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JACCOLD

)> Jaundice (please see notes on abdomen) )> Anaemia (for approach, please refer to haematology) )> Clubbing )> Cyanosis )> Oedema )> Lymphadenopathy )> Dehydration

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Anaemia is a reduction in the concentration of haemoglobin: <13.5g/dl in an adult man <11.5g/dl in an adult female

Anaemia is not a disease itself, but results from an underlying pathological process.

How is anaemia classified?

• Red blood cells with a low mean cell volume (MCV) appear small (microcytic) and pale {hypochromic)

• Those with a high MCV appear large and round or oval-shaped (macrocytic).

• They may be normal in shap~ and size (normocytic, norr:nochromic) but reduced in number.

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Look at the nails; (also koilonychias -dry, brittle, ridged, spoon-shaped nails-can be due to severe iron deficiency anaemia) fingers, tongue, conjunctiva.

Symptoms:

These may be due to the underlying cause or to the anaemia itself.

• Fatigue • Dyspnoea • Faintness • Palpitations • Headache • Tinnitus • Anorexia

Signs:

May be absent even in severe anaemia.

• Pallor • Signs of a hyperdynamic circulation: tachycardia, flow murmurs

(ejection systolic loudest over apex- due to compensatory rise in cardiac output), cardiac enlargement

• Retinal haemorrhages (rare) • Later, heart failure (if myocardial reserve is reduced): here a rapid

blood transfusion may be fatal.

Causes of anaemia:

MICROCYTIC ANAEMIA

/ron deficiency anaemia (iron is essential for haem production) • Chronic bleeding (usually from gastrointestinal or menstrual loss) • Malabsorption e.g. gastrectomy, celiac disease • Hookworm (blood loss) • Pregnancy {increased demand) o NB. Q_ietary~cy alone is rarely ~he sole cause)

I.halas.saeo:ua..m!!lQ.L(an a :-01mal haemoglobin) Sideroblastic anaemia (iron incorporation into haem is abnormal) Long-standing ~naemia of chronic disease

MACROCYTIC ANAEMIA

Megaloblastic bone marrow (oval macrocytes on the blood film) Vitamin 812 deficiency due to:

o Pernicious anaemia (vit 812 deficiency due to lack of intrinsic factor secretion by an atrophic gastric mucosa)

$ Gastrectomy • Ileal disease, e.g. Crohn's disease, ileal resection (>60%) • Poor diet (vegans, very rare)

Folate deficiency due to: _ " Dietary deficiency, especially alcoholics • Malabsorption, especially celiac disease " Increased cell turnover, e.g. pregnancy, leukaemia, chronic

haemolysis, chronic inflammation o Antifolate drugs e.g. phenytoin, methotrexate, sulphasalazine

Non-megaloblastic bone marrow (round macrocytes on the blood film) o Alcohol e Cirrhosis of the liver " Reticulocytosis e.g. haemolysis, haemorrhage e Hypothyrodism • Marrow infiltration o Myelodysplastic syndrome • Myeloproliferative disease

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NORMOCYTIC ANAEMIA

Bone marrow failure: • Aplastic anaemia (bone marrow fatty or empty), e.g. drugs (such as

chloramphenicol, indomethacin, phenytoin, gold, sulphonamides, antineoplastics), radiation, SLE, viral hepatitis, pregnancy, Fanconi syndrome, idiopathic .

• Ineffective hematopoiesis (normal or increased bone marrow cellularity), e.g. Myelodysplastic syndrome, paroxysmal nocturnal haemoglobinuria

• Infiltration, e.g. leukaemia, lymphoma, myeloma, granuloma, myelofibrosis

Anaemia of chronic disease: • Chronic inflammation, e.g. infection (abscess, TB), connective tissue

disease • Malignancy • Endocrine deficiencies, e.g. Hypothyroidism, hypopituitarism, Addison's

disease • Liver disease • Chronic renal failure • Malnutrition

Haemolytic anaemia • . lntracorpuscular defects

e.g. Hereditary sphaerocytosis, E;tlliptocytosis Haemoglobinopathies - sickle cell anaemia, thalassaemia PNH (paroxysmal nocturnal haemoglobinuria) ·

• Extracorpuscular defects e.g. Immune - autoimmune incompatible blood transfusion

Hypersplenism Trauma - marathon runners, prosthetic heart valves Microangiopathic - DIC Toxic- malaria

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Affects fingernails most often but remember to look at the toes.

Cause: Unknown. Possibly due to an increase in blood flow through multiple arteriovenous shunts in the distal phalanges.

What do you look for?

Some signs of clubbing:

1. Shamroth sign: () _ 2. Loss of angle between nail and nail bed (i.e. there is no dip) 3. An exaggerated longitudinal curvature 4. Softening of the nail bed, so the nail feels boggy and there is an increase in nail bed fluctuation (see-saw nails) 5. Interphalangeal depth ratio >1 6. Bulbous swelling of the tip of the finger I toe- "Drumstick" appearance. (There is an increased bulk of soft tissues over the terminal phalanges, very advanced clubbing)

A Remember, clubbing is .a sign of chronic disease, rarely clubbing can develop _ I..:::::::J over several weeks, as 1n empyema. ·

How do you elicit the signs?

1. Look across the nail and nail bed at the "nail bed angle". The angle is normally obtuse'- but disappears in early stages of finger clubbing. 2. Detect nail bed fluctuation: Place both thumbs under pulp of terminal phalanx and try move the nail within the nail bed using your index finger­"spongy feel" . .

What are the causes of clubbing:

Test yourself first: True or False.

Causes of clubbing include:

• Empyema: T: Cause is unknown, probably the result of chronic hypoxia to the nail bed. It is therefore a feature of chronic hypoxic diseases like central cyanotic conditions, chronic suppurative lung disease and a-v shunting.

• Cystic fibrosis: T: Dr.ie to chronic suppuration. • Fibrosisng alveolitis: T: Because of chronic hypoxia. e Asthma: F: Hypoxia characterised by acute episodes rather than

chronic state. e Lymphoid interstitial pneumonitis: T: As a result of chronic hypoxia.

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© Note, if the underlying cause is treated successfully, the clubbing may resolve.

THORACIC

Tumours . Bronchial Ca (usually squamous) Mesothelioma Pleural fibroma Oesophageal Ca Infection Chronic suppurative lung diseases

• Bronciectasis • Empyema • Abscess • Cystic fibrosis

Interstitial lung disease • Fibrosing alveolitis • Asbestosis

AV Shunting • AV malformations in lung

CARDIAC

• Cyanotic congenital heart disease • Bacterial endocarditis • Atrial myxoma

CAUSES OF

CLUBBIN.G

1 RARE CAUSES

Congenital Thyrotoxicosis Pleural fibroma Occupational

• Basket weavers • Drillers

GASTROINTESTINAL

Inflammatory bowel disease • Grahn's • Ulcerative Colitis

Hepatic cirrhosis Gl Lymphoma Malabsorption, e.g. coeliac

UNILATERAL CLUBBING

Axillary artery aneurysm Brachial AV malformations

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Cyanosis is an abnormal blue discolouration of skin and mucous membranes; it is due to the presence of deoxygenated haemoglobin in superficial blood vessels. The haemoglobin molecule changes colour from blue to red when oxygen is added to it in the lungs. If more than 50g/dl of deoxygenated haemoglobin is present in the capillary blood, the skin will have a bluish tinge. Cyanosis does not occur in anaemic hypoxia because the total haemoglobin content is low. So therefore cyanosis is easier to detect in polycythaemia.

Central Cyanosis

Look the tongue. Due to arterial hypoxaemia (there is an abnormal amount of deoxygenated haemoglobin in the arteries and so a blue disoolouration is present in parts of the body with a good circulation, such as the tongue). Always indicates underlying disease (most often cardiac or pulmonary) -so focus on the cardia and respiratory exam. In patients with normal Hb concentration, central cyanosis can be detected when arterial oxygen saturation <90% . Anaemic or hypovolc;:~emia patients rarely have central cyanosis - because severe hypoxia is required to produce the necessary concentration of deoxygenated haemoglobin. Patients with polycythaemia are cyanosed at higher oxygen tensions.

What are the causes of central cyanosis?

1. Decreased arterial oxygen saturation ., Decreased concentration of inspired oxygen: high altitude • Lung disease: inadequate oxygen transfer (may be correctable by

increasing inspired oxygen) e.g. Severe COPD with cor pulmonale, massive pulmonary embolism, pulmonary fibrosis

• Right-to-left cardiac shunt (cyanotic congenital heart disease) i.e. When desaturated blood enters the systemic circulation without passing through the lungs. E.g. PDA, transposition of the great vessels, VSD with a R-L shunt. *

• Also left ventricular failure due to pulmonary oedema. 2. Polycythaemia 3. Haemoglobin abnormalities (rare): methaemoglobinaemia, sulphaemoglobinaemia.

* VSD with a R-L shunt== Eisenmenger's syndrome. Congenital heart defect, first L-R shunt, results in pulmonary hypertension and shunt reversal, then cyanosis . (with or without cardiac failure and respiratory infections). Here cyanosis is not reversed by increasing inspired o.:(ygen.

Peripheral Cyanosis

Look at hands and feet. Occurs when central cyanosis is present, but more commonly seen in poor peripheral circulation i.e. the blood supply to a certain part of the body is reduced and the tissues extract more oxygen than normal from the circulating blood. E.g. the lips in cold weather are often blue, but the tongue is spared.

What are the causes of peripheral cyanosis?

1. All causes of central cyanosis cause peripheral cyanosis 2. Exposure to cold 3. Reduced cardiac output: left ventricular failure or shock 4. Venous or arterial obstruction 5. Raynaud's phenomenon; atheromatous peripheral arterial disease

Causes of acute cyanosis:

Impending emergency!

• Asthma • Foreign body (lumen obstruction) • Pneumothorax • Pulmonary oedema • Hypoventilation due to respiratory depression, e.g. opiate overdose

'Pitting' oedema reflects increased interstitial fluid- results from the disruption of 'Starling forces'. -dictate fluid transit across capillary basement membranes. Pitting oedema occurs in cardiac failure unless the condition has been present for a long time and secondary changes in the lymphatic vessels have occurred.

Usually influenced by the effect of gravity on venous hydrostatic pressure and therefore accumulated in the ankles during the day and

·improves overnight. i.e. 'dependent' oedema.

'Non- pitting' oedema may reflect protein deposition. E.g. myxoedema associated with hypothyroidism.

'Idiopathic oedema' occurs> in women. Typically varies with the menstrual cycle, characterised by marked diurnal variation in weight- reflects variation in capillary permeability rather than extracellular fluid volume.

Clinically:

A substantial volume (litres) of extracellular fluid may accumulate without any clinical signs. Immobile-limbs are often first to be affected, ankle swelling and over the sacrum in bed-bound patients. . Note the upper leveJ .of oedema. - It rises higher up the lower limbs with increasing severity. May affect the genitalia and the abdominal wall. Ascites is common in children, young adults and liver disease. Pleural effusions are common and can be a feature of any cause of generalised oedema. Facial oedema on waking- common in adults with low oncotic pressure. Features of intravascular volume depletion (tachycardia, postural hypotension) may occur when oedema is due to decreased oncotic pressure or increased capillary permeability.

Investigations:

e Do proper cardiovascular examination and abdominal examination. • Test the urine for protein and meas'ure serum albumin level. • If there is ascites or a pleural effusion, do an aspiration (measure

protein, glucose and microscopy of cells) to confirm the diagnosis.

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Causes of oedema:

Low plasma oncotic pressure:

Low serum albumin due to • Increased loss- nephritic syndrome • Decreased synthesis - liver failure • Malnutrition/ malabsorption

Increased capillary permeability:

Leakage of proteins into the interstitium, reducing the osmotic pressure gradient which draws fluid into the lymphatics and blood

• Local - infection/ inflammation • Systemic - severe sepsis • Drug -related, e.g. calcium channel blockers

Increased hydrostatic pressure:

High venous pressure I obstruction • DVT or venous insufficiency - local oedema • "Pregnancy • Pelvic tumour • Congestive heart failure • Intravascular volume expansion (iatrogenic, renal failure, Conn's

syndrome)

Lymphatic obstruction • Infection -filariasis, lymphogranuloma venerum • Malignancy • Radiation injury • Congenital abnormality

A different classification of the causes which may help with the clinical examination: ·

Pitting lower limb oedema

Cardiac: CCF, constrictive pericarditis Hepatic: cirrhosis causing hypoalbuminaemia

. __ Reoal:_n_ephrLti.c_s.yndrome. causing. h~poalhumioaemia __ __ ____ ____ __ -· ___ _ GIT: malabsorption, starvation, protein-losing enteropathy causing hypoalbuminaemia BeriBeri Cyclical oedema

Pitting unilateral lower limb oedema

DVT Compression of large veins by tumour or lymph nodes

Non-pitting lower limb oedema

Hypothyroidism Lymphoedema

• Infectious (e.g. filariasis) o Malignant {tumour invasion of lymphatics) "' Congenital (lymphatic development arrest) • Allergy Gl Milroy's disease (unexplained lymphoedema which appears at puberty

and is more common on females)

Management:

Treat the specific cause Diuretics are commonly used for oedema Where there is sodium retention and generalised oedema, restriction of sodium (and sometimes fluid) intake is rational, with diuretic treatment. Mild fluid retention- will respond to a thiazide or to a low dose loop diuretic, like furosemide. Oedema caused by venous or lymphatic obstruction or by increased capillary permeability, diuretics may be dangerous. -They will cause hypovolaemia, with a secondary hyperaldosteronism and rebound exaggeration of oedema. Rather use compression either continuously or intermittently. Large doses of diuretics, sometimes in combination -in nephrotic syndrome, renal failure and severe cardiac failure.

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lymphadenopathy can be caused by benign or malignant disease. Enlarged lymph glands m~y be an important indicator of haematotogical disease, but are also common in infection and inflammation.

Reactive nodes: expand rapidly and are painful Nodes due to haematological disease: painless

Localised nodes: look for inflammation in the appropriate drainage area, scalp; ear, mouth, face or teeth for the neck, the breast for the axilla, the perineum or external genitalia for inguinal lymph nodes.

Generalised lymphadenopathy: May be secondary to infection, connective tissue disease or extensive skin disease but is more likely to signify underlying haematological malignancy. (ask about weight loss and night sweats, especially for lymphoma)

Investigations: first a FBC, (to detect neutrophili~ in infection or evidence of haematological disease), an ESR and chest x..;ray (look for mediastinal lymphadenopathy) If these findings indicate malignancy, formal cutting neddle or excision biopsy is indicated to confirm diagnosis on histological examination .

Group~ ofJymph nodes to examine: . •·.

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, ·,........: . · 1 .. Cervical and supraclavicular nodes:

Ask the patient to sit and examine the patient from behind. There are 8 groups. Palpate first the submental node- lies directly under the chin Then the submandibular nodes- below the angle of the jaw Next the jugular chain- lies anterior to the sternocleidomastoid muscle Then posterior triangle nodes- posterior to the sternocleidomastoid muscle Occipital nodes in the occipital region Then the postauricular node- behind the ear Next the preauricular node- in front of the ear Lastly the supraclavicular nodes - in the supraclavicular fossa at the base of the sternocleidomastoid muscle.

2. Axillary nodes:

Raise the patient's arms and palpate as high as possible into the axilla. There are 5 groups.

• Central • Lateral (above and lateral) • Pectoral (medial) • Infraclavicular • Subscapular (most inferior}

3. Epitrochlear nodes:

Palpate proximal and slightly anterior to the medial epicondyle. If enlarged, usually indicates pathology. It occurs with local infection, immunocompromised disease, non-Hodgkin's lymphoma or syphilis (rare).

4. Inguinal nodes:

There are 2 groups: o Along the inguinal ligament o Along the femoral vessels

Firm, small, mobile nodes commonly found in normal patients.

5. Popliteal fossa

Very occasionally, popliteal nodes may be found in the popliteal fossa.

Characteristics of lymph nodes:

Site: Localised (local infection, early lymphoma) vs generalised (late lymphoma) Palpate all the groups as above.

Size: Large nodes are usually abnormal (>1cm)

Consistency: Hard: suggest carcinoma deposits Soft: may be normal Rubbery: may be due to lymphoma

Tenderness: Infection or inflammation

Fixation: Nodes that are fixed to underlying structures are more likely to be infiltrated by carcinoma than mobile nodes.

Overlying skin: Inflammation of the skin suggests infection, tethering to the skin suggests carcinoma.

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Causes of lymphadenopathy:

Generalised lymphadenpoathy

Lymphoma (rubbery and firm) .Leukaemia Infections .

• Viral: Infectious mononucleosis, CMV, HIV • Bacterial: TB, Brucellosis, syphilis, streptococcal • Protozoal: Toxoplasmosis • Fungal: Histoplasmosis

Connective tissue diseases, e.g. Rheumatoid arthritis, SLE Infiltration, e.g. sarcoid Drugs, e.g. phenytoin (pseudolymphoma)

Localised lymphadenopathy

Local acute or chronic infection Metastases from carcinoma or other solid tumour Lymphoma, especially Hodgkin's disease

Or if you prefer this classification of possible causes:

1. Infective (see above) 2. Neoplastic

• Primary: lymphomas, leukaemias • Secondary: Lung, breast, thy(oid, stomach • Conne<;tive tissue disorders: RA, SLE

3. Sarcoidosis 4. Amyloidosis 5. Drugs: phenytoin·

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Duration of onset Severity>. NYHA Classification Exacerbating (acto"§:

o nocturnal Sx.

o RQS!tlonaf· S"x -0.;:~~~~ when ~.ing_on_ . s §.;§tJ~ ~.mtliiiQdfsease­

~~ o Co~b· ~. ~aemoms • .9lest pain,

stridor, voice chanse. ankle swelling, conSB'tuHonal Sx

Personal and familv Hx of lung! heart slfi.~se OtherHx:

o fimgloYTlJsnt. bob!z!es, pets. lifUMe o Medication, illicit drug us!

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NYHA Classification of Dvspnoea

I. No limitation of physical activity rr. Slight limitation ordinary

activities .• • Ill. Marked limitation ordinary

activity ..:.. IV . RY ::lt rA.<U

o Sats, Sx respiratory distress, pulsus paradoxus, cyanosis, paradoxical chest movement CVS: - o t JVP, prec~~ia~pu~atiofl, gallop; apex._~ '~<!>.· • .-\ H(:..

• RESP:,., _ . · ~~ --. ~ ......_ _ _ '.,·_.::, \~ - o'· ~ze, creps, ~breath sounds, hyperinflation, trachea - ~:-_, ~'""':. ~ J 'I . .::..~-'C~:·t~::1-;.: ,_,__ EXI§i_ E!Y1fg~: · ., <: _..-~ .. ,,_.iJ:~·r~-,;<lo\c.,-·

• G._ -;;:.....--...) • '"-;r~-H.l-o 1: ema, cyanosis· •, ;. ~

s~ir~~~=-- ~-;;;.o-.--------------------...... ti!IVS!tU!l! ~ • A.ftg

CXR • .eCG

.&t!rlal Blood gas What It tells yotiabou(Q"as flSigCitD 1;,;;•~\1.-:-..

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• Amount of ventiiatlon ..... PaCQr:. 8 kf'a tinder ventilating ·--:-;-- -.. 'PaCOi <-f.B.e.a over ventilating --!. • ,_ • ..., .... : :\~

• Adequate oxygenation · ..... Pa02 > 7 kPa ~~ ··- · , • I~ there a VL$trnlsn'tatch - - ,-,c-:-.;,_ ....... ;t-i.ctt . I~ ,;;;o .. -

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What it m'IB YottaJQtJ~!D -- . .,U ~~~-~~ ..,...~-~ •

• RespiratorY- Coinponent from PaC~

Causes; Instantaneous

• PE Pneumothorax

Acuts lmln - hrs)

· o .-fPaCO~ = respiratory acidosis

• Metabolic component from base excess/deficit o j base excess = metabolic alkalosis

• · Airway disease -+ asthma, COPO • Parenchymal disease ..... pneumonia, pulmon oedema • Pulmon vascular disease -. PE • Cardiac disease

Metabolic acidosis • Hyserla

Subacute ldaysl • Pleural effusion • Lobar collapse • Acute interstitial pneumonia • SVC obstruction • Pulmonary vasculitis

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COPD, asthma Diffuse parenchymal disease Hypoventllatlon

• · Anaemia

• thyrotoxicosis

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Pleural Effusion .~

Definition: ---- ::::> S"C::>O -=- S-\ 0\1\.7 C>u. \\ • fluid accumulation In pleural space ....::::__ -.. · ""JL _ -r \ · """' ,

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Mechanism: J: · • t H. ydro~. tatic p. ressure TRANSUDATE t-W, (.o~.,~.ti\h'd\~Q Do!· I'C&dJ~·h 'S., UU.11"\o. \ ~ 1 ~lli\ql) • ! Oncollc pressure ~ . . r . _ . -l; • ~~I_crovascularpermeabiity } - ~\.>.llo\1c ... ~ ~'\c\~ l ,~d:_e. t\~ Dd·~A.cr..ls .

.C.~ . • teymphatfc oedema U:XIJOATE .

~ Approach: f, \ +tlstory,.axamlnation.CXR (AP and Lateral) V ~ • Does the patient have heart failure?

\ I -~ ... _,0,." ~ - 75 % cardiac effusions resolve within 48 hrs of diuresis

l • <rueural'fap ~\1\\~ U-,10-\a:- -=\fellV:> _ o Note9p):m"arano~'C5Hiuld · I \r\"\CX::~-~ "'---<=.,cu.~ V.J Co r-...-- . o Fluid.Qm!~iiJ..agd.bQ.tj, A-A~t.y ·=< c\t-. \o\-V...iSt<ix::- (lyvu~~ Po-:.+ ~\biJ.\V'o.(0/tXt-ntJv\' · \ "- ~o ~~matfgnantcelfs+~Cu.:S.tW=c\.V.. . ·- c~' ~ 1 tO v\ l . y- S.~ +culture, ~(:) :0-'q . ... -~~ ') ~Oil\. "'-J ~ ~andi§,P~ ~~- __ 0u\.va, V<f~C}I~ t~'c:YJ<:~,T(S

Exudate vs. Transudate o N S - albumin prot > 30g/l = Exudate and <30g/l =

Transudate o Abn or borderline S - albumin -+ use lights criteria

Further Investigations o ~ with pleural contrast -+ dlff benign vs.

malignant.disease o <F,te'jj~ytl!llogy o !fiurther~e-sts -+ <emylase,11glu, .mol, ~Gs. ft:lct, <fungal

·stains o Rtefini1'Did!'sy fo!'iFB'·'titllture-¥1f.iistotogy

Lights Criteria

For and Exudate: Fluid prot/S -prot > 0.5 Fluid LDH/S- LDH > 0.6

. Fluid LDH > % upper limit N S • LDH .

o m~nsraerrthoracost:opy if persistent undiagnosed pleural effusion

Causes: ~rimsUdate:

~ammon

• "!:iHF •

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l'tepatJocChirrosis 1f?E ·-Rerltoneal til a lysis Nepfifrtfd syridrom e Aielectasis

Less Common:

,.....-p\li.JI.oJ-" U'<'.:\~cJ -<~Exudate:

.Somtn2n· • 'tlJlrara•pnenmonjc • 1lMWiti6an!4f

"Ef • "8.8 e 'WSsG!helioma

«ss13o!ifii1oo: • . 'IEmpyflma

:®enstrlctlve pericarditis ~ypothyroldism

Melg's :Syndrome 11;1a!lgnancy·{5%)

!6. other Infections SUbphrenic-abscess - ),s_P,~tic ,

_J.gj§nlc -iitiGto•lmmune !:lisease 4i'..lii!Wfeatltls

'1' \--\}.d\os.-\61\tc f -:: ·Hf ' ~t:, ~--ll\,;~:hue. ~icQ'b; \ ' s '~ v c..o>;: :. Li ue· o.H ~s;_

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Effuslott'ln 'HlY Patient

• ·11S:GstCard!ac Surgery/ Radiotherapy .,r~gJhdU<:ed-"""' amlodarone, bromocrlptine, methotrexate, phenytoin, nitrofurantoin

Commonest causes -+~apo'sf.'Sarcorftagara•;pneumani~B.WCP,itymphoma Dlff Dx includes .... CCF, t!u1d overload, PE, drug related, other infections, leukemia. myeloma

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Definition; • Reversible AW obstruction

AW hyper-responsiveness • Chronic Inflammation

Pathology: • AW obstruction due to ..... smooth muscle contraction, thickened secretions, AW wall thickening • May eventually become Irreversible due to ..... basement membrane thickening, epithelial desquamation,

collagen deposition -+ AW remodelling with smooth muscle hyperplasia and hypertrophy

Aetiology: Immunologic mechanisms-+ atopic Individuals produce lgE specific 8-lymphocytes Genetic factors

• Environmental factors Hygiene hypothesis

Clinical Features: · Cough, Expiratory wheeze, SOB, Chest tightness Ask about-+ nasal obstruction, atopic dermatitis, hay fever, food allergy, GORD, triggers, social sltuatlon/stressors, asp irin sensitivity, family Hx, NOCTURNAL Sx

c\\li-.\C..O.\ \rvo + -::\ c.r \M.c~ ~

. . • • • • • •

Triggers: Dust mites Pets Smoking exercise Cold Infection Drugs -+ B Blockers, NSAIDS Anxiety Pollen

Diaanosis: ~-z::. ·~~is"'! 1) • FEV1 > 15% ·(200 ml) t after inhalation 200 - 400Dg

Salbutamol in 15- 30 mins or 20 % improvement from •

As(llrln lndu!;_ed Astoma .= M K Chronic rhino-conjunctivitis, nasal

)I.C Pt·1S

to Yo=~ baseline 115 7D , 't.). FEV1 >~!after 6 min exercise -s)• 20% diurnal variaUon In PEF on >3 days.!n a week PEF

diary &. r -c...u.:.'<....:;. •

Non - essential Special Investigations:

'FBC + dlff (i eosinophlls) \A.:>e... Ll.k:u.J to .lgE + RAST . _ C'. , 1 ASpergillus precipitins ~~ I ~~~lO{\ •

CXR -t:>\1'-kdtC\'\. ~ \)~\f'\..0 . Metacholine/ histamine challenge Sputum MCS Laryngoscopy

~f-: ~e.

I ~a ·

Day time Sx ..._ < 21 week

Nocturnal Sx <1 I month _,. --

SAB,A No dly preventer

No controler

~I.Gi:>: .

3-4/ week

2~4/month

>80%

D SABzA

! Dose ICS 250-500 Og

Beclamethasone

4_ e.G

•

•

polyps and asthma 'Mechanism .... COXby aspirin 'Mth j leukotriene production by Llpo-

, oxygenase pathway iPG·E,

• 0

•

·em .. f)x

~-~l:lmr"UC::~n ~a~gn~~pir.ati9n ~ · ~r (carcinoid) ~~lll"F.I\t~gU.9D.; •

~1lti'Gitifmtltis I ~0 .~'fi}lP,E

dt :;mmpmmu::LW?:SO .

..... ~Jlt .. CQ.!'\?1? ~~te · -· t

>4/week Contlnous

> 4/ month Frequent

60-80% <60%

D SABzA SABzA

Mod dose ICS ii Dose ICS > +I· 1000 Og

LABzA LABzA

a .. dJ.\+ o:J.~w'O \s ~.Rr:.~ f~-

LRA LRA oc.Cc.-~ ~r-c '-

. Oral prednisone

411\anagement otOhronjc ·Asihma: i'ilon ·Pharmacological:

"'Anergen~avoldaancs Cessatiorr1S·moking

• ~/eight r.edt~ction olliltlmuna~therapy

~

~c) \-\ ~ '2f~ _Ace\ d ~c::.\1( . bdo s

0w~\.!Jt~

~ ~ I

·j_

IJ

[I j

' ! .

I •

atsltfactors: • ~us'lleat.fata11.S1hma

• · ~ag-ss~t;f:~lcatfo.n laltgd~2~se

• tllllfittltf'asthma -Type 1: wide PEF variability __. Type 2: sudden severe attacks on background good control

.,geverltv: Moderate

• rsx ''-J • PEFR 50- 75o/o / • No features ofsevere asthma

May be 0/C after 1 hour after Rx If P.EF > 75% predicted or best

t8ev.ere. · __ \ ~ L""'.J" • emrnR:93·o.i.SO% ·{ L ~% en ~c::o ~ o Ulbl.) • eaz·es . • ~10" • tlfafrulty·w;conwtete sentencelri '4 ,l)reath

e&i~teatanlng • 1'-EF.a&:S3% • ~lh10{'Q2 (need ABG) • PaO, < 8kPa • · <&ormaiC~ • _,..east • ~Is • : Poor respiratory effort . ..

· 'IM!ertif<t'Phone 1CU • . •ocs.~l.ngP.EF .desplte·Rx • «l(4i:I?Sirifri{ftiypoxla • · . GIYP~a • .• _H • · ect1ilUIDon1:1lOO{.;f.E!Sp.;&,(fort • ~c · ·

• ~t!J.Pill.'~fY·'~rrf:!St

~~\t-..0.(~ l-'*b . ..... ·-....-- :-1 " Ju..>d.P~\~.

.... r.,~--... . -· - ··-...(

JJ~E:f ~ Pa.C.Oc..

' . .1~ ~Loc..-

• · •r~Mtcafdlst.tJypotensrohi'-~iTh}'thmla • ~~n

~'f. a.~f~*-._ ______________ __ • ·-f.l;l~ion • .~a·

· !!?fcti'f11qe'i!'!ent • . ~tn.ed~y ) • --~-ll%) . . :~. ·-• ~s:· -~

ita1bMamol5mg nebs-+ repeated doses or contlnous e.g. 5 -10mg /hr

~1pf,ci'fi'dpllliti1B~il'!ttle O.Smg If If poor response or signs of life · threatening asthma ·

1\rrarsteri31as as effeCtive as lVI - 'tJO~g pr~ntso11n-~:aaysr'O"'f::-·" . *iVm'edtlsi!ne"'l®t;qg,fvl ·

Upoor response ·

~lnophYfllne loading dose"'SrilgJkg""'vei'~O!tl'lln . -> maintenance dose O.Srnglkg @ {0.5 x kg) mVhr

.

.. .

. . . c._ .

~-d. ;( ~~~~- '( ~c~

Discbarge When: . • ~e· ~s .and on lflli;!aled:.-medS'~4 :l:lrs \w~ \o \i;@;t}'\}~ =._ \

• ~F•~ro-:p~pteg.~r-ibest • "-'!Minimal ,.P.EF~tilumal variation

·L/C.o\IV._.o..

l/"~ o'f~~ . v-p~ {_ ~ 0 w---\.1.~ v--'f' <A CO~::::> 4-.:::, IM-.....:~\~ V"fh ~ 'T ~ \\* ~

V/' I • c (':. . 4 I I c..,x:v~;,.,_, O'l\, u~u..Al ()-['\, ,o\CLJ~, ~~-

__ ... -... .. -\.- L-.A1S -z _A .. -·· .... . ........ .

+ LAI-c.)

i J_

\ 5

\

Definition: • Acute Infection of lower respiratory tract with Sx of consolidation

Clinical Features: Fever, malaise, cough (productive, non-productive, rusty/green, blood stained)

• Dullness to percussion, L chest movement, bronchial breathing, tachypnoea, crepitations, r vocal fremitus

CAP Ae!loloay:

Typical: •

• •

,. . ~lco.s\y £t·..(; ~ · S. pneumonia: .

o i age, co-morbidity, acute onset. high fever, pleuritic chest pain o Bacteraemic: COPD, alcoholism, OM, dry/ no cough, female o Pleural effusion ·

H. Influenza S. aureus

o Recent Influenza like Rlness o Muii!.Jobar. cavitation, spontaneous pneumothorax

Atypical: • Leglonella spp

o Younger pts, S!Tiokers, >severe Infection, no co-morbidity, neuro Sx, SX of multi­system disease

• Chlamydia pneumonia Mycoplasma pneumonia

o Younger pts, previous Ab, ! multi-system Involvement. o Extra-pulmonary Involvement haemoptysls, skin & joint problems o .·Lymphadenopathy + • Klebsiella pneumonia: o !Plat,leukopenia,male .------~--.... ~ f)'~ic,

t~J- .. \ ; '. CURB-65 .'-. . I <;.-o,S

RjskFactors: /f.il~'~- -~· ~~-~·c;)l<J!:rv_ · .. . • .• .• ,· .. _.t.._\ :,f • · .COnfusion ~ ~~. · . ·\'·?~ -.=Aspiration""·•:.• · · · 7 ··~ · ··· . ;;~~\~. ~ t. ? • · urea~ 7mmo

: ~~hoi =:f~~~ · ·. ! (: . :~;·!~t~~ 60 ~~~\{ Oral steroids .-.:....,_,. !'!;lil.~~~ -\ &. ~-- :..Age > 65 7 -·-- · · · · - · - j Immune suppression .:=;:-· ··.,:::-. /- · ~ C:... 4 °~ "> 'Z'C

• HIV WIW~ ~)'~'d . ch\_i;;_;_.:., • COPD ·· ~a\(~~<4~t~~~~ lSl. ·w. ~..;l\.· \1 .. -~~1,•\.J:'--.... • Institutionalisation ~.· . · : ··.·· .. ..., -~~ ~-- · ::~· ·~'-~'\0'00.\

-~--- . -- •' if',.~~-[Poor er.gg,nostlc Sx: 1 . . .

·-> 2iiave ·t risk" of death and should be Mx as severe pneumonia .• 65 yrs ! • · ·co-extstil"!g disease

Respiratory rate > 30 Confusion

• BP: systolic < 90mmHg, diastolic < 60mmHg .:Hypoxemia

• Urea >7mmolli · Albumin <35 gil

• wee < 4 or> 20 • 'Mes: tve blood culture

• • •

•

•

Radiology: bilateral or multilobar Involvement

0

0

0

~-0

\,

0

..a 0

. o

I \

.FBC + dlff + plat ,u&E + LFT CRP Blood culture

•

•

c~@~ ··6.~·\ .... W'O.OJd.,t:)e 1- "'- a::;:~\~{fr:·co~ic\ov +

Uo.c:::.~\lde ~

Ce~lo;f:blo•U

-z =-~~\ B\oclow-.-~, w-.0-0b ~'oe ~ -=- ~;q\J...careh;:.cu : \)e\J'. t ~ -- -···-·- ····-

,• ~\.>-.~'rc~ ~\b\k:>e.

6

.. ~- --- ----. ........._ Maaagement: .--. :~.;;-=-~~----..

.:~~ l~~ g~l~i. n: l ,~ -'~~- I,

Analgesia , / f"" 'CA~ o.., : 'j ' Nutrition i ;~ - i I

., / / Physiothera:\'y ku\\~-h'-o{; · /

\ ' , · /

en~ibloUcs: \ :; \ z~d,/_./ ,_ \' ' ~ ._ -........ _: -- .r··

· ~ ··>_.-Pfeferred Mild $ _oxm50Qt!:ll:rtds llP

Moderate ORAL: ~oxil 500mg tds po + Erythromycin SOOmg qid po

lVI: Cefuroxlme 750mg Bhr!y + Erythromycin 500mQ 6 hrly

Severe lVI: Cefuroxime 1.5g 8hrly + Erythromycin 500mg 6 hrly

Leglonella ClarlthrornYcln 500mg po /lVI +7- RifamPicin

Chlamydia Clarlthromycln 500mg po I lVI Haem ph flus Amoxil, augmentin, Staph aureus Fiucioxacillln 1 - 2g lVI +/-

Rifampicin 600mg od/bd po/IVI MRSA: Vancomycin 1g bd lVI

mJ1T£n:i;!ikll progress esp. elderly pts ncorrect Dx econdary ex

o Para-pneumonic effusion o Abscess o Empyema o Extra-pulmonary Infection

Inappropriate Ab Atypical pathogen

o TB o PCP

Impaired Immunity o -HIV 0 Cancer 0 .Overwhelming Infection

• •

- GG"l!ptlallzatlon· Criteria • •tures"Ptsevere pneumonia

~oi'b1di1llness

Gl@l'\Q$1$ f!ml\blol:;lal~hs91\<;lation ·

• ~s

Alternative _Erythromycin 500mg qld poOR Clarlthromycln 500mg bd po

lVI: Amplclllin 500mg 6hrly + Erythromycin 500mg 6 hriy OR Clarithromycin 500mg bd

lVI: Augmentln 1.2g tds + Erythromycin 500mg 6 hr!y OR Clarlthromycln 500mQ bd

Tetracycline if C. Bumettil psittaci Cefuroxime Teicoplanin 400mg bd lVI +/· Rifampicin 600mg odlbd po/IVI

~~Jlai!te tRjs~ lgd!xj~ Influenza: ~Chronic lung disease ~ · l ..

• -cardiac, renal, liver disease ~ • Diabetes ~ '

Immune Suppression ~ .. • Age>65 ~

Institutionalisation ~~ Health care workers '#"'~

o Cllln EGG .ALLERGY ,.~

,.lJ.Jtr:~~: I 0 ~

~~· !:'IDa!. Hy;u'j,M.?M, ~ IWQl!!M-Sl-tP2Jg¥1.l9.n .

_i

I •• I_

7

• Other options • ab: • Prophylaxis : BACtr!m 2 tabs d!y pn co, > 200 • ~

Wosocomla! Pneumonia ---{::>\.)~\~(' Definition: ·

•

• . Radiographic lnlfiltrates and ~t of new Sx > 72 hrs post admission

Aetiology: G-ve

• Pseudomonas • l<lebslellla • Bacterodies • Clostridium

f!BOO!'_fi@OCs: • ~0- .

A-~ S--~~ r '~ AuiOJJJ 1?- ~{;C.. -e. - tid;oS\d.a.

• ~~un.g -clfsease;,eo-rnor'bfdliY • ~;t;\11 • Chest or abdomlnalfl.tmJery • Gl.,nlcal'M~atlon • NG feeding · · · • Previous Ab exposure • Steroids/ cytotoxic drugs • Poor dental hygiene

Management: General:

Pts developing Sx < 48hrs post admission most llkel)! C~ and MX accordingly • Assess severity • Oz and IV fluids • Cllndamycln or dprofloxacin In penlcUIIn allergy

Antibiotics· ·Preferred ··Alternative

~~Ill ~itinm)t;;5g·1VI ,fds Flouroquino!one lVI OR .. lmlpenem SOOmg qid lVI OR Meropenem 0.5- 1o Ids lVI

tliiut!Qmonas ~n 500 -750mg bd po Ciproftoxacln 400mg bd lVI "CeffilZiaiMe 2g Ids lVI + Plperaclllin 4g tds lVI + GentamYdn OR tobramvcln lVI ' Gentamycln OR tobramycin.IVI

~eel ~g~l~~~~:~:rin ~lqmf!~lii 8!rfju!tian: . . .

• . ~l1fl'8llon of exogenous material orUggg~mglllnQs r correlation between volume of aspirate and developing pneumonia

- ~~r. · ~~coho!, drug overdose, post-Ictal, massive CVI

o ~3Motor neuron disease. GVI

• ~~-Sl!~e e: 6 !dl\i&9 to stomach or oesophagus · o · Mechanical Impairment of glottic or cardiac sphincter: tracheostomy, bronchoscopy, NG feeding

.• ..-m:»< ~ t volume vomiting, t volume NG feeding, feeding gastrostomy, recumbent position

• ~fflem:ea:li.Oim!?' kif•~ CE::l

Management: ~. Gtumt1sal~s

General supportive measures. suction if aspiration observed steroids - controvertial but may befefit XRDS AI:!.- usually given to prevent 2ndary bacteriallnf - o Cefuroxlme + metronidazole OR·

o Penicillin + .clindamycin ~. -~rJ!I

• Ab necessary -!Q§~mJ~~~lt!m!9Pm.e o · ~~~ -· n . Clt:no· TIS'Etfb\itid

.let ·ifMc1ul .c :-Jt -~!!on . ~ causes lhdOde: saline, barium, ingested fluids, gastric contents, drowning, foreign. body

• Mx .... tracheal sUCtiOn -- -

8

0

H-~ . \r-.<;.\u A-~ IN - \U.yco \-1. u-~

td-\IN:D~\:

. ~ (fulrrlonary·:re] eetJnltion: ~ C!>1r\ · \ _ _ · ,1'\\ p, ~

• Caused by ·J:(i acferiumjuberctifosls .--- ~v.o~ ~"'''V<-' · • Spread from rimary focus to hilar and mediastinal LN (primary focus heals spontaneously)

Direct extension -4fi!tJma!):~ctiveTB ~e\ltal extefislon IN!th rutusion

• . tft.:iamato~enous sprea.d -'fi!Mi/UafTS + ra Meningitis ~.... NddGOcJV

Predisposing Factors: Extremes a~ Primary In~ < 1 yr ago t IB contact -!::!.LV

·~ Co-morbidity: CRF, OM, Malignancy

· GIT disease assoc with malnutrition

etansls: ~ c;.~ S ·

eixgl!lt\'l~S!OOP!~~iQ!JMGS~i:i'ff"ArJ3 (ZN stain) OR l!l.e~~mtms • . ~·

0

. (;;;;l...._""~r;tJrl,:•l\ \. - .~ :.C 'f~"a:.\~

..J_. \0. _, . ~

GfiRiearFeatures • •t!!ahill!l~tiuctlve > 2,Wks +/::@laemgptysls

POO,C!htesolved pneumonia, liilght ·sweats • ~weight

· • tleMhema nodosum • HSM • _,hadenopathy, lobar collapse • •f:lsolldation

@eural~ffuslon • ~yon • •t~!Jiitis

(jijlmtSnary: • . Massive l!ft!emop~is • $l!!gt~lmonale · ... • ~. emphysema • Atypical Mycobacteria lnf,

· aspergiiloma • · fB~M!oteqtaltaiCiflcations • ~t\f:lffuslon • c@qlachl~ctasis

~G!!il!§~ema .tilung .abscess • @!:!Wtii:ti'te'Jungj!l_sease _

{!ami! Qefinlt!on:

• .ent~IFmi1f1NH (2 or> first line drugs) ~~. -\o Mechanisms of Resistance: . ~ .

• ~d through selection of resistant mutants

o ~~l'l'aPY o . ranee

• • • •

Treabnent:

t\-e.J~OJ.-s. l1S f Co~ :C \}J.l~ ~\\S · rtt:-V .

., §

... N I

= 5f 3 ~

H dl :> S!!. < "' -g. ... !£ ==

Deflnltlon: • ~B plus resistance iof!*!JilatiQi!IE!$!and 1 or > lnJectables

.:: "' I

}!} ... ID

i .. i e ·= c .. iil ..

· ~ .. ;;; 0 ::s

0

0

0

Kanamycin Capreomycin Amikacin

0 :> -g. e: CD

10

~ \)ec¥.\o_\k\ --4:> 'eo---:: -t> ~~ . tC:Ca. tat./ lz..l ~s-

, COPD ~ .. _(". ·~ ~u..c>>..s ~focu~lc;,,......._ +

Definition: . / C~ \J\. / s\.t-A. \y~( &:f,' • fg10tphic-prooresslve MV-obs!nJctipn Including ffAtn1!5ern&an0,Chmn'£ br?oC"itis

'l§lxei:IAW,i:ibstruptlon "1:..;;>{~ ·· Cillbim!ll..or·noreverslblllty with bronchodllators Minimal variability in day time Sx Slowly progressive and irreversible deterioration In lung Fx ._. worsening Sx Chronic Bronchitis: dinically cough sputum m_.ost days tor 3 consgcrttlve months for 2 consecutive

~ . Emphysema: Alstaloglcal Ox of'festruction of air space;s distal to tecmloel bronchiole

Pathology: ~ce).\) • ~deoulfg)'a'nd hyperplaslav (squamous hyperplasia with loss of cilia! Fx) -~~,:o.~ .. ei'6'f.llo 'lnflammatlonand·fibrosls ~:a~. o Otw.nysema c~-~~ IV:0.\1"-Cclt-a.t t::Ur~u..\o.' ·

Thickened pulmonary arteriolar wall and remodelling -.due to hypoxia -.. tPulmon VR. Pulmon HT, .j. gaseous exchange

ll'"""""""""'"""""""""""""""'"'""""""""""""""""""""'=""""""'""""""""""'il·-;-ca:>D---=-\ Classification NICE 2004 Aetiology:

Mild ~ FEV1 50- 80% predicted. /"_0

\ ~~ :1·

may or may not be Sx (cough, sputum) L.A. )\u Moderate-. FEV1 30- 49% predicted, d \\JDi O. ·

• • Smoking "'-.

@. _ =· a,-Antitrfpslndeflciency (~.). "==> _ j familial risk

Air pollution/ 2nd hand smoke

• Occupational ~a~\cl \ ~W\1-~ c').b.~ .

Clinical Features: Symptoms:

o .Dyspnoea ,~i:-..dO;y,~@ ~\).;\ • Cough usually chronic + productive

Wheeze L exercise tole ranee

Signs:

• usuallySx Severe -. FEV1 < 30% predicted, usually hypoxic with Sx cor-pulmonale

• •

Tachypnoea -~·. 0.~ '· Use of accessory muscles ·. \\ ~~ ; b ~\ef>.~

• • •

0 Hyperinflation (barrel chest, hyperresonance, t heart sound9 j expiratory time ~ -;= '= -sacs. Pursed Up b~eathlng (auto PEEP) ~ breath sounds +I: basal crepitations t ;i Sx of cor-pulmonale (anckle oedema, t JVP, warm peripheries, pleothoric conjunctiva/face, bounding , pulse, polycythemia, flapping tremor If acute jC02)

~clallnvestigatlons: o ~1ilri\FEx tests ~~FRC+~RV due to air trapping + .1. elastic recoil

~!J1;{;$;tj9% .- Minimall no reversibility -4lf.jy~i:ll'J'fh3tlorowith black lung sign, -~r,st~r~~qibs 1 t, c..\1....\ • ..... J.l.'lle -~U!i!!l~d :heq~!"l'!l~pl)ragms 0..'- \.o.l. ~~cytherola

·.D!ff Ox -Asthma Bronchiectasis .Bronchiolitis LV failure

...;.,.L,llH IAH

e..I..J\.\ 1 (.__M-\ \ 'e_A-1::;:.- ( ~"-.~~~ ~ ~{'.. \.) 0 .

A- As-\\-.\fJ~ "g-~\o~~s C - C7c::,\i:C .§ ~\s L \J fu.~ \.IJ.\e .

P.narmacorQfllc·al: MILD: MODERATE:

SEVERE:

-+flra'e&"d'iir1e'i!Ci!'le, :W~!DID.9'~~-~Jlgig.l;ii5S, education -+'ill,ll!l!&tcJSelmtrram:e; quality of life, .1. hospital admissions -+'-'MO:SS.'iifiGb,!l_~et supplement if catabolic due to WOB

..... 'f9"r-evsnt1lnf.te~te~r;;ilxacetbatlorts :!::

SA82A or lpratropium prn ~ regular lpratropium or LAB2A '; 0 ~ -z._ 0--~C,\J'-(S.-\--

'FEV, <50 add Inhaled steroid} . ~ Oral Theophylline ~ s

. ~

/~0,,. c.' s6\ •b ~~~d':::, i) )\IJ'-..\:~ "'-''-'-'~CO..'\'-"~~

0

~ Combination Rx tpratropium + SA62A Oral steroid trlal: 30mg x 2wks Steroid rasponsive if FEV, improves >15%

~ CD~~~bid'-

0 \"'-~~~y\~-1'-~ s) ~ S\Mo\.~~ G) Oz:

11

' I

Other: \~~ .

L TOT: for pts In resp failure Pa02 <7.3 or normal with any 1 of:

. PACh( .~ •

•

~i'y: • 8t111!1ialtee!h~Joo.II'IIIDlmmy

• tsu~olumnecfllot!OifJ1Jt!ll'gery· • ~~nt~ young pts with a1-:- Antltrlpsln deficiency

ACUTE EXACERBATION of COPD

Aetiology; • BacteriaV vlr:allnfection • Rupture of bullae

· • Ml ~<:~~

~-PE

Management: ~~~' Controlled 0 2 Therapy

24 - 35 % via facemask -+ keep sats 80 ... 90% to balance hypoxia, hypercapnia and pH

~ tlebullsed .Bronchodllators

Severely dyspnoeic pts may benefit Salbutamol Smg 4 hrly +I· lpratroplum bromide

'~ ·steroids

Hydrocortisone 200mg lVI stat then all pts get short course .Prednisone 30 mg po x 2 wks

.! Antibiotics

Only If Sx of lnf e.g. New CXR changes, pyrexia, t CRP

J Antibiotics

Only If Sx of lnf e.g. New CXR changes, pyrexia, t CRP

~ . Physiotherapy

~oResponse Consider lVI Amnlophllline, repeat nebs, consider Intermittent CPAP

'Still No Response Consider Intubation If pH < 7.26 and PaC02 Increasing

/

Oz_ ~'-Sot L{ c._o<t-\e.5l

fo~i.'vJ\'o\tC}S.

p~?\·0~~7'

l)o .~~ · ~ ~ . 4> Avv..·\r-.a.p~y\l ~ -

-& l}2o . ~0~ 4>~~0-b..

12

Interstitial Lung disease Of . ~~0:- \Y"'-\J ~~~e\l·

Definition: ' ·~ ""' Heterogeneous group of diseases{ characterised by alveolar wall thlckenipg}flrflammat§ry cells and) ·. .

-Exudate . .. Sl w r resslve loss of gaseous exchange · \ Progression; fun sti nes ~ ..... ventilation defects and ; exertional dyspnoea _. respiratory failure--( /1 . V0 ~\ ·+ pulmonary · . tJ ~ : ..

Classification·) ~ T( nown etiology: l!"\ l I'"' · ~11 \1\

~aU0t:~ai$.<J~~~e:ubestosjsfthei41Ujr>sis . _ \\. _\......., __ ~A ~/ 'r'- ~~:\ • ~jilimfl!!re : li~otle, bleomycin, sulfasalazlne ,~\:1~ . Cr ~ · • ~l!l::rtlOnS:1jtxtl'tt\sf~~leml9@1lt,ESQIIUS u'o'· ~l

1\ 1 I tr~"-"~ .

~~--'-. .: ...... J(I!I:Ilral '-'-\~ Assoc with S.ystemlc Disease: ·

• •

Whats Important • · Remember to ask about~__, birds, mushrooms,

exposure to malts

Clinical Features: ~cugatlggal,flx frogresslve exertional dyspnoea . Q.!tllil& ~~lg Qi§Rim§.

• Non-productive paroxysmal coygh ~ Abnormal breath sounds ---- _fb....,..,.,.,.,.,...,.....,....,"""',_=....,=="""""""""""'""""""""""'"""':"'i""""'"""'"""""""'"""'~ Restrictive pulmonary spiro~try ---r:> .\ 'f'O::::..o\f~y I Oo'/J\

1fclo y aM->s ~ '· Abnormalities on CXR or CT ~ /' \ r '--\

Special Investigations: .. CXR ABG, FBC, U&E etc. ·Mainly dictated by cljnlcal fiadjags

Sarcoidosis d4Bl22'!12!iiiAJG ... •

Pathology: Non-caseating epltheloid granulomas R!!solve spootaorua~.llx

-M~stations related to ~ or~an Involvement Ca metabolism may be disturbe : =-

o ercalcemla

0

0

Head: - 0

~a=~

,:Diff Ox- Granulomatous Lung Disease • Sarcoi@sis

!B • Wegner's Granulomatosis • Leprosv ~ Brucellosis • Primary billiary cirrhosis • Hypogammagfobulinemia

Fungal infections • Schistosomiasis • lymphoma • · Chron's d!Sei$Se • De Quervain's Thyroiditis

0

0

0

0

0

~~us pemig: l:lli.!i,gb tjnge to nose, cheeks and ears-. assocwith chronic disease vm~naa enooathy

=oru;.gtisrenlargement afsy

~ung~: 0

0

13

~ ·gzakwor"'b • Abdomen:

~ , im£oo!!~~us uw s18 ase

0 ~eghmcaiGinosl§ 1 kldpey 5mgv o · yeercalcurla .

~: • o ·

0. I. II.

Normal Staging

Hllar Lymphadenopathy Hllar Lymphadenopathy+ parenchymal Infiltrates Parenchymal infiltrates

0

· 0

~r:

o§tenoomsts Arthmpa!h'es gpalaggea! boge mtt

Ul. IV. • Progressive Fibrosis, honey-combing, pleural

Involvement • o ~erlph;ql mumgathiM o Skip plaquos o ~ear lpfj!t@tlpn

~ i§isimfJM:J!R'ex Onset either ~e: arthropathy, wallis, hllar Lymphadenopathy, lethargy, fever •

C,b&;a,gj,c: paroxysmal non-productive cough, exertional dyspnoea, extra-pulmonary features . -~~ .

~pecra' JqyesllpaUoo;;: · llnica! Approach:

• MAKE Ox: cllnlcal~lc + HTCT +/~ · • ASSES SEVERII: CXR, m,, PFT;tii...OODS: - :

• U&E,~LFT Immunoglobulins }

·Q

STABLE VS PROGRESSIVE:WSB· Pfi. oJSimetry ACE Urea, OTHER: • •

MAN1FMENT; .STAG I &II:

.. • •

• · S;dOm require Rx. may resolye soon!aneously .. ··Severe systemic features: short course steroids+/- NSAIDS

STAGE Ill & IV: · • ftjmlc steroids --> 40mg prednisone dly for active disease x +I· 4

. , II response then l • Maintenance dose - 5 - 15mg taper off slowly over few months, long

.tenn therapy· over 6- 12 months

Can be T In Active Sarcoidosis

• trnplasma •

• .Coccldiom~cosls • :BI§lgglaiiW:sS • Recuqent lmesuogs

· Maliinancr: • Lymphoma • Mediastinal Tl.ITlours • . Ceukemla

Dusts: - ~ • • ~s

Q:!!mr: Extrinsic anw;ahii Alveglltis •

• .· bvlillilliliiiWiilll;!lll!liirJ.emla

14

ACUTE MASSIVE PE

ajar hemod~namlc effects: "! CO; acute l"l failiifii; d1sordered V/Q

ratio ~eeL 4>

ACUTE SMALU MED PE

.Occlusion of~ · pulmonart aife!Y - limlrction ± effUSion

CHRONIC PE

Chronic occlusion of pulmonary microvasculature; .pulmonary hYPertension, RH tailure.

j~MPTOMS

~

Major~trnycollapse.~rdla, b)1110ti111Slon~4'P{Iop:1hYthrri"P, Gn"~rrt

Severe~sls, no local slg~? ~'),

~ut # -~b;ott<11sed WdiU!fiijlhlagll't;llraiJitat!Ons, «i!Sfon·(usuaUy blood stained)

4f'..effusloncdefects·not matched fMf ~l1!1111atlon $Can

UiiloiW l"'!pO, or ~l!l'iltl,~rr-on (ormal ~il!lsiifitQSllng

-J;'MQ~.A!IJGI<:JGf0PH-f" ~~~.~Ox _y!$t110·atm

l@;~ll)!lve'Dx

--'r-b-0~~

·•

Radilo

~~t~'!! ''Jj¥ need lung ~iifisr : o connrm

,.,.--=. J!'fk·~Fa£to(!·for vt:E 8or ::!!! -____ ,..-. e:ttQer'y

- ~l!:lor

<!l major abd/pelvic, ortho, post-op ICU care

11bgnancy e late trimester, C/S , PET

'ill'l!1i!!i9'1~ncy -4!1 pelvlclabd, advanced or mats

~r;JJmb;probl.ems, ~6billty

G'i/S e Cong HD, CCF, HT, CVP, superficial

venous thrombosis ~agens

• COC, HRT ~U!callaneous

• - i'vlalignancy, neuro disability, thrombotic d/o, obesity, 180, nephritic syndrome, myeloproliferative disorders, dialysis

Special Investigations: investigations add wt to clinical suspicion thus must asses probability of Dx Including clinical pic and risk factors

~ ~ ~Ira! QT. W., Doopler le~ns ~:·= ·~--,.

o If probability ! then -ve result excludes PE o If probability j then +ve result needs further

investigation o -ve resu t unheloful in • robabillt cases

Do not send unstable pt for Dx Investigations. ather Rx. .¥.,~.~?.is first line before CT, but do not delay Rx by > 1 hr

CONSIDER IN PTS WITH !Jnexplalned SOB 9ollapse tiew onset AF SxRHF ~Effusion -· SWI!-·~-----·

l. - F\,j::-0[().! ~Y~:J,_n~ (~~ ~--- __ /-:':

15

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• • •

Clinical Features compatible with PE

: B;!*r~s • -+t- eleu ce~r~

Plus 2 other tacfoiS · 1. Absence o:~lfif:Jw~~n 2. ~ceof or ·

1 + 2 _,. HIGH pre-test probability 1 or 2 _,. INTERMEDIATE pre-test probability Alone __. LOW pre-test probabiUty

E;1anagemeqtl General: . - • Qa 1QPf10

• ~s, baseline bloods (Inc clotting profile)

~palge;!a - opiates but beware Hypotension Mx ~rdiogeglc S~k wl1li lnotropes If Massive PE causes ! RV filling

• • •

Anticoagulation: I lVI~ . .

o 5000 - 1 0 000 IU or BOIU/kg as bolus ...!. _ _ . 1 ( D F-) \I o Maintenance dose 1300 IU/hr or 181Uikg/hr r'1f0~\}<... \L-t-\ LC!:>\\que_

Thrombg!ytlc Th~raf" · l iz iJ/ • o Indicate iF ~tensive, Sx of RHF, acute coDapse ~

o · ~freptg!sfgasFo Odd U over 20 mins with 1 00 000 Ulhr for 24 hrs o ive ~~:~~sfnl£ to prevent circulatory collapse o Stoprc 4 fbmnzb01"515 and restart la'li'.r o .Cf! In actiye bJeedlpp , recent Hx of ICH

Embolec • . o done, . o For acute life tbreaterung massjve P!i

16

Qef\nitlon: ~ ~ • ~A~@·rest~uryngexercise

Classification: 1. Pulmonary Arterial HT:

• -~rlmary pulmonary HT (familial, sporadic) • Related Conditions: HllL.go!le!WD rucu!ar.djsea§e. portal HT, Drugs + toxins

2. Pulmonacy Vegous HAi • . Le sided Heart or Valvular diseas~

. • Extrinsic compression of pulmonary veins 3. Due to Respiratory Diseas; gr Hypnem'w

• COPD. ILD, sleep disordered breathing, chronic exposure to j altitudes, 4. £!Jron!c Thrombo!lc bimease;

• PE. sjck!ft cell disease 5. Disord~U;;t directly affectlna Pulmpnaer: )(aelfMiaturs;

• SarcoidOsis, ~lslosomlss!s • PUT'monary capary haemangiomatosis

Clinical:

~

C5mpto? · • Exertianal Dyspnoe<;~

Eatigu,e Ai1cjli1al che§t oain

a Orthopaoea Syncoe_e

·Haemoptvsis

0

@ 0

0

0

PFT Bloods

0

0

0

0

Management: General:

Anticoagulation Oo '§7goxin a~d diuretics Contraception and immunizations: influenza. pneumococcus

17

18

v '

Lung Cancer

CI;U:.i~ Non·small Cell:

§..qiJamous:, · o most common !YPe

o may present as sin I~ s CXR, but may form multiple cavitatory lesions o often present wi er~lcem

Adenocarcinoma: o Not only smoking related, can occur in sqars or Ubrosis a May be primary or 2ndary from other sites

Alveolar cell carcinoma: o Rare o Fluffy air space shadow on CXR, o triittr sputum production

3rnnll Cell : 20 - 25% of all lung Ca Usually not amendable to surgery, chemo/radio sensitive Untreated extensive SCLC has mean survival +/· 6wks

·~ -.,..11;!> I \ ,.~;...._ \ \'"!:.. 1__~ . ._ ~ ! 0;\'\1'>. ~~ "\ .~"rC'jl{"'-,

t4g ljJ:tas~~ the lung~_:i_il.rea5Citli:fne¥;ut'eQ.i"S, · testes; ovafl.;iflir;~~;~ From the lungs: liver, bone, brain, adrenals, skin

. ... ~ ....... -. •• •• •it • •• - ... -~· ·· ..... . - - "-·"" . .:.·-: .. -·..:.....1

Cliul.c.i!l Features: ~llal Tumour effects:

C..QYgf:l: persistent or change from previous Ha~JlP.tllsis ~In Un-resolvlnq oneumgnla or lobar collapse Wheeze or stridor Siim !Idee pain Pleural effusion Shoulder pain

~~'\O!IOPiastjc Syndromes: --.): • Cachexia and wasting

Dysphagia Pancoast tumou~~ ~igJI@I)

Metastatic Tumour effects;. • c:&.I.Vical/supraclavlcular lymphadenopathy • Palpable liver edge-• Bonspain

Neurologic sequelae

~)· ~: . ... ~ o More common in squamous and adeno. but can occur in any :.1 . ~

0 Hyponatraemja hypo-osmolality price osmolality ttrrt a Causes include: HIV, Post major surgery, carbamezeplme, Fluoxetlne, pneumonia, stroke, psychosis

SCLC o Management: Fluid restriction, Demeclocycline 450mg bd (tetracycline derivative, blocks ADH in Distal

tubule, may be used long term)

.·:~

,'\. -~·) .

Ectopic ACTH: o Pts present with Cushing's syndrome, but due to rapid development the biochemical changes

predominate o Mainbt In SClC

Hypertrophic Pulm eo-arthro at : o 1c ening of periosteum esp. tlbja fiho da radius y!na o ~ny cell tvpe, mostly in squamous and adena

svco: 0

0

0

0

Malignant causes: Lung Ca and lymphoma Benign causes: granulomatous d!seasR !ntra-fboradc gojt~. CVP, pacemaker wires. Clinical Features:

face and upper body oedema with pleothora and cyanotic appearance venous dist~ of upper body and face E#iXJQWQQ;;;:> facial plethora, ~.stridar..qf;t~t.,®i.®A~~ePAX§Jie.ad..fe&!a.w mJn~ Dyspnoea Headache worse on lying down or bending forNard Other Sx of malignancy

Manage according to underlying cause

~~~~(;ial _ lpv~stiqatlans · . CXR ....... UlW"'...:.:::D;

0

0

0

0

0

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&)u~E,;MP; • iipu!!Jm gVtO]I/ 9U -o, pleural tap .-• F.NA or I.N 8 • ~T/MRI } E • Uone Scan ~ ' rerscan 3 I! • Diagnostic t~ :

o Bronchoscopy o Radiologically guided lung biopsy if

Newly enlarging mass not amendable to Bronchoscopy Multiple nodules In pt not known with malignancy

• • • • • •

Persistant undiagnosed single or multiple pulmonary infiltrates • Hilar mass

:3~ ~~(:~Q:

• Staged using TNM system S_(:LC:.

• Staged as limited (ipsilateral hemi thorax and supraclavicular LN) or extensive

e:wenJi. • Stage I and II usually amendable tcJJ.\!~!Y • S..~~Y an..~ Radi~~Y usually reserved tor Inoperable patients ~

• • •

L!!lJ.il§l.i.~J£ may benefit from ~ cpe[1.2tt}W,.iJPY mainstay qf~ may Increase survival t~1_!months in limited disease _Radiotherae~ also u~~· ~

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~ . ,-.::.J.,!, .... ~ . ..... . -.~~-~··,r . .-.. ·oAJ,-.:.....4~ .. jo.o-~1f

~ Pulmonary Oedema { 'I'IIT•"·'· .... ~-~·~.-., .......... ~...,.~~· .. .;1 ,_>.!;~

Q~;tlnltlon :

• fluid accumulation In the lnterstl1ium of the lung

dependant oh hydrostatic and oncotic forces .

A~Y Direct lung Injury: ·· Chest trauma, pulmonary contusion

Aspiration Smoke inhalation Pneumor]ia 02 Toxicity PE I reperfusion injury

CVS Cause~: LYF post Ml or IHD rvl~ Arrhythmias Malignant AT

Injury in T Hydrostatic Pressure: · · · High altitude ·

Neurogenic Re.~expanslon in]t.try

Haematogenous Lung lnlury: Sepsi!l Pancreaitis lVI dn.ig'use eg. her9in

• Cardiopulmonary bypass Multiple transfusions (fluid overload)

SPecial Investigations: CXR

\ \ ") ,;......, .~

0

Blgods 0

ABG Echo

Cardiomegaly, bilateral small shadowing of costo-phrenic angles, kerley ~· ftuid in fissures

U&E, S-Aib, Pro-BI'JP, Cardiac Enzymes ·

=rm ~nd intubation if necessary ~ Sl x 2 tabs if SBP > 100mmHg .&b~esn;Wid%40- 80mg lVI (may need more in renal failure) (ld~hine 2 - 4 mg lVI · ~....&till,,B,Q g[CQythmi.a.s

§£_condJ.J~ qpQ~-f SSP 70 -100mmHg and Sx of shock Dobutamiiie if SBP > 100mmHg and no Sx of shock

Once Stable : • Gnx wejgqL BP and pulse 6 hourly,

~ate~~ ~to oral FurwmtdEf A~~:J. if in LVF, also consider BB and spironolactone Warrarln and disoxin in AF

' . . .. 5 ;_ ;a;;, .,:

:' . . -· -~ :" . - ' .

... '· ...

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Inadequately ~-RJl~ID9.!1Jf Bro,n~_lf.l-.Q.~\0,19l!Qn

P_uJro.9!1~!~).!lfir.«.qoJI s"~Qtlg..!li:Il~9.1'

• Syg.::R.b.m.o.~al;ls~ HeAAti&,~R$~S.lf,

• Asw!.~~

Predisposing Factors: • Dental disease • Diabetes • !LOC • Bronchus Ca • Pneumonia • lmmunocompromised •

C!!gjcgl F;gtures: • ·~ggjgg ftyer, ~oss, m~lalse • CQIIQh Yt1fb pt rg rfent sguffifu • eteyrttig chest om • Haemopty§ls • Apaemla crepitatlops p~ubblnp

Special .lions: • ex

o Walled Gayjtv • s ~~fluid leysl . ~¥ •

o FBC. U&E, CRP, ESR, Blood cultyre lfl

Management: • Antibiotics

o Amoxyl 500mg Bd o Metronidazole 400mg tds o Rx 4 - 6 wks until clnica!!y and radiologically

resolved o Cllndamycin if penicillin allergy o Augmentin if G -ve organisms suspected

Postural drainage • Surgical excision If

o no response to Rx o very large > 6cm o resistant organisms o haemorrhage o recurrent disease

Oiff Ox for. Cavitating Mi!S3..

!=~Y.i!etOr1( -~~ • G~xi~\QJX,m • "Y~!l~~~r~!!?IJlaje~ • inf~~j&$J,9t.§.l!@.i • ASP2.s!J!.~I,l;l.~ ~ Pl:J_IrqqnC!tt.Jnl~ • Rheumatoid nodule

·' -<-J.~.:f'"A .. ~-:~

• Sq,c.£gj9g~l§

• P~lm.~~rxlr.J!I!~L

Bronchiectasis .-m::e:c::.s.m ,_.. .... ;;;;;;:::a~

Definition: Abnormal d~iAA~"g;tQra.b!"QJl~

CQ~~a~~~in~m= . . A'ssocliirediecurrent'CheSt Infections, purulent sputum and airflow obstructron

Iii! . Ole

Genetic Congenital Post infective Immune deficiency Toxins

Cystic Fibrosis 1 'uA( 1;-o. C;P ~ •<J. pulmonary sequestration ' whooping cough, TB, severe pneumonia HIV, CLL, Nephrotic syndrome aspiration, Inhalation gasses/chemicals

Mechanical Insults Associations

foreign body, extrinsic compression by LN. Intrinsic compression by tumour SLE, Ulcerative colitis, Chron's, Marian's

Clinical Features: Symptoms:

"".

Chronic cough iTTTiii sputum production with halitosis, worse in morning Recurrent haemoptysis Dyspnoea · Intermittent Pleuritic chest pain Lethargy/malaise, wt loss, low grade fever

Signs: Coarse lnsp and exp craps Airflow obstruction with wheeze

Special Investigations: -Essential:

· • CXR o [ramline] ring shadows, thickened airway walls

_High Res CT Sputum IY1Q§ PFT _lgA. E,M,G

• Aspergillus __ ~ Second line:

CF sweat test ~uta antibodies Barium swallow if suspect recurrent aspiration

Management! Ganerat Prlncl'ples:

~underlying- condition .(, Bacterial load and prevent 2ndary iniection

o l·ntermlttent during exacerbationS' o Long term In severe disease o iDose forlonger· per!od~

Collooizatlorn o s :·aureus--. H!,fnfluenza ._ M>i Catarrhalis -+ Pseudomonas spp,

Prevent exacerbation: o Keeping airways clean· ..... physic' · o Br.eathing techniques o Exercise regime

Other: 0

0

0

Exacerbation:

Optlmlze;.nutrition Refer for surgery if disease limited to one segment Lung transplantation·

Mlfct disease: o Clprofloxacin 750mg bd if suspect pseudomonas x +I· 2weeks

C Dv'-C-},Q.\J,.(\-C)..J

c __ J.== C\ \~o..\'7 Clys.tx 'S.y\1\.dfc•"'--L

1- 0

\-\'ftfC~cA.W.\.N"'O-~\dp 1)..\~ I'NL\..>.. \l c.'l

Ac..ru-\~.cJ -c\j\.,~e;)&e~

~\J-..N::::N\.•' 0.

/..\.-0\is

T \J'-~"\.d.W <so{ei'~f' ba=.-~

. Ac'Pu.'~ -A--~\-tb s~ . ...\'Q0A\Ic.ili~ ~\N'-0~"-,'C-.. r-t.;_~~ T~ ~\o.'f\Ci\.J,:a.\ +v.~ .

o If early recurrence consider long term antibiotic Rx amoxil 500mg bd or doxycycline 1 OOmg dly Severa Diseas&: ,

o Chronic suppressive Rx to prevent progression o Long term therapy with nebulfsed aminoglycoside to ~ levels of pseudomonas-

.. 23

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....

t\.A.o~-\ ~O'\J'-l\.'-N\0...--..._ SCA.\·c~ a~\oso~\ ~ec..e<;<:;:'l.:l~ d\<SR~ i - "-/c)......._~ co-..\ .. >.C~~o.\J>....P-

_ _ Cystic Fibrosis

DefiniUqn: Muladon is autosomal recessive on long_ arm Chr 7 .... chloride channel mutated Cllll;uy dysfunction · .

Diagnosis: Diagnosed In neonates and small children

Clinical_~

• Often Fam Hx • · Failure to thrive, meconium plugs, rectal prolapse

Resp: o Cough, wheeze. Bronchiectasis. respiratory failure. cor-pulmonale. recurrent infections

GIT: o Pancreatic Insufficiency (DM, steatorrhoea}, distal Intestinal obstruction, gall stones, cirrhosis

Other: o Male Infertility, osteoporosis, vasculitis, arthritis, nasal polyps, sinusitis, HPOA

Spedal invesflgatfons: Genetic screening for CF Sweat test > 60mmol/l Faecal elastase useful screening test for pancreatic Insufficiency

Management: General Principles: ·

Lung function o Maintaining ·good lt.lng Fx• o Aggressive Rx of infections o Refer for transplant when and If necessary

Nutrition o Nutritional support o Monitor weight o Slipplement enzymes

GIT o Annual screening for portal· H-T and Cirrhosis

• Endocrine' o Screening and managing DM and osteoporosis

Fertility advtce Psy-:;nosoCial suppart

/: .. - _ Co-.~o:\o_oc~ ~<-"~u\c&-c·A -------~~Vc. ~\ \p~u,.s -\~0.\S\S.~~Jb\}....Q .. )

~~\d.\\~ \C\ o~eJ.r'-o_ Co::~>h-~ ~\ Ct- c.~o\}..U&.,\ f~\lc{e_ ~oc c~ - ~ \-\.2: 0 ~~ ~s..:; -cp·tWL\.t'a.i ~'i~\...u..~&::>.u."-0_

-ee.Df ~\~\.0L~v--_ \<2.\ct\:LU~ ~)7-c-\cJ.:tcd ~-1' .~ \ ~~~~t0.'\ ... £L~ C\' li"Ol_/~S~ .

Lu'.J'-o... ~i @., ~\~J -\-~ --t:::~:>l:-o-r . , I t - \ -.J ~ t'.::),O\l"C-\J-.0..\ ll'--.~c:=-c...--

df '17 . \ . \'JIIO.,."C~\.,· -E=C.-\o.J:.\ _5

& fQc_\.....\,_{ fc\.1~ eccoc.-:56:::.\J:..(~~

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'· Cardiolog~t . ~- '. ;:!.,. - ~ . • ~- .. . ~ -~ .. ·. -~-· ~;_; ;:~- -?..;";: . -~ ,___ : ':)'7._:--·;~f: !?-.:~~~ ~\·:~ .~-~ ~ : :;

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. ,, ·· . _:· ·-~·

· . _ .:. ·, .

>: .• Infective Eh:cracarditis. ;: ~ ;: .• ,_ :·- , .. . ")' .· . .> RJilmmatle Feve~·~·~:;~::;,:t.~~-~~0-~!:· · · · · · ·;· '> : . . }}' .,> .· ~· .'. ~.:;.

>· Pericardial Diseme . -Acute Pericardios:; :;;;. ~.· :'\'•:;•> ·' : .

. .. . ~·_· .• S .• ~.·.· c·o····p···e··-· ·· .~ '> ' \f{~_:.~;:!~1;~1~ij!,;';~~:· .· .· . ,-- J."!:t' - •. :f-j~. ~.-;.:. -- ._ • . !~·-.{.~-~"::,1-Ji~:~/-{~;.;: ~~·:· ..• ~· .. - · .... ·· · .. - ~:·,_ . ~ -- ; · ·.. ' ,'

-.: .. ·-· .. .,: · .

.-. :: ' . . . · ·· :: _;;_:- ·, ·.· · . . ... ·~: -.. ·-_,(, -. ·:·-.:- ...

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. > ;· ·n!~~ase of H~art IVIusci~~:•~:-_~Dilatei{~ardiomyopailiY,~;;,:>., :': ~-· ~,~~ t: ,:>: · -~ >:<.-: ··_ . : .·· ... · : -~· ;. , ~: .': .. _- ; · .

. . . -~ .. - .

.. -:-<,::' ): :::;Atl.?:er~sderosis;~_:<.~~.-} ·.'>:: . _,··. · ~· · Congenital Heart. Dise·ase·: :_< )>- . ,~~est pain '.. _ . ,

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Atrial Fibrillation Don't miss it in examl!!!!

I ;;:,;:.a;:o::..:;:.:~~~ @ 300- 600bpm. _:The A V node responds intennittently- thus irregular ventricular

·~.__._..__.~~------~=·a. -----Clin importance= a) loss of atrial contraction b) inappropriate fast ventricular response ,:· . c) loss of atnai appendage contractility and emptying- risk of thromboembolism.

i '"¥ fqr {rr~rlllor ~ ..:... Sx: ~"®etomatic, chest pail!. palpitations,sf.ysprioea ~ · • . •,. ----- Sg: Irre'gujar rate, liTe~ar volume

Jli'luucr with APPROACH: Slvanable intensity

blc heart bloclc 1) Dx it clinically!-- Pii!Se oeficlt > Ill ~ l nal /ventricular ectopic 2) DoECG ~ .. l.s

•·· - ,kcnbacn heart 3} Find cause: ECG changes: k(2~. type I) > fu- alcohol? Thyroid sx? I' l)Abscnt P waves

; :> ~-pale? Munnur?CCF? 2)Im:gulac R-R interval

embolic phenomena? ...:.... )> Vitals (esp.BP) )> rug-UCE/I'FI'/Cardiac markers ..... Causes: .AR.ITID'!fAliG. :> ~- left atrial enlargement, A-Alcohol

mitral valve disease, structural R- .Rheumatic val vc disease

aboormalities, poor LV Fx. I - Ischaemic heart disease )> Qat- dilated heart? Infection? T- Thromboembolic = PE

v;) Mx arrhyth~a (rate vs rhythm H- Hypcrtension!HF/Hyperthyroid M- Mitral valvedisease/MI

control) A- Atrial ®".XQ.Q'}8/ Anaemia

. - 5) Mx cause T- Trauma = Post-op

6) Screen for and prevent ex-.........___ I - ~on= Pneumonia/Enodcarditis

7) Explain to pt ----.__ C-'caiWomyopathy/Constricnve ·

~ pericanlitis/Con~enital heart disease

I ·~ Cx: . l~mbolic stroke!! 2li3chycaJ:Sija-mediated

} due .· ·.\.F (<48hrs) Chronic: AF (> 48hrs) . Paroxvsmal AP cardiom~o2ath~. · . to+ sociated illness .URate control vs :rhythm. I )Pill-in-~ocket 3)greatcr uregu anty of .1moruaj. control - No diff in (eg.tlec3llllde PRJ.'l), if ventricular respoose. HR.

ry ill/haemodynamically mortality/morbidity.( RACE infrequint, SBP> 100 muiHg, ··-• e:Oi>ucE>sCdlitc>Emcr&en~ and AFFI&VI trail). no past LV dysfx. Bi~k fug!Qr:; f2r ~!mke:

!<f..§!Q!! (do not'Cida:Yk cii-dcrto I" choice: b-blocker/rate 2) If above not appropriate- -previous strokefl'IA :icoagulation) liDiitmg Ca-blocker. r~lar b-blockcr,. -Hypertension!DM/CCF

•:t anticoag - .heparin 5000- 2ad choice: 3)Anricoagulate -mitral stenlagc>75 Q U N (if DC cardiovcmon digoxinlauuodarone. -atria> Scm/left vent dysfx

'i1iiit time is running out). Don't give b-block & ca- = = Allticoal!u[ants nl ventricular rate: 1" choice- block together = bradycanlia JJ!vcxapam.illmctoprolol. risk.

1oicc...: digQx'fnf'!tlliodaro~. (~JAiiticoag!;!late)- warfarin INR2-3) Alternative-~ esp if

Elt!!(ain to pr: < 65 + no risk factors. -Part of your heart (the small heart

Warfarin= Bl=diQ!U!,ialh;si~ If AF continues despi~ above: chamber) is not conliacting well, thus

f iliO x 109/L AV node ablgion. puim vein ablation.

blood can clot there/or it can move and

0/90 pacing block vessels elsewhere in your body,

Compuance issues even cause your death. It is thus very

Pt choice important to drink your heart meds, as

- well as your bid thinners. Your INR must be maintained (btwn 2-3) inorder to prevent bid clotts, thus you MUST follow up at the clinic.

--r_.;.~..;...:.:.:;.:;::-;:,:,::;:;~a.::m::.:wm:::;::ur;.~ IE until proven otherwise

a tho genesis= [Bacteraenua + Abnonnal cardiac endothelium] ' Portal of entry (oropharynxfiv drug abuser/nosocomial infect)- Bacteraemia- Turbulent flow over diseased valve

- dg1osition of bacteria- ve&etation(clump of fibrin,plts,wbc,bactena)- Endocarditis- Septic emboli. Classification:

( Acute.[SO% on nDrmal valves) ( Sub-acute)(abnormal valves_} Severe febrile ilriieSs: Stigmata of IE ....___...... Pronunent7shanglllg murmur Petechiae -~typical clinical Sg's Cx -Embolization, Cardiac failure/Renal failure

Valve involvement:':MV>>AV>TV>PV]. .

Risk: ~=Prosthetic valves, previous lE, congen heart disease Moderate risk= HOCM, mitral valve prolapset !Ditral regur_[e, thickened leaflets

I) Sx'.1: ~r, rigors, c\J,il!s, night sweats. flu-like sx's, -i1<::1t pain, dyspnoea, cough. ~.1ccnt surge!:(_? IV drug abuser? Poor dental hygien~?_

1) X 2) Exam 3) SII and Organism Isolation 4) Dukes Criteri 5) Mx- Admit to hosp + bedres

Antibiotics Surgery- valvoplasty

Explain to pt. Prophylaxis Prevent Cx

)·-.....:'~"-------------+~~'1\j 1) Bid culture- 3 specimens,@ different times/sites. --5-10% culture newative

'ld- FBC = -~ormocytic normochromic anaemia ·JiliO mboc yto penia

ES RJCRP = increased (for assessing purposes) UCEILFT!Ctvr-

'rJ!:e analysis ~croscopic haetlli!OJila CO- dysrhythmias (conduction defect- abscess/infarct)

.Prolonged P-R interval, ST elevation in AvR 'XR (<:ard10meg@Z5 CHO- :!_eaetat10ns if> 2mm

'"I": rtihiotics{]mrunQli.IB benzylpenicillin+ ~a ....,..- Eoterococ = runoxicil!io

Streptococ =benzylpenicillin (2-4 wks) then amox:icillin Staph= fluclox + genta ColCiella = doxy+ rifampacio Fungi =.flucytosine followed by fluconazole

{ii..~.fi{;r· l;!E due to valve damage ·"'"' Antibiotic failure

· Lar"'e left val vuJar lesion with embolic risk Val~e ri"ng absc~ss = Va.l'ie oerforatiog U nstabk orosthesis wTYcottc ~neunsm

l) Sg: ~/- clubbin_g..QQ%) Cardiac-Murmur~

CCF~ Athralgia Pyrexia (90%) Skin lesions: Osiers nodes (15%)- 'ouch' raised, painful! 3-15mm on

Soles/palms. Janeway lesions- 'pain away' 1-2cm, painless. Soles/palms/fmgers/toes Splinter haemorrhages~)- proximal milbed Petechia~- mucous membranes/skin

Eyes - Roth spots (5%)-~ Splenomegally (40%) CNS- emboli {20%)- focal sg's. Mycotic anearisms (10%) Renal- Haematuria@ Embolic~- emboli .!\abscesses in oroansYbrain, heart, kidney, spleen, GrT,

commonest, prosthetic

ij..A,C.i: .S. + HACE-L<­

(.~o)o I '"~.

1)Prophy!axis:

· 1£ng(righr sided endocarditis))

4)Dukes criteria: 2 Major/! Major+ 3 minoriS Minor

Major: _ <::fve blood culture)

*typical organism in 2 cultures *3 +ve cultures> 12hrs apart

~urn iiivotY'ID +veECHO · '

• -~ar regurge .Minor: Predisposition (Cardiac lesioJJ!iv drug abuser) ~/immunoligical ~ +ve bid culture that do not meet major criteria +ve ECHO that do not meet major crit

"CaUS'e =prj or antibiotics Organism that fail to grow in culture =

*coxiella bumetti (Q fe v:r) •c!amydia *bartonelle \..,,. c,_\.~'-'Sc~-. *legionella

8)Cx:

Dentallorallresploesophageaf procedures: (;£f' (valve insufficiency) S;gJ;mic emhQ]j

Amoxill 2g 1 hr prior GUIGIT: High risk- AmolCil + Genta

Moderate risk- Amoxil/A.mpi

lvfycotic aneurism formation Intracardiac abscess forma tion Rgnal failure --glomerulonephritis due_to immune co.'!:Jple,x_ ~ep'?::i_ti?_n

\./' E"""''oo\~C S~o\~ !,.-/" Cc~ ,

v U)A._c~.,\ 2;o~ \UK

"'/ A~~\ .A;l~:Lv'i:s.'--'\1'. S-.r, f'v\J'-.ct_:\\o<.""-... .

.. -

, I

·/ ~ I '::>'-'\"-! \0"'--"-'j --~- - .

,--- :_i) ( 0 r_ -~ ) '-0 ~ Rheumatic Fever ll!!!!SA-~915e, d-ue to ~!.l!lo~~~tion, ~!_ered by moi~~..EEm!~ry b~ the cell wa.llM ·protei" .is Cifilie1i" c:c~ep pyog~ and_~ardiac myosin and lamioin. _ · -- . t ... S.) Epldemlol~: children and young adults (5-1 Syrs) Aetiology~OfUntreated group A b-haemo)ytic streptococ pharyngitis develop acute rheumatic fever. Pathology! Affects heart. skin. joints CNS

All 3 layers of heart may be affected ~ Rheumatic carditis --: Aschoff nodules --!!ranulomatous lesion with central necrotic Small valVIilar vegetations may develop Synovial membranes acutely inflamed - subcutaneous nodules

' •

l<lrtJve ex - ex nn 6omji/!Cg/daj

APPROACH 1) Hx aprl Exam. 2) S/1 -----' 3) Dx.:... Jones Criteria

-4) Mx · 5) Cx

, •co§!eroids (prednisone) until ESR decrease .-\ nCi streg rx== _

a)immediate"<B~l :Z. MU IMI stat ---- ( Penoxymetilf!]?ettu SOOmg bd x !Odavs

· Macrolide for for pen allergy bjp.IJJP}J)da:ds= ~.h<moxvmeth;tl pc:n, ~mglday x5 yeaa

afut.last attack 1mobiljze joints in severe arthritis lloperidoVdia.zspam for chorea.

Pericardial Diseases

Pericardium = 2 layers: Visceral and Parietal ·- -· -- ....

i._vilt.eA"-Il(_jirep Infect~ ~ent strcp ~ bx of sc:!!!c:t J.~y_cr, +R.tbmat.Slnb. ASOT>200, increase DNase B ~

Major-Polyarthritis (large joints - painfu!J .. ~lcn, tender) ~rdbema Margipatum (Pink raslf2~ Mostly trunk) Subcutaneous Nodules (painless, -~ae.hai1J,over ~endons.joints) ~ (Sydenhams chorea/St. Vitus dance ­spasmodic/~!!tionaV Choreiform,develop late) ~ ne\V/cbangili!Lmunnur -- Cardiomegally/CCf

-Pencardial effusion 1• deg AX block Diastolic mitral WUri!lll((due toy~) -Car%· COombs murmur · u...._ .u_c .. ccc~w

Minor= ~ousrhe'!W~

Arth!algia CRP/ESR jnctt:,W \ Lcvc:ocytosis t- pe_ ~ l'-;\ei;0cl.. _

"60% with can:l.itis = chronic rheumatir..l!elu:t ~ . ··__ -.Mitral{§), Aortic {~.Tricuspid(~ PV ((~ : Bssurrence- precipitated by_~gmm:y, other ~ta:p.~ens,us~-PiJI.. -

Reflec~!t<!.c;Kai!Qn ~~e.!!.@_ great bid vss~!l_r;g .i9_ip._~~~! E.esi..£.~~rnW1g_~s~--:: _21 in normal heart ·

r,

Acute Pericarditis- Inflam of pericardium, primary or secondazy to systemic disease. _.z **

Mx~

1)

Sx:: Chest pain- better when sitting up and leaning forward, worse with detj! br_c;~tJling and SU£iJl~ J!!JSi.tig_n. Fever, malaise Sg: Friction rub- Best@ lower left sternal edg; e~_expiratory,.Jll.hing forward

2) Confirm dx and find cause >ECG!! >Bids :tCXR >ECHO

3) Mx- rx cause and analgesia 4) · Cx- watch out!, it's a

TRRAP!!!!!!

J I) Rx underlying £!liD '2)Analgesia- NSAIDS (ibuprofen 400mg/8h)

J )Steroids/imm~ppressants if relapse llCCllt

Cx=TRRAP *Ta!llP.<??~Ci~ *Recurrence • Re5idUa.l constrictive pericarditis • iiriai ~ic~l-tllii:!ias · ---·-­*Pe.ricarl!ii!.l effusions

1) Hx & Exam 2) Confirm dx and find cause

>ECG!! >Blds >CXR >CT/MRI >ECHO >Endomyocardial biopsy

3) 1\-~;!-R~e fii'ri)lc~l- resection of p~ric.ardium Dturencs & Salt restnct10n

·"'!41-'U&\iHJP za aaa __

ECG = diagnostic: ST elevation (~e shapc;smiley face), in anUiat/inf leads> then ST resolution> T flattening > T inversion> normal T. ST depression in ~ PR segment depression in antllat/inf leads. Bids= FBC,ESR,CRP Cardiac mark~ ~be raised),Vrra{ serologv~d cu tures,atltoaiiti6Qdifls jfjpdicated

~! 0reciniraots TFT ~- pulm infiltrateslcardiomegally­

perica:rdial effuska? ..!ilL() =If oericard effusion susoccted

Etiology ibrous material d osited in ericardial Idioegth!c most common ~s =Ym:l (coxsackie, mumps, hetpes, HIV)

.• Bacterial (S~apb,Strep,Pneumococ.Mcningococ H jnfluem) .TB .. Fungal (Histoplasmosis,Candida)

Post !'vii"' Acute (1-7 days)- 20%ofMI pts, common inantMI · •· Dresslers syndrom-;():10 wlcs)- autoimmune response to cardiac darna~e.

A!ltimyocardial antibodies found Neoplasms= primary twnow-s of heart (mes0tbeljQ[pa}

lofefa.ltatic pericarcf.iti,r (breast, lung hodgkin' s lymphoma, leukaemia, melanoma) .. .

Uraemic Peficarditi~~fcbronic renal failure pts- DIALYSIS!!! Cgllaaeg yascular =~Systemic sclerosis Drugs = Hydralazine/Isoniazid Infiltrative= Sarcoid

~----------------------------------J

Sx = -;bdg pajqJFatirue!Dvspnoea/Palpitations Sg = Mimjcs CCF- ascites/hepato;;plenomeg/oedema

Increased JVP., Kussmauls sg, Friedrich sg (y descent> x Dcscent),jQ,ft, diffuse apex, soft S I &S2. S3, pericardia! Knoc~( early diastolic sound),Jlll!sus paradOx~. AF (30%) Thus-- don' t miss irregular pulse!!

ECG = s~, inverted Tor flat, AF. ~ CXR = small heart, pericardia! calcificatron CT/MRI = if no calcificatiQ.n on cxr, do ct -- if still none- cardiomyopathy? Endomyocardia! bioJlsY - pencarditis vuardiomyopathy -ECHO - Thichened/calcified wa~. Decreased ejection fraction. Bids= Same as acute pericarditis

~: Same as acute pericarditis

j ···l

..

P iRRtffliti iffit;jon- Accumulation of fluid in pericardia\ sac, often complicate acute pericarditis. JL) .

· •• none/similar to

d .:arditis/~oea/cou

h .. ehrenic irritation.­;; .. nused JVP. sgft

i2,apex 1loable fOctipn

~ ·cal

APPROACH: 1) Hx & Exam, monitor vitals!!!!! 2) Conftrm dx and find cause

>ECG >Bids >CXR >ECHO- procdure of choice! >Dx tap: T.r.~nsudate/exu~~~s./m~Jigna~~ cells/bacteria.

3) Mx - Rx Cause -Most tt'o'ye :spqnt,pm•y'y - mild=.serial ECHO, anti-mflaiJl meds..\.lS>~ - se~ere= pericardiocentesis (sonar guided)

- In malignancy -·~r~eia~c~c;u~m~u~laL;;;~~~~ ..i er 4) Continue to monitor pt tam onade

(serial CXRIECHO/response to rx

ECG =-low voltage 0~ Et"ectri~al. altc:mans ·FlatT

CXR"' Enlarged, globular heart ECHO • echo-tiee zone iuO"~heart Bids= same as for acute pmc8Iditis, albumin Dx tap= CS mali eel we hx:ose total

Etiology= Tramp date- ~Cf Jqw

.;·~·t' h~th-uae :ruses similar to

-:'Pericarditis. May develop secondazy to

.r

5} Cx -<gmeonadep m;qij'KP(~

ruprure)

Cardi!f lmmgaqe Cx of effusion. CLINICAL Dx!!l = M:EDIC~ EMERGENCY Palliop )./ \!eased pericanHal pressure- decreased venous return-.E:C!?reasCddlastolic venii'Jc:IJ~- dectcaSed CO-

hyPOtension+ venous congestion. Main prob!CIII"' CfficuLATORY CO LLAPSE.--Common cause for

CABDIAC ARREST

l)Sx "'Dyspnoea, flushed, syncope. sweating ~~- Intubate and ventilate if resp failure Sg = Tac~cardia .,_... ... ~ Maintain Opell airway ~- · . . Bee lriQd =Distended neck veins

.,..... Breathuif):..t 00% 02 (non-rebreathcr mask) · Muffled heart sollllds •· '-. / Intubate- ventilate Hypotension ....

- M . rSATS,RR Classical quartet= Distended neck veins ~;~~ lL cristalloids to 1etn22rarill Hypotension ...

reasetlie~O Tachycardia Diitw same bias as for effusion Pulses Paradoxus ·/·

Monitor .Sf.HR. 6i::Q temp, urice Kuessmauls sg (iric_reased NP during insp) excretiWl Frledreiclr sg v ··

.~ / Impalpble ape:c ./ Electrtcal altemans · ~ •

-u already drawn should be sent

\: APPROACH 1/ '! for same tests as effusion ) Pick it up!!! (dx) ~ricardial fluid away for same

)@$) J)Do em~enc;rcri:n~o:tcsis. · <well. Preferably guid~by d, but do

- 3) Tap it not wait for sonar machine!! I!!!!!! Just do ...... (pericardiocentesis) it!

. . ~4) (Use CVP set, so fluid can be tapped Find cause thron&h it)

5) Further iVIx When the needle is in, in wtll move as the / heart coniiacts- dQp,'$ fl:eak QYlo

. . It( The ~loodi!Juid a,mi.ratcd should @iP 5)Rx undwrl:dog s;a~. Confirm placement by sonar/when

Contact_j!h~sician & cardiothoracic surgeon ASAP. fini~hed.

<:ECricaiiilOtomY::it effusion recurrent.

c onstrictive per car di. tis vs c d" ar 1ac tamponade Constrictive _l)ericarditi3 Cardiac tamponade

Kuslmaul + It m to increa5eaio see ..1 Pulsus Paradoxus 1/3 cases Always Pericardia( knock + -BP Decreased Very decreased

.•. i: t

. )

•. r-

~ Sudden; transient loss ofco!JSciOusness due to decreased cerebral bid flow with sPontaneous recov~

Aetiology=~ vs. -

~acarcfi'~

~ ~~ ~ VT, Torsades, ~Yf, rapid Af ·~=Sicksinus ~dromo, 2/3 degree

V block ·

Mechanical !Qhstmc•i"e L=AS, MS, LA .

myxoma CarQtid stenosis R= PS, PE, PHI' *Tamponade *Myocardjal dysfx­CAD, Lv dysflt

r---. !~=~mgW&n -Visceral tio: syncope, cough syncope,

Valsalva, ocular pressure -CanJtidskwssyncope -Psyc~atnc: panic/anxiety

~--TWStrokc

~

c&izure vs s~ -suGaraciiiioid haemorrhage . :Cemc:U ~n<lY!ostS

Facial colour

Tongue bitting

Aura

Nausea -

· LOC

Reorientation

Todd's paresis

Attacks

Age

CK

. .

SeiztUe Syncope

Cyanotic V""'· Pale ~~~~-ion, ~~:~(escp. ACEI) -:venous 112 g

-~ . /-autonemic nevg~rb Rare

No

Uncommon Common •pnmary = ~ager •secondary · l\1

V ;hl:!l,2volaemia

Repeated

<35

Brief

.~s~l.ir... --. -~OXJa LO~ -hypoglycaemia -L1-~ ~apnia 1--\~ueM.-~ \cJ.~-

Seconds

No

Infrequent

Variable

Normal

. ~-- ... ______ _ _

. .::.-APPROACH :~ l)!{~ruul).~~l!~ = sclude seizure: Qi;~d'Qi;\jjiiiiffi~~M and CNS exam. Focal CNS sg's? 2)FBC/Cl\'IPIUCE/CK/GLUCOSE 3JNormaf"Wm=t:::~~.E.Y.il~F---Ti\t test if recunent _ f.,~l!,\!!~~~~J!:!.@.~--c~io~c-. --J;.CGIE~HOIC~d dgpler/24hr.E£QJ:iolter

(.. Orthostatic_·-----Exclude meds · ..--. ____ _ , ___ :_---Normal CNS exam::::._!lost g~~s_!!onic autonoll!ic ~gi~y-h~a.ttbeat

V.~!i~bil_&t_~tj_ng • .--- - -~~,._ -------Aiinormal CNS enin--Periheral neuropathy (DM}, Sb.Yc:O.rl!-g~ mcl_J;QQ1.~.­

CTIMR1-iffocal eNS sg's

/'..

~'-.lc,.t.lU~ (-c,;;>;,a·~. Valvular Heart Disease

When vou rnentiQn a in!!m!U[- cQmmcnt Qn;!ihlng~;

Intensity 1 = soft,soft (optimal conditions needed) 2 = soft but audible 3 = louder, no thrill

4 = loud, palpable thrill

Benian Murmur. >Soft >Mid-systolic >No tadiatibn. >No added sounds

1) 2) 3) 4) 5) 6) 7) 8) 9)

Tiping (systolic\diastolic) 5 = loud, but still need stet + thrill . location (where it is heard the loudest) 6 = no stet needed Radiation(wher~ __.... Duration (pan/early/late)

~ll of valve l~iQ Intensity ( 1-6) Shape ( cresc::ndo/ decrescendo) >HF Pitch (low- bell of stet; high -diaphragm) >Pu!m.fiT

Variation with rnanuvers >Dysrrhythmias

ns

Added sounds? - (esp .. AF) ~-DG~ -

--o::r~. >Infective Endoc arditis >Stroke

Clinical pearls: In multiple murmurs ·--which l is dominated by clinical sg's? Severity of murmur---Determined bY. duration and not loudness! _&L lou1,11--------Always think of~

Fail ina to hear murmur in· At Listen all down left sternal edge with pt sitting up @ end ~piration. MS.:... Turn pt on left later side, listen around & @apex. .

>Heard @ left sternal edge

II/ 'I •

i -­'\ '

-~

! ....

i ' ' I j ___ _

' i

Mx:

~2et\f\,-§c:f\.\ ~1.-l\CA.. . \~ ( \ v/. J ... .,.._

GA, f'i::.A, J (l vL~ : U c( \.J..V.......Q.. ( c\J\.ciO ch.r-- .

}~DiiiC StcDo~[t Mfost common (attf valvular lesion l§ntricular ?Ysrrhxthm-.J.~ sudden onsgt LHF) J cf: Narrowed va ve ~mficc ('!IDrmal= 3-4cm) •

Severe= <l.Ocm · Critical=~m1

l'uthophys: •obstruction- Prc:~sw:c overload--increase in LV end diastolic pressure--concentric LVH-subendocardial ischaemia-···anginalatrhythmi -· • • •Oiltflow .:>bstruction

"LVHF-f;,:;:u~lm~o~ediiie~J!I<»j-.... }fpMaJ!t ~bauliut.c:n)-C_g

NB: Not all LV outflow obstructio11 of~ r;) . r;:) (b . ·~uenvalvular obstruction- coagemtal fibrous <ffiPhragm above aomc valve+ Menilil reta!d,+ Hypcrcalcaenua =Williaf!IS.s~mc. '"Subvalvufar diaphragm- coogeoital fibrous ring_ · *Hypertrophic cardiomyopathy- septal muscle hypertrophy \-\~. 'u I • ;Ail :::s• '-"'--""-'\

Ae~ • ~=flow through abnormal valve<hjcumjsQ -~ · ~ = degenerative calcified AS "wear & tear"-e~

Rheumatic heart disease- progressive fuSion, tmc1cznmg & calcification , ~aortic invoTvemcnt ,.

APPROACH=-----*-~ 1) Dx it!!!

-2) S/1 and Aetiology

J.+---11---3) Mx 4) Prognosis 5) ex 6) Explain to pt!

(_~~12lead): LVH/strain/Afli.BBB L.JMds. ~Post stcnotic.,illrtic root dil3tatiog. saJcified valv& L . r~casurevalvular area and ~flow/leaflet abnormalities ~ exclude infective endocarditis PimOu@

Sx's= ASD- Angina,syncopc, Dyspnoea illg!na: cc:ertional, dnc ro fir¢ m & ~ ·

Cardia! ischaemia. < Sxr 5urvival. ~e: Fixed CO/arrhythmia. <(jjir surviv!I) ~a: LV fuilu~c & diastolic dysfx ·

PUffi!1 o&ieina. < 2 yr survival

~@ ,lepgb;rnl ~lsu3 paQQI§,QJ finlus (slow upstroke) Ce~ ol

Small volum11e ~ardjag r palpation-~pe ~v displacjD

Maye~ Palpable .§1' Systolic tiii1U (2od right ICS)

Ausqultatiah - . .,.. Tfm'C:CjCCtion systolilmid-sytolic 0 J Location: 2aa right ICS ·"'" Radiation:~ ~ -f 0~ Duration: longer as disease progress Intensity: grade .. . Shape; $fr;sccndo-Decrescendo Pitch: harsh, hisliplt:F,musiCal gualitv @.asex.

- (Girllaviiiilin ellino'1iicna) .... :a

Asvmptomatic- monitor . ~~ .

Heart soundS: reverse spfiffilft S"O"trS27\11m:!l'taZ

. "lli early in discase}-LV hyPertrophy S3(1atcr in disease):L Vdiiate . S"upportive\medical- avoid exmi~g

-lli~ro~~xis :~ jd tnTACfL SYIDQ~"""'-""""'(A V ~..,.,:.::;;:,.. oc b•lloon """""-)

.rnrtff!l!ttions: ~=yncoDe/DVSliggsa ~

Cx of .iurzerv: _re uced CO. bleedin2. A V block. stro~

\;&3rt~{ refir;e r:§i?l

Cx: >IE >AVbiock > VentricullU' dyssrhythmias >Sudden LV failure

Pathophys: AR-Bld flow back into LV-Volume overload--;L V dilatation-increased SV-increascd SBP & decreased DBP-- I )increased wall tension (due to increased SBP & LV dilatation>=jrcssure over!oad-L CJ1ii dyspnoea, PNDJ

-2)decreased coronary perfusion (due to decreased DBP)--- incrcas myocardial 02 deman syncope, angina]

Aetiology: Most common=~ ·

I \:::::> Q Suoravalvular (aortic root disease w_ifudilatation o_f_ascendiM.J!Qruu= ~. ....t. ~-irlli • .,......,..._ -a!l:!..erosclerotic dilatation and aneurism

YrtALS .. csp. BP -cystic medjal necrosis (Marfan, Ethlers Danlos) AfifEROSdEROSJS? {@' -dissec!mg; aoric ~DSID

. Rf. witrkun if acute Fever -ill worlcuo. :systemic HT ~.~ = L VH, !-A enlargement

~ -smhillis

LV c::nlargement, LA enlargement, -other connective tissue disorders (SLE.RA Reiters, ~osil}g_mQ_nd.) Aortic root dilatation Valvular i C c....._~'t'1 ·

JJ.Q.iQ .. GOLD STANDARD -Co~enital abnormalities (bicuspid A V) I t.:= @ ~\.._-:; 13 ~ ·• bt1sdine, exclude autoimmune,~lis~ -Connectiv~ tiSSll~ disorders (!U'R/VRDL t:tc). A.JJ e.. ..;, .,-.,..

-RF, IE, ;erosthetic valve

P' ACUTE A,& ~cute r~euma.tc l~a". m, liOLUC O!SSectlOn, trauma, rauea nmstneuc valve.

l'ro~nos!s: Mild to moderate- few sx's S.xmatomatic- prognosis L APPROACH Sx's:~ea, 2.,11!}~gl!2,ea~J!l:!D~e .. palpi!~ope,~ W<trse Sg's: ·

1) Dx it! ,

s~~~tll ngute Qg,-~· cl:'!"nr. t y due to nvnerdvnamic circulation): live> 1 yr after dx 2) . srrr "TPUrsating-iJUpil • uandolfi sg

aetiology 2.Pu1sating uvula= Mueller sg Cx: 3) Mx 3.Head bobbing= DeMus set sg >CCF

' 4) Prognosis 4.Distcnded neck veins during systole= Corrigan's pulse

:>(8 S.Bou.ndlng pulse >ArrhYthmias 1'\i= 5) Cx 6. Waterhammer pulse (large PP)

?.Pulses Bisflriens (only if AR +AS) , 8.Pulsetile blushing of nail bed= Quincke's sg 9. 'Pistol shot' sound over femoral artery

1\<lt: lO.Systolic-Diastolic femoral murmur= Duroziez's murmur ~,\£Jll9Y£..: -serial ECH~ assess LV 3ize _ !!.Pulsating liver= Rosenbach sg · t,.."-ttc;t\!Wl;i!t®l!WM!ffh@erediqi}ii\Cm 12.Pulsating spleen= Gerhard sg

. -IE proehylaxis . . . ~~~= -restnctlooofactmties Cardiac sg's:

-RxCCF Palpation ~yperdynamic) ~(AV replacement/repair) if: au oe 1sp aced

- 1Sx severe I V"" Auscultation - pt stttlng forward with hands straight ~·Pro=ss o V dilatation / Sl =soft -.

i!='~f<55%@.~,/ ' S2 = so.IVabsent

6,~= Stabalize with IV vasoauators oewre surgery S3 = severe AR 3 murmurs: @ aortic area (2..! (R) ICS) = ejection systolic murmur ~ = Qiastolic nwbl~ (Austin-flint)

@ (L) lower sternal border= mrz=~c7n~ ea ely ntr' ic -( rue roO'aiSease or

@ (R) lower sternal border- dei:rescendo early diastolic = .. . ~e~ ijis'eamt

~~ill's testj Femoral-brachial SBP difference: l0-20mmHg = mild 20-40mmHg = moderate >40 rnmHg = severe

~S-----L V inlet obstruction---Left atrial enlargement---increase in LA pressure---Pulm HT--increase in R V pressure----RHF

Aetiology: Con<>enital - Q Acquired- Rheumatic b~art disease most common L.:Q

APPROACH 1) Dx it! ----tr~ 2) Sll &

aetiology 3) l\rlx 4) Prognosis 5) Cx

P wo.ce · \~t\\i-e:.~-\to o% V\i.?~~.

~~'.\c)~~~ J

~

L

'\

I ·I

.. . __ ; : ..

: . . (

l@IVa1 Regurge iMl@ ~L~

Cx: • ,&!!!!! (an atrium that dilate will fibrillate)

·~ . • Aprte q;p dq;pmPSfr'i1ti0n •m •

Theresto@ _.-:t:;."""

W -I>CC~ Pathophys: Chronic. :MR-gradually increase flow across MV into LA during systole--progxessiv~ecreascd fraction ;d SV flows forward~ (to increase SV & maintain CO )--increase in LV wall tension~ ..

Acute MR. -increase in LA pressure-increase Pulm artery pressure-Pulm oedema-RV failure (acute onset CCF) - .. , -MR causes LV dllatadon-causes allllnlus dilatation-worsens MR!!!

~=~.LVH "1:m' = VH, ill, Pulm HT .£!& "',$SHOICE! ·

ggoJaji ~flail leaflets, vegetations · ~- regurge volume/fraction

Orifice area. · increased L VILA size, EF flow shows abnormal jet

Dxit!. S!I& i).~i:lc aetiology 1---------------Jcu Mx

4) Cx ---~Jf-.,. 5) Explain to pt.

- . ~ cc\~ • ~ -:;;y~ t'O""""--{Mitral Valve Prolapse <MVP>'j3-S%ofpopulation(~ >d') .

Leaflets tll.splacB into LA. during systole

Aetiology: :>~!p;omattus d~:jjc:neratio\1 of chordae & leaflets which are tliilmeci, vo liiillnous & redundant (too big for orifico) >alone, or with c~mnztive tjme dj•c;;; ( eg. Marfan) >May e associated wirtus excavatum mai"bl jzppk wdmm~ other skelern! agnounew es. W*j

Cx: >AF >CCF >Pulm.HT >Pulm oedema >IE

,(flo·~)

E~Q- non-s~ecific T wave ~baxl!!es ~-~stolic 11rola~e ofMV leaflet into LA

·Assess severi!l: of MR CXR- same as MR -

,\fl; APPROACH ~~ll,jil\ij!gj)l\8 withn111 MR = ~nt 1) Dx it!

"--2) Sri& !'III.JiJi91111

··w~mrrianstoai~ ~pxi1~ -aetis!l!l~ , . . g- sys crruc emb?us 3) M.L ~ ·· IE ~Jro~h~laK is,:tanda!li

Jl · l~ 1111.!1 ror MV r~air 4) ~ 5) Ex;elain to et.

Cx: Depend on degree ofMR >Sever MR >IE--

> Arrhy:!hmias >Thromboembolism >Sliaden death

---c Tricusgid valve diseasi:f Tricuspid regurge (TR) and Tricuspid stenosis (TS)

Aetiology: · (IDj.bsuey•js Cgpgmi~rcinoid syndrome, Fib. roelastosis @ ~J!iljit§ti..on (commonest cause)..E.b.gJmatjp, If F&w

-~Y ~,!rcinoj4l,J.;_w!lillil.

t APPROA . ...;:CH~--41--4-1

1) Dx it! !+--l1il--2) S/I &

3) _/ 4)

aetiology Mx Cx

'----·------------'1.............- l;..._----- 5) _m. CCF. Dysrrhythmias, thromboemboli r :..__ Explain to pt.

Jlrlx: Supportive- preload r;:Lgn (diuretics), IE prophylax. TV ill£&.m usually indtcateil by need for other interventions.

u monarv valve disease

Aetiology:

.al rJaz~in (proloriged. non exertional, sta " , ~noea, hiiJe!VentilatioO.: an.'Cie~. ~algitations, r ~gg~~.

:1: sx. 'x ofMR. Sg's-~ck-murmur SJ'!l(IIOm~Barlow s_yntti'Oin~ .MirLov.tnlic_cliclC tensmg of redundant valve tlssue,

Billowmg-o! ::E ,Leaflet in mid-syao !e. ·&fid to !at; sVSioiiC murwy((regurge alter prolapse),

Crescendo. -Manuevers to change LV volume""

S~uad to st~ valsalva --:-decrease ~enous refum-!&ecrease vent. filling--~ cick & louder & lon!!er murmur

Sx;...IW&. -fatigue, pedal oedema, abdo pain (liver congestion), ascites, dyspnoea (may reflect RH for­ward failure)

Sg: C't.f2tid pulse= ip'c$ii!.Af Yv P mcreased

- Promment a-waves in TS Large v-WaVSS in TR Ccy-w;;;.) +ve Heoatoiul!Ular reflux in TR

Precordta L r R V) Palpation Auscu ta ton= All R-sided SQ.unds louder on · <lii§.ii~!Wil5except pulm

ejecilon click! ~-Diastolic rumble 4.n res ~- Pansystolic mt1rmur al,ng

[..lower sternal border ~

I :aiVallo '< mu"'!:'ur -\""" RV S3 L-lower sternal oorder

ABDO- Heoa!Q!ly:ft',illJ¥,),11~~~ 'Ascites

PEDAL O'E'i5EM:A :.:ww::~

~!m Stc~S~ = conacnital, rheumatic )m Re ( R) ifro dilai.ai'ro'?O'I valve ring

Sx : chest painm syncope, dyspnoea, leg oedema = Pulm HT (MS!!!, COPD, PE) Sg l'.S. = sv;tolic ~\!&lllUS (2od UCS),gulw eje~lc =Weum~~ic ~

~ormaDfoud/soft P2, Right S4

t ffi = ~4iiA3tJ:lJjc mpnnm@ ba,s;., Graham ;teel _m\Ul!llrrldiastolic)@ 2•"13n1UCS

~ ''li'icrease wl't~~'ji':"mrQ.eriQheral su~wata ,"'-. APPROACH ECG=~

1) Dxlt! CXR = ~minent Pulm. arteries if !llOlJ;:I.lii

Enlaraed!2 2) SII & ECHO= Diagnostic- RVH, RV dilatation

d:t : aetiology PSIPR by doppler fi12roohvlax!s 3) Mx :J[ = ra~e!y requires ~ (well tolerated if :;ystemic vascular .::;tstance = no!Tillll) 4) Cx-as ~ .::'alve r~!acement if s.e.Y.er:.. TSfTR

5. ~ Balloon va)vu.J:e)1~11 deoendin~n l"'-'!iti\V 5) Explain to pt.

l

Heart Failure Wltat is lteartfai1tu'e?---11a Clinic;jfndrome of t~-!lie due to a ~W-!IIi&f, u.sually accompanJed by n~w,J._a<!!;~ons resulting' in_.._ ~ ~ wa~~ reteos}~,!l" (Packer,M.1989) ---..

Neurohormonal adaptation= Heart cannot maintain an adeqpate CO- Neurohormonal activation (RAAS, vasopressin. endothelia)- Nand H20 retention apd vasoconstrictjon increase aftCiload & intravascillar volume- increase BP & cardiac ~k- myocYte loss- BACK TO SQUIR I!

RHF LHF -Increased M -Pulm oedema (cough, dyspnoea, PND)

l)Dx it!!!!!! 2)S/I

APPROACH

J)Stage heart failure 4)Drugs that reduce symptoms 5)Drugs that reduce mortality 6)Aetiology---Rx 7)Precipitant--RX 8)Risk reduction & prevention of Cx 9)Ciassify according to NYHA 10)Explain to pt!!!!!

-Hepatomeg -CardiomegaUy -Ascites -Pleural effusion -Peripheral oedema -S3 -RightS3 -pulses altemans -IUR sustained -peripheral c:xanosis

·Sj'UCO~

~ lllFraminl!ham lritena forDs: ofCCF (65% sensitivity)

@ least= I Mar or & 2 Minor Major Minor >PND >Peripheral oedema >Possitive IUR >Pleural effusion >Acute Pulm.oedema >Night cough >Rates >Dyspnoea on eicertion >Cardiomegally >Hcpatomegally >Increase venous pressure >HR>I20 .. taglng of HF (A;nerican heart association & American

oilti!ieofcardiolo!?fj ·- >Neck vein distension >Vital capacity < 113ni of normal (L Fx.) lb 611/l:IJi 41 >G-S3

High risk with no Sx's - &: P.J:PCnt remode{fing;/Jx "J!JM."ifiiiiii~DM-~g!IARB

!r Strucrural bean disease, no sx's -A+ !l;b.f.g.g;er ,$.&"' ')' Structural heart disease, previous/current Sx 's-

· 8 + diuretic + alda~terone antas:_onist ±digoxin, + salt < '2BtdwL -"' . "

2)~E/lliJ!fhyroid fx/ECG/CXR- help to establish nature & severity & (de B~ain natriuretic peptide (BNP)- elevated, used as screerung m pt's with

Dyspnoea+ Oedema . ~allpt's!! , Refractory Sx's (on max Rx)- C +.il:9,tr,o.(?.esiLVAD(trqnf=

Salt < Jg/day · • -determine aetiology .­-valvular diseases (eg.MS) ,__ -EF .::>b~% -monitor progression of disease ....--

1 = Diuretics: Loog di~ic (for peri!!heral.'.eulmon~ oe,dem~ Regarded as 1" line in symptomatic""CCF Furosemide- 40mg ~ increase according to diuretic response & BP

l"" Digoxin: ~al-long term Rx reduce Sx's & hospitalization

1- ACEI: - ··

!:f!i'f ~~~i~- impact negatively on survival Still in most guidelines

lrnproves survival in all stages ofHF' Start low: Captopril- 6,25mg tds, increase to 50mg tds

Enalapril- 2,5mg bd, increase to 1 Omg bd

~~~ ~\7e ,_..'-.>o\\.:C. c:l~c:'o:tJJ

' cu.!.)_

-<;.~u.-c..\-u.•la.\ aU)~~ . ._EF-

2 = B-blocker: In haemodinamically stable pt- r~ucs mortality ( carvedilol, metoprolo1 bisoprolol) - Com;rnicus trial- 351 reduction in mortality when carvedilol, 25mg bd was used in pt' s with

L VEF<25%_ . fa -They are not rescue therapy for bedridden pt' s Start low!!!! Monitor BP!!! Carvedilol 3,125 mg bd- 25-50mg bd) -

3 "'ARB's: - A1J effective ~ ACEI. ,©~.ML ~ARB + ACEI together= better. Seldom done due to cost.

4 =Aldosterone antagonists: Spironolactone 25-50mg!day added to ACEI and diuretic=- reduce mortality, in pt's with NYHA lli-N.

6)Aetlo!ogv: 1. Ventricular outflow obstruction = HT ,AS,Pulm HI' ,PS

1 Z.Ventrlcularinflow obstruction= MS, TS l 3_ Ventricular volume overload= 0 LV overload: AR, MR 0RV overload: ASD, VSD 0 Increased CO (hyperdynamic causes, eg anaemia etc) · •I. Reduced contractility= MJ/Myocarditis/Cardiomyopathy/IH.D

5.Arrhythmias =: M, cornoH:te heart block, tachycardia cardiomyopathy 6.Diastolic dysf:c =Constrictive pericarditis. restrictive cardiomY?I!@iY, L VH & {i~~ac tam~_oade

I '· -1._) ':> _\- r--::.<:::,rr;..\( ;-:__ .::.;( '::.. ·(:~~- · ;

·' "" ~~. !.

1 1 t' ) \ ~:-:\_tj'• •L.\.,' ... \ .r '$

:· ~~ :: ~~\-c\ .\_(_ . : ...... .. ·. ·-- !( :c: .~)

---------

1) 1D l'rccip\tant --RX: H· Hypertension r..gudoc~irditis

_£

9) Classify according to NYHA I=No Sx's

A ·Anaemia/ Alcohol/ Atherosclerosis R· Rheumatic fever

. >lnipai:red liver Fx: (due to congestion) >Renal Faj!nrc (hl£Pppgfusjon) >Thromboembolism (stasis)

II= Some Sx's on exertion III= Marked Sx's on exertion IV= Marked Sx 's @ rest

1 1' · ·n,yrotoxicosis li• Failure of complaince A· 1\rth.yttunia.s (· rschcmiallnfarction L· Lung disease: pleural effusioo!COPD E· Endocrine: Cushings/Pheo/aldosterone j D· Diet: increase NaC! intake

IO)Explain to pt his condition!!

>Arrhythmias >Remoddeling

-occurs in: Ml,HI',Cardiomyopathy,Valvular disease

-Includes: .~erw'hX~Locyte lo1s. Fibro.§i~ ,pQatatlon · J

·Rx :"reverse remo'ae!ling" .f\cEJJB-blockers

~BIJ:~RRF secondary to lung. diseasE ware of the blu;;t in HFJU)

Pulm.HT + Hypoxia----RV h;-pertrophy ·---HypopeffilS!On of kidneys---RAAS--Volume overload--RHF

-----,- ._ ( . I Sx = Chest pa~spnoea, S-XJE_ope@Y ANOSED~~ not blueJhwot_corR!!Jw!?J!j!l;l. ~ ee-L lA'N7e\ \-~ I_.LQ.. . Sg = L parasternal heave (RVH) A ~ (_(_

Palpable P2 (Pulm HT) / /..-.. R Ventricular S4 ~ Mid-systolic ejection murmur / . Early diastolic murmur due to PR 0 ~G5\ ~ ~ o.e..... 1jJj a-wave

TR = All s~g;.:'s~:-=,.,-::-:r:-:-==-=:--:;-;c:-:::=:=;::;-;~;;1 ECG = RVH t axLS ev1atlon and dominan in VI ~ (P:.pulmona c m_, an V 1N2 - Right Atrial Enlargement (RAE)

APPROACH= same as Heart failure

Go look for the lung pathology (most commo~il.ro f40/ -~ 110- 12.0J it -"qo i'Hyneitens!~ - Non.;..~ As.. ~,_ C:D- go

':7 \) BP = ~ x:P5'R t-.J · . ~ Sympathetic system, ~G II,

SVxHR ~

Preload, Afterload, Contractility

lr-===~

APPROACH

l)Sx: Headaches ._.­Nausea/Vomiting_.­Poor Vision .......­Convulsions v­Trarisient paralysis.......­Coma.....-Epistaxis <./' "'~'"· \)

Sg· Eagdoscopv ~ ~- L VH, {ti!nboric . . S_!. C@!]jal nerves stro e? --Abdo- bruit, large kidney, renal bruit,

R-F delay

l).Sx's/clinical clues 2)~

-Hx!Exam

11.:~" JV'=-------------------------------;",]6

2).Assessment of BP: '-· :..-> ~

Urine Dftisti:~!! i! -protein/bid . .

-Is HT sustained 3)~creen for other CVS risk factors 4)Exclude secondary causes 5)Detect Target Organ Damage

.l)Ciinical. (office): for Dx, repeat~eperate visits= 140 ~ ~mmHg 2).~bulat&b( BP- to exclude w~oat HT = 2 • 3)How.e (pt monitors own BP) = _135 I

PmmHg 0

-

6)~ ~e.:d: D ~;carate visitsl and jWOUfd pt hem:fit fgn Rx~ ·r~mc + specific tes'fiuided by clinical clues {eg. aldosterone etc). Fasting

. g!ucoseiffimwun. fCO CXR !JtyQ

3)Recommended ~~a, · Uncomplicated HT~/ fudications for targd B < " 0:

Riskfactorsforatherosc ero.ris (DlvL Smoking, ~-""' ·· · ' Dyslipid. Obe.siry)

Detect Target Organ Damage ...

Chronic kidney disease "SeCondary prevention of stroke!TIA !£l;L

~..:Jb.vi-I, MI, HF, Arr_tciii!lli_gj 1in- Stroke (ischeullclhacmorrhagjc), Dementia ~ =MT"croalbuminuria/oroteinuria, ~ure ri phe.q! ~rte£' - ~if.J!.ruLuD.Mll...Cian~ , ""'-... ~ Grade I= Copperwiiing of artery walls ( ~\~~~.-1'<-y

Grade 2 = A V "nipping"- narrowing of 'lesseJj Grade 3 = Ischaemia- Flame shape haemorrhages, cotton wool soots Grade 4 = Paoi~dema ·

f?_;e-vi?fJ..s ~ )JO A :;.c.. .i-f p i 1'b1 ' lr.tflfl.ove fifY'i IN

0:: G ....... ~.==o .

YYJI-1_

95/c

: I ~ 1 i

.,

, _

' !

. ,

)l'rlx:

. .I

..---------------,'18~~ OF 1-J--r 'f Drufk-Irr'Q5

GtAdllHT SBPl:IIO

Subclinical organ damage ·LVH: ACE!, CA. ARB ·Asymptomatic atherosclerosis: CA. ACE! -Microalbumlnur1a: ACEI. ARB -Renal dysfuncUon: ACEI, ARB

Clinical event -Previous stroke: Any BP-lowertng agent -Previous Ml: Ba, ACEI. ARB -Angina pectoris: BB, CA -Heart faQure: Diuretics, BB, ACE I, ARB, anti-aldosterone agents -Atrial fibrillation: Recurrent ARB, ACEI Permanent: BB, non-dlhydropiridlne CA ESRO/proteinuria: ACEI, ARB, loop diuretics Peripheral artery disease: CA

Condition -ISH (elderly): OiureUcs, CA -Metabolic syndrome: ACEI, ARB, CA ..!Jiabetes mellitus: ACEI, ARB

.2. ACJJi-- I

a· 10 ~cx;az. h. V4 "l..o-0 n-A --re12.

IS (A . C:MAf"J/'Jt;.L.

~~~:~ ~-y~;:~rfl-Al-

~·~'~· a·

-Pregnancy: CA. methyldopa, BBr--------l'---------, -Black Individuals: Olun1tlcs, CA

Dise!lses gr Heart Muscle -!)Dilated Cardiomyopathy (DCl'v{) 2)Hypertrophic Obstructive Cardiomyopathy (HOCM) J)Restrictivc Cardiomyopathy (RGrv!) 4 )Myocarditis

First exclude disease secondary to CAD, valvular heart disease, ~genital heart disease gericardial disease before making a Dx.

~;ii;liiiii;i:i.;;iiiil;i~!iiii~iliiiaiithiiaiyii-ii!i¥ncc CCF:~ 5 yr survival

k factor= male, black. ram hx:E) Collaaen vascular disease · 1Mecd'ous (post-viral (Coxsackie), !QY etc), myocarditis ~ (uraemia, nutntiolia:l deficiency) • e..

~cal1m:jrerqtnc::!Jnnn:lf'ftng]-

Ciin picf@systernic!Pulm ~li, arrhythmias, sudden death

Investigations: ECG- ST -T wave abnormalities - Poor R wave ro

ECHO= 4-cbamber ;nJar~!ji!leut D~r-..ssed ~ection fraction NC·TR seC ri@Qi uzlfararjgn

Endomyocardial biopsy- rule out IU-able cause

\. i~iyu~~~~phl~~~;~~~~: ~~~?~Y._~~~-Funexglainedo:.entricular hYeertrophy} f: &

Clin pic: Asymptomatic, ~ea, an~ina, CCF, arrhythmias, sudden death ~

Investigations:

l'r£x: A~id extremes of exertion

!E~opliyi~ = Me teal- B-block ~1- (drug-refractory Sx' s)

-Surgjcal myomectgmY -~estal ethi!,ngl agW,j9,n -1gal -phqmb.g,.pacing

.&.H~as- ~rone.,__ip~E_a-c~~~~fibrillator @en. Qt:;"iy.

Clinpic: >CCF ~ythmias

S/I : ECG~) ~SJ.-Lw.a;L~:.s~ng_es

t{su:is_gbasmis O.w.a~ --

.Qili :,:3:!,ld cardiac enlacagn~

Poorprognosi~' ·--~-:;:. ~-r, ·)e:. (:· . ~·_A.~.:: ' 'i!Lc .J:- ,.:_:. .. ./'-~

ECHO = normal pericardium SfisbtlY.d!<Q"!?.i@;g,illl9Jic.Jx Ji~ .. ~!'?.!!.~~l~,!.

Bjopsv =.1,i~tigauish etialoav

~~; c . , n -' 1 . , , · ·- ( ___ ,,_ 1·· • ( •'.· __ ·,.- ,::_,I...Ui...·L

Exclude~tric.ti.y.e.o,;ri,q;u:slitis .... . ·: .. ~:;.:..( ::. , I c c_......,, ~ ... , ., ·o r--. .. r..

~;ut-';ikl~ ~~~e

'& ·- -- --· ----- I

~ ~ Mvocarditi.s\- Inilam of _:nyocardium, NB cause o~J2C\"L usually self-limiting .

Aetiology: ~pat\llc · ·ecqou~ · Cox<ackie 8, HIY.~ S.Aureus

Acure ~~~~~~;~ ~~A; tQ!laa( ; ~7r(i;e~es · SiY>:i,<;>~

~- :

i ;

.. ,_ ...

I

.-.J

·' l

i .,

.:_

• I

' . ·~

Sfl:

Mx: §upP$rtive Resmct ohysica! avtjyjty m Er!li::me

ATHEROSCLEROSIS- Mu!tifocal tibro rolifer:ativc immunointlammato · case of medium and large size arteries, fuelled by Hpids Cause .. coagulative necrosis. Consequence = Isc cmia/necrosis

,4 .... t • •••

~ Jt.~n•e• oFb!d yqsels:

.therosclerosis ...,.....-~ertensive vascular disease _.,.--

1 ~ l~erosclcroSJS ·Arteriosclerosis ~ &,diss'ections ~ :.'A'!Ii'ei'OSclcrosis ·Syphilitic -Abnormalities of connective tissue

'" Marfan) asculitis.(inf!am. disease) ~

So how do we recognize atherosclerosis?

l)j;ligjcal CVI;!I (MI/StroJs~ 2)Ri5k factor assessment'(.JH~P;-:,U;-.;:p?::ids;:-;;,S;::mo==Jang=,..,,o""M}'..,.,. 3)§vasive testing((An~gra~W) 4if\{on invasjys tc;;tjn2,(Exersice ECG, Sgnar. Heart Ca1~ scan,

MRI. cr. PET scan)

lfhe Story of King Atherosclerosis

J Risk ~actors (T with age,> males, HyPerte~ion, Dvslipj~~smia, Abnormal gluco;e, smoking, ~ty, @acfiYltY, hum resbng p~J.Iiill

lmpaired NO bioactivity

:=::x .J. Endothelial dysFx

£finical Seqre,lae (lschaemic Heut Disease): ;)

•l)Suddcn death

1•2)Heart Failure-

· •3)Dysrrhythm.ias · :..,)Chest Pain =.

J

CHRONIC $TALE ANGINA Fixed Stenosis ( h.l'tC.\J I?") -:clemand'Iid stenosis -related to effort ·predictable -Sx 's over long term ~Sx ·s on minjmal a;nion

c®e:ecrnl ~"duration of exea;ise *degree of ECG chaages !!AbnormU;BP response

~ble plaq · J . "'thick fibrous cap -"'little ioflame.cells *small lipid core

i.,...,;-u,.,._.."'""-:~

~~~~ {-r ·- , E

. .. . ,. ... - · ;•..n.o."'" ...

!2YJJ.amic Stenosis -~upply-leci ISCHaemia ·sx's..at.,mt -unpredictable -sx 's over short term -frequent or nocturnal sx'x cECG changes at rest . -ECG changes w1th sx 's :,elevation of troporun

fun$b(il%kijeCl orous cap

*high inflame. activity *large lipid core

1)...,~ Qcilioc

UNSTABLE AI."! GINA

.MI Sx = Chest pain> 20 min, radiates tg ~ (L), throat, jaw, back ~- . Cold, clamm

Sg = ympa euc- pallor, THR sweating . Vagal-~~ LBP, .J. urine excretion, cold -Iilflam sXJsg- rWcc, tteni·P.

ECG = STEJ.\1IINON STE!\11 Cardiac-markers '(Trop,c:K}

I /--1/..~ _ --_ -;: sc.St,c.

"risk of rupture- thrombosis/arteriospasm {)Q;;·v,, 0)J'.r 1

~~~1Aool--i!Dpmve sualitv of life. .......:S-blockers -.....-:cca- _L , . .,.~ . ( • ~ -...-;Nitrates..&,\\ c~,r\ \ i l t--i.-i\OI'<.J o.~yc .

2) ~~-J~ ACEL B-blocker, Statin

-Reduce risk factors . . -~:t\F cU)arizatiou . . . jlgOf"~ . .·

t:!frneral myocardl!g ox.ygiij~oQ;l

· ·A02

•. . ; ('\\.. ... \a• \ \wo:.v.~c><:o~ A<::. - spmn--Clopid~grel (t\.~X)-:r~J\\,,.;b·cJ _.A=t> \)

if~ Ana!ges1a: Momh,inQ ( Decrease myocardial energy coDSUmption: B-hlqgker

. Coronary Vasodilation: Glycew,l trjgitratc ~~ . Plaque stabilizatioo!V entricular remodelling: Statin & ACEI ~,gj J:j'ON7ITE~U.,

- f-ntitluombin· LMWH - . Gly!!:c~::tein IIBI1Yi\ inhibitors: Abciximab

f!J!S FOl!J~-- . "'fnrom olpis: Streptokinase/ Alteplase/ Reteplase

A'tt'"' •) Qy fX''n i-;,. (2.,6'rl r,.uro~ MAUoR ,.)

:A= Aspirin ACEI Alcohol in moderation

B = BP-:-B-blocking """"C =Cholesterol- Statin

No .£igarettes o.<J> =Diet

Rx Depression ... 'IE= E11.erc~

..

SMcJ .. or-1~ g i)tv1, H-11

:for"""""• ~ J.+:::U) 0'f&l-•Pf0/'>"F£ N. lfi:.

'790:%1 o/- pi~ -v-/1/ ~ d 6'-7/ J ~7-"

~ ,· 0J..! ~ucleJ P~' ~~

P£1 {)'?"'~~l?f ~1 ~ItA. U

1-) &rt£_.1(""1

• '

. -L

~ D~ffDx:

tf ~ardiac: MI . - Myocardial Sischaemia

Mitral valveprolase Myocarditis Pericarditis

-Aortic: Aortic dissection Aortic aneurism

-Oesophageal: Oesopbagitis

-Ma.rsive PE -Mediastinal:

Oesophageal spasm Maliory-Weis syndrome

·\mll'AE[D@ . -Lungs/pleura:

Tracheitis Malignancy

Puhn.infarct Pneumoma Pneumothorax: Malignancy TB ColUleCtivc tissue disease

-Musculoslceletal: Osteoarthritis Costocboodritis (Teitze's disease) Rib fracture Intercostal muscle injury Epidermic myalgia

-Neurological: Prolapsed disk Herpes zoster Thoracic outlet syndrome

Investigations:§§S\ and take it from there . .,., ..,/ .,..,.. ..,/ ...,..... REMEMBER: Common cardiac symptoms"" Chest pain, dyspnoea, palpitations, syncope, oedema. So know your approaches to them!!

... - --· / \.£k::_/" . ------ . - .

... .

\__. c~·,c)\.l c .. .-;.i .s_. . '--- "( U \ !\. t:' CJ.--"-'\.) _:.:::...ll0'-'2-~

£) t...-tfrs 'j 1)

Congenital Heart Diseases ~~~~g,'IJ.~ ~Q~J;:J~!114Pb~~~l}.L.~4§.lL(for cyanotic heart diseases, please refer to paediatrics)

1. r,&u,IQ . .&qmt:na:a:J&~w..«,t.. _extra blood is displaced through a communication. from the left to the right side of the heart, resulting in increased pulmonary blood flow _shunt volume depeo.deot upon three factors: size of detect, pressure gradient between chambers or vessels, peripheral outflow resistance _untreated shunts can result in pulmonary vascular disease, right ventricular hypertension (RVH), and R to L shunts

tt'i'.Tni'Se~~~ ~-.;ostium primum • common in Down Sjludrome ,.ostium secundum· most common type (50-70%) Bli!IUS venosus. defect located at entry of superior vena cava (SVC) into right atnurn ol\~n asymptomatic in childhood

-murmur: often grade 2/6-3/6 pulmonic outflow murmur with widely split and r~~cd S2 . . -·-··· . ~ ~RAD), mil~rtgfit bundle branch biW (itBBB) '-- CXR: increased pulmonary vasculature . niltural history: 80-100% spontaneous closure rate if ASD diameter< 8 mm _if remains patent, congestive heart failure (CHF) and pulmonary hypertension can develop in adult life . management: elective surgical or catheter closure {low risk procedures) b~tween 2-5 years of age

~~l!m~ . patent vessel between descendmg aorta and pulmonary artery limc;tionnl closw-e within frrst 1-15 hours of life, anatomical closure within first IY~ ot hfe 5 · I 0% of ail congenital heart defects , ~(11nmon in premature infants (!13 of infants< 1750 grams) ,;iay b~ asymptomatic or have apneic or bradycardic spells, poor feeding, ~c~~ory muscle use "~~ociated tachycardia, bounding pulses, hyperactive precordium, wide puis~ r~;;ure r,:;;: murmur: onhnuous ".machiner " murmur best heard a.vetbnfraclavicular area} ECO: mays ow RVH ::XR: normal to mildly enlarged heart, increased pulmonary vasculature .liugr.u~is by echocardiography (ECHO) 1utural history: spontaneous closure common in premature infunts, less mmou in term infants nanagement:\iodomethacin,\surgicalligation. or catheter closure 1igll risk ofSBE, antibiotic prophylaxis required until6 months after closure - .

·r:;_" .... " ....... ·~·~·-,....a~ ~ ~~~~~~~ 'o. t_ '"e ~ r a oarrowmg 8t''a'3i'&'aTiffos always at the level of the ductus arteriosus

=commonly associated with_bicuspid aortic valve (50%) ·

tZ'.n.td'€liG~~ ~ _most common congenibl heart defec~

small VSD (majority) • asymptomatic, normal growth and development ~early systolic to ho!osystolic, best heard at left lower sternal border (LLSB) -=='" • ECG and CXR are normal • ~ost close spontaneously, do not aeed surgical closure even if remain patent

moderate to lar~c YSQ =-delayed growth and .dcvelopmen~ decreased e~ercise tolerance, recurrent URTls .~:~p_isqd~, GJ!£.

• murmur: holosystolic at LLSB with thrill, ~d.-diastolic rumble at ae_<:_:x, size ofVSD is inversely related to intensity of murmur • ECG: left ventricular hypertrophy (L..:1!), left atrial hypertrophy (LAH), RVH • CXR: increased pulmonary vasculature. cardiomegaly, CHF • natural history: secondaryjlufmonary hypertension, CHF b¥ 2 months of age • management: treatment of CHF; surgical closure

_few bave high£!? in infancy (160-200 mmHg systolic) but this decreases as coUaterals develop _ if severe, presents with shock in the neonatal period when the ductus closes _often asymptomatic with upper extremity systolic pressures of 140-145 mm Hg _ ~eak pulses, d~creased blo_od ressure in lower extremities, radial-fem~>_ral d'!!~L -- it"asSoctated wtrh other !es10n.s (e.g. PDA, V , can cause CHF _ ECG: R VH early in infancy, L VH later in childhood _ murmur: absent or systolic with late peak at apex, left a;dlla, left back _ management: balloon arterioplasty or surgical correction

comolications : essential hvoe ension

·cv:.\.~o:riC ·c·oNcENrrAL HEART nrsii"As"E"~"'t .3Y5iefii:ic''venolis retuni !e·.:i:ii.!ei-5 systeililC''ciic · ·· ·an"c3irectly _most prominent feature is cvanosis (0 2 sa < 7 5%)

differentiate between cardiac and other causes ot cyanosis with h•roeroxjc test {if ~mprovement ofl'a02 , less likely cardiac cause) _sur1ival depends on mixing via shunts (e .g. A;;b, V .:!0, PDAJ

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I· i"~ . ~ .·.

t t

~ Pituitary Gland ~ DM

E-ndocrinology

~ Adrenal Gland ·Addison's disease -Hyperaldosteronism

~ Diabetes Insipidus ~ Pheochromocytoma ~ Hyperprolactinaemia ~ Thyroid Gland ~ Cushings Syndrome ~ Parathyroid hormone )> Hypercalcaemia ~ Hypoparathyroidism ~ Endocrine Emergencies

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Endocrine

Ptuitary Gland

SPOT diagnosis: Endocrinopathies

1. Thyrotoxicosis: ~' jl.'"e.tiQial m..:t,J!.Oedem!l,,2n.Y;,h~ly~, ~l<!ging eyes (exophthalmos) QUlM4P w ~- W4UV ~ > ....

2. Hypothyroidism: Hajr loss, eyebro loss, cold eale skin, characteristic face

3. Cushing's syndrome: Central obesity and wasted limbs, moon facies, buffalo hump,

4. Addison's disease:

5. Acromecly:

6. Hyperandrogenism: •

7. Hypoptuitarisrn:

supraclavicualr fat gads. purple abdominal striae.

Hyeerejgmentatlon (face, neck, palmae creases).

Acral {distal} and soft tissue overgrowth, big jaws (macrognathia)

hands and feet, thick coarse skin, Coarse facial features.

Hirsutism, temporal baldin~,~

~, yellow thinned skin resu!tjng !g fine wrinkles around the e'(:!

and mouth makjng the gt !oqk glde,t.

8. Pseudohypoparathyroidism: Sho t re~k and_£h and_ltn metacarpals.

9. ~ yeopa rat hyrgi djs m · \_;;D;.;.r.:.y~, s;;.;;c;.;;;a~ly~,.:;P;.;;U;,;.ffy~s~.;:..;;;;.;,;.;.;.;;.;.;.;;--.""'"'"--. ... .-..;;;;;.;;.;;.;.;;;.;,~

{::\·~~~. Ptuitary tumours: Mostly benign adenomas

4

< lcm = microadenoma

>1 em= Macroadengma

The anterior pituitary secretes a number of hormones includi :

I

: • Growth hormone (GH) I ' . Prolactin (PRL) ! • Thyroid-stimulating hormone (TSH} ; • Adrenocorticotrppic hormone (ACTH} ! • Melanocyte-stimulating hormone (MSH) t i • Follicle stimulating hormone (FSH.) ...:,_ __ __ ,. _____ -~~~.. ... \ _......!··· _ .. _. \~-. -· 1 • luteinizing hormo~~-(~H)___ -·· _ -·-·- \ .. \: .. ,CJCA,~'

® Although theoretically a tumour could secrete any of these hormones, the common tumours secrete growth hormone (acromegaly), prolactin (prolactinoma and hyperprolactinaemia), mixed secretions or no secretion at all.

{There are 3 histological type;~

1 . .,S,hromophgb.t':,: (70%)- Non-secretory but cause hypoptuirarism, most secrete PRL, a

few secrete GH or ACTH. Local )Jressure effects jq ~ 2. Acidoghjl (15%)- Secrete PRL or GH. Local Pressure effects in 10% 3. Basophil (15%)- Secrete ACTH. Pocal pressure effects rare.

Patient presentation: . . Local Pressure effect symptoms: Headache, visual field defects ·~. .. On examination:

1. BITEMPORAL HEMIANOPIA DUE TO OPTIC CHIASM COMPRESSION 2. CN palsy Ill, IV, VI a~e to pressure or invasion of the cavernous smus. 3. Dl ==• -4. Disturbance of the hypothalamic centres of Tern erature control, slee etite. 5. Eros in through the floor of the sella tursica causing CSF rhinorr

Sl:

1. MRI/CT scans 2. 'visual"field examination

75 . .....

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3. Blood tests for the hormones are important diagnostic tools- PRL, JGF- 1, ACTH, Cortisol, · TFT's, lH, fSH, testosterone lgvefs jn males. short Synacthgn iAAt. ·

4. Glucose tolerance test if acromegaly suspected. 5. Over night Dexamethasone suppression test if Cusbjngs disease suspected. 6. Water deprivation test if 0( suspected. •

Most tumours are benign but are quite serious because of their position close_ to important brain structures.

J7reatment includ~: a:

1. Hormone replacement as needed: Ensure stroids given before thyroxine as it can induce an adrenal crisis.

Rapid ptuitary enlargement due to haemorrhage into a tumour- causes a sudden mass effect, cardiovascular collapse due to hypgptpjtarjsm aod deatb.

Hx:

1. Headache

Ex:

l.Meningism ,....-

3. Ophthalmoplegia ._,.­

Visual field defects ~

DifferentiaiJit presents like a subarachnoid bleed. \

Treatment: involves urgent steroids (Hydrocortisone lOOmg IV) and surgery. '=-

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It is the diminished secretion of the anterior pituitary hormones ond is most commonly caused by a pi!ujtacx.I!U!Wlru:iuml.uP· The hormones are affected in the following order: Growth Hormone. Gonadotroehlns: FSH and LH. Proladin. Th roid-sti 'ii!ligjiililli;;U::4~1:~· Pnnhypopituirism 1s e iciency o a anterior hormones. usually caused by irr·.adiation or surgery.

tr,!ffi€fr!ii,to~~$:c[~~i] (2£'regs@ .6H ·· Lethargy, central obesity, atherosclerosis, muscle weakness, dry wrinkly skin, osteoporosis, decreased Cardiac output and glucose.

Decreased Gonadotro . hins ema e: Amenorrhoea, ecreased libido, osteoporosis, decreased fertility, hari

loss, breast atrophy, dyspareunia Mole: Erectih: dysfunction, decreased libido,gynaecomastia,hoir loss, hypogonadism. Chronic anaemia may also occur.

Decreased . TSH ~ads to seconaary hypothyroidism. This contributes futher to apathy and cold lntlolerance. In contrast to primary hypothyroidism, fronk myxoedema Is rare, probably because the thyroid retains some autonomous function.

Lo5k gf.dc:lli Re.sults in symptoms of cortical insufficiency. In contrast to primary adrenal insufficiency, aldosterone sectreticn maintains normal K-levels. The patient doesn't become pigmented because ACTH decreases and there is lock of stimulation of melanocytes. Lethargy, Postural hypotension, dilutional hyponatraemia, Pallor, Hair loss.

Lack of Prolactin trare-J;;!lure ;rtctation

Causes: Structural· Primary pituitary tumour, esp adenoma. Craniopharyngioma Meningioma Congenital deficiencies- GnRH(Kallmann's syndrome functional- Chronic systemic illness. Anorexia nervosa. Excessive exercise Head injury, Para-sellar surgery or radiotherapy.

,. 1 ~otha~, .. ~. ~lm ........ .;;a. ..,."fndrc;:,..~,...-; .~cur ...... .u..\:nati~ .... ..... ~;~·- .. meningitis), ischaemia. Pituitary stalk: Trauma, surgery, mass lesian(craniophoryngiomo, meningioma. Pltuatary: Tumour, irradiation, surgery,lnflanunation, lnfiltratlon(Haemnchromatosls, Amyloidosis etc).Sheehan syndrome(pitui~ necrosis after postpCll'tUI'I\ hoemmorage) ~· . ) } \

Investigations: • In acutely unwell patients, the priority is to diagnose and treat '

cortisol deficiency. MRI orCT ACTH clef.- Short ACTH stimulation test or Insulin tolerance test(ci: epilepsy, heart disease, odrenol failure.) lH/FSH def- male- random serum testos~erone,l.H and FSH

Pre-menopausal women - ask If menses Is regular

1 • Post menopausal women - measure FSH c111d LH. 1 Should be >30mU/L

TSh def- measure rardom serum thyroxine. TSH Is often detectable In 2ory hypothyroidism, due to inQCtive TSH lsoforms in blood. Arginine and GH releasing hormone test. Glucagon stimulation test when ITT Is controindicated.

Treatment: Involves hormone replacement and treating the underlying cause • Hydrocortisone for 2ory adrenal failure

Thyroxine if hypothyroid . . Hyp~;~gonadism(for symptoms CUid to prevent osteoporosis). Males: testosterone enanthate 250mg IM every 3 weeks, doily topical gels or mucoodhesive tablets. Female(premenopause): Oestrogen. If GH deficiency Is suspected refer to an endocrinologlst.can give Somqtropin (GH).

~~ The disease is due to the hy£~!"se~reJ!on of.. of :;:t~ hormone from~ P!tuitary rumour in > 99'/. of cpses on IS rarely associate Wfft]C'fii\k w;,gdw;tl!!h.o,£J![p!!!lb i~ne ega carc:in2l<!.!:;IJ!!Wr.Prevolence is 1:1 Qnd it mainlf presents betweenJJJ,. ~tl'ye'Ht! ... GraWfu hormone ~~j~IQ1lljqft.ti~ and ~lseleWlo'?R~~h~p~i!Q lhcrellSed secretion of Insuhn-hke growth factor and 1ts secretion ts tnhtbtted by somato$tatin.

frontal bossing prominent supraorbital ridge enlargement of lips, nose and tongue. , . mandibular 1111largement with prognathism w,..a-o q~c::>­itide.n;dJpm.h;,tW$en.t~i.~~!' lnci§ru; tCAtit...

thickened skin In children and adolescents, initiation of GH hypersecretion prior to epiphyseal long bone closure Is associated with development of pituitary

gigantism

Can also pruent with Local tumor effects Pituitnry enlo.rgement

Complications: Impoireg,glut;g~e .t~(40%), DM (20~.). as tt;:w,!h-hormo"!-J.s counter rerlato~ to in5ulln.

~~~~~:5fr!i~lws:=:;=:~ tJ»;Jru;prgsed BC..pnd jpsu'in re3is1w1Es. ~a\igooll,Sl( - increased risk of colonic polyps that may develop into colon cancer- guidelines suggest a colonoscopYiir50.

Investigations: R11ndom ,@J:I!wth hormoM m;psur.sru;Q!1 grs;mt.b!jlpfuUIS GH Is secreted in a markedly pulsatile manner. GH i~ increased in stress, sleep ond puberty. Decreased In puberty. . Se IG - Is userJ os a screening test for Acromegaly

e c inlcal diag~osis must be confirmed by measuring Gh during an.,ggL glucose tolerance t Usually GH is Inhibited by a rise In glucose and Gh s au e u etectoble(<O ,!i). In llc:romegoly there is a follure to suppress GH. False positives Is. seen In puberty, pregnancy, hepatic 11nd renal dlseo.se, anorexia nervosa and I>M, Prolactin lsvels mgv hG el;vamrJ. AAI of.gltultsc:dgw,. Test gltuitery fungrtgn,for lrL!loJ!l!.!!!!tarlsm fCG · -Xl§Ygl fisld,MU£1Jl:!Y

• Qld phstqaJ!UiWM£~

Treatment • · Trons-@enol$ll sur_g~y Is U!lually the treatment of choice. Cure rate -

B07. in microadenomas and 40% in macroadenomas. 3 months po~t-op', repeat special Investigations to assess GH. If GH remains high, adJuvant medical or radiotherapy may be needed.

•

Medical: Somatostatin 1111Qiogues CSc!~otlde given monthly IM) and lanreotiCie, Dopamine agonist are lessifplul but help in patient~ with prolactin excess. Pegvisomant, a recombinant GH analogue acts liS a 6H receptorantagonlst.rt suppress IGF·l,Gh In R11diotherapy: If surgery iooppropri11te or as adJuvant therapy. J:t ~ toke years to work.

It Is important to do'yearly follow ups· GH. IGF-1 measureriii.mt, 06rT, visual fields, CVS etc. Aim Is to keep GH<5mlJ/L

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~lrsutisrJ Is excessive and increased hair growth.an femQle humans in \ocaticns where 'the. occurre.l\ce of termii\GI hClil' norrtl<lll~ is minimal or absent. For exal1\ple, a beard oG cbeU fl&!t· Hirsutism is a ~m rather than a disease and may be a s1gn of a more serious r;ne.dical indication, especially if it develops well after pu~

The cause of hirsutism can be either an increased level of androgens (male hormones) or an oversensitivity of hair follicles to androgens ; Male borms~es such as tgtost}irgne stimulate hairgrow'th, increase size and intensify the growth and pigmentation·'of hair.

Cutaneous manifestations: 1. ~ 2. etjgJs.pgtterg bafdi.pg( androgenic alopecia)

3. ,Virilisation -condition where androgen levels are high enough to cause additional signs.Virilisation can suggest a poss1bJe ovarian or adrenal neoplasm: · •

• Deepening of voice • Breast atrophy • Increased muscle bulk • Clitoromegaly • Increased libido • Some women also have menstrual dysfunction

Causes: Polycystic ovary syndrome

• Idiopathic hirsutism • Drugs - Danazol • Congenital adrenal hyperplasia (mast often Zl-hydroxylase deficiency)

Hyperthecosis Ovarian tumors Adrenal tumors

• Severe insulin resistance syndromes • Hyperprolactinemia • Cushing's syndrome • Obesity

Special investigaTions: Blood tests may show elevated androgen !eyels.

• CT scan, MRI, pelvic ultrasound-- used to identify cysts or tumors on the ovaries or adrenal glands

Treatment(Depends on how severe the problem):

Determine the cause eg. If on medication that c:an cause Hirsutism- stop meds Tumour - surgery Obesity - lose weight

If no underlying cause is found, a combination of self-care strategies and hair-removal techniques may be used. Psychological

support may also be helpful since hirsutism is often a frustrating and embarrassing eondition.

Eat healthy, exercise and maintain an adequate weight.

Meds Oral contraceptives- ypically choose an OC tha.t contains a progestin with low androgenicity (or an antiandrogen such as cyproterone acetate or drospirenone) Anti- androsers:ioironolactoneJiu1gmi~. and cxproterone acetate-- blocks androge'n receptors in the body !nsulin lowering drugs- metformin, rosiglitazone.Doesn't real! hel si nificantl . Eflorinithine (Vaniqa) is a prescr1pt1on cream a reats unwanted facia hair. t slows new hair growth but doesn't get rid of existing hair. Hair comes back''i'f you stop using the cream

Cosmetic methods ·

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DM results from ~ oLlljii¥!J~b©S rtte~D~;r~ogf!nous Insulin. r¥ee l~f": Insulin"deficienc:yue to set ve a4!8it8f lnsyhn SEER\tin9 . paocrea IC 9 Cells. --=c:> \}__)<::;. ~ ~ \t\.. . fD.-,\-.lXDG D pf1: Insulin defip!iQ(iY as well a~nsulln ;e;!stance occurs~\ ·~ Risk factors for type 2 diabetes: 1 l-\\')l.( 0 """' """ .~

1. Increased age · ~ ~ 2. Glucose intolerance \.' G-7 d- . '8-3. Family history of diabetes .,. oro$ 4. Physical inactivity and calorie excess f7 · ''-' ()

5. increased waist drcumference Ol . G- ""' 6. Increased BMI/Obesity ,c, · '\), e-

f a"''c.. c, c s.c"""'c b.~ "L()...T 1 ::f~~ 14-; 5 · ~ '-b .. <f-.

0~J1)o~~c.... M\QD ~as.D t--~7(1£ ~~C---\-~ (f\.

GAU6E6 or: J!.u~AJ-/ Gll.~ATH'CJ .

k ker/oCJerJdas l5 13 : fJ-ilr.y Je..,.d 0 ,,(J:) I u UI'D~IQ

6 5oJ,o-jo~~ 0-lhLIS PorooebJrLll JVI Nl e;) honer I INI·L

~0 A AlctJh:t/ 1-J J-.n CJ-f rcno1cfa::J~

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l Presenting symptoms of hyperg!ycae@i] 1. Polyuria, frequency and glucosuria 2. Po!ydi~a and dry mouth, thirst 3. Weight ass- insulin defidency 4. 'lrocffi~ s. il&W'Pnagia 6. Blurry vision 7. Burning feet 8. Fatigue 9. Kussmaul's breathing (deep sighing respiration] 10. FUNGAL INFECT10NS esp. candida, UTI's, ABSCESSES

+ Random Plasma Glucose 11.1 mmoi/L

c§.! 6.9m~ [draw In ~morning after ovemlght fast]

2· hour Post ora lerance te > 1 [OGIT =75g glucose Ingested, measure Plasma glucose

OR

If there is any doubt - use the oral glucose tolerance test

Classification of Diabetes Mellitus (DM)

----==-· -( TYPE ~(Insulin Dell~:~~dent\ ( TYPE 2-tNon-IRSUIIn DeDef.dentl Etiology F--'o ~UIIC • genetically.;lliib!d

• Autoimmune Destruction or a-cells

Onset • usual!:.: bef!l!:l: age Jll. • u2:!!!!1Y after !!9! 40 Youno and aOJte

Genetics • associated with .I;! LA DRJ DB:! • 2;ea1er herita~.ll!~ ltJ~Il I¥lls J. and~ • noo.i'lLA-as-sodated • oW% coocordance In . rao: 100% CllOCOCdaiiCe In monozygotic monozygotic twins twins

PathoohvsioloOv • completely lnsulln-deftdent • abnormal insulin seaelion

Risk factors • pe=nal hls!O!)' of autolnvnune e.g. Graves' disease, myastllel1lii

1-§t..vls, Addison's disease. perniclous anemia

Body Hab!IUS • typically pormalto wil$:11

Pharmacological • Absoh•tc lniyl!o resulred

-= Circulating Islet It' 50·85%) CeU Antibodies I'---"'""'

Other Aspects • prone to ketoacld,s!.s

NOT All PATEINlS Willi I.AIE ~OM HAVE TYPE 2

·jr~ ~~- -~ tisSues lilcdy due to recepwc Gnd po;.r· recepTor abnonnanties • lnaeased hepatic gluconeogenesis

·~ • (am!!y blstory ._ pckx abnormAl a!, mse tatenmre • bypertens\Qn • byqnljgldenUa • geslll!ional diabetes me!IIM (GOM)

• camb!natlon of 9011 hypgglycemlc:

l~un

• not !l!O!le to keloacido<ls h! ¢ prone tp

hyper0511101ar coma \-\\-\ S Not excluded wllh keto-acidasls 20% of patients have OM complications at diagncsls

[Diabetes Secondary to Spedfic Et!glogies } i.GeneUc · • ~·Turner's syndrom~, Huntington's' disease, Porphyria,

.,. ndrome. Pradar - WJ!It syndrome genetic defects In 6-ceH function and insulin action

3. Endoainopathles e acromesalv, Cushing'S syn=, :;:cagonoma, !JYperth)UDid!SOt,

Hyperthyroidism, Pheochro to a. Aldostgrgngma

4 •. Drug-Induced . . • 8-agonists. 9lucocorticolds. ~ phenytolp. Protease lnhlbitm ·-· 5. Infections • cytomegalovirus (CMV), congenital rubella, Mumps, Coxsackie

PA'rt!OGENESlS

toxins--~~~~ viruses foods GenetiCs Stress

T -cell activation and lnfiltra lion of Islet cells with mononuclear cells, Maaophages, helper-T, cytotoxlc-T cells and NK cells

Insullnitls [Inflammatory process]

• ~f B-c~!ls leit wlllf!:esent t;J!n!canY as gl~b$· Very slow process. • ~and poorly understOod Interaction between environmental and

genetic factors.

Typ!: !Diabetes Proposed Pathoge1,1esis \

<§!iiitit1t~~ IJul\1le W""' dol- . . \1!!:!!l<

~ . .., ... ~ ~blt&<eiclliltld ....... PlliP!Inl!lsllltioMD Insunn reslstanse In

· rliOIIIiiitc ad!.yase BSSue, liver and Dl!!n!!ld"":*l-911 ~~· elillullon !!l uetoobesity,renal ~ _ failure, TB drugs, OJshlng's,

fEAGt. vcEIUIIA Acromegaly, Cystic Fibrosis, · ~ . PCOS, Werner's syndrome,

~~-=~ '"""·---.. -• syndrome, Pregnancy,

glucose toxicity] + pancreatic B-cell fanure leads to Impaired glucose tolerance · and hyperglycaemla. If the Insulin response is adequate = euglycaemlc. If not = TYPE2 DM!!I

,, 111 J I 111~1.." lOill i ~ .J :> H ' ,cUt t

este'rifiea ralty adds caustng po5t-fecept0rderects ii1Trlsutu\'S adlOj}. 2. Mutation of genes encoding insulin receptors 3. ~Orculating autot~ntibodies to extracellular domain of the insulin receptor.

~tests in DM· ... ( OiaQnostic)

OGTT '· FBG

COMPLICAUONS !=== OF DIABETfS c

Assessment of Glycaemic Control RBG HBAlC Fructosa mine

rl urop atl:ly Infections Macrovascular

Mlcrovascillar (intracellular hyperglycaemja of vascular endothelium causing abnormal · endothelial functioning, this causes increased vessel wall profetn accumulation and microvascular ceil loss fogeffier Wtm vessel occlusion].

Aggravating factors: e:r glycaemic control, inadequate control of hypertension and cholesterol, smo lng, high fat diet

§icrovasc§i · :: . ::::·:::::. :: ")

Accelerated atherosderosis leading to 1. .lliD and coronary artery disease (CAD), 2. CVD1 stroke, 3. pulmonary vascular disease ~ <\. Peri heral vascular disease [amputation, gan rene

Most common cause of deat tn . nee maaovascular disease develops In a diabetic, they have a poorer prognosis for survival than normogtycaemlc patients w1th macrovascuiar disease.

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In : .. '>ner velcp :~' :1:~ 'r sev years ot uM,Tohowul!J the activaoon of RAAS.

• In tltpe 2 patients it is mostlY_ present at diagnosis and follows actiVation of eSNS secondary to lnsulm resistance and hyperinsulinaemla.

• The TARGET is lower for diabetic atlents namely: 130/85 mm !!!! Jarget lipid values in diabetics: LDL < 2.6, HDL > .15 and TGl <2.5 ~L

r:: : ... aP ;;:•• ~· -~~:~::c~::"::::::= .. ::_: . .,. :::J 2. Acute bacterial cystitis and pyelonephritis ..............-3. Emphysematous pyelonephritis---4. Perinephrinic abscess ..-- ·' · 5. Fungal cystJtis-----6. Necrotizing fasditis ...---7. Invasive otitis externa .._---8. Rhinocerebral MUCORMYCOSIS .._.-9. Cholecystlts ,...,-

~(Microvascuia?\_::__::::. Retinopathy ; '- 7 - Nephropathy

- Neuropathy. • major chronic complication of type l and cype 2 OM • pathognomonic lesion i!tbilsement wmbrant thickening • dasslcally causes r,et!n?pathff nephp!PillthY ADd PCU,(Q!P~ • can Involve many other organs, lridudang heart and skin . ·

~ve complications: i 1. Glaucoma ~ 2. Cataracts v--" 3. Retinopathy _...-4. Glycation of the lens protein with cross llnliing 5. Osmotic swelling of the lens A~·~

e . . . · \~ ~ ~j~~;~ Background non-Proliferative: ~ c-..k.k

• tao aneunS{TIS • Scattered exudates (hard, yellow) = leaking vessels

Haemorrhages {flame shaped, dot and blot) • Colton wool spa~ = dead/isc.haernic vessels

venous dif.i'd6!t~Yooping

o onwoo > nous ea mg, oop1ng and duplication

• Intra-retinal mic:ro aneurism (IRMA) 3 .• frglifer;~tive t R••b.qqsi5 Jridis

• ff·XW~'*~e • Fr rous proliferation • Haemorrha es

4. Advance _1a e a_c eye disea~e A~\:::> . -~ . ltefi1iaF~~~e~menf

.. rtuTieSsg·i~F • Neovascular ~!:ucoma

S:.,...Maculpga.tlJ.y • Mag dar Qedema • Exudates within 1 DD of the fovea • Orcinate around the macula • S\,ldden, g!!l~ loss of vision < 61£

(Annual eye screertlng mandaffi 1. Visual acuity

. . 2. Eye examinatlpn (ophthalmoscopy through dllated pupils) When to refer?

l. . Severe ogn-pm'ife@tlve/proliferatlve retinopathy 2. Macular oedema or exudates in dose proximity to the macula 3. ytaract 4. Unexplained reductjon in Visual acuity

• present in 50% of patients after 10 years with OM, B0-100% after 20y. • one of the leading causes of blindness

' c;;p;;;.~ w1M?ro rnwmqn In Tyoe 1 diabetes

1. Increased lomerular filtration rate (GFR) and kidney hypertrophy 2. nuria (3D-300 mg/24h) . 3. (>300mg/24h, positive urine dipstix) 4. isease [ tBUN and Creatinine, T K and fluid overload]

Progresses to cause h'tEertension, persistent proteinuria (macroalbuminuria), Qe[?hrotic syndrome and renal failure. Miaoalbuminuria is an indication for

• common In both t¥Qe 1 pn(f type ? OM • Pathophysiology: metabolic defect th ught to be due to !no-eased

sorbitol and/or decreased rnyolnosltol (eXact mechanisms not understood)

3. MononeU!l?J,;!at!ri [ entra== s '"' •• ~l]t~iie~u~WDQ\i!=;:;.:.§~: =_=:::;:::.:+==:::::::=;.;;;::;~

- Carpal nmnel Syndrome (median n), - Ulnar nerve compression svndrome,

- M2r.Jigia pareshetica (Ia[ cut n of thigh), - · bateral popliteal nerve compression (drop foot) - [;ye; Lateral rectys - Radial ne!Ve - atrophy - Thoracoabdominal radiculopathy

4 . Proximal motor neuropathies • Amyotropathy: especially proximal neuropathy affecting the

quadriceps musdes with weakness and arthropathy. **Screen for neuropathies by usin~tunlng fork for vibration testing and ~ monofilament

Management of Neuropathies: • tight glucose mntrol • anti-depressants (e.g. ijrpj!rjptyline), capsaicin, and anti-epileptics

(e.g. Tegretol, Neurontin) for painful neuropathic sp1dmmes • erythrom~n and domperidone for gastroparesjs • foot care education: Cheds feet dajly, Wash (eet daily Keep toenails short,

Protect feet, Always wear shoes, look inside shoes before putting them on, Always wear socks, Break new shoes gradually

• Alpha lipoic add and Gamma Unoleolc add

4 .. Other Complications _ skjo djsej~se _bone and. joint disease

L.~. -~--

I I i

::::J

~V< ----------------~----------~~- .

r_....._~

U~;a-k~~

~-dill.~

--~ ... .,,.~.--11ato (\'V.nt¥ iti'A1 M!M'I .

Diabetes Control and Complications Trial (OCCT} (1993) demonstrated a 5Q-70% degeag.!Q, rnlqpv;5'\11Ar f1jcat~ In type 1 OM in an nte veiY eated group as compared to a conventionally treated group as well as a mar~? In Y4§Qdar &Wtlons n imith weu-~re u

Current recommendations by ADA!

FBG (before breakfast) 5.0-7.2 mmol/L ll"ostpranlii<tl plasma glucose {2H <HJmrnoiJL-, an:er a mea& u . - ...

ltBAlC ( < 7 °/o '"')

··- : C, ..... 7 :=:::I ton-ph==~cp:;l}teN.e*nC::::;~::::::JI l 1.1 Diet:) '-=i::ifeslyle!; changes to prevent a patient with IGT to develop Type 2 Diabetes:

(58% r~uction) s· pillars of a healthy diet:

• Reduce saturated fat and sugar Intake • lncrease fiber intake • NB Low GI carbs (starch carbs) • Umit salt jntake

~ojd almhol consumptjoo and stop smoking.

• 25:'30min aerobic exercise 3-4x per week · Target heart rate of 60 -70% of maximum

• Exercise im rove glvcaemic control and Insulin se · ivi • _Improve lipi pro I e: 1TGL, 1 LDL, THDL. • Decrease BP • Increase metabolism and helps with weight reduction

Type 1 DM pt Invariably need I!!5ulln Type 2 DM Managed initially wil:h diet and exercise alone- progress to need for oral hypog!ycaemic agentS and jhen insulin depending on Glycaemic control.

\2.1 Oral. hypoglycaemic agentil

• INSUUN AUGMENTING GENTS (If'I£REASE INSUUN SECRETION) 1.-ca. -\o c:.1., cl-~ . .

• ASSISTING AGE TS [REDUCE 91~0SH RESISTANCE]

• INSUUN SELF ~S,.: ~-.~ S..

Principles: L._£:ombining drug = more effective tnan stopping one ~ffit a.10 ISl!rmiO!".ofi

another. 2. ~jp9 a 2"" i!Qfjpt > than Increasing dose of one agent already near

maXImum dosage 3. binations rna be useful but lack expertmental testing 4. Failure of 2 oral agents calls for Insu 1n a one or 1n corn 1nation with oral ~rem.

5. In pt with severe hyperglycaemia: Insulin may be started from the beginning, when tox1c1ty resolves= reduce or withdraw it!

.·- . ~~~SULIN AUG~AGENTS [INCREAsE INSULIN SECitETION]

~ ...... 1. Sulfonylunas: Gliclazlde (Dlamicron), Glibenc!amlde, GlipiZide, Cblopropamide, Tolbutamide.

2. Metglitlnides: Repaglinlde (Novonorm) Nataglinide (Stariix)

Sulfonylurias:

Stimulate release of endogenous Insulin by blocking K·ATPase channels ..... Open Gi channels .... <?.' lnft~-+Insu!ln reJease! NB: ~_,\!d f~ll!!Jg ~;,cells!

S/E: N~~ ausea, GI discomfort C/1:~'

• Type 1 OM - no functioning B- cells left! • Pregnancy • hepatic or renallmoalrment. [Metabolized In liver CYT P450 e

active metabolite excreted by nei'$. - will t risk for Hypogiycaemla. • Also C/I in pt on Warfarin. Warfarin Induces C'!T (!450 enzyme thus

decrease rnetabOtlSffiOF SU and Increase its level in blood -HYPOGLYCAEMIA!

• tan't combine with other SU/ Metglitlnides • NB: SU 1 receptor, SU 2A and B receptors as well on cardiac muscle! SU

will occupy ALL of these receptors causing Ca Influx and thus causing a TACHYCARDIA. It aggravated cardiac Ischemia= called Cardiac Ischemic preconditioning!

Indications: • Use with other Oral Hypoglycaemlc agent

Meglitlnldes: postprandial Glucose Regulators

Stimulate release of endogenous Insulin by binding to ATP dependent K-channel on B- cells. Not SU receptor. (rapid-acting, better post-prandial glucose control)

·- , _ ,_

lt b ic~ u

5/E: hyr>_oglycemia (less frequent than with sulfonylureas)

C/1: pw>ersensithtity djabetjc ke•Ntid~)

~G AG~REDUCJ: INSUUI'l RESISTANCE]

1. Biguanides: Metformin 2.-Thiazolfdinei1'1'8nes: P{oglitazone, Rosiglitazone 3. !!jiGa-§!t.\.5os@jii:Inbibitocy: Acarbose

Biguanides: Metformin {~lucopha~e)

L Reduce luconeogenesis In liver 2. Increase lnsu 1n m 1ate ucose utiliz 3. e uce g ucose a sorption through gut 4. Increase splanchnic glucose utilization 5. Activate Insulin receptors and Glt!T4 recepto(11. When you exerdse- you

move GLUT receptors to cell membrane and make them fuse with the cell membrcme at a permanent level.

Advantages: 1. Weight loss and slight anorexic e~ 2. No Hyooglycaemja 3. Decrease thrombotic risk as it decrease platelet aggregation and decrease

plasminogen activator inhibitor (PAl-l) 4. Positive effect on lipid profile 5. Safe in pregnancy

S/E: lactic addosis ·

• "anorexia, nausea ' 1

\':;>\.-z::... -..,A ~s~\-\~ ..... • diarrhea ~ • Gl discomfort

C/I: • hepatic or renal impairment due to lack of lactic addosis . • alcoholism • ~da~ •

Thiazolidinediones: ~osiglitazone (Avandia)

1.

2.

T~J. -t:-:;...._5 t ~.:=

4. 1-lOA: -aa,..~AA-"i (~ :~. -:;;...-~ ~-~ c:..;;.-~;.,~. :J.

r"9ularors ci hpid and 91~ rr..:Gcus-. - :.-~..,-~ G._ I_. ;;..--~: with improved glucose transpor.-. I<Jaci">SC:l ;-_iO,.at..:: ;~ ~ o-.: decreased glucose production

5. Decrease TGL and increase HDL (decrease viS<:eral fat oy .r.creas.e peripheral fat)

S{E: • Increased TG • weight gain • hepatotoxicity • n.w@ (decrease hb) • fluid retention

C/1: • l!,yer disease (NB do to ALT regularly) • r;gogestiye heart faHure (CHF)

Alpha-Glucosidase Inhibitors: Acarbose {Prandase)

Decrease/delays the digestion/absorption of carbohydrates by preventing the conversion of pqly- and disaccharides to monosaccharides (thus decreasing postprandial rise of glucose). Only use It as .monoth~!!t

S/E: flatulenc(! .Afilfciilliilat cramping ®i.ihl\a

. C/1: hypersensitivity, DKA, infllimmatorv bowel disease (IBD)

Thus: MOA of antihyperglycaemic agents: 1. GIT: decrease digestion of complex sugars- Alpha-Glucosidase

Inhibitors (Acarbose) 2. Pancrease B-cells: Increase Insulin secretion - SU, non-SU secretaloques 3. Liver: Decrease hepatic glucose production - Biguanides,

Thiozolldinediones 4. Increase glucose uptlke in muscles -- Biguanides, Thiozolidinediones

Step care in OM Type 2:

STEP 1: Nutrition- Diet, ~e. lifestyle changes I raining in' self-Mx and self-monitoring of glucose

STEP 2: Add oral agents (monotherapy or combined) STEP ;3: Add or change to Insulin STEP: Intensify Insulin Therapy

What for WHO? High postprandial glucose -Obese pt

. Recently dx type 2 OM Insulin resistance

A~RBOSE.MEGLnlNIDES MiETBJRMINifBM!>2~ If BMI <25 use metformin/SU. GUTAZONES caila'iSOile used.

....su_ GUTAZONES

NB: How to decide what to give: •:• BM[ >25 = metformln ·:· BMi""<25= }letfOrmin/SU - if this falls - combine metformln and SU

and Insulin thereafter if still no response.

2.2 Insulin 4! - l

When to start? HBAlC routinely~. 0 o Indicated pt might benefit from Insulin. 3 monthly HBAlc miiiiliOrlng Is NB! Indications forinsuiln In tYpe i DM:

- After tt!Jure on Oral Hvpog!ycaemlc agents (OHA) alone (mono Of combined tx], combination Insulin + OHA can Improve glycaernic control with less weight gain. Persistent " er I caemia with OHA. Pers1stent w os n ype 1 OM LATENT A OIM E DISEASE IN ADULTS (skinny type 2's)

; .. ~. ·-~-'

OHA SjE Of"~ r~ ~-..; ;., ·-~;~1 ~ cocnpiiai\Ce

- Pt on multiple medications Pt with renal or hepatic Impairment.

- Women plannin~ pregnancy Gestational Dia etes

- Intercurrent events: MI, OJA, Acute illness, surgery

NB: Patients should be educated to self-adjust their insulin dose in light of exerdse and calorie intake to achieve normoglycaemia.

Subcutaneous Insulin Analogues {lOOu/ ml) lnsulin regimens should: .

1. Mimic Insulin profiles of healthy id. (post prandial spikes and basal levels) 2. Maintain effective glycaemic control and avoid complications.

Administration: • subcutaneous injections: lateral thighs, Abdomen, not umbilicus, Lateral

upperarm! Not forearm. • continuous subrutaneous Insulin Infusion pump • IV Infusion (regul11r insulin only)

NB: ** Lipodvstro.PlJY: S/E If only inject at the same spot everytlme - due to the fact that msuhn &s got Growth hormooe propertJes. Absorption from this area is very poor!

p reoarations: TREATMENT ACTION ONSET OF PEAK {H) ouRAnoN

ACJION (H) CH}

CONVENTIONAL HUMAN INSUllN NI'H Intermediate 2-4 4-6 12-16

lente Intermediate 2-4 4-12 12·18 Ultralente Long-Acting 6-10 10-16 18·20 Regular. Rapid (dose 30-60 min 2-4 6-6

dependent) ANALOQUES ·Giarginlne Lonq 2 ·Flat 24 Detemir Long 2 ' Rat 14·16

Uspro (Humalog) Ultra-rapid 5·15 min 60min '1-5 Aspart (Novolog) Ultra-rapid 5-15 min •60 min 4-5

(Novoraoid) Glulislne (Apldral Ultra-raoid 5·15 min 60min 4-5 Also: Soluble Insulin Humuhn S or Actrapid

..

ill ly_ Qo,\x · -

' L I It .......,, ' _;{ . ADN!NISTRATION: (:)1 C:::,- \ \A""-1: .;:<;;. \ "-~ ---t:> \--""-'~ :.l-

C), 2- -O,L._ ~'Co---\) \JJ..\"Z... . 1. Estimate of total daily insulin requirement when starting an adult type 1 u

diabetes patient on insulin = 0.5 - 1.0 unil:sfkg and when starting an adult with type 2 diabetes = 0.2-0.4 units}kg. OR 1 unit insulin for every 1 unit ofBML Athletes and pt near there ideal body weight will require less insulin than obese pt Be aware of the honeymoon period!

2. Design a regimen to suit pt lifestyle

Insulin regimes Traditional onf:e or twice daily Flexible Basal bolus

Basal and at meal times No longer recommended Appropriate:

L Initial be. 2. ~oor understanding of

the disease

~eguires an intelligent an motivated pt 4 injections required daily

Twice dally regime Total daily dose

213 morulog: 2/3 intenncdiatc +

I /3 short acting

A , ~ . ,,;,.1¢ \ \ ~} \ \'• ', • · r . ·.;:: , .~· \ ·

, -~. ~~ .... ~\. \ l-1~

Flexible Basal Bolus regime

Total daily dose

Basal Bolus: 40% of dly dose . NPH/Glarginine

once or twice dly

l13 eveo.iog: 213 intennediate +

1/3 short acting

Meal time bolusses: 60% in 3 divided dosages Regular/ Lis pro/ As part within JO min before meals

. . ~ .,. ... , .

k .•.• -... ' ~'"··· J . •

-" .· .• :_---,· ~ _. ,.,~' .1" - •.

.. ~\-- .... _ ...... -~- .. . . - .. ... j • .· -- ( . ~ , L .. ll. • .-, ·.,- · .• _

. r. " \

:i ilii. ~ il;;.;.ll ~ ~ ·~: 1.. Sl~ot~Gooas.ti!=-~~ .. ~~-2.. DePtl:t Qflnjec;Uon: In~~-;-qn _~-~ 3. Ins:ulln conceritratiQn: 1000/IU ' -" ·-· ·!';"-~~ 4. Insulin dose: higher dose, slower ~'l 5. Insulin mbdng: 6. Heat application or massage: Increase absor,n:.Un. Pr. s.·_;:._;.Q :-,r.i L C>

rub/massage because we don't want to ccel- - · . ~ 7. ercl$e: WI mcrease a rption due tO llasodilataticll. B. ntness Increases lnSlllin requlrem~nts despite redLlced fOOd

Intake. ·

~in;;q~ Patient takes fixed doses of Intermediate- n Insulin {N) but varies doses of ~-gct!ng !n:;uUn egular or Humolog} based on blood glucose reading at time of dose

Pre meal Insulin dose I alucose

Lag time Comments

.:2.8mmoi/L 12U Inject during meal Include > lOg simple 01 2.8-4.4 llU 0 4.4-7.2 No chanQe 0 7.2-8.3 flU 0 8.3-11.1 t2 u 10min ll.l-13.9 t3 u 15 min 13.9-16.7 I t4 u 20mln Test u-ketones 16.7-19.4 I iS U 25mln

lnsulln slldina scale exam ole for 3 daUv lnlectlons Blood glucose

I rmmoi/u Insulin nr of Units

Breakfast Dinner Bed Reaular Humoloo HPH Reautat/Hunlotoo NPH

<3 -2 25 -2 18 3.1-3.9 -1 ·1 4-8 ltametl 12 9 8.1-12.0 +1 +1 12.1·17.0 +2 +2 >17 +3 +3

,. i ,.\ \\ "' ' ' - ,: .· :\, .. !,~ ·\. j ~ -- '" .

< .. .;:·." .l. ' ~t ''

.. : l .. ' .. •- .; . ·' t

....... _ .•

' ' ........ . . ...... { , __ ... -~~) ' ----·· ~} · ... ·-··

I ., .•• ~ ,) . ..... .

... . . .I;~.

-'r : 0: .r: . \. /'·. < :\ .:.7. : .. :.; .... 4-. _ .. :! .

. - l .. . , \

\. . . . ~ .. • \.

---- -- - -·-·•:;t• • pt must be taught to count the grams of Oi they antidpate eating, the

dose of Insulin is adjusted according to this. • Nan• l.U Lispro/Aspart for every~. This should be

individualized!

Glucose Monitoring • frequent self-monitoring and recording of blood glucose is now standard

management - pt should keep a record of home fingerprick glucose records to detect patterns of hyper- or hypoglycaemia.

• hemoglobin Ale (HbAlc or glycosylated hemoglobin) percentage Indicates level of plasma glucose over past 3 rnonths Extremely useful for monitoring patient's long-term diabetes control Goal is to maintain HbAlc within < 7% or <6.5% if patient is at increased arterial risk e.g. prev1ous strok.e or Nl.

• Fructosamine levels reflect control over 2-3 weeks.

Patients coming for F/U. What to do? 1. £ducate and gjve ljfesMe adyice: Promote exerdse, ~ealthy eating and

weight reductjan. · 2. Find oyt about problems/ SE exoerieoced 3. Assess vascular risk:

target <140/80] • D pstix, UKE [creatinine, micro-----=·

Patients Wiih renal disease: B • Encourage to stop smoking • Check cholesterol • dieck Insulin illjectlng sites for Infection or lipodystrophy and advice on

rotating sites. · • loolt for Cx!

/ ~ ~ecJ.·~C)"" ~c:~.~~ ij~X. C l'c ...J c.,._j::}

.- .

tli · ·-~" liS ~-

'-.0 .JU UiJ : (i.\..

Lli til w· t: fliabeU~ Keto-acidosis l .

Symptoms patient presents with: 1. Polyuda. Pol):dip$ia 2 . Wejtjh! !OS:> 3.~ss 4. Nausea and vomiting 5 . ~ps 6. Bluaed vision

1. ~omln.i!Wi"

Signs: 1. J?ehydration 2.~on 3. Tachvcarctja tach~pnoea 4~ Kussmaul's b•eatbi.ng 5. Smell of pcetoae 6. Metahpl!c a,;bfo$1S 7. ~othermia · 8. Confusion. drowsinJlsS c0ma

Cause& and precipitating factorg: 1. New presentalil?n of Insulin

oei)endent OM 2. Known Insulin dependence

DM+ • inappropriate redw:;tjgo in ~

• Co-existing infection • Surgery • Ml • Emgllooal stress

Differential dlagnoeils: Suspect HONK when byperglycaemic without high urine ketones. \--\.k. '? . ·

Diagnostic criteria: 1. GLUCOSE> 13 mmoVL 2. Arterial pH < 7.3 3. Upne Ketones >/= 2 +

[Remember 3's)

M!; 1. ABC 2. ""Fhlid deficit:

(0.6 X Wl{kg) X (S·Na/140))-{0.6 X wt}= 4-6L Replace 3L from ECf with 0.9% NaCI Replace 3l from IVF with dextrose

3. Glucometer reading 4. ~oilfinn read1ng with formal

blood ~iu<:ose 5. Urinee;;t!Qii for kel~s_ 6. If elevated Blood Glucose

positive- giveW of soluble Insulin In 50ml N Saline [1 Ulml). Administer iV@a rata of~. Blood glucose usually falls by 5 mmollhour. Persistent ketonuria - give 10'/o dextrose as fluid replacement of choice combined with Insulin @6U/ho11r

7. Catheleme In no urtne passed Tor 3 hrs.

8. ~to empty stomach In unconscious/semi-conscious pt.

9. CVP ifCY§ compromised 1 0. plasma eMpander it.llf._not

respond with N Saline 11. Antibiollc If suspected no

Primary cause found: Ceflrtaxone 1 g

12. Momlilr blood glucose.IJW,lliy tor 3 hours and therafter every 2-4 hours.

13.0nce Blood sugar< 15mmolll- change to soluble

i !H. ,. uu Insulin Ids or start with N regi{Qe and ensure adequate calorie intake.

14.fluld replacement: • 1 L N Saline over 30

mtn. • Second Liter over 1

hour. • Then foUowed bl,!.

6ags oyer 2, 4, 8 ~· .

15.0nce glucose< 15 mmoi/L Change to 10% dextrose, except when hypoyolaem!c

16.K replacement: NOT in FIRST · 2 L of fluid. There1.1fler

administer K as follows: • < 3 mmol/L give

40mmoiK • ~Lgive20

mmoi·K - · -Hypokalaemia Is a potential cause

of death In pt being tr~a~ed for DK.6.1lt .

17.~-give 5Dm1 -mcaibonate --. to. C2 over3o m1n. ~

A raised WBC count In a pt wltb DKA doeJn't lndlcawd underlying

In f.

18.Heparln anticoagulation as these pt are at Increased risk for developing · Thromboembolism

·Is i Uu liJ .. ijj .

£!;. 1. Cerebral o~fyou l

"Gjyr,ose iooray or when hypotonic fluids are given {Rx with mannitol and 02)

2. ABW3 3. Thromboemboflsm . 4. DIC · -5. AcUte Circulatory failure

NB: When do you change from lnsufin Infusion to Subcut Insulin?

Continue IV infusion until ketones­Conti"r! IV Infusion until 60 ml!}. • after 1 subcut aose. Start of with a short acting Insulin tds before meals. Thereafter (24h), de!Ejrmlne the patlents total dally Insulin requirement and administer 213 before breakfast and the remainder before supper. The Insulin given should comprise% soluble and Y.a lntenned!ate acUng ln$UIIn. Take glucometer readings before a­fast. Lunch and dinner and adjust Insulin accoJd!ngly.

~· AdW'al insuffidSJCV : APDISON'S DISEASE AND CRISIS .·

·Addison's disease = ~ adrenal Insufficiency · (1° and ' 2° ·adrenal lnsuffidency) · _ · · · Addison's crisis = · ~ adrenal insufficiency' = ER!!!' Inability to secrete in'l'eased cortlsoi/ACfH in response to stress {Infection, dehypratlon, surgery) l~rllflg to ~ypovoi. Shoii, Tever, extreme weakness, decreased LOC, nausea,

. vomiting, hypoglycaemial · ' .... ' Hypothalamus

1 CRF

t

I Pituliry I ' ACTH -t-

~ e;-- io l .

·Cortisol and Aldosterone

Destruction of,the adrenal cortex leads to cortisol and aldosterone · . deficiency! '

G:::> l.lS~~o~~o~D~U~·~~~~~~~~ 2. e

rena Is 3. OJ>IlQrtunlstlc lofectjgos ln.Hl'l..(CMy, M~bacterium Avlum) 4. :xarenatliaemorrhagic inrarctlo~ (Waterhouse Friederichsen

S'Pifll&mi In CFI•fCiren, coagulopathy 1n adults) . Slf, Antlphospholipid AB syndrome)

s. Granu!0mi'tous a;wase: Sarcoidosis and TB of adrenals (COmmonest cause worldwide) · .

6. Congenital (late onset congenital adrenal hyperplasia} .

:L Pituitary or Hypothalamic disease [no hyperplgf!lentation as ACfH Intact, aldosterone synthesis nonnal}/ · ·

2. Iatrogenic: Chronic cortlcosteroid usage with suppression of pituitary-adre.:tal axis, now suddenly steroidw1thdrawal.

occurring in rapidly

'· · H. · Influenza, s. ~ureus, Pneumococcal,

B~~~atl~~~l[.!~e, No aldostero!!-e q qtracell!!!!r

-:~~~R~!~H:ydrocortlsone 2Dpma/4 b IV

~ \ .

I Clinical Presentation: .. ,

' ·' '> 1. fatl'l':'e, ~~gla, ~alntlng, weakness, Ancireida. weight!oss 2. Abnorma fx. . ~DGIT DYSEXIIII ·

- Nausea, Vomiting, Abd pain, Dlall'lloea, eo'nstJpation -3. PersonaUty Ch<inqes PsYchosis • . · . . 4. ~meJKn!.on In unexposed skin areas~ ~, Creases of hand$,

~cars, Buccal Mucosa due to ACili secretion and 11:5 0'055 reaction, Wiffi"Melanin. -ln..eBlf:36&Y,lJOT SJ:CONDARY!II ·

5. Dehydration and salt mtvlng, -In PRIMARY, NOT SECONDARY!!! 6. Decease pubic and axlQ;; hair ~ e::les. 7. ~y~IJfenslon RoTra odio::::riUD!l.e NB!!JI ~ 8.~0 __L

l Lab Investigations:

1. ~a, ~(due to ~Aldosterone) 2. -t,Gh.cose ( due to.UCortisol) 3. UKE: Uraemia/ BUN/ Creatinine 4: FBC and Diff Count: Eosinophilia and Ana~Ja (no~c, .

· nonnochromic) ~

5. Increased ca 2+. J.

!

\--!

Diagnosis: 1. ACTH Stimulation test: ~y

· Take plasma Cortisol before and 30min after tetracosactide (Synacthen) 0.150mg IM. (synthetic ACfH) Failure of cortisol to rise > 553mmoi/L after JOmln = Addison's NB: This test will be falsely + In pregnancy and In pt on contraceptive pills due to an Increase in the cortisol binding protein.

2. Basal ACTH will ~ 4rimary Addison's. 9am ACTH will be .t addison's. 3. 7t-hydroiilase antLodjes +in autoimmune disease. 4. AXray/CXray/ cr abdomen: r enlar2ement of adrenals in adrenal

liaemorrh~e, active TB or Metastatic Malignancy. Signs of pastTB = upper zorl'e fibroSis or calcitlcatlon,

5. Iri3ECONDARY: LOW CORTISOL, LOW ACTH, NORMAL K+/ BUN/ CREATININE .

Preci~: f.a"IQ[!: 1. on of medicati"Oi'D 2. llness- Severe infection, Ml, CVI, Severe trauma, surgery without adrenal

support 3. Withdrawal of steroid tx in a pt on long term steroid tx. 4. Administration of drugs impairing adrenal hormone synthesis e.g.

KETOCONAZOLE. 5. Drugs increasing steroid metabolism e.g. Phenytoin and Rifampicin.

l Treatment of Addison's crlslslll ERIII

1. tJ~grocortlsone 1 OOmg IV stat then 50mg 4 hr!y for 24 hours 2. Tamper slowly over next 3 days. 3. Change to oral replacement therapy when oral feeds are tolerated 4. OVERlAP FIRST ORAL AND IASI I~ DQSEI 5 . . 5% Dextrose InN Saline £VI N Saline IV in large volumes! . 6. If Aldosterone Insufficiency give fludrocortlsone Wnen sfilff to oral tx . . 7. Treat the precipitant.

Treatment of Addison's Disease 1. Replace Steroids: 15-25mg hydrocortisone daily in 2-3 deyjded do§p~. Not

· laTe 1n day -INSOMNIA! 2. Fludrocortlsone daily po when signs ·of aldosterone deficiency present. 3. If no response to tx- Consider autoimmune cause. 4. Always warn pt. on just abruptly stopping steroid usage and Increase steroid dose in times of illness or surgery!

i- ;­\ i-- )- -- J-

z~-

j .M~~'Cl--\ Co.~~] .. ~o~\o~ CJ\. -"(::) A \c'b~c~t..u.

.l--

· fo. sc\c'-l..~o.. -e. c~ \s:)

_; __ ' 1-·

I ,_ 1_ ,:

( ~\J~o.~

(_s-Q.~~

· ..

! .

..... ~ ~(./C:s\- ' ->-.·....L_ -t> ''-" ! --~ .. -r:. .::::::: .. . :: 1

.: :: : Hypera'fj\erorus~ :: :. , .

Excess production of aldosterone Independent of the RAAS system causing 1' Na and H20 retention and a -1-renln release.

Patient presentation;

1. Usually Asxs 2. Hypertension - Esp. @ a 'ypung age.

3. ~okalaemla-w~ss·, ~ps, parasthesla, occasionally p~is, polyuria, polydipsia, latent TETANUS!

4. AlkalOsiS --;;patient NOT on ·a diuretic!

5. Na ·•mtldty1' /N

pjffereotlal dlaenosls;

l.~sslve diuretic ~s~ule out. If patient not on a diuretic - consider this diagnosis first!

1. ~pt must ldealy not be on a diuretic, hypotensive, steroids, K, laxatives for 4 weeks) 2. Oonotrelyona ,J..K as >20% can be normokalaemlc. 3./ j1Jdasterone/R8illil RatiO (AR'9)Pt sits upright for 2 hours. Antihypertensives withheld for 2

weeks (Spironolactone for 6 weeks). Alpha blOckers can be used aslt does not affect the test. A 1' ratio (1'Aidosterone)lndlcates hyperaldo5teronlsm. -

4. MRI/CT scan of the adrenals to localize the cause: pn!y done If hyperaldosteronism Is proven. If unilateral ademona shown- e•dslon. lf no nodules or bilateral nodules are seen a trial of Glucocortl~s (GCS) may be used to test for GRS: In GRA the GCS J.ACTH production by neptlve feedback and therefore .J.. aldosterone production.

s. If the above are Inconclusive: Adrenal vein sampllnc may be done. Venous blood sampled from both adtenals and If one side demonstrates Increased aldo5terone an adenoma Is llketv.

6. Adrenal scintigraphy can alternatively be used. If It shows an Increased unilateral uptake of the lsotype, adenoma suspected.

Causes;

@vperaldosteronlsm (Conn's syndrome).

(Think of Conn's In: •!f!PERTENSION ASSO(!ATED WITH HYPOKALAEMIA!!!• Refractory HT depslte 3 antihypertensives • Hypertension before 40years of ase (esp. Women))

1. 2/3 Conn's a~a 2. 1/3 Bilateral adrenal hyperplasia 3. Glucoconlroid-remedlable raldosteronlsm (GRA)

_Al}CS\..o..\ oc)e:-'J\Oii-..A."'- o(

I E) -1>· JJ ~'\.\ \'-

[ACTH regulatory gene element of the 11 B-hydroxylase aene "fuses. to mE: a ,Jcsterc;;e 5\•.u-,;,~c: gene, Increasing_ aldosterone production, and bringing It under the control of ACTH.

@vperaldosteronlsm [Due to high renin from +renal perfusion) ~

1 . .m 2. liver chlrrosls +ascites 3. Nephrotic 5yndrome 4. Renal artery 5tenosls 5. Sodium losing nephritis

6. Barter's syndrome [ congenital cause- derectlve NaO chann~lln the loop or Henle causing a leak)

7. Renin-secreting tumours

Non-aldo5terone mlneralocortkold excess:

1. _Ectopic ACTH syndrome 2. Uquorlce 3. 17 Alpha-hydroxylase/118-hydroxylase defldency 4. Liddle's syndrome_

.~ann's iyndrome: Laparoscoplc adrenalectomy. Give Spironolactone up to 300mg per 24h po 4 wk pre­op to contrOl the BP and to treat the hypokalaemta.

H~: Spironolactone o~e Of' ~e(does not cause svnaectomastla like other 2)

GRA: Dexamethasone lmg.24h po for 4 wks. lf Bp nto 1' after this treatment- swtthCh to Spironolactone as alternative

Adrenal carcinoma; Surgery+/- post-op adrenolytlcthe~py with mUotane- poor prognosis!

PJr~'o.\ ~'r~\(\,~~ -

9 L A-bt-\ (_ \'bs.\ r:~:-:-:::-d ::-:::::-:;:-:. -·. ::-::: -:~-:~et-;'"-·'P~-s:-::-:~.·~--.-d :-: _-:: .. -:.:~

"''volume of diluted urine (>3l/day) due to Impaired H20 absorption as result of ,J:ADH secretion ·from Posterior pituitary gla~

Q ..\.N~ ' ADH produalon by the posterior ptultary gland.

• Polyuria • f'olvdlpsla

• ~ion

• Patient passes 5-20L H20/day • Patient complains of excessive thirst- drinking EVERYTHING!! I

1. ' UKE

2.• Ca 3. • Glucose (exclude DMJ 4. • Serum and Urine osmolalities: Plasma osmol >300mOsmoVkg and Urine osmol <400mOsmol/kg. 5. • Serum Na 1'. Polydipsia might i:ause a dullutlonal hyponatraemla. 6. , WATER DEPRIVATION TEST: Used to establish Ox of Dl and differentiate cranial from

nephroaenlc Dl. Normal: Urine osmol> 600mOsmoVk& Primary polydipsia: Urine concentrates, but less than ROfmal, e.a. >400-600 mOsmol/kg Cranial 01: Urine osmol Increases to> 600 mOsmol/k& after desmopressln. Nephrogenic Dl: No Increase In urine osmol after desmopressln.

~&11Dl~ Diabetes, Diuretics, lithium, Primary Polydipsia {Caused by psychiatric disease: 52P/Manlal

Cranial:

• Structural Hypothalamic lesion or high stalk lesion (trauma/hypophysectomy}

• Infection • ~ar:)~hal! syn_prom~ (Infarction seen after severe hypotension e.g post partum

haemorrhage}

• ldeopathlc -

~-· ,- r- ~- r-- )- . 1- _I_ I

• Genetic defea: Dominant Recessive: DIOMOAO syndrome: Diabetes Insipidus Dlat>etes Optic Atrophy and Deafness (Wolfram's Syndrome}

Nephrogenic :

• Genetic: V2 receptor mutatlon~Aquaporln -2 mutallonACystinosls • Metabolic Abn: Hypokalaemla, Hypercalcaemia

Drug Therapy: Uthlum, Demeclocycllne

• Polsonins: Heavy metals • Chronic Kidney Disease: PCKO, Sickle cell anaemla,lnflltratlve disease.

Treatment;

Cranial Dl:

1. Find the cause: MRI 2. Test anterior ptuitary function 3. DDAVP (Desmopressln} and analoque of ADH via the nasal mucosa. Dose 10..20 mlcrogram/12-

24 hours, usual tV, S microgram In the morning and 10 mlcro&rams @ night.

Nephrogenic 01:

l. Thiazide diuretics e.g. bendroflumethlazlde 2.5-5 ml/day po. 2. NSAIQS: (e.g. lmlometadn 15 mg 8 hrly) aslt lowers Prostagladlns. Prostllstandlns Inhibit the

action of ADH locally. (SE: Reduced GFR}.

~ 1. Urgent UkE and serum and urine osmolalities. 2. Monito";';;rlne output and check UKE twice dly. 3. Oo not lower NA too quickly- risk of Cerebral oedema ;md brain Injury. If Na >170 use 0 .9%

Saline and reduce Na at a rate of leis than 12mmoi/L per day. The use of 0.45% SaDne can be dangerous.

4. Desmopressln 2 micrograms IM [lasts 12-24 hours)

,_ I _, __ ; / ,_ I .· ~

i--

C.:: ... :: ... .... .... s:S~erpro.•~dii:m;~ r· · ···-·r::: ;;;·:. . : .. J Hyperprolactlnaemla Is the. most common dlstur!)ace of the otu!tarv glaod. 1..E

• It presents earlier In females than males due to menstrual disturbances. • Prolactin stimulates Lactation and antago(llze sex Steroids perlphally. Raised levels of Prolactin

lead to secondary hypogonadism, Infertility and osteoporosis as It Inhibits Gonadotrophin releasing hormone (GRH) secretion -leading to a low testosterone, estrogen, FSH and LH level.

• serum prolactin levels> 300 l-l&IL (300 nB/mL) virtually diagnostic o'i"ji;:QiWingma •· prolactin-secreting tumours may be Induced by ~strogens and may grow during pregnanO{

Patleot D!esents with fo!!owlnc complaints: FEMALES

1. Amenorrl)oea or Ollgomenorrhoea 2. Infertility 3. Leaking breasts 4. Decreased llbldg 5. Weight gain 6. ~na 7. Osteoporosis 8. L~re effects; Headacbe

Exami!!!tlon; FEMAUS and MALES

1. Galactorrhoea 2. Hypogonadism

MALES 1. Impotence 2. Reduced facial hair 3. Leaking breasts 4. Osteoporo5ls 5. Local pressure effects: Headache

3. Local pressure effects: VIsual field defects (Bitemporal hemianopia}, CN palsies (Ill, IV, VI) Dlffererola! Ox; Secretion of Prolactin (PRL) stimulated by :

1. Phy51otoslcel: ~' Breat·feedin& stress e.£. post-seizure, S1eeQ, hyooslvcaemla,J!!!!!:­menstrual cycle, TRH, sexual actlviW

2. ~: Phenothlazlnes, estrogens. osychotroo~ (e.g. haloperidol, rlsperldone), antihypertensives (e.g. reserpine, verapamll), alpha -methyldooa,.!!Q!ms, bl&b-dose estrogens, metodopramlde, domperidone, dmetldlne

3. Olieases: PrQI~ (mlao/macroadenoma) ~- Stalk damase: PtultalV adenomas, transection, trauma

Hypothalamic disease: Craniopharyngioma, other tumours Other: hypothyroidism (due to 'tTRH), chronic renal failure (-!,clearance and excretlon),llver cirrhosis.

tRANIOPHARVNGIOMA}Develpos from. Rathke's pouch - situated between the ptultary and the 3'4

ventrlde. Commonest childhood Intracranial tumour, 50% presents in childhood with Growth failure and wltn amenorrhoea, -!, libido, hypothaiamlc symptoms- 01, hyperphagia, sleep disturbances- In adulthood. Treatment Is surgery}

i---- \ - ~---- }-- .1- I --- L_;

~ 1. Basal PRL! Do a non-stressful venepuncture between 9 am and 4 pro.

Causes of basal PRL secretion (>390 mU/l): Secreted from the anterior ptultary. Release Is Inhibited by Dopamine produced In the Hypothalamus. Hyperprolactlnaemla causes:

l.lncreased production from ptultary (Prol,ctinoma} 2. Disinhibition by compression of the ptultary stalk reducing the Dopamine levies 3. Administration of a Dopamine anta!!Onlst

2. Pregnancy test 3. lEI 4. UKE 5. MRI of ptultalV lf no other causes found.

Any level of PRL >5000 probably Indicates a prolactlnoma. Macroadenoma (>Wan}: PRL levels 10.D00-100.000

Treatment lnelucles 1. bromoalptlne or qrbesol!nJ.(Iong-actlng dopamine agonist), 2. SU(&e/V. Compl: Pennanent hormone def, recurrence so reserved for 2"" treatment. 3. +/-radiation

• these tumours are very slow-growing and sometimes require no treatment

MACAOADENOMA.S') !-faiCROADENOMAS ~ . IWZiour >1 an In diameter on MRI • TUZIIOU < Cll'l . Initially be with Bromocrlpllne . 25" of ~t.tlon haV! ISvrnPlOII!ftiC . Slireerv Indicated If Vl$1£11 symptoms, pressure mlcroprollcllnOrn.t • effects which falls to respond to medial tx or . Bromocrlpilne Wid- ~PRL, restore when preanancy Is contemplated- 25% of menstrualtln& cycles and .,. tumour size. macroadenomu expand during precnancy. Doselltreted up: US m1 dly, then lncreue . Post-suiJlery: Radiation or Bromoaiptlne. wkly by 1.25-2.5Z111fd untU Z.5mr/12h.

SE: Nausea, Depression. POitural hypotension. If preananc:y planned- use barrier mothodt untlll periods have acc~~n-ed, If JIASnancy OCCUB, stop bromocrtp«<ne alta' 1• mbsed period. Alternative • carbocollne . SUrsr:ery If Intolerant to Ooznllplne eaonlst.

Hypoprqlactlnemla

• inability to lactate t:""" ~ • may be the first slsn of Sheehan's svndromejj)o5tpaiiUIH pltult&tf fiemorrhai\

,"-· ~--· ) ' .- i-

r'"" IWs-·· ·~ .. ···- rc - z ··~z· - c· -am

level$ are high.

Thyroid functions:

Serum, n ~~: To lliSB';t!flii.JlP.S are more useful measure eFev s.

TBG c.afl Urela~e beeau:!f: and :.av:a i cagent?'JE lpN s levels aJ • aUgh es conla lng Iodine

flll~se TBG as weU. TBG decreaHd when using andwens corticosteroids .I!Jd phenytoin, also low an cRI&ic IIOer !l'lseasa iliid ~ly.

T3 rosin uplake test: Measures lhe unoccupied receptors. Are thus at its lowest wllen hormone

Radloactivt Ttchneslum 88 {r99} or Iodine 1131 or 1 132: measures lha func:lion of tho gland ali well •• tho peUom of uptake.

~ ·:\

- Aalle suppuraUve ·- Subacute: (de Quervaln's

thyrold!Us - painfUl) ·Riedl • ONg Induced • Subacute thyroldiUs • Non-toJdc:

~PP1 "fut 1. linodulargoiter 2. Stngte nodule:

Benign: Adenoma MaUgnant Papillary l~l

Follculllt17%) Anapl .. llc Medullary LymphOml

0~~~ .o ~~~~~~~~~~ o extend retrostemlll o e - ed aslina compres on - s r ysp goaJSVC obalrucUon/Hoaraeoess

ue rea11rent louyngeal nerve Involvement (More Hke!y In CA) o ,W41!11ll5t{ DPnMI (OR upper llmlls with TSH u~detedable) o Bt!ll!19q!gi!A: Tracheal dlsplacernen!/compresslon: ontrathyroldal catc:lllcaUons: retrostemaJ exte~ ·

· o ~No RJ< with annual review (-. toxic mu!Unodular goitre) o ~ Partlallhyrl!idectomy (mediastinal compression/cosmetically unattractive) o ~ 1~20 years later no unconvnon and caMot be prevented

·--i .1-- I ..---~-

Hyperthyroidism:

Symptoms patient presents with:

,_

.16usdo~ AS well as o Weight loss despite a

healthy appetite. o Heat Intolerance, o Diarrhoea o· Polyuria · o lniabUlty o Emotlonalllablllly o Psychosis 0 Itching o Eye discomfort and

DOUBLE VISION o FaUque and Weakness o Loss or Libido

Signs: 1. Tachycardia 2. AF 3. Warm peripheries 4. Fine Tremor 5. Warrn,molst skin 6. Palpitations 7. Palmar erythema 8. Hair thinning

9. lid lag (eyeUds tag behind eye' s decent as patient watches your finger descend slowly) ·

10.11d retraction (sclera mcposed above Iris causing a stare) 11.Nervousnesa 12.Anxlely, Hyperactivity, Dysphoria 13. +/-a goiter 14. +1- thyroid bruits 15.Proxlmal musde weakness 16. Gynaectomastia

Laboratory Investigations: • Ask for T3 and T4 as well as TSH • All will have l TSH except for rare case of TSH-secretlng pituitary

adenoma) • Most wW have t T4, 1% will only have t T3

i_ _'I - \_

b'n · 1 J w p~ng • W.eMi!BI1Ei efei!ISt!:S • OHen at other sites such as ~~nddl:aOll<

Iii~' irMtl-·liGWith Rllll'li~IIMDAIIRdM'eal•"iin QQIIIJIAfAMII

• tt is associated withoeai!!~l:ttqlllA.as andoe!l'l!l'lli:'!l'6i3<iliee. • 'Hi!JM...,_• sfa4h]lf8ii . etiu:el:fitM!R§~aM~Me1f:r• r • OHen reee!wEte p e *eeee:lll'jOor ~:itlrFearlia~ or

carbimazole. Special investigations

1. ""'"and~ 2. ~(<0. 5) 3. T 1131/T99 uptake wilh a diffu~e uptaKe pallern. 4. .., Th) ruii MiMwlalift!'MI-~Iellwlilt' Thyroid autoantibodies 5. JcBWf' ·•·+ *I I on d· +if. r eesr ('jfief"1~tl"'"' 6. fl 4 i._. .... ,GfAA&9 iq C-4+

· 7:' '"' eesllli•toss. Wilh OM)

Patients with exophthalomos have an ll¥!fuss'II""IIMIIiar cf-·=, · r.s..;e.; with dageemaMae ·AL.awsr1a .W••, Infiltration by lymphocytes and macro phages and deposits of.O"Hdi~ll)••rtwWes, fat and oedema.

ttli9i6 [ii oli~f=D Present in 70 Yo orpa ents with Grave's disease:

1. aGM*tinlti; pain: d;esomtoct'&Rtt,._.ephehilf 2 . ......... 3. · O.lfvliiiAl fll!piN...,. 41M8cl and .@armento lltliiil! may iAElieal• ~e

ae .. ;peessieM 4. 'iiwlotjhlhalmQs- protruding eyes 5. ~s - eyes prot(Ude beyond U1e orbit 6. Gogj"?fti"a' oedema 7. MFA till 'llillll'l!lion 8. P~~PiltitiMa 9. \ as& of oetewr "iaMMl 10.~1:JIIouii!Mplagie esp. of upward ga:z:e) due to fibrosis and muscle swelling

Treatment of opthalmopathy: 1 . Rlltllllltlll'llle

2. uaak~eon"lfb59 era m 81'5" 3. MPI8 d 8111£68& 4. 'e•ewt•er,.rApt.y (corneal ulceration) 5. lii.tnmw 'lilt w·s&e.enf!efY (Diplopia) 6. likedpim la ·{decreased acuity, papilloedema)

Patient can be hypo-. eu- or hyperthyroid on presentati~n . Eye signs can be present +I- Grave's Disease but is caused by an autoimmune process similar as found in this condition. ii¥& s~~90'5 m?# 'i ± 'C'!PY'OWSI§IIC t m f . "> &:lit--. liWI!IS"'ISJisitet lrolle~;u 1~ ancll; illphec; to iuliltl'llt+ew-~tlle irl• utslliP!J.ef.Uaewwt..

Q!ffc; stuRI ·t~JagiiNO&t

1 . B!>&ma; 6'fl'illl'll~811 • Nodular goiter , • No eye signs ,

No pretibial myxoedema • • No Thyroid stimulating globulin •

If CA<&re'!l"''!lfaasai!l ece 11 in a..ploll~'ie"21~.1"'1fi .. ..-MIIW!efi•!l.,.gei&•= Mttl'\lllfe$UHII1/'I~Ilf Ujilt'lleffiiS

3. $.ub:y:;vie~· Radioactive iodine is not increased.

4. Jet+ iili&&Btw .. Transient hyperthyroidism caused by iodine intake.

5 .~ Choriocarcinoma, hydatiform mole as Is $ecretes gonadotrophin which binds to the TSH receptors and sUmulates thyroid ~~sue.

c:mn11mi'f1aitlr 1 { Q:e;;::!i:;. : Propranolol for rapid control of symptom~> 2. ~!!WfJ'X'!t tia• Esp. In young patients, mUd hyperthyroidism and a

slightly enlarged goiter, during pregoancy. Thionamides: Thiourea, Propyl-thiouracil (PTU) and neomercazote or Imidazole group (carblmazole):

Carbimat.ole 40.00mg12-4h In devlded doses for 4 weeks reducing it to 20-40mg/day in devided doses for the next 1-2 months.Reduce further according to TFT every 1-2 months until maintainance of 5-20mg/day. Or give carbima:z:ole and thyroxine simultaneously. SE:

• Enlargement of goiter esp. when meds cause hypothyroidism [prevent by giving thyroxine simultaneously, but not together with PTU) Agranulocutosls: leadign to life-threatening sepsis. If pt develops signs of lnfectlon, skin rask, pharyngitis, fever mouth ulcers treatment must be stopped and WBC count performed Immediately.

• Dermatitis, joint pains, myalgia, jaundice, fever, tympadenopathy.

1. Toxic ADENOMA (autonomically functioning adenoma) Single nodule producing 13 and T4

• Isotope scan (T99) shows a HOT nodule and the rest of the gland is suppressed

• Tx: Radioiodine

I Hyperthyroidism I ~ CAUSES

2. Toxic multinodular goiter (Secondary hyperthyroidism) = Plummer disease

SEEN IN ELDERLY PT and Iodine deficient areas! • Cervical swelling. Thyroid nodules secreting thyroid hormones. • Heavy sensation when swallowing • Kinking of the trachea - pt awakens at night with dyspnoea

: :IPtlfi::Sule can cause respiratory distress.

• { : I DISED SALT • MX: Exogenous thyroid hormone: 0.2 mg thyroxine dly. Or

radioactive lotline • Indications f()r surgery:

1. Presst.Jre symptoms: Dysphagia or dyspnoea 2. Cosmetic considerations 3. Fear of malignancy (Esp. When one dominant nodule

palpated) • When Surgery has to be performed:

SUBTOTAL THYROIDECTOMY Patient prepared with bedrest, controlling of cardiac failure if present and a short course or lugol iodine. Add a beta-blocker Wlleo cardiac failure under control. Perform a sutrtolal thyroldedoiny. If cardiac failure is uncontrollable- Tx with radioactive iodine with doses higher than lor Grave's.

l . ~Wsdisease~ O:CitW!f: 61 Dlyroitoxicosisl

Common in ages ~rs old, females> mates ~fpmpgp ditftte C8USed by fij=oletjpg ASH......,..,(

~ 7 disc which also reacts with orbital auloanligens. 8ii£USE 1J Cj :ai• QMfq·mon+r

• W;pa: • SIP'P'$eh)tpe'b\W*'i5Ql • Associated with other autoimmune diseases:~. "f,.pie"'!<@M,

.• eta· !4?1 1 3 61a!6b&fl ·

Symptoms: a. Aexie¥eet'be.,_. b. llacl:;x:iia c. ~and ho&tiPIIII&:a::N d. a., :::aad:'!MtttMiM e. " 11 · !l~ ilm despite a healthy appetite f. Moeall u:-s g. ldrsrpl*o h.~ 1. ~

Signs: a. ~ b ...... c. u,p• ,. d. lllfi!'MW?='a 1i&M1;aadill and flllll sorneUmes an

ejes'ie&'I:SI'I"s •••• ,,.n~l Pulse pressure Increased. Peripheral vasodilatation with f;lilm"p"d'UVPa. In older patients cardiac failure present

e. St1'81 ... qR~III\lkiiJii6 . f. P'fttws a· I a ' U ; et•u often asymmetrical H· a bruit g. !i¥lii fie~ I&: jt\'jt,t, I ·1 a II I

-~signs or symptom • ~EiRII Q?lP • ~nly signs (l!i!l MeiFilslielfand l!lr§) • Ra'e 1 I & illl::eae

No signs .u iji1 • s r pelp ~ d>f!M-·'1011 tissuelnvolvemenl • ~

-flroptosis ( &Je J!fletlllaft!lll'bf !8nMI) becoming pronounced with exophthalmos later- this leada to 111 ::cal alllelt'tlan due to the lnabinty of the eyea to dose properly. -he-ocular muscle inoolvement {Qijllllpla andoioelt _. aeu 1~e due to muscle weakening esp. of sup. rectus musde.

(Rwlorh1'?'e 1afMit

-•omeallnvolvement ~ ·•ghtloss ( p · 11 sf IRe Spll$ li't'lfto) ... 'I++so t a t bahifev ; ''* Sl 1 ''bi'a

.. L.; fm•

t'rlnl<\f'l H)IDOlb\IW!illsJn - 1. Autoimmune o roidism (Hashimoto's atrophic thyroiditis}

2. a ro~erJIC (Radioactive iodine trealment, thyroidectomy, external Irradiation of the neck)

3. Dru~: Iodine excess-causes hypothyroidism causes a goitre in patients \lilttl'i underlying auto-immune thyroiditis, litl1ium, antithyroid drugs, Amiodarone

NB: Association wit~Q1tl.Y!2!gi,O:m. diseas~ : / Turner's syn rome .1" Down's Syndrome -; Cystic fibrosis 'f- Primary Billiary Chirrosis

- amyloidosis, Sarcoidosis,

,;-POEM's syndrome [Pol~nevrQQi!lhy. Orrnow;, En~!l.h~­~in band from erasmacy!~'!!a and ~~!n e;m ~mvrem

Treatment: 1. wQthvrmJQa

If no residual thyroid function 1.5 microgram/kg/day Patients under age 60 without cardiac disease can be started on 50 - 100 microgramsldi!Y and the dose adjusted according to TSH levels. In elderly especially those with CAD the starting dose should be much less (12.5- 25 micrograms/day)

NB: Long term effe.:ts of thyroxine= <;!steogorosis ant! ... ~eeelef'!~~ Artherosclerosis.

r::::::_::.~ r:· _.~:.~ i~bc,l!.ne:E¥.P~~~X!oldis~: ~:. :: :as: ] RAISED TSH WITH NORMAL T4-+ Antibody+

-.Previous lrealmenl for Gra11e's .... Other organ specific autoimmune

disease -+ TSH > 10

If YES: Thyroxine 1realmen1 unlillSH inN range If NO: 6 -12 monthly TSH measurement. If symptomatic a trial or Thyroxine.

,. -· -·· -~ , ...... . """" · · ··- ----~·- ·--· ·· ·-

I ··] =~:;thyroid sick syndrome} I

Acute: Rare, due to suppurative Infection of the thyroid Subacute: De Quervians thyroiditis/ granulomatous thyroiditis- mostly viral

Mosly autoimmune {Hashimoto's) Chronic:

Acute: 1. Bacterial: ~~/Stre,es 2. Fungal: ~erQillilS qndlda 1;1j$NMma eoei!QlQ!i,~ 3. Ra!llali® . 4 . ;ii!Wa[Qrun;,Normal thyroid function, ERS raised, Painful thyroid.

Subacute: Viral {granulomatous) - mumps. coxsackie, influenza. adena and echovirus

Chronic:

11!> Mostly affects middle aged females e · 3 phases:

tl" Painul, Jl' enlarged thyroid ~ Complete resolution

• Tx: NSAIDS and glucocortlcoids when necessary

1. ~~~!mo~'s th~roldltls: MOST COMMON CAUSE OF OTH ~~1fY~r

2~ ~del'ji: Rare, middle aged women. Painless and Insidious course. ymptoms are due to compression. A dense fibrosis develops. There

is usually no thyroid function impairment.

~rnal 'ru: ~ ........._ ~-h..: .. ~ ~ u•aeMIIa.t iostMte. 2. l'thiW'e besrp!wdiGa s .. i&'t11iii!!2 1ilt~tLij ~~ 11(id ·ie"o'hlffAWiQe and i., .. a:t u,.,..,~ - etc+atJeti:J:&taiRe8 . 3. Inhibits conversion of !-thyroxine to l-tri-iodolhyronine (13) in peripheral tissues.

3. a&diz r r Hi"t't 1 1131 1 ex: ~"~~!!WiiMm 4. l'"'~niiiMin II)• Indications: Pressure symptoms already present, fear of

malignancy, failed medical management; cosmetic reasons, pregnancy, Young patients Cx: Damage to Recurrent l nerve - hoarseness and hypoparathyroidism. 7.

8. 9. and poor appetite 10.~II.iiiO,.lll.lllor 11. MengqhR.!ljil , later oligo- and

amenorrhoea 12. Paresthesia 13.11J!pajrM heagng

Examination: • Generai:Dry skin and cool

extremities P~. hands and feet-­~~ (NON-PmtNG -OEDEMA) Diffuse~a D~ coar&Jl.!Wr ROarse viiEs

• Cilrdlo: • Respiratory:

• Musculoskeletal:

• Neurological: • +/- a goiter, signs of

a,,..,..,,.. afiiTt•ikl<oUiua

l Dementia ip elderly Btl Check thyroid !ir~€ ::' ~= . )

1. I§_HJ. free T11· But in secondary hypofhyroidis: T4! and lJN TSH due to lock of t'fieptuitOJY . . .

2. UJS and Scintigraphy are of little value · · 3. Agtl TPO An!jhpdif!S t 4. S-CKf; S..Chol j, s-TGL T 5. Normochromic or maeto 6.

ll!i OIJ ·flCO[' ~--,. 2)1: t

Also called hyperadrenocorticism or hypercorticism. Caused b;t high levels of cortisol in.lhe blood. J[ ... T .. . Causes:

Exos;!J.?US (ACTH ~ due to- feedback) ....... ~~ ............. ,......._

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1. Iatrogenic: Glucgcgrtjcgstergkt; as .medicalion for e.g. Asthma, RA, immunesuppresion after organ transplant. -MOST COMMON

Cushins's syndrome can also be sub-classified according to whether or not the ~o.C" excess cortisol Is dependent on increased ACTH.

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Untreated Cushing's syndrome can lead to heart disease and increased mortality. · -Pseudo Cushing's:

1. Alcohol excess - sUmulales adrenal glands. 2. Major demession -Increases stress response 3. ~y: Simple or as part of Metabolic syndrome

1. PATIENT PRESENT TO YOU WITH:

11. Hypercalcaemia: leading to skin necrosis.

1. ~t gain - central obesity (Lo'lmk and raceanasparing !he limbs}

2. autfl!lo hum~ and supraclavicular fal disltibution: at pnd grOWUl·Blong coUar bon";. and back of neck­lipodystrophy

3. Moon face

4. Sweallng -5. Telangleclllsls (dllaUoo of capWartes)

6. Thlnnlnp ol skin- easy bruise, dryness t~sp. of the hands und other mucous membiunes:

7.Purpura co--

8. Pumle stria (lhe weight gain In Cushing's syndrome streldlus the skin, which Is Uiln and weakened, cau•ing it to hemotrhago} co tho trunk, bullocks, anns, leg a or breasta)

9 pmxjmal mysrte wAakoces (hlps. shoulders)

12. Osteo~orosis (+1- lractures), persistent hypertension due to COtllsors unhanc:emenl of adrenafine s vasoconslticilve eHed

12. Glllcose lntolarance/ lni!\JiirJ resistance or oven OM leading lo lncreMeq lnfectlono and &low wound healing. Also Polyuria and polydipsia

13. Psychological dlsluibances: Euphoria, irritability, Depression. Psychosis, AnXIety.

14. Hyperpl~menlallor: Cushing's due to increas-~OMC ... ACTH una Melanocyte sUmutaGng ormone. ~

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15. Cortisors can exhibit mineralocorticoid activity in higll concentrations wocsening hypertalsioal and leading lo hypokalaemia fcomrnon in ectopic ACTH seaelion).

17. Cushing's may catJse sore and aching joints. particularty in the hip, shoulders, and lower baa;:--

SPECIAL.. INVESTIGATIONS; DO NOT PERFORM RANDOM CORTISOL LEVELS- OF NO VALUE!

1. Confirm !he dlapopsls 2. Localize the source by using laboratory investigations and Imaging studies

Wilen suspect Cu!hing's Syndrome:

~vemight dexamethasone suppression test; Gille the pauent 1 mg dexamethasone@ midnight. check •trum cortisol < and > B am.

_In normal patients: High dose of cortisol causes:: feedback and _lhus j ACTH and 1 Cortisol Jo < 50nmolll. · · ··· · -

In Cushing's syndrome: Failure to suppress cortisol secretion. Thus high levels of cortisol de~t!'d -

OR

~~urinary free cortisol ( N value " 2BDnmoJJ24h)

FALSE +; (Paeudocushing's) seen in Oeptes:slon. Obe~ly. Alcohgf excess and Inducer gf ljv~r _enzymes such as phenytoin, phenobarbital Riramnjcjo as jt lnqeasq ltle rate ol cortisol, j'ijiDlmlllism.

~izeth~ Oo plasma ACTH -If undetectable, adrenal tumor llkelr. Do pllysical exammaUons to detennlne any visual f&ald dale~ If ptuitary lesion is suspected?

• ~ CT scan of adrenals and MRI of pluitary gland to detect presence of adenomas. 'Sdntagraphy of lhe adrenal gland with lodochotosllolscan.

TREATMENT:

, __

If J,Ca 2+ in the blood -7 PTH 1' in response. Secretion inhibited by low serum Mg. Not influenced directly by P043- (except by P04 effect on the ionic calcium levels) PT,tJ secreted by 4 parathyrojd glands situated posterior to thyroid.

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PTH actions: 1. ~~~~S$oclast a£J.l.v~ (bone resorption) releasing Ca 2-t- and P04 3- from the bones. 2. Increases Ca 2+ agd Mg.absgrpti9,41 and decreases P04 3-and~ absorption in the re'nal tubules . 3. Increase active 1.25dih· droxy-cholecalciferol Vita · odu · 4 . Increased Ca 2+ and PO 4 a sorpt1on rom gut 5. NET EFFECT: increased serum Ca 2+ ->increased vit D, decreased PO 4

Patient presents with: 1. Asymptomatic with tCa2+ on routine tests. 2. Symptoms related to 1'Ca2+

• • • • • • •

On examination: 1. Dehydration 2. Pancreatitis

Weakness Tiredness Deprgssjgn -Polyuria and Polydipsia Renal STONES Abdominal pain Bone resorption effects: pain

3. Ulcers (duodenal:gastic = 7:1 MEN 1 causes 1'PTH and Zollinger Ellison syndrome) -4. o~-teogenia apd.osteogomsis.U's 5. 1'BP and when_untx- cardiovascular risk and mortality

Associated with MEN! (multiple endocrine neoplasia)

'ZiiS A&i-·-1 frM'itra a

\§uses and diffSreptjal ~= \ . P[jmal¥ hyperparathyroidism( 1' Ca2+, 1' PTH)

Secondary~( ,j,Ca2+, appr 1' PTH)

~rti'm'Ji-l.-Ca2+, inappr 1'1' PTH)

NB: Malignant hyperparathyroidism:

Investigations: 1. 1' PTH, 1' Ca2+

80-85% = wtitarx adegoma, 15-20% = bygemlasia agd <0.5% = wvcipgma Same as for hypocalcaemia =Malabsorption, Osteomalacia, Rickets, Low Vit 0 intake, chronic renal failure. After prolonged secondary hyperparathyroidism causing glands to act autonomically having undergone hyperplastic or adenomatous changes. C32+ increases unlimitecfby feedbaxk control. Seen in chronic renal failure.

Parathyroid related protein (PTHrP) produced by some squamous cell lung cancers, breast and renal cell carcinomas. This mimics PTH resulting In 1'Ca2+ but -1.- PTH as PTHrP not detected In the assay

[Diefferetials with these tests: Lithium, Thiazides, Familial hypocalcuria, Hypercalcaemia, tertiary hyperparathyroidism.

2. .J,P043- (unless renal failure) 3. 1'ALP levels from bone activity 4. 24h urinary Ca2+1' 5. DEXA bone scan to assess osteoporosis 6. OSTEITIS FIBROSIS CYSTICA = BM fibrosis and cyst formation due to severe resorption : Brown tumours,

Subperiosteal erosions of distal phylanges on hand Xrays, pepper·pott skull on skull Xrays.

Treatment: Surgery prevents #'sand peptic ulcers. Indications for surgery [excision of all4 hyperplastic glands or adenoma:

High serum or urjnarv ~e6.+ 2. Bo,..o.e..djsease 3. 9JJ:gngrgsjc; 4. Renal calculi s. Decreased r:nal functjop'age <50 years

ex of surgery: • Hypoparathyroid!~

• RLN dama,ie (hoarse voice)

• Post·oe symptomatic iCa2+ ·check Ca2.;. tor 11 dmpo~~-Mild symptoms does not validate surical removal:

1. Advise- Increase fluid intake to prevent stones 2. ftN'O'm thiazfdes or high Ca2+ and Vit D intake 3. Rev1ew in 6 months 4. Cincalcet (Increases Parathyroid cells to Ca2+ thus .J..PTH secretion

S7E: Myafgia, decreased testosterone.

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Serum Ca 2+ is about 50% protein bound (mostly albumin) and not exchangeable and alterations in protein content of the blood for any number of reasons may affect the total serum Ca 2+ without altering the ionized form.

Normal total serum Ca 2+ range l{i_25-2.62 mmoi/L)

Defln!tlgn gf Hvpgrnll;;iWllJ.a =Total corrected serum Ca 2+ > 2.62 mmoi/L (10.5 mg/dl) OR Ionized Ca2+ > 1.35 mmol/l (5.4 mg/dl) It Is a· medical emergency!

Sources of ECF Ca 2+ : diet and resorption frgm bgne Loss of Ca 2+ from ECF space viai Gllosses, renal excretion and deposition In bone matrix Calcium regulated mainly by two factors: parathyroid hormone (PTH) and Vitamin D

And Its actions is mainly on three organs: Gl tract1,Bo.ne, all.ti.!s.jd.fMlX

fVltamip oJ. '1recessary for Ca 2+ and PO 4 absorption from Gl

tract Production of 1,25 Dihydroxy-Vit Dis enhanced by PTH and low P04 levels

(§lcitoninJ • Polypeptide secreted by thyroid C cells • secretion enhanced by Ca 2+, Gl hormones,

pentagastrin • major actions: Decreased osteoclastic bone

resorption, increased renal PO 4 and Na+ clearance

ACUTE NET EFFECT: decreased serum Ca2+ when given in pharmacologic doses

Giimeslum l major intracellular divalent cation Ca 2+ is resorbed from the kidney with Mg, and thus Ca 2+ balance is difficult to maintain in Mg deficiency

fbosphorus) Found In all tissues and necessary for most biochemical processes cis well as bone formation

\hrathyrgld HormoQ! ir.!.tUJ Increased Ca 2+, vit D decreased PO 4

~tamin[l ;creased Ca 2+, PO 4

tti@tonin) decreased ca 2+ (In pharmacologic doses}

~-"'.TATIOM BONES, STONES. ryJOANS AND ABDOMINAL GRQANSJ • (kidney):Polyurla, polydipsja . Regal cpfic • (men a I) Lethargy, Depressiog. Orgwsjness Decreased cognjtjye funs;tion • ANS IT)Anorexia, Nausea, Dyspepsia, Constipation, Peptlc ulcer • :J ~atonia. bone pain. • ..l!,mary Hypwgarntbymjdjsm:

1. Asxs • 2. Renal calculi, 3.Hypertension • 4. Acute dehydration • S.Tumours never palpable • 6.Arrhythmlas •

Pathgphysio1ni\' 'increased bone resorption Increased gastrointestinal absorption Decreased renal excretion

Causes: With Normal or 1'PTH levels:

> 90% of hypercalcemia is caused by either parathyroid disease or malignancy. 1. Primary or tertiary Hyperparathyroidism 2. Lithium Induced hyperparathyroidism 3. Familial hypocalciuric hypercalcuria

With .J,.PTH levels: 1. Malignancy: Lung, Breast, Renal, Ovarian, Colonic, Thyroid Multiple myeloma 2. 1' 1,2S(OH)2 Vit D due to intoxication e.g Sarcoidosis 3. Thyrotoxicosis · 4. Paget's Disease with immobilization 5. Milk-alkali syndrome 6. Thiazide diuretics 7. GlucoCS deficiency

Investigations: 1. Serum Ca 2+, P04, PTH, diagnostic imaging for renal calculi and osteopenla

Treatment of Hypercalcemia

Treat acute, symptomatic hype_rcakemia aggressively with rehydration:~nd calciuresis • IV NS infusion (usually requires 4-6 L of fluid) • Only after adequately rehydrated, promote calcluresis with a loop diuretic, i.e. furosemide .. blsphosphonates is the treatment of choice as It inhibits osteoclast activity. It is Indicated in malignancy­

related hypercalcemia. Pamidronate is most commonly used via IV route since poorly absorbed from the Gl tract. It takes several days until full effect but effe~ Is long-lasting. Mithramycin is effective when patient can not tolerate large fluid load (dangerous- hematotoxic and hepatotoxic)

o Calcitonin: inhibits osteoclastic bone resorption and promotes renal excretion of calcium. Combination of calcitonin and steroids rriay prolong reduction in calcium

• Steroids: anti-tumour effects. useful in vitamin D-related hypercalcemia (including sarcoidosis) and hematogenous malignancies (myeloma, lymphoma). Slow to act (5-10 days); need high dose

• Prostaglandin inhibitors Surgical treatment if indicated Avoid immobilization

Clinical presentation:

1. Tetany '

2. Depression •

3. Perioral parasthesia

4. Trousseau's sign [wrist flexion, fingers drawn together if brachial artery occluded with BP cuff] . %

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~~,',,:, 5, N~uromuscular excitability e,g, tapping over the parotid (facial n, ) causes facial muscles to twitch ... , .. '.

6.

7.

[Chvoste!s's sjgnt Chronic Hypocalcaemia= Cataract

ECG: prolonged QT interval.

;.: . .. , . ;-;:· ... Investigations:

'

1. ..L-Ca2+ -.•:·~ .. 2. 1' P043-/N

3. · Normal ALP\

· .. · Causes:

1. · Autoimmune [associated with other autoimmune diseases].

2. .. Congenital- 01 george syndrome

, ·: Tx·i Alfacalcido~

Seeondary: ·: ~ -··.

Due to ra.dlation, surgery (thyroidectomy/parathyroidectomy), hypomagnaesemia.

[!seudohypoparath¥roldlsmJ ·

· .·. Failure of target cells to respond to PT!'f.

SIGNS: Short metacarpars (esp. 4th and sth), round face, short stature. m;nta! retardation; ' . . . i

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l, 1fTH 2. 1"/N ~p 3. ,J... Ca2+

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Tx.= The same as for primary.

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-Endocrine Emergencies:

__*Thyroid 'storm'

-Severe Thyrotox.i·ccrsis, [mortality;::! 10%} -Most commonly caused by infection in an undiagngsed/improRerly treated hyperthyroidism

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-Ciinlcai sx's _ -feve~,agitatiOJhCOnfusi.£n,tachycardia8,cardiac failure( older pt's)

-Treatment JVi(j{J[JtY"O~--IV fluids 10% 8i-Uc;c:6~ / YrrAtvtltl6/ (pa.--n0 CrPi:;

-"§road SPf.GtF'_,~~ -B-blockers(Propanalol)80mg/6hours p/o or 1-5mg/6hours IV -,!tadwgraphic contrast(Sodium Idopate)SOOmg daily p/o will normalise T3 levels within 48-i'l hOurs by illhibttrng the release ()f thyro-id flo-rmo.ne + reducing -conver~ion -ofT 4 to T3 -Dexamethasone 2mg/6hours or Amiodorone have similar effects -Carbimazole 4D-60mg daily p/o inhibits the synthesis of new thyrojd hormone After 10-14 days the pt can be managed on carbimazole alone.

*Mvxodoema Coma

.-.~are flz::sentation of hYRothxroiQ.i:jp [mortality = 50% J - sua Jy in ~.;;_!.LEt's who apQear m)2Sq.edematous ...

-Clinical sx's -decreased LOC,temp as low as 25,convulsions,increase in CSF pressure and proteins

-Treatment -ThroxinelY(not usually available) -Triidoth;y-ronine IV bolus 20 u~ followed by 20u¥/8hours until clinical improvement

-BG<3.5 mmol/1 [mortality 2-4% in insulin treated pt's] -Usually due to overtreatment ofDM(usually insulin)

-Clinical sx'~'s -Autonomic sx's: sweating, trembling, anxiety ~Neuroglycopenic sx's: Confusion, drowsiness, inability to concentrate, speech difficulty -Non-specific sx's: nausea, headache

-llisk factors for developing hypoglvcaemia -strict glycaemic control Jlekery young and very old)

-longstanding diabe~ :ftx of previo,}ls hypo glycaemia -renal imi;lainnent

uM ...

-Treatment -Oral carb treatment (able to swallow) --[adults]30-50ml of20-50% dextrose or g!ucagon lmg 1M · . -[ children]IV'<iextrose 0.2i'1g . -Where intermediate/long actmg medication is used, relapse may occur after initial treatment -Relapse: 10%dextrose infhsion, titrated to pt's BG • ~Co~sciousness not regained: suspect cerebral oede~a ~1lianrutol + oxyg~~ -AdJUSt future pharmacotherapy to prevent future epiSoJl:.~~-----..J

tAdrenal insuf/icienEJ!.

-inadeguate secretion of cortisol and/or aldosterone -Secondary( more common) - l .]withdrawal of gl~ocorticoid therapy

2.]hypothalamic or pituitary disease=

-Primar~(rare) - = 1. ]Addisons disease( due to autoimmune,HIV, TB,malignancy 2.]Congenital adrenal hyperplasia

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-Tests for glucocorticoids -ACTH stimulation test to differe . tia e and secon -Administer 250ug ACTH IM: if cortisol levels fail to respond=a insufficiency -Decreased AC I H = secondary ; increased ACTH = primary

-Clinical sx 's ~yreserif ;vith: circulatory shock .wjth severe hypot;eosigp. hvnorutt.L~!; hxp~1·ka~n;ia, and m some mstanceihrnoglyC:ae~ta and b.Per~alcaew!a .. ·IDJ;l~le Cr~mps, ~usea. Yom.iling. Utarrh~V}Ct,. -Vittilizy in 10-20% of pt' s with auto-immune Addisons

-Treatment -S2,_rtjW,(hydrocortisone)l5m~@ waking and 5mg@ 18:00 p/o -Indivjdual dosages <md responses may vary

. u~ h.v<j,u-~c;nrt i ~OIJt: ~ucr;iw•te 1 nOn.J$ + IV fl nid~(ssline + 10% d.e:x tro:)e f{)r hypo gtyG:ilem ia') ~.JV !Jydrq<;orti~one should continue (0)1 00m~/6hnurs nnD.l GD' svrnptoms QO awav

:-~ ~~;: r. .l':t :.}~ ~~_;--~~~\,·~-~ ~:-~::=~~:~~~-Co ,- . .... ... ; ;~; - .... ·1 ,i:: . .., ~ !'!-• - , .. ..... -F ,. . ... ,..~~ ~"!' ... . ... --~ :";" _ ~.,. - ..... : ·. . • . .• •. : : • : ,. .•• . ; ...... ·, ~ ;. . ... . : ·. • . ~- •.: ~·- . . • • . ·' • ~ ·' . •• :. t - .

---

-Treatment -Cortisol(hydrocortisone)l5mg@ waiGng and 5mg@ 18:00 p/o -Individual dosages and responses may vary -Adrenal crisis is however an EMERGENCY! -IV hydrocortisone succinate lOOmg +IV fluids(saline + 10% dextrose for hypoglycaemia) -fV hydrocortisone should continue @1 00mg/6hours until GIT symptoms go away

-Hazards of glucocorticoid treatment -(see clinical features of ci.tshin's disease)

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The Red cell ~ Erythropoiesis & Haemoglobin }> Anaemias:

-Approac~ -Iron deficiency -Anaemia of chronic disease -Sideroblastic anaemia -Thalassaemia -Haemolytic anaemias -Aplastic anaemia -Megaloblastic anaemia

}> Myeloproliferative disorders ~ TheSpleen

The White cell }> Neutrophil }> Eosinophil ~ Basophil }> Lymphocyte )> Monocyte .

The Platelet & Bleeding disorders

Leukaemia

Lymphomas

Multiple myeloma

DVT

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