Ftplectures Musculoskeletal system Lecture Notes

MUSCULOSKELETAL

Medicine made simple

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Brachial plexus Part-1

Roofs Trunks divisions cords branches

C5 DS SS LP M

C6 UPTD LSS

LTN C7 A M

Serratus ant. C8 R

Winged scapulaT1 mp MABC

MBC U

Robert tree drinks cold beer

DS- dorsal scapular

SS- supra scapular

LP- lateral pectoral

Pect is my FAM-

TD- thoracodorsal n- Latissmus; MEAL- medially rotates, extends my hand, addeducts, latissmus

LSS- lower subscapular nerve

UP- upper subscapular nerve

MBC- medial brachial cutaneous

MABC- medial anti brachial cutaneous

MARMU- musculocutaneous, axillary, radial, medial, ulnar nerve

Musculocutaneous nerve innervates BBC- Biceps, Brachialis and Coracobrachialis

Axillary nerve innervates Deltoids and Teres minor

Radial nerve innervates BEST- Brachioradialis, Extensors, Supinator, Triceps muscle

Median nerve innervates 2 LOAF- 2 lumbricals, oppones pollicis bravis, abductor pollicis bravis and flexor pollicis bravis

Compression of median nerve causes Carpal Tunnel syndrome- caused by excessive use, prednisone, hyperthyroidism.

Hand of benediction due to damage to median nerve- pope sign- ulnar nerve works but median nerve does not function

Ulnar nerve-75% of all muscles in your hand innervated.

Hypothenar nerve, 2 lumbricals, PAD [palmar interossi addeduct] and DAD dorsal interossi [abduct]

Ulnar nerve damage causes claw hand when asked to make a fist.

Gout

- Monoarticular inflammatory arthritis of the joint. - Caused by monosodium urate crystals deposition - Excess uric acid- hyperuricemia - Males more than 50 years and females at menopausal age.

Pathogenesis

- Increased production of uric acid. - HGPRT- hypoxanthine guanine phosphodosyl transferase enzyme deficiency- Lesch

Nyhan syndrome

Catabolism and salvage of purine nucleotides

AMP Ribose 5 phosphate GMP

PRPP synthetase

Adenosine PRPP

IMP

Inosine HGPRT

Hypoxanthine Guanosine

Xanthine

Uric acid Guanine

1. Lesch Nyhan syndrome - It is an X-linked recessive disease so affects males mainly - 9-12 months - Self-mutilation - Involuntary movements - Tourette syndrome- aggression - Uric acid increases- gout due to hyperuricemia - Uric acid stones in kidney.

2. Over activity of PRPP synthetase. 3. Cell turnover 4. Most common cause of hyperuricemia

End stage renal disease Drugs Acidosis Decreased excretion of uric acid

1. Hydrochlorothiazide inhibits Na/Cl channel

- Hyper Glycemia - Lipidemia - Uricemia

Causes increased levels of uric acid

- Calcemia 2. NSAIDS- Aspirin 3. Immunosuppressants

like TAcrolismus and cyclosporine

Pathophysiology of gout

High uric acid- monosodium urate crystals

They deposit in the joint space

IgG binding to uric acid crystals

C3a and C5a get activated

Neutrophils come to the area to swallow antibody-uric acid crystal complex

Lysis of neutrophils causing release of proteolytic enymes

Inflammation Joint pain and swelling podagra

Macrophages engulf uric acid crystals and release IL8, IL6, IL1 and TNF

Clinical features of gout

Asymptomatic hyperurecemia

Acute gouty arthritis Intercritical gout Chronic tophaceous gout

Treatment- leave it alone

Males 40-60 years They develop acute gouty arthritis then they become asymptomatic for the next few years and again develop an episode of acute phase.

They develop tophi

- Acute onset of metacarpophalngeal joint

- Cellulitic changes like Swelling, Erythema, Warmth

- Cartilage destruction

- Soft tissue destruction + inflammatory giant cells + urate crystals

Precipitants - Low

temperature - Dehydration - Stress - Alcohol -

excessive Post healing phase

about 1 week later- skin desquamation

Diagnosis

i. Joint aspiration and synovial fluid analysis- a polarized microscope is used for analysis – needle shaped negatively birefringerent urate crystals.

ii. Serum uric acid level- not much of help as it remains normal during acute gouty arthritis.

iii. X-rays- punched out erosions around bone cortex. iv. Gram stain of the joint to rule out septic arthritis

Treatment

- Avoid anything that predisposes patient to develop hyperuricemia - Stop excess alcohol intake - Decrease purine diet like meats - Reduce obesity by weight loss - Check medication like diuretics, NSAIDS - Acute gout- advise bed rest, start NSAIDS- indomethacin, ibuprofen - Colchicine is alternative of NSAIDS- side effects are nausea, vomiting, abdominal

cramps and diarrhea. It is contraindicated in renal failure and pancytopenia. - Corticosteroids- oral prednisone for 7 to 10 days. - If only one joint involved- intra-articular injection of steroids.

Prophylactic therapy for gout-

NSAIDS [not aspirin] or colchicines is given – 3-6 months and then stopped.

Check for 24 hour uric acid secretion in urine before starting uricosuric drugs.

<800mg/day >800mg/day Undersecretion Oversecretion Uricosuric drugs like probencid and sulfupyrazone

Allopurinol- inhibits Xanthine oxidase

Contraindicated in patients with renal failure or kidney stones

Complications of gout-

i. Nephrolithiasis ii. Destructive arthritis

Pseudogout

- It is the deposition of calcium pyrophosphate crystals inside the joint causing inflammation.

- Seen in older patients with degenerative joint disease. - People at increased risk are those with hemachromatosis, hypothyroidism,

hyperparathyroidism - Diagnosis- joint aspiration. Positively birefringent rod shaped or rhomboid shaped

crystals. - X-rays- cartilage calcification- chondrocalcinosis- white colored rim on bone - Treatment- according to the underlying cause. For symptomatic relief give NSAIDS,

colechicine, intra-articular steroid injection. Joint replacement may be needed.

Shoulder pain evaluation

A patient comes with shoulder pain.

Checking of active and passive movements of cervical vertebrae-

- He is asked by the doctor to bend his head forwards, backwards and side to side. - He is asked to turn the head left and right.

Palpation of cervical vertebrae

- It hurts.

Check the back- active and passive movements

- Bringing both the hands in the front. - Asking to flex forward, backwards and turning on right and left side. - Palpation of the vertebrae from back.

Checking of first and second rib

- Asking to take a deep breath during palpation.

Checking of pectorals

- Pull the right hand back and then left

Check the range of motion of upper body and shoulder muscles

- Ask the patient to lift up both arms [flexion] and then bring them down [extension] - Then the arms should be lifted up from side- abduction and then brought back-

adduction - Then locking of hands at the back- joints undergo internal and external rotation. - Now the doctor will flex, extend, abduct and adduct the arms of the patient. Locking

the arms in the back also and exaggeration of it by the doctor. - Doctor asks the patient to put his fists together in the front. - He pushes the patient down and checks for resistance during abduction, pushes up to

check adduction - Similarly flexion and extension is also checked - Fists are asked to be put on sides to check external rotation by pressure inwards and

internal rotation by pressure outwards.

Empty can test for supra spinatus

- Pressure given downwards and the resistance is checked for supraspinatus

The arms are checked by

- Flexing the arms forward and then returning back by keeping them close to the chest. - Now supination and pronation of arms by the patient and then by the doctor himself.

Now for wrists

- Wrists are flexed, extended and internally rotated and externally rotated. It is called radial deviation and ulnar deviation.

- Now the doctor does the same to understand the strength of flexion and extension on the patient.

Sensory nerve and reflexes

- C5, C6, C7 and T1

Check for reflexes

- Biceps- C5, radialis- C6 and triceps- C7

Spencer test

- Shoulder examination - Make the person lie down. - Check the ribs and the clavicles - Check for internal rotation mainly - Make the person lie down on his side. - Check for flexion, extension, adduction and abduction.

Head and neck physical examination

Patient has sinus pain.

- Ask the patient to bend the head forward and then passively extend the head - As the patient is asked to rotate the head to the right and left and passively acted upon

by the doctor also. - Now the patient’ head is turned from one side to other and checked - He patient has a good range of motion. - Next, the cervical vertebrae are checked C2-C7, - Sinus- check- frontal sinus, maxillary sinus - Lymph nodes- posterior auricular- light to deep palpation, anterior lymph node,

preauricular , submaxillary, submental, sternocleidomastoid muscle- posterior to it are posterior cervical lymph nodes- light to deep palpation, then anterior cervical lymph nodes and supraclavicular lymph nodes.

Ear examination

- Pull the pinna superiorly and posteriorly - Next check nasal sinuses. - Ask the patient to say ‘ah’- check for anterior and posterior faucial pillars and tonsils

Check thorasics

- Ask the patient to put the arms forward and then bend and then backward. Rotate from one side to other. Now side-bend on both the sides.

Check thorasic vertebrae

- Palpate nicely.

Next listen to heart and lungs

- Place the stethoscope on the 2nd intercostal space- falls between the 2nd and 3rd rib to hear S2 sounds. On the other side for pulmonary sounds, then in midsternum for tricuspids, for mitral valve placement on 4th intercostal midclavicular.

- Triangular auscultation- a triangle formed by inferior angle of scapula, medial side of scapula, medial surface of trapezius and base of latissmus dorsi.

- While breathing lung moves from T8 to T10. - Check for rib 1 and rib2.

Check for patient rib function

- Ask the patient to breathe - Check the clavicles. - Flex the sternum.

Crohn’s disease

Another name is regional enteritis.

Definition

It is a chronic trans mural inflammatory disease that can affect any part of the GI tract from mouth to anus. Most commonly affects terminal ileum and cecum. Small intestine= 30%, terminal ileum=40%, colon=25%. More common in Caucasians

Pathology

- The lesions within the bowel are discontinuous skip lesions. - Fistula formation-enteroenteric fistula, enterovesicular fistula-bladder and bowel

connected (bubbles in urine- pneumaturia), fistula connecting bowel and vagina= enterovaginal fistula

- Luminal strictures due to the inflammation of the bowel wall. - Non-caseating granulomas - Creeping fat surrounds the inflamed bowel.

Extra-intestinal manifestation of Crohn’s disease

a. Eyes 1. Episcleritis 2. Anterior uveitis b. Skin

1. Erythema nodosum- painful nodules on their skin which are red in color 2. Pyoderma gangrenosum- huge skin ulcer which does not heal.

c. Arthritis- 1. monoarticular and migratory type 2. ankylosing spondylitis- bamboo spine 3. sacro-iliatis

d. Hypercoagulable state 1. deep venous thrombosis 2. pulmonary embolism 3. stroke

e. osteoporosis f. gall stones [esp. Crohn’s disease] g. primary sclerosing colengitis

Clinical features

1. Non-bloody diarrhea 2. Weight loss and malabsorption 3. Abdominal pain- right lower quadrant mostly 4. Fever, malaise 5. Aphthous oral ulcers

6. Cholelithiasis and nephrolithiasis

They have flare-ups and remissions so they are unpredictable.

Diagnosis

1. Endoscopy- sigmoidoscopy and colonoscopy - Aphthous ulcers – a cobblestone appearance of the bowel wall - Pseudo-polyps or patchy skip-lesions

2. Upper endoscopy

Complications

1. Fistula formation 2. Abscesses inside the GI tract 3. Small bowel obstruction- only reason for surgery 4. Malabsorption of Vit. B12 and bile acids 5. Gall stones- lack of bile acids absorption 6. Nephrolithiasis- Increased oxalate absorption in the colon- calcium bind to form

calcium oxalate stones inside the kidney. 7. Toxic megacolon

Treatment

1. Sulfasalazine- 5-ASA- mesalamine- Block prostaglandins 2. Metronidazole 3. Corticosteroids- systemic prednisone- given in acute exacerbations 4. Immunosuppressive agents like azathioprine or 6, mecaptopurine 5. Bile acid sequesterants- cholestyramine or colestipol 6. Surgical resection-segmental- disease can recur 7. They need a lot of nutritional supplements

Ulcerative colitis

Definition-

It is the Chronic inflammatory disease of the colon or the rectum.

Age-

adolescents, young adults

Site-

Mostly rectal area=10%, rectum+ left colon= 40%, left colon+ right colon, entire colon= 30% [pancolitis], backwash ileitis=10%

Not predictable

Pathology

- No skip lesions. The lesions are continuous. - Limited to mucosa and submucosa - PMNs accumulate in the crypts of the colon. They form crypt abscess.

Clinical presentation

1. Hematochezia/ bloody diarrhea 2. Abdominal pain 3. Frequent bowel movements- small amounts 4. Fever, anorexia, weight loss in severe cases. 5. Tenesmus – rectal dry heaves.

Extra-intestinal

- Pyoderma gangrenosum- skin lesions - Eyes- anterior uveitis - Arthritis- joints

Diagnosis

1. Stool culture- clostridium difficile, ova, parasite 2. Fecal leukocytes- crypt neutrophils are reflected. 3. Colonscopy

Complications

1. Iron deficiency anemia- low ferritin level and iron levels. MCV<70. Microcytic anemia

2. Hemorrhage 3. Dehydrated due to loss of electrolytes 4. Increased risk of developing colon cancer.

5. Primary sclerosing cholengitis- strictures and dilatation in biliary tree. 6. Cholangiocarcinoma- Klatskin tumor if the tumor is in the Y of the biliary tree. 7. Toxic megacolon 8. Depression, narcotic abuse.

Treatment

1. Systemic corticosteroids in case of acute exacerbation. 2. Main drug is sulphasalazine—5ASA, proptysis – 5 ASA enema. 3. Immunosuppressants- Azothiaprine / 6 Mecaptopurine 4. Only cure is total colectomy- then anastomosed to skin.

Polyarthralgia rheumatica

It is common in elderly female patients more than 70 years of age

Cause unknown

Autoimmune process

Genetic predisposition- HLA-DR4 allele

Clinical symptoms-

1. Shoulder and hip pain bilaterally. 2. Morning stiffness is there and worsens without movement. 3. Muscle strength is normal 4. Fever, fatigue, weight loss, malaise and depression 5. Synovitis in knee, wrist- joint swelling. 6. Tenosynovitis- shoulder muscles- SITS- supra spinatus, infraspinatus, teres minor and

subscapular 7. Adhesive capsulitis 8. 10% develop temporal arteritis.

Diagnosis

1. Clinical- bilateral 2. ESR>50

Treatment

1. Corticosteroids 2. Temporary arteritis may cause blindness if not treated.

Anatomy of shoulder and back

Name of the muscle Origin Insertion Nerve Trapezius –superficial muscle

Superior nuchal angle of occipital bone Cervical vertebrae from C1-C7 and thorasic vertebrae from T1 to T12

Lateral part of the clavicle, acromium and the spine of the scapula

Spinal accessory

Latissimus dorsa –superficial muscle (MEAL- medial rotation, extension, addeduction and lats)

T7-T12, lumbar vertebrae, iliac crest, Ribs 9-12

Groove of humerus after spiraling around teres major

Thoracodorsal nerve

Rhomboideus minor Rhomboideus major (retract scapula)

C7 and T1 T2 and T5

Medial border of the scapula Medial border of the scapula

Dorsal scapular nerve for both

Levator scapulae Transverse process of C1 to C4

Superior medial border of the scapula

Deltoids Ant part- lateral third of the clavicle Middle part-acromion Posterior part- spine of scapula

Deltoid tuberosity Axillary nerve from Brachial plexus

SITS muscles

Name Origin Insertion Action Nerve Supraspinatus Greater tubercle

of humerus Suprascapular

nerve Infraspinatus Greater tubercle

of humerus Suprascapular

nerve Teres minor Greater tubercle

of humerus Axillary nerve

Teres major Inferior angle of the scapula

Bicipital groove of humerus

Subscapularis Subscapular fossa

Inferior tubercle of humerus

Primary flexors of arm- anterior deltoids, coracobrachialis muscle

Primary extensors of arm- posterior deltoid, latissmus dorsa

Abduction- middle deltoid till 90 degree, supraspinatus for the first 15 degree

Serratus anterior muscle- stabilizes scapula, laterally rotate- origin- medial aspect of scapula, insertion- ribs 5,6,7 & 8. Nerve – long thorasic nerve

Primary adductors- subscapularis muscle

Adduction- pectoral muscles- nerve- axillary nerve - FAM- flexion, adduction and medial rotation

Internal rotation- pectorals and latissmus

External rotation- infraspinatus and pect minor

Teres major- nerve- subscapular nerve

Rheumatoid arthritis

Definition

It is the chronic inflammatory autoimmune disease of the synovium.

Cause

Unknown

Age of onset-

Females of 20 to 40 years of age.

Pathogenesis

- Foreign body- genetic predisposition. - Fb activate CD4 helper Tcells- which in turn activate plasma cells- antibodies like

IgM- attach and attack to Fc part of IgG antibodies- this complex is called Rheumatoid factor(RF)

- It cause inflammation- chronic inflammatory synovitis - Pannus formation- destruction of cartilage, edgy bone - Increased synovial fluid in the joint space.

Clinical features

- Symmetrical inflammatory arthritis- DIP (distal interphalangeal joint) remains untouched.

- It affects PIP (proximal interphalangeal joint) and MCP (metacarpal phalangeal ) - Morning stiffness due to PM - PIP and MCP affected. - Fever, weight loss, fatigue - Hand deformities- ulnar deviation, Boutonniere’s deformity (PIP is flexed and DIP is

hyper-extended), swan-neck deformity also called the Z-arm (MCP is flexed, PIP is hyperextended and DIP is flexed)

- Cervical spine (C1-C2) is affected in case of rheumatoid arthritis.- ca develop subluxation. Before surgery make sure you do a cervical xray.

Different organs affected-

1. Skin - Subcutaneous nodules present on elbow, occiput, sacrum- classic rheumatoid nodules - Tend to bruise easily as it is thin and atrophic - Ulcers around their hands due to poor blood flow. 2. Heart - Pericardium affected- pericarditis- chest pain due to that especially during bending

front. - Pericardiac effusion. - Predisposed to develop bundle branch blocks

3. Lungs - Pleural effusion- low glucose - Pleuritis - Pulmonary fibrosis- interstitial lung disease - Honeycomb pattern on chest xray 4. Eyes - Scleritis - Scleromalacia- soft sclera- can get perforated and go blind - Dry eyes- Sjogren’s syndrome - Mononeuritis multiplex – infarction of the nerve trunks 5. Blood vessels - Microvascular vasculitis

Felty syndrome

1. Neutropenia 2. Rheumatoid arthritis 3. Splenomegaly

Blood cells

- Low platelets - Lymphadenopathy - Anemia

Diagnosis

1. Rheumatoid factor titre- 80% will have high RF level. It is a non specific test. 2. ESR and CRP- high 3. Anemia of chronic disease- normocytic and normochromic 4. Xrays- bone loss at the finger joints, cartilage eroded, narrowing of the joint space,

bone erosions, a lot of synovial fluid in joint space. 5. Synovial fluid analysis- non-specific- cloudy yellow fluid- WBC>5000 /mm3

Treatment

1. Slow down or prevent bone destruction 2. Watch out for toxicity 3. Exercise- for mobility 4. Pain control- NSAIDS 5. Low dose short term corticosteroids 6. DMARDS- disease modifying anti rheumatoid arthritis drugs- reduce the morbidity

and mortality of the patient.- 6 weeks to work a. Methotrexate- can cause GI ulcers/upset, bone marrow suppressant,

hepatotoxicity, pulmonary fibrosis.

Check renal function and LFT b. Hydroxychloroquine- ADR- vision loss due to retinopathy so carry out eye

examination once in every 6 months. c. Sulfasalazine

All of them require folate replacement.

Second line of drugs- C the GAP 1. Gold 2. Azathioprine 3. Pencillamine 4. Cyclosporine

Last resort- synovectomy or joint replacement therapy

Scleroderma  (systemic  sclerosis)  

Definition-­‐  It  is  a  connective  tissue  disorder  in  which  collagen  is  involved  causing  widespread  fibrosis.  

Pathogenesis  

Fibroblasts  stimulated  by  cytokines-­‐  excess  production  of  collagen  fibers-­‐  women  of  35-­‐50  years  old.  

Types  

Diffuse     Limited    Skin-­‐  Raynaud’s  phenomenon   Face,  neck  and  distal  extremities  Cutaneous  fibrosis-­‐  claw  hands-­‐  sclerodactyly   Facial  contractions  and  claw  hands  GI  tract-­‐  develop  vomiting  from  acid  reflux,  develop  dysphagia,  delayed  gastric  emptying,  constipation,  diarrhea,  esophageal  strictures(  secondary  to  excess  acid  reflux)  

Raynaud’s  phenomenon-­‐  digital  ischemia  

Lungs-­‐  pulmonary  hypertension.  It  can  be  the  major  cause  of  death  

Pulmonary  hypertension  

Heart-­‐  pericardial  effusion,  congestive  heart  failures,  arrhythmias  Kidneys-­‐  rapid  malignant  hypertension-­‐  today  it  is  rare  due  to  ACE  inhibitors    

Better  prognosis  than  diffuse  CREST  syndrome  Calcinosis  Raynaud’s  phenomenon  Esophageal  dysmotility  Sclerodactyly  Telangictasis    

Diagnosis-­‐  ANA-­‐  elevated  Increased  anti-­‐topomerase  1.  Also  called  anti-­‐scl  70  Check  barium  swallow  and  pulmonary  function  test-­‐  restrictive  pattern  as  it  s  ILD  

 ANA-­‐elevated  Anti  centromere  antibody-­‐  specific  to  limited  

 

A  certain  %  of  people  with  scleroderma  can  have  Sjogren’s  syndrome.  

Treatment  

-­‐ No  cure  -­‐ NSAIDS  for  joint  pain  -­‐ H2  blockers  or  proton  pump  inhibitors  for  acid  reflux-­‐  drugs  like  omeprazole,  cimetidine  -­‐ Raynaud’s  phenomenon-­‐  stop  smoking,  avoid  cold,  stay  warm,  calcium  channel  blockers  in  

severe  cases  -­‐ Kidneys-­‐  lisinopril-­‐  ACE  inhibitor  –  to  prevent  renal  hypertension.  

 

Idiopathic inflammatory myopathies

Polymyositis and dermatomyositis

Cause- viral infection or autoimmune. Actual cause is unknown. Genetic susceptibility is there. Immune system is activated which causes chronic inflammation.

Occurrence- mostly in females, rare form in males- inclusion body myositis- distal muscle weaknesses, no autoantibody, low creatinine levels.

Clinical features

-­‐ Symmetrical proximal muscle involvement- weakness. – shoulder girdle, pelvic muscles, neck flexors

-­‐ Myalgia- -­‐ Dysphagia – esophageal muscles affected

Skin rash- dermatomyositis

1. Heliotrope rash- butterfly rash- Around the eyes, bridge of the nose, cheeks- redness and erythema

2. Gotrons papules- MCP, PIP, DIP- affected- red scaly rash. They show a V sign on the front or back of their neck. It is called as the Shawl sign

3. Periungal telangiectasias 4. Arthralgias- joint pain 5. They are at an increased risk of cancer- lung, breast, GI, ovarian, myeloproliferative disorder

Diagnosis

1. CPK- creatinine kinase level is elevated in muscle damage cases, LDH, Aldosterone, AST/ALT-elevated

2. ANA levels high in 50% of the patients. 3. Anti-synthetase antibody/ antiJo-1 antibody 4. Anti-signal recognition particle- worst prognosis if positive 5. Anti-MI2 antibody- good prognosis if positive 6. EMG- 7. Muscle biopsy- best by far. Inflammation around the muscle fibres, lymphocytes

Treatment

1. Corticosteroids 2. Methotrexate, cyclophosphamide, chloramloncil - immunosuppressive agent 3. Physical therapy

Ankylosing spondylitis

Seronegative spondyloarthropathies

- No rheumatoid factor ( anti IgG antibodies) - HLA-B27 (gene for HLA MCH1) - PAIR - Psoriasis arthritis - Ankylosing spondylosis - Inflammatory bowel disease - Reactive arthritis/ Reiter’s syndrome - Common factor for PAIR

i. Asymmetrical oligo-arthritis. ii. Enthesitis – inflammation in the area where tendon meets the bone iii. Inflammatory arthritis- sacro-iliac joint iv. Genetically linked

Ankylosing spondylitis

- Males (HLA-B27) - Bilateral sacroilitis - It starts at a very young age. - Gradually the spine starts fusing- from lumbar to cervical - There may be acute exacerbation

Clinical features

- Lower back pain - Neck pain - Morning stiffness which gets better by exercise. - Enthesitis- tendon of the supraspinatus muscle that goes and inserts into the head of

the humerus, cheilius tendon that attaches to the calcaneous. - Limited spinal movements due to fused spine so prone to fractures even by a small

trauma. - Chest pain due to limited mobility of spine. - Shoulder pain, hip pain - Fever- low grade and weight loss

Extra-articular events

- Anterior uveitis or iridocyclitis

Diagnosis

1. Imaging- X-ray plain film, MRI, CT scan of lumbar and pelvis, 2. Sacral-iliatis 3. Bamboo spine

4. ESR- just let you know about inflammation 5. HLA-B27- not required as such

Treatment

1. NSAIDS- indomethacin 2. Maintain good posture 3. Physical therapy

Warning

Immobilize the neck with C collar to prevent injury to spinal cord.

Complications

1. Restrictive lung disease – FEV1:FVC ratio is increased or normal 2. They may develop Cauda Equina syndrome. 3. More prone to spinal fracture + osteoporosis

Psoaritic arthritis

- 10% of psoarisis patients affected. Gradual onset of arthritis. - Joints affected-upper extremities - Asymmetrical and polyarticular - Treatment by NSAIDS for pain control.

Inflammatory bowel disease

- Ulcerative colitis - Crohn’s disease

Reactive arthritis

Definition

It is an asymmetric inflammatory arthritis of the upper and the lower extremities where the lower ones are affected more.

It is preceded by infection and starts after 4 or 6 weeks.

The infection can be genitourinary (2) of gastrointestinal infection (1,3,4,5) which are namely-

1. Salmonella 2. Chlamydia 3. Campylobacter 4. Yersinia 5. Shigella

Reiter’s syndrome- can’t see, can’t pee, can’t climb a tree

1. Conjunctivitis 2. Urethritis 3. Arthritis

Symptoms

1. Asymmetrical joint pain- Effusion and no mobility 2. Check for previous GI/GU infections 3. Fever, weight loss and fatigue

Diagnosis

1. Synovial fluid analysis- rule out crystals as in gouty arthritis and septic joint.

Treatment

NSAIDS- IST TIME

Immunosuppressive agents- sulfasalazine or azothioprine

Sjogren’s syndrome

- Autoimmune disease - Lacrimal gland, parotid gland affected- destruction of the glands due to lymphocytic

infiltration - Dry eyes, dry mouth- primary Sjogren’s syndrome - Secondary Sjogren’s syndrome- lupus, rheumatoid arthritis, systemic sclerosis,

polymyositis- other rheumatological disease. Dry eyes, dry mouth + any of the above mentioned disease.

- Increased risk of developing non-Hodgkin’s lymphoma- can cause death.

Symptoms-

- Redness, burning sensation in eyes - Blurring of vision - Dry eyes + dry mouth - Arthralgias - Fatigue - Intestinal nephritis, vasculitis and chronic arthritis.

Diagnosis

1. ANA=anti nuclear antibodies-it is not specific as such but 95% of patient show positive ANA

2. Rheumatoid factor is positive 3. Anti Ro (SS-A) or anti La (SS-B)- those with positive anti Ro have higher risk of

developing neonatal lupus. 4. Increased ESR 5. Leucopenia 6. Normocytic, normochromic anemia

Treatment

- Pilocarpine- increase secretions – saliva + tears - Artificial tears - Good oral hygiene - NSAIDS for arthralgia/arthritis

Systemic Lupus Erythematosus

Definition- It is an autoimmune disease

Cause- unknown. Sometimes genetic component, environmental factors

Pathophysiology- antibodies binds to the double stranded DNA- compliments attracted –C3 activation- neutrophils are attracted.

IgG+C3 complex causes inflammation= pain+redness

Race- African Americans are most common patients. Always women at 20’s to 30’s.

Types

Spontaneous lupus Discoid lupus Drug-induced lupus ANA negative lupus

Most common and systemic

Seal- skin lesion on face

Chlorpromazine Anti-nuclear antibodies negative lupus

Hydralazine They may have arthritis and subcutaneous skin lesions

Isoniazid Anti SSA will be positive.

Procainamide Methyl-dopa Quinidine

Increased risk of developing AV blocks in newborn

Clinical features

1. Malar rash- Also called as butterfly rash which is around the cheeks and goes over the bridge of the nose. Discoid lesions are keratotic. Patients are photosensitive so sunscreens are prescribed. They develop oral, pharyngeal and nasal ulcers.

2. Joint pains 3. Fatigue, weight loss and fever 4. Raynaud’s phenomenon- they are prone to develop vasculitis. They get vasospasm when they go

out as their blood vessels are fibrotic. Their extremeties become white or even blue when they move out in cold. The condition is extremely painful.

5. Alopecia- loss of hair 6. Arthritis-arthralgias and myalgias. 7. Heart- pericarditis, Libmann-Sacks non bacterial endocarditis. 8. Lungs- pleural effusions and pleuritis, interstitial pneumonitis- can develop interstitial fibrosis-

and then pulmonary hypertension. 9. Blood- develop vasculitis of blood vessels. RBC- hemolytic anemia, WBC- leucopenia (common

cause of death) and lymphopenia, platelets- thrombocytopenia

10. Kidney- glomerulonephritis, proteinuria (>0.5g/day), hematuria, azotenia (increased BUN/creatnine ratio), cellular casts in urine

11. CNS- develop seizures, headaches, psychosis, depression 12. Transient ischemic attack or stroke (CVA) 13. GI tract- nausea, vomiting, dysphagia, peptic ulcer disease. Can develop Sjogren’s syndrome.

Diagnosis

1. Antinuclear antibody of serum- sensitive but not specific- elevated levels then chances for lupus 2. False VDRL/ RPR test for syphilis- positive- it is due to the presence of anticardiolipin 3. Anti double-stranded DNA antibody test- specific to lupus- not sensitive. 4. Anti-Smith antibody posistive- definite diagnosis 5. Anti-SS DNA- 70% 6. Anti-histamine antibodies- drug induced lupus if positive 7. Anti-Ro (SS-A): La(SS-B)- sjogren’s syndrome, neonatal lupus (AV block/ transposition of great

vessels, ASDs or VSDs), low complement levels (C2/C4) 8. Check for CBC 9. Renal function test 10. Urinalysis – casts, hematuria

Diffuse proliferative glomerulonephritis is usually a type IV- almost developing renal failure

TYPE V- lupus- common cause of renal failure

11. Anticardiolipin+ lupus anticoagulant test – -­‐ Antiphospholipid antibody syndrome -­‐ hypercoagulable state-. It is associated with lupus, scleroderma, -­‐ Deep venous thrombosis- increased risk of pulmonary embolism. Recurrent arterial

thrombosis- recurrent miscarriages. -­‐ Thrombocytopenia, levidoreticularis

Labs

-­‐ PTT prolonged -­‐ Warfarin given

Treatment

-­‐ Long term anticoagulation to keep INR within 2.5-3.5

Treatment modalities

1. Prevention- decrease sun exposure, by wearing sunscreen 2. Pain control –mild cases- NSAIDS 3. Local/systemic corticosteroids- prednisone in acute cases 4. Hydroxychloroquine- for skin, joint and constitutional symptoms. 5. Cyclophosphamide- lupus glomerulonephritis (mesna) 6. Monitor- kidney function and hypertension

7. Patients die due to renal failure, opportunistic infections

Vasculitis

It is the inflammation of blood vessels.

Inflammation- ischemia- decreased perfusion- necrosis- end organ damage

Large vessel vasculitis Medium vessel vasculitis Small vessel vasculitis Aorta, carotid, temporal arteries

1. Temporal arteritis 1. Polyartheritis nodosa 1. Henoch-Schlein purpura 2. Takayasu arteritis 2. Kawasaki’s disease 2. Behcet’s syndrome

3. Wegener’s granulomatosis

3. Hypersensitivity vasculitis

4. Churgs struss syndrome

5. Microcytic polyangitis

Temporal arteritis

- Giant cell arteritis - Unknown cause - Patient population- women above 50 years - Temporal arteries are affected the most. Aorta and carotid arteries can be affected. - Increased risk of developing aortic aneurysm or aortic dissection.

Clinical features

- Severe headaches - Fever, malaise, fatigue- constitutional symptoms - 25% of patient have visual problems- optic neuritis- Amaurosis fugax- can lead to

blindness - Jaw pain- intermittent claudication- during chewing. - Tender temporal artery with palapable nodule. - Decrease pulse - They can have the disease polymyalgia rheumatic.

Diagnosis

- ESR- could be normal - Temporal artery biopsy- most sensitive way to pick up the disease.

Treatment

- Aggressive and immediate treatment as they can turn blind. - High dose corticosteroids- prednisone. - IV steroids if visual problems have started already.

- Check ESR during treatment to know if the corticosteroids are working or not.

Takayasu’s arteritis

- Found in Asian women, - Aortic arch, major branches- subclavian, carotid, - Stenosis of blood vessels - Diagnosis by arteriogram

Clinical features

- Fever, night sweats, malaise, arthralgia, fatigue - Tenderness on the area involved. - Los of radial, ulnar or carotid pulses. - Aortic regurgitation - Stroke, aortic aneurysm, limb ischemia

Treatment

- Steroids - Angioplasty- surgery- a stent placed to maintain patency of the blood vessel.

Churg-Struss syndrome

- Medium vessel vasculitis - Affects many organs- lungs, heart, GI, kidney and skin

Symptoms-

- Shortness of breath- dyspnoea-asthma - Fever, fatigue, weight loss - Skin nodules with palpable purpura

Diagnosis

- Biopsy-lung/skin- eosinophils - P-ANCA[ anti neutrophil cytoplasmic antibody] - Poor prognosis

Treatment

- Steroids

Wegener’s granulomatosus

- Kidney and upper and lower respiratory tract involvement

Symptoms-

- Sinusitis - Bloody or purulent nasal discharge. - Oral ulcers - Cough, hemoptysis, dyspnoea - Rapidly progressing glomerulonephritis - Conjunctivitis/scleritis - Tracheal stenosis

Diagnosis

1. Chest Xray- nodules/infiltrate 2. ESR- elevated 3. Positive C-ANCA 4. Open lung biopsy

Treatment

1. Corticosteroids +Cyclophosphamide 2. Kidney transplant in case of end stage renal failure.

Polyarteritis nodosa (PAN)

- Affects nervous system and GI - Associated with HepB, HIV, drug reactions

Pathophysiology

Decrease in the size of lumen- fibrinoid necrosis- ischemia due to decreased blood flow

Symptoms

- Fever, weakness, weight loss- constitutional symptoms - Abdominal pain - Myalgia - Bowel angina- due to ischemia - Hypertension - Levido reticularis, mononeuritis multiplex

Diagnosis

- Biopsy - ESR - P-ANCA positive - Test for fecal occult blood

Treatment

- Corticosteroids or cyclophosphamide

Behcet’s syndrome

- Recurrent mouth and genital ulcers - Very painful - Arthritis (knees and ankles) - Autoimmune disease - Vasculitic syndrome 1. Eye involvement- conjunctivitis, optic neuritis 2. CNS problems- meningoencephalitis, intracranial hypertension

Diagnosis

Biopsy

Treatment – steroids

Buerger’s disease

- Smokers – young men who smoke cigarettes - Decreased perfusion- necrosis of arm and legs - Limb ischemia and amputation

Symptoms

- painful digital extremities - Cold - Cyanotic - Tingling and numbness - Ulcerations of digits

Treatment

- Stop smoking- prevent the progression of the disease.