dr sara al-ansari, fy1. session overview diabetes mellitus aetiology presentation investigations...

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Dr Sara Al-Ansari, FY1

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Page 1: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Dr Sara Al-Ansari, FY1

Page 2: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Session OverviewDiabetes MellitusAetiologyPresentationInvestigationsDiagnosisManagementComplications

Diabetic ketoacidosis Hyperosmolar hyperglycaemic state Hypoglycaemia

Page 3: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Diabetes MellitusDefinition: A metabolic disorder characterised by chronic hyperglycaemia resulting from defects in insulin production, insulin action or both.

Aetiological classification of DMType 1 DM: (β cell destruction > insulin deficiency)- Immune mediated- IdiopathicType 2 DM: (Characterised by variable degrees of insulin deficiency and resistance).Gestational DMOther specific types

Page 4: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

PresentationCharacteristic symptoms: polyuria, polydipsia, blurring of vision, weight loss, recurrent infections, lethargy.

In its most severe forms, ketoacidosis or a non-ketotic hyperosmolar state may develop and lead to stupor, coma and in absence of effective treatment, death.

Often symptoms are not severe, or may be absent, and consequently hyperglycaemia sufficient to cause pathological and functional changes may be present for a long time before a diagnosis is made

Page 5: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

InvestigationsBedside tests- BM- Urine dipstick: ketones + proteinuriaBlood tests- Fasting/Random glucose, HbA1c, FBC, U&E’s, LFTs, cholesterol,

Amylase, C-peptide, Autoantibodies.- ABGAdditional tests- ECG- CXR- AXR/CT abdomen- Albumin:creatinine ratio

Page 6: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Diagnostic Criteria [WHO Criteria]Diabetes is diagnosed on the basis of history (ie polyuria, polydipsia and unexplained weight loss) PLUS:

Fasting plasma glucose >= 7.0 mmol/L Two-hour plasma glucose level concentration

>= 11.1 mmol/l after 75g anhydrous glucose in an oral glucose tolerance test (OGTT)

A random venous plasma glucose concentration >= 11.1 mmol/l in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis

HbA1c > 6.5% (48 mmol/mol)

With no symptoms diagnosis should not be based on a single glucose determination but requires confirmatory plasma venous determination.

Page 7: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Management of DiabetesConservative Lifestyle – weight reduction, dietician input, regular exercise Smoking cessation

help and advice Foot care Eye checks Patient Education

Medical Type 1: Insulin regimes Type 2: Metformin, Sulphonylureas, Glitazones, DDP4 inhibitors, Insulins Control BP, cholesterol and other risk factors

Surgical Islet cell transplants Complications e.g. amputation

Page 8: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Oral Hypoglycaemic medications

Page 9: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

  Onset Peak Duration Example

Short-acting

30 minutes 2-4 hours 8 hours ActrapidHumulin S

Intermediate

1-2 hours 4-12 hours

16-24 hours

InsulatardHumulin I

Long-acting

1-2 hours 4-12 hours

20-35 hours

Human UltratardHumulin Zn

Analogue 0-15 minutes

1-2 hours 4-6 hours  24 hours

Humalog (Lispro)Novorapid (Aspart)Apidra (Glulisine)Glargine, Levemir

Page 11: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Glucose controlReview the person's HbA1c level and agree an appropriate target

level:If managed by diet alone or by one drug, a target HbA1c of 6.5% (48

mmol/mol) is generally recommended.If the person requires more intensive treatment, a target of less than

7.5% (59 mmol/mol) is generally recommended

Page 13: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Diabetic Ketoacidosis

Ketonaemia > 3.0mmol/l or significant ketonuria (2+ on standard urine sticks)

Blood glucose > 11.0mmol/l or known DM

Bicarbonate (HCO3) < 15.0mmol/l and/or venous pH <7.3

Precipitating factors Omitted/inadequate insulin

dose: Inadvertent - malfunction of

insulin delivery system. Intentional - not

administering insulin when required.

Infection, e.g. pneumonia, UTI. Acute illness. Drugs that alter carbohydrate

metabolism, e.g. corticosteroids, thiazides, sympathomimetics, and second-generation (atypical) antipsychotics.

Page 14: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Symptoms: Polyuria, polydipsia, weight loss, D+V, abdo pain, lethargy, confusion.

Examination Acetone breath. Kussmaul respiration. Dehydration — classify as:

Mild (3%) — only just clinically detectable. Moderate (5%) — dry skin + mucus membranes; reduced skin turgor. Severe (8%) — sunken eyes, prolonged CRT. Shock — severely ill with: ↑HR, poor peripheral perfusion & ↓BP,

indicates decreased cardiac output. Lethargy, drowsiness, or ↓GCS indicates decreased cerebral perfusion. ↓UO indicates decreased renal perfusion.

Assess the person for conditions in which ketoacidosis can have severe consequences: pregnancy, heart failure, renal failure.

Page 15: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Management of DKA Rapid ABC Large bore IV canula and commence IV fluid replacement Full clinical assessment and initial investigation

Blood ketones CBG Venous plasma glucose FBC + U&Es Blood cultures ECG CXR Urinalysis and culture Urinary catheterisation if patient is incontinent and anuric

Fixed Rate insulin infusion - This is made of 50 units of human soluble insulin(Actrapid®, Humulin S®) made up to 50ml with 0.9% sodium chloride solution [0.1 units/kg/hr] Continue long-acting insulin analogues Potassium replacement Reassess the patient Review biochemical and metabolic parameters: Monitor hourly blood glucose and ketones.

Monitor serum K and bicarbonate 2-hourly for the first 6 hours. Diabetes specialist team

Typical deficits in adult• Water - 100ml/kg• Sodium - 7-10mmol/kg• Chloride - 3-5mmol/kg• Potassium - 3-5mmol/kg

Page 17: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Metabolic treatment targets:

↓ blood ketone by 0.5 mmol/L/hour↑ venous bicarb by 3 mmol/L/hour↓ CBG by 3 mmol/L/hourMaintain potassium between 4.0 and

5.5mmol/L If these rates are not achieved, then

the FRIII rate should be increased

Assessment of severity, the presence of one or more of the following may indicate severe DKA:

Blood ketones > 6mmol/LBicarbonate level < 5mmol/LVenous/arterial pH < 7.0Hypokalaemia on admission

(<3.5mmol/L)GCS <12 or abnormal AVPU scaleO2 sats <92% on RA (assuming normal baseline resp function)SBP <90mmHgTachy/bradycardicAnion gap above 16 [Anion Gap =

(Na+ + K+) – (Cl- + HCO3-) ]

Page 20: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Goals of treatment

The goals of treatment of HHS are to treat the underlying cause and to gradually and safely:• Normalise the osmolality • Replace fluid and electrolyte losses• Normalise blood glucose

Other goals include prevention of:• Arterial or venous thrombosis• Other potential complications e.g. cerebral oedema/ central pontine myelinolysis• Foot ulceration

Page 22: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

HypoglycaemiaDefinition: Blood glucose levels decrease to less than 4.0 mmol/L.

Adrenergic effects (early symptoms): sweating, tachycardia, palpitations, pallor, hunger, and restlessness. Apart from sweating, these effects may be suppressed in people taking non-cardioselective beta-blockers (such as propranolol).

Neuroglycopenic effects (late symptoms): confusion, slurred speech, drowsiness, frequent yawning, anxiety, blurred vision, diplopia, and numbness of nose, lips, and fingers. In more serious cases, this can lead to loss of consciousness, seizures, and death.

Hunger, headache, nausea, and tiredness are non-specific symptoms which can be associated with low, high or normal blood glucose.

Page 23: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Mild & Moderate hypoglycaemia is when the person is aware of, responds to and self-treats the hypoglycaemia. They can swallow safely.

Three to six glucose tablets.90–180 mL of fizzy drink or squash.50–100 mL of Lucozade Energy® (contains 26% glucose syrup/100mL).2-4 spoonfuls of sugar added to a cup of drink (for example, water).Sweets such as four large jelly babies, or seven large jelly beans.A glass of fruit juice.Glucose gel (GlucoGel® or Dextrogel®; both contain 10 g of glucose)

The patient should immediately eat some long-acting, starchy carbohydrate (such as a sandwich or some biscuits). Around 10–20 g is recommended but the exact amount will vary from person to person.

Page 24: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Severe hypoglycaemia is when the person is semi-conscious or unconscious or in a coma with or without convulsions and will require parenteral therapy (glucagon or intravenous glucose). These people are unable to swallow safely.

• Protect Airway • 15L O2• IV access• 50ml 50% glucose STAT• (100ml of 20%, 200ml of 10%)• For large insulin OD give 1mg of glucagon SC/IM/IV• Should respond in 10 min• 1L 10% glucose over 4-8h• Aim for BM > 5

Page 25: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

Case ScenarioA 52 year old man presents to his GP as he has been

feeling lethargic and tired for the last few months.  He has over the last 2 weeks also become very thirsty and is drinking more than normal.  He reports no other significant symptoms.  He suffers from hypertension which is managed with ramipril and has no known allergies.  He works as a librarian and drinks socially and doesn’t smoke.  On examination he has a BMI of 32 and full systems examinations are unremarkable. His urine dip shows glucose ++ and a BM done in the surgery registers as 13.  à Diabetes Mellitus type 2

Page 26: Dr Sara Al-Ansari, FY1. Session Overview Diabetes Mellitus Aetiology Presentation Investigations Diagnosis Management Complications  Diabetic ketoacidosis

What are your differentials for this gentleman? (make sure these include all important differentials that must be ruled out)

How would you investigate this man? How would you manage this gentleman? What are the diagnostic criteria for diabetes? What are impaired fasting glucose and impaired glucose

tolerance? What are the micro and macrovascular complications of

diabetes? How does diabetes cause peripheral neuropathy? What drugs are used to manage type 2? What insulin regimes are used to manage type 1?