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PHASE 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Diabetes Mellitus

A

Disease in which the body’s ability to produce or respond to insulin is impaired, resulting in hyperglycaemia -> micro and macrovascular complications

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2
Q

Epidemiology of Type I DM

A
  • Younger onset (<30)
  • More common in northern european ancestry
  • Patients usually lean
  • 10% of DM
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3
Q

Epidemiology of Type II DM

A
  • Older onset (>30)
  • More common in African/Asians
  • Patients usually overweight
  • 90% of DM
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4
Q

Risk factors of Type II DM

A
  • Obesity
  • Increasing age
  • Family history
  • HTN
  • Hyperlipidaemia
  • Alcohol excess
  • Sedentary lifestyle
  • Smoking
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5
Q

Pathophysiology of Type I DM

A
  • Type IV hypersensitivity/cell mediated immune reaction -> T cell against antigen on beta cells
  • Beta cells destroyed
  • HLA DR3/4 gene mutation
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6
Q

Pathophysiology of Type II DM

A
  • Insulin resistance
  • B cells hyperplasia + hypertrophy until exhaustion -> hypoplasia + hypotrophy
  • B cells unable to produce enough insulin to overcome insulin resistance
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7
Q

Signs and symptoms of Type I DM

A
  • Polyphagia (weight loss from lipolysis and muscle breakdown -> hunger)
  • Glycosuria (kidneys not able to reabsorb all glucose)
  • Polyuria (water follows glucose in urine down water conc. gradient)
  • Polydipsia (dehydration from polyuria -> thirst)
  • Ketoacidosis (fruity breath)
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8
Q

Signs and symptoms of Type II DM

A
  • Similar to Type I but longer period
  • Fatigue + blurred vision
  • Neuropathy
  • Raised BP
  • Elevated cholesterol
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9
Q

Investigations for DM

A
  • Fasting plasma glucose (>7mmol/L) or random plasma glucose (>11.1mmol/L)
  • HbA1c >6.5%/48mmol/mol (not used in pregnancy, children, haemolytic disease, type I, pancreatic surgery)
  • Oral GTT 2hr >11.1mmol/mol
  • C peptide reduces in type I, persists in type II
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10
Q

Management of Type I DM

A

Glycaemic control:

  • Diet (low sugar, fat, high starch)
  • Insulin (twice daily with meals) - DAFNE (dose adjustment for normal eating)
  • Exercise encouraged
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11
Q

Management of Type II DM

A
  • Lifestyle changes + regular HbA1c
  • Monotherapy metformin
  • Dual therapy metformin + DPP-4i, pioglitazone, SU, SGLT-2i
  • Triple therapy
  • Insulin
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12
Q

Secondary prevention Type II DM

A
  • Eye screening
  • Foot screening
  • Kidney tests
  • BP checks
  • Reduce CV risks using statins and ACE-i
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13
Q

Metformin mechanism of action

A
  • Sensitises GLUT4 receptors + helps lose weight
  • SE: nausea, diarrhoea, anorexia
  • Don’t give if eGFR < 36ml/min
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14
Q

Pioglitazone mechanism of action

A
  • Increases insulin sensitivity
  • SE: hypoglycaemia, fractures, fluid retention
  • CI: CCF, osteoporosis, weight gain or oedema whilst on the drug
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15
Q

DPP-4i mechanism of action

A
  • Inhibits DPP-4 (enzyme that destroys incretins)

- Incretins stimulate decrease in blood glucose levels

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16
Q

Sulphonylurea (SU) mechanism of action

A
  • Increases insulin secretion

- SE: hypoglycaemia, weight gain

17
Q

SGLT-2i mechanism of action

A
  • Inhibits selective sodium-glucose cotransporter 2
  • Reduced glucose reabsorption in the kidneys
  • SE: yeast infection, UTI
18
Q

Complications of Type II DM

A

Microvascular:
- Diabetic nephropathy
- Diabetic neuropathy
- Diabetic retinopathy (bloodshot eyes and aneurysms)
Macrovascular:
- Arterial disease (stroke, MI, limb ischaemia)
Other:
- Staph. skin infections
- Erectile dysfunction
- Hyperosmolar hyperglycaemic state (HHS)

19
Q

Explain pathophysiology of diabetic ketoacidosis (DKA)

A
  • Increased lipolysis -> ketogenesis in the liver creates acetoacetate and beta-hydroxybutyrate
  • Decrease in blood pH causing renal hypoperfusion due to osmotic diuresis -> coma and circulatory failure
20
Q

Symptoms of DKA

A
  1. Develops over days
  2. Polyuria + polydipsia
  3. Nausea + vomiting
  4. Weight loss
  5. Weakness
  6. Abdominal pain
  7. Drowsiness and confusion
21
Q

Signs of DKA

A
  1. Hyperventilation (Kussmaul breath - deep + laboured)
  2. Dehydration
  3. Hypotension
  4. Tachycardia
  5. Coma
22
Q

Management of DKA

A
  1. Rehydration (IV fluids)
  2. Insulin
  3. Replacement of electrolytes (K+)
  4. Treat underlying cause
23
Q

Other types of DM

A
  1. Maturity-onset diabetes of the young (MODY)
  2. Diseases of the endocrine pancreas
  3. Endocrine causes (acromegaly, Cushing’s)
  4. Drug-induced
24
Q

Maturity-onset diabetes of the young (MODY)

A

Refers to any of several hereditary forms of DM caused by single mutation in an autosomal dominant gene disrupting insulin production (alters beta cell function)

25
Q

MODY 2

A
  • Glucokinase gene mutation
  • GCK = glucose-sensor of beta cells -> controls insulin release
  • Higher set point
26
Q

Patients that might be MODY

A
  • Parent affected with diabetes
  • Absence of islet autoantibodies
  • Evidence of non-insulin dependence (good control on low dose insulin, no ketosis, measureable C-peptide)
  • Sensitive to sulphonylurea
27
Q

Pathophysiology of permanent neonatal diabetes

A
  • Usually rising ATP causes channel closure, but mutation prevents this so beta cells unable to secrete insulin
  • Tx = sulphonylurea - blocks channel
28
Q

Signs of permanent neonatal diabetes

A
  • Small babies
  • Epilepsy
  • Muscle weakness
29
Q

Maternally inherited diabetes and deafness (MIDD)

A
  • Mutation in mitochondrial DNA
  • Loss of beta cell mass
  • Similar presentation to type II
  • Wide phenotype
30
Q

DM causing diseases of the exocrine pancreas

A
  • Hereditary haemochromatosis
  • Pancreatic neoplasia
  • Cystic fibrosis
31
Q

Features of hereditary haemochromatosis

A
  • Autosomal recessive - triad of cirrhosis, diabetes and bronzed hyperpigmentation
  • Excess iron deposited in liver, pancreas, pituitary, heart and parathyroid
  • Most need insulin
32
Q

Features of pancreatic neoplasia

A
  • Common cause of cancer death
  • Require subcutaneous insulin
  • Prone to hypoglycaemia due to loss of glucagon funciton

PHASE 2 (6 decks)

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