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2a high tier > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the aetiology of T1DM?

A

Autoimmune B cell destruction in the pancreas’ islets of Langerhans

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2
Q

What is the pathophysiology of T1DM?

A

Insulin deficiency

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3
Q

What are the risk factors of T1DM?

A
  • genetic predisposition
  • geographical region
  • infectious agents
  • dietary factors
  • other autoimmune diseases e.g. autoimmune thyroid, coeliac disease, Addison’s disease, pernicious anaemia
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4
Q

What is the clinical presentation of T1DM?

A
  • polydipsia
  • polyuria
  • ketosis
  • weight loss
  • blurred vision
  • nausea/ vomiting
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5
Q

What are the differential diagnoses of T1DM?

A
  • monogenetic diabetes
  • neonatal diabetes
  • latent autoimmune diabetes in adults
  • T2DM
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6
Q

How is a diagnosis made in T1DM?

A

Fasting plasma glucose > 7mmol/L
Oral glucose tolerance test > 11mmol/L
Random blood glucose > 11.1mmol/L
HbA1c ≥ 48

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7
Q

What are the interventions in T1DM?

A
  • basal-bolus insulin
  • pre-meal insulin
  • amylin analogue
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8
Q

What is the aetiology of T2DM?

A

Beta cell dysfunction in the islet of langerhans in the pancreas (reduced cell mass)

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9
Q

What is the pathophysiology of T2DM?

A

Peripheral insulin resistance and reduced insulin secretion

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10
Q

What are the modifiable risk factors of T2DM?

A
  • diet high in triglycerides and low in LDLs
  • lack of exercise
  • obesity
  • some medications
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11
Q

What are the non-modifiable risk factors in T2DM?

A
  • family history

- history of gestational diabetes

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12
Q

What is the clinical presentation of T2DM?

A
  • excessive thirst and hunger
  • polyuria
  • nocturnal urination
  • fatigue
  • blurry vision
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13
Q

How is a diagnosis made in T2DM?

A

Fasting plasma glucose >7mmol/L
Oral glucose tolerance test >11mmol/L
Random blood glucose >11.1mmol/L
HbA1c ≥ 48

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14
Q

What are the interventions in T2DM?

A
  • initially lifestyle interventions
  • metformin
  • sulphonylurea
  • insulin
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15
Q

What is the aetiology of diabetic ketoacidosis?

A

Insulin deficiency causing a state of uncontrolled catabolism

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16
Q

What is the pathophysiology of diabetic ketoacidosis?

A

Lack of insulin causes an increase in gluconeogenesis and peripheral glucose uptake by tissues.
This also causes an increase in lipolysis from adipose tissues, hepatic fatty acid oxidation and formation of ketone bodies.

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17
Q

What are the risk factors for diabetic ketoacidosis?

A
  • stopping insulin therapy
  • infection e.g. UTI
  • surgery
  • MI
  • pancreatitis
  • undiagnosed diabetes
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18
Q

What is the clinical presentation of diabetic ketoacidosis?

A
  • excess ketones in urine and breath (characteristic pear drop smell)
  • drowsiness, vomiting and dehydration
  • deep rapid breathing
  • sunken eyes, reduced tissue turgor and dry tongue
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19
Q

What are the differential diagnoses of diabetic ketoacidosis?

A
  • hyperosmolar hyperglycaemic state
  • lactic acidosis
  • starvation ketosis
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20
Q

How do you diagnose diabetic ketoacidosis?

A
  • plasma glucose > 11mmol/L
  • FBC → raised WCC without presence of infection
  • raised capillary/ serum ketones (>3mmol/L)
  • dipstick urinalysis for presence of ketones and glucose
  • raised serum urea and creatinine
  • blood pH < 7.3
  • blood cultures, CXR and urine microscopy and culture to look for infection
  • ECG and cardiac enzymes to look for MI
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21
Q

What are the interventions for diabetic ketoacidosis?

A

MEDICAL EMERGENCY

  • immediate ABC management
  • replace fluid loss with 0.9% saline
  • restore electrolyte loss
  • restore acid-base balance of 24h
  • replace deficient insulin (give insulin + glucose to prevent hypoglycaemia)
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22
Q

What is the pathophysiology of a hyperosmolar hyperglycaemic state?

A

Endogenous insulin levels are reduced enough to inhibit hepatic ketogenesis but not enough to inhibit hepatic glucose production

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23
Q

What are the risk factors of hyperosmolar hyperglycaemic state?

A
  • infection (usually pneumonia)
  • consumption of glucose-rich foods
  • concurrent medication such as thiazides diuretics or steroids
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24
Q

What are the symptoms of hyperosmolar hyperglycaemic state?

A
  • severe dehydration
  • reduced consciousness
  • hyperglycaemia
  • hyperosmolality
  • stupor or coma
  • no ketones in blood or urine
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25
Q

How is a hyperosmolar hyperglycaemic state diagnosed?

A
  • plasma glucose > 11mmol/L
  • dipstick urinalysis shows heavy glycosuria
  • plasma osmolality extremely high
  • serum potassium low
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26
Q

How is hyperosmolar hyperglycaemia state managed?

A
  • lower rate of insulin
  • fluid replacement
  • low molecular weight heparin
  • restore electrolyte loss
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27
Q

What are the causes of hyperthyroidism?

A
  • Graves’ disease
  • toxic multinodular goitre (nodules secrete thyroid hormones)
  • solitary toxic adenoma
  • drug-induced
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28
Q

What are the general symptoms of hyperthyroidism?

A
  • palpitations
  • diarrhoea
  • weight loss and increased appetite
  • oligomenorrhoea ± infertility
  • heat intolerance
  • tremor
  • irritability
  • anxiety
  • diffuse goitre
29
Q

How do you diagnose hyperthyroidism?

A
  • usually a clinical diagnosis
  • thyroid function tests (raised T4/T3 and reduced TSH)
  • thyroid USS
30
Q

What are the interventions for hyperthyroidism?

A
  • beta blockers for rapid control of symptoms
  • anti-thyroid drugs
  • radioactive iodine
  • surgery
31
Q

What is the aetiology of Graves’ disease?

A
  • genetic (HLA-B8)
  • E-coli and other G-ve organisms
  • smoking
  • stress
32
Q

What is the pathophysiology of Graves’ disease?

A

Circulating IgG autoantibodies bind to and activate G protein thyrotropin receptors, causing smooth thyroid enlargement and stimulating T4/T3 production

33
Q

What are the risk factors of Graves’ disease?

A
  • stress, infection, childbirth
  • smoking
  • female sex
  • high iodine intake
  • autoimmune diseases (vitiligo, Addison’s, T1DM, pernicious anaemia)
34
Q

What are the symptoms of Graves’ disease?

A
  • neck swelling
  • opthalmopathy (swollen and protruding red eyes)
  • swelling in extraocular muscles
  • diffuse goitre
35
Q

What are the differential diagnoses of Graves’ disease?

A

Other types of thyrotoxicosis e.g. nodular gland, thyroid tumours

36
Q

How do you diagnose Graves’ disease?

A
  • thyroid function tests → low TSH, high T4 and T3
  • blood tests for anti-thyroid autoantibodies
  • ESR blood test for inflammation
37
Q

What are the interventions for Graves’ disease?

A
  • thionamides (e.g. propylthiouracil) to inhibit excess thyroid hormone production
  • beta blockers to relieve symptoms
  • iodine radiotherapy to destroy some thyroid cells
  • surgery as a last resort
38
Q

What is the aetiology of hypothyroidism?

A
  • autoimmune/ atrophic
  • Hashimoto’s
  • post-partum thyroiditis
  • iatrogenic (after thyroidectomy or radioactive iodine treatment)
  • drug induced
  • iodine deficiency
39
Q

What is the pathogenesis of primary hypothyroidism?

A

Reduced T4 and T3 production

40
Q

What is the pathogenesis of secondary hypothyroidism?

A

Reduced TSH from the anterior pituitary

41
Q

What are the symptoms of hypothyroidism?

A
  • tired
  • low mood
  • cold intolerant
  • weight gain
  • constipation
  • menorrhagia
  • goitre
  • hoarse voice
  • slow reflexes
  • bradycardia
  • cold hands
  • blank expression
  • dry skin and thin hair
42
Q

How is hypothyroidism diagnosed?

A
  • thyroid function tests (high TSH, low T4 and T3)
  • thyroid antibodies
  • FBC
43
Q

How is hypothyroidism managed?

A

Lifelong thyroid hormone replacement

44
Q

What is the main risk factor for thyroid cancer?

A

Radiation

45
Q

What is the presentation of thyroid cancer?

A
  • thyroid nodules
  • increased thyroid gland (hard and irregular shape)
  • dysphagia or voice hoarseness due to tumour compression
46
Q

What is the differential diagnosis of thyroid cancer?

A

Goitre

47
Q

How is thyroid cancer diagnosed?

A
  • fine needle aspiration cytology biopsy
  • thyroid function tests (hypo- or hyperthyroidism need to be treated first
  • thyroid USS
48
Q

What are the interventions for thyroid cancer?

A
  • radioactive iodine
  • levothyroxine to keep TSH reduced
  • chemotherapy
  • thyroidectomy
49
Q

What is the aetiology of Cushing’s syndrome?

A
  • exogenous corticosteroid syndrome (after taking corticosteroids for a disease e.g. IBD)
  • ACTH-secreting pituitary adenomas
  • adrenal adenomas
50
Q

What is Cushing’s disease?

A

When Cushing’s syndrome is caused by a tumour

51
Q

What is the pathophysiology of Cushing’s syndrome?

A

Excess tissue exposure to cortisol

52
Q

What are the risk factors for Cushing’s syndrome?

A
  • exogenous corticosteroid use
  • pituitary adenoma
  • adrenal adenoma
  • adrenal carcinoma
53
Q

What is the presentation of Cushing’s syndrome?

A
  • hyperglycaemia
  • mood and personality changes - depression, lethargy, irritability, psychosis
  • CNS irritability
  • ‘moon face’
  • acne
  • increased susceptibility to infection
  • obesity (central fat distribution with thin extremities)
  • osteoporosis
  • bruises
  • thin skin
  • GI distress
  • men: gynaemastia, erectile dysfunction
  • women: amenorrhoea, hirsutism
54
Q

What are the differential diagnoses of Cushing’s syndrome?

A
  • obesity
  • metabolic syndrome
  • Pseudo-Cushing’s syndrome (caused by alcohol excess)
55
Q

How is Cushing’s syndrome diagnosed?

A
  • random plasma cortisol
    1- overnight dexamethasone suppression test or urine free cortisol
    2- 28h dexamethasone suppression test
    3- plasma ACTH
56
Q

What are the interventions of Cushing’s syndrome?

A
  • stop steroids if iatrogenic
  • resection of pituitary adenoma
  • post-surgical corticosteroid replacement therapy
57
Q

What is the aetiology of acromegaly?

A
  • mostly due to a benign GH-producing pituitary tumour

- sometimes due to hyperplasia (e.g. ectopic GHRH from a carcinoid tumour)

58
Q

What is the pathophysiology of acromegaly?

A
  • excessive growth hormone in adults stimulates skeletal and soft tissue growth
  • local tumour expansion can compress surrounding structures and cause headaches/ visual field loss
59
Q

What are the risk factors for acromegaly?

A

5% associated with multiple endocrine neoplasia-1 (MEN-1)

60
Q

What are the symptoms of acromegaly?

A
  • headaches
  • increased size of hands and feet
  • excessive sweating
  • visual deterioration
  • snoring
  • skin darkening
  • coarsening face with wide nose
  • projecting lower jaw
  • big supraorbital ridge
61
Q

How is acromegaly diagnosed?

A
  • glucose tolerance test (high glucose)
  • plasma GH levels
  • high calcium and phosphate
  • insulin-like growth factor
  • pituitary fossa MRI
  • visual field examination
  • request old photos to see physical changes
62
Q

What are the interventions for acromegaly?

A

1st line = trans-sphenoidal surgery to remove the tumour

  • somatostatin analogues, GH receptor antagonists and dopamine agonists
  • radiotherapy
63
Q

What is the aetiology of Conn’s syndrome?

A
  • excessive aldosterone production, independent of RAAS

- mostly caused by an adrenal adenoma secreting aldosterone

64
Q

What is the pathophysiology of Conn’s syndrome?

A
  • disorder of adrenal cortex characterised by excess aldosterone syndrome
  • results in increased retention of sodium and water, and loss of potassium
65
Q

What are the risk factors of Conn’s syndrome?

A

Hypertension in patients:

  • under 35y with no hypertension FHx
  • with accelerated hypertension
  • with hypokalaemia before diuretic therapy
  • resistant to conventional antihypertensive therapy
  • with unusual symptoms (e.g. sweating attacks or weakness)
66
Q

What are the symptoms of Conn’s syndrome?

A
  • often asymptomatic
  • hypertension
  • hyperkalaemia symptoms (weakness/ cramps, paraesthesia, polyuria, polydipsia)
67
Q

What is the differential diagnosis of Conn’s syndrome?

A

Secondary hyperaldosteronism

68
Q

How is Conn’s syndrome diagnosed?

A
  • hypokalaemia ECG (flat T waves, ST depression, long QT)
  • serum hypokalaemia (not always)
  • plasma aldosterone to renin ratio
  • increased plasma aldosterone levels not suppressed with 0.9% saline infusion
  • CT or MRI of adrenals
69
Q

What are the interventions for Conn’s syndrome?

A
  • laparoscopic adrenalectomy

- aldosterone antagonist e.g. oral spironolactone

2a high tier (10 decks)

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