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Hamzah's endocrine pathology > endocrine pathology > Flashcards

endocrine pathology Flashcards

1
Q

What is the main cause of acromegaly?

A

Increased secretion of GH from a pituitary adenoma (99%)

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2
Q

What is the male:female ratio of acromegaly and what is the UK incidence?

A

M:F

3 per million people/year

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3
Q

What are the symptoms of acromegaly?

A

low libido, headaches, pins and needles in extremities, joint pain, shoes no longer fit

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4
Q

What are the signs of acromegaly?

A

widely spaced teeth, macroglossia, prominent supraorbital ridge, massive growth of hands, feet and jaw

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5
Q

What are the complications of acromegaly?

A

impaired glucose tolerance and DM
Hypertension
Left ventricular hypertrophy
Increased risk of IHD, stroke and colon cancer

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6
Q

What are the diagnostic tests used to confirm acromegaly?

A

Oral glucose test - high glucose suppresses GH secretion. If the lowest GH recording is still above 1 microgram/litre = acromegaly

MRI scan of pituitary fossa
Look at old photos of patient
Visual fields and acuity examinations

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7
Q

What is the treatment for acromegaly?

A

Prevent tumour compression by excising the lesion
Reduce GH and IGF-1 by 1st line treatment = trans-sphenoidal surgery
somatostatin analogues = octreotide
GH antagonists = Pegvisomant

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8
Q

What is Cushing’s disease and syndrome

A 
Increased glucocorticoid (cortisol) levels in the blood. 
chief cause = long term steroid use
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9
Q

What is Cushing’s disease caused by

A

Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma

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10
Q

What are the other causes of Cushing’s syndrome?

A

Ectopic ACTH production - small lung cancers and carcinoid tumours. Leads to pigmentation, weight loss, hyperglycaemia and hypokalemic metabolic alkalosis. Dexamethasone fails to suppress cortisol.

ACTH-independent causes (decreased ACTH due to negative feedback). Iatrogenic, adrenal adenoma. dexamethasone won’t suppress cortisol.

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11
Q

What are the symptoms of Cushing’s syndrome?

A

mood change, muscle weakness, weight gain, acne

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12
Q

What are the signs of Cushing’s syndrome?

A

Central obesity, moon face, buffalo hump, purple abdominal striae, osteoporosis

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13
Q

What are the diagnostic tests used to confirm Cushing’s disease and syndrome?

A

Measure free cortisol in 24hr urine test
overnight dexamethasone suppression test - dexamethasone suppresses ACTH production. if Cushing’s syndrome, there is no suppression
Check ACTH plasma levels - low=adrenal adenoma/carcinoma. high=Cushing’s disease –> inject dexamethasone to confirm
MRI scan of pituitary gland
CT scan of adrenal glands.

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14
Q

What is the treatment of Cushing’s disease and syndrome?

A

Treatment depends on cause
Iatrogenic = stop medications if possible
Cushing’s disease = surgical excision of pituitary tumour
Adrenal steroid inhibitors = metyrapone
Adrenal carcinoma –> radiotherapy

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15
Q

What is Conn’s syndrome and hyperaldosteronism?

pathophysiology

A

Excess production of aldosterone independent of the RAAS
Decreased potassium, increased sodium, increased BP
Aldosterone binds to receptors on the DCT of the nephron:
- stimulates sodium/potassium pumps on principle cells = more sodium in blood and more potassium in urine
- stimulates ATPase pump in alpha-intercalated cells = acidifies urine

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16
Q

What are the causes of primary hyperaldosteronism?

A

Conn’s syndrome = aldosterone-producing adenoma

Bilateral adrenocortical hyperplasia

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17
Q

What is the cause of secondary hyperaldosteronism?

A

Excess aldosterone production in response to high levels of renin

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18
Q

What are the symptoms of hyperaldosteronism?

A

Hypokalaemic signs - constipation, heart rhythm changes, muscle weakness, cramps
Headaches

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19
Q

What are the signs of hyperaldosteronism?

A

Hypertension
Hypernatremia
Metabolic alkalosis

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20
Q

What are the diagnostic tests used to confirm hyperaldosteronism?

A

U&E tests

Measure renin and aldosterone levels:

  • low renin + high aldosterone = primary cause
  • high renin + high aldosterone = secondary cause
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21
Q

How is hyperaldosteronism treated?

A

Conn’s syndrome = laparoscopic adrenalectomy, give spironolactone pre-operatively - potassium sparing diuretic. competitively binds to aldosterone receptors on principle cells and alpha intercalated cells of the DCT.

adrenal carcinoma = surgery

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22
Q

What is the epidemiology of Addison’s disease?

A

rare - 0.8/100,000

destruction of the adrenal cortex leads to cortisol and mineralocorticoid deficiency

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23
Q

what are the causes of Addison’s disease?

A

80% = autoimmune
TB, adrenal metastases, lymphoma, opportunistic infections in HIV

primary adrenal insufficiency = Addison’s disease
secondary adrenal insufficiency cause = iatrogenic - long term steroid use

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24
Q

What are the signs and symptoms of Addison’s disease?

A

lean, tanned, tired, anorexia, weakness, dizziness, nausea/vomiting
pigmented palmar creases and buccal mucosa
postural hypotension

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25
Q

What is the differential diagnosis of Addison’s disease?

A

viral infection or anorexia nervosa (potassium levels are decreased in anorexia but increased in Addison’s disease)

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26
Q

Diagnostic tests and results in Addion’s disease

A

decreased sodium and increased potassium levels - due to decreased mineralocorticoid
decreased glucose levels - due to decreased cortisol

Short ACTH stimulation test

21-hydroxylase adrenal autoantibodies are positive in autoimmune disease

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27
Q

What is the treatment of Addison’s disease?

A

replace steroids - hydrocortisone

mineralocorticoids to correct postural hypotension - fludrocortisone

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28
Q

What do beta cells produce?

A

insulin - decreases blood glucose levels

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29
Q

what do alpha cells produce?

A

glucagon - increases blood glucose levels

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30
Q

3 microvascular problems of hyperglycaemia?

A

retinopathy, neuropathy, nephropathy

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31
Q

3 macrovascular problems of hyperglycaemia

A

stoke, heart disease, limb ischaemia

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32
Q

WHO criteria - diagnosis of DM

A

symptoms of hyperglycemia = polyuria, polydipsia, unexplained weight loss, visual blurring
raised venous glucose - fasting>7, random>11
HbA1c>48mmol/l (6.5%)

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33
Q

Clinical presentations of DM

A

acute presentation = young person with short history of thirst, polyuria and unexplained weight loss
subacute presentation = older patients with same symptoms but less marked over time
retinopathy
type 1 DM = presenting with thirt, polyuria, weight loss
type 2 DM = complications generally seen

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34
Q

Type 1 DM cause

A

autoimmune destruction of beta cells by CD4 and CD8 T-lymphocytes
usually adolescent onset
patient must be given insulin
prone to ketoacidosis and weight loss

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35
Q

Treatment of T1DM

A

insulin, patient education

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36
Q

Type 2 DM cause

A

strongly related to obesity and insulin resistance
- initially the pancreas compensates for insulin resistance by increasing insulin secretion (hypertrophy and hyperplasia) - eventually beta cells suffer secretory exhaustion (atrophy) - insulin levels fall

High prevalence in Asians, elderly and men
onset is usually >40 years

stronger genetic influence than type 1 - twin studies

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37
Q

What are the other causes of DM?

A

drugs, pancreatic issues, Cushing’s disease, acromegaly, pregnancy

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38
Q

3 risk factors for type 2 DM

A

pregnancy, central adiposity, asian background, overweight/obese, >40 years of age, family history

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39
Q

Diagnostic tests for DM

A

fasting blood glucose = >7mmol/l

random blood glucose = >11mmol/l

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40
Q

Treatment of type 2 DM

A

first line = exercise and healthy diet
metformin - increases insulin sensitivity
sulfonylurea - increases insulin secretion = gliclazide

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41
Q

What are the complications of diabetes?

A
  • infection at injection sites
  • MI, stroke - give statins
  • neuropathy - use an ACE inhibitor
  • diabetic retinopathy
  • cataracts
  • diabetic foot
  • BM of capillaries thickens –> hypoxia
42
Q

What is the diagnostic test for hypoglycemia?

A

> 3mmol/l

43
Q

What are the symptoms of hypoglycaemia?

A

Autonomic - sweating, anxiety, palpitations

Neuroglycaemic - confusion, drowsiness, seizures

44
Q

Causes of hypoglycaemia

A

insulin or SU treatment in diabetics

Non-diabetes = EXPLAIN acronym
- exogenous drugs, liver disease, addison’s disease

45
Q

Who are typically at risk of a hyperosmolar hyperglycaemic state?

A

type 2 diabetics

>30mmol/l

46
Q

Treatment of hyperosmolar hyperglycaemic state

A

rehydrate slowly with IV saline

replace potassium when urine starts to flow

47
Q

What happens in diabetic ketoacidosis?

A

there is high plasma glucose but a lack of insulin causes a starvation-like state

48
Q

Signs and symptoms of diabetic ketoacidosis

A

gradual drowsiness, vomiting and dehydration

pear drop smell on breath

49
Q

What can cause diabetic ketoacidosis?

A

infection, surgery, MI, wrong inslulin dose

50
Q

What are the diagnostic tests for diabetic ketoacidosis?

A

acidaemia (pH<7.3)
hyperglycaemia
ketonemia

ECG, chest X-ray
urine dipstick

51
Q

What is present in severe DKA?

A

pH<7.1

blood ketones >6mmol/l

52
Q

Complications of DKA

A

cerebral oedema, hypokalemia, thromboembolism

53
Q

Treatment of DKA

A

give fluids, insulin IV infusion, potassium replacement

54
Q

What is hyperkalemia?

A

plasma potassium >6.5mmol/l

causes myocardial hyperexcitability –> ventricular fibrillation and cardiac arrest

55
Q

Causes of hyperkalemia?

A

insulin deficiency, potassium sparring diuretics, Addison’s disease, ACEi

56
Q

Signs and symptoms of hyperkalemia

A

chest pain, weakness, small P waves on ECG, light headedness

57
Q

Treatment of hyperkalemia

A

non-urgent

  • treat underlying cause
  • polystyrene sulfonate resin - prevents K+ absorption in gut

Urgent treatment

  • IV calcium gluconate - prevents damage to heart
  • IV actrapid (insulin) - drives K+ into cells
58
Q

What is hypokalemia?

A

K+<2.5mmol/l

59
Q

Causes of hypokalemia

A

diuretics, vomiting, diarrhoea, Cushing’s, Conn’s syndrome

60
Q

Signs and symptoms of hypokalemia

A

muscle weakness, hypotonia, hyporeflexia, cramps constipation, small inverted T waves on ECG

61
Q

Treatment of hypokalemia

A

mild hypokalemia = oral potassium supplement

severe hypokalemia = IV potassium

62
Q

What is hyperthyroidism/thyrotoxicosis?

A

Excess thyroid hormone

63
Q

Causes of hyperthyroidism

A 
Graves' disease
Toxic adenoma
Toxic multinodular goitre
Ectopic thyroid issue
Exogenous - iodine excess

Secondary cause = TSH-secreting adenoma in anterior pituitary gland

64
Q

Symtoms of hyperthyroidism

A

Diarrhoea, weight loss, increased appetite, overactivity, tremor

65
Q

Signs of hyperthyroidism

A

fast/irregular pulse, warm skin, fine tremor, palmar erythema, thin hair, eyes wide open

66
Q

Diagnostic tests in hyperthyroidism

A
  • Measure blood levels of TSH, T3 and T4
  • check for thyroid autoantibodies
  • isotope scan
67
Q

Treatment of hyperthyroidism

A

Drugs

  • Beta blockers - propranolol - treats immediate symptoms
  • Anti-thyroid medication - carbimazole - blocks thyroid hormone production and release

Radioiodine

Thyroidectomy

68
Q

Complications of hyperthyroidism

A

Heart failure, angina, AF, osteoporosis

69
Q

What is the cause of Graves’ disease?

A

Autoimmune condition.
Circulating IgG autoantibodies bind to and activate G-protein-coupled thyrotropin receptors
This causes smooth thyroid enlargement and increased hormone production

70
Q

Epidemiology of Graves’ disease

A

0.5% prevalence
F:M = 9:1
Typical age = 40-60 years

71
Q

Graves’ disease triggers

A

stress, infection, pregnancy

associated with other autoimmune conditions=vitiligo, T1DM, Addison’s disease

72
Q

Graves’ specific signs

A

proptosis (bulging of eyeballs), pretibial myxoedema, thyroid acropachy

73
Q

Treatment of Graves’ disease

A

propanol to relieve symptoms

carbimazole and thyroxine for 12-18 months

74
Q

What is hypothyroidism?

A

lack of thyroid hormone

75
Q

Epidemiology of hypothyroidism

A

4/1000/year
F:M = 6:1
women approximately 40-60 years

76
Q

Causes of hypothyroidism

A
  • primary atrophic hypothyroidism - common. Diffuse lymphatic infiltration of the thyroid gland –> atrophy, no goitre
  • Hashimoto’s thyroiditis - autoimmune inflammation of the thyroid. Anti-TPO antibodies and antithyroglobulin antibodies. commoner in older women.
  • iodine deficiency
  • post-thyroidectomy/radioiodine treatment
  • drug induced - lithium inhibits thyroid hormone
  • subacute thyroiditis - temporary hypothyroidism after hyperthyroidism phase
77
Q

what is secondary hypothyroidism?

A

when the pituitary gland doesn’t produce enough TSH

78
Q

What is hypothyroidism associated with?

A

T1DM, pernicious anaemia, Addison’s

79
Q

Symptoms of hypothyroidism

A

tiredness, lethargy, cold intolerance, weight gain, constipation, weakness

80
Q

Signs of hypothyroidism

A

puffy face, dry thin hair, bradycardic, cold hands, defeated demeanour

81
Q

Diagnostic tests for hypothyroidism

A
  • TSH, T3 and T4 plasma levels
  • cholesterol/triglyceride raised
  • macrocytosis
82
Q

Treatment of hypothyroidism

A

Replace thyroid hormone - oral levothyroxine (T4)

83
Q

What does the parathyroid gland secrete?

A

Parathyroid hormone in response to low plasma calcium. secreted by chief cells.

84
Q

What are the effects of parathyroid hormone?

A
  • increased osteoclast activity - more calcium and phosphate
  • increased calcium reabsorption in kidneys
  • decreased phosphate reabsorption in kidneys
  • increases active 1,25-dihydroxyvitamin D production

Overall effect = increases calcium, decreases phosphate

85
Q

Causes of primary hyperparathyroidism

A

solitary adenoma - 80%

hyperplasia - 20%

86
Q

Presentation of primary hyperparathyroidism

A

increased calcium - renal stones, abdominal pain, constipation, weakness,
Asymptomatic
PTH effects - pain, fractures, osteoporosis
Raised BP

87
Q

Tests for primary hyperparathyroidism

A

raised calcium, raised PTH, phosphate decreased (unless renal failure)
DEXA for osteoporosis

88
Q

Treatment of primary hyperparathyroidism

A

increase fluid intake to prevent stones

excision of adenoma

89
Q

What is secondary hyperparathyroidism?

A

High PTH, low/normal calcium

90
Q

Secondary hyperparathyroidism causes

A

Vit D deficiency

chronic renal failure

91
Q

Treatment of secondary hyperparathyroidism

A

Treat underlying cause
Phosphate binders
Vitamin D supplements
Cinacalcet - reduces PTH production

92
Q

When does tertiary hyperparathyroidism occur?

A

occurs after secondary hyperparathyroidism –> hyperplasia of parathyroid gland.

It is seen in chronic renal failure

93
Q

What are the levels of calcium and PTH in tertiary hyperparathyroidism?

A

High calcium

Massively raised PTH

94
Q

Treatment of hyperparathyroidism

A

Parathyroidectomy

95
Q

What is primary hypoparathyroidism?

A

PTH decreased due to parathyroid gland failure.

96
Q

Causes of hypoparathyroidism

A

autoimmune or congenital

97
Q

Tests for primary hypoparathyroidism

A

low calcium, low/normal phosphate

98
Q

Signs of primary hypoparathyroidism

A

hypocalcemic signs - cramps, spasms, seizures, slow heartbeat, numbness/tingling of hands, feet and lips

99
Q

Treatment of primary hypoparathyroidism

A

calcium supplements

calcitriol - vitamin D analogue

100
Q

Secondary hypoparathyroidism

A

Radiation, surgery, hypomagnesaemia

Hamzah's endocrine pathology (3 decks)

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