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My Phase 2a Medicine > Endocrine Conditions > Flashcards

Endocrine Conditions Flashcards

1
Q

What is the difference between primary and secondary thyroid disorders?

A

Primary - due to damage/disease of the thyroid

Secondary - due to damage/disease of the hypothalamus or pituitary

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2
Q

What is hypothyroidism?

A

Thyroid gland doe not produce enough thyroxine

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3
Q

What are the causes of hypothyroidism?

A
  • Autoimmune (atrophic or Hashimoto’s thyroiditis=lymphocyte infiltration)
  • Iodine deficiency
  • post-thyroidectomy
  • thyroiditis
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4
Q

What are the symptoms of hypothyroidism?

A
  • tiredness/lethargy
  • weight gain
  • depressed mood
  • constipations
  • weakness
  • cold intolerance
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5
Q

What are the signs of hypothyroidism?

A
  • Bradycardia
  • slow relaxing reflexes
  • ataxia (lack of voluntary control of muscle movements)
  • dry skin
  • yawning
  • cold hands
  • ascites
  • round puffy face
  • poor movement
  • goitre
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6
Q

What is the treatment for hypothyroidism?

A

Levoxythyroxine.

-check and monitor levels

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7
Q

What is hyperthyroidism?

A

Overactive thyroid gland produces too much T4

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8
Q

What are the causes of hyperthyroidism?

A
  • Grave’s disease (IgG antibodies bind to TSH receptors on thyroid gland)
  • toxic multi/solitary nodular goitre
  • ectopic thyroid tissue
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9
Q

What are the symptoms of hyperthyroidism?

A
  • weight loss
  • sweating
  • diarrhoea
  • increase appetite
  • heat intolerance
  • malaise
  • tremor
  • overactive
  • irritability
  • stiffness
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10
Q

What are the signs of hyperthyroidism?

A
  • tachycardia
  • tremor
  • hyperkinesia
  • warm vasodilated peripheries
  • goitre
  • fast/irregular pulse
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11
Q

What must you do before treatment?

A

Must get biochemical confirmation before treatment

  • raised T4/3
  • suppressed TSH (usually)
  • IgG antibodies to TSH if Grave’s disease
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12
Q

How is hyperthyroidism treated?

A
  • anti-thyroid drugs (carbimazole)
  • radioactive iodine
  • thyroidectomy
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13
Q

What are the complication of hyperthyroidism?

A
  • angina

- heart failure

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14
Q

What is goitre?

A

Swelling in the neck due to enlarged thyroid gland

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15
Q

What are the causes of goitre?

A
  • simple
  • autoimmune
  • thyroiditis
  • nodular
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16
Q

What is acromegaly?

A

Excessive growth hormone secretion from the pituitary gland

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17
Q

What are the causes of acromegaly?

A
  • tumour

- ectopic GH-releasing hormone

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18
Q

What are the symptoms of acromegaly?

A
  • increased ring and hat size
  • large tongue
  • increased sweating
  • loss of libido
  • weight gain
  • tiredness
  • headaches
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19
Q

What are the signs of acromegaly?

A
  • prognathism (jaw protudes forward)
  • interdental seperation
  • thick greasy skin
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20
Q

How is acromegaly diagnosed?

A
  • glucose tolerance test (GH not decrease despite high glucose)
  • IGF-1 levels (raised)
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21
Q

How is acromegaly treated?

A
  • transphenoidal surgery to remove the pituitary tumour
  • somatostatin analogues (somatostatin inhibits GH secretion)
  • GH receptor antagonist
  • radiotherapy
  • dopamine agonists
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22
Q

What are the complications of acromegaly?

A
  • impaired glucose tolerance (DM in 15%)
  • increased blood pressure
  • LV hypertrophy
  • cardiomyopathy
  • arrhythmias
  • neoplasia
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23
Q

What is Addison’s disease?

A

Primary hypoadrenalism. The adrenal cortex does not produce enough mineralcortcoid, glucocorticoid or sexsteroid

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24
Q

What are the causes of Addison’s disease?

A
  • autoimmune (80%)
  • TB
  • adrenal metastases
  • lymphoma
  • adrenal haemorrhage
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25
Q

What are the symptoms of Addison’s disease?

A
  • tiredness
  • weight loss
  • fever
  • malaise
  • weakness
  • anoerexia
  • abdominal pain
  • nausea/vomitting
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26
Q

What are the signs of Addison’s disease?

A
  • skin pigmentation
  • postural hypotension
  • dehydration
  • loss of body hair
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27
Q

How is Addison’s disease diagnosed?

A
  • low Na and high K (due to lack of aldosterone)
  • low glucose (due to lack of cortisol)
  • ACTH stimulation test (cortisol not increase after giving ACTH)
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28
Q

What does SIADH stand for and what is this condition?

A

Syndrome of inappropriate Antidiuretic hormone secretion. Inappropriate secretion of ADH causes water retention and hyponatraemia.

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29
Q

What are the causes of SIADH?

A
  • tumours
  • meningitis
  • head trauma
  • alcohol withdrawal
  • drugs
  • subarachnoid haemorrhage
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30
Q

What are the signs of SIADH?

A
  • evolaemic state (normal blood volume)
  • concentrated urine
  • hyponatraemia
  • normal renal, kidney, thyroid function
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31
Q

What are the symptoms of SIADH?

A
  • confusion
  • nausea
  • irritability
  • fits
  • coma
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32
Q

How is SIADH managed?

A
  • restrict fluid intake to 500-1000ml
  • measure osmolarity of blood
  • demeclocycline (block binding of ADH to receptors of kidney tubules)
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33
Q

What is hypercalcaemia of malignancy?

A

Tumour secretes substances which cause hypercalcaemia

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34
Q

What substance are secreted from tumours which cause hypercalcaemia?

A
  • PTH-related peptide (most common)
  • PTH
  • 1,25-dihydroxyvitamin D
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35
Q

What are the symptoms of hypercalcaemia of malignancy?

A
  • tiredness
  • malaise
  • dehydration
  • abdominal pain (due to renal stones)
  • hypertension (Ca causes vasoconstriction)
  • pain pain/fractures (due to bone resorption)
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36
Q

How is hypercalcaemia of malignancy managed?

A
  • treat malignancy
  • rehydration
  • glucocorticosteroids (inhibit osteoclast resorption)
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37
Q

What is hypokalaemia?

A

Low serum potassium

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38
Q

What are the causes of hypokalaemia?

A
  • diuretics
  • hyperaldosteronism
  • chronic kidney disease
  • reduce K intake
  • vomitting and diarrhoea
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39
Q

What are the symptoms of hypokalaemia?

A
  • asymptomatic
  • muscle weakness
  • atrial/ventricular ectopic beats
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40
Q

How is hypokalaemia managed?

A
  • treat underlying cause
  • withdraw diuretics
  • potassium supplements
41
Q

What is a neuroendocrine pancreatic tumour?

A

Tumour arising from the cells of the islets of Langerhans.

Maybe be hormone secreting or non-functional

42
Q

What are the symtoms of neuroendocrine pancreatic tumours?

A
  • abdominal pain
  • jaundice (if obstructive)
  • depends on hormone secreted
43
Q

What are the 4 type of secretory neuroendocrine tumours and their effects?

A
  • insulinoma -> low glucose
  • glucagonoma -> high glucose
  • gastrinoma -> inc gastric activity
  • somatostatinoma -> dec gastric activity
44
Q

How are neuroendocrine tumours managed?

A
  • CT or MRI
  • biochemical tests for hormones
  • surgical excision
  • chemotherapy
  • antagonists for hormones
45
Q

What is hyperkalaemia?

A

High serum potassium

46
Q

What are the causes of hyperkalaemia?

A
  • decreased excretion (CKD, drugs, acidosis, hypoaldosteronism)
  • increased release from cells (acidosis, vigorous exercise)
  • increased intake (salt, blood transfusion)
47
Q

What are the symptoms of hyperkalaemia?

A
  • cardiac arrest
  • muscle weakness
  • hypotension
  • bradycardia
48
Q

How is hyperkalaemia managed?

A
  • treat the cause
  • supraphysiologcical insulin (drive K into cells)
  • ion exchange resins
  • monitor levels
49
Q

What is hypocalcaemia?

A

low calcium plasma levels

50
Q

What are the causes of hypocalcaemia?

A
  • increased phosphate levels
  • hypoparathyroidism
  • vitamin D deficiency
  • drugs
51
Q

What are the symptoms of hypocalcaemia?

A
  • spasm or twitch
  • paraesthesia (pins and needles)
  • numbness
  • cramps
  • tetany (intermittent muscle spasms
  • convulsions
52
Q

What are the signs of hypocalcaemia?

A
  • prolonged QT interval
  • Chvostek’s sign (gentle tapping over facial nerve causes facial spasm in the same side)
  • Trousseau’s sign (inflation of blood pressure cuff causes spasms of hand and wrist)
  • papiloedema (swelling of optic disc due to increase intercranial pressure)
53
Q

How is hypocalcaemia diagnosed?

A
  • low serum calcium

- clinical history

54
Q

How is hypocalcaemia managed?

A
  • if vitamin D deficient: give colecalciferol or hydroxylated vitamin D
  • oral calcium supplements
  • if PTH deficient: PTH replacement
55
Q

What is hyperparathyroidism?

A

Excessive amount of PTH is secreted from the parathyroid gland.

56
Q

What are the causes of primary hyperparathyroidism?

A

Due to disease of the parathyroid gland

  • adenoma
  • carcinoma
  • hyperplasia
57
Q

What is the cause of secondary hyperparathyroidism?

A

Decrease in plasma Ca causes an APPROPRIATE increase in PTH

  • Vit D deficient
  • CKD
58
Q

What is the cause of tertiary hyperparathyroidism?

A

Increase in plasma Ca causes an INAPPROPRIATE increase in PTH
-prolonged secondary hyperparathyroidism

59
Q

What are the symptoms of hyperparthyroidism?

A
  • asymptomatic
  • weak
  • tired
  • depressed
  • abdominal pain (due to renal stones)
  • bone pain/fractures (due to osteopoenia)
60
Q

What are the signs of hyperparathyroidism?

A
  • increased plasma Ca
  • increased bone resorptions
  • hypertension
61
Q

How is hyperparathyroidism managed?

A
  • PTH, Ca blood tests
  • bone scan
  • increase fluid intake
  • avoid a high Ca and vitamin D diet
  • surgical excision of adenoma
  • surgical excision of hyperplastic glands
62
Q

What is diabetes insipidus?

A

Vasopressinn deficiency or insensitivity which leads to excess excretion of dilute urine with a compensatory thirst

63
Q

What are the symptoms of diabetes insipidus?

A
  • polyuria
  • polydypsia
  • dehydration
  • hypernatraemia symptoms (lethargy, thirst, weakness, irritability, confusion)
64
Q

What are the signs of diabetes insipidus?

A
  • high plasma osmolarity

- low urine osmolarity

65
Q

What are the causes of diabetes insipidus?

A 
Cranial
-idiopathic
-congenital defects
-pituitary tumour
-pituitary trauma
-auto-immune
-pituitary infection
Nephrogenic
-inherited
-drugs (renal damage)
-chronic kidney disease
66
Q

How is diabetes insipidus diagnosed?

A

8hr water deprivation test

  • dilute urine despite dehydration <600 mOsmol/kg
  • if urine osmolarity increases when desmopressin is given - cause is cranial
67
Q

How is diabetes insipidus treated?

A 
Cranial
-MRI
-desmopressin
-test pituitray function
Nephrogenic
-treat cause of CKD
-thiazide diuretics (dec rate of blood filtration by kidneys)
68
Q

What is primary hyperaldosteronism also called?

A

Conn’s syndrome

69
Q

What is primary hyperaldosteronism?

A

increased mineralcorticoid secretion from the zone glomerulosa of the adrenal gland

70
Q

What does hyperaldosteronism result in?

A
  • hypertension
  • potassium loss (aldosterone inc K secretion)
  • sodium retention (aldosterone inc Na reabsorption)
71
Q

What are the causes of primary hyperaldosteronism?

A
  • adrenal adenoma
  • bilateral adrenocortical hyperplasia
  • adrenal acrcinoma
72
Q

What are the symptoms of primary hyperaldosteronism?

A
  • asymptomatic
  • muscle weakness
  • polyuria
  • polydypsia
  • cramps
  • paraesthesia
  • hypertension
73
Q

How is primary hyperaldosteronism managed?

A
  • laparascopic adrenalectomy
  • spironolactone and amiloride (K sparing diuretic - aldosterone antagonist)
  • ca channel blockes
74
Q

What are the complications of primary hyperaldosteronism?

A

-retinal damage
-cardiac damage
due to hypertension

75
Q

What is secondary hyperaldosteronism?

A

High aldosterone secretion due to high renin secretion from kidneys

76
Q

What is cushing’s syndrome?

A

increased glucocorticosteroid in the blood and loss of feedback mechanisms

77
Q

What is cushing’s disease?

A

increased glucocorticosteroid production due to increased ACTH from a pituitary adenoma

78
Q

What are the causes of cushings sydrome?

A
  • pituitary adenoma producing ACTH (cushing’s disease)
  • ectopic ACTH production
  • corticosteroid medication
  • adrenal adenoma/cancer
  • adrenal nodular hyperplasia
79
Q

What are the symptoms of Cushing’s syndrome?

A
  • moon face (redder rounder face)
  • purple striae
  • weight gain
  • hair growth
  • acne
80
Q

What are the signs of Cushing’s syndrome?

A
  • bufalo hump
  • hypertension
  • proximal myopathy
  • moon face
  • easy bruising
  • central obesity
81
Q

How is Cushing’s syndrome diagnosed?

A
  • 48hr low dose dexamethasone test (not dec cortisol levels in CS due to loss of negative feedback)
  • urine cortisol
  • blood cortisol
  • high dose dexamethasone test (indicate CD)
82
Q

How is cushing’s syndrome treated?

A
  • stop corticosteroid medication
  • adrenalectomy
  • surgical removal of tumour
  • metyrapone (inhibits cortisol production)
  • radiation treatment of tumour
83
Q

What is diabetes mellitus?

A

lack of or reduced sensitivity to endogenous insulin resulting in hyperglycaemia

84
Q

What is Type 1 Diabetes Melitus?

A

severe insulin deficiency, usually auto-immune mediated

85
Q

What causes T1 DM?

A
  • auto-immune destruction of beta cells
  • environmental influence
  • linked to HLA-DR3 and HLA-DR4
86
Q

What is the clinical presentation of T1 DM?

A
  • polydipsia (excessive drinking)
  • polyuria (excessive urination)
  • weight loss
  • ketoacidosis
87
Q

What is T2 DM?

A

increased insulin resistance and decrease secretion due to lifestyle

88
Q

What are the risk factors of T2 DM?

A
  • obesity
  • lack of exercise
  • calorie excess
  • alcohol excess
  • low birthweight
89
Q

Does T2 DM have genetic susceptibility?

A

Yes, polygenic links.
80% concordance with identical twins
No major HLA association

90
Q

What is impaired glucose tolernace (IGT)?

A

raised blood glucose levels but not high enough to be classed as DM (7.8mmol/L - 11.1mmol/L)

91
Q

What is impaired fasting glucose (IFT)?

A

raised blood glucose when fasting (6.1mmol/L-7mmol/L)

92
Q

How is DM diagnosed?

A
  • symptoms of hyperglycaemia (polyuria, polydypsia, weight loss, visual blurring)
  • raised venous glucose (fasting >7mmol/L normal>11.1mmol/L)
  • HbAlc
93
Q

What is the clinical presentation of DM?

A
  • polyuria
  • polydypsia
  • weight loss
  • lack of energy
  • visual blurring
  • pruritus vulva (due to infection)
94
Q

What are the complications of DM?

A
  • retinopathy
  • cataracts
  • polyneuropathy
  • erectile dysfunction
  • staphylococcus skin infection
  • atherosclerosis (inc risk of MI and stroke)
  • diabetic foot (dec sensation, ischaemia, infection)
95
Q

What is diabetic foot?

A
  • decreased sensation
  • ischaemia causing ulceration/gangrene
  • infection
96
Q

How is diabetic foot managed?

A
  • regular chiropody
  • rest
  • appropriate footwear
  • amputation
97
Q

What lifestyle changes are involved in the management of DM?

A
  • low sugar and saturated fats
  • high fibre and starchy carbs
  • increased exercise
98
Q

What medications are used to managed DM?

A
  • metformin (first line use to dec blood glucose)
  • suphonylureas and meglitinides (inc insulin secretion)
  • thiazolidinediones (dec insulin resistance)
  • insulin
99
Q

What does insulin based therapy involve in DM management?

A
  • educate patients of lifestyle changes
  • plan to fit lifestyle
  • insulin pumps - continuous subcutaneous insulin
  • long acting recombinant insulin analogues
  • long acting isophane (NICE recommended)
  • ultra fast acting

My Phase 2a Medicine (5 decks)

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