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Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Name the hormones secreted by the anterior pituitary?

A

FSH, LH, GH, TSH, prolactin, ACTH

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2
Q

Where are ADH and oxytocin secreted from?

A

posterior pituitary

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3
Q

What is the function of cortisol?

A

It is a stress hormone. It inhibits the immune system, inhibits bone formation, increases blood glucose, increases metabolism and increases alertness. Therefore there is diurnal variation and it is highest in the morning.

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4
Q

What does GH stimulate and what is the role of this?

A

It stimulates release of IGF-1 from the liver. This is used for increased muscle growth, cell regeneration and production, increased bone density and strength and increased growth of internal organs

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5
Q

Describe the parathyroid axis?

A

PTH is released by the four parathyroid glands in response to low serum calcium (and low magnesium and high phosphate). PTH release results in higher numbers of and increased activity of osteoclasts and therefore there is more reabsorption of calcium from bones to blood. PTH also increases the kidney reabsorption and intestinal absorption of calcium.

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6
Q

Describe the renin angiotensin system?

A

Renin is secreted by the juxtaglomerular cells in the afferent arterioles in response to a low blood pressure. It converts angiotensinogen to angiotensin I in the liver. Angiotensin I is then converted to angiotensin II in the lungs using ACE. ATII causes vasoconstriction and release of aldosterone. Aldosterone then increases the sodium reabsorption in the DT, K secretion and hydrogen secretion. Water is then drawn in and increases volume.

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7
Q

What does prolonged abnormally elevated cortisol result in?

A

Cushing’s syndrome

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8
Q

What are the signs and symptoms of Cushing’s syndrome?

A

symptoms: central obesity, round moon face, buffalo hump, limb proximal muscle wasting, abdominal striae
signs: HTN, cardiac hypertrophy, hyperglycaemia, depression, insomnia, poor skin healing, easy bruising, osteoporosis

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9
Q

What are the signs and symptoms of Cushing’s syndrome?

A

symptoms: central obesity, round moon face, buffalo hump, limb proximal muscle wasting, abdominal striae
signs: HTN, cardiac hypertrophy, hyperglycaemia, depression, insomnia, poor skin healing, easy bruising, osteoporosis

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10
Q

How is Cushing’s syndrome diagnosed?

A

low dose dexamethasone suppression test and if the morning cortisol returns high then do the high dose dexamethasone suppression test
FBC (increased WCC), U&Es, MRI, CT chest and abdomen

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11
Q

How is Cushing’s syndrome treated?

A

Life long steroids or transsphenoidal surgery if there is a pituitary adenoma

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12
Q

Describe the types of Adrenal Insufficiency?

A

Addison’s - damaged adrenals - decreased cortisol and aldosterone - primary or autoimmune
secondary - decreased ACTH due to pituitary damage
tertiary - decreased CRH due to hypothalamic damage

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13
Q

How is adrenal insufficiency diagnosed?

A

short synacthen test - synthetic ACTH given in morning and cortisol measured at baseline and at 8 hours - less than double is indicative

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14
Q

what investigations are done in adrenal insufficiency?

A

FBC, U&Es (decreased na, increased K)
early morning cortisol
ACTH
adrenal autoantibodies
CT/MRI adrenals
MRI pituitary

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15
Q

how does adrenal insufficiency present?

A

fatigue, nausea, cramps, abdominal pain, decreased libido, hyperpigmentation, hypotension

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16
Q

What is an addisonian crisis and how is it treated?

A

when the patient presents with decreased consciousness, hypotension, low BG and sodium, increased K, and is triggered by infection, trauma, withdrawal of steroids etc
treatment - monitoring, IVF resus, correct hypoglycaemia, parenteral steroids, monitor U&Es

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17
Q

How is Adrenal insufficiency treated?

A

hydrocortisone to replace cortisol and fludrocortisone to replace aldosterone

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18
Q

What does anti-TPO positive indicate?

A

autoimmune condition such as grave’s or hashimotos

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19
Q

what does antithyroglobulin indicate?

A

graves, hashimotos or cancer

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20
Q

what do TSH receptor antibodies indicate?

A

Graves

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21
Q

what do you look at in TFTs and describe the results?

A

look at TSH alone first - if abnormal do T3 and T4
hyperthyroidism - high T3 and T4, low TSH
hypothyroidism - low T3 and T4, high TSH if primary, if secondary then low T3,4 and TSH
pituitary adenoma - high TSH

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22
Q

how do you diagnose thyroid disorders?

A

TFTs
thyroid USS and guided biopsy
radioisotope scan

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23
Q

describe the results of a radioisotope scan?

A

diffuse high - Graves
focal high - TMNG and adenomas
low - cancer

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24
Q

what is the primary cause of hyperthyroidism?

A

graves

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25
Q

what are signs specific to graves?

A

exopthalmos, pretibial myxoedema, thyroid eye disease

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26
Q

what is the presentation of hyperthyroidism?

A

anxiety, irritability, tachycardia, weight loss, fatigue, frequent loose stools, sexual dysfunction

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27
Q

a patient presents with viral presentation, symptoms of hyper then hypothyroidism, what is condition and how is it treated?

A

DeQuervains thyroiditis - NSAIDs, BBs - self limiting

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28
Q

what is the management of hyperthyroidism?

A

carbimazole
change to maintenance or add levothyroxine
propylthiouracil
radioactive iodine
surgery

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29
Q

what are the signs of thyroid storm? what is the management?

A

hyperthyroidism + delirium, tachycardia and pyrexia
supportive mx with IVf, BBs and anti-arrhythmias

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30
Q

list the causes of hypothyroidism?

A

hashimotos, iodine deficiency, hypopituitarism, medications

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31
Q

what is the presentation of hypothyroidism?

A

weight gain, constipation, fatigue, dry skin, coarse thinning hair, fluid retention, heavy/irregular periods

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32
Q

how do you investigate hypothyroidism?

A

T3, T4 - low
TSH - increase in primary and decrease in secondary

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33
Q

how do you manage hypothyroidsim?

A

levothyroxine

34
Q

what is the normal glucose range?

A

4.4-6.1mmol/L

35
Q

what is the role of insulin and production process?

A

insulin lowers blood sugar levels
it is produced by beta cells in the islets of langerhans in pancreas
it makes the cells absorb glucose for fuel and the liver and muscles store it as glycogen

36
Q

what is the production and role of glucagon?

A

glucagon is produced in the alpha cells of the islets of langerhans in the pancreas. It increases blood sugar levels through glycogenolysis and gluconeogenesis

37
Q

what is the pathophysiology of T1DM?

A

pancreas stops producing insulin - hyperglycaemia
glucose is not absorbed or stored

38
Q

what is the pathophysiology of DKA and complications?

A

body thinks it is starved so converts fatty acids into ketones
this results in acidic blood as it overcomes the bicarbonate production - ketoacidosis
the hyperglycaemia results in glucosuria - more water removed through osmosis - dehydration and polyuria and polydipsia
lack of insulin result in less K+ being moved into cells - high or normal serum potassium but low overall
hypokalaemia - arrhythmias

39
Q

what are the symptoms of hypoglycaemia?

A

tremor, sweating, pallor, irritability, dizziness

40
Q

what is the presentation of DKA?

A

hyperglycaemia, dehydration, ketosis, metabolic acidosis, K imbalance, altered consciousness, nausea, vomiting, polydipsia, polyuria, acetone breath

41
Q

what are the criteria to diagnose DKA?

A

glucose>11, ketones>3, pH<7.3

42
Q

what is the management of DKA?

A

IV fluids, insulin, glucose, potassium as required

43
Q

what is the long term management of T1DM?

A

insulin - background/long acting and bolus - short acting

44
Q

what are the complications of diabetes?

A

short term - hyper/hypoglycaemia
long term - macrovascular- peripheral ischaemia, stroke, CAD, HTN
micro - retin/neuropathy, glomerulosclerosis
infection related

45
Q

what are the symptoms of hyperparathyroidism?

A

renal stones, painful bones, psychic moans, abdominal groans

46
Q

what are causes of the three types of hyperparathyroidism?

A

primary - tumour of the parathyroid
secondary - insufficient vitamin D or chronic renal failure
tertiary - prolonged secondary - hyperplasia

47
Q

what are the treatments of the three types of hyperparathyroidism?

A

primary - surgical resection
secondary - correct vitamin D and renal transplant
tertiary - remove the additional gland

48
Q

where is adrenaline produced and how does this link to phaeochromocytoma?

A

adrenaline is produced in the chromaffin cells in adrenal medulla - cancer of these is phaeochromocytoma - unregulated excessive adrenaline production

49
Q

what is the presentation of phaeochromocytoma?

A

peaks and troughs of adrenaline
anxiety, sweating, headaches, HTN, palpitations, paroxysmal AF

50
Q

how do you diagnose phaeochromocytoma?

A

24 hour urinary catecholamines
plasma free metanephrines

51
Q

what is the management of phaeochromocytoma?

A

alpha blockers, beta blockers, adrenalectomy

52
Q

what is acromegaly?

A

excessive growth hormone usually from pituitary adenoma

53
Q

what is the presentation of acromegaly?

A

headache, visual field defects such as bitemporal hemianopia, large forehead, brow, jaw, tongue, hands, feet, arthritis, T2DM, HTN, CRC, new skint tags, sweating, hypertrophic heart

54
Q

how do you investigate acromegaly?

A

IGF-1 - raised
OGTT - no fall
ophthamology referral
MRI brain

55
Q

how do you manage acromegaly?

A

transsphenoidal surgery
treat cancer
GH antagonist
somatostatin analogue
dopamine agonist

56
Q

what is the pathophysiology of T2DM?

A

repeated exposure to glucose and insulin leads to insulin resistance - increased requirements - the cells then fatigue and produce less so there is chronic hyperglycaemia

57
Q

what are the risk factors for T2DM?

A

modifiable - obesity, sedentary lifestyle, high carb diet
non-modifiable - older age, ethnicity, family history

58
Q

what is the diagnosis criteria for T2DM?

A

HbA1c>48, random glucose > 11, fasting glucose >7, OGTT>11

59
Q

what is the presentation of T2DM?

A

fatigue, polydipsia, polyuria, weight loss, infections, slow healing, glucosuria

60
Q

what is the management of T2DM?

A

first line - dietary, optimise RFs, monitor complications
first line drug - metformin target 48
2nd line - add pioglitazone, sulphonyurea, incretins, DPP-4 inhibitors, GLP-1 mimetic, SGLT-2i
third line - triple therapy or insulin

61
Q

how does metformin work? name some SEs?

A

biguanine - increases the sensitivity and decreases the production of glucose
diarrhoea, abdominal pain, lactic acidosis

62
Q

how does pioglitazone work and what are some SEs?

A

increases sensitivity to insulin and decreases glucose production
weight gain, fluid retention, anaemia, HF

63
Q

how do sulphonylureas work and what are the SEs?

A

stimulates insulin
weight gain and hypoglycaemia

64
Q

what is SIADH?

A

syndrome of inappropriate ADH secretion
results in inappropriate ADH secretion meaning more water reabsorbed - leads to a euvolaemic hyponatraemia

65
Q

what is the presentation of SIADH?

A

headache, fatigue, muscle aches, cramps, confusion, seizures, level of consciousness decrease

66
Q

what are the causes of SIADH?

A

post op, infection, head injury, meningitis, malignancy, medications such as NSAIDs

67
Q

how is SIADH diagnosed?

A

diagnosis of exclusion
hyponatraemia on U&Es
high urine osmolality
-ve short synacthen test
no diuretics, burns, vomiting, fistula, sweating, CKD, AKI
?CXR, MRI, CT

68
Q

what is a complication of treatment of SIADH?

A

central pontine myelinolysis
osmotic demyelination syndrome
severe, prolonged hyponatraemia treated too fast - encephalopathic and confused - demyelination - paralysis, palsy, cognitive and behavioural changes

69
Q

how do you treat SIADH?

A

check medications
resolve hyponatraemia <10mmol/L per 24 hours
fluid restriction
vaptans

70
Q

what is diabetes insipidus?

A

lack of response to ADH - cannot concentrate urine - polydipsia and polyuria

71
Q

what are the types of diabetes insipidus?

A

cranial or nephrogenic
cranial - lack of production e.g. idiopathic or malignancy
nephrogenic - no response e.g. kidney disease, mutations

72
Q

what is the presentation of diabetes insipidus?

A

polydipsia, polyuria, dehydration, hypernatraemia, postural hypotension

73
Q

how is diabetes insipidus investigated?

A

urine osmolality- decreased
serum osmolality - increased
water deprivation test

74
Q

describe the water deprivation test?

A

no fluids for 8 hours
measure urine osmolality at baselines and then give synthetic ADH
measure osmolality 8 hours after
cranial - low then high
nephrogenic - low then low

75
Q

how is diabetes insipidus managed?

A

treat cause
desmopressin can be given for cranial or under surveillance at high dose for nephrogenic

76
Q

what is primary hyperaldosteronism?

A

adrenals secrete too much aldosterone - serum renin is low

77
Q

what can cause primary hyperaldosteronism?

A

bilateral adrenal hyperplasia, adrenal adenoma (Conns), familial, adrenal carcinoma

78
Q

what is secondary hyperaldosteronism?

A

excessive renin - BP lower in kidneys than rest of body and is usually caused by atherosclerosis

79
Q

how do you investigate hyperaldosteronism?

A

renin aldosterone ratio: high aldosterone and low renin - primary, both high - secondary
BP increase, decreased K+, ABG
CT, MRI, MRA, CTA, USS

80
Q

how is hyperaldosteronism managed?

A

aldosterone antagonist
surgical resection
renal artery angioplasty

Finals (16 decks)

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