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Clinical Years / Progress Test > Endocrine > Flashcards

Endocrine Flashcards

1
Q

treatment of myxoedemic coma

A

hydrocortisone and levothyroxine

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2
Q

treatment of thyrotoxic storm

A

Beta blockers, propylthiouracil and hydrocortisone

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3
Q

when should a second drug be added to metformin in T2DM

A

if HbA1C>58mmol/mol

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4
Q

What diabetic drugs can be continued in pregnancy

A

Only metformin and insulin

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5
Q

causes of Cushing’s

A

iatrogenic (exogenous steroids)
pituiatry ACTH producing tumour (cushings disease)
Ectopic ACTH from lung cancer
Primary adrenal tumour (ACTH independent)

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6
Q

diagnosing Cushings

A
  1. measure increased cortisol and exclude exogenous steroids
  2. Dexamethasone suppresion test. If normal dex suppresses ACTH
    Cushings disease (pituitary) is suppressed by high dose
    Ectopic ACTH/Adrenal tumour is not suppressed
  3. venous sampling at inferior petrosal sinus can detect ACTH from pituitary
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7
Q

what electrolyte abnoramlity is seen in Cushings

A

excess cortisol leads to increased sodium, increased bicarb and decreased potassium

causes metabolic alkalosis

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8
Q

treatment of cushings

A

if operable operate
if not suppress cortisol synthesis using drugs; metyrapone or ketoconazole

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9
Q

causes of nephrogenic diabetes insipidus

management

A

genetic
electrolyte abnormalities (increased calcium, decreased potassium)
lithium
tubulointerstitial disease

thiazides and low salt/protein diet

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10
Q

examples of following diabetic drugs + main side effects

biguanide
sulphonylureas
DPP4inhibitors
SGLT2 inhibitors
GLP1 agonists

A

biguanide - metformin - GI effects and lactic acidosis

sulphonylureas - gliclazide, glimperide - hypo risk, weight gain

DPP4inhibitors - gliptins - pancreatitis

SGLT2 inhibitors - gliflozins - UTIs

GLP1 agonists - glutides

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11
Q

test results in primary hyperparathryoidism

most common cause

A

low phosphate and high PTH and calcium level

solitary adenoma of the parathyroid causing increased PTH

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12
Q

test results in secondary hyperparathryoidism
causes

A

high PTH, low phosphate and low calcium

renal failure
vitamin D deficinecy

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13
Q

test results of tertiary hyperparathyroidism

A

high PTH, high phosphate and high calcium with decreased vit D
caused by end stage renal failure

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14
Q

what can happen if you wihtdraw steroids abruptly

A

precipitate an addisonian crisis

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15
Q

diagnosis of gestational diabetes

A

fasting glucose of >5.6
or 2 hour glucose of >7.8

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16
Q

What hormones do each layer of the adrenal gland produce

A

Zona glomerulosa - mineralocorticoids
Zona fasiculata - glucocorticoids
Zona reticularis - androgen precursors
Medulla - catecholamines

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17
Q

What does metyrapone do?

A

It is a glucocorticoid synthesis inhibitor

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18
Q

How do you measure
- urinary cortisol
- plasma cortisol
- salivary cortisol

A

Urinary - 24 hour collection
Plasma - 9am cortisol, evening or midnight. Midnight most different from normal
Salivary - late night highest specificity for Cushing diagnosis

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19
Q

Treatment of adrenal crisis

A

High dose steroid replacement - IV hydrocortisone 100mg every six hours

IV saline (with dextrose if hypoglycaemic)

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20
Q

Diagnosing adrenal insufficiency
Treatment

A

High dose short synacthen test - give ACTH and see if adrenals respond

Treatment is steroid replacement

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21
Q

What is SIADH?
Diagnosis?
Causes?

A

Syndrome of inappropriate ADH secretion - more water reabsrobed by kidneys leading to dilute serum and concentrated urine

Diagnosis; low serum osmolaltiy with high urinary osmolality

Causes:
Lung diseases
Brain lesions
Drugs e.g. carbamazepine, SSRIs

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22
Q

Symptoms and signs of hyponatraemia

A

Headache dizziness and nausea
Can result in coma if severe
Can be hypovolaemic or hypervolaemic hyponatraemia

Hypovolaemic:
Cool peripheries
Tachycardia
Postural Hypotension
Confusion
Dehydrated

Hypervolaemic:
Tachycardia
Raised JVP
Pulmonary oedema
Ascites
Peripheral oedema

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23
Q

Causes of hyponatraemia

A

Renal loss; addisons, renal failure, excess diuretics

Loss elsewhere; diarrhoea, vomiting, burns, trauma

SIADH, water overload, severe hypothyroid, glucocorticoid insufficiency

Nephrotic syndrome, cardiac failure, cirrhosis, renal failure

24
Q

When does hypernatraemia occur

A

Dehydration without access to water e.g. in elderly demented patients

25
Q

What are the criteria for bariatric surgery

A

BMI of over 40 or 35-40 with other significant disease that could be improved with weight loss
All non surgical measures have been tried
Has been / will receive intensive management in a tier 3 service
Fit enough for surgery

26
Q

What is osteomalacia

A

Softening of the bones secondary to vitamin D deficiency (primary, CKD or other)
Presents with bone pain, fatigue, and proximal myopathy

27
Q

what gastric complications can T1DM cause

A
  • gastroparesis; manage with metoclopramide, domperidone or erythromycin (prokinetic agents)
  • chronic diarrhoea
  • GORD
28
Q

what type of diabetes are C peptide levels raised in

A

type 2

29
Q

what antibodies can be raised in T1DM? (approx 80%)

A

anti-GAD
islet cell antibodies
insulin antibodies

30
Q

what is acromegaly

what is the most common cause

A

excess growth hormone

most commonly due to a pituitary adenoma

31
Q

tests to diagnose acromegaly

A

serum IGF-1 levels

if raised do an oral glucose tolerance test (OGTT) - in acromegaly there is no suppression of GH due to increased glucose

pituitary MRI may demonstrate a pituitary tumour

32
Q

management of acromegaly

A

trans-sphenoidal surgery if possible

if not:
- somatostatin analogues
- GH receptor antagonist
- dopamine agonists effective in minority

33
Q

features of addisons disease

A
  • lethargy, anorexia, weakness, N & V
  • hyperpigmentation (primary addisons)
  • hypotension
  • hypoglycaemia
  • hyponatraemia and hyperkalaemia
34
Q

addisons disease management

A

glucocorticoid and mineralocorticoid replacement therapy

hydrocortisone given daily in 2-3 divided doses
fludrocortisone

35
Q

addisons treatment changes in an intercurrent illness

A

double glucocorticoid

keep mineralocorticoid the same

36
Q

diagnostic criteria T1 DM

A

fasting glucose 7.0mmol/L or more

random glucose (or glucose tolerance test) 11.1mmol/L or more

on one occasion if symptomatic or two if asymptomatic

37
Q

when should SGLT2 inhibitors be used in T2DM

A

after metformin is titrated up

in anyone with or at high risk of CVD

38
Q

2nd drug choice and when T2DM

A

when HbA1C >58 on metformin

in CVD risk - SGLT2 inhibitor

if not at risk - DPP4i, pioglitazone or a sulphonylurea

39
Q

HbA1C targets T2DM

A

48

53 if on a drug that has hypo risk e..g sulphonylurea

40
Q

types of thyroid cancers

A

papillary carcinoma - best prognosis, most common
follicular carcinoma
medullary carcinoma - part of MEN2
anaplastic carcinoma - worst prognosis

41
Q

triple therapy options in T2DM

A

metformin + sulphonylurea + DPP4i (gliptin)

metformin + sulphonylurea + pioglitazone

metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT2i if certain criteria met

42
Q

sulphonylureas:
- names
- main side effect + risk
- pregnancy?

A

gliclazides

weight gain
risk of hypos

avoid in pregnancy and breastfeeding

43
Q

hypoglycaemia with impaired GCS?

A

give IV glucose STAT if access

44
Q

treatment of a prolactinoma

A

cabergoline - a dopamine agonist

dopamine inhibits prolactin release

45
Q

thyrotoxicosis with a tender goitre?

A

subacute (de quervain’s) thyroiditis - typically follows a viral infection

46
Q

phases of subacute thyroiditis

A

1 - tender goitre, hyperthyroidism, ESR raised (3-6 weeks)
2 - euthyroid (1-3 weeks)
3 - hypothyroid (weeks to months)
4 - return to normal

47
Q

which hormones reduce in a stress response e.g. to surgery

A

insulin
oestrogen
testosterone

48
Q

primary hyperaldosteronism

A

hypertension
hypokalaemia - muscle weakness
alkalosis

49
Q

investigation primary hyperaldosteronism

A

plasma aldosterone/renin ratio
- will show aldosterone too high and low renin (negative feedback)

CT abdomen if raised

adrenal venous sampling if CT inconclusive

50
Q

causes of primary hyperaldosteronism

A

bilateral adrenal hyperplasia (most common)
adrenal adenoma secreting aldosterone (conn’s syndrome)

rarely familial or an adrenal carcinoma

51
Q

what is secondary hyperaldosteronsim

A

excessive renin stimulates the adrenal glands to secrete more aldosterone

due to blood pressure in kidneys being disproportionately lower to rest of body
e.g. renal artery stenosis or obstruction
heart failure

52
Q

management of primary hyperaldosteronsim

A

bilateral adrenal hyperplasia - spironolactone (aldosterone antagonist)

adrenal tumour - surgery

53
Q

DKA management

A

isotonic saline first! restore volume

fixed rate insulin infusion (long acting insulin continued, short acting stopped)

potassium may need replacing due to insulin moving it into intracellular place

54
Q

typical presentation of primary hyperparathyroidism

A

typically elderly females with an unquenchable thirst and polydipsia

most commonly due to a solitary adenoma

55
Q

investigation results primary hyperparathyroidism

A

high calcium

high or normal PTH

low phosphate

56
Q

definitive management of primary hyperparathyroidism

A

total parathyroidectomy

Clinical Years / Progress Test (24 decks)

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