endocrine Flashcards

1
Q

what is the x-ray findings of primary hyperparathyroidism?

A

pepperpot skull
osteitis fibrosa cystica

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2
Q

how do SGLT2 inhibitors cause euglycaemic ketoacidosis?

A

it is hypothesised that as these agents lower blood sugar levels by increasing the excretion of glucose the resulting reduction in plasma glucose results in reduced insulin secretion from pancreatic beta-cells and these patients entering a state of relative insulin deficiency. This leads to a lowering of the antilipolytic activity of insulin, and the consequent stimulation of the production of free fatty acids, which are then converted to ketone bodies by beta-oxidation in the liver.

Moreover, insulin stimulates the activity of acetyl-CoA carboxylase, which produces malonyl-CoA, a potent inhibitor of carnitine palmitoyltransferase (CPT-I). Given that CPT-I promotes the transport of fatty acids into mitochondria and hence increases the rate of beta-oxidation, the decrease in the circulating level of insulin promotes the production of ketone bodies through activation of CPT-I.

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3
Q

what is seen on thyroid scintigraphy for de-quverian’s thyroiditis?

A

thyroid scintigraphy: globally reduced uptake of iodine-131

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4
Q

who is statin treatement offered to in type 1 diabetics?

A

atorvastatin 20 mg should be offered if type 1 diabetics who are:
- older than 40 years, or
- have had diabetes for more than 10 years or
- have established nephropathy or
- have other CVD risk factors

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5
Q

what is barrtter’s syndrome?

A

similar to taking a lot of furosemide

defective NKCC2 channel

usually presents in childhood, e.g. Failure to thrive
polyuria, polydipsia
hypokalaemia
normotension
weakness

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6
Q

what are side effects of sufonylureas?

A
  • hyponatraemia secondary to syndrome of inappropriate ADH secretion
  • bone marrow suppression
  • hepatotoxicity (typically cholestatic)
  • peripheral neuropathy
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7
Q

what is the difference between IFg and IGT? (physiologically)

A

impaired fasting glucose (IFG) - due to hepatic insulin resistance
impaired glucose tolerance (IGT) - due to muscle insulin resistance

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8
Q

what is CRP and how is it synthesized?

A

CRP is a protein synthesised in the liver and binds to phosphocholine in bacterial cells and on those cells undergoing apoptosis. In binding to these cells it is then able to activate the complement system. CRP levels are known to rise in patients following surgery. However, levels of greater than 150 at 48 hours post operatively are suggestive of evolving complications.

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9
Q

what are the different type of multiple endocrine neoplasia

A

MEN type 1 - 3Ps : hyperparathyroidism. pituitary, pancreas (insulinoma, gastrinoma)

MEN type 21:
parathyrioid, pheochromocytoma
+
medullary thyroid cancer

MEN type 2b
medullary thyroid cancer + pheochromocytoma

marfanoid body habitus, neuromas

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10
Q

what medications does levothyroxine interact with?

A

iron, calcium carbonate
absorption of levothyroxine reduced, give at least 4 hours apart

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11
Q

what do the results of 9am cortisol suggest when it comes to ? addisons disease

A

sending a 9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

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12
Q

what is the screening test for conn’s syndrome?

A

aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism
should show high aldosterone levels alongside low renin levels

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13
Q

how is hypothyroidism treated?

A
  • serum thyroid-stimulating hormone measured in each trimester and 6-8 weeks post-partum
  • women require an increased dose of thyroxine during pregnancy
    by up to 50% as early as 4-6 weeks of pregnancy
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14
Q

what does the abg look like in cushing’s syndrome?

A

hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.

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15
Q

what is diagnosis in someone with hashimoto’s thyroiditis who has new mass?

A

The presence of a new thyroid mass on a background of longstanding Hashimoto’s thyroiditis should arouse the suspicion of mucosa-associated lymphoid tissue (MALT) lymphoma.

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16
Q

what can precipitate thyroitoxic storm?

A

thyroid or non-thyroidal surgery
trauma
infection
acute iodine load e.g. CT contrast media

17
Q

what is the tx for thyrotoxic storm

A

Hydrocortisone, propranolol, propylthiouracil

Hydrocortisone acts to prevent the peripheral conversion of T4 to T3

Propranolol blocks the effects of thyroid hormones and reduces the heart rate

Propylthiouracil stops the release and production of thyroid hormones and reduces the peripheral conversion of T4 to T3.

18
Q

what are some of the causes of NAGMA?

A

renal tubular acidosis, diarrhoea, hypoaldosteronism, and carbonic anhydrase inhibitors.

19
Q

which renal tubular acidosis is associated with sjogren syndrome

A

RTA type 1

20
Q

which gene is responsible for MODY?

A

HNF1-Alpha

21
Q

what is offered in t1dm and high Bmi after insulin trial?

A

metformin if the BMI >= 25 kg/m²

22
Q

when do you refer immediately to ophthalmology in thyroid eye disease?

A
  • unexplained deterioration in vision
  • awareness of change in intensity or quality of colour vision in one or both eyes
  • history of eye suddenly
  • ‘popping out’ (globe subluxation)
    -obvious corneal opacity
    cornea still visible when the eyelids are closed
    disc swelling
23
Q

what are the features of insulinoma?

A
  • hypoglycaemia: typically early in morning or just before meal, e.g. diplopia, weakness etc
  • rapid weight gain
  • high insulin , raised proinsulin: insulin ratio
  • high C-peptide
24
Q

how does duloxetine work?

A

It is thought to work by increasing serotonin and norepinephrine levels in the pudendal motor nucleus of the sacral spinal segments, thereby increasing urethral muscular tone and closure pressure.

25
Q

how does carbimazole function?

A

This medication blocks thyroid peroxidase thereby preventing the iodination of the tyrosine residue on thyroglobulin. This results in a reduction in excessive thyroid hormone production that results in the signs and symptoms of thyrotoxicosis.

26
Q

why is there acidosis everytime there is hyperkalaemia?

A

Whenever there is hypokalemia, remember the potassium levels in the blood are low. So intracellular potassium tends to come out of the cells.

Whenever 1K+ comes out of the cell 1H+ goes in (there is exchange of potassium and hydrogen ions)

Since H+ is removed from the blood and sent into the cells, there is alkalosis.

If in some other situation, like Addison’s, there is hyperkalemia, the opposite would occur i.e. potassium moves into cells and hydrogen goes out into the blood. This would cause acidosis.

Hence whenever there is hypokalemia there is alkalosis.
Whenever there is hyperkalemia there is acidosis.

27
Q

what are the causes of hypokalemia with acidosis?

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis