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LMCC > Endocrine > Flashcards

Endocrine Flashcards

1
Q

findings in someone with familial hypoalphalipoproteinemia

A

there is less HDL, resulting in premature atherosclerosis and cerebrovascular disease

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2
Q

Tangier disease

A

decreased HDL

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3
Q

lipid/lipoprotein screening should start at age __ or anyone with risk factors

A

40

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4
Q

What scoring system do you do to assess CVD risk and determine if you should start a statin

A

framingham risk score.

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5
Q

if highrisk framingham and not responsive to behavioural modifcation and statin, what other med should you try

A

ezetimibe/pscK9 inhitibor

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6
Q

insulin correction factor

A

100/total daily dose of insulin = change to blood glucose per unit of insulin

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7
Q

how much replacement of potassium if someone with HHS or DKA is hypokalemic

A

give 40mEQ/L K+ before insulin

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8
Q

is liraglutide (GLP1 inhibitor) cardioprotective

A

yes– sglt2 and glp1 inibitors are cardioprotective and have cardiorenal benefit.

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9
Q

management of diabetic nephropathy

A

glycemic control
- sglt2 is nephroprotective
- ARB/ACEi for CKD progression prevention.

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10
Q

use of C-peptide

A

it’s a short peptide that is released when insulin is cleaved into its active form. Increased Cpeptide = endogenous hyperinsulinemia

low/normal Cpeptide= exogenous hyperinsulinemia.

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11
Q

how does GH affect glucose

A

growth hormone is a catabolic hormone that acts to increase blood glucose. Can thus cause symptoms of cardiomyopathy, acanthosis nigracans etc.
GH is pulsatile and there is a nocturnal stage which is why kids need sleep.

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12
Q

GH excess in children vs adults

A

children= gigantism
adults = acromegaly

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12
Q

GH excess in children vs adults

A

children= gigantism
adults = acromegaly

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13
Q

investigations of GH excess

A
  • serum IGF-1 level (will be elevated)
  • glucose suppression test (glucose would suppress GH levels in a health individual).
  • CT/MRI or skull may shouow cortical thickening
    -MRI of sella needed to look for tumor that is screting GH
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14
Q

where is GH secreted

A

anterior pituitary.

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15
Q

treatment for GH excess

A
  1. somatostatin analogue (octreotide)
  2. dopamine agonist (cabergoline)
    - GH receptor antagonist (pegvisomant)
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16
Q

dopamine and prolactin relationship

A

dopamine suppressed prolactin. Therefor anti-dopaminergic properties (ex/ anti psychotics) can cause hyperprolactinemia.

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17
Q

treatments for hyperprolactinemia

A

dopamine agonists are first line (bromocriptine, cabergoline)– have proven effect of shrinking prolactin secreting tumours
- PRL-secreting tumors may possible be resected.

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18
Q

if a person is responsive to exogenous ADH (DDAVP), what kind of diabetes insipidus do they have?

A

they have central DI (not enough ADH being made, but the kidneys are still responsicve to it)

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19
Q

what is cerebral water wasting

A

in a subarachnoid hemorrahge, Na+ is excreted by malfunctioning tubules, mimicking findings of SIADH–> hallmark distinguishing factor is hypovolemia.

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20
Q

criteria for SIADH

A
  1. low sodium
  2. plasma hypo-osmolality (<275)
  3. high URINE Na+ concentration (>40)
  4. urine osmolality of >100.
  5. euvolemia (no edema)
  6. absence of adrenal, renal or thyroid insufficiency
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21
Q

treatment of SIADH

A
  1. serum sodium
  2. treat underlying cause (post-surgical stress, malignancy of small cell carcinomas, inflammatory CNS disease)
  3. fluid restriction
  4. vasopressin receptor antagonists (tolvaptan)– to stop ADH from causing increased water retention and thus hyponatremia
  5. furosemide
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22
Q

visual field defects due to pituitary adenoma

A
  1. visual field defects (bitemporal hemianopsia due to compression of optic chiasm)
  2. diplopia due to oculomotor nerve palsies

*recall that pituitary adenoma can cause any type of problem:
- PRL (galactorrhea, hypogonadism)
- GH (acromegaly in adults, gigantism in children)
- ACTH (Cushing’s disease)
- rare TSH secreting tumors

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23
Q

8I’s of hypopituitarism

A

Infection
Infarction: Sheehans, apoplexy
Invasive; craniopharyngioma, pituitary tumor
Infiltrative: sarcoid, histiocytosis
Infectious: syphillis
Injury: severe head trauma
Immunologic: autoimmune destruction
Iatrogenic: following surgery
Idiopathic: familial forms

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24
Q

Note: Langerhans cell histiocytosis is a rare, multisystem disease that shows a particular predilection for hypothalamo-pituitary axis involvement. Diabetes insipidus is the most frequent permanent consequence of Langerhans cell histiocytosis, developing in around a quarter of patients.

A
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25
Q

explain the insulin tolerance test when testing for hypopituitarism

A

dose of insulin –> hypoglycemia –> increased GH and cortisol (normal response)

GnRH –> increased LH and FSH
TRH –> increased TSH and PRL

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26
Q

primary vs secondary hyperthyroidism

A

primary: TSH is low because the thyroid is releasing T3 and T4 excess causing a negative feedback loop
secondary: problem is at the pituitary. In this case, Tsh being released too much, causing increase in T3 and T4

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27
Q

what antibodies should be assessed in Graves disease

A

TRAb (thyroid stimulating immunoglobulin)

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28
Q

what autoantibodies should be assessed in Hashimotos

A

TSH-receptor antibodies (TRAb and TPOAb)

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29
Q

____ is first line tool for identification of thyroid nodules

A

U/S. Then Fine need Aspiration biopsy.

30
Q

assessing hot nodule

A

radioisotope thyroid scan–> determine whether nodules are hot. Scan takes a picture of the nodule.

31
Q

hot nodule = ___ chance of malignancy. What about cold?

A

hot nodule = LOW chance of malignancy, treat hypertyroidism
cold nodule = further required U/s, then FNAB if concerning sonographic featues.

32
Q

eye signs of graves disease

A

lid lag, retraction, proptosis, diplopia, decreased acuity, puffiness, conjunctival injection

33
Q

treatment for graves/hyperthyroid/thyrotoxicosis

A
  • PTU or MMI (propylthiouracil or methimazole) MMI recommended usually, except in first trimester pregnancy
  • radioactive iodine thyroid ablation for Graves disease eand toxic nodules/adenoma
  • surgery for thyroidectomy or toxic nodules.
  • beta blockers for control of adrenergic symptoms.
34
Q

what do the results of radioactive iodine uptake tell us

A

it assesses if patient is thyrotoxic
if increased uptake: the thyroid is producing a lot of thyroid hormone –> hyperthyroid
if decreased uptake: the gland is leaking preexisting hormone (thyroiditis), or there is exogenous hormone use, or excess iodine intake (amiodraone)

35
Q

an autoimmune disorder characterized by autoantibodies that stimulate the TSH receptor leading to hyperthyroidism

A

graves. May have a diffuse goiter and thyroid bruit secondary to incresed blood flow through the gland.

36
Q

what would the radioactive scan show with graves disease

A

homogenous uptake on thyroid scan.

37
Q

is myxedema coma seen in hyper or hypothyroidism

A

hypothyroidism.

38
Q

effect of ACTH on skin pigmentation

A

ACTH can bind directly to MSH receptors on melanocytes, enhancing melanogenesis

39
Q

MOA of aldosterone

A

mineralocorticoid that acts on the distal tubule to cause Na+ retention and K+ and H+ excretion.

40
Q

layers of the adrenal cortex

A

G: glomerulosa (aldosterone)
F: fasciculata (cortisol)
R: reticularis (androgens

41
Q

how does aldosterone effect arteriolar diameter?

A

causes vasoconstriction in repsonse to decreased blood flow volume, decresaed arterial pressure, reduced Na delivery to macula densa, prostaglandins etc. in order to increse sodium and water volume to blood. Aldosterone also causes ADH release

42
Q

SCREENING testing if you suspect too much cortisol

A

dexamethasone suppression test at NIGHT– then measure plasma cortisol levels the following day. Usually, plasma cortisol will be low the next day because dexamethasone reduces ACTH and thus leads to decreased cortisol. If pituitary gland produces too much ACTH, you will still have high cortisol in the morning because it wasn’t suppressed.

43
Q

diagnosing test after you do a screening test of excess cortisol production

A

24 hour urine free cortisol with no diurnal variation.

44
Q

what is a positive screen for primary hyperaldosteronism

A

an elevated aldosterone: renin ratio.

45
Q

confirming test for primary hyperaldosteronism

A

Aldosterone Supprression Test: ECFV expansion with NS. IV infusion of 500ml/h of NS for 4 hours, then measure plasma aldosterone levels. Plasma aldosterone>277 pmol/L is consistent with PA (too much aldosterone even though it should be suppressed)

46
Q

how does hyperaldosteronism affect potassium?

A

often causes hypokalemia, +/- mild hypernatremia and metabolic alkalosis.

47
Q

primary vs secondary hyperaldosteronism PAC/PRA findings

A

primary HA will have elevated aldosterone and normal/low renin because there is an adrenal adenoma or something that is causinga n increase in aldosterone

secondary HA will have elevated renin which increases aldosterone, so both will be elevated. This is often due to coarctation of the aorta, malignant hypertension or diuretic use, or a renin-secreting tumour.

if there is a decreases in renin and decrease in aldosterone, but there is hypertension or hypokalemia, consider congenital adrenal hyperplasia or cushings.Cortisol acts as a diuretic, which leads to water and potassium excretion and sodium retention. It increases potassium excretion in the intestines as well.

48
Q

treatment of hyperaldosteroneism

A

inhibit action of aldosterone: spironolactone
surgical excision of adrenal adenoma
secondary hyperaldosteronism: treat underlying cause.

49
Q

cushings is cortisone___

A

excess. usually due to ACTH -secreting pituitary tumor, or ectopic ACTH-secreting tumor, bilateral adrenal nodular hyperplasia, or iatrogenic.

50
Q

diagnosis of cushins

A
  1. 24 hour urine free cortisol
  2. low dose dexamethasone suppresion
  3. late night salivary cortisol.

confirm again with another remaining test.

51
Q

treatment of cushings

A

adrenal problem: adrenalectomy with glucocorticoid supplementation.
ketoconazole to reduce cortisol, mitotane can also be used.

52
Q

when to check progesterone level (if you expect it to be elevated)

A

it will be elevated in congenital adrenal hyperplasia, check on day 3 of menstrual cycle.

53
Q

PTH vs calcitonin function

A

PTH: increases phosphate, Ca2+ and calicitriol
calcitonin: decreases Ca2+ and phosphate

54
Q

role of cholecalciferol

A

acts on liver to make vitamine D

55
Q

most common cause of hypercalcemia in healthy out patient

A

primary hyperparathyroidism. superfical excision is the definitive treatment.

56
Q

corrected calcium

A

= (measured Ca2+) + (0.02(40-albumin))

For every decrease in albumin by 10, increase Ca2+ by 0.2

57
Q

psychiatric drug that can cause increase calcium

A

lithium, increases PTH and thus Ca2+

58
Q

high calcium in context of low PTH and high calcitriol

A

granulomatous disease which causes extra-renal production of calcitriol by macrophages in the lung and lymph nodes. (or excessive calcitriol intake)

59
Q

signs of acute hypO calciemia

A

chvostek’s sign: percussion of facial nerve just anterior to the external auditory meatus elicits ipsilateral spasm of the orbicularis.

trousseau’s sign: inflation of BP cuff elicits carpal spasm and paresthesia

60
Q

treatment of acute hypercalcemia

A
  1. increase urinary Ca2+ excretion– fluids and calcitonin
  2. diminish bone resorption– bisphosphonates
  3. decrease GI Ca2+ absorption– corticosteroids can be used in hypercalcemia mediated by 1,25 vitamin D
  4. dialysis (last resort) if heart failure or renal insufficiency.
61
Q

effect of magnesium of calcium

A

hypomagnesemia can impaire PTH secretion and action.

62
Q

what disturbance to calcium causes torsades

A

hypocalcemia

63
Q

muscle differneces between hyper and hypocalcemia

A

hyper: muscle weakness
hypo: tetany, chovsteks, trousseau, seizure, laryngospasm, perioral numbness and paresthesia

64
Q

drug therapy for osteoporosis

A

biphsophonates
rank inhibitors/denosumab
sclerostin inhibitor
SERM/raloxifene (women)
HRT

65
Q

PTH ___ phosphate

A

decreases phosphate.

66
Q

how does fanconi syndrome cause osteomalacia

A

Fanconi syndrome causes a proximal tubular acidosis, which reduces phosphate. thus calcium will be normal, but wihout phosphate, vitamin D cannot properly mineralize the bones.

67
Q

drugs causing gynecomastia DISCKO

A

Digoxin
isoniazin
spironolactone
cimetidine
ketoconazole
oesterogren

68
Q

what tumor is assocaited with myasthemia gravis

A

thymoma

69
Q

CRAB multiple myeloma

A

hypercalcemia
renal injury
anemia
bony lesions.

70
Q

Urine sodium <10 indiciative of

A

RAS system is turned on– so it likely means that you are dry– prerenal injury if creatinine high.

71
Q

what do you expect to see in secondary hyperparathyroidism caused by renal failure?

A

renal failure= cannot excrete phosophate = high PO4
PTH will go up because if phosphate goes up, PTH will go up to down regulate the phosphate. therefore PTH elevated

in kidney dysfucntionm, vitamin D synthesis gets reduced and you accumulate 1,25 (OH)2 vit D.

Calcium stays low until you get tertiary hyperparathyroidism, which is what you see in a transplant situation. PTH was so high for so long, and its become autonomoous, causing really high Calcium.

72
Q

MOA os SGLT2 inhibitos

A

stops the drive of glucose reabsorption in the renal tubule. Cardiovascular benefit, weight loss benefit

73
Q

salt craving and hyperpigmentation, hyperkalemia, ACTH really high.

A

Addison’s disease Low cortisol aka PRIMARY adrenal insufficiency (all the GFR layers are affected)

Low zona glomerulosa = low aldosterone (hyperkalemia)
low fasciculata = low cortisol (hyperpigmentation, tired)
low reticularis= low sex steroids (do a free androgen index aka decreased libido)

Central adrenal insufficiency only affect the fasciculata and the reticularis because they are both under command of ACTH from the pituitary system. Aldosterone/glomerulosa layer will not be affected. therefore in central AI you would only have low sex steroids and low cortisol but no hyperkalemia because the RAS system is intact.

LMCC (19 decks)

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