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UWorld Facts > Endocrine Facts > Flashcards

Endocrine Facts Flashcards

1
Q

Hashimoto thyroiditis - histologic findings

A
  • Intense lymphocytic infiltrate with GERMINAL CENTERS

- Hurthle cells: large oxyphilic cells filled with granular cytoplasm

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2
Q

Subacute thyroiditis (De Quervain) - histologic findings

A
  • granulomatous inflammation

- mixed cellular infiltrate with multinuclear giant cells

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3
Q

Riedel thyroiditis - histologic findings

A
  • FIBROSIS of thyroid gland extending to surrounding structures
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4
Q

Derivatives of neural crest cells: MOTEL PASS

A 
M: melanocytes
O: odontoblasts
T: tracheal cartilage
E: enterochromaffin cells 
L: laryngeal cartilage

P: parafollicular cells of thyroid
A: adrenal medulla
S: schwann cells
S: spiral membrane

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5
Q

Inhibin is under the influence of which hormone?

A

FSH

  • FSH causes increased production of inhibin to act negatively on PITUITARY only to inhibit FSH and LH release
  • decrease FSH or response to FSH by FSH receptors causes low levels of inhibin
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6
Q

Why do you want to check SERUM CREATININE before starting METFORMIN?

A
  • Meformin inhibits hepatic gluconeogenesis —> increased peripheral glucose utilization
  • decreased gluconeogenesis also increase LACTIC ACID because not being metabolized into glucose —> risk for LACTIC ACIDOSIS in patients with significant hepatic or renal deficiency
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7
Q

Statins - side effects

A
  • Myopathy

- hepatotoxicity

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8
Q

Fibrates - side effects

A
  • cholesterol gallstones

- myopathy

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9
Q

Niacin - side effects

A
  • hyperuricemia: GOUT
  • hyperglycemia
  • red, FLUSHED FACE: decreases if use NSAIDs before
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10
Q

Bile acid sequestrates - side effects

A
  • GI upset

- decreased absorption of other drugs and fat soluble vitamins

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11
Q

Ezetamide - side effects

A
  • increased LFTs
  • diarrhea
  • increase hepatotoxicity with statins
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12
Q

Neurophysins

A
  • are carrier proteins for oxytocin and ADH —> shuttle the hormones to the nerve terminal ends for release from posterior pituitary
  • produced in the hypothalamus with the other two hormones
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13
Q

Treatment of CAH

A
  • low dose exogenous corticosteroids to suppress excess ACTH secretion and reduce stimulation of adrenal cortex —> decrease androgen production
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14
Q

Role of beta-blockers in hyperthyroidism

A
  • block beta-1 adrenergic receptors decreasing the stimulation from sympathetic impulses on target organs
  • decrease PERIPHERAL CONVERSION of T3 to T4
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15
Q

side effects of TZD (thiazolelidinediones)

A

Edema: increased Na retention in renal collecting tubes
Weight gain: from edema, also adipose weight gain
Excess fluid can exacerbate heart failure

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16
Q

Clinical difference between Tay-Sachs and Niemann-Pick disease

A

Do not have HEPATOSPLENOMEGALY in Tay-Sachs

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17
Q

What inhibits carnitine acyltransferase?

A

MALONYL-COA

  • carnitine acyletransferase is involved in FATTY ACID OXIDATION —> transfers fatty acids from cytoplasm to mitochondria
  • malonyl-CoA is involved in FATTY ACID SYNTHESIS
  • do not want to break down newly made fatty acids so malonyl-CoA inhibits the transfer of FA into the mitochondria
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18
Q

How are NE and EPI secretion activated in the adrenal medulla?

A

By ACh released from PREganglionic sympathetic neurons —> act on POSTganglionic sympathetic neurons to release EPI and NE

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19
Q

What do you get from deficiency of dihydrobiopterin reductase?

A

Is enzyme needed to reduce BH2 to BH4, a cofactor for phenylalanine hydroxylase and tyrosine hydroxylase. Without it, get:

  • hyperphenylalanemia (PKU)
  • decreased dopamine, NE, Epi and serotonin
  • increased prolactin from decreased dopamine inhibition
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20
Q

Craniopharyngioma

A
  • from remnant of Rathke’s pouch (gives rise to ant. pit.)
  • three components: solid (tumor cells), cysts (“machinery oil” liquid) and calcified component —> THINK CRANIOPHARYNGIOMA WHEN SEE THESE THREE THINGS
  • present in childhood
  • Mass effect and visual deficits, increased prolactin from decreased dopamine inhibition
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21
Q

Why do you get cataracts in galactosemia?

A

Excessive galactose gets converted to galactitol by ALDOSE REDUCTASE —> galactitol accumulates in lens and causes osmotic damage leading to cataract formation

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22
Q

Test for hypothyroidism

A

TSH!

  • more sensitive: shows marked changes to small changes in T3, T4
  • is increased before a low thyroid hormone is seen
  • cannot detect central hypothyroidism but this form is uncommon
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23
Q

Primary adrenal insufficiency - labs

A

Decreased ADOLSTERONE
- hyponatremia, hyperkalemia, hyerchloremia (retain Cl- to maintain electrical neutrality of ECF), non anion gap metabolic acidosis (retain H+ with K+, and Na+ loss)
Do not see increased cortisol with ACTH stimulation

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24
Q

Where is proinsuln cleaved?

A

In SECRETORY GRANULES —> get insulin and C-peptide

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25
Q

Which nerve is at risk of injury during a thyroidectomy?

A

External branch of the superior laryngeal nerve (due to proximity to the superior thyroid artery and vein) —> innervates the cricothyroid muscle

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26
Q

Osteitis fibrosa cystica

A
  • most common characteristic skeletal manifestation of primary hyperparathyroidism
  • affects cortical (compact bone) in appendicular skeleton
  • bone pain
  • subperiosteal erosions affecting the phalanges of the hand
  • granular “salt and peper” skull
  • BROWN TUMOR osteolytic cysts in long bones
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27
Q

Copper reduction test

A

Tests for presence of reducing sugars in the urine: unmetabolized fructose, glucose, galactose

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28
Q

Glucose oxidase dipstick test

A

Used to test for presence of urine glucose

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29
Q

Insulin-mediated glucose transporter

A

GLUT-4

- in skeletal muscle and adipocytes

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30
Q

Insulin-independent glucose transporters

A

GLUT-1, 2, 3, 5

- in liver, brain, kidney, RBC, intestine

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31
Q

GLUT-1 location

A

RBCs and at BBB

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32
Q

GLUT-2 location

A

hepatocytes, pancreatic beta cells, kidney, small intestine

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33
Q

GLUT-3 location

A

Placenta and neurons

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34
Q

GLUT-4 location

A

Spermatocytes and GI tract

35
Q

Effects of HAART on fat redistribution

A
  1. Lipoatrophy: loss of subcutaneous fat in face, extremities and buttocks
    - NRTIs
    - protease inhibitors
  2. Central fat distribution: increased abdominal growth and buffalo hump
    - can be seen with any HIV medication —> can be the result of treating HIV rather than the medication
36
Q

Whipple’s triad

A
  • symptoms of hypoglycemia
  • low blood glucose levels
  • relief of hypoglycemic symptoms when blood glucose levels increase
37
Q

Sheehan syndrome

A

ISCHEMIC NECROSIS of pituitary in case of systemic hypotension after peripartum hemorrhage

38
Q

Adrenal crisis - treatment

A

Immediate stress-dose corticosteroids —> increases cortisol levels (cannot produce on own with adrenal crisis)

39
Q

Diagnosis of 21-hydroxylase deficiency

A

High serum levels of 17-hydroxyprogesterone

40
Q

Pioglitazone - class

A

TZD

41
Q

Niacin - main effect

A

increase HDL

42
Q

Fibrates - main effect

A

decrease Triglycerides

43
Q

Bile acid sequestrants - main effect

A

decrease LDL

44
Q

Ezitimide - main effect

A

decrease LDL

45
Q

Statins - main effect

A

decrease LDL (LOTS)

46
Q

Fish oil - main effect

A

decrease triglycerides but to a lesser degree

47
Q

Ca sensing receptors

A

G-protein couple receptors

- help regulate PTH

48
Q

Familial hypocalciuric hypercalcemia - mutation

A
  • defect CaSR in parathyroid glands and kidneys - can’t sense Ca levels so higher levels of Ca are needed to suppress PTH
  • AD
  • have mildly elevated Ca, decreased urine Ca excretion and high normal or mildly elevated PTH
49
Q

Meglitinides - MOA

A
  • bind and close ATP-dependent K+ channels —> depolarize cell —> increase intracellular Ca —> increased insulin secretion (like sulfonylureas)
  • shorter acting, have to be given more frequently but similar efficacy
  • may have less risk of hypoglycemia
  • still gain weight
50
Q

Repaglinide, nateglinide - class

A

Meglitinides (for diabetes)

51
Q

Molecules with intracellular receptors

A
  • Steroid hormones
  • thyroid hormone
  • vit D
52
Q

Molecules with tyrosine kinase receptors

A
  • Insulin

- IGF-1

53
Q

Molecules that go through JAK/STAT pathway

A
  • growth hormone
  • prolactin
  • erythropoietin
  • cytokines
  • colony stimulating factors
54
Q

McArdle Disease - enzyme deficiency

A
  • myophosphorylase (muscle form of glycogen phosphorylase): breaks alpha-1,4 glycosidic bonds in glycogen
55
Q

How do free fatty acids contribute to insulin resistance?

A
  • increase lipolysis and free fatty acids in INSULIN RESISTANCE
  • increased FFA contribute to insulin resistance even more by: impairing insulin dependent glucose uptake in liver and muscle and increasing hepatic gluconeogenesis
56
Q

Long acting sulfonylureas - name of drugs

A
  • Glyburide
  • glimepuride
    longer acting so increased risk of HYPOGLYCEMIA
57
Q

Short acting sulfonylureas - name of drug

A
  • Glipizide

shorter acting so DECREASED risk of HYPOGLYCEMIA

58
Q

MEN1 - associated cancers

A

3 Ps

  • parathyroid tumors
  • pituitary tumors: prolactin or GH
  • pancreatic endocrine tumors: zollinger-ellison syndrome, insulinomas, VIPomas, glucagonomas
59
Q

MEN 2A - associated cancers

A

2 Ps

  • parathyroid hormone
  • pheochromocytoma
  • MEDULLARY thyroid carcinoma
  • mutation in RET gene
60
Q

MEN 2B - associated cancers

A

1 P

  • pheochromocytoma
  • MEDULLARY thyroid carcinoma
  • oral/intestinal MUCOSAL NEUROMAS
  • mutation in RET gene, associated with marfanoid habits
61
Q

Anastrozole, letrozole, exemestane - class

A

AROMATASE inhibitors

62
Q

Effects of ethanol on gluconeogenesis

A

INHIBITS gluconeogenesis

  • ethanal reduces NAD+ to NADH so increases the NADH/NAD+ ratio —> less NAD+ —> cannot drive reactions that need NAD+
  • HYPOGLYCEMIA (after glycogen stores are used)
63
Q

Metyrapone stimulation test

A
  • Metyrapone blocks cortisol synthesis by inhibiting 11-beta-hydryoxylase which converts 11-deoxycortisol to CORTISOL
  • reduction in cortisol levels causes increase in ACTH
  • increased ACTH causes increased 11-doxycortisol which is converted to 17-hydroxycorticosteroids —> both of these hormones should rise if HPA axis is intact
  • if HPA axis is not intact due to primary or secondary adrenal insufficiency, then these two steroids will NOT INCREASE
64
Q

Causes of hypoglycemia in type 1 diabetes:

A
  • excessive insulin dose
  • inadequate food intake
  • physical activity, exercise
65
Q

Histology of Type 2 diabetes

A

islet amyloid polypeptide (IAPP) deposits

66
Q

Histology of Type 1 diabetes

A

islet leukocyte infiltrate

67
Q

Medullary thyroid cancer - histology

A
  • neuroendocrine tumor that arises from parafollicular calcitonin-secreting C CELLS
  • nests or sheets of polygonal or spindle-shaped cells with extracellular amyloid deposits derived from calcitonin (amyloid stains with CONGO RED)
68
Q

Glargine and Detemir - insulin type

A

Long acting - once a day

69
Q

NPH - insulin type

A

long acting - twice a day

70
Q

Regular insulin

A

short acting

best for IV use

71
Q

Lispro, Aspart, Glulisine - insulin type

A

short acting - best for post-meal hyperglycemia

72
Q

Sympathetic stimulation on insulin release

A

overall DECREASE insulin

  • beta 2 is coupled to Gs and stimulates insulin secretion
  • alpha 2 is coupled to Gi and inhibits insulin secretion —> PREDOMINATES
73
Q

Parasympathetic stimulation of insulin release

A

overall INCREASE insulin

- M3 receptors coupled to Gq and stimulates insulin secretion induced by smell and/or sight of food

74
Q

Pathyphys of exophthalmos and pretibial myxedema

A

Response to AB in Grave’s disease, not due to thyroid hormone
- caused by lymphocytic infiltration, enlargement of the extra ocular muscles by myositis, fibroblast proliferation and overproduction of mucopolysaccharides in response to anti-thyroid antibody

75
Q

Immediate treatment of SEVERE hypoglycemia

A
  • IM glucagon in non medical setting

- IV glucose in medical setting

76
Q

Flutamide - class, MOA

A

Nonsteroid anti-androgen

  • acts as competitive inhibitor of testosterone receptors
  • blocks stimulatory effect of androgens on the primary tumor and the metastases and leads to DECREASE IN SIZE
77
Q

Role of tamoxifen in MEN with prostate cancer

A

Can help prevent gynecomastia in men receiving anti androgen deprivation therapy by modulating estrogen receptors in the breast

78
Q

Enzymes dependent on THIAMINE as cofactor

A
  • pyruvate dehydrogenase: pyruvate to Acetyl-CoA
  • alpha-ketoglutarate dehydrogenase complex: alpha-ketoglutarate to Succinyl CoA
  • transketolase: pentose phosphate pathway
79
Q

Finasteride - MOA, uses

A

Anti-androgen drug

  • inhibits 5-alpha reductase: decreases conversion of testosterone to DHT
  • treatment for BPH and androgenetic alopecia
80
Q

Enzymes that require biotin as a cofactor

A

Carboxylase enzymes
- Biotin acts as a CO2 carrier on the surface of carboxylase enzymes
- acetyl Co-A carboxylase: acetyl CoA to malonlyl CoA
- pyruvate carboxylase: pyruvate to OAA in gluconeogenesis
- propionyl carboxylase
- beta-methylcrontonyl CoA carboxylase
Biotin deficiencies are seen in excessive ingestion of avidin (raw egg whites)

81
Q

Molecules that signal through G-protein

A

TSH, glucagon and PTH

82
Q

Human insulins without any amino acid modifications

A
  • Regular insulin

- NPH

83
Q

Smooth ER

A
  • contains enzymes for steroid and phospholipid synthesis -

- all STEROID PRODUCING cells have highly developed smooth ER

84
Q

Rough ER:

A
  • site of synthesis for secretory, lysosomal and integral membrane proteins

UWorld Facts (12 decks)

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