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USMLE Step 1 Systems > Endocrine > Flashcards

Endocrine Flashcards

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1
Q

Causes of elevated CK

A

Hypothyroidism
Polymyositis, Dermatomyositis
Muscular dystrophies
Statins

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2
Q

What type of insulin given to those with DKA?

A

Regular insulin.

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3
Q

What mediates insulin resistance in overweight/obese individuals?

A

Serum FFA and TAG

FFA increase resistance by serine phosphorylation of insulin receptor and decrease insulin secretion.

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4
Q

Treatment of congenital adrenal hyperplasia.

A

Exogenous corticosteroids to suppress ACTH.

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5
Q

Central (complete vs. partial) vs. Peripheral DI

A

Central: > 10% rise in urine osmolality after vasopressin
Complete: > 50%

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6
Q

What is used to treat graves opthalmopathy and how?

A

Glucorticoids (PTU and methimazole do NOT help)

Opthalmopathy develops bc of edema and infiltration of lymphocytes -> stimulate retroorbital fibroblasts to secrete cytokines and produce glycosaminoglycans -> inflam and accum of glycosaminoglycans -> proptosis.

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7
Q

How to prevent absorption of radioactive iodide isotopes?

A

Administer Potassium Iodide - competitive inhibitor of the Na-iodide symporter.

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8
Q

What glucose transporter is responsive to insulin and where is it located?

A

GLUT4 - on skeletal muscle and adipocytes

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9
Q

How do glucocorticoids affect the liver vs. muscle/adipose tissue?

A

Liver - increase gluconeogenesis and glycogenesis.

Muscle/Adipose - antagonize insulin effects - proteolysis and lipolysis. to provide substrates for making glucose.

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10
Q

Central DI - caused by damage to what?

A

Paraventricular and Supraoptic nuclei of the Hypothalamus

(Post pituitary injuries don’t result in permanent central DI since the hypothalamic neurons will hypertrophy to compensate)

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11
Q

What causes the increased risk of gallstones in pregnant women or those on OCPs?

A
  1. Estrogen induced cholesterol hypersecretion - increases HMG CoA reductase
  2. Progesterone induced gallbladder hypomotility
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12
Q

MOA of acarbose

A

alpha-glucosidase inhibitors - decrease activity of dissacharidases on intestinal brush border.

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13
Q

What hormones are Gs?

A

Glucagon
TSH
PTH

cAMP -> protein kinase a.

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14
Q

What paraneoplastic syndrome is associated with neuroblastoma?

A

Opsoclonus-Myoclonus.

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15
Q

TNFalpha facilitates insulin resistance thru what mechanism?

A

Phosphorylation of serine residues.

This inhibits IRS-1 (insulin receptor substrate) tyrosine phosphorylation by insulin.

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16
Q

Histology of Hashimoto’s thyroiditis?

A

Mononuclear parenchymal infiltration with well-developed germinal center

“looks like a lymph node”

17
Q

Electrolyte abnormalities in primary adrenal insufficiency?

A

HypoNa
HyperK
HyperCl
Non anion gap metabolic acidosis

(think like the aldo antagonist diuretics)

18
Q

In a patient on chronic glucocorticoids presenting with adrenal crisis s/p surgery, what are pt’s levels of CRH, ACTH, and cortisol?

A

Decreased CRH, ACTH, and cortisol!

19
Q

Thyroid hormone receptor is located where?

A

Nucleus!

20
Q

What should diabetics be advised to do to protect against peripheral neuropathy?

A

DAILY foot inspection
(changing socks, snug shoes, testing water first, etc)

YEARLY neurologic evaluation by physician.

21
Q 
How are the following altered in DKA? 
Na
K 
pH
urine HCO3 
urine H2PO4
A

Hyponatremic:

  • osmotic activity of glucose -> Na drops 1.6 mEq/L for every 100 mg/dL rise in glucose
  • hyperglycemia induced osmotic diuresis -> Na and free water losses

HyperK:

  • K/H exchanger
  • but total body K loss

Metabolic Acidosis: Dec. pH

Urine:
Decreased HCO3 = reabsorbed

Increased H2PO4, NH4+: increased secretion of acid buffers (due to H+ secretion from the kidneys)

Hyperglycemia, Hypovolemic

Hyperammonemia: due to muscle degradation.

22
Q

Which antidiabetic drug increases GLUT4 transport to adipocytes?

A

Glitazones

activate PPARalpha -> increase transcription of insulin responsive genes -> GLUT4 translocation to cell membrane (adipocytes, skeletal muscle)

23
Q

Mech of acarbose

A

alpha-glucosidase inhibitor - inhibit intestinal brush border alpha-glucosidases - dec. postprandial hyperglycemia.

Tox: GI disturbance, hepatotoxic (miglitol)

24
Q

What are the GLP-1 analogs and DPP-4 inhibitors? Mech?

A

GLP1: exenatide, liraglutide
DPP-4 inhibitor: -gliptin (inhibit degradation of GLP1)

Mech: increase insulin, decrease glucagon release (in response to glucose, like physiologic), delay gastric emptying

Tox: (X) No hypoglycemia or weight gain (nl physiology)

  • n/v
  • pancreatitis
  • mild urinary or resp infections
25
Q

During fasting, normoglycemic with higher than normal baseline insulin levels = what?

A

Insulin Resistance - DM II

READ THE FUCKING GRAPHS.

26
Q

Labs in PCOS

A

High LH, LH/FSH ratio

Low to nl FSH - bc FSH is dec. compared to LH, can’t aromatize the testos to estrogen.

27
Q

HOW DOES HYPOTHALAMUS REGULATE PROLACTIN?!

A

Dopamine INHIBITS Prolactin.

Hypothalamic destruction => Hyperprolactin!

28
Q

What is the presentation of Type I DM?

A

Subacute with polyuria, polydipsia, polyphagia with weight loss and fatigue.

Young adult, sometimes recent viral infection will be in picture.

29
Q

Histology of medullary thyroid cancer?

A

Polygonal or spindle shaped cells with extracellular amyloid deposits (stain with congo red)

30
Q

Glucagonoma

A
  1. Diabetes
  2. GI sx
  3. Necrolytic Migratory Erythema: erythematous papules and plaques that coalesce, leaving bronze-colored central indurated area with peripheral blistering/scarring.
31
Q

Hyperthyroidism - what lab needs to be checked before treating?

A

PTU and Methimazole can cause agranulocytosis!!

32
Q

Papillary Thyroid Carcinoma - Histo findings

A

Orphan Annie nuclei (Large cells with finely dispersed chromatin)

Psammoma Bodies

Inclusion bodies and nuclear grooves

33
Q

Medullary Carcinoma Histo

A

Sheets of cells with amyloid stroma.

34
Q

Metyrapone test

A

Blocks 11b-hydroxylase (increases 11 deoxycorticosterone but this doesn’t feedback negatively) -> dec cortisol -> increased ACTH -> increased 11 deoxycorticosterone, 17-OHS (its metabolite) if you have normal HPA axis.

35
Q

Pituitary Apoplexy - presentation, tx.

A

Intrapituitary hemorrhage, most often in an underlying pituitary adenoma. EMERGENCY.

Sx:
Chronic sx of pituitary adenoma (h/a, decreased libido)
Acute severe headache, bitemporal hemianopsia
Signs of meningeal irritation may be seen

Will eventually develop cardio collapse due to ACTH deficiency and glucocorticoid deficiency.

Tx:
Glucocorticoids - prevent cardio collapse
Surgery to decompress.

Note: May have similarities to subarachnoid, but the hx of pit adenoma sx and acute cardiovascular collapse favor pit hemorrhage.

36
Q

Polyuria and Polydipsia - what 3 things should you immediately think of?

A
  1. DM
  2. DI
  3. Psychogenic Polydipsia.
37
Q

Pathophysiology of Graves Proptosis/Opthalmopathy

A

Lymphocytes infiltrate orbital tissue -> secrete cytokines that activate fibroblasts -> secrete increasing amounts of glycosaminoglycans/hyaluronic acid -> draws water into orbit resulting in extraocular muscle edema.

Can result in sensations of grittiness, tearing since the lids don’t cover the eyes fully.

Note: neutrophil infiltration would be in like orbital cellulitis.

USMLE Step 1 Systems (11 decks)

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