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Review / Wrong Answers > 5/30 UWorld > Flashcards

5/30 UWorld Flashcards

1
Q

What is the presentation of secondary adrenal insufficiency

A

o Lack of cortisol due to decreased ACTH = weakness, fatigue, weight loss

o Aldosterone synthesis is preserved (controlled by RAAS) à no hypotension or hyperkalemia

o ACTH low = no hyperpigmentation

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2
Q

What is the most common cause of tertiary adrenal insufficiency

A

Usually caused by abrupt withdrawal of exogenous steroids after chronic usage

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3
Q

Describe steps of Gq pathway

A

Binding/activation of Gq = activation of phospholipase C (which stimulates hydrolysis of membrane-bound phospholipids) = PLC releases IP3 and DAG = IP3 liberates intracellular Ca2+ and DAG activates protein kinase C = ultimately leads to smooth muscle contraction

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4
Q

Describe steps of Gs pathway

A

Binding/activation of Gs = activation of adenylate cyclase = adenylate cyclase cleaves ATP to form cAMP = cAMP activates protein kinase A

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5
Q

What are the positive serum markers in neuroblastoma

A

Bombesin and NSE (+)

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6
Q

Differentiate Cushing disease vs. Cushing syndrome

A

Cushing syndrome = increased cortisol

Cushing disease = increased cortisol secondary to ACTH-secreting pituitary adenoma

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7
Q

What is Addison disease

A

Primary adrenal insufficiency due to autoimmune destruction of the adrenal gland

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8
Q

What is Jod-Basedow phenomenon

A
  • Iodine-induced hyperthyroidism
  • Due to a patient with iodine deficiency and partially autonomous thyroid nodule being repleted of iodine
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9
Q

What is Riedel thyroiditis and its presentation

A
  • Thyroid replaced by fibrous tissue
  • Fibrosis may extend to local structures, mimicking anaplastic carcinoma
  • Presentation:
    • Euthyroid or hypothyroid
    • Fixed, hard (rock-like), painless goiter
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10
Q

What are the 2 main types of chronic complications in diabetes

A
  • Nonenzymatic glycosylation (leads to leaky vessels)
    • Small vessel disease
      • Retinopathy
      • Nephropathy
    • Large vessel disease
      • Atherosclerosis, CAD, MI
      • Gangrene
  • Osmotic damage
    • Recall:
      • Glucose -> (aldose reductase) -> sorbitol -> (sorbitol dehydrogenase) -> fructose
    • Sorbitol accumulation in organs with aldose reductase and decreased or absent sorbitol dehydrogenase
    • Sorbitol is an osmol that increases osmotic pressure causing:
      • Neuropathy (glove and stocking)
      • Cataracts
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11
Q

What is the cause/presentation of pseudohypoparathyroidism?

A
  • Due to end organ resistance to PTH due to defect in the PTH receptor
  • Present with:
    • Hypocalcemia
    • Hyperphosphatemia
    • Elevated PTH
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12
Q

What is Albright hereditary osteodystrophy?

A
  • Pseudohypoparathyroidism type 1a (Albright hereditary osteodystrophy)
    • Unresponsiveness of kidney to PTH à hypocalcemia despite elevated PTH
    • Characterized by short stature, short metacarpal, and short metatarsals
    • Autosomal dominant disorder
    • Due to defective Cs protein a-subunit, causing end-organ resistance to PTH
    • Defect must be inherited by mother due to imprinting
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13
Q

Cause and presentation of primary hyperparathyroidism

A
  • Due to parathyroid adenoma or hyperplasia
  • Presentation:
    • THINK: Stones, thrones, bones, groans, psychiatric overtones
      • Hypercalcemia, increased PTH
      • Renal stones
      • Polyuria (thrones)
      • Osteitis fibrosa cystica (cystic bone spaces filled with brown fibrous tissue)
      • Weakness and constipation (groans)
      • Depression (psychiatric overtones)
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14
Q

Pathogenesis and presentation of familial hypocalciuric hypercalcemia

A
  • Due to defective G-coupled Ca2+ sensing receptors (e.g. parathyroids, kidney)
  • Higher levels of Ca2+ are needed in order to suppress PTH
  • Causes excessive renal Ca2+ reuptake, leading to mild hypercalcemia and hypocalciuria with normal to increased PTH levels
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15
Q

What are neurophysins and what might a mutation cause?

A
  • Neurophysin = carrier protein for oxytocin and vasopressin from hypothalamus to posterior pituitary
  • Mutation in neurophysin can lead to defective transport of vasopressin = Central diabetes insipidus
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16
Q

What is pituitary apoplexy (cause, treatment)

A
  • Acute hemorrhage into the pituitary gland
  • Occurs most often in patients with preexisting pituitary adenoma
  • Cardiac collapse caused by ACTH deficiency and subsequent adrenocortical insufficiency
    • Treatment – Medical emergency
      • Glucocorticoid replacement (to prevent life-threatening hypotension)
      • Surgical decompression
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17
Q

What is pseudopseudohypoparathyroidism?

A

Physical exam features of Albright hereditary osteodystrophy but without end-organ PTH resistance (PTH levels normal)

Occurs when defective Cs protein a-subunit is inherited from father

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18
Q

What type of collagen makes up mature scar tissue?

A

Type I

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19
Q

What type of collagen makes up granulation tissue

A

Type III

20
Q

What is the triad of symptoms associated with cardiac tamponade

A

Beck triad: hypotension, increased venous pressure (JVD), distant heart sounds

21
Q

What is one of the more severe consequences of homocysteinuria

A

Increased risk of thrombotic events

22
Q

What is the mutation in Marfan syndrome

A

o Autosomal dominant mutation in fibrillin gene (FBN1) which codes for a protein responsible for the production and maintenance of elastin fibers

23
Q

Describe the steps that occur due to carotid sinus massage

A
  • Causes increased stretch of carotid baroreceptor in order to simulate increased BP = increased afferent firing from the carotid sinus = increased efferent parasympathetic firing = slowed conduction though the AV node = prolonged AV refractory period = slowed HR
24
Q

Why does Verapamil not have any significant effect on skeletal muscle?

A

Unlike cardiac muscle, skeletal muscle does not rely on influx of Ca2+ to stimulate extra calcium release

25
Q

What coronary artery supplies inferior heart

A
  • Posterior descending/interventricular artery arising from RCA
    • Supplies the posterior 1/3 of interventricular septum and most inferior wall of LV
26
Q

Which vasculitides are associated with granulomas?

A

Giant cell (large-vessel)

Takayasu (large-vessel)

Granulomatosis with polyangiits (small-vessel)

Churg-Strauss (small-vessel)

27
Q

What is the most frequent mechanism of sudden cardiac death in the first 48 hours after an acute MI

A

Ventricular fibrillation related to electrical instability in the ischemic myocardium

28
Q

What CV abnormalities are associated with tuberous sclerosis

A
  • Valvular obstruction due to cardiac rhabdomyomas
29
Q

What CV abnormalities are seen in Marfan?

A
  • Aortic insufficiency due to abnormal aortic valve (e.g. aortic dissection and aneurysm)
30
Q
A
31
Q

What is Werdnig-Hoffman disease

A
  • Damage to anterior motor horn secondary to inherited autosomal recessive disease
  • LMN lesion – flaccid paralysis with SYMMETRIC weakness
  • Floppy baby
32
Q

What does the term “shunting” mean

A

Low ventilation and high perfusion (i.e. wasted perfusion)

Blood that is not being oxygenated

33
Q

What is the V/Q ratio at the apex and the base of the lung

A
  • Zone 1 = apex
    • High V/Q (> 1)
      • Low perfusion (gravity pulls down)
      • Wasted ventilation (physiologic dead space)
  • Zone 3 = base
    • Low V/Q (< 1)
      • High perfusion (gravity pulls down)
      • Wasted perfusion (shunting)
34
Q

What happens to V/Q during airway obstruction

A
  • V/Q = 0
    • This is when there is low ventilation and high perfusion
35
Q

What happens to V/Q during blood flow obstruction

A
  • V/Q = infinity
    • This is when there is high ventilation and low perfusion
36
Q

In which V/Q mismatch will giving 100% O2 improve paO2

A

In blood flow obstruction (V/Q = infinity)

100% O2 will not improve paO2 in airway obstruction

37
Q

What are the ways in which CO2 can be transported from tissues to lungs

A
  • CO2 is transported from tissue to lungs in 3 ways:
    • (1) HCO3- (via carbonic anhydrase)
      • 90% of CO2 travels in this form
    • (2) Carbaminohemoglobin – CO2 bound to Hb and N terminus of globin (not heme)
      • CO2 binding favors taut form (O2 unloaded)
    • (3) Dissolved in blood
38
Q

Describe how the body compensates for high altitude, including chagnes in ventilation, renal function, cellular changes, and Hb binding

A
  • Increase in ventilation, thus blowing off CO2
  • Increase in erythropoietin production = increase hematocrit and Hb
  • Increase in 2,3-BPG = increased O2 unloading
  • Cellular changes = increased mitochondria = increased O2 efficiency
  • Increase renal excretion of bicarb to compensate for respiratory alkalosis
39
Q

Describe the presentation of acute mountain sickness

A
  • Headache, fatigue, cerebral edema, pulmonary edema
40
Q

Describe the physiologic changes that occur with chronic mountain sickness

A
  • Increased RBC mass and hematocrit
  • Increased blood viscosity and decreased tissue blood flow
  • Elevated pulmonary artery pressure – due to hypoxic pulmonary vasoconstriction
  • Right-sided heart enlargement
  • Peripheral artery pressure falls
  • Congestive heart failure
41
Q

Treatment for altitude sickness

A
  • Acetazolamide
42
Q

What is the mechanism behind cerebral edema and pulmonary edema due to acute mountain sickness

A
  • Cerebral edema due to hypoxia-induced vasodilation
  • Pulmonary edema due to hypoxia-induced local vasoconstriction
43
Q

Describe the pathogenesis behind decompression sickness

A
  • At deep pressures, nitrogen dissolves in blood
  • As you ascend, nitrogen escapes dissolved state and forms bubbles that can occlude blood vessels
44
Q

Presentation of “the bends” aka decompression sickness

A
  • Pain in joints and muscles of arms and legs
  • Neurologic problems (dizziness, paralysis, syncope)
  • “Chokes” (SOB, pulmonary edema, death)
45
Q

Treatment of decompression sickness

A

Hyperbaric therapy = High pressure room that will re-dissolve the nitrogen in blood

Review / Wrong Answers (140 decks)

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