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3/25 - UW 23 Flashcards

1
Q

Lesion in what part of the brain would lead to a complete contralateral sensory loss?

A

Thalamic VPL and VPM nuclei

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2
Q

How big are lacunar infarcts?

A

Small, approx 5mm

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3
Q

What are two primary causes of lacunar infarcts?

A

Lipohyalinosis and Microatheromas

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4
Q

Oligodendrocyte apoptosis is characteristic of what pathology?

A

MS

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5
Q

What is the gross appearance of MS lesions?

A

Pink patches in white matter tracts, NOT cavities

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6
Q

In what organ does Renin act to convert Angiotensinogen to Angiotensin I?

A

Liver

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7
Q

What are the primary routes of HCV transmission?

A

Inoculation or Blood transfusions (not so much sexual)

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8
Q

Where is the IF-B12 complex absorbed?

A

Terminal ileum

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9
Q

How do OCP prevent pregnancy?

A

Suppression of FSH and LH secretion from anterior pituitary

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10
Q

What enzyme converts heme to biliverdin?

A

Heme oxygenase

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11
Q

How is bilirubin transported to the liver?

A

Bound to albumin

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12
Q

How is bilirubin (unconjugated) converted to bilirubin glucuronide (conjugated)?

A

By UGT (UDP glucuronyl transferase) in the liver

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13
Q

In what disease is UGT deficient in the liver?

A

Crigler-Najjar

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14
Q

What is the effect of 2,3-BPG on Hgb oxygen affinity?

A

Decrease, shifting curve to the right

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15
Q

What type of Hgb doesn’t bind to 2,3-BPG?

A

HbF

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16
Q

What kind of change in FSH levels are seen in menopause?

A

Increase, due to decreased estrogen inhibition

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17
Q

What are the major risk factors for esophageal squamous cell carcinoma?

A

Alcohol, tobacco, foods with N-nitroso compounds (e.g. betel nuts…?)

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18
Q

What are the major risk factors for esophageal adenocarcinoma?

A

Barrett’s esophagus, GERD, obesity, tobacco

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19
Q

Why would mannitol cause pulmonary edema?

A

Because it increases intravascular and intratubular volume. Increased IV volume increases hydrostatic pressure, which may leak into the lungs. I guess.

20
Q

Aside from pulmonary edema, what are some other risks of mannitol over-treatment?

A

Interstitial volume depletion and hypernatremia, Plasma volume expansion and hyponatremia with metabolic acidosis and hyperkalemia

21
Q

When would you see coagulative necrosis?

A

After ischemic injury, except in the brain

22
Q

When and where do you see liquefactive necrosis?

A

Focal bacterial infx (with leukocyte involvement) and CNS infarcts

23
Q

When do you see fat necrosis?

A

Acute pancreatitis, due to lipase release.

24
Q

With what type of necrosis can you see saponification?

A

Fat necrosis, when lipase-digested fatty acids combine with calcium. In acute pancreatitis

25
Q

When do you see caseous necrosis?

A

Tuberculous infx

26
Q

Increased bleeding time with no other abnormalities suggests what disease?

A

von Willebrand’s disease

27
Q

What clotting factor does DDAVP increase the production of? From where?

A

vWF, from endothelial cells

28
Q

Association: DDAVP in bleeding problem…disease??

A

von Willebrand’s disease or hemophilia A

29
Q

What clotting factor does vWF help to stabilize?

A

Factor VIII

30
Q

What is contained in the lamellar bodies of type II pneumocytes?

A

Surfactant

31
Q

What is alveolar atelectasis?

A

Collapse

32
Q

HTN with low renin suggests what pathology?

A

Hyperaldosteronism

33
Q

What electrolyte abnormalities are seen in hyperaldosteronism?

A

HypoK and metabolic alkalosis (due to loss of K and H from increased reabsorption of Na).

34
Q

Why don’t you see hypernatremia in hyperaldosteronism?

A

Because of “aldosterone escape” wherein the increased Na and fluid retention causes a compensatory rise in ANP and hydrostatic natriuresis.

35
Q

What cranial pathology is often seen in ADPKD?

A

Berry aneurysms in the Circle of Willis that can rupture, producing subarachnoid hemorrhages

36
Q

Why would you see neck stiffness in Subarachnoid Hemorrhage?

A

Blood in the subarachnoid space is irritating to the meninges

37
Q

What is the most common cause of post-MI hospital death?

A

Ventricular failure (cardiogenic shock)

38
Q

What is the order of prevalence of atherosclerosis in arteries?

A
  1. Abdominal aorta
  2. Coronary arteries
  3. Popliteal
  4. Internal carotid (carotid sinus)
  5. Circle of Willis
39
Q

How does ANP lower BP?

A

Peripheral vasodilation, natriuresis, diuresis

40
Q

What is ANP’s action in the kidney?

A

Dilates afferent arterioles
Limits proximal tubule Na reabsorption
Inhibits Renin secretion

41
Q

What is ANP’s action in the adrenals?

A

Restricts aldosterone secretion

42
Q

What is ANP’s action in the blood vessels?

A

Arteriolar and venular vasodilation

43
Q

Where does the conversion of vit D to 25(OH)D take place? What enzyme? What is another name for 25(OH)D?

A

In the liver by 25-hydroxylase.

Calcidiol

44
Q

Where does the conversion of 25(OH)D to 1,25(OH)2D take place? What enzyme?

A

In the kidney by a1-hydroxylase

45
Q

In what disease do you see hyperCa secondary to high serum calcitriol?

A

Sarcoidosis

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