3/25 - UW 23

Question 1

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

Answer 1

Thalamic VPL and VPM nuclei

Question 2

How big are lacunar infarcts?

Answer 2

Small, approx 5mm

Question 3

What are two primary causes of lacunar infarcts?

Answer 3

Lipohyalinosis and Microatheromas

Question 4

Oligodendrocyte apoptosis is characteristic of what pathology?

Answer 4

MS

Question 5

What is the gross appearance of MS lesions?

Answer 5

Pink patches in white matter tracts, NOT cavities

Question 6

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

Answer 6

Liver

Question 7

What are the primary routes of HCV transmission?

Answer 7

Inoculation or Blood transfusions (not so much sexual)

Question 8

Where is the IF-B12 complex absorbed?

Answer 8

Terminal ileum

Question 9

How do OCP prevent pregnancy?

Answer 9

Suppression of FSH and LH secretion from anterior pituitary

Question 10

What enzyme converts heme to biliverdin?

Answer 10

Heme oxygenase

Question 11

How is bilirubin transported to the liver?

Answer 11

Bound to albumin

Question 12

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

Answer 12

By UGT (UDP glucuronyl transferase) in the liver

Question 13

In what disease is UGT deficient in the liver?

Answer 13

Crigler-Najjar

Question 14

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

Answer 14

Decrease, shifting curve to the right

Question 15

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

Answer 15

HbF

Question 16

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

Answer 16

Increase, due to decreased estrogen inhibition

Question 17

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

Answer 17

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

Question 18

What are the major risk factors for esophageal adenocarcinoma?

Answer 18

Barrett’s esophagus, GERD, obesity, tobacco

Question 19

Why would mannitol cause pulmonary edema?

Answer 19

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

Question 20

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

Answer 20

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

Question 21

When would you see coagulative necrosis?

Answer 21

After ischemic injury, except in the brain

Question 22

When and where do you see liquefactive necrosis?

Answer 22

Focal bacterial infx (with leukocyte involvement) and CNS infarcts

Question 23

When do you see fat necrosis?

Answer 23

Acute pancreatitis, due to lipase release.

Question 24

With what type of necrosis can you see saponification?

Answer 24

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

Question 25

When do you see caseous necrosis?

Answer 25

Tuberculous infx

Question 26

Increased bleeding time with no other abnormalities suggests what disease?

Answer 26

von Willebrand's disease

Question 27

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

Answer 27

vWF, from endothelial cells

Question 28

Association: DDAVP in bleeding problem...disease??

Answer 28

von Willebrand's disease or hemophilia A

Question 29

What clotting factor does vWF help to stabilize?

Answer 29

Factor VIII

Question 30

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

Answer 30

Surfactant

Question 31

What is alveolar atelectasis?

Answer 31

Collapse

Question 32

HTN with low renin suggests what pathology?

Answer 32

Hyperaldosteronism

Question 33

What electrolyte abnormalities are seen in hyperaldosteronism?

Answer 33

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

Question 34

Why don't you see hypernatremia in hyperaldosteronism?

Answer 34

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

Question 35

What cranial pathology is often seen in ADPKD?

Answer 35

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

Question 36

Why would you see neck stiffness in Subarachnoid Hemorrhage?

Answer 36

Blood in the subarachnoid space is irritating to the meninges

Question 37

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

Answer 37

Ventricular failure (cardiogenic shock)

Question 38

What is the order of prevalence of atherosclerosis in arteries?

Answer 38

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

Question 39

How does ANP lower BP?

Answer 39

Peripheral vasodilation, natriuresis, diuresis

Question 40

What is ANP's action in the kidney?

Answer 40

Dilates afferent arterioles Limits proximal tubule Na reabsorption Inhibits Renin secretion

Question 41

What is ANP's action in the adrenals?

Answer 41

Restricts aldosterone secretion

Question 42

What is ANP's action in the blood vessels?

Answer 42

Arteriolar and venular vasodilation

Question 43

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

Answer 43

In the liver by 25-hydroxylase. | Calcidiol

Question 44

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

Answer 44

In the kidney by a1-hydroxylase

Question 45

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

Answer 45

Sarcoidosis