PREP Questions

Question 1

List 7 causes of upper GI bleed (melena)

Answer 1

Variceal bleeding
Acute liver failure
Peptic ulcer
Erosive gastritis
Esophagitis
Mallory-Weiss tear
Vascular lesions (angiodysplasia, arterial malformation, Dieulafoy lesion)

Question 2

How is prostaglandin related to ulcers?

Answer 2

Endogenous prostaglandins (prostaglandin E2) increase gastric mucus and bicarb secretion

Question 3

Therapy for upper GI bleed after initial stabilization?

Answer 3

Endoscopy - diagnostic and therapeutic with hemostatic clipping, sclerotherapy, thermal coagulation

Question 4

Mechanism of action of PPI

Answer 4

Blocks H-K-ATPase in stomach
Prodrugs - require gastric acid to activate
Increase the pH which may help with platelet aggregation (good for GI bleed)
May help with H. pylori eradication

H2 blocker less effective than PPI at acid suppression

Question 5

Is NG placement recommended for upper GI bleed?

Answer 5

No: not shown to be helpful for endoscopy, may dislodge clot

Question 6

Should octreotide be used for upper GI bleed?

Answer 6

• Mostly used for GI bleed from portal hypertension (presplanchnic vasoconstriction)
• Role in erosive gastritis or peptic ulcer disease is less clear
• Does inhibit gastrin thereby decreasing gastric acid

Question 7

What is train of four ratio?

Answer 7

Magnitude of muscle contraction on 4th pulse / magnitude on 1st pulse

> 0.6 associated with successful extubation

Question 8

What percentage of acetylcholine receptors are blocked with different responses to train of 4?

Answer 8

4 twitches: <75%
3 twitches: at least 75%
2 twitches: 80%
1 twitch: 90%
0 twitches: 100%

NMB should be adjusted to have at least 1 twitch in response to train of 4 if using long term to avoid weakness

Question 9

What are the three mechanisms of action of antiviral agents?

Answer 9

1. Interferons - synthetic form of native immune system (hepatitis B & C)
2. Neuraminidase inhibitors - neuraminidase is found on viruses, helps it enter host cells (oseltamivir)
3. Nucleotide/phosphate analogues (most currently available antiviral agents)

Question 10

Most common toxicities from antiviral agents?

Answer 10

Renal failure, neutropenia, thrombocytopenia

Occurs when antiviral incorporates into host DNA especially mitochondrial DNA affecting renal and hematologic cell lines; can also be due to disruption of host’s nucleotide triphosphate pool and sometimes from crystal precipitation within renal tubules

Question 11

Cidofovir main toxicity

Answer 11

Nephrotoxicity excreted unchanged in the urine, probenecid and hydration help

Question 12

Interferon side effects

Answer 12

Acute: hypotension, tachycardia, headache, myalgia
Chronic: neurologic changes

Question 13

How fast to lower bp in hypertensive emergency

Answer 13

20-25% in fist hour then to normal in next 24-48 hrs
Nicardipine preferred

Question 14

Nitroprusside toxicity

Answer 14

Can convert hemoglobin to methemoglobin
Cyanide binds to electron transport chain
Thiouyanate toxicity in those with renal dysfunction


Question 15

Explain anion gap

Answer 15

Anion gap = [Na] - ([Cl] + [HCO3])
Results from unmeasured anions (albumin)

Normal = 3-11

Causes of increased gap include lactate and ketones (unmeasured anions)

Question 16

What is strong ion difference (SID)?

Answer 16

Strong ion difference = [Na] + [K] + [Ca] + [Mg] - [Cl]

Much of the charge difference (normally 40) is due to weak acids that are dissociated (phosphate, albumin), denoted A-. Rest of SID is made up of acid/base players:

SID = ([A-] + [HCO3-] + [OH-] + [CO3 2-]) - [H+]
Most are small quantities except HCO3
Decrease in SID means acidosis, increase means alkalosis

So:
[Na] + [K] + [Ca] + [Mg] + [H+] =
[Cl] + [A-] + [HCO3-] + [OH-] + [CO3 2-]
Strong ion changes are balanced by HCO3- and H+
H+ is the only cation that isn’t a strong ion so its concentration can change very quickly

If add lactate (A-) then have to add H+ to balance(?)

Question 17

List fibrinolytic/thrombolytic meds and mechanisms

Answer 17

Most work by activating plasminogen to plasmin (breaks down fibrin):
Tissue-type plasminogen activator (tPA)
Urokinase-type plasminogen activator
Streptokinase

In circulation, tPA has a low affinity for plasminogen - only when bound to fibrin does affinity for plasminogen increase
Streptokinase/urokinase-type plasminogen activator bind plasminogen anywhere, increasing risk of systemic bleeding

Alternatives:
Plasmin and its analogues
Mechanical thrombectomy

Treatment of massive PE: heparin bolus (class I), tPA (class I), surgical thrombectomy (class I), endovascular thrombectomy (class IIa)

Question 18

How does warfarin work?

Answer 18

Vitamin K antagonist, inhibits synthesis of new clotting factors and protein C and S (should initiate with heparin given decrease in C/S first)

Question 19

Does vocal cord dysfunction after cardiac surgery get better?

Answer 19

In one study, 70% recovered vocal cord function on follow-up exam

<1% require tracheostomy