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Question 1

Nicardipine vs nifedipine?

Answer 1

They both have marked coronary and peripheral dilatation without AV or SA conduction depression

But nicardipine has minimal effect on cardiac muscle where nifedipine causes moderate depression of the cardiac muscles

Question 2

esmolol

A. metabolism/half life/pharm
B. dosing
C. indications

Answer 2

A. blood borne esterases/9-10 minutes/cardioselective
B. 0.5mg/kg or infusion for HTN
SVT - 500ug/kg -> 50ug/kg/min x4 mins
if not controlled repeat loading dose then 100ug/kg/min for 4 minutes
repeat up to 200-300ug/kg/min
~if longer acting agent needed, use metoprolol

Question 3

RF for steroids induced perianal itching

Answer 3

Female and young age, and with bouls dose.

The mechanism is unknown though it may be related to phosphate ester in chemical structure.

Fentanyl been used to decrease the incidence.

Question 4

Max dose of vancomycin to prevent red man syndrome is

Answer 4

10 mg/min

The reaction (hypotension, Tachy, generalized pruritus, and red rash) related to non-immune mediated histamine release and related to the fast administration of a large molecular drug.

Question 5

Other common anesthetic drug then steroids that causes genital burning and itching?

Answer 5

Fospropofol

It’s a prodrug of propfol in phosphate ester form (which though the cause of itchiness)

Question 6

How histamine H2 receptors antagonists reduces the severity and risk or perioperative aspiration pneumonia?

Answer 6

They block histamine from inducing acidic gastric fluid secretion by partial cells which effectively raises gastric pH and therefore decrease risk of aspiration pnumonitis.

Question 7

Onset of action and duration for H2 blockers

Answer 7

Onset. Duration

Cimetidine. 1-1.5 3-4

Ranitidine. 1 9-10

Famotidine. 1 10-12

In hours. So Ranitidine has longer elimination half life then cimetidine, faster onset, and it is more potent with fewer CV and CNS side effects.

Famotidine has longer half life then both.

Question 8

The triad of cyanide toxicity are …

Answer 8

• Elevated PVO2
• Tachyphylaxis to sodium nitroprusside
• metabolic acidosis

Question 9

Antidote for cyanide poison

Answer 9

Amyl nitrate

Converts Hb to MetHb which binds to cyanide and converting it to nontoxic cyanomethemoglobin

Question 10

Anti thrombotic 2 classes are

Answer 10

Anti platelets (prevent platelet activation/aggregation)

Anticoagulants (reduce fibrin formation)

Question 11

Anti platelets (which they prevent platelet activation/aggregation) are …

Answer 11

Anti platelets (prevent platelet activation/aggregation)

• ASA (irreversibly inhibit cyclooxygenase)
• ADP receptor inhibitors (clopidogrel, prasugrel, ticlopidine, ticagrelor)
• phosphodiestrase inhibitors (cilostazol)
• G2b-3a inhibitors (abciximab, eptifibatide, tirofiban)

Question 12

Anticoagulants (which they reduce fibrin formation) are …

Answer 12

Anticoagulants (reduce fibrin formation)

• AT3 inhibitors (heparin, LMWH)
• heparin-like factor 10 inhibitors (fondaprinux)
• direct factor 10 inhibitors (rivaroxaban,apixaban)
• direct thrombin inhibitors (bivalirudin, hirudin, argatroban, dabigatran)
• Vit K antagonist (warfarin)

Question 13

Diuretics that causes hyperchloremic metabolic acidosis?

Answer 13

Acetazolamide and K-sparing

There is no Diuretics that causes hypo-chloremic

Question 14

Diuretics that causes hypochloremic metabolic acidosis ?

Answer 14

Loop + Thiazides

Contraction alkalosis occur due to a decrease in the extracellular volume around a constant extracellular HCO3. This combined with increased urinary H+ loss result into alkalosis

Question 15

In Rx acute hyperkalemia, what are the driving K intercellular choices?

Answer 15

B-agonists
Insulin+D50
Bicarbonate
Hyperventilation (decreasing plasma CO2 leads to left shift of bicarb buffer system which lowers extracellular H+ and therefore shifts K into cell to maintain electrical neutrality).

Question 16

Enzyme polymorphism and its associated anesthetic medication effect

CYP(2D6)
CYP(3A4)
MC1R

CYP(C19)
CYP(2C9)

Answer 16

(2D6) -> codeine, BB, anti arrhythmic, diltiqzem, tramadol

(3A4) -> most anesthetics, lidocaine, precedex

MC1R -> associated with red hair, leads to increase analgesia

(C19) -> PPI, antidepressants
(2C9) -> phenytoin, warfarin, ibuprofen

Question 17

At what plasma levels of Mg causes ECG changes? What they are?

Answer 17

6-12 mgdL

Par prolongation + wide QRS (these changes occur before loss of deep tendon reflexes)

Question 18

Associated with pain on injection?

Answer 18

Diazepam (not versed)
Etomidate
Methohexital 
Propfol
Rocuronium

The mechanism is not entirely clear but studies point towards increase pain scale with; rapid injection, increase similar concentration of agent, or agents with either very high or low pH (propofol is thought due to release of bradykinin and not due to pH)

Question 19

Chemistry derangements with thiazides

Answer 19

Hypo K, Mg, Na

Hyper Ca, urecemia, glycemia,

Increased TG, cholesterol, LDL production

Question 20

MoA of

Thiazides

Furosemide

Spironolactone

Answer 20

Blocks Na/Cl at DCT

Blocks Na/K/Cl in loop of henle

Blocks aldo receptors in DCT

Question 21

Large amount of licorice (عرق السوس) induces hyper aldosterone like effect through…

Answer 21

Inhibiting 11-beta-hydroxysteroid dehydrogenase which an enzyme converts cortisol to cortisone. Therefore large amount of cortisone act like aldosterone causing all symptoms of Conn syndrome.

Question 22

Mydriatic drug that can cause anticholinergic toxicity?

Answer 22

Cyclopentolate

It’s used for ocular procedures and systemic absorption can cause (dysarthria, Tachy, disorientation, psychotic rxn, and convulsion)

It’s more common with use of 2% solution then 1% mixture

Question 23

Drug used in treatment of glaucoma that can cause sever bronchospasm and bradycardia if systemic absorption occurs?

And other glaucoma treatment drug that can prolong Succinylcholine activity?

Answer 23

Timolol (nonselective BB)

Echothiophate (inhibits plasma butyrylcholinesterase which is called paudocholinesterase, the enzyme responsible for succinylcholine metabolism)

Question 24

When to consider metoclopramide to prevent PONV or aspiration risk? And what’s its contraindication to use?

Answer 24

Diabetic patients undergoing outpatient procedures

First trimester in urgent situations (it counteract the effect of pregnancy progesterone mediated relaxation of LES)

Trauma patients

CI in bowel obstruction

Question 25

Metoclopramide is a

Dopamine….

Seretonin …. at higher doses

Cholinergic … which enhances response of … in GI tissue

Answer 25

Dopamine antagonist

Seretonin antagonist

Cholenergic Agonist, enhances response to ACho (results in accelerated gastric emptying, decrease gastric fluid volume, increases LES tone, increase gastric contraction, and enhances peristalsis in duodenum and jejunum)

It has no effect on gastric pH

Question 26

Glucagon MoA

Answer 26

Increases intracellular cAMP which results in increased intropy and chronotropy

Useful in treatment of BB toxicity because it dose not utilize alpha or beta adrenergic receptors

Question 27

Medications/drug class causes hyperkalemia

Answer 27

Digitalis	
Heparin 	 
Mannitol 
Nonselective β-antagonists
Pentamidine 	 
NSAIDs
Succinylcholine 	
Potassium-sparing diuretics
Triamterene 	 
Trimethoprim

Question 28

LMWH exerts its anticoagulation effect by inactivation of …

The …. is the best test to document the adequacy of anticoagulation with LMWH.

Answer 28

inactivation of factor Xa.

anti-Xa assay

Question 29

St. John’s wort is an herbal medication that is taken by patients to treat depression. St. John’s wort induces P540 …

Answer 29

P450 3A4. This induction causes many anesthetic-related drugs to be metabolized including alfentanil and midazolam.

Question 30

Name the four potassium sparing diuretics? their MoA?

Answer 30

Amiloride, triamterene, spironolactone, and eplerenone.

They work by blocking sodium reabsorption in the cortical collecting tubule and simultaneously increasing potassium reabsorption.

Question 31

How mannitol can exert a renal protective effect?

Answer 31

Mannitol draws fluid into the renal tubule, which allows for continued patency and flushing of debris from the tubule. Accordingly, mannitol can exert a renal protective effect. In addition, mannitol transiently creates an osmotic gradient within the vasculature and can maintain circulating plasma volume and renal perfusion via this effect, further eliciting protective properties.

Question 32

What is the contraindication for mannitol? whats alternative?

Answer 32

Mannitol is relatively contraindicated in patients with congestive heart failure (CHF) due to an initial increase in intravascular volume. Furosemide is the drug of choice when diuresis is recommended in this class of patients.

Question 33

Difference mechanism of diuresis between Mannitol and ANP?

Answer 33

(ANP) induces diuresis via natriuresis,

Mannitol induces diuresis; not via an osmotic effect.

Question 34

Medications that use cGMP as a second messenger

Answer 34

nitroglycerin, sodium nitroprusside, nitric oxide, and sildenafil.

Question 35

Insulin and glucagon receptors use … as a second messenger

Answer 35

cAMP

Question 36

NMDA receptor antagonists include, but are not limited to,

Answer 36

dextromethorphan, ketamine, memantine, methadone, nitrous oxide, and tramadol.

Question 37

The NMDA receptor is an inotropic glutamate receptor that functions as a nonspecific ion channel when activated. Activation only occurs when … is bound to the receptor AND the cell is depolarized. The receptor’s effects are primarily mediated via increased intracellular …

Answer 37

glutamate and glycine

calcium

Question 38

Antihistamine vs Antiacids vs PPI in their onset when given to decrease aspiration risk?

Answer 38

Cimetidine, ranitidine, and famotidine are common H2 blockers that are used to increase gastric pH. Additionally, they can reduce gastric volumes (except for ranitidine). When given orally these medications have an onset of action of approximately 1 hour. The pH raising effects of ranitidine are longer than those of cimetidine. Ranitidine lasts for 9 hours following administration. Intravenous cimetidine and famotidine typically work in under 30 minutes, but are not faster than oral antacid medications. Ranitidine in particular has an approximately 1 hour onset time for both IV and PO administration.

Antacids have a near immediate onset taking effect within 15-30 minutes of oral administration. Antacids work by neutralizing acid in the stomach. However, antacids may increase gastric volume and slow gastric emptying.

Proton pump inhibitors take 2-4 hours to initial effect when administered orally. Peak response may take up to 5 days. Proton pump inhibitors (PPI) act by binding to hydrogen potassium pumps. PPIs cause a permanent inhibition of proton pumps. Synthesis of new pumps takes about 24 hours, which explains the duration of action of PPI medications.

Question 39

Amiodarone’s primary effect is … and itd clinical use for …

Answer 39

blockade of potassium channels. It also blocks calcium and sodium channels to a lesser effect as well as α- and β-adrenergic receptors.

refractory ventricular arrhythmias, sustained SVT with accessory pathway conduction, and atrial fibrillation/flutter/tachycardia with congestive heart failure (CHF). Recall that amiodarone is still the antiarrhythmic agent of choice in the setting of CHF or low ejection fraction.

Question 40

The most common SE of Amiodarone?

Answer 40

bradycardia and hypotension, which occur in approximately 5 to 10% of the population. Risk factors include age >60 and higher dose therapy.

Others; hypothyroidism (20% of patients), life-threatening hyperthyroid storm, pulmonary toxicity (with a pulmonary fibrosis appearance), prolonged QT, and elevated liver function tests (LFTs). Pulmonary toxicity is one of the most lethal side effects of amiodarone therapy. It is dependent on cumulative dosage and may appear up to 45 days following discontinuation of the drug.