Q-Bank- Pharmacology

Front 1

What are some of the side effects of Corticosteroids?

Back 1

Adrenal suppression, immunosuppression, hypernatremia, hypocalcemia, and water retention.

Front 2

Cefaclor is a cephalosporin with side effects that include the development of what "sickness"?

Back 2

Serum-like sickness.

Front 3

List some of the DMARDs (Disease-modifying antirheumatic drugs). How are they thought to slow the progression of RA (rheumatoid arthritis)? Is there ever additional therapy needed to treat RA?

Back 3

Methotrexate, azathioprine, penicillamine, hydroxychloroquine, and chloroquine, organic gold compounds, and sulfasalazine. These compounds may slow or reverse joint damage, but have a slow onset of action. Because it may take 6-8 weeks for these drugs to begin to have an effect, "bridging therapy" is need with corticosteroids.

Front 4

Describe the EKG of atrial fibrillation. What is the initial medication that someone should be put on in the event that they have this abnormality? What about long term care?

Back 4

The EKG of A-fib shows no P wave and is labeled as irregularly irregular because of its fluctuating R-R intervals. You would put a patient who has atrial fibrillation on Diltiazem initially to stabilize their condition. Long-term care would require Warfarin to prevent adverse effects of clotting.

Front 5

What class of antibiotic is Ciproflaxin? Describe the mechanism of action of this antibiotic.

Back 5

Cipro is a quinolone drug, which includes norofloxacin, and ofloxacin among others. These antibiotics act by inhibiting DNA gyrase which is responsible for the insertion of negative supercoils in bacterial DNA in order to allow the open up of the super coil in DNA replication.

Front 6

Name some antibiotic classes that can work by inhibiting folate synthesis. What types of infections are these drugs used for?

Back 6

Trimethoprim and sulfonamides. These drugs may be used in the treatment of UTIs.

Front 7

Explain the mechanism of action of Tetracyclines. What types of infections are they normally used for?

Back 7

Tetracyclines bind to the 30s ribosomal subunit and prevent attachment of aminoacyl-tRNA. They are usually used for cholera, acne, Lyme disease, and Rickettsia among others.

Front 8

How do Aminoglycosides work? Are they used for run-of-the-mill infections? Why or why not?

Back 8

Aminoglycosides inhibit protein synthesis by preventing initiation complex formation, causing misreading of mRNA. They are used for sever Gram (-) rod infections, but are rarely used in simple cases due to their poor side-effect profile, which includes nephrotoxicity and ototoxicity.

Front 9

What are the two most tested side effects of Aminoglycosides?

Back 9

Nephrotoxicity and ototoxicity.

Front 10

Describe the mechanism of Isoniazide.

Back 10

This antibiotic is specific form the treamtent of mycobacterial infection and works by inhibiting the synthesis of mycolic acid.

Front 11

Which antibiotics work through inhibition of bacterial cell-wall synthesis?

Back 11

Penicillins, Cephalosporins, imipenem/meropenem, aztreonam, vancomycin.

Front 12

Which antibiotics work through inhibition of bacterial protein synthesis?

Back 12

Aminoglycosides, Chloramphenicol, macrolides, tetracyclines, streptogramins, linezolid.

Front 13

Which antibiotics work through inhibition of nucleic acid synthesis?

Back 13

Fluoroquinolines, and rifampin.

Front 14

Which antibiotics work through inhibition of Folic acid synthesis?

Back 14

Sulfonamides, trimethoprim, pyrimethamine.

Front 15

Which equation would you used to calculate steady sate concentrations: Loading dose or maintenance dosing? What are the equations for both?

Back 15

You would use the maintenance dosing equation to figure out the steady state concentration.

Loading dose (LD) = Vd x C(plasma)/ f (bioavailability)

Maintenance dose (MD) = Cl (clearance) x C(steady state)/ f(bioavailability)

Front 16

Lactic acidosis is an adverse side effect that has been associated with what diabetic medication? What population of patients are extremely susceptible to developing this side effect?

Back 16

Metformin is the biguanide oral hypoglycemic agent that carries the possibility of producing the adverse side effect of lactic acidosis. This side effect is more likely to occur in patients with renal insufficiency.

Front 17

What is the main indication for Clonidine? What is its mechanism of action?

Back 17

Clonidine is a centrally acting antihypertensive agent typically used in the TREATMENT of REFRACTORY HTN. Clonidine acts centrally as an Alpha-2 receptor AGONIST

Front 18

Which beta blocking agent has an association with the development of dyslipidemias in patients? What other medication class used to treat heart failure, are known for causing dyslipidemias?

Back 18

Metoprolol is a beta-adrenergic blocking agent that is known to cause dyslipidemias in patients. Thiazide diuretics are also associated with causing hyperlipidemias

Front 19

How does Prazosin work and what effects does it have on serum lipids?

Back 19

Prazosin is a selective alpha-1 blocker, and represents a class of antihypertensives that has a favorable effect on plasm lipids, lowering total cholesterol, reducing triglyceride levels, and mildly raising HDL cholesterol.

Front 20

How can we pharmacologically maintain a patent ductus arteriosus in an infant? How can we induce closure?

Back 20

The patency of a ductus arteriosus can be maintained by prostaglandin E. Alprostadil is prostaglandin E1. NSAIDs such as Indomethacin, will close a PDA.

Front 21

Why would a pregnant mother be given corticosteroids?! What benefit does this provide to the fetus? Provide an example of a corticosteroid that would be given.

Back 21

Glucocorticoids can accelerate pulmonary maturation and stimulate production of surfactant when given to the mother prior to delivery of premature infants. Betamethasone is a glucocorticoid that might be given.

Front 22

What medications could improve surfactant production in a premature infant if given to a pregnant mother? Which could inhibit surfactant production?

Back 22

Glucocorticoids accelerate pulmonary maturation and stimulate surfactant production, while Insulin would inhibit surfactant production.

Front 23

In a patient with multiple small bowel masses or intestinal obstructions what type of medication is absolutely contraindicated and why? Given an example of such medication.

Back 23

The use of a drug that stimulates the intestinal tract is absolutely contraindicated in patients with bowel obstruction or the possibility of bowel obstruction. Pressure and perforation can occur behind the obstruction. Metoclopramide is a prokinetic agent that would stimulate GI movement and be contraindicated.

Front 24

What drug uses the blockade of 5HT3 receptors? What is the effect of this?

Back 24

5HT3 results in the strong antiemetic effect of ondansetron.

Front 25

What drug uses the blockade of 5HT2 receptors? What is the effect of this?

Back 25

5HT2 blockade is part of the mechanism of Atypical Antipsychotics such as Clozapine.

Front 26

Which drug used to treat Generalized anxiety disorder, is a partial AGONIST of 5HT-1A receptors?

Back 26

Buspirone, a serotonin 5HT partial agonist, is used in the treatment of GAD (Generalized Anxiety Disorder).

Front 27

What is the mechanism of action of Sumatriptan and what is its clinical indication?

Back 27

Sumatriptan is a serotonin 5HT-1D/1B agonist that is used to abort migraine headaches and is approved for the treatment of migraine without aura, but not for long-term prophylaxis. It is also effective in the treatment of cluster headaches.

Front 28

What is the antidote to Acetominophen poisoning which produces liver toxicity?

Back 28

N-acetylcysteine.

Front 29

What is the antidote to Cholinesterase inhibitor poisoning which produce the symptoms of SLUDE?

Back 29

Atropine.

Front 30

What is the antidote to poisoning with Calcium Channel Blockers?

Back 30

Calcium Chloride.

Front 31

What is the antidote to Iron salts poisoning?

Back 31

Deferoxamine.

Front 32

What is the antidote to Arsenic, gold, mercury, or lead poisoning?

Back 32

Dimercaprol (BAL).

Front 33

What is the antidote to Digoxin toxicity?

Back 33

Digoxin Fab antibody.

Front 34

EDTA is a specific antidote to poisoning with what heavy metal?

Back 34

Lead.

Front 35

What is the treatment/antidote for poisoning with Methanol and Ethylene glycol? Why does it work?

Back 35

Ethanol; to compete for metabolism so the other substances can be excreted without being converted into toxic metabolites

Front 36

What is the treatment for Benzodiazepine toxicity?

Back 36

Flumanzenil.

Front 37

What is the treatment for insulin induced hypoglycemia?

Back 37

Glucagon.

Front 38

Cyanide poisoning from Nitroprusside is treated with what medication? How would you treat Cyanide poisoning from Cyanide instead?

Back 38

Hydroxycobalamin for Niroprusside poisoning. Strict Cyanide poisoning is treated with Nitrite or Sodium Thiosulfate.

Front 39

What is the treatment for Opioid overdose (e.g. Fentanyl)?

Back 39

Naloxone.

Front 40

What is the treatment of Copper poisoning?

Back 40

Penicillamine.

Front 41

What is the treatment for someone with Anticholinergic poisoning?

Back 41

Anticholinesterase inhibitor such as Physostigmine.

Front 42

Warfarin and warfarin-like anticoagulants are treated with what medication?

Back 42

Phytonadione.

Front 43

Organophosphate and anticholinlesterase inhibitors are treated with what medications?

Back 43

Pralidoxime.

Front 44

What are the most common drug induced causes of prerenal azotemia and ARF?

Back 44

Peripheral vasodilators (e.g. ACEIs), and Renal Vasoconstrictors (e.g. NSAIDs).

Front 45

NSAIDs affect which arteriole more: afferent or efferent? What is their effect there?

Back 45

They are thought to have a greater effect on the Afferent arteriole where prostaglandins are thought to play a large role in vasodilation. Thus, NSAIDs have the effect of blocking prostaglandin production and causing vasoconstriction in afferent arterioles.

Front 46

What do peaked T waves mean on an EKG? What is the P wave doing in this situation?

Back 46

Hyperkalemia. Here, the P wave will be absent.

Front 47

What type of immune complexes are present in Henoch-Schonlein purpura?

Back 47

IgA immunocomplexes.

Front 48

How does excess sodium effect arterioles and TPR?

Back 48

Excess sodium enters arteriole smooth muscle cells and opens calcium channels, causing vasocontriction. Thus excess sodium produces vasoconstriction and increases TPR and diastolic BP.

Front 49

What are the most common causes of Renovascular Hypertension in older men and younger women?

Back 49

Older men: atherosclerosis

Younger women: Fibromuscular hyperplasia

Front 50

The renal artery has a "beaded" appearance in renovascular hypertension due to what cause?

Back 50

Fibromuscular hyperplasia.

Front 51

Vitamin K gamma carboxylates clotting factors so that those factors can bind what molecules?

Back 51

Ca2+ and Phopholipid.

Front 52

What do platelets bind to themselves with? What molecule and what receptor for that molecule?

Back 52

Fibrinogen and GpIIb/IIIa.

Front 53

What Gp and factor do platelets use to bind to the endothelium with?

Back 53

GpIb and vWF.

Front 54

What factors are used up in clot formation?

Back 54

Factors I (Fibrinogen), II (Prothrombin), V, and VIII.

Front 55

What factors do Proteins C and S inactivate?

Back 55

V and VIII

Front 56

What does tPA do? What molecule does it work on?

Back 56

It works on converting Plasminogen to Plasmin.

Front 57

What type of Ig antibodies are elicited in response to AB blood groups?

Back 57

IgM

Front 58

What type of Ig antibodies are elicited in response to Rh blood groups?

Back 58

IgG

Front 59

Digoxin is indicated for the treatment of what atrial arrhytmia? What is its general mechanism of action?

Back 59

Atrial Fibrillation, especially when ventricular rate is elevated. The indirect action of digoxin decreases the conduction rate through the AV node and creates depression in the SA node (vagomimetic action).

Front 60

What is a first line agent of choice to treat Paroxysmal Superventricular Tachycardia?

Back 60

Adenosine and Cardioversion.