Pass/fa Pharm Drill Day 7

Front 1

What is the tx for African Trypanosomiasis (aka African Sleeping Sickness)?

Back 1

Suramin

Front 2

What is the tx for Chagas?

Back 2

Nifurtimox

Front 3

What is the tx for PCP?

Back 3

1st: TMP/SMX
2nd: Aerosolized Pentamidine
3rd: Dapsone

NOTE: PCP = PneumoCystis Pneumonia
BUG: Pneumocystis Jiroveci (formerly Pneumocystis Carinii)

Front 4

What is the SE of Aerosolized Pentamidine?

Back 4

Drug-induced pancreatitis

Front 5

What is the tx for Entamoeba Histolytica?

Back 5

Metronidazole

Front 6

What is the tx for P. vivax?

Back 6

Primaquine for latent P. vivax & P. ovale to prevent relapse (otherwise tx = Chloroquine)

Front 7

How do you tx a patient with Malaria who has just returned from New Dehli?

Back 7

Methloquine; Malaria from the indian subcontinent/subsahara is assumed to be resistent to Chloraquine

NOTE: New Dehli is the capital of the Republic of India

Front 8

What is the tx for "Kala-azar"?

Back 8

Pentavir Antimony
Na+ Stipigluconate

NOTE: Kala-azar (aka Dumdum Fever) is Visceral Leishmaniasis, the most severe form of Leishmaniasis

Front 9

What is the tx for Taenia Solium?

Back 9

Niclosamide

Front 10

What is the tx for Clonorchis Sinensis?

Back 10

Praziquental

Front 11

What is the tx for Enterobius Vermacularis?

Back 11

Praziquental & Mebendazole (on day 11 he says Pyrantal Pamoate & Mebendazole)

Front 12

What is the tx for Onchocerca (River Blindness)?

Back 12

Ivermectin

Front 13

What are the Neuroleptics?

Back 13

Fluphenazine
Thioridazine
Haloperidol
Chlorpromazine
Promazine

Front 14

What is the tx for Tourette's?

Back 14

Olanzapine
Promazine

Front 15

What is the MOA of Quetiapine?

Back 15

Quetiapine = Atypical Neuroleptic
Block 5-HT-2 & D2 receptors

Front 16

What drug blocks 5-HT-1D receptors?

Back 16

Nothing, h/w Sumitriptan is a 5-HT-1D AGONIST

Front 17

What drug blocks 5-HT-2, 5-HT-3, & a2 receptors?

Back 17

Mirtazipine

Front 18

What drug blocks 5-HT-3 receptors only?

Back 18

Ondansetron

Front 19

What is/are the SE(s) of Quetiapine?

Back 19

Cataracts

Front 20

What drug has a SE profile of Pigmented Retinopathy?

Back 20

Thioridazine

Front 21

What is/are the SE(s) of Fluphenazine?

Back 21

Hyperthermia due to disruption of the thermo-regulatory center

Front 22

What is the DOC for OCD?

Back 22

Paroxetine

Front 23

What is the MOA of Clomipramine?

Back 23

TCA's: Block 5-HT & NE re-uptake

Front 24

What drugs block [only?] NE re-uptake?

Back 24

Cocaine
TCA's
Maprotiline

Front 25

What heterocyclic inhibits only 5-HT re-uptake?

Back 25

Trazadone

Front 26

What is the DOC for Generalized Anxiety in a pt who is an alcoholic?

Back 26

Busparone

Front 27

What is the MOA of Phenalzine?

Back 27

Non-selective MAO inhibitor

Front 28

What is/are the SE(s) of Chlortinidine?

Back 28

*Hyper-GLUC:
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia

Front 29

What are the 4 main Thiazide Diuretics?

Back 29

Hydrochlorothiazide
Indapamide
Metolazone
Chlortinidine

Front 30

What is/are the SE(s) of Quinidine?

Back 30

Severe rebound HTN

Front 31

What is/are the SE(s) of Methyldopa?

Back 31

Positive Coomb's Test

Front 32

What is/are the SE(s) of Hexamethonium?

Back 32

Sympatholytic
Severe orthostatic Hypotension
Sexual Dysfunction
Parasympatholytic
Constipation
Blurred Vision

Front 33

What is/are the SE(s) of Reserpine?

Back 33

Depression
Diarrhea

Front 34

What is/are the SE(s) of Guanethidine?

Back 34

Sexual Dysfunction
Diarrhea

Front 35

What is/are the SE(s) of Prazosin?

Back 35

1st-dose Orthostatic Hypotension
Priapism

Front 36

What is/are the SE(s) of B-Blockers?

Back 36

Impotence
Exacerbates asthma
Masks hypoglycemia in DM
Cardiovascular efffects (bradycardia, AV block, CHF)
CNS effects (sedation, sleep alteration)

Front 37

What is/are the SE(s) of Hydralazine?

Back 37

*SARS
Salt retention
Angina
Reflex tachycardia
SLE-like sx's

Front 38

What is/are the SE(s) of Minoxidil (OTC Rogaine)?

Back 38

*SHARP
Salt retention
Hypertrichosis (too much hair)
Angina
Reflex tachycardia
Pericardial effusion

Front 39

What is/are the SE(s) of Verapimil?

Back 39

Constipation

Front 40

What is/are the SE(s) of Captopril?

Back 40

*CHAPTOPRIL where ""H"" = Hyperkalemia
C = Cough
H = Hyperkalemia
A = Angioedema
P = Proteinuria
T = Taste change
O = HypOtension
P = Pregnancy problems (fetal renal ?)
R = Rash
I = Incr'd renin
L = Lowers Ang II

Front 41

DAY 7:

Front 42

What happens to EDV when Nitrates are given?

Back 42

Decreased

Front 43

What happens to BP when Nitrates are given?

Back 43

Decreased

Front 44

What happens to Contractility when Nitrates are given?

Back 44

Reflexively Increased

Front 45

What happens to HR when Nitrates are given?

Back 45

Reflexively Increased (reflex tachycardia)

Front 46

What happens to Ejection time when Nitrates are given?

Back 46

Decreased

Front 47

What happens to MVO2 when Nitrates are given?

Back 47

Decreased

Front 48

What happens to EDV when B-Blockers are given?

Back 48

Increased (incr'd time in diastole = incr'd filling time)

Front 49

What happens to BP when B-Blockers are given?

Back 49

Decreased

Front 50

What happens to Contractility when B-Blockers are given?

Back 50

Decreased

Front 51

What happens to HR when B-Blockers are given?

Back 51

Decreased

Front 52

What happens to Ejection Time when B-Blockers are given?

Back 52

Increased

Front 53

What happens to MVO2 when B-Blockers are given?

Back 53

Decreased

Front 54

What happens to EDV when Nitrates AND B-Blockers are given?

Back 54

No change

Front 55

What happens to BP when Nitrates AND B-Blockers are given?

Back 55

Decreased

Front 56

What happens to Contractility when Nitrates AND B-Blockers are given?

Back 56

Decreased

Front 57

What happens to HR when Nitrates AND B-Blockers are given?

Back 57

Decreased (b/c B-Blockers = direct response, while Nitrates = reflexive response)

Front 58

What happens to Ejection Time when Nitrates AND B-Blockers are given?

Back 58

No change

Front 59

What happens to MVO2 when Nitrates AND B-Blockers are given?

Back 59

Decreased

Front 60

What is the 1st line tx for Cocaine-related MI?

Back 60

Benzodiazepines to tx HTN
Nitrates to tx VC/Vasospasm
Aspirin to decrease thrombus formation

Front 61

What is the tx for symptomatic premature atrial contraction?

Back 61

B-Blockers

Front 62

What is the Na+, K+, & Ca2+ ion normal physiology of the heart?

Back 62

1) The Na+/K+ pump exchanges 3K+ (moves inward) for 2Na+ (moves outward)
2) The Na+/Ca2+ antiporter exchanges Na+ (moves inward) for Ca2+ (moves outward)
3) K+ leak channels slowly allow K+ to diffuse (moves outward) to be used again by the
Na+/K+ pump (exchanger)
3) If the resting membrane potential reaches threshhold (approx +90mv) an AP occurs

Front 63

What is the MOA and physiology leading to the effects of Digoxin?

Back 63

1) Digoxin binds the K+ on the Na+/K+ pump preventing Na+/K+ exchange; K+ therefore stays outside the cell while Na+ stays inside the cell;
2) Na+ is then no longer exchanged with Ca2+; Ca2+ accumulates inside the cell;
3) Once threshhold is finally reached and an action potential does occur, the accumulated Ca2+ is released; release of an increased amount of Ca2+ results in an increased ionotropic effect (i.e. increased contractility due to increased ""ions"", Ca2+ in this case)

Front 64

What is the c/u and rationale for Digoxin?

Back 64

CHF b/c increases contractility
Atrial Fibrillation b/c slows conduction @ AV node leading to accumulation of intracellular Na+ which causes ventricles to contract harder (ventricular contractio is due to Na+)

Front 65

What is the toxicity of Digoxin?

Back 65

Torsades De Pointes Arrhythmia (i.e. prolonged QT) b/c of its effects on K+
Yellow vision

Front 66

What is the tx for Digoxin toxicity?

Back 66

1) STOP DIGOXIN ADMINISTRATION!
2) Slowly normalize K+
3) Lidocaine
4) Mg2+
5) Digifab/Digibind
6) Pacemaker once stable (~2wks later)

Front 67

What effects does Digoxin have on the EKG?

Back 67

Decr'd Na+/K+ Pump action --> Incr'd intracellular CA2+ accumulation:
PR Interval: Increased
QT Interval: Decreased
ST segment: Depression
T wave: Inversion (i.e. U wave)

Front 68

What are the Class III anti-arrhythmics?

Back 68

Ibutilide
Sotalol
Bretylium
Amiodarone
Dofetilide

Front 69

What is the MOA and effects of Class III Anti-arrhythmics?

Back 69

Blocks K+ leading to:
AP duration: Increased
QT interval: Increased (repolarization requires K+)
ERP: Increased (b/c blocked K+)

Front 70

What is the break-down metabolite of Amiodarone?

Back 70

Procainamide

Front 71

What class of Anti-Arrhythmic is Procainamide?

Back 71

Class IA

Front 72

Why is Amiodarone listed as a Class IA AND Class III anti-arrhythmic?

Back 72

Class IA: Amiodarone's metabolite, Procainamide, is a Class IA
Class III: Amiodarone's MOA is to block K+

Front 73

What is the MOA & effects of Class IA Anti-arrhythmics?

Back 73

Blocks Na+ AND K+ Channels leading to:
AP duration: Increased
QT interval: Increased (repolarization requires K+)
ERP: Increased (b/c blocked K+)

Front 74

What are the Class IB Anti-arrhythmics?

Back 74

Lidocaine
Mexlotine
Tocanimide
Phenytoin

Front 75

What is the c/u for Phenytoin?

Back 75

Treatment: Tonic-clonic seizures
Phrophylaxis: Status-epilepticus seizures

Front 76

What is the MOA of Phenytoin?

Back 76

Blocks Na+ channels

Front 77

What is the MOA and effects of Class IB Anti-arrhythmics?

Back 77

Blocks Na+ (does NOT affect K+ channels):
AP duration: Decreased
QT interval: No change (repolarization requires K+ and there is no change in K+)
ERP: No change (b/c no change in K+)

Front 78

What is the c/u for Class IB Anti-arrhythmics?

Back 78

1) Post-MI Ventricular Arrhythmias
2) Lidicaine: 3rd step in tx for digioxin toxicity

Front 79

What is the toxicity of Lidicaine?

Back 79

ASYSTOLE --> DEATH
(MOA = blocks Na+ Channels in the heart)

Front 80

What drugs tx Ventricular Arrhythmias and what is the rationale for their use?

Back 80

Class IB Anti-arrhythmics:
Decreased AP = decreased work by the heart
Class III Anti-arrhythmics:
K+ is blocked, thereby slowing repolarization at the AV Node
(i.e. less ventricular firing)

Front 81

What is the rationale for whether or not to use Digoxin for the tx of Ventricular Arrhythmias?

Back 81

Digoxin could be used, but you do NOT want to make the heart contract harder. Therefore, Digixin is not used in the tx of Ventricular Arrhythmias

Front 82

What are the Class IC drugs?

Back 82

Cainide
Flecainide
Propafenone

Front 83

What are the indications for Class IC Anti-arrhythmics?

Back 83

When everything else fails!
Ventricular Tachycardia becomes Ventricutlar Fibrillation
Intractable SVT

Front 84

What is the DOC for SVT?

Back 84

DOC: Adenosine
2nd Line: Verapamil

Front 85

What is the MOA of Adenosine?

Back 85

Opens Ca2+ channels: decr'd Ca2+
Opens K+ channels: incr'd K+ (repolarization --> ""hyperpolarizes"" AV node)

Front 86

Why are Class IC Anti-arrhythmics ONLY given for INTRACTABLE SVT?

Back 86

Class IC Anti-arrhythmics block Na+ channels EVERYWHERE!!
The heart has once chance to ""fire"" & then it will not ""fire"" again (b/c Na+ is blocked)

Front 87

What is the MOA and effects of Class IC Anti-arrhythmics?

Back 87

Class IC Anti-arrhythmics block Na+ channels EVERYWHERE!!
AP duration: no more AP's after ""first fire""
QT interval: No change (repolarization requires K+ and there is no change in K+)
ERP: No change (b/c no change in K+)

Front 88

Why do we use Class IC Anti-arrhythmics, if they are a "last resort"?

Back 88

Toxicity = ""PRO-ARRHYTHMIA""
Any arrhythmia is better than NO arrhythmia at all (i.e. flutter or flatline)
e.g. working on pt for 20 mins & still no HR

Front 89

What is the MOA of Class II Anti-arrhythmics?

Back 89

Class II = B-Blockers:
Decr'd HR
Decr'd Contractility
Decr'd AV node conduction

Front 90

What is the phsyiological bases for why Class II Anti-arrhythmics cause decr'd HR?

Back 90

Class II = B-Blockers:
Beta receptors are blocked --> decr'd stimulation of Gs proteins --> decr'd AC -->
decr'd cAMP --> decr'd PKA --> decr'd SS outflow --> decr'd HR

(NOTE: Step 1 may ask which of the following is affected with B-Blocker tx & the correct answer will be one of the steps in the pathway)

Front 91

Which B-Blockers have intrinsic sympathomimetic activity

Back 91

B-Blockers that ""partially"" block beta receptors AND are also a-agonists (incr'd SS's):
Oxprenolol
Acebutolol
Pindolol
Penbutolol

Front 92

What is the toxicity of Amiodarone?

Back 92

Hepatotoxicity
Corneal deposits
Photodermatitis

Front 93

What is the MOA of Class IV Anti-arrhythmics?

Back 93

Class IV = Cardio-selective CCB's:

Front 94

What are the Class IV Anti-arrhythmics?

Back 94

Verapimil
Diltiazam

Front 95

Why aren't Nefidapine and Amlodipine Class IV Anti-arrhythmics?

Back 95

Though they are CCB's, they are NON-CARDIO selective (they don't affect the heart)

NOTE: These will be ""distractors"" on Step 1

Front 96

Where do Class IV Anti-arrhythmics work?

Back 96

AV Node

Front 97

What node controls atrial contraction?

Back 97

SA Node

Front 98

Which node controls ventricular contraction?

Back 98

AV Node

Front 99

What is the c/u for Class IV Anti-arrhythmics?

Back 99

SVT b/c AV node is just above (i.e. "supra") the ventricle

Front 100

What is the Na+, K+, & Ca2+ ion normal physiology of the heart?

Back 100

1) The Na+/K+ pump exchanges 3K+ (moves inward) for 2Na+ (moves outward)
2) The Na+/Ca2+ antiporter exchanges 2Na+ (moves inward) for Ca2+ (moves outward)
3) K+ leak channels slowly allow K+ to diffuse (moves outward) to be used again by the
Na+/K+ pump (exchanger)
3) If the resting membrane potential reaches threshhold (approx +90mv) an AP occurs

Front 101

What is the MOA and c/u of Adenosine?

Back 101

Opens Ca2+ channels: decr'd Ca2+
Opens K+ [leak] channels: incr'd K+ (repolarization --> ""hyperpolarizes"" AV node)
Clinical use: ventricular arrhythmias (b/c it hyperpolarizes the AV node)