Kaplan Pharm Essentials-Cardiac And Renal

Front 1

Fast Response Fibers:
Na channel blocker ____ slope of phase ___.

K channel blocker ____ duration of phase ___. (affect QT)

Back 1

Decrease; 0

Increase; 3

Front 2

Fast Response Fibers:
Antiarrhythmics have no significant effect on phase _____ & ____.

Back 2

1; 2 (Na channels inactivated)

Front 3

What are the slow response fibers?

Back 3

SA/AV node

Front 4

What type of arrythmia is slow response fibers responsible for?

Back 4

SVT

Front 5

Which phase is missing from slow compared to fast response fiber?

Back 5

Phase 1 & 2

Front 6

What channel does phase 0 of slow response fiber depend on?

Back 6

Ca

Front 7

**Summary of location of action:
Fast fibers:
Na blocker
K blocker

Slow fiber:
CCB
BB

Back 7

Phase 0
Phase 3

Phase 0
Phase 4

Front 8

What is phase 4 in both fast and slow response fibers?

Back 8

Depolarization

Front 9

What is the general function of Na channel blockers?

Back 9

Increase refractory period
(Na+ channel spends most of its time in this state, right after phase 0)

Front 10

What is the general function of K channel blocker?

Back 10

Increase AP duration

Prolong refractory period

Front 11

Why is conduction slower in ischemic heart tissue?

Back 11

Refractory period is longer
(cells are partly depolarized, and this reduces the number of channels able to participate in next depolarization)

Front 12

What channel does Class 1A block?

Back 12

Na & K

Front 13

**What is the class SE of class 1A?

Back 13

Torsades (K+ channel blocker)

Front 14

How is Class 1A different from other class 1 agents?

Back 14

Prefers open/activated state (state dependent blockade) rather than inactive state preferred by all other Class 1 agents

Front 15

What is the problem w/ quinidine in an antiarrhythmic context?

Back 15

It is proarrhythmic

atropine like effect --> M blockade --> increase HR & AV conduction

-zosin like effect --> Alpha 1 blockade --> Reflex tachycardia

Front 16

What do you need to give to patients taking quinidine to make it safer?

Back 16

Digitalis (reduce reflex tachycardia)

Front 17

**What are the SE of quinidine?

Back 17

Cinchonism
-GI
-Tinnitis
-Ocular dysfunction
-CNS excitation

Increase QT (block K+)

Displace Dig

Front 18

Why is procainamide a bit safer than quinidine?

Back 18

Less M & Alpha1 blockade

Front 19

**What is a main SE of procainamide?

Back 19

SLE (in slow acetylators)

Front 20

What active metabolite of procainamide is responsible for the K+ blocking effect?

Back 20

NAPA (N-acetyl procainamide)

Front 21

What channels does class 1B affect?

Back 21

Na

Front 22

What type of tissue does Class 1B drug prefer?

Back 22

Partially depolarized (ischemic) tissue

Front 23

What is the effect of class 1B?

Back 23

Decrease HR (decrease AP duration slightly, but increase diastole)

Front 24

What is the uses for lidocaine?

Back 24

#1 Ventricular Arrhythmia drug

(Post MI, dig toxicity)

Front 25

What is the SE of lidocaine?

Back 25

CNS toxicity (seizures)

Front 26

Why is lidocaine given IV?

Back 26

Extensive first pass metabolism

Front 27

What are other class 1B drugs?

Back 27

Mexiletine/Tocainide (same use as lidocaine, oral)

Phenytoin (used as antiseizure)

Front 28

What does class 1 c drugs block?

Back 28

Fast Na Channels

Front 29

Why is class 1c drug Flecainide not used much?

Back 29

Proarrhythmogenic in post-MI & prophylatic VT pts --> Death!!!

Front 30

1A _____ AP (___ shift)
1B _____ AP (___ shift)
1C _____ AP (___ shift)

Back 30

Lengthen; R

Shorten; L

DN affect; No

Front 31

Which of the following is non-selective, while others are cardioselective BB?

Propranolol
Acebutolol
Esmolol

Back 31

Non-Selective: Propranolol

Cardioselective: Acebutolol, Esmolol

Front 32

What are the uses of BB?

Back 32

SVT

Prophylaxis post-MI

Front 33

**Why is esmolol used only in acute SVT?

Back 33

It only last ~10 min

Front 34

What are the class 3?

Back 34

Amiodarone

Sotalol

Front 35

What makes amiodarone so special?

Back 35

It has all class activity, tx almost anything, and extensive activit --> Low chance of torsades

("Ami"=Friend who always help you)

Front 36

How do you distinguish amiodarone from amiloride?

Back 36

"Lo-ride"=Kidney=K+ sparing

Front 37

**What are the SE of amiodarone?

Back 37

Pulmonary Fibrosis (also bleomycin)
Iodine effect
-"Smurf skin"
-Thryoid dysfunction
-Phototoxicity

Front 38

What additional SE does sotolol have besides torsades?

Back 38

B1 blockade effect

Front 39

What are the cardioselective CCB?

Back 39

Verapamil & Diltiazem

Front 40

What are the CCB used for?

Back 40

SVT

Front 41

What is a prominent GI SE of verapamil?

Back 41

Constipation

Front 42

What does Class 3 Antiarrhythmic do to AP & Refractory?

Back 42

Lengthen

Front 43

MOA of adenosine

Back 43

+ adenosine receptor --> +Gi --> Increase K efflux--> Hyperpolarize SA &AV node

Front 44

Use of Adenosine

Back 44

DOC paroxysmal SVT

Front 45

Use of Mg

Back 45

Torsades (if low Mg)

Front 46

SVT use:

Back 46

Class II, IV, Adenosine, Dig

Front 47

VT use:

Back 47

Class I, III

Front 48

A. fib use:

Back 48

SVT drugs + Warfarin

Front 49

Causes of Torsades

Back 49

K Channel Blocker (Class 1A & 3)
Antypsychotic (Thioridazine)
TCA

Front 50

MOA of alpha2 agonist in anti-HTN

Back 50

Decrease sympathetic outflow

Front 51

Y is alpha2 agonist 2nd line in HTN?

Back 51

Powerful drop in BP --> Rebound HTN & Fatigue/Depression

Front 52

Which alpha2 agonist is used for opiate w/drawal?

Back 52

Clonidine

Front 53

**DOC of HTN in pregnancy?

Back 53

Methyldopa

Front 54

**What test should u run b4 administering methyldopa in pregnant women?

Back 54

Coomb's Test (+=AIHA)

Front 55

**MOA reserpine in HTN

Back 55

Destroy vesicle --> Amine depletion (NE/DA/Serotonin)

Front 56

What is main SE of reserpine?

Back 56

Depression (this forms our theory of depression)

Front 57

MOA alpha1 blocker in HTN

Back 57

Dilate aa AND vv

Front 58

SE of Alpha1 blocker

Back 58

First dose syncope
Orthostatic HypoTN

Front 59

**What is the cause of orthostatic hypoTN?

Back 59

VEIN dilation

Front 60

What is a common cause for pt going off BB?

Back 60

Sexual dysf (leads to rebound tachycardia)

Front 61

Caution in BB use in pts w/:

Back 61

Asthma
DM (reduce insulin release & mask hypoglycemic tachy)
Vasospastic Dz

Front 62

What are primary uses of direct acting vasodilators?

Back 62

Severe HTN

Front 63

Which 3/4 DA vasodilators are arteriolar selective?

Back 63

Hydralazine, Minoxidil,Diazoxide

Front 64

Which 1/4 DA vasodilator act on both aa & vv?

Back 64

Nitroprusside

Front 65

What is MOA of hydralazine?

Back 65

Increase NO

Front 66

Hydralazine SE?

Back 66

SLE in slow acetylator

Front 67

Nitroprusside use?

Back 67

HTN emergency

Front 68

SE nitroprusside?

Back 68

CN toxicity

Front 69

How do u tx CN poisoning in nitroprusside?

Back 69

Coadminister:
-Nitrite: Form MetHb which bind CN --> CyanoMetHb--> resist CN inhibition of complex IV of ETC
-Thiosulfate: Reconvert cyanometHb--> MetHb by forming less toxic thiocyanate ion (SCN)

Front 70

How do u tx metHb as a SE of nitrite tx?

Back 70

Methylene Blue

Front 71

Which drugs directly open K channel --> Hyperpolarization?

Back 71

Minoxidil
Diazoxide

Front 72

SE minoxidil

Back 72

Hypertrichosis (tx baldness)

Front 73

SE diazoxide

Back 73

Hyperglycemia (decrease insulin release)

Front 74

Vasodilator that are arteriolar selective

Back 74

CCB/Hydralazine/K channel opener

Front 75

Vasodilator that are venoselective

Back 75

Nitrate

Front 76

CCB use for HTN

Back 76

Diltiazem (jack of all trade, cover cardio & vessels)

-dipines (vascular selective)

Front 77

**-dipine SE

Back 77

Gingival hyperplasia (also phenytoin/cyclosporin)

Front 78

**DOC primary HTN

Back 78

Thiazide

Front 79

Aliskiren?

Back 79

Renin blocker

Front 80

ACE function?

Back 80

AT1 --> AT2
Bradykinin-->inactivate

Front 81

Where does ATII bind?

Back 81

AT1 receptor (AT II type 1 receptor)

Front 82

AT1 receptor function?

Back 82

Increase aldosterone release (adrenal cx)

Vasoconstriction

Front 83

ACE & ARB suffix

Back 83

-pril

-sartan

Front 84

Use of ACE/ARB

Back 84

HTN
DM nephropathy (Renal protective)
CHF (Cardioprotective)

Front 85

SE ACEI

Back 85

Cough/Angioedema (Bradykinin)

Front 86

SE both ACE/ARB

Back 86

Hyperkalemia (decrease Ald)

Acute RF in renal aa stenosis pt (dilate efferent arteriole --> RF)

Front 87

How does NSAID cause RF?

Back 87

Decrease PG (which dilates aff aa)

Front 88

**Tx of pulmonary HTN

Back 88

Bosentan

Sidenafil

Front 89

MOA Bosentan

Back 89

Endothelin (ET-A) receptor antagonist (endothelin is a powerful vasoconstrictor released by stretched vessels)

Front 90

What are the body's rxn to HF (Decreased CO)?

Back 90

Remodelling (fibrosis & lose myocyte)

Intrinsic compensation (eg: hypertrophy)

Front 91

**How do we prevent cardiac remodelling?

Back 91

Decrease SANS (metoprolol/carvedilol)

Decrease Ald
-ACE/ARB: Decrease production
-Spironolactone: Block receptor

Front 92

What are ionotropes used for primarily?

Back 92

Acute CHF

Front 93

**How does ionotorpe work generally w/ HF?

Back 93

Incease Ca(cytoplasmic) --> Increase Ca release from SR --> Increase contraction

Front 94

**MOA dig in CHF & Arrhythmia

Back 94

CHF: Block Na/K ATPase --> Decrease Na gradient --> Decrease Na/Ca pump activity --> Increase IC Ca

Arr: Block Na/K ATPase in neuron --> Increase Vagal activity --> M2 --> Slow AV/SA

Front 95

**Dig is DOC for:

Back 95

Pt w/ CHF AND SVT (both HF & Arrhythmia)

Front 96

Dig SE

Back 96

Visual (halo/blurry yellow)=CNS

Front 97

Dig DI

Back 97

Diuretics: Hypokalemia (thiazides)

Quinidine & Verapamil (displace dig)

Front 98

How does Inam/mil-rinon work as ionotrope?

Back 98

PDE III I --> Increase cAMP --> Open Ca channel on memebrane

Front 99

Hw does dobutamine & DA work?

Back 99

Sympathomimetic --> + B1 receptor --> increase cAMP --> Open Ca channel on memebrane

Front 100

Dobutamine is a B agonist w/ > activty on B1/B2?

Back 100

B1

Front 101

What is nesiritide?

Back 101

rhBNP

Front 102

What are drugs for acute HF?

Back 102

Dobutamine/DA
PDE III I
Nesiritide

Front 103

Drug for chronic CHF?

Back 103

ACE/ARB (hydralazine (dilate aa) +
Isosorbide dinitrate (dilate vv) if intolerant to ACE)

BB

Diuretic

Poss. Dig

Front 104

2 Types of angina

Back 104

Classic/Stable=Atherosclerosis (effort)

Prinzmetal=Vasospastic (decrease BF)

Front 105

What's special about M3 in vessels?

Back 105

No innervation/circulating Ach, rely only on NO (endothelium derived relaxation factor)

Front 106

What endogenous cpd + receptors that activate NOS?

Back 106

Bradykinin
Histamine
5HT

Front 107

What does NO do?

Back 107

+ Guanylyl cyclase --> relax

Front 108

What is main SE of nitroglycerin?

Back 108

H/A

Front 109

Y can't u wear nitro patch all day?

Back 109

Tachyphylaxis (wear patch 1/2 day only)

Front 110

U can use ____ CCB for angina, but ____ is especially impo for vasospastic angina.

Back 110

ALL; Nifedipine (DOC for Raynauds)

Front 111

**BB are used in ______ angina, but CI in _______ angina.

Back 111

Classic; Prinzmetal

Front 112

POST MI Tx= MONA then ___, ____, ___.

Back 112

Morphine, O2, Nitroglycerin, Aspirin

BB;ACE;Statin

Front 113

cGMP cause myosine LC ______.

cAMP cause myosine LC kinase ______.

Back 113

Dephosphorylation (inactivation)

Phosphorylation (inactivatoin)

Front 114

Loops and thiazides are _____ biochemically --> Will compete w/ ____ for excretion.

Back 114

acids; UA

Front 115

*******************************************Why will loops & thiazides cause hypokalemia?

Back 115

They block proximal resorption of Na --> increase resorption of Na downstream w/ corresponding loss of K

Front 116

***********************************Why will loops and thiazides cause alkalosis?

Back 116

K secretion is coupled to H secretion

(reason K good for u?)

Front 117

What is the use of Carbonic Anhydrase in PCT?

Back 117

Convert CO2 and H2O to:
-H: Power resorption of Na from lumen via antiporter
-HCO3: Absorbed into bloodstream

Front 118

What are CA suffix?

Back 118

-zolamide

Front 119

What are uses of CA?

Back 119

Glaucoma

Acute mountain sickness (>10k ft)

Front 120

**Where does CAI primarily affect?

Back 120

PCT (85% of HCO3 resorption)

Front 121

SE of CAI:

Back 121

Bicarbonaturia/acidosis

Sulfonamide HS

Hypokalemia (K secretion increased b/c Na resorption decreased upstream)

Front 122

**How does loop work?

Back 122

Block Na/K/2Cl symporter in Thick Ascending LOH

Front 123

**What is the importance of K in Thick Ascending LOH?

Back 123

Backleak of K into lumen--> Mg/C1 entry through paracellular space

Front 124

What are the uses for loops?

Back 124

Acute pulmonary edema (DOC: fast)

HTN (but require frequent dosing)

Hypercalcemia

Front 125

What are the loops?

Back 125

Furosemide/torsemide/bumetanide

Ethacrynic acid

Front 126

**When is the only time you use ethacrynic acid?

Back 126

When u want to use a loop but pt have sulfonamide allergy

Front 127

What is the main unpredicted SE for loops?

Back 127

Ototoxicity (esp w/ Ethacrynic acid)

Front 128

MOA thiazide

Back 128

Block lumenal NaCl symporter (lose Na & Cl)--> increase basolateral Na/Ca antiporter (increase Ca)

Front 129

Uses of thiazides

Back 129

HTN

Nephrolithiasis (decrease Ca in urine)

Nephrogenic DI (force Na loss--> increase Na resorption in PCT --> H2O resorption)

Front 130

What is the physiological problem in nephrogenic DI?

Back 130

Uncoupled V2 (vasopressin 2) receptor in CD

Front 131

What are the SE of thiazide?

Back 131

Sulfonamide HS

Hyperglycemia (makes B-cell harder to release insulin b/c K lost)

Hyperlipidemia

Front 132

What are the thiazides

Back 132

HCT

Indapamide

Front 133

**Loops & Thiazides are the MCC of hypo_____ & metabolic ______.

Back 133

K; Alkalosis

Front 134

**Hypokalemia _____ insulin secretion

Back 134

Decrease

Front 135

Where does K-sparing agents work?

Back 135

CD's Na channel

Front 136

How does Na channel (lumenal) in CD work?

Back 136

Allow Na to enter, this entry is driven by Na/K pump at basolateral side

Front 137

How does aldosterone receptor antagonist work?

Back 137

Decrease Tc of Na channels on the lumenal side

Front 138

What are Ald receptor antagonist?

Back 138

Spironolactone/Eplerenone

Front 139

What can spironolactone also be used for?

Back 139

Hirsuitism (antiandrogenic effect)

Epleronone is SELECTIVE at ald, so no antiandrogenic effect (Newer drug w/ more specificity)

Front 140

What are the Na channel blocker that are K-sparing?

Back 140

Amiloride

Triamterene

Front 141

What are the use for K-sparing Na channel blockers?

Back 141

Adjunct to K+ wasting diuretic

Li induced nephrogenic DI

Front 142

What is MOA of Li induced Nephrogenic DI?

Back 142

Li goes through Na channel in the CD, then damage the V2 receptors.

Front 143

AcCoA-->--> ______ --> ______ -->--> Cholesterol

Back 143

HMG CoA; Mevalonic Acid

Front 144

What are statins?

Back 144

HMG-CoA Reductase inhibitor

Front 145

What does statins help w/?

Back 145

Everything

Front 146

**SE of statins:

Back 146

Myalgia (Check CK)
Rhabdomyolysis

Hepatotoxicity (Check LFT)

Front 147

DI of statin:

Back 147

Gemfibrozil (increase rhabdomyolysis)

P450 inhibitors (eg: grapefruit juice) increase toxicity

Front 148

MOA of Bile Sequestrants

Back 148

Prevent recycling of Bile Salt (Bile salt 95% recycled)

Front 149

SE of Bile Sequestrant:

Back 149

Increase VLDL& TG (liver forced to make stuff)

B.S. CI: HyperTG pt

Front 150

What are the B.S. drugs?

Back 150

Cholestyramine

Colestipol

Front 151

What is the main use of Nicotinic acid (niacin, aka vitamin B3)?

Back 151

Increase HDL (by inhibiting VLDL syn)

Front 152

**SE niacin:

Back 152

Pruritis (pretx w/ aspirin)

Front 153

MOA of fibrates:

Back 153

PPAR-alpha agonist (Peroxisome Proliferator Activated Receptor) & regulate Tc--> Activate lipoprotein lipase

SN: -glitazones are PPAR-gamma (g=glucose) activators that are used for DM type II

Front 154

**Primary use of fibrates:

Back 154

Lower TG

Front 155

MOA ezetimibe?

Back 155

Prevent GI absorption of cholesterol --> Decrease LDL

Front 156

What is orlistat and its use?

Back 156

Pancreatic lipase inhibitor; weight loss

(rem: to bring a change of black pants)

Front 157

PDE III inhibitors increase cAMP, causing:
______ in heart contractility.
______ in sm mm contractility.

Back 157

Increase (ionotrope)

Decrease

Front 158

Progression of sedative/hypnotic/anxiolytics:

Back 158

Paradoxical disinhibition --> anxiolysis --> hypnosis --> anesthesia --> Medullary depression --> coma

Front 159

Why is BZD safer than barbiturates/EtOH?

Back 159

BZD effect ceiling at around medullary depression, while Barb/EtOH can go all the way to coma

Front 160

CNS excitatory NT:

Back 160

Glutamine

Front 161

CNS inhibitory NT:

Back 161

GABA, DA, Opioid

Front 162

CNS exc&inhibitory NT:

Back 162

ACh, NE, 5HT

Front 163

BZD/Barb/EtOH all bind to ____ parts of the GABA binding site.

Back 163

Different

Front 164

MOA of:
GABA-A (ionotropic=ion channel)
GABA-B (metabotropic=G-protein)

Back 164

Increase Cl influx (hyperpolarize)
Increase K efflux (hyperpolarize)

Front 165

**Sedative Hypnotics works PRIMARILY on which GABA receptors?

Back 165

GABA-A

Front 166

**MOA BZD VS Barb:

Back 166

BZD: Potentiate GABA
Barb: Prolong GABA duration

"Ben like frequency, Barb like duration"

Front 167

What addn'l activity does barb have at high doses?

Back 167

GABA mimetic

Front 168

**What non-specific BZD receptor antagonist is used to tx BZD OD, but dn work on Barb/EtOH OD?

Back 168

Flumazenil