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IPAP JUNIOR SEM. > PHARM II Block II Specific Trivia > Flashcards

PHARM II Block II Specific Trivia Flashcards

1
Q

What is the greater predictor of CVD in pts older than 50 y/o

SBP or DBP

A

SBP!

Sustained elevated BP is directly correlated: 
Myocardial Infarction
Angina
Heart Failure
Kidney Failure
Early death secondary to CV cause
Retinopathy
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2
Q

What is the differnce between essential and secondary HTN

A 
Essential Hypertension: 
90% (no identifiable cause)
Possibly Genetic
Can only be controlled not cured
Contributed mostly by obesity

Secondary Hypertension:
Results from comorbid disease or is drug-induced
< 10% of individuals have this type
Removal of the offending agent or treatment of comorbid disease should be first step in management
Renal dysfunction from chronic kidney disease or renovascular disease is the most common secondary cause

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3
Q

What is the Tx approach to secondary HTN

A

Removal of the offending agent or treatment of comorbid disease should be first step in management

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4
Q

What is the most common cause of secondary HTN

A

Renal dysfunction from chronic kidney disease or renovascular disease is the most common secondary cause

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5
Q

What is the definition of resistant HTN

A

American Heart Association (AHA) Definition: “When a patient is not at their blood pressure goal despite use of optimal doses of three anti-hypertensives from different classes, ideally including a diuretic”

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6
Q

What is the cause of Isolated Systolic HTN

A

Results from pathophysiologic changes in the arterial vasculature consistent with aging (arteriosclerosis)

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7
Q

What is the criteria for Isolated systolic HTN

A

SBP > 140 and DBP< 90

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8
Q

Higher pulse pressures indicated increased risk of…

A

Arterial stiffness and CV risk

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9
Q

List as many CV risk fxs

A

Age (≥55 years for men to 65 years for women)

Diabetes Mellitus

Dyslipidemia: elevated LDL, total cholesterol or triglycerides; low HDL

Albuminuria: protein in the urine

Family History of Premature CV disease

Obesity (BMI ≥ 30 kg/m2)

Physical Inactivity

Tobacco Use

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10
Q

What is the formual fr BP

A

CO x Total peripheral resistance

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11
Q

MAP calculation

A

(2DBP+SBP)/ 3

Examply 120/80
160+120=280/3=roughly 90

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12
Q

What effect does NO have on peripheral resistance

A

Decreases peripheral resistance

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13
Q

What effect does prostycyclins, Kinins, ANP all have on peripheral vasc resistance

A

All decrease resitance

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14
Q

What effect do thomboxanes, enodthelin both have on perifpheral vasc resist.

A

Increase resistance via vasocon

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15
Q

What is the most influential contributor to homeostatic regullation of BP

A

RAAS system

Sympathetic nervous system activity is regulated largely by negative feedback via the baroreceptor feedback mechanism

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16
Q

What three mechanism stimulate the release of renin

A

Low BP, Low fluid volume in the glomerulus, or increased B1 sympathetic stim.

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17
Q

What is the effect of Angiotesin II

A

Stimulates aldosterone, mild vasocon, and increases NaCL and H2O reabsorption

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18
Q

What are the baroreceptors of the Renin aldo system

A

Juxtaglomeluar cells (these also secrete renin)

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19
Q

What are the important actions of Angio II

A

Vascular smooth muscle (constricts)

Adrenal cortex (aldosterone synthesis and release)

Kidney (increase Na+ re-absorption)

Heart (increase rate)

Brain (increases anti-diuretic hormone release)

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20
Q

What is the MOA of Thiazide and Thiazide like diuertics

A

Mechanism of Action: inhibit sodium and chloride reabsorption in the early distal convoluted tubule (DCT) resulting in water retention in the tubule

Loss of sodium increases urine volume

Lowers BP by increasing Na+ and water elimination

With continued use the volume returns to normal but reduced peripheral resistance (PR) still keeps BP lower

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21
Q

What must pts have in order for thiazide/like medications to work

A

Functioning kidneys (CrCL>30 or SCR<2.5)

Excception when in reduce renal function metolazone works and is the DOC

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22
Q

What is the best tolerated HTN tx class of drugs

A

Thiazide/ Like meds

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23
Q

Diuretics are most effective when combined with…

A

ACEI or ARBs

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24
Q

Combining thiazieds with what other mediations can reduce Hypokalemia

A

Potassium sparing agents

Combinations include

Triamterene/Hydrochlorothiazide (Maxzide and Dyazide)
Amiloride/Hydrochlorothiazide (Moduretic)
Spironolactone/Hydrochlorothiazide (Aldactazide)

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25
Q

What is the MOA for ACEI

A

Inhibits the Renin-Angiotensin-Aldosterone System (RAAS) by inhibiting the conversion of angiotensin I to angiotensin II

Reducing :
Vascular smooth muscle constriction

Aldosterone synthesis and release

Na+ re-absorption

Heart rate

Anti-Diuretic Hormone (ADH) release

Also increase the availability of the vasodilator bradykinin by inhibiting its breakdown

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26
Q

What effect doe ACEI have on bradykinin

A

increase the availability of the vasodilator bradykinin by inhibiting its breakdown

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27
Q

Do ACEI impact heartrate

A

NO!

Lowers blood pressure by reducing peripheral vascular resistance without increasing cardiac output, rate, or contractility

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28
Q

What is the role of bradykinin

A

Bradykinin is involved in the production of nitric oxide and prostaglandins (Ex: prostacyclin)
Nitric oxide and prostacyclin are vasodilators

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29
Q

What is the hypothosised reason for a cough and angioedema with ACEI Tx

A

Bradykinin and a related substance “substance P” are probably responsible for inducing a cough and angioedema

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30
Q

Are ACE effective in African american populations

A

Reduced effectiveness unless combined with a CCB or diuretics

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31
Q

What are the ADE of ACEI

A 
Taste disturbance 
HOTN 
Hyper K+ 
Increased Cr and BUN 
(Up to 20% increase is acceptable)
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32
Q

What is the only C/I to ACEI

A

Renal artery stenosis

Should also monitor K+, Cr, BUN and baseline and two weeks into Tx

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33
Q

When Rx an ACE what is the F/u and monitoring required

A

Monitoring: potassium, serum creatinine, and BUN at baseline and two weeks into therapy

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34
Q

Can ACEI be used in pregnancy

A

Nope preg CaT D

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35
Q

A pt on an ACEI gets pregnant, what do you do

A

DC the ACEI

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36
Q

What is the renal trifecta

A

Diuretics: reduce plasma volume and concentrate blood urine (increase SCr)
+
ACEI/ARB: blocks renal compensation and dilates efferent arteriole
+
NSAIDs: inhibits prostaglandins and bradykinin, producing vasoconstriction of the afferent renal arteriole

Result: drug induced acute kidney injury

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37
Q

What is the MOA of ARBs

A

Antagonize angiotensin II at the AT1 receptor

AT1 predominates in the vasculature

Prevents the vasoconstrictor effects of this receptor

Block aldosterone secretion, leading to decrease salt and water retention

AT2 produces arteriolar and venous dilation

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38
Q

What is the clinical use of ARBs

A

Reserve ARBs for patients that do not tolerate ACEIs

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39
Q

Should ACE and ARbs be used simultaneously

A

NO!

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40
Q

What are the pros and cons of ARBs over ACEI

A

ARBs benefits
-Low/No bradykinin associated cough

-Low/No angioedema issue

ARBs drawbacks
-Cost $$$ compared to ACEIs

-Not as much clinical data as ACEIs

Both ARBs and ACEIs
Category D in pregnancy
Caution with renal stenosis

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41
Q

What is the MOA of Aliskiren

A

Direct Renin Inhibitor (DRI)

Mechanism of Action:

  • Inhibits renin
  • Reduces angiotensin I and II and aldosterone
  • Is not limited by angiotensin II production through non-ACE dependent pathways or indirect activations of AT2 receptors
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42
Q

CAn aliskiren be used in pregnancy

A

No

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43
Q

What are the ADE of aliskiren

A

Adverse Effects

  • Diarrhea (at high doses)
  • Cough and angioedema, but less than ACEIs
  • Hyperkalemia
  • Increased serum creatinine and BUN
  • Hypotension in volume and/or salt depleted patients
  • Hypersensitivity to sulfonamide component
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44
Q

What adrugs should be avoided in aliskirin Rx

A

Avoid combined use of ARBS or ACEI

Avoid NSAIDs (renal trifecta)

Avoid lithium

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45
Q

What is the MOA of A1 blocking agents

A

Mechanism of Action:
Selectively block α1 receptors and prevent vasoconstrictor actions of these receptors

Decrease peripheral vascular resistance and relax both arterial and venous smooth muscle on both arteries and veins (mainly arteries)

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46
Q

Should A1 blockers be used as mono tx fror HTN

A

No and its rarely the 1st step

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47
Q

What med class can be used in pts with BPH and HTN

Or have resistant HTN already on diuretic, BB, and ACEI

A

A1 blockers

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48
Q

Is prazosin acceptable to use in BPH

A

NO it is howeever indicated for PTSD

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49
Q

What are the ADE of A1 Blockers

A 
Ortho HOTN 
Tachy reflex
Edema-prazosin (may require a diuretic) 
HA/Dizzy/wkness
Inhibition of ejaculation
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50
Q

What is the MAO of A2 agonist

A

Stimulate presynaptic α2 receptors in the CNS inhibits (via negative feedback) sympathetic outflow to the heart, kidneys, and peripheral vasculature causing peripheral vasodilation

Reduction of sympathetic outflow will result in a net decrease in blood pressure

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51
Q

A2 agonists are best used with what other drugs

A

best used in combination with agents that have different MOA (diuretics and ACEI) and not with adrenergic blockers

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52
Q

What are the ADE of A2 agonist

A

Drowsiness
Dry mouth
Edema/fluid retention

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53
Q

What are the ADE of clonidine

A

Its and A2 agonsit

So Dry mouth
Sedation
Constipation
Ortho HOTN

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54
Q

Can you abruptly wthdrwl clonidine?

A

NO!

Abrupt withdrawal of doses >1mg/day can result in life-threatening hypertensive crisis mediated by increased sympathetic nervous activity

Withdrawn gradually while other anti-hypertensive agents are being initiated

Symptoms: nervousness, tachycardia, headache, and sweating after omitting 1 or 2 doses

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55
Q

If a pt is taking clonidine and starts to get depressed

What should you do

A

Withdrwl clonidine

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56
Q

Is clonidine safe in geriatrics

A

No

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57
Q

What effect do Clonidine and TCAs have on eachother

A 
Tricyclic antidepressants (TCAs) may block the antihypertensive effect of clonidine and potentiate anticholinergic effects
(Example: amitryptyline)
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58
Q

When methyldopa is used to treat HTN in a pregnant pt

How should it be dosed

A

TID or QID

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59
Q

What is the MOA of Bblockers

A

Mechanisms of Action: antagonize β receptors

Antagonizing β1 receptors in the heart causing decreased cardiac output (decrease rate and force of contraction)

Decrease sympathetic outflow from CNS and inhibit the release of renin secretion from the
Kidney
-Results in the reduction of angiotensin II and aldosterone causing reduced peripheral resistance and sodium and water retention

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60
Q

What are the clinical outcomes of using BB

A

reduce systolic BP by 10-20mm Hg and diastolic pressure by 10-15mm Hg

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61
Q

What are the plethora of uses for BB

A

HTN , Angina, Select arrythmias, CF, MI, Hyperthyroid, Migraine HA, Pheos, Gluacoma

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62
Q

Where are B1 and B2 receptors found

A

β1 receptors are primarily on the heart

β2 receptors
Primarily located at the bronchial tree, skeletal muscle blood vessels, kidney, and liver
-Not very important for the treatment of primary hypertension, but are of concern in asthma and diabetes
-Activated β2 receptors causes bronchial dilation and can increase blood glucose due to glycogenolysis
-β2 receptors antagonist restrict bronchioles and reduce glucose production ( which is a problem for asthma and lung pts)

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63
Q

What is the MOA of ISA BB

A

Partial BB agonsist

Option for patients who need a beta blocker but experience significant bradycardia from a non-ISA agent

-Avoid use post myocardial infarction

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64
Q

Can ISA BB be used in MI

A

NO

Do not use acebutolol pindolol or penbutolol
APP

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65
Q

Which two BB have high lipid soluablilty and what does ADE does this cause

A

Propranolol and Bisprolol

Lipophilic agents enter the CNS better and may result in more cases of:
Drowsiness, mental confusion, nightmares, and depression

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66
Q

If you wanted to avoid CNS S/s of BB which two would you use and why

A

Atenolol and Nadolol

They have the lowest lipid soluability

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67
Q

What effect do BB have on glycemia

A

mask symptoms of hypoglycemia and reduce the ability to recover from hypoglycemia (sympathetic activation of beta receptors)

So avoid in DM

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68
Q

What effect do BB have on Asthma Pts

A

non-cardioselective β-blockers can make bronchoconstriction worse, and block the action of bronchodilators

So caution with proprnolol, nadolol, and timolol
(PNT)

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69
Q

Do BB effect erections

A

Yes may decrease libido or cause ED

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70
Q

What would happen if you rapidly withdrew BB

A

may induce angina, myocardial infarction, and even sudden death in patients with ischemic heart disease

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71
Q

Should BB and CCB be used together

A

may produce bradycardia if used with non-dihydropyridine calcium-channel blockers (Non-DHP CCB) such as verapamil or diltiazem

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72
Q

Can BB be used with NSAIDs

A

may impair the hypotensive effects of beta blockers by interference with the auto regulation of renal blood flow

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73
Q

Can BB be used with clonidine

A

Yes, but increased risk of clonidine withdrawal hypertensive crisis if stopped before beta blocker can be initiated (may have to taper for 1 week)

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74
Q

How long should clonidine be tappered with BB admin

A

1 week, if not it can cause HTN crisis

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75
Q

What is the MOA of mixed A1 and NSBB

A

In hypertension, decrease’s rate and strength of contraction of heart without reflex vasoconstriction (α1 antagonism)

In CHF, decreases afterload by inhibiting vasoconstriction (α1 antagonism) while decreasing SNS tone via β-blockade

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76
Q

What are the two mixed A1 and NSBB

A

Carvedilol and Labetolol

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77
Q

What are the 3 ISABB

A

Acebutolol, Pindolo, penbutolol

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78
Q

What are the 3 B1 selective BB

A

Atenolol, metropolol, bispropolol

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79
Q

What are the three NSBB

A

Propranolol
Nadolol
Timolol

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80
Q

What is the MOA of CCB

A

Block the inward movement (L-type calcium channel) of calcium ions through the L channels of arterial smooth muscle cells and cardiac cells of the coronary and systemic arterial vasculature

Arteriolar vasodilators that cause a decrease in smooth muscle tone and vascular resistance

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81
Q

What are the 2 types of CCB

A

Dihydropyridines (DHP):
-Minimal direct cardiac effect, may cause compensative tachycardia
End in “pine”; amlodipine, nicardipine, felodipine

Non-dihydropyridines (Non-DHP):

  • More selective for myocardium
  • Negative inotrope
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82
Q

What type of CCB are Preferred in patients with fast heart rates and even for rate control with atrial fibrillation who cannot tolerate a beta blockers

A

Non DHPs

  • Verapamil
  • Diltiazem
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83
Q

What is the least selective NONDHP CCB

A

Verapamil

Significant effects on both cardiac and vascular smooth muscle cells

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84
Q

What is the clinical use of Verapamil

A

Angina, supraventricular tachyarrhythmia, and prophylaxis for migraine!! And Cluster headaches!!

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85
Q

What is the clinical use of diltiazem

A

supraventricular tachyarrhythmia (decrease rate in atrial flutter and atrial fibrillation)

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86
Q

What is the major diff between NONDHP and DHP CCB

A

DHPs mostly vasodilate

NonDHPS decease HR, AV node conduction and contractility and also vasodilate

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87
Q

CCB are most effective in what pt population

A

BLACK PEOPLE

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88
Q

Should CCB be used in HF

A

Caution!

Amlodipine touted as safe in patients with hypertension and advanced heart failure

Studies have shown a 38% increased risk of heart failure with amlodipine vs. diuretic

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89
Q

A pt has HTN and Asthma

What drug is best

A

CCB not BB

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90
Q

A pt has HTN and DM

Use what drug

A

CCB not BB ( they mask glycemia)

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91
Q

A pt has HTN and angina

Use what drug

A

CCB

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92
Q

A pt has HTN and PVD

Use what drug class

A

CCB

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93
Q

What is the drug class that can treat Isolated sys HTN

A

CCB

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94
Q

What is dihyropyridines with CCB

A

Watch for ankle edema, flushing, dizziness, headache, and fatigue

Nifedipine: gingival enlargement

Avoid high dose short-acting CCBs because of increased risk of MI due to excessive vasodilation and marked reflex tachycardia (Nifidipine)

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95
Q

You just started a pt on verapamil and now they cany poop, is this normal

A

Yes Verapamil causes constipation

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96
Q

What medications should be avoided when RX CCB

A

Digoxin with Verapamil or Diltiazem
May increase digoxin (anti arrhythmic agent) level by 20-70%

Beta blockers with Verapamil or Diltiazem produce additive negative inotropic effects (bradycardia)

Only Dihydropyridine CCBs can be safely combined with beta blockers
(So dont use verapamil or diltizem with BB)

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97
Q

What is the MOA of hydralazine and minoxadil

A

Direct Arterial Vasodilators
Mechanism of Action: directly relaxes arteries and arterioles in smooth muscle and decreases peripheral vascular resistance and arterial blood pressure

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98
Q

What are the clinical uses of hydralazine

A

Reserves for severe HTN in refractory HTN +3 meds

Or used in HTN emergency to rapidly drop the BP

Can be used safely in pregnant pts

Also used in combo with isosorbide dinitrate to treat HTN and HF in black pts

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99
Q

A pregnant black pt started a recent HTN med but cant remember the name

Today she presetns with a headache, TachyHR, Nausea, diaphories, palpations, and angina, you notice a butterfly like rash on her face that spares the corners of her mouth

What is the medication she most likely started on

A

Hydralazine

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100
Q

What is the clinical use of minoxidil

A

Used when maximal doses of hydralazine are not effective or in patients with renal failure and severe hypertension who do not respond well to hydralazine

Greater reflex sympathetic stimulation and sodium and water retention

Also can be used topically for male pattern baldness

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101
Q

You recently started a pt on hydralazine for refractory HTN

Today they present with Renal failure and severe HTN

What drug should be used now

A

Minoxadil

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102
Q

What are the ADE of minoxidil

A

TachyHR, palpations, angina, sweating, and edema,

Same as hydralazine

ALSO MAJOR HAIR GROWTH

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103
Q

What are the 1st line agents to pharm tx of HTN

A

First-line agents include thiazide/thiazide-like diuretics, CCBs, and ACE inhibitors or ARBs

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104
Q

When mono tx vs 2 drug tx be used for htn

A

Single antihypertensive drug is reasonable in adults with stage 1 hypertension and BP goal <130/80 mm Hg with dosage titration and sequential addition of other agents to achieve the BP target

2 first-line agents of different classes is recommended in adults with stage 2 hypertension

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105
Q

In black adults with hypertension but without HF or CKD, including those with DM, initial antihypertensive treatment should include…

A

Thyazid diuertic or CCB

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106
Q

A pt presents with an elevated BP of 190/130 with LOC, possible aortic dissection, with pulm edema

Think

A

HTN crisis

Admit, TX emergently

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107
Q

What are the S/s of HTN crisis

A 
Stroke
Loss of consciousness
Memory loss
Crushing chest pain/ Heart attack
Damage to the eyes and kidneys
Aortic dissection
Angina (unstable chest pain)
Pulmonary edema
Eclampsia
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108
Q

What is the MOA of nitro

A

Forms free radical NO

Venous dilation more than arterial dialtion

Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure), may modestly reduce afterload

Dilates coronary arteries and improves collateral flow to ischemic regions

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109
Q

What are the 3 clin uses of nitro

A

Acute decomp HF ( WARM AND WET or COLD and DRY- inotrope alt)

HTN emergency ( Ideal choice for pts with ischemic HDz, MI, HTN s/p bypass, pulm edema)

Considered the preferred agent for preload reduction in patients with pulmonary congestion

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110
Q

What is Considered the preferred agent for preload reduction in patients with pulmonary congestion

A

Nitro

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111
Q

Why must nitro be stored in glass bottles

A

PVC tubing and bags may absorb nitroglycerin

Use glass bottles and special non-PVC tubing to administer IV nitroglycerin when possible (pre-mixed bottles)

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112
Q

You are in the ED treating a warm and wet HF pt, your collegue just administered nitro

What are the ADE of nitro tx

A

Severe HA, Vomitting, ICP, and methemoglobinemia

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113
Q

What is the MOA of sodium nitroprusside

A

mixed arterial–venous vasodilator, acts on smooth muscle increasing synthesis of nitric oxide to produce a balanced vasodilating action

Effectsd afterload more

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114
Q

What is considered DOC for most cases of hypertensive emergency

A

Sodium nitroprusside

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115
Q

Your in the ED treating a warm and wet HF pt

Your collegue just administered sodium nitroprusside

labs come back and the pt has poor renal function

What ADE is this pt at risk of

A

Cyanide poisoning

Combines with hemoglobin to produce cyanide and cyanmethemoglobin
Cyanide hepatically metabolized and thiocyanate renally excreted

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116
Q

What are the ADE of sodium nitroprusside

A

HOTN, Cyanide toxic, ICP

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117
Q

What is the MOA of Fenoldopam

A

Direct Dopamine Agonist

D1 agonist that bind with moderate affinity to α2 receptors

Rapid acting vasodilator

Decreases peripheral vascular resistance and BP secondary to increased renal blood flow, and natriuresis/diuresis

6 times more potent as dopamine in producing renal vasodilation

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118
Q

What is the clin use of fenoldopam

A

treatment in hospital, short-term (up to 48hrs) management of severe hypertension when rapid, but quickly reversible, emergency reduction of blood pressure is clinically indicated (HTN CRISIS)

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119
Q

A pt presents with HTN crisis, and you promptyl drop the BP with fenoldopam

What are the ADE you know must be aware of

A

Headache/flushing/dizziness
N/V
Reflex tachycardia
Hypokalemia

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120
Q

What is special about nicardipine

A

It can be in tablets and IV ( Iv dose not require a loading dose)

useful in patients acute with intracerebral hemorrhage/acute ischemic stroke, hypertensive encephalopathy, preeclampsia or eclampsia, acute renal failure, sympathetic crisis, and perioperative hypertension

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121
Q

What is special about enalaprilat

A

ACEI that can be used IV

Only ACEI available in IV formulation

Advantageous in patients who are in need of prolonged BP control

Titration difficult and hypotension can potentially develop in some patients

Avoid in patients with decompensated HF or acute MI, pregnancy, or bilat renal art stenosis

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122
Q

What is special about esmolol

A

Ultra short acting B1 selective BB

Useful in conditions related to severe tachycardia, and increased cardiac output, and severe post-op hypertension

Avoid in patients with decompensated heart failure,

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123
Q

What is special about labetolol

A

Mechanism of action: selective α1 and non-selective beta blocker

Used for both urgency (PO) and emergency (IV)

Does NOT cause reflex tachycardia (no increase in myocardial O2 demand) so it is preferred in coronary artery disease, acute dissection, end stage renal disease, acute intracerebral hemorrhage/acute ischemic stroke or MI

Does not reduce cerebral blood flow

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124
Q

Can enalaprilat cause angioedema

A

Yes

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125
Q

What is diuresis

A

C ondition that causes urine to be excreted, usually associated with large volumes

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126
Q

What is uremia

A

an accumulation of nitrogenous waste products in the blood due to impaired renal filtration

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127
Q

What is tubular secretion

A

process in which the nephrons produce and release substances (ions, acids, and bases) that facilitate sodium ion reabsorption and maintain acid-base balance

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128
Q

How much fluid is filtered at the glomerulas dialy

A

180L

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129
Q

What is a NML GFR

A

About 130mls/mil

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130
Q

What is the best overall index of kidney fx

A

GFR

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131
Q

What is widely used to estimate GFR

A

CrCl

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132
Q

What is the cockcroft-gault equation

A

CrCl= (140-age) x wt (kg) (O.85 for females)

All divided by (Scrx72)

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133
Q

What is the most accurate way to find a CrCl

A

24 hr urine

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134
Q

What is a NML CrCl

A

90-140

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135
Q

ADH works were

A

Collecting ducts

136
Q

Where is the majority of sodium absorbed in the Nephron

A

In the PCT

137
Q

Is the descending loop of henle permiable to sodium

A

No

138
Q

Is the thick ascending loop of henle permeable to water

A

No

139
Q

Where do loop directs have thier greatest effect

A

The thick ascending loop of henle

140
Q

How do loop diruertics work on the loop of henle

A

Loop diuretics inhibit the co-transporter; which reduces the lumen-positive potential, causing an increase in urinary excretion of divalent cations in addition to NaCl

Loop diuretics are the most efficacious of all diuretic classes

141
Q

Is the DCT permeable to water

A

Relatively impermeable to water

142
Q

Where is calcium reabsobped in the nephron

A

In the DCT

143
Q

What part of the nephron do thiazides work at

A

The DCT

144
Q

Where do Sodium Channel blockers and aldosterone agonist work in the nephron

A

Collecting Duct

145
Q

What are the clin used of Diuretics

A

Edema (e.g., secondary CHF, etc.) (i.e., primarily thiazides and loops)

Hypertension (i.e., primarily thiazides)

Acute renal failure

Hypercalcemia (i.e., loops)

Hypercalciuria (with renal stone
formation) (i.e., thiazides)

Glaucoma (i.e., Carbonic Anhydrous Inhibitors)

Mountain sickness (i.e., acetazolamide)

Acute brain injuries (i.e., mannitol)

146
Q

What is the MOA of Carbonic Anhydrous Inhibitors

A

Mechanism of Action: increases sodium and water excretion by inhibiting the enzyme carbonic anhydrase in the proximal convoluted tubular cells

Results in increased Na+ excretion because H+ is no longer being excreted to combine with HCO3-

Loss of HCO3- causes hyperchloremic metabolic acidosis and decreased efficacy after several days therapy

147
Q

After several days o acetazolamide Tx was is the pt at an increased Rsk of

A

Hypercholremic Metabolic acidosis

148
Q

What are the clin uses of Acetazolamide

A

Tx open angle glaucoma (decreases production of aqueous humor)

Or mountain sickness

It works by decreasing the amount of CSF and pH of the CSF where carbonic acid is responsible for secreting bicarbonate
Creates a mild acidosis resulting in hyperventilation
(Prophylaxis)

Can also be used for absene SZR

149
Q

Where is acetazolamide absorbed

A

absorbed well orally, not metabolized in the body, but excreted totally by the proximal convoluted tubules (PCT)

150
Q

Your on a sumit in south america, and you treated your companions with acetazolamide for 5 days prior to accent to reduce SOB, pulm edema, cerebral edema..

One of your hikers has a sulfa allergy, and another has poor kindey function,

What are the ADE of acetazola,ide Tx

A

CNS: drowsiness, anorexia, headache, depression

Allergic rash (sulfonamide derivative)

Hypokalemia

Hyperchloremic Metabolic Acidosis

Kidney Stones: Ca2+ less soluble in an alkaline environment; risk increases 10 fold

151
Q

Can a pt in liver failure take acetazolamide

A

No, should be avoided in pts with cirrhosis

152
Q

Can a pt with COPD take acetazolmide

A

Should be used with caution

153
Q

What is the MOA of mannitol

A

Osmotically active agent (largely confined to the extracellular space) that is filtered by the glomerulus but not reabsorbed causes water to be retained in these segments (PCT) and promotes a water diuresis

Increases urinary output secondary to increased plasma volume delivered to the kidneys resulting from a hypertonic plasma that draws fluid out of the tissues and promotes water diuresis (osmotic gradient that attracts water)

154
Q

What are the two clin uses of mannitol

A

Tx of the oliguric phase of acute renal failure

And ICP

Also can be used to maintain urine flow in toxic states

(MUST BE GIVEN IV)

155
Q

should pts in CHF get mannitol

A

No, it increases vascular fluid and can worsen the condition

156
Q

What are the C/I for mannitol

A

active intracranial bleeding, pulmonary edema, or chronic edema due to cardio insufficiency

157
Q

What is the loop diuretic that is safe to use in pts with sulfa allergies

A

Ethacrynic acid

158
Q

What is the MOA of Loop diuretics

A

increases urinary output by selectively blocking the reabsorption of Na+ and Cl- (i.e., Na+/K+/2Cl- co-transporter) in the ascending loop of Henle

159
Q

What does it mean to be a “high-cieling: diuertic like furosemide

A

Effacacy increases with dose

160
Q

What is teh DOC in reducing extra volume in HF

A

Loop diuretcs

161
Q

What is the drug class of diuretics that can treat
Acute renal failure
Hyperkaleia
Acute hypre Ca2+
Or an Anion overdose (bromide, fluoride, iodide)

A

Loop diuretic

162
Q

What are the ADE of loop diuertics

A

THink all electrolytes will be down

Hypo K, Hypo Ca2+, Acute hypovolemia,

Can cause ototoxicity/ deafness (can be perminint)

Hyperurecemia

Ethacrynic acid and furosemide compete with uric acid for the renal secretory systems (blocking the system can cause or exacerbate gout)

163
Q

What is the only 2 contra/ind for loop diuertics

A

Hypersensitivity to Sulfonamide: except Ethacrynic acid

Anuric patients or patients with severe electrolyte disturbances

164
Q

Should loop diuretics be used with NSAIDs

A

No, they work opposite of eachother

165
Q

What effect do aminoglycoside ABX have on the nephron

A

Nephrotoxic, avoid in use with loop diuretics

166
Q

Which two loop diuretics are most likely to cause hyperurecimaia

A

Both furosemide and ethacrynic acid are more likely to cause hyperuricemia; compete with uric acid for secretion

167
Q

What are the clin uses for Thiazide/like diuretics

A

HTN, HF(edema reduction), Hypercalcemia (useful in tx kidney stones)
DI

168
Q

What diuretic can be used to treat….DI!!!?

A

Thiazides have the ability to reduce polyuria and produce hyperosmolar urine (can substitute for antidiuretic hormone)

169
Q

What is the hypothosis on how thiazides work

A

The most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion

170
Q

What are the 5 main actions of thiazide/ like meds

A 
Increase NA and Cl- excretion 
Loss of K+ 
Loss of Mg+ 
Decreased urinary calcium exceretion 
Reduced PVR
171
Q

As a class, thiazides become inefective at what GFR

A

Less than 30 mlls/min

Except for metolazone which remains effective all the way to 10-20 mls.min

172
Q

What is the only thiazide available for IV admin

A

Chlorothiazide

173
Q

What effect do thiazides have on lipids

A

5-10% increase in LDL

174
Q

When starting a pt on thiazdes, how often should you check thier K+

A

Q 2-4 wks then q6-12 months

If K falls below 3.5 , add a potassium supplemtn or a potassium sparing combo

175
Q

How do thiazides effect diabetes pts

A

Impairs release of insulin and tissue uptake of glucose

Diabetes patients may have difficulty maintaining appropriate blood sugar levels

176
Q

Can pts with a sulfa d/o take thiazides

A

No

They should take a loop diurttic- etharcynic acid

177
Q

Can thiazides be used with ACEI

A

No may cause severe HOTN

178
Q

Can thiazides be used with digoxin

A

No, can causes hypokalemia

179
Q

Can pts on lithium take thiazides

A

No, may cause toxiciity

180
Q

Can pts taking NSAID take thaizides

A

No, it may blunt the diuretic effect

Remember NSAIDs decrease flow to the glomerulus

181
Q

What are the two thiazide and the three thiazide like meds

A

Thiazide:
HTCZ and chlorothiazide

Like:
Chlothalidone
Indapamide
Metolazone

182
Q

What is the MOA of Eplerenone and Spironolactone

A

Aldosterone antagonist

Increases urinary output by blocking the effects of aldosterone in the collecting duct leading to Na+ loss and K+ retention

183
Q

What is the MOA of Amiloride and triamterene

A

Na+ channel inhibitor

Increases urinary output by excreting Na+ and retaining K+ in the collecting duct; does not work on aldosterone

184
Q

What effect does aldosterone have on the heart

A

contributes to cardiac hypertrophy and myocardial fibrosis

185
Q

You have a pt that presents with ascitis, what diuretic is indicated for this pt

A

K+sparing

186
Q

Spironolactone is used off label to treat what GYN condition

A

Polycystic ovarian syndrome

187
Q

What is the DOC (diuretic) for hepatic cirrhosis

A

Spirinolactone

188
Q

How are K sparing diuretcs used in Resistant HTN

A

in combination with a thiazide or loop diuretic (HCTZ or furosemide)

189
Q

How are K+ sparing diuretics used in HF

A

aldosterone antagonists prevents the remodeling that occurs as compensation for the progressive failure of the heart
(Spirinolactone, epelerone)

190
Q

How are potassium sparing diuretics used in secondary hyperaldosteronism

A

spironolactone, more effective in patients with hepatic cirrhosis and nephrotic syndrome

191
Q

What effect does spirnolactone have on adrogens

A

Blocks androgen receptors and inhibits steroid synthesis at high doses

Can be used for polycystic ovary syndrome

192
Q

What are the ADE of sprinolactone

A

Hyper K and gynocomastio in males

Can use epleronone instead for the males

193
Q

What are the contra/ind for K+ sparing diuretics

A

Actic PUD or pregnancy

194
Q

What is the DOC for lithioum induce DI

A

Triamterene

195
Q

What effect does K have on glucose and what is its relevance to K+ sparing diuretics

A

K+ is needed to move glucose across the cell; when K+ levels fall, less glucose moves across the cell and more glucose remains in the plasma

Can cause hyper glycemia

196
Q

Using K+_ sparing diuertics cause gout and how

A

Yes

Can lead to hyperuracemia and a gout flare

Due to secondary competition for uric acid secretion within the organic acid secretory system (i.e., diuretic secreted and uric acid is retained)

197
Q

What area of the heart has the fastest phase 4 depolarization

A

Sinoatrial node

Also has a higher resting potential

198
Q

What is phase 0 of the action potential of the heart

A

rapid depolarization due to influx of sodium ions, generates an action potential (cell depolarizes and begins to contract)

199
Q

What is phase 1 of the action potential

A

early rapid repolarization due to potassium moving out of cell (contraction is in process)

200
Q

What is phase 2 of an action potential

A

plateau phase mainly due to the inward movement of calcium ions into the muscle cell and function in myocardial contraction

201
Q

What is phase 3 of an action potential

A

repolarization, potassium ions move out of cell

202
Q

What is phase 4 of an action potential

A

potassium flows out and sodium seeps into the cell (membrane potential has returned to its resting level and is ready for the next action potential)

203
Q

What is the difference between absolute and relative refractory period

A

Absolute refractory period is the interval during which a second action potential absolutely cannot be initiated, NO matter how large a stimulus is applied

Relative refractory period is the interval immediately following the absolute refractory period, during which initiation of a second action potential is inhibited but not impossible

204
Q

What is re-entry phenomenon/ heartblocks

A

1st degree heart block:
Electrical impulse travel through AV node too slowly, but impulse reaches ventricles
Results in PR prolongation

2nd degree heart block:
Electrical impulses travel slowly through the AV node and occasionally get blocked, causing the ventricles to beat out of sequence

3rd degree heart block:
Electric impulses do not reach the ventricles from the atria, so the ventricles create their own impulse, which causes the ventricles to beat out of sequence with the atria
Can be a life-threatening condition

205
Q

Excessive prolongation of the QTi leads to increased risk of…

A

Torsades de pointes

206
Q

What is the most common cause of QTi prolongation

A

Drug-induced

207
Q

When the QTi is greater than 500 miliseconds what is the pt at risk of

A

Torsasdes

208
Q

Is aflutter a rentry problem

A

Yes

209
Q

Waht are common causes of PSVT

A

digitalis toxicity, caffeine intake, anxiety, alcohol, Wolff-Parkinson-White syndrome

210
Q

Is antiarrhymic thearpy alwasy beneficial

A

CAST trial proved that continued treatment with encainide and flecainide resulted in a 2-3 fold increase in death and challenged the assumption that antiarrhythmic therapy is always beneficial

211
Q

What is the most common system of antiarrhythmic classification

A

Vaughn-Williams Classification

212
Q

What is a class IA drug

A

Na+ channel blocker that:

Lengthen the refractory period
Decrease automaticity in sodium-dependent conduction tissue
Decrease conduction velocity

213
Q

What is a class IB drug

A

Fast Na+ channel blocker

Weak sodium channel blockers
Shortens phase 3 repolarization in ventricular muscle fibers decreases refractory period
Possess local anesthetic activity

214
Q

What is a class IC channel blocker

A

Potent Na channel Blocker

Slows the conduction velocity while having little effect on the refractory period
Useful in both supraventricular and ventricular arrhythmias but are not often used for ventricular arrhythmias due to proarrhythmia risk

215
Q

What is a class II drug

A

BB

Block catecholamines at the beta receptor in the heart to decrease conduction velocity
Lengthen the refractory period
Decrease automaticity

216
Q

What is a Class III drug

A

K+ blocker

Prolongs phase 3 (refractory period in ventricular and supraventricular tissue)

217
Q

What is a class IV drug

A

Ca2+ blocker

Inhibits action potential in SA and AV nodes to prolong the refractory period
Slow conduction
Decrease automaticity

218
Q

What are three Class Ia drugs

A

Disopyramide
Quinidine
Procanamide

All increase the QRS and QT,
Used to tx atrial and vent arrythmias

219
Q

What are two Ib drugs

A

Lidocaine and Mexiletine

Both decrease the Qt interval
Used to treat Vent arrythmias

220
Q

What are 2 class Ic drugs

A

Flecainide and propafenone

Both increase the QRs
Used to treat atrial and vent arrythmias

221
Q

What are 4 class II drugs a

A

Propranolol
metroprolol
Atenolol
Esmolol

Both decrease HR and Increase PR

Used to treat Tachyarrhythmias caused by sympathetic activity, Supraventricular and Ventricular Arrthymias

222
Q

What are 5 Class III drugs

A 
Amioderone 
Sotalol 
Ibutilide 
Dofetilide 
Droedarone

All increase QT interval

Used to treat Atrail and Vent Arrythmias

223
Q

Waht are 2 class IV drugs

A

Verapamil and diltiazem

Both decrease HR and increase PR

Used to treat: Atrial Arrthymias (atrial flutter/fibrillation), reentrant Supraventricular Tachycardia

224
Q

What is the MOA of class I agents

A

Na channel blockers
Blocks voltage sensitive Na channels

Used for ryhtynm control

225
Q

What effect do class Ia have on the refractory preiod

A

Decrease Phase 0 upstroke velocity and prolong repolarization

226
Q

What effect do class Ib have on the refractory period

A

Prolong phase0 mildly and SHORTENS the repolarizatrion period

227
Q

What effect does class Ic drugs have on the refractory period

A

Markedly delays phase0 , with minimal effect of the repolarization period

228
Q

What are the ADE of quinidine

A

N/V/D, Cinchonism ( flushed sweaty skin with ringing of the ears), HOTN, Syncope, and skeletal muscle wkness especially MG pts

229
Q

What is cinchonism

A

An ADE of quinidine

Ninchina is tha alkoloid of quinie

S/s: Flushed, sweaty skin, ringing in the ears
Anticholinergic Properties: blurred vision, tinnitus, headache, disorientation, and psychosis/hallucinations

High doses cause arrhythmias and ventricular tachycardia, which can be fatal

230
Q

When Rx quinidine for a pt with Myasthenia Gravis, what should the provider be aware of

A

Quinidne can deprress all muscle funciton and can exacterbate MG

231
Q

What is the most requently used Class IA agent

A

Procanamide

Used to treat SVT and Vent arrythmias

232
Q

If procanimide is given to quickly, what happenes

A

HOTN

233
Q

What is the active metabolite of procanimide that prolongs the duration of the action potential

A

NAPA (N-acetylprocanamide)

NAPA is secreted by the kidneys so procanaide needs renal dosing adjuctment

234
Q

What are the ADE of procanamide

A

QT interval prolongations, and Syncope

Longer term can produce a lupus type rash/ syndrome
Arthralgia/ arthritis

And serum increases of antinuclear antibodies

235
Q

Disopyramide crosses multiple classes, it is both a Class Ia and also..

A

Class III ( K+ blocker)

236
Q

What is the role of disopyramide

A

ventricular arrhythmias that are refractory or intolerant to quinidine or procainamide

237
Q

What is the class and clin use for Lidocaine

A

Class IB

Use: Terminate Ventricular Tachycardia with a pulse
Prevent ventricular fibrillation after cardioversion
An alternative agent in pulseless VT /VF if amiodarone is not available

238
Q

Can you safely admin lidocaine to a pt with CHF or hepatic Dz ?

A

Yes, however the doseage must be adjucted

HF: Lidocaine’s volume of distribution and total body clearance may both be decreased

239
Q

What is the least cardio toxic medication of the sodium channel blockers

A

Lidocaine

240
Q

Can a pt in 3* HB get lidocaine

A

NO!

241
Q

What is the relationship between lidocaine and amioderone

A

Amiodarone can increase lidocaine levels

242
Q

What is the orally active form of lidocaine

A

Mexiletine

Used for Tx of Vent arrythmias with a previous MI

Also can be used off label to treat DM neuropathy

243
Q

A pt who has an otherwise nml heart + SVT what is the lass of medications for clin use

A

Class Ic

These drugs can not be used in pts with HEART FAILURE OR post MI

(Flecaindie and propfenone)

244
Q

Can flecaindie be used in HF

A

Specific to Flecainide: possesses negative inotropic effects and can exacerbate heart failure

245
Q

What is the clin use of flecainde and what is the pill in pocket approach

A

Maintenance of sinus rhythm of atrial fib and flutter in patients without structural heart disease
“Pill in Pocket Approach”_ take a pill and use it when you feel S/s

246
Q

Flecainide had death that was greater than placebo?

A

Yes, use pill in pocket approach, this med can be dangerous

247
Q

What is the MOA of propafenone

A

Mechanism of Actions: Potent Na+ Channel Blocker

Possess weak beta-blocking properties

248
Q

What is the clin use of Class Ic meds

A

Indicated in patients without structural heart disease for supraventricular arrhythmias; rhythm control of atrial fibrillation or flutter and etc.
“Pill in Pocket Approach”

249
Q

What effect do BB have on refractory periods

A

Diminish phase 4 depoloarizaation

Prolong AV node conduction

250
Q

What is the DOC in Afib / A Flutter

A

BB

251
Q

Post MI patients should be started on β-blocker unless contraindicated to suppress….

A

PVCs

252
Q

Due to its short Half life what B1 selective BB is used intraoperatively for blood pressure, heart rate control, and other acute arrhythmias requiring a beta blocker

A

Esmolol

253
Q

What is the MOA of class III meds

A

Mechanism of Action: K+ Channel Blockers

Prolongs phase 3 (refractory period in ventricular and supraventricular tissue)

Electrophysiological Effects:

  • Prolong duration of action potential and effective refractory period
  • Interfere with the outward K+ currents or slow inward Na+ currents
  • No significant effect on conduction velocity
  • All class III agents have the potential to induce arrhythmias
254
Q

Can Class III meds induce arrhythmias

A

Yes, all class III agents can

255
Q

What is the MOA of amiodernone

A

Contains iodine and is related structurally to thyroxine

Has class I, II, III, IV actions but its main action is prolongation of the action potential and refractory period by blocking potassium channels

Possess both α-blocking activity, anti-angina, and vasodilatory effects

256
Q

What is the DOC for pulseless VT/ Vfib ( cardiac arrest)

A

Amioderone

257
Q

What is the prefered agent in pts with LVDF (HF)

A

Amioderone

258
Q

What are the C/I to amioderone

A

Remember it contains iodine and is structurally similar to thyroxine… so

Iodine hypersensitivity
Hyperthyroidism
Third-degree heart block

259
Q

What are the ADE of Amioderone

A

50% of pts stopped meds due to severeity of ADE

CNS effects: heartblock, HOTN, tremors, ataxia, neuropathy

Pulm Fibrosis
( CXR and Pulm fx tests are required at baseline and q 6-12 months)

Liver toxicity
(Monitor at baseline and q 6 months of tx)

Hypo/hyperthyroid
(Same monitor)

BLUE GRAY SKIN!

Optic neurtitis (monitor for visual impairments)

260
Q

IS dronedarone more or less effective than amiodernone

What makes it differnt

A

Less effective

Derivative of amiodarone: does not posses the iodine moieties that are responsible for thyroid dysfunction like amiodarone

Maintain sinus rhythm in atrial fibrillation/flutter in patients with a history of paroxysmal or persistent atrial fibrillation

261
Q

What is the mechanism of action of SOTALOL, dont get tricked thinking its just a BB )

A

Mechanism of Action: K+ Channel Blockers

Prolongs cardiac action potential

Increases the duration of the refractory period

Potent non selective beta blocker activity (Class II action)

50% beta blocking properties and K+ blocking properties (Class III)

Not classified as a beta blocker

262
Q

What is the DOC for SVT and Vent arrhythmia is pediatric age groups

A

Sotalol

263
Q

What is the black box warning for sotalol

A

Black Box Warning: patient initiated or reinitiated on sotalol should be placed for a minimum of 3 days (on their maintenance dose) in a facility that can provide cardiac resuscitation and continuous ECG monitoring

264
Q

What is the clin use of Ibutilide

A

Rapid conversion of afib to NSR

Careful! It can cause torsades

265
Q

If you give ibutilide, how long must you monitor the pt for torsades

A

Patients require continuous ECG monitoring for 4 hours post infusion or until QTc returns to baseline

266
Q

What is the clinuse of Class III drug Dofetilide

A

Indicated for the conversion of atrial fibrillation/atrial flutter and maintenance of normal sinus rhythm in patients whose arrhythmia is of greater than one week duration and who have been converted to normal sinus rhythm

Reserved for patients in whom atrial fibrillation/atrial flutter is highly symptomatic

So essential you would use ibutilide in the acute phase and then dofetilide in the long term managment

267
Q

You just succesfully converted a pt out of afib with ibutilide.. to maintain this pts therapy what drug should you use

A

Dofetilide,

268
Q

What is the black box warning of dofetilide

A

Black Boxed Warning: hospitalization mandatory for initiation, obtain QTc 2-3 hours after each of the 1st five doses

Restricted to prescribers who have completed a specific manufacturer’s training session

269
Q

Can dofetilide be Rx outpt?

A

NO, requires hospitilization

270
Q

A pt with poor renal function (CrCl) is given dofetilide, what ADE are they now at risk for

A

Dofetilide is excreted renally, so an accumulation of dofetilide can increase the QTi and lead to torsades

271
Q

Where do CCB have thier action in on refractory periods

A

Phase 0

272
Q

What is the MOA of Digoxin

A

Cardiac glycoside (inotrpe)

Inhibts the NA/+ pump

273
Q

What are the clin effects of Digoxin

A

Inotrope and slows SA and AV node through vagus stim.

Slows HR and Av conduction

274
Q

What is the clinical benifit of digoxin

A

Positive inotropic effects, increases the force of myocardial contraction and does not cause increase oxygen consumption

275
Q

A pt has Afib, what drug can be used to prevent RVR

A

Digoxin

276
Q

Should digoxin be used in HF pts

A

No

277
Q

What electroyltes interact with digoxin

A

K+ and Ca2+

Hypokalemic results in increased digoxin binding and thereby enhances its therapeutic and toxic effects
Decreased K+ may cause an increased incidence of arrhythmias, which can lead to ventricular fibrillation and sudden death

Hyperkalemia reduces the effects of digoxin
Increase K+ reduces the enzyme-inhibiting actions of digoxin

Hypercalcemia enhances digitalis induced increases in intracellular calcium, which can lead to calcium overload and increased susceptibility to digitalis induced arrhythmias

278
Q

A pt presents with halos around thier visual fields, what med did they prolly just take

A

Digoxin

279
Q

What is the antidote to digoxin OD

A

Digoxin Immun fab

In patients not suffering from arrhythmias or electrolyte imbalances, discontinue digoxin for 2-3 days and restart if therapy is beneficial

280
Q

What must be done when giving digoxin

A

MONITOR MONITOR MONITOR

281
Q

What is the MOA of adenosine

A

Causes a slowing of the heart rate and AV conduction, which usually terminates the episode of tachycardia

Naturally occuring nucleotide in the body

Increase K and Ca2+ influx

Decreases conduction velocity, prolongs the refractory period and produces automaticity in the AV node

282
Q

What is the Doc in Regular PSVT

A

Adenosine

283
Q

What is the definition of paroxysmal AFib

A

spontaneous self-termination within 7 days of onset

284
Q

What defines persistnet Afib

A

Lasting 7> days

285
Q

What is longstanding persistnet Afib

A

Lasting more than 12 months

286
Q

What are the Tx options for a pt with Afib and no structural HDz

A

If they are in an expiernce hospoital: ablation

If not or med tx is perferred: 
Class IC ( Flecainide and Propfenone)
Dofetilide (Class III) 
Dronedarone (Class III) 
Sotolol (Class III)

If those dont work, you can either go straight to ablation or try amioderone 1st

If amio is unsuccefull, then abaltion

287
Q

Can pts with Afib and structural Hdz get class Ic tx

A

No

288
Q

What BB can be used in a pt with stable HF and needs vent rate control

A

Carvedilol, metoprolol, and bisoprolol

289
Q

Should BB be used in pts with WPW

A

No

290
Q

Can CCB be used in WPW

A

No

291
Q

What two types of drugs can be used to control vent rate

A

BB Class II

And Non DHP CCBs Class IV

292
Q

Is digoxin ever used a mono tx

A

No

Best Effective if additional HR control is needed when a patient is receiving a B-blocker, diltiazem, or verapamil

293
Q

Can digoxin be given to a pt with WPW

A

No

294
Q

What is the CHA2 DS2 VASc score

A

A rubric to asses if pts need anitcoag in afib

CHF (1)
HTN (1)
AGE (2) (>75)

DM (1)
Stroke (2)

Vasc Dz (1) 
Age (1) (65-74) 
Sex cat( 1)

Is score is greater than 2= anticoag tx
If score is 0-1 = consider asprinin

295
Q

What is considered the first line Tx for stable pts with Afib by the AHA

A

Elecctircal cardioversion

296
Q

Prior to coardioverting Afib, what must you do

A

Before converting MUST ensure absence of atrial thrombi!
-Trans Esophageal Echocardiogram (TEE) guided to visualize the atria
or
3 or more weeks of anticoagulation prior to cardioversion

With 4 weeks anticoagulation required after cardioversion regardless of method

297
Q

Regardless of method, what must all pts who are cardioverted from Afib be put on

A

Anticoag

298
Q

Class IC drugs can use the pill and the pocket approach to Afib tx with out structural heart disease… what are the class IC drugs

A

Flecaindie and propafenone

299
Q

How is amioderone used in pts after cardioverision of Afib

A

Initiated outpt after pts have rciveed cardiovert +anti coag

300
Q

What is the drug that can be used to treat Afib in a pt with WPW

A

Amio

301
Q

How do Epi and NE effect HF

A

Contributes to vent remoddeling and ypertrophy

302
Q

What effect does Angio II have on HF

A

Stimulated vent hypertropyy and remodelling

303
Q

What is the effect of BNP

A

Increases in response to stress and stretch of the ventricles

Hemodynamically causes vasodilation of arteries, veins, and coronary arteries

Neuro-hormonally decreases aldosterone, endothelin, and norepinephrine

Renally increases diuresis and naturesis

304
Q

What are the good vs bad effects of Bradykinins and ACE

A

Good” effects:
ACE inhibitors cause increase in bradykinin levels causing
Decreased peripheral vascular resistance

Decreased blood pressure

Bradykinin is involved in the production of nitric oxide and prostaglandins (Ex: prostacyclin)
Nitric oxide and prostacyclin are vasodilators

“Bad” effect:
Bradykinin and a related substance “substance P” are probably responsible for inducing a cough and angioedema
ACE inhibitors increase bradykinin and increase substance P

Note: ARBs do not affect bradykinin levels

305
Q

An elevated BNP is a sign of…

A

HF

306
Q

What are the ACEI that have been approved for HF tx

A

Captopril (50mg)
Enalapril (10mg)
Lisinopril (40mg)

(CEL)

Perindopril
Ramipril
Trandolapril

307
Q

What are the ARBs that have been approved

A

Candastartan (32 mg/day)
Losartan (150 mg./day)
Valsartan (160 mg/day)

(CLV)

308
Q

What is the MOA of sacubactril

A

Sacubitril: neprilysin Inhibitor

Inhibits neprilysin, which increase levels of peptides that are normally degraded by neprilysin

More of these peptides (natriuretic peptides, bradykinin, adrenomedullin) means more vasodilation and sodium loss plus less cardiac and vascular hypertrophy and remodeling

309
Q

A pt has a HFref
You start them on metoprolol, and lisinopril, furosemide, they have a K+ less than 5.0 and a CrCl greater than 30. So you start them on spirinolactone

You are considering wether to switch this pt to an ARNI, what C/I should be considered for initiaion of Rx

A

Contraindications:
Patients with a history of angioedema with a previous ACEI or ARB, concomitant use of an ACEI, and use with aliskiren in patients with diabetes.

Adverse Effects: hypotension, hyperkalemia, cough, dizziness, and renal failure

310
Q

A pt with HfrRF is taking aliskiren for DM, can you safely give this pt an ARNI

A

NO!

311
Q

If you use an ARNI with spirnoloactone what must you monitor

A

The K+ levels, can cause Hyper K

312
Q

Can you use ARNI and NSaid

A

Think of renal trifecta

NSAIDS+ ACE/ARB/ARNI may laed to increase risk of renal impairment

313
Q

How should pts with currnet or recent history of fluid retention be started on BB. ( think of a pt with HFreF

A

With a diuertic

314
Q

What are the BB approved for use in HF

A

Bisprolol (10mg/day)
Carvedilol (25mg/ BID)
or (80mg/day CR)
Metoprolol (200mg/day)

315
Q

When should you use Loop diuretics vs Thiazide./ like diuretics in HF

A

Loop Diuretics: best when fluid overload is excessive, needs to be done quickly, or when the kidney is impaired, GFR below 25 to 30mL/min

Thiazide and Thiazide-like Diuretics: may be used in mild fluid overload/regular management for hypertension

316
Q

What is the cieling effect of furosemide

A

120-200 mg

317
Q

What is the added benifit of K+ sparing diuretics in HF

A

Inhibit cardiac re-modeling = slows ventricular hypertrophy

318
Q

What is the MOA of Nesiritide

A

Human B-type natriuretic peptide (hBNP): neurohormone secreted from the ventricles in response to symptomatic CHF

Causing:

Arterial and venous dilation
Enhanced Na+ excretion
Suppression of the Renin-Angiotensin-Aldosterone System (RAAS) and the sympathetic nervous system

319
Q

What are the ADE of nesiritide

A

HOTN and azotemia

320
Q

Digoxin, dopamine, dobutaine, and milrinone are all examples of what kind of drug

A

Inotrope

321
Q

When is dopamiine used in the Tx of acute DHF

A

Generally avoided in the treatment of ADHF, except where the patient has significant systemic hypotension or cardiogenic shock in the face of elevated ventricular filling pressures

322
Q

What is the MOA of dobuatmine

A

Selective β1 receptor agonist with a small amount of α1 and β2

Clin use; ADHF (cold and dry)
Can be use alt in Cold and wet

323
Q

A pt is unresponsive to or has ADE to dopamine in shrot term severe HF whould be switched to waht drug

A

Dobutamine

324
Q

What is the MOA of milinone

A

Inhibits phosphodiesterase III (PDE3), enzyme responsible for breakdown of cAMP to AMP in the heart and vascular smooth muscle

Positive inotrope, arterial vasodilation and venous vasodilation
Increase in stroke volume = increase CO, with little change in HR
Decrease in SVR
No direct adrenergic effect (useful when patients are using beta blockers)

325
Q

What is the clin use of milrinone

A

Clinical Use: Acute Decompensated Heart Failure (ADHF)

Primarily cold and dry ADHF

Alternative/adjunct to diuretics in cold and wet ADHF

326
Q

What is the recommended salt restritcion in pts with Staged A-D HF

A

Limit salt to 1500mg/day for stages A and B and consider less than 3 g/day for stages C and D

327
Q

What is the NML PCWP and the CHF Optimal PCWP

A

NML 8-12 mmHg

Optimal CHF: less than 18 mmHg

328
Q

What is a cariac index

And what is a NML vs CHF optimal value

A

CI = CO/BSA; the volume of blood pumped by the heart (L/min) divided by the body surface area (m2)

CI is determined by two factors:
HR and SV; CO = HR X SV

Normal: 2.8-3.6
CHF optimal: >2.2

329
Q

What are the S.s of a wet HF pts

A 
D yspnea on exertion or rest
Orthopnea, paroxysmal nocturnal dyspnea
Peripheral edema
Rales
Early satiety, nausea/vomiting
Ascites
Hepatomegaly, splenomegaly
Jugular venous distention
Hepatojugular reflex
330
Q

What are the S/s of a cold HF pt

A 
Fatigue
Altered mental status or sleepiness
Cold extremities
Worsening renal function
Narrow pulse pressure
Hypotension
Hyponatremia
331
Q

What are the two inotropes used for Cold and dry ADHF

A

Dobutaqmine and milrinone

332
Q

What is the recommendation of use of steroids in HFreF

A

use at the lowest dose for the shortest length of time possible

Can cause fluid retention

333
Q

Can yiou use metformin, pioglitazone or saxagliptin in HF pts

A

No

334
Q

What is the DOC for intermittent claudication (muscle pain), for peripheral vascular disease

A

Cilostazol

335
Q

CAn you use Cilostazol in HF pts

A

No

Phosphodiesterase inhibitors have decreased survival rates in patients with class III-IV heart failure

336
Q

Can prazosin cause edema

A

Its an A1 blocker and yes

337
Q

Your hiking and eceryone in your party gets kidney stones, Potassium probles, a rash on the face, met acidodis, and headache.. what drug did you use that caused this

A

Acetazolamide

IPAP JUNIOR SEM. (43 decks)

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