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Pharm supplement > CV > Flashcards

CV Flashcards

1
Q

Adverse effects of Hydrochlorothiazide (HCTZ)

A

hypokalemia, hyponatremia, hypochloridemia
hypotension, hypovolemia
can increase uric acid levels

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2
Q

Effects/uses of Mannitol

A

strong diuresis,
rapid volume excretion needed for increased: ICP and IOP, renal fxn preservation

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3
Q

Blood is hypotonic: meaning, what is given

A

meaning: low solutes in blood, fluid going into cells,
give: hypertonic fluids (3% or 5% NaCl, 10% dextrose water (D10W)

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4
Q

Blood is isotonic: meaning, what is given

A

meaning: blood = same as cells about 280-300
give: isotonic (NS (0.9%), D5W)

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5
Q

Blood is hypertonic: meaning, what is given

A

Meaning: blood has high solutes (>300), risk for cellular dehydration
give: hypotonic (1/2 NS 0.45% NaCl)

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6
Q

Potassium Salts: uses, AE

A

Use: hypokalemia
AE: rapid can cause cardiac arrest, can be irritating to veins

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7
Q

Magnesium Salts: uses, nursing considerations

A

use: hypomagnesemia
considerations: dilute and infuse slowly, monitor for s/s of hyperMg (less activity - breathing, HR, muscles)

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8
Q

Effects of ARBs and direct renin inhibitors (remember they work in slightly different ways)

A

decreased vasoconstriction
increased Na+/H20 excretion and K+ retention
Decreased CV remodeling

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9
Q

AE of ARBs and Direct renin inhibitors

A

hypotension, dehydration, hyperK+
cough (less than ACE)
angioedema
fetal injury

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10
Q

AE of nondihydropyridines

A

constipation, dizziness, facial flushing, head ache, edema
bradycardia, heart block, decreased contractility –> decreased CO

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11
Q

drug interactions with nondihydropyridines

A

beta blockers
digoxin

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12
Q

AE of dihydropyridines

A

flushing, dizziness, HA, peripheral edema, increased myocardial O2 demand

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13
Q

drug interaction with dihydropyridines

A

beta blockers

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14
Q

AE of Hydralazine

A

SLE like syndrome, HA, dizziness, fatigue r/t hypotension

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15
Q

Drug interactions with nitroglycerin

A

hypotensive drug effects can be intensified
Contraindicated w/ PDE5 inhibitors
Caution w/: BB, calcium channel blockers, diuretics

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16
Q

What class are Quinidine and procainamide

A

class Ia antidysrhythmic

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17
Q

use of class Ia antidyrthmics

A

atrial and ventricular arrhythmias

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18
Q

AE of class Ia antidysrhythmics

A

anticholinergic (interact with M receptors)

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19
Q

What class is lidocaine

A

IB antidysrhythmic

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20
Q

Indications for lidocaine

A

post MI and other ventricular arrythmias

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21
Q

Uses of Class IC antidysrhythmics

A

supraventricular tachycardia, and a fib

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22
Q

Can we give desmopressin (DDAVP) for hemophilia A? Why or why not? Describe the mechanism of action of the drug.

A

This drug releases factor 8 clotting factors from the vasculature into the blood, it can be given for hemophilia A because the issue is producing/releasing these factors, so it increases the amount of factor 8 in the blood. It is preferred for mild forms

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23
Q

Understand the general ACC/AHA guidelines for the management of blood cholesterol. (In general, I don’t need you to memorize little details).What is the purpose of these guidelines?

A

The purpose of the guidelines is how to decide who to treat and to what intensity they need to be treated. It separates patients into two categories (high and very high risk), and subdivides high risk by age to determine who should receive the most aggressive statins
Who should be screened
Who is at risk (ASCVD 10 yr risk assessment)
Treatment: lifestyle modifications + low/med/high drug therapy

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24
Q

How should your patient’s HMG-CoA reductase inhibitor dosing be adjusted with acute renal failure?

A

Their CK should be checked, if it is elevated (which it will be) the drug should be discontinued

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25
Q

Discuss HMG-CoA reductase inhibitors and myopathy. What are the s/s? What are the risks? What can happen in severe cases? How do you educate your patients to monitor for this?

A

s/s: aches, tenderness, weakness, can progress to myositis, with increased CK and K+
Risks: female, old age, low BMI, chronic liver or kidney disease, higher statin dose, CYP34A inhibitors, OATP1B1 inhibitors, specific genetics
Watch for s/s: measure CK upon start of therapy and again if symptomatic

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26
Q

What is the difference in mechanism of action between warfarin & heparin? Why do you think a patient would be prescribed one over the other?

A

Heparin works by binding anti-thrombin → suppresses fibrin mesh formation. Heparin works relatively quickly, and can only be given via IV or sub Q injection, so it is typically only given inpatient.
Warfarin inhibits activation of vitamin K so clotting factors 2, 7, 9, and 10 are decreased, leading to lessened clots (decreased fibrin formation). Warfarin can take a while to work, and is oral so it is a medication patients are sent home on to prevent future clots.

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27
Q

Name the 4 classes of antidysrhytmics and describe how they work

A

1 - na+ blockers
A = increase AP, ERF, QT interval
B = decrease AP, ERF
C= increase ERF only in AV node
2 - beta blockers
3 - k+ blockers, delayed repolarization, increased AP duration, increased ERP, prolongs QT,
4 - decrease HR, contractility, conduction thru AV node
Other
Adenosine - hyperpolarizes by opening K+ channel,
Digoxin - na+/k+ inhibitors, increasing ca2+, thus increased contractility,

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28
Q

Name the 4 classes of antidysrhythmics and what they are used for

A

1 - na+ blockers
A = Atrial and ventricular arrhythmias,
B = Post MI and other ventricular arrhythmias
C= SVT and afib
2 - beta blockers - SVT, VT, post MI
3 - Ventricular tachy
4 - SVT
Other
Adenosine - tachycardias where pt is unstable
Digoxin - heart failure and supraventricular dysrhythmias

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29
Q

What is the difference in mechanism of action between the nondihydropyridines and dihydropyridines? How does this difference alter their clinical effects?

A

dihydropyridines only affect the vasculature, can cause reflex tachycardia, contractility increase, while nondihydropyridines affect both the vasculature and the heart rate, decreased contractility and AV node conductivity

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30
Q

List 2 cardioselective beta blockers

A

metoprolol, esmolol

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31
Q

What are the effects of amiodarone

A

delayed repolarization, increased AP duration, increases ERP, prolongs QT

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32
Q

Which HCG reductase inhibitor (statin) would you not give to someone of Asian heritage

A

Rosuvastain

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33
Q

What is Fenofibric acid

A

delayed release preparation of fenofibrate, reduces VLDL

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34
Q

How are monoclonal antibody (PCSK9) inhibitors given

A

sub Q or IV Q2weeks bc long half life (11-20 days)

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35
Q

indications of Exogenous erythropoietic growth factors (Epoetin alfa, Darbepoietin alfa)

A

Anemia d/t kidney d. (decreased endogenous EPO)
Palliation of chemo induced anemia
anemia preoperatively (need to increase H/H for surgery (expected blood loss), usually given with an anti-coagulant

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36
Q

-grel

A

P2Y12 ADP agonists

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37
Q

-teplase

A

thrombolytics

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38
Q

-stim

A

leukopoetic growth factors

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39
Q

-dipine

A

dihydropyridines

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40
Q

-xaban

A

factor 10 inhibitors

41
Q

-parin

A

anticoagulants that activate antithrombin (like heparin)

42
Q

-sartan

A

ARB

43
Q

-pril

A

ACE inhibitor

44
Q

-fibr-

A

fibric acid derivatives

45
Q

What is the half life of thrombolytics

A

5 mins

46
Q

Which part of RAAS contributes to cardiac remodeling?

A

aldosterone

47
Q

Drug that decreases CV M+M
a. nifedipine
b. amioderone
c. diltiazem
d. lisinopril

A

d. lisinopril because it is an ACE inhibitor

48
Q

does sodium nitroprusside cause reflex tachycardia

A

no

49
Q

Hypo/hyper kalemia with digoxin

A

hypo: toxic
hyper: subtheraputic

50
Q

AE of methadone

A

Can cause prolonged QT –> torsades
EKG prior to administration
avoid admin if QT>500 msec

51
Q

Difference between heparin and LWMH

A

because the molecules in LWMH are smaller, there is decreased protein binding and a much longer half life (slower liver clearance), meaning they do not require lab monitoring

52
Q

Indications of heparin

A

rapid anticoagulation
open heart surgery or dialysis to prevent device coagulation
low dose sub q for DVT prevention
treatment of DIC
adjunct to acute MI

53
Q

Indications for direct thrombin inhibitors

A

A fib
Tx DVT/PE
prevention of thrombosis
hip/knee replacement

53
Q

Indications of aspirin

A

CVA, TIA, chronic stable angina, stents, acute MI
inflammation, mild-moderate analgesia, fever reduction, suppression of platelet aggregation

54
Q

Uses of P2Y12 inhibitors

A

prevent stent thrombosis and thrombotic events

55
Q

Uses of PAR1 antagonists

A

w/ aspirin/clopidogrel in reduction of thrombotic events

56
Q

Indication of GPIIb/IIIa receptor antagonists

A

short-term to prevent ischemic events in those with acute coronary syndrome or undergoing PCI

57
Q

alteplase is an exogenous factor of

A

tPA (tissue plasminogen activator)

58
Q

Dosing of factor VIII and IX concentrate

A

by % increase in factor desired in body weight

59
Q

AE of iron supplementation

A

GI disturbances (take with food and water)
leading cause of poisoning fatalities in kids

60
Q

AE of B12 supplementation

A

hypoK+ due to erythrocyte prodxn

61
Q

Difference between epoetin alfa and darbepoetin alfa

A

darbepoetin alfa has a slower clearance and a longer half life so it can be given less frequently

62
Q

Uses of thrombopoetin receptor agonists

A

thrombocytopenia (idiopathic or with liver disease pre-op)

63
Q

Contraindications of cocaine

A

avoid with preexisting CV (tachy, dysrhythmias, MI)

64
Q

dosing of inhalation anaesthetics

A

minimum alveolar concentration (MAC), concentration in the lungs that produces immobility to painful stimuli in 50% of the pop

65
Q

AE of inhalation anaesthetics

A

Malignant hyperthermia dose-dependent HR and cardiac depression
sensitization of depression of pharengeal reflex - aspiration risk
nausea and vomitting

66
Q

Uses of propofol

A

low dose for sedation
ver high dose for anesthesia

67
Q

Uses of ketamine

A

analgesia
dissociative anaesthesia

68
Q

AE of ketamine

A

Psychologic rxns (hallucinations, bad dreams)
–> avoid stimulation

69
Q

Uses of celecoxib

A

osteo and rheumatoid arthritis
ankylosing spondylitis
acute pain

70
Q

contraindications of opioid agonist antagonists

A

since nalbutaphine and butorphanol can increase cardiac work, avoid in MI

71
Q

AE of methylnaltrexone

A

abd pain, nausea, flatulence, diarrhea

72
Q

contraindications of methylnaltrexone

A

GI obstruction

73
Q

AE of Naltrexone

A

IM injection site rxn (can be severe)
rare: hepatotoxicity

74
Q

Drug in the serotonin receptor agonist class

A

sumatriptan (-triptans)

75
Q

Indication for serotonin receptor agonists (triptans)

A

first line for migraine termination

76
Q

How do serotonin receptor agonists (triptans) work?

A

promote vasocontriction and supress CGRT release causing decreased inflamation

77
Q

AE of triptans

A

chest symptoms (transient, not ischemia)
coronary vasospasm
teratogenic

78
Q

contraindications for triptans

A

CAD
printmetals
pregnancy
drug interactions with anything that causes increase NE or seratonin (SSRIs/SNRIs, MAOIs, ergot alkaloids, other triptans)

79
Q

How do seratonin 1F receptor agonists work?

A

block trigeminal ganglia pain transmission
no vasoconstriction
overall not well understood

80
Q

Abortive drug therapies for migraines

A

asprin-like drugs
seratonin receptor agonists (triptans)
seratonin 1 F receptor agonists
ergot alkloids
Calcitonin gene related peptide receptor antagonist

81
Q

Indication for ergot alkloids

A

second line for migraine attack termination

82
Q

AE of ergot alkloids

A

N/V, weakness/myalgia, N/T, teatrogenisis
OD: egotism: ischemia d/t peripheral vasoconstriction causes necrosis

83
Q

contraindications of ergot alkloids

A

sepsis, PVD, renal or hepatic disease

84
Q

AE of Calcitonin gene related peptide receptor antagonist

A

minimal, some nausea and somnolance

85
Q

nursing considerations for Calcitonin gene related peptide receptor antagonist

A

high fat meal can delay aborption by as much as 2 hours

86
Q

Indications for Calcitonin gene related peptide receptor antibodies
- when given
risks

A

prevent migraines, sub Q once per month, risk for antibody formation

87
Q

How is benzocaine different from other local anesthetics

A

benzocaine has the adverse effect of methemoglobinemia, so it is contraindicated in those under 2

88
Q

How is cocaine different from other local ananesthetics

A

Cocaine in addition to blocking na+ channels, cocaine also blocks NE reuptake causing CNS and CV stimulation

89
Q

What makes chloroprocaine different from other local anesthetics?

A

Chloroprocaine is special because it is not effective topically (injection only) and has a short duration of action

90
Q

How do inhalation anesthetics reach their site of action? Where is their therapeutic site of action

A

They reach their site of action through the lungs (concentration, solubility, blood flow and ventilation all play a role in their absorption)
Their therapeutic site of action is the CNS

91
Q

Go through each body system and describe the effects that opioid agonists have. How are these adverse effects managed? (i.e. cough suppression can be managed by teaching your patient to deep breath & cough at intermittent intervals to clear secretions & prevent PNA)

A

Constipation - fiber, fluid, activity, stool softener, laxative
Miosis – usually not a problem
Respiratory depression – monitor, if needed stop opiods and give narcan. Elderly, young and those with respiratory disease are especially at risk
Decreased heart rate – stand up slowly to help avoid and limit orthostatic hypotension
Urinary retention – monitor I/Os
Orthostatic hypotension – educate pts
Cough suppression – educate pts to breath deep and cough, auscultate for crackles
Euphoria, emesis, birth defects, tolerance, neurotoxicity

92
Q

Why do we avoid ergot alkaloids & triptans together?

A

We avoid ergot alkaloids and triptans together because they can cause excessive vasospasm

93
Q

What phramacologic measures can be used to treat heart failure

A

REDUCE PRELOAD (Diuretics ACEi, ARBs, aldosterone antagonists, Venodilation)
REDUCE AFTERLOAD (ACEi, ARBs, BB (controversial, use w/ caution), Arteriole vasodilators)
INCREASE INOTROPY (CONTRACTILITY) (Cardiac glycosides (digoxin), Dopamine/dobutamine (sympathomimetics)

94
Q

How does sodium nitroprusside work? long term AE?

A

Sodium nitroprusside works the fastest and is given IV and works by decreasing both preload and afterload, decreasing O2 demand (and decreasing the resistance on the heart) and has minimal reflex tachycardia. For hypertension emergencies, renally eliminated over days
long term AE: Thiocyanate toxicity causing CNS effects

95
Q

What are the differences between cardiac beta1 blocker action and cardiac calcium channel blocker action?

A

Calcium channel blockers cause arteriole vasodilation, while beta blockers cause decreased renin release. Both BB and nondihydropyridines decrease HR, AV node conductivity and decreased contractility

96
Q

List absolute contraindications for nondihydropyridines

A

Drug interactions: beta blockers, digoxin
Don’t want to use with anything that would cause low contractility

97
Q

Why does digoxin cause increased urine output?

A

Increased cardiac output = improved tissue perfusion = improved renal blood flow = more glomerular filtration = increased UOP!

Pharm supplement (10 decks)

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