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Pharmacology Exam 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Examples of cardiac and vascular disorders:

A
  • Ischemic heart disease
    • Arteriosclerosis
    • Angina
    • Myocardial Infarction (MI)
  • CHF
  • HTN
  • Orthostatic Hypotension (OH)
  • Cardiac arrhythmias
  • Arterial occlusive disease
  • Peripheral vascular disease (PVD)
  • Venous thrombosis
    • DVT
  • Pulmonary embolism (PE)
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2
Q

When does ischemia occur?

How does this affect the heart?

A
  • When there is insufficient blood flow to tissue. Occurs in the heart when the O2 supply doesn’t meet the workload demand.
  • Increase HR and contractility.
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3
Q

What’s the difference between CAD and PAD?

A
  • CAD= Coronary artery disease

- PAD= Peripheral arterial disease

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4
Q

How many people does ischemic heart disease affect in the US?

A

12 million

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5
Q

What is chest pain caused by reduced blood flow to the heart called?

A

Angina pectoris

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6
Q

Angina is any condition that alters oxygen supply to the heart or any condition that increases the oxygen demand to the myocardium.
Examples of this:

A
  • Increased O2 needs to the heart
  • Increased cardiac output
  • Reduced blood flow to the heart
  • Triggers include:
    • physical exertion
    • increase in pulse rate or BP
    • vasoconstriction
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7
Q

Ischemia angina is usually due to CAD or PAD?

A

CAD

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8
Q

How is angina described?
It is considered mild to moderate lasting usually - minutes, up to __ minutes.
What relieves angina?

A
  • Squeezing, burning, pressing, heartburn, indigestion
  • 1-3, 20
  • Nitroglycerin
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9
Q

What are the three forms of angina?

A
  • Exertional:
    • occurs only when load is put on the heart
  • Variant (Prinzmetal’s)
    • Caused by coronary spasm, can occur at rest
    • Would respond well to vasodilator
  • Unstable
    • Occurs before a MI
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10
Q

What are the most common drugs used to treat angina pectoris?

A

Vasodilators:

  • Nitrates
  • Calcium blockers

Cardiac Depressants:

  • Calcium blockers
  • Beta-blockers
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11
Q

What is different about nitrates?

What is their MOA?

A
  • Work directly on vascular smooth muscle instead of through a receptor
  • Decrease preload and afterload→ reduce workload of heart→ reduce O2 demand
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12
Q

What are the forms of nitrate?

What is the drug of choice for acute attacks?

A
  • IV
  • Sublingual-spray, chewable, and oral tablets
  • Topical-transdermal patch

Drug of choice for acute attacks is sublingual

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13
Q

Nitrates don’t work on ____ but rather act directly on smooth muscle.

A

Alpha-1

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14
Q

Does isosorbide dinitrate (ISDN) or isosorbide mononitrate (ISMN) have a longer half life?

A

-ISMN (4-6 hours)

ISDN has a half life of 1 hour

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15
Q

What are the storage guidelines when it comes to nitrates?

What is the dosing of nitrates?

A

Storage:

  • limit light exposure (keep in glass bottle)
  • short shelf life (6m unopened, 3m opened)
  • tingling sensation as drug dissolves= it is active

Dosing:

  • After 1st dose, relief should occur within 1-2 minutes
  • 2nd dose if symptoms still present after 5 minutes (up to 3 doses in 15 minutes)
  • No relief= possible MI
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16
Q

What are the adverse effects of nitrates?

A
  • reflex tachycardia
  • dizziness
  • OH
  • weakness

Be concerned about FALLS.

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17
Q

When should patients start taking nitrates?

A

When they have symptoms, dont wait for a “more severe episode” to take meds.

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18
Q

What are the two other types of angina treatment?

A

B-blockers

Calcium channel blockers

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19
Q

Beta blockers are used for ______ angina along with __________ nitrates.

A
  • stable

- short-acting

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20
Q

Both beta blocker and calcium channel blockers reduce ________ which in return reduces ________ which relieves angina.

A
  • contractility

- O2 demand

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21
Q

Both beta blockers and CC blockers do what?

A

reduce workload of the heart

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22
Q

When a cardiac event is suspected, immediately chew _____ _________ coated aspirin

A

-325mg non-enteric coated aspirin

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23
Q

How many nitroglycerin doses can be administered in 15 minutes?

A

3

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24
Q

What determines the type of cardiac event?

What are the two types of cardiac events and what drugs are used for them?

A

-ECG determines the type of cardiac event

  • STEMI
    • thrombolytic agent
  • NSTEMI
    • heparin
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25
Q

What are the 2 surgical options for unstable angina?

A
  • Coronary artery bypass graft

- Artery angioplasty

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26
Q

ST elevation on a ECG most often means what?

A

thrombus formation that occludes a major artery

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27
Q

What are the zones of injury in a MI?

A

Zone of ischemia:
-Injury is reversible

Zone of hypoxic injury:

  • Surrounds zone of infarction
  • Has the ability to return to normal if adequate circulation is restored

Zone of infarction:

  • deprived of oxygen
  • cells die and tissue becomes necrotic
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28
Q

Is angina reversible?

A

Yes

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29
Q

Venous thrombosis is divided into ________ and __________.

What can be the cause of each?

A

Superficial:

  • Can occur in UE or LE
  • usually due to varicose veins

Deep:

  • 3rd most common CVD
  • those at risk are patients with a recent surgery
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30
Q

Pulmonary emboli can occur ______ _______.

What are the Signs and Symptoms of pulmonary emboli?

A

-without warning

S/Sx

  • possible sudden death
  • pleuritic chest pain
  • diffuse chest discomfort
  • tachypnea (rapid breathing)
  • tachycardia (rapid HR)
  • anxiety, restlessness
  • dyspnea (shortness of breath)
  • persistent cough
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31
Q

What are the three type of antithrombotics?

All antithrombotics have a risk of what?

A
  • Antiplatelets
  • Anticoagulants
  • Fibrinolytics

Bleeding

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32
Q

What is a example of an antiplatelet?

A

Aspirin

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33
Q

Platelet and the coagulation system in thrombogenesis:

A
  1. ) Vascular injury occurs
  2. ) Collagen and VWF are exposed
  3. ) Platelets adhere to collagen VWF, these platelets release ADP and thromboxane A2.
  4. ) ADP and thromboxane A2 recruit more platelets. Platelets are activated. Glycoprotein IIb/IIIa undergo a change resulting in more platelet aggregation
  5. ) Vascular injury exposes tissue factors
  6. ) Tissue factor triggers the coagulation pathway and thrombin generation
  7. ) Thrombin recruits more platelets, and converts fibrinogen to fibrin
  8. ) Fibrin binds platelets together to form platelet/fibrin thrombus
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34
Q

Antiplatelets-Aspirin MOA?

A
  • inhibits COX-1 and COX-2→ decrease production thromboxane A2→ inhibits platelet aggregation
  • at low doses (81mg), primarily inhibit COX-1 for CV protection
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35
Q

Antiplatelets-ADP Receptor Inhibitors (Irreversible) MOA?

What are they commonly referred to as?

A

MOA:
-irreversibly blocks PSY12 receptor on platelets→ blocks ADP binding→ blocks activation of the GP IIb/IIIa receptor complex→ decreased platelet aggregation (for lifespan of platelets, 7-10 days)

-commonly referred to as theinopyridines

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36
Q

Clopidogrel (Plavix) is a ________ and _________ antagonist.

A

noncompetitive and irreversible

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37
Q

What is the biggest concern for antiplatelets?

What is the takeaway?

A
  • bleed

- drug drug interactions can significantly impact the efficacy of these drugs

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38
Q

Antiplatelets-ADP Receptor Inhibitors (Reversible) MOA?

What are the AE?

A
  • Same as irreversible but can be reversed

- Dyspnea, bleeding

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39
Q

Anticoagulants are divided into what 2 parts?

A

Parenteral and PO

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40
Q

Parental is divided into what 4 classes?

PO classes?

A

Parenteral:

  • Heparin
  • Low-molecular weight heparin (LMWH)
  • Fondaparinux (Arixtra)
  • Direct thrombin inhibitors

PO:

  • Vitamin K antagonist
  • Direct thrombin inhibitor
  • Factor XA inhibitors

All of the PO except vitamin K antagonist (Warfarin) are DOACs-all renally eliminated

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41
Q

Fibrin acts as the _____ to create a clot

A

mesh

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42
Q

Heparin route?

MOA?

A
  • IV or subcutaneous

- prevents conversion of fibrinogen to fibrin by potentiating antithrombin

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43
Q

Does heparin have a reversal agent?

A

Yes, protamine sulfate

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44
Q

What is HIT?

A

Heparin induced thrombocytopenia

-Body creates antibodies which bind to heparin→ this activates platelets→ clotting and decreased platelet levels

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45
Q

What is LMWH and what is its MOA?

A
  • Low-molecular weight heparin

- Like heparin, potentiates action of antithrombin but has a greater effect on inhibiting FXa than thrombin

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46
Q

What is preferred, heparin or LMWH?

Does LWMH have a reversal agent?

A
  • LMWH

- Yes, protamine sulfate, andexanet alfa

47
Q

Fondaparinux MOA?

Advantages?

A
  • causes antithrombin-mediated selective inhibition of FXa

- once daily dosing, no risk of HIT

48
Q

S40 for MOA of all 3

A

S40

49
Q

IV Direct Thrombin Inhibitors MOA?

A

binds directly to thrombin with high selectivity→ inhibits conversion of fibrinogen to fibrin

50
Q

Vitamin K Antagonist-Warfarin MOA?

A
  • binds to VKORC1, an enzyme that converts inactive vitamin K to active vitamin K→ deplets vitamin K stores→ inhibits synthesis of factors VII, IX, X, and II, and protein C and S
  • active vitamin K is required for synthesis of factors and proteins
51
Q

Is there a reversal agent for Warfarin?

A

Yes, Vitamin K

52
Q

Does warfarin have an immediate effect?

A

No, usually takes 3-5 days for full effect and longer to stabilize dose

53
Q

Warfirin is a ___ drug, meaning it requires frequent monitoring of INR.
What is the normal INR?
If NRI is low, what is the patient at risk for?
If NRI is high, what is the patient at risk for?

A
  • NTI
  • normal is ~1 (2-3 for a.fib, 2.5-3.5 for mechanical heart valve)
  • If NRI is low- at risk for blood clotting
  • If NRI is high- at risk for bleeding
54
Q

Warfarin has ____ drug and food interactions.

Why is warfirin used so often?

A
  • Many (maintain stable intake of vit K containing foods)

- Cheap

55
Q

PO Direct Thrombin Inhibitor MOA?

AE?

A
  • binds directly and reversibly to thrombin with high selectivity→ inhibits conversion of fibrinogen to fibrin
  • Dyspepsia
56
Q

PO Direct Thrombin Inhibitor has less ___________ bleeding than warfarin but increased ____ bleeding.

A
  • intracranial

- GI

57
Q

Does PO Direct Thrombin Inhibitor have a reversal agent?

A

Yes, idarucizumab

58
Q

Factor XA Inhibitors end in what?

MOA?

A
  • end in -xaban

- selectively and reversibly binds FXa→ stops further coagulation cascade

59
Q

Which example of this inhibitor has more GI bleed than the others and must be taken with food?
Which has the lowest bleed risk?

A

rivaroxaban (Xarelto)

apaxiban (Eliquis)

60
Q

Do Factor XA inhibitors have a reversal agent?

A

Yes, andexanet alfa

61
Q

Monitoring with antiplatelets and antithrombotics?

A

-bleeding and clotting

62
Q

Fibrinolytics MOA?

A

-mimic endogenous tissue plasminogen activator (TPA) which converts plasminogen to plasmin→ plasmin breaks fibrin links in the thrombus

63
Q

Fibrinolytics are the only medicine that does what?

When should it be taken?

A
  • breaks up a clot

- taken after stroke, MI, PE

64
Q

What is a.fib?

A

Irregular rhythm, not necessarily high

65
Q

VTE includes both ____ and _____.

A
  • DVT

- PE

66
Q

What are the prevention measures for VTE?

A
  • LMWH or heparin used for prevention
    • before and after surgery
    • In patients at high risk for VTE
67
Q

Long-term treatment for VTE?

A

1st line- DOAC
2nd line- VKA (warfarin)
3rd line- LMWH

Exceptions:

  • LMWH is 1st line in cancer patients
  • Questionable efficacy in BMI>40
68
Q

AF increases risk of what?

A

stroke (5x more likely)

69
Q

What patients dont recieve anticoagulation-based treatment based on risk vs. benefit?

A
  • CHADSVASC
  • HAS-BLED
    • HTN
    • Abnormal liver or renal
    • Stroke
    • Bleeding
    • Labile INR
    • Elderly
    • Drugs or alcohol
70
Q

Therapeutic concerns about antithrombotic drugs.

A
  • Falls

- Contraindicated PT treatments

71
Q

What is atherosclerosis?

A

-narrowing and hardening of the arteries

72
Q

What is good in terms of LDL and HDL?

A

LDL-low=good
HDL-high=good

lousy vs happy

73
Q

What are the three main classes of atherosclerosis drugs?

A
  • HMG-CoA reductase inhibitors (Statins)
  • Cholesterol absorption inhibitor
  • PCSK9 inhibitor
74
Q

Statins MOA?

AE?

A
  • block HMG CoA reductase= blocks cholesterol synthesis

- Myalgia

75
Q

What is rhabdomyolysis?

A

Breakdown of muscle tissue releasing protein in blood that can cause renal failure.

76
Q

Can statins cause tendon rupture?

A

Currently more case reports so yes and no.

77
Q

Cholesterol Absorption Inhibitor MOA?

AE?

A
  • Inhibits absorption of cholesterol in small intestine

- Generally well tolerated

78
Q

Are statins or cholesterol absorption inhibitors used more often?

A

Statins

79
Q

PCSK9 Inhibitor MOA?

AE?

A
  • inhibits PCSK9= increase LDL receptor expression on hepatocytes= increase LDL uptake for degredation
  • injection site reactions
80
Q

2 other meds to treat artherosclerosis that are less common?

A

Fibrates

Omega 3 fatty acids

81
Q

2018 Cholesterol Guidelines for treatment order

A

1st line=statin
2nd line=ezetimibe added on if remain uncontrolled

Other options:

  • bile acid sequestrants
  • PCSK9 inhibitor

Fibrates and niacin decrease triglycerides but are not supported as add-on therapy

Omega 3 fatty acids not in this guideline

82
Q

Therapeutic concerns for statins

A
  • myositis and myalgia
  • persistent muscle effects
  • rhabdomyolysis
83
Q

There are _____ and _____ to reducing cholesterol.

A

Benefits and risks

84
Q

Therapeutic concerns for statins

A
  • Grapefruit juice inhibits CYP3A4, linked to rhabdomyolysis

- polypharmacy can cause increased competition and increase statin concentration

85
Q

CHF is a ___________ disorder that can be ______ or ______. The heart is unable to pump sufficient blood to supply the needs of the body.

A
  • progressive

- acute or chronic

86
Q

How does CHF affect heart muscle and stroke volume?

A

Hypertrophy in heart muscle

Reduced SV

87
Q

CHF is the most common cause of hospitilization for what individuals?

A

> 65

88
Q

Compensated vs Decompensated CHF

A

Compensated- When a patient is medically stabilized

Decompensated- The patient is unable to maintain adequate circulation. The bodys efforts to compensate backfire, the mechanisms are no longer effective

  • Mild- mild congestion
  • Life-threatening- fluid overload and total heart failure
89
Q

What is left ventricular heart failure?

A
  • Left ventricle doesn’t empty completely
  • Cant accept blood from the lungs
  • Pulm veins become engorged
  • Fluid seeps out of veins and into lungs
  • Results in PULMONARY EDEMA
90
Q

What are the clinical manifestations of left ventricular heart failure?

A
  • Dyspnea
  • Fatigue and muscular weakness
  • renal changes
  • Nocturia
91
Q

Clinical manifestations of right ventricular heart failure?

A
  • Dependent edema
  • Jugular venous distension
  • Abdominal pain
  • RUQ pain
  • Cyanosis
92
Q

Heart failure terminology:
What is HFpEF?
What is HFrEF?

A

HFpEF (HF with preserved ejection fraction):

  • Diastolic heart failure
  • Often related to aging
  • Cardiac hypertrophy

HFrEF (HF with reduced ejection fraction):

  • Systolic heart failure
  • Heart unable to adequately contract= less O2 rich blood pumped into body
93
Q

What is ejection fraction?

A 
% of blood pumped out of left ventricle during each heart beat
RANGES:
-50-75%= normal
-36-49%= below normal
-<36%= low pumping ability
94
Q

What are the goals in HFpEF?

A
  • Manage symptoms with diuretics
  • treat underlying comorbities
  • may add aldosterone antagonist to decrease hospitalization
95
Q

Goals and meds in HFrEF?

A
  • decrease edema and congestion = diuretics
  • increase contractility = positive inotropic drugs (digoxin)
  • decrease preload and afterload = vasodilators

Outcomes = improve QOL by decreasing fatigue, reduce hospitalization, prolong survival

96
Q

HFpEF and HFrEF percentages?

A 
HFpEF = >40%
HFrEF = <40%
97
Q

rEF treatment drugs?

A

ACEi or ARB + beta-blocker + diuretic

98
Q

What HF drug is used more so in African American population?

A

Hydralazine

99
Q

ARNI (angiotensin receptor-neprilysin inhibitor) drug used to reduce mortality in CHF?

A

Entresto

100
Q

When is digoxin used?

What is its MOA?

A
  • only if symptoms not controlled on other therapy; does not reduce mortality
  • inhibits Na+/K+ ATPase pump in myocardial cells = increase intracellular sodium = increase Ca2+ from Na/Ca exchange pump = increased contractility
101
Q

Digoxin is purely used for what?

A

Symptom control

102
Q

Digoxin S/Sx of toxicity?

A

anorexia, nausea, vomiting, visual changes (HALOS AROUND YELLOW-GREEN COLOR SPECTRUM), cardiac arrhythmias

advanced age

103
Q

What is arrhythmia?

A

A disturbance of HR or rhythm due to an abnormal rate of the generation of the electrical impulse from the SA node, or by abnormal conduction of the impulses

104
Q

What is arrhythmia classified by?

A

Origin- ventricular or atrial

Pattern- fibrillation or flutter

Speed/rate- brady or tachycardia

105
Q

Difference between fibrillation and flutter?

A

Fibrillation-irregular HR

Flutter-irregular but higher HR

106
Q

What is responsible for regulating the number of times the heart beats and the rhythm of the beat?

A

Sinoatrial node

107
Q

Where is the SA node located?

A

Upper right portion of heart

108
Q

Clinical manifestation of cardiac arrhythmias:

A

Any significant deviation from the regular range of 60-100

 - Increase or decreased HR
 - Fatigue
 - Dyspnea
 - Syncope
 - Dizziness
 - Angina
 - Diaphoresis (sweating)
 - Palpations
109
Q

Goal of arrhythmia treatment?

A

Restore normal rhythm vs control rate of abnormal rhythm

Overall treatment has declined to potential risk of PROARHHYTHMIA and development of NONPHARM THERAPY

110
Q

S92 Normal Conduction

A

S92 Normal Conduction

111
Q

Amiodarone MOA?

AE?

A
  • prolong the duration of the action potential by blocking K+ channels
  • BLUE discoloration, “LFT, TFT, PFTs”
112
Q

Does amiodarone have a short or long half life?

A

Long, ~50 days can prolong AE even after withdrawal

113
Q

Therapeutic concerns with antidysrhythmic agents?

A
  • Efficacy of the class of drugs (30-60%)
    • Patients may continue to experience arrhythmias while medicated
  • Hypokalemia increases risk or arrhythmia
    • Be aware of dehydration (Diuretics!)
  • Effect on exercise tolerance
    • Negative inotropic effects
    • exercise may cause rhythm disturbance
    • lack of “cool down” period will also contribute to rhythm disturbance

Monitor throughout treatment to avoid over exertion

114
Q

Therapeutic concerns with digoxin?

A
  • NTI
  • Toxicity
    • GI symptoms- nausea, vomiting, diarrhea, ab pain
    • CNS- blurred vision, confusion, lethargy
    • Cardiac- arrhythmia
  • Kidney function

Pharmacology Exam 2 (7 decks)

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