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Pharmacology (SPRING 2024) > UNIT 4 EXAM > Flashcards

UNIT 4 EXAM Flashcards

1
Q

Blood Flow

A

Venae Cavae -> Right Atrium -> Tricuspid Valve -> Right Ventricle -> Pulmonary Trunk -> Pulmonary Arteries -> Pulmonary Capillaries (site of exchange) -> Pulmonary Veins -> Left Atrium -> Bicuspid (Mitral) Valve -> Left Ventricle -> Aortic Semilunar Valve -> Aorta

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2
Q

Important Electrolytes

A

Na+ (sodium): main extracellular electrolyte; fluid balance
K+ (potassium): main intracellular electrolyte; maintains the structure and function of the cell (especially cardiac muscle)
Ca2+ (calcium): mineral associated with bone; aids in muscle contraction and blood coagulation; FOC

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3
Q

Conduction System

A

SA node fires;
signal spreads through the atria to the atrial myocardium;
signal reaches the AV node;
signal travels down the Bundle of His;
signal travels down bundle branches;
signal travels down Purkinje Fibers;
signal reaches ventricular myocardium

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4
Q

SA node

A

(RA) pacemaker; impulse starts here;
auto rhythmicity - heart initiates its own impulse

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5
Q

Conduction

A

coordinates contraction of the heart;
monitored by EKG (ECG)

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6
Q

Phases of Action Potential

A

Phase 4: RMP (-90 mV)
diastole (Na+ outside the cell; K+ inside the cell)

Phase 0: rapid depolarization; Na+ flows into cell; rapid change in voltage from RMV, generates an action potential

Phase 1,2 and beginning of 3: K+ moves out of cell; repolarization occurs, bringing membrane potential back to resting
refractory period - another contraction cannot occur; cannot receive another action potential; prevents continuous contraction - tetany

Phase 2: plateau phase; balance of Ca2+ moving into cell and K+ moving out of cell; muscle contraction occurs

Phase 3: rapid repolarization; Ca2+ channels close, more K+ channels open

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7
Q

EKG/ECG

A

P wave - atrial depolarization
PR segment - AV node delay
QRS complex - ventricular depolarization
ST segment - absolute refractory period (another contraction cannot occur; prevents tetany)
T wave - ventricular repolarization

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8
Q

Control of the Heart

A

Autonomic Nervous System: regulates HR and FOC

SNS: NE
EPI from adrenal medulla
increases HR (chronotropic); increases FOC (inotropic); increases conduction (dromotropic)

PNS: ACH
decrease HR; decrease FOC; decrease conduction (dromotropic)

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9
Q

Normal Sinus Rhythm

A

Normal Rate and Rhythm
Measurements are Accurate
No Extra Beats

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10
Q

Fibrillation

A

quivering;
ineffective contractions

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11
Q

Diseases of the Heart

A

Heart Failure (HF/CHF)

Congestive Heart Failure

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12
Q

Heart Failure (CHF/HF)

A

occurs with activity or at rest;
heart is unable to pump out blood effectively;
more blood enters the heart than leaves;
less blood reaches the organs;
kidneys compensate, resulting in edema, fluid and electrolyte retention;
hypertrophy;
sympathetic nerves compensate: vasoconstriction, increase in HR & FOC

Tx: cardiac glycosides ( increase FOC); beta-blockers, vasodilators, diuretics

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13
Q

Hypertrophy

A

increase in volume of a tissue/organ due to enlargement of component cells

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13
Q

Congestive Heart Failure

A

Left Ventricular Failure - Pulmonary Congestion;
dyspnea, tachypnea, orthopnea, nocturnal dyspnea, pulmonary edema, coughing

Right Ventricular Failure - Venous Congestion
pitting edema; ascites

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14
Q

Possible Actions of Cardiac Drugs

A

1) Chronotropic: positive/negative HR
positive: EPI, atropine
negative: cardiac glycoside

2) Inotropic: positive/negative FOC
positive: cardiac glycosides
negative: calcium channel blockers

3) Dromotropic: positive/negative conduction

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15
Q

Ascites

A

a condition in which fluid collects in spaces within your abdomen

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16
Q

Pitting Edema

A

accumulation of an excessive volume of fluid within the body;
when pressure is applied, a dent is formed

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17
Q

Dyspnea

A

shortness of breath

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18
Q

Tachypnea

A

rapid breathing

19
Q

Orthopnea

A

shortness of breath that occurs while lying down; is relieved when sitting up or standing up

20
Q

The Rights

A
  1. Right Patient
  2. Right Drug
  3. Right Dosage
  4. Right Route of Administration/Form
  5. Right Time
  6. Right Response
  7. Right Documentation
21
Q

Cardiac Glycosides

A

MOA: increase the FOC; accelerate entry of Ca2+ into the cardiac muscle cells; this, in turn, increases kidney fxn; kidneys eliminate excess fluid and electrolytes that cause edema;
decreases HR; slows down AV node conduction

USES: CHF;
arrhythmias: atrial fibrillation and atrial tachycardia

DRUGS: digoxin (Lanoxin)

PATIENT TEACHING/SIDE EFFECTS: interfere with Na+/K+ pump,
hypokalemia occurs that results in arrhythmias, nausea, headache, visual disturbances
check pulse: to administer has to be 60 - 100 bpm

GOAL: increase FOC without increasing oxygen consumption

22
Q

digoxin (Lanoxin)

A

digitalization (administration of the drug):
maintenance dose, low TI, must monitor levels

therapeutic serum levels: 0.5 ng/mL - 2.0 ng/mL
toxic: over 2.5 ng/mL

rapid onset and short duration of action

toxicity: cardiac: slow pulse, irregular pulse
CNS: headache, confusion, visual disturbances (halos around dark objects), delirium
GI: N/V/D

toxicity: give K+ to increase heart’s ability to contract; d/c drug, serum levels

antidote: digoxin immune fab (Digibind)

23
Q

Preload

A

how stretched the chamber is prior to contraction;
venous blood return to the heart

24
Q

Afterload

A

tension required to cause the contraction;
how hard the heart must work to contract

25
Q

Effects of Vasodilators

A

decreased BP, decreased preload and afterload;
decreased blood flow through the heart and body;
decreased work on the heart and oxygen consumption;
increased cardiac output with less effort

26
Q

Vasodilators

A

Nitrates

27
Q

Nitrates

A

vasodilators;

MOA: dilate blood vessels, decrease blood pressure, decrease venous return (preload and afterload); decreases cardiac work and oxygen consumption

USES: HF, angina, CAD, HTN, MI

DRUGS:
1. nitroglycerin (Nitro-Bid, Transderm Nitro, Nitrostat) - sublingual, tabs, transdermal, IV
do not expose to air or light (drug loses its potency)
2. isosorbide (Isordil or Ismo)

PATIENT CAUSE/SIDE EFFECTS: HA, lightheadedness, tachycardia, orthostatic hypotension - be careful with position changes, no ED meds

28
Q

Inadequate Oxygenation

A

brain: dizziness, drowsiness, less alert
lungs: SOB, cough
kidneys: try to compensate; hold on to H2O and electrolytes ->
edema everywhere and in lungs; must give diuretics to eliminate fluid

29
Q

Beta Blockers
(non-selective beta-1 and beta-2)

A

MOA: block beta-1 receptors;
decrease HR, FOC and oxygen consumption;
reverse excessive sympathetic activation (compensatory CHF)

USE: CAD, angina, HTN, CHF, arrhythmias - tachycardia, glaucoma, migraines

DRUGS:
Non-Selective Beta Blockers:
propranolol (Inderal)
nadolol (Corgard)
nebivolol (Bystolic)
Selective Beta-1 Blockers:
atenolol (Tenormin)
metoprolol (Lopressor)
Non-selective beta blockers, alpha-1 blocker:
carvedilol (Coreg)

PATIENT TEACHING/SIDE EFFECTS: drowsiness, GI upset, CNS depression, bradycardia, monitor serum lipid levels, mental depression, monitor glucose levels in diabetic patients, avoid using non-selective BBs with asthma patients - bronchoconstriction

30
Q

Coronary Arteries

A

blood flows to heart muscle

31
Q

CAD (Coronary Artery Disease)

A

blockage -> ischemia occurs
02 demand exceeds the supply
(coronary arteries only)

32
Q

Arteriosclerosis

A

hardening or narrowing of coronary arteries due to an aging process

33
Q

Atherosclerosis

A

buildup of fatty deposits/plaque that has accumulated in walls of arteries

34
Q

Angina Pectoris

A

chest pain caused by reduced/restricted blood flow to the heart caused by arteriosclerosis or atherosclerosis

35
Q

3 Types of Angina

A
  1. Exertional/Stable Classic Angina
  2. Unstable Angina
  3. Prinzmetal/Vasopasm of Coronary Artery
36
Q

Exertional/Stable Classic Angina

A

chest pain/discomfort that occurs with activity or stress; is usually resolved with rest/meds

37
Q

Unstable Angina

A

unpredictable bouts of chest pain, usually occurring at rest; MI is soon to follow; doesn’t respond to rest

38
Q

Prinzmetal/Vasospasm of Coronary Artery (Angina)

A

sudden constriction of the coronary artery; decreased O2 to cardiac muscle; chest pain

39
Q

CAD and Antianginal Drug Therapy

A

Vasodilators/Nitrates - nitroglycerin;
Beta Blockers (BB) - -olol
Calcium Channel Blockers (CCB)

40
Q

Calcium Channel Blockers (CCB)

A

Calcium Antagonists;
Calcium: FOC;

USES: CAD, angina, HTN, tachyarrhythmias

CAUTION: do not use on patients with CHF; already have ineffective pumping

2 Categories: dihydropyridines & nondihydropyridines

41
Q

Calcium Channel Blockers/Antagonists
Dihydropyridines

A

have a vasodilating effect;

MOA: 1. block entry of calcium into cardiac muscle to decrease the FOC; demand for O2 decreases
2. block of entry of calcium into smooth muscle; vessels relax, BP decreases

DRUGS:
1. nifedipine (Procardia)
2. amlodipine (Norvasc)
3. nisoldipine (Sular)

USES: angina, HTN

42
Q

Calcium Channel Blockers/Antagonists
Nondihydropyridines

A

act on cardiac muscle, heart’s conduction cells, and smooth muscle
vasodilators and antiarrhythmics

MOA: 1. block entry of calcium into cardiac muscle; decreased force of contraction; decreased demand for O2
2. block entry of calcium into smooth muscle cells; vessels relax; vasodilation; decreased BP
3. decreased SA node and AV node conduction; decreased conduction velocity of each (Tx: tachyarrhythmias)

DRUGS:
1. verapamil (Cadan)
2. diltiazem (Cardizem)

USES: angina, HTN, tachyarrhythmias

43
Q

Calcium Channel Blockers/Antagonists Side Effects

A

HA, facial flushing (vasodilation), reflex tachycardia, dizziness, hypotension, constipation, xerostomia

44
Q

Calcium Channel Blockers Drug Interactions

A

CCB and BB
slows HR and depresses cardiac activity leading to CHF

45
Q

Myocardial Infarction (MI)

A

1 killer in the US

heart cells - ischemia
necrosis
to follow are CHF and arrhythmias
infarct

every 20 seconds: MI
every minute: 1 MI death
about 697,000 deaths in the US due to MI (1 in every 5 deaths)

46
Q
A

Pharmacology (SPRING 2024) (7 decks)

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