KAAP440 - CP Exam 1

atrophy

reversible reduction in cell size from insufficient blood flow, malnutrition, denervation, reduced, endocrine stinulation

hypertrophy

increase in cell size due to an increased workload

hyperplasia

increased cell number

metaplasia

replacement of one adult cell with another adult cell that can better endure change

dysplasia

deranged cell growth of specific tissue that results in abnormal size, shape, and appearance

toxic cell injury

endogenous/internal (metabolic errors, gross malformations)

exogenous/external (alcohol, lead, carbon monoxide, drugs)

infectious cell injury

viruses, fungi, protozoa, bacteria

physical cell injury

thermal (electrical, radiation) or mechanical (trauma, surgery)

deficit cell injury

lack of basic requirement

aging cell injury

normally lose structure and function over time, may cause atrophy

medulla oblongata

vital functions and senses disruptions

pituitary gland

regulates other glands and response to disruption

reticular formation

help control vital reflexes, cardiovascular function and respiration

nerve signaling

fast specific - single cell sends a nerve impulse to regulate muscles and glands

endocrine signaling

hormones are sent around the body in the bloodstream from the endocrine gland/tissue to target areas, more widespread

local signaling

between adjacent cells as seen in the inflammatory response

stages of disease

exposure or injury → incubation → prodromal → acute phase → remission → convalescence → recovery

how are drugs absorbed?

small intestine → directly to the liver and chemically altered

drug distriibution

following absorption, the drug disperses throughout fluids and tissues of the body to target cells and organs

drug metabolism

occurs mainly in the liver to make th e drug more water soluble

drug excretion

the drug is eliminated mainly through the kidneys, but also in the bile, tears, sweat, and breath

bioavailability

proportion of the does that reaches circulation

therapeutic range

difference between the blood level needed to be effective and the level above that would be toxic

plasma half life

time it takes for the drug amount in the plasma to be reduced by one half; determines how long drugs last in the body

peak plasma concentration

indicates when drug levels in the body are at their highest

beta blockers

class of beta- adrenegic blocking agaents that block the effects of epinephrine/ adreline - lowers HR and BP

adrenergic

nerve cells in which adrenaline acts as a neurotransmitter

beta 1

present in myocardial (heart muscle) tissue

beta 2

present in smooth muscle cells

cardio-selective beta blockers

block B1 adrenergic nerve receptor of the myocardium, directly decreasing activity of the heart and reducing CO

non-cardio-selective beta blockers

block both B1 and B2 receptors affecting heart and smooth muscle lining of kidneys, lungs, GI tract, liver, uterus, vascular smooth and skeletal muscle - reduced CO and renal output

indications for beta blockers

hypertension, angina, arrythmias, acute MI, migraine headaches, anxiety, essential tremor, heart failure

what do cardio-selective drugs end in

olol

beta blockers are most proscribed for

recent/acute MI

beta blocker effects on CO

lower to no change with exercise

beta blocker effects on HR

lower at rest and exercise

beta blocker effects on BP

lower at rest and exercise

beta blocker effects on ECG

reduced ischemia at rest and exercise

beta blocker effects on VO2 max

reduced with acute admin, increased with chronic admin

how many pacemaker sights are there?

SA (60-100), AV (40-60), Purkinje (15-40)

electrical flow of the heart

SA node → AV node → AV bundle → left and right bundle branches → purkinje fibers

4 major determinants of myocardial oxygen demand

HR (high/low), contractile force (EF), muscle mass (how much is viable), ventricular wall tension

myocardial O2 demand

O2 supply to maintain balance

how does exercise effect the amount of O2 demand

increase O2 demand by muscles → HR accelerates contractions (increase SV) → increased cardiac workload

how does myocardial O2 demand increase

hypertension, ventricular dilation, heart muscle hypertrophy

to increase O2 supply

coronary artery perfusion must also increase, tissue hypoxia causes coroary arteries to dilate and increase coronary blood flow

arterial pressures drop when

HR and for of contractions (arterioles) increase

arterial pressure rises when

slowing of the HR, decreased force of contraction → vasodilation

ACE inhibitors (angiotensin-converting enzyme)

slows the activity of the enzyme ACE and inhibits the production of angiotensin II. BP is reduced

angiotensin

a hormone that causes vasoconstriction and an increase in blood pressure

indications of ACE inhibitors

hypertension, coronary artery disease, heart failure caused by systolic dysfunction, diabetic kidney damage, chronic kidney disease, cerebrovascular disease

ACE-inhibitor side effects

generally well-tolerated, dry cough, hypotension, hyperkalemia (inhibiting angiotensin helps retain potassium)

what do ACE inhibitors end in?

pril

effects of ACE on CO

no change w/ exercise

effects of ACE on HR

no change with exercise

effects of ACE on BP

lower at rest and exercise

effects of ACE on ECG

no change with exercise

effects of ACE on VO2 Max

no change in exercise capacity, however improved exercise tolerance

saccular aneurysms

one side of the arterial wall biollowed out/out pouched

fusiform aneurysms

spindle shaped, outpouching encompassing the entire circumfrance

false aneurysm

outpouching occuring when inner layer of a wessel wall is injured and blood leaks through the wall but is contained with the surrounding soft tissue

how do aneurysms develop

slowly, weakness in the middle muscular layer allows both inner and outer layer to stretch outward.

drugs appropriate for treating aneurysms

beta blockers, ACE inhibitors, statins, analgesics, anti platelet medications

cardiac tamponade

rapid rise in pressure usually from blood/fluid accumulation within the pericardial sac that left untreated can lead to cardiogenic shock and death

the pericardium can normally hold up to _____ fluid, ____ in acute situations, up to _______ liters if slow build-up

50 ml, 200 ml, 2000ml/2

causes of cardiac tamponade

effusion, hemorrhage, pericarditis, acute MI, chronic renal failure, drug reaction, connective tissue disorders

signs of cardiac tamponade

hypotension (narrowing pulse pressure), elevated CVP, muffled heart sounds, othopena, diaphoresis, anxiety, restlessness, pluses paradoxus, cyanosis, weak rapid pulse

how to detect cardiac tamponade

chest xray, ECG, pulmonary artery pressure, ECHO

treatment for cardiac tamponade

pericardiocentesis, pericardial window, insertion of a drain

cardiogenic shock

CO severely impairs blood and O2 perfusion to the tissues, serious complication following acute MI in some patients reflected in severe left-sided heart failure

causes of cardiogenic shock

most often caused by severe heart attack

facts of cardiogenic shock

Affects patients whose infarction exceeds 40% of the heart’s muscle mass, Mortality > 85%, most patients die withing 24 hrs, prognosis = poor

signs of cardiogenic shock

Cold, clammy, pale skin, drop in SBP (30 mmHg below baseline), weak peripheral pulses, tachycardia, rapid, shallow respirations, restlessness, confusion, cyanosis, S3 and S4 heart sounds are abnormal

detection of cardiogenic shock

pulmonary artery pressure increased, arterial blood gas analysis, ECG – acute MI, ischemia, aneurysms, ECHO

treatment of cardiogenic shock

1. Increasing cardiac output

2. Improving myocardial perfusion

3. Decreasing cardiac workload

increase cardiovascular status

orthopnea

difficulty in breathing when lying down that improves when upright

Pulsus Paradoxu

abnormal drop in pulse or systolic BP during inspiration

tachypnea

rapid, shallow breathing

preload

volume of blood in ventricles at the end of diastole, increased in hypervolemia and regurgitation of cardiac valves

afterload

resistance left ventricle must overcome to circulate blood, increased in hypertension and vasoconstriction

positive inotropic drugs

increase the strength of muscular contractions, cardiac glycosides, diuretics, DCM

negative inotropic drugs

weaken the force of muscular contractions, beta blockers, calcium channel blockers, HCM

angiotensin II receptor blockers (ARBS)

block the binding of angiotensin II on the angiotensin receptors on muscle surrounding blood vessels to prevent vasoconstriction

indications for ARBS

hypertension, heart failure, renal failure (in diabetes)

side effects of ARBS

hyperkalemia, hypotension, drowsiness, abnormal taste

what do ARBS end with?

sarten

effects of ARBS on CO

increase in some studies

effects of ARBS on HR

decrease to no change with rest and exercise

effects of ARBS on ECG

transient changes in QT interval prologation

effects of ARBS on VO2

increase to no change

coronary artery disease

atherosclerosis of the coronary arteries that reduces the blood supply to the heart muscle. may lead to myocardial ischemia or necrosis

modifiable risk factors for CAD

physical inactivity, smoking, stress, obesity, DM increased LDL and decreased HDL, elevated homocysteine levels, Increased serum fibrinogen, increased uric acid levels, elevated hematocrit, reduced vital capacity, hyperthyroidism, use of hormonal contraceptives

atrial septal defect

flaw in the septum that divides the two atria of the heart

arteriovenous malformation

an abnormal communication between an artery and a vein

stable angina

predictable and relieved by rest or nitrates that vasodilate the blood vessels

unstable angina

more easily induced and may occur during rest periods, so that it’s unpredictable, classified as an acute coronary syndrome and is much more likely to progress to an MI

nitrates

relax arterial and venous smooth muscle, which reduces the amount of blood that returns to the heart (more O2 blood in PNS)

indications for nitrates

angina, acute MI, heart failure, low cardiac output syndromes, hypertension

uses of nitrates

rapid relief as well as extended relief versions to prevent pain, increases arterial lumen to manage hypertension

what do nitrates end with?

nitrate, start with nitric, or start with nitro