Cson F10 Patho Exam 1

Front 1

How is the heart "fed"

Back 1

through the coronary arteries

Front 2

how much of the energy in the blood does the heart use

Back 2

70-80%

Front 3

cardiac output =

Back 3

heart rate X stroke volume

Front 4

stroke volume

Back 4

amount of blood pumped out of the ventricle with each contraction

Front 5

preload

Back 5

amount of myocardial stretch just before systole caused by the pressure created by the volume of blood within the ventricle aka left ventricular end diastolic pressure, LVEDP

Front 6

afterload

Back 6

the amount of resistance to the ejection of blood from the ventricle

Front 7

atherosclerosis

Back 7

accumulation of lipid, or fatty substances in vessel walls

Front 8

most prevalent type of cardiovascular disease

Back 8

coronary artery disease

Front 9

optimal level of HDL cholesterol

Back 9

greater than 40, ideally over 60; this is good cholesterol h=high

Front 10

optimal level of LDL cholesterol

Back 10

less than 130 or 100 for those diagnosed with CAD or at high risk; bad cholesterol L=low

Front 11

optimal level of triglycerides

Back 11

less than 200

Front 12

how does HDL help lower LDL

Back 12

assists with transport of LDL to liver to be processed

Front 13

potential causes of high triglycerides

Back 13

obesity, physical inactivity, excessive alcohol intake, high carb diets, DM, kidney disease and meds (BCP, steroids, high dose beta blockers)

Front 14

non modifiable risk factors for CAD

Back 14

age, gender, family history, ethnicity

Front 15

modifiable risk factors for CAD

Back 15

high cholesterol, smoking, hypertension, hyperglycemia, obesity, physical inactivity, stress

Front 16

3 of the following must be present to have metabolic syndrome

Back 16

large waist (40in or more in men and 34in for women); borderline or high blood pressure; triglycerides above 150; low HDL (<40 for men and <50 for women); high fasting blood sugar (above 100)

Front 17

what can we do to reduce effects of metabolic syndrome

Back 17

exercise, eat fewer calories, eat better calories

Front 18

what is the #1 killer of women

Back 18

CAD

Front 19

what level of vessel narrowing causes myocardial demands to not be met

Back 19

50% or more

Front 20

myocardial ischemia

Back 20

pathologic mechanisms interfere with blood flow through the coronary arteries

Front 21

possible causes of myocardial ischemia

Back 21

atherosclerosis, thrombus formation, vasoconstriction

Front 22

how soon after coronary occlusion does ischemia develop

Back 22

within 10 seconds

Front 23

how long do cardiac cells remain viable under ischemic conditions

Back 23

20 mins

Front 24

what happens if cardiac cells are ischemic for more than 20 mins

Back 24

infarction begins

Front 25

hemodynamic causes of myocardial ischemia

Back 25

obstruction or constriction of coronary vessels, hypotension, decreased blood volume

Front 26

cardiac factors contributing to myocardial ischemia

Back 26

increased heart rate, decreased cardia filling time, valve problems

Front 27

hematologic factors contributing to myocardial ischemia

Back 27

low O2 content in blood (poor oxygenation, respiratory difficulties, trauma, sickle cell)

Front 28

systemic disorders contributing to myocardial ischemia

Back 28

reduced blood flow or availability of oxygen (shock)

Front 29

things that result in increased demand that contribute to myocardial ischemia

Back 29

high blood pressure, myocardial hypertrophy, exercise, stress, hyperthyroidism, anemia

Front 30

acute coronary syndrome

Back 30

sudden coronary obstruction caused by thrombus formation over an atherosclerotic plaque, coronary vasospasm or both (complete occlusion of coronary artery)

Front 31

signs of ACS

Back 31

chest pain, nausea/vomiting, diaphoresis, EKG/lab changes

Front 32

angina pectoris

Back 32

chest pain caused by myocardial ischemia resulting from insufficient coronary blood flow

Front 33

most common caue of angina pectoris

Back 33

atherosclerosis

Front 34

factors precipitating anginal pain

Back 34

physical exertion that increases myocardial demand
exposure to cold which increases vasoconstriction and elevates bp, increasing O2 demand
eating a heavy meal increasing blood to gut and reducing flow to myocardium
stress causing release of adrenaline and increasing bp, heart rate and myocardial workload

Front 35

signs of angina

Back 35

feeling of indigestion
choking/heavy pressure in sternum that may radiate to neck, jaw, shoulders, arms
weakness/numbness in arms, wrists, hands
shortness of breath, pallor, diaphoresis
dizziness, nausea, vomiting

Front 36

what symptoms of angina do the elderly most exhibit

Back 36

dyspnea

Front 37

silent CAD affects who

Back 37

women, elderly, diabetics

Front 38

types of angina

Back 38

stable, prinzmetal, silent ischemia, unstable(preinfarction)

Front 39

stable angina

Back 39

predictable pain on exertion
usually lasts only 3-5 mins after activity is ceased
caused by gradual narrowing and hardening of arterial walls

Front 40

prinzmetal angina

Back 40

unpredictable, caused by vasospasm; almost exclusively at rest, usually treated with CCB

Front 41

silent ischemia angina

Back 41

EKG changes but no reported symptoms; has been linked to mental stress; ST depression may occur on EKG

Front 42

unstable (preinfarction) angina

Back 42

occurs at rest or during minimal activity
increasing severity or frequency
signals atherosclerotic plaque has become complicated
infarction may soon follow
St segment depression and T wave inversion (will resolve as pain is relieved)

Front 43

what percentage of unstable angina proceeds to MI or death

Back 43

20%

Front 44

myocardial infarction

Back 44

myocardial tissue abruptly deprived of oxygen
myocardial cells begin to necrose as the blood flow is interrupted

Front 45

myocardial cells aka

Back 45

myocyte

Front 46

if coronary occlusion is resolved early in an MI the infarction will only involve

Back 46

the myocardium directly beneath the endocardium (non Q wave MI or subendocardial)

Front 47

if a thrombus lodges permanently in a coronary vessel the infarction will involve

Back 47

the myocardium all the way from endocardium to epicardium (Q wave MI aka Transmural MI)

Front 48

this EKG wave change generally represents ischemia

Back 48

Inverted T wave

Front 49

this EKG wave change generally represents injury

Back 49

elevated ST

Front 50

which EKG wave is permanently changed after an MI indicating necrotic cells

Back 50

Q wave

Front 51

describe the patho of cellular injury with MI (8 steps)

Back 51

1. myocardial oxygen reserves are used
2. anaerobic metabolism begins
3. hydrogen ions and lactic acid accumulate
4.acidosis further damages cells, allows lysosomal breakdown
5. conduction and contraction are suppressed
6.K, Ca and Mg rush out of cells
7. catecholamines are released
8. release of angiotensin II

Front 52

gycolysis (step 2 of MI) can only supply _____ of the myocardial energy requirement

Back 52

65-70%

Front 53

catecholamine release during an MI causes

Back 53

unusual sympathetic and parasympathetic responses (irregular heart rhythm)
suppression of pancreatic insulin secretion

Front 54

release of angiotensin II during MI results in

Back 54

vasoconstriction, elevated BP, fluid retention
growth factors also cause myocardium to remodel
causes further catecholamine release and coronary artery spasm

Front 55

loss of K, Ca and Mg (step 6 of MI) leads to what

Back 55

decreased contractility, heart is no longer an efficient pump

Front 56

changes in the heart muscle post MI

Back 56

decreased contractility
abnormal wall motion
poor left ventricular compliance
decreased stroke volume
decreased ejection fraction
increased preload
SA node malfunction

Front 57

what happens to necrotic myocardial tissue

Back 57

after about 6 weeks is replaced by scar tissue

Front 58

signs of MI

Back 58

sudden onset of chest pain with no response to rest or meds
shorness of breath, dyspnea, tachypnea
nausea and vomiting
decreased urinary output
cool, clammy, diaphoretic pale skin
anxiety, restlessness, fear

Front 59

what populations do not usually have the classic signs of MI

Back 59

women (fatigue, tired)
elderly (shortness of breath)

Front 60

most common causes of acquired valve disorders

Back 60

acute rheumatic fever
infective endocarditis

Front 61

what precipitates infective endocarditis

Back 61

bacterial or viral systemic infections
IV drug use

Front 62

acquired forms of valve disorders

Back 62

ischemic, traumatic, degenerative, infectious alterations in function

Front 63

stenosis

Back 63

valve orifice is constricted or narrowed
blood cannot flow through efficiently
pressure in the chamber rises and increases myocardial workload
causes hypertrophy

Front 64

regurgitation aka

Back 64

insufficiency or incompetence

Front 65

regurgitation

Back 65

leaflets fail to completely shut
blood is able to leak back into chamber
increased volume blood must pump
increased workload
dilation and hypertrophy of chambers

Front 66

most common side affected by regurgitation

Back 66

left

Front 67

dilation and hypertrophy of myocardium leads to

Back 67

diminished contractility, reduced ejection fraction, increased pressure and overworked ventricles leading to failure

Front 68

common causes of aortic stenosis

Back 68

inflammatory damage from rheumatic heart disease
congenital malformation
degeneration from calcification

Front 69

with aortic stenosis, pressure will build where

Back 69

in left ventricle

Front 70

signs of aortic stenosis

Back 70

dyspnea d/t left ventricular failure
dizziness and syncope d/t decreased blood flow to brain
angina d/t increased workload, decreased flow to coronary arteries
loud, rough systolic murmur

Front 71

common causes of mitral stenosis

Back 71

rheumatic fever
bacterial endocarditis
congenital (uncommon)

Front 72

with mitral stenosis pressure builds where

Back 72

left atrium

Front 73

with mitral stenosis there is a high risk of developign

Back 73

atrial dysrhythmias
dysrhythmia induced thrombi
pulmonary HTN due to backing up into pulmonary circulation

Front 74

mitral stenosis results when

Back 74

scarring causes leaflets to thicken and fuse
chordae tendineae shorten

Front 75

signs of mitral stenosis

Back 75

dyspnea/pulmonary congestion
fatigue
cough
frequent resp infections
a fib
low pitched murmur at apex

Front 76

common causes of aortic regurgitation

Back 76

rheumatic fever
bacterial endocarditis
HTN
connective tissue disorders
atherosclerosis

Front 77

signs of aortic regurgitation

Back 77

widened pulse pressure
murmur-high pitched blowing sound at 3rd to 5th intercostal space just left of sternum
carotid/temporal pulsations
throbbing pulses
dyspnea
fatigue

Front 78

complications of aortic regurgitation

Back 78

dysrhythmias and endocarditis

Front 79

common causes of mitral regurgitation

Back 79

mitral valve prolapse
rheumatic heart disease
infective endocarditis
CAD
connective tissue diseases
CHF

Front 80

with mitral regurgitation blood flows backwards from ___ to ___

Back 80

left ventricle into left atrium

Front 81

mitral regurgitation results in

Back 81

atrial dilation causing valve structures to stretch, leading to further backflow
left ventricle is eventually affected as well leading to heart failure

Front 82

signs of mitral regurgitation

Back 82

loud pansystolic murmur
palpitations
shortness of breath
cough
symptoms of heart failure-dyspnea, fatigue, weakness

Front 83

most common valve disorder in the US

Back 83

mitral valve prolapse

Front 84

mitral valve prolapse

Back 84

leaflets of the mitral valve billow upward into atrium

Front 85

mitral valve prolapse is more common in

Back 85

women

Front 86

causes of mitral valve prolapse

Back 86

may be due to genetic or environmental disruption of valvular development during 5th or 6th week of gestation
can be assoc with connective tissue disorders
symptomatic may be related to hyperthyroidism

Front 87

signs of mitral valve prolapse

Back 87

murmur or click, palpitations, tachycardia, light headedness, syncope, fatigue, weakness, chest tightness, anxiety, depression, panic attacks, chest pain

Front 88

which valve disorder is often asymptomatic

Back 88

mitral valve prolapse

Front 89

normal bp level

Back 89

<120 and <80

Front 90

pre hypertension bp

Back 90

120-139 OR 80-89

Front 91

stage 1 hypertension bp

Back 91

140-159 OR 90-99

Front 92

stage 2 hypertension bp

Back 92

>= 160 OR >= 100

Front 93

which bp measurement is the focus for treatment according to WHO

Back 93

systolic

Front 94

risk factors for primary HTN

Back 94

family hx, smoking, age, obesity, heavy alcohol consumption, race (blacks), high dietary sodium intake, low dietary intake of K, Ca, Mg; glucose intolerance

Front 95

5 patho theories of primary HTN

Back 95

1. overactive sympathetic nervous system
2. over activity of RAAS
3. defective sodium excretion by kidneys
4.inhibition of na/K pump
5. insulin resistance and endothelial function

Front 96

how does overactivity of sympathetic nervous system potentially contribute to primary HTN

Back 96

overstimulation of alpha and beta adrenergic receptors causes vasoconstriction and increased cardiac output

Front 97

how does overactivity of RAAS potentially contribute to primary HTN

Back 97

affects vascular tone and salt/water retention in the kidneys

Front 98

how does defective sodium excretion by the kidneys potentially contribute to primary HTN

Back 98

water/salt balance is thrown off; aggravated by dietary intake of more than 60mEq of NA/day

Front 99

pre hypertension bp

Back 99

120-139 OR 80-89

Front 100

how does inhibition of Na/K pump potentially contribute to primary HTn

Back 100

Na excretion from cells is inhibited causing intracellular increase; intracellular calcium also rises causing increased contractility of vascular smooth muscle

Front 101

stage 1 hypertension bp

Back 101

140-159 OR 90-99

Front 102

stage 2 hypertension bp

Back 102

>= 160 OR >= 100

Front 103

which bp measurement is the focus for treatment according to WHO

Back 103

systolic

Front 104

risk factors for primary HTN

Back 104

family hx, smoking, age, obesity, heavy alcohol consumption, race (blacks), high dietary sodium intake, low dietary intake of K, Ca, Mg; glucose intolerance

Front 105

5 patho theories of primary HTN

Back 105

1. overactive sympathetic nervous system
2. over activity of RAAS
3. defective sodium excretion by kidneys
4.inhibition of na/K pump
5. insulin resistance and endothelial function

Front 106

how does overactivity of sympathetic nervous system potentially contribute to primary HTN

Back 106

overstimulation of alpha and beta adrenergic receptors causes vasoconstriction and increased cardiac output

Front 107

how does overactivity of RAAS potentially contribute to primary HTN

Back 107

affects vascular tone and salt/water retention in the kidneys

Front 108

how does defective sodium excretion by the kidneys potentially contribute to primary HTN

Back 108

water/salt balance is thrown off; aggravated by dietary intake of more than 60mEq of NA/day

Front 109

how does inhibition of Na/K pump potentially contribute to primary HTn

Back 109

Na excretion from cells is inhibited causing intracellular increase; intracellular calcium also rises causing increased contractility of vascular smooth muscle

Front 110

how does insulin resistance and endothelial function potentially contribute to primary HTN

Back 110

insulin resistance is linked to endothelial cells inability to release vasodilators

Front 111

hypertensive urgency

Back 111

BP must be lowered within hours; generally use fast acting oral HTN meds

Front 112

conditions which cause a HTN emergency

Back 112

acute MI, dissecting aortic aneurysm, intracranial hemorrhage

Front 113

hypertensive emergency

Back 113

bp must be lowered IMMEDIATELY; IV vasodilators and intensive care

Front 114

cardiogenic shock

Back 114

shear inability of heart to function as an adequate pump; cells go into shock because they aren't getting oxygen and nutrients

Front 115

what makes cardiogenic shock different from other forms of shock

Back 115

no fluid shifting or hypovolemia

Front 116

causes of cardiogenic shock

Back 116

MI, left heart failure, myocardial ischemia, myocardial or pericardial infection, drug toxicity leading to heart failure

Front 117

what effect occurs during cardiogenic shock

Back 117

pulmonary congestion

Front 118

signs of cardiogenic shock

Back 118

tachycardia, hypotension, low urine output (late sign), cold clammy skin, weak peripheral pulses, rapid shallow respirations, pulmonary congestion, chest pain, dysrhythmias

Front 119

peripheral vascular diseases

Back 119

vasospasm (raynauds)
inflammation, thrombi, vasospasm (buerger disease)
atherosclerosis (hardening of arteries)
blood pooling (varicose veins)

Front 120

strabismus

Back 120

deviation of one eye from the other; walleyed

Front 121

nystagmus

Back 121

involuntary rhythmic movement of one or both eyes; pendulum, jerk

Front 122

causes of strabismus nystagmus

Back 122

head injury, neuro/cerebral components of disease; strabismus is either a weak muscle somewhere or a stronger one

Front 123

myopia

Back 123

nearsightedness

Front 124

hyperopia

Back 124

farsightedness

Front 125

causes of cataracts

Back 125

age, degeneration, congenital

Front 126

cataract

Back 126

disease of lens
becomes cloudy or opaque
protein starts to clump together

Front 127

leading cause of preventable blindness in the US

Back 127

glaucoma

Front 128

types of glaucoma

Back 128

open angle
closed angle (angle closure)
congenital closure

Front 129

glaucoma = IOP of

Back 129

22mm Hg or above

Front 130

#1 cause of legal blindness in adults

Back 130

macular degeneration

Front 131

macular degeneration

Back 131

degeneration of central portion of macular area

Front 132

drusen

Back 132

yellow spots in macular degeneration seen through pupil at back of eyes

Front 133

wet macular degeneration

Back 133

blood is seen due to pressure and bc new vessels are trying to form

Front 134

causes of age related macular degeneration

Back 134

hypertension, smoking, IDDM

Front 135

main sign of retinal detachment

Back 135

curtain over vision

Front 136

causes of detached retina

Back 136

serious trauma, diabetes (poor circulation weakens retina)

Front 137

types of auditory dysfunction

Back 137

conductive hearing loss
sensorineural hearing loss
meniere disease
ear infection

Front 138

meniere's disease

Back 138

inner ear fluid builds up and causes headaches, vertigo, balance issues, tinnitus, hearing loss, degeneration of area

Front 139

otitis externa

Back 139

inflammation of outer ear caused by staph, psuedomonas, fungus

Front 140

pneumonia

Back 140

acute infection of lower respiratory tract

Front 141

types of pneumonia

Back 141

community acquired, hospital acquired, immunocompromised

Front 142

causative organisms of community acquired pneumonia

Back 142

streptococcus pneumoniae
mycoplasma pneumoniae
haemophilus influenza

Front 143

causative organisms of hospital acquired pneumonia

Back 143

pseudomonas aeruginosa
escherichia coli
staphylococcus aureus

Front 144

causative organisms of immunocompromised pneumonia

Back 144

pneumocystil carinii
mycobacterium tuberculosis
fungi

Front 145

which organism that causes pneumonia usually indicates HIV

Back 145

pneumocystis carinii (bc this is easy for body to beat)

Front 146

subjective signs of pneumonia

Back 146

fever, chills, cough, pleural pain, malaise, hemoptysis, dyspnea

Front 147

objective signs of pneumonia

Back 147

elevated wbcs (usually > 10,000)
elevated temp
chest xray = infiltrates
sputum culture positive

Front 148

differences between pneumonia and COPD

Back 148

pneumonia=bacterial cause, can't receive air in location, short lived
asthma et al = allergen cause, can't get rid of air, ongoing

Front 149

extrinsic (atopic) asthma

Back 149

sensitive to specific external (extrinsic) allergens; in childhood commonly accompanied by other hereditary allergies

Front 150

causes of atopic asthma

Back 150

pollen, animal dander, house dust/mold, kapok or feather pillows, food additives containing sulfites, other sensitizing substances

Front 151

intrinsic (nonatopic) asthma

Back 151

reaction to internal, nonallergenic factors

Front 152

causes on nonatopic asthma

Back 152

irritants, emotional stress, fatigue, endocrine changes, temp variations, exposure to noxious fumes, coughing, laughing, humidity variations, genetic factors, anxiety

Front 153

subjective signs of asthma

Back 153

suddend dyspnea, wheezing, tightness in chest, cough, tachypnea, use of accessory muscles, rapid pulse, hyperresonant lung fields, diminished lung sounds

Front 154

objective signs of asthma

Back 154

decreased vital capacity, increased total lung/residual capacities, serum IgE levels may be increased, increased eosinophils, analysis of sputum usually shows presence of curschmann's spirals (casts) and charcot-leyden crystals; hyperinflation of lungs with areas of atelectasis, sinus tach on EKG, hypoxemia with ABG

Front 155

bronchitis

Back 155

inflammation of the bronchi caused by irritants/infection; classified as acute or chronic

Front 156

chronic bronchitis

Back 156

hypersecretion of mucus and chronic cough for 3 months/year occurring for 2 consecutive years

Front 157

distinguishing characteristic of chronic bronchitis

Back 157

airflow obstruction

Front 158

causes of chronic bronchitis

Back 158

smoking, exposure to irritants, genetic predisposition, exposure to noxious gases, respiratory tract infection, exposure to organic or inorganic dusts

Front 159

12 steps of chronic bronchitis patho

Back 159

1. irritants inhaled over prolonged time
2. irritiants inflame tracheobronchial tree
3. mucus production increases
4. inflammation and increased mucus=narrowed airway
5. epithelial cells and mucus glands hypertrophy
6. goblet cells increase in numbers
7. goblet cell hypersecretion= decreased cilia movement
8. cilia is damaged
9. mucus/debris accumulates in airway
10. increased risk for respiratory infections
11. smooth muscle bronchospasm further narrows airway lumen
12. with airway obstruction, gas is trapped in distal portion of lungs (bronchioles/alveoli)

Front 160

signs of chronic bronchitis

Back 160

productive cough, dyspnea, cyanosis, use of accessory muscles, tachypnea, pedal edema, jugular vein distention, weight gain from edema, wheezing, prolonged expiratory time, rhonchi to auscultation, pulmonary hypertension

Front 161

test results of chronic bronchitis

Back 161

increased residual volume, decreased vital capacity, decreased forced expiratory flow, increased PaO2, positive sputum analysis

Front 162

emphysema

Back 162

abnormal, permanent enlargement of the acini accompanied by destruction of alveolar walls

Front 163

most common cause of death from respiratory disease

Back 163

emphysema

Front 164

characteristics of emphysema

Back 164

obstruction results from tissue changes rather than mucus production
airflow limitatino caused by lack of elastic recoil in lungs

Front 165

causes of emphysema

Back 165

smoking, genetic (inherited deficiency of alpha1 antitrypsin)

Front 166

12 steps of emphysema patho

Back 166

1. primary emphysema inherited
2. decreased inhibition of proteolytic enzymes
3. proteolysis in lung tissues uninhibited
4. regular emphysema-recurrent inflammation=release of proteolyticc enzymes from lung cells
5. irreversible enlargement of air spaces distal to terminal bronchioles
6. alveolar walls destroyed; decreased capillary bed
7. breakdown of elasticity; alveoli unable to recoil normally
8. loss of fibrous and muscle tissue
9. lungs become less compliant
10. enlarged air spaces and less alveolar walls=compromised air circulation
11. bronchiolar collapse on expiration
12. air trapping occurs = overdistention

Front 167

signs of emphysema

Back 167

tachypnea, dyspnea on exertion, barrel chest, prolonged expiration, grunting, decreased breath sounds, clubbed finger/toes, decreased tactile fremitus, decreased chest expansion, hyperresonance on chest percussion, inspiratory crackles/wheezing

Front 168

expected test results of emphysema

Back 168

flattened diaphragm, decreased vascular markings @ lung periphery, overaeration of lungs, vertical heart, enlarged anteroposterior chest diameter, large retrosternal air space, increased hemoglobin (late), increased residual volume, increased total lung capacity, decreased diffusing capacity, increased inspiratory flow, decreased PaO2