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Pathophysiology > Class 2 chapter 19 > Flashcards

Class 2 chapter 19 Flashcards

1
Q

Pericarditis

A

Inflammation of pericardium (outside of heart)

Acute =

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2
Q

Pericarditis manifestations

A 
Decreased CO
Pericardial friction rub
Chest pain (precordial - right where heart is, abrupt onset, sharp, radiates, scapula pain, increases with deep breath/cough)
Relief when sitting forward
ECG changes
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3
Q

Pericardial effusion

A

Accumulation of fluid in the pericardial cavity/space

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4
Q

Cardiac tamponade

A

Compression d/t fluid or blood

Emergency situation

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5
Q

Cardiac tamponade causes

A

Trauma (MVA)
Myocardial rupture post MI
Cardiac surgery
Aortic dissection

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6
Q

Cardiac tamponade manifestations

A

Dependent on amount and rapidity
Limits stroke volume (amount that leaves with every heartbeat) and CO = low SBP (CNS = change in mentation, resps = dyspnea and tachypnea, CVS = chest pain and tachycardia)
Elevated central venous pressure (pressure in R atrium) and jugular venous pressure
Circulatory shock (not getting blood pumped properly to organs)

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7
Q

Cardiac tamponade diagnosis

A

Muffled heart sounds (extra sac of fluid around heart so won’t be able to hear lub dub as easily)
Pulsus paradoxus (>10 mmHg fall with respirations, abnormally large decrease in SBP during inspiration)
ECG (decreased voltage)
Echocardiogram (can see if fluid is around heart)
CT, MRI

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8
Q

Coronary artery disease = coronary heart disease

A

Heart disease caused by impaired flow to coronary arteries

Chronic or acute

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9
Q

Non-modifiable risks for coronary artery disease

A

Sex/gender (men> women, post-menopausal women)
Age
Ethnicity
Genetics

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10
Q

Variant/prinzmetal angina

A 
D/t spasms of coronary artery
Cause is unclear
Often at night
Variable symptoms
Treatment is dependent on findings of investigative diagnostics
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11
Q

Acute coronary syndrome

A

Looking at ST segment elevation (ischemia to heart muscle)
Risk is classified based on ECG changes
1. Unstable angina/non ST-segment elevation myocardial Infarction (non-STEMI)
2. ST-segment elevation MI (STEMI)
All caused by an imbalance in myocardial oxygen supply and demand

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12
Q

Acute coronary syndrome causes

A

Unstable plaque, rupturing to form a clot (thin fibrous cap with fatty core is most unstable)
Coronary vasospasm (spasms of artery)
Atherosclerotic narrowing (progressive)
Inflammation/infection
Secondary causes (anemia - during surgery, fever - makes heart muscle pump harder, hypoxemia)

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13
Q

ST elevation MI

A

Ischemic death of myocardial tissue
Cardiac muscle wall schema and necrosis (subendocardial, transmural = Q wave - big, “stunned” myocardium)
Cell death in 15-20 minutes
Early perfusion and revascularization can prevent necrosis

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14
Q

ST elevation MI manifestations

A 
Crushing/constricting pain; usually abrupt (substernal with radiation to left arm, jaw, neck)
Epigastric distress/nausea
Palpitations
Cool, clammy skin
SOB
Anxiety
Unrelieved by rest/nitro
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15
Q

Myocardial ischemia/necrosis results in

A

Decreased contractile force (decreased CO, coronary artery perfusion, pulmonary vasculature pressure - pressure in system backs up to lungs)
Interruption of conduction (dysrhythmias)

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16
Q

MI diagnosis

A

Based on serum biomarkers
Troponin (rises within 2-3 hours, remains 7-10 days, serial = multiple so you know where they are in heart attack)
Myoglobin (rises within 1 hour, peaks at 4 hours, also from skeletal muscle damage)
Creatine Kinase MB (peaks at 4-6 hours, gone in 2-3 days, specific to cardiac muscle)

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17
Q

Acute MI treatment

A

Oxygen
Pain relief
Reperfusion (fibrionolytics - break up clots, percutaneous transluminal coronary angioplasty PCTA - put balloon in artery and expands to open up artery, stents)
Coronary Artery Bypass Grafting CABG (vein from another part of body and transplant it into heart)

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18
Q

Acute MI complications

A

Arrhythmias – most common cause of sudden death
Reinfarction
Heart failure
Pericarditis
Embolic CVA or Pulmonary embolus
Valve deformities (have to work properly for blood flow)
Septal rupture (separates ventricles)
LV wall aneurysms/rupture
Cardiogenic shock (heart unable to deliver oxygenated blood to brain)
Dressler syndrome

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19
Q

Idiopathic cardiomyopathy

A

Muscle disorders (mechanical - heart failure, electrical - arrhythmias)
Primary
Secondary

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20
Q

HCM manifestations

A

Variable
Decreased stroke volume d/t impaired diastolic filling (dyspnea, chest pain, syncope (passing out) post exertion)
Atrial fibrillation
Lethal ventricular arrhythmias

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21
Q

Endocarditis

A

Any infection of inner lining of heart (usually staphylococcus aureus, vegetative - things starting to grow, involvement of mitral and aortic valves most common)
Acute - relatively healthy individual
Sub-acute/chronic - h/o valve abnormalities

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22
Q

Rheumatic heart disease

A

Caused by rheumatic fever (which occurs after streptococcal pharyngitis, sore throat, fever, NV, joint pain, headache, one or all layers - pancarditis, valves, aschoff bodies - see on heart under microscope)
Immunological response but pathogenesis unclear
Acute, chronic or recurrent
Acute phase = pancarditis (pericardial friction rub, murmur, mitral/aortic valve involvement, arrhythmias)

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23
Q

Rheumatic heart disease diagnosis

A

Evidence of GAS (group A) infection
Elevated WBC, ESR, CRP
Echocardiogram
Ultrasound (can see valve moving and how much blood is going through)

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24
Q

Rheumatic heart disease treatment

A

Antibiotics

Prevention of complications

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25
Q

Valvular disorders causes

A 
Congenital (from childhood)
Trauma
Ischemic damage
Degenerative changes (vegetation growing over time)
Inflammation
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26
Q

Valvular disorders diagnosis

A

Auscultation
Doppler Echo
Ultrasound

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27
Q

Valvular disorders treatment

A 
Preventative
APA (antiplatelet aggregator)
Symptoms
Percutaneous valvuloplasty (fixing valve)
Surgery
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28
Q

Mitral valve stenosis

A

Fibrous, stiff tissue, often causing chordae tendineae to shorten
Incomplete opening obstructs blood flow

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29
Q

Mitral valve stenosis causes

A

RF

Congenital

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30
Q

Mitral valve regurgitation causes

A

RHD (rheumatic heart disease)
Chordae tendineae or papillary muscle rupture
LVH dilates orifice (opening)
Mitral valve prolapse (flops back when shouldn’t)

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31
Q

Aortic valve stenosis

A

Narrowing causing resistance to ejection

Slow progression = compensation

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32
Q

Aortic valve stenosis causes

A

Congenital or acquired

Male, active inflammation

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33
Q

Aortic valve regurgitation causes

A

RHD, ideopathic aortic dilation, congenital, endocarditis, Marfans, HPTN, trauma

34
Q

Chronic aortic regurgitation

A

Slow progression = compensation

LV enlarges but works harder

35
Q

Acute aortic regurgitation causes

A

Acute endocarditis
Trauma
Aortic dissection

36
Q

Heart disease in infants and children

A 
Patent ductus arteriosus
Atrial septal defects
Ventricular septal defects
Pulmonary stenosis
Tetralogy of fallout
Transposition of the great arteries
Coarctation of the aorta
37
Q

Heart disease in infants and children

A 
Patent ductus arteriosus
Atrial septal defects
Ventricular septal defects
Pulmonary stenosis
Tetralogy of fallout
Transposition of the great arteries
Coarctation of the aorta
38
Q

Patent ductus arteriosus

A

Persistent delay >3 months
Normally closes at 24-72hrs
Delay if premature

39
Q

Patent ductus arteriosus manifestations

A

Dependent on size

High pressure from aorta = pulmonary hypertension

40
Q

Ventricular septal defects

A

Most common congenital heart defect (25-30% of all)

41
Q

Ventricular septal defects causes

A

Incomplete separation of ventricles during development invitro
1/3 close spontaneously

42
Q

Ventricular septal defects manifestations

A

Dependent on size
Asymptomatic = heart failure
Tachypnea, tachycardia, pulmonary congestion, failure to thrive

43
Q

Pulmonary stenosis

A

Obstruction of blood flow from RV

44
Q

Pulmonary stenosis causes

A

Pulmonary valve lesions
Pulmonary artery lesions
Combination

45
Q

Tetralogy of fallot

A

Most common cyanotic congenital heart defect (5-7% of all)

  1. Pulmonic narrowing
  2. RV hypertrophy
  3. Ventricular septal defect
  4. Dextroposition of aorta (over-rides RV, attaches to septal defect)
46
Q

Tetralogy of fallot manifestations

A

Cyanosis with increased oxygen demands (crying, feeding, defecation)
Loss of consciousness possible

47
Q

Tetralogy of fallot treatment

A

Knee-chest position

Surgery

48
Q

Transposition of the great arteries

A

RV empties into aorta

LV empties into pulmonary arteries

49
Q

Transposition of the great arteries risk factors

A

Mothers with diabetes

Boys > girls

50
Q

Transposition of the great arteries manifestations

A

Cyanosis

Survival if patent ductus arteriosus or septal defect

51
Q

Coarctation of the aorta

A

Associated with other congenital lesions

52
Q

Coarctation of the aorta manifestations

A

BP lower in legs than in arms
Asymptomatic
Hypertension later in life
LVH

53
Q

Pericarditis causes

A 
Viral
Bacterial
Uremia (kidneys – a lot of toxins in blood)
Neoplastic (cancer)
Radiation
Trauma
Drug toxicity
54
Q

Pericarditis complications

A

Pericardial Effusion
Cardiac Tamponade
Dressler Syndrome (post heart attack)

55
Q

Pericardial effusion causes

A 
Inflammation of pericardium
Infection elsewhere
Neoplasms (tumours)
Cardiac surgery 
Trauma
56
Q

Cardiac tamponade treatment

A

Immediate pericardiocentesis (removal of fluid in pericardium)

57
Q

Dresslers syndrome

A

Pericarditis that happens after heart attack
Usually 4-6 weeks
Self-limiting (rarely leads to tamponade)

58
Q

Dresslers syndrome manifestations

A

Low grade fever
Pleuritic pain
Pericardial friction rub and/or effusion

59
Q

What assists coronary artery flow?

A

Endothelial cells lining arteries
Diastolic pressure in aorta (able to fill arteries)
Time in diastole (the faster your heart goes, the less time to fill arteries)

60
Q

What impairs coronary artery flow?

A

Atherosclerosis

61
Q

Modifiable risks for CAD

A 
Hypertension
Hyperlipidemia
Tobacco use
Diabetes
Obesity
Sedentary lifestyle/physical inactivity
Ability to cope with stress
62
Q

Stable angina

A

Pain/pressure d/t transient ischemia
Precordial/substernal (possible radiation, possible epigastric discomfort)
Often d/t a fixed coronary narrowing
Occurs with exercise/exertion/cold/emotions
Relieved with rest and nitroglycerine (helps to open up arteries in heart and increase flow)

63
Q

Silent MI

A

More likely in the elderly (less myocardium involved, neuropathy - neurological issues because of another disease processes. hypotension, low body temp, vague complaints of discomfort, mild diaphoresis, stroke-like symptoms, dizziness, sensorium changes)

64
Q

Unstable angina/non ST MI manifestations

A

With pre-diagnosis of “stable angina” but more severe or more often than usual
Occurs at rest (or minimal exertion)
Lasts >20 minutes
If biomarkers (blood values) are elevated = non-STEMI
High risk of STEMI

65
Q

Cardiomyopathies

A 
Cardio = heart
Myo = muscle
Pathy = disorder/syndrome/bad stuff
66
Q

Hypertrophic cardiomyopathy (HCM)

A

Leading cause of sudden cardiac death in young adults
Unexplained genetic ventricular septal thickening
Poor diastolic filling
LV outflow obstruction
Left ventricular hypertrophy (LVH)
Disruption of normal conduction pathways

67
Q

Endocarditis risk factors

A

Infection elsewhere
Dental surgery/surgery, IV drug use/contaminants
Immunodeficiency/immunosuppression
Valve prolapse (sudden or congenital)

68
Q

Endocarditis manifestations

A

Signs and symptoms of systemic infection
Heart sound changes (lub dub sounds different)
Symptoms related to embolism

69
Q

Endocarditis complications

A

Emboli (lung, renal, brain)
Valve dysfunction
Arrhythmias

70
Q

When will you hear a murmur?

A

If a valve is stenotic (stiff), you will hear a murmur of blood shooting through the narrow opening when the valve is open
If a valve is regurgitant (going backwards), you will hear a murmur of blood leaking back through when the valve should be closed

71
Q

Mitral valve stenosis manifestations

A

Chest pain, weakness, fatigue, palpitations

72
Q

Mitral valve stenosis complications

A

Arrythmias (atrial fibrillation, atrial tachycardias)

Mural thrombi

73
Q

Mitral valve regurgitation

A

Incomplete closing

Some blood returns to LA during systole

74
Q

Mitral valve regurgitation manifestations

A

Slow process = compensation
Pulmonary congestion
Pansystolic murmur
L Atrial and LV hypertrophy

75
Q

Mitral valve regurgitation complications

A

Atrial fibrillation

Thrombus

76
Q

Mitral valve prolapse

A

Leaflets enlarge, become “floppy”

Associated with connective tissue disorders (mar fan’s syndrome, osteogensis imperfecta)

77
Q

Mitral valve prolapse manifestations

A

“Snap”
Asymptomatic
Chest pain, dyspnea

78
Q

Mitral valve prolapse complications

A

Mital valve regurgitation
Atrial fibrillation
Thrombus

79
Q

Aortic valve stenosis manifestations

A

Chest pain, dyspnea, syncope, heart failure (LV hypertrophy)

80
Q

Aortic valve regurgitation

A

Scarring of leaflet and/or enlarged orifice

Blood flow back into LV during diastole

81
Q

Chronic aortic regurgitation manifestations

A

Blowing sound over valve
Widening pulse pressure (difference between systolic and diastolic)
Korotkoff sounds persist to zero!
Tachycardia or water hammer pulse (heart pumps really hard and strength of pulse is very exaggerated)
“Pounding” of heart when lying down
Eventually orthopnea, dyspnea, paroxysmal nocturnal dyspnea

82
Q

Acute aortic regurgitation manifestations

A

Too quick for compensation
Extreme rise in LVEDP (left ventricular end diastolic pressure) = pulmonary edema (decreased coronary artery perfusion)
Dysrhythmias = lethal

Pathophysiology (13 decks)

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