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Pathophysiology 212 > Chapter 19 > Flashcards

Chapter 19 Flashcards

1
Q

What is pericarditis? What is acute?

A

Inflammatory process of the pericardium

- Signs and symptoms of <2 weeks

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2
Q

In pericarditis, inflammation increases ____________ which means theres an ____________. During healing there is a ____________________.

A
  • capillary permeability
  • increase in fluid
  • deposition of scar tissue
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3
Q

What are the causes of pericarditis?

A
  • viral, bacterial, uremia (kidney failure), neoplastic, radiation, trauma, drug toxicity
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4
Q

What are the manifestations of pericarditis?

A
  • Decreased CO
  • pericardial rub
  • Chest pain (abrupt onset, sharp, radiates, scapula pain d/t irritation of the phrenic nerve, increases with deep breathing coughing, relief when sitting and leaning forward)
  • ECG changes
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5
Q

What are complications of pericarditis?

A
  • pericardial effusion
  • cardiac tamponade
  • dressler syndrome (happens after a heart attack)
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6
Q

What is pericardial effusion? What are the causes?

A

Fluid build up in the pericardial space which causes compression of heart cambers
- inflammation of pericardium, neoplasms, trauma, cardiac surgery

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7
Q

Pericardial effusion can lead to cardiac tamponade. What is cardiac tamponade? What are the causes?

A

Fluid/blood accumulation in the pericardial sac which causes compression
-trauma, heart rupture post MI, cardiac surgery, aortic dissection

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8
Q

What are the manifestations of cardiac tamponade? State the diagnosis/ treatment.

A

Manifestions depend on amount and rapidity (limits Stroke volume and CO= low SBP)
- change in mentation, dsypnea, tachycardia, chest pain, elevated central and jugular venous pressure = cardiac shock

Diagnosis: muffled heart sounds, pulsus paradoxes, ECG, CT, MRI
Treatment: pericardiocentesis, NSAIDS, corticoster.

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9
Q

What is coronary artery disease?

A

Heart disease caused by impaired coronary blood flow

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10
Q

Describe the blood flow in coronary circulation and relate to the metabolic needs of the heart.

A

dsadsa

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11
Q

What assists coronary artery flow? What impairs it?

A

Assist: endothelia cells lining arteries (selective permeability barrier), diastolic pressure in aorta, time is diastole

Impairs: atherosclerosis in common

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12
Q

What are the non-modifiable and modifiable risks for CAD?

A

NM: sex (post menopausal women), age, ethnicity, genetics

M: HT, hyperlipidemia, tabacco, diabetes, obesity, sedentary lifestyle, inactivity, ability to cope with stress

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13
Q

What are the 3 types of chronic Ischemia heart disease?

A
  1. Stable angina pectoris
  2. Silent myocardial ischemia
  3. Varient/prinzmental (vasospastic) angina
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14
Q

Explain stable angina pectoris. (what? location? provokes? relief?)

A

Chest pain or pressure sensation d/t transient ischemia (often a fixed coronary narrowing/obstruction)

  • pain is constricting, squeezing, suffocating
  • location: precordial/substernal (may radiate and cause epigastric discomfort)
  • occurs with exercise, physical exertion, cold, emotions)
  • relieved with rest and nitroglycerine
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15
Q

Explain silent myocardial ischema.

A
  • occurs in the absence of anginal pain
  • impaired blood flow from the effects of coronary atherosclerosis and vasospasm
  • the reason for no pain may be due to: the attack being shorter and not involving as much myocardial tissue, or the person having defects in pain threshold/transmission
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16
Q

Explain variant/ Prinzmental angina.

A

-caused by coronary artery spasms
- cause is unclear
- often at night (nocturnally), during rest, minimal exercise
- variable symptoms (arrhythmias, ECG changes)
Note: more in elderly, neuropathy, hypoten., low temp, stroke like symptoms

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17
Q

What is acute coronary syndrome? and what are its risks classified on?

A

Sudden decrease in blood flow to the heart (all caused by an imbalance in myocardial oxygen supply and demand)
- ECG changes (unstable angina, NSTEMI, STEMI)

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18
Q

Causes of acute coronary syndrome?

A
  • unstable plaque that forms a clot
  • coronary vasospasm (decrease in 02)
  • atherosclerosis/ narrowing
  • inflammation/ infection
  • secondary (anemia, fever, hypoemia)
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19
Q

Explain unstable angina/ NSTEMI?

A
  • You will get one of these depending on how severe the ischemia is
  • is biomarkers are elevated= NSTEMI
  • occurs with rest or minimal exertion
  • lasts more than 20 mins
  • severe, and frequent pain
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20
Q

What is STEMI? (ST elevation myocardial infar.) What are typical manifestations?

A
  • ischemic death of myocardial tissue
  • crushing/ constricting chest pain which is abrupt (may radiate), epigastric discomfort, nausea, vomiting, palpitations, cool clammy skin, SOB, anxiety, tachycardia, elevated HR, BP changes, decre. O2
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21
Q

Is STEMI relieved with rest?

A

NO

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22
Q

in STEMI how long does cell death take? ____________and_____________ can prevent necrosis
Note: ischema and necrosis = stunned myocardium, transmural Q wave

A
  • 15-20 mins

- early perfusion and revascularization

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23
Q

What does myocardial ischemia and necrosis result in ?

A
  • decreased contractile force (decr. CO, coronary artery perfusion, incr. vasculature pressure)
  • interruption of conduction (dysrhythmias)
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24
Q

Why are symptoms in STEMI and NSTEMI so variable?

A

It depends on where the damage is

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25
Q

Explain the difference between males and females in terms of acute coronary syndrome.

A

men: substernal pain with exertion/emotion, relieved with rest/nitro, ST elevation, exercise stress is a diagnosis, surgery= fewer complications, larger vessels
women: generalized/ subtle pain, relief with antacids, less ST elevation, stress/ echo is a diagnosis, surgery= complicated and smaller vessels

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26
Q

Diagnosis is also based on serum biomakers. What is this?

A

When myocardial cells become necrotic, their intracellular contents diffuse out.
Troponin- rise in 2-3 hr, remains for 7-10days
myoglobin- rise in 1 hr, peaks in 4
creatine kinase MB- peaks 4-6 hr, gone in 2-3 days

27
Q

What is the treatment for acute MI? Name some of the pharmacology as well.

A

oxygen, pain relief, reperfusion (fibrinolytics, percutaneous trans luminal coronary angioplasty, stents, coronary artery bypass grafting
-clopdogrel, nitrates, antiplatelet, beta blockers, ace inhibitors, anti-anxiety

28
Q

List some complications of an acute MI.

A

Arrhythmias – most common cause of sudden death, Reinfarction, Heart failure, Pericarditis, Embolic CVA or pulmonary embolus, Valve deformities, Septal ruptures, LV wall aneurysms/ rupture, Cardiogenic shock, Dressler syndrome

29
Q

Define cardio myopathies.

A

disorders of the heart muscles which can either be mechanical (heart failure) or electrical (arrhythmias)

  • can be primary (genetic or acquired) or secondary (associated with other disease)
30
Q

What is the leading cause of sudden death in young adults?

A 
Hypertrophic cardiomyopathy (HCM) 
Note: it is an autosomal dominant disorder
31
Q

What is hypertrophic cardiomyopathy? And what results?

A

unexplained genetic ventricular hypertrophy with septum thickening
- abnormal diastolic thickening, L ventricle outflow obstruction, disruptions of normal conduction pathways

32
Q

What are the manifestations of hypertrophic cardiomyopathy?

A
  • variable
  • decreased stroke volume d/t impaired diastolic filling
  • dyspnea, chest pain, syncope (fainting), A fib, arrhythmias, sudden death
33
Q

What is endocarditis? Explain.

A

Serious/ life threatening infection of the inner surface of the heart (may be acute-normal healthy person or subacute-valve abnormality)

  • staphylococcus aureus is a common cause
  • bulky, destructive vegatative heart lesions from (lesions consist of infectious organisms and cellular debris in fibrin strands of blood clots)
  • involve mitral and aortic valves
34
Q

What are some risk factors for endocarditis?

A

-infection, dental surgery, surgery, iv drug use, contaminants, immunodeficiency, valve prolapse, cardiovascular prostheses/ devices

35
Q

What are manifestations of endocarditis?

A

S&S of systemic infection, heart sound changes, fever accompanied by chills, symptoms related to embolism, anorexia, malaise, lethargy, cough, dyspnea, diarrhea, arthritis

36
Q

What are complications of endocarditis?

A

Embolism, arrhythmia, valve dysfunction

37
Q

What is rheumatic heart disease? What is it caused by?

A

Immune mediated multisystem inflammatory disease

  • caused by rheumatic fever (RF)
  • occurs after streptococcal pharyngitis (sore throat, swollen glands, headache, fever, n&V, joint pain)
  • happens in one or all layers
  • presence of aschoff bodies (lesions in the heart)
38
Q

What is the pathogenesis of rheumatic heart disease?

A

Unclear, but immunological response

-May be acute, chronic, or recurrent

39
Q

Explain the acute phase (pancarditis) of rheumatic heart disease.

A

-involves pericardial friction rub, murmurs, mitrial/aortic valve involvement, arrhythmia

40
Q

What is the diagnosis and treatment for rheumatic heart disease?

A

Diagnosis: evidence of GAS infection, elevated WBC, ESR, CRP, echocardiogram, U/S (can identify lesions)
Treatment: antibiotics (penicillin), anti-inflam, corticosteroids (suppress inflam. response)

41
Q

What is valvular disorders?

A

-disease process affecting 1 or more of the heart valves

42
Q

What are the causes of valvular disorder?

A

congenital, trauma, ischemic damage, degernative changes, inflammation

43
Q

What is the diagnosis and treatment of valvular disorders?

A

Diagnosis: auscultation, doppler echo, U/S
Treatment: symptoms, prevention, APA, percutaneous valvuloplasty, surgery

44
Q

When will you hear murmurs?

A
  • Valve stenosis: blood traveling through open narrow valves
  • valve regurgitant: blood back flow through closed valve
45
Q

What is mitral valve stenosis?

A
  • Narrowing of the mitral valve
  • fibrous, stiff tissue, often causing chordinae tendineae to shorten
  • complete opening obstructs blood flow
46
Q

What are the causes? Manifestations? Complications of mitral valve stenosis?

A

Causes: Rheumatic fever, congenital
Man: chest pain, weakness, fatigue, palpitations (decreased oxygen perfusion)
Comp: arrhythmias (A.fib, PAT), mural thrombi

47
Q

What is mitral valve regurgitation?

A

Incomplete closing of the mitral valve= some blood returns to the L atrium during systole

48
Q

What are the causes? manifestations? complications of mitral valve regurgitation?

A

Causes: RHD, chordae tenineae or papillary muscle rupture, LVH diliates orifice, mitral valve prolapse
Man: slow process (compensation), pulmonary congestion, murmur, L atrial and LV hypertrophy
Comp: A fib, thrombus

49
Q

What is mitral valve prolapse? And what two things is it associated with?

A

-Leaflets enlarge and become floppy

Can be associated with marfan’s and osteogensis imperfecta (connective tissue issue)

50
Q

What are manifestations and complications of mitral valve prolapse?

A

Man: “snap” sound, asymptomatic or chest pain, dyspnea, blood flow issues, tachycardia
Comp: Mitral valve regurgitation, A. fib, thrombus d/t turbulence around the valves)

51
Q

What is aortic valve stenosis?

A

-Narrowing of the aorta causing resistance to ejection

theres slow progression=compensation

52
Q

What are the causes? and manifestations of aortic valve stenosis?

A

Cause: congenital or acquired, male, active inflam.
Man: loud systolic ejection murmur or split S2 d/t stenosis/turbulence, angina, dyspnea, syncope, heart failure (LV hypertrophy)
- You get the splitting sounds because the valves are closing at diff. times

53
Q

What is aortic valve regurgitation? and causes?

A

Scarring of leaflet and/or enlarges orifice (blood flow back into LV during diastole) may be chronic or acute
Causes: RHD, congenital, endocarditis, HT, trauma, marfans, ideopathic

54
Q

What is Chronic aortic regurgitation?

A

slow progression= compensation from the body

-LV enlarges but works better

55
Q

What are the manifestations of chronic aortic regurgitation?

A
  • blowing sound over valve
  • widening pulse pressure (valve is suppose to close to maintain diastolic pressure)
  • korotkoff sounds persist to 0!
  • tachycardia, water hammer pulse (strong systole, weak diastole)
  • pounding heart while laying down
  • orthopnea, dyspnea, paroxysmal nocturnal dyspnea
56
Q

What are the causes ad manifestations of acute aortic regurgitation?

A

Causes: endocarditis, trauma, aortic dissection (wall detachment)
Man: no compensation, extreme rise in left ventricular end diastolic pressure=pulmonary edema, dysrhythmias (lethal because combined with issues like pulmonary edema=low cardiac output)

57
Q

What is patent ductus arteriosus? What are the manifestations?

A

ductus arterioles doesn’t close (>3 months), delay is premature (usually closes @ 24-74 hours)
Man: depends on size, extra pressure in aorta=HT

58
Q

What is atrial septal defects? What are manifestations?

A

Non closure of foramen ovale (usually asymptomatic until in teens)
-blood from L side pushes to R= incr. pressure in the pulmonary system
Man: incr. pulmonary pressure, atrial dilation= dysrhythmias (disrupts electrical conduction)

59
Q

What is cause of ventricular septal defect? Manifestations?

A

incomplete separation of ventricles during in vitro, 1/3 close spontaneously
Man: depends on size, asymptomatic>heart failure, tachypnea, tachycardia, pulmonary congestion, failure to thrive

60
Q

What is pulmonary stenosis (in children)? Causes?

A

partial obstruction of blood flow from RV

Causes: pulmonary valve lesions, artery lesions, combination

61
Q

What is Tetralogy of Fallot? (Hint: 4 things wrong)

A
  1. pulmonic narrowing
  2. RV hypertrophy
  3. ventricular septal defects
  4. dextroposition of aorta (aorta moves- overrides right ventricle but should be over left)
62
Q

What is the manifestations of Tetralogy? Treatment?

A

Man: cyanosis with incr. o2 demands (crying, feeding, defecation, loss of consciousness)

Treatment: knee chest position (less CO needed), surgery

63
Q

What is transposition of the great arteries? Risk factors? Manifestations?

A

-RV empties into aorta
-LV empties into pulmonary arteries
Risk: Diabetic mothers, boys
Man: cyanosis, survival is patent ductus arteriosus or septal defect

64
Q

What is coarctation of the aorta? Manifestations?

A

Associated with other congenital lesions (aorta narrows were it inserts in the ductus arterioles)
Man: BP lower in legs, symptomatic, HT later in life, LVH

Pathophysiology 212 (4 decks)

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