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Pathophysiology 212 > Chapter 19 > Flashcards

Chapter 19 Flashcards

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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
Explain the difference between males and females in terms of acute coronary syndrome.
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
26
Diagnosis is also based on serum biomakers. What is this?
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
What is the treatment for acute MI? Name some of the pharmacology as well.
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
List some complications of an acute MI.
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
Define cardio myopathies.
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
What is the leading cause of sudden death in young adults?
``` Hypertrophic cardiomyopathy (HCM) Note: it is an autosomal dominant disorder ```
31
What is hypertrophic cardiomyopathy? And what results?
unexplained genetic ventricular hypertrophy with septum thickening - abnormal diastolic thickening, L ventricle outflow obstruction, disruptions of normal conduction pathways
32
What are the manifestations of hypertrophic cardiomyopathy?
- variable - decreased stroke volume d/t impaired diastolic filling - dyspnea, chest pain, syncope (fainting), A fib, arrhythmias, sudden death
33
What is endocarditis? Explain.
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
What are some risk factors for endocarditis?
-infection, dental surgery, surgery, iv drug use, contaminants, immunodeficiency, valve prolapse, cardiovascular prostheses/ devices
35
What are manifestations of endocarditis?
S&S of systemic infection, heart sound changes, fever accompanied by chills, symptoms related to embolism, anorexia, malaise, lethargy, cough, dyspnea, diarrhea, arthritis
36
What are complications of endocarditis?
Embolism, arrhythmia, valve dysfunction
37
What is rheumatic heart disease? What is it caused by?
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
What is the pathogenesis of rheumatic heart disease?
Unclear, but immunological response | -May be acute, chronic, or recurrent
39
Explain the acute phase (pancarditis) of rheumatic heart disease.
-involves pericardial friction rub, murmurs, mitrial/aortic valve involvement, arrhythmia
40
What is the diagnosis and treatment for rheumatic heart disease?
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
What is valvular disorders?
-disease process affecting 1 or more of the heart valves
42
What are the causes of valvular disorder?
congenital, trauma, ischemic damage, degernative changes, inflammation
43
What is the diagnosis and treatment of valvular disorders?
Diagnosis: auscultation, doppler echo, U/S Treatment: symptoms, prevention, APA, percutaneous valvuloplasty, surgery
44
When will you hear murmurs?
- Valve stenosis: blood traveling through open narrow valves - valve regurgitant: blood back flow through closed valve
45
What is mitral valve stenosis?
- Narrowing of the mitral valve - fibrous, stiff tissue, often causing chordinae tendineae to shorten - complete opening obstructs blood flow
46
What are the causes? Manifestations? Complications of mitral valve stenosis?
Causes: Rheumatic fever, congenital Man: chest pain, weakness, fatigue, palpitations (decreased oxygen perfusion) Comp: arrhythmias (A.fib, PAT), mural thrombi
47
What is mitral valve regurgitation?
Incomplete closing of the mitral valve= some blood returns to the L atrium during systole
48
What are the causes? manifestations? complications of mitral valve regurgitation?
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
What is mitral valve prolapse? And what two things is it associated with?
-Leaflets enlarge and become floppy | Can be associated with marfan's and osteogensis imperfecta (connective tissue issue)
50
What are manifestations and complications of mitral valve prolapse?
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
What is aortic valve stenosis?
-Narrowing of the aorta causing resistance to ejection | theres slow progression=compensation
52
What are the causes? and manifestations of aortic valve stenosis?
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
What is aortic valve regurgitation? and causes?
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
What is Chronic aortic regurgitation?
slow progression= compensation from the body | -LV enlarges but works better
55
What are the manifestations of chronic aortic regurgitation?
- 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
What are the causes ad manifestations of acute aortic regurgitation?
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
What is patent ductus arteriosus? What are the manifestations?
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
What is atrial septal defects? What are manifestations?
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
What is cause of ventricular septal defect? Manifestations?
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
What is pulmonary stenosis (in children)? Causes?
partial obstruction of blood flow from RV | Causes: pulmonary valve lesions, artery lesions, combination
61
What is Tetralogy of Fallot? (Hint: 4 things wrong)
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
What is the manifestations of Tetralogy? Treatment?
Man: cyanosis with incr. o2 demands (crying, feeding, defecation, loss of consciousness) Treatment: knee chest position (less CO needed), surgery
63
What is transposition of the great arteries? Risk factors? Manifestations?
-RV empties into aorta -LV empties into pulmonary arteries Risk: Diabetic mothers, boys Man: cyanosis, survival is patent ductus arteriosus or septal defect
64
What is coarctation of the aorta? Manifestations?
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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