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CVM II > Cardiac Path I > Flashcards

Cardiac Path I Flashcards

1
Q

What changes are found in the myocardium and chambers of an aging heart?

A

Decreased LV size
Increase epcardial fat
lipofuscin and basophilic degeneration
Fewer myocytes,increased collagenfibers - reduced contractility and compliance

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2
Q

What changes are found in the valves of an aging heart?

A

Aortic and mitral valve annular calcification - stenosis
Fibrous thickening
Mitral valve degeneration - MVP -> increase LA size
Lambl excrescences - bumps

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3
Q

What changes are found in the vasculature of an aging heart?

A

Coronary atherosclerosis

Stiffening aorta - loss of elastic tissue

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4
Q

When does CHF occur? How many people are effected?

A

Occurs when the heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with increased filling pressure
2% of US population

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5
Q

When the body is not getting the oxygen demand, what does the heart initially do to compensate?

A

Frank-starling mechanism
Myocardial hypertrophy
Activation on neurohumoral systems

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6
Q

When do cardiac myocytes become hypertrophic?

A

When there is sustained pressure or volume overload
or
Sustained trophic signals - b-adrenergic

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7
Q

What happens to myocytes in the setting of pressure overload?

A

Myocytes become thicker, LV wall thickness increases

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8
Q

What happens to myocytes in the setting of volume overload?

A

Myocytes elongate, and ventricular dilation is seen

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9
Q

Why is the hypertrophied heart vulnerable to ischemia-related decompensation?

A

because the hypertrophy of myocytes isnt accompanied by a matching increase in blood supply

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10
Q

What is the best measurement of hypertophied heart?

A

weight, not size or length

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11
Q

What is cardiac dysfunction characterized by?

A

Heart failure (systolic/diastolic)
Arrhythmias
Neurohumoral stimulation

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12
Q

What are the causes of LEFT sided HF?

A

Myocardial ischemia
HTN
Left-sided valve disease
Primary myocardial disease

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13
Q

What are the symptoms of LEFT sided HF?

A

Hypertension
Pulmonary congestion/edema/HTN
Atrial fib, stasis, thrombus if LV dysfunction->LA dilation
Reduced renal perfusion - prerenal azotemia
Hypoxic encephalopathy due to reduced CNS perfusion

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14
Q

What is the most common cause of RIGHT sided HF?

A

left-sided failure

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15
Q

What causes isolated RIGHT sided HF?

A

From any cause of pulmonary HTN

  • lung disease
  • Primary pulmonary HTN
  • Pulmonary vasoconstriction
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16
Q

In primary RIGHT - sided HF, what will manifest

A 
Pulmonary congestion is minimal 
Venous system is markedly congested 
- nutmeg liver/hepatomegaly
- Splenomegaly 
- Effusions
- Edema
- Renal congestion
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17
Q

What can ischemia of the heart result in

A

Myocardial infarction
Angina pectoris
Chronic ischemic heart disease, with HF
SCD - arrhythmias

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18
Q

What are more than 90% of IHD secondary to?

A

atherosclerosis

causing chronic vascular occlusion, acute plaque changes leading to thrombus

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19
Q

What are some causes of IHD?

A

Atherosclerosis, increased myocardial demand, hypoxia due to anemia, lung disease, etc

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20
Q

What is Agnina pectoris?

A

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction

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21
Q

What is stable angina?

A

Stenotic occlusion of coronary artery
Squeezing or burning sensation
Exercise induced
Relieved by rest or vasodilators

22
Q

What is Prinzmetal variant angina?

A

Episodic coronary artery spasm
Symptoms unrelated to exertion
Relieved with vasodilators

23
Q

What is unstable (crescendo) angina?

A

Pain, increasing in frequency, duration and severity, eventually at rest
Usually rupture of plaque, w partial thrombus
50% may have myocardial necrosis

24
Q

What are most MIs caused by? What are the other causes?

A

atheromatous plaque

Other causes: embolus, vasospasm, ischemia secondary to vasculitis, shock, hematologic abnormalities

25
Q

What is the clinical presentation of MI?

A 
Prolonged chest pain (>30 min) 
Crushing, stabbing, squeezing, tightness
Radiating down left arm or left jaw
Diaphoresis 
Nausea
25% asymptomatic
26
Q

How much time does complete deprivation of blood flow lead lead to irreversible myocardial injury?

A

20-30 min

27
Q

What happens to ATP and Lactate levels in myocardial tissue during MI?

A

ATP levels are depleted

Lactate increases

28
Q

What three arteries are mainly involved in MI? How frequently?

A

LAD (40-50%)
RCA (30-40%)
LCX (15-20%)

29
Q

Describe Transmural MIs

A

Many MIs occur w/i the distribution of a single coronary a
Fullthickness
Atherosclerosis and acute plaque changes
ST elevation

30
Q

Describe non-transmural subendocardial infarct

A

may involve more territory than a single coronary
Non-st elevation
Causes: lysis of thrombosis, chronic atherosclerotic disease, global hypotension

31
Q

Describe multifocal microinfarction

A

Small vessel microembolization, vasculitis, or vascular spasm (epi or cocaine)
Can cause SCD
non-transmural

32
Q

What stain is used to look for myocardial tissue that has recently suffered MI?

A

Triphenyltetrazolium chloride - TTC
Stains tissue containing lactate dehydrogenase red
Lysed cells become yellow

33
Q

Describe the morphologic changes that occur during an MI in the first 4 hours?

A

Grose: none
Micro: none

34
Q

Describe the morphologic changes that occur during an MI in the 4-24 hours?

A

Gross: dark mottling, pale-cyanotic arease
Micro: coagulation necrosis, eventual PMN

35
Q

Describe the morphologic changes that occur during an MI in 1-3 days ?

A

Gross: yellow-tan, mottling
Micro: coagulation necrosis; many PMNs

36
Q

Describe the morphologic changes that occur during an MI in the 7-10 days following?

A

Gross: yellow-tan, soft
Micro: phagocytosis of dead cells/debris, granulation tissue

37
Q

Describe the morphologic changes that occur during an MI in the 10-14 days following?

A

Gross: red-grey
Micro: granulation tissue, new vessels, early collagen

38
Q

Describe the morphologic changes that occur during an MI in the 2-8 wks following?

A

Gross: grey-white scar
Micro: increased collagen

39
Q

Describe the morphologic changes that occur during an MI in the 2 months following

A

Gross: complete scar
Micro: Dense collagen

40
Q

How is restoring blood flow to area of ischemia accomplished and what is the purpose? What can result

A

Thrombolysis, angioplasty and stent placement, CABG
An attempt to limit infarct size by rescuing at risk myocardium
Contraction band necrosis can occur due to Ca overload and hypertetanic contraction and reperfusion injury can result

41
Q

Describe the levels of CK-MB and Troponin I after MI

A

Detectable in circulating blood 3-12 hrs after infarction
Levels peak at 24 hours
CKMB returns to normal in 48-72 hrs
TI in 5-10 days

42
Q

Half of MI-associated deaths occur w/i the first hour due to what?

A

arrhythmias - result frompermanent damage to conducting system, or from myocardial irritability following infarct

43
Q

What are some complications of MI

A

Arrhythmia
Contractile dysfunction
Fibrinous pericarditis - Neutrophils coming in, friction rub, self limited
Myocardial rupture - weakend wall; 2-4 days post
papillary muscle rupture
Infarct expansion
Ventricular aneurysm - late complication
SCD

44
Q

What are the risk factors for myocardial rupture?

A

increase in age
large transmural anterior MI
First MI
Absence of LV hypertrophy

45
Q

What does rupture of the free wall of the heart cause?

A

pericardial tamonade

46
Q

What does rupture of the septum cause?

A

L->R shunt with right sided volume overload

47
Q

What disease commonly precipitate SCD?

A

Coronary artery disease

48
Q

What is the minimum dx for Left-sided HTN disease?

A

Hx of HTN, left ventricular hypertrophy in thea bsence of other lesions (Valve stenosis, coarctation)

49
Q

Isolated right-sided HTN HD arises in what setting?

A

pulmonary HTN

50
Q

What may acute cor pulmonale arise from?

A

large pulmonary embolus

51
Q

What may chronic cor pulmonale arise from?

A

chronic right venticular pressure overload- CHD or primary lung disease

CVM II (4 decks)

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