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PathoPhys > Lecture 6 - Cardiac > Flashcards

Lecture 6 - Cardiac Flashcards

1
Q

Immunosurveillance is defined by 3 events - what are they?

A

“THE 3 E’S” escape, equilibration, elimination

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2
Q

In regard to tumor immunology: a.) adaptive immunity is involved b.) B cells are involved c.) innate immunity is involved d.) adaptive and innate immunity are involved

A

d

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3
Q

Macrophages: a.) are always deleterious for macrophage growth b.) are helping tumor growth if they are M1 type c.) are helping tumor growth if they are M2 type d.) are deleterious to tumor growth if they are M2 type

A

c

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4
Q

The abscopal effect: a.) is caused by an immune response b.) elicits an immune response c.) doesn’t use an intact immune system d.) happens only when NK cells are available

A

b

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5
Q

humans: a.) acquire their first microbiome in utero b.) acquire their first microbiome at birth c.) acquire their first microbiome a few days after birth d.) acquire their first microbiomes years after birth

A

b

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6
Q

What is the most common end result for a person with ischaemic heart disease (IHD)?

A

heart failure

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7
Q

Ischaemic heart disease: what layer(s) are at risk of ischemia?

A

subendocardial layers

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8
Q

What occurs to coronaries during diastole?

A

blood flow is good; well developed plexus, good blood flow

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9
Q

What occurs to coronaries during systole?

A

blood flow restricted - muscular tension causes collapse of coronaries

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10
Q

how many coronaries are there, and from where do they originate?

A

originate from ascending aorta, 2 main ones (right and left)

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11
Q

Is ischaemic heart disease more likely to occur during systole or diastole?

A

systole - as there is no blood flow, so pathology (ischemia) can possibly occur during this time

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12
Q

What pathology of the heart may cause diastole to get shorter?

A

tachycardia, thus tachycardia is a risk factor for IHD

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13
Q

decreased HR is called?

A

bradycardia

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14
Q

what pathology is the main cause of coronary art disease?

A

atherosclerosis

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15
Q

define atherosclerosis - what does it tend to result in?

A

build up of fat/ cholesterol/ other substance on arterial walls resulting in impeded blood flow tends to result in lesion (plaque) formation, which may burst forming a blood clot - leading to heart attack if in coronaries

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16
Q

atherosclerosis especially effects what part(s) of the heart?

A

epicardial (proximal) parts - intramural branches (which are deeper) show only slight thickening of intima

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17
Q

state the causes of IHD?

A

Complications of atherosclerosis…
1. STENOSIS - Progressive atherosclerotic stenosis
2. THROMBUS - Erosion of atherosclerotic plaque leading to thrombus formation
3. HEMORRHAGE - Rupture of fibrous cap of plaque, leading to hemorrhage into lesion and thrombosis
Other…
1. Embolus formation - due to infective endocartitis, calcific valvular disease
2. Low coronary artery perfusion, which may be due to… a.) shock from hemorrhage b.) severe anemia c.) severe aortic valve disease

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18
Q

define ‘stenosis’?

A

narrowing of passage

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19
Q

Relationship between coronary blood flow and aortic pressure?

A

coronary blood flow is INDEPENDANT of aortic pressure - as ensured by autoregulatory mechanisms

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20
Q

low coronary perfusion is a (more/ less) common cause of IHD?

A

less

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21
Q

In order for symptomatic IHD, by how much must the coronary artery lumens be blocked?

A

75-80% blocked to cause symptoms

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22
Q

State what the following coronary supplies: Right coronary artery

A

R. atrium R. ventricle

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23
Q

State what the following coronary supplies: Right marginal artery

A

R. ventricle apex

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24
Q

State what the following coronary supplies: Left anterior descending artery

A

Both ventricles Interventricular septum

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25
Q

State what the following coronary supplies: Left marginal artery

A

L. ventricle

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26
Q

State what the following coronary supplies: Left circumflex artery

A

L. atrium L. ventricle

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27
Q

Explain how the subepicardium and subendocardium differ in terms of blood flow during heart phases? What can be concluded from this?

A
  1. Subendocardial far more dependent on BF during diastole 2. Subendocardial has far less BF during systole Thus, subendocardial layers are far more prone to IHD!
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28
Q

Compare subepicardial and subendocardial layers: a.) Risk of atherosclerosis? b.) Risk of IHD?

A

a.) Epicardium more prone to atherosclerosis b.) Subendocardium much higher risk of IHD

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29
Q

Coronary arteries have very (many/ few) anastomoses

A

few - thus this increases risk of myocardial infarction

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30
Q

When do most major coronaries fill with blood - how does this occur?

A

during diastole: 1. the SL valves cover the openings to the L. and R. coronary arteries during systole as blood flows away from the aorta 2. backflow of blood closes SL valve, coronary artery openings form, blood flows into coronaries

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31
Q

why are the subendocardial layers more susceptible to IHD?

A

Due to the nature of BF in this area - BF is limited to only occur during diastole (during systole the arteries collapse), thus these periods of no BF increase risk of ischemic complications

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32
Q

What is the most common cause of coronary artery blockage?

A

blood clot due to rupture of plaque fibrous cap - a process of late atherosclerosis

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33
Q

define angina

A

chest pain

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34
Q

what connects the coronary arteries to the subendocardial plexus?

A

intramuscular penetrating arteries

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35
Q

Why is aerobic metabolism used explicitly in the heart?

A
  1. poor ATP reserves 2. as mitochondria make up ~30% cardiac myofiber volume (must use them!)
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36
Q

What is the main fuel used by the heart?

A

Fatty acids! As they store higher energy and can be better exploited under aerobic conditions

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37
Q

t/f: reperfusion of coronaries is always possible

A

false - only if ischemia is brief may reperfusion occur, quickly a ‘critical point’ is hit and from then on ya fucked

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38
Q

define acute myocardial infarction (AMI)

A

reduction in coronary artery blood supply leading to formation of necrotic myocardium - reduction may be sudden, absolute or relative

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39
Q

state the general cause of AMI

A

thrombosis superimposed (OR hemorrhage within an atheromatous plaque in a coronary artery

40
Q

symptoms of AMI?

A
  1. chest pain 2. nausea, vomiting 3. profuse sweating
41
Q

AMI is silent in _% of patients, especially the ___

A

10%; elderly

42
Q

Relationship between atherosclerosis, IHD and AMI?

A

atherosclerosis causes IHD which causes AMI - they all are linked!

43
Q

What determines the severity of AMI?

A
  1. location - which CA effected 2. size - size of occlusion in CA’s 3. presence or absence of anastomosis at site
44
Q

Where are coronary artery anastomoses?

A

Only in intramural part! (mural means ‘wall’, thus within heart wall only not major CA’s)

45
Q

Why are coronary artery anastomoses mostly irrelevant with regard to pathogenesis of atherosclerosis, IHD and AMI?

A

Because often atherosclerotic plaques form within major coronary arteries - where anastomoses are not present. Thus, IHD/ AMI may still develop despite their presence later on in the circuit!

46
Q

State means of clinical observation of AMI?

A
  1. angiograms - good as can confirm blockage within 3-4 hrs of angina 2. ECG’s - good to find site of infarction
47
Q

State means of AMI diagnosis?

A
  1. transient leukocytosis - as this damage triggers some inflammation 2. cardiac enzymes and proteins released from cardiac tissue into blood serum - ie. troponin (early indicator), creatine kinase (later indicator)
48
Q

State the major occurrences of myocardial infraction… a.) Within first 18hrs? b.) Within 1-2 days? c.) Within 3-4 days? d.) Within 1-3 weeks? e.) Within 3-6 weeks?

A

a.) Within first 18hrs = nothing b.) Within 1-2 days = edema, myocyte necrosis, acute inflammatory cell infiltration, muscle pale c.) Within 3-4 days = obvious necrosis, inflammation, yellow rubbery center w/ hemorrhagic border d.) Within 1-3 weeks = granulation tissue, infarcted area paler and thinner e.) Within 3-6 weeks = dense fibrosis, tough white scar

49
Q

State the most common coronaries affected for myocardial infarction’s?

A

50% - left anterior descending artery 30% - right coronary artery 20% - circumflex artery obstruction

50
Q

Define coronary dominance?

A

Which - the left or right coronary artery - supplies the posterior interventricular artery. Most, 60-70% of people are right dominant

51
Q

How is coronary dominance clincially relevant?

A

Left dominant circulation increases mortality rate for those with acute coronary syndrome

52
Q

what is mural thrombosis?

A

many layers of thrombosis in infarcted area “The formation of an abnormal endothelial surface following infarction, occurring in interval of 1 week or more” - google

53
Q

CHID stands for?

A

Chronic Ischemic Heart Disease

54
Q

CHID - clinical features?

A
  1. Angina - particularly during exercise, may be unstable or crescendo 2. Impaired ventricular function following previous infarction; episodes may lead to ventricular and congestive heart failure
55
Q

Describe morphology of someone with CHID?

A

Generally speaking arteries on day to day basis still have some space for blood flow (see slide 19), however… 1. Extensive coronary arterial atheroma 2. 2-3 major coronary artery’s have stenosis 3. may have rupture of fibrous cap (however if this occurs the pathology will progress, due to embolus formation and complete blockage

56
Q

sudden cardiac death most often occurs due to?

A

acute cardiac failure, which occurs due to ischemic heart disease ((((really feeling like we got 52 names for the same thing)))))

57
Q

State the post-mortem findings of those who died due to sudden cardiac death?

A
  1. coronary artery stenosis 2. coronary thrombosis (atleast ~55% of cases) 3. ventricular arrhythmias (assumed)
58
Q

expand the acronym ‘SADS’

A

Sudden adult (arrhythmic) death syndrome ((((could do with some of that rn))))

59
Q

How can sudden cardiac death be prevented?

A
  1. defibrillator (normal or implanted) 2. CPR 3. anticoagulant therapy to reduce thrombosis formation, ie. aspirin, warfarin
60
Q

Define heart failure (HF)?

A

General term used to describe the end-result of various types of cardiac dysfunction leading to inadequate perfusion of heart tissue

61
Q

Prognosis of HF?

A

~3 years to live

62
Q

HF comprises _% of hospitisaiton for those >65

A

20%

63
Q

name some anticoagulant drugs?

A

warfarin, aspirin

64
Q

symptoms of HF?

A

fatigue poor exercise tolerance shortness of breath

65
Q

clinical diagnosis of HF?

A

difficult - no single test echocardiography

66
Q

Pathophysiology of HF - how’s it affect CVS? Compensatory response to this?

A

decreased CO leading to arterial under-filling in response - fluid retention causing increased BV by up to 25%

67
Q

Pathophysiology of HF - state the sequence of events?

A
  1. decreased CO 2. arterial under-filling (decreased BP and BV) 3. mechanoreceptors (both high and low pressure barorec.) detect this 4. affarent impulse via vagus + glossopharyngeal nerves to CCC (medulla) 5. efferent impulse via sympathetic motor nerves (sympathetic chain) 6. tachycardia, increased contractility, vasoconstriciton other effects… - RAAS system
68
Q

t/f: HF may only be acute, not chronic

A

false - may be either, depends on speed of pathological development

69
Q

acute HF occurs within?

A

minutes of myocardial infarct

70
Q

acute HF symptoms?

A

pulmonary edema, shortness of breath

71
Q

chronic heart failure is usually caused by?

A

valvular defects - mitral stenosis, incompetence

72
Q

When may chronic congestive HF develop?

A

after an episode of acute HF

73
Q

t/f: failure of one ventricle during HF will usually occur after the other has

A

true

74
Q

which - left or right HF - is more likely to cause pulmonary edema?

A

left HF - as blood coming from lungs is not taken into left side of heart, thus fluid escapes CVS into lung interstitium leading to pulmonary congestion and edema

75
Q

What are some consequences of right sided HF?

A

Failure to ‘move on’ blood returning from venous circulation… 1. systemic venous congestion 2. raised jugular vein pressure 3. liver enlargement

76
Q

left sided HF - symptoms?

A
  1. pulmonary congestion/ edema 2. elevated pulmonary capillary pressure 3. discomfort breathing (orthopnea) 4. tachycardia 5. cyanosis (blue extremities, lips) 6. paroxysmal nocturnal dyspnea - cannot sleep lying down have to sit
77
Q

right sided HF AKA?

A

Cor pulmonale - alteration in structure and function of right ventricle

78
Q

right sided HF - symptoms?

A
  1. edema in extremeties 2. weight gain 3. distended jugular veins 4. enlarged liver/ spleen
79
Q

right sided HF may be secondary to what?

A

lung disease - ie. lung disease means reduced flow O2 blood to right side of heart thus right heart failure

80
Q

a mitral stenosis would leave to what?

A

increased pulmonary pressure and then right HF

81
Q

t/f: congestive HF involves both L. and R. sides, and thus a combination of systemic and pulmonary signs

A

true

82
Q

causes of HF?

A
  1. IHD 2. Systemic hypertension 3. Valvular heart disease 4. Lung disease (as it causes lack of return to the right side of the heart -> right HF -> congestive HF) note: majority clinical symptoms due to first 3; alone or in combination
83
Q

How much of right HF is consequence of left HF? How much of right HF is purely just right HF?

A

85% consequence due to Left HF, 15% purely just right HF

84
Q

t/f: all clinico-pathological features of HF have clear pathological basis

A

true

85
Q

t.f: all clinico-pathological features of HF are present in HF

A

false - may only be some

86
Q

what is the ‘gold standard’ for diagnosis of HF?

A

echocardiography

87
Q

What is the first symptom of HF?

A

dysponea - shortness of breath (SOB)

88
Q

what physiologically causes SOB in HF?

A

increased blood/ H2O in lungs at expense of air volume

89
Q

define orthopnea - what causes it?

A

shortness of breath whilst supine - caused by increased VR to lungs in this position

90
Q

what is paroxysmal nocturnal dysponea?

A

sudden urgent SOB during sleep

91
Q

**not a question** slides 44,45,46 are crap/ already covered so im not re-writing - just incase ya’ll care i haven’t done these explicitly

A

**not a question** slides 44,45,46 are crap/ already covered so im not re-writing - just incase ya’ll care i haven’t done these explicitly

92
Q

Right heart failure ____ ventral venous pressure and ____ cardiac output

A

increases; decreases

93
Q

oedema causes what (2)

A
  1. Hydrothorax - pleural effusion or low protein transudation 2. High systemic venous pressure - causing: a.) increased transudation fluid from capillaries b.) impaired lymphatic and thoracic duct drainage (can’t flow into vein because venous pressure too high
94
Q

what other organ may be effected heavily by HF?

A

kidneys - as require on blood flow not just for tissue survival but to serve their function (adjust BV, produce urine) thus ‘pre-renal’ renal failure can occur

95
Q

cardiac valves cause _% of HF

A

10%

96
Q

this lecture and unit is fucking horseshit im out

A

lmao

97
Q

explain how heart subendocardial and subepicardial layers differ in blood flow, through systole and diastole (graph)

A

PathoPhys (25 decks)

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