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CPAT CARDIO > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Most common congenital heart disease

A

septal defects

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2
Q

types of congenital heart disease

A

right to left shunt
left to right shunt
obstructions

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3
Q

examples of right to left shunt

A

tetralogy of fallot (most common), transposition of great arteries

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4
Q

4 anatomical features of tetralogy of fallot

A
  1. ventricular septal defect (communication between RV and LV)
  2. obstruction to the RV outflow (pulmonary stenosis)
  3. over-riding aorta (above septal defect)
  4. RV hypertrophy (due to volume and pressure overload due to septal defect)
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5
Q

in the tetralogy of fallot, what factor determines the direction of the shunt

A

the obstruction to the RV outflow - severity of this dictates shunt direction.
Mild: L –> R
Critical: R –> L

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6
Q

Transposition of great arteries

A

anatomical discordance such that the aorta arises from the RV and the pulmonary artery emanates from the LV.
Shunt means better prognosis as there is some mixing of blood.

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7
Q

define right to left shunt and what it is clinically characterised as

A

when deoxy blood form right side of heart mixes with the left. Clinically characterised as cyanosis, since the cells of the body are receiving poorly oxygenated blood.

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8
Q

what is cyanosis often accompanied by

A

clubbing of fingers and toes

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9
Q

define shunt

A

abnormal connection between heart chambers leading to abnormal blood flow.

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10
Q

examples of left to right shunts

A

atrial septal defect, ventricular septal defect, patent ductus arteriosis

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11
Q

consequences of left to right shunts

A

increased pulmonary blood flow which causes increased pressure and volume in pulmonary circulation. this causes pulmonary hypertension and RV hypertrophy.

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12
Q

how does pulmonary artery response to increase pressure and volume associated with left to right shunts

A

vasoconstriction and resistance eventually causes the shunt to shift from a left to right shunt to a right to left shunt with associated cyanosis

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13
Q

atrial septal defect is an example of what kind of shunt

A

left to right shunt

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14
Q

describe atrial septal defect

A

communication of blood between atria.

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15
Q

why is atrial septal defect initially a L-R shunt.

A

It is classified a L-R shunt because initially the pulmonary resistance is less than the systemic resistance and because RV is capable of distension to accomodate increased volume. HT will eventually develop in pulmonary artery and increased resistance will shift it to a R-L shunt.

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16
Q

ventricular septal defect is an example of what kind of shunt

A

left to right shunt.

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17
Q

describe a ventricular septal defect

A

communication of blood between ventricles. this causes significant RV hypertrophy and hypertension in pulmonary artery from birth.

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18
Q

what kind of shunt is patent ductus arteriosus an example of

A

left to right shunt initially, however obstructive pulmonary vascular disease develops and eventually reverses it to a R-L shunt. (Eisenmengers syndrome/reaction)

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19
Q

describe patent ductus arteriosis

A

ductus arteriosus usually connects pulmonary artery and aorta during fetal development and prostaglandins usually shut this at birth. PDA is when the connection fails to close after birth.

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20
Q

What is Eisenmengers syndrome

A

the provess by which a L-R shunt causes increased flow through pulmonary vasculature resulting in pulmonary HT. This leads to elevated right sided pressure and reversal of shunt from L-R to R -L.

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21
Q

What are three examples of congenital obstructions

A

coarctation of aorta
pulmonary stenosis
aortic stenosis

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22
Q

describe coarctation of aorta

A

constriction of the aorta leading to HyperT in upper extremities but HypoT in lower extremities

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23
Q

describe difference between infantile coarctation and adult coarctation

A

infantile: proximal patent ductus arteriosis, symptoms occur early in life, lower body cyanosis.
adult: typical, ridge like infolding of the aorta opposite a closed ductus arteriosis. generally asymptomatic until later in life which manifest as enlarged intercostal arteries, saw tooth notching on ribs, stroke and brain aneuryism

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24
Q

define cardiomyopathy and the types

A

disease intrinsic to heart. types:
dilated (most common)
hypertrophic
restrictive

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25
Q

define dilated cardiomyopathy

A

progressive cardiac dilation and contraction (Systole) dysfunction. Causes - genetic, alcoholism, viral myocarditis, pregnancy

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26
Q

macroscopic features of dilated cardiomyopathy

A

heart is heavy, 2-3x the normal weight, large and flabby (dilation of all 4 chambers), thinned walls and hypocontraction

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27
Q

microscopic features of dilated cardiomyopathy

A

granular mural thrombosis, variable myocyte hypertrophy, abnormal filling (diastole). interstitial fibrosis,

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28
Q

define hypertrophic cardiomyopathy

A

genetic cause, characterised by hypertrophy and abnormal filling (Diastole) mostly due to mutations in genes of the sarcomere

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29
Q

most common genetic mutation underlying hypertrophic cardiomyopathy

A

Arg403-Gln403 in myosin heavy chain beta protein

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30
Q

macroscopic features of hypertrophic cardiomyopathy

A

heart is heavy, thick walled and hypercontracting. hypertrophy - chamber is compromised and cant hold sufficient blood for systemic circulation - compensates by contracting faster. Septal muscle bulges into the LV outflow tract, LA enlarged.

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31
Q

microscopic features of hypertrophic cardiomyopathy

A

disarray, extreme hypertrophy, characteristic branching of myocytes and interstitial fibrosis.

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32
Q

define rheumatic fever/ rheumatic heart disease

A

autoimmune mediated inflammatory disease occuring following group A streptococcal pharyngitis (strep throat).

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33
Q

what levels of the heart to RF/RHD effect

A

may effect heart at all three levels -
endocardium (valves)
myocardium (Aschoff bodies)
pericardium (fibrinous exudates)

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34
Q

what is a macroscopic characteristic of RF/RHD

A

non infectious vegetations (fibrin + platelets) along the mitral valve and thickening/shortening of the chordae tendinae. this results in eventual stenosis and regurgitation. ALSO Aschoff bodies and fibrinous pericarditis.

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35
Q

what are aschoff bodies composed of?

A

collagen surrounded by t lymphocytes and specialised macrophages (Anitschkow cells)

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36
Q

what is the interval between the throat infection and cardiac RHD

A

1-5 weeks, by this time the pharyngeal cultures for GAS are negative.

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37
Q

what is the pathogenesis of acute rheumatic fever

A

antibodies to GAS protein cross react with glycoprotein antigens in heart and joints. antibodies to streptococcal proteins e.g. m protein cross react with cardiac myosin

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38
Q

what are the clinical features of rheumatic fever?

A
  1. polyarthritis of large joints
  2. carditis
  3. subcutaneous nodules
  4. rash
  5. sydenhams chorea/ st vitus dance. uncontrolled movements.
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39
Q

what do aschoff nodules contain

A

swollen eosinophilic collagen surrounded by lymphocytes, occasionally plasma cells and plump macrophages.

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40
Q

what kind of inflammation is rheumatic myocarditis

A

granulomatous (foreign body type)

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41
Q

define infective endocarditis

A

when microorganisms from mouth (dental procedures) or from IV drug use lodge on a damaged valve, which causes large, infected vegetations to form on valve.

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42
Q

consequences of infective endocarditis

A

destruction of valve

embolism to brain, kidney, spleen,

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43
Q

what do the vegetations of infective endocarditis mostly consist of

A

thrombotic debris, immune cells and micro-organisms (usually bacterial)

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44
Q

what are the two types of infective endocarditis

A

acute - rapid destruction of valve, highly virulent organism, not good prognosis, often fatal despite intervention.
subacute - less virulent organism, colonisation of previously deformed valves, recovery likely.

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45
Q

what are the differences between vegetations of infective endocarditis and rheumatic heart disease

A

RHD vegetations are rows of small, warty vegetations along the lines of closure of the valve leaflets and are STERILE. ID vegetations are large, irregular masses on the valve cusps which can extend onto the chordae tendinae and are INFECTIVE.

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46
Q

Define congestive heart failure

A

the pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of metabolising tissues, despite adequate venous filling
AND OR
the heart can only pump adequately when there is an abnormally elevated diastolic volume.

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47
Q

what are the five clinical features of heart failure

A
  1. systolic vs diastolic
  2. high output vs low output
  3. acute vs chronic
  4. right sided vs left sided
  5. forward vs backward.
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48
Q

what is the difference between systolic and diastolic heart failure

A

systolic heart failure is an inability to contract normally

diastolic heart failure is inability to relax and or fill the heart normally

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49
Q

what are 2 examples of systolic heart failure and symptoms

A

ischemic heart disease, dilated cardiomyopathy.

symptoms: weakness, fatigue, reduced exercise tolerance.

50
Q

what are some examples of diastolic heart disease and symptoms

A

constrictive pericarditis, hypertensive/hypertrophic cardiomyopathy, restrictive cardiomyopathy (causes myocardial fibrosis and infiltration). symptoms is increased diastolic BP.

51
Q

what is the difference between high output and low output heart failure

A

low output failure is when the heart cannot pump adequate amounts of blood to tissues.
high output failure is when the heart must pump abnormally large quantities of blood to deliver adequate O2 to tissues.

52
Q

what are some examples of low output heart failure

A

ischemic heart disease, hypertension, dilated cardiomyopathy, vascular disease, pericardial disease.

53
Q

what are some examples of high output heart failure

A

anaemia, hyperthyroidism, pregnancy, pagets disease of bone.

54
Q

what is the difference between acute heart failure and chronic heart failure

A

acute HF is a consequence of sudden imposition of disease

chronic HF occurs slowly, progressively

55
Q

what are some examples of acute heart failure

A

large myocardial infarction, rupture of cardiac valve. clinically associated with sudden hypotension without peripheral edema.

56
Q

what are some examples of chronic heart failure

A

cardiomyopathy, multi-valve disease. clinically associated with normal BP until late in disease and peripheral edema.

57
Q

what is the difference between left sided heart failure and right sided heart failure

A

left sided heart failure results in pulmonary congestion

right sided heart failure results in systemic venous congestion, peripheral edema, congestion of liver and spleen.

58
Q

what is the difference between backward failure and forward failure

A

backward failure leads to venous congestion in the lungs and or systemic viscera
forward failure leads to inadequate LV output

59
Q

what causes pressure overload in the heart

A 
increased systolic pressure
increased systolic wall stress
parallel addition of new myofibrils
wall thickening
this leads to 
concentric hypertrophy (myocytes thickened) and pressure overload.
60
Q

what are some examples of diseases which cause pressure overload in the heart

A

hypertension, aortic stenosis

61
Q

what does volume overload do to the heart

A 
increases diastolic pressure
increases diastolic wall stress
series addition of new sarcomeres
chamber enlargement (stretched)
this leads to 
exxentric hypetrophy (thinner, bigger chamber)
62
Q

example of something which causes volume overload.

A

mitral regurgitation

63
Q

what are some things which cause increased strain on LV

A

myocardial disease (infarction, cardiomyopathy)
valve disease (stenosis, regurgitation or both)
arrhythmias
hypertension

64
Q

what is an organic valve lesions

A

the presence of an intrinsic structural disorder of the valve/cusp/chordae tendinae e.g. mitral stenosis in recurrent RHD.

65
Q

what is functional valvular regurgitations

A

due to an external disease/disorder e.g. tricuspid regugitation occurs in severe heart failure when the right side of the heart is dilated, thus there is stretching of tricuspid valve ring.

66
Q

what is the left ventricular response to strain

A

immediate dilatation - stretching of myocytes which will increase force of contractility.
hypertrophy of lv - limited by ability to perfuse myocytes.

67
Q

describe pulmonary venous congestion

A

congested capillaries in alveolar walls due to poor flow causes alveolar edema and a pink frothy sputum due to RBC extravasation into alveoli. causes pulmonary fibrosis, firm lung parenchyma, brown pigmentation due to deposition of hemosiderin.

68
Q

in what diseases is cardiac heart failure confined to the right side

A

chronic fibrosing lung disease e.g. silicosis. RV and then RA will attempt to compensate via dilatation and hypertrophy. because right side of heart is thinner, it will fail more rapidly.

69
Q

what are the effects of right heart failure

A

congestion of systemic veins, hepatic venous congestion, splenic venous congestion

70
Q

describe chronic venous congestion of the liver

A

slowing of lobular blood flow through the sinusoids from the portal tract to the central vein
nutmeg liver, fatty change in hepatocytes - light, patchy liver

71
Q

what are the manifestations of systemic venous congestion

A

elevation of jugular venous pressure
pitting edema of legs
ascites and effusions (fluid retention around gut)

72
Q

describe biventricular cardiac failure

A

severe dilatation of all chambers

hypertrophy of all chamber walls, most evident in ventricles. wall hypertrophy masked by dilatation.

73
Q

what is the forward component of congestive heart failure

A

may lead to cerebral ischemia and contribute to liver cell damage, peripheral edema

74
Q

how is peripheral edema exacerbated by forward heart failure

A

reduced LV output leads to renal hypoperfusion which activates the renin angiotensin system which increases aldosterone production and NA H20 retention.

75
Q

what is the difference between endothelial stimulation and endothelial activation

A

endothelial stimulation is a rapid reaction to histamine/serotonin which results in either increased permeability or decreased NO production.
endothelial activation is alteration in gene expression and protein synthesis

76
Q

what is the vascular smooth muscle response in atherosclerosis

A

an exaggerated healing response resulting in excessive neointima formation.

77
Q

what are the two VSMC phenotypes

A

contractile (media)

proliferative (migrate into intima)

78
Q

what is the pathogenesis of atherosclerosis

A
  1. endothelial injury
  2. fatty streak formation via accumulation and oxidation of LDL and the initiation of monocyte adhesion and migration
  3. migration of monocytes into the intima and differentiation in macrophages. T cell and VSMC migration into intima. continued LDL oxidation and accumulation.
  4. VSMC proliferation in intima. Increased lipid accumulation, engulfed by macrophages to form foam cells.
  5. advanced lesion - continued localisation of macrophages, VSMCs, T cells and lipids, formation of necrotic core and fibrous cap.
79
Q

histology of atherosclerotic vessel

A

irregular thickness of wall of artery due to thickened intima and thinned media. narrowed lumen. necrotic core, fibrous cap

80
Q

consequences of atherosclerosis

A

aneurysm and rupture
occlusion by thrombus
critical stenosis
embolus

81
Q

what is the difference between a true and false aneurysm

A

true - the wall bulges outward and may be attenuated but is intact
false - the wall is ruptured and there is a collection of blood (hematoma) that is bounded externally by adherent extravascular tissues. adventitia

82
Q

what is a dissection

A

a tear between intima and media of vessel

83
Q

define thrombosis

A

represents the inappropriate activation of normal haemostatic processes, such as formation of a blood clot, in uninjured vasculature, or thrombotic occlusion of a vessel after relatively minor injury.

84
Q

define embolism

A

any intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin. emboli lodge in vessels too small to allow their passage, resulting in infarction and necrosis of distal tissue. often thromboembolism.

85
Q

what is cardiac ischemia usually caused by

A

coronary artery atherosclerosis

86
Q

what are the four clinical manifestations of cardiac ischemia

A
  1. myocardial infarction
  2. angina pectoris
  3. chronic ischemic heart disease
  4. sudden cardiac death.
87
Q

define infarction

A

myocardial death caused by ischemia (lack of O2)

88
Q

define reperfusion

A

restoration of blood flow

89
Q

what is angina pectoris

A

short series of ischemic events marked by recurrent attacks of chest pain. transient with no necrosis. caused by chronic atherosclerotic stenosis which causes ischemia when there is elevated demand on myocardial blood supply (E.g. exercise). treated by potent vasodilators and rest.

90
Q

what are the biochemical features of ischemia

A

shift from aerobic to anaerobic glycolysis - leads to inadequate ATP, build up of lactic acid
poor contractility
necrosis after 20-40 mins of ischemia

91
Q

which area is the least well perfused zone of the myocardium

A

the sub endothelial zone. a sub endothelial infarct is necrosis limited to the inner (Furthest) 1/3-1/2 of the ventricular wall.

92
Q

what is a transmural infarct

A

necrosis of the near to full thickness of the ventricular wall in the distribution of a single coronary artery

93
Q

macro of recent infarct

A

pale area with hyperaemic (red, inflamed) border

94
Q

what are two examples of reperfusion

A 
proteolytic therapies (thrombolysis)
angioplasty.
95
Q

what events occur in a rapid ischemic event

A
  1. change in morphology of plaque (e.g. rupture)
  2. platelets adhere and activate causing release of activators (e.g. serotonin)
  3. coagulation
  4. thrombus evolves to block lumen in minutes
96
Q

what are the two causes of reperfusion injury

A

ROS generated from infiltrating leukocytes (reperfusion induced burst + from electron transport chain 1 and 3)
Ca overload
these both activate proteases (calpain, caspases) which damage cardiac proteins/contractile proteins

97
Q

what is myocardial stunning

A

persistent abnormalities/dysfunction in cardiac contractile proteins for several days after reperfusion.
Myocardial stunning is the reversible reduction of function of heart contraction[1] after reperfusion not accounted for by tissue damage or reduced blood flow. slow recovery as myocytes synthesise new contractile proteins.

98
Q

which proteins are altered during reperfusion injury

A
  1. troponin I/T (regulates Ca contraction of cardiac muscle) - is the target of proteases and is degraded and released into circulation
  2. myosin light chain 2 is cleaved
  3. creatine kinase is released into circulation
  4. c reactive protein is released into circulation.
    damage to these proteins is eventually overcome by synthesis of new proteins - why myocardial stunning is short lived.
99
Q

what is a biomarker for myocardial infarction

A

troponin I/Tin circulation

100
Q

what are the macroscopic features of myocardial infarction over time.

A 
0-4 hrs - none
4-24 hrs - dark mottling
1-7 days - tan infarct centre
7-14 days - hyperemic border, tan center
2-8 weeks - grey/white collagenous scar
2 months - scarring complete(white)
101
Q

what are the microscopic features of myocardial infarction over time

A

0-4hrs - basically none
4-24hrs - coagulation necrosis, pyknosis of nuclei
1-7 days - neutrophil infiltrate
7-14days - macrophages, granulation tissue forms
2-8 weeks - collagen deposition
2 months - dense collagenous scar replaces viable tissue

102
Q

what are the histological features of myocardial infarct at 2 days

A

necrotic myocytes with few recognisable nuclei
infiltration of infalmmatory cells, neutrophils
vascular congestion

103
Q

what are some of the consequences of myocardial infarct

A
  1. chronic contractile dysfunction
  2. arrhythmias
  3. myocardial rupture (weakness of necrotic tissue)
  4. ventricular aneurism
104
Q

what is normal BP

A

120/80

105
Q

what does cardiac output equal

A

CO = HR X SV

106
Q

define the two types of hypertension

A
  1. essential hypertension - most common, no single specific cause can be determined.
  2. systemic hypertension - consistent BP elevation at rest, 140/90, no response to antihypertensive drugs. may be benign (Stable for years) or malignant (Rapid. 1-2 year course, 200/120)
107
Q

what does angiotensin II do?

A

potent vasoconstrictor - constricts golmerulur afferent arterioles - increased TPR, which decreases GFR and increases BP.

108
Q

what does aldosterone do

A

increases NA reabsorption and water reabsorption which increases BV, BP and CO.

109
Q

describe what low BP induces

A
  1. low BP detected by juxtaglomerular cells in afferent arterioles.
  2. stimulates renin which coverts angiotensinogen to angiotensin 1 which is converted to angiotensin 2 by ACE
  3. angiotensin 2 triggers thirst reflex, the secretion of aldosterone by the adrenals, and vasoconstriction.
    aldosterone increases NA and H20 resorption in th ekidney which increases blood volume and CO = increased BP.
    vasoconstriction increases TPR which increases BP
110
Q

what are some secondary causes of systemic hypertension (primary causes is idiopathic)

A

renal: acute arterial stenosis
endocrine: cushin syndrome, estrogen (pregnancy), phaeochromocytoma (Ectopic secretion of hormones e.g. aldosterone)
CV: coarctation of aorta (constriction of aorta leading to LV hypertrophy)
neurological: acute stress

111
Q

describe kidney disease/renal artery stenosis

A

normal response to low BP in the renal arteries is to increase cardiac output to maintain pressure needed for glomerular filtration. in disease, increased CO cannot solve structural problems causing renal artery hypotension so CO remains elevated.

112
Q

what are the effects of HT on heart

A

pressure overload in LV causes concentric LV hypertrophy (wall thickness exceeds 1cm). this deacreases chamber size/ total LV filling volume. causes greater exertion by the heart. reduces diastolic ventricular volume.

113
Q

what are microscopic features of HT on heart

A

hypertrophied myocytes with larger, irregular, hyperchromatic nuclie. areas of ischemia and necrosis. collagenous deposition

114
Q

what are the effects of HT on arterioles

A
  • replacement of smooth muscle by hyaline in wall (esp. in afferent arterioles of kidney) - resulting from extravasation of plasma proteins through injured endothelium.
  • narrowed lumen
  • protein in blood.
115
Q

what are the effects of HT on arteries

A

loss of elastin and smooth muscle cells in the media, replacement by fibrous, hyaline tissue - hypertensive.

116
Q

what is RV hypertrophy

A

cor pulmonale

117
Q

what does cor pulmonale result from

A

pulmonary disease e.g. cystic fibrosis, constrictions, pulmonary vessel disease

118
Q

what are the effects of benign HT on kidney

A
  • afferent arteriole hypertensive damage - hyaline
  • atherosclerosis
  • HT nephrosclerosis
  • ischemia results in loss of glomerular and related nephrons.
  • bilateral finely granular surface, contracted kidneys (fibrosis)
  • enlarged fat filled hilum
  • cortical thinning (loss of nephrons)
  • indistinct cortico-medullary junction
119
Q

what does HT increase the risk of in the brain

A
  • cerebral infarction
  • intracerebral haemorrage
  • berry aneuryisms.
120
Q

what is malignant hypertension

A

rapid rise in BP to 200/120, accompanied by severe headaches, shortness of breath, chest pain, potentially severe organ damage e.g. stroke heart attack

121
Q

what are some causes of malignant hypertension

A

drugs e.g. cocaine, strong anti depressants, oral contraceptives, withdrawal from B blockers, alcohol.

CPAT CARDIO (1 decks)

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