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brs round 2 - help me > cardiology > Flashcards

cardiology Flashcards

1
Q

what is VSD

A

ventricular septal defect

hole between ventricles = mixing of ox + deox blood

LVP > RVP so blood pushed into RV = overloading = right sided HF

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2
Q

what is ASD

A

atrial septal defect

hole in septum between atria

mixing of ox + deox blood

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3
Q

what is tetralogy of fallot

A

large VSD

blood from both ventricles into aorta (overriding aorta) = less ox blood to body

contraction of pulmonary artery = less blood to lung = pulmonary atresia

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4
Q

what is coarctation of aorta

A

contraction of small part of aorta

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5
Q

what precedes aortic stenosis

A

aortic sclerosis (aortic valve thickening without flow limitation)

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6
Q

what is aortic stenosis

A

narrowing of aortic valve - restricts flow of blood from left ventricle into aorta

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7
Q

basic pathophysiology of aortic stenosis [6]

A

fibrosis + calcification of aortic valve = disrupted flow

LV must contract harder to pump blood through

continuous forceful contractions cause concentric (thickening) myocardial hypertrophy

hypertrophic LV = stiff overtime = harder to fill

decreased cardiac output + diastolic dysfunction

pressure overload in LV backs up in LA = dilation + increased back pressure in lungs = pulmonary congestion

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8
Q

what can cause the initial fibrosis and calcification of aortic valve

A

degeneration (age related / >70 yrs) or congenital malformed valves (bicuspid) = wear and tear of valvular endothelium

untreated group A streptococcus (UTI) = anti-strep antibodies that wrongly attack valve endocardium = inflammation

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9
Q

risk factors for aortic stenosis

A

hypertension, LDL, smoking, radiotherapy

old age, CKD, congenital bicuspids, high CRP

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10
Q

causes of aortic stenosis

A

rheumatic heart disease
congenital heart disease e.g. bicuspids
calcium build-up

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11
Q

clinical findings for AS

A

ejection SYSTOLIC murmur (crescendo-decrescendo)

SYNCOPE on exertion (less blood to brain)

ANGINA on exertion (high muscle demand + high pressure)

DYSPNOEA + crackles (pulmonary congestion)

(AS = SSAD)

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12
Q

history of AS

A

rheumatic fever
high lipoprotein
high LDL
CKD
age >65

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13
Q

general investigations for valvular defects

A

ecg
transthoracic echocardiography
cardiac catheterisation
CXR
cardiac MRI

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14
Q

key investigation for AS

A

doppler echo - pressure gradient

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15
Q

severe AS management

A

AVR:

transcatheter valve replacement
surgical valve prosthesis

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16
Q

what is aortic regurgitation

A

diastolic leakage of blood from aorta into left ventricle due to incompetent valve leaflets caused by root dilation or intrinsic valve disease

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17
Q

acute vs chronic AR

A

acute = emergency
(sudden onset pulmonary oedema + hypotension/cardiogenic shock)

chronic = culminates into CHF

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18
Q

5 causes of incompetent leaflets in AR

A

RHD
infective endocarditis
aortic stenosis
congenital heart defects
congenital bicuspid valves

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19
Q

5 causes of aortic root dilation leading to AR

A

marfan’s
connective tissue disorder/collagen vascular disease
ankylosing spondylitis
trauma
idiopathic

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20
Q

general pathophysiology of AR (acute + chronic)

A

valve leaflets close poorly when Aortic Pa > LV in diastole
backflow of blood from aorta to LV
volume + pressure overload in LV = increased preload + afterload

ACUTE = dilation = increased SV due to FS-law

CHRONIC = dilation + eccentric hypertrophy to accommodate high volume
excess stretch = weakens myocardium = SHF
back pressure into atria + pulmonary vasculature = congestion

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21
Q

7 AR clinical findings - acute

A

DIASTOLIC murmur
S3 GALLOP in early diastole (rapid filling + expansion of ventricles)

ANGINA on exertion
FATIGUE
DYS/ORTHOPNOEA + crackles (congestion)

TACHYCARDIA
CYANOSIS

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22
Q

3 AR clinical findings - chronic

A

CORRIGANS (bounding pulse - large SV + exaggerated collapse on diastolic return)

WIDE PULSE PRESSURE

TRAUBE’S (pistol shot pulse)

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23
Q

best non-invasive test to diagnose + grade severity of AR

A

echocardiography

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24
Q

management of AR (acute + chronic)

A

acute = AVR

asymptomatic chronic w/severe AR = vasodilator therapy (delays AVR need)

PREVENTION IS KEY - TREAT RHD + IE

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25
Q

what is mitral stenosis

A

structural abnormality of mitral valve = obstructed flow from LA to LV

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26
Q

9 causes of mitral stenosis

A

(bigger valve than aortic so more causes)

rheum fever
rheum arthritis
amyloidosis
carcinoid syndrome
SLE

ergotonergic/serotonergic drugs
mitral annular calcification (ageing)
whipple disease
congenital valve deformity

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27
Q

basic pathophysiology of mitral stenosis

A

recurrent inflammation = fibrous deposition + calcification of leaflets + cordae tendinae

junctions between leaflets fuse

obstructed blood flow through valve

impaired emptying of atrium = increased LA pressure = congestion

impaired LV filling = low SV + CO = CHF

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28
Q

MS clinical findings

A

diastolic murmur
a-fib
cardiogenic shock
RS-HF
dyspnoea

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29
Q

MS history

A

rheumatic fever
dysphagia
haemoptysis

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30
Q

management of progressive + severe MS

A

progressive asymptomatic = none

severe asymptomatic = none but maybe balloon valvulotomy

severe symptomatic = diuretic + balloon valvulotomy/MVR + beta blockers

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31
Q

what is mitral regurgitation

A

abnormal reversal of blood flow from the left ventricle to the left atrium

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32
Q

acute causes of MR (pips)

A

prolapse
infective endocarditis
prosthetic valve dysfunciton
valvular surgery

RHD (can be acute or chronic)

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33
Q

acute causes of MR

A

SLE
scleroderma
hypertrophic cardiomyopathy
drugs

RHD (can be acute or chronic)

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34
Q

basic pathophysiology of mitral regurgitation

A

impaired closure of the valve closure = back flow of blood from LV to LA

increased vol + pressure in LA

increased volume in LV in next diastole

LV dilation = remodelling = decreased systolic function

decreased SV + CO = CHF
back pressure in LA + lung vasc = congestion

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35
Q

clinical findings in MR

A

HOLOSYSTOLIC murmur - radiates to axilla

S3 heart sound

high serum CREATININE (less O2 to kidneys = damage)

cardiogenic shock or CHF

peripheral OEDEMA

low sats, tachypnoea, wheeze/crackles, frothy sputum (fluid excavation in lungs)

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36
Q

history of MR

A

dyspnoea
signs of CHF

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37
Q

management of acute severe MR

A

valve replacement + repair
prosthetic ring placed to reshape

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38
Q

management of chronic MR

A

chronic severe asymptomatic = watchful waiting for surgery

chronic symptomatic = surgery + meds

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39
Q

whats a cardiomyopathy

A

disease making it harder for heart to pump blood to the body

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40
Q

dilated cardiomyopathy pathophysiology

A

inflammatory damage or toxic damage = eccentric fibrosis + increased volume

LV chamber enlargement without increase in myocardial mass

FS law initially compensates - contractility is okay

gradual over distention + systolic dysfunction

decreased cardiac output + increased end diastolic volume/pressure

volume overload = CHF

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41
Q

primary causes of DCM

A

familial
idiopathic

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42
Q

7 secondary causes of DCM (match mad)

A

myocardial ischaemia
autoimmune
thyroid disease
childbirth
heart valve disease

myocarditis
alcohol
drugs

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43
Q

5 symptoms of DCM

A

dyspnoea/cold extremities (low CO = low ox)

fatigue (low CO = low perfusion)

angina (low coronary perfusion)

sudden cardiac death

peripheral oedema

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44
Q

2 signs of DCM

A

displaced apex HB (enlarged LV)

crackles (pulmonary congestion)

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45
Q

special additional investigations for DCM

A

genetic testing
viral serology

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46
Q

how to manage DCM - 3 key principles

A

diet modification - fluid + sodium restriction

treatment of symptoms (e.g. HF, arrhythmia, thrombotic events)

treatment of underlying diseases

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47
Q

how to treat symptoms of heart failure

A

ACEi
b-blockers
diuretics
ARBs

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48
Q

how to treat arhythmias

A

amiodarone

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49
Q

how to treat thrombotic events

A

anti-coagulants

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50
Q

what is hypertrophic cardiomyopathy

A

increased LV wall thickness not solely explained by abnormal loading conditions

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51
Q

HCM basic pathophysiology

A

thickening or disarray of LV myocardium - mainly at septum

obstructed flow through LV outflow tract

disorganised myocytes disrupt signal conduction

ventricular arrhythmias = sudden cardiac death

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52
Q

5 causes of HCM

A

genetic diseases (auto-dom in 50% cases)
storage diseases
neuromuscular disorders
mitochondrial disorders
malformation syndromes

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53
Q

symptoms of HCM

A

syncope - low CO to head
fatigue - low CO = low ox
angina - low coronary perfusion

MOSTLY PRESENTS WITH SUDDEN CARDIAC DEATH

54
Q

signs of HCM

A

S4 - forceful atrial contraction into hypertrophied LV

crackles - congestion + oedema

systolic murmur - disrupted outflow

55
Q

HCM management

A

symptoms = beta-blockers

if refractory + drugs fail = mechanical therapy with pacemaker/surgery

56
Q

what is restrictive cardiomyopathy

A

chambers of heart become increasingly stiff over time

57
Q

aetiology of RCM (has farcs)

A

associated with systemic diseases e.g.

haemochromatosis
amyloidosis
sarcoidosis
Fabry’s disease
anthracycline toxicity
radiation
carcinoid syndrome
scleroderma

58
Q

basic pathophysiology of RCM

A

deposition of abnormal substances in heart tissue e,g. amyloid proteins

endomyocardial fibrosis = LV wall stiffening = diastolic dysfunction

atrial enlargement = impaired LV filling but volume + wall thickness of LV normal

conduction abnormalities = diastolic HF

adverse remodelling = systolic dysfunction + ventricular arrythmias

reduced LV filling = decreased CO

59
Q

5 signs of RCM

A

easy bruising + weightloss (HF)

ascites + pitting oedema

hepatomegaly

S4 sound

increased JVP

60
Q

RCM added investigations

A

FBC
serology
amyloidosis check

61
Q

management of RCM

A

heart failure meds (ACEi or ARB, diuretics, aldosterone inhibitors)

anti-arrhythmic therapy

immunosuppression

pacemaker

cardiac transplantation

62
Q

what is infective endocarditis

A

infection of the endocardium/vascular endothelium of the heart

typically affects valves
(aortic > mitral > RHS)

63
Q

pathophysiology of IE

A

bacteria in BS = vegetation forms on endocardium

(v = bac inf surrounded by platelets + fibrin)

vegetations on valves = valve cant open/close

(more likely or turbulent flow + underlying damage)

64
Q

major Duke’s criteria for IE diagnosis

A

positive blood culture
ECHO
new valvular regurgitation murmur
coxiella burnetti infection

65
Q

minor Duke’s criteria for IE diagnosis

A

emboli
fever > 38
immunologic (glomerulonephritis, Oslers nodes, Roth Spots)
predisposing heart condition
IV
non-specific blood cultures

66
Q

definitive vs possible endocarditis

A

definitive
2 major
5 minor
1 major + 3 minor

positive gram stain or culture from surgery or autopsy

67
Q

IE risk factors

A

IV drug user
dental surgery
immunosuppressed
congenital heart defect

68
Q

what is cardiac decompression

A

Heart can no longer maintain adequate circulation

69
Q

symptoms of CD

A

SOB
coughing
swelling
fatigue

70
Q

signs of CD

A

raised JVP
lung crackles
oedema

71
Q

complications of CD

A

vascular + embolic phenomena
(stroke, Janeway lesions, splinter/conjunctival haemorrhages)

immunological phenomena
(olsers nodes/roth spots)

72
Q

layers of arteries (out to in)

A

tunica ADVENTITIA - vasa vasorum + nerves

tunica MEDIA - external elastic membrane + SMC

tunica INTIMA - internal elastic membrane + lamina propria (SM + CT) + BM + endothelium

73
Q

structure of capillaries

A

single endothelial layer surrounded by pericytes and BM

74
Q

how capillaries maintain single layer

A

contact inhibition - all cells touch each other which stimulates intracellular pathways that inhibit mitosis

75
Q

functions of endothelium

A

have specific organotypic properties and unique gene expression profiles for diff organs

produce angiocrine factors essential for tissue homeostasis and regeneration

(tissue specific microenvironment determines phenotype of endothelium which determines angiocrine profile)

76
Q

basic steps of angiogenesis

A

driven by hypoxia
pro-angiocrine factors released such as VGEF or FGF
bind capillaries + cause endothelial activation
cells divide + migrate to hypoxic area

77
Q

define angiogenesis

A

formation of neo-vessels from pre-existing blood vessels

78
Q

examples of different angiogenic microenvironments

A

development
menstrual cycle
wound healing

79
Q

pathologies involving angiogenesis

A

cancer
retinopathy
atherosclerosis
chronic inflammation
ischemic diseases
vascular malformations

80
Q

angiogenesis in cancer growth

A

large tumour = hypoxic cells in the centre

release angiogenic factors to stimulate vessel formation via endothelial cells

ANGIOGENIC SWITCH (pro-ang factors > anti-ang)

new vessels facilitate growth + metastasis

very leaky due to messed up microenvironment

81
Q

how discovery of angiogenesis in cancer lead to treatment

A

mow use anti-angiogenic drugs in clinic with chemotherapy

82
Q

von willebrand disease

A

decrease or dysfunction of vWf
characterised by mucosal bleeding

83
Q

why does vwf replacement not work in some patients - still bleeding

A

bleeding from GI tract due to vascular malformations in gut blood vessels

vwf not sufficient to control this bleeding

shows that both clotting factors and vessel properties are necessary for appropriate bleeding/clotting

84
Q

roles of vwf

A

HAEMOSTASIS
mediates platelet adhesion to subendothelium + aggregation

ANGIOGENESIS
endothelial vwf controls BV formation + integrity by regulating GF signalling

85
Q

what is the paradox of angiogenesis

A

promotes plaque growth = blockage = ischaemia

therapeutic angiogenesis prevents damage post ischaemia

86
Q

where is atherosclerosis most likely to occur + why

A

at bifurcation of arteries - where theres turbulent/disrupted flow

87
Q

laminar flow

A

in straight parts of arterial tree - blood flows in parallel layers

increased shear stress - stimulates endothelial mechanoreceptors

upreg of intracellular pathways = increased endothelial nitric oxide synthase (enos)

NO = anti-inflammatory

88
Q

disrupted flow

A

blood flows slow + disordered = decreased shear stress

decreased shear stress = decreased NO production

high MCP + VCAM expression = pro-leukocyte migration

high PDGF production = SMC proliferation

pro-inflammatory

89
Q

basic pathophysiology of atherosclerosis until macrophage activation

A

endothelial activation by turbulent flow or other risk factors

increased permeability = LDL into sub-endothelial space = oxidised (OxLDL)

increased monocyte recruitment via over-expression of VCAM-1 = macrophages

macrophages uptake LDL + become activated

90
Q

what 4 things do activated macrophages do

A

generate FREE RADICALS enzymes like NADPH oxidase + myeloperoxidase - further oxidise LDL + form toxins leading to apoptosis

secrete CYTOKINES (IL-1) and CHEMOKINES (MCP-1) - activate endothelial cells + recruit more monocytes

express GROWTH FACTORS e.g. PDGF + TFG-b (switch VSMCs from contractile to synthetic = collagen synthesis)

activate METALLOPROTEINASES - degrade collagen in arterial wall - weakens fibrous cap of plaque = can rupture

91
Q

what happens after macrophage activation

A

FOAM CELL formation - made by phag of modified LDLs + accumulate in plaque

(plaque = necrotic core of dead foam cells + toxins surrounded by fibroblasts + collagen made by TGF-b)

PLAQUE RUPTURE - plaque unstable due to inflamm + degradation of collagen by MMPs = rupture into blood stream

THROMBUS FORMATION - triggered by plaque contents entering BS

92
Q

what do the free radicals made by macrophages do

A

NADPH oxidase: generates superoxide O2-

Myeloperoxidase: generates HOCL hypochlorous acid (bleach)

generation of H2O2

93
Q

cytokine + chemokine involved in atheroscleorsis

A

cyto: IL-1 = triggers intracellular cholesterol crystals and NFkB
(nfkb = coordinates multiple processes e.g. cell death, proliferation, high CRP)

chemo: MCP-1 (monocyte chemotactic protein) = binds monocyte G-protein coupled receptor CCR2 = increased recruitment

94
Q

contractile vs synthetic VSMCs

A

contractile = normal
(high contractile filaments + low matrix deposition genes)

synthetic = atherosclerotic
(low contractile filaments + high matrix deposition genes) = collagen synthesis

(contractile to synthetic via PDGF and TGF-b)

95
Q

what do MMPs do

A

degrade collagen = weak arteries = plaque erosion/rupture

dead macrophages + fat come into contact with blood = triggers occlusive thrombus

cessation of blood flow = MI (if blocking coronary artery)

96
Q

characteristics of vulnerable and stable plaques

A

large, soft eccentric lipid-rich necrotic core

increased VSMC apoptosis
reduced VSMC & collagen content

thin fibrous cap

infiltrate of activated macrophages expressing MMP

97
Q

when does a macrophage undergo apoptosis

A

when too many toxins (e.g. 1-keto-cholesterol produced by OxLDL) build up + overload foam cell protective mechanisms

release of macrophage TFs + toxic lipids into necrotic core

thrombogenic + toxic material accumulates + walled off until platelet ruptures = meets blood

98
Q

NFkB

A

nuclear factor kappa b

TF - master inflamm regulator

activated by inflammatory stimuli + switched on inflammatory genes (MMP, iNOS, IL-1)

99
Q

iNOS vs eNOS

A

inducible = made in cytosol, lasts much longer, made by activated macrophage

endothelial = made by membrane, made to maintain healthy CVS

100
Q

how do macrophages take up OxLDL

A

scavenger receptor A (CD204) = meant to bind dead cells/gram+ive bacteria

scavenger receptor B (CD36) = meant to bind dead cells/malaria parasites

both accidentally bind OxLDL

101
Q

functions of non-inflammatory and resident macrophages

A

homeostasis (may be parenchymal)

e.g. alveolar = surfactant lipid homeostasis

e.g. spleen = iron homeostasis

102
Q

what is familial hyperlipidaemia

A

auto dom disease that causes massively elevated cholesterol

failure to clear LDL from blood (no ldl receptors in hepatocytes so no uptake or negative feedback to stop production)

get xanthomas (fat deposition in skin)

103
Q

how is the uptake of ldl in atherosclerotic macrophages different to normal uptake

A

normally - uptake via LDL-R inhibited by build up

macrophages in atherosclerosis = second scavenger receptor = not under feedback control

103
Q

how do PCSK9 inhibitors work

A

PCSK9 = protein that degrades LDL receptors when high amounts in cell

inhibitor = increased LDL uptake by cells = -ive FB on cholesterol production

104
Q

how does reverse cholesterol transport work in reducing build up in arteries

A

macrophages have ABCA1 and ABCG1 cholesterol export pumps

bind Apolipoprotein-A on HDL

export cholesterol to HDL which removes it from the arteries and initiates its return to the liver (woopwoop)

105
Q

PDGF vs TGF-b

A

PLATELET DERIVED GROWTH FACTOR:
VSMC chemotaxis, survival + division

TRANSFORMING GROWTH FACTOR BETA:
collagen synthesis + matrix deposition

106
Q

whats the p-wave

A

electrical signal that stimulates atrial contraction (atrial systole)

107
Q

whats the qrs compex

A

electrical signal that stimulates ventricular contraction (ventricular systole)

108
Q

whats the t-wave

A

ventricular repolarisation (relaxation)

109
Q

why is the p-wave wide + short

A

wide = low velocity
short = less muscle

110
Q

electrical conduction through heart process (7)

A

SAN - autorhythmic myocytes causing atrial depolarisation (p)

AVN - depolarises + slows signal down to give time for ventricles to fill

bundle of his - rapid conduction + insulated

bundle branches - septal depolarisation (insulation ends) (q - dep goes up so -ive deflection)

purkinje fibres - ventricular depolarisation
(r then s)

st = fully depolarised ventricles - isoelectric
t-wave = ventricular repolarisation

111
Q

limb leads

A

lead 1: RA to LA
lead 2: RA to LL
lead 3: LA to LL

(rule of Ls)
-ive to +ive
bipolar

112
Q

chest leads

A

VI: 4th ICS -> right of sternum
V2: 4th ICs -> left of sternum
V4: 5th ICS -> mid clavicular line
V3: midway between 2 + 4
V5: 5th ICS -> anterior axillary line
V6: 5th ICS -> midaxillary line

(-ive electrode = middle)
unipolar

113
Q

AV leads

A

aVR: lead 3 to RA
aVL: lead 2 to LA
aVF: lead 1 to LL

unipolar

114
Q

uni vs bipolar

A

unipolar: only one electrode + one virtual electrode

bipolar: 2 electrodes

115
Q

what leads represent the inferior section of the heart and the right coronary artery

A

lead 2
lead 3
avF

116
Q

what leads represent the anterior section of the heart and the left anterior descending artery

A

V3
V4

117
Q

what leads represent the lateral section of the heart and the left circumflex artery

A

lead 1
aVL
V5
V6

118
Q

what leads represent the septal or anteroseptal section of the heart and the left anterior descending artery

A

V1
V2

119
Q

why is aVR pretty useless

A

positive electrode above negative do ECG is upside down

120
Q

how to calculate rate on ECG

A

count boxes between R-waves

small = 0.04s, large = 0.2s

1/no:seconds = beats per second

beats per second x 60 = BPM

121
Q

how does a sinus arrhythmia present on ECG

A

irregular rate - varied R-R intervals

122
Q

atrial fibrillation on ECG

A

oscillating baseline as atria contract asynchronously

irregular rate + slow rhythm
turbulent flow pattern = increased clot risk

123
Q

atrial flutter on ECG

A

regular saw tooth pattern in baseline

ratio of atrial to ventricular beats = 2:1

124
Q

first degree heart block on ECG

A

prolonged PR interval - slower AV conduction

regular rhythm

125
Q

second degree heart block on ECG - mobitz 1 (wenckebach)

A

most p-waves followed by QRS, some not

gradual prolongation of PR interval until beat skipped

regularly irregular

126
Q

second degree heart block on ECG - mobitz 2

A

p waves regular but only some followed by QRS

regularly irregular

127
Q

third degree heart block on ECG

A

regular p-waves + QRS but no relationship between them

p-waves sometimes hidden in QRS

no sinus rhythm = SAN failure - ventricles attempt to take over

128
Q

what causes ST elevation or depression

A

elevation = infarction (hypoperfusion)

depression = ischaemia - coronary insufficiency

129
Q
A

brs round 2 - help me (4 decks)

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