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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 is aortic stenosis

A

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

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6
Q

causes of aortic stenosis

A

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

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7
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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8
Q

general investigations for valvular defects

A

ecg
transthoracic echocardiography
cardiac catheterisation
CXR
cardiac MRI

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9
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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10
Q

acute vs chronic AR

A

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

chronic = culminates into CHF

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11
Q

causes of AR

A

incompetent leaflets in (RHD, infective endocarditis, congenital)

aortic root dilation (marfans)

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12
Q

7 AR clinical findings - acute

A

DIASTOLIC murmur
S3 GALLOP

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

TACHYCARDIA
CYANOSIS

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13
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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14
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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15
Q

what is mitral stenosis

A

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

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16
Q

causes of mitral stenosis

A

rheum fever/arthritis
amyloidosis
carcinoid syndrome
SLE

ergotonergic/serotonergic drugs
ageing
whipple disease
congenital

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17
Q

MS clinical findings

A

diastolic murmur
a-fib
cardiogenic shock
RS-HF
dyspnoea

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18
Q

MS history

A

rheumatic fever
dysphagia
haemoptysis

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19
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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20
Q

what is mitral regurgitation

A

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

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21
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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22
Q

clinical findings in MR

A

HOLOSYSTOLIC murmur - radiates to axilla

S3 heart sound

cardiogenic shock or CHF

peripheral OEDEMA

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23
Q

history of MR

A

dyspnoea
signs of CHF

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24
Q

management of acute severe MR

A

valve replacement + repair
prosthetic ring placed to reshape

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25
Q

management of chronic MR

A

severe asymptomatic = watchful waiting for surgery

chronic symptomatic = surgery + meds

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26
Q

whats a cardiomyopathy

A

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

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27
Q

dilated cardiomyopathy pathophysiology

A

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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28
Q

primary causes of DCM

A

familial
idiopathic

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29
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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30
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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31
Q

2 signs of DCM

A

displaced apex HB (enlarged LV)

crackles (pulmonary congestion)

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32
Q

how to treat symptoms of heart failure

A

ACEi
b-blockers
diuretics
ARBs

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33
Q

how to treat arhythmias

A

amiodarone

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34
Q

how to treat thrombotic events

A

anti-coagulants

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35
Q

what is hypertrophic cardiomyopathy

A

increased LV wall thickness not solely explained by abnormal loading conditions

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36
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

37
Q

5 causes of HCM

A

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

38
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

39
Q

signs of HCM

A

S4 - forceful atrial contraction into hypertrophied LV

crackles - congestion + oedema

systolic murmur - disrupted outflow

40
Q

HCM management

A

symptoms = beta-blockers

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

41
Q

what is restrictive cardiomyopathy

A

chambers of heart become increasingly stiff over time

42
Q

aetiology of RCM (has farcs)

A

associated with systemic diseases e.g. haemochromatosis, amyloidosis

43
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

44
Q

5 signs of RCM

A

easy bruising + weightloss (HF)

ascites + pitting oedema

hepatomegaly

S4 sound

increased JVP

45
Q

RCM added investigations

A

FBC
serology
amyloidosis check

46
Q

management of RCM

A

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

anti-arrhythmic therapy

immunosuppression

pacemaker

cardiac transplantation

47
Q

what is infective endocarditis

A

infection of the endocardium/vascular endothelium of the heart

typically affects valves
(aortic > mitral > RHS)

48
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)

49
Q

major Duke’s criteria for IE diagnosis

A

positive blood culture
ECHO
new valvular regurgitation murmur
coxiella burnetti infection

50
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

51
Q

definitive vs possible endocarditis

A

definitive
2 major
5 minor
1 major + 3 minor

positive gram stain or culture from surgery or autopsy

52
Q

IE risk factors

A

IV drug user
dental surgery
immunosuppressed
congenital heart defect

53
Q

what is cardiac decompression

A

Heart can no longer maintain adequate circulation

54
Q

symptoms of CD

A

SOB
coughing
swelling
fatigue

55
Q

signs of CD

A

raised JVP
lung crackles
oedema

56
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

57
Q

structure of capillaries

A

single endothelial layer surrounded by pericytes and BM

58
Q

how capillaries maintain single layer

A

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

59
Q

what determines endothelium phenotpe

A

tissue specific microenvironment - determines phenotype (by unique gene expression)

determines angiocrine profile

60
Q

basic steps of angiogenesis

A

driven by hypoxia
pro-angiocrine factors released (VEGF or FGF)
bind capillaries + cause endothelial activation
cells divide + migrate to hypoxic area

61
Q

define angiogenesis

A

formation of neo-vessels from pre-existing blood vessels

62
Q

examples of different angiogenic microenvironments

A

development
menstrual cycle
wound healing

63
Q

pathologies involving angiogenesis

A

cancer
retinopathy
atherosclerosis
chronic inflammation
ischemic diseases
vascular malformations

64
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

65
Q

how discovery of angiogenesis in cancer lead to treatment

A

mow use anti-angiogenic drugs in clinic with chemotherapy

66
Q

von willebrand disease

A

decrease or dysfunction of vWf
characterised by mucosal bleeding

67
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

68
Q

roles of vwf

A

HAEMOSTASIS
mediates platelet adhesion to subendothelium + aggregation

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

69
Q

what is the paradox of angiogenesis

A

promotes plaque growth = blockage = ischaemia

therapeutic angiogenesis prevents damage post ischaemia

70
Q

where is atherosclerosis most likely to occur + why

A

at bifurcation of arteries - where theres turbulent/disrupted flow

71
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

72
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

73
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

74
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

75
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

76
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)

77
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)

78
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

79
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

80
Q

NFkB

A

nuclear factor kappa b

TF - master inflamm regulator

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

81
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

82
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

83
Q

functions of non-inflammatory and resident macrophages

A

homeostasis (may be parenchymal)

e.g. alveolar = surfactant lipid homeostasis

e.g. spleen = iron homeostasis

84
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)

85
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

85
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

86
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)

87
Q

PDGF vs TGF-b

A

PLATELET DERIVED GROWTH FACTOR:
VSMC chemotaxis, survival + division

TRANSFORMING GROWTH FACTOR BETA:
collagen synthesis + matrix deposition

88
Q
A

brs round 2 - help me (4 decks)

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