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Medical Studies 1 > CVS Week 4 > Flashcards

CVS Week 4 Flashcards

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USMLE® Step 1 flashcards
1
Q

outline the mechanism of inflammatory heart disease

A

chronic activation of the immune system

Then, immune cells mistakenly target self antigens in heart tissue

Then, inflammation

Then, immune cells release cytokines and other inflammatory mediators that exacerbate tissue damage

Then, fibrosis

Then, myocarditis, endocarditis, pericarditis

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2
Q

what are 3 infective triggers of inflammatory heart disease

A

bacteria

viruses

fungi

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3
Q

what are 3 non infective triggers of inflammatory heart disease

A

autoimmune disorders

hypersensitivity

iatrogenic

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4
Q

describe endocarditis

A

inflammation of endocardium characterised by vegetations composed of platelets, fibrin, microorganisms and inflammatory cells

can be infective or non infective

vegetations lead to severe complications including embolic events and valve destruction

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5
Q

describe myocarditis

A

inflammation of the myocardium, presenting w myocardial necrosis or fibrosis, typically resulting from viral infections, immune responses or toxins

clinically, resembles STEMI but w inflammatory pathology

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6
Q

describe pericarditis

A

inflammation of the pericardium, often presents with sharp pleuritic chest pain, pericardial effusion and diffuse ST elevation on ECG

can lead to cardiac tamponade

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7
Q

outline the pathophysiology of rheumatic heart disease

A

exposure to Streptococcus A

Leads to, Strep A infection

Leads to, acute rheumatic fever

Then, recurrences of ARF

Leads to, rheumatic heart disease

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8
Q

what are 4 symptoms of RHD

A

dyspnea

chest pain

fatigue

palpitations

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9
Q

what are immune complexes

A

molecules formed by binding of multiple antigens to antibodies

a complement binds to these immune complexes

unchecked ICs deposit in tissues and lead to inflammation via complement and neutrophil activation

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10
Q

what is mononuclear-phagocyte system

A

composed of circulating tissue-fixed phagocytotic cells that possess IgG Fc and C3 receptors, bind to circulating ICs that have IgG or C3 in their lattices, and lead to phagocytosis

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11
Q

describe immune complex clearance vs deposition

A

relative concentration of Ag to Ab determines whether complexes will be cleared or deposited into tissue

when Ab and Ag not in equivalence, ICs are not removed efficiently, leading to a pathogenic state

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12
Q

what criteria is used for RHD diagnosis

A

jones criteria

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13
Q

what is included in the major criteria of jones criteria

A

carditis

polyarthritis

chorea

erythema marginatum

subcutaneous nodules

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14
Q

what is included in the minor criteria of jones criteria

A

fever

arthralgia

elevated acute phase reactants

prolonged PR interval on ECG

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15
Q

outline 4 consequences of RHD

A

increased risk of infective endocarditis due to damaged valves

mitral regurg leads to LA enlargement, which increases risk of A-fib and hence risk of stroke

chronic RHD can cause pulmonary HTN

can leads to multi-organ dysfunction due to chronic low Q and systemic embolisation

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16
Q

name 7 common causes of endocarditis

A

staphylococcus aureus

coagulase-negative staphylococcus

viridians group of streptococci

streptococcus bovis

other streptococci

enterococcus species

other e.g fungi, yeast

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17
Q

what are 4 common complications of endocarditis

A

uncontrolled infection

emboli

HF

mycotic aneurysms

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18
Q

describe the pathophysiology of infective endocarditis

A

endothelial damage

then, deposition of platelets and fibrin which forms a thrombus known as non-bacterial thrombotic endocarditis (NBTE)

then, microorganisms like bacteria enter bloodstream and adhere to the thrombus leading to colonisation and growth within the platelet/fibrin matrix, forming vegetations

then, these vegetations grow and cause further valve damage leading to regurg, stenosis, or obstruction and can embolise to distant organs

then, the ongoing infection triggers a systemic inflammatory response

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19
Q

describe the basic approach to managing IE

A

broad-spectrum antibiotics

ID causative bacteria > antibiotic therapy is tailored

patients present w HF > diuretic therapy

surgical intervention in cases of severe valvular dmg

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20
Q

what are 3 clinical signs of IE on the hands/feet/eyes

A

janeway lesions

osler nodes

roth spots

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21
Q

what are septic clinical signs of IE

A

presents on spleen, kidney, lungs, vertebral disc

septic arthritis

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22
Q

what are 3 neurological clinical signs of IE

A

abscess

stroke/bleed

seizures

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23
Q

what is the criteria used for diagnosis of IE

A

modified dukes criteria

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24
Q

how is the modified dukes criteria used to diagnose IE

A

2 majors
or
1 major and 2 minor
or
5 minors

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25
Q

what is included in the major criteria of modified dukes

A

microbiological evidence of endocarditis in blood cultures

positive echo showing vegetation and associated valve dmg

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26
Q

what is included in the minor criteria of modified dukes

A

predisposition to getting endocarditis (valve abnormality)

fever > 38 degrees

vascular phenomena (splinter haemorrhages)

elevated CRP

immunological phenomena (osler’s nodes, roth spots)

blood culture findings not fitting into major criteria

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27
Q

where is the SA node located

A

border b/w SVC and RA

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28
Q

describe the generation of an AP in the cardiac conduction system

A

resting membrane potential of -70mV

then, slow influx of Na+ depolarises the membrane

then, T-type Ca2+ channels open, further depolarising the membrane

then, L-type Ca2+ channels open, further depolarising the membrane

then, membrane potential exceeds threshold and AP occurs

then, K+ channels open, efflux of K+ initiates hyperpolarisation

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29
Q

how is cardiac conduction different to skeletal muscle conduction

A

cardiac muscles capable of automaticity and rhythmicity using their own pacemaker cells that are modified heart cells, not nerve cells

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30
Q

describe in detail the conduction system of the heart

A

generation of AP in SA node which sets pace at 60-100BPM

then, electrical impulse spreads through the atria causing atrial contraction pushing blood into ventricles

then, impulse reaches AV node which delays signal slightly to allow complete ventricular filling

then, impulse goes from AV node to bundle of his which divides into left and right bundle branches, transmitting signal to ventricles

then, purkinje fibres distribute impulse throughout ventricular myocardium, resulting in coordinated ventricular contraction

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31
Q

describe the process of excitation-contraction coupling in cardiac muscle

A

begins w cardiac AP that depolarises sarcolemma (cell membrane of cardiomyocyte)

then, this depolarisation triggers opening of voltage gated L type calcium channels > Ca2+ to enter the cell

then, influx of Ca2+ induces further Ca2+ from sarcoplasmic reticulum via ryanodine receptors (process known as CICR)

then, intracellular Ca2+ binds to troponin > displaces tropomyosin, exposing actin-binding sites for myosin > cross-bridge cycling > muscle contraction

then, relaxation occurs as Ca2+ is pumped back into sarcoplasmic reticulum and out of cell allowing muscle to return to resting state

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32
Q

what is phase 0 of AP in cardiac cell

A

depolarisation

rapid influx of Na+ through V-G Na+ channels

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33
Q

what is phase 1 of AP in cardiac cell

A

initial repolarisation

Na+ channels close and transient outward K+ channels open, causing brief, partial repolarisation

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34
Q

what is phase 2 of AP in cardiac cell

A

plateau phase

balance b/w inward flow of Ca2+ through L type Ca2+ channels and outward flow of K+

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35
Q

what is phase 3 of AP in cardiac cell

A

repolarisation

Ca2+ channels close and delayed rectifier K+ channels open, allowing K+ to exit the cell, restoring membrane to resting state

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36
Q

what is phase 4 of AP in cardiac cell

A

resting potential

maintained by Na+/K+ ATPase pump which restores ionic gradients by expelling Na+ and bringing in K+

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37
Q

outline the modification of AP generation

A

w/o control, SA node = fire 100-110 AP (ie 110BPM)

under rest, parasympathetic NS via vagus nerve releases ACh which reduces HR to 60-80BPM

to increase HR, parasympathetic influence must be reduced and sympathetic NS must be initiated

38
Q

how does parasympathetic stimulation affect HR

A

increases K+ currents and causes hyperpolarisation and slows depolarisation

39
Q

how does sympathetic stimulation affect HR

A

increases Ca2+ currents and causes faster depolarisation

40
Q

what are 3 primary functions of the atria

A

reservoir chamber ie atrial filling

conduit ie passive emptying

booster ie active emptying

41
Q

what are 4 types of AF

A

paroxysmal

persistent

long standing persistent

permanent

42
Q

describe paroxysmal AF

A

spontaneously terminates <7days

43
Q

describe persistent AF

A

continues for >7 days or requires cardioversion

44
Q

describe long-standing persistent AF

A

continuous >12 months

45
Q

describe permanent AF

A

continuous AF in which attempts to restore sinus rhythm have been abandoned

46
Q

what are 6 risk factors for AF

A

ageing

HTN

obesity

alc intake

genetics

cardiac disease

47
Q

describe the role of atrial ectopic firing

A

critical to initiation of AF episodes

may be due to enchanced automacity, ion channel abnormalities and/or altered Ca2+ handling

pulmonary veins have been IDed as primary source of ectopic firing, hence pulmonary vein isolation w catheter ablation is a main control treatment

48
Q

what is atrial fibrillation

A

cardiac arrhythmia characterised by chaotic and irregular electrical impulses in atria, leading to ineffective blood flow into ventricles

no discernable P waves on an ECG

49
Q

what 4 components drive the pathophysiology of AF

A

calcium handling abnormalities within myocardium

electrical remodelling of heart

structural remodelling of heart

autonomic nerve remodelling of heart

50
Q

describe atrial electrical remodelling

A

changes in AP within atria can cause AF and can be due to reduced atrial refractory period, shorter AP duration or heterogeneity in APD across atria

this increases AF vulnerability and maintenance

can alter ion channel expression or function

51
Q

describe atrial structural remodelling

A

atrial volume and pressure overloads can initiate structural maladaptations in the heart such as myocyte hypertrophy, extracellular remodelling, metabolic abnormalities, and fatty infiltration

these adaptations damage and remodel previously healthy myocardium

tends to slow down conduction and favour re-entry

52
Q

what are 7 symptoms of AF

A

palpitations

dyspnea

exercise intolerance

fatigue

chest discomfort

dizziness

syncope

53
Q

describe AF diagnosis

A

ECG used typically

holter monitor can be used (basically a smaller wearable ECG that allows continuous monitoring)

wearable tech like apple watches

54
Q

what are the 4 main treatment approaches for AF

A

rate control

rhythm control

anticoagulation

risk management

55
Q

why would you use rate control as a treatment approach for AF

A

reduce ventricular rate > alleviate symptoms, promote hemodynamic stability, reduce tachyarrhythmic effects

56
Q

what are examples of treatment methods for rate control approach

A

beta blockers

calcium channel antagonists

57
Q

why would you use rhythm control as a treatment approach for AF

A

attempt to achieve and maintain sinus rhythm, reduce AF symptoms, reverse remodelling

58
Q

what are examples of treatment methods for rhythm control approach

A

catheter ablation

anti arrhythmic meds

59
Q

why would you use anticoagulation as a treatment approach for AF

A

reduce risk of stroke with elevated risk score

60
Q

what are examples of treatment methods for anticoagulation

A

factor XA inhibition

direct thrombin inhibitors

61
Q

why would you use a risk management as a treatment approach for AF

A

reduce risk factors promoting maintenance and progression of AF

62
Q

what are examples of treatment methods for risk management

A

weight loss

glucose control

prescribed exercise

63
Q

describe the pathophysiology linking AF and stroke risk

A

cardiac inflammation + cardiac endothelial damage > abnormal atrial flow > blood stasis within the LA > blood clot formation (which is added to by hypercoagulability) > embolisation > ischemic stroke

64
Q

list the common forms of bradyarrhythmias

A

sinus bradycardia

sinus arrhythmia

sinus node ageing

sick sinus syndrome

65
Q

describe sinus bradycardia

A

sinus node discharge rate <50BPM

generally considered benign unless accompanied by other symptoms like presyncope

66
Q

what can cause sinus bradycardia

A

high vagal tone

decreased sympathetic tone

sinus node dysfunction

effects of meds

67
Q

describe sinus arrhythmia

A

phasic variation in cycle length

accompanied by normal P wave morphology and PR interval >120ms

68
Q

describe sinus node ageing

A

intrinsic HR (SA node discharge rate in absence of autonomic activity) progressively declines w increasing age, thus the likelihood of sinus bradyarrhythmias is much higher in elderly patients

69
Q

describe sick sinus syndrome

A

multiple sinus abnormalities including persistent sinus bradycardia, sinus arrest or exit block, combinations of SA and AV node abnormalities, tachybrady syndrom

70
Q

sinus node disease is commonly chracterised by what

A

fibrosis in proximity to SA node and diffuse atrial scar

nodal-atrial discontinuity

inflammatory/degenerative changes

ion channel remodelling

71
Q

an AV block can be classified into what 3 main categories

A

1st degree

2nd degree type 1 and type 2

3rd degree

72
Q

outline 1st degree AV block and its interventional process

A

impulses are conducted but conduction time is prolonged (>200ms)

prolonged PR interval on ECG

nil intervention

73
Q

outline 2nd degree type 1 AV block and its interventional process

A

progressive lengthening of conduction time until an impulse is not conducted

PR interval progressively longer on ECG

nil intervention

74
Q

outline 2nd degree type 2 AV block and its interventional process

A

intermittent block of conduction without prior lengthening of conduction time

PR interval consistent on first few cycles then no AV conduction afterwards on ECG

nil intervention

75
Q

outline 3rd degree AV block and its interventional process

A

complete dissociation b/w atrial and ventricular impulses

PR intervals are not coupled w QRS complexes on ECG

urgent pacemaker needed

76
Q

describe pacing for bradycardia as a management of bradyarrhythmias

A

for patients w symptomatic bradycardia

3 types: single chamber (only atria), dual chamber (atrial and RV), biventricular (atrial and RV and LV)

77
Q

what are 4 cardiac causes of sudden cardiac death

A

CHD

cardiomyopathies

inherited arrhythmias

valvular heart disease

78
Q

what are 8 reversible causes of sudden cardiac arrest (4Hs and 4Ts)

A

hypoxia

hypovolemia

hypokalemia

hypothermia

tension pneumothorax

tamponade

toxins

thrombosis

79
Q

what are some modifiable risk factors for sudden cardiac arrest/death

A

HTN

smoking

obesity

depression

poor diet

heavy alc use

80
Q

what are some non modifiable risk factors for sudden cardiac arrest/death

A

advanced age

male sex

diabetes

family history

congenital abnormalities

specific CV conditions

81
Q

what is ventricular arrhythmia

A

abnormal electrical activity that is arising from the ventricles of the heart, either left or right

82
Q

what are 4 forms of ventricular arrhythmia

A

sustained v-tach

non-sustained v-tach

polymorphic v-tach

torsades de pointes (ballerina)

83
Q

describe sustained v-tach

A

cardiac arrhythmia of >3 consecutive complexes

> 100 BPM

VT >30s and/or requiring termination

84
Q

describe non-sustained v-tach

A

cardiac arrhythmia of >3 consecutive complexes

> 100 BPM

terminates spontaneously <30s

85
Q

describe polymorphic v-tach

A

multiform QRS morphology from beat to beat

indicates ischemia

86
Q

describe torsades de pointes arrhythmia

A

long QT segment

polymorphic

twisting of points

87
Q

what are key assessment factors when diagnosing ventricular arrhythmias

A

HR and regularity

JVP

sternotomy scars

elevated BP

murmurs

oedema

88
Q

describe ECG patterns of ventricular arrhythmias

A

wide abnormal QRS complexes that are not preceded by P waves

V-tach shows regular rhythm w rapid rate while v-fib shows chaotic, irregular rhythm with no distinct QRS complexes, leading to a loss of effective Q

89
Q

what are 6 individual interventions for management of ventricular arrhythmias

A

education of community members

screening

promoting healthy lifestyle

BLS programs

community AED provision

recognition of familial risk > screening

90
Q

what are 6 community interventions for management of ventricular arrhythmias

A

electrical defibrillation

CAD risk management

internal cardioverter defibrillation

anti-arrhythmic meds

specific risk scoring systems

risk assessment of SCD

Medical Studies 1 (16 decks)

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