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Medical Studies 1 > CVS Week 4 > Flashcards

CVS Week 4 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
what is included in the major criteria of modified dukes
microbiological evidence of endocarditis in blood cultures positive echo showing vegetation and associated valve dmg
26
what is included in the minor criteria of modified dukes
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
27
where is the SA node located
border b/w SVC and RA
28
describe the generation of an AP in the cardiac conduction system
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
29
how is cardiac conduction different to skeletal muscle conduction
cardiac muscles capable of automaticity and rhythmicity using their own pacemaker cells that are modified heart cells, not nerve cells
30
describe in detail the conduction system of the heart
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
31
describe the process of excitation-contraction coupling in cardiac muscle
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
32
what is phase 0 of AP in cardiac cell
depolarisation rapid influx of Na+ through V-G Na+ channels
33
what is phase 1 of AP in cardiac cell
initial repolarisation Na+ channels close and transient outward K+ channels open, causing brief, partial repolarisation
34
what is phase 2 of AP in cardiac cell
plateau phase balance b/w inward flow of Ca2+ through L type Ca2+ channels and outward flow of K+
35
what is phase 3 of AP in cardiac cell
repolarisation Ca2+ channels close and delayed rectifier K+ channels open, allowing K+ to exit the cell, restoring membrane to resting state
36
what is phase 4 of AP in cardiac cell
resting potential maintained by Na+/K+ ATPase pump which restores ionic gradients by expelling Na+ and bringing in K+
37
outline the modification of AP generation
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
how does parasympathetic stimulation affect HR
increases K+ currents and causes hyperpolarisation and slows depolarisation
39
how does sympathetic stimulation affect HR
increases Ca2+ currents and causes faster depolarisation
40
what are 3 primary functions of the atria
reservoir chamber ie atrial filling conduit ie passive emptying booster ie active emptying
41
what are 4 types of AF
paroxysmal persistent long standing persistent permanent
42
describe paroxysmal AF
spontaneously terminates <7days
43
describe persistent AF
continues for >7 days or requires cardioversion
44
describe long-standing persistent AF
continuous >12 months
45
describe permanent AF
continuous AF in which attempts to restore sinus rhythm have been abandoned
46
what are 6 risk factors for AF
ageing HTN obesity alc intake genetics cardiac disease
47
describe the role of atrial ectopic firing
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
what is atrial fibrillation
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
what 4 components drive the pathophysiology of AF
calcium handling abnormalities within myocardium electrical remodelling of heart structural remodelling of heart autonomic nerve remodelling of heart
50
describe atrial electrical remodelling
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
describe atrial structural remodelling
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
what are 7 symptoms of AF
palpitations dyspnea exercise intolerance fatigue chest discomfort dizziness syncope
53
describe AF diagnosis
ECG used typically holter monitor can be used (basically a smaller wearable ECG that allows continuous monitoring) wearable tech like apple watches
54
what are the 4 main treatment approaches for AF
rate control rhythm control anticoagulation risk management
55
why would you use rate control as a treatment approach for AF
reduce ventricular rate > alleviate symptoms, promote hemodynamic stability, reduce tachyarrhythmic effects
56
what are examples of treatment methods for rate control approach
beta blockers calcium channel antagonists
57
why would you use rhythm control as a treatment approach for AF
attempt to achieve and maintain sinus rhythm, reduce AF symptoms, reverse remodelling
58
what are examples of treatment methods for rhythm control approach
catheter ablation anti arrhythmic meds
59
why would you use anticoagulation as a treatment approach for AF
reduce risk of stroke with elevated risk score
60
what are examples of treatment methods for anticoagulation
factor XA inhibition direct thrombin inhibitors
61
why would you use a risk management as a treatment approach for AF
reduce risk factors promoting maintenance and progression of AF
62
what are examples of treatment methods for risk management
weight loss glucose control prescribed exercise
63
describe the pathophysiology linking AF and stroke risk
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
list the common forms of bradyarrhythmias
sinus bradycardia sinus arrhythmia sinus node ageing sick sinus syndrome
65
describe sinus bradycardia
sinus node discharge rate <50BPM generally considered benign unless accompanied by other symptoms like presyncope
66
what can cause sinus bradycardia
high vagal tone decreased sympathetic tone sinus node dysfunction effects of meds
67
describe sinus arrhythmia
phasic variation in cycle length accompanied by normal P wave morphology and PR interval >120ms
68
describe sinus node ageing
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
describe sick sinus syndrome
multiple sinus abnormalities including persistent sinus bradycardia, sinus arrest or exit block, combinations of SA and AV node abnormalities, tachybrady syndrom
70
sinus node disease is commonly chracterised by what
fibrosis in proximity to SA node and diffuse atrial scar nodal-atrial discontinuity inflammatory/degenerative changes ion channel remodelling
71
an AV block can be classified into what 3 main categories
1st degree 2nd degree type 1 and type 2 3rd degree
72
outline 1st degree AV block and its interventional process
impulses are conducted but conduction time is prolonged (>200ms) prolonged PR interval on ECG nil intervention
73
outline 2nd degree type 1 AV block and its interventional process
progressive lengthening of conduction time until an impulse is not conducted PR interval progressively longer on ECG nil intervention
74
outline 2nd degree type 2 AV block and its interventional process
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
outline 3rd degree AV block and its interventional process
complete dissociation b/w atrial and ventricular impulses PR intervals are not coupled w QRS complexes on ECG urgent pacemaker needed
76
describe pacing for bradycardia as a management of bradyarrhythmias
for patients w symptomatic bradycardia 3 types: single chamber (only atria), dual chamber (atrial and RV), biventricular (atrial and RV and LV)
77
what are 4 cardiac causes of sudden cardiac death
CHD cardiomyopathies inherited arrhythmias valvular heart disease
78
what are 8 reversible causes of sudden cardiac arrest (4Hs and 4Ts)
hypoxia hypovolemia hypokalemia hypothermia tension pneumothorax tamponade toxins thrombosis
79
what are some modifiable risk factors for sudden cardiac arrest/death
HTN smoking obesity depression poor diet heavy alc use
80
what are some non modifiable risk factors for sudden cardiac arrest/death
advanced age male sex diabetes family history congenital abnormalities specific CV conditions
81
what is ventricular arrhythmia
abnormal electrical activity that is arising from the ventricles of the heart, either left or right
82
what are 4 forms of ventricular arrhythmia
sustained v-tach non-sustained v-tach polymorphic v-tach torsades de pointes (ballerina)
83
describe sustained v-tach
cardiac arrhythmia of >3 consecutive complexes >100 BPM VT >30s and/or requiring termination
84
describe non-sustained v-tach
cardiac arrhythmia of >3 consecutive complexes >100 BPM terminates spontaneously <30s
85
describe polymorphic v-tach
multiform QRS morphology from beat to beat indicates ischemia
86
describe torsades de pointes arrhythmia
long QT segment polymorphic twisting of points
87
what are key assessment factors when diagnosing ventricular arrhythmias
HR and regularity JVP sternotomy scars elevated BP murmurs oedema
88
describe ECG patterns of ventricular arrhythmias
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
what are 6 individual interventions for management of ventricular arrhythmias
education of community members screening promoting healthy lifestyle BLS programs community AED provision recognition of familial risk > screening
90
what are 6 community interventions for management of ventricular arrhythmias
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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