week 4 Flashcards

1
Q

inflammatory heart disease mechanism

A

immune cells attack heart causing inflammation and damage leading to scarring and fibrosis

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2
Q

pericarditis 4 characteristics

A

pleural inflammation
pericardial effusion
ST elevation on ECG
Serious cases leads to pericardial tamponade

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3
Q

myocarditis 3 characteristics

A

myocardium inflammation
elevated troponin and inflammatory markers

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4
Q

endocarditis 2 characteristics

A

endocardium inflammation
often due to vegetations of immune complexes

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5
Q

RHD progression 5

A

Infection
Sore throat and skin sores
Rheumatic fever
Recover and fibrosis or recurrent infection
rheumatic HD

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6
Q

immune complex disease definition and cause

A

antigen antibody complexes which deposit in tissue causing inflammation

occur when there is excessive antigen/antibody present which are not cleared

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7
Q

infective endocarditis and immune complexes

A

immune complexes attack endocardium cause inflammation, seed to structures incl valves

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8
Q

RHD key tissue manifestations

A

brain (chorea), skin (subctuaneous noduels), MSK (arthritis)

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9
Q

complications of RHD

A

emboli - from vegetations
AF
stroke
infective endocarditis

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10
Q

common pathogens implicated in endocarditis

A

staphylococcus aureas
streptococcus viridians

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11
Q

infective endocarditis clinical features (4 main tissue manifestations)

A

Skin: janeway lesions, osler nodes and splinter haemorhages
Joints: Arthritis
Kidneys: Glomerularnephritis
Eyes: conjunctivale haemorhages, ROth spots

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12
Q

major features of infective endocarditis 2

A
  1. positive blood culture
  2. echocardiogram w vegetation
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13
Q

complications infective endocarditus

A

emboli
HF
sepsis

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14
Q

pathology of infective endocarditis 6 steps

A

infection->bacteraemia->seeding and adhesion->immune response->immune complex formation->chronic inflammation

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15
Q

infective endocarditis management 3

A

antibiotics
HF management
Palliative treatment

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16
Q

what calcium channel opens first in pacemaker production and what triggers it

A

the T type calcium channel opens first allowing rapid depolarisation
triggered by influx of sodium reaching minimum threshold

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17
Q

sympathetic influence on HR (not BP) 3

A

adrenaline and noradrenaline release = chronotropy and inotropy increasing calcium channel currents and sodium channel currents

18
Q

parasympathetic activation of heart

A

acetylcholine release
binds to muscarinic receptors
increases potassium channel currents
causing hyperpolarisation

19
Q

4 key causes for AF

A

electrical remodelling
structural remodelling
Ca handling abnormalities
Neural remodelling

20
Q

where do ectopic beats normally come from in AF

A

pulmonary veins

21
Q

what are the key reasons for AF occuring from the four causes listed prior

A

reduced refractory period, shorter AP time

22
Q

reason for palpitations, dyspnoea, exercise intoleance, fatigue, chest discomfort, dizziness and syncope in atrial arhythmias

A

palpitations = irregular heartbeat

dyspnoea+exercise intolerance+fatigue = comprimised CO

chest discomfort = ischaemia

dizziness+ syncope = reduced blood flow to brain

23
Q

4 key drugs in AF management

A

rate drugs: beta blockers calcium channel anyagonists

rhythm drugs: Amiodarone

anticoagulation

risk factor management

24
Q

scoring system used to link AFib and stroke risk

A

CHADVAS2 score
1> men = anticoagulation
2> women = anticoagulation

25
4 types of bradyarrhythmia
sinus bradycardia sinus arrhythmia sinus ageing sick sinus syndrome
26
Bradyarrhythmia diagnoses (ECG AV blocks)
type 1 = prolonged PR intervals type 2 mobitz = continually prolonged until one p wave missing type 2 = intermittent type 3 = comple dissociation between atrial and ventricular impulses
27
list management of bradyarrhythmias
cardiac pacemakers
28
types of pacemakers 3
single chamber dual chamber biventricular
29
sudden cardiac arrest
sudden cessation of cardiac activity
30
sudden cardiac death
sudden and unexpected death occuring within an hour of sympotm onsent or within 24hrs of asymptomatic
31
risk factros for sudden cardiac arrest 3
hypertension smoking obesity
32
types of ventricular arrhythmias 5
polymorphic incl torsades des pointes bidirectional monomorphic ventricular flutter ventricular fibrillation
33
list of basic management in ventricular arrhythmias 4
defibrillation CAD management anti-arrhythmic management risk factor management
34
difference between cardiac blues and depressino
cardiac blues: after MI/surgery, will resolve depression: long term, underlying factor, check FHx and SHx
35
presentation of AFIB on ECG signs 2
irregular irregular rate and rhythm
36
invasive management technique in AF
pulmonary vein catherisation and electrical isolation preventing the regeneration and dissemination of ectopic beats
37
what is the rhythm control drug in afib
amiodarone
38
mech of action in amiodarone
blocks potassium channels in myocardial cells resulting in hyperpolarisation whcih decreases rate of contraction and firing
39
criteria of CHADVAS
C = congestive HF H = hypertension A = age<75 D = diabetes V = vascular disease A = age>75 S = sex
40
reasons for sinus bradychardia 5
increased vagal tone SA remodelling/dysfunction decreased sympathetic medication athlete
41
what does sinus arrhythmia look like on an ecg
will always have p waves but the RR intervals are irregular
42