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M1 > week 4 > Flashcards

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
Q

4 types of bradyarrhythmia

A

sinus bradycardia
sinus arrhythmia
sinus ageing
sick sinus syndrome

26
Q

Bradyarrhythmia diagnoses (ECG AV blocks)

A

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
Q

list management of bradyarrhythmias

A

cardiac pacemakers

28
Q

types of pacemakers 3

A

single chamber
dual chamber
biventricular

29
Q

sudden cardiac arrest

A

sudden cessation of cardiac activity

30
Q

sudden cardiac death

A

sudden and unexpected death occuring within an hour of sympotm onsent or within 24hrs of asymptomatic

31
Q

risk factros for sudden cardiac arrest 3

A

hypertension
smoking
obesity

32
Q

types of ventricular arrhythmias 5

A

polymorphic incl torsades des pointes
bidirectional
monomorphic
ventricular flutter
ventricular fibrillation

33
Q

list of basic management in ventricular arrhythmias 4

A

defibrillation
CAD management
anti-arrhythmic management
risk factor management

34
Q

difference between cardiac blues and depressino

A

cardiac blues: after MI/surgery, will resolve
depression: long term, underlying factor, check FHx and SHx

35
Q

presentation of AFIB on ECG signs 2

A

irregular irregular rate and rhythm

36
Q

invasive management technique in AF

A

pulmonary vein catherisation and electrical isolation preventing the regeneration and dissemination of ectopic beats

37
Q

what is the rhythm control drug in afib

A

amiodarone

38
Q

mech of action in amiodarone

A

blocks potassium channels in myocardial cells resulting in hyperpolarisation whcih decreases rate of contraction and firing

39
Q

criteria of CHADVAS

A

C = congestive HF
H = hypertension
A = age<75
D = diabetes
V = vascular disease
A = age>75
S = sex

40
Q

reasons for sinus bradychardia 5

A

increased vagal tone
SA remodelling/dysfunction
decreased sympathetic
medication
athlete

41
Q

what does sinus arrhythmia look like on an ecg

A

will always have p waves but the RR intervals are irregular

42
Q
A

M1 (13 decks)

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