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BRS Y2 > cardio and respiratory > Flashcards

cardio and respiratory Flashcards

1
Q

when do we hear S1 heart sound

A

closure of mitral and tricuspid valve

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2
Q

when do we hear S2 heart sound

A

closure of aortic and pulmonary valve

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3
Q

when do we hear S3 heart sound

A

congestive cardiac failure
due to rapid filling and expansion of ventricles
early diastole

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4
Q

when do we hear S4 heart sound

A

systemic hypertension, hypertrophic cardiomyopathy, ischemia
atrial hypertrophy/ stiff ventricles
late diastole
due to forcegul atrial contractions

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5
Q

what are some congenital structural heart diseases

A

atrial septal defect
ventricular septal defect
coarctation fo aorta
patent foramen ovale
tetralogy of fallot
patent ductus arteriosus

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6
Q

what are types of valvular defects (4)

A

aortic stenosis
aortic regurgitation
mitral stenosis
mitral regurgitation

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7
Q

what is aortic stenosis preceded by

A

aortic sclerosis

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8
Q

risk factors of atrial stenosis

A

hypertension
LDL
smoking
elevated C reactive protein
CKD
radiotherapy
age

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9
Q

causes of aortic stenosis

A

rheumatic heart disease
congenital heart disease
calcium build up

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10
Q

pathophysiology of aortic stenosis

A

degeneration or congenital malformed valves or anti Streptococcal Av wrongly attack valves leading to inflammation of valve endocardium -> cause fibrosis and calcification of aortic valve –> LV need contract harder to pump blood –> concentric LV myocardial hypertrophy –> hypertrophic LV becomes stiff overtime and harder to fill –> decrease Cardiac output –> diastolic dysfunction –> pressure overload in LV back to LA –> cause LA dilate and lead to increase pressure ij lungs –> pulmonary congestion

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11
Q

symptoms and signs of aortic stenosis

A

ejection systolic murmur
syncope on exertion
angina on exertion
diffuse crackles on auscultation of lungs and dyspnoea

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12
Q

how to diagnose aortic stenosis

A

doppler echo (to detect blood flow and pressure gradient)

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13
Q

management of aortic stenosis

A

transcatheter valve replacement
surgical valve prosthesis

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14
Q

what is aortic regurgitation

A

diastolic leakage of blood from aorta to LV
due to incompetence of valve leaflets resulting from intrinsic valve disease or dilation of aortic root

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15
Q

is aortic regurgitation chronic or acute

A

can be both

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16
Q

what happens in acute aortic regurgitation

A

sudden onset of pulmonary oedema and hypotension or cardiogenic shock

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17
Q

what happens in chronic aortic regurgitation

A

culminate into congestive cardiac failure

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18
Q

causes of chronic aortic regurgitation

A

rheumatic heart disease
infective endocarditis
aortic valve stenosis
congenital heart defects
congenital bicuspid valves

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19
Q

causes of chronic aortic regurgitation

A

Marfan’s syndrome
connective tissue disease
collagen vascular diseases

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20
Q

pathophysiology of aortic regurgitation

A

aortic root dilation / inflammation of valvular endothelium lead to abnormal valve leaflet –> valve leaflet close poorly when aortic pressure is higher than LV during diastole –> back flow of blood from aorta to LV –> acute dilation cause increase stroke vol / chronic LV dilates and eccentrically hypertrophies –> excessive stretching weakens myocardium and unable to contract properly –> systolic heart failure

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21
Q

aortic regurgitation symptoms and signs

A

diastolic murmur
S3 gallop in early diastole, due to rapid filling and expansion of ventricles
angina on exertion
fatigue
increase back pressure in lungs causing pulmonary congestion

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22
Q

presentation of acute aortic regurgitation

A

cardiogenic shock
tachy
cyanosis
pulmonary oedema
diastolic murmur

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23
Q

presentation of chronic aortic regurgitation

A

wide pulse pressure

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24
Q

how to diagnose aortic regurgitation

A

echocardiography

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25
Q

management for aortic regurgitation (for acute and chronic respectively)

A

acute : aortic valve replacement
chronic: vasodilator therapy

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26
Q

what is mitral stenosis

A

obstruction to LV inflow at mitral valve due to structural abnormality of mitral valve
may lead to pulmonary hypertension and right HF

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27
Q

causes of mitral stenosis

A

rheumatic fever
carcinoid syndrome
SLE
mitral anular calcification
amyloidosis
congenital deformity of valve

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28
Q

pathophysiology of mitral stenosis

A

recurrent inflammation –> fibrous decomposition and calcification of mitral valve leaflets ad chordae tendineae –> thicken and shorten of chordae tendineae –> fusion of leaflets, very narrow -> decrease in orifice area -> obstructed blood flow thru MV –> impaired emptying of LA -> impaired filling of LV –> decrease SV and CO –> congestive HF –> increase in RV pressure –> hypertrophy of RV –> right side HF

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29
Q

symptoms and signs of mitral stenosis

A

mid diastolic murmur
afibrillation
right side HF/ cardiogenic shock/ congestive HF
LA enlargement

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30
Q

presentations of mitral stenosis

A

dyspnoea
murmur
dysphagia
opening snap
haemoptysis

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31
Q

how to diagnose mitral stenosis

A

ECG
chest x ray
transthoracic echocardiography

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32
Q

management of mitral stenosis

A

if progressive asymptomatic -> no therapy
severe asymptomatic -> adjuvant balloon valvotomy
severe symptomatic -> diuretic, balloon valvotomy, valve replacement and repair adjunct B-blockers

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33
Q

what is mitral regurgitation

A

caused by disruption in any part of mitral valve apparatus
abnormal reversal of blood flow from LV to LA

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34
Q

causes of acute mitral regurgitation

A

mitral valve prolapse
rheumatic heart disease
infective endocarditis
post valvular surgery
prosthetic mitral valve dysfunction

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35
Q

causes of chronic mitral regurgitation

A

rheumatic heart disease
SLE
scleroderma
hypertrophic cardiomyopathy
drug related

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36
Q

pathophysiology of mitral regurgitation

A

back flow of blood from LV to LA due to impaired closure of valve –> increase vol and pressure in LA –> increase vol push bk into LV in next diastole –> LV dilation due to remodelling –> decrease in LV systolic function –> back pressure in LA and lung vasculature leading to congestion / decrease SV and cardiac output –> congestive HF

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37
Q

symptoms of mitral regurgitation

A

holosystolic murmur
S3 heart sound
decrease in oxygen saturation, wheeze, crackles, tachypnoea
sign of congestive HF

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38
Q

how to diagnose mitral regurgitation

A

ecg
CXR
transthoracic echocardiography
cardiac mri
ct scan

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39
Q

management of acute mitral regurgitation

A

repair or replace supporting valve structures
prosthetic ring to reshape the valve

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40
Q

management of chronic mitral regurgitation

A

asymptomatic -> monitor or surgery
symptomatic –> first surgery plus medical treatment

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41
Q

what is cardiomyopathy

A

makes heart muscle harder to pump blood to rest of body

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42
Q

which types of HF are result of cardiomyopathies (3)

A
  1. dilated
  2. hypertrophic
  3. restrictive
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43
Q

what is dilated cardiomyopathy

A

most common cause of HF
progressive irreversible
cause systolic dysfunction with HF

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44
Q

what is hypertrophic cardiomyopathy

A

genetic CVD
sudden cardiac death in preadolescent and adolescent children
increase in LV wall thickness not solely explained by abnormal loading conditions

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45
Q

what is restrictive cardiomyopathy

A

idiopathic/familial/associated with systemic disorders
restrictive ventricular filling pattern

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46
Q

what is infective endocarditis

A

infection of endocardium or vascular endothelium of heart

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47
Q

main cause of infective endocarditis

A

bacteria entering blood stream and form a vegetation in endocardium

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48
Q

what is the most common bacteria in endocartitis

A

Streptococci

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49
Q

how to diagnose infective endocarditis

A

blood test show anaemia and raised markers of infection
blood cultures isolate a microorganism
echocardiogram show vegetation, abscess, valve perforation, dehiscence of prosthetic valve, regurgitation of affected valve
transoesophageal echo has higher sensitivity than transthoracic

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50
Q

symptoms of infective endocarditits

A

fever
malaise
sweats
unexplained weight loss
new heart murmur

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51
Q

what symptoms of cardiac decompensation in infective endocarditis

A

SOB
frequent coughing
swelling of legs and abdomen
fatigue

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52
Q

what are clinical signs of infective endocarditis

A

raised JVP
lung crackles
oedema

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53
Q

what part of heart does infective endocarditis affect

A

endocardium
valves of heart
most common aortic valve

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54
Q

what is vegetation in infective endocarditis

A

changes to valve thickness or failure in their ability to opena nd close

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55
Q

how IV drugs users are more dangerous to infective endocarditis

A

due to repeated injection more at risk to expose bloodstream to bacteria on surface of skin or use of non sterile needles

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56
Q

what is difference between rheumatic fever and rheumatic heart disease

A

fever: temporary inflammatory condition
heart disease: permanent condition as a sequala of previous rheumatic fever causing permanent damage to heart valves

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57
Q

which bacteria cause rheumatic fever

A

group A streptococci

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58
Q

is there a long lag between rheumatic fever and rheumatic heart disease

A

yes
7 years to 30years

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59
Q

what are the most common valvular dysfunction caused by rheumatic heart disease

A

mitral stenosis

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60
Q

which valve can be affected by acute rheumatic fever

A

aortic valve (more common) and tricuspid
causing regurgitation and then stenosis

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61
Q

clinical signs of mitral stenosis

A

fluid overload eg peripheral oedema
malar flush
hoarse voice
loud S2
RV heave

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62
Q

symptoms of mitral stenosis

A

haemoptysis
fatigue
SOB
paroxysmal nocturnal dyspnoea
palpitation

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63
Q

why is there hoarse voice in mitral stenosis

A

compression of left recurrent laryngeal nerve by dilated left atrium

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64
Q

what are in increased risk in mitral stenosis

A

stroke and embolic events

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65
Q

major Jones’ criteria for rheumatic heart disease

A

presnece of grp A streptococci infection
carditis
arthritis
chorea
erythema marginatum
subcutaneous nodules

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66
Q

minor Jones’ criteria for rheumatic heart disease

A

polyarthralgia
fever
elevated acute phase reacts (CRP/ESR)
prolonged PR interval

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67
Q

pathognomic features of rheumatic heart valves

A

leaflet or chordal thickening
prolapse leaflets
excessive leaflet tip motion during systole

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68
Q

management of mitral stenosis

A

valve commissurotomy (percutaneous or surgical)
valve replacement
management of complications (eg HF and AF) using vit K antagonist

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69
Q

pathogenesis of allergic asthma

A

allergen cause sensitises airway and cause inflammation -> airway remodelling
recruitment of inflammatory cellls into airway
structural change in airway, increase in goblet cells and mucus production
increase amt of matrix and size and amt of smooth muscle cells
narrowed airway

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70
Q

what is the name of abnormal air flow in brocnhocostriction

A

turbulent flow

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71
Q

why some ppl who are sensitised develop asthma

A

hv allergies but not asthma
can be genetically susceptible of allergic asthma

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72
Q

what are the steps in Type 2 Immunity allergic asthma

A
  1. exposure to antigen
  2. allergen binds to lung dendritic cell MHC ll
  3. APC carried by MHC ll to mediastinal lymphocytes
  4. Th0 differnetiate into Th1 and Th2
  5. Th2 differnetiates to IL-4, IL-5, IL-13
  6. eosinophilic airway inflammation
  7. mast cell proliferation, IgE synthesis, mucin secretion
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73
Q

function of IL-4

A

convert B plasma cells to secrete IgE

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74
Q

function of IL-5

A

recruit eosinophils into airways and promote their survival causing eosinophilic airway inflammation

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75
Q

unction of IL-13

A

mucus secretion

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76
Q

what are some tests for allergic sensitisation

A

allergy skin tests
blood tests (for IgE antiobodies to allergens of interest)

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77
Q

tests for eosinophilia

A

blood test
sputum

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78
Q

what is a non invasive biomarker for type 2 airway inflammation

A

fraction of exhaled nitric oxide (FeNO)
>40ppb in adults
>35ppb in children

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79
Q

management of asthma to reduce airway eosinophilic inflammation

A

inhaled corticosteroids (ICS)
leukotriene receptor antagonsits

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80
Q

management of asthma for acute symptomatic relief

A

Beta-2 agonists (smooth muscle relaxation)
anticholinergic therapies (smooth muscle relaxation)

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81
Q

management fo asthma with steroid sparing therapies

A

anti IgE antibody
anti-IL-5 antibody
anti-IL-5 receptor antibody

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82
Q

what is the mechanism of corticosteroids

A

reduce eosinophil numbers through apoptosis
reduce mast cell numbers
smooth muscle relaxation
reduce mucus secretion

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83
Q

what is LABA in approaches to treat asthma symptoms

A

B2 agonists to causing smooth muscle relaxation and dilatation of the airways

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84
Q

pathogenesis of acute asthma attack

A
  1. exposure to allergens eg pollution, smoke, dust
  2. asthma attack
  3. if infection predominating, asthma patients have reduced IFV so increase viral replication
  4. prolonged illness
  5. reduce peak expirating flow rate and increase airway obstruction
  6. increase airway eosinophilic inflammation responsive to corticosteroid
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85
Q

is eosinophil responsive to corticosteroids

A

yes

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86
Q

what is anti-IgE antibody therapy

A

humanised anti-IgE monoclonal antibody
binds and captures circulating IgE to prevent interaction with mast cells and basophils to stop allergic cascade
reduce IgE production

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87
Q

what is omalizumab

A

Anti-IgE antibody
but very expensive

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88
Q

example of anti-IgE antibody

A

omalizumab

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89
Q

example of anti-IL-5 antibody

A

mepolizumab

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90
Q

what is mepolizumab

A

anti-IL 5 antibody

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91
Q

when do we use mepolizumab

A

severe eosinophilic asthma

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92
Q

what is dupilumab

A

anti-IL 4Ra subunit therapy

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93
Q

what is biggest risk factor of male for respiratory failure

A

smoking

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94
Q

what is biggest risk factor of female for respiratory failure

A

household air pollution

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95
Q

what is pulmonary transit time

A

the time taken for blood to pass through the pulmonary circulation

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96
Q

when will we have alveolar deadspace

A

well ventilated + poor perfusion
V/Q ration high

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97
Q

when will we have intrapulmonary shunt

A

poorly ventilated + well perfused
low V/Q ratio

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98
Q

what is minute ventilation

A

tidal vol x breathing frequency

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99
Q

what is alveolar ventilation

A

gas entering and leaving alveoli
(tidal vol - dead space) x breathing frequency

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100
Q

where is V/Q ratio highest

A

apex of lung

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101
Q

what is meaning of compliance of lung tissue

A

tendency to distort under pressure (change in ventilation/change in pressure)

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102
Q

what is meaning of elastance of lung tissue

A

tendency to recoil to its orig vol
(change in pressure/change in ventilation)

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103
Q

risk factor of chronic RF

A

COPD
pollution
recurrent pneumonia
CF
pulmonar fibrosis
neuro-muscular disease

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104
Q

risk factor of acute RF

A

infection (bacteria, viral)
aspiration
trauma
pancreatitis
transfusion

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105
Q

pathology of acute lung injury

A

alveolar macrophages activated by inflammation infection
release more cytokines (IL-6 and IL-8 and TNF alpha)
protein rich oedema build up in lung
inactivation of surfactant
alveoli less efficient at expanding
get migration of neutrophils into interstitium
increase distance between capillary and alveoli
further d.d. for gas exchange –> less efficient

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106
Q

what is the role of salbutamol in treating RF

A

relieve symptoms of asthma and chronic obstructive pulmonary disease (COPD) such as coughing, wheezing and feeling breathless.
relaxing the muscles of the airways into the lungs

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107
Q

what is ARDS

A

acute respiratory distress syndromes
life-threatening lung injury that allows fluid to leak into the lungs

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108
Q

what are some therapeutic intervention to treat underlying disease of RF

A

inhaled therapies (bronchodilators, vasodilators)
steroids
antibiotics
anti virals

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109
Q

what are some therapeutic intervention for multiple organ support

A

cardio: fluids, vasopressors, inotropes, vasodilators
renal: haemofiltration, haemodialysis
immune: plasma exchange, convalescent plasma

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110
Q

consequence of ARDS

A

poor gas exchange
infection (sepsis)
inflammation
systemic effects

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111
Q

what are different types of ventilation

A

volume controlled
pressure controlled
assisted breathing modes
advanced ventilatory modes

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112
Q

what is the scoring system of RF

A

murray score

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113
Q

what is ECMO

A

extracorporeal membrane oxygenation
a form of life support for ppl w injuries for heart or lung

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114
Q

how does ECMO work

A

help remove CO2 and input O2

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115
Q

pathogenesis of lung cancer

A
  1. interaction between inhaled carcinogens and epithelium of upper and lower airways
  2. formation of DNA adducts (cancer causing chemicals)
  3. persisting DNA adducts cause mutation and genomic alterations
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116
Q

what are differnet types of lung cancer (4)

A
  1. sqaumous cell carcinoma
  2. adenocarcinoma (most common)
  3. large cell lung cancer
  4. small cell lung cancer
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117
Q

what are some important oncogenes

A
  1. epidermal growth factor receptor (EGFR) tyrosine kinase
  2. anaplastic lymphoma kinase (ALK) tyrosine kinase
  3. c-ROS oncogene 1 (ROS) receptor tyrosine kinase
  4. BRAD
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118
Q

which gene mutation in lung adenocarcinoma

A

EFGR tyrosine kinase

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119
Q

which gene mutation in non small cell lung cancer

A

ALK tyrosine kinase
c-ROS receptor tyrosine kinase
BRAF

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120
Q

symptoms of lung cancer (6)

A

cough
weight loss
breathlessness
fatigue
chest pain
haemoptysis

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121
Q

neurological features of advanced lung cancer

A

focal weakness
seizures
spinal cord compression
bone pain
paraneoplastic syndromes

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122
Q

what is pemberton’s sign

A

SVC obstruction

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123
Q

what are some imaging for lung cancer

A

CXR
staging CT (chest + abdo)
PET-CT

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124
Q

what is useful to exclude occult metastases

A

PET-CT

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125
Q

what can be used to stage mediastinum and achieve tissue diagnosis and access peripheral lung tumors

A

biopsy

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126
Q

Staging – what is T1-4 for (2)

A

tumor size and location

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127
Q

Staging – what is N0-3 for

A

lymph node involvement (mediastinum and beyond)

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128
Q

Staging – what is M0-1c for (2)

A

metastases + number

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129
Q

what is the grading of patient fitness according to WHO performance status

A

0-5 (asymptomatic to death)

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130
Q

what are the surgery options for lung cancer (4)

A

wedge resection
segmental resection
lobectomy
pneumonectomy

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131
Q

what is another option than surgery for early stage lung cancer

A

radical radiotherapy

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132
Q

what are the systemic treatments for lung cancer (3)

A
  1. oncogene-directed
  2. immunotherapy
  3. cytotoxic chemotherapy
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133
Q

when is oncogene directed systemic treatment used

A

first line treatment for metastatic NSCLC with mutation

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134
Q

mechanism of immunotherapy for lung cancer

A
  1. orig PD-L1/PD-L binding inhibits T cell killing tumor cell
  2. immunotherapy uses anti PD-1 to bind on PD-1 causing PD-1cannot bind to PD-L1 receotor
  3. make it available to T cell to kill tumor cell
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135
Q

when is immunotherapy used

A

first line treatment for metastatic NSCLC with no mutation and PDL > 50%

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136
Q

when is cytotoxic chemotherapy used

A

first line treatment for metastatic NSCLC with no mutation and PDL < 50%
can combine with immunotherapy

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137
Q

side effects of immunotherapy for lung cacner

A

immune-related side effects (thyroid, skin, bowel, liver, lung)

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138
Q

side effects of cytotoxic chemotherapy for lung cancer

A

fatigue
nausea
bone marrow suppression
nephrotoxicity

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139
Q

what are the treatments for early stage disease in lung cancer

A

surgery
radiotherapy with curative intent

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140
Q

what are the treatments for locally advanced disease in lung cancer

A

surgery + adjuvant chemotherapy
radiotherapy + chemo +/- immunotherapy

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141
Q

what are the treatments for metastatic disease in lung cancer

A

with targetable mutation: tyrosine kinase inhibitor

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142
Q

when to use immunotherapy alone for lung cancer

A

no mutation
PDL-1 positive

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143
Q

when to use standard chemotherapy + immunotherapy for lung cancer

A

no mutation
PDL-1 negative

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144
Q

what abnormalities can we check in ECG (3)

A

conduction
structural
perfusion

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145
Q

what is atrial fibrillation

A

irregular and abnormally HR
can be fast or slow

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146
Q

what can be seen on atrial flutter ECG (2)

A

regular saw tooth pattern in baseline
atrial to ventricular beats at 2:1 or 3:1 ratio or higher
*saw tooth not always visible in all leads

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147
Q

what happens in ECG for 1st degree heart block (2)

A
  1. prolonged PR segment / interval caused by slower AV conuction
  2. regular rhythm 1:1 P: QRS
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148
Q

cause of 1st degree heart block

A

slower AV conduction
progressive disease of ageing

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149
Q

what happens in ECG for 2nd degree heart block type 1

A

progressive PR prolongation until missing QRS

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150
Q

characteristic of 2nd degree heart block type 1 heart beat

A

regularly irregular

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151
Q

cause of 2nd degree heart block type 1

A

diseased AV node

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152
Q

what is 2nd degree heart block type 2

A

regular P waves but only some are followed by ARS
no P-R prolongation, PR is normal

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153
Q

characteristic of 2nd degree heart block type 2 heart beat

A

regularly irregular

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154
Q

what happens in ECG for 3rd degree heart block

A

regular P waves and QRS but no relationship between P and R
can hv hidden P waves within bigger vectors

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155
Q

management for 3rd degree heartblock

A

back up pacemaker

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156
Q

cause of 3rd degree heartblock

A

non sinus rhythm

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157
Q

diseases with 3rd degree heart block

A

congenital heart disease, fibrosis, ischaemic heart disease, infections, autoimmune conditions

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158
Q

diseases with 2nd degree heart block type 1

A

drugs, MI, myocarditis

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159
Q

diseases with 2nd degree heart block type 2

A

MI, fibrosis, cardiac surgery, inflammatory conditions, hyperkalaemia

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160
Q

management of 1st degree heart block

A

stopping AV blocking drugs.

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161
Q

management of 2nd degree heart block type 1`

A

stopping AV blocking drugs.

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162
Q

management of 2nd degree heart block type 2

A

cardiac monitoring, temporary pacing, or pacemaker insertion

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163
Q

management of 3rd degree heart block

A

cardiac monitoring, pacing, or permanent pacemaker

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164
Q

what happens in ECG for ventricular tachycardia

A

hidden P waves (dissociated atrial rhythm)
regular and fast rate

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165
Q

what is the risk of ventricular tachycardia

A

deteriorate into fibrillation (cardiac arrest)

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166
Q

can we use defibrillators for ventricular tachycardia and why

A

yes, as it is shockable rhythm

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167
Q

what happens in ECG for ventricular fibrillation

A

fast and irregular heart rate

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168
Q

can we use defibrillators for ventricular fibrillation and why

A

yes, shockable rhyhtm

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169
Q

what happens in ECG for ST elevation

A

ST segment elevated above >2mm isoelectric line
regular rhythm and normal rate

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170
Q

causes of ST elevation

A

infarction (tissue death caused by hypoperfusion)

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171
Q

what happens in ECG for ST depression

A

ST segment depressed above >2mm isoelectric line
regular rhythm and normal rate

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172
Q

causes of ST depression

A

myocardial ischaemia (coronary insufficiency)

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173
Q

what is dilated cardiomyopathy (2)

A

dilated chambers
thin walls with reduced contractility

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174
Q

what will be shown on echocardiogram in dilated cardiomyopathy

A

dilated LV
reduced systolic function (ejection fraction_
hypokinesis

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175
Q

which part of heart does dilated cardiomyopathy typically affect

A

RV and LV

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176
Q

common causes of dilated cardiomyopathy

A

idiopathic
genetic
toxins
pregnancy (peripartum cardiomyopathy)
viral infections (myocarditiis)
tachycardia-related cardiomyopathy
thyroid disease
muscular dystrophies

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177
Q

how to treat dilated cardiomyopathy (5)

A

sodium glucose transporter reuptake inhibitor
diuretics
anticoagulation for AF
cardiac devices
medical HF therapy

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178
Q

examples of sodium glucose transporter reuptake inhibitor to treat dilated cardiomyopathy (2)

A

dapagliflozin
empagliflozin

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179
Q

examples of medical heart failure therapy for dilated cardiomyopathy

A

ACEi
beta blockers
mineralocorticoid receptor antagonsits

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180
Q

symptoms of right heart failure

A

peripheral oedema
eg leg swelling, raised jugular venous pressure

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181
Q

symptoms of left heart failure

A

pulmonary oedema

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182
Q

what is hypertrophic cardiomyopathy

A

genetic disorder

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183
Q

which part of heart hypertrophic in hypertrophic cardiomyopathy

A

LV hypertrophy

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184
Q

cause of hypertrophic cardiomyopathy (what kind of mutation)

A

missense mutation in 1 of at least 10 genes that encode proteins of the cardiac sarcomere

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185
Q

symptoms of hypertrophic cardiomyopathy

A

majority asymptomatic
some present with severe limiting symptoms of dyspnea, angina, syncope, or death

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186
Q

hypertrophic cardiomyopathy pathophsyiolgy

A
  1. genetic, storage disease, neuromuscular or mito disorders, malformation syndromes
  2. thickening and disarray of LV myocardium (can happen in any region of LV)
  3. involve interventricular septum
  4. obstruction of flow thru LV outflow tract
  5. disorganised myocytes disrupt signal conduction
  6. ventricular arrhythmias
  7. sudden cardiac death
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187
Q

therapy for obstructive hypertrophic cardiomyopathy (4)

A

beta blockers
surgical therapy
PTSMA
pacing therapy

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188
Q

beta blocker example for obstructive hypertrophic cardiomyopathy

A

verapamil
diltiazem
disopyramide
cibenzoline

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189
Q

medical therapy for non- obstructive hypertrophic cardiomyopathy with LVEF > 50% (2)

A

Beta blocker
diuretics (low dose)

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190
Q

what is obstructive hypertrophic cardiomyopathy

A

plaque builds up in coronary arteries
cause arteries narrowing

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191
Q

medical therapy for non- obstructive hypertrophic cardiomyopathy with LVEF < 50% (4)

A

Beta blocker
ACEi
Mineralocorticoid receptor antagonist

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192
Q

treatment for non- obstructive hypertrophic cardiomyopathy with therapy resistent

A

cardiac resynchronisation
ventricular assit devices
heart transplant

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193
Q

what is restrictive cardiomyopathy

A

presence of restrictive ventricular filling pattern

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194
Q

causes of restrictive cardiomyopathy

A

idiopathic
familial (troponin I mutations)
haemochromatosis
amyloidosis
sarcoidosis
Fabry’s disease

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195
Q

medical treatment for restrictive cardiomyopathy (4)

A

ACEi
angiotensin receptor ll blockers
diuretics
aldosterone inhibitors

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196
Q

what are management for immunosuppression for restrictive cardiomyopathy

A

steroids

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197
Q

non medical treatment for restrictive cardiomyopathy

A

pacemaker
cardiac transplantation

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198
Q

roles of vascular endothelial cells (2)

A

barrier function
leukocyte recruitment

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199
Q

roles of platelets (2)

A

thrombus generation
cytokines and growth factor release

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200
Q

monocyte-macrophages role (4)

A

foam cell formation
cytokine and growth factor release
major source of free radicals
metalloproteinases

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201
Q

roles of vascular smooth muscle cells (3)

A

migration and proliferation
collagen synthesis
remodelling and fibrous cap formation

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202
Q

role of T lymphocytes (4)

A

macrophage activation – CD4 Th1
macrophage de-activation CD4 Treg
VSMC death – CD8 CTL
B cell / Ab help – CD4 Th2

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203
Q

what is the main inflammatory cell in atherosclerosis

A

macrophages derived from monocytes

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204
Q

roles of inflammatory macrophage

A

adapted to kill microorganism

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205
Q

function of non inflammatory and resident macrophages

A

spleen – iron homeostasis
alveolar resident macrophages – surfactant lipid homeostasis
homeostatic functions at parenchymal

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206
Q

what are oxidised LDLs / modified LDLs

A

chemical and physical modifications of LDL by free radicals, enzymes, aggregation
families of highly inflammatory and toxic forms of LDL in vessel walls

207
Q

steps for modification of subendothelial trapped LDL

A
  1. LDLs leak thru endothelial barrier due to endothelial activation in areas of vortex
  2. LDL trapped by binding to sticky matrix carbohydrates in sub-endothelial layer and becomes susceptible to modification
  3. free radical attacj from activated macrophages (oxidation)
  4. LDL oxidatively modified by free radicals
  5. oxidified LDL phagocytosed by macrophages and stimulates chronic inflammation
    macrophages now known as foam cells
208
Q

what is Familial hyperlipidemia (FH)

A

autosomal genetic disease
failure to clear LDL from blood
elevated cholesterol

209
Q

which enzyme inhibitorknown for lowering plasma

A

HMG-CoA reductase inhibitors

210
Q

which gene degrades the number of LDLreceptors

211
Q

what are ABCA and ABCG

A

cholesterol export pumps
export selective to apolipoprotein A
removes cholesterol from arteries and return to liver

212
Q

what are macrophage scavenger receptor

A

on macrophages to function in endocytosis and degradation of modified (acetylated) LDLs

213
Q

what is CD204

A

macrophage scavenger receptor A

214
Q

what does macrophage scavenger receptor A do (3)

A

binds to oxidised LDL
binds to gram +ve bacteria eg Staphlococci and streptococci
binds tp dead cell

215
Q

what does macrophage scavenger receptor B do (3)

A

binds to oxidised LDL
binds to malaria parasites
binds to dead cell

216
Q

what is CD36

A

macrophage scavenger receptor B

217
Q

what kind of oxidative enzymes do macrophages have to modify native LDL (3)

A

NADPH Oxidase
Myeloperoxidase
generation of H2O2

218
Q

why do we need to generate free radicals to further oxidise lipoproteins

A

bleach further an damage inside of artery to cause plaque to fall apart

219
Q

how are foam cells formed

A

macrophages accumulate modified LDLs to become foam cells

220
Q

how are monocytes recruit in athersclerosis

A

plaque macrophages express inflammatory factors

221
Q

what inflammatory factors are there (2)

A

cytokines
chemokines

222
Q

what are cytokines roles in athersclerosis

A

protein immune hormones that activate endothelial cell adhesion molecules

223
Q

what are chemokines role in athersclerosis

A

small proteins chemoattractant to monocytes

224
Q

what is IL-1

225
Q

role of IL-1

A

triggers intracellular cholesterol crystals and NFkB
coordinate multiple process eg cell death, cell proliferation and elevated CRP

226
Q

is athersclerosis higher or lower in humans with anti-IL-1 antibodies

227
Q

what are monocyte chemotactic protein -1 (MCP-1)

228
Q

role of MCP-1

A

bind to monocyte G-protein coupled receptor CCR2

229
Q

is athersclerosis higher or lower in MCP-1 deficient or CCR2 deficient mice

230
Q

what do macrophages in plaques do (4)

A
  1. generate free radicals that further oxidise lipoproteins
  2. Phagocyte modified lipoproteins and become foam cells
    3a. express cytokine mediates to recruit monocytes
    3b. express chemo-attractant and growth factors for VSMC
    3c. Express proteinases to degrade tissue
  3. macrophage apoptosis
231
Q

in athersclerosis when macrophages release growth factors what is the result

A

recruit VSMC
stimulate them to migrate, survive, proliferate, deposit extracellular matrix

232
Q

role of platelet derived growth factor (3)

A

VSMC chemotaxis
VSMC survival
VSMC division (mitosis)

233
Q

role of transforming growth factor Beta

A

increase collage synthesis
matrix deposition
these make fibrous cap thicker so cells becomes less contractile to maintain BP

234
Q

role of metalloproteinases (MMPs)

A

activate each other by proteolysis
degrade collage and tissue

235
Q

what are the effects of plaque erosion or rupture

A

blood coagulation at site of rupture may lead to an occlusive thrombus and cause cessation of blood flow

236
Q

steps of macrophage apoptosis

A
  1. OxLDL derived metabolites are toxic (eg 7-keto cholesterol)
  2. macrophage foam cells have protective system that maintain survival in face of toxic lipid overloading
  3. when overwhelmed, macrophages die via apoptosis
  4. release macrophage tissue factors and toxic lipids into central death zone called lipid necrotic core
  5. thrombogenic and toxic material accumulates and walled off
  6. platelet rupture and meet blood
237
Q

what are macrophages’ functions in atherosclerosis pathophysiology (6)

A

secrete inflammatory cytokines and chemokines
phagocytose, process and export cholesteral to reverse cholesterol transport
secrete oxidants that damage cells and LDL
accumulate cholesterol and become sick and activated by cholesterol overload
secrete MMPs to degrade fibrous cap collagen
initiate death of VSMC

238
Q

what are characteristics of vulnerable and stable plaque in athersclerosis (4)

A

large soft eccentric lipid rich necrotic core
increased VSMC apoptosis
reduced VSMC and collage content
thin fibrous cap
infiltrate of activated macrophages expressing MMPs

239
Q

signs and symptoms of atherosclerosis

A

death of downstream tissues
loss of function of one side of body (major ischeamic stroke)
severe central crushing chest pain with fear, dizzy, nausea (MI)
angina
thrombogenic and toxic material accumulate, walled off and plaque rupture and meet blood

240
Q

what is nuclear factor kappa B (NFkB)

A

transcription factor
regulator of inflammation

241
Q

what is NFkB activated by (3)

A

scavenger receptor
toll like receptor
cytokine receptors (IL-1)

242
Q

roles of NFkB

A

bind and switch on numerous inflammatory genes (MMPs, IL-1, inducible nitric oxide synthase)

243
Q

what does NFkB act as

A

non-redundant network hub in inflammation

244
Q

what do NFkB do as a network

A

directs multiple genes (multiple different inflammatory stimuli including IL-1 and cholesterol crystals)
then coregulation of differnet inflammatory genes (eg IL-1)

245
Q

what are the kinds of cardiomyopathy (3)

A
  1. dilated cardiomyopathy and HF
  2. Hypertrophic cardiomyopathy (HCM)
  3. restrictive cardiomyopathy
246
Q

mechanism of haemostasis

A

vessel constriction
formation of unstable platelet plug
primary haemostasis
stabilisation of plug within fibrin
secondary hemostasis
fibrinolysis
vessel repair and dissolution of clot

247
Q

what is factor in indirect platelet adhesion

A

platelet bind to Glp1b on VWF

248
Q

what is factor in direct platelet adhesion

A

platelet bind toGlp1a

249
Q

after platelet adhesion, what is released (2)

A

ADP
thromboxane

250
Q

causes of thrombocytopenia

A

bone marrow failure (leukaemia, B12 deficiency)
accelerated clearance (immune ITP, DIC)
pooling and destruction in an enlarged spleen
hereditary absence of glycoproteins or storage granules
acquired (drugs)

251
Q

what is ITP (immune thrombocytopenia purpura)

A

not clot properly
immune system destroy blood clotting platelets

252
Q

what is glanzmannn’s thrombasthenia

A

absence of Gpllb/llla receptor on platelets

253
Q

how aspirin lead to reduce platelet aggregation

254
Q

mechanism of clopidogrel

A

antiplatelet medicine
blocks ADP receptor on platelets

255
Q

does thromboxane A stimulate or inhibit platelet aggregation

256
Q

funciton of VWF in haemostasis

A

bind to collagen and capture paltelets
stabilise factor Vlll

257
Q

does prostacyclin inhibit or stimulate platelet aggregation

258
Q

what are type 1 or 3 Von Willebrand disease

A

deficiency of VWF

259
Q

what is type 2 Von Willebrand disease

A

VWF with abnormal function

260
Q

what are 3 kinds of disorders of primary haemostasis

A
  1. platelets
  2. VWF
  3. vessel wall
261
Q

what are clinical features of disorders or primary haemostasis

A

bleeding
petechiae (bleed underneath skin)
ourpura (paltelet or vascular disorders)
severe VWD (haemophilia like bleeding)

262
Q

tests for disorders or primary haemostasis

A
  1. platelet count
  2. platelet morphology
  3. bleeding time
  4. assays of VWF
  5. clinical observation
    * coagulation screen is normal
263
Q

treatment for failure of production / function in abnormal haemostasis

A

prophylactic
therapeutic

264
Q

treatment for immune destruction abnormal haemostasis

A

immunosuppression
splenectomy for ITP

265
Q

additional haemostatic treatment examples

A

desmopressin (as AVP increase VWF and factor Vlll)
Tranexamic acid

266
Q

what is role of coagulation in secondary haemostasis

A

genereate thrombin lla

267
Q

role of thrombin lla

A

convert fibrinogen to firbin

268
Q

causes of disorders of coagulation factor production

A

hereditary (factor Vlll/lX) haemophilia A or B
acquired (liver disease anticoagulant drug)

269
Q

examples of anti coagulant drug

A

warfarin
direct oral anticoagulants (DOAC)

270
Q

disorders of coagulation causes

A

deficiency in production
dilution (blood transfusion)
increased consumption (DIC,)

271
Q

what is haemophilia

A

failure to generate fibrin to stabilise platelet plug

272
Q

examples of acquired coagulation disorders

A

liver failure (decreased production)
anticoagulant drugs
dilution

273
Q

which coagulation factor not synthesised in liver

A

VWF (in endothelial cell)
factor V (platelets)

274
Q

clinical features of coagulation disorders

A

bruising
bleeding frequently restars after stopped
delayed and prolonged bleed after trauma

275
Q

what are the clinical distinction between bleeding in platelet and coagulation defects

A

platelet/vascular: superficial bleeding into skin, mucosal membranes ; bleed immediate after injury
coagulation: bleed into deep tissues, muscles and joints ; delayed but severe bleeding after injury

276
Q

tests for coagulation disorders

A

PT
APTT
FBC (platelets)
coagulation factor assays

277
Q

which pathway does APTT test

278
Q

which pathway does PT test

279
Q

normal PT
prolonged APTT

A

haemophilia A/B
factor XI or XII deficiency

280
Q

prolonged PT
normal APTT

A

factor Vll deficiency

281
Q

prolonged PT
prolonged APTT

A

liver disease
anticoagulant drug (warfarin)
DIC
dilution

282
Q

warfarin mechanism

A

inhibit Vit K

283
Q

which clotting factors do Vit K affect

A

factors II, VII, IX and X and the anti-clotting proteins, proteins C and S

284
Q

replacement of missing coagulation factors

A

FFP (contain all coagulation factors)
cryoptecipitate (rich in fibrinogen, factor Vlll, VWF, factor Xlll)

285
Q

mechanism of tranexamixc acid

A

antifibrolytic
prevent excessive blood loss from major trauma

286
Q

when can we use tPA (tissue plasminogen activator)

A

stroke to increase fibrinolysis

287
Q

mechanism of heparin

A

anticoagulant

288
Q

what is virchow’s triad (3 factors predispose to thrombosis0

A

blood (venous thrombosis)
vessel wall (arterial thrombosis)
blood flow (both venous and arterial thrombosis)

289
Q

examples of anticoagulant proteins(fibrinolytic factors)

A

protein C
protein S
antithrombin

290
Q

what does factor C do in anticoagulant

A

inactive factor V
inactive factor VLLLa

291
Q

what does antithrombin do

A

act on factor lla (prothrmobin)

292
Q

does higher or lower blood flow incraese risk of thrombosis

293
Q

treatment of venous thrombosis

A

anticoagulant (heparin)
lower procoagulant factors (use warfarin, DOACs)

294
Q

mechanism of unfractionated heparin

A

anticoagulant
enhancement of antithrombin
(inactivate thrombin, factor X, factor IXa, XIa, XIIa)

295
Q

differnece between heparin and warfarin

A

heparin: inject IV
warfarin: oral

296
Q

mechanism of low molecular weight heparin (LWMWH)

A

contain pentasaccharide sequence to bind to antithrombin

297
Q

do we needa monitor if use LWMH

A

no cuz predictable

298
Q

action of warfarin

A

anticoagulant
Vit K antagonists (block recycling of Vit K)
inactive factor II, VII, IX, X, protein C and S

299
Q

how to reverse warfarin action on Vit K (2)

A
  1. Vit K administration (several hrs to work)
  2. infusion of coagulation factor (PCC – factor II, VII, IX, X/ FFP)
300
Q

side effects of warfarin

A

blled
skin necrosis (protein C deficiency)
purple toe syndrome
embryopathy

301
Q

what are the steps in coagulation (3)

A

initiation
propagation
fibrin formation

302
Q

factor IIa role in fibrin formation

A

convert fibrinogen to fibrin

303
Q

how to resistance to warfarin

A

lack patient compliance
diet, increase Vit K intake
reduce binding

304
Q

which has renal impairment, warfarin or DOACs

305
Q

which has faster onset, warfarin or DOACs

306
Q

which need monitoring, warfarin or DOACs

307
Q

what does endothelium control

A

blood vessels function and tissues
tissue hoemostasis and regenration

308
Q

what are organotypic properties

A

tissue specific

309
Q

which cells have organotypic properties

A

endothelial cells
microvasculature

310
Q

basic structure of blood vessels

A

a
Tunica adventitia
Tunica media
Tunica intimia

311
Q

what is vasa vasorum

A

tiny vessels that feed larger vessels

312
Q

structure of capillaries and venules

A

endothelium
mural cells (pericytes)
basement membrane

313
Q

what is used to examine transcriptional signature of individual cells

A

single cell RNA sequence
to study expression of genes at single cell level

314
Q

examples of tissue specific (organotypic) variations of microvasculature

A

fenestrated - kidney
non-fenestrated - lung, skin, muscle, BBB
discontinuous - liver

315
Q

which factor does endothelial cells produce

A

angiocrine factors

316
Q

what of endothelial cell does tissue specific microenvironment influence

317
Q

which type of cell is most abundant in heart and crosstalk with cardiomyocytes

A

endothelial cells

318
Q

when resting, which pathways are endothelium at

A

anti-inflammatory
anti-thrombotic
anti-proliferative

319
Q

when endothelium switched on to activated endothelium, what pathways are they on

A

pro-inflammatory
pro-thrombotic
pro-proliferative

320
Q

how small tumors receive oxygen and nutrients

A

diffusion from host vasculature

321
Q

how large tumors receive c=oxygen and nutrients

A

require new vessels
tumor cells secrete angiogenic factors to stimulate neovessel formation by endothelial cells

322
Q

what is angiogenic switch

A

tumor cells secretes angiogenic factors that stimulate neovessel formation by endothelial cells in adjacent vessels

323
Q

what is the most common hereditary bleeding disorder

A

VWF dysfunction

324
Q

what is VWF disorder characterised by

A

mucosal bleeding

325
Q

treatments for Von Willebrand disease

A

replacement therapy
(VWF, DDAVP)

326
Q

role of VWF in haemostasis

A
  1. mediates platelet adhesion to subendothelium and platelet aggregation
  2. stabilise circulating coagulation factor VIII
327
Q

role of VWF in angiogenesis

A

control angiogenesis byr egulating growth factor signaling (VEGFR2, Ang-2)

328
Q

what happens when there is lack of VWF to blood vessels formation

A

increase angiogenesis

329
Q

endothelial dysfunction in pathogenesis of atherosclerosis mechanism

A

1.leukocyte recruitment
2. permeability
3. shear stress
4. angiogenesis

330
Q

leukocytes adhesion cascade mechanism

A
  1. leukocytes interact with endothelium
  2. leukocytes roll , stop, spread and enter
331
Q

structure of capillary

A

endothelial cells surrounded by basement membrane and pericapillary cells (pericytes)

332
Q

differnece between capillary and post-capillary venule

A

structure similar but post-capillary venules have more pericytes

333
Q

what happens to leukocytes recruitment in athersclerosis

A

leukocytes adhere to activated endothelium of large arteries and get stuck in subendothelial space

334
Q

what happens to monocytes recruitment in atherosclerosis

A

monocyte migrate to subendothelial space, differentiate into macrophages and become foam cells

335
Q

are the flow patterns and hemodynamic forces same in vascular system

336
Q

in straight parts of arterial tree, what is the blood flow described as

337
Q

is the wall shear stress high or low in laminar flow and directional or indirectional

A

high
directional

338
Q

in branches and curvatures of arterial tree, what is the blood flow described as

A

turbulent/ disturbed with non uniform distribution

339
Q

is the wall shear stress high or low in disturbed flow and directional or indirectional

A

low wall shear stress
irregular distribution

340
Q

what does laminar blood flow promote (4)

A
  1. anti-thrombotic, anti-inflammatory
  2. endothelial survival
  3. inhibition of smooth muscle cells proliferation
  4. Nitric oxide production
341
Q

what does disturbed blood flow promote (4)

A

thrombosis, inflammation(leukocyte adhesion)
2. endothelial apoptosis
3. smooth muscle cell proliferation
4. loss of Nitric oxide production

342
Q

protective effects of nitric oxide on cardiovascular system (6)

A
  1. vasodilation
  2. reduce platelet activation
  3. inhibit monocyte adhesion
  4. reduce SMC proliferation in vessel wall
  5. reduce release of superoxide radicals
  6. reduce oxidation of LDL cholesterol
343
Q

what does angiogenesis promote

A

plaque growth

344
Q

what does therapeutic angiogenesis prevent

A

damage post-ischaemia

345
Q

how permeability contribute to early plaque formation

A

increased permeability to lipids increase early plaque formation

346
Q

symptoms of upper respiratory tract infection

A

cough
sneeze
runny or stuffy nose
sore throat
headache

347
Q

symptoms of lower respiratory tract infection

A

productive cough (phlegm)
muscle aches
wheezing
breathlessness
fever
fatigue

348
Q

pneumonia symptoms

A

chest apin
blue tinting of lips
severe fatigue
high fever

349
Q

risk factors of exacerbations of asthma pneumonia

A

respiratory infections

350
Q

what is the most common cause of hospitalisation in pneumonia asthma

A

exacerbations

351
Q

what are the common causative agents of respiratory infections for bacteria (4)

A

Streptococcus pneumoniae
Myxoplasma pneumoniae
haemophilus influenzae
mycobacterium tuberculosis

352
Q

what are the common causative agents of respiratory infections for virus (35)

A

influenza A or B virus
respiratory syncytial virus
human metapneumovirus
human rhinovirus
coronavirus

353
Q

mechanism of bronchitis

A

inflammation and swelling of bronchi

354
Q

mechanism of bronchiolitis

A

inflammation and swelling of bronchioles

355
Q

mechanism of pneumonia

A

inflammation and swelling of alveoli

356
Q

what is the grading potential for bacterial pneumonia outside hospital

A

CRB65
confusion
respiratory rate ( >30breaths/min)
blood pressure (<90 systolic and 60 diastolic)
65 yo

357
Q

what is the grading potential for bacterial pneumonia in hospital

A

CURB-65
confusion
urea (greater than 7mmol)
respiratory rate
BP
65yo

358
Q

what are the bacteria that cause community acquired pneumonia

A

Streptococcus pneumoniae
mycoplasma pneumoniae
Staphylococcus aureus
Chlamydia pneumoniae
Haemophilus Influenzae

359
Q

what are the bacteria that cause hospital acquired pneumonia

A

Staphylococcus aureus
Psuedomonas aeruginosa
E.coli

360
Q

what are the bacteria that cause ventilator associated pneumonia

A

Pseudomonas aeruginosa
Staphylococcus aureus
enterobacter

361
Q

bacteria that cause typical pneumonia

A

Streptococcus pneumoniae
Moraxella
Haemophilus influenzae
catarrhalis

362
Q

bacteria that cause atypical pneumonia

A

Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella pneumoniae

363
Q

what is typical pneumonia

A

most common
caused by most common forms of bacteria

364
Q

what is atypical pneumonia

A

less frequent
distinct bacterial species
slower onset of symptoms and milder

365
Q

what treatments are for bacteria pneumonia (2)

A

supportive therapy
antibiotics

366
Q

what are supportive therapy for bacterial pneumonia

A

oxygen
fluids
analgesia
saline
chest physiotherapy

367
Q

what are examples of antibiotics for bacterial pneumonia

A

penicillin eg amoxicillin
macrolides eg clarithromycin

368
Q

mechanism of amoxicillin

A

beta lactams to bind proteins in bacterial cell wall to prevent transpeptidation

369
Q

mechanism of clarithromycin

A

bind to bacterial ribosome prevent protein synthesis

370
Q

treatment for CURB65 score 0

A

amoxicillin (clarithromycin or doxycycline if penicillin allergic)

371
Q

treatment for CURB65 score 1-2

A

amoxycillin + clarithromycin

372
Q

treatment for CURB65 score 3-5

A

benzylpenicillin IV + clarithromicin PO

373
Q

what is opportunistic pathogen

A

a microbe that takes advantage of a change in conditions (often immuno-suppression)

374
Q

examples of oropharynx bacteria

A

haemophilus spp
Staphylococcus aureus
Streptococcus pneumoniae

375
Q

example of nose bacteria

A

staphylococcus aureus
strep pneumoniae
haemophilus spp

376
Q

what is pathobiont

A

a microbe that is usually commensal but found in the wrong environment that can cause pathology

377
Q

are the virus that cause respiratory infection pathobionts

378
Q

how viral infection cause inflammatory response

A

airway narrowing
fluid and mucus build up in airways and parenchyma
damage to gas exchange surfaces

379
Q

which virus has the most number of serotypes for common cold

A

rhinovirus
followed by coronavirus and influenza virus

380
Q

H1N1 influenza A target

A

haemogglutinin binds to alpha2,6 sialic acid

381
Q

H5N1avina flu target

A

haemogglutinin binds to alpha2,3 sialic acid

382
Q

rhinovirus target

A

ICAM-1 (major)
LDLR (minor)

383
Q

SARS-CoV-2 target

A

spike protein binds to ACE2

384
Q

risk factor of bronchiolitis in infants (2)

A

premature birth
congenital heart and lung disease

385
Q

what is leading cause of infant hospitalisation

A

Respiratory Syncytial Virus (RSV)

386
Q

how Respiratory Syncytial Virus (RSV)
affect infants

A

infect infants
nasal flaring
chest wall retractions
hypoxemia and cyanosis
croupy cough
expiratory wheezing
prolonged expiration
tachypnea

387
Q

what are the physical barriers of upper airway

A

hairs and cilia

388
Q

physical and chemical barriers of epithelial lumen

A

fluid lining lumen
mucociliary escalator
epithelial barrier

389
Q

immune fortification of host

A

innate immune responses
resident immune cell
recruited immune cell

390
Q

characteristics of respiratory epithelium (5)

A
  1. tight junctions
  2. mucous lining and cilial clearance
  3. antimicrobials
  4. pathogen recognition receptors
  5. interferon pathways to promote upregulation of anti-viral proteins and apoptosis
391
Q

which interferon is essential in curbing new viral infections

392
Q

examples of innate immunity cells (5)

A
  1. alveolar macrophages
  2. resident dendritic cells
  3. neutrophils
  4. natural killer cells
  5. monocytes
393
Q

function of CD8-T cells in adaptive immunity

A

provide antigen specific cytotoxic immunity and immunological memory

394
Q

function of B cells in adaptive immunity

A

B cells differentiate into antigen specific antibody secreting cells and memory B cells

395
Q

what are serotypes

A

pathogens which cannot be recognised by serum that recognise another pathogen

396
Q

which part of respiratory tract is enriched for IgA

A

upper
have high frequency of IgA-plasma cells

397
Q

which part of respiratory tract is enriched for IgG

A

lower
thin walled alveolar space allows transfer of plasma IgG into alveolar space

398
Q

what are problems with too much IgG

A

inflammation and damage inXS surfaces

399
Q

which virus has the most serotypes

A

rhinovirus

400
Q

which virus require long lasting antibody mediated immunity

A

rhinovirus

401
Q

which virus cannot be re-infected by same strain

A

influenza virus

402
Q

how does influenza virus avoid antibody mediated immunity

A

influenza strains drift and shift surface antigens

403
Q

which virus can have recurrent infection with the sam serotype or strain

A

Respiratory Syncytial Virus (RSV)

404
Q

which virus has limited mutation of surface antigens

A

Respiratory Syncytial Virus (RSV)

405
Q

why Respiratory Syncytial Virus (RSV)
can be re infected

A

natural antibodies wane rapidly allowing reinfection

406
Q

which virus has no prior exposure

A

SARS-CoV-2

407
Q

what are preventive / prophylactic treatment options for respiratory infection

A

vaccines (only work before or between infections)

408
Q

examples of vaccine

A

major surface antigen (spike protein)
viral vector
mRNA vaccine

409
Q

examples of anti-virals

A

remdesivir (broad spectrum antiviral) to block RNA dependent RNA polymerase activity
paxlovid (antiviral protease inhibitor)
casirivimab and imdevimab

410
Q

which virus is most common cause of asthma and COPD exacerbations

A

rhinovirus

411
Q

which pneumonia is high likelihood after viral infection

A

secondary bacterial pneumonia

412
Q

which bronchiolitis is associated with asthma development

A

viral bronchiolitis

413
Q

what are the 4 clinical parameters of murray score

A
  1. PaO2/FIO2 (on 100% oxygen)
  2. CXR
  3. Positive end expiratory pressure (PEEP)
  4. Compliance
414
Q

which clinical readings in child can use to confirm a diagnosis of asthma

A

exhaled nitric oxide (FeNO)

415
Q

what is intrinsic lung disease

A

alterations to lung parenchyma
interstitial lung disease
lung tissue becomes damaged and scarred

416
Q

what is extrinsic lung disease

A

compress lungs or limit expansion
pleural
chest wall
neurotransmitter (reduced ability of respiratory muscles to inflate/deflate lung)

417
Q

where is interstitial space

A

space between alveolar epithelium capillary endothelium

418
Q

what is alveolar type 1 epithelial cells for

A

gas exchange surface
thin cells

419
Q

what is alveolar type 2 epithelial cells for

A

surfactant tor educe surface tension, stem cell for repair
cell type regeneration (regenerate type 1)

420
Q

what are fibroblasts component in lung parenchyma

A

produce ECM (collage type 1 etc)

421
Q

alveolar macrophage function

A

phagocytose foreign material, surfactant

422
Q

what are different types of interstitial lung diseases (6)

A

idiopathic (IPF,DIP)
autoimmune (CTD associated)
eposure related (hypersensitivity pneumonitis)
cysts or airspace filling
sarcoidosis
others (eosinophilia pneumonia)

423
Q

what are some history of interstitial lung disease

A
  1. progressive breathelessness
  2. non-productive cough
  3. limited exercise tolerance
  4. occupational and exposure history
  5. meds, FHx
424
Q

what are some clinical examination of ILD

A

low oxygen sats
fine bilateral inspiratory crackles
digital clubbing
+/- features of connective tissue disease (skin, joints, muscles)

425
Q

what are blood tests test for in ILD

A

ANA
rheumatoid factor
anti-citrullinated peptide

426
Q

invetsigations in ILD

A

pulmonary function test
blood tests
6-min walk test
high resolution CT scan
bronchoscopy
surgical lung biopsy

427
Q

what is lung physiology in ILD

A

scarring makes lung stiff
reduce lung compliance
reduce lung volume
reduce FVC
reduce diffusing capacity of lung for carbon monoxide
reduce arterial PO2 esp with exercise

428
Q

how is FEV1/FVC ratio like in ILD

A

normal or increased

429
Q

how is FEV1/FVC ratio in obstructive lung disease

430
Q

why is high resolution CT (HRCT) good for ILD diagnosis

A

thin slices and high frequency reconstruction to give good resolution at level of secondary pulmonary lobule (which is the smallest functional lung unit on CT)

431
Q

what color is high density substance in CT

A

white
as bone absorb more x-rays

432
Q

what color is low density substance in CT

A

darker
air absorb few x-rays

433
Q

what CT feature in ILD

A

honeycomb cysts

434
Q

CT features in non-specific interstitial pneumonia

A

more inflammatory
ground glass type area

435
Q

what is implied in honeycomb cysts in CT

A

no gas transfer in these areas

436
Q

what are the general principles of ILD management early disease

A

pharmacological ( immunosuppressive drugs and antifibrotics)
vaccination ‘smoking cessation
education, trials
treat co-morbidities
pulmonary rehabilitation

437
Q

what are the general principles of ILD management late disease

A

supplemental oxygen
lung transplant
palliative care

438
Q

what is idiopathic pulmonary fibrosis

A

progressive
scarring lung disease
unknown cause

439
Q

name a serious event of IPF

A

acute exacerbations
contributes to 50% in hospital mortality

440
Q

does IPF have a good or poor prognosis

441
Q

what are the predisposing factors of IPF (3)

A

genetic susceptibility
environmental triggers
cellular ageing

442
Q

cellular ageing example that contribute to IPF

A

telomere attrition (shortening)
senescene

443
Q

mechanism of IPF

A

aktered microbiome
cause injury to Type 1 and 2 alveolar epithelial cells
fail to regenerate
trigger fibrotic reaction
recruit and activate fibroblasts
XS accumulation of ECM
remodel and honeycomb cyst formed
fibroblasts further proliferate
cause scarring

444
Q

what is spatial heterogeneity in IPF

A

area of normal right next to highly abnormal lung area

445
Q

what is temporal heterogeneity in IPF

A

very active areas of fibrosis next to very inactive or less active fibrosis

446
Q

do antifibrotics slow IPF progression or cure

A

slow disease porgresson

447
Q

example of tyrosine kinase inhibitor

A

nintedanib

448
Q

what is pirfenidone

A

inhibits TGF-β1-induced differentiation of human lung fibroblasts into myofibroblasts, thereby preventing excess collagen synthesis and extracellular matrix production.

449
Q

what are the drug targets for fibrotic pathway

A

alveolar space
epithelium
mesenchyme
endothelium
vascular space

450
Q

what is hypersensitivity pneumonitis (HP)

A

ILD caused by immune mediated response in susceptible and sensitised individuals to inhaled environmental antigens

451
Q

which parts of lungs do HP involve (2)

A

small airways
parenchyma

452
Q

what are the 2 types of HP

A

acute
chronic

453
Q

what is acute HP

A

intermittent
high level exposre
mre abrupt onset

454
Q

what symptoms are in acute HP

A

flu ike symptoms
4-12 hrs after exposure

455
Q

what is chronic HP

A

low level exposure
nonfibrotic / fibrotic

456
Q

what is non fibrotic chronic HP associated with

A

inflammatory

457
Q

what is fibrotic chronic HP associated with

A

higher mortality

458
Q

what are causes of HP

A

antigen exposure and processing by innate immune system
accumulation of lymphocytes and formation of granulomas

459
Q

what are the inflammatory response mediated by in HP

A

T-helper cells
antigen specific immunoglobulin IgG antibodies

460
Q

what are some diagnostic finding on auscultation of HP

A

inspiratory squeaks due to co-exisitng bronchiolitis and distal airway in HP are inflammed

461
Q

what are some diagnostic finding on blood tests of HP

A

specific circulating IgG Ab

462
Q

what are other diagnostic tests for HP

A

HRCT
bronchoalveolar lavage lymphocyte count

463
Q

treatment of HP

A

corticosteroids
immunosuppressants (MMF, azathioprine)
antifibrotic (Nintedanib)

464
Q

what is systemic sclerosis associated (SSc) ILD

A

autoimmune connective tissue

465
Q

characteristic of SSc

A

immune dysregulation ajd progressive fibrosis that affect skin
variable organ involvement

466
Q

who do SSc usually affect

A

young, middle aged women

467
Q

how many % of SSc develops into ILD

A

30-40%
most common death

468
Q

how are clinical features of SSc classified

A

based on skin involvement

469
Q

2 types of SSc

A
  1. limited cutaneous SSc (pulmonary hypertension more common)
  2. diffuse cutaneous SSc (ILD more common)
470
Q

what are the different features of SSc

A

sclerodactyly (skin tightening)
raynaud’s (reduced blood flow to fingers)
telengectasias (dilated or broken blood vessels located near the surface of the skin or mucous membranes)

471
Q

what are the autoantibodies associated with ILD

A

anti-centromere
anti-Scl-70

472
Q

pathogenesis of SSc-ILD (step 1-6)

A
  1. tissue injury
    2.vascular injury
    3.autoimmunity
  2. fibrosis
  3. inflammation
473
Q

tissue injury causes in SSc-ILD

A

1.genetic predisposition
2. gastro-oesophageal reflux
3.oxidative stress
4. environmental stimuli
5. organic solvents
6. virus, silica

474
Q

vascular injury causes in SSc-ILD

A
  1. endothelial cell injury
  2. tissue hypoxia
  3. ineffective angiogenesis
475
Q

autoimmunity causes in SSc-ILD

A

B cell differentiate to plasma cell to release auto antibodies and IL-6
IL-6 is the key in ILD

476
Q

fibrosis causes in SSc-ILD

A

IL_6 stimulate fibrocytes recruited and resident fibroblasts activated
myofibroblasts express aSMA and produce collagen
cause inflammation at last

477
Q

what is the most common pattern in SSc-ILD

A

non-specific interstitial pneumonia (NSIP)

478
Q

management of SSc-ILD

A

corticosteroid is controversial as risk of renal crisis if high dosages
immunosuppressives
antifibrotic (nintedanib)

479
Q

what is polychromatic macrocytes in terms of RBC

A

immature RBC

480
Q

what does reticulocyte count increased indicate

A

anaemia
RBC destruction before mature

481
Q

difference between haemolysis and haemolytic

A

haemolysis: increased destruction of RBC (reduced RBC survival)
haemolytic: RBC lifespan reduced

482
Q

why give folic acid in anaemia

A

increased requirement for erythropoiesis

483
Q

why do splenectomy in anaemia

A

increase RBC lifespan

484
Q

what is DAT test for (Direct antiglobulin test)

A

detects immunoglobulin and/or complement on the surface of red blood cells

485
Q

what is auto-immune haemolytic anaemia (AIHA)

A

immune system mistakes red blood cells as unwanted substance

486
Q

disorders of immune system associated with AIHA (2)

A

systemic autoimmune disease (SLE)
underlying lymphoid cancers (lymphoma)

487
Q

what are the bone marrow response to haemolysis

A

have reticulocytes

488
Q

what are Heinz bodies

A

a type of hemolytic anemia, which happens when your red blood cells break down faster than your body can replace them
indicate oxidant damage

489
Q

what is G6PD role

A

protect red blood cells from damage and premature destruction

490
Q

G6PD deficiency results

A

cause red cells vulnerable to oxidant damage
result in haemolysis

491
Q

what is haemolytic anaemia

A

shortened survival of red cells in circulation causing anaemia

492
Q

causes of inherited haemolytic anaemia

A

G6PD deficiency
abnormalites in cell membrane/ Hb or red cell enzymes

493
Q

causes of acquired haemolytic anaemia

A

extrinsic factors eg micro organism, chemicals, drugs, malaria

494
Q

what is extravascular haemolysis

A

defective red cells are removed by spleen

495
Q

what is intravascular haemolysis

A

acute damage to red cell

496
Q

in inherited haemolytic anaemia, if the site of defect is membrane what example of anaemia is that

A

hereditary spherocytosis

497
Q

in inherited haemolytic anaemia, if the site of defect is at haemoglobin what example of anaemia is that

A

sickle cell anaemia

498
Q

in inherited haemolytic anaemia, if the site of defect is at glycolytic pathway what example of anaemia is that

A

pyruvate kinase deficiency

499
Q

in inherited haemolytic anaemia, if the site of defect is at pentose shunt what example of anaemia is that

A

G6PD deficiency

500
Q

in acquired haemolytic anaemia, if the site of defect is membrane what example of anaemia is that

A

AIHA autoimmune haemolytic anaemia

501
Q

in acquired haemolytic anaemia, if the site of defect is at whole red cell mechanical what example of anaemia is that

A

microangiopathic haemolyic anaemia (MAHA)

502
Q

in acquired haemolytic anaemia, if the site of defect is at whole red cell microbiological what example of anaemia is that

503
Q

in acquired haemolytic anaemia, if the site of defect is at whole red cell oxidant what example of anaemia is that

A

drugs chemical

504
Q

what are investigations for blood in stool

A

faecal immunochemical test (FIT)

505
Q

what is ferritin

A

storage form of iron

506
Q

role of hepcidin

A

inhibit iron absorption

507
Q

what happens when reduce hepcidin

A

increase iron absorption and release storage iron

508
Q

what is microcytic anaemia usually associate with in terms of color

A

hypochromic

509
Q

what is macrocytic anaemia usually associate with in terms of color

A

normochromic

510
Q

2 examples of microcytic anaemia with defect in haem synthesis

A

iron deficiency
anaemia of chronic disease

511
Q

2 examples of microcytic anaemia with defect in globin synthesis

A

alpha and beta thalassaemia

512
Q

lack in what results in megaloblastic anaemia

A

vit B12 and folic acid

BRS Y2 (9 decks)

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