CardioResp Flashcards

1
Q

Preload measurement

A

End diastolic volume
End diastolic pressure
Right atrial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Afterload measurement

A

Diastolic bp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Heart sounds

A

S1: closure of mitral valve
S2: closure of aortic valve
S3(just after S2): congestive HF
S4(just before S1): hypertension etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alveolar cells

A
Type 1(95%): thin, gas exchange
Type 2(5%): secrete antiprotease and surfactant, replicate to replace type 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Function of nasal conchae

A

Warm and humidify air

Filter large particles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lung capacities

A
Tidal volume
Inspiratory capacity
Functional residual capacity
Vital capacity
Total lung capacity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Positive and negative pressure breathing

A

Negative is normal

Positive is CPAP or mechanical ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Shifts in HbO2 sat and PO2 graph

A

Right shift: high temp, CO2, 2,3DPG, acidosis
Left shift: low temp, CO2, 2,3DPG, alkalosis, HbF
Down shift: anaemia
Up shift: polycythaemia
Down and left: HbCO
Severe left shift: myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Endogenous regulation of heart

A

SA node controls pulse
Phase 0: upstroke from Ca influx
Phase 3: repolarisation from K efflux
Phase 4: pre potential from Na influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiac muscle action potential

A
Phase 0: Na influx(depolarisation)
Phase 1: K efflux(early repolarisation)
Phase 2: Ca influx(plateau)
Phase 3: K efflux(repolarisation)
Phase 4: RMP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Exogenous regulation of heart(brain)

A

Vasomotor centre(VMC) in medulla
Sympathetic/paraympathetic on SA node
M2 receptor(ACh)
Beta-1 receptor(NA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Exogenous regulation of heart(kidney)

A

BP detected by baroreceptors
Sympathetic->renin->AT2-> vasoconstriction and raise bp
AT2->aldosterone->Na reabsorption-> blood volume rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Exogenous regulation of heart(blood vessels)

A

Low filling/pressure->low baroreceptor firing->sympathetic activity
Vasoconstrictors: thromboxane A2, adrenaline
Vasodilators: NO, ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Control of lung function

A

4 nuclei in medulla
Dorsal respiratory group: inspiration
Ventral respiratory group: expiration and inhibits apneustic centre
Apneustic centre: stimulates DRG
Pneumotaxic centre: regulates depth and frequency, inspiratory off switch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Afferent lung receptors

A

Irritant: induces cough
Stretch: excessive inflation->DRG & VRG
J: detects oedema->breathing frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type of vessel with highest resistance

A

Arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Variation of perfusion and ventilation in lung

A

Highest at base, lowest at apex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Arteriole vasodilation

A

Active hyperaemia e.g. skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Arteriole vasoconstriction

A

Myogenic autoregulation e.g. GI arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is heart failure(causes, symptoms, tests, treatment)

A

Preserved(<50%) or reduced(<40%) ejection fraction
Causes: hypertension, cardiac damage, valve disease
Symptoms: exertional dyspnoea
Tests: elevated BNP and cardiomegaly
Treat with drugs that reduce heart exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Atrial arrhythmias

A
AF: disorganised electrical activity
WPW: tachycardia and abnormal electrical conductance
Symptoms: palpitations and chest pain
ECG: 
Absent p wave and irregular rhythm(AF)
QRS delta wave(WPW)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Conduction block

A

1: prolonged P-R interval
2: Mobitz 1(increasing) and 2, missing QRS
3: no relationship between P and QRS
Treatment: discontinue AV blocking drugs and implant pacemaker if severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Acute coronary syndrome types, cause, symptoms, biomarker and treatment

A

Angina, NSTEMI, STEMI
Caused by atherosclerosis

Angina: chest pain on exertion
NSTEMI: chest pain, sweating, nausea
STEMI: radiating chest pain, sweating, nausea

High troponin in NSTEMI & STEMI

Treat with vasodilators, coronary stent, CABG, anti platelets, pain relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

COPD comprises of

A

Emphysema: alveolar destruction
Chronic bronchitis: mucus hypersecretion
Small airway disease: small airway fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

COPD cells and mediators

A
Neutrophils secrete proteases (neutrophil elastase and MMP)
Macrophages
T lymphocytes
TNF alpha
IL8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Tetralogy of Fallot

A

Pulmonary stenosis
Right ventricle hypertrophy
Interventricular septal defect
Widening of aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Aortic stenosis causes

A

Rheumatic heart disease

Calcium build up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Aortic stenosis pathogenesis

A

Endocardial injury
Inflammation
Leaflet fibrosis and calcium deposition on valve
Low aortic leaflet mobility

High afterload->left ventricle hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Aortic stenosis presentation

A

Ejection systolic murmur
High LDL
Chest pain
Exertional dyspnoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Aortic stenosis management

A

Aortic valve replacement
Balloon aortic valvuloplasty
Antihypertensive
Statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Aortic regurgitation causes

A

Acute: infective endocarditis, trauma
Chronic: rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Aortic regurgitation pathogenesis

A

Acute:
Infective endocarditis->rupture of leaflets

Chronic:
Rheumatic fever->fibrotic changes-> thickening and retraction of leaflets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Aortic regurgitation presentation

A

Acute:
Tachycardia
Cyanosis
Pulmonary oedema

Chronic:
Wide pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Aortic regurgitation management

A

Treat underlying cause first

Acute: vasodilators and valve replacement/repair

Chronic asymptomatic: drugs if LV function normal

Chronic symptomatic: valve replacement and adjunct vasodilator therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Mitral stenosis causes

A

Rheumatic fever
SLE
Carcinoid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Mitral stenosis pathogenesis

A
Acute cause
Formation of multiple foci
Infiltrate endo and myocardium
Valve thickens, calcifies and contracts
High left atrial pressure
Pulmonary oedema&hypertension
Low left ventricle filling
Low cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Mitral stenosis presentation

A

Dyspnoea
Orthopnoea
Diastolic murmur
Hepatojugular reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Mitral stenosis management

A

Progressive asymptomatic: no therapy
Severe asymptomatic: adjuvant balloon valvotomy
Severe symptomatic: diuretic, valve repair/replacement, beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Mitral regurgitation causes

A
Acute: 
Infective endocarditis
Chronic:
Rheumatic heart disease
SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Mitral regurgitation pathogenesis

A
Infective endocarditis
Abscess formation
Rupture of chordae tendinae
Leaflet perforation
Eccentric hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Mitral regurgitation presentation

A
Dyspnoea
Pan systolic murmur
Fatigue
Orthopnoea
Chest pain
Atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Mitral regurgitation management

A

Acute:
Emergency surgery, diuretics, intra aortic balloon counterpulsation

Chronic asymptomatic: ACEi, beta blockers, surgery if EF<60%

Chronic symotomatic: surgery, intra aortic balloon counterpulsation if EF<30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Dilated cardiomyopathy type of dysfunction

A

Systolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Most common valve disease

A

Mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Dilated cardiomyopathy presentation

A
Dyspnoea
Displaced apex beat
Systolic murmur
Pulmonary congestion
Low cardiac output
High natriuretic peptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Dilated cardiomyopathy management

A

Fluid and Na restrict
Treat underlying cause
Antihypertensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hypertrohpic cardiomyopathy type of dysfunction

A

Thick left ventricular wall

Diastolic

48
Q

Hypertrophic cardiomyopathy presentation

A
S3 gallop
Syncope
Dizziness
Palpitations
Double carotid artery impulse
49
Q

Hypertrophic cardiomyopathy management

A

Check Hb, BNP, troponin levels

Beta blockers
Calcium channel blocker
Pacemaker
Disopyramide

50
Q

Restrictive cardiomyopathy type of dysfunction

A

Normal wall thickness but stiff muscle

Diastolic

51
Q

Restrictive cardiomyopathy presentation

A

Ventricular pressure rises quickly but ventricular volume rises slowly
Low filling
Low cardiac output

Hepatomegaly with pain
Peripheral oedema
Hepatojugular reflux

52
Q

Restrictive cardiomyopathy management

A

Amyloidosis check

Antihypertensive
Antiarrhythmic
Immunosuppression
Pacemaker
Cardiac transplant
53
Q

Broad QRS complex

A

LBBB or RBBB

54
Q

High take off on ST segment

A

Benign early repolarisation

55
Q

Tall T wave

A

Hyperkalaemia

56
Q

Inverted T wave

A

V1-3: RBBB
V4-6: LBBB
V5-6: left ventricular hypertrophy
Widespread: HCM

57
Q

Biphasic T wave

A

Hypokalaemia

58
Q

Asthma cells and mediators

A

Eosinophils
Mast cells
Type 2 lymphocytes
IL4,5,13

59
Q

Asthma allergic sensitisation test

A

Skin test: wheel and flare reaction

Blood test: specific IgE

60
Q

Asthma diagnosis

A

Spirometry FEV1/FVC<0.7
Bronchodilator reversibility >12%
Exhaled nitric oxide(FeNO)>35ppb(child) or 40ppb(adult)

61
Q

Asthma management

A
Inhaled corticosteroids
Leukotriene receptor antagonist
Beta 2 agonist
Anticholinergic therapy
Anti IgE antibody (mepolizumab)
Anti IL-5
Anti IL-5 receptor
62
Q

Most common and most deadly resp infections and most commonly infected age group

A

Common: rhinovirus
Deadly: tuberculosis
Age: 0-10

63
Q

Pneumonia grading

A

CURB65

Confusion
Urea >7mmol/L
Resp rate >30 breaths/min
BP <90systolic or <60diastolic
Age >65
64
Q

Bacterial pneumonia management

A

Supportive: oxygen, fluids, analgesia

Penicillin (amoxicillin)
Macrolides (clarithromycin)

65
Q

Viral bronchiolitis management

A

Supportive: fluids, oxygen, analgesia

Antiinflammatory: steroids, anti IL6, anti IL6R

Vaccine

Antivirals: remdesivir, paxlovid, casirivimab

66
Q

Types of resp failure

A

Type 1: hypoxaemic
Type 2: hypercapnic
Type 3: perioperative
Type 4: intubated and ventilated during shock

67
Q

ARDS symptoms

A

Dyspnoea
Tachypnoea
Cyanosis

68
Q

ARDS pathophysiology

A

Fluid accumulation in lungs not from heart failure
Alveolar injury and surfactant dysfunction
Inflammation: TNF, DAMPs, cytokines
Compliance is reduced

69
Q

ARDS diagnosis

A

Acute onset
Bilateral opacities on imaging
Respiratory failure not caused by heart failure
Decreased PaO2/FiO2 ratio

70
Q

ARDS treatment

A

Mechanical ventilation
Prone position
Fluid management(diuresis)
ECMO

71
Q

Lung cancer epidemiology

A

Age >75
M>F
Smoking history
Genetics

72
Q

Types of lung cancer

A

Squamous cell carcinoma: bronchial

Adenocarcinoma(common): peripheral

Large cell lung cancer

Small cell lung cancer: highly malignant

73
Q

Lung cancer oncogenes

A

BRAF
ALK
ROS1
EGFR

Tyrosine kinase inhibitor for systemic treatment

74
Q

Lung cancer symptoms

A
Weight loss
Haemoptysis
Cough
Breathlessness
Chest pain
75
Q

Lung cancer biopsies

A

Bronchoscopy for central airway

Endobronchial ultrasound and transbronchial needle aspiration of lymph nodes: stage mediastinum

CT guided biopsy: peripheral tumours

76
Q

Lung cancer management

A

Surgery: lobectomy and lymphadenectomy

Radical radiotherapy: SABR

Oncogene systemic

Immunotherapy systemic: block PDL1 but PDL1 must be >50%

Cytotoxic chemotherapy: platinum based regime, good with pembrolizumab(immuno)

Palliative and supportive care

77
Q

Primary haemostasis failure causes

A

Thrombocytopenia(leukaemia, B12 deficiency, ITP, DIC)

Impaired platelet function(aspirin, clopidogrel, NSAIDs)

Von willebrand factor disease(hereditary)

Vessel wall(ageing, vasculitis, scurvy)

78
Q

Primary haemostasis failure symptoms

A

Prolonged bleeding

Petechiae(blanches with pressure):thrombocytopenia

Purpura(doesnt blanch):platelet/vascular disorders

Easy bruising

79
Q

Primary haemostasis failure treatment

A

Replace missing factor/platelets
Stop drugs
Immunosuppression if autoimmune(ITP)
Splenectomy for ITP

80
Q

Secondary haemostasis failure causes

A

Low factor production(haemophilia A/B, drugs, liver disease)

Dilution(blood transfusion)

High consumption(DIC)

81
Q

Secondary haemostasis failure features

A

Haemarthrosis(haemophilia)

Superficial cuts dont bleed

Bleeding into deep tissue, muscle, joints

82
Q

Raised PT, normal APTT

A

Factor VII

83
Q

Normal PT, raised APTT

A

Factors VIII, IX, XI, XII

84
Q

Raised PT and APTT

A

Liver disease, anticoagulants, DIC, transfusion dilution

85
Q

Secondary haemostasis failure treatment

A

FFP: contains all factors

Cryoprecipitate: mainly fibrinogen

Factor concentrates: except factor V

86
Q

Haemophilia treatment

A

Gene therapy

Bispecific antibodies(A):mimics factor VIII

RNA silencing: targets antithrombin

Desmopressin: raises VWF and factor VIII

Tranexamic acid: antifibrinolytic

87
Q

Virchow’s triad thrombosis

A
Blood(venous)
Vessel wall(arterial)
Blood flow(mixed)
88
Q

Thrombophilia presentations

A

Thrombosis at young age
Spontaneous thrombosis
Thrombosis while on anticoagulants

89
Q

Thrombophilia causes

A

Low antithrombin, protein C, protein S
High factor VIII, II
Factor V Leiden
Myeloproliferative disorders

90
Q

Vessel wall and blood flow thrombosis

A

Vessel wall: inflammation

Blood flow: reduced flow increases risk(long haul flight)

91
Q

Heparin

A

Enhances antithrombin: inactivates IIa and Xa

Unfractionated: IV, short half life, greater effect
Low molecular weight: subcutaneous

92
Q

Warfarin

A

Blocks recycling of vit K
Many drug interactions

Side effects: bleeding, skin necrosis, purple toe syndrome, embryopathy

Warfarin montoring using INR

93
Q

DOAC

A
Rapid onset
No food effect
Few drug interactions
No monitoring
Some renal dependence
Reversible with antidotes
94
Q

Layers of vascular endothelium

A

Tunica adventitia
Tunica media
Tunica intima

95
Q

Atherosclerosis risk factors and causes

A
Hypercholesterolaemia
Diabetes mellitus
Smoking
Obesity
Hypertension
Sex hormone imbalance
Ageing
Oxidative stress
Infectious agents
Haemodynamic forces
96
Q

Nitric oxide in different types of flow

A

Laminar: high NO production
Turbulent: low NO production

97
Q

Nitric oxide functions in vessel wall

A
Reduce LDL oxidation
Vasodilation
Reduce platelet activation
Inhibit monocyte adhesion
Reduce superoxide release
98
Q

Where is LDL deposited in atherosclerosis

A

Subintimal space

Binds to matrix proteoglycans

99
Q

Role of macrophages in atherosclerosis

A

Inflammation from LDL deposition
LDL oxidised by free radicals
Macrophage phagocytosis
Foam cell formation, apoptosis after

100
Q

Receptors on macrophage(atherosclerosis)

A

LDL receptors undergo -ve feeback when LDL in cell is high

Scavenger receptors have no feedback so high influx of OxLDL

101
Q

Atherosclerosis enzymes invloved

A

NADPH oxidase(O2-)

Myeloperoxidase(bleach)

Metalloproteinase(MMP): degrades collagen, causing bleeding

102
Q

Atherosclerosis cytokines and chemokines, chemoattractant and growth factor

A

IL-1

Monocyte chemotactic protein(MCP-1)

Platelet derived growth factor(PDGF)
TGF beta

103
Q

Transcription factor in atherosclerosis activated by __ and activates __

A

Nuclear factor kappa B gets activated by scavenger receptors and IL-1

Activates MMP and IL-1 secretion

104
Q

Macrocytic anemia causes

A

B12 deficiency: diet, gastrectomy, pernicious anaemia, Crohn’s

Folate deficiency: diet, proximal jejunum(coeliac disease), high demand

Drugs that inhibit DNA synthesis

Liver disease/ethanol toxicity

105
Q

Haemolytic anaemia causes

A

Membrane integrity: hereditary spherocytosis, autoimmune haemolytic anaemia

Structure and function: sickle cell anaemia

Cellular metabolism: G6PD deficiency

106
Q

Blood test for autoimmune haemolytic anaemia

A

Direct antiglobulin test (DAT)

107
Q

Causes of microcytic anaemia and which chain is affected

A

Iron deficiency(haem)
ACD(haem)
Thalassaemia(globin)

108
Q

Iron deficiency causes

A

Blood loss: menorrhagia, GI

Insufficient intake: vegetarian, coeliac, H. Pylori gastritis

Increased requirement: pregnancy

109
Q

Iron deficiency blood test results

A

Low ferritin
High transferrin
Normal ESR

110
Q

ACD blood test results

A

High ferritin
Low transferrin
High ESR

111
Q

ACD pathology

A

Rheumatoid arthritis, autoimmune disorder, malignancy or TB/HIV
IL-1, TNFa, IL-6
Low erythropoietin, high hepcidin

112
Q

Hb electrophoresis thalassaemia

A

HbA2 is raised: beta thalassaemia

113
Q

MI treatment

A

Anticoagulants
Primary percutaneous coronary intervention
Alternative: thrombolysis or CABG

114
Q

Mild VWD treatment

A

Desmopressin: increases VWF and FVIII

115
Q

Murray score ARDS

A

PaO2/FiO2(on 100% O2)
CXR
PEEP(positive end expiratory pressure)
Compliance(ml/cmH2O)

3 or more->ECMO