Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Give three cardinal signs of anaphylaxis

A

Skin rash
Wheeze and inspiratory stridor
Hypotension

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

List the ABC signs of anaphylaxis

A

Airway:
* Voice hoarseness
* Stridor
Breathing:
* Rapid breathing
* Wheeze
* Fatigue
* Cyanosis
Circulation:
* Pale clammy
* Hypotension
* Faintness
* Confusion
* Reduced consciousness

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

Give the pathophysiology of anaphylaxis

A

IgE-mediated reaction
On first exposure, IgE antibodies are formed specific to the antigen presented.
IgE antibodies attach to high-affinity Fc receptors on basophils and mast cells.
On subsequent exposure, binding of antigen to the IgE antibodies leads to bridging and triggers the degranulation of mast cells.

Cause release of:
Histamine
Prostaglandin D2
Leukotrienes
Platelet-activating factor
Tryptase
Nitric oxide
Eosinophil and neutrophil chemotactic factors

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

Give the effects of adrenaline on alpha-1, beta-1, and beta-2 receptors

A

Alpha-1 receptors - peripheral vasoconstriction, which reduces hypotension and mucosal oedema.

Beta-1 receptors - increase the rate and force of cardiac contractions and reduce hypotension.

Beta-2 receptors - reducing inflammatory mediator release from mast cells and basophils and causing bronchodilation.

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

Define the four types of hypersensitivity

A

Type 1 IgE-mediated hypersensitivity
* IgE is bound to mast cells via Fc portion. When an allergen binds to these antibodies, cross linking of IgE induces degranulation

Type 2 IgG-mediated cytotoxic hypersensitivity
* Cells are destroyed by bound antibody, either by activation of complement or by Tc cell with Fc receptor for the antibody

Type 3 Immune complex-mediated hypersensitivity
* Antigen-antibody complexes are deposited in tissues, causing activation of complement, which attracts neurtrophils to the site

Type 4 Cell-mediated hypersensitivity
* Th1 cells release cytokines, which activate macrophages and cytotoxic T cells and can cause macrophage accumulation at the site

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

List the variables in QRISK

A

Demographic information
Age
Gender
Ethnicity
Postcode

Clinical information (13)
Angina or heart attack in 1st degree relative < 60 years age
Smoking status
Diabetic status
Rheumatoid arthritis
Systemic lupus erythematosus
Chronic kidney disease (stage 3, 4, 5)
Atrial fibrillation
Migraine
Erectile dysfunction
Severe mental illness
Under treatment for hypertension
Atypical antipsychotic medication
Regular steroid tablets

Others
Cholesterol/HDL ratio
Systolic blood pressure
BMI = Weight / Height squared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give the management plan for a QRISK < 10%

A

Lifestyle modifications
Advise smokers to stop and non-smokers to avoid passive smoking.
Advise weight loss if the person is overweight or obese.
Advise the person to adopt a diet that helps to reduce CVD risk, including:
* Eating unsalted nuts, seeds, legumes, fish, fruit, vegetables and fibre
* Reducing sugars, saturated fats, and salt
* Increase mono-unsaturated fats
Advise the person to keep alcohol consumption within the recommended limits - no more than 14 units per week spread over 3 days or more
Advise the person to be physically active and to avoid prolonged sedentary behaviour, including:
* At least 75 minutes per week of vigorous intensity aerobic activity
* At least 150 minutes per week of moderate intensity aerobic activity

Review relevant co-morbidities

Advice that a further risk assessment should be considered in 5 years.

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

Give the management plan for a QRISK > 10%

A

Lifestyle modifications
If lifestyle modification is ineffective or inappropriate, offer Atorvastatin 20 mg daily

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

List the risk factors for CVD

A

Non-modifiable
Age
Male sex
Family history
Ethnicity (increased risk in South Asian or sub-Saharan African, reduced risk in South American or Chinese)

Modifiable
Smoking.
Low HDL cholesterol and high non-HDL cholesterol.
Sedentary lifestyle.
Unhealthy diet.
Alcohol intake above recommended levels.
Overweight and obesity.

Comorbidities
Hypertension.
Diabetes mellitus (and pre-diabetes/metabolic syndrome).
Chronic kidney disease.
Dyslipidemia (familial and non-familial).
Atrial fibrillation.
Rheumatoid arthritis, systemic lupus erythematosus, and other systemic inflammatory disorders.
Influenza.
Serious mental health problems (schizophrenia, post-traumatic stress disorder).
Periodontitis.

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

Define typical, atypical, and non-anginal chest pain

A

Typical angina - 3 out of 3 following features of chest pain
Atypical angina - 2 out of 3 following features of chest pain
Non-anginal chest pain - 1 out of 3 following features of chest pain

Features of chest pain:
Heavy, tight, gripping central or retrosternal pain that may spread to jaw and arms
Pain occurs with exercise/ emotional stress
Pain eases rapidly with rest/GTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List the severity classification criteria of stable angina

A

Class I = Angina with strenuous activity. No angina during ordinary activity
Class II = Angina during ordinary activity
Class III = Angina during low level activity
Class IV = Angina at rest/ any level of exercise

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

Define unstable angina

A

Acute coronary syndrome
Angina of recent onset <24 hrs

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

Define Prinzmetal’s angina

A

Angina at rest due to coronary vessel spasms
More frequent in women

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

Define Microvascular angina

A

Exercise induced angina
Coronary artery normal during angiography

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

Give the pathophysiology of atherosclerosis

A
  1. Endothelial dysfunction triggered by smoking, hypertension or hyperglycaemia.
  2. Pro-inflammatory, pro-oxidant, proliferative changes in the endothelium.
  3. Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL).
  4. Macrophages phagocytose oxidised low-density lipoprotein.
  5. Smooth muscle proliferation and migration from the tunica media into the intima.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the acute and chronic presentations of atherosclerosis

A

Acute:
Stroke
TIA
Thoracic aortic rupture
Thoracic aortic dissection
Abdominal aortic occlusion (rare)
Renal artery occlusion (rare)
Acute mesenteric ischaemia
Acute coronary syndrome
Acute peripheral arterial occlusion

Chronic:
Recurrent TIAs
Vascular dementia
Worsening renal function
Renovascular hypertension
Chronic mesenteric ischaemia
Abdominal angina
Stable angina
Abdominal Aortic Aneurysm
Chronic limb ischaemia
Intermittent claudication

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

List the differential diagnosis for chest pain

A

Cardiac causes:
Acute coronary syndrome
Stable angina
Thoracic aorta dissection
- Sudden tearing chest pain radiating to the back
Pericarditis / cardiac tamponade
- Sharp constant sternal pain, relieved by sitting forward
Acute congestive heart failure
Arrhythmias
- Chest pain with palpitations

Pulmonary causes:
Pulmonary embolism
- Acute onset breathlessness, pleuritic chest pain, cough, haemoptysis, syncope
Pneumothorax / tension pneumothorax
- Sudden onset chest pain, breathlessness, tachycardia, pallor
Community acquired pneumonia
- Cough, sputum, wheeze, dyspnoea, pleuritic chest pain
Asthma
- Wheeze, breathlessness, cough
Lung / lobar collapse
- Localised chest pain, breathlessness, cough
Lung cancer
- Chest / shoulder pain, haemoptysis, dyspnoea, weight loss, anorexia, hoarseness, cough
Pleural effusion
- Localised chest pain, progressive breathlessness

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

List the risk factors for angina

A

Hyperlipidaemia
Diabetes mellitus
Smoking
Age
Family Hx.
Obesity
Hypertension

Environmental factors for angina
Heavy meals
Cold weather
Emotional stress
Exercise

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

Name the first line investigations for angina

A

12-lead resting ECG
Haemoglobin
Lipid profile
Fasting blood glucose / HbA1c

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

List the ECG changes that may indicate ischaemia or previous myocardial infarction

A

ST depression (ischemia)
Pathological Q waves (prior infarction)
Left bundle branch block
T-wave abnormalities (T-wave flattening / elevation / inversion)

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

List the management options for stable angina

A

Symptom relief:
Sublingual glyceryl trinitrate (GTN)

Regular medications
1. beta-blockers or calcium channel blockers
2. if intolerance/contraindicated:
- long acting nitrates (isosorbide mononitrate)
- ivabradine
- ranolazine
- nicorandil
if symptomatic switch or both
3. plus 2 other anti-anginals
4. revascularisation by PCI or CABG

Drug treatment for secondary prevention
Low dose aspirin 75mg
If stroke / peripheral arterial disease: continue clopidogrel
ACEi for people with stable angina and diabetes mellitus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When should nitrates not be used in

A

Acute MI with low filling pressure, acute circulatory failure (shock, vascular collapse), or very low blood pressure.
Hypertrophic obstructive cardiomyopathy, constrictive pericarditis, cardiac tamponade, low cardiac filling pressures, or aortic/mitral valve stenosis.
Diseases associated with a raised intracranial pressure (for example following a head trauma, including cerebral haemorrhage).
Severe anaemia.
Closed-angle glaucoma.
Severe hypotension, or hypovolaemia

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

List the anti-anginal medications

A

Vasodilators
* Isosorbide mononitrate
* Glyceryl trinitrate
Beta-blockers
* Bisoprolol
Calcium-channel blockers
* Verapamil, diltiazem, amlodipine
Ivabradine
Nicorandil
Ranolazine
Aspirin

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

When should bisoprolol be used cautiously

A

COPD
AV conduction block
Acute heart failure

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

List the side effects of bisoprolol

A

Fatigue
Peripheral vasoconstriction (cold peripheries)
Erectile dysfunction
Bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

When are verapamil and diltiazem contraindicated

A

Severe bradycardia
LV failure with pulmonary congestion
2/3 degree AV block

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

List the side effects of Verapamil, Diltiazem, Amlodipine

A

Verapamil: constipation
Diltiazem: ankle oedema
Amlodipine: ankle oedema, reflex tachycardia

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

List the side effects of Ivabradine

A

Bradycardia
Phosphenes

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

When is Ivabradine contraindicated

A

Sick sinus syndrome
AV block

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

List the side effects of Nicorandil

A

Headaches
Flushing
Oral ulceration

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

List the side effects of Ranolazine

A

Constipation
Dizziness
Lengthened QT

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

When should acute coronary syndrome be suspected

A

Any patient with acute chest pain which includes pain in arms, back, jaw that
* Lasts longer than 15 minutes
* Is associated with nausea and vomiting, marked sweating, breathlessness
* Is either new in onset or occurs as sudden worsening of known stable angina

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

List the causes of acute coronary syndrome

A

atherosclerosis
stress-induced (Tako-Tsubo) cardiomyopathy
coronary vasospasm without plaque rupture
coronary dissection due to connective tissue defects
drug induced (amphetamine, cocaine)
thoracic aorta dissection

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

List the 6 types of MI

A

1 - MI spontaneous with ischaemia. due to primary coronary event
2 - MI secondary to ischaemia, due to increased demand and reduced supply
3 - MI in sudden cardiac death
4a - MI in PCI
4b - MI in stent thrombosis
5 - MI in CABG

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

Give the early management of STEMI

A

300 mg loading dose aspirin as soon as possible and continue indefinitely unless contraindicated
Immediately assess eligibility for reperfusion therapy. Otherwise medical management.

Reperfusion therapy:
Angiography with follow-on primary PCI
* Offer if presenting in 12 hours of symptoms and PCI can be delivered in 120 mins
* Consider if presenting more 12 hours after symptoms and continuing myocardial ischaemia or cardiogenic shock
* Consider radial in preference to femoral access

Drug therapy for primary PCI:
* Offer prasugrel with aspirin if not already taking oral anticoagulant
* Offer clopidogrel with aspirin if taking an oral anticoagulant
* Offer unfractionated heparin with bailout GPI for radial access
* Consider bivalirudin with bailout GPI if femoral access needed

Fibrinolysis
* Offer if presenting in 12 hours of symptoms and PCI not possible in 120 mins

Drug therapy for fibrinolysis:
* Give an antithrombin (heparin) at the same time
* Offer ticagrelor with aspirin unless high bleeding risk
* Clopidogrel with aspirin, or aspirin alone for high bleeding risk

Medical management
* Offer ticagrelor with aspirin unless high bleeding risk
* Clopidogrel with aspirin, or aspirin alone for high bleeding risk

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

Give the early management of NSTEMI/Unstable Angina

A

Initial antiplatelet therapy - 300 mg loading dose aspirin as soon as possible and continue indefinitely unless contraindicated
Initial antithrombin therapy - fondaparinux unless high bleeding risk or immediate angiography
Use GRACE to predict 6-month mortality and risk of cardiovascular events:
Low risk (predicted 6-month mortality ≤ 3%)
* Consider conservative management without angiography
* Offer ticagrelor with aspirin unless high bleeding risk
* Clopidogrel with aspirin, or aspirin alone for high bleeding risk

Intermediate or higher risk (predicted 6-month mortality > 3%)
* Offer immediate angiography if clinical conditions are unstable.
* Otherwise, consider angiography (with follow-on PCI if indicated) within 72 hours if no contraindications such as comorbidity or active bleeding
* Offer prasugrel with aspirin if not already taking oral anticoagulant
* Offer clopidogrel with aspirin if taking an oral anticoagulant
* Offer systemic unfractionated heparin in catheter laboratory if having PCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

List the variables involved in GRACE risk score

A

Age
Heart rate/pulse
Systolic BP
Creatinine
Cardiac arrest at admission YES/NO
ST segment deviation on ECG YES/NO
Abnormal cardiac enzymes
Killip class (signs/symptoms)
* I - No congestive heart failure
* II - Presence of S3 gallop or bibasilar rales or both
* III - Pulmonary oedema
* IV - Cardiogenic shock

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

List the complications of MI

A

Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler’s syndrome
Embolism
Recurrence, regurgitation

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

List the causes of pericarditis

A

Idiopathic (most common)

Viral
Coxsackie virus
HIV
EBV
CMV
Mumps
Herpes

Bacterial
TB
meningococcal
staphylococcal
streptococcal
pneumococcal
mycoplasmosis
borreliosis
chlamydia
h.influenzae

Fungal
candidiasis
histoplasmosis
coccidioidomycosis

Post myocardial injury syndrome
myocardial infarction (Post-MI early, Dressler’s syndrome late)
surgery
radiation

Myxoedematous pericarditis
Chylopericardium
Uraemic pericarditis

Malignancy
primary malignancy of heart
mesothelioma
metastatic pericarditis
Breast / lung carcinoma
Lymphoma
Leukaemia
Melanoma

Autoimmune
rheumatic fever
SLE
RA
scleroderma

Drug induced
procainamide
hydralazine
doxorubicin
isoniazid
cyclophosphamide

Familial idiopathic pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

List the presentations of Dressler’s syndrome

A

Fever
Pleuritic pain
Pericardial effusion
Raised ESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Give the management of Dressler’s syndrome

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the pathophysiology of Dressler’s syndrome

A

autoimmune reaction against antigenic proteins formed as the myocardium recovers

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

When does Dressler’s syndrome occur

A

Tends to occur around 2-6 weeks following a MI.

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

List three complications of pericarditis

A

Chronic recurrent pericarditis
Cardiac tamponade
Constrictive pericarditis

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

Give the natural history of acute pericarditis

A

<4-6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

List the presentations of acute pericarditis

A

Pleuritic chest pain that is exacerbated by movement, relieved by sitting forward
Pericardial friction rub
Pericardial effusion

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

List the ECG features in acute pericarditis

A

Saddle shaped ST elevation
PR depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Define Recurrent pericarditis

A

Recurrence after an initial episode of acute pericarditis with an intervening symptom-free interval of ≥4 to 6 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Define Incessant pericarditis

A

Signs and symptoms lasting >4 to 6 weeks but <3 months without remission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Define Chronic pericarditis

A

Signs and symptoms persisting for >3 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What can constrictive pericarditis be caused by

A

TB
hemopericardium
rheumatic heart disease
bacterial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

List the investigations considered in pericarditis

A

ECG
* upwards concave ST-segment elevation globally with PR depressions in most leads
* J-point depression and PR elevation in leads aVR and V1
Serum troponin - Elevation reflects myocardial involvement
Pericardiocentesis - Urgent in cardiac tamponade
CRP - Elevated
Serum urea and electrolytes - Elevated levels of urea suggest a uraemic cause
FBC - Leukocytosis in acute or infectious aetiology
LFT - Liver congestion may be present if the patient is developing cardiac tamponade.
CXR - Normal / Increased cardiothoracic ratio if large pericardial effusion is present (> 300mL)
Transthoracic echocardiography
* pericardial effusion
* absence of left ventricular wall motion abnormalities
* thickened and/or bright appearance of pericardium if actively inflamed
* evidence of respiratory variation in ventricular filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Give the management for acute pericarditis

A

70~90% self limiting
NSAIDS (aspirin / ibuprofen) + PPI + Colchicine
Exercise restriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

List the high risk groups that may require inpatient management of pericarditis

A

Fever > 38C
Subacute onset
Large effusion
Cardiac tamponade
Unresponsive to therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

List the clinical features of pericardial effusion

A

Soft distant heart sound
Obscured apex beat
Pericardial friction rub due to pericarditis early on, then quieter as fluid accumulates - best heard over the left sternal border with the patient leaning forwards at end-expiration
Pulsus paradoxus - decrease in systolic blood pressure of >12 mmHg during inspiration
Ewart’s sign - dull percussion below L scapula angle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

List the ECG changes in pericardial effusion

A

Sinus tachycardia.
Low QRS voltage.
Electrical alternans.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Name the first line investigation for pericardial effusion

A

Transthoracic echocardiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Give the CXR feature of pericardial effusion

A

water-bottle-shaped cardiac silhouette with distinct pericardial fat stripe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

List the clinical features of cardiac tamponade

A

Tachycardia
Tachypnoea
Hypotension
Elevated jugular venous pressure
Distended neck veins
Kussmaul’s sign (a rise in venous pressure with inspiration)
Pulsus paradoxus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Give the Beck’s triad of cardiac tamponade

A

Hypotension
Distant heart sounds
Elevated jugular venous pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

List ECG changes in cardiac tamponade

A

low QRS voltages
electrical alternans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

List the management approaches in cardiac tamponade

A

Pericardiocentesis under echocardiographic guidance
Surgery drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What population groups do infective endocarditis most commonly affect?

A

Elderly
Young IVDU
Young congenital heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

List the aetiology for infective endocarditis

A

Dental procedures/disease - viridian groups streptococcus (s. mutans, s. milleri, s. oralis, s. sanguis)
Native prosthetic valve endocarditis
* early theatre/ICU acquired (staph. aureus, staph. epidermidis)
* late community acquired (staph. aureus, viridian group strep)
IVDU
Prolonged IV catheter dwelling
Prolonged hospital stay (enterococcus faecalis)
Underlying GU disease
Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

List the common causative micro-organisms for infective endocarditis

A

Viridans group streptococci (s. mutans, s. milleri, s. oralis, s. sanguis)
Staphylococcus aureus
Enterococci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

List the diagnostic criteria for infective endocarditis

A

Modified Duke Criteria
Major
Consistent positive culture for typical microorganisms of IE
Echocardiography
* wall motion abnormalities
* abscess
New prosthetic valve dehiscence / valvular regurgitation

Minor
Predisposition
* IVDU
* predisposing heart disease
Vascular phenomena
* Janeway lesions
* intracranial haemorrhage
* conjunctival haemorrhage
* arterial emboli
* septic pulmonary infarction
* mycotic aneurysm
Immunological phenomena
* Osler’s nodes
* Roth spots
* Glomerulonephritis
* Rheumatic fever
Microbiological evidence
Fever > 38

Definite IE =
2 major
1 major + 3 minor
0 major + 5 minor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

List the clinical features of infective endocarditis

A

General
* Malaise
* Clubbing
Skin
* Janeway lesions
* Osler nodes
* Splinter haemorrhage
* Petechiae
Neurological
* Mycotic abscess
* Cerebral emboli
Eyes
* Roth spot
* Conjunctival haemorrhage
Splenomegaly
Renal - Haematuria
Cardiac
* Murmur
* Cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Give the first line investigation for infective endocarditis

A

TTE Echocardiography:
* abscess
* vegetation
* valvular dysfunction
* Assess ventricular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What may be seen on ECG in aortic root abscess

A

PR prolongation / heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What may been seen on CXR in infective endocarditis

A

pulmonary oedema in L side disease
pulmonary emboli/abscess in R side disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What may been seen on FBC in infective endocarditis

A

Reduced Hgb
Elevated CRP, ESR, WCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

List the management for infective endocarditis

A

Suspected staph. IE (IVDU / Recent IV device / cardiac surgery)
* Vancomycin + gentamicin
Staph. IE
* Vancomycin / benzylpenicillin / flucloxacillin + gentamicin
Clinical IE not suspected Staph.
* Penicillin + gentamicin
Strep. IE
* IV benzylpenicillin + gentamicin
Enterococcal IE
* IV amoxicillin + gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Give two types of bradycardia

A

Sinus bradycardia
AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

List the intrinsic and extrinsic causes for sinus bradycardia

A

Extrinsic causes
Hypothermia
Hypothyroidism
Cholestatic jaundice
Increased ICP
Drugs
* Beta-blockers
* Digitalis
Neurally mediated syndromes (syncope / presyncope)
* POTS
* Vasovagal attack
* Carotid sinus syndrome

Intrinsic causes
Post-MI ischaemia / infarction of the sinus node
Sick sinus syndrome
* Idiopathic
* IHD
* Myocarditis
* Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Define types of heart blocks

A

1st degree AV block
Prolonged PR interval longer than 0.2 seconds
Every atrial depolarisation followed by ventricular depolarisation

2nd degree AV block
* Mobitz I: progressive PR prolongation until a P wave fails to conduct - Blockage in AVN
* Mobitz II: regular PR, intermittently failed to conduct - Blockage in infra-nodal level eg. His-Purkinje
* Fixed ratio: every 2/3 P waves conduct

3rd degree AV block
All atrial activity failed to conduct to ventricles
Life maintained by spontaneous escape rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

List causes of 3rd degree AV block

A

Congenital
* Structural heart disease eg. transposition of great vessels
* Autoimmune
Idiopathic fibrosis
* Lev’s disease (progressive distal His-purkinje fibrosis)
* Lengrene’s disease (proximal His-purkinje fibrosis)
Ischaemic heart disease
Non-ischaemic heart disease
* idiopathic cardiomyopathy
* calcific aortic stenosis
* infiltrations (amyloidosis, sarcoidosis, neoplasm)
Cardiac surgery
* aortic valve replacement
* CABG
* VSD repair
Iatrogenic eg. radio frequency AV ablation
Drug induced
* b-blockers
* amiodarone
* digoxin
* non-dihydropyridine CCB
Infections
* endocarditis
* Chaga’s disease (Trypanosoma cruzi)
* Lyme disease
Autoimmune eg. SLE, RA
NMD eg. DMD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

When does escape rhythms occur?

A

when supraventricular impulse arriving at AVN/ventricles less than intrinsic rate of ectopic pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

List the causes for broad complex escape rhythm

A

Lev’s
Lengrene’s
IHD
Myocarditis
Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Give the ECG characteristics of right bundle branch block

A

MARROW
Tall late R in V1
Deep S in I, V6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Give the ECG characteristics of left bundle branch block

A

WILLIAM
Tall late R in I, V6
Deep S in V1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

List the causes for right bundle branch block

A

Pulmonary embolism
Pulmonary stenosis
Pulmonary HTN
MI
Fallot’s tetralogy
Congenital cardiac disorders
Conductive tissue fibrosis
Chaga’s disease (Trypanosoma cruzi)
Isolated congenital anomaly - 5% healthy population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

List the causes for left bundle branch block

A

(Extensive LV disease)
Aortic stenosis
MI
HTN
Severe coronary disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

List the four classes of anti-arrhythmics

A

Class I Na+ channel blockers
Ia (moderate) - procainamide, quinidine
Ib (weak) - phenytoin, lidocaine
Ic (strong) - propafenone, flecainide

Class II beta-blockers
Propanolol
Metoprolol

Class III K+ blockers
Amiodarone
Sotalol

Class IV Ca+ blockers
Verapamil
Diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

List three characteristics of POTS

A

Exaggerated heart rate: increase >30 bpm, or an absolute increase to 120 bpm within 10 minutes of standing or head-up tilt

Symptoms of cerebral hypoperfusion: light-headedness, blurred vision, cognitive difficulties, generalised weakness in response to postural change

In the absence of orthostatic hypotension and cardiac causes of sinus tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Explain the pathophysiology of AV nodal reentrant tachycardia

A

There are two pathways within the AV node:
The slow pathway: a slowly-conducting pathway with a short refractory period.
The fast pathway: a rapidly-conducting pathway with a long refractory period.

Mechanism of re-entry in “slow-fast” AVNRT:
1. A premature atrial contraction (PAC) arrives while the fast pathway is still refractory, and is directed down the slow pathway
2. The ERP in the fast pathway ends, and the PAC impulse travels retrogradely up the fast pathway
3. The impulse continually cycles around the two pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

List the ECG features in AVNRT

A

Regular tachycardia ~140-280 bpm
Narrow QRS complexes (<120ms)
P waves invisible or immediately before / after QRS (due to spontaneous A and V activation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

List the ECG features in AVRT

A

Pre-excitation
* Short PR interval

Orthodromic AVRT
* Normal QRS duration
* Retrograde P wave after QRS

Antidromic AVRT
* Wide QRS with delta wave
* P wave rarely seen
* If P wave visible, it is retrograde and occurs just before QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

List the ECG features in Wolff-Parkinson-White syndrome

A

Shortened PR interval < 0.12 s
Delta wave
QRS prolongation > 0.12 s
Discordant ST and T changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Give the acute and chronic management for AVNRT and AVRT

A

Acute
Hemodynamically unstable (hypotension / pulmonary oedema) - cardioversion
Hemodynamically stable
* vagal manoeuvres eg. carotid massage
* valsava manoeuvres
* facial immersion in cold water
If physical unsuccessful - IV adenosine

Long term:
Radio-frequency ablation of accessory pathway
Class Ic antiarrhythmic - flecainide, propafenone
Beta-blockers
Class III antiarrhythmic - sotalol, dofetilide, azimilide
Verapamil, diltiazem
Multichannel blocker - amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

List the side effects of IV adenosine

A

bronchospasm
flushing
chest pain
sense of impending doom
heaviness of limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

List the side effects of amiodarone

A

Long QT syndrome
Polymorphic ventricular tachycardia
Interstitial pneumonitis
Hyper / hypothyroidism
Abnormal liver biochemistry
Sun sensitivity
Slate grey discoloration
Corneal deposition
Optic neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

List three most common causes for atrial fibrillation

A

Hypertension
Coronary artery disease
Myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Define paroxysmal, persistent, and permanent AF

A

Paroxysmal AF - episodes > 30 seconds but < 7 days (often < 48 hours) that are self-terminating and recurrent.

Persistent AF - episodes > 7 days (spontaneous termination unlikely after this time) or < 7 days but requiring pharmacological or electrical cardioversion.

Permanent AF - AF that:
* Fails to terminate using cardioversion
* Is terminated but relapses within 24 hours
* Longstanding AF (usually > 1 year) in which cardioversion has not been indicated or attempted (accepted permanent AF).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

List the causes of AF

A

Cardiac causes
Congestive heart failure.
Rheumatic valvular disease.
Atrial / ventricular hypertrophy.
Wolff–Parkinson–White syndrome.
Sick sinus syndrome.
Congenital heart disease.
Inflammatory / infiltrative disease (pericarditis, amyloidosis, myocarditis).

Non-cardiac causes
Pulmonary embolism
Thyrotoxicosis
Diabetes mellitus
Acute infection
Autonomic neural dysfunction
Electrolyte depletion
Hypokalemia
Hyponatremia
Cancer
Primary lung cancer involving the pleura and pericardium
Breast cancer and malignant melanoma metastasising to the pericardium

Dietary and lifestyle factors
Excessive caffeine intake.
Alcohol abuse
Obesity
Smoking
Medication exposure
Thyroxine
Bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

List the complications of AF

A

Stroke and thromboembolism
Heart failure
Uncontrolled AF
* Tachycardia-induced cardiomyopathy
* Critical cardiac ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

List the clinical features of AF

A

Breathlessness.
Palpitations.
Chest discomfort.
Syncope or dizziness.
Reduced exercise tolerance, malaise/listlessness, decrease in mentation, polyuria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

List the differential diagnoses of an irregular pulse

A

Atrial flutter
Atrial extrasystoles
Ventricular ectopic beats
Sinus tachycardia
Supraventricular tachycardias
* atrial tachycardia
* atrioventricular nodal re-entry tachycardia
* Wolff-Parkinson-White syndrome
Multifocal atrial tachycardia (severe pulmonary disease)
Sinus rhythm with premature atrial or ventricular contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

List the ECG features of AF

A

Irregularly irregular rhythm
No P wave
Fine oscillations at baseline - f wave
Ventricular rate 160-180
Rapid irregular QRS rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

List the acute management of AF

A

Treat provocation factor eg. chest infection, thyrotoxicosis, alcohol intoxication
Cardioversion
* direct DC shock
* flecainide, propafenone
* IV antiarrhythmic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Give the first line rate control treatment in AF

A

beta blockers OR rate-limiting CCB (diltiazem / verapamil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

When should an anticoagulation be offered in AF?

A

CHA2DS2VASc score of 2 or above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

List the anticoagulation offered in AF.

A

Factor Xa inhibitor:
* Apixaban
* Edoxaban
* Rivaroxaban
Factor IIa (Thrombin) inhibitor:
* Dabigatran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

List the variables in CHA2DS2VASc score

A

Congestive heart failure (1)
Hypertension (1)
Age > 75 (2)
Diabetes Mellitus
Stroke/TIA (2)
Vascular disease (1)
* prior myocardial infarction
* peripheral arterial disease
* aortic plaque
Age 65~74 (1)
Sex = female (1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

List the complications of sustained ventricular tachycardia

A

Syncope / presyncope
Hypotension
Cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Give the ECG feature in ventricular tachycardia

A

Rapid broad ventricular rhythm > 0.14 s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Give the management of ventricular tachycardia

A

Hemodynamically unstable - DC cardioversion
Hemodynamically stable
* IV beta-blocker
* Class I / amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Define torsades de pointes

A

A form of polymorphic ventricular tachycardia occurring the context of QT prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

List the causes of long QT syndrome

A

Congenital
Electrolyte abnormalities:
* Hypokalaemia
* Hypomagnesaemia
* Hypocalcaemia

Drug causes
Antiarrhythmic
* Class Ia: quinidine, disopyramide
* Class Ic: propafenone, flecainide
* Class III: sotalol, amiodarone
Tricyclic antidepressant
Phenothiazine
Antipsychotics
* Chlorpromazine
* Haloperidol
* Droperidol
* Quetiapine
* Olanzapine
* Amisulpride
* Thioridazine
Quinolones
Macrolides
* Erythromycin
* Clarithromycin
Chloroquine
Hydroxychloroquine
Quinine
Methadone
Poisons - inorganic phosphate insecticides

Other causes
Bradycardia
Acute MI
Mitral valve prolapse
Diabetes
Prolonged fasting
CNS disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

List the clinical features of long QT syndrome

A

Syncope
Palpitations
Ventricular fibrillation
Sudden death
Polymorphic ventricular tachycardia - Torsades de Pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

List the managements in long QT syndrome

A

Correct electrolyte disturbances
Stop causative drugs
Maintain HR with AV pacing
IV isoprenaline
Magnesium sulphate given over 10-15 mins for acquired long QT

111
Q

Give the ECG feature in ventricular fibrillation

A

shapeless rapid oscillations

112
Q

List presentations in ventricular fibrillation

A

pulseless
unconscious
respiration cessation

113
Q

List the chest auscultation areas

A

Aortic area - R sternum, 2nd ICS
Pulmonary area - L sternum, 2nd ICS
Erb’s point - L sternum, 3rd ICS
Tricuspid area - L sternum, 4th ICS
Mitral area - L midclavicular line, 5th ICS

114
Q

When may the S4 heart sound be present?

A

(Blood forced into a stiff / hypertrophic ventricle)

Aortic stenosis
Hypertrophic cardiomyopathy
Heart failure

115
Q

Give the normal and symptomatic mitral valve area

A

Normal mitral valve area: 4~6 cm2
Symptomatic when area <2 cm2

116
Q

List the causes of mitral stenosis

A

Rheumatic heart disease (most common) -following group A beta-haemolytic strep (S. pyogenes) infection
Congenital mitral stenosis
Lutembarcher’s syndrome (Combination of acquired mitral stenosis, ASD)
Mitral annular calcification
Metastasis

117
Q

Give the pathophysiology in mitral stenosis

A

LA pressure increases in order to maintain CO, leads to LA hypertrophy
Increased pressure in pulmonary vein, artery and RH
Increased pulmonary capillary pressure causes pulmonary oedema
Pulmonary HTN causes
* RH hypertrophy, dilation, failure
* Eventually tricuspid regurgitation

118
Q

List the clinical symptoms in mitral stenosis

A

Dyspnoea (increased pLA, vascular congestion, P oedema) / Orthopnoea / Paroxysmal nocturnal dyspnoea
Peripheral oedema (P HTN, RH failure)
Haemoptysis
Large LA predisposes to:
* Atrial fibrillation (palpitations)
* Systemic emboli

119
Q

List the signs in mitral stenosis

A

Mitral facies
Small volume regular pulse in early stenosis
Atrial fibrillation
Jugular venous distention - RH failure
Tapping impulse parasternally on L side

120
Q

List the auscultatory findings in mitral stenosis

A

Mid-diastolic rumbling murmur
Opening snap
Load S1 if valve is pliable (doesn’t occur in calcific M stenosis)
Tapping apex beat
Pulmonary HTN
* Right parasternal heave
* Loud pulmonary component of S2

121
Q

Give the gold standard investigation in mitral stenosis

A

TTE

122
Q

List the management options for mitral stenosis

A

Diuretics - Reduce LA pressure, relieve mild symptoms
* Furosemide
* Bumtanide
Balloon valvotomy

123
Q

List the causes of mitral regurgitation

A

Common
Rheumatic Heart Disease
Infective endocarditis
Ischaemic heart disease
Myxomatous disease

Diseases of myocardium - DCM, HCM
Rheumatic autoimmune disease eg. SLE
Collagen diseases - Marfan’s, EDS
Drugs
* DPA agonists
* Centrally acting appetite suppressants

124
Q

Give the pathophysiology of mitral regurgitation

A

LV hypertrophy (50%)
LA dilation

125
Q

List the clinical features in mitral regurgitation

A

Dyspnea and orthopnea
Fatigue and lethargy (reduced CO)
Congestive cardiac failure (late RH failure)
Cardiac cachexia
Subacute IE, thromboembolism

126
Q

List the auscultation findings in mitral regurgitation

A

Pansystolic murmur (regurgitation during systole)
Mid-systolic click
Laterally displaced apex beat (apex radiates to axilla)
Systolic thrill
Soft S1 (incomplete apposition of M valve)
Prominent S3 (blood rush to LV during early diastole)

127
Q

Give the normal and symptomatic aortic valve area

A

Normal aortic valve area = 3~4 cm2
Symptomatic when ¼ normal area

128
Q

List the causes for aortic stenosis

A

Calcific aortic valvular disease (most common)
Bicuspid aortic valve
Rheumatic fever
Chronic Kidney Disease
Paget’s disease of the bone
Radiation
SLE

129
Q

What is bicuspid aortic valve associated with?

A

aortic root dilation
aortic coarctation
aortic dissection

130
Q

Give the pathophysiology of aortic stenosis

A
  1. obstructed LV emptying
  2. increased pLV, LV hypertrophy
  3. relative ischaemia, angina
  4. arrhythmia
  5. LV failure
131
Q

List the symptoms of aortic stenosis

A

Triad of: (SAD - Syncope, Angina, Dyspnoea)
Fatigue

132
Q

List the signs in aortic stenosis

A

Carotid pulse - pulsus tardus et parvus (slow and weak pulse)
Narrow pulse pressure
Apical heave
Thrills in aortic region
Reduced or absent S2 over aortic area
Radiation of murmur to carotid artery

133
Q

List the auscultatory findings in aortic stenosis

A

Crescendo decrescendo systolic ejection murmur
Soft S2 (immobile aortic valve)
Systolic ejection click (valve immobile and calcified)
Prominent S4

134
Q

List the causes in aortic regurgitation

A

Bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis

135
Q

Give the pathophysiology in aortic regurgitation

A
  1. blood reflux from aorta to LV during diastole
  2. increased volume of blood pumped in aorta to maintain CO,
  3. LV dilation and hypertrophy, increased O2 demand
  4. decreased coronary perfusion due to diastolic runoff during diastole
  5. eventually cardiac ischaemia
136
Q

List the presentations in aortic regurgitation

A

Aangina pectoris
Dyspnoea (exertional)
Displaced apex beat

137
Q

List the auscultation findings in aortic regurgitation

A

Diastolic blowing murmur at L sternal border (Austin Flint murmur)
Large volume pulse
Collapsing pulse
Wide pulse pressure
Prominent carotid pulsations (Corrigan’s sign)
Displaced apex beat

138
Q

Give the classification of heart failure

A

HF with reduced ejection fraction (HFrEF): LVEF ≤40%
HF with mildly reduced EF (HFmrEF): LVEF 41% ~ 49%
HF with preserved EF (HFpEF): LVEF ≥50%

139
Q

List the four most common causes of heart failure

A

Coronary artery disease
Hypertension
Valvular heart disease
Myocarditis

140
Q

List the causes for chronic heart failure

A

Myocardial disease
Coronary artery disease (most common).
Hypertension.
Cardiomyopathies:
* Familial.
* Infective.
* Autoimmune
* Toxins
* Pregnancy.
* Infiltrative (sarcoidosis, amyloidosis, haemochromatosis, connective tissue disease).

Valvular heart diseases

Pericardial disease:
Constrictive pericarditis.
Pericardial effusion

Congenital heart disease.

Arrhythmias

High output states
Anaemia.
Thyrotoxicosis.
Phaeochromocytoma.
Septicaemia.
Liver failure.
Arteriovenous shunts.
Paget’s disease.
Thiamine (vitamin B1) deficiency.

Volume overload
End-stage chronic kidney disease.
Nephrotic syndrome.
Obesity.

Drugs including:
Alcohol.
Cocaine.
NSAIDs, beta-blockers, and CCBs (may worsen pre-existing heart failure).

141
Q

List the complications of chronic heart disease

A

Arrhythmias
* Atrial fibrillation
* Ventricular arrhythmias
Depression
Cachexia
Anaemia
Chronic kidney disease
Acute kidney injury
Sexual dysfunction
Sudden cardiac death

142
Q

List the typical symptoms in chronic heart disease

A

Breathlessness
Peripheral oedema
Fatigue, decreased exercise tolerance
Lightheadedness, history of syncope

143
Q

List the risk factors in chronic heart disease

A

Coronary artery disease
Hypertension
Atrial fibrillation
Diabetes mellitus
Drugs, alcohol
Family history of:
* heart failure
* sudden cardiac death under the age of 40 years

144
Q

List the signs in chronic heart failure

A

Tachycardia
Elevated JVP
Cardiomegaly
Laterally displaced apex beat, S3, S4
Tachypnoea, pleural effusion, basal crepitations
Peripheral oedema, ascites
Tender hepatomegaly

145
Q

Give the first line investigation in chronic heart failure

A

NT-pro-BNP / BNP levels - Elevated

146
Q

List CXR findings in chronic heart failure

A

Cardiomegaly (increased cardiothoracic ratio)
Pulmonary congestion
Pulmonary vascular congestion (vascular redistribution, Kerley B lines)

147
Q

List the treatment algorithm in chronic heart failure

A

Symptomatic treatment: loop diuretics
1. First line: ACEi + beta-blockers
2. If ACEi intolerant: ARB
3. If ACEi and ARB intolerant: hydralazine + nitrate
4. Consider:
Digoxin
Ivabradine

148
Q

List the drugs that should be avoided in HFrEF

A

Non-dihydropyridine calcium-channel blockers - Diltiazem, Verapamil
Class Ic antiarrhythmics - Propafenone, Flecainide
Thiazolidinediones - Pioglitazone
Dipeptidyl peptidase-4 (DPP-4) inhibitors - alogliptin, linagliptin, saxagliptin, sitagliptin
NSAIDs

149
Q

List the causes of secondary hypertension

A

Vascular:
Renal artery stenosis
Coarctation of aorta
Pre-eclampsia

Renal:
Chronic kidney disease
Chronic pyelonephritis
Diabetic nephropathy
Glomerulonephritis
Nephrotic syndrome
Polycystic kidney disease
Obstructive uropathy
Renal cell carcinoma

Endocrine:
Pheochromocytoma
Primary hyperaldosteronism
Cushing’s syndrome
Acromegaly
Hyperthyroidism
Hypothyroidism
Hyperparathyroidism

Drugs:
Alcohol
Ciclosporin.
Cocaine, amphetamine, and other substances of abuse.
Combined oral contraceptive.
Corticosteroids.
Erythropoietin.
Leflunomide.
Liquorice — present in some herbal medicines.
NSAIDs
Oestrogens (hormone replacement therapy)
ADHD stimulants
* methylphenidate, atomoxetine, dexamfetamine, lisdexamfetamine.
Sympathomimetics
Venlafaxine

Others
Pregnancy
Connective tissue disorders
* Scleroderma
* Systemic lupus erythematosus
* Polyarteritis nodosa
Retroperitoneal fibrosis
Obstructive sleep apnoea

150
Q

List the hypertension staging system

A

Stage 1
Clinical 140/90-159/99
ABPM 135/85-149/94

Stage 2
Clinical 160/100-180/120
ABPM 150/95

Stage 3
Clinical 180/120 mmHg or higher

151
Q

Define malignant hypertension

A

Severe increase in blood pressure to 180/120 mmHg or higher with signs of retinal haemorrhage and/or papilloedema

152
Q

List the risk factors for hypertension

A

Increasing age
Gender
* Women <65 years tend to have a lower blood pressure than men.
* Between 65–74 years women tend to have a higher blood pressure
Ethnicity - black African / Caribbean more likely
Genetics
Social deprivation
Co-existing diabetes / kidney disease
Lifestyle
* Smoking
* Excessive alcohol consumption
* Excess dietary salt
* Unhealthy diet
* Obesity
* Lack of physical activity
Anxiety and emotional stress

153
Q

List the complications for hypertension

A

Heart failure.
Coronary artery disease.
Stroke.
Chronic kidney disease.
Peripheral arterial disease.
Vascular dementia.

154
Q

List the fundoscopy findings in hypertensive retinopathy

A

Arteriolar narrowing
Arteriolar venous nipping (constriction of veins at crossing points)
‘Cotton wool spots’ on the retina (due to ischaemic changes)
Flame haemorrhages or papilloedema

155
Q

When should secondary hypertension be suspected

A

Young (<40 years)
Rapid onset
Sudden change in blood pressure when previously well controlled on a particular therapy
Resistant hypertension

156
Q

When should same-day specialist referral be made in hypertension?

A

A clinic blood pressure of 180/120 mmHg and higher with
* Signs of retinal haemorrhage and/or papilloedema (accelerated hypertension)
* Life-threatening symptoms (new onset confusion, chest pain, signs of heart failure, acute kidney injury)

Suspected pheochromocytoma
* labile or postural hypotension, headache, palpitations, pallor, abdominal pain, diaphoresis

157
Q

List the medical treatment for hypertension

A

Step 1 treatment
ACEi / ARB first line in
* Age < 55 and not of black African or Caribbean origin.
* T2DM
CCB first line in
* Age > 55, no T2DM
* Of black African or Caribbean origin, no T2DM
* If CCB untolerated - offer indapamide (thiazide-like diuretic)
If there is evidence of heart failure - indapamide (thiazide-like diuretic)

Step 2 treatment
If not controlled with ACEi/ARB
* CCB
* Indapamide (thiazide-like diuretic)
If not controlled with CCB
* ACEi/ARB
* Indapamide (thiazide-like diuretic)

Step 3 treatment
Combination of
* ACEi/ARB
* CCB
* Indapamide (thiazide-like diuretic)

Step 4 treatment
If blood potassium level 4.5 mmol/L or less - low-dose spironolactone
If blood potassium level > 4.5 mmol/L - alpha-blocker / beta-blocker

158
Q

List the contraindications for ACEi

A

Angio-oedema
Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women

159
Q

List the adverse effects for ACEi

A

Reduced ACE:
Hyperkalaemia
Renal impairment
Hypotension

Increased Kinin (ACE inactivates bradykinin)
Cough
Angio-oedema
Anaphylactoid reaction

160
Q

List the contraindications for ARB

A

Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women

161
Q

List the adverse effects for ARB

A

Renal impairment
Hyperkalaemia
Angio-oedema
Dizziness

162
Q

List the risk factors for peripheral arterial disease

A

Smoking
Diabetes mellitus
Advanced age
Hypertension
Hypercholesterolaemia
Atherosclerotic disease
Chronic kidney disease
High serum homocysteine

163
Q

List the Fontaine stages of peripheral arterial disease

A

Stage I: asymptomatic
Stage IIa: mild claudication
Stage IIb: moderate to severe claudication
Stage III: ischemic rest pain
Stage IV: ulceration or gangrene

164
Q

Give the first line investigation and findings in peripheral arterial disease

A

Ankle-brachial index
* < 0.5 severe arterial disease
* 0.5 ~ 0.8 presence of arterial / mixed / venous disease
* 0.8 ~ 1.3 no evidence of significant arterial disease
* > 1.3 maybe arterial calcification

165
Q

List the 6Ps of acute limb ischaemia

A

Pain
Paralysis
Paraesthesias
Pulselessness
Pallor
Perishingly cold

166
Q

List the causes of acute limb ischaemia

A

Thrombotic
* Chronic atherosclerotic stenosis
* Hypercoagulation
* Prosthetic / venous grafts de novo
Emboli
* Cardiac thrombus
* Cardiac arrhythmias

167
Q

List the interventions for acute limb ischaemia

A

Endovascular
* Percutaneous catheter-directed thrombolytic therapy.
* Percutaneous mechanical thrombus extraction.
Surgical interventions
* Surgical thromboembolectomy.
* Endarterectomy.
* Bypass surgery.
* Amputation if the limb is unsalvageable.

168
Q

List the complications form acute limb ischaemia

A

Compartment syndrome - reperfusion of ischaemic muscles can cause oedema and increased compartmental pressure
Reperfusion injury - products of cell death are released when blood flow to the ischaemic limb is restored.
* Rhabdomyolysis
* Cardiac dysrhythmia
* Acute kidney injury
* Multiorgan failure
* Disseminated intravascular coagulation

169
Q

List the risk factors for chronic limb ischemia

A

Smoking
Diabetes
Hypercholesterolaemia
HTN

170
Q

List the signs in chronic limb ischaemia

A

Cold dry skin, lack of hair
Diminished / absent pulses
Ulceration associated with dark discolouration / gangrene

171
Q

List the management in chronic limb ischaemia

A

Risk factor management
Naftidrofuryl oxalate (5 HT antagonist, vasodilator, reduce lactic acid build up)
Surgery when severe, disabling:
* angioplasty
* bypass

172
Q

List the clinical presentation for varicose veins

A

Lower extremity pain
Fatigue
Itching and/or heaviness
Worsen with prolonged standing
Associated with dilated tortuous veins

173
Q

List the complications for varicose veins

A

Chronic venous skin changes
Superficial venous thrombosis
Venous ulceration
Bleeding

174
Q

List the pathophysiology of varicose veins

A

Incompetent valves
Blood pass from deep to superficial venous system
Venous hypertension, dilation of superficial veins

175
Q

List the risk factors for varicose veins

A

Increasing age
Family history
Female sex
Pregnancy
Contraceptive pills
Obesity
Prolonged standing or sitting
History of deep vein thrombosis

176
Q

Give the first line investigation and findings for varicose veins

A

Duplex ultrasound
* Reflux
* Valve closure >0.5 second in the superficial system and >1.0 second in the deep system

177
Q

List the intrinsic and temporary risk factors for deep vein thrombosis

A

Intrinsic risk factors
Age > 60 years.
Male sex.
A history of DVT.
Overweight / obese.
Cancer.
Heart failure.
Acquired / familial thrombophilia.
Inflammatory disorders (eg. vasculitis, inflammatory bowel disease).

Temporary risk factors
Significant immobility.
Significant trauma or direct trauma to a vein (eg. intravenous catheter).
Hormone treatment (eg. hormone replacement therapy).
Pregnancy and the postpartum period.
Dehydration.

178
Q

What is the most serious complication for deep vein thrombosis

A

pulmonary embolism

179
Q

List the presentations in deep vein thrombosis

A

Asymmetrical leg swelling
Unilateral leg pain
Superficial vein dilation
Calf warmth / tenderness / swelling / erythema

180
Q

List the variables in Wells score

A

Active cancer (Treatment or palliation within 6 months)
Bedridden recently >3 days or major surgery within 12 weeks
Calf swelling >3 cm compared to the other leg (Measured 10 cm below tibial tuberosity)
Collateral (non varicose) superficial veins present
Entire leg swollen
Localised tenderness along the deep venous system
Pitting edema, confined to symptomatic leg
Paralysis, paresis, or recent plaster immobilisation of the lower extremity
Previously documented DVT
Alternative diagnosis to DVT as likely or more likely

181
Q

List the investigations and findings for deep vein thrombosis

A

Wells score ≥2: DVT likely - Venous ultrasound
* Abnormal B-mode image: inability to fully compress lumen of vein using ultrasound transducer
* Abnormal Doppler: reduced or absent spontaneous flow

Wells score <2: DVT unlikely
1. D-dimer level (results available within 4 hours)
2. If elevated: Venous ultrasound

182
Q

List the investigations required before starting anticoagulation

A

Full blood count
Urea and creatinine
Liver function tests
Clotting screen (prothrombin time (PT) and activated partial thromboplastin time (aPTT))

183
Q

List the management approach for deep vein thrombosis

A

Suspected DVT - Apixaban (interim therapeutic anticoagulation)

Confirmed proximal DVT - Receive anticoagulation for at least 3 months
First line: Apixaban / rivaroxaban
Alternatives
* LMWH for at least 5 days followed by dabigatran / edoxaban
* LMWH concurrently with a vitamin K antagonist for at least 5 days

184
Q

List the management approaches in phlegmasia cerulea dolens

A

Anticoagulation with low molecular weight heparin or unfractionated heparin
Vascular surgery
Elevated affected leg

185
Q

List the risk factors for pulmonary embolism

A

Personal / family history of DVT.
Recent surgery.
Significant immobility.
Active cancer.
Antiphospholipid antibody syndrome.
Lower limb trauma.
Recent myocardial infarction.
Increasing age.
Pregnancy
Oral contraception
Hormone replacement therapy
Cigarette smoking
Long-duration travel
Obesity

186
Q

List the symptoms for pulmonary embolism

A

Dyspnoea
Tachypnoea
Pleuritic chest pain (normally localised to one side)
Features of DVT
Cough and haemoptysis
Retrosternal chest pain (RV ischaemia)
Syncope / presyncope (RV failure)

187
Q

List the ECG features in pulmonary embolism

A

Sinus tachycardia
S1Q3T3
* Deep S wave in lead I
* Q wave in III
* Inverted T wave in III
T wave inversion V1~3
RBBB
Right axis deviation
P pulmonale

188
Q

List the variables in Two-level PE Wells score

A

Clinical features of deep vein thrombosis (leg swelling, pain, palpation of the deep veins) +3
Heart rate > 100 bpm +1.5
Immobilisation +1.5
Previous DVT or PE +1.5
Haemoptysis +1
Cancer +1
An alternative diagnosis is less likely than PE — plus 3 points.

189
Q

Give the interim therapeutic anticoagulation in pulmonary embolism

A

apixaban

190
Q

List the investigation approaches for pulmonary embolism

A

Two-level PE Wells score > 4: PE likely
* 1st line: CT pulmonary angiogram

Two-level PE Wells score < 4: PE unlikely
* D-dimer within 4 hrs
* If positive, arrange CTPA

191
Q

Give the pathophysiology of superficial vein thrombophlebitis

A

Thrombus formation in a superficial vein, and inflammation in the tissue surrounding the vein.

192
Q

List the aetiologies for superficial vein thrombophlebitis

A

Vessel wall damage
Catheterisation
IV drugs
Sclerotherapy
Inflammatory vascular diseases

Stasis
Varicose veins
Immobilisation

Hypercoagulability
Oral contraceptive medicines
Inherited or acquired thrombophilia

193
Q

List the clinical signs in superficial vein thrombophlebitis

A

Pain
Tenderness
Induration
Warmth
Erythema
Palpable cord along the course of a superficial vein

194
Q

Give the first line investigation and finding in superficial vein thrombophlebitis

A

Duplex ultrasonography
* Lack of compressibility or intraluminal thrombus in the superficial veins

195
Q

Where does aortic aneurysms most commonly affect?

A

Abdominal
Iliac
Popliteal
Femoral
Thoracic

196
Q

Give the definition of aortic aneurysm

A

Permanent pathological dilation of the abdominal aorta with a diameter over 1.5 times the expected anteroposterior diameter of that segment given the person’s sex and body size.

197
Q

List the risk factors for aortic aneurysms

A

Increasing age
Male sex
Smoking
Hypertension
Positive family history
Diabetes mellitus
Chronic obstructive pulmonary disease

198
Q

What may aortic aneurysms be secondary to?

A

Atherosclerosis
Trauma
Infection (syphilis, E. coli, salmonella, mycotic aneurysm)
Genetic (MFS, EDS)

199
Q

When is AAA screening offered?

A

all men the year they become 65 years old.

200
Q

List the possible outcomes and actions after AAA screening

A

No aneurysm found (less than 3.0 cm) — no further scans are required.
Small AAA (3.0 cm to 4.4 cm) — the person is placed under surveillance and a repeat scan offered in 12 months.
Medium AAA (4.5 cm to 5.4 cm) — the person is placed under surveillance and a repeat scan offered in 3 months.
Large AAA (5.5 cm or larger) — the person is referred to a vascular surgeon.

201
Q

List the symptoms of rapid expansion or rupture of AAA

A

Severe epigastric pain radiating to back
Hypotension
Tachycardia
Profound anaemia
Sudden death

202
Q

Give the definition for aortic dissection

A

Dissection in aortic wall intima, causing blood flow into a new false channel composed of the inner and outer layers of the media.

203
Q

List the acute aortic syndromes

A

Aortic dissection
Intramural haematoma
Penetrating aortic ulcers

204
Q

List the predisposing factors in aortic dissection

A

Autoimmune rheumatic disorders
MFS
EDS

205
Q

List the Stanford classification of aortic dissection

A

Type A: Dissection proximal to L subclavian artery origin
Type B: Dissection distal to L subclavian artery origin

Type B dissection has a better prognosis

206
Q

List the DeBakey classification of aortic dissection

A

Type 1: extends to abdominal aorta (ascending + descending)
Type 2: localised to ascending aorta (ascending)
Type 3: Tear originates distal to the left subclavian artery and extends through the thoracic aorta (3A) or extends beyond the visceral segment (3B) (descending)

207
Q

List the signs of aortic dissection

A

Sudden onset of severe central chest pain that radiates to the back and arms

Shock
Neurological symptoms secondary to loss of blood to spinal cord
Aortic regurgitation
Cardiac tamponade
Coronary ischaemia
Absent peripheral pulses
Distal dissection:
* Acute kidney disease
* Visceral ischaemia
* Acute lower limb ischaemia

208
Q

Give the CXR sign of aortic dissection

A

widened mediastinum

209
Q

List the medical treatment for aortic dissection

A

IV beta-blockers to achieve
* Heart rate <60 beats per minute
* Systolic blood pressure (SBP) 100-120 mmHg
IV opioids
* Pain relief, decrease sympathetic tone and facilitate haemodynamic stability.
If heart rate and SBP not adequately controlled
* Add vasodilator eg. sodium nitroprusside

210
Q

What is the most common form of cardiomyopathy

A

Hypertrophic cardiomyopathy

211
Q

Give the inheritance of hypertrophic cardiomyopathy

A

Autosomal dominant
* MYH7 (beta-myosin heavy chain)
* MYBPC3 (myosin binding protein C)

212
Q

Describe the pathology in hypertrophic cardiomyopathy

A

abnormal, thickened, disorganised collagen matrix
septal thickening from myocyte hypertrophy

213
Q

Give the complication for hypertrophic cardiomyopathy

A

HFpEF - diastolic dysfunction

214
Q

Give the presentation in symptomatic hypertrophic cardiomyopathy

A

Dyspnoea
Chest pain
Syncope with exertion
Cardiac arrhythmias
Sudden death

215
Q

List the physical examination findings in hypertrophic cardiomyopathy

A

Double apical impulse
Brisk carotid upstroke (jerky carotid pulse)

216
Q

List the auscultation findings in hypertrophic cardiomyopathy

A

Systolic ejection murmur at lower left edge
* accentuated by exercise and standing
* lessened by lying supine or squatting
S4

217
Q

List the ECG findings in hypertrophic cardiomyopathy

A

Prominent Q waves in leads II, III, aVF, V5, V6

218
Q

List the managements in hypertrophic cardiomyopathy

A

Symptomatic:
Chest pain, dyspnoea: beta-blockers +/- verapamil
LV outflow tract obstruction: disopyramide

219
Q

Describe the pathology in arrhythmogenic cardiomyopathy

A

progressive replacement of myocardium with fibro-fatty material

220
Q

Describe the Mendelian inheritance of arrhythmogenic cardiomyopathy

A

Autosomal dominant

221
Q

List the ECG findings in arrhythmogenic cardiomyopathy

A

T inversion and broad QRS in V1-3
Epsilon wave - small positive deflection buried in the end of the QRS complex
RBBB

222
Q

List the Task force criteria for arrhythmogenic cardiomyopathy diagnosis

A

Structural abnormalities of RV and RV outflow tract
Fibro-fatty replacement of myocytes on tissue biopsy
Repolarisation and conduction abnormalities on ECG
Ventricular tachycardia / extrasystoles on Holter monitoring
Family Hx. of ACM in first / second relative
Premature sudden death < 35 years due to ACM

223
Q

List the management approaches in arrhythmogenic cardiomyopathy

A

Non-life threatening arrhythmias - beta blockers
Symptomatic arrhythmias - amiodarone / sotalol
Refractory / life threatening arrhythmias - ICD
Intractable arrhythmia / cardiac failure - cardiac transplantation

224
Q

List the causes of dilated cardiomyopathy

A

Familial DCM - Autosomal dominant

Sporadic DCM causes
Myocarditis
* Coxsackievirus
* Adenovirus
* Erythrovirus
* HIV
* Mycobacteria
* Chaga’s disease (Trypanosoma Cruzi)
Toxins
* Alcohol
* Chemotherapy
* Heavy metal
Autoimmune disorders
Endocrine disorders
Neuromuscular disorders

225
Q

List the clinical features in dilated cardiomyopathy

A

Heart failure (HF-rEF)
Cardiac arrhythmias
Conduction defects
Thromboembolism
Sudden death

226
Q

List the ECG findings in dilated cardiomyopathy

A

AF
Ventricular premature contractions
Ventricular tachycardia

227
Q

List the four types of shock

A

Hypovolaemic
Cardiogenic
Distributive
Obstructive

228
Q

List the causes of shock

A

Hypovolemic
Haemorrhage
Fluid depletion

Cardiogenic
Myocardial infarction
Atrial fibrillation
Ventricular tachycardia
Bradyarrhythmias
Toxic substances
Excessive rise in blood pressure
Infection
* Pneumonia
* Infective endocarditis
* Sepsis
Acute mechanical cause
* Myocardial rupture
* Chest trauma
* Acute valvular incompetence

Distributive
Sepsis
Anaphylaxis
Brainstem or spinal injury (neurogenic)

Obstructive
Pulmonary embolism
Cardiac tamponade
Tension pneumothorax

229
Q

List the clinical presentations in shock

A

Hypotension
SBP < 90 mmHg
MAP < 65 mmHg
Decrease ≥40 mmHg from baseline

Skin changes
Sweating and cyanosis of the skin, lips, or tongue
Cold or clammy peripherally

Oliguria (<0.5 mL/kg/hour)

Mental status changes
Agitation, confusion, and distress
Unresponsiveness

General features
Airway compromise
Dyspnoea
Hypoxaemia
Fever
Hypothermia

230
Q

Define sepsis

A

Life-threatening organ dysfunction due to a dysregulated host response to infection.

231
Q

List the most common causative organisms

A

Staphylococcus aureus
Pseudomonas species
Escherichia coli

232
Q

List the risk factors for sepsis

A

Extremes of age
Frail
Immunocompromised
* Diabetes mellitus
* HIV
* Cirrhosis
* Sickle cell disease
* Asplenia
* Drug treatment eg. anticancer, oral corticosteroids
Trauma, surgery, or other invasive procedures in the past 6 weeks
Any breach of skin integrity (cuts, burns, blisters, skin infections)
IV drug or alcohol misuse
Indwelling lines or catheters
Women who are pregnant, are post-partum, or have had a termination of pregnancy or miscarriage in the past 6 weeks

233
Q

List the complications for sepsis

A

Death
Organ dysfunction and failure
* Acute kidney injury
* Cholestasis
* Heart failure
* Acute respiratory distress syndrome
* Acute lung injury
Recurrent and secondary infection
Coagulopathy
* Thromboembolism
* Disseminated intravascular coagulation
Reduced quality of life
Neurological sequelae
* Focal neurological deficits and hearing loss in bacterial meningitis
* Polyneuropathy in sepsis and multi-organ failure
Psychological

234
Q

List the signs for sepsis

A

New-onset confusion, disorientation, agitation
Temperature
* Fever
* Hypothermia
Respiratory distress
Hypotension
Capillary refill time and oxygen saturation - poor peripheral perfusion
Skin changes
* Mottled or ashen appearance; pallor or cyanosis of the skin, lips, or tongue; cold hands or feet.
* Non-blanching petechial rash - meningococcal disease
* Breach of skin integrity or infection
A weak high-pitched or continuous cry (in children under 5 years of age).
Dehydration

235
Q

List the sepsis six

A

Take
Blood Cultures
Lactate
Urine output

Give
Fluids
Antibiotics
Oxygen

236
Q

List the four AHA stages of heart failure

A

Stage A: at risk for heart failure
People who are at risk for heart failure but do not yet have symptoms or structural or functional heart disease
Stage B: pre-heart failure
People without current or previous symptoms of heart failure but with either structural heart disease, increased filling pressures in the heart or other risk factors
Stage C: symptomatic heart failure
People with current or previous symptoms of heart failure
Stage D: advanced heart failure
People with heart failure symptoms that interfere with daily life functions or lead to repeated hospitalizations

237
Q

List the four AHA classes of heart failure

A

Class I
No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation or shortness of breath.
Class II
Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, shortness of breath or chest pain.
Class III
Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, shortness of breath or chest pain.
Class IV
Symptoms of heart failure at rest. Any physical activity causes further discomfort.

238
Q

Give the first line investigation in heart failure and potential actions

A

Elevated NT-pro-BNP / BNP levels
> 2000 ng/litre - TTE within 2 weeks
400~2000 ng/litre - TTE within 6 weeks
< 400 ng/litre (47 pmol/litre) - heart failure less likely

239
Q

Compare Janeway lesions vs Osler’s nodes

A

Janeway lesions: painless, blanching red macules on the thenar/hypothenar eminences
Osler’s nodes: painful raised erythematous lesions, typically on the pads of the fingers

240
Q

What is the gold standard investigation for heart failure

A

TTE

241
Q

List the CXR signs of heart failure

A

Cardiomegaly (increased cardiothoracic ratio)
Pulmonary congestion
Pulmonary vascular congestion (vascular redistribution, Kerley B lines)

242
Q

List the ECG signs of heart failure

A

LV hypertrophy
Atrial enlargement
Conduction abnormalities eg. LBBB
Underlying coronary artery disease

243
Q

What can serum natriuretic peptides be reduced by

A

Obesity
African or African–Caribbean family background
Diuretics
ACEi
Beta‑blockers
ARBs
Mineralocorticoid receptor antagonists

244
Q

List the causes of high levels of serum natriuretic peptides other than heart failure

A

Age over 70 years
Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Pulmonary embolism (hypoxaemia)
Renal dysfunction [eGFR < 60 ml/minute/1.73 m2]
Sepsis
COPD
Diabetes
Cirrhosis

245
Q

List the treatment algorithms in heart failure

A
  1. ACEi + beta-blockers
    * Symptomatic treatment: loop diuretics
  2. ARB
  3. hydralazine + nitrate
  4. Digoxin / ivabradine
246
Q

List the drugs that should be avoided in HFrEF

A

Non-dihydropyridine calcium-channel blockers - Diltiazem, Verapamil
Class Ic antiarrhythmics - Propafenone, Flecainide
Thiazolidinediones - Pioglitazone
Dipeptidyl peptidase-4 (DPP-4) inhibitors - alogliptin, linagliptin, saxagliptin, sitagliptin
NSAIDs

247
Q

List the causes of acute heart failure

A

IHD
Valvular heart disease
HTN
Acute / chronic kidney disease
Atrial fibrillation

248
Q

List the symptoms and signs of acute heart failure

A

Dyspnoea / Orthopnoea / Paroxysmal nocturnal dyspnoea
Ankle swelling
Reduced exercise tolerance
Fatigue
Elevated jugular venous pressure
S3 (gallop rhythm)
Pulmonary crepitations

249
Q

List the hypertension severity staging

A

Stage 1
Clinical 140/90 ~ 159/99
ABPM 135/85 ~ 149/94

Stage 2
Clinical 160/100 ~ 180/120
ABPM 150/95

Stage 3
Clinical 180/120 mmHg or higher

250
Q

Give the definition of malignant hypertension

A

Severe increase in blood pressure to 180/120 mmHg or higher with signs of retinal haemorrhage and/or papilloedema

251
Q

List the secondary cause for hypertension

A

Vascular
* Renal artery stenosis
* Coarctation of aorta
* Pre-eclampsia
Renal
* Chronic kidney disease
* Chronic pyelonephritis
* Diabetic nephropathy
* Glomerulonephritis
* Nephrotic syndrome
* Polycystic kidney disease
* Obstructive uropathy
* Renal cell carcinoma
Endocrine
* Pheochromocytoma
* Primary hyperaldosteronism
* Cushing’s syndrome
* Acromegaly
* Hyperthyroidism (increased systolic BP)
* Hypothyroidism (increased diastolic BP)
* Hyperparathyroidism
Drugs
* Alcohol
* Ciclosporin.
* Cocaine, amphetamine, sympathomimetics
* ADHD stimulants
* Venlafaxine
* Combined oral contraceptive, oestrogens
* Corticosteroids.
* Erythropoietin.
* Leflunomide.
* NSAIDs
Pregnancy
Connective tissue disorders
* Scleroderma
* Systemic lupus erythematosus
* Polyarteritis nodosa
Retroperitoneal fibrosis
Obstructive sleep apnoea

252
Q

List the risk factors for primary hypertension

A

Increasing age
Gender
* Women <65 years tend to have a lower blood pressure than men.
* Women 65–74 years tend to have a higher blood pressure
Ethnicity - black African / Caribbean more likely
Genetics
Social deprivation
Co-existing diabetes / kidney disease
Lifestyle
* Smoking
* Excessive alcohol consumption
* Excess dietary salt
* Unhealthy diet
* Obesity
* Lack of physical activity
Anxiety and emotional stress

253
Q

List the complications for heart failure

A

Heart failure.
Coronary artery disease.
Stroke.
Chronic kidney disease.
Peripheral arterial disease.
Vascular dementia.

254
Q

List the symptoms and signs for hypertension

A

Usually asymptomatic
May present with
* Headaches
* Nosebleeds
* Visual symptoms
* Neurological symptoms

255
Q

When should secondary hypertension be suspected

A

Young (<40 years)
Rapid onset
Sudden change in blood pressure when previously well controlled on a particular therapy
Resistant hypertension

256
Q

List the fundoscopy findings for hypertensive retinopathy

A

Arteriolar narrowing
Arteriolar venous nipping (constriction of veins at crossing points)
‘Cotton wool spots’ on the retina (due to ischaemic changes)
Flame haemorrhages or papilloedema

257
Q

List the treatment algorithms for hypertension

A

Step 1 treatment
ACEi / ARB first line in
* Age < 55 and not of black African or Caribbean origin.
* T2DM
CCB first line in
* Age > 55, NOT T2DM
* Black African or Caribbean origin, NOT T2DM
* If CCB untolerated - indapamide (thiazide-like diuretic)
If there is evidence of heart failure - indapamide

Step 2 treatment
If not controlled with ACEi/ARB
* CCB
* Indapamide (thiazide-like diuretic)
If not controlled with CCB
* ACEi / ARB
* Indapamide (thiazide-like diuretic)

Step 3 treatment
Combination of
* ACEi / ARB
* CCB
* Indapamide (thiazide-like diuretic)

Step 4 treatment - resistant hypertension
* K+ 4.5 mmol/L or less - low-dose spironolactone
*K+ > 4.5 mmol/L - alpha-blocker (doxazosin, terazosin) / beta-blocker

258
Q

List the contraindications for ACEi

A

Angio-oedema
Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women

259
Q

List the adverse effects for ACEi

A

Reduced ACE:
* Hyperkalaemia
* Renal impairment
* Hypotension
Increased Kinin (ACE inactivates bradykinin)
* Cough
* Angio-oedema
* Anaphylactoid reaction

260
Q

List the contraindications for ARB

A

Diabetes mellitus
eGFR < 60 mL/minute/1.73 m2
Pregnant / planning a pregnancy
Breastfeeding women

261
Q

List the adverse effects for ARB

A

Renal impairment
Hyperkalaemia
Angio-oedema
Dizziness

262
Q

List the Thiazide diuretics. What channel do they act on?

A

Hydrochlorothiazide
Bendroflumethiazide

Na+Cl- co-transporter in DCT

263
Q

List the Loop diuretics. What channel do they act on?

A

Furosemide
Bumetanide

NKCC channel on the in thick ascending limb of loop of Henle, cause Na+, K+, Cl- loss in urine

264
Q

What channel does spironolactone act on

A

ALD-Na+ channel DCT

265
Q

What channels does amiloride act on

A

ENaC, collecting duct

266
Q

List the contraindications for spironolactone

A

Addison’s disease.
Acute renal insufficiency, significant renal compromise, anuria.
Hyperkalaemia.

267
Q

List the causes of ejection systolic murmurs

A

High cardiac output state
* severe anaemia
* fever
* athletes (bradycardia → large stroke volume)
* pregnancy
* thyrotoxicosis
* liver cirrhosis
* arteriovenous fistula.
Pulmonary flow murmur (increased RV stroke volume)
* atrial septal defect
* pulmonary regurgitation
Aortic flow murmur (increased LV stroke volume)
* aortic regurgitation
Valvular stenosis
* aortic stenosis
* pulmonary stenosis
Other valve abnormalities
* mechanical aortic or pulmonary valve
* aortic sclerosis (turbulent flow without significant pressure gradient)
Subvalvular obstruction
* hypertrophic obstructive cardiomyopathy
* subaortic membrane

268
Q

List the causes of pan systolic murmurs

A

Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

269
Q

List the causes for bradycardia in sinus rhythm

A

Sleep
Athletic training
Hypothyroidism
Medication:
* Beta-blockers
* Digoxin
* Verapamil, diltiazem

270
Q

List the causes for tachycardia in sinus rhythm

A

Exercise
Pain
Excitement/anxiety
Fever
Hyperthyroidism
Medication:
* Sympathomimetics, e.g. salbutamol
* Vasodilators

271
Q

List the causes for elevated JVP

A

Heart failure
Pulmonary embolism
Pericardial effusion
Pericardial constriction
Superior vena cava obstruction

272
Q

When may Kussmaul’s sign be seen

A

(paradoxical rise of JVP on inspiration)
Constrictive pericarditis
Severe right ventricular heart failure
Restrictive cardiomyopathy

273
Q

List the causes for displaced apex beat

A

(LV systolic dysfunction)
Heart failure
Aortic regurgitation
Mitral regurgitation

274
Q
A

Medicine (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions