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Hamzah's cardio pathology > Hamzah's cardio pathology > Flashcards

Hamzah's cardio pathology Flashcards

1
Q

Define angina

A

recurrent transient episodes of chest pain due to myocardial ischaemia

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2
Q

Types of angina

A

classic/stable - induced by effort, relieved by rest
unstable (crescendo) - increases rapidly in severity, occurs at rest. Massive risk of MI
Decubitus - occurs when lying down
Prinzmetal - occurs at rest = coronary artery spasm

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3
Q

Aetiology of angina

A 
atheroma = main cause
others = anaemia, coronary artery spasm, aortic stenosis
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4
Q

Pathogenesis of angina

A

myocardial ischaemia occurs when demand outstrips supply. stenosis of a coronary artery impairs coronary blood flow when myocardial oxygen demand increases.

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5
Q

Risk factors for angina

A

diabetes, smoking, hyperlipidaemia, hypertension, family history, lack of exercise

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6
Q

Clinical presentation of angina

A

central crushing chest pain
comes on exertion and relieved by rest
exacerbated by cold weather, heavy meals, anger
radiates to arms and neck
other symptoms = dyspnoea, nausea, sweating, faintness

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7
Q

Differential diagnosis of angina

A

ACS, pericarditis, myocarditis, aortic dissection, GORD

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8
Q

Diagnostic tests for angina

A

ECG - normal but may show ST depression and flat/inverted T waves
Exercise ECG tests
coronary artery angiography

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9
Q

Treatment of angina

A

modify risk factors - stop smoking, weight loss, control hypertension
secondary treatment to prevent MI, stroke = low dose aspirin

symptomatic treatment = sublingual GTN spray, beta blockers, calcium channel blockers

surgery = PCI, CABG

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10
Q

What do acute coronary syndromes include?

A

unstable angina - no infarction
NSTEMI - subendocardial infarction
STEMI - transmural infarction

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11
Q

Pathophysiology of ACS

A

rupture, erosion of the fibrous cap leads to platelet aggregation and the formation of a platelet rich clot. Vasoconstriction occurs due to serotonin and thromboxane A2 release by platelets. This leads to ischaemia of myocardium

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12
Q

Symptoms of ACS

A

acute central chest pain (20 mins+)

sweating, dyspnoea, palpitations

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13
Q

Signs of ACS

A

Distress, Pallor/sweatiness, high/low pulse, hyper/hypotension. 4th heart sound

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14
Q

Differential diagnosis of ACS

A

angina, pericarditis, myocarditis, aortic dissection, pulmonary embolism, oesophageal reflux/spasm

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15
Q

Diagnostic tests for ACS

A

Blood - FBC, U&Es, lipids
ECG - pathological Q waves
Cardiac enzymes - cardiac troponin T and I - peak at 24-48 hrs

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16
Q

Treatment of ACS

A

=MONA
morphine, oxygen, nitrates, aspirin (300mg).

High risk STEMI/NSTEMI = MONAT
morphine, oxygen, nitrates, aspirin, T-clopidogrel/Ticagrelor

beta blockers, anti-coagulant (FONDAPARINUX)

PCI if high risk

secondary treatment = ACEi, statins

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17
Q

Acute STEMI treatment

A

aspirin, pain relief, antiemetic, oxygen, restore coronary perfusion - PCI or CABG, thrombolysis

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18
Q

Complications of MI

A

Heart failure, rupture of IV septum, mitral regurgitation, arrhythmias, pericarditis - Dressler’s syndrome

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19
Q

When is hypertension clinically treated?

A

sustained BP>160/100

>140/90 on 2 separate occasions - treat if at increased risk of coronary events, have DM or end-organ damage

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20
Q

Aetiology of hypertension

A

Essential hypertension = primary hypertension - hypertension with no underlying cause - genetics, obesity, high salt intake

Secondary hypertension = hypertension that is the result of a specific and potentially treatable cause - renal disease, endocrine disease (Conn’s, Cushing’s, pheochromocytoma, acromegaly), coarctation of aorta, steroids, pregnancy

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21
Q

Risk factors for hypertension

A

age, family history, male gender, African or Carribean origin, high salt intake, obesity, smoking

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22
Q

Pathogenesis of hypertension

A

Complex - multiple factors interact to produce hypertension
sustained hypertension promotes atherosclerosis, increases the work of the LV (–> LV hypertrophy) and increases the risk of LV failure, intracerebral haemorrhage and chronic kidney disease

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23
Q

Clinical presentation of hypertension

A

check for retinopathy, check for end organ damage, signs of underlying disease (renal disease, Cushing’s, low femoral pulse=coarctation)

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24
Q

What is malignant or ‘accelerated’ hypertension?

A

Rapid rise in BP leading to vascular damage.

Fibrinoid necrosis of vessel wall results in end organ damage in kidneys, retina and cardiovascular system.

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25
Q

Diagnostic tests for hypertension

A

ABPM - excludes white coat effect and is 24hrs
Home BP monitoring.
To quantify overall risk –> fasting glucose, cholesterol
ECG –> look for end organ damage
U&Es –> exclude secondary causes
24hr urinary metanephrines

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26
Q

Treatment of hypertension

A

treat underlying cause
target BP = 140/85 and for diabetics = 130/80

non-pharmacological = reduce weight, low-fat diet, low-salt diet, stop smoking, exercise

pharmacological = ACEi, thiazide diuretics (Bendroflumethiazide), beta-blockers, ARBs, Calcium channel blockers

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27
Q

Define heart failure

A

Where cardiac output is inadequate for the body’s demands

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28
Q

Aetiology of heart failure

A

systolic = IHD, MI, cardiomyopathy

diastolic = tamponade, constrictive pericarditis, systemic hypertension

valvular disease, anaemia, ventricular septal defect

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29
Q

Define acute heart failure

A

new onset acute characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypoperfusion

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30
Q

Define chronic heart failure

A

develops or progresses slowly. venous congestion is common but arterial pressure is well maintained until very late

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31
Q

What is low output heart failure?

A

cardiac output is low and fails to rise with exertion. Causes = pump failure and excessive afterload

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32
Q

What is high output heart failure?

A

rare. the heart is pumping the right amount of blood but this is not enough to meet the demands of the body. causes = anaemia, pregnancy, hyperthyroidism

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33
Q

New York Classification of HF

A
  1. Heart disease present but no undue dyspnoea from ordinary activity
  2. Comfortable at rest; dyspnoea during ordinary activities
  3. Less than ordinary activity causes dyspnoea - limiting
  4. Dyspnoea present at rest; all activity causes discomfort
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34
Q

What is systolic heart failure?

A

the ventricles can’t pump hard enough. <40% of ejection fraction

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35
Q

What is diastolic heart failure?

A

not enough blood fills into ventricles during diastole (same ejection fraction but lower SV and total volume)

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36
Q

Aetiology of left sided heart failure

A

IHD
hypertensive heart disease - increased afterload - LV hypertrophy
dilated cardiomyopathy - chamber grows and muscle gets weaker over time

diastolic

  • LV hypertrophy - less room for blood to fill
  • aortic stenosis
  • hypertrophic cardiomyopathy
  • restrictive cardiomyopathy = LV can’t stretch and fill
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37
Q

Pathogenesis of left sided heart failure

A

low cardiac output = low BP
low BP stimulates baroreceptors and reduces renal blood flow
sympathetic overdrive + RAAS
In the short term, BP is restored as well as afterload and preload
In the long term, the heart has to work harder and so LV hypertrophy occurs
LV hypertrophy reduces the volume of the ventricular cavity - reduced stroke volume

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38
Q

Clinical presentation of LHF

A

symptoms = dyspnoea, poor exercise tolerance, fatigue, orthopnoea, PND, cold peripheries, weight loss, muscle wasting

signs = pulmonary oedema, frothy pink sputum, cyanosis

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39
Q

Diagnostic tests for LHF

A

FBC, U&Es, ECG, echocardiogram

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40
Q

Causes of RHF

A

left ventricle failure - high pressure in pulmonary artery makes it harder for right ventricle to pump blood –> biventricular heart failure

left-right cardiac shunt - septal defect causes blood shunt from left to right. increases fluid volume of right side of the heart causes hypertrophy and becomes susceptible to ischaemia (systolic dysfunction) and smaller volume (diastolic dysfunction)

Chronic lung disease and cor pulmonale - in response to hypoxia the PA constrict which raises PBM. This makes it harder for the right ventricle to pump blood out - RV hypertrophy

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41
Q

Effects of RHF

A

systemic vein congestion - jugular venous distension

blood backs up to spleen and liver. can causes ascites and cardiac cirrhosis

pitting oedema in legs

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42
Q

Clinical presentation of RHF

A

peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis

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43
Q

Management of heart failure

A

Acute HF = medical emergency - oxygen, diamorphine, furosemide, GTN spray

Chronic HF = healthy lifestyle changes

treat underlying cause
treat exacerbating factors (infection, anaemia, high BP)

drugs = diuretics, ACEi, Beta-blockers, Mineralocorticoid receptor antagonists (spironolactone), digoxin, vasodilators

surgical intervention = revascularisation in IHD (PCI or CABG), valvular replacement, heart transplant, implanted autonomic cardiac defibrillator or pacemaker

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44
Q

What is an abdominal aortic aneurysm?

A

a permanent dilation of the abdominal aorta of more than 3cm in diameter

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45
Q

Causes of AAA

A

most = aortic atherosclerosis,

can also be caused by CT disorders (Marfans), trauma

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46
Q

Pathogenesis of AAA

A

proteolytic enzymes weaken the media of the aorta leading to aneurysmal change

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47
Q

Clinical presentation of AAA

A

unruptured aneurysms are often asymptomatic but may cause abdominal or back pain

ruptured AAA present as a surgical emergency with abdominal pain and shock

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48
Q

Diagnostic tests of AAA

A

ultrasound scan or CT scan

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49
Q

Treatment of AAA

A

elective surgical repair considered for aneurysms with a diameter greater than 5.5cm
surgical replacement of the aneurysmal section with prosthetic graft
endovascular repair with stent insertion if surgery not possible

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50
Q

What is an aortic dissection?

A

a tear in the tunica intima leading to blood flow into the tunica media. This forms a false lumen in the diseased media

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51
Q

Aetiology of aortic dissection

A

most are related to hypertension

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52
Q

Types of aortic dissection

A

Type A - 75% - involves the ascending aorta or aortic arch

Type B - 25% - involves the descending aorta

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53
Q

Pathogenesis of aortic dissection

A

caused by hypertension - tears the tunica intima
dissections may propagate in the blood flow direction (=anterograde) or against the normal flow of blood (=retrograde)
Dissections may re-enter the aortic lumen at a distant site (- creating a double-barrelled aorta) or rupture externally into the pericardial cavity, pleural cavity or peritoneal cavity

54
Q

Presentation of aortic dissection

A
  • abrupt onset of severe, tearing chest pain

- involvement of branch arteries may involve unequal arm pulses and blood blood pressures

55
Q

Investigation of aortic dissection

A

Chest x-ray = widened mediastinum
CT scan
TOE - transoesophageal echo
MRI scan

56
Q

Treatment of aortic dissection

A

surgical repair

urgent control of BP = IV esmolol

57
Q

What is acute pericarditis?

A

inflammation of the pericardium

58
Q

Aetiology of pericarditis

A 
idiopathic
viruses - coxsackie, echovirus
bacteria - TB, staphs, streps, Lyme disease
autoimmune - SLE
Dressler syndrome
metabolic - uremic pericarditis
59
Q

Clinical presentation of pericarditis

A

central chest pain. Worse on inspiration or lying flat. Relieved by sitting forward

60
Q

Diagnostic tests for pericarditis

A

ECG - concave (saddle shaped) ST segment elevation and PR depression
Blood tests - FBC, ESR, U&Es, cardiac enzymes, echocardiogram
pericardial friction rub heard on auscultation

61
Q

Treatment of pericarditis

A

NSAIDs or aspirin with gastric protection for 1-2 weeks
colchicine - inhibits neutrophil migration
treat underlying cause

62
Q

What is a pericardial effusion?

A

The accumulation of fluid in the pericardial sac

63
Q

Causes of pericardial effusion

A

pericarditis, myocardial rupture

64
Q

Clinical features of pericardial effusion

A

dyspnoea, chest pain, signs of local structures being compressed, nausea (diaphragm), cardiac tamponade signs

65
Q

Diagnostic tests for pericardial effusion

A

Chest X-ray
ECG changes - low voltage QRS complexes
Echocardiography

66
Q

Treatment of pericardial effusion

A

Treat underlying cause
Pericardiocentesis
- diagnostic –> send bacteria to labs
Therapeutic –> cardiac tamponade

67
Q

What is constrictive pericarditis?

A

the heart is encased in a rigid and stiff pericardium.

If inflammation persists, immune cells cause fibrosis of serous pericardium

68
Q

Clinical features of constrictive pericarditis

A

RVHF signs = hepatomegaly, increased JVP, ascites, oedema

69
Q

Diagnostic tests for constrictive pericarditis

A

chest X-ray - small heart and pericardial calcification

CT/MRI scan

70
Q

Management of constrictive pericarditis

A

surgical excision

71
Q

What is cardiac tamponade?

A

A pericardial effusion that raises intrapericardial pressure. This reduces ventricular filling and thus leads to a drop in cardiac output.

72
Q

Cardiac tamponade signs

A

increased pulse, decreased BP, pulsus paradoxus (abnormally large decrease in SV and BP during inspiration), increased JVP

73
Q

Diagnostic tests for cardiac tamponade

A

Beck’s triad = falling BP, rising JVP, muffled heart sounds
ECG - low voltage QRS complex
Echocardiogram

74
Q

Management of cardiac tamponade

A

pericardial effusion needs urgent drainage

send fluid for culture, ZN stain/TB culture

75
Q

What is infective endocarditis?

A

infection of the heart valves or other endocardial lined structures within the heart

76
Q

Where does infective endocarditis infection occur?

A

mitral or aortic valves, prosthetic valves, right sided is more common in IVDU, pacemakers

77
Q

Aetiology of infective endocarditis

A

usual cause = prior antibiotic therapy

strep viridans, staph aureus, rarely=candida(fungi)

78
Q

Risk factors for infective endocarditis

A

prosthetic valves, congenital valve defects, IVDU

79
Q

Pathophysiology of infective endocarditis

A

mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valves. the valves are destroyed by virulent organisms –> regurgitation.

vegetations are a source of embolus

80
Q

Epidemiology of IE

A

disease of the elderly, IVDU, young with congenital heart disease, anyone with prosthetic heart valves

81
Q

Clinical presentation of IE

A
  • systemic fever signs = fever, night sweats, weight loss, malaise
  • valve destruction –> heart murmurs and HF
  • splinter haemorrhages under nails
  • Roth’s spots in retina
82
Q

Diagnostic tests for IE

A

blood cultures may remain negative due to prior antimicrobial therapy
Blood tests - high ESR/CRP
TOE - identifies vegetations and valvular dysfunctions

83
Q

What is the Duke Criteria for IE?

A

Diagnosis requires 2 major or 1 major and 3 minor or 5 minor criteria

84
Q

Major criteria for IE

A

positive blood culture, vegetation on endocardium, new murmur

85
Q

Minor criteria for IE

A 
predisposing factors - IVDU
fever - more than 38C
vascular signs 
immunological signs
equivocal blood cultures
86
Q

Treatment for IE

A

Anti-microbial
Treat complications - emboli, HF, arrhythmias
surgery if infection cannot be treated with antibiotics or severe complications.

87
Q

Drug order for hypertension

A

<55 = ACEi/ARB –> CCBs/thiazide diuretics/

> 55/Black = CCBs –> ACEi/ARB/thiazide diuretic

88
Q

Peripheral vascular disease

A

occurs due to atherosclerosis causing stenosis of arteries.

89
Q

Chief feature in peripheral vascular disease

A

intermittent claudication

90
Q

Modifiable risk factors of peripheral vascular disease

A

hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia

91
Q

Non-modifiable risk factors of peripheral vascular disease

A

age, male gender FH

92
Q

What is intermittent claudication?

A

pain in a muscle or group of muscles due to ischaemia which is exacerbated by exercise and relieved by rest

93
Q

What is critical ischaemia?

A

severe obstruction of the arteries which markedly reduces blood flow to extremities and has progressed to the point of pain

94
Q

Fontaine classification of peripheral vascular disease

A
  1. Asymptomatic
  2. Intermittent claudication
  3. Ischaemic rest pain
  4. Ulceration/gangrene (critical ischaemia)
95
Q

Symptoms of peripheral vascular disease

A

Cramping pain in calf, thigh or buttock after walking for a given distance (claudication distance) and relieved by rest.
ulceration, gangrene and foot pain at rest = critical ischaemia
burning foot pain at night relieved by hanging legs over side of bed

96
Q

Signs of peripheral vascular disease

A
  • Absent femoral, popliteal or foot pulses
  • Cold white legs
  • Atrophic skin
  • Punched out ulcers
  • Postural colour change
  • Capillary refill time >12 seconds = sever ischaemia
97
Q

Diagnostic tests for peripheral vascular disease

A

Exclude DM and artheritis (C-reactive protein, ESR, CRP)

FBC, U&Es, ECG, lipids, ankle-brachial pressure index

98
Q

Imaging in peripheral vascular disease

A

Colour duplex USS - non-invasive and easily available

MR/CT angiography - provides location and extent of stenosis

99
Q

Risk factor modification of peripheral vascular disease

A

Smoking cessation, BP control, cholesterol control, clopidogrel (reduces cardiovascular risk)

100
Q

How is claudication managed?

A
  • Supervised exercise programmes - reduce symptoms by improving collateral blood flow (2hrs/week for 3 months) - patient to exercise to point of maximum pain
  • Vasoactive drugs - naftidrofuryl oxalate - only if revascularization is not an option
101
Q

Revascularization in peripheral vascular disease

A
  • Percutaneous transluminal angioplasty (PTA) - balloon inflated in narrowed segment and stent inserted
  • Surgical reconstruction - arterial bypass graft (autologous vein grafts are superior to prosthetic grafts)
102
Q

Causes of mitral stenosis

A

Majority = rheumatic heart disease

congenital, malignant carcinoid

103
Q

Pathophysiology of mitral stenosis

A

narrowing of mitral valve prevents free flow of blood from the left atrium to the left ventricle during ventricular diastole

104
Q

Complications of mitral stenosis

A

left atrial hypertrophy, pulmonary hypertension, RVHF, pulmonary oedema, breathlessness, AF

105
Q

Symptoms of mitral stenosis

A

Begin when mitral valve orifice is less than 2cm squared (normal=4-6cm)
- dyspnoea, fatigue, palpitations, chest pain, systemic emboli, coughing up blood

106
Q

Signs of mitral stenosis

A

malar flush on cheeks
low volume pulse
AF
mid-diastolic murmur

107
Q

Diagnostic tests in mitral stenosis

A

ECG - AF, P-mitrale 0 broad bifid P waves

CXR - LA enlargement, PO, Mitral valve calcification

Echocardiogram = diagnostic

108
Q

Treatment of mitral stenosis

A
  • treat complications
  • beta blockers in AF
  • anticoagulate with warfarin to prevent embolus
  • diuretics - decrease preload
  • balloon valvuloplasty
  • mitral valve replacement
109
Q

What is mitral valve regurgitation?

A

mitral valve doesn’t close properly

110
Q

Aetiology of mitral regurgitation

A

developed world = prolapsing mitral valve
developing wall = rheumatic heart disease

infective endocarditis, LV dilatation, annular calcification, CT disorders, ischaemic heart disease

111
Q

Pathophysiology of mitral regurgitation

A

mitral valve prolapse –> abnormal valve leaflets balloon into LA during ventricular systole

IHD –> ischaemic papillary dysfunction and widening of mitral valve annulus to to LV dilatation

Eventually there is development of LVHF

112
Q

Symptoms of mitral valve regurgitation

A

dyspnoea, fatigue, palpitation, IE symptoms (if this is the cause)

113
Q

Signs of mitral valve regurgitation

A

AF, displaced apex beat, RV heave, soft S1

114
Q

Diagnostic tests for mitral valve regurgitation

A

ECG - AF and p mitrale (bifid P waves)
CXR - enlarged LA, pulmonary oedema
Echocardiogram –> assess LV size and site using doppler echo
Cardiac catheterization ==> confirms diagnosis

115
Q

Treatment of mitral valve regurgitation

A 
control pulse - AF - beta blockers
diuretics
surgery - MV replacement or repair
anticoagulant if AF
Mild disease = serial echo every 1-5 years
116
Q

Aortic stenosis

A

narrowing of aortic valve - most common valve disease

117
Q

Causes of aortic stenosis

A

most = calcification of norml valve - elderly

calcification of bicuspid aortic valve - middle aged

rheumatic heart disease

118
Q

Pathophysiology of aortic stenosis

A

Obstruction to LV emptying results in LV hypertrophy

This can lead to angina, arrhythmias and LV failure

119
Q

Symptoms of aortic stenosis

A

classic triad = angina, syncope, HF

symptoms = dyspnoea, dizziness, faints, systemic emboli (if IE present)

120
Q

Signs of aortic stenosis

A

SYSTOLIC EJECTION MURMUR

slow rising pulse with narrow pulse pressure, LV heave, aortic thrill, ejection click

121
Q

Differential diagnosis of aortic stenosis

A

hypertrophic cardiomyopathy, aortic sclerosis

122
Q

Diagnostic tests in aortic stenosis

A
  • ECG - p mitral, depressed ST and T wave inversion
  • CXR - LVH, calcified aortic valve, post stenotic dilation of ascending aorta
  • Doppler echocardiography - assesses pressure gradient across the valve
  • cardiac catheter - assesses LV function (risk = emboli)
123
Q

Treatment of aortic stenosis

A

valve replacement

124
Q

What is aortic regurgitation

A

The diastolic flow of blood from the aorta into the LV

125
Q

Causes of aortic regurgitation

A

diseases which dilate the aortic root = Marfan’s, IE, rheumatic fever

Acute = IE, aortic dissection, chest trauma
Chronic = rheumatic heart disease, Marfan's, bicuspid aortic valve, hypertension
126
Q

Pathophysiology of aortic regurgitation

A

dilatation of the aortic root pulls the annulus of the aortic valve and prevents the tight closure of the valve leaflets

chronic regurgitation –> LV hypertrophy –> LVHF

127
Q

Symptoms of aortic regurgitation

A

exertional dyspnoea, orthopnoea, PND, palpitations, angina, syncope, CHF

128
Q

Signs of aortic regurgitation

A

HIGH PITCH EARLY DIASTOLIC PULSE

collapsing (water hammer) pulse, wide pulse pressure, displaced apex beat

129
Q

Diagnostic tests for aortic regurgitation

A

ECG –> LVH
CXR –> cardiomegaly and dilatation of ascending aorta, PO
Echocardiogram = diagnostic
Cardiac catheterization

130
Q

Treatment of aortic regurgitation

A
  • reduce systolic hypertension - ACEi
  • monitor –> echo every 6-12 months
  • valve replacement

Hamzah's cardio pathology (2 decks)

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