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

Hamzah's cardio pathology COPY 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, cornory 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

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

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

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
34
Q

What is systolic heart failure?

A

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

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)

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
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

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

39
Q

Diagnostic tests for LHF

A

FBC, U&Es, ECG, echocardiogram

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

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

42
Q

Clinical presentation of RHF

A

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

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

44
Q

What is an abdominal aortic aneurysm?

A

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

45
Q

Causes of AAA

A

most = aortic atherosclerosis,

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

46
Q

Pathogenesis of AAA

A

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

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

48
Q

Diagnostic tests of AAA

A

ultrasound scan or CT scan

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

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

51
Q

Aetiology of aortic dissection

A

most are related to hypertension

52
Q

Types of aortic dissection

A

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

Type B - 25% - involves the descending aorta

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

Hamzah's cardio pathology (2 decks)

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