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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
Diagnostic tests for hypertension
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
26
Treatment of hypertension
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
27
Define heart failure
Where cardiac output is inadequate for the body's demands
28
Aetiology of heart failure
systolic = IHD, MI, cardiomyopathy diastolic = tamponade, constrictive pericarditis, systemic hypertension valvular disease, anaemia, ventricular septal defect
29
Define acute heart failure
new onset acute characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypoperfusion
30
Define chronic heart failure
develops or progresses slowly. venous congestion is common but arterial pressure is well maintained until very late
31
What is low output heart failure?
cardiac output is low and fails to rise with exertion. Causes = pump failure and excessive afterload
32
What is high output heart failure?
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
New York Classification of HF
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
What is systolic heart failure?
the ventricles can't pump hard enough. <40% of ejection fraction
35
What is diastolic heart failure?
not enough blood fills into ventricles during diastole (same ejection fraction but lower SV and total volume)
36
Aetiology of left sided heart failure
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
Pathogenesis of left sided heart failure
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
Clinical presentation of LHF
symptoms = dyspnoea, poor exercise tolerance, fatigue, orthopnoea, PND, cold peripheries, weight loss, muscle wasting signs = pulmonary oedema, frothy pink sputum, cyanosis
39
Diagnostic tests for LHF
FBC, U&Es, ECG, echocardiogram
40
Causes of RHF
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
Effects of RHF
systemic vein congestion - jugular venous distension blood backs up to spleen and liver. can causes ascites and cardiac cirrhosis pitting oedema in legs
42
Clinical presentation of RHF
peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis
43
Management of heart failure
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
What is an abdominal aortic aneurysm?
a permanent dilation of the abdominal aorta of more than 3cm in diameter
45
Causes of AAA
most = aortic atherosclerosis, | can also be caused by CT disorders (Marfans), trauma
46
Pathogenesis of AAA
proteolytic enzymes weaken the media of the aorta leading to aneurysmal change
47
Clinical presentation of AAA
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
Diagnostic tests of AAA
ultrasound scan or CT scan
49
Treatment of AAA
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
What is an aortic dissection?
a tear in the tunica intima leading to blood flow into the tunica media. This forms a false lumen in the diseased media
51
Aetiology of aortic dissection
most are related to hypertension
52
Types of aortic dissection
Type A - 75% - involves the ascending aorta or aortic arch Type B - 25% - involves the descending aorta
53
Pathogenesis of aortic dissection
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
Presentation of aortic dissection
- abrupt onset of severe, tearing chest pain | - involvement of branch arteries may involve unequal arm pulses and blood blood pressures
55
Investigation of aortic dissection
Chest x-ray = widened mediastinum CT scan TOE - transoesophageal echo MRI scan
56
Treatment of aortic dissection
surgical repair | urgent control of BP = IV esmolol
57
What is acute pericarditis?
inflammation of the pericardium
58
Aetiology of pericarditis
``` idiopathic viruses - coxsackie, echovirus bacteria - TB, staphs, streps, Lyme disease autoimmune - SLE Dressler syndrome metabolic - uremic pericarditis ```
59
Clinical presentation of pericarditis
central chest pain. Worse on inspiration or lying flat. Relieved by sitting forward
60
Diagnostic tests for pericarditis
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
Treatment of pericarditis
NSAIDs or aspirin with gastric protection for 1-2 weeks colchicine - inhibits neutrophil migration treat underlying cause
62
What is a pericardial effusion?
The accumulation of fluid in the pericardial sac
63
Causes of pericardial effusion
pericarditis, myocardial rupture
64
Clinical features of pericardial effusion
dyspnoea, chest pain, signs of local structures being compressed, nausea (diaphragm), cardiac tamponade signs
65
Diagnostic tests for pericardial effusion
Chest X-ray ECG changes - low voltage QRS complexes Echocardiography
66
Treatment of pericardial effusion
Treat underlying cause Pericardiocentesis - diagnostic --> send bacteria to labs Therapeutic --> cardiac tamponade
67
What is constrictive pericarditis?
the heart is encased in a rigid and stiff pericardium. | If inflammation persists, immune cells cause fibrosis of serous pericardium
68
Clinical features of constrictive pericarditis
RVHF signs = hepatomegaly, increased JVP, ascites, oedema
69
Diagnostic tests for constrictive pericarditis
chest X-ray - small heart and pericardial calcification | CT/MRI scan
70
Management of constrictive pericarditis
surgical excision
71
What is cardiac tamponade?
A pericardial effusion that raises intrapericardial pressure. This reduces ventricular filling and thus leads to a drop in cardiac output.
72
Cardiac tamponade signs
increased pulse, decreased BP, pulsus paradoxus (abnormally large decrease in SV and BP during inspiration), increased JVP
73
Diagnostic tests for cardiac tamponade
Beck's triad = falling BP, rising JVP, muffled heart sounds ECG - low voltage QRS complex Echocardiogram
74
Management of cardiac tamponade
pericardial effusion needs urgent drainage | send fluid for culture, ZN stain/TB culture

Hamzah's cardio pathology (2 decks)

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