Vascular system Flashcards

1
Q

Pharmacology and drugs in cardiovascular disease: What common cardiovascular conditions require drug therapy

A

hypertension
ischaemic heart disease and other atheromatous diseases
Heart failure
Arrhythmia

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2
Q

Pharmacology and drugs in cardiovascular disease: What are most cases of hypertension caused by?

A

Essential hypertension - no secondary cause

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3
Q

Pharmacology and drugs in cardiovascular disease: What sort of end organ damage can happen as a result of hypertension?

A

Brain: thrombotic, thromboembolic and haemorrhagic stroke, multi-infarct dementia, hypertensive encephalopathy
Heart: LVH, LV failure, coronary artery disease
Kidney: renal failure
Eyes: hypertensive retinopathy

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4
Q

Pharmacology and drugs in cardiovascular disease: What are the major risk factors for cerebrovascular atherosclerosis?

A
Hypertension
smoking
diabetes
hyperlidimedia 
obesity
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5
Q

Pharmacology and drugs in cardiovascular disease: What is the prognosis of hypertension related to and how can it be improved?

A

Related to level of systolic and diastolic blood pressures
Related to age, sex and other risk factors such as hyperlipidaemia and diabetes
Worse if there is evidence of end-organ damage
Improved with antihypertensive therapy

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6
Q

Pharmacology and drugs in cardiovascular disease: What non pharmacological treatments of hypertension are there?

A
Weight reduction
Reduce salt intake
Reduce fat intake
Reduce alcohol intake
Exercise
Smoking cessation
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7
Q

Pharmacology and drugs in cardiovascular disease: What common antihypertensive drugs are there?

A
Thiazide diuretics
ACE inhibitors
Angiotensin II receptor antagonists
Beta blockers
Calcium channel blockers
Alpha blockers
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8
Q

Pharmacology and drugs in cardiovascular disease: What do thiazide diuretics do?

A

Inhibit reabsorption of NaCl in proximal and early distal tubules of nephron

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9
Q

Pharmacology and drugs in cardiovascular disease: What is the most commonly used thiazide?

A

Bendroflumethiazide most commonly used thiazide

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10
Q

Pharmacology and drugs in cardiovascular disease: Which thiazide Is used in combo with loop diuretics for severe congestive heart failure?

A

Metolazone

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11
Q

Pharmacology and drugs in cardiovascular disease: Which drug is cheap and recommended for first line use?

A

thiazides

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12
Q

Pharmacology and drugs in cardiovascular disease: What are the side effects of thiazide diuretics?

A

Side effects include electrolyte disturbance, rash and postural hypotension- risk of low blood pressure on standing up

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13
Q

Pharmacology and drugs in cardiovascular disease: What sort of system is a cardiovascular drug system?

A

positive feedback

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14
Q

Pharmacology and drugs in cardiovascular disease: What do ACE inhibitors do and what are the side effects?

A

e.g. ramipril - most commonly used now, ramipril reduced risk of CV event in HOPE study

Inhibit the conversion of angiotensin I to angiotensin II

Relatively infrequent side effects except for dry cough: hypotension, rash, hyper-kalaemia, renal failure (especially in the presence of renal artery stenosis), angioedema, ageusia

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15
Q

Pharmacology and drugs in cardiovascular disease: What can be an effect of ACE inhibitors?

A

Bradykinin build up (as ACE causes bradykinin degradation) causing the dry cough

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16
Q

Pharmacology and drugs in cardiovascular disease: What are angiotensin II receptor antagonists used for?

A

Similar effects to ACE inhibitors but do not influence bradykinin metabolism so do not cause dry cough

Examples:
Losartan, valsartan, candesartan, irbesartan

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17
Q

Pharmacology and drugs in cardiovascular disease: What do beta blockers do and what are the side effects?

A

Reduce heart rate, blood pressure and cardiac output

Variable selectivity for cardiac b1 receptors to target just the heart receptors

Relative contraindications: asthma (beta receptors involved in bronchoconstriction so beta blockers can affect this), uncontrolled heart failure, bradycardia

Side effects: fatigue, hypotension, cold peripheries, bronchospasm, impotence. can also increase blood sugar

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18
Q

Pharmacology and drugs in cardiovascular disease: What do calcium channel antagonists do and what are the side effects?

A

Vasodilators – reduce systemic vascular tone

Two main types:

  • Verapamil and diltiazem – cause bradycardia, inhibit AV node conduction, negative inotropes
  • Amlodipine, lercanidipine …dipine – may cause a reflex tachycardia

Side effects: oedema, flushing, headache, dizziness, hypotension

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19
Q

Pharmacology and drugs in cardiovascular disease: What is stable angina?

A

CV episodes brought on predictably by increased stress/exercise

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20
Q

Pharmacology and drugs in cardiovascular disease: how can you treat an episode of angina?

A

Beta blockers
Nitrates
Calcium channel blockers
Potassium channel activators

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21
Q

Pharmacology and drugs in cardiovascular disease: How do beta blockers treat angina and what problems are there if there is cardiac failure or abrupt withdrawal?

A

Lower myocardial oxygen demand by reduce heart rate, blood pressure and myocardial contractility
May exacerbate cardiac failure (need to be introduced slowly) and peripheral vascular disease (claudication), and cause bronchospasm
Abrupt withdrawal may lead to arrhythmia, worsening angina or myocardial infarction

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22
Q

Pharmacology and drugs in cardiovascular disease: How do nitrates work to treat angina and what are the side effects?

A

Oral, sublingual (GTN tabs/spray), buccal, transdermal and intravenous forms used commonly
Symptomatic relief of angina
Produce nitric oxide at the endothelial surface leading to vascular smooth muscle relaxation and arteriolar and venous dilatation
Reduce myocardial oxygen demand (lower preload and afterload) and increase myocardial oxygen supply (coronary vasodilatation)
Side effects: headache, flushing, postural hypotension

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23
Q

Pharmacology and drugs in cardiovascular disease: How do calcium antagonists treat angina and which ones should be avoided in heart failure?

A

Lower myocardial oxygen demand by reducing blood pressure and myocardial contractility and increase myocardial oxygen supply by dilating coronary arteries and lateral arteries
Verapamil and diltiazem should be avoided in heart failure

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24
Q

Pharmacology and drugs in cardiovascular disease:How do potassium channel activators treat angina and what are the side effects?

A

Nicorandil
Arterial and venous dilating properties
No problems with tolerance as seen with nitrates

Can cause mucocutaneous and anal ulceration – relegated to second-line therapy

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25
Q

Pharmacology and drugs in cardiovascular disease: What do anti-platelet drugs do?

A

Inhibit platelet aggregation and arterial thrombus formation, thus preventing heart attack, stroke and CV death

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26
Q

Pharmacology and drugs in cardiovascular disease: What anti-platelet drugs exist and what do they do?

A

Aspirin – blocks platelet cyclo-oxygenase (COX1) and the production of thromboxane A2, a platelet activating substance
Clopidogrel, prasugrel and ticagrelor – platelet ADP (P2Y12) receptor inhibitors; used alone or, more often, in combination with aspirin
Dipyridamole – mainly used in combination with aspirin to prevent stroke

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27
Q

Pharmacology and drugs in cardiovascular disease: What are statins and what do statins do? Give some examples of statins

A

Hydroxymethyl-glutaryl (HMG) CoA reductase inhibitors

Lower LDL cholesterol and may increase HDL cholesterol

Examples:
Simvastatin, pravastatin, atorvastatin, rosuvastatin, …..statin

Reduce risks of myocardial infarction, stroke and CV death

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28
Q

Pharmacology and drugs in cardiovascular disease: What is heart failure?

A

an imprecise term describing the state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of an elevated filling pressure

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29
Q

Pharmacology and drugs in cardiovascular disease: Why does pulmonary and/or peripheral oedema develop?

A

due to high atrial pressures and salt/water retention caused by impaired renal perfusion and secondary aldosteronis

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30
Q

Pharmacology and drugs in cardiovascular disease: What are some symptoms of heart failure?

A

Shortness of breath, swelling of feet and legs, chronic lack of energy, difficulty sleeping due to breathing problems, confusion and or impaired memory, increased urination at night, cough with frothy sputum, swollen or tender abdomen with loss of appetite

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31
Q

Pharmacology and drugs in cardiovascular disease: What drugs can be used for chronic heart failure?

A

Diuretics
ACE inhibitors
Beta Blockers
Aldosterone antagonists

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32
Q

Pharmacology and drugs in cardiovascular disease: What are tachyarrhythmias and what are the different types?

A

Abnormal rapid heart rhythms

Different types depending on origin in heart of abnormal electrical activity including:
Atrial fibrillation (AF) or atrial flutter with rapid ventricular rate response
Supraventricular tachycardia (SVT)
Ventricular tachycardia (VT) - more serious in people with structural heart problems

high BP and alcohol are triggers

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33
Q

Pharmacology and drugs in cardiovascular disease: What does Digoxin do?

A

Blocks Na+ / K+ ATPase => Ca+ +

increases vagal tone – slows conduction in atrial fibrillation

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34
Q

Pharmacology and drugs in cardiovascular disease: What drugs can be used for controlling tachyarrhythmia?

A

Class Ia,b,c – disopyramide, flecainide, procainamide
Class II – beta blockers
Class III – amiodarone, dronedarone, sotalol
Class IV – calcium antagonists (verapamil, diltiazem)

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35
Q

CV disease: What things could go wrong?

A

Develop chest pain (angina or MI)
Develop a tachycardia (get palpitations or breathlessness) or bradycardia (get dizzy, blackout)
Develop heart failure (breathlessness, sometimes very acute and very severe)
Suddenly die (Ventricular tachycardia or fibrillation)
Get endocarditis

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36
Q

CV disease: What questions should you ask when faced with patients with definite or possible cardiovascular disease?

A

Will they tolerate my treatment?Almost always yes

Will my treatment complicate their condition or treatment? Very Rarely

Will their condition or treatment complicate my treatment? Often, particularly bleeding risk

Should I tell anyone about them? Yes; if you uncover cardiac symptoms (chest pain, breathlessness, blackouts, dizziness) or signs (irregular pulse, high/low BP, swelling)

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37
Q

CV disease: What are common causes of heart failure?

A

Conditions that affect the efficiency of the pump (reduce cardiac output) cause heart failure
Common causes; previous heart attacks (MI), high blood pressure, genetic causes, alcohol, drugs (chemotherapy – Hodgkin’s etc), idiopathic

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38
Q

CV disease: What is the standard assessment used for pump function?

A

Transthoracic echocardiography

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39
Q

CV disease: What are the symptoms of heart failure and why do they occur?

A

Reduced cardiac output increases fluid pressure in lungs (left heart failure), reduces venous return to the heart via vena cava (right heart failure) and compensatory responses cause fluid retention and vasoconstriction.

This causes;
Breathlessness (increased fluid pressure in lungs)
Swelling (increased fluid pressure in venous system)
Also; dizziness, tiredness, weight loss

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40
Q

CV disease: What are the clinical signs of heart failure?

A
Low blood pressure
High pulse rate
Crepitations in lungs
Raised jugular venous pressure
Pitting ankle oedema / ascites
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41
Q

CV disease What are the causes of valve disease?

A
Degeneration (ie it just happens)
Rheumatic fever
Congenitally abnormal valve
Endocarditis
Papillary muscle rupture after MI
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42
Q

CV disease: What are the symptoms of valve failure?

A

Same as heart failure

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43
Q

CV disease: What organisms usually cause endocarditis?

A

Streptococcal or Staphlococcal

44
Q

CV disease: What does endocarditis feel like?

A

Like a really bad systemic infection (night sweatsfever, rigors, weight loss) but with the bonus of infected lumps flying around your blood stream (causing embolic complications) and your heart valves being eaten away (causing valve regurgitation and heart failure)

45
Q

CV disease: What can infective endocarditis cause?

A

Valve damage and embolism - cerebral abscesses, retinal emboli, digital emboli

46
Q

CV disease: How is tachycardia and bradycardia defined?

A

(tachycardia, >100bpm) or too slow (bradycardia <60bpm).

47
Q

CV disease: What does it mean if the QRS complexes are closer together?

A

Faster the heart rate

48
Q

CV disease: What does a narrow QRS, fast rate/ Wide QRS, fast rate mean?

A

Narrow complex tachycardia

broad complex tachycardia

49
Q

CV disease: What are the risk factors for coronary artery disease?

A
Smoking
High cholesterol
High blood pressure
Diabetes
Overweight
Poor diet
Lack of physical activity
Other atherosclerotic conditions (stroke, peripheral vascular disease)
Family history
Genetics
Male sex
Age
50
Q

CV disease: When does angina occur?

A

When coronary artery disease becomes obstructive, this can cause angina. The “plaque/s” that cause angina are stable; a strong fibrous cap protects the blood from exposure to the lipid core of the lesion, preventing thrombosis.

51
Q

CV disease: What is angina?

A

Angina is a recurrent feeling of chest pressure/heaviness/pain/indigestion, sometimes radiating to the arm, neck, or back

52
Q

CV disease: What is angina almost always precipitated by?

A

exertion or stress (circumstances where the heart needs a greater blood supply)

53
Q

CV disease: When does MI occur?

A

when an atherosclerotic plaque in a coronary artery ruptures, triggering thrombus formation. This causes permanent death of some myocardium (unlike angina)

54
Q

CV disease: How can you tell if someone has coronary artery disease?

A

Exercise ECG - easy but inaccurate
Myocardial perfusion scan - slightly more accurate
Angiography, either by CT or invasive angiography

55
Q

CV disease: How do you treat coronary disease?

A

Lifestyle modification; stop smoking, take more exercise, eat heart healthy diet (5-7 veg/fruit/d, low processed food, oily fish, olive oil, nuts/seed), lose weight

Cholesterol lowering (statin treatment usually)

Antiplatelets (usually Aspirin) lowers MI risk

Address other risk factors; blood pressure, diabetes

These improve prognosis but do not reduce angina frequency

56
Q

CV disease: How do you treat coronary artery disease that is also causing angina?

A

No need to treat further if not bothersome

Medication to reduce anginal attacks; nitrates (spray or long acting tablets, betablockers, calcium channel blockers, nicorandil, ivabradine, ranolazine)

If medication not working/side effects; stenting or coronary artery bypass grafting

These improve angina but do not improve prognosis

57
Q

CV disease: How do you tell if it is a MI or trapped wind?

A

Two key investigations; ECG and serum Troponin measurement

If the ECG shows ST elevation it is an ST elevation MI

If the ECG is normal or shows other changes (ST depression, T wave inversion) it may be a Non-ST elevation MI (NSTEMI). Or trapped wind.

In both STEMI and NSTEMI the serum troponin will be raised (but may take some hours to rise, so often treat as MI until results known)

58
Q

CV disease: How do you manage STEMI and NSTEMI?

A

Immediate dual antiplatelet therapy (DAPT; aspirin plus Ticagrelor, Prasugrel, or Clopidogrel) and pain relief. Paramedics usually give the Aspirin and opiates. Oxygen should be avoided and nitrates are useless for MI.

Anticoagulation for 24-72hrs; Heparin, Fondapariux or similar

Both STEMI and NSTEMI should have angiography and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications

59
Q

CV disease: What is the secondary prevention for STEMI and NSTEMI?

A

Secondary prevention; DAPT for a year then Aspirin alone, Statin, Betablocker for a year, ACE inhibitor, and treatment of any complication (heart failure, arrhythmia, etc).

Cardiac rehabilitation; exercise, education, diet, smoking cessation

60
Q

CV disease: How do you investigate heart failure?

A

Mainstay is transthoracic echocardiography to detect ventricular impairment.
Also newer test for elevated serum B-type Natriuretic Peptide (BNP)
Other tests include cardiac MR

hypertrophic cardiomyopathy - commonly passed down, affects younger people more

61
Q

CV disease: What is the treatment of heart failure?

A

Treatment is predominantly medical (drugs)
ACE inhibitors, Betablockers, Aldosterone Antagonists (Spironolactone or Eplerenone), Diuretics, Ivabradine.

Correction of other causes (anaemia, thyroid dysfunction)

Management of complications (arrhythmia)

Some Heart Failure patients benefit from Cardiac Resynchronisation Therapy (CRT – special form of pacemaker)

62
Q

CV disease: How do you investigate valve disease?

A

Diagnosis usually by transthoracic echocardiography

Transoesophageal echocardiography gives better images particularly of mitral valve but is not pleasant for the patient

63
Q

CV disease: How is valve disease treated?

A

If valve disease symptomatic (usually breathlessness) then valve surgery probably appropriate (done by cardiothoracic surgeon, not cardiologist)

Valve can be replaced with metallic prosthesis, biological prosthesis (tissue from animal or human donor) which requires open heart surgery on bypass. Metallic valves require lifelong warfarin, and this can only be stopped if bridged with Heparin. (Anticoagulation for e.g. AF can often be stopped without bridging Heparin).

For aortic stenosis we now sometimes use TAVI (transcatheter aortic valve implantation)

64
Q

CV disease: How are arrhythmias investigated?

A

Diagnosis made by ECG at time of symptoms (easier said than done; often needs multiple 24hr recordings, home recorders, smartphone apps or implanted loop recorder)

Other investigations look for causes (echo for heart failure, valve disease, angio for coronary artery disease, family screening/testing for genetic conditions etc)

Treatments vary according to specific type of arrhythmia

65
Q

CV disease: What is the treatment of bradyarrhythmia?

A

pacemaker insertion

66
Q

CV disease: What does the ECG record?

A

p wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation

67
Q

CV disease: What devices can be used for bradycardia?

A

Dual chamber pacemaker - not for tachycardia or VF

68
Q

CV disease: What device treats tachycardia or VF?

A

Implantable Cardioverter/Defibrillator. Treats ventricular tachycardia or VF. Can also pace bradycardias

69
Q

CV disease: What device treats tachycardia or VF?

A

Implantable Cardioverter/Defibrillator. Treats ventricular tachycardia or VF. Can also pace bradycardias

70
Q

CV disease: What device treats heart failure and paces bradycardia?

A

Cardiac resynchronisation therapy (CRT) - debrillator

71
Q

CV disease: When should you defer dental treatment?

A

Urgent treatment rarely warrants deferral; risk of deterioration is theoretical in almost all situations

Stable angina (predictable chest pain, not unstable) is not a reason to defer treatment; but increasing pain, or pain at rest may well be.

Stable heart failure (breathless on exertion but can lie flat at night, is on treatment) is not a reason to defer, but increasing breathlessness and/or oedema may be.

Recent MI (within 6 weeks); defer until 3-6 months post MI, longer if possible.

Frequent attacks of disabling tachycardia

If patients are awaiting stents or bypass or valve surgery, but are stable, then can proceed with treatment

72
Q

Ischaemic heart disease and hypertension: What are the causes of ischaemic heart disease?

A

atherosclerosis
myocardial hypertrophy
small vessel disease

73
Q

Ischaemic heart disease and hypertension: What are the risk factors that predispose to the thrombosis?

A

change in vessel wall,
change in blood flow
change in the constituents of the blood

74
Q

Ischaemic heart disease and hypertension: What are the risk factors for atherosclerosis?

A

smoking
hypertension
diabetes - not controlled
hyperlipidaemia - lots of lipid in the blood

75
Q

Ischaemic heart disease and hypertension: How does atherosclerosis happen?

A

endothelial cells of the vessel walls damaged over many years due to plaque - blood clot forms but endothelial cells can grow over the top, this happens repeatedly till the vessel is occluded

76
Q

Ischaemic heart disease and hypertension: how does left ventricular hypertrophy cause heart disease?

A

Bigger muscle means blood supply cannot increase to meet the needs of a larger heart

77
Q

Ischaemic heart disease and hypertension: how do small vessel changes cause heart disease?

A

at arteriolar level
• inappropriate vasoconstriction
– reduced production of nitric oxide – increased destruction of nitric oxide

78
Q

Ischaemic heart disease and hypertension: what does ischaemic heart disease look like?

A
  • regional transmural myocardial infarction • subendocardial myocardial infarction
  • chronic ischaemia
79
Q

Ischaemic heart disease and hypertension: What is a regional transmural myocardial infarction?

A

acute occluding event in one of the three main coronary arteries
lack of collateral circulation from the other vessels

  • angiogram to find blockage and fit stent
80
Q

Ischaemic heart disease and hypertension: What is a subendocardial myocardial infarction?

A

severe coronary artery atherosclerosis in all three main coronary arteries

some sudden reduction in blood flow e.g. hypotension during an operative procedure

81
Q

Ischaemic heart disease and hypertension: What is chronic ischaemia?

A
  • ‘fixed’ atherosclerotic lesions • angina
  • myocardial fibrosis
  • hibernating myocardium
  • stunned myocardium
82
Q

Ischaemic heart disease and hypertension: What are the complications of myocardial infarction?

A
  • sudden death
  • arrhythmias
  • cardiac failure
  • mitral incompetence
  • pericarditis
  • cardiac rupture
  • mural thrombosis
  • ventricular aneurysm
  • pulmonary emboli
83
Q

Ischaemic heart disease and hypertension: What are some causes of sudden death?

A
  • arrhythmias such as ventricular fibrillation

* rational for acute coronary care services

84
Q

Ischaemic heart disease and hypertension: What is cardiac failure?

A
  • arrhythmias

* loss of myocardium and so reduced pump function

85
Q

Ischaemic heart disease and hypertension: What is mitral incompetence?

A
  • rupture or necrosis of papillary muscles

* pan systolic murmur

86
Q

Ischaemic heart disease and hypertension: How may a cardiac rupture happen?

A
  • weakening of wall due to muscle necrosis and acute inflammation
  • 3-7 days after infarction
  • rupture into pericardial sac
  • rupture of interventricular septum
87
Q

Ischaemic heart disease and hypertension: What is a mural thrombosis?

A
  • thrombosis on the abnormal endothelial surface following infarction
  • 7-14 days after infarction
  • embolisation to any arterial site
88
Q

Ischaemic heart disease and hypertension: What is a ventricular aneurysm?

A
  • stretching of newly-formed collagenous scar tissue
  • 4 weeks or more after infraction
  • may be associated with cardiac failure
  • may contain thrombus
89
Q

Ischaemic heart disease and hypertension: What is the clinical importance of hypertension?

A
  • commonest cause of heart failure in most countries
  • major risk factor for atherosclerosis
  • major risk factor for cerebral haemorrhage
90
Q

Ischaemic heart disease and hypertension: What are the causes of primary hypertension?

A

Adrenalin - stress
renin angiotensin aldosterone
sodium control

91
Q

Ischaemic heart disease and hypertension: What are the causes of secondary hypertension? (can control this)

A
• renal
– renin dependent
– salt and water overload
• endocrine
– Cushing’s (too much corticosteroid - adrenal tumour or steroidal medication), Conn’s (aldosterone), phaeochromocytoma (tumour of adrenal centre of the the medulla  causes adrenaline and noradrenaline into blood stream)
• coarctation of aorta • drug therapy
– corticosteroids, NSAIDs
92
Q

Ischaemic heart disease and hypertension: What are the differences between benign and malignant causes of hypertension?

A
• benign
– long asymptomatic period
– increased frequency of complications later
• malignant
– markedly raised diastolic pressure 
– symptomatic
– rapidly fatal if untreated
93
Q

Ischaemic heart disease and hypertension: What are the effects of hypertension?

A
  • heart failure
  • kidney failure
  • cerebral haemorrhages = ‘strokes’
  • accelerated atherosclerosis
  • sclerosis of smaller vessels
  • microaneurysms and haemorrhages
94
Q

Pathology of valvular heart disease: What can go wrong with heart valve?

A

Stenosis - narrowed valve

incompetence - doesn’t close properly so get back flow of blood

95
Q

Pathology of valvular heart disease: What causes valve problems?

A

rheumatic fever
calcific aortic valve disease
age related degeneration

96
Q

Pathology of valvular heart disease: What is rheumatic fever?

A

Allergic reaction to streptococcal pharyngitis

immune reaction to it

cross reaction with self antigens ( look the same)

occurs in the different parts of the heart

TYPE 4 hypersensitivity lymphocyte mediated

97
Q

Pathology of valvular heart disease: Where is valve fibrosis more likely to occur?

A

90% mitral valve

40% aortic valve

98
Q

Pathology of valvular heart disease: What is calcific aortic valve disease? ???

A

usually produces stenotic aortic valves which produce left ventricular hypertrophy leads to inadequate coronary artery perfusion —> MI

99
Q

Pathology of valvular heart disease: What type of prosthetic heart valves are there?

A

Biological

  • human
  • porcine

artifical

  • tilting disc
  • ball and cage
100
Q

Pathology of valvular heart disease: What are the advantages and disadvantages of artificial prosthetic heart valves?

A
  • turbulent flow around - red blood cells break down
101
Q

Pathology of valvular heart disease: What are the complications of prosthetic valves?

A
• complications
– haemolysis
– coagulation
–anti coagulation therapy 
–mechanical failure- ball goes into blood stream 
– calcification 
–infective endocarditis

prosthetic valves are the same as rheumatic valves

102
Q

Pathology of valvular heart disease: How does infective endocarditis happen?

A

Bacteria from the mouth enter the blood stream and settle on the valves of the heart

rheumatic fever (already damages the valves) can predispose to infective endocarditis

103
Q

Pathology of valvular heart disease: Where can infective endocarditis occur?

A

• any abnormal heart valve
–all pathologies mentioned so far
–prosthetic heart valves

• tricuspid valve
–intravenous drug users

bacteria meshed in fibrins = vegetations - on the heart valves

104
Q

Pathology of valvular heart disease: What are the complications of infective endocarditis?

A

• local
–valve incompetence
– myocarditis

• systemic
– emboli
–general effects of systemic infection
–glomerulonephritis (immune complex deposition)

105
Q

Pathology of valvular heart disease: What organisms cause infective endocardititis?

A

Streptococcis viridan
staphylococcus aureus
aspergillus - fungi