Brainscape's Knowledge GenomeTM

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


See full index

Revision Notes - Year 1 > Chronic Stable Angina - 126 > Flashcards

Chronic Stable Angina - 126 Flashcards

0
Q

Define stable angina

A

Predictable - symptoms brought on by exertion and stops within minutes when exertion ceases.

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

Define Angina

A

Chest Pain or pressure caused by activities that increase myocardial O2 demand. Pain caused by metabolic acidosis.

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

Define unstable Angina

A

Unpredictable - symptoms come on at rest - acute coronary syndrome.

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

Define class 1 and class 4 angina

A

Class 1 only comes on during strenuous physical activity

Class 4 comes on at rest

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

What causes myocardial ischaemia?

A

Insufficient supply - coronary atheroma (fatty lumps inside lining of artery walls) causes a fixed reduction in maximum supply and ischaemia develops at times of high demand.

Over-demand - eg aortic stenosis, hypertrophic cardiomyopathy, hypertension.

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

What are the risk factors for angina?

A

smoking, diet (high in fat/low in antioxidants), hypertension

also family history, hyperlipidaemia, diabetes mellitus, obesity, sedentary lifestyle, age and M>F

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

What are the symptoms of angina?

A

Retrosternal crushing pain, radiates (jaw, arms, back, neck), Stops within minutes of exertion stopping, shortness of breath

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

What are the differential diagnosis for angina?

A

Reflux oesophagitis, PE, pneumothorax, aortic disection, costochondral pain, pleuritis, varicella zoster.

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

what investigations should be carried out on a patient with suspected angina?

A

ECG (at rest and on exercise stress test - ischaemia shows as ST depression), blood profile, echocardiography (sonogram to show ventricular function and damage), perfusion scintiscan (radioisotopes injected to find stenosis and asses perfusion), Angiography (assess revascularisation - v. invasive)

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

how should angina be managed?

A

1) lifestyle modification - exercise, smoking, drinking, diet
2) Medical therapy - drugs & treat underlying diseases like diabetes, hypertension, hyperlipidaemia
3) Revascularisation - Percutaneous Coronary Intervention (PCI) (balloon dilatation & bare metal/ drug eluting stents), Coronary Artery Bypass Graft (CABG)

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

What pharmacological options are available for the management of angina?

A

1) Reduce demand on heart - Beta Blockers eg atenolol or metoprolol (reduce HR and contractability), Nitrates eg GTN (vasodilator via NO), CA2+ Channel Blockers eg amlodopine (vasodilator), Nicorandil (K+ channel blocker - donates NO = dilator)
2) Reduce plaque - Statins
3) Inhibit thrombosis - aspirin & clopidogrel

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

What are the mechanisms for cell injury due to hypoxia

A

Reduction in ATP (influx of CA2+ & efflux of K+), membrane damage, O2 derived free radicals.

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

What is the structure of atheromatous plaques?

A

Core - lipid (cholesterol)
Fibrous cap - collagen, elastin, smooth muscle cells & proteoglycan stroma
Shoulder zone (inbetween) - T lymphocytes & macrophages

stable plaques are concentric, rich in stroma and smooth muscle
unstable plaques are accentric, rich in lipid & macrophages, inflammed and have endothelial cell injury.

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

what does darcy’s law for laminar flow state?

A

perfusion = pressure difference / resistance

resistance proportional to viscosity and length. inversely proportional to radius (R = 8 x viscosity x l / pi x r^4)

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

how is transient turbulent flow heard on auscultation?

A

murmur

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

how is turbulent flow heard on auscultation?

A

bruit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Vessel resistance occurs due to friction between fluid layers, how does this happen?

A

parabolic distribution - fluid moving in concentric layers, outer layer does not move at all (no slip condition due to contact with endothelium) and central layer moves fastest.

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

why is viscosity least in smallest vessels?

A

Fahraeus-Lindqvist Effect - Axial streaming (RBCs migrate to centre of lumen, plasma left near wall where friction is greatest) and Bolus Flow (RBC diameter takes up whole of capillary and sweeps along plasma).

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

why is viscosity lower at high flow rates (high shear rates)?

A

RBC aggregation into rouleaux (stacks) when shear low but when shear high the RBC flow freely.

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

give three methods of measuring blood flow

A

1) Tissue clearance - time for radioactive substance to decline after injected into small area of tissue
2) Plethysomography - pressure cuff occludes veins in limb and initial swelling in limb measured
3) Fick’s principle - constituents of blood measured before and after an organ and compared to normal increase/decrease in that organ

20
Q

what is the normal hematocrit value in the blood?

A

45%

21
Q

what are the three ways that blood flow is controlled locally?

A

1) Autoregulation - blood flow maintained through an organ across range of BPs due to myogenic response (muscle contraction narrows lumen). eg kidneys
2) Metabolic Hyperaemia - adjustment of perfusion to organ according to demand (changing metabolic rate). Greatest control of blood flow.
3) Human Alerting response

22
Q

which blood vessels provide most resistance?

A

arterioles - blood flow control exert most at this level of circulation.

23
Q

What is the lowest level of hierarchy of blood flow control mechanisms?

A

Intrinsic autoregulation - Myogenic response (vascular smooth muscle contracts in response to increased BP - stretch depolarises, Ca2+ influx, contraction

24
Q

What is the intermediate level of the hierarchy of blood flow control?

A

Intrinsic Reactive Regulation

1) Metabolite control - products of respiration act as vasodilators (k+, CO2, adenosine)
2) Autacoid Control - autacoids (histamine, prostaglandins) released in damaged tissue - inflammation and dilation
3) Endothelial controls - endothelium excrete vasodilators like NO especially at high shear.

25
Q

what is the highest level of hierarchy of blood flow control?

A

Extrinsic regulation (for the benefit of the whole organism)

1) vasomotor nerves - sympathetic vasoconstrictors (noradrenaline), sympathetic vasodilators (acetylcholine) and parasympathetic vasodilators (acetlycholine)
2) Hormones - adrenaline (vasodilation of fight or flight organs) and Renin/Angiotensin II (vasoconstriction, aldosterone release to increase water reabsorption in kidneys)

26
Q

Describe the three models of stress

A

1) Stimulus model - external demands
2) Response model - response to stimulus (internal)
3) Transactional model - both stimulus and response perspectives

27
Q

Describe General Adaptation Syndrome

A

Phase I - Alarm reaction mobilises resources
Phase II - Resistance, cope with stressors
Phase III - Exhaustion, reserves depleted

28
Q

What is the body’s reaction to stress?

A

activation of sympathetic nervous system, adrenaline and noradrenaline release, release of corticosteriods

29
Q

What acronym explains how to manage a patient suspected of an ACS (acute coronary syndrome)? What does it stand for?

A 
MONA 
M - morphine (or diamorphine)
O - oxygeb
N - nitrates (GTN spray)
A - anti-platelets (aspirin)
30
Q

What are the MI-5 drugs?

A 
Aspirin
Clopidogrel
ACE-inhibitor (ramipril)
B-blocker (bisoprolol)
Statin (simvastatin)
31
Q

What is the mechanism of action of aspirin?

A

Irreversibly inhibits COX-1 and COX-2 enzymes. This inhibits the formation of thromboxane A2 -> inhibiting platelet aggregation

32
Q

What are the side effects of aspirin?

A

GI irritation
GI haemorrhage
Bronchospasm

33
Q

Name some contraindications for aspirin

A

Hypersensitivity
Active peptic ulcer
Haemophilia (and other bleeding disorders)

34
Q

What is the mode of action of clopidogrel?

A

Irreversibly blocks P2Y12 components of adenosine receptors on platelet surface

35
Q

Is clopidogrel usually used as a mono therapy or dual therapy?

A

Dual - may be prescribed as a monotherapy in patients that cannot tolerate aspirin.
Is used with aspirin as a dual therapy.

36
Q

What are some side effects and contraindications for clopidogrel?

A

GI irritation
GI haemorrhage

Contraindications: active bleeding

37
Q

Name some drugs that interact with clopidogrel to reduce its antiplatelet effect

A

Carbamazepine
Fluconazole
PPIs

38
Q

What are prasugrel and ticagrelor?

A

Anti-platelet drugs with a similar mode of action to clopidogrel. They can both be used with aspirin. Both contraindicated with active bleeding and can cause GI haemorrhage

39
Q

What is the mechanism of action of ramipril?

A

Inhibits angiotensin converting enzyme (ACE) and prevents the formation of angiotensin II - this prevents vasoconstriction and the formation of aldosterone

40
Q

What are some side effects of ACE inhibitors such as ramipril?

A

Dry cough, hyperkalaemia, renal impairment, angioedema, hepatic impairment

41
Q

What type of drugs do ACE inhibitors interact with?

A

Diuretics

42
Q

What is the mechanism of action of beta blockers?

A

Reduces sympathetic drive, causing a reduction in HR and myocardial contractility.

43
Q

What are some side effects of beta blockers?

A 
Bronchospasm
Bradycardia
Cold extremities 
Sleep disturbance
Fatigue
Sexual dysfunction
44
Q

What drugs could be given in patients unable to tolerate beta blockers?

A

Diltiazem or verapamil

45
Q

How do statins work?

A

Inhibit HMG CoA reductase, which is an enzyme involved in cholesterol synthesis. Inhibition of HMG CoA reductase lowers LDL-c levels by slowing production of cholesterol in the liver and increasing the liver’s ability to remove LDL-c

46
Q

What are some common side effects of statins?

A

Headache
Altered liver funcion
Myalgia

47
Q

What do statins interact with?

A

Grapefruit juice!
Clarthromycin
Fluconazole
Fusidic acid

Revision Notes - Year 1 (41 decks)

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