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Human diseases stage 3 > CVS > Flashcards

CVS Flashcards

1
Q

Explain how blood is carried through the heart and body and by which vessels, which valves (start at left atrium)

A

pulmonary veins - left atrium – mitral/bicuspid valve – left ventricle - aorta - systemic arteries – capillaries for gas exchange –venules – systemic veins - vena cava - right atrium –tricuspid valve - right ventricle – pulmonary valve - pulmonary artery - pulmonary capillaries (alveolar gas exchange) - pulmonary venules – pulmonary veins - left atrium

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2
Q

Name the 1) atria-ventricular and 2) ventricle-arterial valves. What are the 2 type of valve failure

A

1) Mitral/ bicuspid (left) tricuspid (right)
2) aorta (left) pulmonary (right)

Stenosis (narrowing) and regurgitation/ incompetence (backward leaking)

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3
Q

Coronary arteries: what they do, the main ones, when flood flow is highest, meaning of end arteries

A

-supply the myocardium
-left and right, circumflex, left anterior descending coronary arteries
-most blood flow when muscle is relaxing
-end arteries= no link between right and left so blockage can lead to coronary thrombosis and MI as nothing else supplies that area

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4
Q

Explain what happens in phase 0-4 in cardiac action potential

A

Phase 0: Fast sodium entry (Na+ channels)
Phase 1: Inactivation of sodium channels. K efflux
Phase 2: Slow calcium influx (L-Ca++ channel)
Phase 3: Efflux of K +
Phase 4: Resting membrane potential. Spontaneous diastolic drift (Na + and Ca++ entry)

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5
Q

Explain the cardiac cycle, from Sino-atrial node to ventricular contraction

A

-SA node in right atrium= electrical impulse begins here, depolarising which sends a signal for atria to contract
-Bachmann’s bundle send impulse from R to L atrium
-Atrial systole, squeezing blood into ventricles
-AV node detects atrium contraction, and has a 2s physiological delay to allow time to fill
-Bundle of His (AV bundle) transmit signal and cause ventricular systole
-Purkinje fibres cause further distribution of impulses and ensures ventricles contract at same time

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6
Q

Explain the waves on a ECG

A

-P waves= atrial depolarisation (SA to AV)
-PR segment= impulse held at AV node (physiological delay)
-QRS complex= ventricular depolarisation and up walls
-ST segment= ventricule depolarized waiting to be repolarized
-T wave= ventricular repolarising, back to resting potential

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7
Q

What is the lubb and dupp sound you hear

A

-blood hitting AV valve as it closes before ventricular contraction
-blood hitting aortic valve as it closes after ventricular contraction

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8
Q

Healthy systolic and diastolic blood pressure values

A

Systole <120 mmHg
Diastolic < 80 mmHg

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9
Q

What is atherosclerosis. List conditions it can cause (coronary, peripheral and cerebral)

A

-stenosis and calcification of the arteries due to thickened intima with lipids, cells and fibrous tissues, creating atherosclerotic plaques. Can cause thrombus, blockage, embolism, aneurysms

-Coronary= angina, MI, heart failure
-Peripheral= claudication, gangrene, small bowel ischameia & infraction, aortic aneurysm
-Cerebral= ishchameic stroke, aneurysm causing haemorrhage stroke

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10
Q

Risk factors for atherosclerosis

A

age (50+), sex (males), post-menopausal (less eostrogen to protect arteries), smoking (toxins damage endothelium, make platelets sticky), diabetes (glucose damages vessels), hypertension, hyperlipidameia (high LDL), hypercholestrolemia, unhealthy diet (fat, sugar, salt), lack of exercise, obesity

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11
Q

What is an aneurysm and 3 complications

A

Localised and permanent weakening of blood vessel wall which causes dilation. Most are due to atherosclerosis. Complications:
1. Ruptures and cause internal haemorrhage
2. Blood clots, causing thrombosis or embolism and infarction
3. Fistula to adjacent structures

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12
Q

Difference between fusiform and saccular aneurysm

A

o Fusiform – whole vessel dilates (common in abdominal aortic aneurysm)
o Saccular – sac on the side of a blood vessel

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13
Q

What is a Berry aneurysm. consequence.

A

-most common type of intracranial aneurysm, representing 90% of cerebral aneurysms
-aneurym in the circle of wills. Increases pressure as nowhere to go which compresses the brain and causes pain. Can cause subarachnoid haemorrhage if it ruptures. can cause haemorhagic stoke, causing sudden severe headache or major brain damage

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14
Q

What is a thrombus and embolus

A

-thrombus= blood clot within the circulation (tissue damage=collagen exposure=clot)
-embolus= thrombus (or other mass) detaches and moves through circulation until it lodges in a smaller vessel

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15
Q

What is infarction. The 3 types (cerebral, coronary, peripheral). Causes.

A

-death of tissue due to interruption of the blood supply and ischemia
1. Coronary= myocardial infarction - heart attack
2. Cerebral = ischaemic stroke
3. Peripheral= Gangrene

-due to a thrombosis, embolism, atherosclerosis, vasculitis, compression due to tumor or injury, vessel spasms, blood hyper viscosity

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16
Q

What are the 3 ischaemic heart diseases. Definitions.

A

-caused by coronary atherosclerosis and thrombosis
1. Angina: reversible ishaemia due to coronary narrowing, from atherosclerosis
2. Myocardial infarction: irreversible damage due to coronary thrombosis causing blockage
3. Heart failure: heart cannot pump properly due to damage from angina and MI

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17
Q

How pain is the same and differs in stable angina and Acute coronary syndrome (MI) -site, radiation, nature, severity, association features, length, onset, relieving factors

A

Both central heavy/tight/gripping/ dull aching pain due to ishemia. Can radiate to arms, neck, jaw, back, upper abdomen. Breathless

Stable angina= pain on exertion. Relieved by rest and GTN. Lasts <5 mins
MI= severe pain at rest. Associated with sweating, nausea. 20 mins to hours. GTN ineffective

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18
Q

List causes of heart failure. What is the most common heart failure

A

-cardiomyopathy- muscle disorders, not squeezing hard enough
-valve disease - stenosis, regurgitation
-arrhythmias (usually atrial fibrillation)
-left ventricular systolic dysfunction = most common due to high pressure system

-damage from MI - ischaemia
-Hypertension - myocardial damage as has to work harder
-aortic stenosis

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19
Q

Symptoms of heart failure (caused by the raised BP and poor CO)

A

1-breathless -worse lying flat and exercising (pulmonary oedema)
2-ankle swelling (peripheral oedema- interstitial fluid leakage into tissues causing fluid build-up)
3-neck veins stick out (raised jugular venous pressure)

-tiredness, faintness, confusion
-irregular heart beat
-white rim around iris (cholesterol deposits)
-cyanosis
-pitting oedema
-ascites
-pleural effusion

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20
Q

What is a normal heart beat bpm. what is tachycardia, bradycardia, cardiac arrest

A
  • Normal rhythm of the heart called sinus rhythm = 60-100BPM
  • Tachycardia = too fast (>100)
  • Bradycardia = too slow (<60)

-cardiac arrest= no heart beat, or chaotic rhythm,

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21
Q

What is a heart block/ atrio-ventricular block

A

impaired conduction through AV node and His-Purkinje system resulting in ventricular bradycardia (too slow), delay between atrium and ventricle conducting (atrium is normal activity)

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22
Q

What is atrial fibrillation and causes.

A

-uncoordinated atrial activity with irregular ventricular activity, causing irregular heart beat which is often too fast HR
-causes: ischaemic heart disease, valve disease (esp mitral), hyperthyroidism, hypertension, age.

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23
Q

What is a stoke and the 2 types. which is more common.

A

-when blood supply to part of the brain is cut off
1. Ischaemic= blood clot (atheroscleoris, thrombosis, embolism) causing occlusion. 85% of cases
2. Haemorrhage= ruptured aneurysm

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24
Q

What is a mini stroke. What is the usual cause

A

-transient ischameic attack (TIA), where supply to brain is temporarily interrupted, lasting few mins to up to 24 hours.
-can become a stoke, which is occlusion of cerebral arteries causing significant necrosis of brain tissue and permanent symptoms.
-usually secondary to atheroma of carotid artery causing stenosis

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25
Q

What is claudication and gangrene. symptoms

A

-Peripheral vascular diseases caused by atherosclerosis, thrombus, embolism

-claudication (narrowing) = walk a few feet then get pain in calf
-gangrene (blockage) = severe pain on walking. Swelling. Purple. Loss of sensation. Pain at night

-impaired blood flow during exercise due to blockage, causing anaerobic respiration. Build up of lactic acid causing pain

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26
Q

What are the layers of the vessels

A
  1. Tunica intima: endothelium, basement membrane, internal elastic membrane
  2. Tunica media: smooth muscle, external elastic membrane
  3. Tunica externa: advertía
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27
Q

Explain the fatty streak stages in atherosclerosis development. What are foamy macrophages

A

intracellular fat accumulates in wall and small extracellular lipid pools- damaged and permeable endothelium - lipids enter intima - monocytes enter and convert to macrophages - LDLs enter - macophages take up LDLs but cannot digest the fat so fill with fatty droplets in the intima = foamy macrophages

-can resolve
-clinically silent

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28
Q

Explain the fibrolipid plaque formation in atherosclerosis development

A

-smooth muscle cells (of the tunica media) migrate into area of lipid accumulation (tunica intima).
-This is followed by fibroblasts, cell proliferation and more lipid uptake.
-Collagen forms as a repair process but causes fibrotic wall that cannot contract
-lymphocytes and cytokine drive inflammatory process

The layer of lipid with the fibrous cap is the fibrolipid plaque which causes a buldge in the lumen

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29
Q

Explain a complicated lesion in atherosclerosis development. Complications of it

A

-plaque becomes so large that it occludes the vessel
-ulceration - endothelial layer separates and breaks down
-thrombus formation over plaque due to blood exposed to collagen causing platelet activation
-haemorrhage into plaques
-plaques fissure and rupture
-embolism- bits break off and enter circulation
-calcification
-aneurysm - fibrosis

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30
Q

How statins work to treat atherosclerosis. Name drug examples

A

simvastatin, atorvastatin
-reduces LDL synthesis by inhibiting HMG CoA reductase

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31
Q

How fibrates work to treat atherosclerosis. Name a drug

A

-clofibrate
Decreasing bad LDL and increasing good HDL (helps carry LDL to liver)

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32
Q

How Cholestyramine treats high cholesterol

A

Cholestyramine
converts more cholesterol to bile acid so reduces LDL. Removes bile acid
treats billery itch - build up of bilirubin

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33
Q

What is angioplasty, atherectomy, endarterectomy and other surgery options to manage atherosclerosis

A

-Angioplasty – stick a balloon into vessel and dilate it
-Atherectomy – use a bur to get rid of plaque coring vessel
-Endarterectomy – remove diseased vessel and repair it
-Stent – expands vessel wall (increasing lumen) to re-establish blood flow
-Bypass graft – replace with vein

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34
Q

What is a haematoma

A

-damaged vessel causes blood leakage into the tissues
-can form a localised hard mass under the surface of your skin - looks purple

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35
Q

What are the 3 determinants for a thrombus [Virchow’s triad]

A
  1. Change in endothelial lining of vessel
  2. Change in blood flow pattern - no longer laminar
  3. Change in blood constituents - more sticky platelets
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36
Q

What is the main pre-disposing factor of an arterial thrombus. How it forms

A

pre-existing vessel wall with atheroma

-Platelet aggregation on the atheroma
-Clotting cascade activation creating fibrin
-RBCs trap within fibrin layer
-Layer of platelets on top of this, more clotting, fibrin and RBCs. This continues until artery blocks

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37
Q

What are lines of Zahn in histology

A

-a characteristic of thrombi.
- lighter layers of platelets and fibrin
-darker layers of RBCs

38
Q

Where and when a venous thrombosis is likely to occur. Risk factors

A

-as a result of stasis, most likely at valves
-tends to occur with burns/ trauma, surgery, cardiac failure, pregnancy (foetus compresses veins), immobility, long haul flights, contraceptive pill
-coagulation disorder. Increased WBC, thicker blood,
-age, lack of movement, obesity, cancer, heart failure

39
Q

DVT: management. What molecules are risen, who’s at higher risk

A

-lower limb surgery= immobility
-patients with malignancy= hypercoguable state

D-dimers are raised

anticoagulants, calf compression and stockings

40
Q

2 causes of left atrial thrombosis

A

atrial fibrillation
mitral stenosis

41
Q

4 fates of a thrombus

A
  1. Lysis - dissolves and resolution
  2. Retraction and recanalisation -shrinks creating space for blood flow. Epithelium lines thrombus and returns to normal with some scarring
  3. Organisation - fibroblasts and scarring
  4. Embolism
42
Q

What material can form an embolus

A

-thrombus, atheromatous debris, vegetations on valves, infective endocarditis, broken bone, gas, amniotic fluid, tumour, IV foreign material

43
Q

What is Caisson’s disease

A

Aka the Bends in divers
-Increased pressure traps air in blood which create bubbles under decompression
- fatigue, joint and muscle aches, cloudy thinking, numbness and weakness.

44
Q

Main causes of pulmonary embolism

A

-DVT in leg, travels through venous system through the heart and blocks pulmonary artery in lung
-also from pelvic veins

45
Q

What is a saddle pulmonary embolism

A

-large blood clot gets stuck in the bifurcation of the main pulmonary artery
-hilium gets blocked, putting extra strain on right side of heart
-causes sudden death due to hemodynamic collapse

46
Q

What is a wedge infarction of the lung caused by. Symptoms

A

-type of pulmonary embolism that blocks the lung lower down so cuts off half of the lung and causes infarction
-chest pain when exhaling. Breathlessness

47
Q

Causes of pulmonary hypertension

A

-embolism - tiny bits break off and lodge in different areas
-left heart failure, congenital heart disease, connective tissue disease, coronary artery disease, high blood pressure, liver disease (cirrhosis), COPD

48
Q

what happens to the myocardium during MI. <6 hours. 6-24 hours. 24-48 hours. Several days. Several weeks

A

<6 hours: no visible changes (only ECG changes)
6-24 hours: pink cardiomyocytes start to lose their nuclei
24-48 hours: Pale cells. neutrophils infiltrate and macrophages phagocytose dead cells
Several days: hemopericardium
Several weeks: grey cells and fibrotic. Granulation tissue trying to repair, ingrowth of small blood vessels, fibroblast and collagen, scarring

49
Q

What is haemopericardium and causes. what it leads to

A

blood accumulates in the pericardial cavity
-due to trauma, aortic dissection, anticoagulation, MI
-causes tamponade (decreased CO and shock) and circulatory collapse.

50
Q

What is a false aneurysm

A

-AKA arterial pseudoaneurysm
-not weakened and bulged. It is due to trauma which has caused blood to leak out of vessel into surrounding tissue, causing a haematoma

51
Q

What is the most common place for an aneurysm

A

Aorta due to being the largest and highest pressure

52
Q

Where is a dissecting aneurysm. who is it more common in

A

-in the thoracic aorta
-more common in elderly and Marfan’s syndrome

53
Q

Treatment for stable angina

A

-lifestyle measures
-nitrates (GTN spray) for attacks
-anti-hypertensives = beta blockers, Ca antagonists, potassium channel activator
-antiplatelets=aspirin
-lipid lowering= statins

54
Q

Treatment for acute coronary syndrome (STEMI, NSTEMI and unstable angina)

A

-STEMI= emergency PCI (usually stenting) with dual anti platelet afterwards. [MONA= morphine, oxygen, nitrate, aspirin]
-NSTEMI or unstable angina =antianginals, anticoagulants, lipid lowering, reducing hypertension, statins

-PCI – percutaneous coronary intervention (or surgical Coronary Artery Bypass Grafting) for severe or resistant cases.

55
Q

What are the 3 types of acute coronary syndrome [NSTEMI, unstable angina, STEMI]. differences

A
  1. Unstable angina: partial occlusion of artery, no permanent damage to heart
  2. NSTEMI = Non-ST-elevation myocardial infarction
  3. STEMI = ST-elevation MI. Classic heart attack causing extensive damage
  • NSTEMI usually results from narrowing, transient occlusion, or microembolization of thrombus.
    -STEMI -due to complete occlusion of coronary blood vessel. Defined based on ECG criteria. Usually use stented to treat
56
Q

Acute and chronic complications of MI

A
  • Acute/early – ishaemia of internal organs, cardiac arrest/death, arrhythmias, heart failure, cariogenic shock (hypotension) rupture of muscle, aneurysm.
  • Chronic/late – arrhythmias, heart failure, angina, recurrent MI.
57
Q

List ways of investigating cardiac issues

A

-ECG, chest x-ray, cardiac MRI, CT scan, myocardial perfusion scan, ultrasound, stress testing, coronary angiogram, toponins
-Urea and electrolytes, thyroid function, Brain natriuretic peptide (rise in heart failure)

58
Q

What an ECG will show in angina attack and an MI

A

-stable Angina= ST depression
-MI = ST elevation or T inversion

59
Q

What protein is released due to cell death in MI

A

troponin
(not in angina as although there is reduced blood flow there is no cell death)

60
Q

Causative factors of valvular heart disease

A

rheumatic fever, congenital, degenerative, infective/ sterile endocarditis, Marfan’s syndrome

61
Q

Treatment for valvular heart disease, and what specifically for aortic stenosis

A

-Treat symptoms – e.g. diuretics for heart failure, anti-arrhythmics
-lifelong warfarin
-Surgical valve repair or replacement – (mechanical or tissue)
-Transcatheter Aortic Valve Implantation (TAVI) if aortic stenosis and too weak for heart surgery.

62
Q

What classes of meds needed for AF

A

-increased risk of thrombi-embolism and strokes – so give warfarin
-heart rate control - beta blockers, calcium channel blockers
-rhythm control - only within 48 hours as don’t want to risk a thrombus flying off and causing embolism. Eg. digoxin

63
Q

How AF increases risk of heart failure and stoke

A

-AF has irregular heart beat which causes turbulent blood flow. Can cause a mural thrombus on the wall of the atria due to microstasis, which can ping off and embolise and cause a stroke.

-When HR is fast, less time is spent in diastole so less time for heart to fill so less blood pumped out of heart. Lower CO means less blood supplied to coronary arteries so higher chance of heart failure

64
Q

What proportion of the heart cycle is in systole and diastole

A

1/3 in systole
2/3 in diastole

65
Q

Why you pee lots when drink alcohol

A

Alcohol inhibits ADH which is involved in fluid retention. so inhibiting the causes fluid to pass out into urine

66
Q

Sodium and potassium levels of blood in normal and in kidney failure

A

-normal kidney= increases sodium into blood so water retention. Decreased potassium, going into urine
-kidney failure = decreased sodium, and increased potassium = hyperkalaemia. (But they don’t pee more)

67
Q

Most common valvular heart diseases. What occurs at the valves when they are diseased

A

-ASMR = aortic stenosis and mitral regurgitation
-calcified tissue accumulates in the valve which distorts the valve and causes it to become ulcered, unable to function properly

68
Q

What illness progresses to rheumatic fever.

A

-upper respiratory tract infection
-it occurs 2-3 weeks after Step throat (Scarlett fever) when left untreated.
-Group A haemolytic strep infection (s.pyogenes)

69
Q

Diagnostic criteria for Rheumatic fever.

A

-rheumatic fever causes inflammation at multiple sites causing:
- carditis, arthritis, chorea, erythema marginatum (red skin patches), subcutaneous nodules, arteritis

70
Q

Pathogenesis of rheumatic fever causing carditis. Ways it affects the heart

A

-Rheumatic fever causes cardiac damage, making patient susceptible to IE if bacteria enter bloodstream

-antibodies produced in response to strep which cross-react with antigens on cardiac muscle and heart valves. This causes:
-vegetations on heart lining = endocarditis
-inflammation of cardiac muscle (myocarditis) creating Aschoff bodies which are immune cells between muscle fibres
-fibrous pericarditis - fibrin between pericardium and heart wall
-ruptured cord tendinae

-fibrosis, vegetations, fusion, calcification of heart valves. Embolism to coronary vessels

71
Q

Causes of infective endocarditis, who are at risk

A

-usually need a pre-existing vascular or congenital defects in order to develop IE, as irregular structure increases risk of developing infection if have bacteraemia
-eg. rheumatic fever, structural congenital defect, cardiomyopathy, previous IE, prosthetic heart valve, valvular heart disease, aortic stenosis, IV drug abuse
-source of bacteraemia eg. staph aureus, staph epidermis

72
Q

The thrombosis process than occurs in infective endocarditis. What are the local effects on the heart

A

-damaged endocardium due to certain factors is more susceptible to infection
-exposed collagen = platelet and fibrin deposition =vegetation
-bacteraemia causes bacteria (or fungi) to colonise this vegetation on endocardium
-Bacteria proliferate, vegetations grow, creating small nodule of platelets, fibrin, bacteria, phagocytes
=results in thrombus, embolism to coronary vessels and distant sites, causing infection and ischaemia. Arrhythmias, deteriorating valve function, murmurs, heart failure
-usually affects the valves

73
Q

what is the criteria called that is used for diagnosing IE. How many majors and minors are needed

A

DUKES CRITERIA :
2 MAJOR
1 MAJOR 3 MINOR
5 MINOR

74
Q

Signs and symptoms of infective endocarditis

A

-heart murmur
-weight loss
-splenomegaly (enlarged spleen)
-splinter haemorrhages - embolism in nail bed
-glomerulonephritis & haematuria - embolism in kidney
-Roth spots -embolism in retina
-embolism in limbs/ brain/ heart
-finger clubbing
-chronic anaemia, leucocytosis
-flu-like- high temperate, cough, sweats, pale, SOB, fatigue, muscles and joint pain

75
Q

What condition is splinter haemorrhages found in and how they occur

A

IE
embolisms of the small vessels in nail beds

76
Q

Diagnosis of IE

A

-new or changing heart murmur
-Blood test - Full blood count, Erythrocyte sedimentation rate (high)
-Blood cultures - negative in 14% of cases
-transosophgeal ultrasound
-clinical features

77
Q

Treatment for IE

A
  1. Antimicrobial: High dose and long course of IV antibiotics for 6 weeks
    -Penicillin + gentamicin
  2. surgical removal of valve
78
Q

Prophylaxis advice for IE in dentistry

A
  • Dental procedures that cause bacteremia = extraction, deep scale
    – NICE guidlelines say should not be using prophylactic antibiotics in dentistry as there is little evidence that it works and concern of allergic reactions
    -only consider for those at high risk, such as HIV, & some other immunocompromised
    -Liaise if in doubt
  • Preventative measures such as OH encouraged
79
Q

Does IE more commonly affect LHS/RHS. Which valves are affected

A

-95% cases LHS
-Mitral and aortic affected equally

80
Q

What organisms cause IE. Which are most common. and the most common in acute IE

A

-Bacterial is most common - staph, oral & faecal strep,
-Also HACEK - Hamophilius, Actinobacillus, Cardiobacteramia hominis, Eikenella corrodens, Kingella
-Also fungal - candida, aspergillus
-Acute = staphylococcus aureus most common

81
Q

What is RHS endocarditis usually caused by. which valve is affected

A

-5% cases
-tricuspid valve
-usually secondary to IV drug abuse or immunsuressed
-usually due to staph from skin eg. staph epidermis

82
Q

In medicine, why antibiotic prophylaxis used for IE. what is usually given

A

-given before procedure that release bacteria into blood stream to prevent bacteria forming a vegetation on endocardium and becoming infected
-usually 3g amoxicillin 1hr before treatment

83
Q

What erythrocyte sedimentation rate shows

A

sign of inflammation and illness
-measure red cell time from one side of tube to another
-more ill means thicker blood means longer time taken = Higher ESR

84
Q

Signs of IE that occur in the hands

A

-Splinter haemorrhage in finger nails (if >8 years old very likely IE, otherwise trauma)
-Osler’s nodes - red-purple raised lumps on fingers or toes, tender to touch
-Skin rash. -due to chronic Osler’s nodes
-Pupura
-Finger clubbing
-Janeway lesions - red lesions on fingers, similar to Osler’s nodes

85
Q

Signs of IE that occur in the eye

A

-Roth spots= sub-conjunctival haemorrhages (white of eye is now bright red – blood in eye becomes oxygenated)
-unilateral blindness (embolic)

86
Q

Arguments against prophylaxis in dentistry for IE

A

-no consistent association between IV procedure and development of IE. The clinical effectiveness of prophylaxis is not proven
-regular tooth brushing presents a greater risk of IE than a single dental procedure
-people with perio, if they eat something, bacteria enter blood stream, but they don’t take antibiotics every time they eat or brush
-not cost effective and may lead to a net loss of life - Fatal anaphylaxis from antibiotics is more than the chance of IE

Inform patient it is highly unlikely that they will get IE. Discuss risks and benefits of prophylaxis. Importance of good OH to prevent. Explain symtpoms of IE and when to seek advice. Same risk of undergoing invasive procedures such as body piercing or tatooing

87
Q

Diagnosis fo claudication. what is ABI

A

-history: pain in calf on walking for a while, but resolves at rest
-Measure blood pressure in legs: Ankle-brachial pressure index ABI <0.9. Use Hand Held Doppler machine and blood pressure cuff

88
Q

If untreated, what claudication can cause

A

-pain at rest and walking
-critical ischameia = MI or stroke
-may need amputation

89
Q

Why diabetes increases risk of CVD

A

accelerates atherosclerosis

90
Q

Non-cardiac causes of heart failure

A

-anaemia- need to pump larger volume of blood to get same about of oxygen
-hyperthyroidism -causes vasodilation, higher blood demand
-fluid overload from IV therapy, renal failure
-pulmonary hypertension, COPD (increases RHS heart pressure)
-Arteriovenous shunts – abnormal connections between coronary arteries and venous side of the heart

91
Q

signs of anterior, middle and posterior cerebral artery stoke

A

Anterior= hemiparesis (weakness), behavioral changes, aphasia, apraxia.
Middle= unilateral weakness, speech deficit
Posterior= visual changes

92
Q

Bacteria from the oropharynx and the gut causing IE

A

strep viridans
strep faecalis

Human diseases stage 3 (9 decks)

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