Brainscape's Knowledge GenomeTM

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


See full index

xRandom > Cardio Week 4 > Flashcards

Cardio Week 4 Flashcards

1
Q

where does right and left coronary arteries arise from

A

base of aorta

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

where does most coronary venous blood drain

A

via coronary sinus into right atrium

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

what is the intrinsic ways in which O2 is supplied to coronary arteries

A

decreased PO2 causes vasodilation, metabolic hyperaemia matches flow to demandAdenosine (ATP) also potent vasodilator in attempt to increase blood/O2 supply

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

what is the extrinsic ways in which O2 is supplied to coronary arteries

A

sympathetic stimulation of heart results in dilation despite constrictor effect (over ridden by metabolic hyperaemia as result of HR and SV) and circulating adrenaline causes vasodilation

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

when does peak coronary blood flow occur

A

diastole (due to high pressures in left ventricles and subendocardial vessels not compressed)thus shortening diastole - decreased coronary flow

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

the grey matter consists of most of brains neurone cell bodies. What happens during hypoxia

A

loss of consciousness after few seconds of ischaemia and irreversible damage in 3 minutes

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

which two structures anastomose to form circle of willis (major cerebral arteries arise from here)

A

basilar (formed by two vertebral arteries) and carotid arteries

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

what is the adaptation to cerebral circulation if MABP rises/falls

A

rises - vessels constrict to limit blood flow

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

when does autoregulation of cerebral circulation fail

A

if MABP falls below 60mmHg or rises above 160mmHg (below 50 - confusion, fainting, brain damage)

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

what is the value for normal intracranial pressure (ICP)

A

8-13mmHg

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

how to calculate cerebral perfusion pressure (CPP)

A

MAP - ICP increased ICP (injury or tumour) decreases CPP and cerebral blood flow

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

what is the blood brain barrier permeable to

A

O2 and CO2

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

how does glucose cross BBB

A

facilitated diffusion using specific carrier molecules since brain has obligatory requirement for glucose

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

what is BBB exceptionally impermeable to and what does this help protect brain from

A

hydrophillic substances such as ions, catecholamines, proteins etc - protect from fluctuating levels of ions etc in blood

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

how is the pulmonary circulation protected from pulmonary oedema

A

absorptive forces exceed filtration forces

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

what is the result of hypoxia on the pulmonary circulation

A

causes vasoconstriction (opposite to systemic) in order to divert blood from poorly ventilated areas of lung

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

what happens to skeletal muscle circulation during exercise

A

local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity and adrenaline causes vasodilation

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

what is the advantage of large veins in limbs lying between skeletal muscle

A

contraction of muscle aids venous return

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

what is the cause of varicose veins

A

blood pools in lower limb veins if venous valves become incompetent - doesnt lead to reduced CO due to chronic compensatory increase in blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is cardiomyopathy

A

any disease of cardiac muscle that often results in changes of chambers or thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is dilated cardiomyopathy

A

big heart (2-3x normal), heart is flappy and floppy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is causes of dilated cardiomyopathy

A

genetics, toxins, booze, nutritional deficiency, doxorubicin (chemotherapy), cardiac infection or pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the clinical features of dilated cardiomyopathy

A

general picture of HF, lowered exercie tolerance, SOB and chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is hypertrophic cardiomyopathy

A

big solid heart, diastolic dysfunction since heart cannot relax so eventual outflow obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is causes of hypertrophic cardiomyopathy

A

genetic (beta myosin heavy chain, myosin binding protein C and alpha tropomysin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the signs of hypertrophic cardiomyopathy

A

bulding IV septum, outflow tract obstruction, LV luminal reduction, disorganised myofibrils (swirls) - can cause sudden death in athletes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is restricted cardiomyopathy

A

causes lack of compliance - stiff heart, doesn’t fill well so diastolic dysfunction but can look normal and there is biatrial dilation as result of back pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the causes of restricted cardiomyopathy

A

deposition of something in myocardium (iron, amyloid, sarcoid, tumours and fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is amyloidosis

A

abnormal deposition of an abnormal protein, have tendency to form beta pleated sheets and body cant get rid of it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what does amyloidosis look like in heart

A

paleness and expansion but it is also pan systemic (effects different systems eg renal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is amyloid

A

a pink waxy material, stains positively for congo red, exhibits apple green birefringence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is arrhythmogenic right ventricular dysplasia (type of cardiomyopathy)

A

genetic disease, right ventricle becomes replaced by fat, not contractile to prone to arrhythmias and therefore sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is myocarditis

A

inflammation of heart - thickened beefy myocardiun

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the main viral causes of myocarditis

A

coxsackie A and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are non infectious causes of myocarditis

A

after infection eg rheumatic fever, after strep throat, after drug or systemic lupus erythermatosus (SLE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is rheumatic fever

A

classic mitral stenosis with thickening and fusion of valve leaflets, short and thick chord tendinae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is pericarditis

A

inflammation of pericardial layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are infectious causes of pericarditis

A

ECHO virus, bacteria (extension from elsewhere - pneumonia), fungi (post transplant) and TB (caseous material in sac)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is non infectious causes of pericarditis

A

immune mediates (rheumatic fever), idiopathic, uraemic (renal failure) post MI (dresslers syndrome) and SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are complications of pericarditis

A

pericardial effusion, tamponade, constrictive pericarditis, cardiac failure, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is endocarditis

A

affects heart lining but generally refers to inflammation of valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what are causes of infectious endocarditis

A

can occur normally in valves, virulent organisms, bacterial or fungal, IV drug abuse and septicaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are causes of non infectious endocarditis

A

rheumatic fever, SLE, non bacterial thrombotic endocarditis, carcinoid heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

who does endocarditis usually effect

A

people with abnormal valves eg previous rheumatic heart disease or prosthetic valves, congenial defects, MV prolapse or calcific disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the pathology of endocarditis

A

aggregates of organisms on heart valves called vegetations, bacteria excite acute inflammation and bacterial and inflammatory cells produce digest valve leaflets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the microbiology of endocarditis

A

HACEK (haemophilus, actinobacillus, cardiobacteria, eikenella, kingella) IV drug users (candida, staph aurerus) and prosthetic valves (epidermidis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the complications of endocarditis

A

arrhythmia, acute vascular incompetence, high output cardiac failure, abscess, fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is the systemic manifestations

A

olsers nodes, laneway lesions, roth spots, splinter haemorrhages, septicaemia, systemic septic emboli (brain, kidney, spleen), mycotic aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what are carcinoid tumours

A

neoplasms of neuroendocrine cells (see them in any mucosa) and release hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what markers do carcinoid tumours produce

A

excess 5HIAA, serotonin, histamine, bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the consequence of carcinoid tumours

A

flushing of skin, nausea, vomiting, diarrhoea, ride sided cardiac valve disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the most common tumour of the heart

A

atrial myxoma, can cause ball/valve obstruction, may cause tumour emboli, may develop endocarditis and is associated with systemic fever and malaise - IL6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is the clinical signs of angina

A

pressing, squeezing, heavy pain, radiation to arms and jaw, exertion, stress, cold wind, after meals, relieved by rest or GTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is differential diagnosis of chest pain which can be associated with GI tract

A

reflux - burning, provoked by foodpeptic ulcer pain - epigastic, point of finger gestures relieved by antacids oesophageal spasm biliary colic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is differential diagnosis of chest pain which can be associated with MSK

A

injury - tender, prolonged, exacerbated by moving nerve root pain

56
Q

what is other differential diagnosis of chest pain

A

pericarditis (central, posture related) or pleuritic pain (focal, exacerbated by breathing, sharp, catching)

57
Q

what chest pain can be counted as emergency

A

MI (ongoing), pulmonary embolus (breathless, dull - may also be pleuritic) and dissection of aorta (tearing, excruciating, severe then eases)

58
Q

what is perfusion imaging

A

non invasive test that shows how well blood flows through heart muscle - show areas of less blood flow cons - radiation, false readings

59
Q

what is CT angiography

A

non invasive, uses x-ray to visualise arterial and venous vessels though body

60
Q

what is an angiography

A

invasive, sheath inserted into artery, catheter advanced from wrist/groin to coronary ostium, X ray contrast injected to outline coronaries

61
Q

give a quick summary of drugs used in CHD

A

aspirin - anti platelet B blocker - slow HR, reduced O2 demand statin - reduce cholesterol ace inhibitor - reduces BP

62
Q

what vessels are used in coronary artery bypass (medial sternotomy)

A

long saphenous vein, internal mammary artery

63
Q

what are potential complications of coronary artery bypass

A

death, stroke, MI, AF, infection, cognitive impairment, sternal malunion, renal failure, failure to recover

64
Q

which patients are suitable for both CAB and PCI

A

multi vessel disease, diabetes, left main disease, co-morbidities

65
Q

what is percutaneous coronary intervention (PCI)

A

cardiac catheterisation which is insertion of catheter and injection of contrast dye into coronary arteries - used to open narrowing arteries or those blocked by plaque

66
Q

how does PCI work

A

guidewire down vessel, balloons threaded over wire,, stents implanted

67
Q

how is STEMI treated with revascularisation

A

primary PCI

68
Q

how is acute coronary syndrome treated with revascularisation

A

angiography with a view to revascularisation

69
Q

how is chronic stable angina treated with revascularisation

A

revascularisaion for severe symptoms or high risk (CABG vs PCI should be determined by discussion)

70
Q

what is the definition of a aneurysm

A

dilation of a vessel by more than 50% of its normal diameter (1.2-2.0cm normal aortic)

71
Q

what is true aneurysm

A

vessel wall is intact (all 3 layers)

72
Q

what is false aneurysm

A

there is breach in vessel wall (surrounding structures act as vessel wall)

73
Q

what are the different shapes of aneurysms

A

saccular (bubble on top), fusiform (within vessel) and mycotic (arises secondary to infectious process involving all 3 layers - common in IV drug users)

74
Q

what causes the medial degenerations which result in aortic abdominal aneurysm

A

regulation of elastin/collagen in aortic wall, aneurysm dilation, increase in aortic wall and progressive dilation

75
Q

what is the risk factor for AAA

A

age, gender (6:1 men to women) smoking, hypertension

76
Q

what is signs of symptomatic (25% of AAA) AAA

A

pain (mimic renal colic), trashing, rupture

77
Q

what occurs during AAA rupture

A

sudden onset of epigastic/central pain, may radiate through to back, collapse, 75% not make it to hospital

78
Q

what may AAA look like upon examination

A

may look well, hypo/hypertensive, pulsatile, expansile mass which may be tender, transmitted pulse

79
Q

when would you intervene in asymptomatic AAA

A

> 5.5cm AP diameter as this is when risk of rupture rapidly increases

80
Q

what does a duplex ultrasound do in AAA

A

used in asymptomatic for surveillance of diameter and involvement of iliac arteries - only tells us there is AAA not its exact diameter

81
Q

how is CT scan used in AAA

A

IV contrast in arterial system - lets see aneurysm morphology - shape, size, iliac involvement (only imaging to identify ruptured AAA)

82
Q

how is an open repair of an AAA undertook

A

laparotomy, clamp aorta and iliacs, use dacron graft (polyester)

83
Q

how is an endovascular aneurysm repair (EVAR) undertook

A

exclude AAA from inside vessel, inserted via peripheral artery, X ray guided, modular component - needs life long follow up

84
Q

what is acute limb ischaemia

A

sudden loss of blood supply to limb due to occlusion of native artery or of bypass gradt

85
Q

what is the clinical features of ischaemia

A

pain, pallor (pale then mottled), paraesthesia, paralysis, pulseless, perishingly cold

86
Q

what happens after 0-4 hours of ischaemia

A

white foot, painful, sensory motor deficit - salvageable

87
Q

what happens after 4-12 hours of ischaemia

A

mottled, blanches on pressure - partially reversible

88
Q

what happens after >12 hours of ischaemia

A

fixed mottling, non blanching, compartments tender/red, paralysis - non salvageable

89
Q

what is the management of acute limb ischaemia

A

ABC, FBC (U/Es, coag +/- troponin), ECG, CXR, anticoagulation

90
Q

what triad leads to tissue ulceration, necrosis and gangrene in diabetes

A

diabetic neuropathy, peipheral vascular disease and infection

91
Q

what may diabetic foot sepsis be a result of

A

simple puncture wound, infection from nail plate or from neuro-ischaemic ulcer

92
Q

NOTE

A

learn compartments of foot

93
Q

what are the clinical findings of diabetic foot sepsis

A

pyrexia, tachycardia, tachypnoeia, confused, kussmaul breathing

94
Q

what are the local signs of diabetic foot sepsis

A

swollen, tenderness, ulcer with puss extruding, erythema (redness), patches of necrosis, crepitus in soft tissue of foot

95
Q

how is diabetic foot sepsis managed

A

treated as vascular surgery emergency also antibiotics taking into account polycrobial nature of diabetic foot infection

96
Q

what is the aftercare of diabetic foot sepsis

A

diabetic foot problems can be prevented with adequate education, foot assessment and pressure offloading footwear

97
Q

how is chronic ischaemic disease developed

A

damage to artery wall (smoking, BP, glucose, cholesterol) and plaque formation

98
Q

what is intermittent claudication

A

muscle ischaemia on exercise - angina of the legs

99
Q

how can intermittent claudication be tested for

A

ankle brachial pressure index!!, also duplex ultrasound, CT angiography (invasive) and catheter angiography

100
Q

what does the results of ABPI tell us about claudication

A

normal - 0.9-1.2claudication - 0.5-0.85severe - 0-0.45

101
Q

what is the slow progression treatment of intermittent claudication

A

smoking, lipid lowering, anti-platelets, hypertension, diabetes, lifestyle issues

102
Q

what drugs used in intermittent claudication

A

cilostozol, pentoxifylin

103
Q

what is involved in an inflow bypass

A

anatomic or extra anatomic using prosthetic (Dacron, ePTFE) or own vein

104
Q

what causes critical limb ischaemia

A

if claudication doesn’t stop - can progress to this

105
Q

what is pain at rest a sign of

A

toe/foot ischaemia (lying and sleeping)

106
Q

what is ulcers and gangrene a sign of

A

severe ischaemia and damage (trauma and footwear)

107
Q

what is the findings of a clinical examination in critical limb ischaemia

A

cool to touch, absence of peripheral pulses, colour change, worse at night

108
Q

where does a DVT normally form

A

venous valve pockets and other sites of presumed stasis

109
Q

what does a distal vein thrombosis refer to

A

DVT of calves

110
Q

what does proximal vein thrombosis refer to

A

DVT of popliteal vein or femoral vein

111
Q

what causes a hypercoaguable state

A

malignancy, pregnancy, oestrogen therapy, inflammatory bowel disease, sepsis, thrombophilia

112
Q

what causes endothelial injury

A

venous disorders, venous valvular damage, trauma/surgery and indwelling catheters

113
Q

what causes circulatory stasis

A

left ventricular dysfunction, immobility or paralysis, venous insufficiency or varicose veins, venous obstruction from tumour, obesity or pregnancy

114
Q

what causes provoked VTE

A

surgery, hospitalisation (reversible) or cancer (irreversible)

115
Q

what is the consequences of VTE

A

fatal, reoccurrence, post thrombotic syndrome (pain, oedema, eczema, varicose veins, venous ulcerations) or chronic thromboembolic pulmonary hypertension (initially asymptomatic followed by dyspnoea, hypoxaemia, right heart failure)

116
Q

what is the test of exclusion in PE

A

D dimer - breakdown product of cross linked fibrin - valuable first line screening test for suspected VTE with low Wells scoreif undetectable - excludes PE

117
Q

what Wells score makes PE likely

A

> 4

118
Q

what is the first line of imaging in suspected VTE

A

CT angiogram

119
Q

what other tests can be used

A

CXR (normally in PE) and V/Q scan (mismatched perfusion defects - small PEs and pregnancy)

120
Q

what is the pharmacological interventions of DVT and PE

A

anticoagulation (prevent clots), thrombolysis (destroy clots) and analgesia (pain relief)

121
Q

what is the mechanical interventions of DVT and PE

A

graduated compression stockings (prevent post thrombotic syndrome for 2 years) and IVC filters (proximal DVT or PE who can’t have coagulation or who can but it keeps reoccurring despite target INR or LMWH - con they often thrombose)

122
Q

what specific drugs are used in DVT and PE

A

apixaban, rivaroxaban, dabigatran and endoxaban and frogmen (esp for DVT caused by cancer)

123
Q

when should thrombolysis be considered for DVT

A

symptomatic ileofemoral DVT symptoms less than 14 days duration and good functional status, life expectancy of 1 year or more and low risk of bleeding

124
Q

when should thrombolysis be considered for PE

A

consider pharmacological systemic thrombolytic therapy for patients with PE and haemodynamic instability, do not offer for stability

125
Q

what is a haemorrhagic stroke

A

bleeding occur inside or around brain tissue

126
Q

what causes haemorrhagic stroke

A

raised BP and weakened vessel wall due to structural abnormalities like aneurysm, arteriovenous malformation (AVM) or inflammation of vessel wall (vasculitis)

127
Q

what is ischaemic stroke (common)

A

clot blocks blood flow to brain - can be thrombotic, embolic or hypo perfusion (due to reduced flow of blood due to stenosed artery rather than occlusion of artery)

128
Q

what are the non modifiable risk factors for stroke

A

age, family history, gender, race and previous stroke

129
Q

what is the potentially modifiable factors for stroke

A

hypertension, hyperlipidaemia, smoking, history of TIA (temporary occlusion), AF, diabetes, congestive HF, alcohol excess, obesity, physical inactivity and poor socioeconomic status

130
Q

narrow window treatment of ischaemic stroke

A

thrombolysis or thromboectomy

131
Q

how to prevent next stroke if its atheroembolic or due to thrombus

A

antiplateles, statins for high lipids, diabetes and hypertension management

132
Q

how to prevent next stroke if its due to AF

A

anticoagulate ASAP via warfarin or direct oral anticoagulants (inhibit factor X and thrombin)

133
Q

what is a surgery used to manage stroke

A

haematoma evacuation - relief of raised intracranial pressure of carotid endarterectomy

134
Q

what imaging is used in stroke

A

CT brain +/- angiography - only way to differentiate between ischaemic and haemorrhagic stroke

135
Q

what is an atheroembolism

A

embolism from a thrombus forming on a atherosclerotic plaque - platelet rich clots - and infarcts in same side of carotid artery carotid scanning, CT/MR angiography of aortic arch

136
Q

what is a cardioembolism

A

embolism from clot formed in heart (usually left atrium) - clotting factor rich clots - infarcts bilaterally ECG (AF and LVH) or ECG bubble contrast study to look for interatrial connection

137
Q

what should you question in a haemorrhagic shock

A

young - investigate for underlying aneurysm and AVNmultiple haemorrhages - question vasculitis, moya moya disease, cerebral amyloid angiopathy

xRandom (26 decks)

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