CVS clinical cases Flashcards

1
Q

if someone has swelling in lower limb which is painful and is common with people on long flights

A

DVT

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2
Q

what can DVT lead to if the symptoms are sudden breathlessness and pain to breath

A

pulmonary embolus

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3
Q

why specifically can a lower limb start to swell

A

DVT causes disruption to normal circulation and forms block of vessel leads to stasis of blood which leads to plasma leaking out the vessel and causing oedema

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4
Q

what does a DVT look like

A

swelling, pain, tender, inflammation, warmth

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5
Q

which veins are most at risk to DVT

A

femoral, popliteal, tibial vein, lesser saphenous, greater saphenous, iliac

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6
Q

how does immobility lead to DVT

A

lower limb muscles aid in return on blood to the heart

without it you only have the valves and little pressure from the heart

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7
Q

what is a thrombus

A

blood clot

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8
Q

what is virchows triad

A
theory concerning homeostasis 
thrombosis was the result of a delicate interplay between three factors which promote coagulation 
these are 
1 changes in blood flow 
2 changes in the vessel wall 
3 changes in blood constituents
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9
Q

what is stasis

A

stagnation or cessation of blood flow

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10
Q

in stasis why is blood prone to clotting

A

platelets are in contact with the endothelium - clotting factors are not diluted by fast blood flow
inflow of anticoagulants uis slowed

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11
Q

what changes in the vessel wall can lead to DVT

A

damage to the lining of the vein due to inflammation (vasculitis)
chemotherapy

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12
Q

what causes changes in blood flow to result in DVT

A
thrombophilia - abnormal factor V leiden which makes clotting more likely 
cancer 
smoking
contraceptive pill 
pregnancy
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13
Q

what is an embolus

A

material such as blood clot, fat, air, amniotic fluid or foreign body carried by the blood and lodged in a mother area

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14
Q

what is a venous thromboembolism

A

DVT

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15
Q

why is oxygen saturation lowered in pulmonary embolism

A

V/Q mismatch

there is ventilation but no perfusion of blood due to clot

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16
Q

how does D -Dimer test for DVT/VTE

what are the problems with the test

A

when you have a DVT you get large amount of D-dimer which is a product of fibrin breakdown
sesntivte test but not specific to DVT - can be caused by other diseases such as eclampsia, kidney disease, infection, liver disease

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17
Q

what techniques can be used to test for VTE

A

doppler ultrasund
V/Q scan
computed tomography pulmonary angiogram (CTPA)

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18
Q

what treatments are there for DVT or pulmonary embolism

A
warfarin (pills) - monitored 
low molecular weight heparin (anticoagulant) - acute action (sub cutaneous) 
Xa inhibitors 
- rivaroxaban 
- apixaban 
- edoxaban
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19
Q

what is warfarin

A

Warfarin inhibits the effective synthesis of biologically active forms of the vitamin K-dependent clotting factors: II, VII, IX and X, as well as the regulatory factors protein C, protein S and protein Z.
anticoagulant - used in cases of thrombophilia

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20
Q

how would you reverse warfarin

A

give Vit K

in extreme cases give large amounts of prothrombin

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21
Q

what advice would you give someone to reduce DVT and pulmonary embolism

A
stop smoking
lose weight 
regular walking 
keep hydrated 
compression stocking
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22
Q

what is a cerebral infarction

A

stroke

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23
Q

what is a stroke and what can it be caused by

A

rapidly developing loss of brain function due to disturbance in the blood supply to the brain
it can occur via blockage by thrombus (ischaemic stroke)
or by haemorrhage (haemorrhage stroke)

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24
Q

what is a cerebral haemorrhage

A

rupture of a blood vessel can produce bleeding
when an aneurysm ruptures - 15-20% of all strokes and are deadly
best preventative by controlling high blood pressure

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25
Q

what is a TIA

A

mini stroke
temporary disruption of the circulation to part of the brain due to embolism or thrombosis to brain arteries
most common symptoms are loss of vision in one eye and weakness or numbness in one limb or part of limb
patient recovers within 24 hours

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26
Q

what are the symptom of stoke and how can it be identified

A
weakness of the arm or leg 
slurring of speech (dysarthria) 
drooping of the corner of the mouth 
dysphagia 
expressive dysphagia (struggle to speak or understand others)
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27
Q

what is FAST

A

face
arm
speech
time

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28
Q

what are the signs of a stroke or TIA

A

signs detected by clinician
sings of atrial fibrillation
hypertension
possible bruit (turbulent flow caused by atherosclerosis in coronary artery)

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29
Q

what are the risk factors of stroke

A
advanced age 
hypertension 
previous stroke or TIA 
diabetes 
high cholesterol 
smoking 
atrial fibrillation
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30
Q

what are the possible rules of blood clot in stroke

A

aorta - brachiocephalic artery - right common carotid artery - right internal carotid artery

aorta - left common carotid artery - left internal carotid artery

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31
Q

what investigations can you do for stroke

A

CT can of head
ultrasound of carotid artery may show evidence of narrowing (TIA)
echocardiogram of the heart to see if clot in atria
ECG may show evidence of atrial fibrillation

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32
Q

on a CT scan what are the visual difference of a haemorrhage compared to infarction

A

haem - white area to show bleeding

infarction - cell death - dark swollen area

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33
Q

why would someone with stroke be given digoxin

A

cardiac glycoside which increases the refractory period decreasing rate in atrial fibrillation
reduces rate of heart but increases force of contraction so no loss in CO

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34
Q

how can stroke be prevented

A

early intervention of high blood pressure

early detection of atrial fibrillation

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35
Q

what is lisinopril

A

ACE inhibitor which reduce risk of stroke as reduce blood pressure
all things ending in -pril reduce blood pressure
stop conversion of AG1 - AG2 which means less vasoconstriction and less water retention

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36
Q

what is the difference between and symptom and a sign

A

symptoms is what the patient indicates from the disease

sign is what the clinician picks up on not apparent to the patient

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37
Q

what are the clinical symptoms and signs of myocardial infarction

A

symptoms:
severe crushing generalised in the chest by sudden onset
pain often spreads to arm and neck
associated with nausea, vomitting, sweatiness and breathlessness
signs:
distressed, low blood pressure and fast heart rate
could have pulmonary oedema

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38
Q

what is the difference between angina and MI

A

angina is reduced oxygen to the heart which can be exacerbated but MI is an specific block of the coronary system which shuts off blood to the heart and there is tissue death

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39
Q

what are the three factors of angina

A

constricting discomfort in the front chest and neck, jaw, shoulders
precipitated by physical exertion
received by rest of GTN within about 5 minutes

typical angina is all three
a-typical is 2 of the 3
non-anginas chest pain is one or zero

40
Q

what is the biological cause of angina

A

usually due to flow limiting atherosclerosis resulting in schema of the heart
usually in normal situations you don’t have pain but when there is need for stress on the heart such as exercise there atherosclerosis stops blood flow and causes pain

41
Q

what happens during a heart attack

A

atheroma causes narrowing of coronary vessels
if becomes unstable a piece may brea off and form a clot
this starves the heart of O2 causing muscle damage

42
Q

what is a type 1 MI

A

plaque rupture with (non)occlusive thrombus

43
Q

what is a type 2 MI

A

atherosclerosis and O2 imbalance

vasospasm

44
Q

what are the two causes for heart arteries to narrow

A

atherosclerosis - fatty plaques in inner walls obstructing blood flow
coronary thrombosis

45
Q

which part of vichrows triad is affected in MI

A

changes in the vessel wall

46
Q

what are the risk factors in MI and angina

A
dyslipidaemia 
smoking 
diabetes 
hypetension 
male sex 
increasing age 
family history 
obesity
47
Q

what investigations can be done to find angina or MI

A

ECG - look at ST segment - if ST elevation then there is coronary artery completely blocked
raised troponin in blood
echo cardiogram shows reduced contraction inaffected area
coronary angiogram

48
Q

what surgical intervention can be done to manage atherosclerosis or blocking of CA

A

thrombolytic drugs or primary percutaneous intervention

49
Q

what is simvastatin and why is it given to people at risk of MI

A

inhibition of HMG CoA reductase and therefore reduces production of cholesterol

50
Q

what other drugs can be given to patients with angina or MI risks

A
beta blocker s- propranolol 
prolong diastole 
increase coronary filling time
reduce sympathetic activity
aspirin - blocks thromboxane 
clopidogrel - ADP receptor antagonists on platelets 9for stabel angina)
51
Q

what is fallots tetralogy

A

lack of o2 to the body - it has 4 common effects

52
Q

what does congenital mean

A

present from the birth

it does no mean genetic

53
Q

what is an example of congenital being not genetic

A

congenital syphilis

54
Q

what are the normal heart sounds

A

s1 is lub - closure of tricuspid and mitral valves

s2 is dub - closure of aortic and pulmonary valves

55
Q

what are heart murmurs and give examples

A

additional sounds in the heart
aortic stenosis causes more sound during systole
aortic regurgitation - sound during diastole

56
Q

what is a ventricular septal deficit

A

allows oxygenation blood to mix with deoxygenated mood causing the heart to work harder to provide enough oxygen to the body tissues

57
Q

when does ventricular septal defect occur

A

can be present at birth and outgrown or acquire later such as during heart attack
can occur alone or with other congenital heart defects

58
Q

what are the four characteristics of fallots teratology

A

pulmonary stenosis (narrowing)
overriding aorta
VSD
right ventricular hypertrophy

59
Q

what is the route of blood in teratology of the heart

A

RA - RV - lungs - LA - LV - RV - Pulmonary artery - lung etc

60
Q

why would someone appear blue in Fall - TerAT

A

cyanosis - blue / purple colour of the skin due to tissues near the surface of the skin being starved of O2

61
Q

what is a tat spell

A

acute episode of hypoxia

shortness of breath - cyanosis

62
Q

what causes a tat spell

A

initiated by events that cause decreased systemic vascular resistance leading to increased venous return and increased shunting through the VSD

63
Q

what do older children in a Tat spell usually do

A

crouch or squat which increases systemic resistance and allows reversal of shunt

64
Q

what are the symptoms and sings of teratology of the heart

A

difficulty feeding
failure to gain weight
retarded growth of phyla development

65
Q

what is the shunt operation in surgical treatment of fallot of the heart

A

shunt from aorta or branch of artery from the arm to the pulmonary artery - ie more blood back to lungs for re-oxygenation (could be subclavian artery to pulmonary artery)
palliative

66
Q

what is the blalock thomas taussig procedure

A

total repair - curative - of teratology of fallot

67
Q

when is corrective surgery carried out for teratology of the heart, what is the mortality and when does it do

A

around 6 months old
less than 5% mortality
receive right ventricular flow - repair VSD and resection of muscle

68
Q

what happens if ToF goes untreated

A

rapid increase in RV hypertrophy due to pulmonary stenosis
lead to HF
35% mortality in first year of life
50% mortality in first 3 years of life

69
Q

what happens if ToF undergoes total surgical repair

A

improved haemodynamics and often good to excellent cardiac function
no exercise tolerance
progressive leaky pulmonary valve
survival rates much improved

70
Q

what are the signs of ToF

A

heart murmur
clubbing
polycythemia
tat spells

71
Q

what are the symptoms of ToF

A

low blood SaO2 = cyanosis
difficulty feeding
failure to gain weight
retarded growth

72
Q

what is aortic stenosis

A

narrowing of the aortic valve

73
Q

what are the symptoms of aortic stenosis

A

heart murmur
angina pectoris
difficulty breathing
syncope - fainting

74
Q

what are the three common symptoms of valve diseases

A

lightheadedness
chest pain
short of breath

75
Q

why does breathlessness occur in aortic stenosis

A

narrowing of aortic valve so hypertrophy of LV

stiffening of LV and diastolic impairment (impair filling)

76
Q

why do you feel lightheaded in an aortic stenosis

A

Lv baroreceptors sense high LV pressure

indue hypotension, bray cardia which lads to syncope

77
Q

what is the mechanism of fainting in aortic stenosis

A

MAP increases due to pressure from hypertrophy of LV - increased Barorecerptor firing - decrease in symptoms tone and increases in para symptoms

78
Q

why do you have chest discomfort in aortic stenosis

A

increased LV demand for oxygen from hypertrophy - low perfusion and increased demand in some patients with CAD

79
Q

why does exercise exacerbate symptoms in aortic stenosis

A

increased O2 requirements, increased heart rate

greater impact of obstruction to flow from heart

80
Q

what is the heart murmur of aortic stenosis and where is it best heard

A

right sternal boarder
second intercostal space
systolic ejection murmur

81
Q

what is the clinal term to describe narrowing of heart valve

A

stenosis - abnormal narrowing of structure - most aortic stenosis’ are congenital bicuspid

82
Q

how does blood pressure differ in aortic stenosis

A

always higher in every region of LA and LV it becomes less when in the aorta

83
Q

if left untreated what happens with aortic stenosis

A

heart failure - 2 year average survival
syncope - 3 year average survival
angina - 5 year average survival

84
Q

what are the clinal signs of aortic stenosis

A

loud ejection systolic heart murmur
reduced pulse pressure
forceful apex beat

85
Q

what surgical interventions are there for aortic stenosis

A

if the LV strats to dilate then surgery is considered
the aortic valve can be replaced by open chest surgery or percutaneous route
valves are either made from metal or plastic (prosthetic) or pig valves (tissue valves)

86
Q

what are the primary and secondary intervention of aortic stenosis

A

with artificial valves require life long anticoagulant treatment with warfarin
patients with tissue valves do not require warfarin

87
Q

how can flu be associated with systolic heart failure

A

myocarditis - inflammation of the heart muscle - inflammatory cardiomyopathy
caused by infection, immunology, drugs

88
Q

what are viral causes of myocarditis

A
adenovirus 
parovirus 
coxackie virus 
HIV 
enterovirus 
rubella 
polia 
CMV
89
Q

what does myocarditis do to the heart muscle

A

heart muscle becomes thick and swollen

90
Q

what are the symptoms of systolic heart failure

A

tiredness, breathlessness - especially when lying flat or suddenly at night (paroxysmal nocturnal dyspnoea)
ankle swelling
passing lots of urine at night

91
Q

what are the clinical signs of systolic heart failure

A

tachycardia - greater than 110
hypotension - less than 100 systolic
pitting oedema

92
Q

why does tachycardia and hypotension occur in systolic heart failure

A

enlarged ventricles fill with blood

the ventricles pump out less than 40-50% of the blood

93
Q

what would a blood test show of someone with systolic heart failure

A

raised BNP - brain natriuretic peptide

94
Q

what would an x ray show for someone with systolic heat failure

A
A - alveolar oedema 
B - Kelry B lines (interstitial oedema)
C - cardiomegaly 
D - dilated prominent upper lobe vessels
E - pleural Effusion
95
Q

what do inotropic agents do

A

increases force of contraction o the heart - increases ventricular performance and EDV

96
Q

what is an LVAD

A

left ventricular assist device

helps pump heart - need warfarin as risk of thrombosis

97
Q

what treatments are there for systolic heart failure

A

furosemide (loop diuretic), ACE inhibitor (ramipril), beta blocker (propranolol)