week 3 Flashcards

1
Q

how do semilunar valves operate (what is their key differentiation from AV valves)

A

They close and open according to pressure gradients

They lack papillary muscles and chordae tendinae

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2
Q

what are the three layers of valves

A

fibrosa (innermost)
spongiosum
Ventricularis/atrialis (superficial)

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3
Q

what is sound 1

A

av valves closing

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4
Q

what is sound 2

A

SL valves closing

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5
Q

what is sound 3

A

rapid ventricular filling

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6
Q

what is sound 4

A

atrial contraction and turbulent blood in filled ventricles

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7
Q

what are pathological causes for the splitting of second heard sound

A

bundle branch blocks

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8
Q

frank starling mech 7 steps

A

greater venous return
greater end diastolic volume
greater preload
greater muscle tension
greater force of contraction
greater ejection fraction
greater cardiac ouput

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9
Q

what regulates cardiac work

A

baroreceptor reflex
arterial pressure

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10
Q

physiological responses to exercise in terms of circulation 4

A
  1. vasodilation of skeletal muscle BVs
  2. vasoconstriction of GIT
  3. Increased muscle pumping
  4. sympathetic activation: noradrenaline and adrenaline release
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11
Q

arterial pressure

A

cardiac output is inversely proportional to peripheral resistance

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12
Q

parasympathetic response in cardiac control

A

vagal
acts on sa and av node, reduces rate of firing
fast action

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13
Q

sympathetic response

A

causes chronotropy and inotropy through noradrenaline release
also causes vasoconstriction

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14
Q

baroreceptor mech

A

baroreceptors in aortic arch and coronary sinues
signal to cardio centre in medulla
either parasympathetic or sympathetic result

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15
Q

key vasoconstricors 3

A

adrenaline
vasopressin/ADH
angiotensin 2

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16
Q

key vasodilators 2

A

tissue derived vasodilators (metabolically driven) ex. adenosine

endothelium derived vasodilators ex. nitric oxide

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17
Q

what is the autoregulatory method for blood flow to the brain

A

myogenic mechanism: increased intravascular pressure->cerebral arteries constrict to prevent excessive blood flow, decreased intravascular pressure-> dilate to increase blood flow

metabolite concentrations will also influence

18
Q

three broad groups for HF causation and their subgroups

A

myocyte related: ischaemia, toxins, trauma, CAD, myocarditis
Conduction related: Arrhythmias
Loading related: Hypertension, PAD

19
Q

Pathophysiology mech of HF 6 steps

A

index event
reduced cardiac output
compensatory mechanisms
secondary organ damage
LV remodelling
further decline

20
Q

the 3 compensatory mechanisms in HF onset

A

RAAS activation
Sympathetic activation
Natiuretic peptide release

21
Q

what are the physical changes in HF that occur

A

LV remodelling including dilatation, hypertrophy and fibrosis

22
Q

history symptoms of HF 5

A

swelling
dyspnoea
orthopnoea
fatigue
exercise intolerance

23
Q

clinical symptoms in HF 3 right sided

A

raised JVP
added S3 sound
pitting oedema

24
Q

what does an echocardiogram assess in HF 3

A

LV ejection
dilatation
diastolic function

25
Q

reason for dyspnoea in HF

A

reduced cardiac ouput
backflow
increased pulmonary pressure
pulmonary congestion and oedema
increased blood air barrier
impaired gas exchange

26
Q

reason for peripheral oedema in HF

A

low cardiac output->backflow->increased venous pressure->fluid enters interstitium

27
Q

acute management of HF

A

furosemide
Sublingual GTN
supportive care ex. oxygen

28
Q

role of sublingual GTN in acute HF management

A

vasodilator to reduce preload and afterload

29
Q

long term drug management Hf

A

ARNI
beta blocker
Mineralcorticoid receptor antagonist
SGLT2 inhibitors

30
Q

what can worsen HF (think in terms of 3 broad categories CVD, health, external)

A

CVD: Arrhythmias, MI, CAD structural abnormalities

Health: Infection, hypertension

External: Drugs, chemo, diet

31
Q

drugs which precipitate HF 4

A

some chemotherapy drugs
tricyclic antidepressants
NSAIDs
calcium channel blockers

32
Q

r sided HF complications 5

A

L. HF
Peripheral oedema
hepatic congestion->cirrhosis
renal congestion->renal dysfunction
abdominal congestion->ascites

33
Q

l. sided complications 5

A

pulmonary oedema
pulmonary congestion
pulmonary hypertension
fatigue
exercise intolerance

34
Q

reasons for valvular regurgitation to occur (physiological) 3

A

abnormal leaflet closure
muscle dissection
congenital/structural abnormalities

35
Q

reasons for valvular stenosis to occur (physiological)

A

calcification
stenosis pre/para valvular

36
Q

pathological reasons for valvular disease 7

A

ageing
RHD
infective endocarditis
Medications
trauma
Connective tissue disorders
congenital abnormalities

37
Q

characteristics of aortic stenosis 4

A

systolic, radiates to carotids, loudest on phonocardiogram, highest pressure

38
Q

characteristics of aortic regurgitation 3

A

early diastolic murmur, second loudest on phonocardiogram, greatest volume

39
Q

characteristics of mitral regurgitation 5

A

pan systolic murmur, low pressure, higher volume, radiates to axilla, third loudest

40
Q

role of clinical geneticist

A

medical doctor

41
Q

role of genetic counsellor

A

non directive advise about tests and diagnoses

42
Q

people involved in the multidisciplinary genetics team 3

A

genetics counsellor
clinical geneticist
psychologist