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
reason for dyspnoea in HF
reduced cardiac ouput backflow increased pulmonary pressure pulmonary congestion and oedema increased blood air barrier impaired gas exchange
26
reason for peripheral oedema in HF
low cardiac output->backflow->increased venous pressure->fluid enters interstitium
27
acute management of HF
furosemide Sublingual GTN supportive care ex. oxygen
28
role of sublingual GTN in acute HF management
vasodilator to reduce preload and afterload
29
long term drug management Hf
ARNI beta blocker Mineralcorticoid receptor antagonist SGLT2 inhibitors
30
what can worsen HF (think in terms of 3 broad categories CVD, health, external)
CVD: Arrhythmias, MI, CAD structural abnormalities Health: Infection, hypertension External: Drugs, chemo, diet
31
drugs which precipitate HF 4
some chemotherapy drugs tricyclic antidepressants NSAIDs calcium channel blockers
32
r sided HF complications 5
L. HF Peripheral oedema hepatic congestion->cirrhosis renal congestion->renal dysfunction abdominal congestion->ascites
33
l. sided complications 5
pulmonary oedema pulmonary congestion pulmonary hypertension fatigue exercise intolerance
34
reasons for valvular regurgitation to occur (physiological) 3
abnormal leaflet closure muscle dissection congenital/structural abnormalities
35
reasons for valvular stenosis to occur (physiological)
calcification stenosis pre/para valvular
36
pathological reasons for valvular disease 7
ageing RHD infective endocarditis Medications trauma Connective tissue disorders congenital abnormalities
37
characteristics of aortic stenosis 4
systolic, radiates to carotids, loudest on phonocardiogram, highest pressure
38
characteristics of aortic regurgitation 3
early diastolic murmur, second loudest on phonocardiogram, greatest volume
39
characteristics of mitral regurgitation 5
pan systolic murmur, low pressure, higher volume, radiates to axilla, third loudest
40
role of clinical geneticist
medical doctor
41
role of genetic counsellor
non directive advise about tests and diagnoses
42
people involved in the multidisciplinary genetics team 3
genetics counsellor clinical geneticist psychologist