Cardiovascular System Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What BP is hypertension classed as?

90% of HT is what?

A

140/90+

-90% is idiopathic

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2
Q

Name 3 effects HT can have on vessels.

A
  • atheroma and aneurysm and microaneurysms
  • elastic reduplication of lamina in arterioles
  • retinal capillary damage
  • nephrosclerosis, glomerulosclerosis
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3
Q

What is hyaline arteriosclerosis?

A

Plasma exudes into intima/deep layers of arterioles

Glassy pink on histology

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4
Q

What is a false aneurysm?

A

-breach in wall, blood leaks out but is contained in adventitia, expands

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5
Q

3 Types of Aneurysm

A
  • Berry/saccular - @CofW bifurcations, rupture subA
  • microaneuysm - HT in cerebral arteries
  • Abdo Aortic A - usually post atheroma
  • Stretched Aortic Ring - by infection or aortic dissection
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6
Q

What is aortic dissection?

A
  • elderly with medial degeneration/Marfan’s
  • tear in intima so blood enters aortic wall forming a parallel tract
  • Vessel dilates, may rupture through adventitia
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7
Q

What is a stroke?

3 associated factors:

A

-sudden onset of neurological deficit due to CV

HT, smoking, AF, high cholesterol

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8
Q

80% of strokes are ischemic, where/why might these occur?

A
  • thromboembolic/mural thrombus
  • 1ry occlusion of intracerebral artery
  • lacunar (lenticulostriate perforating artery occlusion)
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9
Q

Why might a haemorhhagic stroke occur? What may it cause in the brain?

A
  • rupture of cerebral microaneurysm

- midline shift as blood compresses brain

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10
Q

What is the penumbra areas of brain?

A
  • infarct area necroses but adjacent areas may have some compensation from other branches
  • if perfusion is restored <3hrs this ‘penumbra’ can be salvaged
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11
Q

Why are stroke cerebral lesions ‘soft’?

A

Liquefaction necrosis after MOs clear it they leave cystic spaces and nearby gliosis may be seen

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12
Q

What is a TIA?

A

neurological deficit lasting <12-24hrs. (Increases risk of stroke)

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13
Q

What are the brains requirements for blood?

A
  • constant high flow of O2 rich blood
  • supply that can change with need
  • extracts lots of O2 at rest (vulnerable to hypoxia)
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14
Q

Name 2 special structural features of brain circulation?

A
  • Circle of Willis - colaterals if stenosis occurs
  • BBB tight endothelial junctions, selective control
  • high capillary density
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15
Q

How does the brain modulate its BP/blood flow e.g. in case of high blood pressure?

A

Caroitid sinus baroreceptors monitor stretch, CN IX
NTS -> CVLM -> RVLM -> decreases symp at IML point
Decrease HR, SV and BP

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16
Q

Cerebral arterioles dont have baro-reflex vasoconstriction, how do they regulate pressure/flow?

A

Myogenic autoregulation (high BP causes vasoconstricts to keep flow the same.

17
Q

Explain metabolic autoregulation of cerebral arteries.

A
  • increased pCO2/increased H+ causes vasodilation

- and low O2/hypoxia releases vasodilating metabolites

18
Q

Explain regional hyperaemia of cerebral arteries.

A
  • increased K+ (ECF) hyperpolarises the VSMC

- hence they are relaxed = vasodilation in active areas

19
Q

Name a vasoconstrictor abundant in perivascular nerves

Name a metabolite released in hypoxia causing vasodilation.

A

5HT-v.constrictor

Adenosine - v.dilates

20
Q

Perivascular nerves have nociceptive fibres that mediate pain of vascular headaches, what would they do in e.g. a migrane?

A

-less release of vasoconstrictors (5HT)
-more vasodilators e.g. Sub P and CGRP
(also you get inflammation of extracerabral arteries)

21
Q

What is the mechanism of action of Sumatriptan given to treat migranes?

A

5HT1B agonist - causes vasoconstriction

decreases inflammation and pain

22
Q

What does the BBB keep in/out?

A

Keeps in - NTs

Keeps out - neuroactive chemicals

23
Q

At what 3 places is the BBB defective at?

A
  • area postrema of CTZ - drugs, toxins, Ang II enter
  • subfornicular organ of hypothal - Ang II - thirst
  • paraventricular osmoreceptors -> +/- ADH
24
Q

What happens with herniation due to a space occupying lesion?
AKA?

A

-RVLM compressed which increases its activity
-more symp, higher BP –> activates baroreflex
-more vagus, decreased HR = reflex bradycardia
Cushing’s reflex

25
Q

Cerebral Artery Vasospasm reduces flow and can cause a stroke. What local agents may cause it?

A
  • local vasoconstrictors: 5HT, NPY (perivascular nerves)

- endothelin1 from damaged endothelium

26
Q

What can be used to treat Cerebral Artery Vasospasm?

A
  • VGCa2+C blockers e.g. amlodipine

- ETA receptor blockers e.g. bosentan