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Pre-Med 2022-2023 > CFB L3 > Flashcards

CFB L3 Flashcards

1
Q

Define blood pressure

A

The force exerted by blood on walls of blood vessels.

Definition of blood pressure reflects large arteries

In patients, measured in brachial artery
- aorta
-brachial arteries

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2
Q

State the units of BP

A

mm Hg (millimitres mercury)

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3
Q

What does a BP of 120 mm Hg tell us?

A

This is the force the blood exerts on wall of vessel. Also, this force can cause a column mercury to rise by 120 mm

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4
Q

What is systolic pressure?

A

Highest pressure in arteries when the heart contracts, heart beats + blood flows into it

Normal: 120 mm Hg

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5
Q

What is diastolic pressure?

A

Lowest pressure in arteries

When heart is relaxing between heart beats / contractions

Normal: 80 mm Hg

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6
Q

Define pulse pressure

A

Also known as arterial pulse

Difference beteween systolic pressure + diastolic pressure.

Felt as pulsation by palpating eleastic arteries

Occurs during systole, ventricles contract, blood ejeceted into arteries, they then expand.

Pulse pressure directly proportion to stroke volume,

High pulse pressure = high stroke volume

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7
Q

Why is Mean Arterial Pressure taken ?

A

Alternative value to pulse pressure (arterial pulse)
MAP

Blood ressure in aorta / arteries fluctuates with each heart beat

Pulse pressure fluctuates

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8
Q

What is MAP?

A

Avg of systolic and diastolic pressure

Avg BP in arteries during 1 cardiac cycle ( 1 heart beat)

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9
Q

How do you calculate MAP?

A

(2x diastolic) + (1 x systolic) / 3

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10
Q

What is a healthy MAP ?

A

70 - 110 mm Hg

<60 mm Hg - organ hypoxia, organ ischemia

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11
Q

What happens if MAP is too low?

A

<60 mm Hg - organ hypoxia, organ ischemia, NO FILTRATION IN KIDNEYS

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12
Q

How is blood pressure regulated?

A
  1. Neural control
  2. Hormonal control
  3. Local factors

These factors control heart rate, blood volume, stroke volume

This allows consistent control of blood pressure

NHL

(NHS took an L)

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13
Q

Where is neural control of blood pressure regulated?

A

Cadiovascular centre
(bundle of neurones in medulla oblongata)

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14
Q

State the location of the cardiovascular centre

A

Medulla oblongata

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15
Q

State the function of the cardiovascular centre

A

Control heart rate
Control ventricular contractility
Control blood vessel diamater

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16
Q

State the four centres in the cardiovascular centre

A

There are 4 groups of neurones the CV centre:

Cardiostimulatory centre - stimulates heart function
Cardioinhibitory centre - inhibits heart function
Vasodilator centre - reduces diameter of blood vessels
Vasocontrictor centre - expands diameter of blood vessels

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17
Q

What are the inputs of the CV centre?

A

Inputs = impulses towards CV centre

INputs from higher brain centres:
-Cerebral cortex
-Limbic system
-Hypothalamis

Input from sensory receptors:

-Barroreceptors
-Chemoreceptors
-Proprioreceptors

  1. Barroreceptors - detect changes in BP
  2. Chemorecepors - detect changes in O2 + CO2 levels of blood (blood acidity)
  3. Proprioceptors - detect changes in muscle + joint movement
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18
Q

State sympathetic efferents from the CV centre

A
  1. Electrical signals sent via cardiac accelearotr nerves to heart to increase heart rate and increase ventricular contractility
  2. Electrical signals sent via vasomotor nerves to blood vessels, vasoconstriction of blood vessels
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19
Q

State parasympathetic efferents from CV centre

A

Electrical signals sent via vagus nerve to heart to decrease heart rate

20
Q

Describe sympathetic stimulation of the heart

A
  1. Sympathetic stimulation occurs via the spinal nerves (cervical to upper thoracic T1-T4)
  2. Fibres reach pacemaker + most of myocardium
  3. Activation leads to release of stimulatory neurotransimitter - noradrenaline
  4. Noradrenaline binds to beta adrenergic receptors
  5. Increase in Ca 2+ influx
  6. Increases heart rate + contraction force
21
Q

Describe what happens during parasympathetic activation

A

By Vagus nerve
Fibres reach the pacemaker + some of myocardium
Activation leads to release of ACh
ACh binds to cholinergic muscarinic receptros
Acivating them
Closes Ca2+ channels
Decreases heart rate + force of contraction

22
Q

Why is MAP more clinically relevant than SBP?

A

Better representation of perfusion pressure faced by organs

23
Q

Why is neural function only required for altercations to heart rate and ventricular contractility

A

Heart beats independent of neural regulation and the CV centre, therefore, neural regulation is only needed to alter

-heart rate
-ventricular contractility
-diameter of blood vessels

24
Q

State the function of barroreceptors

A
  • Stretch receptors found in wall of blood vessels
    -Mechanoreceptor sensory neurones that are excited when stretched
    -When stretched / distended (by changes in BP), send electrical impulses to CV centre
    -Found in carotid sinus and arotic arch

Detect changes in blood pressure (in major arteries)

25
Q

State the function and location of chemoreceptors

A

Detect change in blood chemistry - Detect changes of CO2 and O2 levels in the blood (blood acidity)

Found near carotid and aortic barroreceptors - in aortic and carotid bodies

26
Q

State the function of proprioceptors

A

Detetct changes in joint + muscle movements

27
Q

State the parasympathetic efferents from the CV centre

A

Electrical impulses sent via vagus nerve to heart, decreases ventricular contractility and thereofore, heart rate

28
Q

Explain how the CV centre controls blood vessel diameter

A

Narrowing diameter: (When Low BP + generally, arterials have “vasomotor” muscle tone”)

CV centre innervates smooth muscle of blood vessels (mainly arterioles)

It does this by sympathetic nerves from the vasoconstrictor centre - vasomotor nerves

Upon activation, vasomotor nerves release a neurotransmitter, noradrenaline

Noradrenaline binds to alpha-adrenergic receptors,
leading to constriction of vessels (Ca2+ and cAMP mediated)

Vasomotor nerves constantly innervate smooth muscle of arterioles, allowing them to maintain muscle tone and regulate BP

29
Q

Describe the location of vasomotor nerves

A

Branch from spinal cord, go through all thoracic and first 2 lumbar nerves

30
Q

Explain how the CV centre controls blood vessel diameter

A

Widening diamater (when high BP)

Vasomotor nerves constantly innervate smooth muscle of arterioles, allowing them to maintain muscle tone - therefore, in constant state of moderate contriction - “vasomotor tone”

When high BP, detected by barrorecptors in aortic arch + carotid sinus

Impulse sent to vasodilator centre in CV centre, stimulates vasodilator centre which inhibits vasoconstrictor centre

Leads to widening of vessels as activity of vasocontrictor centre is surpressed (activity of vasomotor nerves therefore surpressed)

31
Q

Describe the distrobution and power of the sympathetic vasodilator nerves

A

All segments of circulation

More powerful
-spleen
-gut
-kidney
-skin

Less powerful

-skeletal muscle
-cardiac muscle
-brain

32
Q

State the hormones involved in control of BP

A

Renin-Angiotensin aldosterone system (RAAS)

ADH

Adrenaline, Noradrenaline

ANP - atrial natiuretic peptide

33
Q

Describe how the RAAS system leads to an increase in BP

A

Angiotensinogens is released into blood. Produced in liver

Upon low blood pressure, low renal perfusion, reduced Na+ delivery, kidney secretes renin which cleaves angiotensinogens to produce angiotensin 1

Angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme) in lungs

Angiotensin II
-Potent vasoconstrictor, increases BP
-Stimulates adrenal cortex to release aldosterone, which increases water + sodium reabsorption, increasing blood volume, increasing blood pressure
-Stimulates release of ADH, increases permeability of kidney tubules (collecting ducts), increases reabsorption of water, increasing blood pressure

Angiotensin II stimulates thirst sensation

34
Q

Which cells in the kidney produce ACE?

A

Juxtaglomerular cells

35
Q

State the function of adrenaline and noradrenaline in BP regulation

A
  1. Both secreted by the adrenal medulla and sympathetic nerve fibres
  2. Both hormones and neurotransmitters
  3. Both increase ventricular contractility, heart rate, cardiac output + BP
  4. Both increase vasoconstriction in arterioles + veins, increasing TPR and BP
36
Q

State where ADH is produced

A

Posterior pituirary gland

37
Q

What stimulates the release of ADH?

A

Hypervolemia (reduced blood vol)
High blood plasma osmolarity
Angiotensin II

38
Q

Explain how ADH regulates blood pressure

A

Osmoreceptors in hypothalamus detect
-hypovolemia
-high blood plasma osmolarity - less water in blood

This causes less water to diffuse into osmoreceptors, they then contract, increasing afferant neural firing, stimulating posterior pituitary gland to secrete ADH

ADH increases the permeability of the kidney tubules (collecting ducts) to water, therefore, increasing the amount of water reabsorbed from urine to the blood

By planting “water channels” called aquaporins 2 channels in the membrane of collecting duct, dct

Transport water through tubular cells back into blood

This leads to decrease in plasma osmolarity, increase in blood vol, therefore, increase in BP

ADH = vasoconstrictor, increases BP

COMBINED EFFECT, increased blood volume + vasocnstriction - high BP

HIGH URINE OSMOLARITY - LESS WATER IN URINE, URINE CONCENTRATED

39
Q

State the two principle sites of action during ADH regulation of BP

A

Kidneys

Blood vessels

40
Q

State factors stimulating ADH release

A

Ang II
Thirst
Decreased atrial receptor firing
Sympathetic stimulation of barroreceptors
Hypovolemia / high plasma osmolarity

41
Q

Describe the role of ANP in reg of BP

A

Produced + stored in atrial myocytes

Secreted in response to atrial stretch secondary to hypervolemia and thus hypertension

Increases renal excretion of water, reduces blood vol, reduces BP

VASODILATOR

42
Q

Describe the physiological effects of ANP

A
  1. Constricts efferent glomerular arteriole, incrrease glomerular capillary pressure, increase GFT, increase Na+ + H2O excretion
  2. Decrease sodium reabsorption in DCT, more Na+ H2O excretion
  3. Decrease renin secretion, inhibits RAAS
  4. Reduces responsiveness in alpha-adrenergic receptors in blood vessels to adrenaline, vasodilation
  5. Inhibits sympathetic output from CV, reduced CO
  6. Acts on hypothalamus to reduce ADH release
43
Q

Define auto-regulation

A

Body tissues automatically regulate their blood flow + according to metabolic demand for oxygen, nutrients, disposal of waste materials

44
Q

Describe how local factors play a role in reg of BP

A

Physical factors
TEMP: warming = vasodilation
cool = vasoconstriction

Chemical mediators
WBC, metabolically active, vasodilators - bradykinin, hisyamine, H+, NO

platelets -less metabolically active, vasoconstrictors, serotonion, prostaglan F2 alpbha, thromboxane A2

45
Q

True or false

“NO is a vasodilator released by vascular endothelial cells”

A

True

Pre-Med 2022-2023 (57 decks)

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