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SEM2 BIOSCIENCE > Case 6 > Flashcards

Case 6 Flashcards

(48 cards)

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1
Q

Total peripheral resistance can be effected in 3 main ways. What are these?

A

Viscousity of blood
Vessel length
Vessel radius

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2
Q

At rest, vessel radius is determined entirely by what ‘arm’ of the nervous system?

A

Sympathetic

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3
Q

What is sympathetic tone?

A

The degree of normal, partial vasoconstriction that varies in individuals

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4
Q

Baroreceptors in carotid sinus send impulses to the nucleus solitarius via what nerve?

A

Glossopharyngeal

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5
Q

Baroreceptors in aortic arch send impulses to the nucleus solitarius via what nerve?

A

Vagus

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6
Q

What are the three brainstem centres that control blood pressure on a minute by minute basis?

A

Cardiac accelerator nerve
Vasomotor centre
Cardiac inhibitory nerve

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7
Q

What nerve conduct impulses from the cardiac accelerator and vaso-motor centres?

A

Sympathetic efferent fibres

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8
Q

What nerve conducts impulses from the cardiac inhibitory centre?

A

Vagus nerve (parasympathethic)

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9
Q

Outline the steps in which blood pressure is controlled after baroreceptors have sensed an INCREASE in blood pressure

A

Increase in rate of firing to cardiac accelerator and vaso-motor centres

CA and VM centres inhbited causing vasodilation
CI centre activated slowing HR

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10
Q

Outline the steps in which blood pressure is controlled after baroreceptors have sensed an DECREASE in blood pressure

A

Decrease in rate of firing to CA and VM centres

CA and VM centres activated causing vasoconstriction
CI centre inhibited increasing HR

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11
Q

What brain stem centre is responsible for vagal tone?

A

Cardiac inhibitory centre

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12
Q

What is vagal tone?

A

The degree of parasympathetic activation (via vagus nerve) at any given time

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13
Q

What is the blood pressure response to the valsalva manoeuvre? Why is this important clinically?

A

Increase in thoracic pressure occludes the IVC:

Venous return decreases > EDV decreases > stroke vol decreases > BP drops

BP adjustments can cause clots to be fired off, causing pulmonary embolism

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14
Q

What is the effect of NO on vascular smooth muscle?

A

Vasodilation

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15
Q

What is the effect of endothelin on vascular smooth muscle?

A

Vasoconstriction

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16
Q

What are 3 stimuli that precede renin release in the kidney?

A

Decrease in Na+ perfusion
Sympathetic activation
Decreased Na+ in distal tubule

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17
Q

From what cells is renin released?

A

Juxtaglomerular cells

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18
Q

Where is angiotensinogen produced and found?

A

Produced in the liver, found in the plasma

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19
Q

In what organ is angiotensin I converted into angiotensin II?

A

Lungs

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20
Q

What are the functional effects of angiotensin II?

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A

Vasoconstriction
Increase in thirst
Anti-diuretic hormone production

21
Q

Outline how aldosterone is synthesised. What are its main biological functions?

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A

Angiotensin II stimulates the adrenal glands to synthesise aldosterone.

Aldosterone is a mineralocorticoid increases Na+ and H20 in the kidney, increasing blood volume

22
Q

What is the function of atrial natriuretic peptide? Where is it secreted?

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A

Secreted by atria

Functions to LOWER blood pressure by decreasing blood volume

Promotes Na+ and H20 excretion by increasing rate of glomerular filtration

23
Q

What are the stimuli for atrial natriuretic peptide release?

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A

Atrial stretch
Elevated angiotensin II
Sympathetic activation

24
Q

What are the stimuli for anti-diuretic hormone release? Where is it release from?

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A

Released from posterior pituitary

Decrease in blood osmolarity
Elevated angiotensin II
Sympathetic activation
Atrial/venous stretch

25
What are the effects of anti-diuretic hormone?
Increase in H20 resorption from collecting duct NB. no ions are resorbed meaning ADH changes blood osmolarity
26
How does alcohol effect ADH?
Alcohol inhibits release of ADH from posterior pituitary No water resorption therefore decreased blood volume
27
Catecholamines (noradrenaline and adrenaline) are released from the adrenal medulla in response to stress. What receptors on what cells can these molecules bind to activate the RAAS pathway?
B1 adrenoreceptors on surface of juxtaglomerular cells in the kidney
28
Define hypertension...
An increase in peripheral resistance when cardiac output is normal
29
What is the most common cause of secondary hypertension?
LV hypertrophy Blood pressure raised in response to decreased cardiac output
30
How can renal disease cause secondary hypertension?
Renal artery stenosis decreases renal perfusion Hyperaldosteronism increases blood volume
31
How can vascular disease cause secondary hypertension? (4 ways)
Atheroma Peripheral arterial disease LV hypertrophy Aortic coarctation
32
What is aortic coarctation?
Narrowing of the aorta usually where the ligamentum arteriosum inserts
33
What are the endocrine causes of secondary hypertension?
Parathyroid/thyroid disease | Cushings syndrome
34
A renal profile is ordered to investigate causes of hypertension. What does this measure?
Electrolytes (Na+, K+, Cl-, Ca2+) Plasma glucose Creatinine/ creatinine:albumin ratio Glomerular filtration rate
35
Why is it important to repeat investigations following anti-hypertensive treatment?
Diuretics and ACE inhibitors can cause severe electrolyte imbalances, therefore levels should be monitored
36
NICE recommendations suggest starting antihypertensives on any patient with a ten year CV risk percentage of more than....
20% Due to decrease to 10% upon new recommendations
37
Pathogenesis of hypertension is thought to be caused by what?
Raised cardiac output causes vasoconstriction in the small arteries. Thought to be a protective response to prevent capiliary damage from high pressure
38
What is the most important pathophysiological mechanism in the development of hypertension?
Endothelial dysfunction
39
How does endothelial cell dysfunction cause hypertension?
Increased secretion of endothelin causes endothelin receptor activation Endothelin receptors increase intracellular Ca2+ levels promoting smooth muscle contraction
40
What molecules stimulate endothelin release?
Angiotensin II ROS (smoking) Anti-diuretic hormone
41
How is smoking pro-inflammatory in respect to the cardiovascular system?
Increases IL1 and TNFa produced by endothelium Increases leukocyte adhesion Increases rate of LDL modification Antagonises the effects of NO (meaning no vasodilation)
42
What is the most cost effective smoking cessation tool?
Nicotine replacement therapy
43
Anaerobic exercise mainly uses what molecules as substrates?
Creatine phosphate | Glycogen
44
How is lactic acid metabolised after exercise?
Conversion to glucose/glycogen (Cori cycle) | Metabolism to O2 and H20
45
Sustained aerobic training improves what cardiac parameter?
Stroke volume
46
How may the gross structure of the heart change following sustained aerobic training?
Eccentric left ventricular hypertrophy- associated with cardiac remodelling in response to sustained cardiac overload
47
What is VO2 max? How is it calculated?
Maximal amount of oxygen the body can use during a specified time frame Testing by incremental exercise of increasing difficulty until anaerobic threshold is reached
48
What equation is used to calculate VO2 max? What principle underlies this equation?
Fick equation VO2 = Q (a-v) 02 subtracting arterial O2 from venous O2 gives you the amount of O2 used by the body

SEM2 BIOSCIENCE (13 decks)

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