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SEM2 BIOSCIENCE > Case 6 > Flashcards

Case 6 Flashcards

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?

A

Vasoconstriction
Increase in thirst
Anti-diuretic hormone production

21
Q

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

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?

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?

A

Atrial stretch
Elevated angiotensin II
Sympathetic activation

24
Q

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

A

Released from posterior pituitary

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

25
Q

What are the effects of anti-diuretic hormone?

A

Increase in H20 resorption from collecting duct

NB. no ions are resorbed meaning ADH changes blood osmolarity

26
Q

How does alcohol effect ADH?

A

Alcohol inhibits release of ADH from posterior pituitary

No water resorption therefore decreased blood volume

27
Q

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?

A

B1 adrenoreceptors on surface of juxtaglomerular cells in the kidney

28
Q

Define hypertension…

A

An increase in peripheral resistance when cardiac output is normal

29
Q

What is the most common cause of secondary hypertension?

A

LV hypertrophy

Blood pressure raised in response to decreased cardiac output

30
Q

How can renal disease cause secondary hypertension?

A

Renal artery stenosis decreases renal perfusion

Hyperaldosteronism increases blood volume

31
Q

How can vascular disease cause secondary hypertension? (4 ways)

A

Atheroma
Peripheral arterial disease
LV hypertrophy
Aortic coarctation

32
Q

What is aortic coarctation?

A

Narrowing of the aorta usually where the ligamentum arteriosum inserts

33
Q

What are the endocrine causes of secondary hypertension?

A

Parathyroid/thyroid disease

Cushings syndrome

34
Q

A renal profile is ordered to investigate causes of hypertension. What does this measure?

A

Electrolytes (Na+, K+, Cl-, Ca2+)
Plasma glucose
Creatinine/ creatinine:albumin ratio
Glomerular filtration rate

35
Q

Why is it important to repeat investigations following anti-hypertensive treatment?

A

Diuretics and ACE inhibitors can cause severe electrolyte imbalances, therefore levels should be monitored

36
Q

NICE recommendations suggest starting antihypertensives on any patient with a ten year CV risk percentage of more than….

A

20%

Due to decrease to 10% upon new recommendations

37
Q

Pathogenesis of hypertension is thought to be caused by what?

A

Raised cardiac output causes vasoconstriction in the small arteries.

Thought to be a protective response to prevent capiliary damage from high pressure

38
Q

What is the most important pathophysiological mechanism in the development of hypertension?

A

Endothelial dysfunction

39
Q

How does endothelial cell dysfunction cause hypertension?

A

Increased secretion of endothelin causes endothelin receptor activation

Endothelin receptors increase intracellular Ca2+ levels promoting smooth muscle contraction

40
Q

What molecules stimulate endothelin release?

A

Angiotensin II
ROS (smoking)
Anti-diuretic hormone

41
Q

How is smoking pro-inflammatory in respect to the cardiovascular system?

A

Increases IL1 and TNFa produced by endothelium
Increases leukocyte adhesion
Increases rate of LDL modification
Antagonises the effects of NO (meaning no vasodilation)

42
Q

What is the most cost effective smoking cessation tool?

A

Nicotine replacement therapy

43
Q

Anaerobic exercise mainly uses what molecules as substrates?

A

Creatine phosphate

Glycogen

44
Q

How is lactic acid metabolised after exercise?

A

Conversion to glucose/glycogen (Cori cycle)

Metabolism to O2 and H20

45
Q

Sustained aerobic training improves what cardiac parameter?

A

Stroke volume

46
Q

How may the gross structure of the heart change following sustained aerobic training?

A

Eccentric left ventricular hypertrophy- associated with cardiac remodelling in response to sustained cardiac overload

47
Q

What is VO2 max? How is it calculated?

A

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
Q

What equation is used to calculate VO2 max? What principle underlies this equation?

A

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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