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Physio II > Long Term BP Control-Exam 1 > Flashcards

Long Term BP Control-Exam 1 Flashcards

1
Q

What is the main function of long term bp control?

A

Keeps MAP constant over long period; tied into control of body fluid volume

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2
Q

What does increased volume in arteries and veins result in?

A

Pressure in arteries and veins will increase, assuming no change in vascular compliance

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3
Q

What does increased venous return result in?

A

Increased preload, increased SV, increased CO, increased bp; assuming no change in SVR

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4
Q

Small changes in cardiac output can cause what?

A

Large change in blood pressure

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5
Q

5 to 10 % increase in CO can raise MAP from 100mmHg to what?

A

150 mmHg

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6
Q

What is the relationship between CBV and MAP?

A

Increasing CBV will increased MAP

Decreasing CBV will decrease MAP

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7
Q

Fluid Intake = Fluid Output

A

Constant CBV

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8
Q

Fluid Intake > Fluid Output

A

Increased CBV

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9
Q

Fluid Intake < Fluid Output

A

Decreased CBV

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10
Q

Salt Intake = Salt Output

A

Constant CBV

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11
Q

Salt Intake > Salt Output

A

Increased CBV

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12
Q

Salt Intake < Salt Output

A

Decreased CBV

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13
Q

Under normal circumstances, fluid and salt output is controlled by what organ?

A

Kidneys

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14
Q

What is the normal fluid intake?

A

2300 mls /day

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15
Q

What amount of fluid intake is synthesized by oxidation of carbohydrates?

A

200 mls /day

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16
Q

What amount of fluid intake is ingested fluids?

A

2100 mls/ day

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17
Q

What is the normal fluid loss/ output?

A

2300 mls / day

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18
Q

What amount of fluid loss is insensible loss via respiratory tract and skin (not sweat)?

A

700 mls/ day

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19
Q

What amount of fluid loss is sweat?

A

100 mls / day

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20
Q

What amount of fluid loss is feces?

A

100 mls/ day

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21
Q

What amount of fluid loss is urine?

A

1400 mls/ day

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22
Q

Renal Output Equation

A

Output = Filtration - Reabsorption

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23
Q

What factors affect filtration?

A

MAP, Renal Blood Flow, pressure in glomerular capillaries, oncotic pressure in glomerular capillaries

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24
Q

What factors affect reabsorption?

A

Concentration of angiotensin II, aldosterone, ADH (all increase rate of absorption)

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25
Q

What does 50 mmHg on the pressure diuresis curve refelct?

A

0 Urine Output

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26
Q

What does 90mmHg on the pressure diuresis curve reflect?

A

Normal U/o

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27
Q

What does 150 mmHG on the pressure diuresis curve refelect?

A

U/O over 4x normal

28
Q

What happens short term and long term with increased SVR?

A

Acute: Change in MAP
Chronic: MAP returns to normal, no change in SVR

29
Q

What will happen to the renal function curve if intrarenal vascular resistance is increased?

A

Shift of the renal function curve to the right which will result in a change in the baseline MAP; problem is change in renal vascular resistance not the change in overall SVR

30
Q

BeriBeri

A

body does not have enough thiamine (B1)

31
Q

Paget’s disease

A

involves abnormal bone destruction and regrowth, which results in deformity.

32
Q

What does renin start as?

33
Q

Where is prorenin produced/ stored?

A

Juxtaglomerular cells (walls of afferent arterioles) of the kidneys

34
Q

What causes the splitting of prorenin into renin?

A

Decrease in pressure

35
Q

Where is renin released?

A

Lumen of the afferent arterioles; circulates to the rest of hte body

36
Q

How long does renin remain in the blood?

A

30 to 60 minutes, where it acts on the plasma protein called renin substrate (angiotensinogen) to release angiotensin I

37
Q

What’s another name for renin substrate?

A

Angiotensinogen

38
Q

Angiotensin I

A

mild vasoconstrictor; produces minimal changes in vascular constriction

39
Q

Where is angiotensin I carried to?

40
Q

What happens to angiotensin I when it is carried to the lungs?

A

ACE mediates formation of angiotensin II

41
Q

Where is ACE present?

A

Endothelial cells

42
Q

How long does angiotensin II persist before being deactivated by variety of blood/tissue enzymes known as angiotensinases?

A

Persists for 1-2 minutes

43
Q

Angiotensin II

A

potent vasoconstrictor of arterioles/ minor constriction of veins
Interacts w/ kidneys resulting in increasing salt and water reabsorption
Causes adrenal gland to secrete aldosterone

44
Q

What does aldosterone do?

A

Increases salt and water reabsorption

45
Q

What is the response time of the renin-angiotensin system vasoconstrictor?

A

20 minutes; will take secondary effect several days for maximal effect

46
Q

Is it easier to excrete water or salt?

47
Q

What is the definition of hypertension?

A

MAP greater than 110 mmHg
Diastolic > 90 mmHg
Systolic > 135 mmHg

48
Q

Why does HTN shorten lifespan?

A

Excess workload on the heart
Damage to blood vessels of brain
Injury to kidneys

49
Q

What are the causes of HTN?

A

Volume loading
Renin-Angiotensin imbalance
Combination volume loading / vasoconstriction

50
Q

Types of HTN

A

Primary

Essential

51
Q

Goldblatt HTN

A

Renin-Angiotensin Imbalance
Only one kidney and it has a constriction of renal art.
Kidney senses decrease in pressure and renin/angio system stimulated

52
Q

Two-Kidney Goldblatt

A

HTN will occur even if one kidney normal, other kidney has obstruction of renal artery

53
Q

What will happen to the obstructed kidney in two-kidney Goldblatt?

A

Increases reabsorption of water and salt due to lower pressure in tubular capillaries; release renin resulting in overall increase in angiotensin ii and aldosterone

54
Q

What occurs with renal pressure in two-kidney goldblatt?

A

Normal in obstructed kidney
Higher than normal in non-obstructed kidney

B/c angiotensin ii will increase SVR and MAP

55
Q

What happens with salt and water reabsorption in two-kidney goldblatt?

A

Angiotensin ii and aldosterone will increase salt and water reabsorption for both kidneys

56
Q

What percent of HTN patients have essential HTN?

57
Q

What is the cause of essential HTN?

58
Q

What are the symptoms of essential HTN?

A

Excess weight gain/ obesity account for large percentage of risk for developing HTN (65 - 75% )

59
Q

What is typically the first line of Tx in essential HTN?

A

Weight loss/ exercise

60
Q

What are the main characteristics of essential HTN?

A

Increased CO
Increased sympathetic activity (kidneys)
Increased levels of angiotensin ii and aldosterone
Impairment of renal function

61
Q

Why is there increased CO in essential HTN?

A

Support extra fat tissue

Support increased metabolic demand of major organs

62
Q

Why is there increased sympathetic activity of kidneys in essential HTN?

A

Hormone released from fat cells stimulate regions of hypothalamus that provide excitatory stimulation of vasomotor center

63
Q

How much are levels of angiotensin ii and aldosterone increased in obese patients?

A

2- 3x normal

64
Q

Why is there impairment of renal function in essential HTN?

A

Requires higher pressure to remove normal amounts of salt and water
Must give drugs that improve renal function, can’t just decrease MAP

65
Q

Tx for Essential HTN

A

Lifestyles modifications
Vasodilator drugs
Drugs that reduce reabsorption of salt and water

66
Q

What is the primary target of vasodilator drugs in essential HTN?

A

renal arterioles; inhibits sympathetic signals to kidneys, block sympthetic neurotransmitter on renal vasculature and renal tubules, direct relaxation of renal vasculature smooth muscle, block action of renin-angiotensin system

67
Q

Why do you tx essential htn with drugs that reduce resorption of salt and water?

A

Blocks active transport of sodium in tubules

Physio II (14 decks)

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