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Block 2 Week 5 > Osmotic and Volume Regulation > Flashcards

Osmotic and Volume Regulation Flashcards

1
Q

When do you get ADH release?

A

when you have low plasma volume or high plasma osmolarity

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2
Q

If you have low plasma volume, how does ADH know to be released?

A

Venous, atrial and arterial low pressure will trigger reflexes mediated by cardiovascular baroreceptors to let the brain know to release ADH

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3
Q

Once you have an increase in ADH what happens to the body?

A

Plasma ADH increases, tubular permeability to water increase and thus water reabsorption increases

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4
Q

If you consume 1 liter of water what will happen?

A

your plasma osmolality will go done, your adh release will go down and you will excrete water

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5
Q

If you consume 1 liter of isotonic saline what will happen?

A

Your EFV will increase, your ADH will decrease, you will excrete water and your plasma osmolality increases and then finally your ADH increases

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6
Q

How do you regulate the EFV?

A

via Na reabsorption. more salt the greater the EFV.

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7
Q

So when you have 67% of sodium leaving and 67% of water leaves then you will still have the same (blank) ie. Ratio of salt to water inside the proximal tubule.

A

concentration

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8
Q

What factors effect the kidney to regulate extracellular fluid volume?

A

GFR, Aldosterone, natriuretic hormone, peritubular pressure

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9
Q

Systems that release extracellular fluid volume regulatory factors are what?

A

neural and internal elements

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10
Q

What sense changes in blood volume?

A

venous stretch receptors
baroreceptors
intrarenal elements

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11
Q

Regulation of volume requires first regulating (blank) followed by regulating water

A

sodium

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12
Q

A decrease of EFV leads to what?

A

Increased Na reabsorption-> increase Plasma osmolarity -> increased ADH-> increased water reabsorption-> increased EFV

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13
Q

If you have decreased EFV then what will increase becaues of it?

A

sodium reabsorption

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14
Q

If you have increased EFV then what will decrease because of it?

A

sodium reabsorption

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15
Q

Why does excess sodium consumption lead to an increase in ECF volume?

A

Due to maintainance of reabsorption percentage and concentration

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16
Q

When you have excess sodium consumption what happens?

A

your sodium plasma concentration increase which increases your plasma osmolarity which increases your ADH and thirst and water reabsorption as well as shifts fluid from IC to EC compartments and then your ECF volume increases

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17
Q

Where is the receptor for aldosterone located?

A

intracellularly

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18
Q

If you have a decrease in sodium or blood volume what hormone will be released?

A

aldosterone

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19
Q

What makes sodium channels and conductance of sodium channels increase?

A

aldosterone

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20
Q

In addition to aldosterone increasing sodium channels and conductance of sodium channels, what else does it do?

A

Increase sodium potassium pump effectiveness to allow for better sodium reabsorption and increased potassium secretion

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21
Q

What does aldosterone do to potassium, hydrogen, and sodium?

A

increases potassium excretion
increases sodium reabsorption
increases hydrogen excretion
Increase bicarbonate reabsorption

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22
Q

If you have excessive aldosterone what will you be in alkalosis or acidosis?

A

alkalosis

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23
Q

What does an increase in Angiotensin II and Increase in Plasma K cause?

A

Increase in aldosterone (subsequent increase in Na reabsorption, K excretion, H excretion)

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24
Q

What will an increase in Adrenocorticotropic hormone (ACTH) cause?

A

Increase in aldosterone (subsequent increase in Na reabsorption, K excretion, H excretion)

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25
Q

What will a decrease in Sodium cause?

A

Increase in aldosterone (subsequent increase in Na reabsorption, K excretion, H excretion)

26
Q

What will cause an increase in aldosterone?

A

increase in angiotensin II
Increase in Plasma K
Increase in ACTH
decrease in Plasma Na

27
Q

What will hypoaldosteronemia cause?

A

Adrenal insufficiency (addison’s disease)
acidosis
hyperkalemia
hypotensin (salt wasting)

28
Q

What will hyperaldosteronemia cause?

A

Alkalosis
Hypokalemia
Hypertension (usually not over volume expansion)

29
Q

What is the disease associated with adrenal insufficiency?

A

addison’s disease

30
Q

If you have decreased salt plasma and increased potassium and hydrogen in plasma what is going on?

A

you have adrenal insufficiency so addison’s disease

31
Q

If you have problems with your regulation of Na K transport in the distal renal tubule what is most likely the culprit?

A

you have aldosterone problems and will have decreased plasma salt and increase potassium plasma concentration

32
Q

What is primary hyperaldosteronemia?

A

when you directly increase your amount of aldosterone such as an adrenal tumor

33
Q

If you have primary hyperaldosteronemia what happens?

A

you will have increased aldosterone which will lead to hypertension and subsequent reduction in renin release

34
Q

What is secondary hyperaldosteronemia?

A

When decreased pressure or volume causes an increase in aldosterone (i.e like renal artery stenosis)

35
Q

What happens if you have secondary hyperaldosteronemia?

A

you will have decreased pressure which will increase renin release and increase ang II and increase aldosterone

36
Q

If a patient has primary hyperaldosteronemia (a tumor making increased aldosterone) what will be common symptoms associated with it?

A

hypokalemia
metabolic alkalosis
hypertension
diminished plasma renin activity

37
Q

Does renin regulation come before or after increases in adolsterone in primary hyperaldosteronemia?

A

after

38
Q

Does renin regulation come before or after increases in adolsterone in secondary hyperaldosteronemia?

A

before

39
Q

What stimulates aldosterone release and causes a direct increase in proximal Na reabsorption?

A

angiotensin II

40
Q

What acts via membrane receptors coupled to guanylate cyclase?

A

Atrial natriuretic factor (anti-aldosterone)

41
Q

What decreases sodium reabsorption in the collecting duct?

A

Atrial natriuretic factor (anti-aldosterone)

42
Q

What increases GFR at the glomerulus?

A

Atrial natriuretic factor (anti-aldosterone)

43
Q

What decreases the effects of renin, angiotensin II and aldosterone?

A

Atrial natriuretic factor (anti-aldosterone)

44
Q

What does this:

  • acts via membrane receptors coupled to guanylate cyclase
  • decreases sodium reabsorption in the collecting duct
  • increases GFR at the glomerulus
  • decreases the effects of renin, angiotensin II and aldosterone?
A

Atrial natriuretic factor (anti-aldosterone)

45
Q

(blank) is the excretion of excess sodium in the urine.

A

natriuresis

46
Q

angiotensin II contracts the (blank) arteriole.

A

efferent

47
Q

Where does aldosterone work? (slide 18)

A

from early distal to almost end of collecting duct

48
Q

Where does ADH work?

A

from late distal to end of collecting duct

49
Q

Where does ANP work?

A

at the end of collecting duct and glomerulus

50
Q

Where does angiotensin II work?

A

efferent arteriole and proximal tubule

51
Q

(blank) handling in the kidneys is predominantly regulated by arterial baroreceptors to maintain effective circulating volume (ECV) i.e. that part of the extracellular fluid that is in the arterial system and thus is available for perfusing tissues.

A

sodium

52
Q

sodium handling in the kidney is predominantly regulated by (blank)

A

arterial baroreceptors

53
Q

Explain what happens to the body when a person undergoes CHF?

A

decrease in cardiac output-> shift of blood volume from arterial to venous side-> baroreceptors sense decrease in ECV-> save sodium-> increase in plasma osmolality-> increase ADH-> save water-> Increase EDEMA!

54
Q

How do you maintain sodium balance with progressive nephron loss?

A

intake has to equal outflow. therefore if you have decrease filtered load you must have increased fractional excretion rate to maintain na excretion rate

55
Q

sodium consumption and excretion remain in balance with progressive nephron loss due to an increase in (blank).

A

fractional excretion.

56
Q

If you have 10 nephrons and then only 5 what will happen to your filtered load? What will happen to your fraction excretion? What will happen to your excretion rate?

A

it will decrease
it will increase
it will be maintained

57
Q 
If you decrease your nephrons what will happen to the following:
plasma HCO3
Plasma pH
Plasma Creatinine
Plasma BUN
Posm
Max Uosm
Min Uosm
A 
hco3-decrease
ph, decreases
Creatinine Increases!!
BUN Increases!!
Posm increases!!
max decreases
min increases
58
Q

creatinine formation and excretion remain in balance with loss of nephrons due to an increase in (blank).

A

plasma creatinine

59
Q

Creatinine’s filtered load will equal its (blank) regardless of nephron amount.

A

excretion rate

60
Q

If you have reduced GFR for creatinine what will happen?

A

you will increase your creatinine plasma concentration

61
Q

(blank) release is stimulated by reduced tissue oxygenation

A

erythropoietin

62
Q

What causes an increase in need for tissue oxygenation?

A

1: low blood volume
2: anemia
3: low hemoglobin
4: poor blood flow
5: pulmonary disease

Block 2 Week 5 (7 decks)

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