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Systems Physiology > Renal Physiology III a > Flashcards

Renal Physiology III a Flashcards

1
Q

*Understand the relationship between extracellular Na and ECF

A

a

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2
Q

*Understand the mechanisms of body Na regulation

A

a

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3
Q

*Understand the mechanisms of body water regulation

A

a

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4
Q

*Understand the regulation of Na excretion/reabsorption and extracellular volume in physiological and pathological conditions

A

a

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5
Q

How is fluid volume regulated? What is it linked to? What is mostly composed of ECF and Intracellular fluid?

A

regulation of fluid volume tied to regulation (changes) of body Na (Sodium) content
Most of sodium is in Extracellular fluid (ECF)
Most of K+ is Intracellular
This occurs due to Na+/K+ ATPase pump

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6
Q

What happens when to ECF when there are changes in Na?

A

any changes in Sodium will cause alteration in the amount of fluid in extracellular space.
A NET total LOSS of body sodium will lead to DECREASE in ECF volume
a Net increase in body sodium- lead to increase in body fluid volume

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7
Q

What are the factors affected when there is a change in total body Na+?

A

Change in total body sodium fluid will affect ECF volume which affects plasma volume, blood volume, venous pressure, atrial pressure, ventricular pressure, stroke volume, cardiac output, arterial blood pressure
if you increase total body Na+, you increase All of these factors.

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8
Q

What are the monitored variables? What monitors them? What happens when baroreceptors are stimulated?

A

Monitored variables: Venous pressure, atrial pressure, ventricular pressure and arterial blood pressure
these variables are monitored by baroreceptors.
Baroreceptors stimulated: you get reflex alterations that can affect the kidneys
changes in arterial blood pressure will change renal perfusion pressures, which have direct effect on kidney

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9
Q

What happens when you increase perfusion pressure?

A

Increase in Renal perfusion pressure, INCREASES GFR.

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10
Q

How is sodium excretion determined? What is the equation?

A

Sodium excretion= Sodium Filtered- Sodium Reabsorbed

Na+ Excretion= (GFR x P Na (Na+ plasma concentration)- Sodium reabsorbed.

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11
Q

How can you adjust sodium excretion?

A

To adjust Na+ excretion, you can Control Plasma Sodium, GFR and Sodium reabsorption.

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12
Q

What is GFR, sodium reabsorption and plasma sodium regulated by?

A

GFR and Na reabsorption is Regulated by KIDNEYs

Plasma Sodium- regulated by the Food you eat and sodium it contains

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13
Q

Explain Sodium Balance by comparing the difference between positive and negative sodium balance. How does this relate to how much water is retained or excreted?

A

A person is considered:
Positive Na+ Balance: when Sodium Excretion is LESS than Na ingested
Negative Na+ Balance: Na Excretion is MORE than Na+ ingested.
if there is a positive sodium balance, you RETAIN water
negative sodium balance- you are Excreting water

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14
Q

Which factors control GFR and sodium reabsorption in response to altered bodily Na+ (sodium) balance?

A

Factors that control GFR and Na+ reabsorption:

  1. Extrarenal baroreceptors (carotid sinuses, in arteries, cardiac chambers, great veins)
  2. Renal Juxtaglomerular apparatus- specifically intrarenal baroreceptors and Macula Densa which control the secretion of renin
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15
Q

how is GFR extrinsically controlled?

A

Extrinsic control of GFR is through:

  1. Renal sympathetic nerves:
    a) Increased Renal sympathetic nerve activation, increased Renal Arteriolar Constriction, Decreased P GC (hydrostatic pressure of glomerular capillary) and Decreased GFR.
    b) Increased Renal sympathetic Nerve activation, increased renal arteriolar constriction and Decreased renal blood flow, increased average oncotic pressure GC (pi) and decreased GFR
  2. Renin-Angiotensin system:
    Increased Renin release, increased Plasma Ang II, increased constriction of renal arterioles and Decreased GFR and Renal blood flow
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16
Q

What are the local and direct control of GFR?

A

Local/Direct control of GFR:

  1. Autoregulation- (fine tuning of GFR) allows maintenance of relatively constant GFR over a wide range of perfusion pressures. (most important: Tubular glomerular feedback)
  2. Prostaglandins (humans have VASODILATORY prostaglandins (pg2, pgi2); help modulate angiotensin and Sympathetic nerve constriction
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17
Q

What are the various controls of tubular Na+ reabsorption?

A

Tubular sodium reabsorption mediated by:

  1. Aldosterone
  2. renal sympathetic nerves
  3. Angiotensin II
  4. Pressure Natriuresis
  5. ANP
  6. ADH - antidiuretic hormone (minor effect)
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18
Q

What is the role of Aldosterone?

A

Aldosterone- steroid hormone that is released by Adrenal Cortex
Aldosterone is stimulated by:
INCREASE in PLASMA K+ concentration,
Increase in plasma ACTH (adrenocorticotropic hormone), increase in PLASMA Angiotensin II.

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19
Q

What is aldosterone stimulated by?

A

INCREASE in Plasma K+ concentration

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20
Q

What factors increase Aldosterone?

A

Anything that increases Angiotensin II will INCREASE Aldosterone.
Factors that increase Ang II
1. RENIN
2. Sympathetic Nerves increase renin secretion
also hemorrhage increases Sympathetic Nerves, further increasing more Renin
3. Decreased delivery of Na+ and Cl- to Macula Densa
-Decreased delivery fluid to Macula Densa will increase renin and increase Ang II
Decreased amounts of fluid (Dehydration, loss of water) going into kidney, lead to decreased delivery of Na+/Cl- to macula Densa and hence more renin which increases Ang II and increase Aldosterone.

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21
Q

What increases sympathetic nerve activity?

A

A hemorrhage, or drop in blood pressure will increase sympathetic nervous system, which will lead to secretion of renin.

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22
Q

What is the main function of aldosterone?

A

Aldosterone acts in Collecting duct and INCREASES Na+ Reabsorption
-causes increase number of Na+ channels, so increased Na+ reabsorption.

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23
Q

What are major effects of a Hemorrhage?

A

Hemorrhage can cause:
decrease in pressure, decrease in Cardiac Output,
Stimulate intrarenal baroreceptors, increase sympathetic nervous activity, reduce Na/K+ delivery to macula densa. All of these factors increase renal secretion, which increase plasma renin, increase plasma Ang II and increase release of plasma aldosterone and INCREASE Na+ reabsorption.
This Na+ reabsorption will increase ECF, which reduces the effects of Hemorrhage.

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24
Q

What does Na+ reabsorption do to Extracellular fluid?

A

Na+ reabsorption increases Extracellular fluid, which will help reduce deleterious effects of hemorrhage

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25
Q

What are the Tubular effects of Renal sympathetic nerves?

A

Tubular effects of Renal Sympathetic nerves:

  1. Stimulates Renin secretion via direct action on Beta-1 receptors of granular cells
  2. Directly stimulates Sodium reabsorption in PROXIMAL tubule cells.
    3a) Renal sympathetic nerves can also affect Peritubular capillary Starling forces and constriction of arterioles will decrease RBF more than GFR. This results in Decreased peritubular capillary hydrostatic pressure and increasing peritubular oncotic pressure. (filtration fraction increased) , which increases Na+ reabsorption.
    3b) Decreased GFR and increased Sodium reabsorption in proximal tubule will decrease Na+ delivery to macula densa and increase Renin secretion (positive feedback)
26
Q

What are the Tubular effects of Ang II?

A

Tubular effects of Ang II:
1. Direct effects: Ang II acts directly on proximal tubule cells to STIMULATE Na+ reabsorption. This occurs by stimulating the Na+/H+ exchanger in proximal tubule
2. Effects on Filtration Fraction and peritubular capillary Starling forces. INCREASES filtration fraction and thus increases Na+ and Water reabsorption in proximal tubule
3, Increase Aldosterone secretion

27
Q

What is the role of Atrial Natriuretic Peptide (ANP)?

A

Atrial Natriuretic Peptide (ANP)- small peptide hormone secreted by Cardiac Atrial cells. ANP is released during distension or expansion of atria and plasma volume expansion. ANP is released and acts directly on inner medullary collecting ducts to INHBIT sodium reabsorption.
ANP increases sodium Excretion

28
Q

What is the role of Antidiuretic Hormone (ADH)? What kind of effect does it have with Sodium reabsorption?

A 
Antidiuretic hormone (ADH, aka Vasopressin) increases Reabsorption of Na+ from the thick ascending limb, distal tubule and collecting duct.  This is a minor function of ADH.
ADH has MINOR effect  on Na+ reabsorption
29
Q

Define water secretion and discuss what controls it. What controls ADH secretion?

A

Water secretion- is the difference between the volume filtered (GFR) and the volume reabsorbed
Main determinant of water excretion- RATE of water reabsorption. This is determined by ADH levels.
ADH secretion is controlled by baroreceptors and osmoreceptors.

30
Q

What is the cellular action of ADH?

A

ADH works in COLLECTING DUCT (like aldosterone)
ADH binds to its receptor, which increases Adenyl clyclase activity, form cyclic AMP. You then make channels Aquaforin tubes (water channels)
With greater water channels you get more water to be reabsorbed provided by Gradient for water reabsorption.
If the medullary interstial has LOW osmolarity, so NO gradient or DRIVING FORCE for water to go through (no matter how many water channels you have)

31
Q

Explain what occurs when decrease plasma volume and how it affects other factors.

A

If you decrease plasma volume (like dehydration, diarrhea, hemorrhage) , you Decrease Venous, atrial and arterial pressure, you will INCREASE stimulation of cardiovascular baroreceptors , increase plasma ADH.
Increase plasma ADH leads to increase collecting duct permeability to H20 and Increased H20 reabsorption and decreased water excretion.

32
Q

Explain what occurs physiologically during a thirst response. How is thirst mediated?

A

Thirst response:
Reabsorption of water ALONE Cannot restore total body water to normal levels. This can only be achieved by INCREASING water ingestion/intake
baroreceptor Centers which mediate thirst are located in HYPOTHALAMUS
The feeling of thirst drives one to obtain and ingest water is stimulated by both REDUCED plasma volume and by INCREASED body fluid Osmolarity.

33
Q

Explain how Angiotensin II stimulates thirst?

A

Angiotensin II stimulates thirst by DIRECT effect on the brain. Ang II stimulates ADH release from posterior pituitary, which increases reabsorption.

34
Q

What occurs during the Euvolemia ? How is renal NaCl excretion controlled?

A

Euvolemia:
Na reabsorption by proximal tubule and Loop of Henle is regulated so that a relatively constant portion of filtered Na is delivered to distal tubule.
These two segments reabsorb approx. 90% sodium and ensure that approx. 10% gets delivered to distal tubule
Reabsorption of remaining filtered sodium by distal tubule nd collecting duct is regulated so that amount ingested in diet is at steady state.

35
Q

What is the mechanism for maintaining constant Na+ delivery to distal tubule during euvolemia?

A

Mechanisms that maintain constant Na+ delivery to distal tubule during euvolemia:

  1. Autoregulation
  2. glomerular tubular balance
  3. Sympathetic activity to maintain GFR and increase Na+ reabsorption in proximal tubule
  4. Ang II to maintain GFR and increase Na+ reabsorption in proximal tubule
  5. Local metabolites (prostaglandins, NO, dopamine) which try to maintain GFR>
36
Q

What occurs during glomerular tubular balance?

A

Glomerular tubule balance: mechanism where there are NO nerves or Hormones involved. It tries to maintain the excretion fraction or percentage of sodium reabsorbed in proximal tubule constant.
it maintains the AMOUNT of NA+ and Water reabsorbed (65% of filtration of filtered load)

37
Q

What are the mechanisms for regulating Na+ reabsorption in distal tubule and collecting duct?a

A

Mech for regulating Na+ reabsorption in distal tubule and collecting duct:
- Aldosterone
-ANP
ADH (minor function)

38
Q

Explain how Na+ excretion is controlled with volume contraction

A

Control of Na+ Excretion with Volume contraction:
salt and water loss due to diarrhea, will have decrease in plasma volume (part of ECF), decrease pressure in veins, heart and arteries, increase activity of renal sympathetic nerves, via extraneal baroreceptor reflex, increase constriction of afferent and efferent arterioles and DECREASE GFR.
When you decrease GFR, you decrease volume of fluid excreted which will help with your salt and water loss.
Decrease pressure in veins, heart, and arteries, decrease perfusion pressure of kidneys which will activate intrarenal baroreceptors and increase renal secretion.
sympathetic nervous activity increases renin, increasing Angiotensin II. The increase Ang II increases constriction of afferent and efferent arterioles and decrease GFR, which decreases salt and water loss.
salt and water loss due to diarrhea increases arterial oncotic pressure (lose volume, amount of protein increases, increasing plasma oncotic pressure, decreases GFR.

39
Q

What occurs in patient with congestive heart failure?

A

Patient with congested heart failure has DECREASED Cardiac Output. Renal perfusion pressures are Decreased. GFR is decreased with Increased activity of renin-angiotensin-aldosterone system and renal sympathetic nerves. This tends to increase retention of sodium even when a patient is in positive sodium balance and can cause EDEMA.

40
Q

What are the main factors that affect congestive heart failure?

A

Factors affecting Congestive Heart Failure:

  1. sympathetic nervous stimulation
  2. activation of renin-angiotensin system
  3. increase ADH release
  4. Increased Aldosterone release
41
Q

What are symptoms of water imbalance?

A

Symptoms of water imbalance:
1)Hyponatremia- as plasma Na+ concentration of less than 135 mEq/L with corresponding osmolarity to <275 mOsm/L. The most common cause of this is the dysregulation of ADH secretion
The dysregulation is called syndrome of inappropriate ADH secretion (SIADH).
There are multiple reasons for this syndrome, but the end result is INCREASED ADH release from the posterior pituitary. This results in high levels of water reabsorption from collecting duct and hyponatremia.

42
Q

What is Hypernatremia?

A

2) Hypernatremia- plasma Na+ concentration >145 mEq/L with corresponding osmolarity > 295 MOsm/L.
There are many different causes for hypernatremia but we are focused on those as a result from ADH dysregulation.

43
Q

What is central diabetes insipidus and what causes it?

A

Central diabetes insipidus: this is due to DECREASED ADH release from posterior pituitary. This causes a massive output of hyposomotic urine and subsequent hypernatremia.

44
Q

What is Nephrogenic Diabetes insipidus?

A

Nephrogenic Diabetes Insipidus- plasma ADH is relatively normal but the tubule response to circulating hormone is severely depressed. Once again, there will be INCREASED hypoosomotic urinary output, and subsequent hypernatremia.

45
Q

What is filtration fraction? What happens when it increases?

A

Filtration fraction- GFR/Renal blood flow. If filtration fraction increases with sympathetic nervous activity, increases peritubular capillary oncotic pressure , which is driving force for increased reabsorption of fluid in peritubular capillaries into ECF volume.

46
Q

What is a driving force for Na+ reabsorption?

A

Driving force: Increase for peritubular capillary oncotic pressure (which helps increase Na+ reabsorption).

47
Q

What is an important function of Angiotensin II by itself?

A

Angiotensin II by itself has profound effect on Na+ reabsorption. This occurs through Na+/H+ exchanger in proximal tubule.

48
Q

What substance has a minor effect on Na+ reabsorption?

A

ADH (vasopressin) has a MINOR effect on Na+ Reabsorption

49
Q

what is main determinant of how much water is excreted?

A

The RATE of water reabsorbed determines how much water is excreted

50
Q

What happens to ADH if medullary interstitial has LOW osmolarity>

A

If medullar interstitial has LOW osmolarity, NO water gradient, NO driving force for water to go through.

51
Q

Where is ADH secreted from?

A

ADH is secreted from POSTERIOR pituitary. ADH is a small peptide

52
Q

What are the two main factors that affect ADH release

A

Effects:

  1. Changes in baroreceptors
  2. Water osmolarity- ingest water, ECF osmolarity decrease, ADH secretion decreases, Plasma ADH decreases, permeability to water decreases and less water is reabsorbed. More water excreted.
53
Q

What happens to ADH if you increase osmolarity?

A

Increase osmolarity: lose water, more ADH secreted, more water reabsorbed, ECF volume expands.

54
Q

What other factors that activate thirst response? How does Angiotensin II also stimulate thirst?

A

reduced plasma volume and increased body-fluid osmolarity will activate thirst response.
Angiotensin II stimulates thirst by direct effect on the brain (neurological effects) Ang II will also stimulate ADH release form posterior pituitary which increases water reabsorption.

55
Q

What happens when there is a reduction in plasma volume?

A

Reduction in plasma volume, through various mechanisms will stimulate Angiotensin II, which by itself stimulates salt and water reabsorption in the kidneys, but can also stimulate thirst response.

56
Q

What is euvolemia?

A

Euvolemic- person has normal amounts of body fluid

57
Q

Under normal euvolemic conditions, what occurs when there is greater filter load?

A

The greater filtered load, the greater the reabsorption (to a point). It will try and maintain percentage of Na+ and water that is reabsorbed (65% reabsorbed). This a fine tuning mechanism for maintaining Na+ delivery to distal tubule

58
Q

What occurs when there is a decrease in pressure by itself? what happens when there is an increase in Angiotensin II

A

Decrease in pressure by itself will decrease perfusion pressure. Decrease in perfusion pressure will decrease GFR.
Increase in Ang II will increase activity of sympathetic nerves, increases filtration fraction, which increases salt and water reabsorption

59
Q

What are causes of heart failure? What is unique about heart failure mechanism?

A

Heart failure can be caused by old age, arrhythmia, disease, virus infection, bacterial infection, heart attack, or lack of oxygen.
Heart failure is causing a compensatory mechanism by kidneys, which makes heart failure worse as it can cause edema.
The mechanism- compromised cardiac function will lead to decreased arterial blood pressure, and increase baroreceptor reflex, increase sympathetic outflow, which will increase sodium retention and increase ECF volume. Increase sympathetic outflow, increases renin release. renin release increase Ang II which by itself increases Na+ reabsorption. Increase Na+ reabsorption increases ECF volume in vascular compartment which increases preload and worsens heart failure.

60
Q

What is main cause of syndromes of water imbalance?

A

main cause: dysregulation of ADH secretion. There is a continuous ADH release. Hence increase ADH release, increase water reabsorption, which dilutes Na+ and get hypnatremia.

61
Q

What is hyponatremia caused by? Hypernatremia?

A

Hyponatremia- caused by problem with TOO MUCH WATER
heart failure associated with hyponatremia (as you reabsorb Na+, you are reabsorbing more water than salt)
Hypernatremia- When you have TOO much SODIUM in blood. It is caused by excessive thirst and seen in people who do not drink enough water.

62
Q

What occurs during Central diabetes insipidus? How does this differ from nephrogenic diabetes insipidus?

A

Central diabetes insipidus - due to Decrease in ADH release from the posterior pituitary. This causes massive output of Hypoosmotic urine and subsequent HYPERNATREMIA.

Nephrogenic diabetes insipidus- plasma ADH is relatively normal but the TUBULE response to circulating Hormone is severely DEPRESSED
Once again, there will be increasing hypoosmotic urinary output and subsequent HYPERNATREMIA.

Systems Physiology (19 decks)

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