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Physiology > Unit 4 - Renal Physiology > Flashcards

Unit 4 - Renal Physiology Flashcards

1
Q

Where are Glucose carriers located in a nephron?

A

proximal collecting tubule

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2
Q

transepithelial transport

A

5 barriers to being reabsorbed:

  1. luminal membrane of tubular cell
  2. pass through cytosol to get to other side of cell
  3. cross basolateral membrane of tubular cell to interstitial fluid
  4. diffuse through interstitial fluid
  5. penetrate capillary wall to enter blood
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3
Q

juxtaglomerular apparatus

A

macula densa cells: part of tubule
- monitor & respond to changes in osmolarity of filtrate

granular cells: modified smooth muscle of afferent arteriole
- serve as baroreceptors sensitive to blood pressure

mesangial cells: contain contractile elements

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4
Q

Three forces that influence glomerular filtration

A
  1. glomerular capillary blood pressure - favors filtration
  2. plasma colloid osmotic pressure - opposes filtration (exerted by plasma proteins)
  3. Bowman’s capsule hydrostatic pressure - opposes filtration
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5
Q

what is filtered load?

A

the quantity of any substance filtered per minute (mg/min)

FL = plasma concentration X GFR of substance

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6
Q

define tubular maximum (aka transport maximum)

A

the maximum reabsorption of a substance. Any quantity filtered beyond it tubular maximum, is not reabsorbed & will show up in urine.

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7
Q

Renin-Angiotensin-Aldosterone system (TAAS)

A
  • promotes salt and water retention

- leads to a rise in arterial blood pressure

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8
Q

granular cells

A
  • part of the juxtaglomerular apparatus
  • respond to:
    - fall in NaCl
    - ECF volume
    - arterial blood pressure - if falls, secrete renin
  • secrete RENIN
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9
Q

Renin

A
  • activates ANGIOTENSINOGEN to become ANGIOTENSIN I.

- brings about increased Na+ reabsorption in distal & collecting tubules

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10
Q

angiotensinogen

A
  • plasma protein synthesized by LIVER
  • present in plasma
  • secretion of RENIN activates it to become ANGIOTENSIN I
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11
Q

Angiontensin I

A
  • when passing through lungs, it’s converted to ANGIOTENSIN II by ANGIOTENSIN-CONVERTING ENZYME (ACE)
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12
Q

Angiotensin II

A
  • tells adrenal cortex to secrete ALDOSTERONE
  • increases TPR by constricting systemic arterioles
  • stimulates thirst
  • stimulates vasopressin
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13
Q

Aldosterone

A

increases Na+ reabsorption by:

  1. inserting add’l Na+ channels into luminal membranes
  2. adding Na+-K+ pumps into basolateral membranes

promotes Na+ reabsorption & K+ secretion

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14
Q

hypoventilation would lead to:

A

respiratory acidosis

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15
Q

in which case is the pH lower: hypo ventilating or hyperventilating

A

after hypo ventilating = respiratory acidosis

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16
Q

body’s response to metabolic alkalosis

A

body retains more carbon dioxide

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17
Q

3 components of filtration membrane

A
  1. capillary endothelium
  2. basement membrane
  3. filtration slits of podocytes
18
Q

which part of the tubule is always impermeable to water?

A

ascending limb

19
Q

a decrease in concentration of plasma proteins will _______ filtration pressure?

A

increase

20
Q

How will auto regulation respond to a drop in GFR?

A

dilation of afferent arteriole to increase blood flow & glomerular pressure

21
Q

What would loss of plasma proteins do to GFR?

A

will decrease oncotic pressure (works against filtration) -> GFR would increase

22
Q

What would dehydrating diarrhea do to GFR?

A

would increase oncotic pressure -> GFR decrease

23
Q

Autoregulation of GFR

A

Happens in the kidneys; regulate between 80 - 180 mmHg MAP

  1. myogenic: adjust diameter of afferent arteriole
  2. tubuloglomerular feedback:
24
Q

Autoregulation of GFR: tubuloglomerular feedback for Low GFR

A

detect changes in NaCl concentration
1. for low salt (to increase GFR): macula densa detect low salt; intrarenal baroreceptors -> granular cells to release RENIN - > increased Na+ reabsorption -> increased water retention -> increased BP -> increased GFR

25
Q

Autoregulation of GFR: tubuloglomerular feedback for high GFR

A

high salt concentration (to lower GFR): macula densa cells detect high salt -> release ATP & adenosine -> cause granular cells to constrict afferent arteriole -> lower GFR

26
Q

GFR Regulation - 3 pathways

A

All control afferent arteriole diameter & extrinsic overrides intrinsic

Intrinsic control
1. autoregulation

Extrinsic control - make adjustments to BP which affects GFR

  1. Neural regulation
  2. Hormonal control
27
Q

GFR regulation: Extrinsic: Neural reg

A
  1. sympathetic control - if stimulated b/c too low, causes a system wide constriction of arterioles, which increases BP and therefore GFR

if too high - sympathetic activity is reduced

  1. baroreceptor reflex - baroreceptors in aortic arch & carotid sinus detect low BP; triggers RAAS, which increases BP and GFR
28
Q

GFR reg / extrinsic / neural regulation

A
  1. sympathetic control

2. baroreceptor reflex

29
Q

GFR reg / extrinsic / hormonal regulation

A
  1. Angiotensin II - increase BP

2. ANP - atrial natriuretic peptide - decrease BP

30
Q

renal threshold

A

the plasma concentration at which transport maximum is reached
substance will begin to appear in urine

31
Q

obligatory reabsorption occurs where?

A

Refers to H20 reabsorption done osmotically
80% done this way
1. proximal collecting tubule (PCT)
2. Loop of Henle

32
Q

facultative reabsorption occurs where?

A

Water reabsorption that requires ADH to be present
20% done this way
1. distal collecting tubule (DCT)
2. collecting ducts
This step determines whether grin will be concentrated or diluted

33
Q

Countercurrent Multiplier

A
  1. establishes the gradient - juxtamedullary nephron
  2. preserves the gradient - vasa recta
  3. uses the gradient - DCT, collecting tubules
34
Q

micturition

A

voiding bladder or urination
a spinal reflex
internal sphincter: smooth muscle; contracts
external sphincter: skeletal; relaxes

35
Q

ADH

A

released from posterior pituitary

osmoreceptors in kidneys & hypothalamus dectect osmotic changes

36
Q

ph of blood

A

7.35 - 7.45
< 7.35 = acidosis - depression of CNS
> 7.45 = alkalosis - over excitability of nervous system

37
Q

Mechanisms for Acid-Base Balance in body

A
  1. Chemical buffer systems
  2. Respiratory buffer systems
  3. Renal mechanisms
38
Q

Chemical buffer systems

A

Should resist changes in H+ concentrations

  1. bicarbonate: H2CO3 / HCO3-
  2. phosphate: NaH2PO4 / Na2HPO4
  3. protein buffer : Hb
39
Q

respiratory acidosis

A 
too much CO2 / hypoventilation
to fix:
buffer:  take up H+
no respir
renal:  excrete more H+, conserve HCO3-
40
Q

respiratory alkalosis

A 
not enough CO2 / hyperventilation
to fix:
buffer:  give up more H+
respir:  restrict hypervent
renal:  conserve H+, excrete more HCO3-
41
Q

metabolic acidosis

A

caused by HCO3- deficit / severe diarrhea, diabetes mellitus
to fix:
buffer: take up H+
respir: blow off add’l H+ generating CO2
renal: excrete more H+, conserve HCO3- (except w/kidney disease)

42
Q

metabolic alkalosis

A 
caused by excess HCO3- / prolonged diarrhea, ingestion of too many antacids
to fix:
buffer:  liberate more H+
respir:  hyperventilation restricted
renal:  conserve H+, excrete more HCO3-

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