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Pathophys Exam II > Renal Mod 2 > Flashcards

Renal Mod 2 Flashcards

1
Q

what substances does the glomerulus filter in healthy indvls?

A 
water
electrolytes
creatinine
glucose
nitrogenous wastes (urea & uric acid)
small AA
bicarbonates (HCO3-)
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2
Q

what substances are not normally filtered in glomerulus in healthy individuals?

A

blood cells

most proteins/peptides - some smaller sized proteins/AA do pass thru filter

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3
Q

3 layers of glomerular filtration

A
  1. fenestrated endothelium (pores)
  2. basement membrane (basal lamina)
  3. podocytes (epithelium)
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4
Q

size of pores in fenestrated endothelium

A

70-90nm

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5
Q

function of basement membrane (basal lamina)

A

no pores or slits

acts as a screen/physical barrier

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6
Q

size of slits of podocytes

A

filtration slits approx 25nm

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7
Q

how do RBCs/WBCs compare to glomerular pores

A

cell size:
RBCs approx 8 micrometers in diameter = 8000nm
WBCs approx 8-15 micrometeres = 8-15000nm

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8
Q

how does the endothelium filter?

A

pores of the endothelium allow small molecules to easily pass though and block blood cells

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9
Q

how does the basement membrane filter

A
  1. physically

2. membrane charge

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10
Q

how does the basement membrane filter physically?

A

membrane only permits very small molecules to pass thru into Bowman’s space (4-8nm easily pass, >8nm blocked)

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11
Q

how does the basement membrane filter based on membrane charge

A

membrane is negatively charged

therefore it repels small molecules that physically could pass thru but have a negative charge = proteins

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12
Q

example of albumin and membrane charge of basement membrane

A

lots of albumin in blood
easily passes thru endothelium
albumin is negatively charged tho - so not a lot should get thru into urine (only expect small amounts)

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13
Q

affects of pathology to the capillary membrane

A

a dz/damaged capillary allows :

  1. proteinuria
  2. hematuria
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14
Q

what is proteinuria and what does it indicate?

A
  1. proteinuria: excess levels of protein in urine - d/t loss of glomerular basement charge or size barrier, proximal tubule damage
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15
Q

what is hematuria and what does it indicate?

A
  1. hematuria - any condition in which blood is foun din the urine
    - sign of glomerular capillary dz as well as other kidney pathologies (stones, tumor, infections)
    - often associated with inflammatory condition of kindey
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16
Q

consistent finding in nephritic syndrome

A

hematuria

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17
Q

consistent finding in nephrotic syndrome

A

proteinuria

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18
Q

if proteinuria is present, what would other labs look like?

A
  1. hypoalbuminemia
  2. edema (result of altered albumin in blood)
  3. hyperlipidemia/-uria
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19
Q

if you have hematuria - what would other labs look like?

A

oliguria - low urine output/production

azotemia - elevated BUN and creatinine in blood

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20
Q

permeability of glomerular capillaries vs skeletal muscle

A

50x greater than capillaries of skeletal muscle

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21
Q

total surface area of glomerular capillary endothelium

A

0.8 m2

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22
Q

the surface area of capillary/mesangial cells can be functionally altered by what?

A

by the contraction of mesangial cells

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23
Q

whatwill the contraction of mesangial cells do?

A

effectively decreased the capillary surface area

less surface results in less filtration (decr GFR)

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24
Q

substances that sitmulate contraction of mesangial cells

A
  1. angiotensin II
  2. ADH
  3. NOrepinephrine
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25
Q

substances that stimulate relaxation of mesangial cells

A

ANP

dopamine

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26
Q

what is glomerular filtrate

A

solution that is filtered thru glomerular capillary

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27
Q

the sum of what four pressures will influence GFR?

A
  1. hydrostatic pressures of glomerulus and Bowman’s capsule

2. osmotic pressures in glomerulus and Bowman’s capsule

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28
Q

what is the glomerular capillary hydrostatic pressure

A
  1. major force in filtration, decreases at end of glomerular capillary
  2. opposed by hydrostatic pressure in Bowmna’s capsule
  3. clinical - extreme systolic BP changes will influence
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29
Q

what is Bowman’s capsule hydrostatic pressure

A
  1. small and fairly constant at beginning and end of glomerular capillary
  2. clinical - increased if obstructive pathology (stones), edema of kidney itself (renal capsule limited volume to allow swelling)
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30
Q

what is glomerular capillary colloidal osmotic pressure

A
  1. decreases at end of glomerular capillary which maximizes filtration at the end of capillary
  2. clinical - changes in plasma proteins (hypoproteinemia)
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31
Q

what is Bowman’s capsule colloidal osmotic pressure

A

NOT a factor unless diseased/damaged glomerular capillary

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32
Q

what is tubular reabsorption?

A

reabsorbs substances (filtrate) from the tubular portion of nephron back into capillary system (peritubular capillaries)

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33
Q

what is tubular secretion

A

secretes substances (filtrate) from the capillary system (peritubular capillaries) into the tubular portion of the nephron

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34
Q

what is the PCT

A

proximal convoluted tubule

15mm long, single layer of cells along wall with microvilli (brush border) along the lumen

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35
Q

what is the primary function of PCT?

A

resorption of sodium

-water, electrolytes and other substances are co-transported with sodium back into blood stream

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36
Q

what other substances are reabsorbed in the PCT?

A

the PCT reabsorbs majority of the glomerular filtrate

  • 60-70% of water and sodium
  • 50% of urea is reabsorbed
  • 90-100% of glucose, amino acids, bicarb and other electrolytes
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37
Q

two pathways sodium is reabsorbed from the PCT into PCT cell

A
  1. co-transport

2. active exchange

38
Q

how is sodium reabsorbed from the PCT via co-transport into PCT cell

A

with glucose, AA, water, electrolytes and other substances

–gradient formed by active transport of sodium out of PCT cell drives this pathway

39
Q

how is sodium reabsorbed from the PCT via active exchange into PCT cell

A

exchange of Na+/H= as part of mechanisms to reabsorb bicarb

  • Na+ is transported from PCT lumen in to PCT cell in exchange for H+ ion
  • H+ ion that is transported into the lumen combines with bicarb as part of pathway to reabsorb filtered bicarb into blood stream (does not contribute to increased blood or urinary acid levels - recycling)
40
Q

what are carbonic anhydrase inhibitors?

A

inhibit this pathway to block Na+ absorption in the PCT

41
Q

how is sodium transported from PCT cell into peritubular capillaries

A

active transport via sodium/potassium pump
-creates the sodium gradient eneded to facilitate flow of sodium and co-transporters from the PCT lumen into the PCT cell

42
Q

steps for glucose resorption in the PCT?

A
  1. glucose is transported from PCT lumen into PCT cell

2. glucose transported from PCT cell into peritubular capillaries

43
Q

how is glucose transported from PCT lumen into PCT cell

A
  1. glucose is co-transported with sodium via specialized carriers
  2. glucose and sodium are transported from PCT lumen to PCT cell
  3. co-transport is dependent of the sodium gradient formed by active transport of sodium out of PCT cell
44
Q

how is glucose transported from PCT cell into peritubular capillaries?

A

passively diffuses into blood stream via glucose carriers (GLUT)

45
Q

what is glucose transport limited by?

A

number of available carriers

46
Q

if there is too much glucose in the filtratrate then what?

A

PCT can’t reabsorb all the glucose

47
Q

what is transport maximum

A

Tm - max rarte a substance can be transported across a cell wall

48
Q

what plasma glucose level corresponds with transport max of glucose in PCT

A

> 350 mg/dl

49
Q

in diabetes, elevated plasma glucose will:

A

increase glucose filtered at the glomerulus
increased glucose of filtrate flowing thru PCT
if too much glucose in filtrate then transport max is reached and glucose is excreted in the urine

50
Q

what is the glucose renal threshold

A

refers to plasma values at which glucose first appears in urine

51
Q

plasma glucose levels greater than what correspond with glucose dumping into the urine

A

180-200mg/dl

normal (100mg/dl)

52
Q

functions of the loop of Henle

A
  1. reabsorbs 25% of sodium filtered by glomerulus along with other glomerular filtrate that was not reabsorbed in PCT
  2. regulate the osmotic state of the medullary interstitial fluid and the filtrate leaving the loop of Henle - urine concentration
53
Q

where in the loop of Henle is sodium reabsorbed?

A

occurs in ascending limb only

54
Q

sodium transport from loop of Henle lumen into PCT cell

A

sodium is co-transported with both Cl and K

-transport of Na/Cl/K is dependent on gradient formed by active transport of sodium out of loop of Henle cell

55
Q

sodium transport from loop of Henle cell into peritubular capillaries

A

active transport via sodium/potassium pump
-this pathway creates the sodium gradient needed to facilitate flow of sodium and co-transporters from loop of Henle lumen into loop of Henle cells

56
Q

what happens in descending limb of loop of Henle

A
  • a combo of water permeability out of loop and minimal sodium permeability out of loop creates a hyperosmotic filtrate as in descends in the loop of Henle
  • this allows water to be reabsorbed and does not allow sodium to be reabsorbed
57
Q

what happens to osmolarity of the tubular fluid as it descends to the bottom of the loop of Henle

A

increases

58
Q

what happens in ascending limb of loop of Henle

A

aka diluting segment
-a combo of limited water permeability out of loop and increased sodium permeability out of loop creates a hypo-osmotic filtrate as in ascends in the loop of Henle

59
Q

how does the thickness of the ascending loop of Henle change?

A

starts thin and becomes thick

60
Q

purpose of thick ascending loop of Henle

A

impermeable to water so water stays inside the loop of Henle

-permeable to sodium - so sodium leaves the loop

61
Q

the osmolarity of the tubular fluid leaving the loop of Henle is __________ than when it first entered the loop of henle

A

hypo-osmotic (more diluted)

62
Q

what are loop diuretics

A

ex. furosemide - inhibit the Na/K/Cl co-transport mechanism
- increase osmotic concentration of tubular fluid as it leaves the loop of Henle and decreases the medullary interstitial fluid
- the change of these two concentration results in diuresis and massive natriuresis

63
Q

additional effects of loop diuretics

A

inhibiting the Na+ resorption in the loop of Henle:

  • resorption of K+ is also inhibitied and thus hypokalemia is a secondary effect
  • resorption of Ca+ is also linked to Na+ resorption thus hypocalcemia
64
Q

where does the DCT begin

A

macula densa

65
Q

function of macula densa at beginning of DCT

A

sense NaCl levels as part of feedback
-if increase in NaCl then macula densa signals afferent arteriole to constrict and slow RBF and GFR which filters less sodium

66
Q

function of DCT

A
  1. dilution/concetration of urine
    - early DCT: continue to dilute tubular fluid
    - late DCT: begin process of concentrating fluid for urine output
  2. regulate sodium, potassium, and calcium homeostasis
  3. contribute to regulation of acid-base balance via absorption/secretion of ions
67
Q

early DCT aka

A

cortical diluting segment

68
Q

what does the early DCT do?

A

reabsorbs sodium and impermeable to water further diluting the tubular fluid

69
Q

how does early DCT reabsorb sodium?

A
  • reabsorbs 5% of sodium filtered in the glomerulus
  • sodium transport from early DCT lumen to early DCT cell
  • –transport of NaCl is dependent on gradient formed by active transport of sodium out of early DCT cell
70
Q

how is sodium transported from early DCT cell into peritubular capillaries?

A

active transport via sodium/potassium pump (same as PCT/ascending loop of Henle)
this creates the sodium gradient needed to facilitate flow of sodium and co transporters from early DCT lumen into early DCT cell

71
Q

how do thiazide diuretics work

A

inhibit Na/Cl co transporter which inhibits Na/Cl reabsorption in early DCT

72
Q

secondary effect of thiazide diuretics

A
  • has opposite effect on Ca+ = reabsorption is increased and may result in hypercalcemia
  • calcium is normally reabsorbed into bloodstream from DCT cell as a sodium/potassium exchange
  • also hypokalemia and metabolic alkalosis
73
Q

two cell types located in both late DCT and collecting duct

A
  1. principle cell: reabsorb sodium and water, secrete potassium
  2. alpha - intercalated cells: secrete H+ ions
74
Q

function of late DCT

A

regulate final urine concentration

maintain acid base homeostasis

75
Q

how does the late DCT and collecting duct reabsorb sodium?

A
  1. reabsorption of sodium occurs in principle cells
  2. transport of sodium from late DCT lumen to late DCT cells
  3. transport of sodium from late DCT/collecting duct cells to peritubular capillaries
76
Q

how is sodium transported from late DCT lumen to late DCT cells?

A
  1. aldosterone stimulates sodium reabsorption and potassium secretion
  2. aldosterone stimulates increased sodium uptake into late DCT cell which in turn stimulates sodium/potassium pump to transport sodium into peritubular capillary
  3. increased activity of the sodium/potassium pump will promote potassium secretion from late DCT into the late DCT lumen
77
Q

how do K sparing diuretics work

A
  • K sparing diuretics inhibit K secretion from principle cells in late DCT/collecting duct
  • antagonizes aldosterone influence on principle cells and blunts sodium reabsorption
78
Q

how does the late DCT and collecting duct reabsorb water?

A

if ADH is present then principle cells of late DCT increase permeability to water

79
Q

how do intercalated cells of the late DCT and collecting duct reabsorb K?

A

only occurs if significantly low dietary intake of K

80
Q

how does the late DCT and collecting duct contribute to acid-base regulation

A
  1. H+ is secreted into late DCT lumen from intercalated cells
  2. in the DCT lumen, the H+ combines with non-bicarb buffers in two pathways
  3. this creates a new bicarb which is reabsorbed from the intercalated cells into the peritubular capillaries
81
Q

what are the two pathways that H+ combines with non bicarb buffers

A
  1. H+ combines with ammonia to form ammonium and is then excreted in the urine
  2. H+ combines with a dibasic phosphate to form monobasic phosphate and then excreted in the urine
82
Q

how does the body attempt to compensate for an acidic environment in the blood stream?

A

excretion of H+ in the urine and adding bicarb to the blood stream

83
Q

collecting duct function

A

-ultimately determines the final concentration of urine to be excreted by increasing the concentration of the tubular fluid as it passes thru the collecting duct

84
Q

how does the collecting duct determine the final concentration of urine

A
  • tubular fluid entering the distal DCT and collecting duct is hypotonic
  • collecting duct reabsorbs Na+ and H2O to increase concentration of urine as in late DCT
85
Q

what 2 things stimulate reabsorption of Na+ and H2O

A

aldosterone and ADH

86
Q

fluid concentration in PCT

A

300 mOSM

87
Q

Loop of Henle fluid concetration

A

start: 300mOsm
descending: gradual increase to 1200 mOsm
ascending: gradual decrease
finish: 100 mOsm

88
Q

fluid concentration of DCT

A

early: continues to dilute 100 mOsm
late: begins to concentrate
finish: 150 mOsm

89
Q

collecting duct fluid concentrations

A

start: 150mOsm
finish: 1200mOsm (depending on body’s needs and circumstances)

90
Q

healthy kidney approximately how much water is reabsorbed

A

98-99%

91
Q

how much water is filtered in glomeruli vs how much urine output on average

A

180L filtered vs 1L output

Pathophys Exam II (5 decks)

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