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Exam 3 physio > Lecture 2 Renal > Flashcards

Lecture 2 Renal Flashcards

1
Q

two modes of transport across tubular epithelial cells in a nephron are
transcellular and paracellular, what are these two?

A

transcellular- transport THROUGH tubular cells

paracellular- transport BETWEEN tubular cells

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2
Q

Osmosis results in solvent drag, what is solvent drag

A

solvent drag results from solutes being carried by water in paracellular transport

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3
Q

how can osmosis (rate of water diffusion) be regulated

A

by aquaporins

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4
Q

3 types of transported proteins and their definition

A

uniporter- 1 molecule moves
symporter (cotransport)- 2 molecules moved same direction
antiporter - 2 molecules moved in opposite directions (against concentration gradient)

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5
Q

endocytosis is what?

exocytosis is what?

A

endocytosis is transport into a cell
exocytosis is transport out of cell
BOTH BY Vesicles!

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6
Q

where is the ONLY spot in the nephron where Na is NOT reabsorbed?

A

Na NOT reabsorbed in the Thin Descending Limb of LoH

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7
Q 
Na reabsorption %s
in PCT?
Thin ascending limb?
thick ascending limb?
DCT?
Collecting duct
A 
PCT-65%
Thin AL: 7% 
Thick AL: 20%
DCT: 5%
Collecting duct: 2-3%
SO KIDNEYS Excrete VERY LITTLE Na
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8
Q

The PCT reabsorbs several things

name them and how they are reabsorbed

A

Glucose, AAs= Na symporters
Active transport on basal side keeps Intracellular Na low
Water and solutes via paracellular transport
Na reabsorption in conjunction with Bicarbonate using Na/H antiporter

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9
Q

How is Na reabsorption done in PCT?

A

in conjunction with bicarbonate reabsorption using Na/ H antiporter
BUT reabsorption not direct H is secreted and HCO3 is absorbed

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10
Q

what rxn facilitates the absorption of bicarbonate

A

Carbonic Anhydrase produces H and HCO3 in tubule cells allowing HCO3 to be moved to blood and H is transported back into tubule so it recombines with filtered HCO3
LEADING To NET EFFECT of bicarbonate REABSORPTION

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11
Q

End of PCT what happens

A

2/3 of Na, Cl, and water reabsorbed and small proteins
K and divalent cations reabsorbed by solvent drag
AAs and glucose reabsorbed
Bicarbonate reabsorbed due to Na/ H antiporter
secretion of organic ions (IE organic drugs)

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12
Q

how much of filtered NaCl and water are reabsorbed in the LoH

A 
NaCl= 25% reabsorbed 
Water= 15% reabsorbed
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13
Q

what is the permeability of salt and water in the the THIN Descending Limb

A

Thin DL= impermeable to SALT, Permeable to water

Bc it has aquaporins

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14
Q

permeability of salt and water in THIN ASCENDING LIMB

A

THIN ASCENDING LIMB
PERMEABLE to SALT (passive reabsorption)
IMpermeable to water

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15
Q

the ascending THICK limb has what to dilute fluid

A

Na K 2CL symporter in apical membrane

NaK ATPase in basolateral membrane

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16
Q

Paracellular transport of monovalent and divalents NOT DUE to Solvent Drag in THICK ascending limb
TRUE or FALSE
why?

A

TRUE! due to voltage gradient!!

Tubular fluid becomes positive due to Cl reabsorption so cations diffuse along an electrical gradient

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17
Q

fluid leaving LoH is hyposmotic then how do we get the formation of hyperosmotic urine?

A

renal countercurrent mechanism establishing an osmotic gradient allowing water to be reabsorbed in the collecting ducts by the actions of ADH (vasopressin)

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18
Q

In the absence of ADH what happens

A

no water reabsorption in collecting ducts so urine stays hyposmotic

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19
Q

how does the osmolarity of the blood leaving the kidneys to veins stay the same (normal)

A

bc peritubular capillaries are permeable to NaCL and water so plasma osmolarity changes as the capillaries follow the loop but returns to normal by the end

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20
Q

how does the DCT reabsorb about 8% of the filtered NaCl ?

A

VIA a Na Cy symporter in the apical membrane and a Na K ATPase in the basolateral membrane

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21
Q

describe reabsorption of K, H , and water in DCT

A

variable!

22
Q

What 2 types of cells are in the latter DCT and the collecting duct?

A

Principal cells and Intercalated cells

23
Q

what are principal cells in the late DCT and collecting duct for

A

Principal cells have ENaC channels that reabsorb Na and secrete K
Na reabsorption drives paracellular Cl absorption
K secreted due to Na K ATPase activity in basal membrane

24
Q

What are intercalated cells involved in

A

Intercalated cells involved in acid base balance and help REABSORB K!

25
Q

what is euvolemia

A

Euvolemia is normal blood volume

26
Q

how is euvolemia maintained

A

hormonal and neural responses

27
Q

What hormone is released by the Posterior Pituitary to regulate Blood Volume and what osmolality level does it responds to

A

ADH
release is stimulated by changes in osmolality of blood specifically to changes above a set osmolality of 275-290 mOsm/ kg of H2O

28
Q

A dec in blood volume is sensed by what? (x2)

A
  1. low pressure barareceptors in LEFT atrium and large pulmonary vessels respond to DEC blood volume
  2. High pressure baroreceptors in AORTIC arch and CAROTID sinus respond to DEC in Blood Pressure (i.e. low Blood volume)
29
Q

Actions of ADH?

A

ADH INC permeability of Late DISTAL tubule and Collecting duct to water by INC aquaporins into apical membrane
INC permeability of medullary collecting duct to urea

30
Q

when is ADH released

A

when plasma level low or osmolality is HIGH

31
Q

If ADH is low (diuresis) what happens?

A

ADH LOW = solutes reabsorbed in LATE DCT and collecting duct but NO water absorbed so URINE IS DILUTE and plentiful

32
Q

what happens when ADH is high (antidiuresis)

A

ADH HIGH= water reabsorbed as fluid passes thru collecting duct and URINE IS CONCENTRATED up to 1200!
so urine excretion is low but concentrated!
ADH INC urea transporters thus causing reabsorption of water

33
Q

renin - angiontensin- aldosterone system stimulates events that INC reabsorption of Na and H2O but how?

A

renin INC in response to DEC perfusion pressure and DEC NaCl delivery to Macula dense or SYMP input to JGA
renin converts angiotensinogen to angiontensin 1
angiontensin 1 converted to angiotensin 2 by ACE

34
Q

what does Angiotensin 2 do?

A

Angiotensin 2 causes vasoconstriction, stimulate release of ADH, INC Symp activity, and INC aldosterone secretion

35
Q

what does the release of aldosterone from the adrenal cortex do?

A

Aldosterone INC NaCl reabsorption in the DCT and collecting duct by INC transport protein synthesis

36
Q

what are natriuretic peptides

A

hormones secreted when the heart dilates (during volume expansion)

37
Q

atrial natriuretic peptides come from what

A

atria

38
Q

brain natriuretic peptides come from what

A

THE VENTRICLES!

39
Q

what are the effects of natriuretic peptides

A

VASODILATION of afferent arterioles ( INC GFR)
VasoCONSTRICT Efferent Arterioles (INC GFR)
inhibit renin and aldosterone
INHIBIT ADH secretion
NET Effect INC excretion of NaCl and Water

40
Q

why is regulation of K important for Kidney

A

K is a major determinant of membrane resting potential therefore it can affect electrically excitable cells

41
Q

what is hyperkalemia and result

A

INC K thus depolarizes Vm

42
Q

what is hypokalemia and result

A

DEC K thus hyper polarizes Vm

43
Q

what can changes in K cause

A

cardiac arrythmias

44
Q

How is K regulated (x2)

A

Ingested K is fast shifted into cells by Insulin, E and Aldosterone
Kidney excretes 90-95% of ingested K

45
Q

K if freely filtered in glomerulus so how much is reabsorbed in PCT and how

A

PCT reabsorbed 67^ of K thru solvent drag and paracellular transport

46
Q

how is K reabsorbed in the Thick Ascending lim?

A

by Na K 2Cl simperer and paracellular transport (NOT SOLVENT DRAG!)

47
Q

in the Late distal tubule and collecting duct what happens to K

A

K is secreted by principal cells depending on ATpase activity, K gradient and apical K permeability
or in cases of Low K intercalated cells reabsorb K

48
Q

when body K is depleted what happens

A

Intercalated cells in late distal tubule and collecting ducts reabsorb K

49
Q

If plasma K is INC what happens

A

INC K stimulates aldosterone release and aldosterone INC Na K ATPases in principal cells thus causing more K to be secreted

50
Q

Inc Flow rate has what effect on K and why

A

INC flow rate = INC K secretion due to local response of bending of cilia and INC Flow favors INC Na reabsorption this favoring INC K secretion

51
Q

when plasma concentrations of K are low what does DCT and cortical collecting duct do?

A

reabsorb K

52
Q

if plasma K high what happens

A

DCT and collecting ducts INC secretion of K

Exam 3 physio (4 decks)

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