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Hailey - CRRAB II > Muster Week 2 > Flashcards

Muster Week 2 Flashcards

1
Q

Filtered substances can be ____ or ____

A

REABSORBED or SECRETED as needed to maintian homeostasis

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2
Q

Amount filtrate into nephron PT

A

125 mL/min

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3
Q

SECRETION

A

peri-tubular capillary to lumen

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4
Q

REABSORPTION

A

lumen to peri-tubular capillary

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5
Q

proximal tubule is made of…

A

proximal tubule cell SINGLE CELL LAYER (but still cell membrane)

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6
Q

____ of all the filtered solute and water are reabsorbed within the proximal tubule!

A

2/3
goes in at 300 mosmol –> leaves as 300 mosomols = ISO-OSMOTIC

“literally sucking up what just put into it”

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7
Q

Mechanisms to move substances

A
  1. diffusion (generally down a gradient)
  2. channels
  3. transports (uniporters/multiporters) (active, 1* or 2*)
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8
Q

Primary active transport requres ______

A

ATPase, energy

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9
Q

Secondary active transport

A

one of solutes moves down EM/conc gradient, which drives other
“drag other along for the ride”

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10
Q

stoichiometry drives _____

A

charge difference

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11
Q

basolater Na/K transporter is ________ transport

A

ACTIVE transport
requires energy

ONLY ON BASOLATERAL (serosal, anti-luminal, blood side)

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12
Q

luminal Na+ channel is

A

PASSIVE

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13
Q

What is K+ doing?

A

RECYCLING

allows pump to keep moving/working

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14
Q

Na-glucose trnasporters are also known as…

A

SGLT (sodium-glucose linked transporters) in two flavors, 1 and 2
***90% of glucose reabsorbed in PT occurs via SGLT 2 (1:1)

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15
Q

2* active transport is regulated by:

A
  1. increased CO2
  2. increased angiotension II
  3. increased SNS drive
  4. decreased pH
    = ACIDOSIS
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16
Q

Na/H pump responds directly to ______

A

acidosis

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17
Q

_____% of glucose is brought across at luminal border by _____

A

100% of glucose is brought across luinal border by SGLT 2 = NO GLUCOSE IN URINE

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18
Q

___, ___, and ___ are all being pumped UP their EM gradient

A

glucose, a.a.s, phosphorus pumped UP EM gradient by 2* ACTIVE TRANSPORT
- all facilitated by Na* transport (symporters)

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19
Q

High Na+ in interstitium drives _____

A

Na+ concentration gradient into peritubular capillaries

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20
Q

transport maximum (Tm)

A

Na+/glucose transporter saturation point…additional glucose will NOT be able to be reabsorbed and will REMAIN IN URINE
~15mM glucose

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21
Q

glucosuria

A

when Tm (or glu in urine?) reaches about 15mM = ABNORMAL

not a test for DM

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22
Q

Why isn’t glucosuria test for DM?

A

Becuase Tm is transport mediated, so could have totally normal serum [glu] but glu in urine = SOMETHING IS WRONG WITH TRANSPORTER IN PT (not just high glu everywhere)

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23
Q

osmotic diuresis

A

Na/glu transporter has reached Tm –> excrete rest of glu out –> H20 follows –> osmotic diuresis

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24
Q

Cl- transport, think

A

Cl- recycling
formate recycling

“that’s just the way Cl- is handled” it is recycled using FORMATE = FORMATE ANTIPORTERS = formate is recycling too
and PARACELLULAR TRANSPORT through tight junctions

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25
Q

late section of PT

A
  • formate anti-porters
  • favorable concentration gradient of Cl- for transcellular movement
  • EM gradient allowing some para-cellular movement of sodium as well
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26
Q

CA is present two places

A
  1. brush border

2. in cell

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27
Q

HCO3- transport

A

1 DESTROYED: 1 RECLAIMED (put back in blood)
= BICARBONATE REABSORPTION/RECLAMATION

bicarb is created and put back into the blood stream

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28
Q

CA

A

CO2 + H20 –> H2CO3 –> HCO3- + H+
= makes bicarb and protons

the reaction occurs without carbonic anhydrase (CA) but CA cranks it up 100x

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29
Q

Na/HCO3- symporter

A

on capillary bed side –> 3 HCO3-: 1 Na+ BOTH GOING OUT

= puts bicarbonate back in blood

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30
Q

If PT defect…

A

see in urine:

  • BICARB (ACIDOTIC)
  • PHOSPHOROUS can’t be reclaimed
  • VITAMIN D also
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31
Q

H20 transport in PT

A
  1. diffusion (minor player)
  2. aquaporins
  3. paracellular transport

*for all solute reabsorbing, water follows –> no change in osmolality

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32
Q

ATN

A

ACUTE TUBULAR NECROSIS

  • damage to PTs –> Na+, Cl-, bicarb, glu = everything in pee that PT isn’t taking up
  • see casts
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33
Q

As fluid leaves the glomerulus –> slight increase in oncotic pressure (filtration of solute and water)

A

slight increase in oncotic pressure (filtration of solute and water)

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34
Q

hydrostatic pressure within capillary drops due to

A

resistance

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35
Q

Net filtration pressure of capillary uptake

A

forces of filtration - forces of reabsorption
(P pc + PI i) - (P i - PI pc)
(20 + 6) - (33 + 3) = -10mmHg

NEGATIVE 10mmHg = OPPOSITE OF FILTRATION = REABSORPTION

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36
Q

____% of Na, Cl, H20, reabsorbed by end of PT

A

66%

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37
Q

____% glucose reabsorbed by end of PT

A

100%

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38
Q

____% HCO3 reabsorbed by end of PT

A

80%

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39
Q

Why need to filter 180L/day?

A

We are putting toxic waste metabolites into urine, NEED THIS COPING MECHANISM TO RID TOXINS
(otherwise would be very pointless and excessive)

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40
Q

Not all substances filtered have channels or transports, so they must either:

A

diffuse across cell membrane OR be excreted

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41
Q

Polar substances

A

have CHARGE

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42
Q

Non-polar substances

A

have NO charge

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43
Q

Polar substances’ fate

A

no transporter/channel/diffusion –> trapped in lumen –> “PEE OR POOP IT OUT, THAT’S IT!”

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44
Q

Non-polar substances’ fate

A

Non-polar CAN diffuse across cell membrane –> reabsorption

Ex: O2, steroid hormones, CO2, cholesterol

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45
Q

If given a toxic substance, would you want it to be polar or non-polar?

A

You would want it to be POLAR SO CAN EXCRETE IN URINE/POOP

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46
Q

Liver transformation is…

A

give dursg that are non-polar –> liver –> cyp450 –> polarized drug –> can excrete

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47
Q

If interaction to CYP450…have to do what to dosing?

A

Interaction with CYP450 –> decreased ability –> decrease dosing

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48
Q

WOA and WOB are both:

A

secreted AND reabsorbed

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49
Q

WOA and WOB we WANT to keep

A

monocarboxylic acids: pyruvate, ketone bodies, lactate

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50
Q

Keep WOA and WOB by…

A

adding carboxylate to them –> kidney recognizes carboxylic group –> allows to attach to transporter –> gets into cell –> pumped out

***this pump can become saturated, HAS A TM

51
Q

OAT and OCT

A

organic anion transporter
organic cation transporter
*DEPENENT ON BOUND TO ALBUMIN

active transport

52
Q

WOA and WOB transport into lumen…

A

facilitated diffusion

53
Q

WOA and WOB into cell from blood…

A

active transport (OAT and OCT)

54
Q

WOA and WOB (as MCA’s) into cell…

A

Na+/MCAs symporter

55
Q

MCA’s back into capillary…

A

MCA transporter

56
Q

orthostatic hypotension is a sign of ________

A

volume depletion

57
Q

Key functions of Loop of Henle

A
  1. reabsorbs 25% of filtered sodium
    (add to 66% Na reabsorbed in PT)
  2. Na is reabsorbed IN EXCESS of water = JUST THE SOLUTE = INCREASES [H20]
    –> allows for the excretion of urine with osmolality that is DIFFERENT than plasma
58
Q

Parts of nephron NOT permeable to H20

A

Thin and thick ascending limbs of Loop of Henle, distal tubule

NO AQUAPORINS

59
Q

PT mOsms
deep medullary space mOsms
end of thick ascending limb mOsms

A 
PT: 300 mOsms
Deep medullary space: 1400 mOsms
(huge draw for H20 out of the tubule)
(bottom of loop)
End of thick ascending loop: 100 mOsms
(ascending not permable to H20, but Na+/K+/CL- pump)
(top of loop)
60
Q

Thick ascending limb

A

channels set up nice gradient

- Na/K/2Cl carrier!

61
Q

Important functions of Na/K/2Cl carrier:

A
  1. reabsorbs 20% of filtered Na!
    (add to 66% from PT, 25 from loop of henle!)
  2. all sites MUST be occupied
  3. Na+ reabsorption is NOT linked to organic solutes (glucose, phosphorous)
  4. affinity for Na+ and K+ is VERY HIGH –> Cl- is RATE LIMITING
62
Q

Na/K/2Cl blocker

A

Lasix (furosemide)

63
Q

Lasix indicated for

A

CHF
NaCl retensive patients

-give along with low Na+ diet so can affect this 25% reabsorption and make a difference

64
Q

Na/K/2Cl transporter mutation

A

Bartter syndrome

  • 25% more Na, K, and 2Cl are hitting urine than should
  • genetic mutation
65
Q

Bartter syndrome

A
  • 25% more Na, K, and 2Cl are hitting urine than should
  • genetic mutation
  • present EARLY IN LIFE
  • growth retardation
  • mental retardation
  • VOLUME DEPLETION with LOW BP
  • HYPOkalemia
  • METABOLIC ALKALOSIS
  • normal or elevated urinary calcium excretion
66
Q

Why get elevated urinary calcium excretion in Bartter syndrome?

A

paracellular Ca2+ transport can only work in Na/K/2Cl pump works

67
Q

Distal tubule key features

A
  1. reabsorbes about 5% of filtered sodium
    (add to 66% in PT, 25 in loop of henle, 20% in ascending limb!) by NA-CL PUMP
  2. tubular reabosroption of Na+ varies with Na+ delivery (limited if don’t have enough Na+)
  3. iMPERMEABLE TO WATER so contributes to URINARY DILUTION
  4. contribues to calcium reabsorption
68
Q

NaCl transporter mutation

A

Gitleman syndrome

*better than mutation in Na/K/2Cl transporter because this one only takes care of 5% more Na+ reabsorption

69
Q

Gitleman syndrome

A
  • genetic mutation in NaCl transporter
  • normal BP
  • METABOLIC ALKALOSIS
  • HYPOcalciuria
  • HYPOmagnesemia
  • HYPOkalemia
70
Q

Na/Cl transporter blocker

A

hydrocholorothiazide

*will improve HTN but not to same degree as Lasix

71
Q

Can manipulate kidney Na+ reabsorption for HTN tx because

A

Na+ = BV = BP

PIVOTAL

72
Q

The collecting duct key features:

A
  1. variable sodium reabsorption
    * **FIRST AREA that is DIRECTLY CONTROLLED to DETERMINE URINARY ELECTROLYTE CONCENTRATION
  2. principal cell: BIG KAHUNA BURGER
  3. intecalated cell
73
Q

primary role principal cell

A

BIG KAHUNA BURGER

  • contributes to Na, Cl, and K reabsorption/excretion
  • ENaC (epithelial Na+ channel)
  • RMPK (renal outer medullary K+ channel)
74
Q

primary role intercalated cell

A
  • H+, HCO3-, and K+ reabsorption/excretion
75
Q

Of filtered load of Na+, ____% is controlled

A

5%

76
Q

If reabsorb 4.9% of controlled amount filtered load of Na+, excrete:

A

excrete 0.1% of filtered load = 1g Na+ (25mM)

77
Q

If reabsorb 0% of controlled amount filtered load of Na+, excrete:

A

excrete 5% of filtered load = 50g Na+ (1250mM)

78
Q

Primary mechanism of controlling salt reabsoption (that 5%) (and K+ secretion) in principal cells is via…

A

the hormone ALDOSTERONE

79
Q

Primary regulator of this secretion of aldosterone is…

A

angiotensin I and ultimately, angiotensin II

80
Q

RAAS SYSTEM

A

RENIN –> ANGIOTENSIN I –> ANGIOTENSIN II –> ALDOSTERONE

and ADH

81
Q

3 primary physiologic signaling pathways that stimulate renin release:

A
  1. SNS (NE)
  2. decreased stretch in afferent arteriole
  3. decreased Cl- delivery to macula densa
82
Q

Renin release stimulated by these clinical manifestations:

A
  1. hypovolemia
  2. low Na diet
  3. low body NaCl
  4. anything that causes high SNS
83
Q

Primary actions of angiotensin II

A
  1. ULTIMATELY stimulates ALDOSTERONE
  2. systemic vasconstricotr
  3. stimulates PT reabsorption of Na+
  4. increases SNS
84
Q

Aldosterone and principal cell key points:

A
  1. aldosterone stimulated by angiotensin II
  2. lipophilic so FREELY crosses cell membrane
  3. binds to intracellular Rec –> ultimately INCREASES TX OF CELLULAR PROTEINS
  4. proteins INCREASE ACTIVITY or NUMBER of both the luminal Na+channel ENAC and Kchannel ROMK and basolateral Na/K/ATPase

*renin responding to low Na+ state –> aldosterone –> more doorways –> reabsorbs as much Na+ as possible

85
Q

aldosterone causes

A
  • increased Na- reabsoprtion

- K secretion

86
Q

aldosterone stimulus for release

A
  • low Na+ states

- high K+ states

87
Q

K+ sparing diuretics:

A
  1. amiloride

2. triamterene

88
Q

disease of upregulation of ENaC

A

Little’s syndrome

  • ENaC always on –> ramp up insertion when stimulated by aldo –> reabsorbing Na+ soo much –> no response to aldo any longer
  • present: Na+ sensitive HTN
89
Q

FENa

A

excreted / filtered x 100

90
Q

clearance

A

excretion rate / plasma concentration

91
Q

Cr cl in ____ Na+

A

high Na+

= trying to clear

92
Q

NaCl = ____

A

volume

water follows

93
Q

GFR (creatinine clearance) varies with salt intake:

A

high salt –> increased filtered load of Na+ –> increased Na+ excretion

94
Q

aldosterone is stimulated by ___ salt stores

A

low salt stores

high salt –> reduced aldo –> fewer ENaC channels to reabsorb Na+ –> Na+ excretion increases

95
Q

PT, Na+/H+ antiporter is regulated by RAAS:

A

high salt –> reduced renin –> reduced Na+ reabsorption –> Na+ excretion increases

96
Q

Two primary functions of K+

A
  1. cell metabolism (protein and glycogen synthesis)
  2. (ratio of intracellular/extracellar potassium) PRIMARY DETERMINANT OF RMP (ie the necessary state for generation of APs)
97
Q

___% of K+ is stored intracellularly

A

98%

98
Q

key regulators of immediate/short term extracellular K+

A
  1. insulin (activate Na/K ATPase, promotes SKmus uptake)

2. catecholamines (beta-2 receptors stimulate Na/K ATPase)

99
Q

cell and channels that facilitate renal excretion of K+

A 
PRINCIPAL CELL 
Na/K ATPase pump
ROMK channels (K+)
ENaC channel (Na+)
BK channel (K+)
100
Q

location of K+ reabsorption and contribution of each tubular segment

A

PT: 55-67% via tight junctions
thick ascending limb/loop of henle: 25%
principal cell in distal tubule: 10%
alpha-intercalated cell in collecting: 10% (actively reabsorbed)

101
Q

location of Ca++ reabsorption and contribution of each tubular segment

A

PT: 65% paracellular across tight junctions
thick ascending limb/loop of henle: 20-25% paracellular
distal tubule: 10% transcellular

102
Q

actions of hormones that stimulate K and Ca secretion

A

ALDOSTERONE

  1. increases activity of Na/K ATPase pump
  2. increases presence of ROMK channel
  3. occurs in normal or mildly elevated K+ (directly)

PTH

  1. directly release Ca++ from bones
  2. increase from kidneys
  3. activates increased absorption of Ca++ in gut

***increased angiotensin II activates increase in aldo

103
Q

clinical stimuli of hormones that stimulate K and Ca

A

HIGH K+ STATES/DIET: aldo secreted, also BK channels open (two channels facilitating excretion of K)

LOW K+ DIETS: limited stimulation of aldo, no activity of BK channel, limited/decreased presence ROMK

104
Q

actions of PTH on bone

A

a. DIRECTLY stimulates immediate release of stored skeletal Ca++ ==> increase serum [Ca++]
b. stimulates bone reabsorption (preserve trabecular bone at expense of cortical bone)
* this DIRECTLY releases PO4- as well as Ca++

105
Q

actions of PTH on kidney

A

a. increased production of ACTIVATED VIT D
* this increases gut reabsorption of Ca++
b. increases Ca++ reabsoprtion
c. DECREASES renal PO4- absorption (INCREASES EXCRETION/SECRETION PO4-) –> activates make more vit D

106
Q

actions of PTH on intestines

A

a. increased activated VIT D from kidney –> ULTIMATELY increases gut reabsorption of Ca++

107
Q

cellular mech of Ca++ reabsorption

A
  1. activated PTH
  2. stimulates more Ca channels to open (from lumen)
  3. Ca++ NEEDS TO BIND TO CALBINDIN
  4. Ca++ through calcium ATPASE
108
Q

difference between ROMK and BK channels

A

ROMK: ALDO increases presence RMOK
*inhibited by Mg++
BK: always there, not usually open
**ONLY OPEN WHEN HAVE LOTS K+ THAT NEEDS TO GET OUT (high K+ states = diets)

109
Q

clinical situation when ROMK channels present

A

volume depleted

–> ang II –> aldo –> ROMK –> K out to lumen

110
Q

clinical situation when BK channels present

A

d

***BK channels NOT present: low K+ diets

111
Q

clinical presentations/dz when all intracell K suddenly released

A
  • digitalis OD
  • rhabdomyalisis (breaks down SK muscle, which holds K+_ –> release K
  • crushed SK muscle
  • femoral clot –> opened –> K+ flooded = REPERFUSION = hyperkalemia –> renal failure
112
Q

control K by:

A
  1. distributing between spaces (hiding it)

2. control excretion

113
Q

factors that regulate the Na/K ATPase pump

A
  1. insulin (eat –> increase insulin –> activate pump –> increase K in)
  2. catecholamines
  3. plasma K
  4. exercise –> sudden increase K released from myocytes
  5. cell breakdown
  6. chronic diseases
114
Q

other factors that regulate K in short term

A
  1. plasma concentration: cellular uptake increased when serum K is up
  2. exercise: myocytes release K during exercise
  3. pH: increase in systemic H+ (metabolic acidosis) –> H+ into cells –> K+ out –> hyperkalemia
115
Q

sequelae of active reabsorption of K+ in alpha intercalated cell

A
  • K+ is exchanged for H+ ====> free floating H+ in lumen = ACIDIC PEE
  • lots of H+ must be processed reabsorb K+
  • also requires the reabsorption of bicarb!

= hard work to reclaim K+, has a price (acidic urine, increased HCO3-)

116
Q

___% of all Ca++ bound to _____

A

40% of all Ca++ is bound to ALBUMIN

117
Q

___% of Ca++ is bound to other stuff

A

10% (like phosphate, citrate)

118
Q

___% of Ca++ is available as ionized Ca++ (free calcium) (unbound)

A

50%

  • this is the amount Ca++ (free calcium) body is trying to manage
  • PTH responds to free calcium, not total body calcium
119
Q

You eat _ mM calcium a day, but only absorb ___ mM

A

eat 20mM a day, only absorb 4mM

120
Q

risk factors for calcium oxalate stone formation

A
  • high salt diet
  • maybe calcium supplements
  • reducing dietary calcium can increase stone formation…
121
Q

reduced iCa++ stimulates production of…

A

PTH

122
Q

primary hyperparathyroidism

A 
increase in PTH = ROUGE PTH always on
(separate from sensing Ca++)
- trashes bone --> increase Ca++ release
- increased PO4- excretion --> decreased [PO4-]
- increased gut absorption
- increased vit D
- serum [Ca++] high
123
Q

other reasons have increased Ca++, decreased PO4-, but normal/unchanged PTH

A
  • cancer (mimics PTH)

- granulomatous disease (converts + vit D –> so much calcium with elevated vit D) (eg sarcoidosis)

Hailey - CRRAB II (6 decks)

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