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Renal Physiology Flashcards

1
Q

Positive Balance

A

input > output

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2
Q

Negative Balance

A

input < output

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3
Q

Functional unit of kidney

A

nephron

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4
Q

2 parts of nephron

A

Glomerulus + Tubule

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5
Q

3 filtration layers of glomerulus

A

Endothelial cells (fenestrated)
Basement membrane (protein mesh)
Podocytes (filtration slits w/ foot processes)

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6
Q

5 segments of nephron (in order)

A

Proximal Tubule
Loop of Henle
Distal Tubule
Collecting Tubule
Collecting Duct

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7
Q

Afferent Arteriole –>

A

Glomerular Capillaries

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8
Q

Efferent Arteriole –>

A

Peri-tubular capillaries

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9
Q

Glomerulus function

A

filtration
drives fluid into Bowman’s Capsule

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10
Q

Glomerulus has a high (negative/positive) charge to repel ______ from being filtered.

A

negative
proteins

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11
Q

Primary site of reabsorption

A

proximal tubule

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12
Q

Proximal Tubule functions

A

reabsorption + secretion

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13
Q

Parts of Loop of Henle + Functions

A

Thin Descending: water reabsorption
Thick Ascending: solute reabsorption

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14
Q

Function of Distal/Collecting Tubule

A

regulate reabsorption/secretion

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15
Q

What is juxtaglomerular apparatus?

A

part of distal tubule that communicates with glomerulus to regulate blood flow / filtration

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16
Q

Macula Densa function

A

sense change in Na+ filtration –> contact JG cells

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17
Q

Juxtaglomerular cells

A

vascular smooth muscle cells that release Renin (stimulated by macula densa)

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18
Q

Renin function

A

increases arterial pressure for more filtration into Bowman’s Capsule

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19
Q

4 Components of Nephron Function

A

glomerular filtration
tubular reabsorption
tubular secretion
urine excretion

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20
Q

3 primary functions of glomerular filtration

A
  • maintain normal body fluid comp
  • rapid excretion waste
  • huge mag of blood filtration (60x per day)
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21
Q

What two factors influence rate of filtration

A

physical properties
pressure differences

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22
Q

What is the main physiological regulator of filtration?

A

Capillary Hydrostatic Pressure

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23
Q

Force that drive fluid from glomerular capillaries –> capsule

A

capillary hydrostatic pressure

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24
Q

2 Forces that are driving fluid from capsule –> glomerular capillaries

A

capsule hydrostatic pressure
capillary osmotic pressure (plasma proteins)

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25
Q

Definition of GFR (glomerular filtration rate)

A

volume plasma filtered per unit time

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26
Q

GFR equation

A

GFR = Kf x NFP

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27
Q

What two factors determine GFR?

A

Kf (filtration coefficient)
NFP (net filtration pressure)

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28
Q

What determines Kf (filtration coefficient)?

A

permeability + surface area

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29
Q

What determines NFP (net filtration pressure)?

A

pressure differences between capillaries + capsule

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30
Q

Glomerular capillaries have a (higher/lower) permeability, surface area, and pressure differences than systemic capillaries.

A

higher

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31
Q

Resistance in glomerular capillaries is (greater/less) than systemic capillaries.

A

greater

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32
Q

Physiologically, if the afferent arteriole constricts, that will (increase/decrease) GFR.

A

decrease

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33
Q

Physiologically, if the efferent arteriole constricts, that will (increase/decrease) GFR.

A

increase

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34
Q

What 4 diseased states alter GFR?

A

hemorrhage
heart failure/hypovolemic shock
diabetes mellitus
urinary obstruction

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35
Q

How does the body alter GFR during hemorrhage?

A

constricts afferent + efferent arteriole = reduce GFR & retain blood volume

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36
Q

How does the body alter GFR during Heart failure?

A

decreased CO –> decreased renal blood flow/pressure –> decreased GFR

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37
Q

How is GFR altered during Diabetes Mellitus?

A

BM thickens –> lose permeability (Kf down) = decreased GFR

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38
Q

How is GFR altered during urinary obstruction?

A

increased urinary pressure –> increased hydrostatic pressure = decrease GFR

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39
Q

Function of Reabsorption

A

move water/solute from tubule –> peritubular capillaries

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40
Q

Function of Secretion

A

move substances from peritubular capillaries –> tubule

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41
Q

Paracellular pathway

A

movement through tight junctions between cells

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42
Q

Transcellular pathway

A

movement through cells (luminal/apical –> basolateral)

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43
Q

Simple Diffusion

A

across electrical/chemical gradient

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44
Q

Facilitated Diffusion

A

across gradient + transport protein

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45
Q

Primary Active Transport

A

uses ATP directly (against gradient)

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46
Q

Secondary Active Transport

A

downhill movement of one solute drive uphill movement of another

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47
Q

Simple Diffusion example

A

chloride

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48
Q

Facilitated Diffusion example

A

urea

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49
Q

Primary Active Transport example

A

Na/K ATPase

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50
Q

Secondary Active Transport example

A

Na+/glucose tranporter

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51
Q

Secondary Active Transport example

A

Na+/glucose transporter

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52
Q

Speed of movement of carrier-mediated transport controlled by (3):

A

specificity (how specific carrier is to substance)
competition (between substrates)
saturation (how bound transporters are)

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53
Q

Transport Maximum (Tm)

A

maximum amount of solute in system where all transporters are bound
(“maxed out”)

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54
Q

Afferent arterioles constricting causes (increase/decrease) renal blood flow & (increase/decrease) GFR.

A

decrease flow
decrease GFR

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55
Q

Efferent arterioles constricting causes (increase/decrease) renal blood flow & (increase/decrease) GFR.

A

decrease flow
increase GFR

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56
Q

Afferent + Efferent arterioles constrict (during hemorrhage) causes:

A

decrease in renal blood flow + decrease GFR = conserve blood volume

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57
Q

Pressure in the glomerular capillaries is (higher/lower) than systemic capillaries to allow for _____.

A

higher
filtration

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58
Q

Pressure in the peritubular capillaries is (higher/lower) than systemic capillaries to allow for _____.

A

lower
reabsorption

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59
Q

(Autoregulation/Tubuloglomerular Feedback) is at the level of the individual nephron, while (autoregulation/tubuloglomerular feedback) effects vascular supply to all nephrons.

A

tubuloglomerular feedback
autoregulation

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60
Q

What is renal autoregulation?

A

global regulation of blood flow
affects vascular supply to all nephrons
responds to changes in arterial pressure

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61
Q

What is the mechanism of renal autoregulation?

A

increase in pressure –> afferent arteriole constricts = decreased GFR + renal blood flow

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62
Q

What is the mechanism for tubuloglomerular feedback?

A

decrease pressure –> increase GFR (back to normal)
^release Renin + Angiotensin II locally which constricts efferent arteriole

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63
Q

3 factors cause Renin secretion

A

-decreased tubular Na+
-changes in arteriolar pressure
-SNS

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64
Q

NE release stimulates B-adrenergic receptors on JG cells which releases ______ via (indirect/direct) mechanism of controlling GFR/blood flow.

A

Renin
direct

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65
Q

NE release stimulates ______ on tubular cells to increase _____ reabsorption in the proximal tubule. This is a (direct/indirect) mechanism in controlling renal blood flow/GFR.

A

Na/K ATPase
Na+
indirect

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66
Q

Another way SNS controls renal blood flow/GFR: SNS innervates afferent + efferent arterioles. NE release stimulates ___ receptors which constricts arterioles and (increases/decreases) blood flow/GFR.

A

a-adrenergic
decreases

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67
Q

What 3 things does Angiotensin-II stimulate?

A
  • vasoconstriction
  • aldosterone production
  • ADH production
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68
Q

What do ADH + Aldosterone do?

A

help maintain blood volume (by increasing reabsorption of Na+ & H2O)

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69
Q

Sodium reabsorption transport mechanism

A

primary active transport

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70
Q

Chloride reabsorption transport mechanism

A

passive + active transport

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71
Q

H2O reabsorption transport mechanism

A

passive transport

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72
Q

___ + ___ reabsorption is coupled to ___. reabsorption.

A

Chloride + H2O
Sodium

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73
Q

Where is sodium reabsorbed in the tubule?

A

proximal tubule (majority)
ascending loop (1/4)
distal/collecting tubule (regulation)

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74
Q

Na+/K+ ATPase is on the (apical/basolateral) membrane.

A

basolateral

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75
Q

Order of reabsorption (by location)

A

tubular lumen –> tubular cells –> interstitial fluid –> peritubular capillaries

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76
Q

Movement of solutes from the ISF –> peritubular capillaries is primarily by:

A

passive / bulk flow

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77
Q

Na+ transport on apical membrane - proximal tubule (3 types)

A

Co-transport w/ organic substances
Counter-transport w/ H+ ions
Paracellular diffusion (passive)

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78
Q

What 2 specific transporters are used to transport Na+ across apical membrane by co-transport w/ organic substances?

A

Na+/glucose transporter (2nd active)
Na+/amino acid transporter (2nd active)

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79
Q

What specific transporter does Na+ use as counter-transport w/ H+ ions in the proximal tubule?

A

Na+/H+ exchanger (2nd active)

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80
Q

What 3 types of transport does Na+ use in Loop of Henle?

A

Co-transport w/ K+ & Cl- ions
Counter-transport w/ H+ ions
Paracellular diffusion (passive)

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81
Q

What specific transporter does Na+ use (co-transport w/ K+ & Cl- ions) in Loop of Henle?

A

NKCC (Na/K/Cl co-transporter)

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82
Q

What counter-transport does Na+ use in the Loop of Henle?

A

Na+/H+ exchanger

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83
Q

What two modes of transport does Na+ use in the Distal/Collecting Tubule?

A

Co-transport w/ Cl- ions
Na+ specific ion channels

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84
Q

What specific co-transporter w/ Cl- ions does Na+ use for transport in distal/collecting tubule?

A

NCC (Na, Cl co-transporter)

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85
Q

What specific transporter does Na+ use in the distal/collecting tubule that is a Na+ specific ion channel?

A

ENAC (epithelial sodium channel)

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86
Q

3 inhibitors that are drugs used to target sodium transporters

A

SGLT inhibitors (Na/glu transporter)
NHE inhibitors (Na/H+ exchanger)
NKCC inhibitors (Na/K/Cl co-transporter)

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87
Q

What disease does SGLT inhibitors treat?

A

diabetes / hyperglycemia

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88
Q

How do SGLT inhibitors treat diabetes/hyperglycemia?

A

allow to excrete more glucose

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89
Q

What disease do NHE inhibitors treat?

A

hypertension

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90
Q

How do NHE inhibitors treat hypertension?

A

vasodilate vasculature & protect kidney

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91
Q

What drug is an NKCC inhibitor?

A

Furosemide (a diuretic)

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92
Q

How does NKCC inhibitor (furosemide) work?

A

blocks reabsorption of Na+ which blocks reabsorption of water –> excrete more

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93
Q

Two diuretics that work further down in the tubule (less effective potentially)

A

NCC inhibitors
ENAC inhibitors

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94
Q

How is Cl- reabsorbed in the proximal tubule?

A

passive, paracellular flow
Na+ reabsorption causes negative charge in lumen –> Cl- wants to leave!

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95
Q

How is Cl- reabsorbed in the Loop of Henle?

A

Co-transported (NKCC) - secondary active

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96
Q

How is Cl- reabsorbed in the distal tubule?

A

co-transported with Na+
NCC (secondary active)

97
Q

Which part of the tubule has low permeability to H2O? (no water is reabsorbed)

A

ascending loop of henle

98
Q

Which two parts of the tubule does water permeability vary?

A

cortical part of distal tubule
collecting tubule/duct

99
Q

What two ways is water reabsorbed across the tubular epithelium?

A

simple diffusion (paracellular)
facilitated diffusion (transcellular w/ aquaporins!!!)

100
Q

What are aquaporins?

A

water-selective channels
allow for rapid movement of water from tubule –> ISF

101
Q

Aquaporins are present on the (apical/basolateral) membrane.

A

TRICK QUESTION! Both!

102
Q

How does water move from the tubule to ISF?

A

Na+ reabsorption causes concentration gradient in (more in ISF) so water moves from tubule –> ISF (via aquaporins + simple diffusion)

103
Q

What is the primary driver of H2O from ISF –> peritubular capillaries?

A

capillary osmotic pressure (more proteins so sucks water in)

104
Q

Match osmolality of fluid to location in tubule: proximal tubule | bottom loop of henle | distal/collecting tubule

A

Proximal Tubule: isosmotic (1:1 H2O/solute moving)

Loop: hyperosmotic (concentrated - water has been reabsorbed)

Distal/Collecting: hypoosmotic (dilute b/c solutes reabsorbed)

105
Q

Loop of Henle mechanisms of urine concentration/dilution by location (thin descending | thin ascending | thick ascending)

A

Thin descending: high water / low solute permeability
Thin ascending: just moving fluid
Thick ascending: low water / high solute permeability

106
Q

What is meant by Counter-Current Flow?

A

parts of Loop of Henle work in coordination

Na+ reabsorption (thick ascending) –> water reabsorption (thin descending) b/c concentration gradient

107
Q

At the end of the Loop of Henle, urine is (concentrated/dilute) and volume of water is (high/low).

108
Q

Where does ADH have its effect in the tubule?

A

distal tubule/collecting duct

109
Q

What does ADH do (antidiuretic hormone)?

A

increases water reabsorption in the distal/collecting tubule
stimulates aquaporins to move to apical membrane

110
Q

Low ADH –> (high/low) water reabsorption –> (dilute/concentrated) and (lower/higher) volume urine.

A

low
dilute
higher

111
Q

High ADH –> (high/low) water reabsorption –> (dilute/concentrated) and (lower/higher) volume urine.

A

high
concentrated
lower

112
Q

What is Na+ balance regulated by? (2)

A

GFR
amount Na+ reabsorbed

113
Q

What are 2 challenges to Na+ homeostasis?

A

changes in GFR
changes in Na+ intake

114
Q

3 ways kidney compensates for changes in GFR

A
  1. autoregulation (whole kidney)
  2. tubuloglomerular feedback (local)
  3. glomerulotubular balance
115
Q

Explain glomerulotubular balance

A

amount of Na+ filtered is matched with amount of Na+ reabsorbed (so reduces Na+ loss if filtration increases)

116
Q

Where does feedback of glomerulotubular balance occur?

A

proximal tubule

117
Q

What is aldosterone? What is it produced by?

A

mineralocorticoid (steroid)
produced by adrenal glands

118
Q

Where does aldosterone have its effect?

A

late distal tubule/collecting duct

119
Q

Function of aldosterone

A

increases Na+ reabsorption (and therefore K+ secretion)

120
Q

(T/F) Aldosterone controls whether or not all sodium in the body is secreted/absorbed.

A

False: only controls 2-3%
max aldosterone = NO Na+ excreted
min aldosterone = 2-3% filtered Na+ is excreted, rest reabsorbed

121
Q

Which two Na+ transport mechanisms does aldosterone increase synthesis of to increase reabsorption?

A

Na/K ATPase (basolateral)
ENAC (apical)

122
Q

4 factors that stimulate aldosterone secretion

A

decreased plasma Na+
increased K+
increase plasma ACTH
large increases in Angiotensin II (hemorrhage)

123
Q

How does aldosterone contribute to the response to hemorrhage?

A

increase Na+ reabsorption –>
increase H2O reabsorption = conserve blood volume

124
Q

What is ADH? What secretes it?

A

peptide hormone that increases water reabsorption in late distal tubule/collecting duct

secreted by pituitary

125
Q

What 3 things regulate ADH secretion?

A
  1. Baroreceptors
  2. Osmoreceptors
  3. Angiotensin II
126
Q

Baroreceptors sense changes in _____ and (activate/inhibit) ADH secretion.

A

blood volume
inhibit

127
Q

Osmoreceptors sense changes in ____ and (activate/inhibit) ADH secretion.

A

osmolality/concentration
stimulate

128
Q

High elevations in Angiotensin II (hemorrhage) can directly (stimulate/inhibit) ADH secretion.

129
Q

How does ADH increase water reabsorption in the late distal tubule/collecting duct?

A

ADH binds to receptor –> Gs signaling activates Protein Kinase A = aquaporins move to apical membrane

130
Q

Water diuresis (urine volume + concentration)

A

high volume urine
hypoosmotic (dilute)

131
Q

Osmotic diuresis (urine volume + concentration)

A

high volume urine
isosmotic (not dilute)

132
Q

Causes of water diuresis

A

increased water intake, drugs, disease/inury

133
Q

Causes of osmotic diuresis

A

disease, drugs (mannitol)

134
Q

(Diabetes Mellitus/Diabetes Inspidus) can cause water diuresis.

A

Diabetes Insipidus

135
Q

(Diabetes Mellitus/Diabetes Insipidus) can cause osmotic diuresis.

A

Diabetes Mellitus

136
Q

How does increased water intake cause water diuresis?

A

increased blood volume / decreased osmolarity –> decreased ADH = decreased water reabsorption

137
Q

What kind of drugs have a central effect on ADH?

A

glucocorticoids

138
Q

What kind of drugs have a nephrotoxic effect on the kidney (ADH not effective)?

A

antifungal agent (amphotericin B)

139
Q

Which drug blocks NKCC for clinical treatment?

A

furosemide

140
Q

Which drug blocks NCC for clinical treatment?

A

hydrochlorothiazide

141
Q

Which drug blocks ENAC channels and are K+ sparing?

142
Q

Which drug is an aldosterone antagonist and K+ sparing?

A

spironolactone

143
Q

What are the 2 types of diabetes insipidus?

A

Central
Nephrogenic

144
Q

In (central/nephrogenic) diabetes insipidus, ADH production is normal but not effective.

A

nephrogenic

145
Q

In (central/nephrogenic) diabetes insipidus, ADH secretion is reduced.

146
Q

Who does Diabetes Mellitus induce osmotic diuresis?

A

increased glucose –> increased urine osmolality = water retained in tubule

147
Q

How does mannitol induce osmotic diuresis?

A

shifts small amount of water in the wrong place (treat glaucoma, head injury)

148
Q

Clearance

A

amount of plasma cleared of a substance over time

149
Q

Excretion

A

amount of substance coming out in urine

150
Q

What substance does clearance = GFR?

A

inulin
no reabsorption, no secretion

151
Q

What substance is when clearance is LESS than GFR?

A

Na+
some reabsorbed, none secreted

152
Q

What substance is clearance = 0?

A

glucose
everything is reabsorbed

153
Q

What substance does clearance = renal blood flow?

A

PAH
not reabsorbed, is secreted so 100% is excreted

154
Q

What substance uses clearance to determine GFR? (and therefore kidney function)

155
Q

Not reabsorbed | Secreted =

A

clearance > GFR

156
Q

Not reabsorbed | Not secreted =

A

clearance = GFR

157
Q

Partially reabsorbed | Not secreted =

A

clearance < GFR

158
Q

Fully reabsorbed | Not secreted

A

clearance &laquo_space;GFR (clearance = 0)

159
Q

Name 2 exogenous substances that can used to measure GFR (and therefore renal function)?

A

Inulin
Iohexol

160
Q

Inulin

A

standard agent for GFR measurement
sugar in wheat, injected, takes a while for excretion
Needs electrochemical equipment

161
Q

Iohexol

A

iodinated contrast agent, fast clearance, nephrotoxic
cannot give repeatedly
uses CT scanning

162
Q

What two endogenous substances are used to measure GFR (and therefore kidney function)?

A

creatinine
SDMA

163
Q

Creatinine

A

easily measured, not injected
slightly overestimates GFR

164
Q

SDMA

A

amino acid, sensitive to early kidney dysfunction
Need IDEXX equipment

165
Q

____ & ____ are two essential nutrients that need to be (reabsorbed/secreted).

A

glucose
amino acids
reabsorbed

166
Q

Urea is (reabsorbed/secreted).

A

TRICK QUESTION: both!

167
Q

Glucose & Amino acids are completely reabsorbed in the ______ via _____ transport and coupled to _____ reabsorption.

A

proximal tubule
secondary active
Na+

168
Q

Explain why/how glucose + amino acids use secondary active transport for reabsorption.

A

downhill movement of Na+ is used to move them uphill against their concentration gradient
need Na+ reabsorption to move

169
Q

What are the 2 Na/glu transporters on the apical membrane of the proximal tubule? Which is majority?

A

SGLT1 & SGLT2 (majority)

170
Q

Match SGLTs with:
specificity (high/low)
competition (high/low)
efficiency (high/low)

A

high specificity (only bind glucose)
low competition (no substrate comp)
highly efficient (high Tm)

171
Q

Tm (</>) glucose filtered.

A

> (much greater, none excreted)

172
Q

Match Amino Acid Transporters with:
specificity (high/low)
competition (high/low)
efficiency (high/low)

A

low specificity (multiple AAs)
high competition (multi substrates comp)
low efficiency (less than glucose)

173
Q

Tm (</>) filtered amino acids.

A

> (greater but lower than glucose)

174
Q

What process is the small amount of protein filtered reabsorbed by?

A

endocytosis

175
Q

What type of transport does protein get reabsorbed through?

A

primary active transport

176
Q

What is urea?

A

nitrogen waste product made by protein metabolism

177
Q

The amount of urea excreted depends on (aldosterone/ADH/angiotensin).

178
Q

What type of transport does urea use for reabsorption?

A

passive transport (w/ urea transporters)

179
Q

Urea is coupled to _____.

A

water (and therefore sodium)

180
Q

What substance is recirculated to help increase hyperosmotic medulla for increased urine concentration/water conservation?

181
Q

ADH (increases/decreases) urea transporters –> (increased/decreased) reabsorption –> (increased/decreased) excretion.

A

increased
increased
decreased

182
Q

Increased urine flow –> (increased/decreased) urea concentration gradient –> (increased/decreased) reabsorption –> (increased/decreased) urea excretion.

A

decreased
decreased
increased

183
Q

Azotemia

A

increase in blood urea nitrogen (BUN) with or without increase in blood creatinine

184
Q

3 types of azotemia

A

pre-renal
renal
post-renal

185
Q

Explain pre-renal azotemia

A

decreased blood flow to kidneys (dehydration) –> increased BUN

186
Q

Explain renal azotemia

A

decreased functional nephrons –> increased BUN (from toxin)

187
Q

Explain post-renal azotemia

A

urinary blockage (urolithiasis) –> increased BUN

188
Q

Organic ions are (reabsorbed/secreted).

189
Q

Where are organic ions secreted?

A

proximal tubule

190
Q

What type of transport is used for organic ion secretion?

A

active transport

191
Q

Two types of organic ions

A

cations
anions

192
Q

List 2 types of cations (organic ion type)

A

neurotransmitters
histamine

193
Q

Match to organic ion transporter properties:
specificity (high/low)
competition (high/low)
efficiency (high/low)

A

low specificity
high competition
inefficient (low Tm - easily excreted)

194
Q

(T/F) The ratio of K+ filtration to reabsorption = 1:1

195
Q

What type of transport does K+ reabsorption use in the proximal tubule?

A

passive/paracellular transport

196
Q

What type of transport does K+ reabsorption use in the Loop of Henle?

A

secondary active transport
(via NKCC using energy from Na/K ATPase)

197
Q

What kind of transport does K+ reabsorption use in the distal/collecting tubule?

A

primary active transport
(via H+/K+ ATPase)

198
Q

Where is K+ reabsorbed?

A

proximal tubule (most)
thick ascending loop (some)
distal/collecting tubule (little)

199
Q

Where is K+ secreted?

A

ONLY in distal tubule / collecting duct

200
Q

How is K+ secreted?

A

K+ specific channels (ROMK) on apical membrane

201
Q

Where is K+ balance primarily regulated?

A

distal tubule/collecting duct

202
Q

What 4 factors influence K+ secretion?

A
  1. Na/K ATPase activity
  2. Concentration gradient
  3. Electrical gradient
  4. Permeability of apical membrane to K+
203
Q

How does Na/K ATPase activity influence K+ secretion?

A

up ATPase activity = up K+ secretion

204
Q

How does electrical gradient influence K+ secretion?

A

more Na+ reabsorbed = increased K+ secretion

205
Q

How does concentration gradient influence K+ secretion?

A

more K+ gradient = increased K+ secretion

206
Q

How does permeability of apical membrane influence K+ secretion?

A

more K+ channels (ROMK) = increased K+ secretion

207
Q

(T/F) K+ reabsorption increases when K+ intake decreases.

A

False
reabsorption rate constant & not influenced by changes in K+ intake

208
Q

What is the only way to change K+ excretion?

A

regulation of K+ secretion in the distal/collecting tubule

209
Q

How does K+ secretion increase in the distal/collecting tubule directly?

A

stimulates Na+/K+ ATPase on basolateral membrane

210
Q

How does K+ secretion increase in the distal/collecting tubule indirectly?

A

stimulates aldosterone release –> K+ secretion, Na+ reabsorption

211
Q

What substance is the primary controller of K+ secretion (and therefore K+ excretion)?

A

aldosterone

212
Q

What are the effects of increased plasma K concentration on aldosterone

A

increased aldosterone secretion

213
Q

2 mechanisms by which aldosterone increases K+ secretion in response to K+ intake

A

increase synthesis of Na/K on ATPase (basolateral)
increase ROMK expression (apical)

214
Q

4 ways the two above mechs increase K+ secretion by aldosterone

A
  1. increase Na/K ATPase activity
  2. Increase concentration gradient
  3. increase electrical gradient
  4. increase apical permeability
215
Q

Without aldosterone, there would be a huge (increase/decrease) in K+.

216
Q

Aldosterone secretion = increased __ reabsorption and increased __ secretion.

217
Q

If Na+ load increases, what happens to K+?

A

increased K+ secretion/excretion

218
Q

What two ways goes Na+ handling impact K+ excretion?

A

increased Na+ load
increased Na+ flow

219
Q

If Na+ flow increases, what happens to K+?

A

if less Na+ reabsorbed, less H2O is reabsorbed = K+ concentration diluted in distal/collecting tubule = increased K+ secretion

220
Q

What do diuretic drugs do to Na+? K+?

A

Na: increase load + flow
K: increase secretion, decrease reabsorption

221
Q

Which drug inhibits NKCC (in loop of henle)

A

Furosemide

222
Q

Which drug inhibits NCC (early distal tubule)?

223
Q

Two causes of diuresis

A

disease (diabetes mellitus)
diuretic drugs

224
Q

How does alkalosis influence K+ secretion?

A

increases secretion (body tries to retain K+ to keep positive charge but increases K+ gradient)

225
Q

What important renal enzyme stops functioning outside of physiological pH levels?

A

Na/K ATPase

226
Q

3 examples of intracellular fluid buffers in blood

A

hemoglobin (primary)
organic phosphates
proteins

227
Q

3 examples of extracellular fluid buffers in blood

A

bicarbonate (primary)
phosphate
proteins

228
Q

How do the lungs control the HCO3-CO2 buffer system?

A

PCO2
increase resp in acidosis to decrease CO2
decrease resp in alkalosis to increase CO2

229
Q

What do the kidneys do to control HCO3-CO2 buffer system?

A

increase HCO3 in acidosis
decrease HCO3 in alkalosis

230
Q

What 2 mechanisms does the kidney use to increase HCO3- when the body is in acidosis?

A
  1. increase reabsorption of HCO3
  2. add “new” HCO3 in
231
Q

Increase HCO3 = (increase/decrease) pH

232
Q

Increase PCO2 = (increase/decrease) pH

233
Q

Metabolic/kidney compensation during acid-base disorders is (fast/slow) while Respiratory/lung compensation is (fast/slow)

234
Q

Where are the majority of H+ ions secreted?

A

proximal tubule

235
Q

What transport process + transporter are used for H+ transport across the apical membrane?

A

Na/H+ exchanger (secondary active)

236
Q

HCO3 reabsorption is coupled to H+ secretion (directly/indirectly)

A

indirectly
do not reabsorb the same HCO3- ion that was filtered

237
Q

Explain excretion of titratable acid

A

H+ is excreted as an acid (by combining = urine is acidified

238
Q

Explain excretion of ammonia

A

H+ combines with ammonia (NH3) + chloride = excreted as a salt

Physiology (6 decks)

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