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Physiology > Renal 5 > Flashcards

Renal 5 Flashcards

1
Q

Regulation of Tubular
Reabsorption
Essential to maintain a precise balance between

A

GFR and tubular reabsorption.

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2
Q

Tubular reabsorption controlled by (3)

A

Local Control
Mechanisms, Nervous System, and Endocrine
System

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3
Q

Reabsorption of some solutes can be individually

—.

A

adjusted

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4
Q

Local Control Mechanisms (3)

A

Tubuloglomerular Feedback Response (TGF)
Glomerulotubular Balance (GTB)
Arterial Pressure (pressure natriuresis/diuresis)

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5
Q

Systemic Control Mechanisms (2)

A

Hormones

Sympathetic Nervous System

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6
Q

Hormones (5)

A
  • aldosterone
  • angiotensin II
  • antidiuretic hormone (ADH)
  • atrial natriuetic peptide (ANP or ANF)
    ₋ parathyroid hormone
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7
Q

TGF Response: Autoregulation of GFR. (3)

A

Keeps GFR constant
Afferent and Efferent arteriolar resistance related to flow rate of NaCl by macula
densa
Example: GFR increase-increased NaCl to macula densa- TGF response decreases
GFR

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8
Q

Glomerular Tubule Balance (GTB): Autoregulation

of PT reabsorption rate (4)

A

PT reabsorption rate related to tubular load
As tubular LOAD increases, rate of
REABSORPTION increases.
Depends on changes in peritubular capillary and
renal interstitial fluid Starling’s forces.
Example: GFR increase-GT balance increases PT
Na+/H20 reabsorption to maintain Na+/H20
balance

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9
Q

Together these two mechanisms help to

A

prevent overloading of the distal tubule

segment when GFR increases due to pressure changes or other disturbances

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10
Q

Assures — may be maintained

A

Homeostasis

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11
Q

Small increases in MAP can cause marked increases in urinary (2)

A

Na+ and H2O excretion.

 Mechanisms not understood

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12
Q

Normal kidney function and pressure natriuresis mechanisms assure that

A

large changes in salt and water intake accommodated with only minor changes in ECF volume, CO, and MAP

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13
Q

Aldosterone: Cellular Mechanism

Stimulates

A

Na+ reabsorption and

K+ Secretion

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14
Q

Aldosterone: Cellular Mechanism

onest and duration

A

slow onset

long duration

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15
Q

Aldosterone: Cellular Mechanism

increases (2)

A

number and activity

activity

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16
Q

Control of Aldosterone Secretion

increase (2)

A

 Increased plasma K+

 Angiotensin II

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17
Q

Increase
 Increased plasma K+
 Angiotensin II
(changes associated with

A

Na+
and volume depletion or low
blood pressure)

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18
Q

Control of Aldosterone Secretion

Decrease (2)

A

 Atrial natriuretic peptide
(ANP/ANF)
 Increased Na+ concentration
(osmolarity; weak)

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19
Q 
Decrease
 Atrial natriuretic peptide 
(ANP/ANF)
 Increased Na+ concentration 
(osmolarity; weak)
(changes associated with
A

increased Na+ and volume or

high blood pressure)

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20
Q

Other Effects of Aldosterone (3)

A

Increases H+ secretion by intercalated cells of late distal & cortical
collecting tubule membrane: excess aldosterone levels may cause
metabolic alkalosis.
Increases Na+ reabsorption and K+ secretion by sweat and salivary
glands.
Increases Na+ absorption by intestinal (colon) mucosa.

21
Q

Angiotensin II:
Cellular Mechanism
major regulator of (2)

A

na and water reabsorption

22
Q

Angiotensin II:
Cellular Mechanism
occurs in most

A

nephron segments

23
Q

Angiotensin II:
Cellular Mechanism
stimulus (2)

A

decreased MAP

decreased ECFvol

24
Q 
Angiotensin II: 
Cellular Mechanism
effector responses (6)
A

 Stimulates aldosterone production.
 Directly increases Na+ reabsorption (proximal, loop, distal,
collecting tubules).
 Increases H+ secretion
 Constricts efferent arterioles and increases GFR
 Constricts systemic arterioles, increasing TPR and MAP
 Increases Aldosterone secretion from Zona Glomerulosa

25
Q

ADH: Cellular
Mechanisms
increases

A

water reabsorption

26
Q

ADH: Cellular
Mechanisms
location

A

late DT and CD

27
Q

ADH: Cellular
Mechanisms
Stimulus (2)

A

increased ECFosm

decreased MAP

28
Q

ADH: Mechanisms of Action (3)

A 
 Increases H2O permeability via 
activation of Gαs Protein linked 
receptor
 Activates cAMP
 Increases the synthesis and insertion 
of AQP-2 into luminal membrane.
29
Q

Atrial Natriuretic Peptide (ANP)
increase
decrease

A

increase GFR

decrease na reabsorption (increase na excretion)

30
Q

ANP

Stimulus

A

 Secreted by cardiac atria in
response to stretch (increased
blood volume).

31
Q

ANP: Effector Responses (4)

A 
Effector Responses
 Directly inhibits Na+ and H2O 
reabsorption in PT
 Increases GFR (dilates afferent, 
constricts efferent arterioles).
 Inhibits renin release and 
aldosterone formation.
 Helps to minimize blood volume 
expansion (CHF).
32
Q

hormone:
site of action:
effect:

A
33
Q

hormone:
site of action:
effect:

A
34
Q

hormone:
site of action:
effect:

A
35
Q

hormone:
site of action:
effect:

A
36
Q

SNS Decreases (2) Excretion

A

Na+ and H2O

37
Q

SNS Decreases Na+ and H2O Excretion: (4)

A 
 Constricts arterioles.
 Stimulates renin release.
 Decreases GFR and renal blood 
flow.
 Directly stimulates Na+ 
reabsorption via α receptors on 
tubule epithelial cells in PT and 
TAL.
38
Q

Total Ca++ amount in body

A

1100 g,  99% stored in bones

39
Q

Total Body Ca++ (3)

A
  • 0.1% ECF
  • 1% ICF/IC compartment
  • Majority in bone
40
Q

ECF — tightly regulated

A

Ca++

41
Q

Ca

Critical for: (6)

A 
⁻ Normal cell function
⁻ Neural transmission
⁻ Membrane excitability
⁻ Bone structure
⁻ Blood Coagulation
⁻ Intracellular signaling
42
Q

— Ca++ is form most

important for functions in body

A

ionized

43
Q

–% of Plasma

Ca++ Filtered

A

60

44
Q

–% of Filtered Ca++

Reabsorbed in PCT

A

65

45
Q

—%
Reabsorbed in
Loop of Henle

A

25-30

46
Q

—% Reabsorbed
in Distal and
Collecting Tubule

A

4-9

47
Q

–% Excreted

A

1

48
Q

PTH Regulates Ca++ Reabsorption in (2)

A

TAL and DT

49
Q

Luminal

Absorption (3)

A 
50% by para-
cellular bulk 
flow; passive
Favored by +8 mV 
luminal charge
50% transcellular; 
entry passive

Physiology (53 decks)

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