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Histology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

4 ways that solute moves across membranes

A

diffusion, facilitated diffusion, active transport, & secondary active transport

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2
Q

Describe simple diffusion

A

w/ conc gradient
passive
membrane must be permeable to solute
continues until equilibrium

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3
Q

What increases the rate of (simple & facilitated) diffusion

A

larger gradient & a more permeable membrane

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4
Q

Ex of simple diffusion

A

paracellular reabsorption of Cl- in late proximal tubule

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5
Q

What is the membrane permeable to

A

lipid soluble & sm polar molecules

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6
Q

What is the membrane impermeable to

A

charged & lg polar molecules

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7
Q

Describe facilitated diffusion

A 
w/ conc gradient
passive
membrane is not permeable to solute
utilizes transporters/ pores
continues until equilibrium
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8
Q

Ex of facilitated diffusion

A

Na+, K+, & Cl- transport via NKCC1 in macula densa to monitor glomerular filtration

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9
Q

Describe active transport

A 
against conc gradient
active
transporter moves solute across membrane
transporter itself hydrolyzes ATP
does not continue until equilibrium
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10
Q

Ex of active transport

A

movement of Na+ at basolateral membrane of proximal tubule by Na+K+ATPase
(occurs in other nephron sections)

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11
Q

Describe secondary active transport

A 
against conc gradient
active
transporter moves solute across membrane
uses potential energy generated by ATP-dependent processes elsewhere in the cell
does not continue until equilibrium
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12
Q

Ex of secondary active transport

A

movement of glucose & amino acids at the luminal membrane of the proximal tubule
both moved against conc gradient into the cell
energy from Na+ moving w/ conc gradient into the cell via the same transporter
Na+ gradient was established by Na+K+ATPase burnig ATP

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13
Q

1 way solvent moves across membrane

A

osmosis

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14
Q

Define osmosis

A

movement of water across a semi-permeable membrane from a dilute to a concentrated solution

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15
Q

For there to be osmosis, what has to happen

A

whatever solute creates the difference in water cannot move across the membrane

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16
Q

What does an ineffective osmole do

A

if membrane is soluble to solute, then
solute diffuses until its equillibrium is met
creates two solutions of equal water conc

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17
Q

What does an effective osmole do

A

if membrane is not soluble to solute, then
solute cannot diffuse across the membrane
creates a diffference in water conc to drive osmosis

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18
Q

What is molarity/molality used to define

A

conc of a solution (in terms of solute)

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19
Q

Molarity/molality is the driving force for what

A

solute

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20
Q

Molarity units

A

mol/L

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21
Q

Molality units

A

mol/kg

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22
Q

What is osmolarity/osmolality used to define

A

conc of a solution (in terms of solvent)

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23
Q

Osmolarity/osmality is the driving force for

A

water

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24
Q

Osmolarity units

A

conc of osmotically active solute/L

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25
Q

Omolality units

A

conc of osmotically active solute/kg

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26
Q

NaCl would equal how many osmoles & why

A

2 osmoles

b/c NaCl dissociates into two potentially osmotically active osmoles

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27
Q

Water moves in what direction in terms of osmolarity

A

from low to high osmolarity

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28
Q

Tonicity defines what

A

conc of effective osmoles in a solution

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29
Q

Can tonicity be expressed numerically

A

no, only comparitively

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30
Q

A hypertonic solution has what

A

higher effective osmolarity than another

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31
Q

A isotonic solution has what

A

equal effective osmolarity as another

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32
Q

A hypotonic solution has what

A

lower effective osmolarity than another

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33
Q

Location of kidneys

A

dorsal
slightly posterior in lumbar region
retroperitoneally located

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34
Q

Comparison of left vs right kidneys

A

righty high & tighty

lefty low & loosy

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35
Q

Kidney shape in cats, dogs, sheep, & goats

A

kidney bean

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36
Q

Kidney shape in pigs

A

squashed w/ poles stretched

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37
Q

Kidney shape in equine

A

larger & heart-shaped

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38
Q

Kidney shape in cattle

A

deeply fissured & scalloped; brain-shaped

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39
Q

Components of kidney capsule

A

collagen membrane w/ smooth muscle (elasticity)

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40
Q

Capsule is important for

A

structural integrity of kidney

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41
Q

Hilum is what

A

cleft where renal artery enters & renal vein/ureter leave

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42
Q

Describe cortex (in comparison to medulla)

A

darker staining
cells have more cytoplasm
more extensive vasculature

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43
Q

Describe medulla (in comparison to cortex)

A

lighter staining
more interstitial fluid
high osmolarity

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44
Q

Location of renal pyramid

A

base in outer cortex

apex in inner medulla

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45
Q

Renal pyramids fuse in some species to form

A

renal crest

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46
Q

Renal papilla is what

A

apex of renal pyramids

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47
Q

Renal pelvis functions as

A

funnel that collects urine

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48
Q

Color & location of renal pelvis

A

off-white

at center of kidney

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49
Q

Renal pelvis is an extension of what

A

ureter

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50
Q

Parts of nephron found in cortex

A 
renal corpuscle
proximal convoluted tubule
proximal straight tubule
(later) part of distal straight tubule
distal convoluted tubule
(earlier) part of collecting duct
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51
Q

Parts of nephron found in medulla

A

loop of henle

(earlier) part of distal straight tubule
(later) part of collecting duct

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52
Q

What is found in the cortical labyrinth of the cortex

A

renal corpuscle
proximal convuluted tubule
distal convoluted tubule

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53
Q

What is found in the medullary rays of the cortex

A

proximal straigh tubules
distal straight tubules
collecting ducts

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54
Q

What is found in the outer medulla

A

loops of henle
distal straight tubule
collecting ducts

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55
Q

What is found in the inner medulla

A

collecting ducts

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56
Q

Microscopic distal tubule

A

touches vascular part of glomerulus

includes macula densa

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57
Q

Microscopic afferent/efferent arteriole

A

cannot differentiate b/w them

smooth muscle at vascular pole of glomerulus

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58
Q

Microscopic glomerulus

A

bundle of capillaries

lumens of blood vessels & some RBCs

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59
Q

Intraglomerular mesangial cells function

A

support capillaries

contractile & phagocytic

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60
Q

Extraglomerular mesangial cells function

A

support capillaries

renin-angiotensin system

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61
Q

Microscope intraglomerular mesangial cells

A

found inside glomerulus

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62
Q

Microscope extraglomerular mesangial cells

A

found outside glomerulus

near vascular pole

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63
Q

Urinary space function

A

where filtrate emerges

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64
Q

Microscope urinary space

A

surrounds glomerulus

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65
Q

Microscope Bowman’s capsule

A

thin squamous epithelium surrounding glomerulus

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66
Q

Parietal layer of Bowman’s capsule

A

does not touch capillaries

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67
Q

Visceral layers of Bowman’s capsule

A

touches capillaries

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68
Q

Visceral layer of Bowman’s capsule is adapted into a layer of

A

podocytes

help w/ filtration

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69
Q

Urinary pole of renal corpuscle

A

where proximal tubule leaves

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70
Q

Vascular pole of renal corpuscle

A

where afferent arteriole enters & efferent arteriole leaves
close to distal tubule

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71
Q

Secondary processes of podocytes are called

A

pedicels

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72
Q

Pedicels do what structurally

A

wrap around capillaries

interdigitate w/ other phagocytes/ pedicels

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73
Q

Components of filtration apparatus

A

fenestrated capillary
basal lamina of visceral layer
slit diaphragm

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74
Q

Fenestrated capillary has what that acts as what

A

pores

filter/sieve

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75
Q

Basal lamina of visceral layer is secreted by

A

podocytes/pedicels

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76
Q

Lamina densa externa & interna are composed of what

A

laminin, fibronectin, & polyanions

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77
Q

Lamina densa rara is composed of what

A

collagen

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78
Q

Slit diaphragm is what & secreted by what

A

protein sheet full of holes

podocytes

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79
Q

Structure of proximal tubule

A

tall cuboidal epithelium
thick brush border of microvilli
caniculi

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80
Q

Proximal tubule has what features in the cytoplasm of the epithelial cells

A

many mitochondria

lysozymes

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81
Q

Lysozymes do what

A

break up what is absorbed

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82
Q

Shape & location of nuclei in proximal tubule

A

spherical

central & basolateral

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83
Q

Function of proximal tubule

A

active reabsorption

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84
Q

Does proximal or distal tubule have a larger diameter

A

proximal

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85
Q

Structure of loop of henle

A

simple squamous epithelium

few microvilli

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86
Q

Loop of henle has what features in the cytoplasm of the epithelial cells

A

few mitochondria

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87
Q

Descending limb of loop of henle is permeable/impermeable to what

A

permeable to water

impermeable to Na+

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88
Q

Ascending limb of loop of henle is permeable/impermeable to what

A

permeable to Na+

impermeable to water

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89
Q

Function of loop of henle

A

passive reabsorption

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90
Q

Structure of distal tubule

A

low cuboidal epithelium

minimal brush border of microvilli

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91
Q

Distal tubule has what features in the cytoplasm of the epithelial cells

A

fewer mitochondria

straight tubule has more mitochondria than convoluted tubule

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92
Q

Shape & location of nuclei in distal tubule

A

oval

apical

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93
Q

How does the permeability of the early & late distal tubule vary

A

early distal tubule is always impermeable to water

late distal tubule is permeable to water only w/ a diurectic

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94
Q

Function of distal tubule

A

active reabsorption

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95
Q

Does the proximal or distal tubule have stronger reabsorption

A

proximal tubule

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96
Q

Where are collecting tubules found

A

from outer cortex to renal papillae

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97
Q

Features of collecting tubules as they move deeper into the medulla

A

empty into each other

increase in diameter

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98
Q

Cells of cortical part of collecting duct & their features

A

principal cells w/ microvilli & mitochondria

intercalated cells w/ more mitochondria; extend past principal cells

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99
Q

Function of principal cells

A

minimal active reabsorption

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100
Q

Function of intercalated cells

A

active reabsorption

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101
Q

Type A intercalated cells function

A

excrete H+ & resorb HCO3-

help w/ K+ reabsorption

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102
Q

Tybe B intercalated cells function

A

excrete HCO3- & resorb H+

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103
Q

Medullary part of collecting duct has what cells

A

outer has both principal & intercalated cells

inner has only principal cells

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104
Q

Papillary part of collecting ducts has what cells

A

only principal cells

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105
Q

Collecting ducts are impermeable to what

A

water

unless diurectic is present

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106
Q

Size of cells in collecting duct in comparison to other parts of the nephron

A

in b/w proximal & distal tubule

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107
Q

Shape & location of nuclei in collecting ducts

A

oval (large)

near lumen or central

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108
Q

Unique feature of nuclei in collecting ducts

A

halo

due to cytoplasm not being dense

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109
Q

Do collecting ducts have a brush border

A

no

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110
Q

Function of collecting ducts

A

varying degrees of active reabsorption

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111
Q

Function of juxtaglomerular apparatus

A

samples tubule constituents & feedbacks onto glomerulus to change filtration rate

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112
Q

Macula densa is located where

A

at junction of straight & convoluted distal tubules

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113
Q

The macula densa is a specialized patch of cells that are

A

densely packed
tall
no basal lamina

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114
Q

Extraglomerular mesangial cells do what in relation to the juxtaglomerular apparatus

A

receive signal from macula densa

pass signal to juxtaglomerular cells

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115
Q

Juxtaglomerular cells are specialized what

A

smooth muscle cells full of granular renin inclusions

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116
Q

Function of ureter

A

convey urine from kidney to bladder via peristalsis

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117
Q

Special epithelium of urinary system is what & has what features

A

transitional epithelium

protection & distension

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118
Q

Lamina propria is what

A

fibrous connective tissue covered by mucosa

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119
Q

Mucosa serves as a layer b/w what

A

acidic urine & tissues

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120
Q

Mucosa is what when the structure it covers is full

A

not folded

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121
Q

Are there mucus glands in the mucus of the ureter

A

no

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122
Q

Ureter has how many layers of lamina propria

A

one

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123
Q

What are the smooth muscle layers of the ureter

A

1- outer circular layer
2- inner longitudinal layer
3- near bladder, additional outer longitiduinal layer

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124
Q

Structure of adventitia

A

outer fibrous coat

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125
Q

Function of adventitia

A

elasticity & protection

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126
Q

Function of bladder

A

muscular & elastic bag that stores urine

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127
Q

Bladder has how many layers of lamina propria

A

two

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128
Q

What are the smooth muscle layers of the bladder

A

1- thin inner longitudinal layer
2- thick middle circular layer
3- thin outer longitudinal layer

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129
Q

Smooth muscle layers of bladder are collectively called

A

dextrusor muscle

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130
Q

What is the internal sphincter of the bladder

A

thickening of middle circular layer of dextrusor

smooth muscle

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131
Q

Function of internal sphincter

A

contracted during 1st phase of micturition

involuntary

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132
Q

What is the external sphincter of the bladder

A

skeletal muscle

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133
Q

Function of external sphincter

A

voluntary

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134
Q

Function of urethra

A

conveys urine from bladder during voiding

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135
Q

Features of urethra lamina propria

A

large & porous

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136
Q

Are there mucus glands in the mucus of the urethra

A

yes, called glands of Littre

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137
Q

What are the smooth muscle layers of the urethra

A

1- inner circular layer
2- outer longitudinal layer
3- inner longitudinal layer that is lost as urethra leaves the bladder

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138
Q

Dominant layer of smooth muscle

A

circular layer

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139
Q

How do fenestrated capillaries filter on the basis of size

A

hold back RBC & plasma proteins > 3.6 nm in diameter (like albumin)

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140
Q

How do fenestrated capillaries filter on the basis of charge

A

laminin & fibronectin (polyanionic glycoprotein glycocalyx) repel neg molecules

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141
Q

How does the lamina rara filter on the basis of size

A

densa-> holes in nephrin (collagenous protein) let molecules < 2 nm pass easily while molecules > 4 nm are excluded completely

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142
Q

How does the lamina rara filter on the basis of charge

A

interna/externa-> laminin, fibronectin, & heparan sulfate (polyanionic non-collagenous proteins) repel neg charged molecules

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143
Q

How does the slit diaphragm filter on the basis of size

A

holes in nephrin (collagenous protein) let molecules < 2 nm pass easily while molecules > 4 nm are excluded completely

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144
Q

How does the slit diaphgram filter on the basis of charge

A

supporting podocytes (covered in polyanionic glycoportein glycocalyx) repel neg charged molecules

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145
Q

The ultrafiltrate is described as being what due to the filtration apparatus

A

mostly protein free

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146
Q

Describe how a neutral molecule/protein would get through the filtration apparatus

A

large molecules have difficulty crossing due to size

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147
Q

Describe how a cationic molecule/protein would get through the filtration apparatus

A

large molecules have difficulty crossing due to size

more molecules get through compared to a neutral molecule since the neg charge of the filtration barrier attracts them

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148
Q

Describe how an anionic molecule/protein would get through the filtration apparatus

A

large molecules have difficulty crossing due to size

less molecules get htrough compared to a neutral molecule since the neg charge of the filtration barrier repels them

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149
Q

Some proteins get through the filtration barrier, but how good is the nephron at reabsorbing them

A

not good

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150
Q

A non-functioning kidney would have what distinct clinical sign

A

protein lost in the urine

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151
Q

Name 4 Starling’s forces

A

hydrostatic pressure of capillaries & Bowman’s space (denoted w/ P)
oncotic pressure of capillaries & Bowman’s space (denoted w/ π)

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152
Q

What is oncotic pressure

A

osmotic pressure caused by colloids

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153
Q

Hydrostatic pressure of capillaries (Pc) is due to

A

(pushes out)
blood pressure in capillaries pushes out
generated by resistance difference b/w afferent & efferent arterioles in combination w/ pressure of blood due to left ventricular contraction

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154
Q

Hydrostatic pressure of Bowman’s space (Pbs) is due to

A

(pushes in)

fluid in Bowman’s space pushes against the walls of the glomerulus

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155
Q

Oncotic pressure of capillaries (πc) is due to

A

(pushes in)

protein in capillaries generate an osmotic pull of fluid into the capillaries

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156
Q

Oncotic pressure of Bowman’s space (πbs) is due to

A

(pushes out)

small amount of protein in Bowman’s space that exerts a negligible osmotic pull

157
Q

What is the largest Starling’s force that drive filtration

A

Pc

158
Q

Is filtration higher at the efferent or afferent end

A

afferent

159
Q

Why does Pc decrease at the efferent end

A

some energy has been used up

160
Q

Why does πc increase at the efferent end

A

plasma has left the capillaries

colloids have stayed

161
Q

If blood can enter glomerulus more easily than it can leave it, then

A

Pc increases

GFR increases

162
Q

What causes Pc & GFR to increase

A

dilated afferent arterioles

constricted efferent arterioles

163
Q

If blood can leave the glomerulus more easily than it can enter it, then

A

Pc decreases

GFR decreases

164
Q

What causes Pc & GFR to decrease

A

dilated efferent arterioles

constricted afferent arterioles

165
Q

What is Kf

A

area available for filtration * permeability of the membrane

166
Q

Heartworm affects Kf how

A

reduces filtration area
reduced Kf & GFR
kidney failure

167
Q

Changes in Pc result from

A

systemic hyperextension or pre-renal obstruction

168
Q

What happens to Pc & GFR in acute renal failure

A

Pc decreases due to impaired renal perfusion

thus, GFR decreases

169
Q

Relationship b/w Pc on GFR is indirect or direct

A

direct

170
Q

Relationship b/w πc & Pbs on GFR is indirect or direct

A

indirect

171
Q

What would affect πc

A

plasma protein levels increasing (increased πc & decreased GFR)
plasma protein levels decreasing (decreased πc & increased GFR)

172
Q

During liver impairment, what is the effect on πc

A

πc decreases

thus, GFR increases

173
Q

Obstructions (uroliths or plugs) do what to Pbs

A

Pbs increases

thus, GFR decreases

174
Q

Uroliths or plugs occur can lead to

A

acute renal failure

175
Q

Autoregulation has what functions

A

prevents fluctuations in bp to protect the delicate glomeruli from being slammed due to spikes in bp
prevents changes in Pc that would affect GFR by controlling bp in order to control the amount of filtrate sent to the tubules

176
Q

Renal autoregulation works in what range

A

80-180 mmHg

177
Q

Trigger for myogenic mechanism

A

fluctuations in bp change transmural pressure in afferent arteriole

178
Q

Function of myogenic mechanism

A

protective

prevents damage to glomeruli caused by spiking bp

179
Q

Increased bp causes what response in myogenic mechanism

A

vasoconstriction of afferent arteriole & decreased blood flow to the glomerulus

180
Q

Decreased bp causes what response in myogenic mechanism

A

vasodilation of afferent arteriole & increased blood flow to glomerulus

181
Q

Speed of myogenic mechanism

A

rapid changes (1-2 sec) in response to rapid bp changes

182
Q

Trigger for tubuloglomerular mechanism

A

fluctuations in bp change GFR, meaning distal tubule fluid composition is altered

183
Q

Function of tubuloglomerular mechanism

A

regulatory

prevents a change in GFR

184
Q

Speed of tubuloglomerular mechanism

A

slow changes (10-12 sec) in response to slower bp changes

185
Q

Steps of tubuloglomerular filtration to reduce GFR when bp is high

A

1) increased Na+, K+, & Cl- sensed by NKCC2 on apical surface of macula densa
2) macula densa releases ATP and/or adenosine
3) ATP/adenosine activate receptors on extraglomerular mesangial cells
4) increased intracellular Ca2+ in extraglomerular mesangial cells cause same response in afferent arteriole smooth muscle & juxtaglomerular cells
5) afferent arteriole smooth muscle contracts
6) juxtaglomerular cells inhibited from releasing renin

186
Q

Steps of tubuloglomerular filtration to increase GFR when bp is low

A

1) decreased Na+, K+, & Cl- sensed by NKCC2 on apical surface of macula densa
2) macula densa releases PGE2
3) PGE2 causes afferent arteriole dilation & stimulates juxtglomerular cells to release renin, which then increases angiotensin II
4) angiotensin II in bloodstream

187
Q

As a result of tubuloglomeralr filtration functioning to increase GFR when bp is low, what does angiotensin II in the bloodstream do

A
  • causes systemic vasoconstriction
  • preferentially contracts efferent over afferent arteriole
  • increases PGE2 production from macula densa
  • negatively feedbacks onto contralateral kidney to stop renin release
188
Q

Nephron reabsorption forms what

A

ultrafiltrate carried in the lumen

189
Q

What is contained in the ultrafiltrate

A

waste & important molecules

190
Q

Important molecules in tubular fluid moves across the epithelial lining of the nephron & into where

A

bloodstream via peritubular capillaries

191
Q

Reverse process of reabsorption is

A

secretion

192
Q

What is secretion

A

waste sent from blood into nephron

forms urine

193
Q

Describe the trancellular route

A

reabsorption through cytoplasm of tubular cells

194
Q

Is trancellular route active or passive transport

A

active & passive transport

195
Q

Describe the paracellular route

A

reabsorption b/w tubular cells across tight junctions

196
Q

Is paracellular route active or passive transport

A

passive transport

197
Q

What is the key molecule for reabsorption

A

Na+K+ATPase

198
Q

Tonicity of ultrafiltrate from glomerulus/Bowman’s space compared to epithelial cells & blood is

A

isotonic

199
Q

Since ultrafiltrate is isotonic w/ epithelial cells & blood, all transport would need to be active; how does Na+K+ATPase remedy this

A

generates an electrochemical gradient to allow reabsorption

200
Q

Where is Na+K+ATPase located

A

basolateral membrane of tubules

201
Q

Describe Na+K+ATPase modality

A

pumps 3 Na+ out of cell for 2 K+ into cell

low intracellular [Na+], so this movement is against its gradient

202
Q

Na+K+ATPase allows for reabsorption where (down electrochemical gradient)

A

luminal membrane of tubules

203
Q

% of what proximal tubule reabsorbs/ secretes

A 
Reabsorbs:
67% of filtered water, Na+, &amp; solutes
99% of filtered glucose &amp; AAs
90% of filtered bicarbonate
Does not secrete
204
Q

Describe how reabsorption occurs in first half of proximal tubule

A

1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters via Na+H+ antiporter & Na+ glucose/ AA/ PO4(3-) symporter (luminal membrane)
3) Water follows Na+ down osmotic gradient (luminal membrane)

205
Q

Glucose, AA, & PO4(3-) are moved where by what after the initial reabsorption across the luminal membrane at the first half of the proximal tubule

A

moved across basolateral membrane by specific transporters & into peritubular capillaries

206
Q

How did the solute movement in the first half of the proximal tubule promote water following Na+ entry

A

solute movement increased osmolarity inside proximal tubule cells compared to tubular fluid

207
Q

Describe how reabsorption occurs in the second half of proximal tubule

A

1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters down electrochemical gradient via Na+H+ antiporter
3) Cl- enters down electrochemical gradient via Cl- anion antiporter & Cl- also moves via paracellular route
4) lumen +ve PD drives Na+ movement paracellularly

208
Q

How is Cl- moved on the basolateral membrane of the second half of the proximal tubule

A

K+Cl- symporter

209
Q

Why is Na+ & Cl- transport encouraged in second half of proximal tubule

A

reabsorption of water in 1st half concentrated Na+ in 2nd half
H+ & anion leave cell separately, fuse, & diffuse back into cell, effectively recycling themselves for transport to continue

210
Q

After proteins are partially degraded by enzymes in luminal membrane, what happens

A

reabsorbed by exocytosis

211
Q

Proteins are further degraded by enzymes in lysozymes into AAs & go where

A

across basolateral membrane

212
Q

Protein reabsorption can become easily saturated, leading to what

A

proteinuria (protein in urine)

213
Q

% of what loop of henle reabsorbs/ secretes

A

Reabsorbs:
25% of filtred NaCl (ascending loop)
15% of filtered water (descendng loop)
Does not secrete

214
Q

Active or passive transport in loop of henle

A

passive

215
Q

% of what distal tubule & collecting duct reabsorb/ secrete

A 
Reabsorbs:
7% of filtered NaCl
8-15% of filtered water (w/ diuretic)
Secretes:
K+ &amp; H+
216
Q

Describe how reabsorption occurs in the initial part of distal tubule

A

1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters cell via NKCC1 symporter & Na+H+ antiporter (luminal membrane)
3) +ve transmembrane PD allows cations (Na+, K+, & Ca2+) to move down electrochemical gradient via paracellular route (luminal membrane)

217
Q

Does water follow solutes in initial part of distal tubule

A

no, not even with ADH

218
Q

How does K+ & Cl- get across basolateral membrane in initial part of distal tubule

A

transporters

219
Q

What inhibits NKCC1 symporter

A

loop diuretics

220
Q

Describe how reabsorption occurs in the later part of distal tubule

A

1) Na+K+ATPase generates Na+ gradient (basolateral membrane)

2) Na+ enters cell via Na+Cl- symporter (luminal membrane)

221
Q

Does water follow Na+ in later part of distal tubule

A

yes, but only w/ ADH

222
Q

What inhibits Na+Cl- symporter

A

thiazide diuretics

223
Q

Describe how reabsorption occurs in principal cells of collecting ducts

A

1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters cell via Na+ channels
3) K+ leaves through K+ channels
4) Na+ reabsorption generates neg PD that allows Cl- to be absorbed via paracellular route

224
Q

Does water follow N+ in principal cells of collecting duct

A

yes, but only w/ ADH

225
Q

What inhibits Na+ channels

A

amiloride diuretics

226
Q

Describe how reaborption occurs in intercalated cells of collecting ducts

A

secrete H+ & HCO3-

227
Q

How does osmolarity or [Na+] differences play a role in reabsorption in descending limb of loop of henle

A

osmolarity of tubular fluid is always lower than the osmolarity of interstitia surrounding it so water moves out

228
Q

How does osmolarity or [Na+] differences play a role in reabsorption in ascending limb of loop of henle

A

[Na+] of tubular fluid is always higher than the [Na+] of interstitia surround it so Na+ moves out

229
Q

Why is the loop of henle described as being a countercurrent multiplier (2 reasons)

A

1) fluid in one limb moves countercurrent to fluid in the other
2) effect of one limb multiplies effect of the other

230
Q

Example of how descending limb affects ascending limb

A

water reabsorption in descending limb amplifies Na+ reabsorption in the ascending limb

231
Q

Fluid leaving proximal tubule is

A

iso-osmotic

232
Q

Fluid leaving loop of henle to distal tubules is

A

hypotonic

233
Q

Describe how reaborption occurs in loop of henle

A

1) active reabsorption of Na+ in early distal tubule creates an osmotic gradient, causing water to leave the descending limb
2) medullary interstitium osmolarity increases, so water keeps moving passively out of descending limb
3) at hairpin loop, water reabsorption has concentrated Na+ above interstitial concentration, so a Na+ gradient is formed
4) Na+ passively leaves ascending limb into interstitium, contributes to interstitial osmolarity that allowed water reabsorption in descending limb
5) Na+ reabsorption decreases tubular fluid osmolarity until it is less than the interstitium

234
Q

At the hairpin loop, what is the tonicity difference b/w tubular fluid & interstitium

A

iso-osmotic

osmolarity of tubular fluid is equal to the interstitium

235
Q

High tubular osmolarity at hairpin loop is due to

A

Na+

236
Q

High interstitial osmolarity at hairpin loop is due to

A

Na+ & urea

237
Q

What does low ADH mean

A

diuresis -> water expelled

238
Q

What does high ADH mean

A

antidiuresis -> water retained

239
Q

Stimuli for ADH (3 of them)

A

1) high ECF osmolarity sensed by shrinking omoreceptors
2) low ECF volume sensed by baroreceptors
3) omoreceptors & baroreptors stimulate thirst center

240
Q

Explain the modality of ADH

A

increases expression of aquaporins in medullary collecting duct (NOT CORTICAL) & later parts of distal tubule

241
Q

Is it true that there is always some level of ADH present & what does this mean

A

yes, so nephron sections are always permeable to a degree

242
Q

What does diuresis result in

A

1) high volume of dilute urine
2) ADH low/ zero
3) water is not reabsorbed into distal tubule or medullary collecting ducts
4) instead, water stays in tubular fluid & is expelled in urine
5) loss of ECF water to reduce ECF volume & increases ECF osmolarity

243
Q

What does antidiuresis result in

A

1) low volume of concentrated urine
2) water is reabsorbed in distal tubules & collecting ducts
3) retains ECF water to increases ECF volume & decrease ECF osmolarity

244
Q

Urea is constantly produced where

A

glomerulus

245
Q

Water reabsorption in descending limb of loop of henle causes there to be what relationship b/w [urea] in distal tubule compared to interstitia surrounding it

A

more urea in distal tubule compared to interstitia

246
Q

What happens to urea in distal tubule & cortical collecting duct

A

cannot leave

247
Q

What happens to urea in medullary collecting duct

A

cannot leave without ADH

248
Q

Is urea an effective or ineffective osmole at the collecting duct

A

ineffective

249
Q

Is urea an effective or ineffective osmole at the loop of henle

A

effective

250
Q

What is the result of urea being an effective osmole at the loop of henle

A

increased interstitial [urea] increases interstitial osmolarity around loop
more water than normal is pulled from descending limb
leads to a low volume of concentrated urine (antidiuresis)

251
Q

When urea is added to medullary interstitium, what prevents toxic accumulation

A

when ADH levels are reduced, less urea accumulates
ascending loop is slightly permeable to urea so it can recycle it
vasa recta is permeable to urea & recycles it

252
Q

Modality of vasa recta

A

removes water in countercurrent multiplier function from interstitium & keeps Na+ in interstitium

253
Q

What happens in the ascending limb of vasa recta

A

permeable to Na+ & water
H2O moves down osmotic gradient into ascending limb & is carried from medulla to blood
H2O removed from descending limb of vasa recta & descending limb of loop of henle

254
Q

What happens in the descending limb of vasa recta

A

permeable to Na+ & water
Na+ circulates from ascending to descending limb
keeps Na+ in medulla to maintain a high interstitial osmolarity

255
Q

Main ion contributor to ECF & main osmole

A

Na+

256
Q

Higher [Na+] means

A

higher ECF osmolarity

257
Q

Lower [Na+] means

A

lower ECF osmolarity

258
Q

Increase in amount of Na+ means

A

increase in ECF volume

259
Q

Decrease in amount of Na+ means

A

decrease in ECF volume

260
Q

Kidneys are the only site of ECF Na+ regulation, therefore they are critical in regulating

A

ECF osmolarity & volume

261
Q

During high ECF osmolarity/ high [Na+], what happens

A

fluid moves out of ICF (cells shrink)

262
Q

During low ECF osmolarity/ low [Na+], what happens

A

fluid moves into ICF (cells swell)

263
Q

What is hypernatremia

A

high ECF [Na+]

high ECF osmolarity

264
Q

Clinical signs of hypernatremia

A

rupture of cerebral vessels/ hemmorhage
muscle weakness
behavioral changes/ ataxia
coma -> death

265
Q

Regulation of hypernatremia

A

omoreceptors shrink, causing increased ADH release & thirst response

266
Q

What is hyponatremia

A

low ECF [Na+] concentration

low ECF osmolarity

267
Q

Clinical signs of hyponatremia

A

cerebral/ pulmonary edema
muscle weakness
incoordination & seizures

268
Q

Regulation of hyponatremia

A

omoreceptors swell, causing reduced ADH release

269
Q

Is changing Na+ amount the only way to affect ECF volume

A

no

270
Q

How do the kidneys regulate ECF volume

A

by changing Na+ amount

271
Q

What is hypovolemia

A

low ECF volume

low circulating volume (hypotension)

272
Q

Clinical signs of hypovolemia

A

hypovolemic shock

organ damage

273
Q

Regulation of hypovolemia is by

A

sympathetic nervous system (baroreceptors) & renin-angiotensin system (juxtaglomerular apparatus)

274
Q

Describe regulation of hypovolemia

A

1) baroreceptors (stretch receptors) sense decreased volume & send signals to the brain
2) sympathetic flow to kidney increases
3) norepinephrine is released
4) stimulates renin release from Juxtaglomerular apparatus to activate renin-angiotensin system

275
Q

What does norepinephrine stimulate during hypovolemia regulation

A

causes vasoconstriction of efferent tubule more than afferent tubule (increases GFR)
alters Starling’s forces to increase Na+ reabsorption in proximal tubule (even though more Na+ is being filtered)
causes juxtaglomerular cells to release renin

276
Q

How does Starling’s forces increase Na+ reabsorption in proximal tubule during hypovolemia regulation

A

since GFR increases, so does Pt (tubules)
since a greater amount of plasma is filtered, less makes it to the capillaries so Pc (capillaries) decreases
since GFR increases, not much protein goes through the filtration barrier so πt (tubules) does not change
since GFR increases, elevated filtration increases protein conc in peritubular capillaries so πc (capillaries) increases

277
Q

Angiotensin II as a result of renin-angiotensin system in hypovolemia does what

A

constricts efferent arteriole to increase Na+ & H2O uptake
stimulates Na+H+ antiporter to increase Na+ uptake
stimulates ADH release to increase H2O uptake
stimulates aldosterone to increase Na+ uptake

278
Q

Aldosterone is secreted where

A

from glomerulosa cells of adrenal cortex

279
Q

What does aldosterone stimulate

A

increased Na+ channels in principal cells of collecting duct
increased Na+K+ATPase
increased NKCC1

280
Q

What is hypervolemia

A

high ECF volume

increased capillary hydrostatic pressure (hyperextension)

281
Q

Clinical signs of hypervolemia

A

ascites & pulmonary edema

282
Q

What is natiuresis

A

renal excretion of Na+

283
Q

Where are atrial natrioretic peptides synthesized

A

atrial myocytes

284
Q

Where are brain natiuretic peptides synthesized

A

cardiac ventricles

285
Q

Regulation of hypervolemia is by

A

natiruetic peptide release (baroreceptors)

286
Q

Where are baroreceptors found

A

heart, aorta, & carotid sinus

287
Q

Describe regulation of hypervolemia

A

1) natiuretic peptide release constricts efferent arterioles & dilates afferent arterioles, which increases GFR, thus increasing Na+ & water load entering tubules
2) inhibits renin release from juxtaglomerular apparatus to prevent renin-angiotensin system (RAS)
3) inhibits ADH release by inhibiting RAS
4) inhibits aldosterone release by inhibiting RAS & acting directly on adrenal cortex
5) inhibits NaCl reabsorption in collecting duct by inhibiting Na+ channels

288
Q

Main ion contributor to ICF

A

K+

289
Q

Inside cells, function of K+

A 
important osmole (maintains cell volume)
cofactor for enzymes
290
Q

Outside cells, function of K+

A

small amount, but critical that it is maintained

291
Q

Where can kidney regulate K+

A

extracellular only

292
Q

What does the conc gradient of K+ set

A

resting membrane potential

293
Q

Why does K+ govern resting membrane potential

A

Na+ channels have low permeability

K+ channels are leaky

294
Q

Result of leaky K+ channels

A

inside of cell more neg than outside as K+ follow conc gradient
eventually, inside of cell is so neg that K+ can no longer move out
membrane potential set b/c charge attraction for K+ = conc gradient for K+ moving out of the cell

295
Q

What is hypokalemia

A

less K+ outside cell

296
Q

Result of hypokalemia

A

conc gradient for K+ to move out is larger
inside cell gets more neg -> lower resting potential
to reach threshold, excitable cells need more Na+ so it is more difficult to generate AP

297
Q

Symptoms of hypokalemia

A

muscle weakness, respiratory problems, cardiac arrythmia, & renal dysfunction

298
Q

What is hyperkalemia

A

more K+ outside cell

299
Q

Result of hyperkalemia

A

conc gradient for K+ to move out is smaller
inside of cell gets less neg -> higher resting potential
at first, AP is easier to generate
but then Na+ channels are unable to reset b/c the membrane potential is not low enough
excitable cells become unexcitable

300
Q

Symptoms of hyperkalemia

A

muscle weakness & cardiac dysfunction

301
Q

Describe external K+ homeostasis

A

K+ from diet must be excreted in urine/ feces
if it does not excrete enough -> hyperkalemia
if it secretes too much -> hypokalemia

302
Q

Where does K+ come from

A

diet or parenteral fluids

303
Q

Where is K+ lost at

A

90% via kidney (kaliuresis) & 10% via GI (colon helps when kidney is sick)

304
Q

GI/renal problems can result in

A

hypokalemia or hyperkalemia

305
Q

Describe internal K+ homeostasis

A

adjusts for rapid changes in K+ by translocating K+ from ECF to ICF or vice versa
acid base balance plays a role

306
Q

Why is internal K+ homeostasis necessary

A

kidneys & gut work slowly, so body needs buffers in place to allow these organs to catch up

307
Q

What hormones facilitate translocation of K+ in internal regulation

A

insulin promotes movement of K+ into cells by stimulating Na+K+ATPase (prevents hyperkalemia)
catecholamines -mainly epinephrine- promote K+ uptake into cells (B2 stimulation of Na+K+ATPase) & out of cells (alpha receptor)

308
Q

How does acid base balance play a role in internal K+ homeostasis

A

high H+ promotes movement of K+ out of cells to maintain electronegativity & low H+ promotes movement of K+ into cells

309
Q

Why is bicarbonate administered to treat hyperkalemia

A

reduces H+ & pushes K+ into cells

310
Q

What parts of the nephron determine K+ balance

A

distal tubule & collecting duct

311
Q

Describe paracellular movement of K+ in proximal tubule

A

K+ movement in late part of tubule where transepithelial PD become lumen pos & cell junctions are leaky

312
Q

Describe transcellular movement of K+ in proximal tubule

A

movement facilitated by K-Cl symporter at basolateral membrane & K+ channels at luminal membrane

313
Q

% of K+ that proximal tubule reabsorbs

A

67%

314
Q

Describe paracellular movement of K+ at distal straight tubule

A

movement b/c transepithelial PD is lumen pos

315
Q

Describe transcellular movement of K+ at distal straight tubule

A

movement faciliated by NKCC1 at luminal membrane & K+ channels at basolateral membrane

316
Q

% of K+ that distal straight tubule reabsorbs

A

20%

317
Q

Principal cells in collecting duct illicit what re K+

A

K+ secretion

318
Q

How do principal cells in collecting duct cause K+ secretion

A

1) Na+K+ATPase generates Na+ gradient
2) Na+ enters via Na+ channels to make lumen more neg, causing K+ to want to move into the lumen
3) K+ leaves through K+ channels down gradient
4) Luminal membrane is more permeable than basolateral membrane, so most K+ enters the lumen but some does go back to the serum

319
Q

Alpha intercalated cells in collecting duct illicit what re K+

A

K+ absorption

320
Q

How do alpha intercalated cells in collecting duct cause K+ absorption

A

1) H+ leaves through H+ATPase & H+K+ATPase in luminal membrane
2) K+ enters cell via luminal membrane
3) K+ channels at basolateral membrane return K+ to ECF

321
Q

Beta intercalated cells in collecting duct illicit what re K+

A

reversed, so do not absorb K+ like alpha intercalated cells

322
Q

What are the factors that determine K+ handling

A

increase in size of conc gradient b/w cell & tubular fluid
tubular flow rate affects secretion
lumen electronegativity

323
Q

Increased plasma [K+] leads to hyperkalemia, so K+ is moved where which causes what

A

translocated into ICF
this increases K+ gradient in renal cells so K+ is pushed into the lumen
stimulates aldosterone

324
Q

Stimulation of aldosterone during hyperkalemia results in

A

increase in amiloride sensitive channels, which increases Na+ uptake
neg lumen & pos cell result in K+ secretion into lumen
Na+K+ATPase is stimulated

325
Q

What stimulates aldosterone

A

hyperkalemia & angiotensin II

326
Q

What inhibits aldosterone

A

natriuretic peptides

327
Q

Low tubular flow rate decreases K+ secretion, resulting in

A

K+ persists in tubular fluid (hyperkalemia)

K+ gradient reduced at luminal membrane

328
Q

High tubular flow rate increases K+ secretion, resulting in

A

already secreted K+ is washed away (hypokalemia)

high conc gradient for K+ maintained for secretion

329
Q

Under low flow rate, what increases K+ channel activity (hyperkalemia)

A

ADH increases K+ channel activity

330
Q

When does ADH act to increase K+ channel activity

A

occurs when water deprived or in extended periods of antidiuresis
flow rate reduced to conserve H2O

331
Q

What can occur when ADH acts to increase K+ channel activity

A

hyperkalemia

332
Q

Under high flow rate, what decreases K+ channel activity (hypokalemia)

A

ADH is low

333
Q

What can occur when ADH does not act to increase K+ channel activity

A

hypokalemia (K+ wasting)

334
Q

Increased lumen electronegativity does what re K+

A

increases K+ secretion

335
Q

What increases lumen electronegativity

A

Na+ reabsorption or presence of ions like SO4, HCO3, or penicillin

336
Q

Decreased lumen electronegativity does what re K+

A

decrease K+ secretion

337
Q

What are the factors that influence renal K+ handling

A 
Na+ intake
Acidosis
Alkalosis
Loop-, Thiazide-, &amp; osmotic diuretics
Amiloride-like diuretics
338
Q

How does Na+ intake affect renal K+ handling

A

dietary Na+ increases tubular [Na+], which increases Na+ reabsorption & increases K+ secretion (low intake does the opposite)

339
Q

What effect does ECF osmolarity have on K+ as a result of Na+ intake

A

increased ECF osmolarity generates hypokalemia & decreased osmolarity generates hyperkalemia

340
Q

How does acidosis affect renal K+ handling

A

increases serum [H+] so H+ moves into cells & K+ leaves to maintain electroneutrality
since luminal membrane is not permeable to K+ under acidosis, K+ is dumped into ECF -> hyperkalemia

341
Q

How does alkalosis affect renal K+ handling

A

decreases serum [H+] so H+ moves out of cells & K+ enters to maintain electroneutrality
luminal membrane not permeable to K+ under alkalosis, so K+ is dumped into ICF -> hypokalemia

342
Q

How does Loop-, Thiazide-, & osmotic diuretics affect renal K+ handling

A

increase flow rate & [Na+] in collecting duct

results in increased K+ secretion -> hypokalemia

343
Q

How does Amiloride-like diuretics affect renal K+ handling

A

inhibit Na+ uptake in collecting duct
this inhibits K+ secretion -> hyperkalemia
(K+ sparing diuretics)

344
Q

Define acid

A

proton (H+) donor
increases [H+] conc of a soln
low pH

345
Q

Define base

A

proton (H+) acceptor
decreases [H+] conc of a soln
high pH

346
Q

Normal physiological pH

A

7.35-7.45

347
Q

Define acidemia

A

pH < 7.35

348
Q

What is severe acidemia

A

pH < 7.2

349
Q

Define alkalemia

A

pH > 7.45

350
Q

What is severe alkalemia

A

pH > 7.6

351
Q

Define acidosis

A

processes by which acidemia occurs

352
Q

Define alkalosis

A

proceses by which alkalemia occurs

353
Q

Simplified equation for partial pressure of CO2

A

dCO2 -> H+ + HCO3-

354
Q

Is CO2 an acid or base

A

acid

355
Q

How does a low ventilation rate regulate acid/base balance

A

increases ECF pCO2 which increases [H+] that can lead to respiratory acidosis

356
Q

How does a high ventilation rate regulate acid/base balance

A

decreases ECF pCO2 which decreases [H+] that can lead to respiratory alkalosis

357
Q

Equation that represents the relationship b/w lung ventilation rate & acid/base balance

A

Henderson-Hasselbalch equation

358
Q

Rapid changes of acid/base balance that manipulate pCO2 occur where

A

lungs & tissues

359
Q

What are strong ions

A

ions that completely dissociate at a normal physiological pH

360
Q

Strong cations

A

Na+, K+, Ca2+, & Mg2+

361
Q

Strong anions

A

Cl-, lactate, & SO4(2-)

362
Q

What does the strong ion difference reflect

A

in normal plasma, [strong cations] > [strong anions]

363
Q

How does SID decrease & how would this affect ECF

A

strong anions added or strong cations removed

ECF neg

364
Q

How does SID increase & how would this affect ECF

A

strong cations added or strong anions removed

ECF pos

365
Q

Slow changes of acid/base balance that manipulate SID occur where

A

kidneys, gut, & tissues

366
Q

If [SID] decreases, ECF is less positive & what happens

A

pos charge is required for balance
H+ > OH-
metabolic acidosis

367
Q

If [SID] increases, ECF is more positive & what happens

A

neg charge is required for balance
OH- > H+
metabolic alkalosis

368
Q

What are weak acids

A

acids that partially dissociate at physiologial pH

369
Q

Ex of weak acids

A

proteins (albumins & globulins)

phosphates

370
Q

Eq for weak acids

A

HA -> H+ + A-

371
Q

What is Atot

A

Weak acid buffers in a system

372
Q

Eq for Atot

A

HA + A-

373
Q

If Atot increases, what happens

A

increased [H+]

metabolic acidosis

374
Q

If Atot decreases, what happens

A

decreased [H+]

metabolic alkalosis

375
Q

Does [H+] determine pH

A

no, only pCO2, [SID], & Atot determine pH

376
Q

Are the factors determining acid/base balance independent or dependent

A

independent

377
Q

Kidney goal in acidemic animal

A

increase ECF [SID]

378
Q

What does kidney do in an acidemic animal

A

decrease Cl- reabsorption & increase Na+ reabsorption (alkalosis)

379
Q

When kidneys increase ECF [SID] in an acidemic animal, what happens to urinary [SID]

A

decreases

urine becomes more acidic

380
Q

What is the kidneys response to urine becoming more acidic

A

synthesis & secretion of NH4+ to maintain electroneutrality

381
Q

Kidney goal in alkalemic animal

A

decrease ECF [SID]

382
Q

What does kidney do in an alkalemic animal

A

decreases Na+ reabsorption & increase Cl- reabsorption (acidosis)

383
Q

When kidneys decrease ECF [SID] in an alkelmic animal, what happens to urinary [SID]

A

increases

urine becomes less acidic

384
Q

What is the kidneys response to urine becoming less acidic

A

synthesis & secretion of NH4+ is suppressed to maintain electroneutrality

385
Q

What allows animals to sense abnormal ECF volume

A

baroreceptors (stretch receptors) in left atria/pulmonary vessels & in aortic arch/sinus

386
Q

What do baroreceptors in left atria & pulmonary vessels sense

A

volume change

on venous side where most of the volume is

387
Q

What do baroreceptors in the aortic arch & sinus sense

A

pressure changes
on arterial side where most of the pressure is
(more important than venous baroreceptors)

388
Q

If baroreceptors on arterial side stretch, what happens

A

no ADH is released

389
Q

If baroreceptors on arterial side do not stretch, what happens

A

ADH is released

Histology (4 decks)

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