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Respiratory and Kidney > Renal > Flashcards

Renal Flashcards

1
Q

total body water

A

45% and 75% of body weight

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2
Q

variations in TBW

A

inverse with age
inverse with fat
lower in females

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3
Q

lean body mass

A

body weight exclusive of storage fat

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4
Q

compartments of total body water

A

plasma, interstitial, intracellular

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5
Q

extracellular fluid

A

plasma and ISF, separated by capillaries

1/3 of total, plasma 1/4, ISF 3/4

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6
Q

intracellular fluid

A

2/3 of TBW

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7
Q

transcellular fluid compartment

A

fluid in transit in lumina of epithelial organs, cerebrospinal fluid, intraocular fluid

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8
Q

organs that communicate with external environment and ECF

A

alimentary canal
lungs
kidneys
skin

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9
Q

major ECF ions

A

Na and Cl

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10
Q

major ICF ion

A

K due to Na/K ATPase

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11
Q

protein concentration

A

highest in plasma because capillaries are not permeable to proteins

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12
Q

pH of ECF and ICF

A

ECF=7.4

ICF=7.1

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13
Q

dilution methods for determining distribution

A

C=Q/V

characteristics-nontoxic, neither synthesized nor metabolized, does not cause shifts in fluid distribution

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14
Q

measuring plasma volume

A

serum albumin with radioactive iodine

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15
Q

measuring extracellular fluid volume

A

inulin, some lost in urine

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16
Q

measuring total body water

A

antipyrine or deuterated water or tritated water

lost by all routes

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17
Q

alterations in body fluid compartments

A

enter or leave by ECF
ICF and ECF are in osmotic equilibrium
shifts occur primarily by water and not solutes

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18
Q

isosmotic water shifts

A

change in ECF only
increase in saline infusion
decrease with hemorrhage

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19
Q

hyperosmotic water shifts

A

cells shrink
water loss or Na retention
losing more water by severe sweating, excess renal water loss with decreased ADH
gaining more salt than water by ingestion of salt tablets

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20
Q

symptoms of hyperosmolarity

A

early-lethargy
progresses to twitching, seizures, coma, and death
could result in cerebral hemorrhages

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21
Q

hyposmotic water shifts

A

cells swell
water gain or Na loss
gaining water in SIADH or excessive thirst
loss of salt by lack of aldosterone

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22
Q

symptoms of hyposmolarity

A

serizures, coma

premenopausal women do not fully recover

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23
Q

brain osmotic adaptation

A

cerebral swelling will increase the flow of brain ISF toward the CSF decreasing the amount of swelling, too fast infusion of Na leads to cell shrinkage

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24
Q

functions of kidneys

A 
regulation of water and electrolyte balance
removal of foreign chemicals
regulation of arterial blood pressure
secretion of erythropoietin
secretion of active vitamin D
gluconeogenesis
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25
Q

renal corpuscle contents

A

Bowman’s capsule-end of uriniferous tubule
Bowman’s space-receiving filtrate of blood
Glomerulus-tuft of capillaries which nearly fills Bowman’s capsule
Glomerular mesangial cells-phagocytic, nonphagocytic (contractile)

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26
Q

layers of of glomerular membranes

A

endothelium-fenestrated capillary
basement membrane-barrier to large proteins and lipids
epithelium-podocytes, forms filtration slits bridged by pores

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27
Q

tubule

A

epithelial cells with tight junctions

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28
Q

proximal tubule

A

site of reabsorption, distinguished by large surfae area (apical brush border of microvili, basolateral infoldings and interdigitation)
mitochondria line basolateral membrane

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29
Q

Henle’s loop

A

countercurrent direction of flow, influence electrolyte and water transport

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30
Q

distal tubule

A

returns to cortex and makes contact with afferent and efferent arterioles of the parent renal corpuscle, site of JGA

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31
Q

JGA cell types

A

macula densa-provide information on volume, flow or NaCl
granular cells-smooth cells in afferent that secretes renin
extraglomerular mesangial cells-phagocytic, communicate with granular via gap junctions

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32
Q

collecting tubule

A

tubular fluid from distal tubules from cortex to inner medulla, fine tuning of composition, fuse together near tip of papillae to form papillary ducts of Bellini

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33
Q

cell types of collecting duct

A

principal-ADH, ANP, aldosterone
alpha intercalated-secretes H
beta intercalated-secretes HCO3

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34
Q

cortical nephrons

A

no thin ascending loop of Henle

short loops

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35
Q

juxtamedullary nephrons

A

thin segment may reach tip of papillae
larger glomeruli
concentrated urine

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36
Q

nerve supply to kidney

A

sympathetic only, vasoconstriction of arterioles, basement membrane of PT, loop of Henle, DT, CD which enhances sodium reabsorption

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37
Q

lymphatic network

A

only in cortex

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38
Q

blood supply to kidney

A

interlobar, arciform, interlobular, afferent, capillary, efferent, peritubular capillaries or vasa recta, interlobular veins

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39
Q

glomerular filtration

A

protein-free plasma from glomerular capillaries into Bowman’s capsule, no active transport, physically sieving blood

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40
Q

tubular secretion

A

transfer of materials from peritubular capillary plasma to the tubular lumen

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41
Q

tubular reabsorption

A

transfer of materials from lumen of tubule to peritubular capillary plasma

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42
Q

blood flow to kidneys

A

renal blood flow is 20% of CO
renal plasma flow subtracts hematocrit
GFR is 125

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43
Q

filtration fraction

A

GFR/RPF

normally 20%

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44
Q

colloid osmotic pressure

A

increases during the trip from afferent to efferent arteriole, blood leaving will not have highest colloid osmotic pressure of any blood in the kidney

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45
Q

GFR calculation

A

Kf (Pc-Pb-oncotic c)

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46
Q

Kf changes physiologically

A

ADH causes decrease in Kf and decrease in GFR
angiotensinogen decreases Kf
ANP increases Kf and GFR

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47
Q

pathologic changes to Kf

A

thickening due to autoimmune diseases

destruction of glomerular capillaries decreases SA

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48
Q

glomerular capillary pressure

A

determined by relative resistance of afferent and efferent arterioles, determined by hormones and neural input

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49
Q

changing afferent arteriole resistance

A

vasodilation increases flow and increases GFR

vasoconstriction decreases flow and decreases GFR

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50
Q

changing efferent arteriole resistance

A

vasodilation increases blood flow but decreases GFR and filtration
vasoconstriction decreases blood flow and increases GFR and filtration fraction

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51
Q

changing afferent and efferent

A

constricting both will inhibit renal blood flow but increase GFR and FF

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52
Q

hydrostatic pressure in Bowman

A

required to drive flow of urine, high pressure causes decrease in GFR (diuretics, prostatic hypertrophy, tumors, kidney stones)

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53
Q

autoregulation of glomerular filtration rate

A

80-180 mmHg both GFR and RBF remain constant, myogenic and tubuloglomerular feedback mechanisms

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54
Q

myogenic mechanism

A

change in pressure in arterioles stretch leads to contraction

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55
Q

tubuloglomerular feedback

A

macula densa senses flow through NaCl delivery, constriction by mesangial cells reduce GFR, without reduction system would be overwhelmed and would result in loss of water and electrolytes

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56
Q

measurement of glomerular filtration rate

A

measured by chemical that is not bound to plasma proteins or electrically charged
inulin-all filtered is excreted

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57
Q

GFR and clearance

A

UV/P=clearance

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58
Q

renal clearance

A

volume of plasma from which all of a substance has been removed and excreted into uring per unit of time

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59
Q

inulin clearance

A

independent of plasma inulin concentration and urine flow (U/P remains constant)

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60
Q

endogenous substance to approximate GFR

A

creatine, small amount of secretion

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61
Q

significance of inulin clearance

A

maximal volume of plasma that can be cleared of a substance exclusively by filtration into the nephron per minute

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62
Q

changes in clearance relative to inulin

A

above inulin means something has been secreted

below inulin means something has been reabsorbed

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63
Q

single ratio

A

TF/P concentration in tubular fluid over plasma of inulin

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64
Q

water content from inulin

A

only water is changed, 1-(1/ratio) for amount of water reabsorbed

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65
Q

fractional excretion

A

mass excreted/mass filtered
used to calculate reabsorption or secretion
double ratio when compared to inulin

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66
Q

double ratio

A

greater than 1 is secreted

less than 1 is reabsorbed

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67
Q

diffusion

A

requires electrochemical gradient, downhill transport

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68
Q

facilitated diffusion

A

requires electrochemical gradient and carriers

exhibits specificity, saturability, and competition, downhill transport

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69
Q

primary active transport

A

requires carriers
exhibits specificity, saturability, and competition
uphill transport, requires energy

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70
Q

secondary active transport

A

requires carriers
exhibits specificity, satruability, and competition
one uphill another downhill
cotransport or countertransport

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71
Q

paracellular

A

diffusion between cells

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72
Q

transcellular

A

across the cell

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73
Q

glucose in proximal tubule

A

apical with Na, basolateral facilitated diffusion

requires gradient established by Na/K ATPase

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74
Q

transport maximum

A

limit to amounts of material the active transport system can transport per unit of time, saturation of carriers

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75
Q

threshold

A

plasma concentration at which glucose first appears in the urine

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76
Q

splay

A

appearance of glucose in the urine before Tm is reached
due to kinetics-maximal activity is substrate dependent
not all nephrons have the same Tm

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77
Q

glucose clearance

A

C=0
plasma begins to be cleared of glucose as the plasma glucose threshold is exceeded
higher plasma glucose concentration the greater the clearance of glucose becomes

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78
Q

excretion of glucose

A

direct proportion to amount filtered minus level of reabsorption

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79
Q

high concentrations of glucose

A

approaches the clearance of inulin

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80
Q

glucose reabsorption mechanism

A

increase plasma glucose blocks reabsorption of xylose because affinity for glucose>xylose

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81
Q

renal glycosuria

A

glucose in urine as a result of defective missing transport mechanism

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82
Q

diabetes mellitus

A

glucosuria due to the lack of insulin

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83
Q

pregnancy

A

increase GFR leads to glucose in urine

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84
Q

reabsorption of amino acids

A

Clearance=0
reabsorbed and exhibit considerable splay
kidneys do not regulate plasma concentrations

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85
Q

reabsorption of organic nutrients

A

filtered and reabsorbed in proximal tubule

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86
Q

citrate reabsorption

A

normal in urine

complexes with Ca

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87
Q

alpha ketoglutarate reabsorption

A

active reabsorption, does not regulate alpha keto

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88
Q

beta ketoglutarate reabsorption

A

regulated by kidneys, excretion high in uncontrolled diabetes mellitus and starvation

89
Q

vitamin C

A

active reabsorption, marked splay

90
Q

low filtration of proteins

A

filtration low due to steric hindrance, viscous drag, and electrical hindrance

91
Q

viscous drag

A

lining of pore retards forward movement of protein

92
Q

electrical hindrance

A

charges on glomerular membranes are negative, dont restrict crystalloids but do restrict negatively charged proteins

93
Q

mechanism of protein transport

A

taken in by pinocytosis, apical vesicles fuse to form vacuoles which then join with lysosomes

94
Q

smaller polypeptides

A

completely filterable, peptidases located on luminal membrane catabolize to amino acids

95
Q

parathyroid hormone

A

produced in parathyroid glands, released by low plasma Ca concentration, increase plasma concentration through bone resorption, active vitamin D, increase Ca reabsorption, increase phosphate excretion

96
Q

calcium components

A

most bound to proteins (albumin)
ionized and active
10% complexed with anions

97
Q

calcium changes with H concentration

A

acidosis increases Ca concentration

alkalosis can cause hypocalcemic tetany

98
Q

calcium in proximal tubule

A

paracellualr and transcellular (Ca ATPase on basolateral side)

99
Q

calcium in thick ascending limb of Henle

A

paracellular, claudin and paracellin contribute to tight junctions to regulate paracellular diffusion

100
Q

calcium in distal tubule

A

transcellular, binds to calbindin and then Na/Ca antiporter of Ca-ATPase basolateral

101
Q

phosphorous

A

mostly unbound and freely filtered, cotransport with Na, basolateral mostly with P-anion antiporter

102
Q

regulation of phosphate balance

A

changes in intake alter number and activity of NPT2 transporters

103
Q

parathyroid hormone and phosphate

A

stimulates removal of NPT2 from brush border membrane of the proximal tubule

104
Q

secretion of organic anions

A

active secretory pathway in proximal tubule, OAT, can be inhibited by probenecid,
can be anti with alpha keto or facilitated diffusion

105
Q

secretion of cations

A

low specificity and maximal transport rate, hydrogen antiporter

106
Q

PAH

A

used to measure effective renal plasma flow, no reabsorption

107
Q

Ppah

A

as P increases teh secretory mechanism becomes saturated and less plasma is cleared of PAH (clearance decreases)

108
Q

high and low Ppah

A

high filtration major begins to approach Cin

low secretion major

109
Q

effective renal plasma flow

A

Cpah

110
Q

actual renal plasma flow

A

RPF=Cpah/Epah (extraction)

111
Q

urate

A

derived from metabolism of ingested and endogenous nucleoproteins
reabsorbed in proximal tubule
secretion in late proximal tubule
secretion in homeostatically regulated

112
Q

hyperuricemia in gout

A

decrease filtration
increase reabsorption
decrease secretion
increased production

113
Q

potassium

A

reabsorbed in proximal tubule, thick ascending, distal convoluted
principal cell when stimulated by aldosterone will secrete K

114
Q

mechanisms of K transport

A

PT-active and passive (mostly passive)

DT-reabsorption and secretion,, determined by gradient between principal cell and tubule fluid

115
Q

flow of tubule fluid

A

fast flow, high gradient leads to K secretion, diuretics high speed increases K secretion, low potassium intake fast flow but no impact on K secretion

116
Q

electrical gradient on K secretion

A

Na reabsorption makes lumen negative

poorly reabsorbed anion promotes K secretion

117
Q

aldosterone

A

stimulates secretion of K and reabsorption of Na by increasing luminal Na and K channels and Na-K-ATPase activity

118
Q

K secretion in alkalosis

A

increased secretion from principal cells

119
Q

acute acidosis

A

decrease K secretion and acute potassium retention

120
Q

chronic acidosis

A

increases flow and results in K depletion

121
Q

weak acids

A

acidosis urine-reabsorbed

alkalosis-excreted (used in aspirin poisoning)

122
Q

weak bases

A

acidosis-excreted

alkalosis-reabsorbed

123
Q

sodium reabsorption

A

most is active and transcellular

water reabsorption from osmolarity differences

124
Q

sodium in proximal tubule

A

greatest sodium, chloride, and water reabsorption

Na with glucose and amino acids, counter with H

125
Q

glomerulotubular balance

A

changes in GFR result in proportional change in filtered load of Na, constant fraction

126
Q

osmotic diuresis

A

increased urine flow that is due to extra amount of non-reabsorbed solute within the tubular lumen
mannitol, diabetes mellitus

127
Q

sodium in loop of henle

A

ascending reabsorbs sodium and chloride

128
Q

Bartter’s syndrome

A

mutations in Na-K-Cl cotransporter

129
Q

sodium in distal convoluted tubule

A

regulated by aldosterone
Na,Cl cotransport
collecting duct-sodium channels

130
Q

Gitelman’s syndrome

A

mutation in Na-Cl cotransporter

131
Q

Liddle syndrome

A

mutation in epithelial sodium channel

132
Q

reabsorption of water

A

collecting duct depends on ADH, V2 adds aquaporins

133
Q

obligatory water loss

A

even if you don’t drink water, you excrete water to get ride of solutes-0.43 L/day

134
Q

countercurrent multiplication

A

medullary interstitial fluid is hyperosmotic

in presence of ADH water diffuses out due to difference in permeability of ascending and descending limb

135
Q

descending limb

A

permeable to water (reabsorbed)

136
Q

ascending limb

A

reabsorbs sodium and chloride

137
Q

result of countercurrrent

A

dilute tubular fluid regardless of final concentration of the urine

138
Q

urea contribution to hyperosmolarity

A

recycled from collecting duct

139
Q

urea handling

A

PT-moves along gradient passively
loop of henle-secreted
DT-low permeability
CD-diffusion with UT-AI (activated by ADH)

140
Q

vasa recta

A

prevents wash out of osmotic gradient, carries the salt and water entering

141
Q

free water clearance

A

generated in the ascending loops of henle
low ADH-hyposmotic urine
high ADH-hyperosmotic urine
used to compare the rate of solute excretion with the rate of water excretion

142
Q

positive free water clearance

A

urine is dilute (no ADH)

143
Q

negative free water clearance

A

urine is concentrated (ADH present)

144
Q

water balance

A

urine is isotonic to plasma C=0

145
Q

Na balance

A

input greater than output is positive

input less than output is negative

146
Q

adjustments to sodium excretion

A

baroreceptors in low pressure decreased GFR and increased sodium reabsorption

147
Q

sweating or diarrhea

A

plasma concentration increases net decrease in GFR

148
Q

increase in sodium intake

A

decreases plasma protein concentration and increases GFR

149
Q

hemorrhage

A

decrease in plasma protein but also decrease in arterial pressure overall decrease in GFR

150
Q

renal interstitial hydrostatic pressure

A

increased pressure leads to decreased water and sodium reabsorption
decreased pressure leads to increased reabsorption

151
Q

sympathetic

A

stimulates renin through B1 receptors, stimulates sodium reabsorption, stimulates constriction that decreases GFR and RBF (RBF more than GFR) further renin secretion

152
Q

angio II

A

increases aldo, decreases renal interstitial pressure, direct on tubular cells

153
Q

pressure natriuresis

A

renal arterial pressure increases, increase sodium and water excretion with little change in GFR

154
Q

ANP

A

increase plasma volume leads to distention of cardiac atria

cGMP inhibits Na luminal channels, decreases renin, decreases angio, increases GFR by dilating mesangial cells

155
Q

baroreceptor control of ADH

A

decrease in volume leads to firing of baroreceptors and secretion of ADH

156
Q

osmoreceptors control of ADH

A

increased osmolarity stimulates ADH secretion, more sensitive

157
Q

extracellular buffers

A

CO2/HCO3

158
Q

concentration of H

A

direct to PCO2, indirect to HCO3

159
Q

other extracellular buffers

A

HPO4 and protein

160
Q

intracellular buffering

A

movement of H through HPO4

161
Q

hyperventilation

A

low PCO2 leads to alkalosis

162
Q

hypoventilation

A

high PCO2 leads to acidosis

163
Q

renal defense to acidosis

A

secretes H
conserve bicarb
excretion of NH4

164
Q

renal defense to alkalosis

A

decrease secretion of H

decrease reabsorption of bicarb

165
Q

causes of metabolic acidosis

A

diabetic ketoacidosis
diarrhea
renal failure

166
Q

anion gap

A

Na+K-Cl-HCO3, noramlly 16, used to identify cause of metabolic acidosis

167
Q

normal anion gap

A

diarrhea and pancreatic juice

168
Q

causes of metabolic alkalosis

A

ingestion of antacids

vomiting

169
Q

causes of respiratory acidosis

A

depression of respiratory centers

pulmonary edema

170
Q

causes of respiratory alkalosis

A

anxiety and fear

171
Q

combined complex

A

compensation for primary acid/base disorder

172
Q

combined simple

A

second acid base disturbance compounding the first acid base disturbance

173
Q

renin

A

produced in liver, secreted by JG cells

174
Q

control of renin secretion

A

decreased blood pressure or extracellular volume by baroreceptor (myogenic), macula densa senses low NaCl delivery, increased sympathetic, AII negative feedback

175
Q

angio II

A

split from Angio I by ace in lung, produced intrarenally

176
Q

control of angio II secretion

A

related to level of renin

177
Q

actions of angio II

A

direct stimulation of Na in PT
stimulates aldo
stimulates ADH
vasoconstriction leading to increase in FF

178
Q

prostaglandins

A

derived from arachidonic acid, PGE2 is major renal, produced in glomerular and vascular endothelium, medullary and cortical collecting tubule cells (main site), renomedullary cells

179
Q

production of prostaglandins

A

vasoactive hormones activate phosphatidylinositol turnover which leads to DAG which leads to arachidonic acid

180
Q

action of prostaglandins

A

minimize ischemia by dilating

181
Q

bradykinin

A

produced within kidney, produced by kallikrein in plasma

182
Q

actions of bradykinin

A

vasodilation and natriuresis/diuresis

183
Q

ADH

A

formed in supraoptic and paraventricular nuclei of hypothalamus, stored in posterior pituitary, rapidly metabolized in liver and kidney

184
Q

release of ADH

A 
increased hyperosmolarity (osmoreceptors)
depletion of circulating volume (baroreceptors)
185
Q

SIADH

A

surgical patients with persistent rise in ADH due to stress/pain, water retention post op

186
Q

diabetes insipidus

A

intense thirst and excretion of large amounts of diluted urine

187
Q

central diabetes insipidus

A

decreased secretion of ADH, administer exogeneous ADH

188
Q

nephrogenic diabetes insipidus

A

decrease ability to concentrate urine due to resistance to ADH

189
Q

actions of ADH

A

V2 increases number of water channels
V1 vasoconstriction to increase TPR
prostaglandins counteract the V2 mechanism

190
Q

aldosterone

A

produced in zona glomerulosa

191
Q

release of aldo

A

regulated by angio II
increased K in plasma
increased ACTH

192
Q

actions of aldo

A

increase Na/K channels and Na/K ATPase on basolateral from principal cells
H secretion from intercalated

193
Q

mineralocorticoid escape

A

rise in ECF which effectively decreases Na reabsorption in proximal tubule

194
Q

ANP

A

from myocytes, particularly right atrium

195
Q

release of ANP

A

increased stretch of atrium

196
Q

actions of ANP

A

relaxation
inhibits Na reabsorption (dopamine necessary)
inhibits ADH
increases FF and GFR
inhbitis aldo, vasopressin and angio II outside of the kidney

197
Q

vitamin D

A

fat soluble, skin, liver and kidney to activate

198
Q

production of vitamin D

A

PTH and hypophosphatemia

199
Q

actions of vitamin D

A

increase calcium and phosphate reabsorption, decrease PTH, increase bone resorption

200
Q

PTH

A

from parathyroid gland

201
Q

release of PTH

A

low plasma Ca concentration

202
Q

actions of PTH

A

bone resorption, promotes vitamin D formation, increases Ca reabsorption, increases phosphate excretion

203
Q

Erythropoietin

A

glycoprotein growth factor, peritubular capillary endothelial cells

204
Q

release of EPO

A

decreased oxygen deliver (anermia, hypoxemia)

205
Q

actions of EPO

A

acts on erythroid precursor cells in bone marrow to increase eryhropoiesis

206
Q

gain of hydrogen

A

generation of H from CO2
production of nonvolatile acids from metabolism of protein
loss of bicarbonate in diarrhea
loss of bicarb in urine

207
Q

loss of hydrogen

A

recombination of H and bicarb
utilization of H
loss in vomit
loss in urine

208
Q

volatile acid

A

carbonic acid because it can be excreted by lungs

209
Q

production of fixed acids

A

oxidation of sulfhydryl groups
hydrolysis of phosphoesters
incomplete breakdown leading to lactic acid and ketone bodies

210
Q

intracellular buffers

A

phosphates and proteins

211
Q

extracellular buffers

A

CO2/HCO3

212
Q

bicarbonate conservation

A

freely filterable, reabsorbed indirectly, carbonic anhydrase in brush border

213
Q

acid excretion

A

secretion of hydrogen ions which combine with non-bicarbonate buffers or catabolism of glutamine excreted as ammonium

214
Q

glutamine-ammonium

A

metabolized in PT secreted into lumen and HCO3 enters blood, secreted in collecting duct by nonionic diffusion and diffusion trapping as well as antiporters

215
Q

hydrogen balance PT

A

reabsorbs bicarb

produce and secrete ammonium

216
Q

hydrogen LOH

A

reabsorbs bicarb

217
Q

DCT and CD

A

reabsorbs bicarb in type A
produces titratable acid type A
secretes bicarb type B

218
Q

NAE

A

net excretion of acid
ammonium+titratable-urinary bicarb
positive gain bicarb
negative loss bicarb

Respiratory and Kidney (2 decks)

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