Renal Flashcards
1
Q
total body water
A
45% and 75% of body weight
2
Q
variations in TBW
A
inverse with age
inverse with fat
lower in females
3
Q
lean body mass
A
body weight exclusive of storage fat
4
Q
compartments of total body water
A
plasma, interstitial, intracellular
5
Q
extracellular fluid
A
plasma and ISF, separated by capillaries
1/3 of total, plasma 1/4, ISF 3/4
6
Q
intracellular fluid
A
2/3 of TBW
7
Q
transcellular fluid compartment
A
fluid in transit in lumina of epithelial organs, cerebrospinal fluid, intraocular fluid
8
Q
organs that communicate with external environment and ECF
A
alimentary canal
lungs
kidneys
skin
9
Q
major ECF ions
A
Na and Cl
10
Q
major ICF ion
A
K due to Na/K ATPase
11
Q
protein concentration
A
highest in plasma because capillaries are not permeable to proteins
12
Q
pH of ECF and ICF
A
ECF=7.4
ICF=7.1
13
Q
dilution methods for determining distribution
A
C=Q/V
characteristics-nontoxic, neither synthesized nor metabolized, does not cause shifts in fluid distribution
14
Q
measuring plasma volume
A
serum albumin with radioactive iodine
15
Q
measuring extracellular fluid volume
A
inulin, some lost in urine
16
Q
measuring total body water
A
antipyrine or deuterated water or tritated water
lost by all routes
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
18
Q
isosmotic water shifts
A
change in ECF only
increase in saline infusion
decrease with hemorrhage
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
20
Q
symptoms of hyperosmolarity
A
early-lethargy
progresses to twitching, seizures, coma, and death
could result in cerebral hemorrhages
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
22
Q
symptoms of hyposmolarity
A
serizures, coma
premenopausal women do not fully recover
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
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
25
renal corpuscle contents
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)
26
layers of of glomerular membranes
endothelium-fenestrated capillary
basement membrane-barrier to large proteins and lipids
epithelium-podocytes, forms filtration slits bridged by pores
27
tubule
epithelial cells with tight junctions
28
proximal tubule
site of reabsorption, distinguished by large surfae area (apical brush border of microvili, basolateral infoldings and interdigitation)
mitochondria line basolateral membrane
29
Henle's loop
countercurrent direction of flow, influence electrolyte and water transport
30
distal tubule
returns to cortex and makes contact with afferent and efferent arterioles of the parent renal corpuscle, site of JGA
31
JGA cell types
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
32
collecting tubule
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
33
cell types of collecting duct
principal-ADH, ANP, aldosterone
alpha intercalated-secretes H
beta intercalated-secretes HCO3
34
cortical nephrons
no thin ascending loop of Henle
| short loops
35
juxtamedullary nephrons
thin segment may reach tip of papillae
larger glomeruli
concentrated urine
36
nerve supply to kidney
sympathetic only, vasoconstriction of arterioles, basement membrane of PT, loop of Henle, DT, CD which enhances sodium reabsorption
37
lymphatic network
only in cortex
38
blood supply to kidney
interlobar, arciform, interlobular, afferent, capillary, efferent, peritubular capillaries or vasa recta, interlobular veins
39
glomerular filtration
protein-free plasma from glomerular capillaries into Bowman's capsule, no active transport, physically sieving blood
40
tubular secretion
transfer of materials from peritubular capillary plasma to the tubular lumen
41
tubular reabsorption
transfer of materials from lumen of tubule to peritubular capillary plasma
42
blood flow to kidneys
renal blood flow is 20% of CO
renal plasma flow subtracts hematocrit
GFR is 125
43
filtration fraction
GFR/RPF
| normally 20%
44
colloid osmotic pressure
increases during the trip from afferent to efferent arteriole, blood leaving will not have highest colloid osmotic pressure of any blood in the kidney
45
GFR calculation
Kf (Pc-Pb-oncotic c)
46
Kf changes physiologically
ADH causes decrease in Kf and decrease in GFR
angiotensinogen decreases Kf
ANP increases Kf and GFR
47
pathologic changes to Kf
thickening due to autoimmune diseases
| destruction of glomerular capillaries decreases SA
48
glomerular capillary pressure
determined by relative resistance of afferent and efferent arterioles, determined by hormones and neural input
49
changing afferent arteriole resistance
vasodilation increases flow and increases GFR
| vasoconstriction decreases flow and decreases GFR
50
changing efferent arteriole resistance
vasodilation increases blood flow but decreases GFR and filtration
vasoconstriction decreases blood flow and increases GFR and filtration fraction
51
changing afferent and efferent
constricting both will inhibit renal blood flow but increase GFR and FF
52
hydrostatic pressure in Bowman
required to drive flow of urine, high pressure causes decrease in GFR (diuretics, prostatic hypertrophy, tumors, kidney stones)
53
autoregulation of glomerular filtration rate
80-180 mmHg both GFR and RBF remain constant, myogenic and tubuloglomerular feedback mechanisms
54
myogenic mechanism
change in pressure in arterioles stretch leads to contraction
55
tubuloglomerular feedback
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
56
measurement of glomerular filtration rate
measured by chemical that is not bound to plasma proteins or electrically charged
inulin-all filtered is excreted
57
GFR and clearance
UV/P=clearance
58
renal clearance
volume of plasma from which all of a substance has been removed and excreted into uring per unit of time
59
inulin clearance
independent of plasma inulin concentration and urine flow (U/P remains constant)
60
endogenous substance to approximate GFR
creatine, small amount of secretion
61
significance of inulin clearance
maximal volume of plasma that can be cleared of a substance exclusively by filtration into the nephron per minute
62
changes in clearance relative to inulin
above inulin means something has been secreted
| below inulin means something has been reabsorbed
63
single ratio
TF/P concentration in tubular fluid over plasma of inulin
64
water content from inulin
only water is changed, 1-(1/ratio) for amount of water reabsorbed
65
fractional excretion
mass excreted/mass filtered
used to calculate reabsorption or secretion
double ratio when compared to inulin
66
double ratio
greater than 1 is secreted
| less than 1 is reabsorbed
67
diffusion
requires electrochemical gradient, downhill transport
68
facilitated diffusion
requires electrochemical gradient and carriers
| exhibits specificity, saturability, and competition, downhill transport
69
primary active transport
requires carriers
exhibits specificity, saturability, and competition
uphill transport, requires energy
70
secondary active transport
requires carriers
exhibits specificity, satruability, and competition
one uphill another downhill
cotransport or countertransport
71
paracellular
diffusion between cells
72
transcellular
across the cell
73
glucose in proximal tubule
apical with Na, basolateral facilitated diffusion
| requires gradient established by Na/K ATPase
74
transport maximum
limit to amounts of material the active transport system can transport per unit of time, saturation of carriers
75
threshold
plasma concentration at which glucose first appears in the urine
76
splay
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
77
glucose clearance
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
78
excretion of glucose
direct proportion to amount filtered minus level of reabsorption
79
high concentrations of glucose
approaches the clearance of inulin
80
glucose reabsorption mechanism
increase plasma glucose blocks reabsorption of xylose because affinity for glucose>xylose
81
renal glycosuria
glucose in urine as a result of defective missing transport mechanism
82
diabetes mellitus
glucosuria due to the lack of insulin
83
pregnancy
increase GFR leads to glucose in urine
84
reabsorption of amino acids
Clearance=0
reabsorbed and exhibit considerable splay
kidneys do not regulate plasma concentrations
85
reabsorption of organic nutrients
filtered and reabsorbed in proximal tubule
86
citrate reabsorption
normal in urine
| complexes with Ca
87
alpha ketoglutarate reabsorption
active reabsorption, does not regulate alpha keto
88
beta ketoglutarate reabsorption
regulated by kidneys, excretion high in uncontrolled diabetes mellitus and starvation
89
vitamin C
active reabsorption, marked splay
90
low filtration of proteins
filtration low due to steric hindrance, viscous drag, and electrical hindrance
91
viscous drag
lining of pore retards forward movement of protein
92
electrical hindrance
charges on glomerular membranes are negative, dont restrict crystalloids but do restrict negatively charged proteins
93
mechanism of protein transport
taken in by pinocytosis, apical vesicles fuse to form vacuoles which then join with lysosomes
94
smaller polypeptides
completely filterable, peptidases located on luminal membrane catabolize to amino acids
95
parathyroid hormone
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
calcium components
most bound to proteins (albumin)
ionized and active
10% complexed with anions
97
calcium changes with H concentration
acidosis increases Ca concentration
| alkalosis can cause hypocalcemic tetany
98
calcium in proximal tubule
paracellualr and transcellular (Ca ATPase on basolateral side)
99
calcium in thick ascending limb of Henle
paracellular, claudin and paracellin contribute to tight junctions to regulate paracellular diffusion
100
calcium in distal tubule
transcellular, binds to calbindin and then Na/Ca antiporter of Ca-ATPase basolateral
101
phosphorous
mostly unbound and freely filtered, cotransport with Na, basolateral mostly with P-anion antiporter
102
regulation of phosphate balance
changes in intake alter number and activity of NPT2 transporters
103
parathyroid hormone and phosphate
stimulates removal of NPT2 from brush border membrane of the proximal tubule
104
secretion of organic anions
active secretory pathway in proximal tubule, OAT, can be inhibited by probenecid,
can be anti with alpha keto or facilitated diffusion
105
secretion of cations
low specificity and maximal transport rate, hydrogen antiporter
106
PAH
used to measure effective renal plasma flow, no reabsorption
107
Ppah
as P increases teh secretory mechanism becomes saturated and less plasma is cleared of PAH (clearance decreases)
108
high and low Ppah
high filtration major begins to approach Cin
| low secretion major
109
effective renal plasma flow
Cpah
110
actual renal plasma flow
RPF=Cpah/Epah (extraction)
111
urate
derived from metabolism of ingested and endogenous nucleoproteins
reabsorbed in proximal tubule
secretion in late proximal tubule
secretion in homeostatically regulated
112
hyperuricemia in gout
decrease filtration
increase reabsorption
decrease secretion
increased production
113
potassium
reabsorbed in proximal tubule, thick ascending, distal convoluted
principal cell when stimulated by aldosterone will secrete K
114
mechanisms of K transport
PT-active and passive (mostly passive)
| DT-reabsorption and secretion,, determined by gradient between principal cell and tubule fluid
115
flow of tubule fluid
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
electrical gradient on K secretion
Na reabsorption makes lumen negative
| poorly reabsorbed anion promotes K secretion
117
aldosterone
stimulates secretion of K and reabsorption of Na by increasing luminal Na and K channels and Na-K-ATPase activity
118
K secretion in alkalosis
increased secretion from principal cells
119
acute acidosis
decrease K secretion and acute potassium retention
120
chronic acidosis
increases flow and results in K depletion
121
weak acids
acidosis urine-reabsorbed
| alkalosis-excreted (used in aspirin poisoning)
122
weak bases
acidosis-excreted
| alkalosis-reabsorbed
123
sodium reabsorption
most is active and transcellular
| water reabsorption from osmolarity differences
124
sodium in proximal tubule
greatest sodium, chloride, and water reabsorption
| Na with glucose and amino acids, counter with H
125
glomerulotubular balance
changes in GFR result in proportional change in filtered load of Na, constant fraction
126
osmotic diuresis
increased urine flow that is due to extra amount of non-reabsorbed solute within the tubular lumen
mannitol, diabetes mellitus
127
sodium in loop of henle
ascending reabsorbs sodium and chloride
128
Bartter's syndrome
mutations in Na-K-Cl cotransporter
129
sodium in distal convoluted tubule
regulated by aldosterone
Na,Cl cotransport
collecting duct-sodium channels
130
Gitelman's syndrome
mutation in Na-Cl cotransporter
131
Liddle syndrome
mutation in epithelial sodium channel
132
reabsorption of water
collecting duct depends on ADH, V2 adds aquaporins
133
obligatory water loss
even if you don't drink water, you excrete water to get ride of solutes-0.43 L/day
134
countercurrent multiplication
medullary interstitial fluid is hyperosmotic
| in presence of ADH water diffuses out due to difference in permeability of ascending and descending limb
135
descending limb
permeable to water (reabsorbed)
136
ascending limb
reabsorbs sodium and chloride
137
result of countercurrrent
dilute tubular fluid regardless of final concentration of the urine
138
urea contribution to hyperosmolarity
recycled from collecting duct
139
urea handling
PT-moves along gradient passively
loop of henle-secreted
DT-low permeability
CD-diffusion with UT-AI (activated by ADH)
140
vasa recta
prevents wash out of osmotic gradient, carries the salt and water entering
141
free water clearance
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
positive free water clearance
urine is dilute (no ADH)
143
negative free water clearance
urine is concentrated (ADH present)
144
water balance
urine is isotonic to plasma C=0
145
Na balance
input greater than output is positive
| input less than output is negative
146
adjustments to sodium excretion
baroreceptors in low pressure decreased GFR and increased sodium reabsorption
147
sweating or diarrhea
plasma concentration increases net decrease in GFR
148
increase in sodium intake
decreases plasma protein concentration and increases GFR
149
hemorrhage
decrease in plasma protein but also decrease in arterial pressure overall decrease in GFR
150
renal interstitial hydrostatic pressure
increased pressure leads to decreased water and sodium reabsorption
decreased pressure leads to increased reabsorption
151
sympathetic
stimulates renin through B1 receptors, stimulates sodium reabsorption, stimulates constriction that decreases GFR and RBF (RBF more than GFR) further renin secretion
152
angio II
increases aldo, decreases renal interstitial pressure, direct on tubular cells
153
pressure natriuresis
renal arterial pressure increases, increase sodium and water excretion with little change in GFR
154
ANP
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
baroreceptor control of ADH
decrease in volume leads to firing of baroreceptors and secretion of ADH
156
osmoreceptors control of ADH
increased osmolarity stimulates ADH secretion, more sensitive
157
extracellular buffers
CO2/HCO3
158
concentration of H
direct to PCO2, indirect to HCO3
159
other extracellular buffers
HPO4 and protein
160
intracellular buffering
movement of H through HPO4
161
hyperventilation
low PCO2 leads to alkalosis
162
hypoventilation
high PCO2 leads to acidosis
163
renal defense to acidosis
secretes H
conserve bicarb
excretion of NH4
164
renal defense to alkalosis
decrease secretion of H
| decrease reabsorption of bicarb
165
causes of metabolic acidosis
diabetic ketoacidosis
diarrhea
renal failure
166
anion gap
Na+K-Cl-HCO3, noramlly 16, used to identify cause of metabolic acidosis
167
normal anion gap
diarrhea and pancreatic juice
168
causes of metabolic alkalosis
ingestion of antacids
| vomiting
169
causes of respiratory acidosis
depression of respiratory centers
| pulmonary edema
170
causes of respiratory alkalosis
anxiety and fear
171
combined complex
compensation for primary acid/base disorder
172
combined simple
second acid base disturbance compounding the first acid base disturbance
173
renin
produced in liver, secreted by JG cells
174
control of renin secretion
decreased blood pressure or extracellular volume by baroreceptor (myogenic), macula densa senses low NaCl delivery, increased sympathetic, AII negative feedback
175
angio II
split from Angio I by ace in lung, produced intrarenally
176
control of angio II secretion
related to level of renin
177
actions of angio II
direct stimulation of Na in PT
stimulates aldo
stimulates ADH
vasoconstriction leading to increase in FF
178
prostaglandins
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
production of prostaglandins
vasoactive hormones activate phosphatidylinositol turnover which leads to DAG which leads to arachidonic acid
180
action of prostaglandins
minimize ischemia by dilating
181
bradykinin
produced within kidney, produced by kallikrein in plasma
182
actions of bradykinin
vasodilation and natriuresis/diuresis
183
ADH
formed in supraoptic and paraventricular nuclei of hypothalamus, stored in posterior pituitary, rapidly metabolized in liver and kidney
184
release of ADH
```
increased hyperosmolarity (osmoreceptors)
depletion of circulating volume (baroreceptors)
```
185
SIADH
surgical patients with persistent rise in ADH due to stress/pain, water retention post op
186
diabetes insipidus
intense thirst and excretion of large amounts of diluted urine
187
central diabetes insipidus
decreased secretion of ADH, administer exogeneous ADH
188
nephrogenic diabetes insipidus
decrease ability to concentrate urine due to resistance to ADH
189
actions of ADH
V2 increases number of water channels
V1 vasoconstriction to increase TPR
prostaglandins counteract the V2 mechanism
190
aldosterone
produced in zona glomerulosa
191
release of aldo
regulated by angio II
increased K in plasma
increased ACTH
192
actions of aldo
increase Na/K channels and Na/K ATPase on basolateral from principal cells
H secretion from intercalated
193
mineralocorticoid escape
rise in ECF which effectively decreases Na reabsorption in proximal tubule
194
ANP
from myocytes, particularly right atrium
195
release of ANP
increased stretch of atrium
196
actions of ANP
relaxation
inhibits Na reabsorption (dopamine necessary)
inhibits ADH
increases FF and GFR
inhbitis aldo, vasopressin and angio II outside of the kidney
197
vitamin D
fat soluble, skin, liver and kidney to activate
198
production of vitamin D
PTH and hypophosphatemia
199
actions of vitamin D
increase calcium and phosphate reabsorption, decrease PTH, increase bone resorption
200
PTH
from parathyroid gland
201
release of PTH
low plasma Ca concentration
202
actions of PTH
bone resorption, promotes vitamin D formation, increases Ca reabsorption, increases phosphate excretion
203
Erythropoietin
glycoprotein growth factor, peritubular capillary endothelial cells
204
release of EPO
decreased oxygen deliver (anermia, hypoxemia)
205
actions of EPO
acts on erythroid precursor cells in bone marrow to increase eryhropoiesis
206
gain of hydrogen
generation of H from CO2
production of nonvolatile acids from metabolism of protein
loss of bicarbonate in diarrhea
loss of bicarb in urine
207
loss of hydrogen
recombination of H and bicarb
utilization of H
loss in vomit
loss in urine
208
volatile acid
carbonic acid because it can be excreted by lungs
209
production of fixed acids
oxidation of sulfhydryl groups
hydrolysis of phosphoesters
incomplete breakdown leading to lactic acid and ketone bodies
210
intracellular buffers
phosphates and proteins
211
extracellular buffers
CO2/HCO3
212
bicarbonate conservation
freely filterable, reabsorbed indirectly, carbonic anhydrase in brush border
213
acid excretion
secretion of hydrogen ions which combine with non-bicarbonate buffers or catabolism of glutamine excreted as ammonium
214
glutamine-ammonium
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
hydrogen balance PT
reabsorbs bicarb
| produce and secrete ammonium
216
hydrogen LOH
reabsorbs bicarb
217
DCT and CD
reabsorbs bicarb in type A
produces titratable acid type A
secretes bicarb type B
218
NAE
net excretion of acid
ammonium+titratable-urinary bicarb
positive gain bicarb
negative loss bicarb
