physiology final Flashcards
(362 cards)
2
Q
What is the job of the kidneys?
A
maintain the constancy of the body’s internal environment
3
Q
How do they accomplish this?
A
By regulating the volume and composition of extracellular fluids
4
Q
What do they use to excrete metabolic end products?
A
Nephrons
5
Q
What else are the kidneys involved with?
A
regulation of the total amount of many important substances in the extracellular matrix.
6
Q
What are the 7 main functions of the kidneys?
A
1- regulation of the concentration of numerous ions. 2- excretion of organic compounds. 3- fluid balance. 4- acid-base balance. 5- blood pressure regulation. 6- erythrocyte volume regulation. 7- Vitamin D activation
7
Q
How do the kidneys accomplish #1? (from previous ?)
A
excretion or preservation of Na, Cl, K, Ca, PO4 - balance their intake, production or excretion through other routes
8
Q
How is #2 accomplished?
A
1) elimination of substances like urea and creatinine in amounts equaling their production rates. 2)elimination of drugs, FO, and toxins
9
Q
3?
A
1)regulate water. 2) regulate osmotic pressure of EC fluids. 3) produce urine
10
Q
4?
A
excretion of H+ or HCO2 as needed
11
Q
5
A
renin-angiotensin system and renal-body fluid balance system
12
Q
6>
A
through formation and release of erythropoetin
13
Q
7?
A
vitamin D hydroxylation to render it useful.
14
Q
How much more salt than water do humans typically consume each day?
A
20-25%
15
Q
How is that excess salt/water disposed of?
A
Urine
16
Q
What sensors determine how much is to be excreted?
A
water volume sensors, salt sensors, osmolality sensors,
17
Q
How do these sensors instruct the kidneys on what to do?
A
via hormones.
18
Q
Where does all the action in the kidney take place?
A
Nephrons
19
Q
What is a nephron encased in?
A
a maze of peritubular capillaries
20
Q
What are the components of a nephron?
A
1) Glomerular capsule, 2) PCT, 3) loop of Henle, 4) DCT, 5) collecting duct
21
Q
What are the components of the vasculature of a nephron?
A
1) intralobular artery. 2) afferent arteriole 3) glomerulus 4) efferent arteriole 5) peritubular capillaries 6) venule and intralobular vein
22
Q
What are the 3 versions of a nephron?
A
1) superficial. 2) mid-cortical. 3) juxtamedullary
23
Q
What 3 activities do kidneys engage in?
A
1) filtration 2) reabsorption 3) secretion
24
Q
Where is the bulk of the work done?
A
in glomeruli and PCTs
25
Q
What remains in the final end of the tubules?
A
urine
26
How does blood enter the kidney and nephron?
through Renal artery
27
What does the blood return to circulation through?
renal vein
28
The nephron is said to "clear" what?
the blood of unwanted substances - removes unwanted agents from the plasma
29
What is clearance?
the amount of plasma cleared of a given substance
30
How can glomerular filtration rate be measured?
by looking at the clearance of something that is freely filtered and not reabsorbed at all.
31
How can you measure cortical perfusion?
by looking at the clearance of something that is secreted from the peritubular capillaries into the nephric tubules
32
What establishes a natural filtration and absorption process?
normal blood pressure and osmotic drives
33
How does blood pressure move water?
creates a hydraulic "push"
34
How does osmotic drive move water?
osmotically active solutions "draw" water toward them.
35
What happens to pressure through the nephron?
steadily falls
36
What are two critical locations for pressure ?
1) Glomerular capillaries. 2) peritubular capillaries
37
What happens in glomerular capillaries?
High BP like arteriole end of a system capillary
38
What happens in the peritubular capillaries?
Low BP like venule end of systemic capillary
39
What do high pressure beds create?
net outward flow (loss)
40
What do low pressure beds create?
net inward flow (gain)
41
What order does fluid flow through PCT and Peritubular cap beds?
PCT first, then into peritubular.
42
How does osmolality and glomerulus set up return of water?
glomerulus loses fluid but keeps cells and proteins, peritubular caps are very osmotically active - draws fluid back from nephric tubules.
43
Does water resorption become easy or difficult?
Increasingly difficult.
44
What is glomerulonephritis?
disorder of renal glomeruli - collection of diseases that effect the glomerular membrane.
45
What is the most common subtype?
inflammatory processes - diffuse proliferative form
46
What is the most common cause?
Post-streptococcal glomerulonephritis
47
What are the clinical features?
Oliguria (decreased urine output. Edema. HTN. Foamy urine. Brown urine
48
Lab findings?
Glomerular caps appear damaged. Hematuria. Proteinuria. Immunofluorescence shows granular deposits.
49
What does chronic form lead to?
renal failure - steady loss of glomeruli
50
What does renal function begin with?
production of glomerular filtrate
51
What is the overall strategy in the urinary system?
filter huge amounts of blood and recover nearly all of the good stuff.
52
How much renal blood flow is there?
1000 - 1200 ml/min to kidneys
53
How much cardiac output does this equal?
20-25%
54
What is this known as?
The renal fraction
55
What is glomerular filtrate?
the amount of plasma "lost" from blood volume when delivered to glomeruli
56
how much is produced from glomeruli filtation?
160 - 180 l/day (2x ones body weight)
57
How much is recovered after glomeruli filtration?
1 -2 l/day leaves as urine. = recovery rate of 99%
58
What type of membrane is on glomeruli?
consists of type 2 capillaries and a visceral bowmans capsule covering of podocytes`
59
describe the permeability of glomeruli capillary beds?
several hundred times more permeable than the typical type 1 kind
60
What does this allow for?
Substantial filtering
61
What determines what passes through?
size, molecular shape and charge.
62
what does the endothelium block?
formed elements fenestrations much smaller than platelets
63
What does the basement membrane block?
proteins negatively charges basement membrane materials repel negatively charged plasma proteins
64
what are slit pores?
space between pedicels that allows the remains to flow through.
65
What is glomerular filtration a function of?
pressure across the glomerular membrane.
66
what is the capillary blood pressure?
60 mmHg = outward force
67
What is the colloidal osmotic pressure?
32 mmHg = inward force
68
What is the capsular pressure of filtrate?
18 mmHg = inward, backward force
69
is capillary force higher or lower than systemic capillary blood pressure?
very high
70
When does colloidal osmotic pressure rise?
as filtration continues
71
What is the net driving force?
adding up forces 60 + (-)32 + (-)18 = 10 mmHg OUT
72
what is total filtration?
NDF x Kf (filtration coefficient) = GFR
73
what is the GFR
glomerular filtration rate
74
What would the GFR be for the above info?
12.5 ml/min/mmHg X 10 mmHg = 125 ml/min
75
What would the GFR be for an entire day?
125 ml/min X 60 min X 24 hr = 180 liters/day
76
What would affect this total?
increased or decreased glomerular pressure.
77
How do fluctuations in BP alter GFR?
They probably don't alter it much. (unless it's an extremely dramatic change)
78
What is the autoregulation range?
when MAP is between 80 and 180 mmHg
79
What kind of innervation is significant to the kidneys?
Sympathetic
80
Is it more extensive to afferent or efferent?
afferent
81
What substances can cause renal arterial vasoconstriction?
Angiotensin 1. vasopressin/ADH, epi, norepi, thromboxane A2, endothelin
82
which cause vasodilation?
Acetylcholine, ANP, dopamine, histamine, nitric oxide, some prostaglandins
83
What does an increase or decrease in plasma colloidal osmotic pressure cause?
in hypoproteinemia it causes edema in systemic capillaries
84
What happens with an increase of decrease in bowmans capsule pressure?
tubule obstructions or severe kidney stones will cause fluid to back up and increase pressure
85
what happens with an increase or decrease in glomerular capillary permeability?
thickening or plugging of membrane pores
86
What happens with an increase or decrease in glomerular capillary total surface area?
glomerular destruction will decrease available membranes for GFR. (seen with nephric disease that remove functional tissue.
87
What is final Glomerular filtrate normally similar to?
Plasma minus its proteins.
88
What is glomerulonephritis?
a disorder of renal glomeruli usually due to inflammatory processes, most commonly as a diffuse proliferative form
89
What does post-streptococcal glomerulonephritis result in?
deposition of circulating immune complexes that further attract neutrophils
90
What happens to the G membrane?
becomes clogged and inflammatory reaction make it worse
91
What are the clinical features?
oligouria due to loss of filtration. Edema and HTN due to fluid accumulation
92
What are the lab findings?
G capillaries appear damaged -> hematuria. Foaming of urine from proteinuria. Thickening of G membrane
93
Is there treatment?
yes. Mild can heal on own. Eliminate HTN. dialysis
94
What is Fanconi's syndrome?
a collection of very uncommon diseases that involve the kidneys
95
What do all forms affect?
The behavior of the nephron, especially PCT
96
What does this result in?
deficient renal tubular excretion
97
What are common sources of this problem?
alteration in transporters. Disturbances in cellular energy metabolism. Changes in permeability
98
Clinical signs?
in children: polydipsia, malnutrition, infection. Adults: pain in weight bearing joints, dehydration
99
Lab findings?
aminoaciduria, cystinuria, glycosuria, phosphaturia. Hypokalemia, metabolic acidosis, hypercalciuria
100
What is the principle activity in the nephric tubules?
recovery of most filtrate.
101
What is the primary function of the rest of the nephron?
reabsorption of glomerular filtrate
102
What are the 4 mechanisms of tubule exchange?
1) some substances actively resorbed. 2) some actively secreted. 3) some passively resorbed 4) some passively secreted
103
What is the flow rate of G filtrate suggestive of?
where most of the work is done.
104
Where is flow rate highest?
PCT
105
2nd highest?
Loop of Henle
106
3rd highest?
DCT
107
4th highest?
collecting duct
108
What does flow rate begin and end at within the PCT?
125 ml/min and falls to 45 ml/min
109
What does flow rate fall to at end of DCT?
15 ml/min
110
What does flow rate fall to at end of CD?
0.7 ml/min
111
How much urine does this work result in each day?
1 l/day. (0.7 X 60 X 24)
112
How much nephric flow takes place in PCT?
2/3 of all flow. (70% of water resorption)
113
What 3 kinds of basic solutes does the kidney process in the tubules?
1) Nutritionally important substances. 2) ions/electrolytes 3) metabolic end-products
114
What does the recovery of specific filtered solutes reveal?
reveals what part of the nephron does what.
115
How are nutritionally important solutes absorbed?
to completion
116
What kind of transport is the basic mechanism of glucose?
secondary active transport
117
What is co-transport of Na+ and GLU made possible by?
Na+/K+ exchange pump (requires ATP)
118
How does GLU moves across the basal side into the ECM?
facilitated diffusion. (with GLUT2 protein)
119
What does GLU transportation require?
Energy
120
What is total GLU absorption a function of?
The number of transporters. (which is a function of surface area)
121
How much is normally absorbed?
All of it. Absorbed to completion
122
What is TMG?
total glucose that can be absorbed... tubular transport max
123
What does this represent?
The number of funtioning nephrons.
124
What is the estimated amount?
350 mg/min
125
What is this AKA?
tubular absorption capacity.
126
What does this mean?
tubules can reabsorb 350 mg of glucose every minutes
127
Where is it done?
PCT
128
What is the renal threshold of glucose?
where glucose might appear in urine
129
How can renal threshold be calculated?
by using TMG (375..round up from 350?). a GFR of 125. and plasma glucose concentration of 100 mg/100ml = (375/1)x(1min/125ml)x(100/100) = 300mg/100ml of plasma.
130
Is this quantity higher or lower than normal plasma glucose levels?
higher.
131
What does that mean?
no glucose should be in the urine.
132
What does this say about the kidneys?
That they are not meant to control the concentration of blood glucose.
133
What happens to the amount of GLU resorbed compared to filtered load?
they match up.... to a point
134
When will excretion happen?
When the TMG is reached.
135
What is the actual renal threshold for glucose?
180 - 200 mg/dl
136
What is this number due to?
splay or bending in the theoretical curve.
137
What does splay represent?
nephron variability
138
What is there a specific transporter for?
each kind of sugar and for each kind of facilitated diffusion on the basal surface
139
Where are larger carbohydrates broken down?
PCT
140
What enzyme does this?
surface amylase. (and maltase)
141
What are they broken down to?
simple sugars
142
How are some large carbohydrates brought across the tubule wall, and what is their fate?
Pinocytosis.. lysosomal destruction
143
How are amino acids moved across?
similar to simple sugars (and glucose). By secondary active transport.
144
Where are larger peptides broken down?
PCT.
145
What breaks them down?
surface peptidases
146
What are they broken down to?
to amino acids.
147
What are all the previous substances considered to be?
nutritionally important.
148
Where have all of the previous substances been reabsorbed, and to what extent?
in the PCT and to completion
149
When do the rest of the tubules become important?
When processing substances that the PCT did not complete
150
What is the average intake of salt per day?
8-15 g/day
151
What is the most common cation of the ECM?
Na+
152
Why are there multiple methods for Na+?
because it is linked to the cotransport of many solutes.
153
Wherre does the Na+/K+ exchange pump move Na+ to?
exterior of the cell on the basal surface.
154
Why does Cl- generally follow Na+?
for electrogenic reasons.
155
How much Na+ and Cl- are resorbed in the PCT?
65 percent
156
Where else, and how much, are they resorbed?
25% in asc. Limb of loop of henle. 5% in DCT. 5% in CD.
157
What does the amount of resorption equal?
the amount of salt intake (until there is excess)
158
How can reabsorption be INDIRECTLY controlled?
by body osmolality
159
What hormone controls this?
aldosterone
160
What does aldosterone work through to achieve this?
BP regulatory scheme.
161
What does increase aldosterone lead to?
increased Na+ resorption
162
What does decreased aldosterone lead to?
decreased Na+ resorption
163
How does aldosterone work?
it works on DCTs by altering the number of Na+/K+ exchange pumps and their activity
164
What kind of regulation is this?
Distal nephron function
165
What else does Na+ (and Cl-) effect?
the macula densa
166
When does it effect the macula densa?
as filtrate passes through the DCT (the densa cells communicate with JG cells)
167
What does increased Na+ do to JG cells?
stimulates them to decrease secretion of renin (and angiotensin) and decrease aldosterone
168
What does decreased Na+ do to JG cells?
stimulates them to increase secretion of renin (and angiotensin) and increase aldosterone
169
What does changing Na+ intake do? (big picture)
alter water retention, lead to changes in BP, and CV changes that will lead to altering Na+ retention
170
What are the kidneys the prime regulators of?
body sodium (and chloride) content
171
What is ANF?
atrial natriuretic factor (or peptide... ANP)
172
What does it do?
its a hormone from the right atrium and has a potent effect on kidneys. Acts as a diuretic.
173
When is it released?
with atrial stretch.
174
What does a release of ANF cause?
increased production of urine and thereby decrease blood volume
175
What else does this hormone cause?
decreased renin release. Decreased aldosterone secretion
176
What is potassium?
a potentially dangerous cation
177
Where is K+ processed?
It is variably processed by nephric tubules.
178
What much match K+ intake?
urinary excretion
179
Where is 98% of K+ found?
inside cells (internal K+ balance)
180
What factors effect K+ balance within cells?
many factors: notably, stimulants and acid/base chemistry of the ECF
181
What factors increase K+ levels in the ECF? And what do they lead to?
hyperosmolarity, cell lysis, exercise, acidosis. They lead to Hyperkalemia
182
What factors decrease K+ levels in the ECF? What does this lead to?
Hypo-osmolarity, insulin, alkalosis. Leads to Hypokalemia
183
What are two kinds of alpha and beta adrenergic agonists?
norepi and epi.
184
How do norepi and epi have variable effects on cells?
they enhance or inhibit the Na+/K+ exchange pump.
185
What do some alpha antagonists cause?
decrease in plasma K+ levels
186
What do some beta antagonists cause?
increase in plasma K+ levels (propanolol)
187
How is processing of K+ accomplished?
By way of active pumps and simple channels.
188
How much resorption of K+ is done in PCT?
70 percent
189
Where else is it resorbed and how much?
20% in loops of henle, and 10% in DCT (and upper CD)
190
What mechanism for K+ resorption is used in PCT?
passive. With NaCl and water
191
Where does the critical action of resorption of K+ take place?
DCT
192
What does the primary mechanism for K+ resorption depend on?
the DCT cell sub-type.
193
What are the two sub-types?
Alpha-intercalated and principle.
194
What determines which sub-type is used?
body needs. And electrochemical gradient that drives K+
195
which sub-type is used with decreased K+ intake?
Resorption = alpha-intercalated cells
196
which sub-type is used with increased K+ intake?
Secretion = principle cells
197
Which is the main action?
principle cells
198
What factors affect the principle cells?
Dietary K+, Aldosterone, Acid-base, flow rate, luminal anions
199
What does this insure?
that K+ levels do not rise too high in the blood
200
What does increase aldosterone cause with K+? and how?
decrease K+. by minimizing secretions in DCT
201
What is the prime regulator of the body's K+ content?
the kidneys, duh
202
How much more H2O does the average human consume than is needed?
20-25%
203
What is the average intake of H2O per day?
2.5 Liters
204
Which is tougher to manage -> H2O disposal, or H2O retentions?
Retention
205
How much H2O is resorbed in the PCT?
70%
206
Where else is H2O resorbed?
15% in loops, 5% in DCT, 10% in CD
207
How does the nephron adjust body water levels?
By producing either a dilute or concentrated urine
208
What kind of urine does excess body water lead to?
dilute urine... increased urine volume
209
What kind of urine does lack of body water lead to?
concentrated urine... decreased urine volume.
210
What is osmolality?
measure of the tendency of a solution to induce osmosis.
211
What is the average body fluid osmolality?
300 mOsm... body/blood osmolality
212
Which portion of the tubules is relatively impermeable to water?
CD
213
What is the average osmolality in the PCT?
300 mOsm
214
What is the average osmolality in the DCT?
100 mOsm
215
What about in the CD?
can fall to 50 mOsm (very dilute, but not 0 because of regular waste)
216
What does this mean?
Whatever is left in the DCT will probably flow out with urine
217
What has to happen to the CDs to maintain renal concentration?
they need to become more permeable to give water a reason to want to leave.
218
Where does the bulk of water recovery happen?
in the PCT and into peritubular capillaries.
219
What do the medullar peritubular capillaries recover?
The resorbed water from the CD
220
How many nephrons are JM?
15%
221
Do animals with high urine concentration ability have more or less JM nephrons?
much higher.... i.e. hopping mouse has 85% JM
222
What is related to renal concentration ability in animals?
loop number and length.
223
What are counter-current systems?
pipes that double back on itself. - they have special properties.
224
What do counter-current systems involve?
allowing a tubule to communicate with itself.
225
How is this communication accomplished?
through the loops of henle!
226
In kidneys, instead of heat (his analogy for CC systems) what is magnified?
osmolality
227
What about loops of henle make this possible? (specific feature)
thick ascending segments and counter-current flow
228
What is possible through the thick ascending loops?
actively pumping NaCl into the interstitium
229
Step 1:
filtrate goes through thick ascending loops and pumps NaCl out to interstitium (CC multiplier)
230
Step 2:
after increase in NaCl , new filtrate enters descending limb - H2O leaves to saline interstitium = further concentrates tubule
231
Step 3:
Subsequent filtrate reach thick asc loops, NaCl pumping out still, Solute REENTERS desc limb = further concentrating it
232
Step 4:
Subsequent filtrate in thin limb has vigorous H2O removal (hypertonicity). = Thin limbs equilibrate with interstitium
233
Step 5
Dilute tubular fluid passes to distal nephron. Exposed to hypertonic medullary interstitium. = Powerful osmotic drive for H2O to leave.
234
Step 6:
ADH present. H2O leaves to interstitium = concentrated urine in tube. Antidiuresis now makes concentrated urine.
235
What determines the degree of hypertonic medullary interstitium (high osmolality)?
the length of the loops
236
What is the saltiest place in the human body?
Medullay pyramids.
237
What important structures insure all of this happens?
The vasculature in the area.
238
What do vasa recta do?
serve to preserve and accentuate the effect. Also recover NaCl from filtrate
240
Step 1:
blood descends in medullary interstitium. H2O leaves and NaCl enters = Increase in osmolality of vasa recta blood.
241
Step 2:
Blood returns from deeper medulla is high concentrated and loses its NaCl to the upper interstitium and H2O enters.
242
What do ascending vasa recta do?
Serve to capture resorbed H2O from CDs
243
Where do they send this?
to the body
244
Why is ADH critical?
changes the permeability of the CDs.
245
What does an increase in ADH cause?
water recovery ? increased urine
246
What does decreased ADH cause?
water loss ? decreased urine
247
Where is ADH synthesized?
in neuro-secretory cells of the paraventricular nuclei and supraoptic nuclei of the hypothalamus
248
Where do they project axons to?
posterior pituitary
249
Where does ADH land on the kidneys?
receptors (V2) of the CD
250
What does this cause?
insertion of reserve pools of cytoplasmic aquaporin-2 proteins.
251
What is increased when this happens?
increases permeability of these cells. Also increases synthesis of aquaporins
252
What do the membranes of epithelial cells lack in tubules that are relatively impermeable to water?
aquaporins.
253
What is diabetes insipidus?
failure of ADH
254
What does it cause?
excessive excretion of large amounts of dilute urine. Excessive thirst.
255
What are the causes of diabetes insipidus?
insufficient secretion of ADH, inheritance of mutated gene for ADH V2 r/c, inheritance of mutated gene for aquaporin-2
256
How much filtrate could be lost each day with DI?
20 liters
257
What is pyelonephritis?
an infection of the kidneys; more common in adult females.
258
What causes pyelonephritis?
bacteria condition of the renal medullary pyramids originating from reflux in urine from bladder.
259
What are the acute symptoms of pyelonephritis?
fever. Burning urine. Aching ab pain.
260
What kind of urine do you find in pyelonephritis?
dilute urine...
261
Why?
Invasion of bacteria in the medullary pyramids lessen their ability to produce hypertonic osmolality.
262
What is urine concentration and diuresis determined by?
changes in body chemistry
263
What is water diuresis?
common experience involving increased urine output due to water causing the posterior pituitary to lessen the amount of secreted ADH.
264
What is water intoxication?
When water intake exceeds the bodies ability to expel it
265
What is the normal max diuresis?
About 16 ml/min.
266
What is considered too much intake of water?
when intake exceeds a sustained rate of 1 l/hour.
267
What can happen at this point?
brain edema ? convulsions, death
268
What kind of urine is produced with diabetes mellitus?
sweet urine!
269
Why is it sweet?
because the Tmg of the PCTs is exceeded.
270
How much urine is produced in diabetes mellitus?
a large amount due to osmotic load on the nephrons. (known as osmotic diuresis)
271
What is hydrogen disposed as?
as an acid
272
What 3 mechanisms manage hydrogen concentration?
Blood plasma buffers. Respiratory ventilation. Renal excretion of an acid or alkaline urine.
273
How does blood plasma buffers manage H concentration?
rapidly- taking seconds to accomplish , with minimal gain due to temporary binding of hydrogen
274
How does respiratory ventilation manage [H]?
Slower taking minutes to an hour with higher gain due to change in plasma chemistry (as HCO3)
275
How does renal excretion of an acid or alkaline urine manage [H]?
slow, taking hours to days with the highest gain since it results in true elimination from body.
276
How do the kidneys regulate [H+]?
by increasing or decreasing [HCO3]
277
Where is filtered bicarbonate primarily resorbed?
in the PCT
278
Where is resorption of bicarbonate finished?
in the distal nephron
279
Where is the final acidity completed?
in the distal tubules. Therefore it is the most important determinant in the final pH of the urine.
280
What actively secretes H+?
the nephron
281
How is H+ ultimately lost?
as H2O in urine
282
Is urine normal acidic or basic? And why?
slightly acidic because all the HCO3- is resorbed, leaving the urine with a lower pH
283
What is the normal pH of urine?
6.5 - 7 can vary
284
What is the range of pH urine could be within?
4.5 - 8.5
285
Why won't it fall below 4.5?
That is the level when active secretion is exceeded.
286
What are acids and acidifying salts as diuretics?
some of these supply nephrons with a filtered acid load that counteracts the ability to secrete H+
287
What does this lead to?
ability to exchange Na+ is somewhat compromised (also, with increased Na+ comes increased H2O loss)
288
What is acidosis?
increase in H+ (decreased pH)
289
What does this cause?
as H+ rises it exceeds available HCO3- to titrate against ? acid urine
290
What is alkalosis?
increasesd HCO3-
291
What does it lead to?
as HCO3- rises it exceeds available H+ secretions ? alkaline urine
292
What 2 chemical systems handle the buffering of H+ in distal nephron?
phosphate buffer. Ammonium buffer.
293
What is the phosphate buffer?
HPO4-2 + H+ ? H2PO4-
294
What is the ammonium buffer?
NH3 + H+ ? NH4+
295
Where is ammonia produced?
from glutamine in the nephron
296
Why does urine sometimes smell like ammonia?
ammonia ion being converted back to ammonia when exposed to air (has to sit in open air for a long time)
297
What is urea?
a common waste molecule from the end-stage of protein catabolism.
298
Why does urea use the aquaporin channel?
To diffuse in the collecting ducts.
299
How quickly does urea move through the tubule cells?
much slower than water.... so it tends to just pass out with urine.
300
What is BUN?
Blood-urea-nitrogen. Measure of urea in blood. (higher than normal shows abnormal renal function)
301
Where is calcium found?
extracellular
302
Where is phosphate found?
intracellular fluid
303
How is calcium balanced?
With net loss from body.
304
What normally regulates calcium?
parathormone in the parathyroid gland.
305
What does calcitonin make the kidneys do?
excrete Ca2+
306
What do the kidneys have a natural tendency to do with calcium and phosphate?
keep (reabsorb) PO4-2 and excrete Ca+2
307
What is this modified by?
parathormone in the parathyroid gland.
308
What does regular PTH secretion lead to?
kidney keeps Ca2+ and lets PO4-2 go
309
What is the net effect of this?
increase serum Ca2+
310
What do all forms of Fanconi's syndrome affect?
the normal behavior of the nephron
311
Which portion of the nephron is mostly affected?
PCT
312
What do the diseases that produce this result in?
abnormal renal tubular excretion (as electrolytes and nutrients spill into the urine)
313
What are the clinical signs and symptoms of Fanconis in children?
children: polydipsia, malnutrition, susceptibility to infection.
314
What are the clinical signs and symptoms of Fanconis in adults?
pain on weight-bearing joints, dehydration, polyuria.
315
If left untreated what might this lead to?
Muscle-wasting and death
316
What does pyelonephritis do to the medulla?
fould the ability of the ascending loops to do their job.
317
What is the result?
failure of the renal concentration mechanism. ? large volume dilute urine.
318
What does hemostatic maintenance of the ICF involve?
stabilized with appropriate nutrient delivery, waste removal, and ionic/osmotic balance.
319
What surrounds this compartment?
ECM, which also has to be maintained.
320
What maintains the ECF?
The blood
321
What is the average percent of body fluid in adults?
60%
322
What is it in infants?
80%
323
What about in the elderly?
40-50%
324
Which compartment decreases with age?
interstitial compartment
325
Which compartments remain fairly stable throughout life?
Plasma, and intercellular compartments.
326
Why do women have less water than males in their body?
Because they have more fat which is low in water.
327
Where does our water intake come from? And how much from each?
Drink = 50%, food = 35%, oxidation = 15%
328
How does water exit our body? And how much from each?
Urine = 60%, sweat & ventilation = 35%, stool/feces = 5%
329
What do the kidneys do in response to diarrhea?
conserve fluid as to balance the body.
330
what kind of urine would the distilled water group produce?
large volume dilute
331
What kind of urine would the isotonic solution group produce?
balanced isotonic urine
332
What kind of urine would the 10% salt water group produce?
decreased volume, concentrated urine.
333
What does the body do when the osmolality of blood rises or falls?
manages concentrations of salt and water to correct the change
334
What hemostatic mechanisms are activated when osmolality of blood rises?
Secretion of ADH. Thirst. Lesser players
335
What are the lesser players?
decrease renin ? decrease aldosterone ? decrease Na+ reabsorption; and decrease ANF ? decrease renal flow.
336
How is ADH released?
neurons from the supra optic nuclei emanate from hypothalamus to post. Pituitary
337
What are these neuronal cell bodies sensitive to?
osmolality of blood.
338
What happens to these neurons when osmolality of blood rises?
secrete ADH. ADH enters blood. Goes to renal CDs. Lands on V2 r/c. Cells add aquaporin. ? promotes H2O reabsorption into vasa recta.
339
What happens to the osmolality of urine when the above takes place?
it goes up.
340
what happens to the osmolality of the blood at this point?
Returns to normal.
341
What else do these neurons stimulate?
the thirst center
342
What is the blood volume and systemic BP like when osmolality of blood is rising?
both are low.
343
THUS ?
increase osmolality ? increase ADH secretion ? water retention (anti-diuresis)
344
the opposite is also true ?
decrease osmolality ? decrease ADH ? water loss (diuresis)
345
What can a water deficit be caused by?
excessive sweating or osmotic diuresis.
346
What might this result in?
fluid shifting from intracellular to extracellular compartment
347
What can water excess be caused by?
Excessive drinking, excessive ADH
348
What might this result in?
fluid shifting from extracellular to intracellular compartment.
349
What homeostatic mechanisms are activated when blood volume falls?
secrete ADH, secrete renin angiotensin and aldosterone, decrease ANF ? decrease renal flow.
350
What else will a fall in blood volume cause?
fall in BP
351
What 2 things will a rise in renin cause?
increase angiotensin 1&2 ? systemic constriction ? increase BP. AND increase aldosterone ? increae Na+ reabsorption in distal nephron ? decrease fluid loss
352
THUS ?
decrease blood volume ? increase renin/angiotensin & aldosterone ? increae BP and decrease water loss
353
Salt deficit from vomiting, diarrhea, excessive sweating results in what?
fluid shifting from extracellular to intracellular compartment.
354
Salt excess from excessive intake can result in?
fluid shifting from intracellular to extracellular compartment
355
What is incontinence?
The failure to store urine when desired
356
What is incontinence a disorder of?
involving a lack of control of the urinary bladder
357
When does renal function end?
when there is an accumulation of urine in the bladder. (after having left the renal calyces, pelvis, and ureters.
358
What kind of reflex is micturation?
autonomic spinal cord reflex though it can be inhibited.
359
What happens to pressure as urine accumulates in the bladder?
internal pressure rises
360
When do ramp signals begin in the bladder?
When fluid reaches 30-50 ml. - rises rapidly when over 300-400 ml
361
When does active signaling begin?
100 ml, but very strong by 300 ml
362
What is the secondary nerve associated with micturation?
pudendal n
363
What does the pudendal do during micturation?
inhibits internal urethral sphincter.
364
What neurophysiological or anatomical factors can cause incontinence?
destruction of sensory fibers to CNS. Crush injury to sacral region of spinal cord. Injury to region above sacral region.
