Renal-Chapter 29 Flashcards
What are the ranges of urine osmolarity in cats and dogs?
Dog: 50-2400 mOsm/L
Cat:50-3300 mOsm/L
An increase in ADH would have what effect on urine?
More concentrated urine
A decrease in ADH would have what effect on urine?
More dilute urine
Give renal mechanism for excreting dilute urine (normal conditions)
-Does body excrete xs amount of solutes?
After water ingestion, 30 min later, it gets absorbed.
Urine flow rate increase
Urine osmolarity decrease
Excretion of a large volume of dilute urine
Total amount of solute excreted and plasma osmolarity remain relatively constant. Body does not excrete xs amount of solutes.
Give renal mechanism of dilute urine excretion when ADH levels are very low
-What parts are sensitive to ADH?
Tubular fluid remains isosmotic in PT
Descending LOH tubular fluid becomes more concentrated as it flows into the inner medulla
Ascending LOH tubular fluid is diluted (regardless if ADH is present or not)
Tubular fluid in DT and CT is further diluted in the absence of ADH
CT are sensitive to ADH
ALOH is not sensitive to ADH
In general, how do kidneys conserve water if there is water deficit?
Excrete concentrated urine
Excrete solute and reabsorb water
Which species would have higher urine osmolarity threshold? Beavers or desert species. Why?
Desert species=10,000 mOsmoles/L
Beaver- 500 mOsmoles/L
Desert species have a higher urine concentrating capacity and more juxtamedullulary nephrons to converse water in drier environment.
How much concentrated urine must a human excrete a day?
-What does excretion consist of?
600 mOsm
- Waste products of metabolism
- Ingested solutes
What is formula for obligatory urine volume?
Mandatory concentrated urine to be excreted/Maximum urine concentrating ability
The higher the concentrating ability, obligatory urine volume is
Higher or lower?
Lower`
If you drank 1 L sea water of 1200 mOsm/L how would you compensate for that?
Automatically have to get rid of 600 mOsm/L but you’ve ingested 1200 mOsm of NaCl water.
600+1200= 1800 mOsmol to get rid of
1800/1200 (max urine concentration ability)
You’ve have to drink 1.5 L of water to compensate dehydration.
What does urine specific gravity measure?
estimates urine solute concentration ability
How is urine specific gravity different from osmolarity?
Specific gravity takes into account the number and SIZE of the solute molecules.
What can alter urine specific gravity?
Large molecules like glucose and AB can give false results suggesting that the urine is very concentrated
What are normal values of urine specific gravity for humans, dogs, cats
Humans: 1.002-1.028
Dog:1.001-1.070
Cat:1.001-1.080
Requirements for excreting concentrated urine
High level of ADH
High osmolarity of the medullary interstitium
Why does there need to be a high level of ADH for excreting concentrated urine?
ADH causes water reabsorption at a greater rate than solute reabsorption thus creating concentrated urine
Why is a high osmolarity of medullary interstitium necessary for excreting concentrated urine?
Interstitium osmolarity of cortex=300 mOsm/L
medulla=1200-1400 mOsm/L (more concentrated)
Osmotic gradient necessry for water reabsorption…
Use countercurrent mechanism
T/F Concentrated urine depends on the anatomical arrangement of LOH
True
T/F Collecting ducts move through medulla and contain filtrate from single nephron
Contains filtrate from multiple nephrons
Thin descending LOH
- Does it have active transport of Na+
- Is it permeable to water, NaCl, and Urea
- No active transport
- Permeable to water, NaCl, urea (everything is normally passive
Thin ascending LOH
- Is there an active transport for NaCl
- Is it permeable to water, NaCl, urea?
- No active transport to NaCl
- Impermeable to water
- Permeable to NaCl and urea
Thick ascending LOH
- Does it have active NaCl transport***
- Is it permeable to water and urea?
- Has active NaCl transport capable of establishing a 200 mOsm/L concentration grandient
- Impermeable to water and urea
Explain how the countercurrent multiplier system in LOH produces hyperosmotic renal medulla
As fluid moves through the loop, Na and Cl is pumped out of the ascending limb raising interstitial fluid osmolarity UP TO 200 mOsm/L GRADIENT.
Water then moves from descending LOH by osmosis and concentrates filtrate.
This repeats until ma is reached (~1200 mOsm/L) at deepest medullary point.
When do cortical collecting ducts become high permeable to water?
After passage through LOH
and HIGH ADH levels
Explain role of collecting ducts in excreting concentrated urine
Water is reasborbed into cortical interstitium and carried away by peritubular capillaries
Most of water reabsorbed in corte helps preserce medullary interstitial osmolarity
Further water reabsorption in medulla but small compared to cortex.
T/F Urea contributes to the hyperosmotic renal medullary interstitium. If so when?
T
About 40 percent (500 mOsm/L)
When kidney forms maximum concentrated urine
How is urea reabsorbed in MCD?
Stimulation of ADH
Urea will be passively reabsorbed by facilitated diffusion through urea transporters
T/F DT and CCD are permeable to urea
F
They are impermeable
Outline the flow of urea through tubules when ADH is high
50 percent is immediately reabsorbed (at proximal tubule)
Concentration increases through LOH and water is reabsorbed faster
DT/CCD impermeable to urea but water moves out
Since ADH is present, MCD is permeable to urea
Urea diffuses down concentration gradient into interstitial fluid and re-enters and recirculates to help maintain concentration gradient
T/F Countercurrent exchange in the vasa recta preserves hypoosmolarity of renal medulla
Preserves HYPEROSMOLARITY in renal medulla
T/F Medullary blood flow is high. Higher than 5 percent of total kidney flow
False
Medullary blood flow is low, less than 5 perent of total kidney flow
Medullary blood flow advantages (2)
Sufficient to supply metabolic needs of tissue
Minimzes solute loss/washout
What area acts as a countercurrent exchange
Vasa recta
Explain the countercurrent exchange in the vasa recta
Plasma flowing down the descending LOH of the vasa recta becomes more HYPEROSMOTIC (due to diffusion of water out of the blood and diffusion of solutes from renal interstitial fluid into the blood)
In the ascending LOH of the vasa recta, solutes diffuse back into the interstitial fluid and water diffuses back into the vasa recta.
Why and where does the environment become HYPEROSMOTIC during countercurrent exchange in the vasa recta?
Descending LOH
Because diffusion of water out of blood and diffusion of solutes from renal interstitial fluid into the blood.
Water is being pulled out of tubule and exchange of solutes/H2O is possible due to slow blood flow in this area.
ADH causes an increase or decrease of osmolarity of tubular fluid
INCREASE
What are the two primary mechanisms for ECF Na+ and osmolarity regulation?
Osmosreceptor-ADH system
Thirst mechanism
How can you estimate plasma osmolarity from plasma Na+
P(osm)= 2.1 X Plasma Na+
Where is ADH made?
Neurons of hypothalamus
What releases ADH?
Posterior pituitary
Explain how osmosreceptor-ADH system works
There’s a water deficit
Increase ECF osmolarity
Osmoreceptors SHRINK and there’s increase in ADH secretion
Increase in plasma ADH
Increase in water permeability in DT and CT
Increase water reabsorption
Decrease water excretion
What are two cardiovascular reflexes also have effect on ADH release
Arterial baroreceptor
Cardiopulmonary reflex
What does arterial baroreceptor reflex monitor
Pressure changes
What does the cardiovascular reflex monitor?
-What are 2 features
Monitor volume changes
Afferents into sensory area
Projections to hypothalamus
An increase in ADH would have what effect on arterial pressure, blood volume, and urine
Decrease in arterial pressure
Decrease in blood volume
Urine is decreased flow and concentrated
Is ADH release mechanism more sensitive to osmotic stimuli or pressure/volume stimuli?
Osmotic stimuli
Would nausea, vomiting, nicotine, and morphine stimulate or inhibit ADH release?
Stimulate
Want to retain more water
Would alcohol and caffeine inhibit or stimulate ADH release?
Inhibit ADH release (diuretics)
Would ingesting water increase or decrease ADH release?
decrease
Nausea effects…
- ADH
- Blood volume
- Blood pressure
- Plasma osmolarity
Increase ADH
Decrease blood volume
Decrease pressure
Increase plasma osmolarity
Increase thirst (dryness of mouth) effects
- Plasma osmolarity
- Blood volume
- Blood pressure
- Angiotensin II
Increase plasma osmolarity
Decrease blood volume
Decrease blood pressure
Increase angiotensin II
Decrease thirst (gastric distention) effects
- Plasma osmolarity
- Blood volume
- Blood pressure
- Angiotensin II
- Decrease osmolarity
- Increase blood volume
- Increase blood pressure
- Decrease angiotensin II
T/F The area along AV3V that promotes ADH release also stimulates thirst and involve the same nuclei
F
Same area but involves different nuclei
What are some stimuli for thirst?
Increase ECF osmolarity
Another name for anteroventral region of the third ventricle (AV3V)
Thirst center
Electrical stimulation of AV3V center induces what type of behavior
Drinking behavior
Injection of hypertonic salt solution stimulates what type pf behavior
Thirst
Outline stimuli for thirst mechanism
There’s increased ECF osmolarity due to increased plasma Na+ concentrations, causing intracellular dehydration in the thirst centers
Decreases in ECF volume and arterial pressure
Angiotensin II acts on subfornical organ to stimulate thirst and on kidney to increase Na+ and water reabsorption (in response to low pressure/volume)
Dryness of mouth and membranes
Excessive thirst is called
polydipsia
Diabetes mellitus
- osmolarity
- urine output
- prevalent in
High concentrations of glucose and causes increase in osmolarity
Increase urine output
Increase water excretion
Increase thirst
More prevalent in older animals
More prevalent that diabetes insipidus
Diabetes insipidus
-2 types
Central diabetes insipidus
Nephrogenic diabetes insipidus
Central diabetes insipidus
- Problem
- Origin
- Rx
Inability to produce or release ADH
May be congenital or injury-induced
Treatment-synthetic ADH, desmopressin
Nephrogenic diabetes insipidus
- Problem
- ADH
Renal tubules excrete dilute urine-which may be due to failure of countercurrent mechanism to to form hyperosmotic medulla or inability to respond to ADH.
ADH is normal
Can be caused by diuretics, lithium, tetracyclines, or renal diseases that damage renal medulla
What is “meter” fluid intake?
Thirst that is relieved immediately after drinking- before water has been absorbed.
Distention of the GI tract can relieve what?
How is this beneficial?
Relieve thirst
Prevents over-hydration
T/F Animals drink almost exactly the amount necessary to return plasma osmolarity to normal.
T
When is the thirst mechanism activated?
What is this also known as
When Na+ concentration is increased 2 mEq/L above
Threshold for drinking
Explain the relationship of the integrated responses of Osmoreceptor-ADH and thirst mechanism
- What do they both do
- If one fails
- If both fails
Osmoreceoptor-ADH and Thirst mechansm both work to regulate osmolarity.
If one fails, the other can ordinarily control osmolality
If both fail, there s no mechanism to increase water ingestion or conserve water
T/F Angiotensin II and aldosterone have potent effects on renal Na+ reasbsorption/excretion
T
Low Na+ intake stimulates or decreases ang II and aldosterone formation?
Low intake of Na+ stimulates angiotensin II and aldosterone formation.
T/F Angiotensin II and aldosterone have ptent effect on ECF Na+ concentrations. Why?
F
They increase both sodium and water reabsorption…so volume changes but concentration does not
ADH-thirst mechanism compensates
The normal ECF volume and sodium concentration is a balance between
Sodium excretion
Sodium intake
What are 2 major stimuli that increase salt-appetite
Decreased sodium concentration in ECF
Crculatory insufficiency (often caused by decreased blood volume or blood pressure)
T/F Salt appetite it thought to be under control of neuronal mechanisms similar to thirst
T
