Final Exam - Renal 4 Flashcards
Describe tubule osmolarity from beginning to end of the nephron?
PCT: Osmolarity is ~300, or the same as plasma, because water and solute reabsorption are balanced.
Desc. LOH: Very permeable to water, tubule osmolarity will match interstitial osmolarity as water is being reabsopred to keep both sides of the membrane equal.
Asc. LOH: Impermeable to water, but 25% of solutes are being reabsorped, decreasing the osmolarity all the way down to ~100 at the end of the thick ascending loop (diluting segment).
DCT: Intercalated and prinicpal cells begin reabsorping water and NaCl, creating a tubule osmolarity of ~300.
Collecting duct: Water is again reabsorped to cause the renal interstitum osmo to match the tubule osmo.
Describe what is occuring in the picture below?
- The renal interstitum is not highly concentrated-which decreases water reabsorption.
- There is also no water reabsorption in the DCT and collecting duct, causing very dilute urine, meaning there is no ADH.
- Without ADH the renal interstium is not as concentrated because urea is not being reabsorped.
Explain the mechanism of creatinine’s tubular fluid concentration as it progresses through the nephron as shown below.
PCT: Creatinine is filtered and secreted but not reabsorped - it’s concentration increases here due to water reabsorption
LOH & DCT: Osmolarity decreases here in the diluting segment due to solute reabsorption without water reabsorption
Collecting Duct: Osmolarity increases again as water is reabsorped and creatinine is not.
Explain the reduction in osmolarity for Na, K, and Cl in the distal loop of henle as shown below?
In the thick ascending loop of henle (diluting segment), Na+, K+, and Cl- are being actively reabsorped via the NKCC2 transporter, reducing their tubular concentration.
Explain why each compound’s osmolarity is what is shown on the below graph.
- PAH levels reach 585 because there is a large amount of it in small volume of urine. (90% secreted, not reabsorbed)
- Inulin is completely filtered and not reabsorped or excreted.
- Glucose and amino acids are completely reabsorbed in the PCT
- Proteins are almost completely endocytosed by PCT cells.
Define diuresis?
Di meaning 2
The excretion of water and the dissolved electrolytes
Where do diuretics cause fluid loss from?
The ECF
4/5 ISF, 1/5 plasma
Explain how diuretic therapy is effective at lowering blood pressure long-term?
Diuretics remove a portion of our ECF via diuresis. 4/5 is lost from the ISF and 1/5 is removed from the plasma. On sustained therapy, the body is able to maintain this new “normal” of fluid volume long term, effectively lowering blood pressure.
Why are vasodilators usually not effective at treating hypertension long-term?
The body has many controllers over vascular resistance (AT II, ADH, Epi, Norepi) and will still be able to increase it’s vascular resistance despite vasodilator therapy.
How does a healthy person’s body handle changes in salt intake?
How is blood pressure effected?
Normally, an increase in salt/water intake also leads to increased excretion.
If Na+ levels are high, AT II and aldosterone levels decrease, allowing for more Na+ and water excretion.
This system keeps blood pressures stable despite changes in salt/water intake.
In a patient with high levels of ANG II, how would their blood pressure be effected by increased Na+ intake?
If ANG II levels cannot be repressed, then an increase in Na+ intake would lead to an increase in Na+ and H2O reabsorption.
This means that blood pressure will increase with increased Na+ intake.
How would a person’s blood pressure with blockade of ANG II respond to increased Na+ intake?
At baseline they would have diffiuclty maintaining a normal pressure because they would be unable to reabsorp Na+ and water. Also due to having low aldosterone levels (ANG II causes aldosterone release from adrenal glands).
An increase in Na+ intake would increase blood pressure only temporarily because it will not be reabsorped and excreted.
How does anesthesia affect the blood pressure of people who are on ACEi?
People with very high Na+ intake?
- During the OR they will likely become hypotensive and their body will not be able to regulate it, meaning we will have to supplement their blood pressure, with difficulty.
- People with high Na+ diets have chronic suppression of ANG II. When we shut off their control centers in the OR or they lose blood, they have great difficulty compensating.
Describe the pathophysiology and effects of unilateral renal artery stenosis?
Stenosis causes decreased glomerular pressure and GFR. This leads to less NaCl+ arriving at the macula densa and more renin and ANG II being released.
ANG II increases EA resistance which increases filtration, increases Na+ and water reabsorption, and increases MAP.
This causes hypertension in the unaffected kidney, causing it to reduce renin levels to compensate. But, this overwhelmed by the affected kidney renin levels.
Overall, this leads to systemic hypertension, leading to glomerular capillary damage, and renal dysfunction
Treatments for renal artery stenosis?
- ACEi
- Renin blockers
- ARB’s
Prevents “cross-talk” of ANG II on unaffected kidney - Removing kidney if drugs are ineffective to prevent destruction of both kidneys