Renal 2 Flashcards
Briefly describe the two intrinsic renal mechanisms for autoregulation of GFR and renal blood flow
- myogenic (rise in pressure in aff. arteriole causes it to vacoconstict and therefore increase resistance and decrease glomerular hydrostatic pressure)
- tubuloglomerular mechanism ( change in blood pressure changes GFR and fluid flow through the proximal tubule which the macula densa senses via cilia and NaCl. macula dense sends signal to nearby smooth muscle cells of afferent arteriole to vasodilate/constrict and increase/decrease renin)
How can tubuloglomerular feedback help prevent excessive fluid losses if there is damage to kidney proximal tubules?
If proximal reabsorption is damaged then there will be excessive water and NaCl delivered to distal tubule. The feedback will cause vasoconstriction and lower GFR and prevent excessive fluid loss from damaged nephrons
Give proposed reason why autoregulation is useful. Can autoregulation still protect the kidney in patients with severe systemic hypertension?
Autoregulation fails at really high and really low arterial blood pressure. Autoregulation is useful because it allows for a constant regulation at GFR/RBF even when there is a rise/decrease in systemic blood pressure.
Give the names of the autacoids/hormones which can vasodilate the afferent and efferent arterioles. Which hormones/autacoids cause vasoconstriction?
- PGE2/PGI2: cause vasodilation and oppose norepinephrine.
- Norepinephrine/epinephrine: vasoconstrictors. Sympathetic nerves to kidney release them. Constrict both the afferent and efferent arterioles.
- Endothelin: vasoconstrictor released by damaged vascular endothelial cells
- Angiotensin II: circulating hormone and autacoid in kidney. Vasoconstrictor in general circulation and typically the efferent arteriole. Afferent not affected because of vasodilators. Decreased BP tends to increase this.
Explain why drugs that inhibit prostaglandin synthesis can cause renal damage. Be able to recognize the common drugs that inhibit prostaglandin synthesis.
- NSAIDS like aspirin, ibuprofen, naproxen inhibit prostaglandin synthesis
- The decrease in prostaglandin synthesis leaves unopposed vasoconstriction of nor. and sympathetics which would lead to ischemia. Chronic renal disease patients put more stress on good nephrons because some don’t work if taking NSAIDS you could have immediate renal failure. Loss of ability to concentrate urine because meduallary arteries rely on prostaglandins for blood.
Outline the renin-angiotensin-aldosterone system. Where is each produced?
Kidney releases renin bc of low BP Renin breaks angiotensiogen (from liver) into Angiotensin I Angiotensin converting enzyme breaks Angiotensin I into Angiotensin II(kidney) Angiotensin II causes renal retention by increasing proximal tubule transpot of Na (by way of Na/H transporter). It also is a general vasoconstrictor, increases sympathetic tone, thirst and and ADH release. Angiotensin II increases aldosterone from adrenal cortex Aldosterone increases renal reabsorption of Na
State which cells produce most renin and how renin release is controlled. Which division of the autonomic nervous system innervates the cells that produce renin? What is the effect of increased/decreased nervous stimulation?
Kidney releases renin in response to low blood pressure (direct effect on renal baroreceptor cells) and in response to sympathetic stimulation of B1 adrenergic receptors on granular cells/renal baroreceptors
Outline the pathway from angiotensinogen to angiostensin II. Where do renein and angiotensin converting enzyme ACE act in this pathway?
Renin breaks angiotensinogen into angiotensin I
AVE converts angiotensin I into angiotensin II which causes renal retention of salt and water (by increasing proximal tubule transport of Na through increased activity of NaH transporter) and vasoconstriction to increase blood pressure
Describe the effect of angiotensin II (and the related angiotensin III) on the following:
- vascular smooth muscle
- adrenal cortex
- efferent arteriole
- proximal tubule
- thirst center
- release of ADH
- sympathetic tone
Vascular smooth muscles = vasoconstrictor
Adrenal cortex = release aldosterone
Efferent arteriole = vasoconstrictor
Proximal tubule = increases Na reabsorption
Thirst center = increases
release of ADH = increases
Sympathetic tone = increases
State the two main sources of erythropoietin production. Which organ makes the most (~90%) erythropoietin?
Kidney and liver but mostly kidney
Give the effect of erythropoietin on RBC production.
Stimulates the production, maturation, and release of RBC from the bone marrow
Give the major stimuli for erythropoietin secretion.
Hypoxia
Describe the role of the kidney in making the active form of vitamin D. What is the major action of the active form of vitamin D? (What is its effect on the intestine? On the kidney? Which effect is more important?)
vitamin d3 cholecalciferol is converted in the kidney to 1,25dihydroxy vitamin d (calcitriol)
the final hydroxylation step is in the kidney and is stimulated by PTH
vitamin d active increases absoption of calcium and phosphate in the intestine (most important) and also stimulates reabsorptionof calcium and phosphate and suppresses PTH synthesis in parathyroid gland
Describe the effect of parathyroid hormone on the kidney.
Stimulates activation of Vitamin D and increases renal-tubular calcium reabsorption, but reduces renal reabsorption of phosphate
Describe how chronic renal failure affects the patient’s bones.
Low GFR (lower excretion) which causes and increase in phosphate in plasma increases PTH increase bone resorption renal osteodystrophy
