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Renal Physiology
Constanzo-Renal Physiology
| Question | Answer |
|---|---|
| kidney organ functions | 1)excretory organ 2)regulatory organ 3)endocrine organ=>makes renin, erthyropoietin, 1,25-dihydroxycholecalfiferol |
| papilla | innermost tip of kidney inner medulla empties into pouches called minor and major calyces=>extensions of ureter |
| nephron and structure | functional unit of kidney bowman's space=>proximal convoluted tubule=>proximal straight tubule=>loop of Henle(thin descending limb,thin ascending limb, thick ascending limb)=>distal convoluted tubule=>collecting ducts |
| glomerular capillary network | arises from afferent arterioles surrounded by bowman's capsule ultrafiltration across GCN into bowman's space the first step in urine formation |
| superficial cortical nephrons | glomeruli located in outer cortex contain short loops of Henle=>only descend into outer kidney medulla |
| juxtamedullary nephrons | glomeruli near corticomedullary border glomeruli larger than superficial and have higher GFR contain long loops of Henle=>descend deep into inner medulla and papilla=>essential for concentration of urine |
| renal vasculature | renal artery=>interlobar arteries=>arcuate arteries=>cortical radial arteries smallest arteries: afferent arterioles=>glomerular capillaries=>efferent arterioles=>peritubular capillaries |
| afferent arterioles | deliver blood to glomerular capillaries |
| glomerular capillaries | ultrafiltration occurs when blood crosses into Bowman's space |
| efferent arterioles | delivers blood to peritubular capillaries |
| peritubular capillaries | surrounds nephrons=>reabsorbs solutes and water its blood flows into small veins then renal vein delivers nutrients to epithelial cells in superficial nephrons specialize into vasa recta in juxtamedullary nephrons |
| vasa recta | specialized peritubular capillaries long hairpin-shaped blood vessels that follow same course as loops of Henle=>serve as osmotic exchangers to produce concentrated urine |
| total body water | water accounts for 50-70% body weight=>varies inversely correlates with fat content=>why women have lower TBW |
| 60-40-20 rule | 60% body weight is water 40% is ICF 20% is ECF |
| ICF | 40% body weight=>water inside cells major cations K+, Mg2+ major anions proteins and organic phosphates (ATP,ADP,AMP) |
| ECF | 20% body weight=>water outside cells(interstitial compartment and plasma) major cation Na+ major anion Cl-, HCO3- |
| plasma | aqueous component of blood=>constitutes 55% of blood volume |
| hematocrit | portion of blood volume occupied by RBCs=>averages at 45% of blood volume average is higher in males |
| plasma protein | makes up 7% of plasma volume |
| interstitial fluid | ultrafiltrate of plasma=>same composition as plasma without protein and blood cells |
| ECF volume contraction | ↓ in ECF volume, blood volume, arterial pressure ↑ fractional reabsorption in proximal tubule=>kidneys try to restore ECF volume can cause contraction alkalosis |
| ECF volume expansion | ↑ in ECF volume, blood volume, and arterial pressure=>can lead to edema ↓ fractional reabsorption in proximal tubule=>kidneys try to excrete excess NaCl and water |
| isosmotic volume contraction-diarrhea | large fluid volume lost from GI=>loss of isosmotic fluid leads to: ↓ in ECF volume=>↓ in arterial pressure; ↑ hematocrit and plasma protein concentration no change in osmolarity in either ICF or ECF; no change in ICF volume |
| hyperosmotic volume contraction-water deprivation | hyperosmotic fluid lost from ECF both ICF and ECF volumes ↓; both ICF and ECF osmolarity ↑ plasma protein concentration ↑; hematocrit unchanged(RBC concentration ↑ offsets ↓ in cell size) |
| hyposmotic volume contraction-adrenal insufficiency | aldosterone insufficiency=>excretion of excess NaCl in urine both ICF and ECF osmolarity ↓; ICF volume ↑; ECF volume ↓ plasma protein concentration and hematocrit both ↑ |
| isosmotic volume expansion-infusion of NaCl | all isotonic NaCl solution added to ECF=>↑ in ECF volume but no change in osmolarity both plasma protein concentration and hematocrit will ↓ |
| hyperosmotic volume expansion-high NaCl intake | ↑ in total amount of solute in ECF both ICF and ECF osmolarity ↑; ECF volume ↑; ICF volume ↓ both plasma protein concentration and hematocrit ↓ |
| hyposmotic volume expansion-SIADH | excess ADH secreted=>excess water reabsorption in collecting ducts both ICF and ECF volumes ↑ and osmolarities ↓ plasma protein concentration ↓; hematocrit unchanged(RBC concentration ↓ offset by size ↑) |
| renal clearance | volume of plasma completely cleared of substance by kidneys per unit time C=([U] x V)/[P] renal clearance of a substance ↑ as urinary excretion ↑ |
| clearance of albumin, glucose, inulin | albumin=0 glucose=0 inulin=GFR |
| clearance ratios | =1.0=>substance is a glomerular marker <1.0=>substance not filtered OR filtered then reabsorbed(Na+,Cl-,HCO3-, phosphate, urea, glucose, AA) >1.0=>substance is filtered and secreted(organic acids and bases, sometimes K+) |
| alpha-1 receptors | produced vasoconstriction when activated by SNS more found on afferent than efferent arterioles=>↑ SNS activity ↓ both RBF and GFR |
| angtiotensin II | potent vasoconstrictor of both afferent and efferent (more sensitive) arteriole=>low levels ↑ GFR high protective effect on GFR=>offset by ACE inhibitor stimulates Na+-H+ exchange in proximal tubule |
| prostaglandins | cause vasodilation of both afferent and efferent arterioles when stimulated by SNS=>effects are protective of RBF=>modulates vasoconstriction NSAIDS interfere with protective effects on renal function following hemorrhage produced locally in kidne |
| dopamine | at low levels dilates cerebral, cardiac, splanchnic, and renal arteries; constricts skeletal muscle and cutaneous arterioles has protective vasodilatory effect on blood flow=>low dosage administered to treat hemorrhage |
| autoregulation of RBF | 1)myogenic hypothesis=>stretch activated Ca2+ channels 2)tubuloglomerular feedback=>macula densa cells of JG apparatus |
| layers of glomerular capillary wall | 1)endothelium=>large pores for filtration of fluid, dissolved solutes, plasma proteins 2)basement membrane=>most significant barrier=>doesn't allow plasma proteins through 3)epithelium=>podocytes,foot processes, filtration slits |
| negative charge on glomerular capillary barrier | negatively charged glycoproteins=>fixed negative charges on endothelium, lamina rara interna and externa, podocytes and foot processes, filtration slits of epithelium adds electrostatic component to filtration=>important for large solutes |
| hydrostatic pressure in glomerular capillaries | force that favors filtration pressure remains constant along entire length of capillary |
| hydrostatic pressure in Bowman's space | force that opposes filtration originates from fluid present in lumen of nephron |
| oncotic pressure in glomerular capillaries | force that opposes filtration determined by protein concentration progressively ↑ as fluid filtered out of capillary=>eventually reaches a point where glomerular filtration stops |
| changes in hydrostatic pressure of glomerular capillaries | caused by changes in resistance of afferent and efferent arterioles |
| changes in oncotic pressure of glomerular capillaries | produced by changes in plasma protein concentration ↓ can be caused by nephrotic syndrome |
| changes in hydrostatic pressure of Bowman's space | can be produced by obstructing urine (ex. ureteral stone or constriction of ureter) |
| filtration fraction | FF=GFR/RPF=>fraction of RPF filtered across glomerular capillaries ↑ in FF=>↑ in protein concentration and oncotic pressure in peritubular capillaries |
| glucosuria | excretion/spilling of glucose in urine occurs occurs in 1)diabetes mellitus=>lack of insulin 2)pregnancy=>GFR ↑=>filtered load ↑ 3)Na+-glucose transporter abnormality |
| [TF/P] ratio | compares concentration of substance in tubular fluid to its concentration in systemic plasma = 0=>no absorption/secretion occurred OR water and solute proportionally absorbed <1=>solute>water reabsorption >1=>solute |
| positive Na+ balance | excretion is less than intake |
| negative Na+ balance | excretion is greater than intake |
| proximal convoluted tubule and Na+ reabsorption | reabsorbs 67% of filtered Na+and water=>isosmotic reabsorption reabsorbs 100% glucose and AA 85% HCO3- reabsorbed most phosphate, lactate, citrate reabsorbed |
| early proximal convoluted tubule | Na+ reabsorbed primarily with HCO3-, AA, glucose=>produces lumen-negative potential difference |
| late proximal convoluted tubule | Na+ reabsorbed with Cl- (concentration is high)=>creates lumen-positive potential difference |
| glomerular tubular balance | ensures constant fraction of filtered load reabsorbed ↑ in GFR=>↑ filtration fraction=>↑ oncotic pressure in peritubular capillaries=>↑ reabsorption in proximal tubule and vice versa |
| importance of high oncotic pressure in peritubular capillaries | most important driving force for reabsorption of isosmotic fluid in proximal tubule |
| contraction alkalosis | metabolic alkalosis secondary to ECF volume contraction=>stimulates RAA system=>ATII stimulates Na+-H+ exchange=>stimulates reabsorption of HCO3- |
| loop of Henle | has three segments: thin descending limb, thin ascending limb, thick ascending limb responsible for countercurrent multiplication=>important for concentration and dilution of urine |
| thin descending loop of Henle | high permeability to small solutes(NaCl,urea) and water in countercurrent multiplier water moves out of lumen and solutes move in=>tubular fluid progressively gets hyperosmotic as it flows down |
| thin ascending loop of Henle | permeable to NaCl but impermeable to water in countercurrent multiplication solute moves out of lumen=>tubular fluid progressively gets hyposmotic as it flows up ascending limb |
| thick ascending limb of Henle | actively reabsorbs Na+=>mechanism load-dependent with Na+-K+-2Cl- cotransporter(loop diuretic site)=>some K+ diffuses back to lumen=>lumen-positive potential difference=>drives reabsorption divalent cations impermeable to water=>diluting segment |
| early distal tubule | reabsorbs Na+ with Na+-Cl- cotransporter=>inhibited by thiazide diuretics impermeable to wate=>coritcal diluting segment |
| loop diuretics | act on Na+-K+-2Cl- cotransporter in thick ascending limb of loop of Henle prod. profound kaliuresis=>↑ K+ excretion=>hypokalemia ↑ flow rate dilutes [K+]=>↑ K+ secretion inhibits Ca2+Mg2+ reabsorption=>used to treat hig |
| thiazide diuretics | acts on Na+-Cl- cotransporter in early distal tubule=>causes kaliuresis=>↑ K+ excretion=>hypokalemia ↑ flow rate=>dilutes K+ concentration=>↑ K+ secretion ↑ Ca2+ reabsorption=>why used to treat hypercalciuria |
| late distal tubule and collecting duct | fine tunes reabsorption of Na+ and water=>hormonally regulated by aldosterone and ADH respectively 2 cell types: principal cells and intercalated cells(alpha and beta) |
| principal cell | found in late distal convoluted tubule and collecting ducts contains Na+ channels=>gradient maintained by Na+-K+ ATPase reabsorbs: Na+ and water secretes: K+ regulated by aldosterone, ADH, K+-sparing diuretics |
| alpha-intercalated cells | found in late distal convoluted tubule and collecting ducts contains H+-K+ ATPase that reabsorbs: K+ secretes: H+ |
| beta-intercalated cells | found in collecting ducts reabsorbs: H+ secretes: HCO3- |
| aldosterone | acts directly on principal cells=>↑ Na+ reabsorption thru synthesis of proteins involved in Na+ reabsorption ↑ K+ secretion by principal cells=>secondary effects of Na+ reabsorption and ↑ K+ channels secreted adrenal cortex |
| ADH | ↑ water permeability of principal cells with aquaporins ↑ urea permeability in inner medullary collecting ducts ↑ activity of Na+-K+-2Cl- cotransporter=>↑ Na+ reabsorption and enhances single effect step of CCM |
| K+-sparing diuretics | acts on principal cells to inhibit all actions of aldosterone(Na+ reabsorption and K+ secretion)=>produce mild diuresis DO NOT CAUSE KALIURESIS=>used into combination with loop and thiazide diuretics ex)spironolactone, amiloride, triamterene |
| effective arterial blood volume (EABV) | portion of ECF volume contained in arteries and "effectively" perfusing the tissues=>generally changes with ECF volume(except in edema) kidneys detect changes in EABV |
| sympathetic nerve activity-regulation of Na+ balance | activated by baroreceptors in response to ↓ in arterial pressure=>causes vasoconstriction of afferent arterioles and ↑ proximal tubule Na+ reabsorption |
| atriopeptin (ANP) | secreted by atria in response to ↑ in ECF volume=>causes vasodilation of afferent arteriole and vasoconstriction of efferent arteriole=>↑ GFR ↓ Na+ reabsorption in late distal tubule and collecting ducts |
| brain natriuretic peptide (BNP) | ↑ GFR and ↓ renal Na+ reabsorption secreted by cardiac atrial cells and brain=>marker for CHF |
| renin-angiotensin-aldosterone system | activated in response to ↓ arterial pressure |
| total body K+ | 98% in ICF 2% in ECF gradient maintained by Na+-K+ ATPase |
| hyperkalemia | shift of K+ out of cells produces ↑ in blood K+ concentration |
| hypokalemia | shift of K+ into cells produces ↓ in blood K+ concentration |
| insulin and K+ | stimulates K+ uptake into cells by ↑ activity of Na+-K+ ATPase =>ensures ingested K+ doesn't stay in ECF and produce hyperkalemia deficiency of insulin seen in type I diabetics and leads to hyperkalemia and vice versa |
| H+-K+ exchange | useful because ICF has considerable buffering capacity for H+ exchange necessary to maintain electroneutrality |
| alkalemia | produces hypokalemia because H+ leaves cells and K+ enters cells |
| acidemia | produces hyperkalemia because H+ enters cells and K+ leaves cells |
| beta2-adrenergic receptors and K+shift | ↑ Na+-K+ ATPase activity=>causes K+ shift into cells=>can produce hypokalemia ex)albuterol |
| alpha-adrenergic receptors and K+ shift | cause K+ shift out of cells=>can produce hyperkalemia ex)propanolol |
| hyperosmolarity and K+ shift | causes K+ shift out of cells |
| cell lysis and K+ shift | produces hyperkalemia because large amount of K+ released into ECF ex)burn, rhabdomyolysis, malignant cells destroyed during chemo |
| exercise and K+ shift | causes K+ shift out of cells=>helps in local control of blood flow=>directly dilates skeletal muscle arterioles to ↑ local blood flow strenuous exercise can result in hyperkalemia |
| positive K+ balance | excretion is less than intake=>hyperkalemia can occur |
| negative K+ balance | excretion is more than intake=>hypokalemia can occur |
| alkalosis and K+ | ↑ K+ secretion causes hypokalemia |
| acidosis and K+ | ↓ K+ secretion and causes hyperkalemia |
| luminal anions and K+ | large anions in lumen of distal tube and collecting duct ↑ K+ secretion=>they ↑ eletronegativity of lumen=>↑ electrochemical driving force for K+ secretion |
| phosphate distribution | localized primarily in bone matrix (~85%) 10% in plasma protein-bound 90% in plasma not bound to plasma proteins |
| parathyroid hormone | (PCT) ↑ Ca2+ excretion=>inhibits Na+-phosphate cotransport=>phosphaturia (DCT) ↑ Ca2+ reabsorption PTH receptor coupled to adenylyl cyclase via Gs protein=>defect in this pathway causes psuedohypoparathyroidism |
| pseudohypoparathyroidism | inherited disorder with a defect in a protein involved in PTH receptor pathway renal cells resistant to PTH=>both urinary phosphate and cAMP ↓ |
| calcium distribution | most contained in bone (~99%) most bound in ICF 40% in ECF bound to plasma proteins |
| corticopapillary osmotic gradient | gradient of osmolarity in the interstitial fluid of the kidney size of gradient depends on length of loop of Henle and level of ADH |
| countercurrent multiplication | a function of the loops of Henle role formation of corticopapillary: deposit NaCl into interstitial fluid of deeper regions of kidney builds up corticopapillary osmotic gradient in repeating two-step process 1)single effect 2)flow of tubular f |
| single effect step of countercurrent multiplication | ↓ osmolarity of ascending limb of loop of Henle ↑ osmolarity of descending limb of loop of Henle and osmolarity of interstitial fluid enhanced by ADH=>↑ activity of Na+-K+-2Cl- cotransporter |
| urea recycling | contributes to establishment of corticopapillary osmotic gradient function of inner medullary collecting ducts |
| countercurrent exchange | passive process that maintains corticopapillary osmotic gradient |
| demeclocycline | used to treat SIADH=>inhibits ADH action on principal cells |
| central diabetes insipidus | posterior pituitary gland depleted of ADH stores=>can be caused by head injury large volumes of dilute urine excreted=>plasma osmolarity ↑ to abnormally high levels treat with ADH analogue 1-deamino-8-D-arginine vasopressin (dDAVP) |
| 1-deamino-8-D-arginine vasopressin (dDAVP) | ADH analogue used to treat central diabetes insipidus |
| nephrogenic diabetes insipidus | defect in receptor/pathway of ADH large volumes of dilute urine excreted=>plasma osmolarity ↑ to abnormally high levels treated with thiazide diuretics=>↓ GFR=>↓ total volume of water excreted |
| free water clearance | distilled water free of solutes (+)hyposmotic urine=>low/ineffective ADH levels (-) hyperosmotic urine=>high ADH levels =0 no solute-free water excreted |
Created by:
kphom001
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