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Renal Physiology

Constanzo-Renal Physiology

QuestionAnswer
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