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126 Cards in this Set
- Front
- Back
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T/F ureters pass over the uterine artery and under the ductus deferens
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False
"Water under the bridge" Ureter passes under the the uterine artery and under the ductus deferens (retroperitoneal) |
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juxtaglomerular cells
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synthesizes, stores, secretes renin, in response to low renal blood pressure, and increased sympathetic tone (Beta1)
specialized endothelial cells in the wall of afferent arteriole |
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macula densa
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specialized cells lining wall of distal tubule at its point of return to vascular pole
senses concentration of NaCl of distal convoluted tubule, low concentration of Na will activate, two effects: 1.decreases resistance to flow in afferent arteriole to increase GFR 2. increases renin release |
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mesangial cell
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contractile smooth muscle cells that regulates filtration through capillary
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podocytes
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wrap around capillaries and creates a filtration barrier - preventing large proteins from passing through
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% of body weight taken up by total body water, ICF, ECF
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60-40-20 rule
60% total body water 40% ICF 20% ECF (1/4 plasma + 3/4 insterstitial fluid) |
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NaCl and K concentration of
ECF ICF |
ECF is high in NaCl and low in K
ICF is low in NaCl and high in K |
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how do you measure plasma volume
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radiolabled albumin
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how do you measure ECF volume
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inulin
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glomerular filtration barrier composition
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filters by size and charge
1. fenestrated capillary endothelium (filters by size) 2. fused basement membrane with heparin sulfate (neg charge barrier) 3. Epithelial layer of podocyte foot proceses |
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nephrotic syndrome
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charge barrier of basement membrane is lost
-> albuminurea, hypoproteinemia, generalized edema, hyperlipidemia |
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Renal clearance equation
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C = UV/P
U = urine concentration of X V = urine flow P = plasma concentration of X C < GFR, net tubular resorption C > GFR, net tubular secretion C = GFR, no net secretion or reabsorption |
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Glomerular filtration rate (GFR)
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use inulin to measure - neither reabsorbed or secreted
GFR = UV/P = Cinulin |
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effective renal plasma flow (ERPF)
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measure with PAH because it is both filtered and actively secreted - all PAH is excreted
ERPF = UV/P = Cpah RBF = RPF/(1-Hct) underestimates true RPF by 10% |
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filtration fraction
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FF = GFR/RPF
normal is 20% estimate GFR from creatinine estimate RPF from PAH |
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T/F Angiotensin II preferentially constricts the afferent arteriole
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FALSE
preferentially constricts the efferent arteriole decreasing RPF, increasing GFR - FF increases inhibited by ACE inhibitor |
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T/F Prostaglandins constrict afferent arteriole
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False
prostaglandins dilate afferent arteriole increases RPF, increase GFR so FF stays the same inhibited by NSAIDs |
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afferent arteriole constriction effect on RPF, GFR, and FF
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dec RPF
dec GFR FF stays the same |
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efferent arteriole constriction effect on RPF, GFR, and FF
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dec RPF
inc GFR inc FF |
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increased plasma protein concentration constriction effect on RPF, GFR, and FF
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RPF stays the same
GFR decreases (more oncotic pressure keeps fluid plasma) FF decreases |
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decreased protein concentration effect on RPF, GFR, and FF
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RPF stays the same
inc GFR (less oncotic pressure means more fluid leaves) inc FF |
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constriction of ureter effect on RPF, GFR, and FF
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RPF no change
dec GFR (increased pressure in tubule) dec FF |
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free water clearance
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Free water (C[h20]) = total urine (V) - water occupied with solute (C[osm])
C[osm] = U[osm]V/P[osm] with ADH C[h20] < 0 (negative free water clearance means retention of water) without ADH C[h20] > 0 (excretion of free water) isotonic urine C[h20] = 0 (often with loop diuretic) |
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Filtered load = ?
excretion rate = ? reabsorption = ? secretion = ? |
filtered load = GFR X Px
Excretion rate = V x Ux reabsorption = filtered - excreted secretion = excreted - filtered |
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glucosuria
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starts at plasma glucose of 160-200mg/dl (threshold)
at 350 mg/dl all transporters are sturated |
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Hartnup disease
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deficiency of neutral amino acid (tryptophan) transporter in proximal tubule
-> pellagra |
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parathyroid hormone
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secreted in response to decreased plasma Ca++ or increased plasma phosphate or decreased plasma 1,25 Vit D
proximal tubule - inhibits Na+/phosphate cotransport, decreases phosphate reabsorption early distal tubule - enhances Ca+/Na+ exchange - Ca++ absorption increases 1,25 Vit D production to increase Ca+ and phosphate absorption in intestine |
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angiotensin II action on renal tubules
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proximal tubule: stimulates Na+/H+ exchange --> increases Na+ and H20 reabsorption
thick ascending limb: stimulate NaK2Cl |
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aldosterone effects on renal tubules
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secreted due to decrease in blood volume (via AT II) and increased K+
principle cells (Late DCT/collecting duct): 1. activation of basolateral - Na+/K+ pumps - reabsorb Na+ , secrete K+ 2. increases number of Na+ channels (ENaC) on luminal side to increase permeability for Na+ into the cell 3. increases the number of luminal membrane K+ channels to allow K+ secretion ____ alpha-intercalated cells (Late DCT/collecting duct): 1. increases H+ secretion via H+-ATPase for acid/base balance |
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ADH
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secreted from posterior pituitary due to increased plasma osm, or decreased blood volume
insertion of aquaporin (H2O channel) on luminal side of principle cells (Late DCT/Collecting duct) without ADH, its impermeable to water |
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early proximal tubule
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contains brush boarder
reabsorbs all glucose, AA reabsorbs most bicarb, NaCl, and H2O generates ammonia which buffers H+ PTH and ATII act here |
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thin descending loop of henle
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passive reabsorb water due to medulla hypertonicity
impermeable to sodium concentrating segment makes urine hypertonic |
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thick ascending loop of henle
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active reabsorb of Na+. K+, Cl- (NaK2Cl transporter)
indirectly reabsorbs Mg+ and Ca+ loop diuretics act here impermable to H2O makes urine less concentrated |
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early distal convoluted tubule
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active reabsorption of Na+ and Cl- (NaCl transporter)
thiazides, PTH act here diluting segment |
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late distal convuluted tubule/collecting duct
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2 types of cells: alpha intercalated and principal cells
reabsorbs Na+ in exchange for K+ and H+ aldosterone and ADH act here |
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TF/P
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TF/P compares concentration of a substance in tubular fluid to plasma
TF/P = 1 means there has been no reabsorption or that reabsorption occurs exactly with water reabsorption TF/P <1 means reabsorption of substance is faster than reabsorption of water - concentration of TF is less than plasma TF/P > 1 then reabsorption of substance is slower than reabsorption of water OR there is net secertion |
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what events cause secretion of renin
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decreased BP (JG cells)
decreased Na+ to macula densa cells inc sympathetic tone |
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Renin-angiotensin-aldosterone system
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activated by low BP
antiotensinogen (made by liver) convert to AT I (via Renin made in kidney) convert to AT II (via ACE made in lung and kidney) AT II has many effects including release of aldosterone RAAS aims to control blood volume and BP |
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effects of Angiotensin II
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1. general vasoconstricion -> increases BP
2. constrict efferent arteriole (increases FF - preserves renal function) 3. secrete aldosterone from adrenal gland (increased water reabsorption in kidneys) 4. secrete ADH from posterior pituitary (increased water reabsorption in kidneys) 5. increased proximal tubule Na+/H+ activity ((increased water reabsorption in kidneys) 6. stimulates thirst through hypothalamus |
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erythropoietin
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released in response to hypoxia from endothelial cells of peritubular capillaries
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1,25 (OH)2 vitamin D
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active form of vitamin D converted by the kidney
increased Ca++ and phosphate absorption in intestine stimulated by PTH |
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Renin
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secreted by JG cells due to decreased renal arterial pressure and increased renal sympathetics
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prostaglandins
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paracrine secretion vasodialates afferent arterioles to increase GFR
NSAIDs can cause renal failure by inhibiting this |
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atrial natriuretic peptide (ANP)
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secreted due to increased atrial pressure, sensed by stretch receptors
causes increased GFR and Na+ filtration, and NO Na+ reabsorption -> lose Na+ and water -> decreased blood volume |
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potassium shift out of cell
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causes hyperkalemia
due to: 1. insulin def (dec Na+/K+ ATPase) 2. beta adrenergic atagonist (dec Na+/K+ ATPase) 3. acidosis (K+/H+ exchanger) 4. hyperosmolarity 5. digitalis (dec Na+/K+ ATPase) 6. cell lysis |
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potassium shift into cell
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causes hypokalemia
due to: 1. insulin (inc Na+/K+ ATPase) 2. Beta adrenergic agonist (inc Na+/K+ ATPase) 3. alkalosis (K+/H+ exchanger) 4. hypo-osmolarity |
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metabolic acidosis
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decreased bicarb (primary disturbance)
causes a compensatory decrease in pH and decreased in Pco2 see hyperventilation |
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metabolic alkalosis
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increased bicarb (primary disturbance)
compensatory increase in pH and Pco2 see hypoventalation |
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respiratory acidosis
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increased Pco2 (primary disturbance)
compensatory decrease in pH and increase in bicarb see increased renal bicarb reabsorption |
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respiratory alkalosis
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decreased Pco2 (primary disturbance)
compensatory increase in pH and decrease in bicarb see decrease renal reabsorption of bicarb |
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anion gap
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for metabolic acidosis differential diagnosis
anion gap = Na+ - (Cl- + HCO3-) increased anion gap means exogenous source of acid: MUDPILES - methanol uremia diabetic ketoacidosis paraldehyde iron tablets lactic acidosis ethylene glycol salicylates normal: diarrhea glue sniffing renal tubular acidosis hyperchloremia |
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renal tubular acidosis type 1
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distal
defect in collecting tubule ability to excrete H+ associated with hypokalemia, risk for calcium kidney stones |
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renal tubular acidosis type 2
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proximal
defect in proximal tubule bicarb reabsorption see with hypokalemia and hypophosphatemic rickets |
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renal tubular acidosis type 4
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hyperkalemic
due to hypoaldosteronism or decreased response to aldosterone -> hyperkalemia -> decreased ammonia secretion decreased urine pH |
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RBC casts
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see in globmerulonephritis, ischemia, or malignant hypertension
RBC casts indicate hematuria is renal origin |
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WBC casts
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tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
WBC casts indicate pyuria is renal origin |
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what kind of casts do you see in bladder cancer? kidney stones?
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you dont' see casts, only RBC
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what kind of casts do you see in acute cystitis?
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no casts, only WBC
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granular casts
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muddy brown
see in acute tubular necrosis |
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Waxy casts
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see in advance renal disease and chronic renal failure
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hyaline casts
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nonspecific, most common type of cast
solidified Tamm-Horsefall mucoprotein |
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Nephritic Syndromes
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nephr(I)tic syndrome = (I)nflammatory process (different from nephrOtic)
if involves glomeruli -> hematauria, RBC casts in urine associated with azotemia, oliguria, hypertension, proteinuria |
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Acute poststreptococcal glomerulonephritis
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often see in children 2-4 weeks after streptococcal throat/skin infection
peripheral and periorbital edema...resolves on its own see enlarged glomeruli - hypercellular, lots of neutrophiles "lumpy-bumpy" apperance subepthelial immune complex on EM granular appearance on IF indicating immune complex vs direct Ab binding strep infection will have +ASO and decreased serum complement |
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rapidly progressive (crescentic) glomerulocephritis (RPGN)
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crescent moon shape - consisting of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages
caused by goodpasture syndrome, wergner granulomatosis, microscopic polyarteritis poor prognosis |
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goodpasture syndrome
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type II hypersensitivity - antibodies to glomerular basement membranes
linear IF male dominant disease hematuria, hemoptysis |
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andibody in wergner's granulomatosis
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c-ANCA
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andibody in microscopic polyangiitis
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p-ANCA
p for polyangiitis |
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diffuse proliferative glomerulonephritis
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due to SLE or MPGN (membraneoproliferative glomerulonephritis)
most common cause of death in SLE subendothelial DNA-anti-DNA immune complex -> wire looking of capillaries granular IF - IgG-based immune deposits and C3 |
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Berger's disease (IgA glomerulopathy)
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related to Henoch-Schoenlein disease
increased IgA synth - immune complex formation in mesangium often associated with URI or acute gastroenteritis - most common nephritic syndrome, several days after |
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alport syndrome
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mutation in type IV collagen -> split basement membrane
nerve disorder, ocular disorder, deafness COL4A5 gene |
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nephrotic syndrome
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nephrOtic syndrome presents with prOteinuria - frothy urine, noninflammatory
also see hyperlipidemia, fatty casts, edema increased risk of thromboembolism and risk of infection due to loss of Ig |
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membranous glomerulonephritis (diffuse membranous glomerulopathy)
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diffuse capillary and glomerular basement membrane thickening
spike and dome appearance on EM, subendothelial apperanace granular IF see with SLE, drugs, infections, tumors |
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minimal change disease (lipod nephrosis)
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most common in children
looks normal in LM EM see foot process effacement - loss of albumin, but not Ig trigger by recent infection |
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amyloidosis
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congo red stain, apple green birefringince under LM
see with multiple myeloma, chronic conditions, TB, rheumatoid arthritis |
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diabetic glomerulonephropathy
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nonenzymatic glycosylation (NEG) of GBM - causes increased perm and thickening
NEG of efferent arterioles increases GFR - seem mesangial expansion nodular glomerulosclerosis (Kimmelsteil-Wilson lesion) |
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focal segmental glomerulosclerosis
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most common glomerular disease in HIV patients. very severe in HIV patients
segmental sclerosis and hylinosis, IgM/C3 deposition |
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membranoproliferative glomerulonepritis
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can presents as nephritic syndrome but progresses to CRF
type 1: HBV or HCV - has "tram-track" appearance due to GBM splitting from mesangial ingrowth type 2: C3 nephritic factor - "dense deposits" - stabalized C3 convertase -> decreased serum C3 subendothelial immune complex with granular IF |
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kidney stones types, complications
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calcium
struvite uric acid cystine all cause hydronephrosis and pyelonephritis treat/prevent with fluid intake |
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calcium kidney stones
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most common kidney stone
calcium oxalate (normal or decreased pH) or calcium phosphate (increased pH) see with conditions that cause hypercalcemia often with vit C or ethylene glycol abuse radiopaque |
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ammonium magnesium phosphate (struvite) kidney stones
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2nd most common kidney stone
caused by infection with urease positive bugs (proteius vulgaris, staphylococcus, klebsiella) often form staghorn calculi which serves as breeding area for UTI |
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staghorn calculi
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forms as a nidus for UTIs
created by struvite kidney stones |
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uric acid kidney stone
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associated with hyperuricemia (gout)
see with diseases that cause high cell turnover - leukemia, myeloproliferative disorders- IV/allopurinol to prevent tumor lysis syndrome radioLUCENT |
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cystine kidney stone
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2ndary to cystinuria - high cystine levels in urine
hexagonal shape may for cstine staghorn calculi treat with alkinizaiton of urine |
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renal cell carcinoma
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most common renal malignancy
50-70yo originates in renal tubule - polygonal clear cells see hematuria, 2ndary polycythemia, flank pain, fever, weightloss often see paraneoplasic syndrome - ectopic EPO, ATCH, PTHrP, prolactin associated with von Hipple-Lindau - deletion ch3 invades IVC and spread hemotogenously -> lung, bone |
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wilms tumor (nephroblastoma)
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most common renal malignancy in children
deletion of tumor supressor WT1 gene on ch11 large flank mass and hematuria - contain embryonic glomerular structures part of WAGR complex |
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WAGR complex
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wilm's tumor, aniridia, genitourinary malformation, retardation of mental motor
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transitional cell carcinoma
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most common tumor of urinary tract
painless hematuria - bladder cancer Pee SAC - phenacetin, smoking, aniline dyes, cyclophosphamide |
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acute pyelonephritis
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affects cortex, leaves glomeruli and vessels
see WBC casts fever, CVA tenderness, nausea, vomit chronic - coarse, asymmetric corticomedullary scarring, blunted calyx - see eosinophilic casts (thyroidization) |
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chronic pyelonephritis
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coarse, asymmetric corticomedullary scarring, blunted calyx
see eosinophilic casts (thyroidization) |
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drug induced interstitial nephritis
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acute interstitial renal inflammation
pyuria (usually eosinophil) and azotemia 1-2 weeks after use of drug fever, rash, hematuria, CVA tenderness diuretics, NSAIDS, penicillin, sulfonamide, rifampin act as haptens - hypersensitvity |
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diffuse cortical necrosis
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acute generalized infarction of cortices of both kidneys
due to combo of DIC and vasospasm |
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acute tubular necrosis
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most common cause of acute renal failure in hospitals
associated with renal ischemia, crush injury, toxins see loss of cell polarity, epithelial cell detachment, necrosis, granular casts 3stages inciting event maintainence (low urine) recovery- plyuric, BUN and serum creatinin fall; rsik for hyokalemia |
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renal papillary necrosis
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sloughing of renal papillae - gross hematuria, proteinuria- may be triggered by infection, immune stimulus
associated with 1. diabetes mellitus 2. acute pyelonephritis 3. chronic phenacetin use 4. sickle cell anemia |
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acute renal failure
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defined as decline in renal function with increased creatinine and BUN over several days
due to: 1. prerenal azotemia - due to decreased RBF causes decreased GFR - Na/water retained along with BUN/creatinine 2. intrinsic renal damage - acute tubular necrosis or ischemia/toxin creates debris which blocks tubules, impaired perfusion 3. postrenal - outflow obstruction (needs to be bilateral) |
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chronic renal failure
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due to hypertension and diabetes
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Consequences of renal failure
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Na/H2O retention
hyperkalemia metabolic acidosis Uremia Anemia -no EPO Renal osteodystrophy Dyslipidemia Growth retardation and developmental delay |
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Uremia
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increased BUN and creatinine
-nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction |
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Renal osteodystrophy
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failure of vitD hyroxylation -> Ca wasting and PO4 retention -> secondary hyperPTH
subperiosteal thinning of bones |
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fanconi syndrome
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decreased proximal tubule transport of AA, glucose, phosphate, uric acids, and electrolytes
due to wilsons, glycogen storage disease, drugs, congenital |
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ADPKD (autosomal dominant polycystic kidney disease) formerly adult polycystic kidney disease
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multiple, large, bilateral cystic that destroy the parenchyma
auto dom mutation in APDK1 or APDK2 on chromosome 4 death from chronic renal failure, HTN associated with polycystic liver disease, berry aneurysm, mitral valve prolapse |
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ARPKD (autosomal recessive polycystic kidney disease) formerly infantile polycystic kidney disease
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infantile presentation of PKD in parenchyma
auto rec associated with congenital hepatic fibrosis. significant renal failure in utero -> potter's |
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dialysis cyst
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cortical and medullary cysts due to longstanding dialysis
RCC risk |
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simple cyst
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benign, incidental finding in cortex only
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medullary cystic disease
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medullary cysts -> fibrosis and progressive renal insufficiency - cant concentrate urine
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Na+ disturbances
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too low - disorientation, stupor, coma
too high - irritability, delirium, coma |
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Cl- disturbances
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too low - 2ndary to metabolic alkalosis, hypokalemia, hypovolemia, inc aldosterone
too high - due to non-anion gap acidosis |
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K+ distrubances
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too low - U waves on ECF, flat T waves, arrythemias, paralysis
too high - peaked T waves, wide QRS, arrythemia |
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Ca++ distrurbances
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too low - tetnus, neuromuscular problems
too high - delerium, renal stones, abdominal pain |
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Mg2+ disturbances
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too low - neuromuscular problems, arrhythemia
too high - delirium, decreased DTR, cardiopulm arrest |
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PO43- (phosphate) distrubances
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too low - low mineral ion product causes bone loss - osteomalacia
too high - mineral ion product causes renal stone, metatstic calcification |
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Pronephros
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exists until week 4 then degenerates
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Mesonephros
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develops by 5th week
functions as interim kidney and eventually becomes Bowman's capsule, glomerulus, mesonephric duct drains into hindgut, tubules function then degenerate ducts persist: male ductus epididymis, ductus deferens, ejaculatory duct; female -ureters |
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Metanephros
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first appears at 5 weeks and persists
ureteric bud is a diverticulum of mesonephric duct the metanephric mass forms from mesoderm |
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Kidney development
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ureteric bud penertrates metanephric mass -> bud dilates to form renal pelvis -> pelvis splits into cranial and caudal major calayces -> continues to divide into collecting tubules
upon formation of collecting ducts the metanpehric mass induces tissue cap cells to ffrom nephrons as kidneys develop they ascend into the abdomen |
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Bladder development
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urorectal septum divides the cloaca into anorretal canal and urogenital sinus (protrusion of endoderm by week 7 -> upper and largest part becomes urinary bladder
mucosa of trigone of bladder is initially formed from mesodermal tissue -> replaced by endodermal epithelium, smooth muscle from splanchnic mesoderm |
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Potter's syndrome
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bilateral renal agenesis -> oligohydraminos -> limb deformaties, facial deformaties, pulmonary hypoplasia
due to malformation of ureteric bud |
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Horseshoe kidney
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inferior poles of kidney fuse and kidneys can not fully ascend as they trapped by infererior mesenteric artery
normal function, associated with Turner syndrome |
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Patent urachus
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failure of allantois to obliterate
causes urine to drain through umbilicus |
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Mannitol
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osmotic diuretic -> increased tubular fluid osmolarity, increased urine flow
use: shock, drug overdose, increased intracranial/intraocular pressure SE: pulmonary edema, dehydration, contradindicated in anuria, CHF |
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Acetazolamide
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carbonic anhydrase inhibitor -> self-limited NaHCO3 diuresis, and reduction of total-body HCO3 stores
uses: glaucoma, urinary alkinization (acidic drugs or toxins), metabolic alkalosis, altitude sickness SE: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy |
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Furosemide
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sulfonamide loop diuretic - inhibits cotransport system (Na/K/2Cl) of thick ascending loop of henle -> prevents concentration of urine
stimulates PGE release- inhibited by NSAIDs increase Ca secretion use: edematous states, HTN, hypercalcemia SE: Ototoxicity, Hypokalemia, Dehydration, sulfa Allergy, interstitial Nephritis, Gout - OH DANG! |
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Ethacrunic acid
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phenoxyacetic acid derivative - essentially same as furosemide but without sulfa allergy
can be used to treat hyperureicemia |
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Hydrochlorothiazide
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inhibits NaCl reabsorption in early distal tubule
decreased Ca excretion uses: HTN, CHF, idiopathic hypercalciuria, nephrogenic DI SE: hypokalemic metabloic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalciemia, sulfa allergy |
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Spironlactone
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competitive aldosterone receptor antagonist in cortical collecting duct -K sparing diuretic
use: hyperaldosteronism, K edpletion, CHF ES: hyperkalemia -> arrhythmias, gynecomastia, antiandrogen effects |
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Triamterne, amiloride,
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block Na channels in CCT
use: hyperaldosteronism, K edpletion, CHF ES: hyperkalemia -> arrhythmias, |
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ACE inhibtors
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catopril, enalapril, lisinopril
inhibit ACE -> decreased angiotensin II and preventing inactivation of bradykinin (vasodilator) increased renin release due to loss of feedback inhibition use: HTN, CHF, diabetic renal disease toxicity: cough, angioedema, taste changes, hypotension, detal renal damage, rash, *hyperkalemia* avoid with bilateral renal artery stenosis - prevent constriction of efferent arterioles -> dec GFR -> inc serum creatinine ARBs- -sartans- same effects without cough |
