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220 Cards in this Set
- Front
- Back
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List the layers of the kidney starting from the outermost layer.
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Capsule, Cortex, Medulla, Pelvis, Ureter
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In relation to the uterine artery and vas deferens, where do the ureters pass?
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The ureters pass under both uterine artery and vas deferens
Water(ureters) under the bridge(artery/vas) |
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Name the major branches of the renal artery leading to the glomerulus.
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Renal artery, Interlobar arteries, Interlobular arteries, afferent arteriole
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Which kidney is usually taken in a transplant and why?
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The left because it has a longer renal vein.
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Juxtaglomerular cells are located in which structure?
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Afferent arteriole
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Total body water makes up what percentage of total body weight?
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60% total body water; 40% nonwater mass
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What percentage of total body water makes up the extracellular fluid? Intracellular?
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1/3 Extracellular; 2/3 intracellular
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Plasma volume accounts for what percentage of the extracellular fluid? Interstitial volume?
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Plasma volume is 25 percent of extracellular fluid. The remaining 75 percent consists of interstitial volume
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Which ion(s) have a higher concentration in the extracellular fluid?
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Na and Cl
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Which ion(s) have a higher concentration in the intracellular fluid?
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K
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Total body water(TBW) - Extracellular fluid(ECF) = ?
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TBW-ECF = Intracellular fluid
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How do you measure plasma volume?
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Radiolabeled Albumin
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How do you measure Extracellular volume?
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Inulin
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What is normal Osmolarity?
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290 mOsm
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What is the 60-40-20 rule? (with regards to % of Body weight)
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60% Total body water; 40% ICF; 20% ECF
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What is the formula for renal clearance?
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Cx= UxV/Px, where C= clearance of X, U= urine concentration of X, P= plasma concentration of X, and V= urine flow rate
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If Cx<GFR, what does that mean? If Cx>GFR?
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Cx< GFR indicates net tubular resorption of X, while Cx> GFR indicates net tubular secretion. (If Cx = GFR, there is no net secretion or resorption)
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What three structures make up the gloumerular filtration barrier and what is their mechanism of filtration?
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1. Fenestrated capillary endothelium (size barrier)
2. Fused basement membrane with heparan sulfate (negative charge barrier) 3. Epithelial layer consisting of podocyte foot processes |
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The basement membrane is lost is which general class of kidney diseases?
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Nephrotic syndrome
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What are the symptoms of nephrotic syndrome?
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Albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia
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What is the formula for GFR?
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GFR= Uinulin xV/Pinulin=Cinulin
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What is the formula for Renal Blood flow?
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RBF=RPF/(1-Hct)
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Why is PAH clearance used for determining effective renal plasma flow?
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PAH is both filtered and actively secreted. All PAH entering the kidney is excreted
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What is the formula for Effective renal plasma flow?
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UPAH xV/PPAH=C PAH
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What is the formula for Filtration Fraction?
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FF=GFR/RPF. GFR can be estimated w/ creatinine. Use PAH for RPF
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What is the formula for filtered load?
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GFRx plasma concentration
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Which renal vascular structure do NSAIDs act on, and what is the effect?
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NSAIDs act on the Afferent arteriole. They cause vasodilation.
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What is the effect on RPF, GFR, and FF with NSAID use?
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Increase RPF, Increase GFR, FF remains constant
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Which renal vascular structure do ACE inhibitors act on, and what is the effect?
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ACEI act on the efferent glomerular arteriold. They cause vasoconstriction
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What is the effect on RPF, GFR, and FF with ACE inhibitor use?
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Decrease RPF, Increase GFR, Increase FF
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What is the effect on RPF, GFR, and FF with afferent arteriole constriction?
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Decrease RPF, Decrease GFR, No change with FF
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What is the effect on RPF, GFR, and FF with efferent arteriolar constriction?
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Decrease RPF, Increase GFR, Increase FF
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What is the effect on RPF, GFR, and FF with increased plasma protein concentration?
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No change RPF, Decrease GFR, Decrease FF
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What is the effect on RPF, GFR, and FF with decreased plasma protein concentration?
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No change RPF, Increase GFR, Increase FF
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What is the effect of RPF, GFR, and FF with constriction of the ureter?
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No change RPF, Decrease GFR, Decrease FF
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What is the formula for free water clearance?
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CH2O=V-C OSM, V=urine flow rate; COSM=UOSMV/POSM
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What is the effect of ADH on free water clearance (CH2O)? Without?
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CH2O < 0 w/ ADH (retention of free water); CH2O> 0 without ADH (excretion of free water)
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What is effect of loop diuretics on free water clearance?
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CH2O = 0 (isotonic urine)
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Where is glucose absorbed in the kidney? What percentage of glucose is normally absorbed?
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Normally, 100 percent of glucose is absorbed in the proximal tubule
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At what does glucosuria begin? At what plasma glucose concentration is the transporter saturated? What diagnosis could that lead to?
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Plasma glucose greater than 200 mg/dL is when glucosuria starts, and it's a clue to diabetes. At 350 mg/dL, the glucose transporter is saturated
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Where are amino acids absorbed in the kidney, and via which process (passive/active)?
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Proximal tubule via secondary active transport. Three distinct carrier systems; competitive inhibition possible.
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Which section of the Nephron contains a brush border?
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Proximal tubule via secondary active transport. Three distinct carrier systems; competitive inhibition possible.
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What type of absorption occurs in the proximal tubule? (hypotonic, hypertonic, isotonic)
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Isotonic
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What is the effect of PTH on the proximal tubule?
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Inhibits the Na/Phosphate cotransport, leading to increased phosphate excretion
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What is the effect of Angiotensin II on the proximal tubule?
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Stimulates Na/H exchange, leading to increased Na and water excretion
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What enzyme converts CO2 and H2O into carbonic acid?
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Carbonic anhydrase
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Where is HCO3 resorbed in the kidney and by what process?
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Proximal tubule. HCO3 combines w/ H+ (via Na/H transport) forming H2CO3 in the lumen of the proximal tubule. H2CO3 then dissociates into CO2 and H20. The CO2 is then resorbed and combined with water in the cells of the proximal tubule via carbonic anhydrase. Once again, H2CO3 is formed, dissociates, and HCO3 is transported into the blood via a specific transporter
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Which ions/molecules are resorbed in the proximal tubule?
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Na, Cl, HCO3, K, H2O, glucose, amino acids
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Which ions/molecules are secreted in the proximal tubule?
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H, Organic acids/bases
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What occurs in the thin descending loop of Henle?
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Passive reabsorption of water via medullary hypertonicity. Makes urine hypertonic
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The thick ascending loop of Henle actively reabsorbs which ions transcellulary?
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Na, K, Cl
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Which ions are reabsorbed paracellularly in the thick ascending loop of Henle?
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Mg, Ca
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What is the tonicity of urine in the thick ascending limb and why?
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Hypotonic due to the impermeability of water and active reabsorption of ions (see other slides)
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Where is the Na/K/2Cl transporter located?
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Thick ascending loop of Henle
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What is the effect of PTH on the early distal convoluted tubules?
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Increase Ca/Na exchange leadingn to increased Calcium absorption
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Which ions are reabsorbed in the early distal convoluted tubule?
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Na and Cl
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What is the tonicity of urine in the early distal convoluted tubule?
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Hypotonic
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Which proteins are inserted into the lumen due to ADH secretion
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Aquaporins
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What is the effect of ADH in the collecting tubules?
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Acts of V2 receptors to increase aquaporin channels in the membrane, thereby increasing water resorption and making urine hypertonic
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Which ions are exchanged in the collecting tubules?
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Reabsorb Na in exchange for secreting K and H,
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What is the effect of aldosterone on the collecting tubules?
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Insertion of Na channels on the luminal side
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Which molecules have a relative concentration along the proximal tubule >1? (Tubular Fluid/Plasma, or TF/P)
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PAH>Creatinine>Inulin>Chloride>K+(barely >1)
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What does it mean to have a relative concentration along the proximal tubule > 1?
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solute is reabsorbed more slowly than water, and there is net secretion of solute
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Which molecule is the best indicator of GFR?
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Inulin (Creatinine has slight secretion, and is the best indicator endogenously)
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Which molecule has a relative concentration along the renal tubule equal to 1 and what does that mean? (Tubular fluid/plasma = 1)
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Na; It means that solute and water are reabsorbed at the same rate, and solute is neither reabsorbed nor secreted
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Which molecules have a relative concentration along the renal tubule (TF/P) < 1 and what does that mean? Tubular Fluid/Plasma)
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Inorganic phosphate, HCO3, Amino acids, and glucose; It means that solute is reabsorbed more quickly than water
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Which ion drives water reabsorption in the proximal tubule?
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Na
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Name three things that will cause the release of renin.
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Increase in blood pressure, decrease in Na delivery, increased sympathetic tone
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Which cells recognize an increase in blood pressure in the kidney?
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Juxtaglomerular cells
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Which cells recognize a decrease in Na delivery in the kidney?
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Macula densa cells
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Where is angiotensinogen made?
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Liver
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Angiotensinogen is converted to Ang I by what?
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Renin
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Where is Ang I converted to Ang II and by which enzyme?
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Lung; by ACE
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What are the effects of Ang II on vascular smooth muscle?
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Incr. BP by acting at Ang II rec
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What are the effects of Ang II on the efferent arteriole of the glomerulus and what is the net effect?
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Vasoconstriction leading to incr FF to preserve renal function in low-volume states
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What are the effect of Ang II on the adrenal gland and what the net effects of that?
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Increase aldosterone release, which activates the Na/K pump and opens Na channels in the principal cells leading to Na and H20 reabsorption
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What are the net effects of ang II acting on the pituitary?
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Increase ADH release, increasing aquaporin channels in principal cells, leading to net water reabsorption
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What are the net effects of ang II on the proximal tubule?
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Increase Na/H exchange in the proximal tubule leading to increased water reabsorption
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What are the effects of Ang II on the hypothalamus?
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Stimulate thirst
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Where is ANP released from and what is its effect?
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ANP is released from the atria in response to increased volume. It acts as a check on the renin-angiotensin-aldosterone system
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What is effect of renin on GFR?
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Decreased GFR
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How does ANP effect GFR?
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Decreased Renin, therefore Increases GFR
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Which hormone primarily regulates blood volume?
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Aldosterone
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Which hormone primarily regulates osmolarity
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ADH
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What is the effect of Ang II on baroreceptors?
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Decreases baroreceptor function to limit the reflex bradycardia that would accompany its pressor effects
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Which cells secrete renin?
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JG cells
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Erythropoietin: Source and Stimulus
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Peritubular capillaries; Hypoxia
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1,25-OH-Vitamin D: Source and Function
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Proximal tubule; ↑Intestinal Resorption of Ca and Phosphate
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Parathyroid Hormone: Renal effect
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↑Ca reabsorption (DT)/↓Phosphate reabsorption (PT); Stimulates 1,25-OH VitD production
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Renin: Source and function
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Juxtaglomerular cells; ↓Renal arterial pressure/↑SNS discharge (β1 effect)
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What controls afferent arteriole tone and what is the result
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Prostaglandins → Vasodilation → ↑GFR
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Effect of NSAIDs on renal vascularture
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⊣ Prostaglandin production (Normally vasodilate afferent arteriole)
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Atrial Natriuretic Peptide (ANP): Stimulus and Effect
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↑Atrial pressure; ↑GFR and Na filtration → ↓Volume
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Angiotensin II: Stimulus
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Synthesized in response to ↓BP
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Angiotensin II: Effect
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Constricts Efferent arteriole → ↑GFR and ↑FF w/ Compensatory Na reabsorption (DT) (Preserve renal function in low-volume state w/o loss of volume)
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ADH (Vasopressin): Stimulus
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↑Plasma Osmolarity and ↓Blood Volume
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ADH (Vasopressin): Effect
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Binds Principal cells → ↑Water Channels → ↑Water reabsorption
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Aldosterone: Stimulus
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↓Blood volume (via ATII) and ↑Plasma Potassium
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Aldosterone: Effect
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↑Na reabsorption; Indirect ↑K secretion, ↑H secretion
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Henderson-Hasselbach equation
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PH = pKa + log (HCO3 / 0,03xPco2)
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Metabolic Acidosis: Abnormal lab value and compensatory response
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↓pH / ↓Pco2 / ↓HCO3; Hyperventilation
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Metabolic Alkalosis: Abnormal lab value and compensatory response
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↑pH / ↑Pco2 / ↑HCO3; Hypoventilation
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Respiratory Acidosis: Abnormal lab value and compensatory response
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↓pH / ↑Pco2 / ↑HCO3; ↑Renal [HCO3] reabsorption
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Respiratory Alkalosis: Abnormal lab value and compensatory response
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↑pH / ↓Pco2 / ↓HCO3; ↓Renal [HCO3] reabsorption
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Winter's Formula
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Quantification of respiratory compensation in response to metabolic acidosis (Pco2 = 1.5(HCO3) + 8 (+/-2))
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Causes of Metabolic Alkalosis (with compensation)
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Diuretic use, Vomiting, Antacid use, Hyperaldosteronism
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Causes of Respiratory Alkalosis
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Hyperventilation, Aspirin Ingestion (early)
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Causes of Respitatory Acidosis
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Hypoventilation – Obstruction, Lung Disease, Opioids/Narcotics/Sedatives, Weak respiratory muscles
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Causes of Metabolic Acidosis + ↑AG
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MUDPILES – Methanol, Uremia, DKA, Paraldehyde/Phenformin, Iron/INH, Lactic Acidosis, Ethylene glycol, Salicylates
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Causes of Metabolic Acidosis + ↓AG
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Diarrhea, Glue sniffing, Renal tubular acidosis, Hyperchloremia
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Anion Gap calculation
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Na – (Cl + HCO3)
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What is the cause of Type 1 renal tubular acidosis?
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Defect in H/K ATPase in Collecting tubule → Can't secrete H → HYPOkalemia
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What is the cause of Type 2 renal tubular acidosis?
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Defect in PT HCO3 reabsorption → HYPOkalemia
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What is the cause of Type 4 renal tubular acidosis?
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↓Aldosterone → HYPERkalemia ⊣ Ammonia excretion in PT; Ultimately: ↓Urine pH d/t ↓buffer
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Significance of casts in urine
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Hematuria/Pyuria of a NON-renal origin
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Injury producing RBC casts
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Glomerular inflammation (Nepritic), Ischemia, Malignant HTN
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Injury producing WBC casts
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Tubulointerstitial disease, Acute pyelonephritis, Glomerular disorder
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Injury producing Granular (or Muddy brown) casts
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Acute Tubular Necrosis
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Injury producing Waxy casts
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Advanced renal disease/Chronic renal failure
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Significance of RBC/NO casts in urine
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Bladder cancer
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Significance of WBC/NO casts in urine
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Acute cystitis
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Nephritic syndrome: Describe
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Inflammatory process of the glomeruli → Hematuria, Azotemia, RBC casts, Oliguria, HTN, Proteinuria
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Causes of Nephritic Syndrome
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Acute Post-Streptococcal glomerulonephritis, Rapidly progressive (crescentic) glomerulonephritis, Diffuse proliferative glomerulonephritis, IgA glomerulonephropathy (Berger's disease), Alport's syndrome
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Acute post-streptococcal glomerulonephritis: LM findings
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Enlarged/Hypercellular glomeruli w/ Neutrophils and a “lumpy-bumpy” appearance
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Acute post-streptococcal glomerulonephritis: EM findings
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Subepithelial immune complex (IC) humps
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Acute post-streptococcal glomerulonephritis: Classical presentation
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Child with peripheral/periorbital edema which resolves spontaneously
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Rapidly progressive glomerulonephritis: LM and IF findings
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Crescent-moon shaped – Also seen in: Goodpasture's syndrome, Wegeners Granulomatosis, Microscopic Polyarteritis
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Goodpasture Syndrome: IF findings
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Linear IF due to Anti-GBM Ab (Type II hypersensitivity)
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Goodpasture Syndrome: Presentation characterstics
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Male dominant with hematuria/hemoptysis (d/t lung involvement)
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Wegener's granulomatosis: associated IF antibody
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C-ANCA
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Microscopic polyarteritis: associated IF antibody
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P-ANCA
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Diffuse proliferative glomerulonephritis: Causative process
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Subendothelial DNA-anti-DNA immune complexes → Wire looping of capilaries
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Most common cause of death in systemic lupus erythematosus?
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Diffuse proliferative glomerulonephritis
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Berger's disease: Causative process
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↑IgA → Immune complex deposition in mesangium (IgA glomerulopathy) – Often following Upper Respiratory Infection
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Alport's Syndrome: Causative process
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Mutation in Type IV collagen → Split basement membrane
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Alport's Syndrome: Associated pathologies
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Nerve disorder, Ocular disorder, Deafness
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Presentation of Nephrotic Syndrome
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Massive proteinuria (>3.5g/day), Hyperlipidemia, Edema
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Causes of Nephrotic Syndrome
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Membranous glomerulonephritis, Minimal change disease, Amyloidosis, Diabetic glomerulonephropathy, Focal segmental glomerulosclerosis, Membranoproliferative glomerulonephritis
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Membranous glomerulonephritis: LM findings
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Diffuse capillary and GBM thickening
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Membranous glomerulonephritis: EM findings
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“Spike and dome”
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Membranous glomerulonephritis: Causes
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Drugs, Infections, SLE
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Most common cause of adult nephrotic syndrome
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Membranous Glomerulonephritis
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Minimal change disease: LM findings
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NONE
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Minimal change disease: EM findings
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Food process effacement
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Minimal change disease: Presentation
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Most commonly in children, often postinfectious
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Minimal change disease: Treatment
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Corticosteroids
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Amyloidosis: LM findings
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Congo red stain, apple-green birefringence
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Amyloidosis: Associated pathologies
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Multiple myeloma, TB, Rheumatoid athritis (chronic conditions)
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Diabetic glomerulonephropathy: Causative process
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Nonenzymatic glycosylation of: GBM → ↑Permeability/Thickening; Arterioles → ↑GFR → Mesanglial damage, wire looping
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Diabetic glomerulonephropathy: LM findings
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Kimmelstiel-Wilson “wire loop” lesions
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Focal segmental glomerulosclerosis: LM findings
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Segmental sclerosis and hyalinosis
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Most common glomerular disease in HIV patients?
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Focal segmental glomerulosclerosis
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Membranoproliferative glomerulonephritis: IF findings
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Subendothelial immune complexes with granular appearance
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Membranoproliferative glomerulonephritis: EM findings
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“Tram track” appearance = GBM splitting d/t mesanglial ingrowth
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Membranoproliferative glomerulonephritis: Associated infections
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Hepatitis B > Hepatitis C
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Complications of kidney stones
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Hydronephrosis, Pyelonephritis
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Major types of kidney stones
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Calcium, Ammonium-Magnesium-Phosphate (Struvite), Uric acid, Cystine
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Most common kidney stones?
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Calcium (-oxalate, -phosphate or -both)
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Calcium kidney stones – precipitating conditions
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Hypercalcemia (Cancer, ↑PTH, ↑VitD, Milk-alkali syndrome)
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What is the most common cause(s) of Calcium-Oxalate kidney stones?
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Ethylene glycol (antifreeze) or Vitamin C abuse
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Kidney stone type caused by infection w/ Urease(+) bugs
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Ammonium-magnesium-phosphate (struvite)
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Complications of Ammonium-magnesium-phosphate (Struvite) kidneys stones
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Staghorn calculi which can be nidus for UTIs
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Precipitating condition for Ammonium-magnesium-phosphate kidney stones
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Alkaluria
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Uric acid kidney stones: associated pathology
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Hyperuricemia (gout), Diseases with increase cell turnover (i.e. Leukemia, Myeloproliferative disorders)
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Radiologic appearance of Uric acid kidney stones
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ONLY kidney stone that is radiolUcent
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Cystine kidney stones: causative condition
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Secondary to Cystinuria
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Cystine kidney stones: Treatment
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Alkalinization of urine
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Imaging characteristics of Cystine kidney stones
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Hexagonal shape and faintly radiopaque
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Renal Cell Carcinoma is associated with what neurocutaneous disorder?
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von Hippel-Lindau disease
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What are the clinical findings in renal cell carcinoma?
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hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss
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Most common renal malignancy of early childhood:
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Wilm's Tumor
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What gene deletion is associated with Wilm's Tumor?
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WT1 Tumor Suppression Gene on Chromosome 11
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What are the four anomalies of the WAGR complex?
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Wilm's Tumor, Aniridia, GU malformation, Retardation
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Most common tumor of urinary tract:
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Transitional Cell Carcinoma
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Risk factors for Bladder Cancer:
|
Phenacetin, Smoking, Aniline dyes, Cyclophosphamide (Pee SAC)
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White Cell Casts are diagnostic for what?
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Acute Pyelonephritis
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What renal disorder is associated with obstetric catastropies?
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Diffuse Cortical Necrosis
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What drugs typically cause drug-induced interstitial nephritis?
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penicillin, NSAIDS, and diuretics
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What is the mechanism behind drug-induced interstitial nephritis?
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Drugs act as haptens inducing hypersensitivity
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What is the most common cause of acute renal failure?
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Acute tubular necrosis
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What are the three main causes of acute tubular necrosis?
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ischemia, trauma, and toxins
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What are the three stages of acute tubular necrosis?
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inciting event, maintenance (low urine), and recovery
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What are the four main causes of renal papillary necrosis?
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diabetes, acute pyelonephritis, chronic Tylenol use, and sickle cell anemia
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Will excretion of sodium be higher in prerenal or renal acute renal failure?
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Renal acute renal failure
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Will BUN/Cr ratio be higher in prerenal or renal acute renal failure?
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prerenal acute renal failure
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What are the two main causes of chronic renal failure?
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diabetes and hypertension
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Consequences of renal failure:
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anemia, renal osteodystrophy, hyperkalemia, metabolic acidosis, uremic encephalopathy, sodium and water excess (CHF and edema), chronic pyelonephritis, and HTN
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What is Fanconi's syndrome?
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a defect on proximal tubule transport
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What are the complications of Fanconi's syndrome?
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rickets, osteomalacia, hypokalemia, and metabloic acidosis
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What gene mutation causes adult polycystic kidney disease?
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Autosomal dominant mutation in APKD1
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What are the extrarenal manifestations of adult polycystic kidney disease?
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Polycystic liver disease, berry aneurysms, mitral valve prolapse
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What is the inheritance pattern for infantile polycystic kidney disease?
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autosomal recessive
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What is medullary sponge disease?
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collecting duct cysts with a good prognosis
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What are the ECG findings in hypokalemia?
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U waves, flattened T waves
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What are the ECG findings in hyperkalemia?
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peaked T waves, wide QRS interval
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What is the mechanism of mannitol?
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an osmotic diuretic that causes increased tubular fluid osmolarity, which increases urine flow rate
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The use of mannitol is contraindicated in what patients?
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CHF and anuria
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What enzyme is inhibited by the diuretic, Acetazolamide?
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Carbonic anhydrase
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What are the uses for Acetazolamide?
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Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
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Where is the site of action of Furosemide?
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Inhibits the Na, K, 2 Cl co-transport system in the thick ascending loop of Henle
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Excretion of what electrolyte is increased by Furosemide?
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Calcium (Loops Lose calcium)
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Uses of Furosemide?
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CHF, cirrhosis, nephrotic syndrome, pulmonary edema, HTN, hypercalemia
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Toxicity of Furosemide:
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Ototoxicity, Hypokalemia, Dehydration, Allergy (Sulfa), Nephritis, Gout (OH DANG!)
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What type of diuretic is Ethacrynic Acid?
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A Loop Diuretic (same mechanism as furosemide)
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Clinical uses of Ethacrynic Acid?
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Diuresis in patients allergic to sulfa drugs
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What is the mechanism of Hydrochlorothiazide?
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Inhibits NaCl reabsorption in the early distal tubule and it decreases calcium excretion
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Toxicity of Hydrochlorothiazide:
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Hyperglycemia, Hyperlipidemia, Hyperuricemia, and Hypercalcemia
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Spironolactone, Triamterene, Amiloride, Eplerenone
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Potasium Sparing Diuretics (The K+ STAys)
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What is the mechanism of Spironolactone?
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Competitive Aldosterone Receptor Antagonist
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What are the clinical uses of Potassium Sparing Diuretics?
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Hyperaldosteronism, Potassium depletion, and CHF
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Which diuretic causes gynecomastia?
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Spironolactone
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Which diuretics cause acidemia?
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carbonic anhydrase inhibitors and potassium sparing diuretics
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What diuretics cause alkalemia?
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Loop diuretics and thiazides
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Which diuretic increases urine calcium concentration?
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Loop diuretics
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Which diuretic decreases urine calcium concentration?
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Thiazides
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What enzyme is inhibited Captopril, enalapril, and Lisinopril?
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Angiotensin-converting enzyme
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How do ACE inhibitors effect renin release?
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Increase renin release
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Uses of ACE inhibitors?
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HTN, CHF, and diabetic renal disease
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Toxicities associated with ACE inhibtors:
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Cough, Angioedema, Proteinuria, Taste changes, HypOtension, Pregnancy problems, Rash, Increased renin, Lower AT II (pneumonic: CAPTOPRIL), and also hyperkalemia
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What is the mechanism for Losartan?
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AT II receptor antagonist (benefit: does not cause cough!)
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