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142 Cards in this Set
- Front
- Back
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which kidney taken from donor if there's a choice and why?
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L kidney, b/c it has longer renal vein
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which part of renal vasculature is important to RAA system?
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the JG cells in the Afferent Arteriole
-the JG cell secrete Renin in response to decr Renal BP, decr Na delivery to Distal Tubule (sensed by the Macula Densa), incr sympathetic tone (β1 stim) |
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type of epithelium in bladder
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Transitional Cell Epithelium
-also all the way up to Renal Calyses- Renal Calyx, Renal Pelvis, Ureter, Bladder all have transitional cell epithelium) |
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relationship btw Ureters, Uterine artery / Ductus Deferens?
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Ureters pass under the Uterine a (in F), under Ductus Deferens (in M)
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break down the %'s of total body weight in terms of water
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40% nonwater, 60% TBW
-60% → 40% or 2/3 ICF, 20% or 1/3 ECF -of ICF → 5% or 1/4 Plasma, 15% or 3/4 Interstitial Vol -the %'s are the % of Body Weight: so 60% body weight is TBW, 40% is ICF, 20% is ECF, 5% is plasma, 15% is interstitial |
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nrl osmolarity in body/plasma, etc
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290 mOsm
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what is Glomerular filtration barrier made of, and what happens in Nephrotic Syndrome
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made of:
-Fenestrated capillary endothelium (size barrier) -Fused Basement Membrane of Heparan Sulfate -Epithelial layer of Podocyte foot processes charge barrier lost in nephrotic syndrome |
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how calculate renal clearance of a substance x
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Cx = UxV/P
C = Clearance, U = Urine [x], V = urine flow rate, P = plasma [x] |
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what if, for clearance:
Cx < GFR Cx > GFR Cx = GFR |
Cx < GFR: net tubular reabsorption of x
Cx > GFR: net tubular secretion Cx = GFR: neither secretion or reabsorption |
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what substance use to calculate GFR ~accurately
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Inulin
-it is freely filtered, and neither reabsorbed or secreted -Creatinine is used more often clinically tho, but slightly OVERestimates GFR b/c it is both filtered & ~secreted |
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equation to relate GFR, Urine [inulin], urine flow rate, Plasma [inulin], Clearance of inulin
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GFR = [(Urine[inulin]*V) / Plasma[inulin]) = Clearance of inulin
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what can be used to estimate renal plasma flow?
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PAH can estimate Effective Renal Plasma Flow (ERPF) b/c it is both filtered & actively secreted in Prox Tubule; all PAH entering the kidney is excreted
ERPF = (Urine[PAH]*V)/Plasma[PAH] Renal Blood Flow = RPF/(1-Hct) |
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how calculate Renal Blood Flow?
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RBF = RPF "ERPF" / (1-Hct)
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calculate Filtration Fraction?
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FF = GFR / RPF = Creatinine/PAH
-nrl FF = 20% |
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GFR / RPF is used for?
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GFR / RPF = FF = Creatinine/PAH
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how do Prostaglandins & NSAIDs work on Renal Plasma Flow
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PG's DILATE the Afferent Artery
-this → incr RPF & incr GFR, so FF is constant (FF = GFR/RPF) -NSAIDs inhibit PG production, so decr GFR, decr RPF, decr Filtration amount, but not FF |
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where does Angiotensin II work in the kidney?
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AT II works to constrict the Efferent arteriole
-this incr GFR, but decr RPF, so FF incr (FF = GFR/RPF) -ACE-I stop this b/c stop production of Angiotensin in lung |
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Afferent arteriole constiction vs Efferent arteriole constriction
(effects on GFR, RPF, FF) |
Afferent arteriole constiction
-decr GFR, decr RPF, NO change FF (FF = GFR/RPF) Efferent arteriole constriction -incr GFR, decr RPF, incr FF (FF = GFR/RPF) |
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effects on GFR, RPF, FF of incr Plasma protein concentration vs decr Plasma protein concentration
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incr Plasma Protein [ ]
-decr GFR, no change RPF, so decr FF (FF = GFR/RPF) decr Plasma Protein [ ] -incr GFR, no change RPF, so incr FF (FF = GFR/RPF) |
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effect of Ureter contriction on GFR, RPF, FF
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Ureter constriction:
-decr GFR, no change RPF, so decr FF (FF = GFR/RPF) |
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how calculate Clearance H2O, and how affected by ADH
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C(osm) = (U(osm)*V) / P
if C(H2O) < 0: w/ ADH, retention of free H2O if C(H2O) > 0: w/o ADH, excretion of free H2O as in Diabetes Insipidus if C(H2O) = 0: isotonic urine, common for Loop Diuretics |
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C(H2O) < 0:
C(H2O) > 0: C(H2O) = 0: |
C(H2O) < 0: retaining free H2O; ADH onboard
C(H2O) > 0: clearing free H2O, no ADH; diabetes insipidus C(H2O) = 0: isotonic urine, common w/ Loop Diuretics |
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how calculate Filtered Load of x and Excretion Rate of x
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Filtered Load = GFR * Px
Excretion Rate = V * Ux |
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behavior of glucose in kidneys
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at nrl plasma levels, all Glc filtered is reabsorbed by Na/Glc cotransport
-at plasma Glc 160-200, glucosuria begins (threshold) -at Glc 350, all transporters fully saturated |
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where are Amino Acids reabsorbed, and what is one big deficiency of AA reabsorption
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AA use Na-dependent transporters in PT
-Hartnup's Disease = deficiency of neutral AA (Tryptophan) transporter → Pellagra (diarrhea, dermatitis, dementia, amino aciduria) |
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inability to reabsorb Tryptophan in renal tubule can → what complication
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Hartnup's Disease
-autorecessive -can → Pellagra |
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where does PTH work, and what does it do?
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PTH inhibits Na/PO4 cotransport in the Proximal Tubule
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what does AT II do in the kidney
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AT II:
-constricts the Efferent arteriole -stimulates Na/H exchange in Prox Tubule → incr Na & H2O reabsorption → contraction alkalosis |
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what happens in terms of ion changes in Tk Ascending Loop of Henle
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Na/K/2Cl cotransporter brings in those ions, indirectly brings in Mg & Ca
-impermeable to H2O -makes urine LESS concentrated as it ascends **just before, the Thin Descending Loop of Henle passively reabsorbs H2O via Medullary Hypertonicity...THIS is the MOST [ ]'d part of the nephron (the thin descending limb) w/o ADH present |
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diluting segment?
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Distal Convoluted Tubule
*Na/K/2Cl are reabsorbed in Tk Asc Limb of Loop making urine less concentrated, but DT is the "diluting segment" DT is also where Ca/Na occurs by PTH influence |
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where in nephron does PTH act, and what's it do?
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PTH acts on DCT to induce the Ca/Na exchanger → Ca reabsorbed, Na secreted into cell
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what/where does Aldosterone do in Kidney, and why affect K?
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in Collecting Ducts, Aldosterone induces insertion of Na chnnls into luminal side of Principle cell → Na reabsorption → drives Na/K ATPase to bring Na into blood, K into cell → K out of cell into urine
-thus, Aldosterone stim's Na UPTAKE into blood, and K EXCRETION |
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what/where does ADH act in kidney
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ADH induces binds V2-R to cause Aquaporin2 chnnls to be inserted to the Luminal side of Principle cells of Collecting Ducts to → H2O reuptake
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substance made in kidneys that would be useful after a major bleed?
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Erythropoietin (EPO)
-made in response to hypoxia from endothelial cells of peritubular capillaries |
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pathway of Vitamin D sythesis
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7-dehydrocholesterol is converted by UV light in skin to Cholecalciferol (Vit D3) → to Liver, where 25-hydroxylase converts this to 25-OH Vit D (25-hydroxycholecalciferol) → to Kidney where PTH stim's 1α-hydroxylase to convert that to 1,25-(OH)2-Vit D (dihydroxycholecalciferol)
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how does PTH affect kidney?
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-PTH induces Na/Ca exchange in DCT to bring in Ca
-PTH inhibits Na/PO4 cotransport in PCT to → PO4 excretion -PTH stim's 1α-hydroxylase to make 1,25-(OH)2-Vit D |
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actions of Aldosterone on:
Na K H HCO3 H2O |
Aldosterone's effects on:
Na: renal reabsorption K: renal secretion H: renal secretion HCO3: renal production H2O: renal reabsorption -so, b/c H secretion and HCO3 production, Aldosterone → Alkalosis |
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what's Atrial Natriuretic Peptide, where made, what do, etc?
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ANP:
-secreted from atria in response to incr atrial P → incr GFR & incr Na filtration w/ no compensatory Na reabsorption in distal nephron to give Na & Vol loss |
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insulin deficiency, beta-adrenergic antagonists, acidosis, hyperosmolarity, digitalis, cell lysis can all cause what ionic disturbance
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insulin deficiency, beta-adrenergic antagonists, acidosis, hyperosmolarity, digitalis, cell lysis can all cause K shifting OUT of cells, aka HYPERKALEMIA
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insulin, beta-adrenergic agonists, alkalosis, hypo-osmolarity can all cause what ionic disturbance
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insulin, beta-adrenergic agonists, alkalosis, hypo-osmolarity can all cause K shifting INTO cells, aka HYPOKALEMIA
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easy Henderson-Hasselbach for checking acid-base phys
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pH = pKa + log [HCO3]/0.03*PCO2
***and pKa of this system is 6.1*** |
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Anion Gap =
-what's nrl? |
Anion Gap = Na - (Cl+HCO3)
-nrl AG = 8-12 |
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some possible causes of Respiratory Acidosis
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airway obstruction, acute lung disease, chronic lung disease, opioids, narcotics, sedatives, respiratory muscle weakening
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some causes of incr Anion Gap met Acidosis
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incr Anion Gap Met Acidosis
MUDPILES: Methanol Uremia Diabetic ketoacidosis Paraldehyde or Phenformin Iron tablets or Isoniazid Lactic acidosis & hypoxia Ethylene glycol Salicylates |
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some causes of nrl Anion Gap met acidosis
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nrl AG acidosis:
-diarrhea, glue sniffing, renal tubular acidosis, hyperchloremia |
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some causes of respiratory alkalosis
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respiratory alkalosis:
-hyperventilation, early ASA ingestion |
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some causes of metabolic alkalosis
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diuretic use (contraction alkalosis), V, antacid use, hyperaldosteronism
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difference btw Type 1 & 2 Renal Tubular Acidosis?
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Type 1 ("Distal") Renal Tubular Acidosis
-defect in collecting tubule's ability to excrete H; urine pH > 5.3 -a/w Hypokalemia & risk of Ca-kidney stones vs Type 2 ("Proximal") Renal Tubular Acidosis -defect in Prox Tubule HCO3 reabsorption -a/w Hypokalemia, Hypophosphatemic Rickets |
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difference btw Type 1 & 4 Renal Tubular Acidosis?
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Type 1 ("Distal") Renal Tubular Acidosis
-defect in Collecting Tubule's ability to excrete H -a/w hypokalemia and incr risk of Ca-kidney stones vs Type 4 ("Hyperkalemic") Renal Tubular Acidosis -Hypoaldosteronism or Lack of Collecting Tubule response to Aldosterone → Hyperkalemia → inhibition of ammonia excretion in Prox Tubule -decr urine pH |
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difference btw Type 2 & 4 Renal Tubular Acidosis?
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Type 2 ("Proximal") Renal Tubular Acidosis
-defect in Prox Tubule HCO3 reabsorption -a/w hypokalemia and hypophosphatemic rickets vs Type 4 ("Hyperkalemic") Renal Tubular Acidosis -hypoaldosteronism or lack of collecting tubule response to aldosterone → hyperkalemia → inhibition of ammonia excretion -decr urine pH due to decr buffering capacity |
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RBC casts in urine DDx
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glomerulonephritis, ischemia, malignant HTN
**nephritic type of glomerulonephritis (<3.5g protein per day) |
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WBC casts in urine DDx
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**Acute Pyelonephritis**, tubulointerstitial inflamm (acute tubulointerstitial nephritis), transplant rejection
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Granular ("muddy brown") casts in urine DDx
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Acute Tubular Necrosis
-another name for this type of cast is "Renal Tubular Cell Cast" |
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Waxy casts in urine DDx
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advanced renal disease / Chronic Renal Failure
-tubules nrl'ly make a waxy substance, so w/ decr flow → waxy cast |
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Fatty casts in urine DDx
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Nephrotic Syndrome (>3.5g protein per day)
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nephritic syndrome would have what casts in urine
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RBC casts in Nephritic Syndrome (<3.5g protein per day)
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nephrotic syndrome would have what casts in urine
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Fatty casts in Nephrotic Syndrome (>3.5g protein per day)
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Hematuria, RBC casts, Oliguria, HTN, mild proteinuria
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Nephritic Syndrome
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child had pharyngitis about 2 wks ago. now has hematuria, puffy face, hematuria, (-) ASO titers. what expect to see on Light Micro, EM, and IF?
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this kid has Poststreptococcal Glomerulonephritis
-LM: lumpy-bumpy appearance to glomeruli -EM: **subepithelial** IC deposits -IF: **granular** deposits -(-)ASO nrl, incr anti-DNaseB (+), (+) streptozyme -resolves spontaneously |
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glomerulus w/ lumpy-bumpy light microscopy, subepithelial humps, granular IF, what could this be?
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Acute Poststreptococcal Glomerulonephritis
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hematuria, RBC casts, TN, IF shows linear deposition, what would LM & IF show?
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this is Goodpasture syndrome, causing Rapidly Progressive Cresentic Glomerulonephritis
-LM & IF: crescent-moon shaped deposits of fibrin & plasma proteins w/ glomerular parietal cells, monocytes, macrophages |
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35 y.o F w/ rash on both sides of her nose and arthralgias, develops hematuria w/ RBC casts. what expect to see on kidney Bx?
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this is SLE causing Diffuse Proliferative Glomerulonephritis
-Subendothelial DNA/anti-DNA IC's → "wire-looping" of capillaries -Granular IF of Ig's and Complement |
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LM & IF shows mesangial deposits of IC's, what is this
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mesangial IC deposits c/w IgA Glomerulopathy, "Berger's Disease"
-expect Granular Mesangial deposits of IgA...IgA1 NOT IgA2 -recurrent episodes common after viral infections, URI, acute gastroenteritis |
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mutation in Type IV collagen causing nerve disorders, ocular disorders, deafness, what kidney manifestation expect?
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Alport's Syndrome- "can't see, can't pee, can't hear"
-b/c d/o of Type IV collagen → split basement membrane, and nephritic syndrome |
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IF: granular IC deposition, EM: subepithelial humps, LM: lumpy-bumpy hypercellular
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Acute Poststreptococcal glomerulonephritis
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IF: linear pattern, LM & IF: cresent-moon shape lymphocytic infiltrate
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Rapidly Progressive Cresentic Glomerulonephritis
(Goodpasture, Wegener's, Microscopic Polyarteritis) |
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LM: subendothelial deposits w/ wire-looping, IF: granular
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Diffuse Proliferative Glomerulonephritis (SLE)
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IF: mesangial IC deposits
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IgA Glomerulopathy (Berger's disease)
*Diabetic Glomerulopathy is also Mesangial, but not IC* |
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nephritis, deafness, cataracts
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Alports Syndrome
-mutation in Type IV collagen -"can't see, can't pee, can't hear" |
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after invasive vascular procedure, have S/Sx of renal failure & toe gangrene
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Atheroembolic Renal Disease
-cholesterol can be released from larger arteries during procedure, and lodge/block renal arterioles |
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during chemo, pt develops acute renal failure S/Sx, what could be causing this?
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Tumor Lysis Syndrome
-tubular obstruction w/ Urate crystals |
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LM: diffuse capillary & GBM thickening, EM: spike & dome w/ subepithelial deposits, IF: granular
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Membranous Glomerulonephritis (Diffuse Membranous Glomerulopathy)
-the M/C cause of nephrotic syndrome in adults -subepithelial deposits |
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m/c cause of nephrotic syndrome in adults
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Membranous Glomerulonephritis ("Diffuse Membranous Glomerulopathy")
-subepithelial deposits |
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m/c cause of nephrotic syndrome in kids
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Minimal Change Disease
-LM: nrl glomeruli, EM: foot process effacement/fusion -selective albumin loss, not globulins, due to GBM polyanion loss -responds to corticosteroid Tx |
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child w/ proteinuria, LM shows nrl glomeruli
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Minimal Change Disease
-if looked at EM: foot process effacement/fusion -loss of albumin due to GBM polyanion loss due to T cell cytokines |
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nephrotic syndrome, LM shows a glomerular deposit that stains apple-green w/ Congo red
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Amyloidosis
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LM: mesangial expansion, GBM thickening, nodular glomerulosclerosis, ovoid hyaline PAS (+) deposits
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Diabetic Glomerulonephropathy
-Nonenzymatic glycosylation (NEG) of GBM → incr permeability & GBM thickening -the "nodular glomerulosclerosis w/ ovoid, hyaline PAS (+) deposits = Kimmelstiel-Wilson disease |
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LM: segmental sclerosis, hyalinosis, IgM & C3 deposits
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Focal Segmental Glomerulosclerosis
-IF: IgM & C3 -Podocin (NPHS2) mutation -degeneration & disruption of VECs -M/C glomerular disease in HIV/IVDA pts |
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subendothelial ICs w/ Granular IF, EM: 'tram-tracking' appearance
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Membranoproliferative Glomerulonephritis, Type I
Type II is due to overactive C3 Convertase due to autoAb that binds it and prevents degredation |
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2 causes of Subepithelial deposits in glomeruli
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1) Acute Poststreptococcal Glomerulonephritis (Nephritic)
2) Diffuse Membranous Glomerulonephritis (Nephrotic) |
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2 causes of Subendothelial deposits
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1) Diffuse Proliferative Glomerulonephritis (nephritic)
2) Membranoproliferative Glomerulonephritis (nephrotic) |
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2 causes of Mesangial deposits
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1) Berger's Disease ("IgA Glomerulopathy")
2) Diabetic Glomerulopathy |
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easy way to prevent Urolithiasis
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Urolithiasis = Kidney stones
-easy way to prevent is high fluid intake b/c low urine Vol → incr risk of stones |
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m/c type of kidney stones, and most common type of that group
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Calcium kidney stones = m/c type
-of these, Ca-oxalate stones are m/c -what can lead to this? cond's that cause hypercalcemia (cancer, incr PTH, incr Vit D, milk-alkali syndrome) |
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high PTH and Vit D can → what obstructive process in kidneys
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high PTH and Vit D can → hypercalcemia → hypercalciuria and Ca kidney stones
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Proteus vulgaris common complication in kidneys
-what can incr the risk of this complication |
Proteus vulgaris → high risk of Ammonium-Mg-PO4 stones ("struvite stones")
-b/c Urease (+)!! -can form Staghorn Calculi that can serve as nidus for UTIs -worsened risk by Alkaluria |
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Staphylococcus, Klebsiella can cause what problems in kidney (besides UTI)
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along w/ Proteus vulgaris, Staph & Klebsiella are Urease (+), thus, can lead to formation of Ammonium-Mg-PO4 "struvite" stones
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pt w/ gout is at risk for what type of kidney problem
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Uric acid kidney stone formation
-common when incr cell turnover in general, such as Leukemia, Myeloproliferative d/o |
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how does ASA affect uric acid excretion
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all but extremely high doses of ASA decrease tubular uric acid secretion
-aka, this keeps uric acid w/in the body, bad b/c can cause Sx like typical Gout -only extremely high doses can stim uricosuria (& remember ASA can be toxic) |
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hematuria, palpable flank mass, incr Hct, fever in 55 y.o M
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Renal Cell Carcinoma
-RCC is the m/c renal malignancy -it can invade IVC and spread hematogenously -originates in renal tubular cells → polygonal clear cells -other Sx incl fever, wt loss -the incr Hct is due to ectopic EPO secretion, can also secrete ACTH, PTHrP, PRL |
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pt presents w/ incr Hct, Cushing's-like Sx, incr Ca, incr PRL, what could this be?
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Renal Cell Carcinoma
-incr Hct due to ectopic EPO secretion -Cushing's like Sx due to ectopic ACTH production -incr Ca due to incr PTHrP & PRL |
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m/c cause of a palpable flank mass in children
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Wilm's tumor (Nephroblastoma)
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renal manifestation of von Hippel-Lindaue disease
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Renal Cell Carcinoma
-vHL disease = hemangioblastomas of retina/cerebellum/medulla, multiple bilateral RCC, Pheochromocytoma -due to deletion of tumor suppressor VHL gene on chr 3 |
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testicular enlargement in a 65 y.o pt w/ hematuria, flank pain, fever, palpable flank mass
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this pt can have a Renal Cell Carcinoma
-if the RCC is on the L side, it can → Varicocele -this is b/c L gonad drained by L Gonadal v, which feeds into L Renal v, that goes into IVC (vs R Gonadal v goes right into IVC) |
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what would a Renal Cell Carcinoma look like histologically/grossly
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Histo: nests of cells w/ clear cytoplasm; arises from Prox Tubular cells → clear cells w/ Lipid & Glycogen, giving it its yellow color on gross exam
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m/c cause of palpable flank mass in child w/ possible hematuria
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Wilms' tumor
-sporadic type is m/c -genetic a/w deletion of tumor suppressor WT1 on Chr 11 -can be part of WAGR complex: Wilms tumor, Aniridia (no iris), Genitourinary malformations, mental-motor Retardation |
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child w/ mental/motor retardation, absent iris, and palpable flank mass is m/l to also have what
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Genitourinary malformations
WAGR complex Wilms tumor, Aniridia (no iris), Genitourinary malformations, mental/motor Retardation -the palpable flank mass in question = Wilms' tumor (m/c renal tumor in kids) |
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possible cause of renal amyloid deposition in a pt back pain
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Multiple Myeloma
-multiple myeloma can cause renal amyloid deposition |
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painless hematuria
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Transitional Cell Carcinoma
-m/c tumor of UT (can be in renal calyces, pelvis, ureters, bladder) -a/w problems in your Pee SAC: Phenacetin, Smoking, Aniline dyes, Cyclophosphamide |
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hematuria and SCC in foreigner
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Schistosoma hematobium
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cystitis vs pyelonephritis
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Cystitis
-infection of bladder -dysuria, incr freq, suprapubic pain -NO fever, NO flank pain, NO WBC casts Pyelonephritis -infection of Kidneys -(+)Fever, (+) Flank Pain/CVA tenderness, (+) WBC casts -E coli = m/c, then Enterococci |
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fever, flank pain, incr freq and dysuria in 28 y.o woman
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Acute Pyelonephritis
-UA: WBC casts!!, pyuria, bacteriuria, hematuria, CVA tenderness, N/V -F > M b/c F have shorter urethra |
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~2.5 wks after routine Tx for pharyngitis, pt develops fever, oliguria, rash, UA is (+) for eosinophils
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Acute Drug-Induced Tubular Interstitial Nephritis
-Type I & IV Hypersensitivity rxn to Rx that acts as a hapten -m/c Rx's causing: PCN (esp Methicillin), Rifampin, Sulfonamides, NSAIDs, diuretics -1-2 wk after admin, fever, rash, hematuria, CVA tenderness, eosinophiluria -BUN:Cr </= 15 |
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renal manifestation possible after pt suffered from DIC after an abruptio placentae
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Diffuse Cortical Necrosis
-acute generalized infarction of cortices of bilat kidneys w/ Medullary sparring -likely caused by combo of vasospasm & DIC -a/w obstetric catastrophes & septic shock |
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hospitalized pt develops oliguria, and renal tubular cell casts, what's going on?
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Acute Tubular Necrosis
-m/c is Ischemic ATN, caused m/c by Prerenal Azotemia due to Hypovolemia -ischemia damages endothelial cells → decr Vasodilators, incr Vasoconstrictors, thus decr GFR -ischemic damage → detach. of tubular cells into lumen → obstruct & gives charac Pigmented Renal Tubular Cell Casts -most ischemia-sensitive portions of nephron = Strt portion of PT, Medullary portion of Tk Ascending Limb |
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2 areas of nephron most ischemia-sensitive, and what's charac finding of Acute Tubular Necrosis
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1) St portion of PT and 2) Medullary part of Tk Ascending Limb = 2 most ischemia-sensitive parts of nephron
-charac finding of ATN is Pigmented Renal Tubular Cell Casts |
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BUN:Cr > 15-20
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Prerenal Azotemia
-decr Blood Flow to the kidneys (decr CO, hypotension, etc) -this → decr GFR -decr GFR means more time for Urea to be reabsorbed, Cr is NOT reabsorbed, so incr BUN, same Cr, BUN:Cr much greater (>15-20) -will also have Urine Osm > 500, Urine Na < 10, Fe(Na) <1% |
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BUN:Cr is </= 15
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Renal Azotemia
-ATN, CRF is causing back-up of both BUN & Cr in blood, and losing BUN extra-renally -thus BUN:Cr < 15 -also: Urine Osm < 350, Urine Na > 20, Fe(Na) > 2% |
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BUN:Cr >15, w/ nrl Renal Blood Flow
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Postrenal Azotemia
-urinary tract obstruction below the kidneys (BPH, stone, ca) -back up of Urea into blood, Cr can't be reabsorbed, so BUN:Cr > 15 -also Urine Osm < 350, Urine Na > 40, Fe(Na) >4% |
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some possible conseuences of Renal Failure
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-Na/H2O retention
-Hyperkalemia (common cause of death b/c → arrhythmia) -metabolic acidosis -Uremia...Sx: N, anorexia, Pericarditis, Asterixis (hand-flapping), Encephalopathy, Platelet dysfunction -Anemia (bad EPO production) -Renal Osteodystrophy (bad 1α-hydroxylase production of 1,25-(OH)2-Vit D) -Dyslipidemia -Growth retardation & developmental delay (in kids) |
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decr Prox Tubule transport of AA, Glc, PO4, Uric Acid, Protein, Electrolytes
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Fanconi's Syndrome
some common complications: -decr PO4 reabsorption → Rickets -decr HCO3 reabsorption → Metabolic acidosis (Type 2 RTA) -decr early Na reabsorption → incr distal Na reabsorption → hypokelemia |
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Subarachnoid hemorrhage in pt w/ Bilateral flank mass
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Auto-Dominant Polycystic Kidney Disease (ADPKD)
-ADPKD → berry aneurysm → subarachnoid hemorrhage -multiple, large, bilateral cysts that destroy renal parenchyma -Sx incl Flank pain, Hematuria, HTN, Urinary infection, Progressive Renal Failure, Stones |
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what gene mutation expect in a pt w/ flank pain, hematuria, HTN, bilateral large flank masses w/ heart murmur
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APKD1 or APKD2 for Polycystin
-this is ADPKD -cysts can decr glomerular perfusion → incr RAA system that → HTN |
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gene mutation in ADPKD vs ARPKD
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ADPKD = APKD1 or APKD2 for Polycystin
-develops later in life (4th-5th decade) ARPKD = Fibrocystin mutation -develops early in life (can be present in infant) |
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infant w/ bilateral flank masses, can → early onset HTN, portal HTN, progressive renal insufficiency
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ARPKD
-mutation in Fibrocystin gene -if significant renal failure in utero, can → Potter's Syndrome -Potter's Syndrome = bilateral renal agenesis → oligohydramnios → limb deformities, facial deformities, pulmonary hypoplasia |
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electrolyte disturbance → disorientation, stupor, coma
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hyponatremia
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neurologic irritability, delerium, coma
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hypernatremia
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2ndary to met alkalosis, hypokalemia, hypovolemia, incr aldosterone, what ion disturbance get?
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hypochloremia
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ion disturbance 2ndary to non-AG acidosis
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hyperchloremia
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ECG: U waves, flattened T waves, arrhythmias, paralysis
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hypokalemia
*remember, K follows the T waves- flattened T waves, hypokalemia, peaked T waves, hyperkalemia |
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ECG: peaked T waves, wide QRS, arrhythmias
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hyperkalemia
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ion disturbance causing tetany & neuromuscular irritability
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hypocalcemia
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Chvostek's sign (+) and Trousseu's sign (+)
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hypocalcemia
Chvostek's = tap cheek, get twitching of facial muscles Trousseu's = BP cuff on for 3 min, get carpopedal spasm |
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ion disturbance causing delirium, renal stones, abdominal pain
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hypercalcemia
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ion distrubance causing neuromuscular irritability, arrhythmias
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hypoMg
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ion disturbance causing delirium, decr Deep Tendon Reflex (DTR), cardiopulm arrest
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hyperMg
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osmotic diuretic that incr tubular fluid osmolarity
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Mannitol
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MoA of diuretic that can cause Hyperchloremic Met Acidosis, neuropathy, hypoK
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Acetazolamide
-Carbonic Anhydrase Inhibitors -CA usually causes H excretion & HCO3 absorption, thus inhibition → NaHCO3 diuresis -"ACIDazolamide → ACIDosis" |
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MoA of diuretic that can cause HypoK, Ototoxicity, Gout, Dehydration
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Loop Diuretics (incl Furosemide, Bumetanide)
-these inhibit Na/K/2Cl cotransporter -also cause incr Ca excretion "Loops Lose calcium" -SE: Ototoxicity, HypoK, Dehydration, Allergy (sulfa), Nephritis, Gout ("OH DANG"); can also → Met Alkalosis |
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uses of Furosemide & other Loop Diuretics
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-inhibit Na/K/2Cl co-transporter in Loop of Henle
-for Edematous states (incl CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hypercalcemia -SE: Ototoxicity, HypoK, Dehydration, Allergy (sulfa), Nephritis, Gout |
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since Loop Diuretics cause sulfa allergies, what is one that does NOT cause this
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Ethacrynic Acid is a loop diuretic that's a Phenoxyacetic acid derivative (not sulfonamide), so good for diuresis in pts w/ sulfa allergy
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MoA of Thiazides
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Thiazides
-inhibit NaCl reabsorption in the early DT, reducing diluting capacity of nephron -does NOT lose Ca ("Loops Lose Ca, Thiazides don't") -b/c does NOT lose Ca, good for older F at risk of osteoporosis -incr Na & K excretion, decr dilution, decr ClearanceH2O -SE: Hypokalemic Met Alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC) |
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diuretic causing hyperglycemia, hyperuricemia, hypokalemic met alkalosis has what MoA
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Thiazides
-block NaCl reabsorption in early DT -decr Ca excretion (Loops Lose calcium, Thiazides don't) |
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K sparring diuretics incl
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Aldosterone-I: Spironolactone, Eplerenon
-Na-chnnl-I: Triamterene, Amiloride SE: hyperK, endocrine effects (androgen antagonist, thus → gynecomastia; this is more for Spironolactone & Eplerenone (Aldosterone blockers)) |
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gynecomastia in pt on diuretic
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probably on either Spironolactone or Eplerenone (aldosterone antagonists also have anti-androgen effects)
-K-sparring diuretics incl: Spironolactone & Eplerenone (Aldosterone-blockers), Triamterene & Amiloride (Na-chnnl-blockers) |
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drugs that can cause gynecomastia
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Some Drugs Create Awesome Knockers:
Spironolactone, Digitalis, Cimetidine, chronic Alcohol use, Ketoconazole; estrogens, weed |
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diuretics causing acidosis
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Carbonic Anhydrase Inhibitors, K-sparring
CA-Inhib's: decr HCO3 reabsorption K-sparring: aldosterone blockade prevents K & H secretion, also, more K around exchanges in cells for H |
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diuretics causing alkalosis
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Loop diuretics, Thiazide diuretics:
-Volume contraction → incr AT II → incr Na/H exchange & incr HCO3 reabsorption -K loss → K exits all cells in exchange for H entering -in low K state, H (instead of K) is exchanged for Na in collecting tubule → alkalosis & paradoxical aciduria |
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Loop diuretics vs Thiazides effect on Ca
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Loop Diuretics: "Loops Lose Ca, Thiazides don't": abolish lumen-(+) potential in Tk Ascending Limb → decr paracellular Ca reabsorption → hypocalcemia and incr Urine Ca
Thiazides "Loops Lose Ca, Thiazides don't": vol depletion → upreg of Na reabsorption → enhanced paracellular Ca reabsorption in PT & Loop of Henle; thiazides also block luminal Na/Cl cotransport in DCT → incr Na gradient → interstitial Na/Ca exchange → hypercalcemia |
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diuretics giving SE of cough, proteinuria, taste changes, hypotension, hyperkalemia
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ACE-Inhibitors (Captopril, Enalapril, Lisinopril..."-pril")
-for HTN, CHF, diabetic renal disease -SE: Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Preg problems, Rash, Incr'd renin, Lower angiotensin II; HyperK *option if need ACE-I but develop cough = ARB's ("-sartan"), b/c they are AT II-R antagonists, not ACE-I, so don't incr Bradykinin and don't → cough |
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best HTN diuretic for DM?
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ACE-I (captopril, enalapril, lisinopril "-pril")
-shown to decr progression of diabetic renal disease |
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Tx of Rhabdomyolysis
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NOT diuretics
-Tx w/ Rehydration |
