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73 Cards in this Set
- Front
- Back
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Renal arteries/veins
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Renal arteries POSTERIOR to renal veins
R renal artery > L renal a Renal veins ANTERIOR to renal arteries Both drain directly into IVC L renal vein = inferior phrenic v, suprarenal v, gonadal v Thus when renal v thrombosis on L side, obstruction impedes venous flow from L testis --> L sided varicocele! |
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Fluid compartments
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TB weight = 40% non water, 60% TBW (water)
TBW = 1/3 ECF, 2/3 ICF ECF = 1/4 plasma (measure w/ albumin), 3/4 interstitial ECF - PV = ISF Reg osmolarity = 290mOsm |
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Renal Cl
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Cx = UxV / Px
Cx < GFR = net reabsorption of X Cx > GFR = net secretion of X Cx = GFR = no net reab/sec of X |
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GFR
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Inulin calculates GFR: freely filtered, neither reabs/secreted
GFR = Ui x V / Pi = Ci = Kf[(Pgc - Pbs) - (pigc - pibs)] thus changes in plasma protein affect GFR and thus affect FF b/c FF = GFR/RPF Creatinine CL ~ GFR |
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Effective renal plasma flow
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Estimate using PAH clearance
- filtered - actively secreted in PT - lowest [PAH] = Bowman's space - inc [PAH] through thick asc. limb ERPF = Up x V / Pp = Cp Renal blood flow (RBF) = RPF / (1-Hct) |
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Ureteral constriction
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Anatomically narrowed @ 3 major points: * Renal stones may lodge at these junctures
1. Uteropelvic junction 2. Crossing external iliac vessels 3. Traversing bladder wall |
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Filtration
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FF = GFR/RPF
thus FF = GFR / [(1-Hct)(RBF)] PG's dilate afferent arteriole (NSAIDs antagonize) Angio II constricts efferent arteriole (ACE-I antagonize) |
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Free H20 Cl
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CH20 = V - Cosm
Cosm = Uosm x V / Posm With ADH, CH20 < 0 Without ADH, CH20 > 0 Isotonic urine, CH20 = 0 |
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Glucose
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Completely reabsorbed in PT
Plasma glucose = 200 --> glucosuria Plasma glucose = 350 --> Tm |
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Amino Acid Cl
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PT
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Glucose Transporters
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Stereoselective
D glucose entrance > L-glucose entrance |
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GLUT4
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INSULIN SENSITIVE
skeletal, cardiac muscle adipocytes stored in cytoplasmic vesicles insulin --> inc # of transporters in membrane --> inc ratio glucose uptake |
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GLUT 2
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liver, small intestine, kidneys
facil glucose EXPORT out of cells |
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GLUT 1
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RBCs
CNS |
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GLUT 3
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placenta, brain, kidney
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GLUT5
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spermatocytes, GI tract
fructose transport too |
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Proximal Tubule
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Brush border
Reabsorbs all glucose, AA's Most bicarb, Na+, H20 Secretes ammonia (buffer for secreted H+) PTH - inhib Na+/PO4 cotransport --> PO4 excretion ATII - stim Na+/H+ exchange --> inc Na+ and H20 reabsorption Acetazolamide & Mannitol site of action |
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Thick Asc Loop
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Actively reabsorp Na+, K+, Cl-
Indirectly induce paracellular reab Mg2+, Ca2+ IMPERMEABLE TO H20. Diluting segment! Makes urine HYPOTONIC Furosemide action (loops) |
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Thick Desc Loop
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Passive H20 reabsorption via medullary hypertonicity
Impermeable to Na+ Makes urine HYPERTONIC |
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DCTubule
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Active Na+, Cl- reaborption
Diluting segment Makes urine HYPOTONIC PTH --> inc Ca+/Na+ exchange --> Ca+ reabsorption Thiazide & K-sparingdrug site of action |
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CT
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Reabsorb Na+ in exchg for K/H secretion (reg by aldosterone)
Aldosterone --> insertion of Na+ channels on luminal side ADH --> V2 receptors --> insertion of aquaporin H20 channels on luminal side 1* site of K+ regulation: Hypokalemia --> alpha intercalated cells reabsorb extra K+ via H/K-ATPase |
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Factors that Increase K+ secretion --> Hypokalemia state
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1. High K+ dietary consumption
2. Aldosterone (reab Na+ at expense of K+) 3. Alkalosis - K+ is lost to preserve H+ 4. Thiazides & Loops |
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Pathogenesis of Nephrotic Syndrome
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1. Increased perm of glomerular cap wall --> massive urine protein loss
2. Proteinuria --> dec sr Albumin - inc liver albumin synth CAN'T fully compensate --> dec colloid Posm in blood --> fluid moves into interstitial tissue --> EDEMA 3. Fluid shift: circulation --> interstitium = depletion of BV --> ADH secretion --> inc aldosterone secretion (2* hyperaldosteronism) --> inc Na+ & H20 retention --> exacerbates edema 4. Liver: inc synth proteins/lipoproteins, dec catabolism due to low plasma levels of lipoprotein lipase and abn transport of circ lipid particles (inc chol, TG, VLDL, LDL, Lpa, apoprotein) 5. Inc lipoproteins followed by lipiduria |
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Macula densa cells
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In DCT
Sense Na+ delivery |
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Juxtaglomerular cells
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In renal afferent arteriole
Sense BP Secrete renin if dec BP |
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Tubular Fluid / Plasma
TF / P Along distance of PT |
TF/P > 1 when:
- Solute reabsorbed more slowly than H20 - Net secretion of solute - PAH, Cr, Inulin concen's increase along distance of PCT b/c H20 reab TF/P = 1 - solute & H20 are reab at SAME rate - Solute neither reab/secreted - K, Na TF/P < 1 - solute reab more quickly than H20 - Glucose, AAs, HCO3, Pi ** Cl- absorbed distal to where Na+ reab, so rel concen inc |
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ANP
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Secreted from: Inc atrial P
Causes: Inc GFR & Na+ filtration w/ no compensatory Na+ reab in distal nephron Net Effect? Na+ & Volume loos |
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PTH
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Secreted in response to: Dec [Ca2+]
Causes: Inc [Ca2+] reab in DCT, Dec PO4 reab in PCT, inc 1,25(OH2) production --> Inc Ca2+ and PO4 reab from GI |
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ATII
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Synth in response to Dec BP
Cuases efferent artiole constriction --> inc GFR & FF Compensatory Na+ reab in distal nephron |
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ADH
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Secreted in response to inc plasma Osm & dec BV
Binds to receptors on principal cells --> inc # H20 channels --> Inc H20 reab |
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Aldosterone
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Secreted in response to: Dec BV (via ATII) + Inc K
Causes inc Na+ reab, Inc K+ secretion, Inc H+ secretion |
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Anion Gap
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= Na- (Cl + HCO3)
If Inc AG -- > MUDPILES If Nl --> Diarrhea, RTA, hyperchloremia |
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Respiratory Acidosis equations
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HCO3 = 0.1 x pCO2
HCO3 = 0.4 x pCO2 |
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Respiratory Alkalosis equations
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HCO3 = 0.2 x pCO2
HCO3 = 0.5 x pCO2 |
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Metabolic acidosis
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pCO2 = 1.2 x HCO3
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Metabolic alkalosis
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pCO2 = 0.6 x HCO3
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Kussmaul Respiration
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Assoc w/ DKA
Compensatory respiratory alkalosis via dec CO2 |
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Renal Tubular Acidosis
Type 1 |
Defect in H/K ATPase of CT --> can't secrete H+ --> hypokalemia
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RTA Type 2
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Defect in PT HCO3 reab.
Hypokalemia |
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RTA Type 3
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Hypoaldosteronism --> Hyperkalemia --> Inhib of ammonia excretion in PT
Decrease in urine pH due to decrease in buffering capacity |
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Granular casts
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ATN
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Waxy casts
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Advanced renal dz/ CRF
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Ethylene glycol
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Causes ARF sx's 24-72 h post-ingestion (high AG met. acidosis)
Found in antifreeze, coolants, hydraulic brake fluid Rapidly absorbed from GI Metab to glycolic acid --> toxic to renal tubules Oxalic acid --> precip as Ca2++ oxalate crystals in tubules **Tubular epithelial cells have excellent regenerational capacity |
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Post-streptococcal Glomerulonephritis
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Pts: Children usu; peripheral/periorb edema
LM - enlarged glomeruli, hypercellular, neutrophils, LUMPY BUMPY EM - subepithelial immune complex humps IF - granular |
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Rapidly Prog Crescenteric Glomerulonephritis (RPGN)
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LM/IF - CRESCENT MOON
Assoc w/ 3 types: 1. Type I: Goodpasture syndrome - Type II HSR, GBM Abs (hematuria/hemotypsis), LINEAR IF 2. Type 3: Wegener's granulomatosis - cANCA; pauci-immune 3. Type 2: Microscopic polyarteritis - pANCA; immune-complex mediated. |
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Diffuse proliferative Glomerulonephritis
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SLE-assoc - MCC death in SLE
DNA-anti DNA immune-complexes WIRE LOOPING capillaries Granular IF |
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Berger's Dz
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IgA glomerulopathy
Inc IgA synth Immune complex deposition in mesangium Post URI - coca cola colored urine usually in children |
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Alport's Syndrome
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Type IV collagen mutation -> SPLIT BM
Nerve disorders, Ocular disorders, Deafness SEE NO EVIL, HEAR NO EVIL, PEE NO EVIL |
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Membranous glomerulonephritis
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= Diffuse membranous glomerulopathy
SLE assoc. MCC adult nephrotic syndrome LM = capillary + GBM thickening EM = SPIKE & DOME IF = granular |
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Minimal Change Dz
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LM - NORMAL glomeruli
EM - FOOT PROCESS EFFACEMENT Post-infectious in children Responsive to corticosteroids (-) charge selectivity lost in GBM --> albuminuria |
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Amyloidosis
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LM - Congo red, apple-green birefringence
Assoc w/ MM, chronic dz, TB, RA |
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Diabetic glomerulonephropathy
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Nonenzym glycosylation GBM & efferent arteriole --> Inc perm + thickening; prev w/ ACE-I's & ARBs
Inc GFR Mesangial damage LM - Kimmelstein Wilson WIRE LOOP lesions Early detection: Microalbuminuria screening |
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Focal segmental glomerulosclerosis
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LM - segmental sclerosis + hyalinosis
MCC glomerular dz in HIV pts |
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Membranoproliferative glomerulonephritis (MPGN)
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Immune-complexes w/ granular IF
EM - TRAM TRACK APPEARANCE w/ GBM splitting caused by mesangial ingrowth Usu progresses to CRF Assoc w/ HBV > HCV |
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Ammonia Magnesium Phosphate
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2nd most common kidney stone
Caused by infec w/ urease + bugs (Proteus, Staph, Kleb) Staghorn calculi --> nidus for UTIs Worsened by alkaluria |
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Renal Cell CA
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Assoc w/ chr 3 del
prominent vascularity Clear cells (high lipid content, not a lot of polymorphism, well differentiated) Originate from epithelium of PCT |
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WAGR complex
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Wilm's Tumor
Aniridia (no iris) GU malformation MR Chr 11, WT1 gene |
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Chronic pyelonephritis
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Tubules can contain eosinophilic casts = kidney thyroidization
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Drug-Induced interstitial nephritis
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Acute renal inflammation
GLOMERULI IN TACT Fever, rash, eosinophilia, hematuria 2wks post-tx admin Assoc w PCN, NSAIDs, diuretics --> induce hapten hypersensitivity |
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ATN phases
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1. Inciting event
2. Maintenance (low urine) = oliguric 3. Recovery - assoc w/ severe hypokalemia due to dehydration |
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Chronic phenacetin use
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Can cause renal papillary necrosis (sx's include gross hematuria, proteinuria)
Acetaminophen = phenoacetin derivative |
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Fanconi's syndrome
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Dec PT transport of AAs, glucose, phosphate, uric acid, protein, and electrolytes
Congen/Acquired Causes: Wilson's Dz Glycogen storage dz Drugs (cisplatin, expired tetracycline) Complications: Rickets, Metabolic acidosis, inc distal Na+ reab --> hypokalemia |
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ADPCKD
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AD mut in APKD2
Assoc w/ polycystic liver dz, berry aneurysms (HTN), MVP |
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ARPKD
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AR
Assoc w/ hepatic cysts + fibrosis |
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Medullary cystic Dz
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Medullary cysts
Small kidney on ultrasound Poor Px |
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Medullary Sponge Dz
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CD cysts
Good Px |
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Renal oncocytomas
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VERY RARE tumors
Originate from CD Large well-differentiated neoplastic cells w/ tons of mitochondria |
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Na+ Disturbance
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Low Na:
disorientation stupor coma Hgih Na: irritability delirium coma |
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Cl- Disturbance
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Low Cl:
2* to met alkalosis hypokalemia hypovolemia inc aldosterone High Cl: 2* to non-anion gap acidosis |
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K+ Disturbance
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Low K:
U waves (ECG) Flat T waves Arrhythmias Paralysis High K: Peaked T waves wide QRS arrhythmias |
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Ca2+ Disturbance
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Low Ca+:
Tetany, neuromusc irritability High Ca+: Delirium, renal stones, abd pain |
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Mg
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Low Mg:
NM irritability Arrhythmias High Mg: Delirium Dec DTRs Cardiopulm arrest |
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PO4
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Low PO4:
Low-mineral ion product causes bone loss, osteomalacia High PO4: Renal stones Metastatic calcification |
