191888
Description
Flashcards by Jaimie Shah, updated more than 1 year ago
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Created by Jaimie Shah
over 10 years ago
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| Question | Answer |
| Causes of Yellow urine color | Urochrome (pigment from blood) |
| Causes Green color Urine | Asparagus, B vitamins, Pseudomonas |
| Causes Milky white urine | Chyluria, Schitosomiasis, Phosphaturia |
| Causes Blue Urine | Amitryptiline, Cimetidine, Triamterene, Methylene blue dye |
| Causes Black/brown urine | Alkaptonuria, flagyl |
| Causes orange urine color | Rhubarb, senna, carrot juice, pyridium |
| Causes Port wine color urine (deep purple) | Prophyria |
| Define Hematuria (false +/- dipstick causes) | -x>2RBC/ HPF -Dipstick false neg: vit C>2g/d -Dipstick false +: semen, myoglobin, alkaline urine, oxidizing cleanse solutions |
| Suggests Glomerular Hematuria | dysmorphic rbc (>80%, small, MCV<70) RBC Casts Acantocytes >5% Proteinuria>1g U.alb/T.pro>0.59 mg/mg |
| Pseudo-Hematuria (dipstick for heme) | Supernatant neg for heme: Betalaine in beets Phenazopyridine (urinary analgesic) Vegetable dye Melanin Porphyrin Hydroxycobalamin Phenolphthalein (OTC laxative) |
| pseudo-hematuria (dipstick heme positive) | Myoglobin: plasma clear, haptoglobin normal, cpk is high Hemoglobin: plasma red, haptoglobin high and cpk normal |
| Define Pyruia | x>5 WBC/HPF |
| Causes of Sterile Pyruia | Inflammatory d/o: AIN, NSAIDs, eosinophiuria Chronic tubulointerstitial d/o Analgesic abuse Mycobacterium or viral infection Kidney transplant rejection GU malignancy |
| Define GFR | equal to sum of filtration rate of all nephrons 125 ml/min of plasma filtered per day Avg GFR men: 120-130ml/min Avg GFR women: 110-120ml/min |
| limitations to using Cre to estimate GFR | 1. diseases may lower Cre: liver dz, malnutrition, adv. age 2. 15% Cre secreted and no filtered so overestimates GFR 3. med inhibit tubular secretion: Bactrim, Cimetidine, Fluocytosine, Cefoxitin, probenecid (expected increased in Cre) |
| 24 U CrCL | 20-25mg/kg/d men 15-20mg/kg/d women |
| Microalbuminuria (nl excrete 1g Cre/d) | 30-300mg of albumin/24hr U.alb/Cre:(30mg/1g Cre-300mg/1g Cre) -Exercise and fever can increase protein excretion transiently |
| Urinary proteins include | HMW albumin LMW immunoglobulins Tamm-Horsfall proteins |
| Dipstick detected proteinuria | x>300mg/24hrs |
| Proteinuria risk factor for... | CV disease All cause mortality Non-dipping HTN Greater chance CKD to progress |
| Orthostatic Proteinuria | benign, age<30 Proteinuria only during the day; no risk of CRF, no tx |
| Essential HTN | normal BP: <120/80 Pre HTN: 120-139/80-89 HTN stg 1: 140-159/90-99 HTN stg 2: >160/>100 |
| Essential HTN | 31% adults in US have it- Screen every 2 years if normal BP, and annually if pre-HTN; Thiazides initially treatment |
| When it is okay to start two meds in HTN? | Can start two meds with Stage 2 HTN except in elderly where this could cause orthostatic HTN |
| BP goal with CRF, DM, CAD | sys<130 and dia<80 |
| BP goal in CRF and urine pro/cre>1mg/mg | BP<125/75 |
| patient with white coat HTN | do 24hr BP monitoring |
| lifestyle changes for HTN | DASH Diet (x8wks): dec. sys 11 and dia 5; Weight loss: dec. by 5-7/10kg; dec. ETOH: dec by 2-4; low Na diet: dec. by 4-9; Can wait 6-12mo before starting meds |
| white coat HTN | three office BP>140/90 and two non office BP<140/90 w/o end organ damage; daytime avg BP <135/85 rarely assoc. with LVH |
| Nocturnal BP and non-dippers | BP should dec. by 15% at night; if not RF for: LVH, proteinuria prog in DM, and screen for Sleep apnea as cause |
| Essential HTN workup | EKG UA Glucose Hct Cre K Ca Lipids u.alb/cre ratio |
| isolated Systolic HTN | Occurs in elderly due to diminished arterial complicance; increased risk of MI, LVH, RI, CVA, CV mortality; tx: thiazides, DHP CCB (ex amlodipine), imdur |
| resistant HTN | BP above goal despite 3 meds: be sure at optimal doses, one med is diuretic, Chlorthalidone better than HCTZ, if GFR<30ml/min change HCTZ to loop |
| Resistant HTN | Controlled BP on 4 meds: consider secondary causes; RF include: old age, black race, DM, Excess ETOH, BMI>30; 4th agent= spironolactone |
| Secondary HTN | Severe and refractory HTN; an acute rise in BP over stable BP; HTN before puberty; Age<30 in non-obese, non-AA with confirmed neg FHx of HTN |
| Causes of Secondary HTN | Primary Renal Dz OCP Pheochromocytoma Primary Hyperaldo Cushing's Syndrome Sleep Apnea Coarctation of Aorta Hypothyroid Primary HPTH Genetic d/o |
| OSA related CV effects | systemic HTN Mild Pulm HTN CAD with severe OSA Nocturnal Cardiac Arrythmias (Tx to reduce risk of nocturnal vent arrythmias and reduce systemic HTN) |
| OCP hypertension | typically mild could be malignant HTN; cause unknown; RF- HTN in prior pregnancy and family hx of HTN; HTN returns to normal in 2-12mos; less common in new preparations due to dec. estrogen |
| Coarctation of Aorta | Narrowing aorta distal to Subclavian arteries: so different BP in UE/LE, Interscapular murmur, CXR (notches in post ribs, 3 sign of aorta), CT/MRA helpful---- increased risk of IC aneurysms, assoc. with Turner's and Tx is surgery |
| Pheochromocytoma (clinical manifestations) | Classical Triad (HA, Tach, Sweat), Anxiety, Tremor, HTN, Pallor, Ortho Hypotension |
| Pheochromocytoma Associations | MEN 2A (med. thyroid Ca, pheo, Primary HPTH), MEN 2B (med. thyroid Ca, Pheo, Mucosal Neuroma)- Both AD, Pheo usu B/L here |
| Pheochromocytoma (Clinical Pearls) | -95% inta-abd -10% are malignent (less in MEN 2) -10% familial -Light bulb on T2 MRI |
| Other diseases Associated with Pheo | VHL, NF1, Paragangliomas of head and neck |
| Phemochomocytoma (diagnosis) | 24 urine metanephrines and free metanephrines and serum unfrac free catecholamines; (equivocal case) clonidine suppression test-nl response=50% reduction in plasma catecholamines with .3mg clonidine.; Imaging: CT, MRI, MIBG (esp if extraadrenal or looking for Mets) |
| Pheochromocytoma Treatment | Phenoxybenzamine (nonspp, irreversible, LA, DOC preop) v. Doxazosin (selective, less side effects, used in metastatic disease); then add BB (propanolol) always secondary |
| Pheochromocyoma HTN emergency | Niroprusside or Nicardipine or Pentolamine (SA alpha blocker) |
| Pheochromocytoma mimicking disease | Sympathomimetic drugs- cocaine, PCP, amphetamines; MAO inhibitors (phenelzine and selegiline) + Tyramine containing foods (fermented cheeses, imported beers, chianti, soy sauce, avocados) |
| HTN + Hypokalemia | Primary Hyperaldo, Renovasc Disease, Cushing Syndrome, Licorice ingestion, Surreptitious diuretic use, Congenital Adrenal Hyperplasia, Liddle syndrome, Renin secreting tumor |
| primary hyperaldo causes | Aldo prod Adenoma, B/L adrenal hyperplasia, Unilateral Hyperplasia, Familial hyperaldo type 1, Familial hyperaldo type 2, Aldo prod adrenal Carcinoma |
| When to scree for Primary Hyperaldo? | HTN and hypokalermia, Severe/resistant HTN, HTN and adrenal incidentaloma, HTN and FHx or HTN or CVA<40, HTN in 1st degree rel with primary hyperaldo |
| Primary Hyperaldo Diagosis | PRA (renin)-low; PAC (aldo)/PRA is >20-30; Confirm with high aldo after 3d Na load; CT adrenals; Adrenal vein Sampling |
| Primary hyperaldo (clinical features) | HTN; Hypokalermia; Metabolic Alkalosis (inc. H+ sec); Mild Hypernatermia; Mild hypomagnesemia; Lack of edema |
| Primary Hyperaldo (treatment) | surgery if unilateral w/ preop spironolactone; B/l use MC antag: spironolactone or epelerenone; use glucocorticoid for GRA |
| Fibromuscular Dz | noninflammatory, nonatheromatous cause of arterial stenosis, mostly in the renal and internal carotoid |
| FMD features | Mild hypokalemic, metabolic alkalosis; high renin and high aldo; 3 types: medial (string of beads on angio), perimedial, intimal |
| FMD treatment | suspect if refractory HTN, CVA, female<50, low K; tx: ACE or ARB and PTA, no stents |
| Gene defects of HTN | GC responsive hyperaldo; Apparent MC excess; Progesterone induced HTN; Liddle Syndrome; Gordon Syndrome |
| GC responsive Hyperaldo | Aldo stimulated more by ACTH than angio2, so aldo is high and renin is low; Autosomal Dominant; Hyperaldo look alike and tx is steroids (suppress ACTH sec so can't increase Enzyme activity that would increase aldo production) |
| Apparent MC excess | 11-betaOH DH def- it inactivates cortisol to cortisone; so active cortisol acts like aldo at receptors |
| Apparent MC excess presentation and treatment | -HTN, vol. expanded, hypokalemia, met. alkalosis; -low renin, and aldo levels; -respond to spironolactone and amiloride and dexamethasone; -Can get if eat licorice (chewing tobacco) |
| Progesterone induced HTN | rare, runs in families, defect in receptors so progesterone can stimulate aldo receptors. |
| Liddle Syndrome | increase Na reabs in collecting tubule (genetic-Autosomal Dominant) |
| liddle syndrome presentation | low K, metabolic alkalosis, strong FHx of HTN; renin and aldo supressed due to increased Na; decrease in urinary aldo secretion |
| Liddle syndrome treatment | Amiloride or triamterene (these two block the Na channel directly), not spironolactone (because this disease is no aldosterone mediated and this med competes with aldo to alter it's effects so no helpful here) |
| Gordon syndrome | WNK 1 and 2 mutation cause increase in NaCl abs in distal collecting tubule (AD); See low renin and aldo, HYPERKALEMIA and Metabolic ACIDOSIS |
| gordon Syndrome tx | Thiazide and low Na diet |
| HTN emergency | BP>180/120 + organ failure (encephalopathy, CHF, MI, eclampsis, angina, aortic dissection) |
| HTN emergency tx | IV meds, decreased BP 25% presenting value in first 60mins, if stable- then aim for BP 160/100 over next 2-6hrs. |
| HTN emergency- Stroke | (IC bleed)treat Sys >200 or MAP>150, treat if sys>180 or MAP >130 with care to sys-160 or MAP-110; (ischemic Stroke) if no lysis tx for BP >220/120, if lysis then tx so SBP<180 |
| Cyanide Toxicity (nipride) | s/s: hyperpnea, vertigo, change in MS, Coma, seizures, Tachypylaxis impending sign of toxicity; lab clues: lactic acidosis, increased base deficit (common in RF/ESRD) |
| when to do a renal Bx? | Hematuria, Proteinuria, Unexplained RF |
| Relative contraindications to renal Bx | bleeding diathesis, uncontrolled BP, uncooperative pt, atrophic kidney, skin infection or active kidney infection |
| Nephrotic Syndrome | low albumin, proteinuria, Edema, hyperlipidemia, lipiduria |
| Nephrotic Syndrome causes | MCD, FSGS, Diabetes, Paraproteinemia, Membranous, other; (no blood in urine) |
| Nephrotic syndrome complications | protein malnutrition IV hypovolemia AKI Hypercoaguable infection |
| Nephrotic syndrome Treatment | ACE/ARB, Loop diuretics, Statins, Treat underlying cause |
| MCD under microscope | Normal on LM; minimal IGM in mesangium on IF; Foot process effacement on EM |
| MCD associations | Drugs (NSAIDs, ampicillin, lithium, d-penacillamine, pamidronate, interferon), Atopy (bee stings), Neoplasm (Hodgkins), SLE |
| MCD tx | steroids +/- cyclosporin +/- rituximab; (most impt prognostic factor is response to steroids) |
| FSGS under scope | IF: IM deposition |
| Primary FSGS | Most common in black patients, presents with NS, and renal bx needed for dx |
| Five variants of FSGS | Collapsing, Cellular, Tip (more steroid responsive), perhilar (likely 2/2 obesity), classical |
| Treatment of FSGS | Steroids (failure inc risk of ESRD)- if resistant try cyclosporin and low dose prednisone; Add ACE/ARB; relapses common when treatement stopped |
| What type of FSGS commonly relapses after transplant? | 50% of collapsing and classical form |
| what enzyme in FSGS indicates it is idopathic, causes foot process effacement, and predicts recurrence after transplant? | SuPAR (amiloride inhibits uPAR protein) |
| Causes of Secondary FSGS | Ureteral reflux, HIV, Heroin, Parvovirus, Interferon, Cyclosporin, pamidronate, anabolic steroids, IGA nephropathy, Obesity |
| Features of obesity induced FSGS | Nephrotic range protein but no NS, Perihilar variant, can regress with weight loss, rarely leads to ESRD |
| Risk factors for progression of Diabetic Nephropathy | HTN, Proteinuria, Race, Family hx, Smoker, poorly controlled DM |
| How often do you check Micoalbuminuria after Dx of DM1 + 2 | In DM2 you check anually after Dx, in DM1 you check 5 years after dx then anually |
| How do medications change as kidney disease progresses in DM | Be wary of oral agents accumulating if kidneys fail (low BS with Sulfonylurea overdose), and decrease insulin req as uremia progresses |
| Prevention of DM nephropathy | sugar control, lower lipids, stop smoking, BP control, inhibit RAS system |
| Membranous Nephropathy is seen most in which population | Caucasions |
| What is seen under the Microscope with Membranous Nephropathy | LM: diffuse thickening of the GBM; IF:"spikes"on silver stain-deposits of IgG in capillary wall; EM: subepithelial dense depositis |
| Do you screen for malignancy in MN | it is reasonable to do so |
| MN associations | Gold, Penicillamine, captopril, NSAIDs, SLE, Hep B, Hep C, Syphilis, Malig (lung and stomach), chronic GVHD, Primary billiary cirrhosis, Autoimmune (psoriasis, RA, Sjogrens); Although 75% cases are idopathic |
| treatment of MN | Ace/arb for all; cyclophosphamide+steroids or cyclosporin +/- steroids or Rituximab |
| Multiple Myeloma Cast Nephropathy | 2/2 excess prod, sec and filtration of LMW light chain fragments of Igs-->in ALH and DCT they aggregate and cyrstalize to then perforate the tubule-->granulomatous rxn |
| what light chain seen most with Multiple Myeloma cast nephropathy | kappa>lambda (dx IF staining and renal bx) |
| other causes of Renal injury in patient with Multiple Myeloma | Hypercalcemia, Hyperuricemia, type 1 cryoglobulinemia, Hyperviscosity syndrome |
| Clinical Dx of MM renal failure | low anion gap, proximal RTA, fanconi syndrome, discrepancy of dipstick proteinuria and measured 24hr |
| tx of MM RF | chemo: bortezomib, thalidomide, dexamethasone; IVF; bisphosphonates; plasmapheresis (doesnt change outcomes); HD |
| Systemic Amyloid all have the following | congo red +, has amyloid P component, has 10nm non-branching fibrils on EM |
| Sources of Amyloid proteins | primary: variable portions of light chains; secondary: protein A no an IG; Familial: transthyretin |
| Presentation of primary Amyloidosis | Fatigue, weight loss, easy brusing (fac X def), Macroglossia, Arrythmias (depot in septum), 90% monoclonal Lambda |
| Dx of amyloid | fat pad bx or bx of organ involved |
| tx of amyloid | Melphalan and prednisone; stem cell transplant |
| Describe Monoclonal IG depostion disease (LCDD and HCDD) | clonal plasma cell proliferative d/o with depostion in extracellular organs. often see increase plasma cells in BM, NS is common, typically Kappa deposition |
| Bx in LCDD and HCDD | Dx= nodular sclerosing glomerulopathy; multiple myeloma develops in 40% of patients |
| tx of HCDD and LCDD | same as in multiple myeloma |
| basic points about Fibrillary GN | poor prog, fibrils 18-22nm, heavy proteinuria, progress to ESRD, no proven benefit to immunosuppersion |
| basic facts on Immunotactoid GN | 30nm parallel arranged, monoclonality more than fibrils, low complements |
| HIV related Renal d/o | HIVAN, HIVICK (IGA gen against HIV deposit, diffuse proliferative GN), thrombotic Microangiopathy |
| HIVAN clinical manifestations | NS (collapsing FSGS), normotensive, large kidneys with microcysts, rapid progression, mostly in AA, Low CD4 is a greater risk factor than high viral load |
| tx of HIVAN | HAART, steroids, ACE/ARB, transplant (need no AIDs, CD4>200, viral load<50) |
| HAART related nephropathy | Nucleotide RTI: tenofovir; Nucleoside RTI (stavudine, zidovudine, didanosine)- see fanconi syn, lactic acidosis, rhabdo; non nucleoside RTI (efavirenz) has no nephrotoxicity |
| HIV and the kidney | can cause ATN 2/2 meds (pentamidine, foscarnet, cidofovir, ampho B); Cyrstal depot (acyclovir and sulfadiazine); stones (indinavir, atazanavir); post infectious GN, IgA |
| Benign familial hematuria on Bx | thinning of the BM (possible increased risk of FSGS, CRF and kidney disease in relatives) |
| Most common GN in the world | IGA |
| s/s of IgA nephropathy | synpharyngitic gross hematuria (50%), micro hematuria (40%), NS (10%), AKI, HTN |
| renal Bx of IGA nephropathy | mesangial proliferation, depot of underglycosylated IGA1 |
| IgA nephropathy associations | celiacs, cirrhosis, HIV, MCD, AS, IBD (rare in AA and common in Native americans) |
| poor prognostic factors of IgA nephropathy | 15% get ESRD 10y after Dx--Male sex, proteinuria>500mg-1000mg/d, HTN, diffuse disease with intersitial fibrosis |
| tx IgA nephropathy | steroids, Ace/Arb, fish oil, if cresentic GN can try solumedrol and IV cytoxan |
| Henock Schonlein Purpura | Most common vasculits in kids, Immune mediated, IgA1 deposition |
| tetrad of HSP | palpable purpura w/o thrombocytopenia, arthritis/arthralgias, Abd pain, often preceded by URI and Renal failure is common |
| complication of HSP | intussusception more common in kids, and RF more common in Adults (tx ?steroids) |
| RPGN clincally | rapid loss renal fxn, active urine sediment, no edema or HTN |
| RPGN on staining | linear staining of IgG on GBM and TBM if good pastures'; granular staining of IgG if SLE; Nothing on stain if Pauci-immune |
| Good pastures renal Bx and lab Dx | Bx: cresentic GN on LM, on IF linear IgG1 and IgG3; lab dx: elisa for Anti GBM abs |
| treatment good pastures's | plasmapheresis, pulse steroids, cyclophosphamide, transplant (recurrent linear depot but usually Asx) |
| anti GBM seen in what disease after transplant | Alport's |
| Clinical picture of Wegner's | Pulm involvement; renal- segmental necrotizing GN; sinus involved; skin: purpura, nodules, ulceration |
| IF patterns that give ANCA's their names | Peirnuclear (MPO-abs) and cytoplasmic (PR3-abs) |
| tx of wegner's and Microscopic Polyangitis | steroids+ cyclophosphamide, plamaphereisis; relapsed pts- rituxan for 4 weeks and steroids for 6 months |
| If on a random test a patient is ANCA postive what do you do? | Does not warrant treatment |
| ANCA serology associations | Wegner's, Microscopic Polyangits, Churg-strauss, good pastures, Meds-PTU and Hydralazine, GI- UC and PSC |
| define polyarteritis nodosa | systemic necrotizing vasculitis of medium sized arterioles |
| clinical picture of Polyarteritis Nodosa | fatigue, weakness, fevers, arthralgias, skin-ulcers and erythematous nodules, mononeuritis multiplex, renal failure, Abd pain, NOOO LUNG EFFECT! |
| Dx polyarteritis nodosa | bx organ involved, no definite lab abnormality (ANCA negative), Mesenteric and renal angio for microaneurysms |
| Tx PAN | steroids +/- cytoxan |
| Antiphospholipid AB clinically | can have lupus nephritis with thrombi, venous and arterial thrombi, livido, low plts, frequent miscarriages. |
| Drug induced lupus key points | INH, Hydrlazine, Procanamide; rarely involves kidneys; antihistone ab positive |
| Churg strauss clinical picture | allergic rhinitis, asthma, periperal eosinophillia, skin-purpura and ulcers, renal dz |
| treatment Churg strauss | steroids + cyclophosphamide |
| Basics Post infectious GN | Renal failure 4 weeks after URI, hypocomplement common, active urine sediment, self limited disease |
| Renal Bx of Postinfectious GN | diffuse proliferative GN; IF: IgG and C3 deposition; EM: subepithelial humps (the antigen is strep pyogenes exotoxin B) |
| Renal failure and low complement | SLE, Infectious GN, post strep GN, MPGN, Cryoglobulinemia, Shunt nephritis, HCDD, CFHR5 nephropathy |
| Hep C glomerular lesions | type 1 MPGN with crygolbulinemia, MPGN w/o cryo, MN, IgA nephropathy, ANCA vasculitis, Fibriliary GN, DM |
| Cryglobulinemia | three types with different collections of monoclonal and polyclonal IgM and IgG immunoglobulins |
| Cryoglobulinemia clincally | need>2% cryocrit for renal dz; it's an activation of the classical pathway you see skin purpura, neuropthy, MPGN (intraglomerular deposits), abn LFTs, low C4 and NORMAL C3, +RF |
| Cryo tx | interferon + ribiviran (rituximab if severe dz) |
| MPGN renal pathology | Lobulation, split BM- "tram tracking", type 1: deposits in mesangium and subendothelial space, type 3: deposits in subepi and subendo spaces. |
| MPGN 2 acquired form | autoantibody to alternative pathway C3 convertase |
| MPGN2 familial form | factor H def (CFHR5 nephropathy)- synpharnygetic hematuria |
| Hep B renal manifestations | MN (Sub epi depot of Hep B eAg), PAN, MPGN 1/3, IgA, Mesangial Proliferative, MCD/FSGS |
| Hep B treatment | alpha interferon + lamivudine and Entecovir |
| Lead toxicity, what do you see? | Fanconi syndrome (prox tube injury); Triad: HTN, RF, Gout |
| tx lead toxicity | chelation |
| Cadmium toxicity buzz words | battery plan worker; Proximal>distal injury; Hypercalcuria; Ca oxalate stones; No known treatment |
| Arsenic posining buzz words | drinking water, Bangladesh, tx is chelation |
| Mercury poisoning buzz words | assoc with MN, Sxs- Mad as a hatter, Tx is chelation |
| Star fruit kidney injury | popular in asia, thailand, and south america; causes oxalate nephrotoxicity and stones |
| Ephedra affect on kidney | alpha receptor stimulator, clinically causes HTN and radiolucent kidney stones |
| Blue Cohosh | causes HTN and coronary vasoconstriction |
| Noni Juice | causes hyperkalemia bad ESRD patients |
| Licorice poisoning | causes low K, HTN and metabolic acidosis, and low renin and aldo levels (inhibits enzyme actions) |
| St. John's wart | activates P450 system so can make cyclosporin levels subtheraputic |
| Grapefruit juice | inhibits P450, can cause cyclosporin toxicity |
| Melamine | food additive no longer in the US, can intra tubular depot and see stones and renal failure |
| Causes of AIN | NSAIDs and PPI (often w/o rash, fever and eosinophilia), Infection (legionella, leptospirosis, strep), TINU, Sarcoid, Idopathic |
| AIN presentation | See: rash, perp eosinophillia, eosinophiluria, RF, fevers; Urine sedement= WBC, RBC, WBC casts, and Hansel's stain- u. eosino; <1g proteinuria |
| AIN tx | remove offending agent and steroids (renal Bx= def diagnosis) |
| tubulointerstitial nephritis and uveitis syndrome | Cause ukn, you see Uveitis usually painful and anterior after RI (AIN picture), renal US can show marked swelling |
| TINU renal findings | self limited, steroids used for progression, and prognosis dependent on fibrotic changes |
| Renal Manifestations of Sjogren's | leading cause of intersitial nephritis in caucasion in U.S., assoc with hep C; other renal effects: distal RTA, Fanconi, NDI, MN, MPGN; tx is steroids |
| Lithium nephrotoxicity (not acute, chronic cause) | CTIN: NDI and Distal RTA 1; risk factors are dose and duration- GFR decreases slowly over 20y, may be irreversible |
| Sarcoid renal involvement | Hypercalciuria and hypercalcemia with elevated vit D; Granulomatous intersital nephritis |
| Sarcoid renal presentation | Kidney stones, nephrocalcinosis, ESRD, Pyuria, mild proteinuria, wbc casts, nephromegaly (tx steroids) |
| AKI definition | rapid decline in renal function by prog azotemia +/- oliguria; increase Cre of 0.3mg/dl or 1.5 fold increase in Cre at 48hrs |
| ATN findings | Muddy brown granular casts, FeNA>2%, FeUrea>35%, UNa>40 |
| Fe NA | (UNa x PCre)/(PNa x UCre) x100 |
| what does Fe Na tell us | if >2% tells us it's ATN, if <1% suggests prerenal azotemia |
| Fe Mg tells us what | if >2% suggestive of renal tubular wasting |
| Fe PO4 tells us what | if >5% suggestive of renal tubular wasting |
| Fe of Bicarb tells us what | >15% is a prox RTA (type 2), and <10% Distal RTA (all other types) |
| ATN causes | Severe prerenal azotemia, hypoTN, Neprotoxins- Aminoglycosides, Ampho B, Cisplatinum, IV contrast, Pentamadine, Foscarnet, Cidofovir (tx is supportive) |
| Aminoglycoside nephrotoxicity | in decreasing order: gentamicin, tobramycin, amikacin, netilmicin |
| Risk factors for Aminoglycoside nephrotoxiciy | prolonged duration of tx, advanced age, hypovolemia, sepsis, elevated levels |
| Aminoglycoside nephrotoxicity renal presentation | usu 5-7 days of tx, freely filtered and injures proximal tubule cells; Mild proteinuria, granular casts, nonoliguria due to loss of renal concentrating ability, Electorlyte abn: low Mag, low K, Low Ca and Low Phos |
| Ampho B nephrotoxic presentation | tubular injury and renal vasoconstiction, electrolyte abn: low K, Low Mag, Met acidosis (distal RTA- type 1), NDI (polyuria) |
| Ampho B nephrotoxicity prevention | salt load, avoid other nephrotoxins (cyclophosphamide, aminoglycosides), lipid based formulations |
| Cisplatinum nephrotoxin clinical picture | non-oliguric RF, usu after first 2 weeks of tx, Thrombotic microangiopathy- weeks to mo post tx; low mag, Fanconi like syndrome salt wasting |
| Cisplatinum RF and Prevention | RF: high dose with peak plasma concentration, baseline RI, other nephrotoxins; Prevention: lower doses, IV saline |
| Cisplatinum nephrotox tx | stop agent, add carboplatinum instead, try amifostine |
| foscarnet nephrotoxicity | starts 6-15 days after tx, bland UA, hypocalcemia (drug binds free Ca), can cause Seizures |
| Cidofovir nephrotoxicity | dose dependent and seen in 50% in patients and is contraindicated with proteinuria or Cre>1.5; Usu fanconi syndrome, RF reversible but some go to ESRD |
| Pentamadine renal picture | ATN, Hperkalemia (effects principal cells), Tubular tox-hypomagnesemia, hypocalcemia; tx is to stop the drug |
| Rabdo on labs | elevated CPK, PO4, AST, ALT, Cre, UA + for blood, U. micro neg and U. Myoglobin+ |
| Rhabdo causes | exertional, Metabolic and Mitochondria myopathies, malig hyperthermia, NMS, CO poisoning, ETOH abuse (low phos and RF-->Rabdo), lyte abn (low k/low phos), Statins, |
| Rabdo tx | IVF and avoid Ca replacement (b/c IV calcium will sit in rabdo muscles and leach out to cause rebound hypercalcemia) |
| Tumor Lysis syndromes | A relase of K, Phos, and nucleic acids->uric acid; hypocalcemia; uric acid and phos ppt in tubules form crystals |
| Clinical points on Tumor lysis syndrome | higher risk in NHL and Burkit |
| Tx of tumor lysis syndrome | Prevent with IVF; Allopurinol inhibit XO to decrease Uric Acid production- but can cause xanthine stones; ?alkalinize urine prevent uric acid stones but can cause Ca/Phos stones; Rasburicase changes uric acid to allantoin more soluble in uric acid (dont use in G6PD def) |
| NSAID renal effects | AKI due to dilation of afferent arteiole, HTN, AIN, NS (MCD), CRP (papillary necrosis), hyperkalermia, hyponatremia |
| Define Hepatorenal syndrome | abs of other cause of renal failure, proteinuria<500, no sign of hematuria, inactive urine sediment, lack of improvement of renal function with IVF |
| HRS pathogensis | perp and splanchnic vasodilation-->Activation of the RAS-->renal vasoconstriction-->Na and water retention-->Ascites (circle continues) |
| Tx options of HRS | tx underlying cause, Midodrine (sys vasoconstrict) + octreotide (- splanchnic vasodilation), transplant, TIPs, Dialysis |
| define abdominal compartment sydrome | intra abdominal pressure >20 associated with one or more organ failures (measure bladder pressures) |
| another cause of sterile pyuria | Analgesic Nephropathy (stopping agents wont reverse damage but can stabalize kidney function) |
| Papillary Necrosis Causes | Pyelonephritis, Urinary obs, Analgesic Nephropathy, Radiaiton nepritis, DM, Sickle Cell disease, TB |
| Sickle Cell disease renal manifestations | Hematuria, renal infarct and papillary necrosis, renal medullary carcinoma, impaired concentrating ability, AKI, FSGS, RTA |
| Sickle Cell nephropathy treatment points | Use Ace/Arb for HTN/proteinuria, Keep BP<130/80, Goal Hgb is 10 with adv CRF/ESRD |
| Types of stones | Calcium oxalate, Calcium phosphate, Uric Acid, Struvite, Cystine, medications |
| Medication induced stones | Protease inhibitors (indinavir, Atazanavir)--can be missed on CT w/o contrast, Acyclovir, sulfadiazine, Triamterene, Allopurinol--Xantine stones, Ceftriaxone in kids |
| Dx and Tx of Kidney stones | Helical CT w/o contrast (if protease inhibitor will need contrast), and US if pregnant; tx: IVF, strain urine, Analgesia, Tamsulosin |
| Indications for stone removal | stone doesnt pass in 2-4wks, infection, complete obs and anuria, intractable sxs (N/V), stones >1cm |
| Calcium Oxalate stone risk factors | Hypercalcuria (>4mg/kg/d), Hyperoxaluria (>36mg/d), Hyperuricosuria (>750mg/d), Hypocitraturia (<200 mg/d), Low calcium or fluid intake, High oxlate, animal protein, sodium, and vitamin C intake, Hypomagnesemia, family history |
| Ca oxalate stones treatment | increase water intake (2-2.5L/d), maintain dietary Ca (1-4g/d), decrease oxalate intake (rubarb, spinach, coke, tea), Inc dietary citrate, HCT (inc Ca sec so dehydrate so pt inc Na reabs and Ca w/ it), reduce animal pro intake, limit sodium intake (Ca follows Na into the urine), limit sucrose and fructose (inc Ca excretion) |
| Ca oxalate stones | 4 sided prisim stones |
| Uric Acid stone overview | 5-10% stones in US, Radiolucent, no abnormalities in uric acid metabolism, Hyperuricosuria and diarrhea increase risk, Acidic urine promotes Uric acid precipitation |
| Uric Acid stone Associations | Diabetes, Gout, Polycythemia vera (inc uric acid production), Chronic Diarrhea, Metabolic sydrome |
| Uric Acid stone treatment | maintain UOP, Alkalinize urine (Kbicarb, Kcitrate), Allopurinol (when alkalinzation doesnt work or not tolerated) |
| uric acid stone | four sides crystal biofringent positive |
| staghorn calculi causes | Uric Acid, struvite or cystine stones |
| Staghorn calculi from stuvite crystal | coffin lid crystals that ppt with alkaline urine (pH>7) |
| Staghorn calculi tx | Antibiotics and stone removal |
| Cystine stones general | (AR), impaired prox tubule reabs so increased excretion, starts in early childhood |
| Cystine stones dx | 6 sided crystals in urine, + cyanide nitropruside test means >75mg/L, and 24hr urine shows >400mg/d |
| Cystinuria treatment | high fluid intake, alkalinize urine, restrict Na, meds to make cystine more soluble (Penicillamine, Tiopronin, Captopril) |
| SE of Penicillamine | MN, fever, rash, leukopenia |
| Captopril SE | limited use due to hypotension |
| Cystinosis basics | AR typically in children, this is due to increased production of IC/lysosme cystine formation---leads to fanconi syndrome and RF |
| Dx cystinosis | elevated cystine content in peripheral blood leukocytes |
| Tx of cystinosis | Cysteamine (forms complex to allow cystine to exit cells) or renal transplant |
| Dent's disease basics | Men only really, sx in childhood (x-linked recessive); polyuria, nocturia, microhematuria; due to mutation in voltage gated CL channels so see hypercalcuira, stones, RF, and rickets |
| How do you treat Dent's disease | treat the hypercalcuira that results from genetic change |
| Dx DI (C/N) | do water restriction test and if equivocal measure ADH |
| Changes in Pregnancy | decrease BP, increased HR, chronic hyperventilation, hyponatermia, hypoosmolar, Protein extcretion increased, Lower BUN, Lower Cre, Lower uric acid |
| DI treatments (C/N) | (C): Desmopressin, Chlorpropamide, Carbamazepine, Clofibrate; (N): Thiazides (dehydrate you first so later Na reabs increases and H2O as well), NSAIDs |
| What do you give for SLE flare in preg | prednisone and azathioprine (no cellcept of cytoxan) |
| Hypokalemia causes based on spot U. K | if U. K is <20 than extrarenal and if >20meq/L than renal loss |
| How do you define preexiting HTN in pregnancy | BP>140/90 seen before preg and present before 20th week of preg or persists longer than 12 weeks postpartum; increased risk of pre-eclampsia |
| Causes of Hypokalemia | Pseudo, K shift from ECF to ICF, Renal losses, GI losses, Inadequate K intake |
| Gestational hypertension | HTN w/o proteinuria, develops more than 20wks gestation, resolves within 12 weeks postpartum |
| pseudohypokalemia define | abnormal uptake of K into metabolically active cells (ex AML) |
| Pre-eclampsia clinical diagnosis | HTN>140/90, proteinuria after 20wks gestation, Cre>0.8, Uric acid>5.5, BUN 10-20, decreased renin, decreased GFR, decreased Na excretion, hypocalcuria and decreased urate excretion |
| Cause of cellular shifts in hypokalemia | Alkalosis, Insulin, Thyroid hormone, Barium poisoning, Hypothermia, Hypokalermic periodic paralysis |
| pre-eclampsia risk factors | nullparity, past history of pre-eclampsia, pregestational DM, family hx |
| hypokalemic periodic paralysis define | intermittent acute attacks of muscle weakness with low K; triggered by large carb meals, assoc with low mag or phos, is Autosomal Dominant, and can be acquired in thyrotoxicosis |
| Pre-eclampsia renal bx | a variant of thrombotic microangiopathy (proteinuria increases with time) |
| Hypokalemia via renal loss causes | Primary hyperaldo, causes of ECV contraction that stim renin/aldo (diuretics, barter/gitlemans'), primary renin increase (not dehydrated like malig HTN, Renin sec tumor, RAS), MC-like syndrome (cushings, cogenital adrenal hyperplasia) |
| HELLP syndrome | represents a severe form of pre-eclampsia--hemolysis (elevated LDH), elevated LFTs, low platelets, HTN and usu in third trimester |
| Acute fatty liver of pregnancy | HELLP plus hypoglycemia and coagulopathy, third trimester, almost all have N/V/decreased appetite x10d, mod renal dys |
| pHUS and TTP | usually develops post partum, severe renal dys, TTP can happen at anytime |
| Antihypertensive medications safe in preg | labetalol, methyldopa, hydralazine, Nifedipine |
| TTP clinical pentad | thrombocytopenia (large platelets), Microangiopathic hemolytic anemia (coombs neg, high LDH, schistocytes, neurosymps, renal insufficency, fevers |
| TTP etiologies | Ecoli, HIV, Chemo (mitomycin C, Cisplatinum, Bleomycin, gemcitabine), preg, OCP w/ estro, Ticlid, Plavix, cyclosporin, valacyclovir, APLA, CV surgery |
| TTP tx | plasma exchange with plasma infusion (not effective with EColi) |
| Most solid renal mass | RCC, fat poor AML, oncocytoma, angiolipoma, Metanephric adenoma, Renal TCC, lymphoma |
| renal cysts that need interevention? | Bosniak 2f need repeat US in 6mo; Bosniak 3-4 surgery |
| Tuberous sclerosis | AD, formation of angiolipomas in skin, brain or kidneys; can see seizures, mental retardation, facial angiofibromas and shagreen patches; increased risk of RCC |
| VHL buzz words | AD, retinal angiomas, cerebellar hemangioblastoma, RCC leading cause of death; most need B/L nephrectomy and assoc with pheo |
| Acquired renal cystic disease | increased with duration on HD and PD- 5% malig potential so far to screen these patients |
| alport's syndrome clinical presenation | Persistent microscopic hematuria, Progressive nephritis , High frequency sensorineural hearing loss, Ocular abnormalities |
| renal bx of alport's | LM: nonspecific; Early lesion: GBM thickening; Established lesion: thickened GBM plus basket weaving |
| hypertensive Nephrosclerosis | gradually progressive renal failure, non-nephrotic range proteinuria and ACE/ARB treatment of choice with proteinuric CRF |
| contrast nephrotoxicity | RF begins 12-24hrs after contrast, decline is mild or transient |
| contrast nephrotoxicity risk factors | Diabetes mellitus, Age > 75, Baseline renal insufficiency/dehydration, CHF, Multiple myeloma, High dose and high osmolality contrast agents |
| Fabry's disease basics | Lysosomal storage disease, x linked, def lysosomal hydrolase alpha galactosidase---accumulate Gb3 globotriaosylceramide in podocytes (ESRD by 55) |
| Fabry's disease clinical manifestations | severe neuropathic limb pain, telangiectasias and angiokeratomas (symmetric and truncal), corneal deposits, Polyuria, polydipsia, RF, prog cardiac disease and cerebral involvement |
| Fabry's disease renal manifestations | polyuria, polydipsia, proteinuria, oval fat bodies, renal sinus cysts on imaging, prog renal failure |
| Fabry's disease Bx | Vacuolization of podocytes and distal tubular epithelial cells on LM; EM: Gb3 accumulates in Lysosomes as lamellated structures (myeloid bodies= zebra bodies) |
| Fabry's disease Dx | low alpha galactosidase A in leukocytes |
| Fabry's disease Tx | Fabrazyme for 6-12 mo |
| nail patella syndrome | AD, 60% abs patella, dystrophic nails, renal disease (moth eaten GBM, coarse fibrils of collagen in lamina densa) |
| Causes of Nephromegaly | HIVAN, Diabetic Nephropathy, Infiltrative d/o (lymphoma, leukemia), Sarcodosis, ADPKD, Obstructive uropathy |
| Hyponatremia workup | 1.) measure S.osmo: normal then pseudohypoNa (hyperprotein or hyperlipid), hyperglycemia, or renal failure; low then true hyponatremia. 2.)Measure U.Osmo: if<100 then primary polydipsia or reset osmostat; if >150 other causes of hypo Na with impaired water exctretion (SIADH). 3.)Measure U. Na: if <15-20 then vol depleted, CHF, or cirrhosis; if >40 SIADH or Na wasting |
| SIADH lab abnormalities | hyponatremia, urine osmo> serum osmo, high urine Na, low serum osmo, hypouricemia |
| SIADH tx | Hypertonic saline, fluid restrict, demeclocycline, NACL tablets, Loop diuretics, Vasopressin agonists (tolvaptan-PO, conivaptan-IV) |
| cerebral salt wasting and hyponatremia | usu a few days after neuroSx, low plasma osmo, high urine osmo, high urine Na, difficult to differentiate from SIADH but will show + orthostatics to indicate dehydration |
| Hyponatremia due adrenal insuff | hyponatremia b/c of inc. ADH, hyperkalemia due to decreased aldosterone, Mild non-anion gap metabolic acidosis |
| Exercise induced Hyponatremia | due to presistent secretion of ADH, tx is 100ml bolus of 3% saline; tell ppl to drink to thirst not drink excess fluid intake when they run because that with the increased ADH will hurt them |
| Ecstasy and Hyponatremia | stimulates thirst and increases ADH secretion, decreases GI motility so you retain water; need to give 100ml of 3% saline |
| Polyuria definition and causes | output>3.0L/d; Primary polydipsia (U.osmo<250), Central DI (Uosmo<250), NephroDI (Uosmo<250), BPH, Salt waste nephropathies, Osmotic Diuresis (Uosmo>300-500) |
| primary polydipsia causes | Phenothiazines cause thirst, Infiltration with Sarcoid, Psychogenic |
| causes of central DI | idiopathic, trauma, pituitary surgery, Hypoxic encephalopathy, rare to be familial |
| Nephrogenic DI causes | X linked, AR/AD, Lithium, Chronic Hypercalcemia |
| Treatment of DI (C/N) | Central: desmopressin, Chloropropamide, Carbamazepine, Clofibrate; Nephro: Thiazides, NSAIDs |
| Hypokalemia cause based on U. K | U. K> 20 renal losses, U.K<20 non renal losses |
| Causes of Hypokalemia | Pseudo, K shifts, Renal losses, GI losses, Inadequate intake |
| Explain pseudohypokalemia | abnormal uptake of K into metabolically active cells (ex AML) |
| Hypokalemia- causes of cellular shifts | alkalosis, insulin, thyroid hormone, Barium poisoning, Hypokalemic periodic paralysis, hypothermia |
| Hypokalemic periodic paralysis define | random attacks of muscle weakness with low K, usu after large carb meal, often seen with low mag/phos, autosomal dominant, but can be acquired with thyrotoxicosis |
| Causes of Renal loss of K | primary hyperaldo, relative contraction of ECV (diuretics, Bartters, gitelman), primary renin increase (malig HTN, RAS, renin sec tumor--no signs of dehydration), MC-like syndrome (cushings, cong adrenal hyperplasia) |
| Causes of Hyperkalemia | Pseudo, increased intake, Cellular shift, impaired renal excretion |
| Causes of pseudohyperkalemia | shift out of cells (increase plt, wbc or hemolysis), temperature dependent |
| increased intake causing hyperkalemia | Noni juice/coconut, salt substitute, Pica Syndrome |
| increased intake causing hyperkalemia | Noni juice/coconut, salt substitute, Pica Syndrome |
| Cellular shifts causing hyperkalemia | rhabdo, medications, DKA, hyperkalemic periodic paralysis |
| Impaired renal excretion causing hyperkalemia | Pseudohypoaldo type 1 and 2, obstruction, Medications (heparin, cyclophosamide, Pentamadine, amiloride, triamterene), renal failure |
| Hyperkalemia tx | IVF, Cation resin (not in pts with bowel sx will cause necrosis), insulin and glucose, HCO3, B2 agonists, Ca gluconate or Cl |
| Hyperkalemia EKG progression | Peaked T waves, prolonged PT int, atrial aystole, prolonged QRS, Sine wave |
| Anion gap normal and adjusted | Normal AG is 12; For every 1 gm of albumin below 4 the corrected anion gap is 2.5 less; for every 1gm of albumin above 4 the corrected anion gap is 2.5 higher |
| Delta AG/delta HCO3: if you have an AG metabolic acidosis | if delta HCO3 exceeds delta AG by 3 or more then you have elevated AG MA and normal AG MA; if delta HCO3 less than delta AG by 3 or less then elevated AGMA and metabolic alkalosis |
| Is the primary metabolic acidosis compensated for? | PCO2 decrease should = 1.5 (HCO3) + 8 +/- 2 |
| Is the primary metabolic alkalosis compensated for? | PCO2 should increase .75 for every 1 increase in HCO3 |
| Is the respiratory Acidosis compensated for? | (acute) for every 10 increase in PCO2, then HCO3 increases by 1; (Chronic) for every 10 increase in PCO2 then HCO3 increases by 4 |
| Is the respiratory alkalosis compensated for? | (Acute) for every 10 decrease in PCO2 then HCO3 decreases by 2; (Chronic) For every 10 decrease in PCO2 then HCO3 decreases by 4 |
| what should you always order if there is an acid base disturbance | ABG and Chem 7 |
| Causes of metabolic alkalosis | GI losses (NGT and vomit), renal losses (primary aldo excess, loop or thiazide diuretic, hypercalcemia, milk alkai syndrome), intracellular shift, Alkali admin, Contraction alkalosis (occurs with large amts of loss HCO3 free fluid), admin nonreabsorbable anions, Mag def |
| Urine electrolytes affected in Metabolic alkalosis | U. Na may not tell you vol status because of increased HCO3 that is excreted Na is pulled with it so increased in urine; use U. Cl instead for vol status with met alkalosis |
| U Cl > 40meq/L tells causes of metabolic alkalosis | primary MC excess, Diuretics early on, Alkali load, Bartter's or Gitelman's, severe hypokalemia |
| U Cl < 25meq/L tells causes of metabolic alkalosis | vomitting, diuretics late, factitious diarrhea, post hypercapnia, CF, Low Cl intake |
| Bartter's syndrome Basics | (AR) impaired TALH salt abs so salt wasting/vol depletion, low to nl BP, elevated renin/aldo, low K, alkalosis, hypercalcuria , high to normal urine Cl; tx spironolactone and NSAIDs, KCl |
| Gitelman's syndrome Basics | (AR) defect in NaCl cotransporter in the DCT, see metabolic alkalosis, hypokalemia, normal to low BP, high renin and aldo, salt cravings, hypocalcuria and hypomagnesemia (hard to tell from thiazide); Tx: K, Mg, Amiloride +/- ACE |
| Gitelman's syndrome Basics | (AR) defect in NaCl cotransporter in the DCT, see metabolic alkalosis, hypokalemia, normal to low BP, high renin and aldo, salt cravings, hypocalcuria and hypomagnesemia (hard to tell from thiazide); Tx: K, Mg, Amiloride +/- ACE |
| Causes of elevated AG | -fall in unmeasured cations (Ca, Mg, K); -elevation in unmeasured anions (albumin); ketoacidosis (alcohol, diabetic, starvation); lactate; renal failure; toxins (ethylene glycol, Methanol, Propylene glycol, salicylate, pyroglugamic acid) |
| Normal AG hyperchloremic MA | GI loss (diarrhea), RTA (1,2,4, CKD, Adrenal insuff, hyporenin hypoaldo, PHA 1 and 2), Toluene ingestion |
| Normal AGMA: how to tell GI v Renal | Urine AG= Urine Na+K - Cl; if 0 or + then RTA; if negative then diarrhea |
| RTA type 1 basics | Decrease H secretion distally in collecting tubules |
| RTA type 1 cause | Autoimmune (Sjogrens, RA), Hereditary in children, Ifosphamide, Meds (ampho B, ifosphamide, lead, Li, outdated tetracycline, toluene, glue sniffing), medullary sponge kidney |
| Dx distal RTA type 1 | Normal AG hyperchloremic MA, urine PH>5.3, Urine AG 0/+, Fe HCO3 is constant <3% despite IV infusion (Rx alkali) |
| Distal RTA clinically | Associated with stones, hypercalcuria, Hyperphosphotemia, Hypocitraturia, Nephrocalcinosis (no stones in RTA 2) |
| Proximal RTA 2 basics | Decreased proximal HCO3 reabsorption, self limited with HCO3 around 14-20, distal acidification is normal |
| Causes of Proximal RTA type 2 | Multiple Myeloma, ifosfamide, topomax, carbonic anhydrase, heavy metals (lead and cadmium), Hereditary (Cystinosis, tyrosinemia, Wilson's) |
| Dx of type 2 proximal RTA | normal AGMA, urine PH<5.3, urine AG 0/+, Fe HCO3>15-20% with HCO3 infusion; Rx is alkali more than RTA 1 |
| Type 4 RTA basics | Hypoaldosteronism (nl promotes Na reabs, distal K and H secretion) |
| Type 4 RTA basics | Hypoaldosteronism (nl promotes Na reabs, distal K and H secretion) |
| Type 4 RTA dx | metabolic Acidosis, hyperkalemia, urine pH<5.3 |
| Causes of type 4 RTA | Aldo def (primary, renal dz with DM, ACE, obstruction) v . Aldo resistance (meds: amiloride, spironolactone, triamerene, TMP, Pentamadine) |
| Salicylate intoxication clinically | Early: tinnitus, vertigo, N/V, diarrhea; Late: mental satus changes, coma, pulm edema, death; Resp alkalosis leads to elevated AGMA and increased ketogenesis |
| Tx of Salicylate intoxication | Alkalinization- keep serum PH 7.5-7.55, keep blood glucose approx 200, dialysis for level >100 |
| Methanol intoxication | breaks down to formaldyhyde deposits in eye and basal ganglia; you see Weakness, nausea, HA, deceased vision, blindness, coma, death |
| Dx Methanol intox | order levels, suspect with high AGMA, high osmo gap ((calc Posm= 2xNa + gluc/18 + BUN/2.8)- measured osmo gap) |
| tx methanol intoxication | Fomepizole, Dialysis (if MA, end organ damage, CNS dys or level>50) |
| Ethylene glycol intox basics | see drunkness to coma, oxalate crystals ppt later, thachypnea, pulm edema, Can prolong QTc via effects on Ca |
| Dx ethylene glycol intoxication | levels, highAGMA, elevated osmo gap |
| tx ethylene glycol intoxication | Fomepizole, pyridoxine, thiamine, HCO3 drip for ph<7.3, HD |
| Isopropyl alcohol overdose | S/S is a CNS depressant, does not causes an elevated AGMA; No AG but elevated OG; tx supportive |
| propylene glycol tox basics | caused from certain drips: lorazepam, phenobarb, dilantin, diazepam; elevated AG and OG |
| Diethylene glycol toxicity buzz words | causes elevated AGMA, difacial plegia |
| Valproic acid toxicity clinically | lethargy and coma, Hyperammonemia, hepatic dys, low plts, leukopenia AKI; can dialyze if severe toxicity |
| Metformin toxicity | drug induced lactic acidosis; HD can remove drug |
| Causes of elevated osmo gap | ethylene glycol, Methanol, RF, Lactic acidosis, alcoholic ketoacidosis, DKA, Isopropyl alcohol, formaldyhyde ingestion (normal OG<10) |
| Causes of Hypocalcemia | loss of ionized Ca from ECF, disturbances in PTH secretion, sepsis, fluoride poisoning, bisphosphonates |
| Hypercalcemia S/S | Depression, lethargy, coma, consitpation, pancreatits, muscle weakness, renal (NDI, stones, nephrocalcinosis, AKI, CRF, RTA), shortened QT |
| Hypercalcemia work up | measure iPTH plus PTHrp, phos, 24U Ca: elevated iPTH (primary HPT, FHH, lithium); suppressed iPTH and elevated PTHrp (malig) if not elevated; check vit D (increased then granulomatious disease or increase D intake and lymphoma; if low malig, thyrotoxicosis, immobilization, paget's and milk alkali) |
| Hypercalcemia tx | Saline, calcitonin, Bisphosphonates, glucocorticoids, Dialysis, Diuretics |
| Causes of hypophosphatemia | shift intracellular, decreased intestinal abs, increased urinary excretion |
| hyphosphatemia work up | measure Phos and 24 U. phos: if renal losses then Fe phos greater than 5% and 24 hour>100, measure serum Ca: (high primary HPT, low then vit D def, if normal then primary renal phos wasting so measure FGF23) |
| Causes of hyperphosphatemia | Increased Phos load, Renal failure, increased tubular reabs |
| renal osteodystrophy- osteitis fibrosa cystica | burn turnover increased due to secondary HPT |
| renal osteodystrophy- adynamic bone disease | decreased bone turnover (oversuppression of PTH--so in treatment allow PTH secretion to increase) |
| Renal osteodystrophy- osteomalacia | reduction in bone turnover, increase in osteoid, mostly due to aluminum accumulation in bone and Fe overload or vit D def |
| Hypomagnesemia diagnostic approach | Exclude renal waisting: 24h UMg<20 and feMg<2%; if greater than check 24 UCa and if >250 then diuretics and nephrotoxins and HHN, but if <150 then gitelman's and thiazides, if in the middle than EGF |
| Hypomagnesemia S/S | weakness, anorexia, nausea, hypokalemia, hypocalcemia, prolonged PR int, Prolonged QRS, decreased T waves |
| Hypomagnesemia causes | decreased abs or inadequate intake, meds (cisplatinum, loop, thiazides, PPI, ampho B, Calcineurin inhibitors), EtOH/acute pancreatitis, Hypercalcemia (HPT), DM, Renal losses |
| Hypomagnesemia renal losses | loop, bartter's, FHHNC, AD hypocalcemia, Nephrotoxins (aminoglycosides, CNI, cisplatinum, pentamadine, cefuximab) |
| Causes of hypermagnesemia | Overdose (epsom salt, laxatives), iatrogenic with pre-eclampsia, mild HPTH, FHH, Lithium ingestion, theophylline intox, tumor lysis |
| Hyper mag s/s | decreased DTR, lethargy, drowsy, somnolence, hypotensive, brady, muscle paralysis, complete heart block, cardiac arrest |
| tx hypermagnesemia | stop supplment if renal fxn normal and if in RF start dialysis |
| Peritonitis in PD patient | S/s- abd pain, cloudy effluent, fevers; Dx- PD WBC > 100 and >50% PMN, consider intraabd event if PD amylase>50 |
| Peritonitis in PD patient bugs and tx | Coag neg staph, S. aureus, GN, fungal if refractory (remove catheter); Empiric therapy: Cefazolin or vanc + ceftazidime or aminoglycoside |
| PD exit site infection bugs | s. aureus, Pseudomonas, keep on abx till site is clean |
| PD general points | if blood dialysate often due to trauma or GYN- treat with heparin; increases eosinophils in PD usu after catheter placement and fungal infections. There will also be free air often secondary to PD |
| PD more general points | if R pleural effusion after staring PD then likely defect in diaphragm; diet in pts is low phos, low NA, and +/- restrict fluids; encapsulating peritoneal sclerosis transfer pt to HD |
| Bladder Ca types and risk factors | TCC: smoking, analine dyes, age>50, cytoxan; SCC: stones, chronic inflammation; ACar: congenital defect, chronic inflammation |
| Complications of CKD | volume, metabolic acidosis, hyperkalemia, renal osteodystrophy, HTN, hyperphos, anemia, dyslipidemia, access |
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