Nephro Flashcards
(105 cards)
1
Q
acute renal failure
A
- inc BUN and Creat over hrs to days
- hours:rhabdo, contrast induced RF; constricts aferent art and its toxic to renal tubules
- aminoglycoside(5-10days), post strep(1-2wks)
2
Q
- azotemia vs uremia
- why bleeding diathesis in uremia
A
- azotemia: renal insuff; buildup of azoles; NO DIALYSIS
- uremia: very severe RF; need dialysis;worse; acidosis, mental status changes, highK, fluid overload, anemia, hypoCa, pericarditis;bleeding diathesis (bc platelets dont degran so alpha and dense granules dont work, tx with DDAVP releases platelet factors temporarily); uremia prevents degran of WBC so infxns
3
Q
aminoglycoside toxicity
A
- in weeks
- space intervals to dec chances of toxicity not dec dose
- need to accumulate toxicity over days
- one dose wont cause RF
- peak kills organism; trough = toxicity thats why you space intervals otherwise you get ototoxicity
4
Q
pre/post/intra renal
A
- pre=dec perfusion; decBP, RA stenosis, dec volume, dec albumin
- post= dec drainage or dec fwd flow; GFR most det by hydrostatic pressure of glomerular cap pushing into glom space; dec GFR is hydrostatic press of bowmans spce inc instead (stone in bladder or both ureters, strictures, tumors, obstrxn)
- in prev both, kidney is normal; can transplant it and it will have normal fxn
- intra=tubular or glomerular prob and kidney itself is defective
5
Q
ARF dx
A
- BUN high in all forms of renal failure
- can be falsely high with inc protein load in diet or GI bleed
- BUN falsely low with malnut, liver dis, or SIADH
- Creatinie is main measure of renal fxn; closest to gfr; inulin not naturally in body; slightly overest GFR bc some tubular secrxn of creat; creat is met prod of skeletal muscle; creat can be false low from dec muscle mass so adjust creat clearance for weight; creat inc .5-1pt/day even if pt anuric; .5–>1.5–>2 kidney dead
6
Q
prerenal azotemia
A
- due to hypovolemia, hypotension (shocks), third spacing(addisons low aldo, peritonits, osmotic diuresis), low albumin nephrotic syn leads to dec renal perf
- chf, constrictive pericarditis, coarc of aorta: have edema and fluid overload but no perfusion of kidney so inc bun and creat
- BUN:cr = 20:1; low flow so theres inc time for urea to be absorbed but creat same amt excreted
- urine Na low (500 bc UNa low and concentrated urine; spec gravity inc shows Uosm inc
7
Q
renal art stenosis
A
BUN:CR = 10:1
-this effect is highly exagerrated with acei which markedly diminishes renal perfusion bc theres high aldosterone state in RAStenosis
8
Q
hepatorenal syn
A
- renal failure due to hepatic failure
- kidneys are normal
- intense constriction of afferent arteriole= dec renal perfusion (bc defect is in afferent its lab values are like prerenal)
- bun:cr 20:1, urine Na low, Fe low
- no improvement in renal failure after 1.5L saline is dx of this
- tx: tx underlying hepatic syndrome; fix liver kidney lives
9
Q
ACEi effect on kidney
A
- acei induced renal failure is from vasodilation of efferent arteriole: dec GFR
- rise in BUn:cr if theres underlying renal insufficiency
- severe decline in renal fxn in bl renal art stenosis when starting acei
- overall dec progression to uremia and renal failure bc dec in intraglom htn
- dec proteinuria by 35-45%
- brief dec in gfr and long term benefits
10
Q
kidneys afferent and efferent control
A
- afferent dilation by prostaglandins; inh by nsaids and cause vasoconstrxn (no good in Dm, HTN)
- efferent constriction inc gfr and its by angiontenin II; acei dialtes efferent and dec gfr
11
Q
hepatopulm syn
A
- kindeys normal
- marked changes in sat levels with changes in body positions=orthodeoxia
- o2 sat drops when they sit up and theres an inc in A-a gradient
12
Q
postrenal azotemia
A
- dec outflow of urine with bl obstrxn; stone in bladder obstructs both kidneys
- bladder ca, prostate hyper, bl ureteral dis(retroperitoneal fibrosis), neurogenic bladder (DM, MS); bl strictures
- Cr rises only when lost at least 70-80% of renal fxn
- initially 20:1 like prerenal then as permanent damage occurs it will lower to 10:1 such as in ATN
- early discovery imp; complete recovery possible until 10-14days of obstrxn
- ATN is mcc in hosp pts
- DX: distended bladder, bl hydronephrosis on renal sono or CT, or finding large vol of urine after passing foley
- after voiding there should be no more than 50mL of urine left in bladder
13
Q
retroperitoneal fibrosis cause
A
-bleomycin, methotrexate, & methylsurgide(migraine med)
14
Q
chemo man mneumonic
A
ears: cisplatin=deaf
arms: vincristine = periph neuropathy
lungs: bleomycin, busulfan
kidneys: cisplatin
bladder: cyclophosphamide=hemm cystitis
legs: vinblastin=peripheral neuropathy
15
Q
acute tubular necrosis
A
- allergic, toxin, pigments (myoglobin, HB), crystals, calcium
- from hypoperfusion of kidney leading to such severe ischemia theres cell death ot from toxic inj to kidney like aminoglycosdie or amphotericin. this is from sepsis or after cardiac or aortic sx
- from combo of both ischemia and toxic inj; if ischemia is severe then tubular cells necrose and slough off into urine and become granular, muddy brown or pigmented casts
- longer duration of hypotension/hypoperfusion, the greater chance of ATNl; risk inc with toxic inj; ex risk of rhabdo causing renal failure is inc when theres hypoperf of kidney
16
Q
three phases of atn
A
- prodromal: time between acute inj and onset of renal failure
- oligouric: <100ml/24hrs
- postoliguric= diuretic phase when all water not prev excreted will now leave the body in vigorous polyuria
17
Q
ATN dx
A
- initial clue BUN:Cr close to 10:1
- hugh urine sodium, high FeNa,low osm bc dead cells dont work
- isosthenuria:osm same as serum osm
18
Q
ATN tx
A
- hydration to make sure no prerenal
- diuretics like furosemide or mannitol dont reverse ATN
- nothing reverses it, like a sunburn, see if it corrects itself
- if life threatening then dialysis used
- dopamine doesnt work (inc splanchnic and renal perf)
19
Q
allergic interstitial nephritis
A
- hsa fever, rash, eosinophils in urine, and happens in one dose
- allergies:kidney, stevens johnsons, drug induced hemolysis
- pcn, ceph, quinolones, sulfa(thiazides, lasix, acetazolamide), allopurinol, rifampin; nsaids,PPI
- infxns: leptospirosis, legionella, cmv, ricketssia, strep, SLE, sjogren, sarcoid, cryoglobulinemia
- joint pain common cuz AIN acts like serum sickness
- lab eosinophilia, eosinophiluria, hematuria, proteinuria, inc IgE levels,
- best initial test: UA looking for white cells but it cant distinguish eosin from wbc
- most accurate: hansel stain or wright stain of urine
- single most accurate: kidney bx but not necessary
- resolves spontaneously after stopping agent; if BUN and creat continue to rise then short course of steroid
20
Q
rhabdomyolysis
A
- sudden severe crush injury(K out of cells), seizures, severe exertion, hypokalemia(bc causes musc to breakdown to inc K), hypophosphatemia, statins
- massive hemoglobinuria to cause RF only in ABO incompatibility
- pigmetn toxic to tubules and it precipitates
- toxicity degree related to duration of contact of tubular cells with Hb or Mb; compounded by dehydration so person who run a marathon has myoglobin release and poor kidney perfusion
21
Q
rhabdo lab tests
A
- most imp is EKG or K level with severe crush inj or seizure bc acidosis and highK can cause arrhythmia; if peaked T waves give calcium gluconate or Ca choride
- best initial test is UA: dipstick positive for blood but no RBCs seenbc hb/MB reacts with an agent on stick and comes out as if RBCs present
- confirmed with high serum CPK enormously high 10,000-100,000. n<500
- met acidosis with dec serum bicarb, high phosphate from musc breakdown, low Ca from deposits of ca in damaged muscles
- very rapid rise of creatinine
- tx: hydration and mannitol as diuretic to dec duration of contact; alkalinize urine with bicarb may help stop precip of pigment in tubule
- inc K but no ekg changes: insulin/glucose, or bicarbonate
22
Q
myeloma
A
bence jone proteins cause tubular damage
- myeloma more commonly cause of nephritic
- myeloma: inc ca, amyloid, bence jones, ab clog the glomerulus
23
Q
oxalate
A
- mcc ethylene glycol OD suicide with antifreeze
- met acidosis with high anion gap with renal insuff
- dx: oxalate crystals on Ua; envelope shape
- Tx acute: ethanol or fomepizole infusion to prevent formation of ethylene metabolite oxalic acid; then disalysis used to removve the ethylene glycol; sodium bicarb canbe given to correct acidosis
24
Q
crohns
A
-ch. hyperoxaluria and kidney stones bc of fat and Ca malabs
25
methanol vs ethanol s.e.
- methanol=optic neuritis "drank myself blind"
| - ethanol: renal prob with ca oxalate stones
26
urate
- tumor lysis syndrome
- this is why pts with leukemia or lymphona get vigorous hydration and allopurinol prior to getting chemo (allopurinol inh xanthine to hypoxanthine to uric acid)
- oxalate stones usually precipitate in alkalined urine
- uric acid stones precip in acidic urine
- allopurinol alkalinizes urine too so it reduces risk of uric acid nephopathy
- gout does it by same mech but slower
27
hypercalcemia
- mcc primary hyperparathyroidism
- sx if theres stones or renal impairment
- <5mm stone passed spontaneously
- stellate=star shaped
- staghorn-sx
28
toxins
- need more time >5days
- no therapy to reverse any sepecific cause
- no test to confirm, just check history
29
aminoglycosides
- tobramycin is least nephrotoxic vs genta and amikacin
- dec K and Mg predispose to toxicity
- has postab effect so one dose daily is only needed
30
amphotericinB
-renal toxic and distal renal tubular acidosis
-high creatinine and dec Mg bicarb K.
-
31
atheroembolic dis
- renal failure after vasc catheter like angioplasty
- eosinophilia, low complement, blue discolor of fingers and toes, livedo reticulris(blue fishnet stocking of veins)
- most acc test: skin biopsy to see chol crystals
- no tx
32
contrast materials
- renal failure in 12-24hrs after use
- rise in creat peaks at 3-5days after injury
- bun:cr may be 20:1 bc it cuases afferent vasoconstrxn like prerenal
- prevent with hydration and n-acetylcysteine
33
50 year old male hx of SCD, nsaids, flank pain, fever, ua shows necrotic material
- papillary necrosis
- dx= spiral ct
- tx none
34
papillary necrosis
- hx of scd, db, urinary obstrxn, ch pyelonephritis
- SUDDEN onset flank pain, hematuria, pyuria, fever
- necrotic material in urine
- no growth of org onculture
- dx is ct scan (bumpy contours in renal pelvos where papilla sloughed off)
- no tx
35
prevention of contrast induced renal failure
- must hydrate with 1-2L normal saline over 12 hours before the procedure
- bicarb and n-acetyl cysteine also shown to dec risk
- diuretics dont work
36
glomerulonephritis
- everywhere
- low urine sodium adn Fe<1% bc intense vasoconstrxn causes urine retention of Na
- single most imp dx test is renal bx; renal bx guides tx unline in tubular dis
37
wegeners
- vascular dis
- GI, LUNGS,URI, jts, skin, eye, kidneys
- c-anca
- ch upper and lower resp illness not resp to ab
- high esr, anemia, inc wbc
- rheum factor + in 50%
- best initial test:antiproteinase 3 ab=canca
- most acc test: bx kidney/lung for granulomas
- tx cyclophosphamide and steroids
38
churg strauss
- asthma, eosinophils, inc eosinopils, allergic rxns
- + PANCA=antimyeloperoxidase
- most acc lung bx granulomas&eosinophils
- tx glucocorticoids and cyclophosphamide
39
goodpastures
- idiopathic d/o of only lung and renal
- anti basement membrane ab
- 1/3 have no lung inv and just hematuria and proteinuria
- hemosideren laden macrophages
- best initial test: level of anti basement memb ab to type IV collagen
- single most acc test: lung/kidney bx showing linear depostis on immunoflorescence
- tx: plasmapheresis and steroids. cyclophos may help
40
polyarteritis nodosa
- every organ EXCEPT LUNG
- most acc test: bx
- tx cyclophosphamide and steroids
- hep B in 10-30% PTS
- Abd pain mimicing mesenteric anemia and the pain occurs with eating; angiogram of vessels inv in GI tract can eliminate need for bx
- SURAL NERVE is freq location for bx
- panca only in a minorty of pts
- tx steroids and cyclophosphamide
41
henoch schonlein
- no lung.uri involved
- igA deposits in mult tissues getting renal insuff, skin lesions, gi sym, tetrad of palapable purpura,
- acc test: bx of inv tissue but rare bc most often resolves spontaneously
- next best step? nothing, self limited
- steroids can be used if dis progressive
- bx= leucocytoclastic effect (WBC attack
42
IgA nephropathy (Berger dis)
- presents with mild hematuria that resolves spont in 30%pts; ~40-50% progress ESRD
- from igA deposits but only in kidney
- asian pt with recent URI or pharyngitis who gets hematuria 1-2days later (poststrep occurs 1-2weeks later)
- igA inc in only 50%pts, complement levels normal, dx bx bc igA level not reliable
- tx: acei/arbs with proteinuria, with massive proteinuria use steroids
- fish oil value marginal
43
postinfectious glomerulonephritis
- any infxn
- poststrep occur with either throat or skin infxn with strp pyogenes although rheumatic fever only occurs with strains causing pharyngitis
- smoky, cola or tea colored urine from hematuria, red cell casts, proteinuria
- periorb edema and htn common
- best initial test: Antistreptolysin test (ASO), and antihyaluronic test (AHT)
- C3 low, antiDNAase
- most acc test: bx showing "humps" on electron microscopy from igG and C3 depostis
- tx supportive withmx of fluid overload and htn with diuretics
- alot resolve spontaneously so bx rare
44
Thrombotic thrombocytopenic purpura vs hemolytic uremic syndrome
- TTP: clinical dx pentad(hemolytic anemia, uremia, thrombocytopenia+fever, neuro prob; dont need all 5); HIV and ticlopidine; if severe tx plasmapheresis; dipyridamole can help by preventing platelet aggregation
- HUS:triad (hemolytic anemia, uremia, thrombocytopenia);inc creat; kids ecoli O157:H7 food poisoning; mild dis resolves spont; no ab to pt with possible HUS bc release more toxins as it dies with ab
- anemia is both is intravasc abn blood smear; LDH and retic count high, haptoglobin dec; dec metalloproteinases
- dont transfuse platelets bc can worsen cns and renal prob by giving more platelets as a substrate to precipitate. small platelet plugs atre the cause of the prob
- platelet plugs are stabilized by vwf and factor 8; metalloproteinases cut vwf to release platelet plug
- TTP and HUS= dec metalloproteinases
- thrombin-->fibrin-->tissue stab factor; plasmin destroys fibrin plug and turns it into d dimers
- plasmapharesis puts on metalloproteinases to cut platelet plug
45
crypglobulinemia
- renal dis from cryoglobulinema assoc with chronic hep b&c
- also joint pain, neuropathy, purpuric skin lesions
- no GI inv
- assoc with inc ESR, low complement, confirmed with a test for cryoglobulins
- +rheumatoid factor
- tx: mx hep with interferon and ribavirin
- severe dis pulse doses of steroids and occaional plasmapheresis
46
cryoglobulin vs cold agglutinins
- cryoglobulin =renal dis
| - cold agglutinins: epstein barr, mycoplasma, hemolytic anemia
47
diabetes
- dipstick + for albumin bw 150-300 mg/24hrs = trace amts
- microalbuminuria abn but <300mg
- tx albuminuria is acei to prevent progression of proteinuria
48
SLE
- dsDNA inc, complement dec in flareups
- acc test: bx: essential to guide therapy
- sclerosis: scarring, no tx
- proliferative dis: use steroids with mycophenolate; MYCOPHENOLATE superior to cyclophosphamide
49
alport syn
-combo of glomerular with eye/ear dis
50
idiopathic rapidly progressive glomerulonephritis
- only in the kidney
- idiopathic form: crescent formed in kidney and ANCA neg
- dx bx
- tx: steroids and cyclophosphamide
51
amyloidosis
- AL: plasma cell dyscrasia from light chains; mult myeloma
- AA: amyloid made as proteinaceous material in assoc with mult ch infxns or inflamm conditions
- amyloid builds up in kidney and GI,Nerves,Muscles, heart restrictive cardio rhythm do and heart block, large tongue MACROGLOSSIA
- dx biopsy; aspirate abd fat pad or take a sample of rectum; congo red staining shows green birefringence
- tx difficult; melphalan and prednisone can control protein production
52
nephrotic syn
- protein >3.5, high liopind, edema, low serum albumin level
- edema from salt and water retention by kidney and low oncotic pressure
- high lipid prob from loss of lipoprotein markers on chylomicrons.LDL; high lipid shows maltese cross on Ua
- massive proteinuria and low albumin
- glomerular basement mem loses neg charge so lose proteins
- hypercoag state from loss of natural anticoag proteins ex antithrombin, protein c, protein s
- loss of iron, copper zinc from loss of transferrin adn ceruloplasmin
- dx single spot urine for albumin and creatinine
- bence jones not found on dipstick(only albumin) need to di urine immune electrophoresis
- most acc test: bx
tx: steroids ; next best step add cyclophosphamide or mycophenolate; acei used in all but doesnt reverse underlying dis
53
membranous
-mc nephrotic syn in adults; assoc with cancer like lymphoma/breast ca/infxns/nsaids/hepbc
54
nil lesion
- minimal change dis
- mc in kids
- light microscopy normal and electron microscopy needed to see fusion of foot processes
- improved with steroids
55
mesangial
- mostly idiopathic, steroid resistant nephrotic stn; immunoflorescence shows igM deposits in expanded mesangium
- membranoproliferative: assoc ch hepatits and low serum complement levels; dipyridamole and aspirin used therapeutically; cryoglobulins tx with interferon adn ribavirin
- focal segmental: heroin and HIV; limited response to steroids; ESRD in 5-10yrs
56
age mammography, pap, colonoscopy
-mammo 40yo
-pap 20yo
-colon: 50yo
-
57
urinanalysis
- proteinuria: dipstick only determines albumin; microalb is bw 3-300mg/24hrs; proterinuria can be seen normally under 1g/day resolving spont; from prolonged standing aka orthostatic proteinuria dx by splitting the 24 hour urine sample (no protein in first 8 hours and then find it in hte second part)
- hematuria: rbcs any cause in bladder/kidney; stones, ca, trauma, cyclophosphamide, bleeding do, cystitis, prostitis. in glomerular dis the ebcs change shape and are dysmorphic
- nitrites: gram neg bac reduce nitrate to nitrite on dipstick
- bacteriuria: in pregnant women asymp bacteriuria can progress to pyelonephritis
58
casts
- hyaline: dehydration
- red cell: glomerulonephritis
- broad, waxy: chronic renal failure
- granular: "dirty or muddy", acute tubular necrosis
- white cell: pyelonephritis, intersitital nephritis
59
ESRD dialysis: mcc, indications, anemia, hypocalcemia
- mcc dm and htn;glomerulonephritis, cystic dis,interstitial nephritis
- indications: fluid overload refractory to diuretics, acidosis, pericarditis, encephalopathy, myoclonus, wrist or foot drop, hyperkalemia; or uremia (n/v,bleeding diathesis)
- hemodialysis used 85%, peritoneal dialysis 15% bc peritonitis (put ab into catheter tube)
- anemia: loss of EPO, normocytic normochromic
- hypocalcemia/hyperphosphatemia: lose vitD prodxn tx with vit D replacement; high phosphate from inability to excrete it tx with phosphate binders (calcium carbonate, calcium acetate) (sevelamer and lanthanum are two phosphate binders with no aluminum or calcium used when calcium level abn high from vit D replacement)
- aluminum containing ones shouldnt be used bc assoc with cns accumulation and dementia as well as bone abn
60
cinacalcet
-cinacalcet simulates effectof calcium on parathyroid (shuts down PTH and dec phosphate)
61
osteodystrophy
- osteitis fibrosa cystica: inc pth removes calcium from bones; bone suffers acidosis by removing calcium from bones;
- hypermag: from dec excretion: dec intake
62
htn and atherosclerosis
-renal dis causes rapidly progresive coronary art dis; mcc death on dialysis (MI/coronary dis); goal of BP <130/80
63
infection
-dec degranulation in uremic environment; 2nd MCC death, mc org is staphbc constantly penetrating skin for silysis
64
bleeding
- uremia induced platelet dusfunction
- tx with desmopressin releasing vwf and factr 8 which inc platelet aggregation and adherence; estrogen or cryoprecipitate rarely used
65
renal transplant
- live related donor: 95% at 1yr, 72% at 5 years
- cadaver donor: 88% at 1 yr, 58% at 5 years
- dialysis: 30-40% at 5 yrs
- DM on dialysis: 20% at 5years
- post transplant renal graft rejection prevented by cyclosporine, tacrolimus, adn mycophenolate (all inh T cell fxn)
66
fluid and electrolytes hypoNa
- hyponatremia: low Na <135 from inc water retention or urinary sodium loss
- serum osm= 2xNa + (BUN/2.8) + gluc/18 = 2xNa +10
- neurologic sym; sym depends on how fast the levels dropped
- an acute drop in Na 15-20pts can be seizure or coma
- tx: fluid restriction (mild hypoNa with no sym); moderate (normal saline + loop); severe w/seqizures (3%hypertonic saline
- rate of rise imp to stop central pontine demyelinosis (rate no more than 0.5-1 mEq per hour) no more than 12 pt rise in 12-24hrs; can be corrected as rapidly as 2mEq/hr if pt seizing and its urgent
- fludrocortisone used for cerebral salt wasting disease
67
hyponatremia classification
- hypervolemic: CHF, cirrhosis, nephrotic
- eubvolemic: low Na, low osm
- hypovolemic
68
pseudohypoNa
- total body Na level normal and sodium blood level artificially low
- hyperglycemia: Na dec 1.6 for every 100mg/dL inc in glucose above normal; high gluc causes water to shift out of cells without Na which drops Na level; mannitol adn sorbitol do the same
- hyperlipidemia: lab error
- inc 100glu=dec 1.6Na
69
hypervolemic states (inc ECF)
- dec in intravasc volume causing inc in ADH secretion from post pit : CHF, nephrotic and low albumin, cirrhosis, renal insuff
- perception of intravasc vol dec = ADH inc
70
hypovolemic states=dec ecf
-loss of na thru body fluids and replaced with free water ex sweating, GI n/v, skin burns cystic fibrosis, diuretics, renal sodium los, addisons, acei
71
causes of hypovolemic low Na
| urine Na <10
- dehydration
- vomiting
- diarrhea
- sweating
72
causes of hypovol low Na
| urine Na >10
- diuretics inc Na/Cl reabs
- acei
- renal salt wasting
- addisons
- cerebral sodium wasting
73
euvolemic states
-not dehydrated or vol overload, no edema, no orthostasis, no skin turgor
-psychogenic polydipsia
-hypothyroid
-diuretics
-acei
0endurance exercise
-SIADH
-PSEUOD PSYCHO SIADH
74
28M ho bipolar on lithium, drinks 18L/day, urinates 18L/day, Na normal 140
```
-Na low = psychogenic
Nahigh: nephrogenic DI
-Na normal you cant tell Uosm low in bioth, Una low in both
-nocuria = neph DI
-no nocturia in psychogenic
```
75
SIADH
- Causes: brain lung drugs and Ca
- UNa high, Uosm high = dx
- single most acc test: inc ADH level
- tx fluid restrxn for mild and give hypertonic saline for severe
- chronic where cause cant be corrected: demeclocycline or lithium ; inh effect of adh on kidney tubule adn lead to water diuresis by inducing neph DI
76
hyperNa
- skin, urine, Gi loss and DI
- Dx: CDI vs NDI: watching for dec in urine vol after ADH admin
- tx: acute give isotonic fluids IV; CDI five vasopressin (can be all routes except nasal); NDI ( diuretics or nsaids inh prostaglandind which impair concentrating ability and inc axn of adh at the kidney)
- dec K and inc Ca cause it bc kidney deosnt concentrate
77
hypoK
- causes: GI, inc entry into cells with alkalosis (K in H out), inc insulin, b act (inc axn of Na/K/Atpase Na out K in so bb inc K, digoxin blocks Na/K/ATPase so inc K), b12 replaced in b12 def ppl(rapid prodxn of cells causes dec K), trauma pts have inc b act, uine losses (diuretics, conn, licorice, barter lose Na/k liek lasix, cushings inc aldosterone, Mg dep K channels = dec Mg then huge urine loss of K)
- sym: weakness, arrhythmias, rhabdo; k nec for ADH effect on kidney and hypoK pts present with neph DI
- dec K = Uwaves = purkinje fiber repol
- inc K = peaked T waves
- Dx = ekg
- tx: IV max 10-20mEq/h bc more causes arrhythmia, dont use dextrose bc stim insulin which lowers K adn shifts K into cells; oral no max for oral erplacement but kidney excretes faster than gut absorbs it; total body req is give 4-5mEq per kg per pt
78
hyperK
- inc intake orally or IV with impaired exretions, movement from cells to ECF(acidosis, psuedohyperk, .1decpH = inc 0.7K, insulin def, tissue breakdown, periodic paralysis waxing adn waning with inc or dec K), dec urine excretion renal failure, hypoald, addisons, K sparing, nsaids)
- weakness with K at >6.5, abn cardiac condxn is mcc death, hypoventilation
- tx: calcium chloride/gluconate protect heart not dec K levels, membrane stabilization; sodium bicarb alkalosis drives K into cells but dont give in same IV line as Ca bc forms CaCO3; glucose and insulin drives K in takes 30-60 min to work; diuretics and beta agonists take long tho; kayexelate (cation exchange resin) absorbs 1Meq K per g and releases 1Meq Na. given with sorbitol to prevent constipation, only causes redist not removes from body; dialysis
79
renal tubular acidosis
- Distal (type 1): cause (SCD, autoimm, familial, ch hepatits), BASIC urine ph >5.4, secondary hyperald and hypoK, nephrocalcinosis and nephrolithiasis, BASIC URINE=STONES; dx (acid load test give ammonium Cl which should lower ph but pH remainds high; pts get hypok bc kidney cant excrete H so secretes K instead; tx oral bicarb bc bicarcb reabs in proximal tubule still works and K replacement
- proximal: cause (fanconi, wilsons, amyloid, myeloma, acetazolamide, vit d def, secondary hyperparath etc),unable to absorb bicarb, inital pH basic then turns acidic when body loses enough bicarb, lowK, serum bicar 18-20; malabs glu phosphate urate aa; BONE LESIONS (OSTEOMALACIA AND RICKETS); DX pt unable to absorb bicarb loading and have basic urine in presence of acidemia; normal ppl dont excrete bicarb until serum bicarb >24; tx give K, mild volume depletion will enhance prox bicar reabsoprtion; thiazides and large amts bicarb used; DIURETICS TO DEC VOL OF BODY
- type IV hyporeninemic/hypoaldosteronism: cause (aldosterone def or adrenal insens to angio II which normally stim aldosterone, dm, addisons, scd, renal insuff), HIGH K, hyperchloremic met acidosis(nonAG), Dx high urineNa with oral salt restrxn; tx fludrocortisone(high mineralocorticoid effect and simmilar to aldosterone)
80
Alkalosis
$ metabolic: 1pt increase bicarbonate there's .7 inc in pCO2; volume contraxn leads to inc aldosterone which excretes H so there's met alkalosis
- H ion loss: steroids (acts like Aldo), Gi loss vomiting NG tube, renal loss(cons cushings, ACTH inc, licorice, barters), dec chloride intake causing bicarb absorbed more bc Cl is anion and bicarb is anion so it inc bicarb to compensate , diuretics
-bicarb retention: bicarb admin, contraxn alkalosis, milk alkali syndrome
- H moves into cell: hypokalemia
$ respiratory
- hyperventilation: dec pCo2: anemia, PE, sarcoidosis, anxiety, pain; progesterone stim brainstem to breathe, catecholamines, hypoxia, cirrhosis, preg all inc RR
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renal tub acidosis summary
I distal = cant excrete H; urine basic, dx give acid; tx give bicarb, low K, STONES
II = proximal = low K, unable to absorb bicarb, urine acidic, no stone, dx (give bicarb, urine bicarb bc cant absorb it, acid blood makes bones weak and demin them), tx diuretic
IV: HIGH K, dm dec aldo dec renin, normal AG met acidosis
-I, II, IV all have normal AG met acidosis bc all have inc Cl
- 2 normal AG met acidosis = RTA and diarrhea; dsitinguish these bc with H out of kidney forms NH4Cl so Cl level measure it in the urine for AG; Diarrhea met acid intact to excrete acid so Cl incin urine and urine AGneg; RTA kid cant excrete h and Cl so AG positive ;
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Anion gap
(Na- k) - (hco3-Cl)
| Normal is 8-14
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Acidosis
$metabolic
- low anion gap: myeloma, low albumin level, lithium
- albumin are negative charge ; for every 1pt dec albumin there's 2pt dec in AG bc the cations inc
- myeloma dec AG bc it's cations so anions inc to compensate
$respiratory
- hypo ventilation of any cause: copd, pickwickian, obesity, suffocation, opiates, sleep apneakyphoscoliosis, myopathies etc
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Increased anions gap
Methanol, Uremia, DK(beta hydroxybutyrate and acetobacter te is alternate fuel source from fatty acids, bc glucose can't be absorbed bc dec insulin), Paraldehyde, Propylene glycol, Isopropyl alcohol, INH, Lactate(sepsis ischemia), Ethylene glycol
85
nephrolithiasis
- 70% oxalate, 10% ca phosphate, struvite (Mg/aluminum/phosphate from infxns like Klebsiella and proteus, uric acid are radiolUcent, cysteine, indinavir from proteus and HIV med
- inc calcium = stones
- dec oxalate= stones bc no oxalate to bind Ca
- hypercalciuria: MCC hyperparathyroid, inc vit D with sarcoid and other granulomatious dis, familial
- idiopathic renal hypercalciuria, resorptive from hyperpara and mult myeloma, met dis to bone, hyperCa of malignancy
- hyperoxaluria: with fat malabs, fat binds to calcoium so oxalate reabs in greater amounts
- hypocitrate: citrate binds calcium and prevents ca reabs but low citrate leads to inc in calcium absorption, hypocitrate from any acidotic state
- MVA male needs blood fast, citrate bound up Ca and caused a seizure
- Urate: formes in acidic and with gout, heme malig, crohns
- infxn: forms highly alkaline environment and makes struvite stones
- Dx: xray, US, strain urine, check serum and urine ca, IV pyelogram always wrong, helical spiral CT no contrast needed for stones (contrast used for masses, absecesses and tumors)
- office stable pt: sono
- ED: xray first choice, spiral CT best test
- TX: analgesia, hydration; shockwave lithotripsy for stones <2cm; uteroscopy, percut removal
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hereditary cystic disease: adult polycystic kidney dis
- death not from aneurysm but ESRD; stones infxns--> dialysis
-presents: flank, hematuria, infxns, calcukli
-extrarenal manif: hepatic cysts, colonic diverticula, htn, instracranial aneurysm, MVP
-mc site of cysts beside kidney is liver
-should we screen for aneurysms? no
-DX: us and CT scan
Tx: nonspecific
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simple cysts
- smooth wall, no debris in center: expectant management; very common 60-70% of all renal masses
- irr walls or debris: aspiration to exclude cancer
- dialysis causes cysts
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htn guidelines medical tx
-normal 120/80: wt loss; 1kg = 1mmHg systolic
-pre htn: sys 120-139, dias 80-89
-htn stage 1 140-159/90-99
>160/>100 = two meds needed
-meds: albetalol, nitroprussidm, IV enalapril
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DASH
-inc fruits, vegs, low fat dairy, low fat diet
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pt with severe htn diast >100
-start on meds; >160/>100 start 2 meds
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HTN drug of choice
1. diurtetic = mortality benefit
2. if diuretic fail: ass 2nd drug
- BB good for MI, avoid in dep, asthma, copd, heart block
- ccb good with migraine
- ace/ard good with dm
- dec left vent sys fxn: bb/ace
- preg: alpha methyl dopa, labetalol, hydralazine, ccb; NO ACE/ARB; DIURETICS CONTRAIND FOR LOW BIRTH WT BC SHUNTS BLOOD AWAY FROM PLACENTA
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hypertensive emergenc
- sym of end organ damage with dias .120-130
- malignant: encephalopathy or nephropathy with accompanying papilledema as seen on fundoscope
- resistant htn: failure to reach bp control with those on full doses of 3 drug regimen
- TX: nitroprusside and labetalol is 2 best; nitroglycerin preferred in those with MI
- dont dec bp by no more than 25% within the first 1-2hrs
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secondary htn
- with identifiable cause
-RAS mcc; conns (dec K muscle weakness), cushings, pheoChromocy toma, coarct (UE >LE bp), close of rena art (bruits), contraceptives, cong adrenal hyperplasia (hairy)
screen who?: htn young or very old, labs, remain htn depsite therapy
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RAS
-atherosclerotic in old, fibromusclurar dysplasia in yound women
DX; abd US, captopril renogram positive test is when theres dec uptake ex dec gfr, arteriogram is still best method to confirm,
-tx: percut transluminal angioplasty, surgical resection, aci if everything fails
-1. is US, captopril nuclear display which is inacc with renal insuf or duplex us which is least acc in obese pt, or MRA which is most acc
-angiography and arterioscopy is most accurate
-best initial tx: renal art angioplasty adn stent; fails? stent replacement, fails? sx,, fails sx again? acei
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conns
- primary hyperaldopsterone, mc unilateral adenomas
- HTN assoc with hypoK found on routine screening; symptoms of hypoK muscular weakness, polyuria, or polydipsia from neph DI
- DX: elevated aldo in urine and blood
tx: sx resection in those with an adenoma, potassium sparing diuretics in those with hyperplasia
- primary hyperaldosterone: aldosterone inc but renin normal
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pheochromocytoma
-benign tumor of adrenal gland
-presentation: episodic HTN
DX: urine VMA, metapnephrines and free urinary catecholamines. Plasma catecholamine is helpful. CT/MRI used to localize tumor
tx: alpha blocker followed by removal
-epinephrine --> metanephrine --> VMA
-CT neg --> MIBG scan (detects occult pheo when ct is negative; picked up thru enterochromaffin tissue and excreted through there)
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Cushings
- ACTH hypersecretion by a pituitary adenoma
-presentation: htn, truncal obesity, buffalo hump, menstrual abn, striae, impaired healing from pit releasing acth --> inc cortisol --> inc vasc reactivity to NE and epi
DX: dexamethasone suppression test and e24 hour urine cortisol are best initial tests; not CT first bc alot of ppl have deformities on pit but the prob is in the adrenal actually
tx: sx resection best when possible
- in endo, should start with hormone test whenever possible
-cushings ecchymosis (impaired formation of collagen in skin)
-screening: 11pm 1mg dexamethasone suppression test; if neg excludes the dis, if pos then have disease but dk etiology
-etiology: high acth levels (pit prob), low acth levels (adrenal or ectopic production)
-striae and impaired healing: bc glucocorticoids inh protein prodxn bc changes them to glucose so theres dec proteins
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antihypertensive medications diuretics
- CHF (ace and bb first), edema, African american; contraind in dm, gout, hyperlipid
- thiazides: hctz, chlorthalidone, metalozaone, indapamide
loops: furosemide, bumetanide, torsemide
- pottasium sparing: spirinolactone, amiloride, triamterene
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bb
- mc used metoprolol and atenolol
- MI, supravent arrhythmia, migraines glaucoma anxiety(resting tachy), CHF from diastolic failure
- se: heart block, bradycardia, raynauds, dep, impotence, fatigue, dec hdl, hyperglycemia
- contraind: asthma, copd, av condxn defect, chf from systolic failure, dm masking hypoglycemia
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acei
- dm bp goal 130/80; chf as afterload reduction, postMI with left ventricular impairment
- s.e: cough, edema, neutropenia, hyperK, taste disturbance, anaphylactoid rxns
- contraind: pregnancy, bl RAS
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CCB
- angina pectoris, supravent arrhythmia, migraine, raynauds, esophageal spasm
- s.e.: edema, constipation, heart block, refelx tachy
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arbs
- intolerant to ace
| - contraind in preg
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methyldopa
-s.e.: gives hepatits and coombs positive hemolytic anemia
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direct vasodilators
- hydralazine (lupus), minoxidil (hirsutism, fluid retention, pericardial effusion)
105
alpha blockers
- terazosin, doxasin, prazosin
- use: pts with lipid disorders (dec LDL, inc HDL), BPH
- s.e.: syncope after first dose, dizziness, headache
