Nephrology Flashcards
Pre Renal causes of Acute Kidney Injury (AKI)
MI, CHF
nephrosis, cirrhosis, gastrosis - all lower albumin
diuresis, dehydration, diarrhea, and da hemorrhage
fibromuscular dysplasia, renal artery stenosis
presentation of fibromuscular dysplasia in AKI
young women with secondary HT and renal failure
Post Renal causes of AKI
obstruction levels
- ureters - cancer and stones
- bladder - cancer, stones, neurogenic bladder
- urethra - cancer, stones, BPH, kinked foley, etc
Intra renal causes of AKI
glomerulonephritis
Acute interstitial nephritis (AIN)
Acute tubular necrosis (ATN)
glomerulonephritis and AKI
intrarenal cause
RBC casts - r/o nephrotic syndrome (>3.5 g protein per day and increased cholesterol and edema)
AIN and AKI
WBC casts, WBCs eosinophils
caused by infections and rxn to meds
- TMP-SMP, PCNs and cephalosporins
ATN and AKI
muddy brown casts
ischemia or exposure to toxins
IV contrast or myoglobin
–> tx = vigorous IVF
ATN phases
prodrome - increased Cr
oliguric - decreased urine output
polyuric - increased urine output
AKI workup
increased Cr –> r/o pre renal –> check:
- BUN/Cr –> if >20 = prerenal
- Una —> if <10 = prerenal
- Fena —> if <1% = prerenal
- Feurea —> if < 35% = prerenal
if Pre Renal –> volume down –> IVF
–> volume u –> diuretics
AKI workup if not pre renal
r/o post renal –> US or CT –> hydroureter or hydronephrosis –> if post renal –> tx = foley/ nephrostomy/sx—- > if NOT post renal –> intra renal
AKI workup if not post renal
Intrarenal –> Hx and PE –> UA –> Dx
- may have to do a biopsy to –> Dx
Acute indications for hemodialysis
A - acidosis E - electrolytes - Ca and K+ I - intoxications O - overload U - uremia
CKD stages
I - GFR >90
II - GFR 60-89
III - GFR 30-59 - complication management
IV - GFR 15-29 - prepare for dialysis - put in AV fistula if HD is next step
V - GFR <15 - ESRD - perform dialysis
types of dialysis
HD - 3/wk - 4hrs in length
Peritoneal dialysis - every night - 6-8hrs in length
preventing progression of CKD
HTN - goal <130/<80 - ACE-I or ARB
DM - goal A1c <7 - blood glucose 80-120 - oral meds (not metformin or insulin)
Proteinuria - ACE-I or ARB + low protein diet
complications of CDK
Anemia secondary hyperparthyroidism mineral bone disease volume overload metabolic acidosis
anemia of CKD
kidneys make EPO - decreased EPO - decreased Hgb
pt asymptomatic Hgb <12
dx - of exclusion
tx - iron supp, EPO, transfusions - goal Hgb >10
secondary hyperparathyroidism of CKD leading to mineral bone dz path
increased PO4 + decreased Ca –> increased PTH –> increased bone reabsorption –> mineral bone disease
presentation and dx of secondary hyperparathyroidism in CKD
asymptomatic, if Ca x PO4 >55 -> risk for caclphylaxis (ulcerations of skin)
dx - BMP - Ca and PO4
tx of secondary hyperparathyrodism in CKD
phosphate binders - sevelarer - decreased PO4 —> decreased PTH
calcimimetics = cinacalecet
Ca and Vit D
Volume overload in CKD
Metabolic acidosis in CKD
tx - loop diuretics and add thiazides if needed
met acid - bicarb - 10-20 –> tx - oral bicarb
tx of hyponatremia
mild - dz specific
moderate - IVF
severe - 3% NaCl
tx of hypernatremia
mild - PO H2O
moderate - IVF
Severe - D5W (half of nml saline)
signs and symptoms of various Na levels
mild - asymptomatic
moderate - N/V, confusion, HA
severe - coma, seizure
workup of hyponatremia
serum osm –> nml = isotonic/pseudohyponatremia (lab problem fats and protein
serum osm –> high –> hypertonic hyponatremia –> every 100 BG above 100 needs Na corrected by 1.6
serum osm –> low –> hypontonic hyponatremia –> Hx and PE
serum osm formula
2xNa + (glucose/ 18) + (BUN/2.8) = nml 280
if blood glucose = 500 and Na = 140 the corrected sodium =
500 = 4 x 100 –> 4 x 1.6 = 6.5
140 + 6.5 = 146.6
hypotonic hyponatremia
volume up – diuresis
volume down - IVF
evolemic - RATS
evolumic causes
R - rental tubular acidosis - UA
A - addisons dz - cortisol
T - thyroid dz - TSH
S - SIADH - dx of exclusion –> volume restriction, gentle diuresis, and if all else fails demeclocycline
UNa = surrogate for
Uosm = surrogate for
UNa - surrogate for aldosterone
Uosm - surrogate for ADH
limitations to dropping sodium to not cause osmotic demylinating syndrome
0.25 per hr
4-6 per day to reduce symptoms
except in severe correct until seizures stop
PTH affects on bone
reabsorption of bone by osteoclasts
increased Ca
increased P
PTH affects on kidney
1,25 Vit D turned on
reabsorption of Ca = increased Ca
excretion of P = decreased P
PTH affects on gut
absorption of both Ca and P
increased Ca
increased P
artifical vit D - from granulomas (TB or sarcoid) can affect gut
most Ca is bound to albumin except 1% free ionized so corrected albumin formula
nml albumin = 4
nml Ca = 10
change in 1 for albumin = 0.8 change in Ca
albumin =3 then Ca = 9.2
signs of hypocalcemia
tetany
perioral tingling
trousseaus sign - bp cuff carpal pedal spasm
chvosteks sign - cheek tap facial N
workup of hypocalcemia
check albumin - if corrected - no problem
if still low –> ionized Ca –> if low –> tx = IV Ca - gluconate or carbonate
hypercalcemia workup
recheck Ca –> if still high –> hyper Ca –> tx if symptomatic
hypercalcemia signs
bones, moans, groans, stones, and psychiatric overtones
bone pain
kidney stone
abd pain
AMS
tx of hypercalcemia
IVF IVF IVF IVF then bisphosphinates unless super super high Calcitonin
types of hyperparathyroidism
primary - autonomous - single adenoma
secondary - early CKD
tertiary - multiple adenomas
pt presentation in hyperparathyroidism and dx
pathologic fxs, decreased bone density, brown tumors - eat away the bone
increased PTH –> increased Ca + decreased PO4
dx differentiation of primary secondary and tertiary hyperparathyroidism and tx
sestamibiscan
- primary - single adenoma with other glands atrophied
- tertiary - multiple large adenomas
tx - resect and watch out for low Ca after sx due to other glands left behind being atrophied
HyperCa in cancer path
mets –> invades bone –> release Ca and PO4 –> increased Ca and increased PO4decreased PTH
PTHrP –> scc lung cancer –> “PTH” kidney wins –> increased Ca decreased PO4 but –> decreased PTH
when is a vit D test needed
hypervitaminosis D
- causes - vti D3 po heavy diet but more common = granolomatous dz –> increased Ca + increased PO4 –> decreased PTH
check 1,25 vit D level
hypercalcemia due to immobilization
increased Ca –> decreased PTH –> increased PO4
familial hypercalcemic hypocalcuria
asymptomatic - increased Ca –> urine Ca decreased
hypoparathyroidism
iatrogenic - thyroid sx botch or parathyroid resection and only atrophied glands left over
autoimmune
pt presentation in hypoparathyroidism
tetany
perioral tingling
post op day 1
dx of hypoparathyroidism and Tx
decreased PTH –> decreased Ca
tx - IV Ca
pseudohypoparathyroidism
end organ resistance to PTH (insensitivity)
increased PTH –> increased Ca and decreased PO4
vit D def
lack of dairy and/or sunshine - all day inside no dairy diet
osteopenia, dexa scan -2.0
25-vit D level
tx - Ca and high dose vit d –> if severely osteopenic –> bisphosphonates
CKD and hypoCa
early on impairment of vit D formation –> secondary hypoparathyroidism –> tx Ca + vit d + cinacalet
late stage –> hyper PO4
pancreatitis and HypoCa
sequestration
ominous sign
causes of HyperK
low aldosterone state ingestion + CKD Iatrogenic ESRD Artifact Hemolysis
low aldosterone state causes of Hyper K
ACE-I
ARBs
Aldosterone antagonist
workup of hyperkalemia
recheck –> if still high –> EKG –> unstable –> emergent
–> stable –> urgent tx
EKG signs of hyperkalemia
peaked T waves
wide QRS
emergent tx of hyperkalemia
stabilize - CaCl (min) stabilzied cardiac myocytes
temporize - shift K into cells - insulin + D50 or sodium bicarb or beta agonist
decreased total body K+ - loop diuretics, kayexalate (stool) or hemodialysis
Causes of hypokalemia
renal losses - hypoaldosterone, diuretics (thiazides, loops), genetics (barters, gittlemens)
GI losses - Vomiting, Diarrhea
workup of hypokalemia
recheck K –> EKG –> replete
repletion to tx hypokalemia
oral > IV
peripheral line <10mEq/hr - since it burns
central line <20mEq/hr - induces hyperkalemic symptoms on EKG
if all else fails Mg
10mEq leads to what change in serum K+
0.1 change to K+
presentation of kidney stone pt
colicky abd pain that radiates into the groin
+/- hematuria
N/V
extreme pain
workup of kidney stone
U/A –> microscopic blood –> non con CT –> radiopaque stone or hydronephrosis –> tx
tx of kidney stone
<5mm - IVF, pain meds
<7mm - IVF, pain meds, medical explosive therapy - CCB and alpha blockers
>1.5cm - sx - proximal laparoscopic - distal PAN
>3cm - sx
strain urine and repeat in 6wks
tx of septic stone and an inbetween stone
inbetween stone
- proximal - lithotripsy
- distal - uretoscopy
septic
- nephrostomy tube (proximal)
- stenting (distal)
calcium oxalate stones
radio opaque
risk factors - increased Ca urine, increased Oxalate urine
modify - thiazide, decreased oxalate - decreased red meats - increased citrate - fruits/veggies
struvite stone
magenesium ammonium phosphorus
radioopaque
proteus - urease splitting
staghorn
tx - abx, remove stone burden
uric acid stone
radiolucent
gout or tumor lysis
- gout - allopurinol
- TLS - rasburicase
cysteine stone
radiolucent
genetic
simple cysts in kidney
asymptomatic - found incidentally
small, no loculations, no septations
do nothing
complex cysts in kidney
large, septations, loculations, different echogenecities - heterogenous
flank mass - infection -> pyelo
flank pain - rupture -> hematuria
dx and tx of complex kidney cyst
dx - CT scan unless pregnant US
tx - dz specific
renal cell carcinoma (RCC)
flank pain, flank mass, hematuria
dx - CT scan - DONT biopsy –> hematoma
tx - nephrectomy
paraneoplatic syndromes of RCC
anemia
polycythemia vera
spread hematogenously –> DVT
AR PCKD
newborns
anuric, renal failure day 1
palpable flank masses bilaterally
dx - US - biopsy (radially oriented cysts)
tx - supportive
AD PCKD
adults
asymptomatic –> HTN –> ESRD
palpated cysts –> flank pain
infected -> pyelo
replaces the kidneys normal parenchyma
dx and tx of AD PCKD
dx - CT and then biopsy
tx - supportive –> transplant
complications of AD PCKD
cysts in liver and pancreas (hepatitis and pancreatitis)
berrys aneursyms (SAH) –> screens with MRI angiogram, CT angiogram, angiogram
causes of resp acidosis
opiod overdose
asthma, COPD - air trapping
muscular strength - vent long term, OSA
causes of resp alkalosis
hyperventilation
- pain anxiety
- hypoxemia
causes anion gap metabolic acidosis
M - methanol U - uremia D - DKA P - propanylglycol I - isoproyl glycol L - lactic acidosis E - ethylene glycol - crystals in urine S - salicyclates
causes of metabolic alkalosis
volume responsive - diuretics, dehydration, emesis, NG suction
non volume responsive - HTN -> + -> hyperaldo -> renal artery stenosis
(if not HTN - barters or gittlemens)
causes of non anion gap metabolic acidosis
neg urine anion gap - diarrhea
+ urine anion gap - renal tubular acidosis
ABG workup for pH < 7.4
acidemia
- -> CO2 >40 - resp acidosis
- -> CO2 <40 - metabolic acidosis -> check anion gap (Na-Cl-CO2)
——-> if non anion gap –> check urine anion gap (Na + K + Cl)
ABG workup for pH >7.4
if CO2 < 40 –> resp alkalsosi
if CO2 >40 –> met alka –> check urine Cl -
—–> if Cl <10 –> volume responsive
—–> if Cl nml –> check HTN
In resp acidosis a change of 10 in CO2 leads to what change in bicarb
acute - change in bicarb 1
chronic - change in bicarb 3
in resp alkalosis a change of 10 in CO2 leads to what change in bicarb
acute - change in bicarb 2
chronic - change in bicarb 4
normal anion gap = 12 = what in albumin
albumin x 3
winters formula and interpretation
1.5 x bicarb + 8 +/- 2
CO2 Calculated > expected = resp acidosis
CO2 Calculated < expected = resp alkalosis
bicarb add on formula and interpretation
anion gap - 12(nml gap) + bicarb lab value
calculated bicarb >24 = metabolic alkalosis
calculated bicarb <24 = metabolic acidosis
focal segmental glomerulosclerosis
blacks and hispanics
HIV and heroin use
nephrotic range proteinuria
rapid development of renal failure
central DI
decreased ADH production
causes - trauma, hemorrhage, infection and tumors
water deprivation test –> desmopressin given –> nml results large increase
nephrogenic DI
ADH resistance at the kidney level
causes - lithium, cidofovir, amphotercin, tubulointerstital dz
water deprivation test –> desmopressin given –> no change
lithium Nephrogenic DI tx
salt restriction and stop lithium
indications for urgent dialysis
A - acidosis - pH < 7.1 - refractory to medical therapy
E - electrolyte imbalance - refractory to medical tx
I - ingestion - toxic alcohol, salicylcalte, lithium
O - overload - volume refractory to diuresis
U - uremia - symptomatic
tx of asterexis without liver cirrhosis
dialysis
winters formula = expected
- if PCO2 higher =
if PCO2 lower =
if PCO2 > expected = resp acidosis
if PCO2< expected = resp alkalosis
causes of metabolic alkalosis that is saline responsive
vomiting gastric suctioning diuretics laxatives volume depletion
causes of metabolic alkalosis that is saline resistant
primary hyperaldosteronism
cushings syndrome
severe hypokalemia <2
SLE glomeruloneprhitis
renal failure with erythrocyte cats
proteinuria
significantly low serum C3
HTN
heavy vomiting leads to what electrolyte abnormalities
decreased Cl and K
hypochloremic metabolic alkalosis with hypokalemia
complications of nephrotic syndrome
hypercoagulable state –> venous or arterial thrombus - renal Vein thrombosis (MC) –> membranous glomerulopathy
HTN
protein malnutrition, vit D def
iron resistant microcytic anemia
management of uric acid stones
highly soluble in alkaline urine - potassium citrate can help
MCC of death in dialysis patients and renal transplant pts
cardiovascular dz
causes of AKI
acyclovir - cryalluria – obstruction
sulfonamides
MTX
ethylene glycol
protease inhibitors
Tumor lysis syndrome
acute interstitial nephritis
rash
eosinophilia, eosinohpiluria
WBC casts
Aspirin overdose metabolic state
mixed respiratory alkalosis
and
metabolic acidosis
refractory hypokalemia can be caused by
hypomagenisum due to the removal of the inhibition of renal potassium secretion
causes of pre renal AKI
decreased renal perfusion
- volume depletion, HF, cirrhosis, sepsis, pancreatitis
RAS
NSAIDs
causes of primary adrenal insufficiency (addisons dz)
TB histoplasmosis coccidomycosis cryptoccocic sarcoidisis
presentation of primary adrenal insufficiency
increased K - due to decreased aldosterone secretion
decreased cortisol
decreased adrenal sex hormones
- kidney losing Na while retaining K and H –> non anion gap metabolic acidosis
acute organ rejection tx
IV steroids
simple renal cysts
thin
smooth
unilocular
no septae
benign
malignant renal cysts
multilocular mass
irregular walls
thickened septae
causes of resp alkalosis
hyperventilation
high altitude
salicylate intoxication
ADR of loop diuretics
decreased K
metabolic alkalosis - loss of H ions
pre renal kidney injury
management of uncomplicated cystitis
nitrofuranotin 5 days (doesnt require culture)
TMP SMP 3 days
Fosfomycin single dose
management of complicated cystitis
fluoroquinolones (5-14 days)
management of pyelonephritis
cipro or IV Cipro
pathological hallmark of diabetic nephropathy
nodular glomerulosclerosis
memnranoproliferative glomerulonephritis
dense intramembranous deposits that stain C3 - caused by persistent activation of the complement pathway
AL amyloidosis
causes - MM, waldenstrom macroglobulinemia light chains (usually lambda)
AA amyloidosis
chronic inflammatory conditions - RA, TB
beta 2 microglobulin apoliporpotein or transthyeritn
crescent formation glomerulonephritis is indicative of
Rapidly progressing GN
diabetic nephropathy leads to hyalinosis that affects
both the afferent and efferent arteiroles
linear deposits on immuofluourescne are typical for
antiglomerular basement membrane dz = goodpasture syndrome
granular deposits are present in
immune complex GN - lupus, IgA nephropathy
older woman with RA hx with glomuerula deposits seen on special staining =
amylodosis
causes of papillary necrosis
NSAIDS N - NSAIDS S- sickle cell A- analgesic abuse I- infection (pyelo) D- DM
adverse rxns of thiazides
hyperglycemia
increased LDL and TGL
decreased K, Mg, Na
increased Ca - decreased Ca excretion in urine
best dietary advice to reduce risk of recurrent calcium oxalate stones
decreased Na diet - leads to decreased Ca excretion
nml Ca diet
lots of fluids
abnormal hemostasis in chronic renal failure
platelet dysfunction - increased bleeding time
nml PT, PTT, INR
nml platelets
DOC - DDavp
causes of non anion gap metabolic acidosis
diarrhea
fistulas
carbonic anyhydrase inhibitors
renal tubular acidosis
ureteral diversion
renal tubulular acidosis (type 4)
non anion gap metabolic acidosis
hyperkalmeia
out of proportion to the renal function
leading cause of ESRD
diabetic nephropathy
increased extracellular matrix
BM thickening
mesangial explosion and fibrosis
intimal thickening and luminal narrowing of renal arterioles with evidence of sclerosis is indicative of what cause
HTN
metabolic alkalosis with decreased urine Cl
vomiting
Nasogastric aspiration
prior diuretic use
metabolic alkalosis with increased urine Cl
hypo/euvolemic = bartter, gittleman
hypervolemic - primary hyperadlosteronism, cushing dz, ectopic ACTH
membranous nephropathy
adenocarcinoma
NSAIDs
Hep B
SLE
membranoproliferative glomerulonephritis
Hep B
Hep C
Lipodystrophy
minimal change disease
NSAIDs
Lymphoma (hodgkins)
IgA nephropathy
preceding URI by approx 5 days
MCC of GN in adults
pts have recurrent episodes of hematuria
Amikacin - adr
nephrotoxic
subepithelial humps consisting of C3 and decreased serum C3
PSGN
alport
x linked defect in type 4 collagen formation
hearing loss, ocular abnormalities, hematuria
progressive renal insufficiency
horseshoe kidney complications
ureteropelvic junction obstruction
renal stones
VUR
chronic UTIs
dipstick in pyelo will show
+ nitrites
+ leukocyte esterase
muddy brown casts =
ATN
RBC casts =
glomerulonephritis
WBC casts
interstitial nephritis
or
pyelonephritis
fatty casts =
nephrotic syndrome
broad and waxy casts =
chronic renal failure
most sensitive screening test for nephropathy
random urine for microalbumin/ creatinine ratio
obstructive uropathy presentation
flank pain
low volume voids with or without occasional high volume voids
`
hepatorenal syndrome risk factors and precipitating factors
risk factor - cirrhosis
precipitating factors - reduced renal perfusion, GI bleed, vomiting, sepsis, excessive diuretics, reduced GFR - NSAID use
hepatorenal syndrome dx and tx
dx- renal hypoperfusion labs
tx - splachnic vasoconstrictors can help (octreotide, midoadrine, NE), liver transplant
management of iatrogenic hyponatremia and acute hyponatremic encephalopathy
hypertonic (3%) saline
acetazolamide
diuretic that inhibits proximal renal bicarbonate resorption
used in pts with hypervolemia and metabolic alkalosis
medications that can cause hyperkalemia
Non selective beta adrenergic blockers
ACE-I, ARBS
K sparing diuretics (amilioride)
digoxin
NSAIDs
Trimethoprim
drugs that cause interstitial nephritis
PCNs
cephalosporins
sulfonamides
NSAIDs
rifampin
phenytoin
allopruinol
cryoglobulinemia
palpable purpura
glomerulonephritis
arthralgias, hepatosplenomegaly, peripheral neuropathy
hep C hx
acute therapy indications for hyperkalemia
only if K >7.0 or abnormal ECG
hypovolemic hypernatremia tx
0.9% saline until euvolemic –> 5% dextrose in water
characteristic findings in SIADH
serum osmolality <275
urine osmolality >100
euvolemic pt
decreased Na
N/V AMS
rapid correction of hyponatremia can lead to
osmotic demyelination syndrome
mannitol use
treating ICP and higher intraocular pressure
sodium bicarb uses
severe metabolic acidosis and hyperkalmia
RCC can cause
varicocele
workup includes - CT abd
SSRIs have what kidney side affect
SIADH
when rapidly correcting hypernatremia complication =
cerebral edema
Lab findings of PSGN
decreased C3
increased Creatinine
increased Anti DNase
increased ASO
largest risk factor for CKD =
diabetic microangiopathy
initial therapy for Renal artery stenosis (RAS)
ACE-I or ARB
Stenting only if flash pulmonary edema or HF is present
when should metformin never be given
acutely ill pts with acute RF, liver failure or sepsis
since it can increase the risk of lactic acidosis
most common findings of AKI
weight gain and edema - due to positive water and sodium balance
MCC of AKI = pre renal failure
NSAIDs affect on arterioles
constricts AFFERENT arteriole
ACE-I affect on arterioles
EFFERENT arteriole vasodilation
pathophys of pre renal failure
decreased RBF -> decreased GFR -> decreased clearance of metabolite (BUN, Cr, Uremic toxins) -> increased Cr and increased BUN
rhabdo pathophys
skeletal muscle breakdown -> release of muscle fiber contents (myoglobin) into blood stream -> nephrotoxic –> AKI
increased CPK increased K increased uric acid
decreased Ca
tests for post renal failure
palpate bladder
US - obstruction, hydronephrosis
Catheter - large volume of urine
course of ATN
oliguric phase - azotemia and uremia (10-14days)
diuretic phase - urine output >500 - due to fluid overload
recovery phase - recovery of tubular function
urine osmolality
dehydration -> increased reabsorption -> make concentrated urine
ATN and urine osmolality - patho phys
tubular cells are damaged and cannot reabsorb water (or sodium) -> so urine cannot be concentrated –> low urine osmolality
radiographic contrast affects on kidney
can cause ATN - very rapidly by causing spasm of the AFFERENT arteriole
small kidneys
UA with broad casts
Hx of HTN
edema
CKD
urine output <500
without uremic symptoms
AKI
azotemia =
increased BUN >60
mcc of secondary HTN
renal failure
tx of hyperphosphatemia
calcium citrate
complications of CKD
hyperkalemia
pulmonary edema secondary to volume overload
infections
dialyzable substances
lithium
salicyclic acid
ethylene glycol
magnesium containing laxatives
pathophys behind hypoalbuminemia seen in nephrotic syndrome
hepatic albumin synthesis cannot keep up with renal losses
key features of nephrotic syndrome
proteinuria
hypoalbuminemia
hyperlipidemia
type I RTA
inability to secrete H+ –> non anion gap metabolic acidosis
renal stones
type IV RTA
hyperkalemia
acidic urine
hartnup syndrome
AR - def of AA transproter - decreased absorption of tryptophan
pellagra, dermaitits, diarrhea, ataxia and psych disturbances
causes of renal artery stenosis
atherosclerosis - elderly man
fibromuscular dysplasia - young female
look for bruit on exam
2nd MCC of ESRD
nephrosclerosis
causes of hyperoxaluria
severe steatorrhea of any cause
small bowel dz - crohns
pyridoxine def
risk factors for prostate cancer
age
black
high fat diet
family hx
exposures to herbacide and pesticides
indications to perform a TRUS for prostate cancer
PSA >10
DRE abnormal
prostate mets to
the bone and if there are urinary obstruction issues on findings = late dz course
RCC
2x more common in men
sporadic
risks = smoking, phenacetin, ADPKD, chronic dialysis,eposure to heavy metals
bladder cancer
90% caused by transitional cell carcinoma
risks - smoking, industrial carcinogens, aniline dyes, azo dyes, long term cyclophosphamide
mc testicular tumor
seminous
choriocarcinoma testicular tumor facts
embryonal tumors facts
chorion = increased beta HCG
embry = increased AFP
epididmytitis
children and elderly = e coli
young men = gonorrhea or chlamydia
3 reasons for oliguria
low blood flow to kidney
kidney problems
post regnal obstruction - tx foley
why is glucose given along with saline
to prevent muscle breakdown
lactated ringer
excellent for replacement of intravascular volumes
MC used for trauma resuscitation fluid
DO NOT USE IF INCREASED K
do not combine blous fluids with dextrose due to
hyperglycemia cause or hyperkalemia
signs of volume overload
elevated jugular venous pressure
pulmonary rales - due to pulm edema
peripheral edema
calculating maintenance fluids
100 x first 10kg
50 x second 10kg
20 x remaining 10kg
divide this number by 24
aldosterone basic function
increased Na reabsorption
ADH basic function
increased H2O reabsorption
low urine sodiu < 10 implies
increased Na retention by kidneys to compensate for extra renal losses - such as diarrhea, vomiting, nasogastric suction
decreased Na –> decreased osmolality <280 –>
assess ECF
if low –> assess urine Na
low = extra renal losses - D/V high = renal loss excessive diuretics
excess exogenous glucocorticoids
hypervolemic hypernatremia
Diabetes insipidus and Na
isovolumic hypernatremia
tx of hypervolumic hypernatreia
give diuretics (furosemide) D5W to remove excess sodium
pH affects on metabolites
increased pH - increased Ca binding to albumin
increased pH - decreased K and vice versa
acute pancreatitis and renal insufficiency affects on Ca
decreases ca
renal - due to decreased production of 1,25 dihydroxyvitamin D
hypocalcemia symptoms
rickets and osteomalacia
tetany
hyperactive DTR
chvosteks signs/trousseaus sign
prolonged QT
ECG affect with hypercalcemia
shortened QT interval
multiple myeloma
increased Ca due to release of osteoclastic activating factors and lysis of bone tumor cells
random causes of increased Ca
thiazides
lithium
SCC
saroidosis
signs of hypercalcemia
stones bones groans moans and psych overtones
ECG changes with hypokalemia
t wave flattens out
if severe t wave inverts
u wave appears
causes of hypokalemia
gi losses - v/d/ nasogastric suction
renal losses - diuretics, RTA not type IV, excessive glucocorticoids, mg def
bactrim and amphoterecin B
B2 agonists
K and digoxin
hypokalemia predisposes pts to doxin toxicity
IV KCL can be given if K
K <2.5
causes of hyperkalemia
renal failure K+ sparing diuretics ACE - I insuline def addisons dz
prolonged use of a tourniquet with or without repeatedly clenching fist
ECG changes in hyperkalemia
peaked t waves
prolonged PR interval
widened of QRS with T wave
hyperkalemia workup
check gfr -> if nml -> check aldosterone level ->
if low –> hypoaldosteronism
nml to high –> K+ sparing diuretics
kay exalate
GI potassium exchange resin - leads to decreased K absorption in the gut
hypomagenisum leads to
difficulty treating hypokalemia and hypocalcemia
causes of hypomagensium
GI - malabsorptive, steatorrhea states (MCC)
acoholism
SIADH
drugs - gentamicin, amphotercecin B cisplatin
ECG changes in decreased Mg
torsades de pointes
cause of increased Mg
renal failure (MCC) rhabdo
MCC of severe hypophosphatemia
DKA and alcohol abuse
effects of acidosis
right shift –> increased O2 delivery to tissues
depresses CNS
decreased pulm blood flow
arrhythmias
impairs myocardial function
hyperkalemia
effects of alkalosis
decreased cerebral blood flow
left shift - decreased O2 delivery to tissues
arrythmias
tetany seizures
salicylate (aspirin)
primary resp alkalosis
primary metabolic acidosis
metabolic alkalosis with volume contraction
due to fluid loss - vomiting or diuretics
metabolic alkalosis with volume expansion
usually due to pathology of adrenal gland
increased PaCO2 –>
increased cerebral blood flow –> increased CSF pressure –> CNS depression
and vice versa
