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UROLOGY / NEPHROLOGY - UROLITHIASIS = Pathoma (UROLOGY / NEPHROLOGY -…
UROLOGY / NEPHROLOGY - UROLITHIASIS = Pathoma
UROLOGY / NEPHROLOGY - *UROLITHIASIS = kidney stones
*PAthoma Notes
classic LOIN to GROIN colicky intermittent pain
unilateral is key also
*Types of Calcium Stones
calcium salts are most common
--> calcium oxelate
--> calcium phosphate
*Types of Calcium Stones
calcium salts are most common
--> calcium oxelate
--> calcium phosphate
note you can get kidney stones in CHRON's since OXELATE is mainly found in the GUT and binds to fats and is excreted
--> in Chrons you get poor fat absorption
--> thus oxelate doesn't bind to fats and is brought throuhg the systemic circulation to the kidney and forms
KIDNEY CHRONES STONES
*ammonium Mg+ Phosphate stones
usually caused by urease positive bacteria
--> proteus MAXIMUS
--> Klebsiella
STAGHEAD STONES
--> recall PROTEUS MAXIMUS tortured by UREASE pencil
--> his KIDNEY fire lights the STAGHEAD KIDNEY STONE STOVE
*Uric acid kidney stones
note these are not visible on XRAY
seen with GOUT and hyper uricemia
tx = hydrate with water + alkalinization of the urine
*Cysteine kidney stones
these are rare and happen in kids
they are important since gives Dx of cysteinuria
--> need to fix the metabolism first
note that cuysteine kidney stones are the KDI version of ammonium Mg+ phos in adults
--> they both have the same tx
--> both can have staghorn kidney stones
*Cysteinuria in Kids
note the COLA amino acids all use the same ransporter int he GI and in the kidney for reabsorption
C = cysteine
O = ornithine
L = lysine
A = arginine
Cysteine is the only one that is important
--> Cysteinuria = kidney stones
*End stage kidney disease
based on GFR?
3 most common causes of end stage renal disease
--> diabetes
--> HTN
--> glomerular disease
characteristics of CKD
uremia
--> recall that uremia is a part of MUD PILES
--> increased anion gap metabolic acidosis
anemia
--> note that EPO is produced in the kidney
--> EPO is produced the renal PEROTUBULAR INTERSTITIAL CELLS
--> are these the same as the juxtaglomerular cells?
HYPO CALCEMIA
URemia
note that uric acid STOPS both platelet adhesion and platelet activation
recall that uremia is a part of MUD PILES
--> increased anion gap metabolic acidosis
HYpocalcemia in renal failure
3 causes
osteodystrophy = kidney cannot excrete phosphate
--> get conitnuous PTH that tries to get rid of the Phos
--> bone releases Ca2+ continuously
osteomalacia
--> bone osteoid is layed down properly, but there isn't enough Ca++ to mineralize the bone
--> get bowing and weak bones
--> rickets in kids
osteoporosis
--> since CKD is metabolic acidosis constantly
--> your body compensates by taking excess H+ ions and storing them in your bones
--> this displaces the Ca++ ions
--> osteoporosis slowly over time
tx and outcomes of End stage kidney disease
dialysis or kidney transplant
note that by the time you reach end stage CKD you kidney are shrunk
--> you are at a higher risk of getting kidney cysts
--> cysts on a shrunken kidney is much worse that PCKD
--> HIGH risk for RCC in dialysis
*AKI PAthoma
azotemia = increase in nitrogenous things in the blood
--> BUN and Creatinine
divide AKI = azotemia into:
--> prerenal
--> intrarenal
--> postrenal
PRE renal = BUN : creatine ratio > 15
--> since there is less blood to the kidney
--> RAAS gets activated
--> aldosterone and ADH absorb water
--> high amounts of BUN comes with water in ADH
Intra renal = BUN : creatine ratio < 15
POST renal = BUN : creatine ratio VARIES
--> has increased ratio in early stage
--> decreased BUN /Cr ratio in late stage
PRE renal = BUN : creatine ratio > 15
RAAS activation in pre renal
--> since there is less blood to the kidney
--> RAAS gets activated
--> aldosterone and ADH absorb water
--> high amounts of BUN comes with water in ADH
RAAS is working so you get
low urine Na+
normal osmolarity > 500 ml
--> you can still concentrate urine
*POST renal AKI
BUN : creatine ratio VARIES
--> has increased ratio in early stage
--> decreased BUN /Cr ratio in late stage
Early stage POST RENAL AKI
has increased ratio in early stage
tubular function remains intact AT FIRST
--> normal osmolarity
--> normal Na+
LATE stage POST RENAL AKI
EVERYTHING fails in late stage of POST RENAL AKI
can't absorb BUN anymore
--> decreased BUN /Cr ratio in late stage
lose tubular function
--> low tubule osmolairty
--> high Na+ since can't absorb it
*INTRA renal AKI
intrarenal TUBULAR NECROSIS is the most common cause of AKI
--> you get necrotic cells that plug the tubules and decrease GFR
Intra renal = BUN : creatine ratio < 15
KEY finding in TUBULAR NECROSIS = brown necrotic epithelial cell casts
--> they get shaped from the tubule as it gets destroyed
2 main causes of INTRA RENAL
--> ATN = acute tubular necrosis
--> AIN = acute interstitial nephritis
*ATN = Acute TUBULAR NECROSIS
HISTOLOGY of acute intrarenal TUBULAR NECROSIS
note the red = necrotic tubule
--> loss of nuclei organized around the edges of the tubule lined against the basement membrane
the blue = nomal tubule with normal nuclei at edges
think of PRE and INTRA RENAL as the 2 extremes and POST renal as the mixed version of the two between early and late stage
PRE RENAL
--> EVERYTHING in the kidney is WORKING and RESPONDING
--> high BUN / Cr > 15
--> low Na+ since it is absorbing
--> normal > 500 osmolarity
INTRA RENAL
--> NOTHING in the kidney is WORKING and RESPONDING
4 more items...
*AIN= Acute Interstitial NEPHRITIS
DRUG hypersensitivity Rxn
--> NSAIDS
--> penicillin
--> diuretics
note that diuretics are the highest causes of both gout and AIN
this inflammation of the interstitium
--> it can spread over into the tubules
Histology of AIN
note the tubules are fine here but there are inflammatory cells in the surrounding interstitium
presentation of AIN
eosinophils are pathonognomic for AIN
--> makes sense since it is a hypersensitivity reaction
tx is to stop the drug
--> note this usually happens a few weeks after starting the drug and may give rashes
AIN can lead to renal papillary necrosis = RPN
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