renal Flashcards
what is the effect of dehydration on FF (filtration fraction)
decrease circulating BV (diarrhea and vomiting) –> dec renal plasma flow
which will result in the relase of renin –> inc angiotensin II –> efferent glomerular arterioles constriction to maintain the GFR
know that the dec in GFR in hypovolemia is less than the decrease in RPF
so the ratio (FF) GFR/RPF increases
Excretion = ?
Excretion = (filtration + secretion) - reabsorption
loss of HCO3- in the proximal tubules
diagnosis
type 2 RTA
same mechanism as suppressing the carbonic anhydrase enzyme
cant reabsorb bicarb –> acidosis
2 questions on boards
canagliflozin
moa
side effect
sodium glucose co-transport inhibitors (SGLT-2 inhibitors)
in the PCT. –> inc renal excretion of glucose
side effect: glucosuria –> UTI, genital mycotic infections
explain how ADH works
know its water soluble (binds to membrane receptors)
vs
aldosterone = lipid soluble (goes into cell)
it stimulates V2 receptors (through cAMP) in the late distal tubules and collecting ducts –> facilitates insertion of water channels (Aquaporin) in the renal collecting ducts –> inc free water reabsorption
know that ADH activates V1 receptors (by IP3 mechanism) –> vasoconstriction –> vascular resistance.
a pt with orthostatic hypotension due to blood loss.
what will happen
inc ADH
how is lithium nephrotoxic
inhibits the renal actions of vasopressin
(blocks aquaporin function!!!!) thus pt will develop diabetes insipidus
on the boards
pt with confusion, stupor, N/V, seizures or coma
pt has hyponatremia.
what paraneoplastic syndrome is causing this
SIADH
from small cell carcinoma
“pt has cerebral edema from retaining water. this is causing the symptoms”
hyponatremia
(confusion, stupor, N/V/ seizures or coma)
can be cause by?
SIADH
addisons disease
SSRI or diuretics
CHF, nephrotic syndrome, liver cirrhosis ( will have normal NA, however there is more h2o in body diluting it) thus can give loops.
on the boards
elderly pt with dementia and dehydration
(this isthe most common cause of ?)
hypernatremia.
excessive losses of water from the Urinary tract, seen in pts with uncontrolled diabets mellitus also.
on the boards
water losses associated with extreme sweating or severe watery diarrhea
can cause
hypernatremia
on the boards
pt with ST depression, flattened T waves and U waves on EKG palpitation and Muscle spasm and Weakness.
diagosis
hypo kalemia
what are the meds that cause HYPOKALEMIA
know this
ampohtericin B
cisplatin
loops
thiazide
pt has disseminated histoplasmosis
and is on amphotericin B
now he has arrythmia, what is the cause
hypokalemia and hypomagnesia from amphotericin.
what drugs can cause HYPERKALEMIA
ace inhibitors and ARBS
K sparing
Nsaids (ibuprofen)
cyclosporin and tacroimus
Pentamidine (used in HIV)
Q
HIV pt treated for SJS with pentamidine
what electrolyte innbalance do you expect?
hyperkalemia
on the boards
HYPERKALEMIA symptoms
on the boards
pt with malaise
palpitations
and muscle weakness
EKG = peaked T waves and Widening of the QRS complex
pt is depressed and hasnt gone to his hemodialysis sessions
now he has muscle weakness and palpations
and get an eKG whats the cause?
hyperkalemia
Cisplatin
Gentamicin
Amphotericin B
PPi induced
all these cause?
hypomagnesemia
hypomagnesemia may cause potassium wasting in the urine –>
hypokalemia
magnesium has what effect on PTH
stimulus secretion coupling of PTH
thus hypomag will dec PTH secretion –> hypocalcemia
what is the main factor in secondary HTN due to renal artery stenosis
renin
thus avoid ACE inhibitors
low na (sensed by macula densa) or low perfusion in the (afferent arterioles)
stimulate the release of renin from the JG cells.
renin will due what?
acitvate angiotensin –> aldosterone system –> vasoconstriction, Na, and water retention
pt with BUN =80, Cr = 2.
True volume depletion.
what kind of acute kidney injury?
pre renal azotemia
bc BUN: Cr ratio> 20
80/2 = >20
68 yo man with hx of CHF - no leg edema and his creatinine is 1.2
seen in a walk in clinic for back pain and started on ibuprofen
two days later he developed leg swelling, sob and his creatinine is 2.8.
what is the most likely cause of his symptoms
blocking progstaglandin effect on the afferent arterioles
(prerenal azotemia)
normally prostaglandins normally cause vasodilation of the aff arterioles of the glomeruli
AKI with inc creatinine is seen in prostaglandin dependent pt
e.g. CHF who started on NSAID
why will AKI pt on ace inhibitors have increase in creatinine and K
angiotensin II keeps the tone of the efferent arteriole.
ACE inhibitor will dilate the efferent decreasing glomerular pressure thus less creatinine is filtered out
tumor lysis syndrome
can cause POST renal AKI
how
metabolites of nucleic acid turnover –> increase during cell destruction –> inc URIC ACID –> renal and ureteric stones.
- uric acid precipitates in the ACIDIC medium in the DCT and collecting ducts.
prevention hydration and alkalinization of urine,
interstitial edema and infiltration with mononuclear cells (lymphoctes and macrophages)
and
eosinophils in urine
seen in interstitial nephritis
on boards
pt started on antibiotics (B-lactam) or allopurinol, or cimetidine
classic triad
fever
rash
eosinophilia and eosinophil in urine
what are the two important drugs (on boards) that cause
post renal azotemia
acyclovir
indinavir
what are the two important drugs (on boards) that cause
post renal azotemia
acyclovir
indinavir
hexagonal kidney stone
cystine
for the boards
the only stone that is radiolucent on xray
uric acid
(even though first aid say cystine stones)
referred pain to the groin and the scrotum may be seen in male pts with ureteric colic
renal calculi (kidney stone)
causes of metabolic alkalosis
vomiting and nasogastric suction –> HCL loss
- dec serum chloride –> dec urinary chloride
thiazides and loops diuretics –> renal Na loss (followed by Cl-)
- inc HCO3- reabsorption to maintain electric neutrality
- volume contraction induced by diurectic –> inc aldosterone -> inc H loss
primary hyperaldosteronism
normal anion Gap metabolic acidosis
RENAL TUBULAR ACIDOSIS
DIARRHEA
REMEMBER that the pt will be dehydrated and that will stimulate?
release of ADH
in renal tubular acidosis
why are they all
normal anion gap metabolic acidosis
bc hypercholermic
boards
which diuretic induced normal anoion agap acidosis
acetazolamide
what kidney tumor metasizes to lung where you see
CANNONBALL lesions
renal clear cell carcinoma
wilms tumor arises from embryonal renal cells of?
metanephros
bleeding time is prolonged in pts with uremia (Chronic kidney disease) why?
due to platelet dysfunction not thrombocytopenia
what is the most common cause of CKD in the US or they could ask what is the most common cause of hemodialysis in the US
type 2 DM
followed by persistent HTN
in minimal change disease
you get (albumin) proteinuria why?
loss of the negative charges on the basement membrane
albumin is negative charged so it normally doesnt cross.
the negatively charaged glycosaminoglycans
(such as heparan sulfate)
dehydration
your
RPF ___
GFR ___
FF___
RPF DEC DEC
GFR dec
FF inc
membranous nephropathy
good question!!!
what is the most common nephropathy associated with
renal vein thrombosis???
membranoproliferative GN
hepatitis C virus infection
minimal change disease (lipoid nephrosis) is associated with lymphoma
membranous nephropathy is associated with?
solid tumors
EM: spike and dome
membranous nephropathy
in minimal change disease
how does hodgkins lymphoma effect the glomerulus
the lymphokines from the T lymphocytes cause fusion of the podocytes
Boards (presentations)
- african american male, drug abuser, could be homeless
obese, NOT diabetic
2. heavy proteinuria in an obese caucasian individual
3.chronic vesico-ureteric reflux
EM: no immune complex deposition - effacement of foot processes
FSGN
(focal segmental sclerosis)
on boards
tx of minimal change disease
A. prednisone
B. prednisone and cyclophosphamide
prednisone
Q on boards
what is the most common SECONDARY cause of nephrotic syndrome in adults
diabetic nephropathy
trick question
diabetic pt,
his blood pressure in your clinic is always 110/70. however, on UA he has microalbuminurea.
what is your next best step in tx?
start ACEI or Arbs even if normotensive
diabetic nephropathy can induce what type of RTA?
type 4 RTA with hyperkalemia
pathogenesis
know that glomerular hyperfiltration is caused by dec ristance in both the afferent and efferent arterioles (aff> eff)
-diffuse BM thickening and mesangial cell overproduction -> microalbuminuria (the earliest clinical sign)
persistentHYPERGLYCEMIA is an important factor in pathogenesis of microalbuminuria
diabetic nephropathy
what is the earlier clinical sign of diabetic nephropathy
microalbuminuria
Q
HIV associated nephropathy
what is the pathology
collapsing focal glomerulosclerosis with tubular microcyst formation
A focal segmental variant
Question!!!!
treament of HIV -associated nephropathy
ACE -inhibitor
glomerular pathology in eclampsia
Endothelial dysfunction
glomerular endotheliosis
(diffuse endothelial swelling + fibrinogen deposition on the endothelial side of the capillaries) –> proteinuria (endothelial proliferation)
this is the cause of the proteinuria in eclampsia pt
pt with elampsia
develops confusion, has cerebral edema
what is the cause of this
not HTN
but do to damage
endothelial cells in the cerebral vessels.
