AAW - renal/acid base Flashcards
6 months old presents with FTT, oliguria, recurrent UTIs, enlarged unilateral renal pelvis, normal ureters, and uremia.
what you think
ureteropelvic junction obstruction - most common site of obstruction in young ones because it is the last to canalize
common in males
where do sickle cells damage the kidney
in the vasa recta, the arteries that follow the loop of henle
they damage here because the blood osmolarity is very high here
What does furosemide do to the GFR and how
it increases the GFR:
blocks NKCC
NKCC is present in ascending limb AND macula densa
Macula densa gets less sodium into the cells because NKCC is blocked
kidney thinks that there is low sodium and high water because no sodium gets into the cell
macula densa secretes renin to constrict efferent arteriole to increase GFR to get rid of what it thinks is excess water
how does acetazolomide cause an increase in Na secretion in the proximal tubule
it stops the hydrogen ion from being made inside the proximal tubule cell, which is normally antiported for the sodium that is in the lumen
what is the only diuretic that acts totally upstream of the macula densa
carbonic anhydrase inhibitor - acetazolamide
why do you get acidotic on acetazolomide
because you cannot convert the bicarb in the lumen to CO2 in order for it to be reabsorbed by the proximal tubule cell, so the bicarb gets peed out
what does Captopril do to potassium levels
they could cause hyperkalemia because of decreased RAAS
RAS vs RAAS
RAS - renal artery stenosis
RAAS - renin-angiotensin-aldosterone system
what hypertensive drugs are contraindicated in renal artery stenosis and why
lisinopril, catalopril, other ACEs
because when the body isn’t able to perfuse the kidneys because of stenosis, the normal response of the kidney is to actiave RAAS so that the efferent arteriole constricts, PRESERVING kidney flow
someone’s urine output is lets say 150ml/min and you give ADH and it doesn’t change. why
type 2 DM
hyperglycemia prevents proximal tubule reabsorption of glucose, increases delivery of fluid to loop of henle, overloading the loop and reducing it’s gradient, which causes ADH resistance.
how does proteus increase the pH in the urine
splits urea into ammonia using urease
what do you kidneys do to bicarb if you chronically live at high altitude
your kidney responds to your chronic respiratory alkalosis by secreting more bicarb
What is the molecule in the basement membrane of the glomerulus that has a negative charge
Heparan Sulfate
Hartnup Disease
Autosomal recessive
Deficiency of neutral amino acid (tryptophan) transporters in proximal tubule and in enterocytes
Get pellegra like symptoms
treat with high protein diet and nicotinic acid
what diuretic can cause hypercacemia/hypocalcuria and why
thiazide
works on distal convoluted by blocking Na Cl contransporter on luminal side
this causes a decrease in sodium in the cell
Na/Ca antiporter on the basalateral side is upregulated to get more sodium back into the cell, which throws Ca out into the blood
Where do you find carbonic anhydrase enzyme in the proximal tubule?
In the proximal tubule cell cytoplasm and in the luminal brush boarder.
what diuretic can cause hypocalcemia/hypercalcuria and why
loop
loops increase sodium in distal lumen
Na/Cl activity increases
more Na in tubular cell
no need to use Na/Ca transporter on basolateral side
chlorthalidone
blocks NaCl cotransporter
thiazide
Hydrochlorothiazide
blocks NaCl cotransporter`
what is the “only other time” that your body is making activated vitamin D if the kidneys aren’t doing it?
granulomatous disease like sarcoid or wegeners
can cause hypercalcemia
contraction _______
(alkalosis or acidosis)?
explain how it could happen
alkalosis
Volume contraction -> aldosterone ->H+ secretion at collecting duct
volume contraction -> AT II -> HCO3− reabsorption at proximal convoluted tubule
could happen from a diuretic (like thiazide) or other loss of fluid
Tx for nephrogenic DI
Thiazides (paridoxical)
Amiloride (paridoxical)
Indomethacin (constricts afferent arteriole reducing renal flow)
why do people with kidney dysfunction get secondary hyperparathyroidism
usually in ESRD
get decreased secretion of PO4 and decreased activation of vit D
(the parathyroids are trying to compensate for the low serum Ca and the high serum PO4, but usually they can’t quite return the levels to normal)
Causes of metabolic alkalosis
Mech
–Vomiting
–Loop diuretics (and sometimes thiazides)
–Antacid use
–Hyperaldosteronism (primary, cushing, bartter)
You go “BLAH” when you vomit
“VLAH”
loops cause alkalosis because you get more Na in the collecting tubule, causing an upregulation of aldosterone -> Na is exchanged for K in the principle cell, then you resorb the K by excreting H in the intercalated cell
Hyperaldosteronism causes alkalosis because of the same mech.
if there is no change in volume status (like in primary hyperaldosteronism, cushing, bartters) then the alkalosis with be (saline unresponsive) - treat with potassium
if they are hypovolemic, treat with saline
what makes a metabolic alkalosis (chloride responsive) or (saline responsive)
list causes
it occurs when you are hypovolemic
you see low Cl in the urine because the body is reuptaking ions to combat the hypovolemia
Tx is normal saline.
Vomiting or nasogastric suction Diuretics Posthypercapnia Cystic Fibrosis Low chloride intake
what does your blood glucose have to get to in order to see glucoseuria
about 200mg/dlL
WAGR
wilms tumor
Anirida
Genital abnormalities
mental and motor Retardation
assc with deletion of chromosome 11
when do you see abundant clear cells in the kidney
renal cell carcinoma
kidney condition assc with asbestosis
RCC
von hippel lindau disease
Assc with mutant tumor suppressor gene VHL, resulting in constitutive expression of HIF 1a
Normally functioning VHL aids in ubiquitin apoptosis
autosomal dominant
Assc cancers: *BILATERAL RCC, Cavernous hemangiomas in skin, mucosa, organs;
hemangioblastoma (high vascularity with hyperchromatic nuclei) in retina, brain stem,
cerebellum; and pheochromocytomas
a bunch of eosinophillic cells packed with mitochondria, you think:
oncocytoma (mitochondria are present because the name of the tumor!) (a prof said this, and we still can’t figure out why)
often benign
hamartomatous blood vessels in the kidney mean what
angiomyolipoma, benign tumor
assc with tuberous sclerosis
in the kidney, when would you see circular grouping of dark tumor cells surrounding pale neutrofibrils
these are called homer-wright bodies, and they are found in neuroblastoma, a tumor of the medulary adrenal
if you take a biopsy of the kidney and see embryonic glomerular structures, what is it
Wilms tumor
IgA nephropathy diseases
HSP
Bergers
DDx for hypercalcemia
cancer (squamous cell lung producing PTHrP)
hyperparathyroid
thiazide
dipstick is positive for blood but you see no blood in a high power field. what is it
myoglobinurea
usually occurs after intense physical activity/rhabdo
miliary
(of a disease) accompanied by a rash with lesions resembling millet seed.
i.e. in miliary TB
it means that the TB has spread (happens in immunocompromized patients)
Ziehl-neelsen is used to look for what
acid fast bacteria
like TB - an bacillus
fungal lung infection from latin america
what is a characteristic finding of the yeist
paracoccidioidomycosis
see “multiply budding” or “pilot’s wheel” yeast forms
how to calculate the GFR from a 24 hour urine collection
V = urine flow (mL/min) Uc = urine creatinine (mg/ml) Pc = plasma creatinine (mg/ml) CCr = clearance of creatinine ~= GFR
CCr = V * Uc / Pc
alveolar gas equation
PA02 = PI02 - PACO2/R
oxybutynin
muscarinic antagonist
inhibits urination
muscarinic antagonists that help you not wet your pants
oxybutynin
darifenacin
solfenacin
tolterodine
they only help with urge incontenance, not stress incontinence
bethanechol
cholinergic agonist
helps incontinence by contracting the detrusor muscle
bumetanide
loop diuretic
used when furosemide doesnt work
neostigmine
anticholinesterase
would treat incontinence by increasing cholinergic activity and contracting the detrusor
individuals with defiviencies in the alternative complement pathway are at increased risk of disease from what
neisseria
lambert eaton syndrome
anto-antibodies against calcium channels, which produce muscle weakness
Coughing and peeing blood with no Hx of infection
What is the most likely diagnosis
Goodpasture’s
see linear deposits of IgG in the glomeruli
what embryologic structure forms the adult kidney
Ureteric bud induces the development of the metanephros, which becomes the kidney
What does DIC do to the kidneys
causes diffuse cortical necrosis
head injury and polyurea
what are you thinking
damage to the pituitary decreases the amount of vasopressin getting to the kidney
diabetes insipidus
what causes type 1 renal tubular acidosis
how can you tell its type 1
what happens physiologically
“distal tubular acidosis”
amphotericin B, analgesic nephropathy, congenital abnormalities
only renal tubular acidosis where urine pH is >5.5
assc with hypokalemia
defect in alpha intercalated cells -> cannot secrete H+ into the lumen
what causes type 2 renal tubular acidosis
how can you tell its type 2
what happens physiologically
“proximal tubular acidosis”
fanconi syndrome, carbonic anhydrase inhibitors (“close that gap, #2!”)
type 2 because you have urine pH is less than 5.5 and you get hypokalemia
you get decreased absorption of bicarb in the proximal tubule, but the alpha intercalated respond by secreting acid so your urine pH is actually low
what does urate do to the kidney
how can you stop it from doing what it does
causes an acute tubular necrosis (nephrotoxic)
urate is a salt of uric acid seen in things like tumor lysis syndrome
allopurinol before chemo
what nephropathy is associated with lupus
membranous nephropathy
spike and dome depostits next to the podocytes
hep b,c, solid tumors, SLE, or drugs like NSAIDS
C3 nephritic factor in the blood is assc with what kidney things
what does it do
type two membranoproliferative glomerulonephritis
AKA dense deposit disease
it stabilizes C3 convertase which causes the overactivation of complement which can cause inflammation and drive the glomerulonephritis
nitrites in the urine
what does it mean
bacteria are there
bacteria convert nitrates into nitrites
atrophic tubules with eosinophilic material resembling thyroid tissue in the kidney
chronic pyelonephritis
hemangioblastomas in the cerebellum and cysts in the kidney
what is the genetic defect specifically
loss of the VHL tumor suppressor gene, which leads to increased IGF-1 (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF)
when do you see blastema cells
in a wilms tumor
they are immature kidney mesenchyme
kidney tumor, hypoglycemia, muscular hemihypertrophy, organomegaly
beckwith-wiedemann syndrome
assc with mutations in WT2 gene cluster, particularly IGF-2
7 year old girl with what looks like she is on a huge dose of a loop diuretic, with family history of kidney problems
bartter’s syndrome
defective NKCC
what does PTH do to phosphate levels and where in the kidney does it work to do this
What does PTH do to Ca levels and where in the kidney does it work to do this
decreases them by inhibiting resorption in the PROXIMAL convoluted tubule
(it causes calcium resorption in the distal convoluted tubule)
tryptophan gets converted into niacin with the help of what other vitamin
B6, pyridoxine
what type of diabetes insipidus does lithium produce
nephrogenic DI
mech of sulfamethoxazole
inhibition of dihydropteroate synthase
common causes of interstitial nephritis
the P’s
Pee (diuretics) Pain free (NSAIDs) Penicillins and cephalosporins Proton pump inhibitors rifamPin
acute transplant rejection of a kidney is caused by what type of cells
CD8
non linear mesangial deposits of IgA in the kidney after a respiratory disease
bergers disease
assc with celiac disease
chromosome defective in wilms tumors
11
deletion of the WT1 tumor suppressor gene
what is seen in the urine in a patient with cystinuria
what is the treatment
COLA cystine orntithine lysine arginine
and the cystine can for hexagonal cystine stones
Tx: urinary alkalizing agents (potassium citrate, acetazolamide), chelating agents (penicillamine, which also treats Cu, Pb and Au tox, but CAUSES membranous nephropathy, didn’t you know?)
cola colored urine and orbital edema after being sick
post strep GN
hypercellular inflamed glomeruli on HandE, mediated by immune complex deposition, subepithelial humps on EM
what cells secrete renin
juxtaglomerular cells
antihypertensive medication that causes drowsyness and depression without altering electrolytes
clonidine, guanfacine
obstructive jaundice
what happens to your urine bilirubin levels
what happens to your urine urobilinogen levels
urine bilirubin levels rise (conjugated) because the bilirubin in the gall bladder backs up, etc, etc
urine urobilinogen levels DECREASE because the bilirubin cannot get to the gut in obstructive jaundice, where bacteria normally convert bilirubin to urobilinogen
what does secretin do
increases levels of bicarb in the stomach
