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69 Cards in this Set

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where do the ureters pass under?
the uterine artery and the ductus deferens

water UNDER the bridge
60% of TBW is water...how does intra and extra cellular compare? which is high in K
1/3 is extracellular fluid

2/3 in intracellular fluid (high in K)

HIKIN': HIgh K INtracellular
extracelluar fluid is how much of total body water? and for it how much is plasma volume and how much is interstitial volume (how do you measure each too)
1/4 is plasma (measure with radiolabeled albumin)

3/4 is interstitial (measured with inulin)
normal GFR is what?
100ml/min
formula for renal clearance?
C = UV/P

U: urine concentration
V: urine flow
P: plasma concentration
what can be used to measure GFR because it is freely filtered and neither reabsorbed nor secreted?
inulin
the glomerular filtration barrier has three components, name em. which is lost in nephrotic syndrome
1) fenestrated capillary endothelium (size barrier)
2) Fused basement membrane with heparan sulfate (negative charge barrier)
3) Epithelial layer with podocyte foot processes

Charge barrier is lost in nephrotic syndrome

Full Cup For Being My Endless Lover
60-40-20 rule
60% total body water
40%ICF
20%ECF
creatinine clearance is only an approximate measure of GFR, why?
it slightly overestimates the GFR because creatinine is moderately secreted by the renal tubules
filtration fraction formula
GFR/RPF
what do prostaglandins do to the afferent arteriole?

what does Angiotensin II do to the efferent arteriole?
PGs dilate the afferent arteriole

Angiotensin II preferentially constrict the efferent arteriole
how will NSAIDS affect blood flow in the kidney? how about ACE inhibitors?
NSAIDS block PG formation so that will prevent the afferent arteriole from being dilated

ACE inhibitors block Angtiotensin II formation preventing efferent arteriole constriction

that doesnt answer the question...oh well
formulas

Filtered load and excretion rate
filtered load = GFR x P

Excretion rate = V x U

P: plasma concen.
V: urine flow
U: urine concentration
where is glucose absorbed when at normal levels?

at what levels do glucosuria begin? at what levels are transporters fully saturated
completely reabsorbed in the PROXIMAL tubule by Na/glucose transporters

glucosuria: 160-200 mg/dL
saturation: 350mg/dL
Hartnups disease: def. seen, results in what?
deficiency of neutral amino acid (tryptophan) transporter.

results in pellagra

HarTNuP
Hard to reabsorb Trytophan, a Neutral amino acid resulting in Pellagra
where are amino acids reabsorbed and by what?
in the PROXIMAL tubule by sodium-dependent transporters
in the early proximal tubule what is reabsorbed? what are the effects of PTH and AT II?
All glucose and amino acids. Most bicarb, Na, Cl, H2O

PTH: inhibits the Na/phosphate cotransporter leading to INCREASE phosphate excretion

AT II: increases Na/H exchange leading to INCREASE Na and H2O reabsorption
thin descending loop of henle: reabsorbs what? impermeable to what? aka what?
passively reabsorbs water
impermeable to Na
aka the concentration segment

a THIN dam holds no WATER
thick ascending loop of Henle: reabsorbs what? impermeable to what? does what to urine?
actively reabsorbs Na, K, Cl via NKCC pump (indirectly leading to absorption of Mg and Ca paracellularly)
Impermeable to H20
dilutes urine

THICK dam holds WATER
early distal convoluted tubule: reabsorbs what? aka what? effect of PTH?
actively reabsorbs Na and Cl
aka diluting segment

PTH: INCREASE calcium reabsorption via increasing Ca/Na exchanger
Collecting tubules: reabsorb what? effects of aldosterone and ADH
reabsorb Na in exchange for K and H

Aldosterone: inserts Na channels to increase Na reabsorption (and thus dump K)

ADH: acts at V2 receptors to cause insertion of aquaporin H2O channels on luminal side
three triggers from the RAAS system?
DECREASE in BP
DECREASE in delivery of Na to the macula densa cells
INCREASE in sympathetic tone
action of AT II 6 of em
hits AT receptors on vascular smooth muscle----INCREASE BP
constricts the efferent arteriole---INCREASE FF to preserve renal function
increase aldosterone----increase Na and thus H2O reabsorption
increase ADH---increase H2O reabsorption
increase proximal tubule Na/H activity---increase H2O reabsorption
stimulate hypothalamus---thirst
ADH primarily regulate what? how about aldosterone?
ADH---osmolarity
Aldosterone---blood volume
JGA and its two components and their jobs?
JG cells---secret renin in response to decrease in renal blood pressure, decrease Na delivery to distal tubule and an increase in sympathetic tone

Macula densa---Na sensor

in a nutshell: maintains GFR via the RAAS system
kidney has endocrine functions what are they, 4 of em
Erythropoietin--release in response to hypoxia
1,25-(OH)2 vitamin D--make active vit. D which increases intestinal reabsorption BOTH of Ca and phosphate
Renin--from JG cells
Prostaglandins---vasodilate afferent arteriole to increase GFR
how can NSAIDS kill your kidney?
inhibiting the formation of prostaglandins which causes the afferent arteriole to dilate and maintain GFR in times of dire need
PTH has a couple of effect on the kidney which almost counteract each other...detail them
it works on the proximal tubule to increase the excretion of phosphate

it also indirectly increases phosphate reabsortion in the gut by stimulating the formation of vit. D in the kidney
ANP: source, cause for release, effect and result
from the atria
released in response to increase in atrial pressure
causes an increase in GFR and Na filtration with NO compensatory Na reabsorption in distal nephron
results in Na and volume loss
PTH: cause for release, effect and result
released in response to decrease in Ca, increase in phosphate, decrease in active vit. D
Causes increase in Ca reabsorption, decrease in phosphate reabsorption, increase in vit. D production
results in increase in Ca and phosphate absorption in the gut
AT II: cause for release, effect and result
release in response to decrease in BP
results in increase if efferent arteriole constriction---increases GFR and FF WITH a compensatory Na reabsorption in proximal and distal nephron
results in preservation of renal function in low-volume state
causes of a K shift INTO cell...4 of em
high insulin
Beta adrenergic agonist
alkalosis
hypo-osmolarity
causes of a K shift OUT of cell..6 of em
insulin deficiency
Beta adrenergic antagonists
acidosis
hyperosmolarity
digitalis
cell lysis (duh)
the respiratory compensation in response to metabolic acidosis can be calculated using what?
Winters formula

PCO2 = 1.5 (HCO3) + 8 +/- 2
Anion gap formula?
AG=Na - (Cl + HCO3)
pt has wide AG acidosis...causes?
MUDPILES
Methanol
Uremia
DKA
Paraldehyde or Phenformin
Iron tablets or INH
Lactic acidosis
Ethylene glycol
Salicylates
Type 1 RTA: defect, associated risks
defect in collecting tubule ability to excrete H
assoc. with hypokalemia and risk of calcium containing kidney stones

"distal"
Type 2 RTA: defect, associated risks
defect in proximal tubule HCO3 reabsorption
associated with hypokalemia and hypophosphatemic rickets

"proximal"
Type 4 RTA: defect, associated risks
defect (lack thereof) in collecting tubule response to aldosterone
risk of hyperkalemia and inhibition of ammonium excretion in proximal tubule, leads to decrease in urine pH d/t buffering capacity

"hyperkalemic"
RBC cast sign of? 3 things
glomerulonephritis, ischemia, malignant HTN
WBC cast sign of ? 3 things
tubulointerstitial inflammation, actue pyelonephritis, transplant rejection
granular (muddy brown) casts sign of?
acute tubular necrosis
waxy cast sign of what?
advanced renal disease
hyaline casts sign of?
nonspecific
what mediates the damage in nephritic syndrome?
immune-complex deposition activates complement; C5a attracts NUETROPHILS which mediate the damage
what is the most common cause of death in SLE?
diffuse proliferative glomerulonephritis
what kind of stones CAN NOT be seen on xray?
uric acid stones
what leads to formation of staghorn calculi?
infection with urease-positive bugs (proteus mirabilis, staph, klebsiella)

or cysteine-based stones
what is the most common renal malignancy? where does it originate? what increases its incidence? classic triad
renal cell carcinoma, originates in the renal tubular cells, smoking

triad: hematuria, flank pain, palpable mass
what kind of stones are commonly seen in kids? what can they form?
cysteine, form staghorn calculi
what is part of the pathogenesis of renal cell carcinoma (gene deletion)
loss of VHL (3p) tumor suppressor gene, leads to increased IGF-1 (promotes growth)
a disease associated with VHL inactivation and thus renal cell carcinoma
von Hippel-Lindau syndrome
in nephrotic syndrome what component of the filtration barrier gets lost?
the charge barrier
traumatic crush injuries can lead to an elevation of what electrolyte?
potassium due to it being release from muscles when they are crushed and their cellular contents are spewed out.
what is the imaging study of choice for kidney stones?
abdomen/pelvis CT
what bug is the most common cause of pyelonephritis?
e coli
what is the primary use of mannitol?
decrease intracranial pressure
how would heart failure affect your acid/base balance?
cause metabolic alkalosis due to a lower level of blood being delivered the kidney activating the RAAS system. this will lead to increase in aldosterone, this will lead to K dumping. low K levels will cause a shift of K out of cells and H into cells leading to an increase in the pH
bicarb (and inorganic phosphorus, amino acids and glucose) are absorbed faster than water in the proximal tubule so its concentration is higher in the plasma than the tubule
just remember that
SIADH will lead to what kind of levels of Na in the urine and plasma?
high urine sodium levels
low (diluted) sodium levels in blood
what is the DOC for patients with SIADH
demeclocycline (an ADH antagonist)
a patient with renal cell carcinoma also has von hippel-lindau syndrome what is a pertinent finding on physical examination elsewhere in the body?
retinal angiomas
bugs that cause struvite kidney stones?
urease-producing organisms, including Proteus, Pseudomonas, Providencia

The P's make it so you can Pee

less commonly: klebsiella, staph and mycoplasma
increased redness of skin and mucosal membranes occurs due to polycythemia when a patient has renal cell carcinoma
make that connection!
ADPKD will do what to the BUN and creatinine levels? anemia Y or N?
INCREASE THEM

YES for anemia
losartan blocks what two things on its way to decrease blood pressure?
vasoconstriction and aldosterone release
which will help decrease chances of getting a kidney stone: increase or decrease sodium intake?
DECREASE Na intake
henoch-schonlein purpura present with rash on butt and extensor surface of legs...it is due to IgA deposits where and follow what kind of illness?
in the mesangium and it follows a viral URT infection
what parasite is associated with transitional cell carcinoma, how do you Rx it?
shistosoma

Rx with praziquantel