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163 Cards in this Set

  • Front
  • Back
What organs are retroparitoneal?
Descending colon
Ascending colon
Kidney and ureters
What is the course of the ureter?
Ureters pass under uterine artery and under ductus deferens
What is the role of the Proximal convoluted tubule?
Resorption of all glucose, amino acids, and filtered proteins and 80% of Na and H2O
What percentage of body weight is water?
What percentage of the water in our body is extracellular?
What percentage of the fluid is plasma?
plasma proteins- albumin and globulins
Breakdown the fluid calculations of the body?
ECF-PV (Plasma volume) =Interstitial volume

TBW is highest in men and babies and fat people
60-40-20 rule
60% water
40% ICF
20% ECF

Plasma volume measured by albumin
What are the cations and anions of ICF and ECF
Anions- protein and organic phosphates
Cations- K and Mg

anions- Cl HCO3
Cation- Na
What measures TBW?
titrated H2O
What measures ECF?
WHat measures plasma?
RISA- radiolabeled albumin
Evans blue
How does ECF and ICF change in OSMs and Liters in the following:
Lost in desert
adrenal insufficiency
Diarrhea- decreased ECF volume, no Osm change
Lost in a desert- loss of volume on both sides, increase in osms (sweat is hypoosmotic)
Adrenals- loss of ECF volume, gain of ICF volume; loss of Osm
How does ECF and ICF change in OSMs and Liters in the following:
infusion of isotonic NaCl
Excessive NaCL
Infusion of Isotonic NaCL- increase in ECF
Excessive NaCl- increase in ECF volume, decrease in ICF; increased Osm
SIADH- increase in volume all around, decreased Osms.
What is the formula for calculating clearance?
Volume of plasma from which the substance is cleared per unit time.
If C<GFR reabsorbtion
If C>GFR secretion
If C=GFR no net secreation or reabsorption
What is the Renal blood flow?
25% of the CO
directly proportional to pressure difference
Inversely proportional to resistance.
Flow and GFR are indirectly proportional
How does the kidney autoregulate blood flow?
Myogenic- renal arteries contract in response to stretch.
Tubuloglomerular feedback- increased pressure increases delivery to the macula densa.
RBF is constance over arterial pressures from 80 to 200 because of this.
How do you measure calculate Renal plasma flow?
measure clearance of paraaminohippuric acid.
- filtered and secreted by the renal tubuels.
clearance measures RBF
How is RBF calculated?
How does the kidney filter work?
1. Fenestrated capillary- size barrier
2. Fused Basement membrane w/ heparan sulfate- negative charge barrier
3. Epithelial layer of podocyte foot processes
What makes up the charge barrier of the kidney filter?
When is it lost?
Heparan sulfate
lost in:
nephrotic syndrome-> albuminuria, hypoproteinemia, generalized edema, hyperlipidemia
How is GFR calculated?
clearance of inulin/creatinine
GFR decreases w/ age
What is the filtraction fraction
fractio nof RPF that's filtered
increased filtration-> increased protein concentration of peritubular capillary blood.
What is the relationship between starling forces and GFR?
Kf changes in glomerular disease
Pgc increases w/ dilation of afferent arteriole, or constriction of effecrent
Pbs increased w/ ureter constriction or stone
Pigc- increased along the length of the capilarry; increased by increases in protein concentration
What are teh changes in the GFR, RPF and FF in the following:
constriction of the afferent arteriole
Constriction of the efferent arteriole
increased plasma protein
ureteral stone
afferent- down, down, none
efferent- up, down, up
protein- down, none, down
stone- down, none, down
What constricts the afferent arteriole?
What dilates the afferent arteriole?
What constricts the efferent arteriole?
Ang II
What dilates the efferent arteriole?
How is Glucose reabsorbed?
filtered load increased w/ increased plasma glucose
reabsorption from na-gcose cotransport in proximal tubuel.
At less than 200 mg/dl all can be reabsorbed. above-> glucosuria
at > 350, carriers are saturated and no more can be reabsorbed-> Threshold, Tm
What is the relative clearance of common proteins?
PAH>K>inulin>urea>Na>glucose, AA, HCO3
What is the role of the Early proxmial convoluted tubule?
workhorse- all the gcose, AAs adn most of the bicarb, Na, water.
Na,glucose; Na,AA co-transporters
Na,H countertransporter

Secretes ammonia as buffur for secreted H.
What is the role of the thin descending loop of Henle?
passively reabsorbs water via medullary hypertonicity (impermeable to Na)
What is the role of the thick ascending loop of henle?
actively reabsorbs Na, K, and Cl and indirectly reabsorbs Mg, Ca, Impermeable to H2O
Diluting segment

has the Na, K, 2Cl pump that's blocked by furosemide. Like Barters
What is the role of the early distal convoluted tuble?
actively reabsorbs Na, Cl.
Ca absorb regulated by PTH

Thiazides work here. on the Na, Cl- pump
What is the role of the collecting tubule?
reabsorb Na in exchange for K or H- aldosterone
all channels.
ADH works on the principal cell on V2 receptor

Intercalated cell secretes H
Wha tis the relationship of Na in the tubular fluid to that of it in the plasma?
TF/P = 1
What is the role of carbonic anhydrase?
catalizes HCO3 reaction.
acetazolamide inhibs this reaction -> inhibition of HCO3 reabsorption
What happens in the late proximal convoluted tubule?
HCO3, AA, and Gcose is filtered.
Na reabsorbed with Cl.
What factors affect K secretion?
Dietary K
- high K-> k secretion
- increases K secretion
- acidosis- decreases K secretion
- alkalosis- increases K secretion
Thiazides and loop diuretics- increase secretion
How do you calculate the clearance of free water?
V=urinary flow rate
What are the actions of Angiotensin II?
release of aldosterone from adrenal cortex
release of ADH from posterior pituitary
Stimulates hypothalamus-> thirst
overall increase in BP and intravasc volume
ANP is a check on the system.
What is the role of the juxtaglomerular apparatus?
JG cells are modified smooth muscle of afferent arteriole and the macula densa, an Na sensor secrete reinin leading to increased angiotensin II and aldosterone in reponse to decreased bp, na and increased symp tone.
What is the role of ANF on the tubules?
secretes w/ increased atrial pressure
causes increased GFR and Na secretion
What is the role of PTH on the tubules?
acts to:
increase Ca reabsorption in DCT
decrease P reabsorp in the PCT
What is the role of Aldosterone on the tubuels?
Increased Na reabsorption and increases K secretion at Collecting tubules
What cells secrete epo?
endothelial cells of peritubular capillaries
What is the kidney's role in Vit D?
1alpha-hydroxylade converst 25-> 1,25
How can NSAIDs cause acute renal failure?
in high vasocnstrictive states, prostas help dilate the afferent arteriole.
NSAIDs inhib.
What serves as extracellular and intracellular buffers?
Phosphate- minor

Proteins- imidazole, alpha amino groups, Hemoglobin
What are some fixed acids made that can be overproduced in disease?
lactic acid
salicylic acid
What is teh compensation for Metabolic acidosis?
Pco2=1.5 HCO3 + 8 +/- 2
What is the converstion for metabolic alkalosis?
Pco2 up .7; up 1 HCO3
What is the conversion for Acute resp acidosis?
up 1 HCO3 for 10 Pco2
What is the conversion for chronic resp acidosis?
up 3.5 HCO3 for every 10
what is the conversion for acute resp alkalosis?
down 2 HCO3 for every 10
What is the conversion for chronic resp alkalosis?
down 5 HCO3 for every 10
How do you calculate the anion gap?
Na - (Cl + HCO3)
normal is 12
What is Potter's syndrome?
bilateral renal agenesis-> oligohydramnios-> limb deformities, facial deformities, pulm hypoplasia. Malformation of ureteric bud
Potter can't Pee
How does a horseshoe kidney develop?
inferior poles fo both kidneys fuse. As they ascend from the pelvis during fetal development, horse shoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen
What does an RBC case indicate?
glom inflammation (nephritic), ischemia, or malig HTN
What do WBC casts indicate?
tubulointerstitial disease, acute pyelonephritis, glom disorder
What do granular casts indicate?
acute tubular necrosis
What do Waxy Casts indicate?
advanced renal disease/CRF
what do hyaline cases indicate
they are not specific
What do casts indicate?
hematuria/pyuria is of renal origin.
WBCs-> acute cystitis
RBCs-> bladder cancer
What are the symps of Nephritic syndrome?
hematuria, HTN, oliguria, azotemia

What are the Sx of Nephrotic syndrome?
proteinuria (massive)- >4 gm
peripheral and periorbital edema
hyperlipidemia, hypercholesterolemia- increased hepatic synth
Minimal Change Disease
most commmon nephrotic in kids.
lipoid nephroiss
lipid-laden renal cortices
normal glomeruli- light microscopy
fused foot processes- electron microscope
Rx- steroids
Focal Segmental Glomerulosclerosis

clinically similar to minimal change disease
older pts
sclerosis w/in capillary tufts of deep juxtamedullary glomeruli w/ focal or segmental distribution
- Focal some, but not all glomeruli
- segmental- only part of the glomerulus
Membranous glomerulonephritis
what is the cause?
Who does it affect?
What are some things that can help Dx?
What is a complication?
commonest cause of nephrotic in adults
immune complex
high incidence in teenagers and yougn adults
when nephrotic has azotemia
thickened capillary walls.
electron-dense immune complexes in intramembranous and epimembranous locations
- spike and dome appearance
granular flourescense
can cause renal vein thrombosis
What diseases can occur with membranous glomerulonephritis?
gold salts
What is seen in membrounous glomerulonephritis w/ light microscopy?
diffuce cap and BM thinckening
what is seen w/ immunoflourecense w/ membranous glomerulonephritis?
granular pattern
What is seen on EM w/ membranous glomerulonephritis?
spike and dome
Diabetic nephropathy
often manifests as nephrotic syndrome
increased thickness of glomerular BM.

increased mesangial matric
- diffuse glomerulosclerosis
- nodular glomerulosclerosis nodular accumulations of mesangial matrix (Kimmelstiel-Wilson lesions)
Renal amyloidosis
subendo and mesangial amyloid deposits
associated w/ RA and multiple myeloma
SLE and nephropathy
nephrotic syndrome w/ nephritic features
Type I- none observable
type II- mesangial form. FSGS, w/ increased mesangial cells and quantitative increase in mesangial matrix.
Type III- focal proliferative, less than half the glomeruli.
Type IV- prototype
most severe
all glomeruli
nephrotic and nephritic
thrombosis and proliferation
endothelial prolif
subendothelial deposits

Type V- indistinguisable from membranous golmerulonephritis
What are the characteristics of nephritic syndrome?
inflamm rupture of glomerular capillaries w/ resultant bleeding into the urinary space; proteinuria and edema may be present but are usually mild.
Hematuria- casts; smokey brown urine
Poststrep golmerulonephritis
most frequently seen in kids. Peripheral and periorbital edema. Recovers on its own.
follows an infection- nephritogenic strains of group A B-hemolytic strep
Immune complexes
Decreased C3
What are the gross, light microscopy and EM findings of poststrep glomerulonephritis?
punctate hemorrhages
enlarged, hypercellular, swollen, bloodless glomeruli w/ prolif of mesangial and endothelial cells.
glom BM of normal thickness and uniformity despite inflam changes
electron-dense "humps" on the epithelial side of the BM (supepithelial localization)
Lumpy-bumpy immunofluorescense
Rapidly progressive glomerulonephritis (RPGN)
nephritic syndrome; rapid renal failure in wks.
50% post strep
10 % goodpastures
Pauci-immune- no immune complexes. ANCA

type I- anca -
type II- anti-BM
type III- anca +

Histo is the crescent of bowman's space.
anti basement membrane disease
linear immunoflourescence
- Nephritic
- pneumonitis w/ hemoptysis
- men in mid-20s
- crescents
What is focal glomerulonephritis?
focal and segmental but not FSGS.
prolipheraltive, not nephrotic
immune complex disease, occurs as a manifestation of various disorders, SLE, subacute bacterial endocarditis, polyarteritis nodosa, goodpastures, wegener granulomatosis and IgA nephropahty
what is alport syndrome?
hereitary nephritis w/ nerve deafness and ocular disorders- lens dilocation and cataracts
nephritic syndrome- end-stage renal disease by 30
mutation in the alpha chain type IV collagen
irregular glomerular basement membrane thickening w/ foci of splittin of the lamina densa
What is IgA nephropathy?
Berger disease
common. after a URI
deposition of IgA in the mesangium.
benign recurrent hematuria in kids following an infection
henoch-Schonlein disease
what is membranoproliferative glomerulonephritis?
slow progression to chronic renal disease
BM thickened, cell prolif
reduplication of glomerular BM into two layers from mesangial matrix expansion into glomerular capillary loops. tram-track appearance
Type I - immune complex
type II- Dense deposit disease
C3 is reduced. dense deposits on membrane
caused by an IgG antibody
What is the cause of calcium stones?
most common
calcium oxalate, calcium phosphate, or both
cancer, PTH, vit D, milk -alkali
What is a renal colic?
excruciating pain caused by acute distention of the ureter from transit of a small stone.
What is hydronephrosis?
progressive dilation of the renal pelvis and calyces
What are th characteristics of UTIs?
increasesd in women- shorter urethra, increased in preggers
hematogenous spread to kidney or external entry
E. Coli
What predisposes one to UTI?
gyne abnlties
What are the clinical symps of UTIs?
Urinary frequency
Pyuria- neutrophils
what is the cause of ammonium magnesium phosphate stones (Struvite)?
2nd most common from urease-+ bugs- Proteus vulgaris, staph, klebsiella
staghorn calculi
What is the cause of Uric acid stones
hyperuricemia- gout
icnreased cell turnover- leukemia MPDisoders
What is the cause of cystine stones?
Radiolucent cystinuria
Drug induced interstitial nephritis
penicillin derivatives, nsaids, diuretics
acute interstitial renal inflam
Renal papillary necrosis
ischemic necrosis of the tips of the renal papillae
most often associated w/ DM
sometimes acute pyelonephritis

long-term persistent about of phenacetin
Acute tubular necrosis
most common cause of acute failure
reversible 2 wks
hyperkalemia in initial oliguric phase-> hyperkalemia. ATN must be distinguished from oliguria from prerenal causes like reduced blood volume
renal ischemia from htn or shcok from spepsis, trauma, or hemorrhage
crush injury w/ myoglobinuria
Ethylene glycol
What is Fanconi syndrome?
manifestation of generalized dysfunction of the proximal renla tubules
may be hereditary or aquired
characterized by impaired reabsorption of glucose, AAs, phosphate, and bicarb

genetically determined impaired tubulaar reabsorption of cystine
manifest clinically by cystine stones
genetically determined impaired tubular reabsorption of tryptophan
Chronic pyelonephritis
coarse asymmetric corticomedullary scarring and deformity of the renal pelfvis and calyces
inflam infiltrate, interstitial fibrosis and atrophy
What can cause diffuse cortical necrosis?
ischemic infarction of the cortices
obstetric catastrophes
septic schok
end-organ vasospasm and DIC
what is the milk-alkali syndrome?
hypercalemia from self medication of peptic ulcer w/ milk and absorbable antacids.
Adult polycystic kidney disease
15-30, genetic defect at birth
AD inheritance and is the most common inherited disorder of the kidney

bilateral, greatly enlarged
partial replacement of renal parenchyma

associated with:
berry aneurysm
cystic disease of liver and other
How does adult polycystic kidney disease manifest clinically?
palpable renal masses
progression to renal failure
Infant polycystic kidney disease
cysts present at birth
AR disorder.
closed cysts that are not in continuity w/ collecting system
simple renal cyst
common asymptomatic lesion
uremic medullary cystic disease
serious, uncommon form of cystic disease
medullary sponge kidney
multiple small medullary cysts and impaired tubular function, usually w/o renal failure; renal stones may form in the dilated ducts
may be complicated by infection
Acquired cystic disease
long-term dialysis therapy
multiple cysts, glomerular and tubular atrophy and scarring
increased incidence of renal cell carcinoma
What are the major clinical characteristics of uremia?
Acidosis- sulfates, phophates, organic acids
abnl control of fluid volume-> CHF
HTN- renin
Neuro- diminished mental function to convulsions and coma
Uremic encephalopathy
- anorexia, nausea, vomiting
- bleeding
- skin urochrome
- fibrinous pericarditis
What are the major causes of acute and chronic renal failure?
acute- hypoxia
chronic- HTN or DM
Acute renal failure
1. Prerenal azotemia- decreased RBF-> down GFR.
2. intrinsic- acute tubular necrosis or ischemia. Patchy necrosis -> debris -> obstruction -> down GFR. (Granular casts)
Postrenal- obstruction (stones, BPH, neoplasia) Only if bilateral
In acute renal failure, what are the measurements of urine osms, urine Na, FeNa, BUN/Cr for Prerenal, intrinsic and Postrenal disease?
Urine osms, urine Na, FeNa, BUN/Cr
Prerenal- high osm, low urine Na, FeNa, BUN/Cr>20
Renal- under 350, >20, >2%, <15
PostRenal- under 350, >40, >4%, >15
Renal adenoma
small and asymptomatic
derived from renal tubules
precursor to carcinoma
renal angiomyolipoma
hamartoma of fat, smooth muscle, blood vessels
tuberous sclerosis
Renal cell carcinoma
most common malig
more in men, 50-70
higher in cigarette smokers
chromosome 3 deletion (von Hippel-Lindau)
originates in Renal tubules
invades renal veins or the vena cava and can extend up the vena cava
early hematogenous dissemination
polygonal clear cells
flank pain, palpable mass, and hematuria
- Fever, 2ry polycythemia, ectopic ACTH, PRL, Gonados, renin, PTH
Wilms tumor
most common renal malig in kids
WT1 on chrom 11
WAGR- Wilms, ANiridia, Genitourinary malform, mental motor retard.
palpable flank mass
primitive emetanephric tissue
immature stroma, primitive tubules, and glomeruli, and mesencymal elements- ct, cartilage, bone, striated muscle
What is teh denys-drash syndrome
abnlties of WT1 gene, intersex disorder, nephropathy and wilms
What is Beckwith-Wiedemann syndrome
WT-2 deletion -imprinting from Moms

hemihypertrophy, macroglossia, organomegaly, neonatal hypoglycemia, various embryonal tumors
Transtitional cell carcinoma
most common tumor of collecting system
renal calyces, pelvis, ureter, or bladder
renal pelvis- phenacetin
can recur
local extension
- benzidine or B-naphthylamine
- cigs
- long-term cyclophosphamide use
Squamous cell carcinoma of the kidney
Schistosoma haematobium infection
renal calculi
What happens w/ low serum Na?
What happens with high serum Na?
neurolgic: irritability, delirium, coma
when do you see low serum Cl?
2ry to met alk
when do you see high serum Cl?
2ry to non-anion gap acidosis
what are the effects of low serum K?
U waves on ECG, flattened Ts, arrhythmias, paralysis
What are the effects of high serum K?
peaked Ts, arrhythmias
What are the effects of low Ca?
tetany, neuromusc irritability
What are the effects of high Ca?
delirium, renal stones, ab pain
What are the effects of low Mg?
neuromusc irritability
What are the effects of high Mg?
down DTRs, cardiopulm arrest
What are the effects of high P?
High-mineral ion product -> mets calcification, renal stones
What are the effects of low P?
low mineral ion product-> bone loss
What is the mechanism of Mannitol?
osmotic diuretic
increased tube fluid osm
increased urin
What is the clinical use of mannitol?
Shock, drug OD, decrease intracranial/intraoc pressure
What are the SEs of mannitol?
pulm edema, dehydration
contraindicated in anuria, CHF
What is the mechanism of Acetazolamide?
blocks carbonic anhydrase
self-limited NaHCO3 diuresis and reduction in HCO3 stores. Acts at the proximal convoluted tubule.
What is the clinical use of Acetazolamides?
Glaucoma, urinary alkalinization, met alk, altitude sickness
What are the SEs of Acetazolamide?
Hyperchoremic met acidosis, neuropathy, NH3 tox, sulfa alergy
What is the mechanism of Furosemide?
blocks Na, Cl, K channel
abolishes hypertonicity of medulla, prevents concentration of urine
increase Ca excretion
What is the clinical use of furosemide?
Edematous states
CHF, cirrhosis, nephrotic syndrome, pulm edema, HTN, HyperCa
What are the SEs of Furosemide?
What is the mechanism of Ethacrynic acid?
Phenoxyacetic acid derivative (not sulfonamide)
like furosemide
What is the clinical use of Ethacrynic acid?
diuresis in pts w/ sulfa allergy
What are the SEs of Ethacrynic acid?
same as furosemide (OH DANG) w/o the G
What is the mechanism of HZT?
thiazide diuretic. Inhibs NaCl reabsorp in early distal. decreases Ca excretion
What is the clinical use of HZT?
HTN, CHF, idiopathic hyperCa, nephrogenic DI
What are the SEs of HZT?
sulfa allergy
What is the mechanism of spironolactone?
competitive aldosterone receptor antag in corticla collecting tubule
K sparing
What is the clincal use of spironolactone?
hyperaldosteronism, K depletion, CHF
What are the SEs of spironolactione?
antiandrogen effects
What is the mechanism of Triamterine, Amiloride?
block Na channel of the CCT
K sparing
What is the clincal use of Triamterine, Amiloride
K depletion
What are the SEs of triamterine, amiloride
What is the mechanism of Ace inhibitors?
inhibit ACE
decrease angiotensin II adn prevent inactivation of bradykinin- a botent vaso dilator
renin release is increased from decreased inhibition
What is the clincal use of ACE inhibitors?
HTN, CHF, diabetic renal disease
What are the SEs of ACE inhibitors?
Tast changes
Preg problems
Increased Renin
Lower angiot II

and hyperkalemia
What diuretics cause an increase in urine NaCl
all of them
What diuretics cause an increas in urine K
all but thos that make it STAy
What diuretics cause an increase in pH in blood?
loop, thiazides

carbonics, K casue lower blood pH
What diuretics cause an increase in urine Ca?
thiazides decrease