• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/93

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

93 Cards in this Set

  • Front
  • Back
Henderson Hasselbach equation
pH = pKa + log [HCO3] / .03 PCO2
Winter's formula

for Compensation of metabolic acidosis
PCO2 = 1.5 (HCO3) + 8 (+/-2)
Metabolic alkalosis compensation
PCO2 increases 0.7 mmHg for every 1 mEq/L HCO3-
Respiratory acidosis acute compensation
increase 1 mEq/L HCO3- for every 10 mm Hg increase in pCO2
Respiratory acidosis chronic compensation
increase 3.5 mEq/L HCO3- for every 10 mmHg increase in PCO2
Respiratory alkalosis acute compensation
decrease 2.0 mEq/L HCO3- for every 10 mmHg decrease in PCO2
Respiratory alkalosis chronic compensation
decrease 5 mEq/L HCO3- for every 10 mmHg decrease in PCO2
Potter's syndrome
bilateral renal agenesis --> oligohydramnios --> limb deformities, facial deformities, pulmonary hypoplasia

caused by malformation of the ureteric bud

not compatible with life

decrease in amniotic fluid leads to renal system that fails to excrete fluid swallowed by fetus
Horseshoe kidney
inferior poles of both kidneys fuse

as they ascend from the pelvis during fetal development, horseshoe kidneys get trapped under the inferior mesenteric artery and remain low in the abdomen

kidney functions normally
RBC casts
glomerular inflammation (nephritic syndromes), ischemia, or malignant hypertension
WBC casts
tubulointerstitial disease, acute pyelonephritis, glomerular disorders
Granular ('muddy brown') casts
acute tubular necrosis
Waxy casts
advanced renal disease/chronic renal failure
Hyaline casts
nonspecific
What do you see in urine of a patient with bladder cancer?
RBCs, no casts
What do you see in urine of a patient with acute cystitis?
WBCs, no casts
Focal segmental glomerular sclerosis
LM: segmental sclerosis and hyalinosis

clinically similar to minimal change disease, but happens in older patients

sclerosis within capillary tufts of deep juxtamedullary glomeruli with focal or segmental distribution

more severe disease in HIV patients
spike and dome appearancw
neprhotic...membranous glomerulonephritis
Membranous glomerulonephritis
immune complex disease of unknown etiology

major primary cause of nephrotic syndrome

teenagers and young adults

suspect with nephrotic syndrome and azotemia

THICKENED CAPILLARY WALLS (diffuse capillary and BM thickening)

IF: granular pattern

EM: spike and dome

immune complexes in intramembranous and epimembranous (subepithelial) locations

granular immunoflourescence: IgG or C3 (granular is general characteristic for immune complex diseases)

associations can sometimes be seen in hep B, syphilis, or malaria infections
most common cause of neprhotic syndrome
membranous glomerulonephritis
Diabetic nephropathy
nephrotic syndrome

EM: striking increase in thickness of the glomerular BM; increase in mesangial matrix...diffuse glomerulosclerosis and NODULAR GLOMERULOSCLEROSIS: KIMMELSTEIN WILSON NODULES (nodular accumulations of mesangial matrix...acellular ovoid nodules in the periphery of the glomerulus)

basement membrane thickening
Renal amyloidosis
IF: congo red stain, apple-green birefringence

subendothelial and mesangial amyloid deposits

characteristic criss-cross fibrillary pattern of amyloid by EM

most often associations with chronic inflammatory disease such as RA, TB or plasma cell disorders (like MM)
Lupus nephropathy
renal component of SLE!

severity of renal lesion often determines overall prognosis in patients with SLE

NEPHROTIC

has 5 different patterns

LM: membranous glomerulonephropathy

WIRE LOOP LESION; resulting from immune complex deposition and gross thickening of teh GBM as well as endothelial cell proliferation

subendothelial immune complex deposition
Nephrotic syndrome in general
massive proteinuria (frothy urine), hypoalbuminemia, peripheral and periorbital edema, hyperlipidemia
Nephritic syndrome (in general)
inflammatory rupture of the glomerular capillaries, with resultant bleeding into the urinary space

Oliguria, azotemia, hypertension, hematuria
Hematuria in nephritic syndrome
from leakage of red cells directly from glomerular capillaries into the Bowman space; many of the red cells are aggregated into the shape of the renal tubules and embedded in a proteinaceous matrix forming red cell casts that can be observed in urine

SMOKY BROWN URINE...red cell casts can degenerate and become pigmented granular casts
Acute poststreptococcal glomerulonephritis
NEPHRITIC SYNDROME

LM: glomeruli enlarged and hypercellular, neutrophils

LUMPY BUMPY

EM: subepithelial humps

IF: granular pattern
LUMPY BUMPY
acute poststreptococcal glomerulnephritis
most often follows or accompanies infection (tonsillitis, streptococcal impetigo, infected insect bites) with nphritogenic strains of group A beta hemolytic streptococci
poststreptococcal glomerulonephritis (acute proliferative glomerulonephritis)
Urinary red cells and red cell casts, azotemia, decreased serum C3 and increased titers of antistreptococcal antibodies (antistreptolysin..ASO), anti-DNAase B...
poststreptococcal glomerulonephritis
Lumpy bumpy

subepithelial localization

electron dense humps

glomerular BM of normal thickness and uniformity despite the extensive inflammatory changes
poststreptococcal glomerulonephritis (acute proliferative glomerulonephritis)

...most frequently seen in children; peripheral and periorbital edema; resolves spontaneously
Rapidly progressive (crescentic) glomerulonephritis
NEPHRITIC!

crescent moon shape

rapid course to renal failure; the number of crescents indicates prognosis
Goodpasture's syndrome
Type II hypersensitivity

NEPHRITIC

IF: linear pattern, anti GBM antibodies

pneumonitis with hemoptysis (hemorrhagic pneumonitis); peak incidence is men in their 20's

RPGN crescenteric morphology with linear immunofluorescence

hemoptysis and hematuria
Alport's syndrome
hereditary nephritis

nerve deafness and ocular disorders such as lens dislocation and cataracts

split basement membrane

collagen IV mutation
Berger's disease
IgA nephropathy

IF and EM: mesangial deposits

most often characterized by benign recurrent hematuria in children, usually following infection, lasting 1-2 days, and usually of minimal significance

mild disease; often postinfectious; common cause of recurrent hematuria in young patients
Membranoproliferative glomerulonephritis
EM: subendothelial humps

NEPHRITIC

TRAM TRACKS

slowly progresses to renal failure; disease is marked by reduplication of glomerular BM into two layers, due to expansion of mesangial matrix into the glomerular capillary loops...results in a characteristic tram-track appearance...best seen with silver stains
Tram tracks
membranoproliferative glomerulonephritis
Calcium stones
most common kidney stones (75-85%)

calcium oxalate, calcium phosphate or both...

conditions that cause hypercalcemia: cancer, increased PTH, increased vitamin D, milk-alkali syndrome

can lead to hypercalciuria and stones

tends to recur
Radiopaque...can result from antifreeze or vitamin C abuse
oxalate crystals

(calcium oxalate crystals)
Ammonium magnesium phosphate stones
2nd most common kidney stone

caused by infection with urease-positive bugs (proteus vulgaris, staphylococcus, Klebsiella)

can form staghorn calculi that can be a nidus for UTIs

formed in alkaline urine

worsened by alkaluria
2nd most common kidney stone
ammonium magnesium phosphate

struvite

staghorn calculi

nidus for UTIs
Staghorn calculi
ammonium magnesium phosphate

struvite

2nd most common kidney stone

urease positive bugs: proteus vulgaris, staphylococcus, klebsiella
Uric acid stones
stong association with hyperuricemia (like gout); often seen as a result of diseases with increased cell turnover, such as leukemia and myeloproliferative disorders

CANNOT be seen on x-ray or CT
Cystine stones
most often secondary to cystinuria

hexagonal shape

faintly radiopaque

treat with alkalinization of urine
most common renal malignancy
Renal cell carcinoma
Renal cell carinoma
frequently invades renal veins or IVC and spreads hematogenously

most common in men ages 50-70

increased incidence with smoking and obesity

originates in renal tubule --> polygonal clear cells
associated with von-Hippel-Lindau
RCC!!

gene deletion in chromosome 3
Clinical manifestations of RCC
hematuria, palpable mass, secondary polycythemia, flank pain, fever and weight loss
Associated paraneoplastic syndromes with RCC
EPO, ACTH, PTHrP and prolactin
Wilms' tumor
most common renal malignancy of early childhood (2-4 years old)

presents with huge, palpable flank mass, hemihypertrophy

contains embryonic glomerular structures (primitive glomeruli, fibrous CT, cartilage, bone, striated muscle)
Deletion of tumor suppressor gene on chromosome 11
WT1 on chromosome 11

Wilms tumor!!
WAGR complex
Wilms tumor, aniridia, genitourinary malformation and mental motor retardation
Transitional cell carcinoma
most common tumor of the urinary tract system (can occur in renal calyces, renal pelvis, ureters and bladder)

painless hematuria is suggestive of bladder cancer

in renal pelvis: phenacetin

phenacetin, smoking, aniline dyes and cyclophosphamide
Associated with phenacetin, smoking, aniline dyes and cyclophosphamide
transitional cell carcinoma
Affects cortex with relative sparing of glomeruli/vessels

white cell casts in urine is pathognomonic

presents with fever, CVA tenderness
acute pyelonephritis
coarse, asymmetric corticomedullary scarring, blunted calyx

tubules can contain eosinophilic casts

thyroidization of kidney

lymphocytes
chronic pyelonephritis
acute generalized infarction of cortices of both kidneys

likely due to a combination of vasospasm and DIC

associated with obstetric catastrophes (like abruptio placentae) and septic shock
diffuse cortical necrosis
drug induced interstitial nephritis
acute interstitial renal inflammation

fever, rash, eosinophilia, hematuria 2 weeks after administration

drugs (like penicillin derivatives, NSAIDs, diuretics) act as haptens including hypersensitivity
Acute interstitial renal inflammation
acute drug induced interstitial nephritis...think penicillins
most common cause of acute renal failure
acute tubular necrosis
acute tubular necrosis
REVERSIBLE!

but fatal if left untreated

associated with renal ischemia (like shock), crush injury (myoglobinuria), toxins

death most often occurs during initial oliguric phase (cardiac standstill from hyperkalemia...needs to be distinguished from oliguria due to prerenal causes like reduced blood volume or dehydration)

recovery in 2-3 weeks

direct toxicities: mercuric chloride, gentamicin and ethylene glycol
Microscopic stuff with acute tubular necrosis
loss of cell polarity, epithelial cell detachment, necrosis, granular (muddy brown) casts

three stages: inciting event --> maintenance (low urine) --> recovery
renal papillary necrosis
ischemic necrosis of the tips of the renal papillae

associated with: diabetes mellitus, acute pyelonephritis, chronic phenacetin use (acetaminophen is a phenacetin derivative), and sickle cell anemia
prerenal azotemia
decrease in renal blood flow (like hypotension) leads to decrease in GFR

Na/H2O and urea are retained by kidney

Urine osmolality is increased; urina sodium is <10; Fe Na is less than 1%; BUN/Cr ratio is greater than 20
Intrinsic renal (acute renal failure)
generally due to acute tubular necrosis or ischemia/toxins...patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubules...this leads to decreased GFR...urine has epithelial/granular casts
urine osmolality is <350, urine Na is > 20, Fe Na is greater than 2%; BUN/Cr ratio is less than 15
intrinsic renal stuff
Post renal
outflow obstruction (stones, BPH, neoplasia)

develops only with bilateral obstruction

urine osmolality is less than 350, urine Na is greater than 40, Fe Na is >4% and BUN/Cr ratio is greater than 15

(prerenal is greater than 20)
2 forms of renal failure
acute: often due to acute tubular necrosis

chronic: due to hypertension and diabetes
uremia
clinical syndrome marked by increase in BUN and increase in creatinine and associated symptoms
Consequences of renal failure
1. anemia (failure of EPO production)
2. renal osteodystrophy (failure of active vitamin D production)
3. hyperkalemia, which can lead to cardiac arrhythmias
4. metabolic acidosis due to decrease in acid secretion and decrease in generation of HCO3-
5. uremic encephalopathy
6. sodium and water excess which leads to CHF and pulmonary edema
7. chronic pyelonephritis
8. hypertension
Fanconi's syndrome
defect in proximal tubule transport of amino acids, glucose, phosphate, uric acid, protein and electrolytes

complications include rickets, osteomalacia, hypokalemia and metabolic acidosis

(proximal renal tubules...impaired resorption of glucose, amino acids, phosphate and bicarbonate)
Clinical manifestations of Fanconi syndrome
glycosuria, hyperphosphaturia and hypophosphatemia, aminoaciduria and sytemic acidosis
Coarse, asymmetric corticomedullary scarring
chronic pyelonephritis
Adult polycystic kidney disease
multiple, large bilateral cysts that ultimately destroy the parenchyma; presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure
AD mutation in APKD1
adult polycystic renal disease!
death from uremia or hypertension

associated with polycystic liver disease, berry aneurysms and mitral valve prolapse
PCKD
infantile polycystic kidney disease
infantile presentation in parenchyma

AR

asspociated with hepatic cysts and fibrosis
cortical and medullary cysts resulting from long-standing dialysis
dialysis cysts
benign, incidental finding...cortex only
simple cysts
Medullary cystic disease
medullary cysts

ultrasound shows small kidney

poor prognosis
Medullary sponge disease
collecting duct cysts

good prognosis

multiple small medullary cysts; impaired tubular function without renal failure
Disorientation, stupor, coma
low serum Na
Neurologic: irritability, delirium and coma
high serum Na
secondary to metabolic alkalosis, hypokalemia, hypovolemia and increase aldosterone
low serum Cl-
secondary to non-anion gap acidosis
high serum Cl-
U waves on ECG, flattened T waves, arrhythmias, paralysis
low serum K+
peaked T waves,wide QRS and arrhythmias
high serum K+
tetany, neuromuscular irritability
low serum calcium concentration
delirium, renal stones, abdominal pain, not necessarily calciuria
high serum Ca++
neuromuscular irritability, arrhythmias
low serum magnesium
delirium, decreased DTRs, cardiopulmonary arrest
high serum Mg++
Low mineral ion product causes bone loss, osteomalacia
low serum phosphate
High mineral ion product causes metastatic calcification, renal stones, met calcifications
high serum phosphate