PATH - General Flashcards
Potter sequence (syndrome)
Oligohydramnios–>compression of
developing fetus–>limb deformities, facial anomalies (eg, low-set ears and
retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs–>pulmonary hypoplasia (cause of death).
POTTER sequence associated with: Pulmonary hypoplasia Oligohydramnios (trigger) Twisted face Twisted skin Extremity defects Renal failure (in utero)
“Babies who can’t “Pee” in utero develop Potter sequence”
Multicystic cystic dysplastic kidney
Ureteric bud fails to induce differentiation of metanephric mesenchyme–>nonfunctional kidney consisting of cysts and connective tissue.
Often diagnosed prenatally via ultrasound.
Renal tubular acidosis
A disorder of the renal tubules that leads to normal anion gap (hyperchloremic) metabolic acidosis.
Distal renal tubular acidosis (type 1)
Urine pH > 5.5
Defect in ability of α intercalated cells to secrete H+–>no new HCO3− is
generated–>metabolic acidosis
Associated with *hypokalemia, INC risk for calcium phosphate kidney stones
Proximal renal tubular
acidosis (type 2)
Urine pH INC excretion of HCO3− in urine and
subsequent metabolic acidosis
Associated with *hypokalemia, risk for hypophosphatemic rickets.
Hyperkalemic renal tubular acidosis (type 4)
Urine pH *hyperkalemia–>DEC NH3 synthesis in PCT–>DEC NH4+
excretion.
Casts in urine
Presence of casts indicates that hematuria/pyuria is of glomerular or renal tubular origin
RBC casts
Glomerulonephritis, malignant hypertension.
WBC casts
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
Fatty casts (“oval fat bodies”)
Nephrotic syndrome.
Associated with “Maltese cross” sign.
Granular (“muddy brown”) casts
Acute tubular necrosis
Waxy casts
End-stage renal disease/chronic renal failure
Hyaline casts
Nonspecific, can be a normal finding, often seen in concentrated urine samples
Hydronephrosis
Distention/dilation of renal pelvis and calyces
Usually caused by urinary tract obstruction, other causes include retroperitoneal fibrosis,
vesicoureteral reflux
Serum creatinine becomes
elevated only if obstruction is bilateral or if patient has only one kidney
Leads to compression and
possible atrophy of renal cortex and medulla
Stress incontinence
Outlet incompetence–>leak with INC intra-abdominal pressure (sneezing, lifting)
Urgency incontinence
Overactive bladder–>leak with urge to void immediately
Mixed incontinence
Features of both stress and urgency incontinence
Overflow incontinence
Incomplete emptying–>leak with overfilling
INC postvoid residual (urinary retention) on catheterization or ultrasound
Urinary tract infection
acute bacterial cystitis
Inflammation of urinary bladder.
Presents as suprapubic pain, dysuria, urinary frequency, urgency.
Systemic signs are usually absent
-E coli (most common).
-Staphylococcus saprophyticus—seen in sexually active young women
-Klebsiella.
-Proteus mirabilis—urine has *ammonia scent.
Acute pyelonephritis
Affects *cortex with relative sparing of glomeruli/vessels.
Neutrophils infiltrate renal interstitium
Presents with fevers, flank pain (costovertebral angle tenderness), nausea/vomiting, chills
Complications include chronic pyelonephritis, renal papillary necrosis, perinephric abscess,
urosepsis.
Chronic pyelonephritis
result of recurrent episodes of acute pyelonephritis
Coarse, asymmetric corticomedullary scarring, blunted calyx.
Tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney).
Diffuse cortical necrosis
Acute generalized cortical infarction of *both kidneys.
Likely due to a combination of vasospasm and DIC.
Associated with obstetric catastrophes (abruptio placentae), septic shock
Renal osteodystrophy
Hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic renal disease–>2° hyperparathyroidism
Causes subperiosteal thinning of bones
Acute kidney injury
acute renal failure
an abrupt decline in renal function as measured by INC creatinine and INC BUN.
