Chapter 33: Disorders of Renal Function Flashcards
Exam 2 (16 cards)
Calcium Stones (Oxalate or Phosphate)
Calcium stones are the most common type, making up 70-80% of all kidney stones. They often form in individuals with high levels of calcium in the blood, which can result from conditions like hyperparathyroidism.
Risk Factors: Consuming sweetened beverages can increase the risk, as these drinks may elevate calcium levels in the urine and eating a lot of antiacids
Magnesium Ammonium Phosphate Stones (Struvite)
Struvite stones are associated with alkaline (basic) urine and often develop in people with urinary tract infections (UTIs) caused by bacteria that produce ammonia and carbon dioxide by breaking down urea
Uric Acid Stones
Uric acid stones form in people with high levels of uric acid, such as those with GOUT or individuals who consume a diet high in purines (found in foods like red meat, shellfish, and organ meats).
Cystine Stones
Cystine stones are rare and typically found in children with a genetic disorder that affects cystine transport in the kidneys. This disorder is inherited in an autosomal recessive pattern, causing decreased reabsorption of cystine, which leads to stone formation.
Nephritic syndrome Pathophysiology
clinical manifestations of glomerular inflammation
-inflammatory process damages CAPILLARY WALL
* sudden onset of hematuria, oliguria, decreased GFR
acute post-infectious glomerulonephritis
immune response to group A beta hemolytic streptococci
-azotemia, oliguria, “coke-colored” urine
-hematuria
Nephrotic Syndrome Manifestations
Proteinuria
Lipiduria: damage to the glomerular basement membrane- increase permeability
nephrotic syndrome manifestations
Hyperlipidemia
Edema:
Increased Susceptibility to Infections & decreased colloidal osmotic pressure
Loss of Ions, Hormones, and Binding Proteins
nephrotic syndrome manifestations from damage to glomerular basement membrane
increased: permeability, protein in urine, lipids in blood and urine
decrease: protein in blood
results: edema, hyperlipidemia, increased infections, decreased ions and hormones
systemic causes of glomerulonephritis: lupus
-systemic lupus erythematosus
*type II immune complex-mediated disorder
*vasculitis and glomerulonephritis
*common complication: lupus nephritis
** deposition of immune complexes within glomerular wall
systemic causes of glomerulonephritis: diabetic nephropathy (diabetic glomerulosclerosis)
-major cause of CKD
-most common cause of kidney failure resulting in dialysis
-thickening of glomerular capillary basement membrane
possible mech:
-defective GBM synthesis
-increased blood glucose causing increase GFR, glomerular pressure, enlarged glomerular capillary pores
**angiotensin II
microalbuminuria
-30-300 mg of albumin in urine Q 24 hours
-dysuria, increased urinary frequency, urgency
acute pylenonephritis
bacterial infection of kidney parenchyma and renal pelvis
acute pylenonephritis causative agen
gram negative bacteria
-E. coli, proteus, klebsiella
acute pylenonephritis two routes
-* ascending infection from lower urinary tract
-blood stream: SEPSIS caused by STAPHYLOCOCCUS AUREUS or infective endocarditis
acute pylenonephritis patho
outflow obstruction + incompetence of vesicoureteral orifice
-vesicoureteral reflux
acute pylenonephritis: manifestations
abrupt onset of shaking, chills, fever, constant ache in lower back
-unilateral or bilateral pain
-maliase, N/V, abdominal pain
-lower urinary tract symptoms: dysuria, increased urinary frequency, urgency