Definitely on exam Flashcards
What is the most common form of idiopathic acute glomerulonephritis? What happens? What is key sign in this? _______ proliferation is _________
IgA nephropathy - IgA binds mesangial cells and causes proliferation of mesangial cells and causes pressure on vessel, making it smaller (reduced GFR) Key sign: Hematuria 24-48 hours after URI or viral gastroenteritis
-Mesangial proliferation is reversible
Virchow’s Triad
- venous stasis
- hypercoagulability
- endothelial injury
MOST COMMON CAUSE of acute glomerulonephritis, and what does it result in?
- membranous nephropathy (primary and secondary causes)
- primary: circulating antibodies are either deposited or fromed in situ on podocytes
- secondary: hepatitis, SLE, drugs, some canceres
- Results in: proteinuria and nephrotic syndrome
Remember nephrotic = massive proteinuria, hypoalbuminemia, hyperlipidemia, and edema - remember increase in lipids d/t low albumin stimulating liver to produce more lipoproteins
__________ ___________ is when immune complexes are in the mesangial matrix and lead to proliferation of mesangial cells. What is it associated with?
mesangial proliferation
-It is idiopathic or associated with IgA nephropathy, lupus nephritis, or diabetic nephropathy
Most common cause of acute renal failure in children? What is it associated with? What happens? What is the MOST important thing to know? What are the two major symptoms?
- Hemolytic-uremic syndrome
- Associated with bacterial or viral agents (E.coli)
- Arterioles of the glomerulus become swollen and occluded with fibrin clots
- Decreased GFR, damage to RBCs from narrowing of vessel lumen, acute hemolytic anemia occurs. TWO MAJOR SYMPTOMS: hematuria, proteinuria
- Tx: control HTN, hyperkalemia and seizures from toxin accumulation (dialysis maybe, fluids, blood transfusions)
-Most important: Child w/prodromal GI illness w/diarrhea that comes in w/bruising and purpura –> think about hemolytic uremic syndrome
Diagnostic tests for glomerulonephritis?
- CBC
- Biochemical blood analysis - BUN, creat, total protein, albumin, serum electrolytes, cholesterol, etc.
- Examination of the urine - red cells, red-cell casts, proteinuria
- ASO titer (anti streptolysine O) - to see if this is post-strep glomerulonephritis b/c this would mean + ASO titer
- kidney scan or biopsy
Tx for glomerulonephritis (nothing on slide bolded)
- antimicrobial therapy if there is an infection present
- loop diuretic therapy
- BP drugs to control HTN and statins to control high lipid levels
- Vasodilator drugs like hydralazine if needed
- Immunosuppressive agents - corticosteroids
- Anticoagulants to control fibrin crescent formation in rapidly progressive
Nephritis vs Nephrotic Syndrome (not bolded)
**REMEMBER that clinical manifestations of acute glomerulonephritis may be nephrotic, nephritic or both
- Nephrotic syndrome: massive proteinuria, hypoalbuminemia, hyperlipidemia (high lipids d/t lipoproteins being produced in liver as a result of low albumin levels). ONLY microscopic amounts of blood or no blood in urine.
- Nephritic syndrome: red cell casts, white cell casts (if these are present always think RENAL cause). Varying degrees of protein in urine but usually not severe.
Nephrotic Syndrome - what are some secondary causes? Also remember that with loss of proteins what happens?
- proteinuria, hypoalbuminemia, hyperlipidemia and EDEMA
- Just know that it can be PRIMARY or SECONDARY
- Secondary causes: DM, SLE, IgA nephropathy (Berger disease), drugs, malignancies, and vascular disorders
- remember that with loss of proteins you lose immunoglobulin and therefore have an increased susceptibility to infection ‘
- also remember loss of negative charge means loss of proteins
- also remember increase in ADH and aldosterone because decrease plasma oncotic pressure and decreased plasma volume
What is the first clinical manifestation of nephrotic syndrome?
Periorbital edema - if this appears, especially in children, always consider nephrotic syndrome
Nephritis syndrome
What can happen?
Tx and symptoms similar to nephrotic
- Characterized by microscopic hematuria with RBC casts
- Proteinuria is not severe
- HTN, uremia, and oliguria can occur
- Can co-occur w/nephrotic syndrome
- Associated with: infections, rapidly progressive, mesangial proliferative, IgA nephropathy, lupus nephritis, diabetic nephropathy
Most common secondary causes of chronic glomerulonephritis. Chronic usually starts with acute*
What is not effective in tx of chronic?
Onset?
DM and SLE
- onset usually 10-20 years after dx
- begins with renal insufficiency and progresses to nephrotic syndrome and then ESRD
- CORTICOSTEROIDS are NOT effective
What is the most common cause of chronic kidney disease and end-stage renal failure?
- Diabetic nephropathy - thickening and fibrosis of basement membrane (podocytes), expansion of mesangial matrix, epithelial cell changes
- You would not use immunosuppresive agents to tx like you would with lupus nephritis.
What causes osteoarthritis?
Loss and damage to articular cartilage, new bone formation (osteophytosis), changes in subchondral bone, MILD synovitis, thickening of joint capsule
-Inflammation causes destruction in these areas
What is the hallmark of OA?
-loss of proteoglycans = cartilage absorbs too much fluid and is less able to handle stress
-proteoglycans - stiff quality of articular cartilage (reduces friction), and regulates movement of synovial fluid through cartilage - acts as a pump, assuring there is always fluid through cartilage, even after prolonged weight bearing
-decrease use of joint = decrease in proteoglycans
-**OA causes an alteration of pumping action - cartilage absorbs TOO much fluid and becomes less able to withstand stress of weight bearing
