Pathology Questions Flashcards
Name the renal syndrome:
Results from glomerular injury and is dominated by the acute onset of gross hematuria and RBC casts, mild proteinuria, azotemia, edema, and HTN.
Nephritic Syndrome
What is the classic disease that presents with Nephritic Syndrome?
PSGN Post-Streptococcal Glomerulonephritis
Name the renal syndrome: Glomerular syndrome characterized by heavy proteinuria (>3.5 g/day), hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria.
Nephrotic Syndrome
Name the Renal Syndrome: Associated with severe glomerular injury, and results in acute kidney failure within days/weeks. Manifested by microscopic hematuria, dysmorphic RBCs and RBC casts, and mild to moderate proteinuria.
Rapidly Progressive Glomerulonephritis
Name the renal syndrome: Recent onset of oliguria/anuria, and azotemia (elevated BUN). Can result from Pre-renal, Intra-renal, or Post-renal causes.
Acute Kidney Injury
Name the renal syndrome: Bacteruria and pyuria. Pain with urination.
UTI Can involve only the lower urinary tract or the kidney (pyelonephritis) or the bladder (cystitis)
Name the renal syndrome: Gradual increase in plasma creatinine levels over time, to greater than 50% of baseline.
Chronic Kidney Injury
Name the renal syndrome: Hematuria with no RBC casts. Hypercalcuria.
Nephrolithiasis
What is the main prognostic indicator of a nephrotic syndrome?
Degree of proteinuria
How do you treat Nephrotic syndromes?
Depends on whether it is a primary syndrome or secondary to systemic disease. Primary: CORTICOSTEROIDS, immunosuppression SECONDARY: Treat the underlying cause: HTN, diabetes, etc… cause they won’t respond to steroids or immune suppression.
Immune deposits in the _________ layer of the glomerulus produces Nephrotic syndrome symptoms.
SubEPIthelium. Example: Membranous Nephropathy
What glomerular disease is weird, in that it deposits Subepithelially but produces a Nephritic syndrome? How does it do this?
Post-Streptococcal Glomerulonephritis Originally deposits in the subdendothelium and mesangium, eliciting an immune response and causing damage, but late in the disease, deposits in the subEPIthelium.
T/F: Subepithelial immune complex deposits occur post-infection of some sort.
TRUE! Membranous Nephropathy: 80% are because of autoantibodies against podocytes, and the rest are due to Hep B, syphillis, etc…. Post-Strep Glomerulonephritis (self-explanatory)
Subendothelial and mesangial deposits occur how? Do they present with nephrotic or nephritic syndrome?
Circulating immune complex deposition or in situ immune complex formation. Subendothelial and mesangial deposits cause a nephritic syndrome.
Which part of the GBM is mostly responsible for the filtration SIZE barrier?
Lamina Densa
Which part of the GBM is responsible for the CHARGE barrier to filtration?
Lamina Rara Interna (negatively charged… keeps albumin in the capillaries. Albumin is small enough to filter otherwise)
Which filters easier, a + charged ion or a (-) charged ion?
+ ions are attracted to the - charge of the GBM and filter easier.
How are crescents formed?
Proliferation of the parietal cells of Bowman’s capsule, and the infiltration of Bowman’s space by macrophages/monocytes.
Rapidly progressive glomerulonephritis (RPGN) is a SYNDROME not a specific disease. It is characterized by what?
Progressive loss of renal function, nephritic characteristics, and severe oliguria. CRESCENTS in the glomeruli
What types of RPGN are curable?
RPGN can arise from many glomerular diseases. It can be cured via PLASMAPHORESIS in the case of Anti-GBM Goodpasture’s Wegener’s (ANCA) RPGN due to immune complex deposition does not respond to plasmaphoresis.
The most common cause of death from lupus is….
Renal Failure
A 3 year old boy presents with sudden onset of irritability, weakness, pallor, and oliguria. His mom says he had a stomach virus a week ago, with bloody diarrhea. Physical exam indicates hepatosplenomegaly, dehydration, and blood test revealed thrombocytopenia and schistocytes. What does he have?
Hemolytic Uremic Syndrome
Describe the 2 types of Hemolytic Uremic Syndrome.
Acquired: Kids under 5 with E.coli H7:O157 GI infections. SHIGA TOXIN. The glomerular epithelium has receptors for Shiga toxin, and its binding causes injury and activation: little clots! 10% inherited: Aquired mutation in Factor H (complement regulator). In these patients a minor endothelial injury results in uncontrolled complement activation. ATYPICAL HUS
Finding microangiopathic hemolytic anemia and thrombocytopenia in a older adult with no other explanation for them = what diagnosis? How do you treat them?
Thrombotoc Thrombocytopenic Purpura TTP= ADAMTS13 deficiency (via lack of enzyme or antibody to it) Treat with PLASMAPHORESIS
