Sweep 1.4 Flashcards
some lung tumors can produce
ADH, ACTH, PTH (looks like parathyroid tumor)
• Pneumoconioses- a group of lung disorders caused by ———————–
inhalation of dusts; size, shape and conc. of particles are important factors and particles induce scarring
Pneumoconiosis: Coal workers-
nodular/diffuse fibrosis with coal macules; progressive massive fibrosis
Pneumoconiosis: o Silicosis-
most prevalent occupational disease in world – due to inhalation of silicone.
• Interstitium- formed by
collagen and blood vessels between tubules and glomeruli
Azotemia- elevation of ————– due to decreased —————-
blood urea nitrogen and creatinine levels
filtration of blood through the glomeruli (decreased glomerular filtration rate)
• Uremia- association of ———– with clinical signs and symptoms, including ——————–
azotemia
gastroenteritis, peripheral neuropathy, pericarditis, dermatitis, hyperkalemia and metabolic acidosis
o Acute nephritic syndrome: results from
glomerular injury and is characterized by acute onset of hematuria, mild to moderate proteinuria, azotemia and hypertension
o Nephrotic syndrome:
glomerular syndrome characterized by heavy proteinuria (>3.5g/day), hypoalbuminemia, severe edema, hyperlipidemia and lipiduria
o
Acute renal failure: sudden onset of
azotemia with oliguria/anuria
• Autosomal dominant (adult) polycystic kidney disease-
o Clinically-
1/500 people; characterized by multiple expanding cysts in both kidneys; gradual onset of renal failure in adult, hematuria, pain in flank around 4th decade, hypertension and UTIs; BIG KIDNEYS
• Autosomal dominant (adult) polycystic kidney disease- o Etiology-
defective gene is PKD1→ encodes polycystin-1
• Autosomal dominant (adult) polycystic kidney disease- o Extrarenal pathology-
1/3 of pts have cysts in liver, aneurysms may develop in circle of Willis
• Autosomal dominant (adult) polycystic kidney disease- o Histopathology-
cysts arise from all levels of nephron
• Autosomal recessive (childhood) polycystic kidney disease-
o Clinicaly-
rare; renal failure develops from infancy to several years of age; due to mutation in PKHD1 gene (defective protein)
• Autosomal recessive (childhood) polycystic kidney disease- o Extrarenal pathology-
liver cysts and progressive liver fibrosis
• Autosomal recessive (childhood) polycystic kidney disease- o Pathology-
numerous small uniform-size cysts from collecting tubules in cortex and medulla
o Mechanisms of glomerular injury-
immune complex deposits in glomerular basement membrane or mesangium, can be circulating immune complexes, or autoantibodies to glormerular components
o Path evaluation of kidney biopsies- PAS, trichrome and Jones stain
• Immunofluorescence- looking for immune deposits
• Electron microscopy- ID of immune complexes, cell and basement membrane morphological changes
o Nephrotic syndrome- heavy proteinuria, hypoalbuminemia, severe edema; caused by increase glomerular capillary permeability to plasma proteins
o Mechanisms of glomerular injury-
immune complex deposits in glomerular basement membrane or mesangium, can be circulating immune complexes, or autoantibodies to glormerular components
o Path evaluation of kidney biopsies-
PAS, trichrome and Jones stain
Path eval of kidney biopsies: • Immunofluorescence- looking for
immune deposits
Path eval of kidney biopsies• Electron microscopy-
ID of immune complexes, cell and basement membrane morphological changes
Path eval of kidney biopsies: o Nephrotic syndrome-
heavy proteinuria, hypoalbuminemia, severe edema; caused by increase glomerular capillary permeability to plasma proteins
• Minimal change disease- most common cause of
nephrotic syndrome in children
Minimal change disease: o Path-
normal appearing glomeruli by light microscopy, no immune complexes; USE EM to see epithelial foot processes
Minimal change disease: o Therapy-
good response to corticosteroid therapy
• Focal and segmental glomerulosclerosis-
fibrotic change going on; common cause of nephrotic syndrome in adults; may be idiopathic or secondary to other glomerular diseases, scarring
• Focal and segmental glomerulosclerosis-
o Path-
segmental sclerosis of some glomeruli characterized by increased mesangial matrix collagen with obliteration of capillary loops
• Focal and segmental glomerulosclerosis-
o Therapy-
poor response to corticosteroid treatment- renal failure in 50% after 10 yrs
• Membranous nephropathy (glomerulonephritis)- most common in adults age ———–; may be
30-50yrs
primary and limited to kidney or secondary to infection malignancy, SLE (systemic lupus erethemat) or drugs
Membranous nephropathy: o Path-
immune complexes in the epithelial side of GBM demonstrable by immunofluorescence and EM
Membranous nephropathy: o Therapy-
poor roseponse to corticosteroid treatment with 40% developing renal failure in 2-20 yrs
• Glomerular disease in diabetes mellitus-
minimal proteinuria progresses over 10-15 yrs to severe proteinuria
Glomerular Disease in diabetes mellitus: o Path-
thick glomerular basement membranes, diffuse increase in mesangial matrix and formation of mesangial nodules (the latter is nodular glomerulosclerosis or Kimmelstiel-Wilson lesion).
Nephritic Syndrome: • Characterized by
acute onset of hematuria, oliguria/azotemia, and hypertension
Nephritic Syndrome: • Proliferation of cells within ——— accompanied by ————→severe capillary wall injury, results ————–
glomeruli
inflammatory cells
in blood passing into urine as well as GFR
Acute postinfectious (poststrep.) glomerulonephritis- common to occur soon after
S. pharyngitis infection
Acute postinfectious (poststrep.) glomerulonephritis o Path-
proliferation of endothelial and mesangial cells with neutrophil infiltrate; immune complexes in GBM and mesangium
Acute postinfectious (poststrep.) glomerulonephritis • Progression to chronic renal disease in more likely in
adults
• IgA Nephropathy-
usually in children and young adults; hematuria 1-2 days after non-specific upper respiratory tract viral infection
IgA Nephropathy: o Path- increased
IgA, can lead to Henoch-Schönlein purpura; mesangial deposition of immune complex with IgA, occasionally crescent epithelial cell proliferation (push glomerular tuft off to the side)
• Crescentic/Rapidly Progressive Glomerulonephritis-
acute clinical syndrome, progressive loss of renal function, severe oliguria; death from renal failure in weeks to months if untreated
Crescentic/Rapidly Progressive Glomerulonephritis: o Path-
crescentic glomerulonephritis due to proliferation of epithelium with histiocyte infiltration
Crescentic/Rapidly Progressive Glomerulonephritis: • Several different disorders-
Anti-GBM antibody disease (12% of cases), Immune complex disease (44% of cases), Pauci-immune, lack of anti-GBM or immune complexes (44% of cases)
Crescentic/Rapidly Progressive Glomerulonephritis: o May be associated with
antibodies directed against a glomerular basement antigen
Chronic (End-Stage) Renal Disease-
• Loss of ———– leading to ————,
glomeruli and tubules
fibrosis
Chronic renal disease:
damaged glomeruli become completely sclerotic (global sclerosis)→ adaptive changes→injury and progressive renal failure
Chronic renal disease: o Routine exam-
proteinuria, hypertension or azotemia
chronic renal disease: o Therapy-
without treatment→ poor prognosis, renal dialysis and kidney transplant necessary for patient survival
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • ——————– of kidney and renal pelvis caused by —————————
Suppurative inflammation
bacterial infection, affects tubules, interstitium and pelvis→typically secondary to bacterial infection
Acute Pyelonephritis- aka Tubulointerstitial nephritis
o Infection from urinary bladder→
renal pelvis and kidney
Acute Pyelonephritis- aka Tubulointerstitial nephritis: o Less common route in infection→
hematogenous spread of bacteria
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Predisposing conditions-
female, pregnant, immunosuppressed, diabetes mellitus
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Clinically-
sudden onset of pain at costovertebral angle and systemic infection, dysuria, frequency and urgency
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Path-
patchy insterstitial tubular neutrophilic inflammation
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Etiology-
predisposing conditions
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Prognosis-
repeated bouts of acute inflammation of continuous inflammation may lead to chronic pyelonephritis
chronic pyelonephritis: o Characterized by
mononuclear inflammatory infiltration and irregular scarring
Drug- Induced Interstitial Nephritis-
• Path-
hypersensitivity to drugs; interstitial infiltration of mononuclear inflammatory cells; often with neutrophils and eosinophils; granulomas may be present NO GLOMERULI INVOLVEMENT; large doses of analgesics may lead to interstitial nephritis with papillary necrosis
Acute Tubular Necrosis-
• Clinical-
rapid onset of renal failure, reduced urine output, electrolyte imbalances, reversible over a period of wks as damaged tubular epithelium regenerates
Acute Tubular Necrosis- • Etiology-
injury to tubular epithelial cells from ischemia or a toxin
Acute Tubular Necrosis- • Pathology-
dilation of tubules, interstitial edema, necrosis of epithelium
Acute Tubular Necrosis- • Treatment-
dialysis, supportive care
Acute Tubular Necrosis- • Prognosis-
full recovery unless preexisting kidney disease
• Arterionephrosclerosis- contributing factors are —————, may lead to —————-
hypertension and diabetes
gradual onset of chronic renal failure
Arterionephrosclerosis: o Path-
kidneys are symmetrically atrophic with moderate reduction in size, kidney surface has an even fine granularity and cortex is thin
Arterionephrosclerosis: o Histopathology-
narrowing of lumen of arterioles and arteries caused by hyaline type of arteriolosclerosis
Arterionephrosclerosis: • Clinic:
- Tubular atrophy and interstitial fibrosis
* Global sclerosis of glomeruli
• Arterionephrosclerosis associated with
malignant hypertension
Arterionephrosclerosis
o Clinical-
relatively rapid onset of renal failure with increased intracranial pressure leading to headache, nausea, vomiting and visual impairment
o
Arterionephrosclerosis
Path-
arterioles show hyperplastic arteriolosclerosis, reducing blood flow and causing necrosis of glomeruli
• Thrombotic Microangiopathies-
Defect:
o TTP- acquired defect in ADAMTS13
• Widespread involvement of other organs in
TTP
Thrombotic microangiopathies: o HUS-
endothelial cell injury due to Shiga-toxin from E. coli or Shigella→ platelet activation
• Renal involvement predominates; occurs most often in children
Thrombotic microangiopathies
o Path-
similar in both disorders with microthrombus formation in capillaries
————-; may form ———- of pelvis and calyceal system
staghorn calculi”
cast
Types of stones-
• Magnesium ammonium phosphate-
pts have persistently alkaline urine; infection proteus predisposes to these stones
Types of stones-
• Uric acid- occur in
pts with gout, leukemia (high cell turnover) or persistently acid urine
