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Questions and Answers
What is the primary cause for acute postinfectious glomerulonephritis (APIGN)?
Which condition is referred to as lupus nephritis?
What physiological change occurs due to glomerular inflammation?
What immediate effect does obstruction in the glomeruli have?
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Which symptom is associated with the loss of protein due to nephritis?
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What is the role of antibody-antigen complexes in glomerular nephritis?
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Which organism is NOT associated with acute postinfectious glomerulonephritis?
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What is a primary effect of decreased glomerular filtration rate (GFR)?
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What is one of the main consequences of the formation of antigen-antibody complexes in the kidneys?
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Which cell types are predominantly involved in the inflammatory response of glomerular injury?
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What is a defining characteristic of chronic glomerulonephritis?
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What is the relationship between systemic lupus erythematosus (SLE) and lupus nephritis?
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Which populations are reported to be at higher risk for developing lupus nephritis?
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What is a major clinical feature of antiglomerular basement membrane disease?
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What is the role of plasmapheresis in the treatment of anti-GBM disease?
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Which factor is NOT associated with the development of nephritis?
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What common sign is associated with lupus nephritis?
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What is typically observed in the kidneys of patients with chronic glomerulonephritis?
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Which condition is known to potentially trigger the development of anti-GBM disease?
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What effect does nephritis have on sodium and water retention?
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Which of the following is a consequence of the slow, progressive destruction of the glomeruli in chronic glomerulonephritis?
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Which clinical manifestation is indicative of severe hypertension resulting from nephritis?
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Which of the following therapies is commonly used to address sodium and water retention in nephritis?
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What symptom is associated with encaphalopathy resulting from acute hypertension in nephritis patients?
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Which treatment is appropriate for managing acute inflammation and progressive edema in nephritis?
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Which clinical manifestation suggests a presence of infection in a patient with nephritis?
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Which of the following symptoms is least likely to be associated with acute postinfectious glomerulonephritis?
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What primarily contributes to the increase in edema associated with acute glomerulonephritis?
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Which symptom indicates the progression of acute glomerulonephritis to a more severe condition?
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The presence of head pain, nausea, and vomiting may indicate what serious complication of acute glomerulonephritis?
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What is a key time frame for the onset of symptoms after the initial infection in acute postinfectious glomerulonephritis?
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Which symptom is most indicative of acute glomerulonephritis progressing to pulmonary edema?
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What color is the urine typically associated with acute postinfectious glomerulonephritis?
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Which of the following is a consequence of sodium and water retention in acute postinfectious glomerulonephritis?
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Which clinical manifestation is commonly associated with severe hypertension in nephritis patients?
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Which sign suggests increased intracranial pressure in a patient with acute glomerulonephritis?
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Which symptom is least likely to indicate the onset of acute postinfectious glomerulonephritis?
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Which therapeutic approach is typically used to manage moderate edema in nephritis patients?
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Which symptom is NOT typically linked to the presence of infection in nephritis?
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What dietary change is recommended for patients experiencing sodium and water retention due to nephritis?
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Which of the following treatments may be used in an emergency for severe hypertension in nephritis patients?
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Study Notes
Nephritis
- Inflammation of the kidneys
- Classified based on location or cause
Glomerulonephritis
- Inflammation of the glomerular capillary membrane
- Types include:
- Acute postinfectious glomerulonephritis (APIGN)
- Lupus nephritis
Acute Postinfectious Glomerulonephritis (APIGN)
- May develop after infection with:
- Group A beta-hemolytic streptococci (impetigo or strep throat)
- Staphylococcus
- Pneumococcus
- Coxsackie virus
Lupus Nephritis
- Occurs in patients with systemic lupus erythematosus (SLE)
- Autoimmune attack on the kidneys
- Accounts for 37-45% of SLE cases
- More common in Black, Hispanic, and Asian populations
Pathophysiology
- Antibody-antigen complexes deposit in the glomerular capillary wall
- Triggers inflammation and obstruction
- Glomerular membranes thicken
- Decreases glomerular filtration rate (GFR)
- Increased vascular permeability leads to protein and red blood cell loss in urine
- Fluid and sodium retention causes edema
- This process is known as acute proliferative glomerulonephritis
Chronic Glomerulonephritis
- End stage of other glomerular disorders:
- Rapidly progressive glomerulonephritis (RPGN)
- Lupus nephritis
- Diabetic nephropathy
- Slow and progressive glomerular destruction
- Gradual decline in renal function
- Kidneys decrease in size and become granular
- Nphrons are lost
Antiglomerular Basement Membrane Disease (Anti-GBM Disease)
- Autoantibodies attack the lungs and kidneys
- Early recognition and treatment are critical for prognosis
- Genetic susceptibility and environmental factors contribute to development
Diagnosis of Anti-GBM Disease
- Based on:
- Symptoms
- Physical examination
- Laboratory findings
- Kidney biopsy
- Chest x-ray
Treatment of Anti-GBM Disease
- Plasmapheresis to remove antibodies
- Immunosuppression
Etiology
- Each type of nephritis has a distinct cause
- Lupus nephritis: Autoimmune disorder (SLE)
- Glomerulonephritis: Infection, diabetes mellitus, or SLE
- Tubulointerstitial nephritis: Injury to renal tubules and interstitium (drugs, toxins, radiation)
Risk Factors
- Diabetes mellitus and hypertension due to vascular damage
- Infections
- Drug abuse
- Chronic overuse of analgesics
- SLE (more frequent in Black populations, earlier onset, and more severe in Black, Hispanic, and Asian populations)
- Premature birth
- Trauma
- Family history of kidney disease
- Conditions like SLE, sickle cell disease, AIDS, and congestive heart failure
Prevention
- Exact cause is unknown
- Reduce risk by:
- Practicing good hygiene (to prevent viral infections)
- Managing diabetes and blood pressure
- Quitting smoking
- Maintaining a healthy weight
Glomerulonephritis
- Onset: Can be insidious with microscopic hematuria and proteinuria resolving on its own.
- Abrupt onset: Pain, fever, tiredness, facial puffiness.
- Progressive: Increased edema, shortness of breath, decreased urination, hypertension.
- Acute postinfectious glomerulonephritis: Occurs 10 - 14 days after infection, characterized by hematuria, proteinuria, sodium/water retention, and azotemia.
- Urine Appearance: Often brown or cola-colored.
- Sodium and Water Retention: Leads to hypertension and edema.
- Edema: Primarily in the face, especially around the eyes.
- Other Manifestations: Fatigue, anorexia, nausea, vomiting, headache.
Clinical Manifestations and Therapies
-
Sodium and Water Retention, Hypertension, Mild to Moderate Edema:
- Therapies: Diuretics, antihypertensives, sodium restriction, low-protein diet.
-
Severe Hypertension (Extremely High Blood Pressure with Cerebral Dysfunction:
- Therapies: Emergency care with IV diazoxide, hydralazine, or Labetalol.
-
Progressive Edema, Acute Inflammatory Processes (Ascites, Pulmonary Effusion):
- Therapies: Immunosuppressive therapy (cyclophosphamide, azathioprine), corticosteroids, sodium restriction.
-
Encephalopathy Resulting from Acute Hypertension (Headache, Nausea and Vomiting, Irritability):
- Therapies: Antihypertensives, analgesics, additional therapies.
-
Presence of Infection (Sodium and Water Retention, Fever, Malaise, Edema):
- Therapies: Antibiotics, bedrest, sodium restriction, antipyretics.
Acute Glomerulonephritis
- Signs and symptoms:
- Insidious onset with microscopic hematuria and proteinuria
- Abrupt onset of pain, fever, tiredness, and facial puffiness
- Increased edema, particularly in lower legs and ankles
- Shortness of breath due to pulmonary edema
- Decreased urination
- Acute hypertension (HTN) with headache, nausea, and vomiting
- Acute postinfectious glomerulonephritis:
- Occurs 10 to 14 days after infection
- Characterized by hematuria, proteinuria, sodium and water retention, and azotemia (high blood nitrogen levels)
- Urine often appears brown or cola-colored
Clinical Manifestations and Therapies for Nephritis
-
Sodium and water retention, HTN, and Mild to moderate edema:
- Treatment includes:
- Diuretics
- Antihypertensives
- Sodium restriction
- Low-protein diet
- Treatment includes:
-
Severe HTN (extremely high blood pressure with cerebral dysfunction)
- Treatment includes:
- Emergency care with IV diazoxide, hydralazine, or labetalol
- Treatment includes:
-
Progressive edema, acute inflammatory processes (ascites and pulmonary effusion)
- Treatment includes:
- Immunosuppressive therapy (cyclophosphamide, azathioprine)
- Corticosteroids
- Sodium restriction
- Treatment includes:
-
Encephalopathy resulting from acute HTN (headache, nausea, vomiting, and irritability)
- Treatment includes:
- Antihypertensives
- Analgesics
- Additional therapies as needed
- Treatment includes:
-
Presence of infection (sodium and water retention, fever, malaise, edema)
- Treatment includes:
- Antibiotics
- Bedrest
- Sodium restriction
- Antipyretics
- Treatment includes:
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Description
This quiz covers the essentials of nephritis and its specific type, glomerulonephritis. Learn about their classifications, causes, and pathophysiology. Delve into acute postinfectious glomerulonephritis and lupus nephritis, including their effects on kidney function.