Nephrology and Respiratory Quiz
58 Questions
1 Views

Choose a study mode

Play Quiz
Study Flashcards
Spaced Repetition
Chat to lesson

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

Which symptom is most characteristic of nephrotic syndrome?

  • Hematuria
  • Oliguria
  • Hypertension
  • Massive proteinuria >3.5 g/24 hrs (correct)

    • What is the most common cause of primary glomerulonephritis?

  • Minimal change disease
  • IgA nephropathy (Berger disease) (correct)
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy

    • Which of the following is associated with nephritic syndrome?

  • Periorbital edema
  • Dysmorphic RBCs in urine (correct)
  • Hyperlipidemia
  • Frothy urine with fatty casts

    • What is a common clinical manifestation of nephrotic syndrome?

    <p>Frothy urine</p> Signup and view all the answers

    What is the primary underlying cause of nephrotic syndrome?

    <p>Podocyte damage</p> Signup and view all the answers

    Which type of glomerulonephritis is often associated with respiratory tract infections?

    <p>IgA nephropathy (Berger disease)</p> Signup and view all the answers

    Which of the following features best describes nephritic syndrome?

    <p>Oliguria</p> Signup and view all the answers

    Which laboratory finding is most indicative of nephritic syndrome?

    <p>Presence of acanthocytes in urine</p> Signup and view all the answers

    What type of immune response is primarily involved in infection-related glomerulonephritis?

    <p>Type 3 hypersensitivity</p> Signup and view all the answers

    Which condition is characterized by a rapid decline in renal function and often presents with hematuria?

    <p>Goodpasture syndrome</p> Signup and view all the answers

    What indicates acute respiratory acidosis on an arterial blood gas (ABG)?

    <p>Decreased pH and increased PaCO2</p> Signup and view all the answers

    What is the formula used to calculate HCO3- in acute respiratory acidosis?

    <p>HCO3- = (24) + \[(PaCO2 - 42)/10\]</p> Signup and view all the answers

    Which condition primarily causes chronic respiratory alkalosis?

    <p>Pulmonary embolism during pregnancy</p> Signup and view all the answers

    What is the normal range for arterial blood gas pH?

    <p>7.35-7.45</p> Signup and view all the answers

    Which of the following represents a potential cause of acute respiratory acidosis?

    <p>CNS infections</p> Signup and view all the answers

    What effect does an increase in PaCO2 have on blood pH?

    <p>Decreases pH</p> Signup and view all the answers

    Which of the following is NOT a metabolic component in acid-base balance?

    <p>Carbon dioxide (CO2)</p> Signup and view all the answers

    What happens to bicarbonate (HCO3-) in acute respiratory alkalosis?

    <p>Decreases by 2 mmol for each PaCO2 10 mg below 42</p> Signup and view all the answers

    Which condition can cause severe magnesium deficiency?

    <p>Licorice ingestion</p> Signup and view all the answers

    What is the normal range of HCO3- in arterial blood gas results?

    <p>22-26 mEq/L</p> Signup and view all the answers

    Which clinical manifestation is NOT typically associated with Alport syndrome?

    <p>Hypertension</p> Signup and view all the answers

    What is a common light microscopy finding in diffuse proliferative glomerulonephritis?

    <p>Wire looping of capillaries</p> Signup and view all the answers

    Which type of immunofluorescence finding is associated with membrano-proliferative glomerulonephritis?

    <p>Granular pattern</p> Signup and view all the answers

    What is a typical cause of rapidly progressive glomerulonephritis?

    <p>Autoimmune diseases</p> Signup and view all the answers

    Which medication is NOT commonly associated with acute interstitial nephritis?

    <p>Corticosteroids</p> Signup and view all the answers

    What does electron microscopy reveal in Alport syndrome?

    <p>Irregular thinning of GBM</p> Signup and view all the answers

    What is a hallmark finding in light microscopy for acute interstitial nephritis?

    <p>No changes in the glomerulus</p> Signup and view all the answers

    Which of the following conditions commonly results in postrenal acute kidney injury?

    <p>Benign prostatic hyperplasia</p> Signup and view all the answers

    What is the primary purpose of corticosteroids in the treatment of tubulointerstitial disorders?

    <p>To address underlying autoimmune processes</p> Signup and view all the answers

    What laboratory finding is usually associated with acute interstitial nephritis?

    <p>Increased creatinine</p> Signup and view all the answers

    What characteristic finding on renal ultrasound may be observed in acute interstitial nephritis?

    <p>Increased echogenicity</p> Signup and view all the answers

    Which mechanism is primarily implicated in analgesic nephropathy?

    <p>Toxin-induced ischemia</p> Signup and view all the answers

    What is the mechanism of injury in rapidly progressive glomerulonephritis related to Goodpasture syndrome?

    <p>Type II hypersensitivity reaction</p> Signup and view all the answers

    In conditions of postrenal acute kidney injury, what is a common cause of urinary flow obstruction?

    <p>Ureteral stones</p> Signup and view all the answers

    What is the likely cause of metabolic acidosis when bicarbonate loss exceeds net acid excretion?

    <p>Renal tubular acidosis</p> Signup and view all the answers

    Which anion gap condition is characterized by a decrease in bicarbonate accompanied by Cl-?

    <p>Normal anion gap metabolic acidosis</p> Signup and view all the answers

    What is the effect of carbonic anhydrase inhibitors like acetazolamide?

    <p>Decrease bicarbonate reabsorption</p> Signup and view all the answers

    Which condition can lead to high anion gap metabolic acidosis?

    <p>Ketoacidosis</p> Signup and view all the answers

    What is increased with each 1g/dL decrease in serum albumin concentration concerning corrected anion gap?

    <p>2.5 mmol/L</p> Signup and view all the answers

    Which of the following is a common adverse effect of thiazide diuretics like hydrochlorothiazide?

    <p>Hypotension</p> Signup and view all the answers

    What is the primary action site of loop diuretics like furosemide?

    <p>Thick ascending loop of Henle</p> Signup and view all the answers

    An increase in urinary anion gap (UAG) typically indicates which of the following?

    <p>Decreased renal ammonium excretion</p> Signup and view all the answers

    Which diuretic agent primarily functions by antagonizing aldosterone receptors?

    <p>Spironolactone</p> Signup and view all the answers

    Under what condition is the anion gap calculated as Na+ minus (Cl- + HCO3-)?

    <p>While identifying metabolic acidosis</p> Signup and view all the answers

    What is a common cause of normal or non-anion gap metabolic acidosis elucidated by HARDASS?

    <p>Addison's disease</p> Signup and view all the answers

    Which electrolyte imbalance is most likely to occur in patients taking potassium-sparing diuretics?

    <p>Hyperkalemia</p> Signup and view all the answers

    During which phase of kidney processing does mannitol largely exert its effects?

    <p>Proximal convulated tubule</p> Signup and view all the answers

    Which of the following is NOT a common adverse effect of loop diuretics?

    <p>Hyperuricemia</p> Signup and view all the answers

    What is a key characteristic of asymptomatic bacteriuria?

    <p>Detection during unrelated screening</p> Signup and view all the answers

    Which of the following symptoms is primarily associated with uncomplicated cystitis?

    <p>Suprapubic discomfort</p> Signup and view all the answers

    What is a common urinary analysis finding in cases of pyelonephritis?

    <p>Leukocyte casts</p> Signup and view all the answers

    Which treatment is contraindicated during the first trimester of pregnancy for urinary tract infections?

    <p>Sulfonamides</p> Signup and view all the answers

    What is the primary goal in treating men with a urinary tract infection?

    <p>Eradicating prostatic infection</p> Signup and view all the answers

    Which statement accurately describes uncomplicated pyelonephritis?

    <p>Occurs in immunocompetent, nonpregnant females</p> Signup and view all the answers

    What distinguishes complicated pyelonephritis from uncomplicated pyelonephritis?

    <p>Association with risk factors like pregnancy</p> Signup and view all the answers

    What is the recommended treatment duration for uncomplicated pyelonephritis?

    <p>7 days of oral ciprofloxacin</p> Signup and view all the answers

    Which complication is associated with emphysematous pyelonephritis?

    <p>Gas formation in renal tissues</p> Signup and view all the answers

    Which factor increases the risk of developing urinary tract infections?

    <p>Immunosuppression</p> Signup and view all the answers

    Study Notes

    Nephrotic Syndrome

    • Characterized by edema, proteinuria, hypoalbuminemia, and hyperlipidemia.
    • Edema typically starts in the periorbital region and progresses to peripheral edema.
    • Hypoalbuminemia results from decreased serum albumin levels.
    • Hyperlipidemia includes increased triglycerides and cholesterol, as well as lower HDL levels.
    • Massive proteinuria, exceeding 3.5 g/24 hours, is a hallmark of nephrotic syndrome.
    • Frothy urine with fatty casts is characteristic.
    • Increased risk of blood clots (hypercoagulable state) due to antithrombin III loss in urine.
    • Increased risk of infections due to loss of immunoglobulins (IgGs) in urine and compromised soft tissues from edema.
    • Etiology: podocyte damage impairs the charge barrier, leading to proteinuria.
    • Examples: Focal segmental glomerulosclerosis, minimal change disease, membranous nephropathy, amyloidosis, diabetic glomerulonephropathy.

    Nephritic Syndrome

    • Characterized by hematuria, hypertension, oliguria, and rapid decline in renal function.
    • Hematuria presents with red blood cells in urine, sometimes with acanthocytes.
    • Hypertension is defined as systolic blood pressure greater than 140 mmHg and/or diastolic pressure greater than 90 mmHg.
    • Rapidly progressive glomerulonephritis is characterized by a rapid decline in renal function within days to weeks, caused by conditions like Goodpasture syndrome, lupus nephritis, and vasculitis.
    • Etiology: glomerular inflammation and damage to the glomerular basement membrane, leading to leakage of red blood cells into urine and the presence of dysmorphic red blood cells.
    • General pathophysiology: inflammation and cytokine release damage glomerular capillaries, resulting in a porous glomerular basement membrane. This leakage of proteins and red blood cells creates nephritic sediment detectable on urinalysis.
    • Examples: infection-associated glomerulonephritis, Goodpasture syndrome, IgA nephropathy (Berger’s disease), Alport syndrome, membranoproliferative glomerulonephritis.
    • Mechanism: Type 3 hypersensitivity reaction with consumptive hypocomplementemia.
    • Common in children 2-4 weeks following group A streptococcal pharyngitis or skin infection.
    • Adults may experience this condition following staphylococcus infections.
    • Light microscopy shows enlarged and hypercellular glomeruli.
    • Immunofluorescence reveals granular (starry sky appearance) deposits due to IgG, IgM, and C3 deposition along the glomerular basement membrane and mesangium.

    IgA Nephropathy (Berger’s Disease)

    • Mechanism: occurs concurrently with respiratory or gastrointestinal infections.
    • Characterized by IgA vasculitis, the most frequent cause of primary glomerulonephritis, affecting males in their 20s and 30s.
    • Clinical manifestations include gross hematuria, flank pain, and proteinuria, often triggered by infections.
    • Light microscopy shows mesangial proliferation.
    • Immunofluorescence reveals IgA-based immune complex deposits in the mesangium.
    • Electron microscopy shows mesangial immune complex deposition.

    Diffuse Proliferative Glomerulonephritis

    • Mechanism: often associated with Systemic Lupus Erythematosus (SLE).
    • DPGN and Membranoproliferative Glomerulonephritis (MPGN) can manifest as both nephritic and nephrotic syndromes.
    • Light microscopy reveals "wire looping" of capillaries.
    • Immunofluorescence shows granular deposits.
    • Electron microscopy reveals subendothelial, sometimes subepithelial or intramembranous IgG-based immune complexes, often with C3 deposition.

    Alport Syndrome

    • Mechanism: X-linked dominant condition with Type IV collagen mutation, leading to glomerular basement membrane alterations.
    • Clinical manifestations include eye problems (retinopathy, anterior lenticonus), glomerulonephritis, and sensorineural hearing loss (SNHL) (cant see, cant pee, cant hear a bee).
    • Light microscopy shows an irregular pattern of thinning and thickening, as well as splitting of the glomerular basement membrane.
    • Immunofluorescence is initially negative; irregular deposits of IgG, IgM, and/or C3 may be observed later.
    • Electron microscopy reveals a "basket-weave" appearance due to irregular thickening and longitudinal splitting of the glomerular basement membrane.

    Membranoproliferative Glomerulonephritis

    • Mechanism: Type 1 is often secondary to Hepatitis B or C virus infection.
    • Type 2 is associated with C3 nephritic factor, an autoantibody that stabilizes the C3 convertase and leads to persistent complement activation and decreased C3 levels.
    • Light microscopy shows mesangial ingrowth and glomerular basement membrane splitting, resembling "tram tracking" on H&E and PAS stains.
    • Immunofluorescence reveals granular deposits.
    • Electron microscopy reveals subendothelial immune complex deposits in Type 1.
    • Type 2 shows intramembranous deposits, also known as dense deposit disease.

    Rapidly Progressive (Crescentic) Glomerulonephritis

    • Mechanism: poor prognosis with multiple causes, including Type II hypersensitivity reaction in Goodpasture syndrome.
    • Light microscopy reveals crescent moon shapes formed of fibrin and plasma proteins, including C3b, with glomerular parietal cells, monocytes, and macrophages.
    • Immunofluorescence shows linear deposits due to antibodies against the glomerular basement membrane and alveolar basement membrane in Goodpasture syndrome, characterized by hematuria and hemoptysis.
    • Negative immunofluorescence or pauci-immune (no IgG or C3 deposition) is characteristic of granulomatosis with polyangiitis (PR3-ANCA/c-ANCA), eosinophilic granulomatosis with polyangiitis, or microscopic polyangiitis (MPO-ANCA/p-ANCA).
    • Granular immunofluorescence suggests poststreptococcal glomerulonephritis (PSGN) or diffuse proliferative glomerulonephritis (DPGN).
    • Electron microscopy in Goodpasture syndrome reveals breaks in GBM, necrosis, and crescent formation without deposits.
    • Pauci-immune cases usually lack deposits. If immune complex deposits are present, the presentation is typically more severe.
    • In PSGN, dome-shaped subendothelial and subepithelial electron-dense deposits (humps) are observed.

    Acute Interstitial Nephritis (AIN)

    • Acute inflammation of the renal interstitium and tubules, causing a decline in renal function over days to weeks.
    • No changes in the glomerulus are observed.
    • Etiology: Medications (antibiotics, NSAIDs, proton pump inhibitors, loop diuretics), infection (mycoplasma), autoimmune disorders (Sjogren syndrome, sarcoidosis, SLE), and other causes like nonsteroidal anti-inflammatory drugs, penicillins, sulfa drugs, antineoplastic agents, lithium, and antiviral agents.
    • Pathogenesis: immune-mediated tubulointerstitial damage is the most likely cause.
    • Drugs can act as haptens leading to Type IV hypersensitivity reactions.
    • Acute obstruction: crystals (from medications, uric acid) or proteins (light chains) can obstruct tubules.
    • Characterized by immune-mediated infiltration of the interstitium, leading to lethal/sublethal injury to ducts.
    • Often accompanied by tubular dysfunction with or without acute kidney injury.
    • Reversible due to the regenerative capacity of tubules with preserved basement membranes.
    • Clinical features: morbilliform rash, fever, arthralgias, and flank pain.

    Acute Kidney Injury (AKI)

    • A sudden loss of renal function causing an increase in creatinine and BUN (blood urea nitrogen).
    • Etiology:
      • Prerenal causes: any condition that leads to decreased renal perfusion (Hypovolemia, hypotension, decreased circulating volume (CHF, cirrhosis, acute pancreatitis), renal artery stenosis, and drugs).
      • Postrenal causes: bilateral obstruction of urinary flow that results in Postrenal AKI.

    Postrenal AKI

    • Acquired obstructions: Benign prostatic hyperplasia (BPH), Iatrogenic (catheter-associated injuries), Tumors, Stones, Bleeding
    • Neurogenic Bladder: due to conditions like multiple sclerosis, spinal cord lesions, or peripheral neuropathy.
    • Congenital malformations

    Chronic Tubulointerstitial Nephritis

    • A chronic inflammatory condition affecting the renal tubules and interstitium that may progress to end-stage renal disease (ESRD) over months or years.
    • Characterized by insidious onset.
    • Pathophysiology:
      • Analgesic nephropathy: NSAID use leading to vasoconstriction of medullary blood vessels, papillary ischemia and papillary necrosis, and increased risk of urothelial carcinoma.
      • Precipitation of light chains in renal tubules: causing tubular obstruction, interstitial scarring, fibrosis, and tubule atrophy.
    • Etiology:
      • Medications: analgesic nephropathy, NSAIDs, acetaminophen, cyclosporine, tacrolimus, cisplatin, ifosfamide, cidofovir, tenofovir, lithium.
      • Toxins: lead, cadmium
      • Systemic disease: multiple myeloma, Sjogren syndrome, SLE, sickle-cell disease.
      • Metabolic disease: hyperuricemia, hypercalcemia, hyperoxaluria, hypokalemia.

    Acid Base Disorders

    • Metabolic acidosis: Low pH and low HCO3-, excess acid or loss of base

    • Metabolic alkalosis: High pH and high HCO3-, Loss of acid or gain of base

    • Respiratory acidosis: Low pH and high PaCO2, hypoventilation

    • Respiratory alkalosis: High pH and low PaCO2, hyperventilation

    • Anion gap: difference between cations and anions.

    • Workup: CBC, Blood chemistry, Electrolytes, Urine, Osmolality, Blood gases.### Anion Gap

    • The anion gap measures the difference between unmeasured anions and unmeasured cations in the blood.

    • Anion gap is calculated by subtracting the sum of chloride (Cl-) and bicarbonate (HCO3-) from the sodium concentration (Na+).

    • A normal anion gap is 8-16 mEq/L.

    • A high anion gap indicates an excess of unmeasured anions.

    • Examples of conditions that cause a high anion gap include:

      • Glycols (osmolal gap)
      • Oxoproline (chronic acetaminophen use)
      • Lactate (lactic A acidosis, hypoxic; lactic B, non-hypoxic)
      • D-lactate (exogenous lactic acid, short bowel, carbohydrates, bacteria)
      • Methanol (and other alcohols, osmolal gap)
      • Aspirin (late effects)
      • Renal failure
      • Ketones (diabetic, alcoholic, starvation)

    • A normal anion gap implies that the decrease in serum [HCO3-] is matched by an equal increase in serum [Cl-].

    • A high anion gap can be corrected based on serum albumin levels.

    Metabolic Acidosis

    • Metabolic acidosis occurs when the body produces too much acid or loses too much base.
    • There are two main types of metabolic acidosis:
      • High Anion Gap (AGap) - caused by excess unmeasured anions.
      • Normal Anion Gap (non-AGap) - caused by excess chloride ions.
    • Renal causes for metabolic acidosis include:
      • Renal tubular acidosis (RTA) - failure of net acid excretion.
    • Extrarenal causes for metabolic acidosis include:
      • Chronic diarrhea - loss of bicarbonate and other alkali buffers.
    • Other causes of hyperchloremic (non-AGap) metabolic acidosis include:
      • Hyperalimentation (NaCl solutions, Parental nutrition).
      • Addison Disease (H+/ATPase pump, lack off).
      • Renal tubular acidosis.
      • Diarrhea (loss of bicarbonate, pancreatic, etc).
      • Acetazolamide (carbonic anhydrase inhibitors, impaired reabsorption).
      • Spironolactone (Na/H+ waste, sodium in urine, increase H+).
      • Saline infusion (NaCl).

    Urinary Anion Gap (UAG)

    • The UAG is calculated by subtracting the sum of chloride (Cl-) and potassium (K+) from the sodium concentration (Na+).
    • A normal UAG is a positive value of 30 to 50 mmol/L.
    • Negative value indicates increased renal excretion of unmeasured cation.
    • A positive UAG suggests renal losses of alkali.
    • A negative UAG suggests extrarenal loss of alkali.

    Diuretic Agents

    • Diuretics are medications that increase urine production by promoting fluid excretion from the body.
    • Hydrochlorothiazide: targets SLC12A3 or NCC, Calcium-activated potassium channel subunit alpha-1
    • MoA: inhibition of Na+-Cl- cotransporters (NCC) in the early distal convoluted tubule.
    • AE: Hypotension, Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia.
    • Indapamide: acts on the proximal segment of the distal tubule of the nephron.
    • MoA: inhibits the Na+/Cl- cotransporter, leading to reduced sodium reabsorption.

    Loop diuretics:

    • Ethacrynic acid and Furosemide
    • Site of action: thick ascending loop of Henle; (SLC12A1 or NKCC2).
    • MoA: blockage of Na+-K+-2Cl- cotransporter; increased PGE release: dilation of renal afferent arterioles.
    • AE: Ototoxicity, Hypokalemia, Hypomagnesemia, Dehydration, Allergy (sulfa), metabolic Alkalosis, Nephritis, Gout.

    Potassium-sparing diuretics:

    • Amiloride & Triamterene
    • Site of action: late distal tubule to the collecting duct.
    • MoA: direct inhibition of the epithelial sodium channels (ENaC) in the distal convoluted tubule and the collecting duct.
    • AE: hyperkalemia, metabolic acidosis.
    • Spironolactone & Eplerenone
    • Site of Action: distal convoluted tubule; Inhibits mineralocorticoid receptors.
    • MoA: inhibition of the mineralocorticoid receptor prevents the expression of ENaC, Na+/K+ ATPase in the basolateral membrane, and activation of Sgk1 and CAP1.
    • AE: endocrine disturbances; men: antiandrogenic effects (gynecomastia, ED); women: amenorrhea (lack of menses); general: hyperkalemia; metabolic acidosis.

    Osmotic Diuretics:

    • Glycerol and Mannitol.
    • Site of action: glomerulus, proximal convoluted tubule, descending limb in loop of Henle.
    • MoA: elevates blood plasma osmolality, resulting in an enhanced flow of water from tissues into interstitial fluid and plasma.
    • AE: dehydration, hypo/hypernatremia, pulmonary edema.

    Carbonic anhydrase inhibitor:

    • Acetazolamide & Dorzolamide
    • Site of Action: proximal tubule, thick ascending limb of the loop of Henle, late distal convoluted tube.
    • MoA: Inhibits carbonic anhydrase.

    Urinary Tract Infections (UTIs)

    • UTIs are common infections, particularly in women.
    • Asymptomatic Bacteriuria (ASB): No symptoms, usually detected during screening urine culture.
    • Cystitis: Inflammation of the bladder, characterized by:
      • Dysuria
      • Urinary frequency and urgency
      • Nocturia
      • Hesitancy
      • Suprapubic discomfort
      • Gross hematuria
    • Complicated UTIs: Infections with systemic illness, occurs with:
      • Anatomical predisposition to infection
      • Foreign body in urinary tract
      • Factors predisposing to a delayed response to therapy
    • Diagnosis: Urinalysis, Urine culture, Imaging (CT, US).
    • Treatment:
      • Uncomplicated cystitis: Nitrofurantoin, TMP-SMX, Fosfomycin, Pivmecillinam, Fluoroquinolones, B-lactams.
      • Complicated UTIs: Antibiotics with guidance by in vitro susceptibility test.
      • Pregnant women: Nitrofurantoin, ampicillin, cephalosporins; avoid sulfonamides and fluoroquinolones.

    Pyelonephritis

    • Pyelonephritis is inflammation of the kidney, often caused by an ascending UTI.
    • Pathogens: Commonly caused by gram-negative bacteria (E. coli, P. aeruginosa, KP, Proteus mirabilis), gram-positive bacteria.
    • Risk factors: More in women, pregnancy, urinary tract obstruction, cystitis, antibiotics, immunosuppression, renal transplant.
    • Clinical Features:
      • Mild: Low-grade fever, lower-back or costovertebral-angle pain.
      • Severe: High fever, rigors, nausea, vomiting, flank pain.
      • Bilateral papillary necrosis: Rapid rise in serum creatinine.
    • Treatment: Fluoroquinolones for uncomplicated cases; oral ciprofloxacin, oral TMP-SMX.

    Studying That Suits You

    Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

    Quiz Team

    Related Documents

    Renal Final Exam PDF

    Description

    Test your knowledge on nephrotic and nephritic syndromes, along with related respiratory conditions. This quiz covers key symptoms, lab findings, and underlying causes in nephrology, as well as arterial blood gas interpretation. Challenge yourself and deepen your understanding of these important medical concepts.

    More Like This

    Use Quizgecko on...
    Browser
    Open
    Browser
    Browser