Medicine Marrow Pg No 795-804 (Nephrology)
53 Questions
0 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 of the following is NOT an etiological factor of Chronic Tubulointerstitial Disease?

  • Agrochemicals
  • Heavy metals
  • Vitamin C deficiency (correct)
  • Heat stress

    • Hypertension and edema are early features of Chronic Tubulointerstitial Disease.

    False

    What condition can Chronic Tubulointerstitial Disease progress to if left untreated?

    End Stage Renal Failure (ESRF)

    Chronic Tubulointerstitial Disease often leads to ________ in urine, which is typically absent or only mildly present.

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

    Match the clinical features with their corresponding impacts:

    <p>Anemia = Decrease in red blood cells Proteinuria = Presence of protein in urine Edema = Swelling of body tissues Hypertension = High blood pressure</p> Signup and view all the answers

    Which of the following is NOT a cause of Acute Kidney Injury?

    <p>Diabetes Mellitus</p> Signup and view all the answers

    Oliguric pre-renal failure can develop due to renal vasodilation.

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

    What is the most common type of acute kidney injury?

    <p>Non-oliguric failure</p> Signup and view all the answers

    Acute Tubular Necrosis (ATN) can be caused by __________ and __________.

    <p>Ischemia, Toxins</p> Signup and view all the answers

    Match the following causes of Acute Interstitial Nephritis with their categories:

    <p>Drugs = Hypersensitivity reactions Infections = Hypersensitivity reactions Lymphoma = Infiltration Sarcoidosis = Infiltration</p> Signup and view all the answers

    What is the primary management approach for contrast induced acute kidney injury?

    <p>Adequate hydration</p> Signup and view all the answers

    Atherosclerotic plaques can cause large vessel occlusions in athero-embolic renal disease.

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

    What features might indicate a diagnosis of athero-embolic renal disease?

    <p>Blue toe syndrome, livedo reticularis, retinal hollenhorst plaque</p> Signup and view all the answers

    The increase in creatinine levels in contrast induced AKI typically occurs within __________ hours.

    <p>24-48</p> Signup and view all the answers

    Match the following features with their corresponding condition:

    <p>Blue toe syndrome = Athero-embolic renal disease Livedo reticularis = Athero-embolic renal disease Creatinine increase = Contrast induced AKI Normal creatinine = 7-10 days after Contrast induced AKI</p> Signup and view all the answers

    What is a common clinical feature associated with poor end-organ perfusion during sepsis?

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

    Hypercalcemia is typically seen in acute kidney injury (AKI).

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

    Name one of the predominant causes of pre-renal failure in sepsis.

    <p>Widespread systemic vasodilation</p> Signup and view all the answers

    The recovery phase of acute tubular necrosis (ATN) is characterized by __________.

    <p>volume overload</p> Signup and view all the answers

    Match the following conditions with their associated pathophysiological effects:

    <p>ATN = ↑K and acidosis Sepsis = Widespread systemic vasodilation Hypernatremia = Not seen in AKI IVC diameter = Determines fluid requirement</p> Signup and view all the answers

    Which of the following is a clinical feature of acute interstitial nephritis (AIN)?

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

    Renal biopsy in acute interstitial nephritis typically shows glomerular abnormalities.

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

    What is the mainstay treatment for drug-induced nephropathy after stopping the offending agent?

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

    In NSAIDs induced nephropathy, the ____ secretion is stimulated leading to increased potassium excretion.

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

    Match the following drugs with their characteristics related to drug-induced nephropathy:

    <p>NSAIDs = Leads to hyperkalemia and oliguria Aminoglycosides = Causes oxidative stress in proximal tubules PGE2 = Stimulates RAAS Drug administration method = Single dose to prevent AKI</p> Signup and view all the answers

    Which type of Cardiorenal Syndrome occurs due to chronic heart failure leading to renal dysfunction?

    <p>Chronic cardiorenal</p> Signup and view all the answers

    Birefringent, biconvex elongated cholesterol crystals are typically found in microscopic examinations of Cardiorenal Syndrome.

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

    What common laboratory finding is indicated by elevated levels of white blood cells in Cardiorenal Syndrome?

    <p>Elevated white blood cell count</p> Signup and view all the answers

    Acute kidney injury leading to acute cardiac dysfunction is classified as _____ cardiorenal syndrome.

    <p>Acute renocardiac</p> Signup and view all the answers

    Match the following types of Cardiorenal Syndrome with their descriptions:

    <p>1 = Acute cardiorenal 2 = Chronic cardiorenal 3 = Acute renocardiac 4 = Chronic renocardiac</p> Signup and view all the answers

    Which drug category is associated with causing prerenal failure?

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

    In Acute Tubular Necrosis (ATN), urine output is typically decreased.

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

    What type of urine microscopy finding is characteristic of ATN?

    <p>Muddy brown epithelial casts</p> Signup and view all the answers

    In prerenal failure, the BUN/Creatinine ratio is typically greater than __________.

    <p>20</p> Signup and view all the answers

    Match the following drugs with their associated condition:

    <p>Aminoglycosides = ATN PPIs = AIN Indinavir = Intratubular obstruction Cisplatin = ATN</p> Signup and view all the answers

    What is the first line treatment for Acute Kidney Injury?

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

    Diuretics are recommended for the prevention of Acute Kidney Injury.

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

    Name a condition that can lead to Uric Acid Nephropathy.

    <p>Hematological malignancies</p> Signup and view all the answers

    The passive leg raising test measures ______ before and after the procedure.

    <p>IVC (Inferior Vena Cava)</p> Signup and view all the answers

    Match the following symptoms with their corresponding conditions:

    <p>Oliguric AKI = Acute Kidney Injury High S. uric acid = Uric Acid Nephropathy Increased S. K+ = Acute Kidney Injury Passive Leg Raising Test = Blood volume assessment</p> Signup and view all the answers

    Which of the following can result from acute kidney injury?

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

    KDIGO Class I indicates a urine output of 12 hours.

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

    Name one newer marker in Acute Kidney Injury.

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

    Acute Tubular Necrosis (ATN) is primarily classified under __________ AKI.

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

    Match each cause of Pre-renal AKI to its description:

    <p>Intravascular volume depletion = Due to blood loss or excessive fluid loss Reduced effective intravascular volume = Due to conditions like cirrhosis or cardiac failure</p> Signup and view all the answers

    Which of the following is a cause of Post Renal AKI?

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

    Hyperkalemia can be a resultant condition of acute kidney injury.

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

    What is the most common cause of hospital-acquired acute kidney injury?

    <p>Pre-renal AKI</p> Signup and view all the answers

    Which of the following is a treatment option for rhabdomyolysis?

    <p>IV Rasburicase</p> Signup and view all the answers

    Muscle cramps with dark-colored urine are clinical features of rhabdomyolysis.

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

    Name two risk factors associated with rhabdomyolysis.

    <p>Electric shock, Alcohol use</p> Signup and view all the answers

    A significant enzyme increase in rhabdomyolysis is detected using a CPK assay greater than ________ units.

    <p>1500</p> Signup and view all the answers

    Match the following causes with their descriptions:

    <p>Seizures = Muscle contractions leading to injury Hypothyroidism = Hormonal imbalance affecting muscle metabolism Statins = Medications that can lead to muscle breakdown Glycogen Storage Disease Type 5 = Metabolic disorder leading to muscle weakness</p> Signup and view all the answers

    Study Notes

    Chronic Tubulointerstitial Disease (CKDu)

    • Etiological factors include heat stress, agrochemicals, fluoride in groundwater, heavy metals (e.g., cadmium), and communicable diseases.
    • CKDu often progresses without noticeable symptoms until the later stages.
    • Swelling (edema) and high blood pressure (hypertension) are common symptoms that appear later in the disease process.
    • Protein in the urine is often subtle or not significantly present.
    • Levels of certain markers from the kidney tubules can be elevated, suggesting damage.
    • Common in the eastern coast of India and among middle-aged men.

    Acute Kidney Injury (AKI)

    • AKI can be caused by NSAIDS, Rhabdomyolysis, and polyuria (contrast induced AKI).
    • Non-oliguric failure is the most common type of AKI.
    • Oliguric pre-renal failure occurs only with renal vasoconstriction.
    • The tubuloglomerular feedback loop detects low glomerular filtration rate (GFR) and triggers a response.
    • Low GFR leads to reduced urine output.
    • ATN (Acute Tubular Necrosis) is caused by ischemia, toxins (endogenous and exogenous), and drugs.
    • AIN (Acute Interstitial Nephritis) results from hypersensitivity reactions to drugs, infections, or infiltrations.

    CONTRAST INDUCED AKI

    • Reduced incidence has been observed by using low volume iso-osmolar contrast (lohexol/lopamidol).
    • Pathology includes medullary hypoxia leading to tubular injury.
    • Creatinine levels increase within 24-48 hours, peak at 3-5 days, and return to normal in 7-10 days.
    • Management typically doesn't require medication.
    • Adequate hydration is key for prevention.

    ATHERO-EMBOLIC RENAL DISEASE

    • AKA Cholesterol embolism.
    • Commonly seen in patients with extensive aortic atherosclerosis after endovascular intervention.
    • Atherosclerotic plaque breaks off, embolize distally, and cause multiple small vessel occlusion.
    • Clinical features include subacute renal failure over several weeks and skin manifestations such as blue toe syndrome and livedo reticularis.
    • Mesenteric ischemia and retinal Hollenhorst plaques may also be observed.
    • Patients with atherosclerotic embolism have an increased risk of developing ESRD.
    • Prognosis tends to be poor.

    ATN

    • ATN involves three distinct phases: tubular injury, tubuloglomerular feedback, and recovery.
    • In the tubular injury phase, there is a loss of solutes and water.
    • The tubuloglomerular feedback phase results in decreased urine output, elevated phosphorus levels, decreased calcium levels, and reduced GFR.
    • The recovery phase often involves volume overload.
    • ATN is often characterized by acidosis (NAGMA) and increased potassium levels.

    Sepsis

    • Sepsis can lead to AKI through pre-renal mechanisms, including widespread systemic vasodilation and microvascular dysfunction.
    • Causes of septic AKI include urosepsis, CRBSI (Catheter-related Blood Stream Infection), and DM nephropathy with soft tissue infection.
    • The inflammatory cascade triggered by PAMPS and DAMPS contributes to oxidative stress and potential damage to tubular cells.
    • Septic AKI can also occur in renal allograft recipients, patients with UTIs, and in the post-operative period.
    • Clinical features include signs of poor end-organ perfusion, such as increased heart rate, cool skin, decreased urine output, and restlessness.
    • Investigations for septic AKI involve assessing IVC diameter, lactate levels, and fluid responsiveness.
    • Treatment of septic AKI focuses on fluid resuscitation and management of sepsis.

    AIN (ACUTE INTERSTITIAL NEPHRITIS)

    • Hypersensitivity reaction-mediated renal injury leading to reversible AKI.
    • Characterized by rash, eosinophilia, and asymptomatic renal failure.
    • Edema and hypertension are typically absent.
    • Investigations include assessing renal function tests, urinalysis, and renal biopsy.
    • Treatment generally involves stopping the offending agent and administration of steroids.

    DRUG INDUCED NEPHROPATHY

    • NSAIDs:
      • Pathophysiology: Inhibit PGE2/PGI2 production, leading to stimulation of RAAS and aldosterone-mediated potassium excretion.
      • Clinical features: Oliguria, decreased fractional excretion of sodium (FeNa < 1), and disproportionate hyperkalemia.
    • Aminoglycosides:
      • Pathophysiology: Cationic amino groups bind to anionic megalin in the proximal convoluted tubules, accumulating in lysosomes and causing oxidative stress.
      • Clinical features: Non-oliguric AKI occurs 5-10 days after drug administration.
    • Prevention: Single-dose administration of aminoglycosides is recommended to reduce risk of kidney injury.

    CARDIORENAL SYNDROME

    • Five types of CRS are recognized based on the interplay between cardiac and renal dysfunction.
    • CRS can be caused by systemic conditions, such as snake bite, placental abruption, and pancreatitis.
    • Microscopic findings often include birefringent, biconvex, elongated cholesterol crystals.

    ACUTE KIDNEY INJURY

    • AKI is characterized by an abrupt decrease in renal function over several hours to days.
    • KDIGO classifies AKI based on urine output and creatinine levels.
    • Newer markers for AKI include NGAL, KIM-1, L-FABP, and IL-18.
    • Pre-renal AKI is the most common type in hospital settings and results from intravascular volume depletion or reduced effective intravascular volume.
    • Renal AKI encompasses conditions like ATN and AIN, while post-renal AKI is caused by obstruction of urine flow.
    • Additional causes of AKI include rhabdomyolysis, acute pancreatitis, and compartment syndrome.

    Treatment of AKI

    • First-line treatment for AKI involves fluid resuscitation with crystalloids.
    • For severe AKI, second-line treatment includes vasopressors, such as norepinephrine, dopamine, dobutamine, or corticosteroids.
    • Diuretics are not typically used for prevention or treatment of AKI.

    Renal Nephritis

    • URIC ACID NEPHROPATHY (AKA Tumor Lysis Syndrome):
      • Caused by rapid multiplication of tumor cells in hematological malignancies.
      • Results in elevated uric acid filtered by the glomerulus.
      • Clinical features include oliguric AKI, elevated uric acid levels, electrolyte imbalances, and acidosis.
      • Treatment includes intravenous rasburicase, dialysis, and preventive measures.

    Rhabdomyolysis

    • Causes:
      • Electrical shock
      • Electrolyte imbalances (low potassium or low phosphate)
      • Seizures
      • Alcohol, cocaine, heroin use
      • Statins, zidovudine
      • Glycogen storage disease type 5 (McArdle disease)
      • Hypothyroidism
      • Polymyositis/dermatomyositis
    • Pathophysiology: Injury to proximal tubular cells, vasoconstriction, and tubular obstruction with uric acid.
    • Clinical features: Muscle cramps, high-colored urine, non-oliguric AKI, proximal muscle swelling, and urine with pigmented granular casts.
    • Investigations:
      • Elevated creatine phosphokinase (CPK) levels (> 1500 units):
        • Rise occurs after 2-12 hours.
        • Persistent elevation for 3-5 days suggests compartment syndrome.
      • Elevated potassium, phosphate, magnesium, and uric acid levels.
      • Decreased calcium levels.
      • Acidosis (HAGMA)
      • FENA (Fractional Excretion of Sodium)
    • Treatment:
      • Intravenous fluids
      • Sodium bicarbonate
      • Mannitol
      • Dialysis (if necessary)

    Pre-renal AKI vs. ATN

    Feature Prerenal AKI ATN
    Urine output Normal ↓
    Urine albumin - +
    Urine microscopy - Muddy brown epithelial casts
    BUN/Creatinine ratio >20 40

    Studying That Suits You

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

    Quiz Team

    Description

    This quiz covers key concepts about Chronic Tubulointerstitial Disease (CKDu) and Acute Kidney Injury (AKI), including their etiological factors, symptoms, and mechanisms. Test your knowledge of how these kidney conditions manifest, especially in specific populations and under certain circumstances.

    More Like This

    Use Quizgecko on...
    Browser
    Open
    Browser
    Browser