Lectures

Collecting Duct (CD): Pathophysiology

by Carlo Raj, MD
(1)

Questions about the lecture
My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides CD Pathophysiology RenalPathology.pdf
    • PDF
      Download Lecture Overview
    Report mistake
    Transcript

    About the Lecture

    The lecture Collecting Duct (CD): Pathophysiology by Carlo Raj, MD is from the course Diseases of the Nephron. It contains the following chapters:

    • Transport Mechanism: Collecting Duct (CD)
    • Different Channels in Different Ducts
    • Role of Aldosterone
    • ATPase Pump
    • The Other Renal Tubular Acidoses
    • Conn's Syndrome
    • Summary of Clinical Findings

    Included Quiz Questions

    1. Aldosterone and Antidiuretic hormone
    2. Angiotensin II and Aldosterone
    3. Parathyroid hormone and aldosterone
    4. Parathyroid hormone and antidiuretic hormone
    5. Renin and Antidiuretic hormone
    1. Osmoreceptors of the hypothalamus
    2. Tropic receptors of the anterior pituitary
    3. V2 receptors in the collecting duct
    4. V1 receptors on blood vessels
    5. Chemoreceptors of the aortic root
    1. Basolateral V2 receptor of the principal cell
    2. Luminal aquaporin on the principal cell
    3. Basolateral aquaporin of the intercalated cell
    4. Luminal V2 receptor of the principal cell
    5. Basolateral V2 receptor of the intercalated cell
    1. Luminal sodium channel
    2. Basolateral Na-K-ATPase
    3. Luminal aquaporin channels
    4. Basolateral K/H exchanger
    5. Luminal potassium channel
    1. Epithelial sodium channel on luminal membrane of intercalated cell
    2. Aquaporins on luminal membrane of principle cell
    3. Vasopressin 2 receptor on basolateral membrane of principle cell
    4. H+K+ ATPase on luminal membrane of intercalated cell
    5. Na-K+ATPase on basolateral membrane of principle cell
    1. Aciduria
    2. Increased urine pH
    3. Metabolic acidosis
    4. Increased resting membrane potential
    5. Elevated bicarbonate levels in the plasma
    1. Hyperventilation
    2. Hypoventilation
    3. Increased excretion of hydrogen
    4. Increased excretion of bicarbonate
    5. Increased production of bicarbonate
    1. Decreased aldosterone activation promotes sodium excretion.
    2. Inhibition of ATII vasoconstriction of peripheral resistance arterioles
    3. Inhibition of ATII promotes hydrogen retention.
    4. Decreased aldosterone activation promotes potassium retention.
    5. Inhibition of ATII increases venous capacitance.
    1. Increased urine pH
    2. Hypokalemia
    3. Respiratory acidosis
    4. Increased sodium reabsorption
    5. Metabolic alkalosis
    1. Carbon dioxide byproduct from the TCA cycle.
    2. Carbon dioxide that passively diffuses into the cell from the urine.
    3. Carbon dioxide that passively diffuses into the cell from the blood.
    4. New bicarbonate is formed in the proximal collecting duct.
    5. It is recycled from the carbonic anhydrase reaction.
    1. Hyperkalemia
    2. Hypokalemia
    3. Hypocalcemia
    4. Hyponatremia
    5. Hypernatremia
    1. Ammonia
    2. Hydrogen Phosphate
    3. Uric Acid
    4. Creatinine
    5. Ketoanions
    1. It causes severe anion gap metabolic acidosis.
    2. It presents with xeropthalmia.
    3. It is associated with type 1 renal tubular acidosis.
    4. It is associated with Ssa and Ssb antibodies.
    5. It may promote dental caries.
    1. RTA type IV
    2. RTA type I
    3. None present with hyperkalemia
    4. All present with hyperkalemia
    5. RTA type II
    1. RTA type IV
    2. RTA type I
    3. None present with severe acidosis
    4. All present with severe acidosis
    5. RTA type II
    1. None are correct
    2. Increased ECF osmolarity
    3. Increased ICF osmolarity
    4. Decreased ICF volume
    5. Increased ECF volume
    1. Increased urinary sodium excretion
    2. Increased urinary potassium excretion
    3. Metabolic alkalosis
    4. Hypokalemia
    5. Hypernatremia
    1. Impaired excretion of H+ in the collecting duct
    2. Deficiency of aldosterone
    3. Impaired bicarbonate production
    4. Disordered bicarbonate reabsorption
    5. Aldosterone resistance
    1. Pitting edema
    2. Secondary Hypertension
    3. Metabolic alkalosis.
    4. Polyuria
    5. Muscle weakness
    1. Decreased plasma renin activity
    2. Hyponatremia
    3. Decreased urine volume
    4. Hypertonic urine
    5. Hyperkalemia
    1. Plasma renin activity
    2. Angiotensin
    3. Cholesterol
    4. Desmolase
    5. ACTH
    1. Zona glomerulosa of adrenal cortex
    2. Zona fasciculata of adrenal cortex
    3. Zona reticulate of adrenal cortex
    4. Juxtaglomerular apparatus
    5. Anterior pituitary
    1. Decreased filtration fraction
    2. Decreased effective arterial blood volume
    3. Increased reabsorption
    4. Decreased hydrostatic pressure in the peritubular capillaries
    5. Decreased hydrostatic pressure in the glomerular capillaries
    1. …urinary sodium excretion return to match levels of intake.
    2. …plasma renin activity acts via negative feedback to decrease aldosterone concentration.
    3. …aldosterone potency decreases due to overproduction.
    4. …aldosterone activity is decreased by introducing drugs such as spironolactone.
    5. …aldosterone receptors become oversaturated and are removed from the membrane.
    1. Vasopressin
    2. Angiotensin II
    3. Calcitriol
    4. Parathyroid hormone
    5. Aldosterone
    1. It is protein rich fluid.
    2. It is not found in patients with Conn’s syndrome.
    3. It is fluid in the extracellular compartment.
    4. It is sodium rich fluid.
    5. It is transudative fluid.
    1. ANP
    2. ADH
    3. Renin
    4. Angiotensin II
    5. Aldosterone
    1. It occurs with decreased filtration fraction.
    2. It is due to inhibition of distal sodium reabsorption in the kidney.
    3. It is a plausible explanation for the pitting edema in a patient with Conn’s syndrome.
    4. It is associated with decreased renal plasma flow.
    5. It is caused by decreased hydrostatic pressure in the peritubular capillary.

    Author of lecture Collecting Duct (CD): Pathophysiology

     Carlo Raj, MD

    Carlo Raj, MD


    Customer reviews

    (1)
    5,0 of 5 stars
    5 Stars
    5
    4 Stars
    0
    3 Stars
    0
    2 Stars
    0
    1  Star
    0