2023-11-05T04:28:24+03:00[Europe/Moscow] en true <p>as kidney function declines, there is a decrease in phosphate elimination-hyperphosphatemia; PTH hormone is released because of hypocalcemia; this decreases phosphate reabsorption</p>, <p>as kidney function declines, there is a decrease in phosphate elimination-hyperphosphatemia; this leads to PTH stimulation (independent of calcium); calcium reabsorption occurs and phosphate reabsorption decreases</p>, <p>the decline in kidney function results in hyperphosphatemia; this impairs vitamin D bioactivation directly/indirectly through FGF-23; causes Vit D deficiency and impaired calcium uptake</p>, <p>the decline in kidney function results in impaired vitamin D activation; leading to hypocalcemia </p>, <p>d</p>, <p>c</p>, <p>b</p>, <p>a</p>, <p>kidneys can still respond to PTH hormone and decrease phosphorus reabsorption due to increased renal tubular secretion </p>, <p>kidneys can no longer respond to PTH hormone; this results in sustained PTH secretions which further compromises bone health </p>, <p>decreased; decreased </p>, <p>hydroxyapatite; bone/tooth enamel</p>, <p>PTH; FGF23</p>, <p>2.7-4.5 mg/dL</p>, <p>&gt;5mg/dL</p>, <p>decreased renal tubular secretion despite elevated levels of PTH and FGF23</p>, <p>calcium acetate, calcium carbonate, ferric citrate, lanthanum, sevelamer </p>, <p>b</p>, <p>d</p>, <p>d</p>, <p>metabolic acidosis; due to left over Cl ion</p>, <p>calcium gluconate, calcium chloride</p>, <p>calcium carbonate, calcium citrate </p>, <p>reduced GI absorption, reduced tubular reabsorption, coma, epilepsy</p>, <p>peptic ulcer disease, history of alcoholism </p>, <p>sodium phosphate</p> flashcards
MBD- Pathology & Pharmacology

MBD- Pathology & Pharmacology

  • as kidney function declines, there is a decrease in phosphate elimination-hyperphosphatemia; PTH hormone is released because of hypocalcemia; this decreases phosphate reabsorption

    Explain Pathway 1 of CKD-MBD.

  • as kidney function declines, there is a decrease in phosphate elimination-hyperphosphatemia; this leads to PTH stimulation (independent of calcium); calcium reabsorption occurs and phosphate reabsorption decreases

    Explain Pathway 2 of CKD-MBD.

  • the decline in kidney function results in hyperphosphatemia; this impairs vitamin D bioactivation directly/indirectly through FGF-23; causes Vit D deficiency and impaired calcium uptake

    Explain Pathway 3 of CKD-MBD.

  • the decline in kidney function results in impaired vitamin D activation; leading to hypocalcemia

    Explain Pathway 4 of CKD-MBD.

  • d

    Which is strictly the result of a vitamin D deficiency?

    a) pathway 1

    b) pathway 2

    c) pathway 3

    d) pathway 4

  • c

    Which is the result of hyperphosphatemia-induced Vit D deficiency?

    a) pathway 1

    b) pathway 2

    c) pathway 3

    d) pathway 4

  • b

    Which is the result of hyperphosphatemia-induced hyperparathyroidism?

    a) pathway 1

    b) pathway 2

    c) pathway 3

    d) pathway 4

  • a

    Which is the result of hyperphosphatemia-induced hypocalcemia?

    a) pathway 1

    b) pathway 2

    c) pathway 3

    d) pathway 4

  • kidneys can still respond to PTH hormone and decrease phosphorus reabsorption due to increased renal tubular secretion

    How do the kidneys respond to PTH hormone in early CKD?

  • kidneys can no longer respond to PTH hormone; this results in sustained PTH secretions which further compromises bone health

    How do the kidneys respond to PTH hormone in Late CKD?

  • decreased; decreased

    Hyperphosphatemia will lead to _____ Vitamin D activation and _______ calcium absorption.

  • hydroxyapatite; bone/tooth enamel

    Phosphorus + calcium = ?

    What is this the primary structural component of?

  • PTH; FGF23

    _______ & _______ reduce tubular reabsorption of Phosphorus.

  • 2.7-4.5 mg/dL

    What are the normal serum levels of phosphorus?

  • >5mg/dL

    Hyperphosphatemia=

  • decreased renal tubular secretion despite elevated levels of PTH and FGF23

    What is the most common cause of hyperphosphatemia?

  • calcium acetate, calcium carbonate, ferric citrate, lanthanum, sevelamer

    What are the calcium binders? (5)

  • b

    Which dissociates into ions that bind phosphate?

    a) ferric citrate

    b) lanthanum

    c) calcium acetate

    d) Sevelamer

  • d

    Which exchanges Cl ions for phosphate?

    a) ferric citrate

    b) lanthanum

    c) calcium acetate

    d) Sevelamer

  • d

    Which acts in the intestinal lumen?

    a) ferric citrate

    b) lanthanum

    c) calcium acetate

    d) Sevelamer

  • metabolic acidosis; due to left over Cl ion

    AE of Sevelamer?

  • calcium gluconate, calcium chloride

    What are the IV calcium supplements? (2)

  • calcium carbonate, calcium citrate

    What are the oral calcium supplements? (2)

  • reduced GI absorption, reduced tubular reabsorption, coma, epilepsy

    What are the most common causes of hypophosphatemia? (4)

  • peptic ulcer disease, history of alcoholism

    Which patients will have reduced GI absorption of Phosphorus? (2)

  • sodium phosphate

    What is the most common strategy to treat Hypophosphatemia?