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Pharm > Bone Mineral > Flashcards

Bone Mineral Flashcards

1
Q

Osteoclast
Osterblast
Osteocyte

A

Osteoblast- responsible for removal of bone matrix

Osteoblast- produce protein matrix and control mineralization

Osteoclast- buried in newly formed bone and connect w one another to form a system which controls the rate of ion transport and regulates the rate of mineralization in new bone matrix

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2
Q

Bone composition

2 major mineral constituents

A

Calcium, phosphate

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3
Q

Ca disposition in body

A
  • very small amt of ca exists in the free or active form
    • 99% exist in crystalline form in your skeleton and teeth
    • 1% exist in 2 main compartments
      • 0.9% intracellularly within the soft tissues
      • 0.1% extracellularly
  • complexed w phosphates, citrate, or other anions (15%)
  • bound to serum proteins, primarily albumin (40%)
  • ionized or biologically active (45%)
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4
Q

Phosphate disposition in body

A
  • 85% exists in crystalline forms in your skeleton and teeth

- not as tightly regulated as calcium

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5
Q

Regulators

Regulators of calcium and phosphate homeostasis

A

2 primary hormones responsible for tight control of mineral homeostasis

  • parathyroid hormone
  • vt D

Secondary hormonal regulators of mineral homeostasis

  • calcitonin
  • glucocorticoids
  • estrogen
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6
Q

PTH

Primary regulator –single chain peptide hormone secreted by the parathyroid gland

A
  • main goals of PTH
    Increase calcium
    Decrease phosphate
  • collectively targets 3 main areas
    Bone
    Kidney
    Intesine
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7
Q

PTH effects on kidney

A
  • increase calcium and magnesium
    Reabsorption at the distal tubule
  • decrease phosphate reabsorption at the distal tubule (as well as amino acids, bicarbonate, sodium, and chloride)
  • stimulation of renal production of calcitriol
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8
Q

PTH effects on the intestine

A

-PTH has no direct effect on intestine
-indirectly promotes absorption of calcium
From small intestine through its stimulation of renal activation of vt D

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9
Q

Vitamin D

  • primary regulator
    Hormone/vitamin which is derived either endogenously or exogenously
A
  • when pts are not exposed to UV light, may supplement w vt D
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10
Q

Vt D

Activation of vitamin D: endogenous production

A

Liver does initial hydroxylation, kidney does 2nd hydroxylation which is required for activation

Calcitriol is the active form

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11
Q

Vt D

Main goals of vt D

A

Increase calcium

Increase phosphate

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12
Q

Vt D

Collective sites of action

A
  • intestine
    Inc absorption of calcium
    Inc absorption of phosphate
  • bone ( acts indirectly)
    Inc responsiveness of bone to PTH
    May inc calcium and phosphate resorption
    May inc bone formation
  • kidney
    Dec calcium and phosphate excretion
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13
Q

Secondary regulators of bone mineral homeostasis

A
  • hormonal
    Calcitonin
    Glucocorticoids
    Estrogens
- non hormonal
Bisphosphonates
Plicamycin (mithramycin)
Thiazide diuretics
Loop diuretics
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14
Q

Disordes of bine mineral homeostasis

A 
Hypercalcemis
Hypocalcemia
Hyperphosphatemia
Hypophosphatemia
Osteoporosis
Paget's disease- chronic disorder of adult skeleton in which localized areas of bone become hyperactive softened and enlarged bone
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15
Q

Disorder of ca homeostasis

Assessment of ca concentrations

  • normal total serum concentration=
    8. 5 -10.5 MG/DL
A

Calcium must be adjusted for hypoalbuminemia

  • corrected calcium=
    measured calcium +0.8 (4.0-albumin). Or
  • corrected calcium=
    (Measured calcium- albumin) +4.0

Normal ionized serum calcium concentrations=4.6 to 5.1 MG/DL
Critically ill pts; varying affinities

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16
Q

Disorders of calcium homeostasis

Other factors affecting calcium concentrations

A

-alkalosis:
Decreased calcium concentrations
Calcium protein binding increased

-acidosis
Increased calcium concentrations
Calcium protein binding decreased

17
Q

Hypercalcemia

Signs and symptoms

A

Neurological effects
– Fatigue
– Weakness
– Lethargy

Gastrointestinal effects
– Anorexia
– Nausea/vomiting
– Constipation

Renal effects
– Polyuria
– Nephrolithiasis
– Increase excretion of electrolytes (due to polyuria)

Cardiovascular effects
– EKG changes (shortened QT)
– Bradyarryhthmias; cardiac arrest

Extraskeleton calcification

18
Q

Hypercalcemia: Etiology

A
  • Primary hyperparathyroidism
  • Multiple endocrine disorders
    – MEN-1 or Werner’s syndrome
    -Parathyroid hyperplasia
  • granulomatous diseases (TB/sarcoidosis)
    • extrarenal production of calcitriol
  • pharmacological agents
    • Thiazide diuretics (hydrochlorothiazide); not acute
      – Vitamin D supplementation
    • lithium ( inc PTH hormone concentrations and raises calcium set-point)
19
Q

Pharmacologic management of hypercalcemia

A

Calcium concentration assessment
– Total calcium

20
Q

Pharmacologic management of hypercalcemia

Initial considerations

A
  • Elimination of potentiating agents (thiazides, calcium supplementation, lithium)
  • Symptomatic relief of constipation, nausea/vomiting, and pain
    (Stool softeners, analgesics: Remember pain meds can cause
    constipation)

-Increased mobilization

21
Q

Pharmacologic management of hypercalcemia

Hydration with normal saline (0.9% sodium chloride)

A
  • Amount infused depends on degree of
    hypercalcemia
  • In acute management usually 2-6 liters in the first 24 hours
  • anticipate a 1.6-2.4 mg/dl decrease in calcium concentrations w normal saline alone
22
Q

Intro to bone mineral homeostasis

Homeostasis
Balance

A

Homeostasis- immediate
Adjustments required to maintain constant free calcium concentrations on a minute to minute basis

Balance- long term
Adjustments to maintain a constant amt of total calcium concentration within body

23
Q

Pharmacologic management of hypercalcemia

Loop diuretics
-Mechanism of action

A

-Decrease calcium concentrations through
increased elimination of calcium in the kidney

-Inhibit calcium reabsorption in the ascending loop of henle

-Agents include:
-Furosemide
-Bumetanide
-Toresemide

24
Q

Pharmacologic management of hypercalcemia

Bisphosphonates
– Mechanisms of action

A
  • Bind to hydroxyapatite in calcified bone matrix and thereby inhibit crystal dissolution
    to the mineralized matrix Agents used in acute management of hypercalcemia
    -Inhibit attachment of osteoclasts to the mineralized matrix
  • agents used in acute management of hypercalcemia
    – Pamidronate
  • Zoledronic acid
25
Q

Pharmacologic management of hypercalcemia

Bisphosphonates
-Pamidronate (Aredia®)

A
  • Most commonly used bisphosphonate in the treatment of hypercalcemia
  • Dosage: Depends on the degree of hypercalcemia
    – Usually given as 60 or 90 mg infusion over 4 to 24 hours Onset and Duration
  • onset and duration:
    – Calcium concentrations begin to decline in 3 days
    – Nadir reached in 7 days
    – Normalization of calcium occurs in 60 to 90% of patients
    – Wait at least 7 days following administration to give another dose.

Side effects
– Transient pyrexia
– Rash
- renal dysfunction

  • nausea
  • fatigue
26
Q

Pharmacologic management of hypercalcemia

Calcitonin (Intravenous)

A

– Hormone produced by the C cells of the thyroid gland

– Main goals of calcitonin
DECREASE calcium
DECREASE phosphate

– Collective sites of action

 – bone (primary site of action)
      – Short term effects: decrease calcium movement from bone fluid
      - long term effects: decrease bone r sorotion through inhibition of osteoclasts

 - kidney
      - decrease phosphate and calcium reabsorption ( as well as other ions)
27
Q

Pharmacologic management of hypercalcemia

Corticosteroids

A

– Steroid molecules produced and released by the adrenal cortex
– Administered exogenously for a multitude of applications
– Collective sites of action of glucocorticoids Intestine
- intestine:
– Antagonize vitamin D stimulated absorption of calcium and phosphate
- Kidney: increase renal excretion of calcium
– Bone
– Inhibit bone collagen synthesis
– Increase bone resorption

28
Q

Pharmacologic management of hypercalcemia

Corticosteroids

A

– Dose:
Hydrocortisone 200 to 300 mg daily for 3 to 5 days (or equivalent); generally see decrease in calcium within 7 days

– Potential usefulness of corticosteroids in treatment of hypercalcemia is limited to granulomatous disease (i.e., tuberculosis, sarcoidosis) and lymphoproliferative disorders

– Adverse effects
Hyperglycemia
Infection
Sodium/Water retention
Hypokalemia

29
Q

Hypocalcemia Signs and symptoms

Central Nervous System
– Fatigue
– Confusion
– Hallucinations

A

Neuromuscular
– tetany: due to enhance peripheral neuromuscular irritability; manifests as parathesias
around mouth and extremities, muscle spasms, cramps
– Muscle spasms/cramps
– Parasethesias

Cardiovascular
– Prolonged QT intervals
– AMI
– Hypotension

Dermatologic
– Hair loss
– Eczema
– Psoriasis

30
Q

Hypocalcemia: Etiology

A

Hypoparathyroidism
Vitamin D deficient states

– Rickets
– Liver/Renal disease
Malabsorption

31
Q

Pharmacologic management of hypocalcemia

A
  • Hypocalcemia associated with hypoalbuminemia does not need treatment

Acute symptomatic hypocalcemia
- Treatment is usually via the intravenous route
- Goal of therapy is to administer 200-300MG
of elemental calcium intravenously until symptoms are controlled

32
Q

Pharmacologic management of hypocalcemia

Agents

– Calcium chloride: 1g (270mg elemental Ca)
- Disadvantages –potential for extravasation and tissue necrosis

A

– Calcium gluconate: 2 to 3 grams
(180 to 270 elemental Ca)
Disadvantages –small amounts of elemental calcium per volume and less predictable increases in plasma ionic calcium

– Precautions with intravenous calcium administration
-Administer no faster than 30 to 60 mg of elemental calcium per minute
-Rapid administration associated with hypotension, bradycardia
and cardiac asystole
- If patient’s symptoms return then may consider slow infusions of calcium (i.e., 15 mg/kg over 4 to 6 hours) or continuous 24 hour infusions)

33
Q

Pharmacologic management of hypocalcemia

– Calcium supplementation with oral calcium salts
Calcium salts differ in percentage of elemental calcium (further discussion/explanation in osteoporosis)

A

– Vitamin D supplementation
Vitamin D may need to be added to therapy in patients with malabsorption or concomitant vitamin D deficiency

  • Agents
    – Many vitamin D analogues are available
    – Only dihydrotachysterol 1,25
    Pharmacologic management of hypocalcemia
    Chronic hypocalcemia
34
Q

Pharmacologic management of hypocalcemia

A

– Adverse effects associated with chronic vitamin D and calcium administration
Hypercalcemia
Hypercalciuria
Nephrolithiasis
– Increase urinary excretion of calcium
– The addition of thiazide diuretics (which inhibit calcium excretion) may decrease the risk of nephrolithiasis as well as decrease calcium and vitamin D requirements**
-
alpha hydroxyvitamin D3 (alfacalcidiol) do not require
dihydroxyvitamin D3 (calcitriol) and
-
hydroxylation in the kidney to produce the physiologically active form of the hormone

Pharm (19 decks)

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