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Endocrine > Parathyroid Disoders - Exam 3 > Flashcards

Parathyroid Disoders - Exam 3 Flashcards

1
Q

Where are the parathyroid glands located? How many? Describe their appearance.

A

posterior thyroid gland

4 glands located on the posterior thyroid gland

Size -grain of rice to pea-sized
Shape - smooth surface, oval or bean-shaped
Normally not visible or palpable on neck exam

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2
Q

Parathyroid Hormone (PTH), which plays a key role in regulating _____ level. ____: synthesize and release PTH. ______ are less abundant, larger, acidophilic, nonfunctional

A

extracellular calcium

Principal (chief) cells

Oxyphil cells

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3
Q

Amounts of _____ and ____ increases with age

A

adipocyte deposits

oxyphil cells

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4
Q

Describe the textures of the thyroid and parathyroid glands

A

thryoid is bumpy

parathyroid is smooth

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5
Q

What is the net effect of PTH? ______ in the serum interacts with _____ on the surface of cells in the parathyroid glands and kidney

A

increase serum calcium

Ionized Calcium (aka free calcium, NOT bound to albumin)

calcium-sensing receptors (CaSR)

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6
Q

What do high calcium levels stimulate? What about low calcium levels?

A

stimulates CaSR receptors → PTH suppression

CaSR receptors are not stimulated → PTH release

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7
Q

What is PTH’s response to low calcium? minutes? hours? days?

A

minutes: release of preformed PTH

hours: PTH mRNA expression → increased PTH synthesis

days: parathyroid cell replication → increased parathyroid gland mass

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8
Q

What are the 4 functions of calcium?

A

-maintain skeletal strength

-regulates contraction of muscle

-cellular signaling (especially neurons)

-secretion of hormones and enzymes

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9
Q

Where are the 3 areas that calcium is stored?

A

1: bone as hydroxyapatite

#2: intracellular fluid
#3: Extracellular fluid

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10
Q

Bone: majority (99%) of the calcium in bone is stored as _____

A

hydroxyapatite

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11
Q

What is the job of calcium that is stored in the intracellular fluid?

A

Intracellularsignaling (second messengers), enzyme activation, muscle contraction

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12
Q

What is important to note about the calcium that is stored in extracellular fluid?

A

50% of the calcium is bound to proteins and only has minimal fluctuation

50% is unbound and fluctuates freely

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13
Q

______ is serum calcium that is not bound to proteins. How is serum calcium balance maintained?

A

Ionized calcium

by release of calcium from intracellular storage or influx from extracellular fluid

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14
Q

What 3 organs are responsible for maintaining the narrow balance of EXTRAcellular calcium and phosphorus? What are the responsibilities of each?

A

intestines: absorb dietary Ca

kidneys: reabsorb or excrete Ca as needed

skeletal system: reservoir for Ca, releases and reserving as needed

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15
Q

What is the function of phosphorus?

A

Helps form several major body components: skeleton (its part of hydroxyapatite), cell membranes, DNA/RNA and ATP

balance of several vitamins and minerals

pH regulation and enzyme activation

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16
Q

Most phosphorus in the body is as the ______. Name 3 places phosphorus is stored?

A

phosphate ion, PO4

Bone - majority (85%) in bone as hydroxyapatite

Intracellular/Soft Tissues - (14%) of overall body phosphorus. Phosphate ion, several parts of cellular structures and enzymes.

Extracellular Fluid - Blood, extracellular matrix
1% of overall body phosphorus, mainly as the ion PO4

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17
Q

_____ enhances the intestines ability to absorb calcium and phosphorus

A

vitamin D

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18
Q

In a normal healthy person, how are calcium and phosphorus related? What 3 major hormones maintain this balance?

A

inverse relationship, when calcium increases phosphorus decreases

PTH

Vit D (Calcitriol)

Calcitonin

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19
Q

What are the effects of PTH on bone? on kidney?

A

Bone:
Stimulates release of Ca2+
Stimulates release of PO4-

Kidney:
Increased Ca2+ reabsorption
Increased PO4- excretion
Stimulates production of calcitriol (1,25 Vitamin D)

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20
Q

How does PTH effect calcitriol?

A

Converted from inactive 25-OH Vitamin D by kidneys under the influence of PTH to its metabolically active form

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21
Q

What are the effects of calcitriol on the intestines?

A

Increased calcium absorption
Increased phosphorus absorption

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22
Q

What are the effects of calcitriol on bone?

A

Enhances effects of PTH on bone to promote more calcium release

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23
Q

Where does calcitonin originate? When is it released? What is the effect of calcitonin on the body?

A

calcitonin-secreting cells (C cells) in the thyroid

Calcitonin is released by the thyroid when C-cells become overstimulated by elevated calcium levels

Works in opposition to PTH
Suppresses renal reabsorption of Ca2+ → increased Ca2+ excretion
Inhibits osteoclasts in bone → decreased release and increased storage of Ca2+

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24
Q

What does the total serum calcium measure? What is normal? Which is the metabolically active form?

A

protein bound Ca plus free Ca

8.5-10.5

40-50% is protein bound to albumin

ionized calcium is free and considered metabolically active 4.4-5.4

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25
Q

What does high serum calcium mean? low serum calcium?

A

High - bone breakdown (elevated PTH, cancer), supplementation, kidney dz, meds

Low - low PTH, low vitamin D, kidney disease

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26
Q

____ and ___ could cause a serum calcium to look falsely elevated. _____ could cause it to look falsely low.

A

hemoconcentration and elevated serum proteins

low serum proteins

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27
Q

Abnormal _____ requires a corrected calcium level! Under what conditions is the corrected calcium calculation NOT accurate?

A

albumin

serum calcium + [0.8 x (4.0 - albumin)]

acid/base disorders
Acidosis - decreased calcium binding to albumin
Alkalosis - increased calcium binding to albumin

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28
Q

_____ is the current standard for dx of hyperparathyroidism. Is it accurate?

A

Serum Parathyroid Hormone (PTH)

very sensitive and specific test

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29
Q

What is the process of Vit D becoming active in the body? aka what forms of Vit D and what organs are required?

A

The LIVER converts D2/D3 (which is normally the form pts take PO) to 25-OH Vit D, which is metabolically inactive

The KIDNEY then takes 25-OH Vit D and converts it to active 1,25 Vit D (calcitriol)

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30
Q

_____ form of vit D is the result when you order a “Vit D level”

A

Serum 25-hydroxy vitamin D

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31
Q

**Which form of Vit D supplement is synthesized in skin, found in animal-derived diet food?

A

D3 (Cholecalciferol)

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32
Q

**Which form of Vit D supplement is derived from plant sources?

A

D2 (Ergocalciferol)

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33
Q

______ Metabolically active form of vitamin D. What is the normal range? What does a high level indicate? low level?

_____ is a result that could make it look falsely evelated

A

1,25 Vitamin D (Calcitriol)

20-76 pg/mL

High: excess supplementation, hyperparathyroidism, extrarenal production (granulomatous disease, lymphoma)

low: CKD, severe vitamin D deficiency, heritable diseases, tumor-induced osteomalacia, HIV protease inhibitors

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34
Q

What does a high serum phosphorus indicate? Low indicate? ______ are reasons why it could be falsely elevated?

A

High: hypoparathyroidism, kidney disease, supplementation, acidosis, cell lysis, several other conditions

Low: Low - hyperparathyroidism, malabsorption or poor diet, certain medications, low vitamin D, several other conditions

high levels of lipids, protein, or bilirubin

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35
Q

What is important to note about a serum phosphorus?

A

can bounce all over the place within the normal range

highest: in late morning in May/June
Lowest: in the evening in the winter

Also varies with food, antacids, renal function, menopause, pregnancy, bedrest

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36
Q

______ naturally found in various cells; especially active in tooth eruption and mammary gland development. Pathologically secreted by cancer cells and attaches to _____ receptors. What is the effect? What does a high test indicate?

A

Parathyroid Hormone Related Protein (PTHrP)

PTH

Results in a PTH-like effect on the bone and kidney

High - Humoral Hypercalcemia of Malignancy

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37
Q

90% of hypercalcemia results from _____ and ______. What are the other potential causes of hypercalcemia?

A

hyperparathyroidism due to adenoma and lithium

malignancy

vit D related aka too much vit D

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38
Q

What are the parathyroid related causes of hypercalcemia?

A

**Adenoma- MC-excess secretion of PTH due to increased parathyroid mass
Lithium: decreases parathyroid gland sensitivity to calcium

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39
Q

What cause of hypercalcemia decreases parathyroid gland sensitivity to calcium?

A

lithium

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40
Q

What cause of hypercalcemia is due to osteolysis, release of PTH-related protein (PTHrP)?

A

malignancy

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41
Q

What cause of hypercalcemia is due to increased GI calcium absorption and bone calcium release?

A

increases in Vit D aka they are supplementing too much

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42
Q

What are some causes of high bone turnover that could lead to hypercalcemia? What is the major one?

A

hyperthyroid: thyroid hormone stimulated bone resorption
immobilization
**thiazides: decreases urinary calcium excretion in addition to bone resorption

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43
Q

______ decreases urinary calcium excretion in addition to bone resorption. What does it lead to?

A

thiazides

hypercalcemia

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44
Q

What are some causes of renal failure that can lead to hypercalcemia? What is the major one?

A

Tertiary hyperparathyroidism
**Milk-alkali syndrome

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45
Q

_____ hyperplasia of the parathyroid glands from prolonged CKD persisting in elevated PTH (even if calcium normalizes with CKD treatment). What can it lead to?

A

Tertiary hyperparathyroidism

hypercalcemia

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46
Q

_____ Calcium carbonate supplementation to treat osteoporosis or dyspepsia - combination of hypercalcemia, metabolic alkalosis, renal impairment. What can it lead to?

A

**Milk-alkali syndrome: rates are increasing

hypercalcemia

47
Q

Bone pain
kidney stones
constipation
stomach ulcers
fatigue
confusion
AMS
Shorted QT interval
Diminished reflexes
Bradycardia
Hypertension

What am I?
What is a highlighted symptom?

A

Hypercalcemia
**Shorted QT interval

48
Q

In calcium related disorder the _______ the more prominent the symptoms

A

more rapid the elevation the more prominent the symptoms

49
Q

What is the tx for hypercalcemia?

A

identify and treat the underlying cause

rehydration: IV NS 500-1000 mL/h x 2-4 hrs, as tolerated

Loop Diuretics: IV furosemide

Corticosteroids

Bisphophonates and/or Calcitonin

50
Q

Tx of hypercalcemia, what do we need to monitor for when using loop diuretics?

A

Monitor for SE of hypokalemia, hypomagnesemia

Risk of paradoxical increase in Ca2+ due to bone resorption

51
Q

Tx of hypercalcemia, why are we using corticosteroids?

A

Decreases conversion of inactive to active vitamin D
Especially beneficial when excess calcitriol is a contributing factor

52
Q

Tx of hypercalcemia, why are we using Bisphosphonates, Calcitonin?

A

Decreases release of calcium from bone
Especially beneficial in chronic cases where PTH is elevated

53
Q

What are the two MC causes of hypocalcemia?

A

MC causes of hypocalcemia are impaired production of PTH and/or vitamin D

54
Q

What are some causes of hypocalcemia with a low PTH? Is this considered primary or secondary hypoparathyroidism? What does this cause?

A

Parathyroid agenesis

Parathyroid destruction: surgical, radiation, cancer, autoimmune

Reduced parathyroid function: Low magnesium - required for PTH production and release

primary

hypocalcemia

55
Q

What are some causes of hypocalcemia with a high PTH? Is this considered primary or secondary hypoparathyroidism? What does this cause?

A

**Vitamin D deficiency: Nutritional, poor UV exposure, kidney disease, liver disease

**tissue injury

PTH resistance (PTH receptor mutations)

Malabsorption

Medications: calcium chelators, bisphosphonates

secondary: aka the parathyroid gland is fine, something else is the source of the error

hypocalcemia

56
Q

anxiety
irritability
seizures
hyperactive reflexes
cramps
Chvostek sign
Trousseau sign
dysrhythmias
prolonged QT interval

What am I?

A

hypocalcemia

57
Q

_____ Facial twitching, especially perioral, induced by gently tapping the ipsilateral facial nerve just anterior to the ear

A

Chvostek’s sign

58
Q

____ Carpal spasm induced by inflating BP cuff around the arm (must achieve pressure 20 mmHg above obliteration point for 3-5 min)

A

Trousseau’s sign

59
Q

What labs would you want to evaluate on pt with hypocalcemia?

A

Parathyroid hormone (PTH)
Vitamin D (both 25-OH Vitamin D and 1,25 Vitamin D/calcitriol)
Albumin
Creatinine
Calcium (correct if necessary)
Phosphorus
Magnesium

60
Q

What is the treatment for hypocalcemia? Severe?

A

identify and treat underlying cause

Calcium replacement (give Vit D if needed)
______________

IV Calcium - 10% calcium gluconate 10-30 mL IV over 10-20 min

IV Magnesium if also low

Vit D if needed

61
Q

**What can IV calcium cause that you need to be mindful of?

A

IV calcium can cause vasoconstriction and possible ischemia

62
Q

_____ excessive PTH secretion leading to hypercalcemia, hypophosphatemia. It is the MC cause of ______. What is the MC pt demographic?

A

Primary Hyperparathyroidism

hypercalcemia

black then white women over 50-65 years old

63
Q

Primary Hyperparathyroidism is usually caused by a ______

A

parathyroid adenoma

64
Q

often asymptomatic
discovered incidentally
secondary to hypercalcemia: Bone pain, constipation, fatigue, altered mental status, bradycardia, kidney stones/nephrocalcinosis

What am I?
Can you usually feel a mass?

A

Primary Hyperparathyroidism

Parathyroid adenoma is not typically palpable on exam unless it is a carcinoma then you can in 52% of patients

65
Q

What will the calcium and PTH lab values look like in primary hyperparathyroidism? What will labs look like if carcinoma is present?

A

corrected or ionized calcium: will be elevated

PTH: will be elevated
____

corrected or ionized calcium: If carcinoma present - levels often ≥ 14.0 mg/dL

**PTH: If carcinoma present - PTH often >5x ULN

66
Q

What is the way to confirm your dx of primary hyperparathroidism?

A

elevated PTH in the presence of elevated ionized/corrected calcium

67
Q

What do you do if PTH is normal/minimally high compared to Ca?

A

check 24 hr urine Ca

check for familial hypocalciuric hypercalcemia

68
Q

**What is familial hypocalciuric hypercalcemia? What condition is it associated with?

A

are autosomal dominant d/o causing decreased function of calcium-sensing receptors on parathyroid and renal cells , so that higher than normal serum calcium concentrations are needed to suppress PTH release

primary hyperparathyroidism

69
Q

If the 24 hour urine calcium is above _____ is (includes/excludes) FHH. If it is less than _____, what does it tell you? What medications must be help prior to testing?

A

200-300

excludes: so probably primary hyperparathryoidism

less than 200: FHH or primary hyperparathyroidism with vit D deficiency

Must stop loop and thiazide diuretics prior to testing

70
Q

_____ helps differentiate primary from secondary hyperparathyroidism. What does the results indicate?

A

Serum phosphorus

Normal to Low (< 2.5 mg/dL) - primary hyperparathyroidism

High (>4.5 mg/dL) - secondary hyperparathyroidism

71
Q

What will Serum 25-OH Vitamin D and eGFR look like in primary hyperparathyroidism?

A

Serum 25-OH Vitamin D - may be low in hyperparathyrodism due to excessive conversion of 25-OH vitamin D to 1,25 vitamin D (calcitriol)

eGRF: just checks the status of the kidneys aka looking for renal dysfunction

72
Q

Is imaging needed to dx primary hyperparathyroidism?

A

NOT needed to dx

only needed if you are thinking sx

73
Q

_____ is the most used imaging for soft tissues in the neck. When is Nuclear Medicine Parathyroid Scan used? When are CT-4D scans used?

A

Neck US

to check function of Hyperfunctioning parathyroid glands light up brighter than normal tissue

Uses CT imaging to capture rapid uptake and washout of parathyroid adenomas
Mainly used if US and parathyroid scan are indeterminate or if concern for ectopic parathyroid tissue (adenomas, carcinomas)
aka measured over time and looking for metabolic activity

74
Q

What is the tx for asymptomatic primary hyperparathryoidism?

A

Geared at keeping bones healthy and minimizing symptoms

Adequate hydration - 6-8 glasses of water/day

Encourage physical activity: reduces bone resorption

Avoid medications that aggravate hypercalcemia: Thiazides, lithium, high doses of vitamin A

Moderate intake of calcium (1000 mg/d) and vitamin D (400-800 IU/d)

routine monitoring of labs: serum calcium, 25-OH Vit D, PTH
renal function labs
24-hr urine for calcium

DEXA scans

75
Q

What medications should a pt with primary hyperparathyroidism avoid?

A

Thiazides, lithium, high doses of vitamin A

76
Q

What is the DEFINITIVE treatment for asymptomatic primary hyperparathyroidism? What are the requirements? What happens if they are symptomatic?

A

surgery

only have to meet ONE criteria:
Kidney stones or nephrocalcinosis
Bone disease (osteopenia, osteporosis, pathologic fracture)
Persistent urinary calcium >400 mg/dL
Serum calcium >1 mg/dL above ULN
Age <50 years old

same criteria PLUS symptomatic or anyone who wants a cure and is healthy enough for surgery

77
Q

What is the management for symptomatic nonsurgical primary hyperpararthyroidism whose bone density is WNL? What are the SE? What does it NOT do?

A

cinacalcet (Sensipar)

nausea, arthralgia, diarrhea, myalgia, paresthesia

Does not improve bone density or reduce calciuria

78
Q

_____ binds to CaSRs in parathyroids, thereby decreasing PTH secretion. What lab do you need to monitor? and when?

A

cinacalcet (Sensipar) aka its calcium receptor blocker

Recheck serum calcium one week after initiating!

79
Q

What is the management for symptomatic nonsurgical primary hyperpararthyroidism whose also has osteoporosis? What does it NOT do?

A

Bisphosphonates:

oral: alendronate (Fosamax), ibandronate (Boniva)

IV: pamidronate (Aredia), zoledronic acid (Reclast)
_____

Oral versions do not significantly impact hypercalcemia or hypercalciuria!

IV: Can temporarily treat hypercalcemia

80
Q

_____ bind to hydroxyapatite and, when resorbed by osteoclasts, impair ability of osteoclasts to continue to resorb bone
Also decrease numbers of active osteoclasts by inhibiting osteoclast progenitor development and encouraging osteoclast apoptosis.

Oral version, what is the pt education?
When is the IV version used?

A

Bisphosphonates

oral: Patient must be able to remain upright for 30 minutes after ingestion

IV: Can temporarily treat hypercalcemia
May be used to help prepare patients with severe hypercalcemia for surgery

81
Q

Which management for primary hyperparathyroidism can cause a slight reduction in serum calcium specifically when given to postmenopausal women? Is it first line?

A

Estrogen Replacement: aka protective effect on CA in the bones

NOT first line

82
Q

_____ selective estrogen receptor modulator (SERM). Estrogen agonist in the bone to decrease bone resorption. Estrogen antagonist in the uterus and breast to reduce cancer risk. Is it a first line tx? What condition?

A

Raloxifene (Evista)

NOT first line to treat primary hyperparathyroidism

83
Q

What are complications of primary hyperparathyroidism?

A

Weakened bones → osteopenia, osteoporosis, pathologic fractures (treat with Prolia, DEXA scan q 2 years, vertebrae at highest risk of fracture)

Vit D deficiency

renals effects: nephrolithiasis, nephrocalcinosis, CKD

84
Q

____ excessive PTH secretion leading to hypercalcemia, hypophosphatemia that is caused by an underlying chronic abnormal stimulus or disease. What is the MC etiology?

A

Secondary Hyperparathyroidism

chronic kidney disease

85
Q

Why is chronic kidney disease the MC cause of secondary hyperparathyroidism? What is the 2nd most common cause?

A

Poor renal reabsorption of calcium (hypocalcemia)

Inhibited excretion of phosphate (hyperphosphatemia)

Inadequate renal conversion of 25-OH Vit D to 1,25 Vit D
______

Vit D deficiency

86
Q

What is the MC pt demographic for secondary hyperparathyroidism?

A

Black/Hispanic elderly women

87
Q

HTN
edema
abnormal laboratory values: Low Vit D
LESS likely to have classic s/s of hyperparathyroidism
s/s of hypocalcemia: hyper- reflexive

What am I?
What will BUN/Creatine/eGFR show?
PTH/Calcium/Phosphorus/1,25 Vit D?

A

secondary hyperparathyroidism

BUN/Cr: will be elevated
eGFR: will be decreased

PTH - elevated
Calcium - low to normal
Phosphorus - high in CKD; low in vitamin D deficiency
1,25 Vitamin D - low in CKD and vitamin D deficiency

88
Q

When would you order imaging on a pt with secondary hyperparathyroidism?

A

to look for complications

aka bone pain to look for pathologic fractures

89
Q

What is the management of secondary hyperparathyroidism?

A

refer to nephro if CKD is present

Vit D supplementation specifically 1,25 Vit D (Calcitrol aka the one that you do NOT need good kidneys for because it is already active)

90
Q

What is the MC cause of hypoparathyroidism? What are other causes?

A

typically involves some damage to the parathyroids usually some time of neck sx

autoimmune, radiation, infection, infiltration of cancer etc

90
Q

______ group of disorders characterized by kidney and/or bone resistance to PTH. What will calcium, phosphate and PTH lab values look like? What is the treatment?

A

Pseudohypoparathyroidism

decreased calcium
increased phosphate
increased PTH

calcium and vitamin D therapy to maintain normal serum calcium levels

akak kidney/bones are not responding to PTH

91
Q

You can see ____ associated with hemochromatosis, Wilson’s disease and/or Riedel thyroiditis

A

Hypoparathyroidism

92
Q

functionally hypoparathyroidism is associated with _____ levels. What will severely low levels do to PTH? low? high?

A

abnormal magnesium levels

Severe hypomagnesemia (<0.5) - “false block” of CaSR which SUPPRESS PTH

Mildly low magnesium - INCREASE PTH release

High magnesium - SUPPRESS PTH release

93
Q

_____ causes a “false block” of CaSR which suppresses PTH

A

Severe hypomagnesemia (<0.5)

94
Q

______ is directly proportional to how abnormal the calcium level is. What is the hallmark symptom?

A

Hypoparathyroidism

tetany due to neuromuscular irritability
mild: paresthesias
severe: spasms, seizure

can see Trousseau’s and Chvostek’s signs

95
Q

neurodegeneration, poor dentition, cataracts are all s/s of _____

A

chronic hypoparathyroidism

poor dentition (calcium leaving the teeth)

96
Q

What is the ACUTE management of hypoparathyroidism? What is the goal?

A

maintain the airway
IV calcium gluconate 10% if there is tetany, seizures, bronchospasm, laryngospasm, prolonged QT interval, refractory heart failure

Goal of serum calcium 8-9 mg/dL

start PO Calcitriol (1, 25 Vit D) and calcium when the pt can tolerate aka swallow the medication

if needed: Magnesium supplementation

97
Q

What forms are available for Calcitriol?
Cholecalciferol D3? Ergocalciferol D2?

A

Calcitriol:
capsules
solution
injection

Cholecalciferol:
capsule only

Ergocalciferol:
capsules
solution

98
Q

What do you give for hypomagnesium in the case of acute hypoparathyroid management?

A

Dosing for moderate-severe hypomagnesemia:

magnesium sulfate IV 1-2 g every 6 hours

Transition to magnesium oxide 400 mg 1-2 times daily PO

99
Q

What is the management of chronic hypoparathyroidism? What is the monitoring for each?

A

Oral calcium: monitor serum calcium q 3-6 months: need to keep calcium on the LOWER end of normal

Vit D and Magnesium supplement PRN

???Pts who are intolerant of, or refractory to calcium/Vit D-> PTH replacement therapy: Teriparatide (Forteo); (administered SQ), Synthetic PTH (1-34), Palopegteriparatide (prodrug)??

____
Urine and serum calcium, serum creatinine, phosphorus, 25-OH vit D
Every 3-6 months initially, then every 6-12 months

consider renal US if persistant hypercalciuria

100
Q

What is the prevention of hypoparathyroidism?

A

cryopreserved parathyroid tissue that are then injected into the brachioradialis, pectoralis or SCM

101
Q

______ Fat soluble vitamin, often from plant sources. What routes does it come in?

A

ergocalciferol D2

solution
capsule/ tablet

102
Q

___ and ___ MOA Stimulates calcium and phosphorus absorption in small intestine.
Stimulates calcium reabsorption at renal tubule.
Stimulates secretion of calcium from bone into the blood.

A

Vit D3 and D2

103
Q

____ - Peak effect approximately 1 month with daily dosing. Metabolism - liver, kidney. Elimination - urine

A

Vit D2: Ergocalciferol and Vit D3: cholecalciferol

104
Q

What are the SE of Vit D2/D3 and Calcitriol? CI?

A

SE: hypercalcemia - constipation, confusion, fatigue, arrhythmias

CI: Allergy to medication
Hypercalcemia
Hypervitaminosis D

105
Q

_____ Fat soluble vitamin, often from animal sources. What routes does it come in?

A

Vit D3: Cholecalciferol

solution
capsule/tablet

106
Q

____ is the metabolically active form of Vit D. What routes does it come in? What kind of pt is it good for? Who usually prescribes it?

A

1,25 Vitamin D (calcitriol)

Solution
Capsule
IV

good choice for pt’s who have bad kidneys

nephro rx only due to the higher chance of it causing problems due to its already active form

107
Q

______ MOA binds to and activates vitamin D receptor in kidney, parathyroid, intestine, bone. Decreases PTH levels, stimulates calcium absorption, can enhance the effects of PTH on bone.

A

1,25 Vitamin D (calcitriol)

108
Q

When does 1,25 Vitamin D (calcitriol) start working?

A

begins working in 2 hours as compared to Vit D2/3 that takes a month to start working

109
Q

_____ is oral calcium salt and is used in hypocalcemia prevention/treatment. What is a potential SE?

A

calcium carbonate

hypercalcemia

110
Q

_____ is IV calcium salt and is given in severe hypocalcemia. What is a potential SE?

A

Calcium Gluconate

hypercalcemia: aka it works too well

111
Q

_____ is an antacid and electrolyte. When do you exercise caution when giving to _____ pt. **What is a SE?

A

Magnesium Oxide

Caution if renal impairment

Diarrhea GI irritation

112
Q
A

Endocrine (14 decks)

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