Hypercalcemia and Hypocalcemia Flashcards
What two hormones are responsible for calcium homeostasis?
What three organs play a role?
PTH and Vitamin D
Bone, Small intestine, and kidney
Hypercalcemia- Clinical Manifestations
- GI:
- Neuro/Psych
- Cardio
- Renal
Hypercalcemia- Clinical Manifestations
- GI: N/V/Constipation
- Neuro/Psych: fatigue, AMS, weakness, depression, anxiety, coma
- Cardio: HTN, shortened QT interval, digoxin tosicity
- Renal: impaired water handling, volume depletion, renal failure
- chronically nephrolithiasis and nephrocalcinosis
**stones, bones, abdominal groans, and psychic moans
Hypercalcemia
- mild:
- moderate:
- severe:
Hypercalcemia
- mild: <12 mg/dL
- asymptomatic or mild, nonspecific symptoms
- moderate: 12-14 mg/ dL
- well tolerated chronically. an acute rise can cause significan symptoms
- severe: >14 mg/dL- significan symptoms
if we have hypercalcemia AND a normal or HIGH PTH
- what are the 4 possible causes:
if we have hypercalcemia AND a normal or HIGH PTH the causes are:
- Primary hyperparathyroidism
- tertiary hyperparathyroidism
- familial hypocalciuric hypercalcemia (FHH)
- Lithium
if we have hypercalcemia and low or low normal PTH
- What are possible etiologies?
hypercalcemia and low or low normal PTH
- Increased GI absorption of Ca
- Excessive Bone Resorption
- Decreased excretion of Ca
Familial Hypocalciuric Hypercalcemia (FHH)
- cause:
- inheritance:
- Clinical Findings:
- Management
Familial Hypocalciuric Hypercalcemia (FHH)
- cause: inactivating mutation in CaSR
- inheritance: AD with high penetrance
- Clinical Findings: benign disorder with no/subtle symptoms
- Management: management; avoidance of hypercalcemic precipitants
How does lithium cause hypercalcemia?
lithium changes the set point for PTH release
Treatment of Hypercalcemia
- increase urinary Ca excretion:
- inhibit bone resorption:
- decrease intestinal absorption:
- Dialysis
Treatment of Hypercalcemia
- increase urinary Ca excretion:
- IVF hydration- acute setting
- loop diuretics they increase excretion once the volume has been restored
- inhibit bone resorption: bisphosphonates and calcitonin
- decrease intestinal absorption: glucocorticoids
- Dialysis
Calcitonin
- What receptor does it affect?
- administration:
- period of treatment:
- adverse effects:
Calcitonin
- What receptor does it affect? GPCR receptor that activatesa G alpha S that activates adenylate cyclase
- administration: IM or SubQ
- period of treatment: short term treatment due to tachyphylaxis
- adverse effects: allergies (concentrated from salmon) and increased cancer risk with long-term list
Bisphosphonates
how can they treat hypercalcemia?
- MOA:
- Adverse Effects:
Bisphosphonates
- MOA: impedes osteoclast activity and stimulates apoptosis
- Adverse Effects: long term use can increase the risk of osteonecrosis of the jaw. Potential for nephrotoxicity
**Delayed onset of effects so in severe hypercalcemia its usually given with saline and/or calcitonin
How can glucocorticoids treat hypercalcemia?
- Vit D
- when are they used?
- what is a major side effect of glucocorticoids?
How can glucocorticoids treat hypercalcemia?
**Prednisone is most commonly used
- glucocorticoids reduce vit-D stimulated calcium absorption
- they are used in hypercalcemia associateed with overproduction of calcitriol (granulomatous disease and some cancers) or Vit D intoxication
- glucocorticoids can increase blood sugar (trigger diabetes) increase triglycerides and cholesterol, and increase your risk of ulcers and gastritis
HYPOcalcemia Clinical Manifestations
- Neuro/Psych
- Cardio
- eyes
- Skin
- Severity
HYPOcalcemia Clinical Manifestations
- Neuro/Psych: acroparesthesias, tetany, confusion, seizures
- Cardio: QT prolongation
- eyes: papilledema, cataracts
- Skin: dermatitis
- Severity: depends on degree and rate of decline
Treatment:
- symptomatic/acute:
- chronic
Treatment:
- symptomatic/acute- this is a medical emergency.
- IV calcium
- chronic- depends on the etiology
- give oral alcium +/- vitamin D
