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Clin Med Exam 3 > Hypercalcemia/Hypocalcemia - Randor > Flashcards

Hypercalcemia/Hypocalcemia - Randor Flashcards

1
Q

what body systems use calcium?

A

nervous system (maintains BP), muscular system (muscle contraction), skeletal system (99% found in bone as hydroapatite)

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2
Q

what is the total serum ca?

A
  1. 5-10.5 mg/dL

- only 45% is what we are using

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3
Q

when is it important to have total serum ca?

A
  • The only time it is important is if you see a patient that is hypocalcemic need to look at their albumin
  • If hypoalbumnemic then need to calculate to correct it poor mans way, but best way
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4
Q

what are the 2 mediators of calcium and phosphate balance?

A

parathyroid hormone (PTH) & Calcitriol (active form of vitamin D)

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5
Q

what does PTH do for ca?

A

Secreted by parathyroid gland

Net effect:

  • Increase serum calcium
  • Decrease serum phosphate
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6
Q

what does calcitriol do?

A
  • Enhances intestinal cells to absorb calcium and phosphate into the serum
  • Derived from diet or from UV light
  • Required enzymatic steps in the liver and kidney to become active Vitamin D

Net effect:

  • increase serum ca
  • increase serum phosphate
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7
Q

what else helps mediate serum calcium, but to a lesser extent?

A

calcitonin

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8
Q

how is PTH synthesized and secreted by parathyroid gland for low serum Ca?

A

In response to low serum Ca++:

  • Bone – PTH stimulates bone resorption (osteoclastic) which leads to increase in serum Ca++
  • Kidney – PTH promotes Ca++ resorption and stimulates hydroxylation of 25-hydroxyvitamin D (calcidiol) via an enzyme
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9
Q

how is PTH synthesized and secreted by parathyroid gland for high serum Ca?

A

In response to high serum Ca++:

-Parathyroid hormone decreases it’s production

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10
Q

net effects of PTH?

A

Increased serum calcium decreased PTH

Decreased serum calcium increased PTH

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11
Q

Ca/phosphate homeostasis in bone

A
  • PTH activates osteoclastic activity to increase serum Calcium
  • PTH inhibits osteoblastic activity
  • Active vitamin D promotes osteoblastic activity
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12
Q

Ca/phosphate homeostasis in kidney

A
  • Reabsorbs Calcium
  • Secretes Phosphate in the urine
  • Increases serum alpha hydroxylase in order to convert Calcidiol into active Vitamin D (calcitriol)
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13
Q

Ca/phosphate homeostasis in gut

A

Calcium and phosphate are transferred to blood via ingested food - thanks to activated vitamin D (calcitriol)

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14
Q

what is the most common cause of hypocalcemia & why?

A

CKD

-b/c of renal failure don’t get alpha hydroxylase so don’t get active vitamin D form

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15
Q

what causes vitamin D deficiency?

A

CKD #1 cause

-Kidneys not working, so not responding to PTH to reabsorb serum calcium and kidneys not making alpha hydroxylase to make Vitamin D active

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16
Q

what are causes of hypocalcemia?

A

Parathyroid:
-thyroidectomy (also lose parathyroid gland), iodine therapy

Vitamin D Deficiency:
-CKD (#1 cause)

Hungry Bone Syndrome

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17
Q

why is hypocalcemia from hypoparathyroidism uncommon?

A

b/c hypocalcemia from hypoparathyroidism requires all 4 parathyroid glands to be affects

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18
Q

causes of hypoparathyroidism?

A

Parathyroidectomy or thyroidectomy

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19
Q

what are the symptoms of hypocalcemia + hypoparathyroidism?

A
  • emotional lability (irritable, depressed)
  • paresthesia (personal, hands, get)
  • shortness of breath (diaphragmatic spasms)
  • voice changes (laryngospams)
  • vision changes (cataract formation) -> chronic
  • personality changes (may be irreversible)
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20
Q

Physical exam findings of hypocalcemia (hypoparathyroidism)?

A

Tetany - repetitive discharge of peripheral nerves after single stimulus

  • Chvostek’s sign (tap on cheek and get face twitch)
  • Trousseau’s sign (bp cuff -> carpal spasms and adduction of the thumb)

Hyperreflexia, muscle stiffness, seizures

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21
Q

what are the “cats” of hypocalcemia?

A
  • Convulsions
  • Arrhythmias
  • Tetany (Chvostek’s sign & Trousseau’s sign)
  • Spasms and stridor
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22
Q

what is seen on EKG for hypocalcemia?

A

QTc prolongation (leads to arrhythmias)

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23
Q

labs for hypocalcemia?

A

Vitamin D levels (calcidiol)

BUN/Cr, Phosphate, Magnesium, Albumin, LFTs, PT/INR

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24
Q

why get vitamin D levels in hypocalcemia?

A

b/c need to see if there is any calcitriol (won’t be any)
-in order to get calcidiol, the liver has to work -> calcidiol goes to kidney -> calcidiol will look normal, but won’t get converted to calitriol b/c kidney not working

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25
Q

why check BUN/Cr in hypocalcemia?

A

Check renal function b/c #1 cause of hypocalcemia is CKD

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26
Q

why check Magnesium levels in hypocalcemia?

A
  • Important to always assess
  • If mag is low you will never be able to replete K or Ca
  • If patient is hypokalemia need to replete Mg first
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27
Q

treatment for hypocalcemia?

A

Oral Ca:

  • ca carbonate (2 doses)
  • ca citrate

IV Ca:

  • Ca gluconate
  • Ca chloride (only given when pt dying)

Vitamin D

  • Calcitriol (active form)
  • Vitamin D2 (ergocalciferol)

Mg prn
Diet rich in Ca
Avoid diuretics

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28
Q

what are the indications to give IV Ca for hypocalcemia?

A
  • Severe symptoms (tetany, seizures)
  • Prolonged QT interval or arrhythmia
  • Suspected abrupt decrease from normal
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29
Q

what are the indications to give vitamin D for hypocalcemia?

A

Hypocalcemia secondary to Hypoparathyroidism, Hungry Bone Syndrome, Vitamin D Deficiency

30
Q

what is a common metabolic emergency and most common electrolyte abnormality in adults in malignancies?

A

hypercalcemia

31
Q

what causes hypercalcemia?

A

S.H.A.M.P.O.O

Sarcoidosis (increases ca in your system)

Hyperparathyroidism (most common)

Alkali Milk Syndrome (excessive dietary intake of ca like tums)

Metastasis (most common)

Paget disease

Osteogenesis imperfect

Osteoporosis

32
Q

what is alkali milk syndrome defined by?

A

hypercalcemia, metabolic alkalosis, and renal insufficiency

33
Q

how does metastasis cause hypercalcemia?

A

Malignancies secrete PTH related peptide that isn’t regulated by regular parathyroid and causes more bone breakdown

34
Q

what else causes hypercalcemia, besides SHAMPOO?

A

D.I.R.T

  • D Vitamin intoxication
  • Immobility
  • RTA (renal tubular acidosis)
  • Thiazides
35
Q

what is the most common cause of hypercalcemia?

A

hyperparathyroidism

seen in MEN 1, 2A, 2B

36
Q

what are the causes of primary hyperparathyroidism?

A

hyperparathyroidism and hypercalcemia

Single parathyroid adenoma (80%)

37
Q

what are the causes of secondary hyperparathyroidism?

A

overproduction of PTH due to chronic abnormal stimulus

Chronic renal failure

  • Will have elevated PTH and hypocalcemia b/c not talking to the kidneys
  • Parathyroid senses hypocalcemia and continues to produce PTH without it ever reaching the kidney

(hyperparathyroidism and hypocalcemia)

Vitamin D Deficiency

38
Q

what are the causes of tertiary hyperparathyroidism?

A

state of excessive secretion of PTH after longstanding secondary
-Renal Transplant patient

39
Q

are exam findings contributory to diagnose hypercalcemia?

A

No!

Most of the time exam is non-contributory (no reliable physical findings of hypercalcemia that are sensitive or specific enough to diagnose hypercalcemia)

40
Q

Exam findings of hypercalcemia?

A

Skin: pruritus, skin tenting (dehydration) - b/c peeing out extra Ca

Cardiac: HTN, LVH - Hear S4 and displaced PMI for LVH

GI: anorexia, N/V, constipation, abdominal pain

Renal: renal colic (kidney stones)

MSK: bone fractures (wrist and vertebrae most common)

Neuro/Psych: paresthesias, diminished DTR (reflexes diminished), muscle weakness, depression

41
Q

hypercalcemia dx

A
  • Calcium level
  • PTH (elevated)
  • 24 hour urinary calcium excretion
  • Chloride, phosphate
  • PTHrP
  • BUN/Creatinine (check for renal failure)
  • Calcitriol or Calcidiol

-ECG: AV block, shortened QTc can go into cardiac arrest

42
Q

are imaging studies used to make the dx for primary hyperparathyroidism?

A

Imaging studies are not used to make the diagnosis of primary hyperparathyroidism, may be used to guide the surgeon

43
Q

hyperparathyroidism image findings?

A

Sestamibi scan: tells you where it’s occurring
-Uptake of abnormal parathyroid adenoma

Ultrasound of the neck tells you where it’s occurring

MRI/CT at bottom of list

Bone density measurement by DXA (dual xray absorptiometry) to assess amount of bone loss-focus on lumbar spine, hip, and distal radius

44
Q

X-ray findings for hyperparathyroidism?

A

Osteitis Fibrosa cystica – subperiostal reabsorption of the distal phalanxes

“salt and pepper” appearance of skull

Brown Tumor of long bones

45
Q

hyperparathyroidism txt for asymptomatic pts

A
  • Stay active, avoid immobilization, drink plenty of fluids
  • Modest dietary calcium
  • Vitamin D recommendation based on age
  • Bisphosphates (take Ca out of serum and back into bones; also used in osteoporosis)
  • Discontinue Thiazides, Vitamin A, Calcium containing antacids

Asymptomatic patients and not candidate for surgery, require annual serum calcium and creatinine; Bone Density Scan done 1-2 years

46
Q

what is the mainstay of txt if young and symptomatic or pregnant?

A

surgery

47
Q

what patients are candidates for surgery even if asymptomatic?

A
  • <50 y.o
    -elevated serum Ca (>1.0 ULN)
    -CrCl <60
    24hr urine Ca >400
    -nephrolithiasis
    -osteoporosis
    -vertebral fracture
48
Q

treatments for symptomatic but poor surgical candidates/declining surgery/awaiting surgery?

A
  • Fluids – IV fluid to pee out extra calcium and dilute yourself
  • Furosemide (loop diuretic)
  • IV Bisphosphonates – work faster
  • Calcitonin – thyroid creates this, is quick but has weak effect
  • Cinacalcet
  • Propranolol may help reduce cardiac symptoms
49
Q

hypercalcemia txt medications?

A
  • Normal Saline – decreased the calcium levels through dilution, allows for expansion of ECF volume
  • Loop Diuretics – used with hydration will increase calcium excretion
  • Bisphosphonates – inhibit osteoclastic activity
  • Calcitonin – inhibits bone removal by osteoclasts, and promotes bone formation by osteoblasts

-Steroids – vitamin D toxicity, myeloma, sarcoidosis
Magnesium

50
Q

examples of bisphosphonates used for hypercalcemia?

A

pamidronate

zoledronic acid

alendronate

risedronate

51
Q

what has a genetic predisposition in families with MEN1 and 2A?

A

parathyroid cancer

52
Q

symptoms of parathyroid cancer?

A
  • consistent with mass effect and hypercalcemia

- suspected if symptoms are severe, Ca levels >14, PTH levels 5x normal, palpable parathyroid gland

53
Q

what is Paget’s disease?

A

localized disorder of bone remodeling with excessive resorption followed by disorganized bone formation

  • Bones become weaker, larger and more vascular
  • When fracture, bleed heavier
54
Q

what bones are commonly affected in Paget’s disease?

A

Pelvis, lumbar spine, femur, thoracic spine, sacrum, skull, and tibia

55
Q

when is Paget’s disease usually found?

A

incidentally on imaging or elevated Alk Phos

56
Q

what are the phases of Paget’s disease? (HINT: 3)

A

(1) Lytic
(2) mixed lytic and blastic
(3) sclerotic

57
Q

Lytic phase of Paget’s disease?

A

first phase of Paget’s disease

osteoclasts that are more numerous and larger than normal, burn turnover rate is 20 x higher

58
Q

Mixed lytic & plastic phase of Paget’s disease?

A

second phase of Paget’s disease

rapid increase in bone formation from numerous osteoblasts, new bone is haphazardly laid

59
Q

Sclerotic phase of Paget’s disease?

A

third phase of Paget’s disease

bone formation dominates and it’s formed in a disorganized (woven) pattern and therefore weaker than normal bone

The woven pattern allows for bone marrow to be infiltrated by excessive fibrous connective tissue and blood vessels, leading to a hypervascular bone state.

60
Q

s/sx of Paget’s disease?

A

70-90% are asymptomatic (often an incidental finding)

Pain is the most common symptom (orthopedic pain)

Pathologic fractures (heavy bleeding)

Osteoarthritis

Nerve impingement (rare)

Bones become soft -> bowed tibias, kyphosis

If skull is involved -> HA, increased hat size (if involves skull may develop hearing loss issue or deafness)

61
Q

Dx of Paget’s Disease

A

incidental either by radiographic or elevated alkaline phosphatase

62
Q

what blood levels can you use to assess for bone turn over rate in Paget’s disease?

A

Serum N-terminal Propeptide of Type 1 collagen (NTx)

Serum BetaC-terminal propeptide of Type 1 collagen (betaCTx)

only seen in ACTIVE Paget’s disease, so these test may not be useful

63
Q

what else should be checked when diagnosing Paget’s disease?

A

serum calcium, vitamin D and serum phosphate should be checked

64
Q

what will you see in stage 1 of paget’s disease on imaging?

A

Stage 1: Osteolytic phase driven by excessive osteoclast bone resorption

Seen as areas of bone loss on x-ray

65
Q

what will you see in stage 2 of paget’s disease on imaging?

A

Stage 2: Combined lytic/sclerotic phase due to osteoclast-induced activation of osteoblasts. Newly formed bone appears disorganized and structurally weaker.

Radiographically, there is thickening of the cortices, exaggerated trabecular markings, and loss of the corticomedullary distinction.

These changes are commonly referred to as having a “cotton-wool” or “picture-frame” appearance (for the skull and vertebrae, respectively)

66
Q

what will you see in stage 3 of paget’s disease on imaging?

A

Stage 3: Osteosclerotic “burnt-out” phase due to declining bone turnover

Bones appear enlarged and dense on imaging

67
Q

Radionuclide bone scans (aka bone scintigraphy) and Paget’s disease

A

if patient has ACTIVE Paget’s disease, will have increased uptake in the areas of bone affected, but if patient does NOT have active Paget’s disease, then the bone scan will be normal

68
Q

Paget’s disease complications

A
  • Pain
  • Arthritis
  • Disability
  • Vertebral collapse/Fracture
  • Cranial nerve palsies
  • Hearing loss
  • Paralysis
69
Q

Paget’s disease txt

A

Surveillance: Asymptomatic patients

Medication: IV zoledronate 5mg over 15mins

70
Q

when do you measure serum alk phos when treating Paget’s disease?

A
  • MEASURE SERUM ALK PHOS AT 3-6 MONTHS TO ASSESS TO SEE IF RESPONDING TO TREATMENTS
  • Once value plateaus, it can be measured once or twice a year as a marker of bone activity

Clin Med Exam 3 (6 decks)

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