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DEMS Unit 4 > Disorders of Ca metabolism > Flashcards

Disorders of Ca metabolism Flashcards

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1
Q

PTH effects

A

directly on kidney/bone; indirect on GI via vit D

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2
Q

which form of vitamn D comes from animal vs plants

A
  • D3 from animals/we make in skin

- D2 from plant source (also has molecules inhibiting absorption)

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3
Q

major vitamin D store

A

25 hydroxyvitamin D– fat soluble— big reservoir

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4
Q

is hydroxylation regulated

A

No; based on mass effect

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5
Q

what regulates creation of 1, 25 (OH)2 vit D

A

PTH

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6
Q

parathyroid disorders vs vitamin D disorders

A
  • vitamin D disorders: Ca and phosphate go in same direction since it increases Ca and phosphate absorption
  • parathyroid disorders: moves Ca and P in opposite directions
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7
Q

vit D actions

A

increase Ca and P absorption

- at higher leves, increases bone resorption

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8
Q

Calcitonin

A

smaller hormone reducing Ca by reducing osteoclastic activity mainly

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9
Q

how do we regulate serum Ca/detect low Ca

A

Parafollicular C cells/parathyrod cells/renal tubular cells all have Ca sensor receptor– signals to inside of cell what level of Ca is

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10
Q

Hypercalcemia disorders

A
  • primary hyperparathyroidism
  • hypercalcemia of malignancy
  • granulomatous disorders (express 1alpha hydroxylase enzyme–so high 1, 25 vit D)
  • vit D/A intoxication
  • hyperthyroid
  • thiazide diuretics
  • Milk-Alkali syndrome
  • immobilization
  • adrenal insufficiency
  • acute renal failure
  • family hypocalciuric hypercalcemia
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11
Q

most common hypercalcium disorder

A

primary hyperparathyroidism,

hypercalcemia of malignancy

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12
Q

what do you order after see high Ca to help with diagnosis

A

PTH–

  • PTH elevated in hyperparathyroidism and low in all other except familial hypocalciuric hypercalcemia
  • low PTH– more likely malignancy
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13
Q

brown tumors

A
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14
Q

hyperparathyroidism causes

A

85% due to adenoma and the other 3 are atrophied
- 15% due to hyperplasia–usually familial and 4 glands affected
-

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15
Q

clinical features of primary hyperparathyroidism

A
  • > 50% asymptomatic
  • sk disease
  • kidney disease
  • GI disease
  • psych disease
    (Bones, Stones, Groans, Moans)
  • arthritis, muscle weakness, Band Keratopathy, HTN , anemia
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16
Q

most common sxs of primary hyperparathyroidism

A

NO SXS!!

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17
Q

Osteoclastoma

A

benign “brown tumor”

- severe hyperparathyroidism–once tumor removed, osteoclast dies and spot filled in

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18
Q

Band keratopathy

A

band of Ca deposition of cornea medially/laterally– circumferential

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19
Q

Primary hyperparathyroidism

A
  • elevated serum Ca
  • low serum Phosphate
  • elevated PTH (nl, midnl or elevated)
20
Q

hos often familial vs sporadic HPT

A

90% sporadic (can be hyperplastic)

10% familial (can be hyperplastic)

21
Q

familial cases of HPT

A

Familial HPT, MEN 1, MEN 2

22
Q

MEN1-

A
  • pituitary tumors (multiple), pancreatic islet tumors (multiple), parathyroid hyperplasia
  • germline mutation in Menin gene
23
Q

MEN2

A

medullary thyroid carcinoma (more aggressive)

  • pheochromocytoma
  • parathyroid hyperplasia
  • mutaiton in Ret gene (GDNF receptor)–abnormally expressed
24
Q

treat HPT

A
  • surgery – adenoma- (1 gland)– minimally invasive
  • for hyperplasia remove 3 1/2 and can leave insitu or removed and - reimplanted to be more available if it becomes overactive in future
  • Calcimimetic Drug (Cinacalcet): not curative, but f not good surgical candidate
  • Anti-resorptive Bone Drug( bisphosphonate, denosumab)
25
Q

Secondary hyperparathyroidism

A

elevated PTH in response to stimuli–low Ca orhigh serum P or low vitamin D

  • PTH elevated, but Ca low or low nl; phos high or high nl
26
Q

Hypercalcemia of Malignancy

A
  • Lung Canver (sq cell esp)
  • Breat Cancer
  • Head and neck
  • Kidney
    -Bladder
  • Pancreatic
    Ovarian
    Multiple Myeloma
    Lymphoma–express alpha hydroxylase–convert vit D to active form– hyperabsorb Ca
27
Q

hypercalcemia mediators

A 
in malignancy due to PTH related Peptide
- TGFbeta
-TNF
Interleukin 1, 6
TANK-L
DKK-1
1, 25 (OH)2 vit D
28
Q

PTHrp

A
  • protein made by gene expressed in placenta, lactating breasts, skin
  • possibly role in Ca crossing placenta and transporting Ca from maternal circulation to milk
  • first 13 amino acids the same as PTH, this is the part that binds to the receptor
29
Q

Hypercalcemia of malignancy

A

high Ca, low PTH, high PTH-RP or other mediators (1, 25, hydroxy vit D)

30
Q

Familial hypocalciuric hypercalcemia

A
  • inactivating mutations in Ca sensor receptor, so it doesn’t sense Ca levels–PT just continues to make PTH and kidneys continue to hold onto Ca
  • elevated Ca (mild)
  • mild elevated serum PTH
  • decreased Urine Ca and low Ca/Creatinine ratio (
31
Q

treatment for Familial hypocalciuric hypercalcemia

A

NOTHING–not harmful

32
Q

Causes of hypocalcemia

A

vitamin D deficient, hypoparathyroidism, pseudohypoparathyroidism, hypomagnesemia, renal failure, liver failure, acute pancreatitis, hypoproteinemia

33
Q

most common hypocalcemia cause

A

vitamin D deficiency

34
Q

Labs in hypocalcemia

A
    • elevated PTH, except for hypoparathyroidism(low)
35
Q

how much Ca bound to Ca

A
  • 50% bound to protein
  • 50% free/ionized
  • if low Ca in hospital, most likely due to low serum proteins
36
Q

what to consider on hospitalized pt with low Ca

A
  • most often due to low serum proteins, so do corrected serum total calcium
  • add 0.8 mg/dl to total Ca for every 1g/dl Albumin is
37
Q

sxs of hypocalcemia

A

paresthesias( lips/fingers), muscle cramps, muscle weakness, Chvostek’s Sign/Trousseau’s sign (both when more recent)

-may have sxs if acute but if chronic may have few sxs

38
Q

Trousseau’s sign

A

sign of acute hypocalcemia– when putting on BP cuff, will have carpopedal spasm

39
Q

Chvostek’s Sign

A

when tapping facial nerve in someone who has hypocalcemia, corner of lip will twitch

40
Q

Vit D disorders

A
  • Acquired deficiency (poor intake/inadequate sunlight)
  • Acquired 1,25(OH)2 vit D def (renal disease, hypoparathyroidism)
  • Congenital 1 alpha hydroxylase deficiency – “Vit D dependent Ricket’s Type 1:
  • Congenital Vitamin D receptor Deficiency - Vit D dependent Rickets Type 2 –give enough vit D will responsd
41
Q

Labs on vit D deficiency

A

low Ca, Low, P, low 25 OH vit D
elevated PTH
Alk phos up if osteomalacia

42
Q

Pseudofracture

A

not actual fracture–demineralizaiton where artery crosses bone
- commonly tibia, femoral neck
“Milkman’s fracture”

43
Q

treat vit D def

A
  • replete with high doses vitamin D then maintain on 1000 units a day
44
Q

hypoparathyroidism

A

low Ca, high P, low PTH

45
Q

spontaneous hypoparathyroidism in young ppl

A
  • autoimmune, oft associated with adrenal insufficiency and mucocutaneous candidiasis due to T cell immunodeficiency
46
Q

pseudohypoparathyroidism

A
  • inability to respond to PTH on membrane bound receptor. Have inactivating mutation in alpha Gs subunit–PTH can bind but no signalling
  • oft associated with Albright’s Hereditary Osteodystrophy: shortnening 4/5th metacarpals
    (but can occur without pseudohypoparathyroidism)
47
Q

labs on Pseudohypoparathyroidism

A
  • low Ca
  • high P
  • ## high PTH

DEMS Unit 4 (16 decks)

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