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DERS (endocrine) > L29- Endocrine Pathology VII (Ca, PO4, Mg) > Flashcards

L29- Endocrine Pathology VII (Ca, PO4, Mg) Flashcards

1
Q

list the normal serum values of the following:

  • Ca++
  • PO4-
A

Ca: 2.2-2.6 mmol/L

PO4: 0.8-1.4 mmol/L

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2
Q
  • (1) amount of Ca in body in Kg, predominately in (2) form
  • 50% serum Ca is in (3) form, and the other half is in (4) form
  • total Ca levels are affected by the concentration of (5)
  • ionized Ca levels are affected by (6)
A

1- 1 Kg
2- 98% in bone, hydroxyapatite crystals

3- ionized Ca
4- bound to albumin

5- protein
6- pH (inc ionized Ca with acidosis / low pH —- dec in alkalosis)

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3
Q

describe general Ca function in ECF

A
  • regulates neuromuscular excitability

- acts as co-factor for clotting factors

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4
Q

describe general Ca function in cells

A
  • regulate activity of many enzymes

- exerts 2nd messenger hormonal function

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5
Q

list the hormones controlling Ca levels

A

PTH
1,25-dihydroxycholecalciferol (vitD)
calcitonin

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6
Q

describe role of PTH in Ca metabolism

A

-responds to low serum Ca (ionized form)

Actions:

  • bone for Ca/PO4 release
  • kidney for inc Ca reabsorption, dec PO4 reabsorption
  • kidney for vitD activation
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7
Q

describe the role of vitD in Ca metabolism

A

-activated by liver and kidney

Actions:

  • enhances Ca/PO4 absorption in the GIT
  • bone for Ca/PO4 resorption
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8
Q

describe the role of Calcitonin in Ca metabolism

A

(not involved??)
????
responds to high serum Ca (ionized)

Actions:

  • inc osteoblast activity (Ca/PO4 deposition)
  • dec Ca reabsorption and GIT absorption
  • dec vitD activation
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9
Q

list the 2 main causes of hypercalcemia

A

(90% of all cases)

1) hyperparathyroidism (most common)
2) malignant disease

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10
Q

list the ‘other’ (not main 2 causes) of hypercalcemia

A
  • excess vitD (vitD intoxication)
  • granulomas (Tb, lymphoma, sarcoidosis –> vitD activation)
  • high bone turnover: Thyrotoxicosis, Paget’s disease
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11
Q

Hypercalcemia clinical features:

  • (1) mainly
  • (2) renal
  • (3) MSK
A

1- asymptomatic (50%)

2- polyuria, stones, nephrocalcinosis (Ca crystal deposition in kidney –> renal failure)

3- muscle weakness; rarely demineralization, subperiosteal bone resorption, bone cysts (osteitis fibrosa cystica)

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12
Q

Hypercalcemia clinical features:

  • (1) mainly
  • (2) neurological
  • (3) GI
A

1- asymptomatic (50%)

2- psychiatric / neurological Sxs (MDD, lethargy, seizure)

3- anorexia, constipation, pancreatitis, peptic ulcer

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13
Q

list primary causes of hyperparathyroidism

A
  • solitary adenoma (mainly)

- hyperplasia, carcinoma (rarely)

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14
Q

describe secondary hyperparathyroidism

A

rxn of parathyroid glands to hypocalcemia not aused by parathyroid pathology

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15
Q

describe tertiary hyperparathyroidism

A
  • PTH incs to maintain normocalcemia in vitD deficiency
  • parathyroid hyperplasia occurs
  • PTH secretion becomes independent of Ca levels

-seen most often in renal failure patients (no vitD activation)

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16
Q

hyperparathyroidism is prominent component in ______ congenital disorders

A

MEN1, MEN2 (multiple endocrine neoplasia syndromes)

17
Q

Parathyroid (adenoma/carcinoma) is more popular and it is (usually/not) functional. Prognosis depends on (3).

A

1- adenoma
2- functional
3- extent of invasion and presence of metastasis

18
Q

list the main genes related to parathyroid tumors

A
  • MEN1 mutation

- cyclin D1 gene rearrangement

19
Q

functional adenoma or carcinoma of the parathyroid can be complicated by the following hypercalcemia sequelae

A
  • bone resorption

- foci of hemorrhage, necrosis

20
Q

Parathyroid Adenoma:

  • gross appearance
  • histological appearance
A

Gross:

  • typically well-circumscribed, soft, tan nodule
  • invested by delicate capsule
  • confined to single gland

Microscopy:

  • predominantly chief cells with rim of compressed non-neoplastic parathyroid tissue separated by fibrous capsule
  • minimal nuclear pleomorphisms, forming follicle, no anaplasia
21
Q

Parathyroid Carcinoma:

  • gross appearance
  • histological appearance
A

Gross:

  • enlarge one of glands
  • gray-white, irregular mass
  • dense fibrous capsule

Microscopy:

  • uniform cells resembling normal cells arranged in nodular / trabecular pattern
  • only reliable Dx is invasion or metastasis
22
Q

hypercalcemia investigations

A

plasma levels of:

  • Ca++ (total)
  • PO4-
  • ALP
  • PTH
23
Q

hypercalcemia management

A
  • correct dehydration
  • furosemide
  • bisphosphates
  • calcitonin
24
Q

list the causes of hypocalcemia

A
  • hypoalbuminemia: low total plasma Ca, but normal ionized Ca
  • Chelation by EDTA
  • PTH related: hypoparathyroidism, pseudohypoparathyroidism, hypomagenesemia
  • vitD metabolism defect: Ricketts, osteomalcia, CRF, vitD resistant rickets. liver disease, anticonvulsion therapy
  • acute pancreatitis
25
Q

list the clinical features of hypocalcemia

A
  • inc neuromuscular excitabiliy –> tetany, paresthesia, muscle cramps
  • prolonged hypocalcemia, associated with cataract, mental retardation, psychosis, inc intracranial P, seizures
26
Q

describe hypocalemicia investigation results

A

-dec serum Ca

Primary hypoparathyroidism: dec Ca, dec PTH, inc PO4

VitD deficiency: dec Ca, inc PTH, dec PO4

27
Q

list the many general causes of hypoparathyroidism

A
  • Congenital absence
  • Autoimmune syndrome
  • Thyroidectomy, neck surgery
  • Pseudohypoparathyroidism
28
Q

describe associations with congenital absence of parathyroid glands

A

-isolated
OR
-DiGeorge –> thymic and congeniral heart defects

29
Q

autoimmune syndromes causing hypoparathyroidism are usually associated with….

A

adrenal or ovarian failure (associated with other autoimmune issues)

30
Q

describe pseudohypoparathyroidism

A
  • dec responsiveness of target organs b/c PTH receptor issue

- sex-linked: males 2x more likely than females

31
Q

Hypoparathyroidism:

  • (1) skeletal features
  • (2) other features
A

1- short stature, short metacarpals, short metatarsals

2- cataracts, mental retardation, testicular atrophy

32
Q

list the many hypophosphatemia causes

A

Reduced absorption / Malabsorption

Inc cellular uptake: treated DKA, hyperalimentation alkalosis

Inc excretion: hyperparathyroidism, hypomagnesemia, renal tubular defects, dialysis

Dilution- volume expansion

Chronic alcohol abuse

33
Q

hypophosphatemia Sxs

A
  • muscle weakness
  • Hemolysis: due to 2,3-diphosphoglycerate (2,3-DPG) depletion
  • Respiratory failure: severe hypophosphatemia (critically ill Pts)
  • Rhabdomyolysis: skeletal muscle breakdown –> Myoglobin release –> ARF
34
Q

hyperphosphatemia causes

A
  • artefact: hemolysis or delay in separation of blood samples
  • CRF
  • hypoparathyroidism
35
Q

hyperphosphatemia effects

A

-high plasma Ca, PO4-

=> metastatic calcification (Ca salt deposition in normal tissue)

36
Q

hypomagnesemia:

  • (1) associations
  • (2) causes
A

1- hypocalemia, hypokalemia

2- malabsorption, malnutrition, alcoholism, diuretics, chronic mineralocorticoid excess

37
Q

hypomagenesemia Sxs

A 
tetany
agitation
ataxia
tremors
convulsions
38
Q

hypermagenesemia causes

A

renal failure

39
Q

hypermagnesemia effects

A

levels >6mg/L => respiratory paralysis and cardiac arrest

DERS (endocrine) (8 decks)

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