Lecture #4 -- Parathyroid Physiology Flashcards Preview

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Flashcards in Lecture #4 -- Parathyroid Physiology Deck (79):
1

How is intracellular calcium controlled?

Pump-leak transport system
--Calcium leads into cytosolic compartment and is actively pumped into storage sites in organelles

2

What are the three definable fractions of calcium in serum

Ionized Calcium -- 50%
Protein Bound Ca -- 40%
Ca complexed to serum constituients -- 10%

3

What is protein bound Ca bound to

90% Albumin
Remainder to globulins

4

What serum constituients is Calcium complexed to?

Citrate and Phosphate

5

Explain the relationship of EC Ca binding to pH

Acute Alkalosis --> more Ca binding, less ionized Ca
Vice versa

6

Normal blood Ca range?

8.5-10 mg/dL

7

What type of Ca is biologically active?

Only free, ionized Ca

8

Physiological importance of Calcium?

Calcium salts provide structural integrity of skele.
Essential for biochemical processes (neura, muscular, coagulation, hormonal secretion, enzymatic rxns)

9

Where is most Ca found? What does it look like there?

99% Ca is found in the bone in hydroxyapatite crystals

10

Describe the process of Vitamin D synthesis

Occurs in keratinocytes
7dehydrocholesterol photoconverted to pre-D3
pre-D3 spontaneously converts to D3

11

How is Vitamin D3 production controlled

UV rays degrade previtamin D3 if present too long
1,25 dihydroxy-D feeds back to inhibit production

12

Two sources of vitamin D

Produced by skin + UV
Diet

13

Why is Vitamin D a shitty vitamin?
Why is D a shitty hormone?

Bad vitamin -- synthesized de novo
Bad hormone -- not produced/secreted by gland

14

First hydroxylation of in D3 processing takes place...
What about the 2nd?
What do these make?

in the liver, yielding 25-hydroxy D
in the kidney, making 1, 25 dihydroxy-D

15

Enzyme responsible for generation of 1,25 dihydroxy-D

Mitochondrial P450 enxyme -- 1 alpha hydroxylase

16

1-alpha hydroxylase is inhibited by

1, 25 dihydroxy-D

17

Effects of PTH on Vit D synthesis

Stimulates 1-alpha hydroxylase

18

Where does Vitamin D promote Ca absorption?

Duodenum > Jejunum > Ileum

19

Ca absorption is greatest at ____ pH

low pH

20

Blood supply of parathyroid glands?

Thyroid Arteries

21

Clevage of the C-terminal end of PTH yields...

.a biologically inactive peptide

22

How is PTH release regulated?

G protein coupled Receptor
Activated Phospholipase C, Inhibits Ad. Cyclase
Increase in intracellular Ca, decreased cAMP
These conditions don't allow PTH exocytosis

23

Overall action of PTH?

Increase plasma Ca levels
Decrease plasma phosphate levels

24

Three sites of PTH action

- Stims Bone Ca Resorption
- Stims Kidney Ca reabsorption, P excretion
- Stimulates 1, 25 Dihydroxy-D synth

25

Specific sites in nephron on kidney activities

Ca reabsorbed in distal tubule
P resorption inhibited in the prox (?)

26

What happens when PTH is secreted continuously?
Once Daily?

If cont., Gs in ost.blast increases cAMP, PLS, inhibits fxn
If once daily, the opposite

27

PTH half life?

2-3 minutes

28

Where is PTH broken down?

Liver (2/3) and Kidney (1/3)

29

Intake range of Ca?
Why is this okay?

200-2000 mg
Fractional gut absorption will adapt to deprivation or overload

30

General daily Ca balance

350 absorbed in intestine
750 lost in feces
200 lost in urine

31

Normal PO4 plasma concentration?

3-4.5 mg/dL

32

Low Calcium levels in the blood will ______ PTH release

Increase

33

High levels of 1,25 dihydroxy D and Ca have what regulatory power

Inhibition of transcription of PTH

34

Cell type with Calcium sensing receptor (CaSR)

Parathyroid Chief Cells

35

What is a Calcium Sensing Recptor (CaSR)

GPCR or Gplc and Gi varieties
Makes inositol 1,4,5-triphosphate
Increases intracellular Ca
Found in thyroid C Cells, Kidney, Brain

36

Where does calcitonin come from?
What does it do?

Parafollicular C cells of the thyroid
Inhibits osteoclast resorption and promotes renal Ca excretion

37

Big picture purpose of Calcitonin?

Decreasing plasma Ca

38

How can parafollicular (C) cells be distinguished in the thyroid?

They are large, pale cytoplasm, and have small secretory granules

39

What stimulates Calcitonin secretion?

High plasma Ca

40

Molecular method of Calcitonin action

Increased cAMP concentration to inhibit osteoclast motility and cell shape
This inactivated them

41

T or F. Calcitonin is necessary for human survival.

It probably isn't

42

Calcitonin is used clinically to treat.....

hypercalcemia

43

List some bone formation stimulants

GH, Insulin-like growth factos, insulin, estrogen, androgens, Vit D

44

Common bone formation inhibitor?

Cortisol

45

Common bone reabsorption inhibitors?

Estrogen, Androgen, Calcitonin

46

Three types of hypocalcemia

Hypoparathyroid
Nonparathyroid
PTH resistance

47

Causes of hypoparathyroid hypocalcemia

PostoperativeIoiopathic
Post Radiation
Autoimmune

48

Causes on Non-parathyroid hypocalcemia

Vit D Deficiency or Resistance
Malabsorption
Liver Disease
Kidney Disease

49

Causes of PTH resistance hypocalcemia

Pseudo-hypoparathyroidism

50

When should we expect to see Parathyroid Hormone Related Protein

Important in deveopment of hypercalcemia of malignancy
Also involved in development and lactation

51

Primary effects of Hyperparathyroidism

Hypercalcemia
Depressed neuromuscular excitability, lethargy, anorexia, muscle weakness, dulled mentation, constipation, renal stones, ulcers

52

Primary effects of Hypoparathyroidism?

Hypocalcemia
Increased neuromuscular excitability, hyperreflexia, decreased D3 synth, convulsions

53

Effects of Vitamin D toxicity?

Excess bone reabsorption and gut absorption of Ca
Increase in plasma Phos

54

Effects of Vitamin D deficiency?

Decreased plasma (buffered by PTH)
Decreased Bone Mineralization (Rickets/Osteomalacia)

55

Causes of primary hyperparathyroidism?

80% adenoma
15% parathyroid hyperplasia
other -- parathyroid carcinoma

56

Labs in Primary Hyperparathyroidism?
PTH, Ca, P, Urinary cAMP, Alkaline Phosphotase

Increase PTH
Increase Calcium
Decrease Pho
Increase Urinary cAMP
Increased alkaline phosphate

57

treatment for primary hyperparathyroidism?

Surgical excision of the gland
Cinacalcet (Sensipar) for non-surgical candidates

58

Cause of secondary hyperparathyroidism?

Excess PTH production in resp. to problem outside PT

59

Two commonly seen sources of secondary parathyroidism?

Chronic Renal Failure
Gastric Bypass Surgery

60

What causes secondary hyperparathyroidism in renal insufficiency>?

Decreased P excretion by kidneys
Increased serum phosphate binds free Ca
Lower free Ca level stimulates PT to produce PTH
Bone Resorption

61

Labs in secondary hyperparathyroidism
PTH, Ca, P, Alkaline Phos.

Increased PTH
Decreased Calcium
Increased P
Inc. alkaline phosphatase

62

Three primary causes of hypoparathyroidism?

Autoimmune hypoparathyroidism, surgical excision, digeorge syndrome

63

Features of a DiGeorge syndrome patient?

Abnormal faces
Congenital heart defects
Hypoparathyroidism with hypocalcemia
Cognitive, Behavioral, and psychiatric problems
Increased Susceptability to infections

64

Physical exam findings in a hypoparathyroidism patient?

Perioral numbness/tingling
Tetany, carpopedal spasms
Trosseau's Sign
Chvostek's Sign
Decreased PTH, Ca

65

How is hypoparathyroidism treated?

Calcitrol and Ca supplements
NatPara

66

What is pseudohpoparathyroidism

End Organ Resistance to PTH
Hypocalcemia and Increased PTH
Give patient short stature and short 4th and 5th digits

67

Review the charts on diagnosing with PTH and Ca levels

That'll probably be testable

68

What is osteoporosis?

Disease characterized by low bone mass and micro-architectural deterioration of boen tissue

Causes reduced bone strength and increased fracture risk

69

Presentation of Rickets, Osteomalacia

Insufficient mineralization of bone
Rickets is in children before growth-plate fusion
Osteomalacia occurs in patients of any age

70

Causes of Rickets, Osteomalacia?

Nutritional Def (D, Calcium Chelators, Antacid overuse)
GI Abs. Defects (Gastrectomy, Biliary disease, liver probs)
Renal tubular defects
Renal osteodystrophy

71

Clinical features of Rickets

Convulsions, Failure to Thrive, Tetany
Stunted Growth
Ricketic Rosary
Spinal Curvature
Bowing of Long Bones

72

Clinical features of Osteomalacia

Aches and Pains
Muscle Weakness
Loss of Height, Stree Fractures

73

What is Paget's Disease?

A disease of bone remodeling
Accelerated bone resorption and formation causes bone to be disorganized with more vascularity

74

Cause of Paget's Disease?

Unknown
Blamed on a Virus

75

How would you treat Paget's disease?

Bisphosphonates to decrease bone turnover

76

Clinical manifestations of Paget's disease?

Bone/Joint Pain
Deformity
Spontaneous Fractures
Hearing Loss

77

Other name for osteogenesis imperfecta

brittle Bone Disease

78

What is Osteogenesis imperfecta?

heritable disorder of connective tissue with 4 subtypes

79

Hallmark features of Osteogenesis imperfecta?

Bone fragility
Tendency to fracture with minimal trauma