Exam 4 Week 3 Flashcards

1
Q

Forms of plasma calcium and pH effect

A
  1. Free/ionized 45%
  2. Bound to albumin 40%
  3. Bound to anions (PO4) 15%
    Increased pH=increased negative charge=increased binding and therefore hypocalcemia
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2
Q

Signs of hypocalcemia

A
Hyperexcitibility:
Cramps
Pain
Paresthesias
Carpopedial spasm/tetany
Seizures
Chvostek sign (cheek)
Trousseau (triceps, spasm)
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3
Q

Signs of hypercalcemia

A
Hypoexcitibility
Nephrolithiasis
Nephrocalcinosis
CNS disturbances (depression/seizure)
Constipation, PUD
Acture pancreatitis (enzyme activation)
Osteitis fibrosa cystica (fibrosing bone)
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4
Q

Vitamin D overview and functions

A

D3: sun exposure, animal products
D2: plants
Increase diet absorption of Ca2+ and PO4
Enhances bone mineralization

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5
Q

Vitamin D stimulation

A

High PTH
Low Ca2+
Low PO4
All stimulate 1,25-OH production

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6
Q

Functions of calicum

A

Structural: in bone/teeth (99%)
Biochemical: signaling, EC coupiling, exocytosis (1%)

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7
Q

Functions of PO4

A
Bone
High energy compounds
Membrane phospholipids
Regulation
DNA/RNA backbone
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8
Q

PTH Release:
Cell
Stimulus
Mech

A
Chief cells
Stimulated by low serum Ca
7 TM Ca sensor coupled to Gq
IP3/DAG/Ca influx
ER builds and releases PTH in vesicles
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9
Q

Vit D3 synth and PTH input

A

Skin (made)
Liver (25-OH) - storage form, helpful in deficiency lab
Kidney (1,25-OH) - active (24,25 = inactive)
PTH regulates at level of kidney

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10
Q

Vit D3 effect on gut epithelium

A

Increased Ca and PO4 absorption
Ca happens via increased BL transporter, calbindin, and apical pump
Happens via VDR/RXR and VDRE binding on DNA

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11
Q

Dietary Ca absorption

A

Passive: Paracellular, b/t tight jxns in D, J, I
Active: active transport in (TRPV6), intracellular transport (calbindin), pump out (PMCA)

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12
Q

Low dietary intakes ______ calcium absorption

A

Increases , but can only do so much

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13
Q

Ca gut absorption increased by (physio vs. dietary)

A

Physio: Vit D, increased physiologic demand
Dietary: Gastric acid, lactose, protein intake
BONE MINERAL DEPLETION CANNOT STIMULATE ABSORPTION

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14
Q

Ca gut absorption decreased by (physio vs. dietary)

A

Physio: Vit D def, steatorrhea (soap formation)
Dietary: Gastric alk, Oxalic acid, phytic acid

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15
Q

Main age of peak bone mass determination

Increase in RDA values?

A

Teens (30-50% accrued in teenage years)
Teens and elderly have increased RDA
Pregnancy and lactation do not

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16
Q

Calcium diet and supplements

Indications?

A
  1. Dairy is best
  2. Calcium carbonate (tums) taken with meals
  3. Calcium citrate malate taken between meals
    Only when needed! Risks with supplementation over 800mg/d of dietary intake: MI, stroke, death
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17
Q

High risk calcium groups

A
  1. Teens
  2. Premies (3rd trimester Ca placenta crossing)
  3. Peri-menupausal
  4. Bariatric surgery patients
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18
Q

Osteoporosis highlights
Genetics vs. variability
DASH diet effect

A

70% genetic, 30% variable

Decreased Na leads to less Ca loss (increased Ca)

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19
Q

Symptoms of hypercalcemia

Signs

A
Bones: bone pain
Stones: CaO kidney stones
Groans: GI upset
Moans: Psych
Signs: brown tumor, band keratopathy
20
Q

Hypercalcemia with high PTH

A

1˚ parathyroidism (higher urine Ca, more likely to have stones)
FHH (low urine Ca)

21
Q

Hyperparathyroidism treatments

A

Surgery (adenoma vs. hyperplasia)
Calcimemtic: Cinacalet
Anti-resorptive drug: Bisphosphonate, denosumab

22
Q

Secondary hyperparathyroidism causes

A

Renal failure, vitamin D def, Ca def

23
Q

Hypercalcemia of malignancy: cancer types and secretion type

A

Lung CA - systemic release leading to symptoms
Breast CA - local release: needs to met to bone for symptoms
Head and neck CA

24
Q

Main mediator of hypercalcemia of malignancy

Actions?

A

PTH-related peptide

Increases Ca from bone, but doesn’t act on kidneys and therefore phos will be high

25
Q

Hypocalcemia causes

A

Main: hypo-proteinemia

Vit D def, renal/liver failure, acute pancreatitis

26
Q

Hypoalbuminemia Ca correction (Ca will appear low but it probably isn’t)

A

For every 1g < 4g, add .8 to serum Ca

27
Q

Hypercalcemia of malignancy: s/s

A

Polyuria, polydipsia
N/V
AMS/coma

28
Q

Symptoms of hypocalcemia

A

Cheek/triceps sign
Weakness/cramps
Parasthesias (especially peri-oral)

29
Q

Lab values differentiating vit D deficiency and hypoparathyroidism

A

Vit D def: high PTH, low phos

Hypoparathyroidism: low PTH, high phos

30
Q

2 main causes of osteomalacia/rickets

A

Vitamin D def

Hypophos (diet or renal wasting)

31
Q

Clinical features of osteomalacia vs. rickets

A

Osteo: adults, pseudofx, bone pain, fx
Rickets: bowing, short stature, weakness

32
Q

Causes of hypoparathyroidism and lab values

A

Surgical injury
Autoimmune
Low Ca, High PO4, Low PTH

33
Q

4 types of vitamin D deficiency

A

Acquired vit D def: decreased diet or sun
Acquired 1,25 OH def: renal dz
1-a-OH def: vitamin D dependent rickets type 1
Vit D receptor def: vitamin D dependent rickets type 1

34
Q

Pseudohypoparathyroidism and lab values and classic signs

A

receptor deficiency
Low Ca, High PO4, High PTH
Short stature, decreased 4th/5th digit size

35
Q

Types of Rickets

A

1-a-OH def: vitamin D dependent rickets type 1
Vit D receptor def: vitamin D dependent rickets type 1
Hypophos rickets: vit D resistant rickets, PO4 wasting (95% congenital rickets)

36
Q

Paget’s etiology

A

Genetic + chronic paramyxovirus infection

37
Q

Paget’s stages

A
  1. Reabsorption (High CTX, NTX)
  2. Balance (High CTX, NTX and alkphos)
  3. Formation (Low CTX, NTX and High/low alkphos)
38
Q

Radiographic findings in Paget’s

Bone scan findings

A

Osteolytic lesions (blade of grass)
Thickened and disordered trabeculate
Bone scan: increased uptake

39
Q

Paget’s histology

A

Increased osteoclast number and nuc per cell
Increased peripherial osteoblasts
Disordered bone

40
Q

Path findings Graves dz

A

Hyperplasia, scalloping of colloid

41
Q

Path findings Hashimoto

A

Mononuclear inflammation
Onc metaplasia
Germinal center formation

42
Q

How to define inclusion criteria for SR/MA

A
P = population
I = intervention
C = control/comparison
O = outcomes
S = study design
43
Q

Methodology of SR

A
  1. Focused question
  2. Complete and explicit data search
  3. Unbiased selection
  4. Critical appraisal
  5. Synthesis of data (if part of study design)
44
Q

SR specific bias

A

Publication bias (+ results more likely to be published)

45
Q

Heterogenity in MA: clinical difference options

A
  1. Don’t do MA
  2. Ignore = fixed effects
  3. Allow = random effects
  4. Explore variability