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
Hypocalcemia causes
Main: hypo-proteinemia | Vit D def, renal/liver failure, acute pancreatitis
26
Hypoalbuminemia Ca correction (Ca will appear low but it probably isn't)
For every 1g < 4g, add .8 to serum Ca
27
Hypercalcemia of malignancy: s/s
Polyuria, polydipsia N/V AMS/coma
28
Symptoms of hypocalcemia
Cheek/triceps sign Weakness/cramps Parasthesias (especially peri-oral)
29
Lab values differentiating vit D deficiency and hypoparathyroidism
Vit D def: high PTH, low phos | Hypoparathyroidism: low PTH, high phos
30
2 main causes of osteomalacia/rickets
Vitamin D def | Hypophos (diet or renal wasting)
31
Clinical features of osteomalacia vs. rickets
Osteo: adults, pseudofx, bone pain, fx Rickets: bowing, short stature, weakness
32
Causes of hypoparathyroidism and lab values
Surgical injury Autoimmune Low Ca, High PO4, Low PTH
33
4 types of vitamin D deficiency
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
Pseudohypoparathyroidism and lab values and classic signs
receptor deficiency Low Ca, High PO4, High PTH Short stature, decreased 4th/5th digit size
35
Types of Rickets
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
Paget's etiology
Genetic + chronic paramyxovirus infection
37
Paget's stages
1. Reabsorption (High CTX, NTX) 2. Balance (High CTX, NTX and alkphos) 3. Formation (Low CTX, NTX and High/low alkphos)
38
Radiographic findings in Paget's | Bone scan findings
Osteolytic lesions (blade of grass) Thickened and disordered trabeculate Bone scan: increased uptake
39
Paget's histology
Increased osteoclast number and nuc per cell Increased peripherial osteoblasts Disordered bone
40
Path findings Graves dz
Hyperplasia, scalloping of colloid
41
Path findings Hashimoto
Mononuclear inflammation Onc metaplasia Germinal center formation
42
How to define inclusion criteria for SR/MA
``` P = population I = intervention C = control/comparison O = outcomes S = study design ```
43
Methodology of SR
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
SR specific bias
Publication bias (+ results more likely to be published)
45
Heterogenity in MA: clinical difference options
1. Don't do MA 2. Ignore = fixed effects 3. Allow = random effects 4. Explore variability