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LAST TEST!!! > L85- Calcium and PTH > Flashcards

L85- Calcium and PTH Flashcards

1
Q

How is serum ionized and total calcium influenced by Albumin and pH? Describe the trends

A

Albumin - binds Ca and is part of total Calcium measured

  • low albumin state lowers the Total but not the ionized calcium

pH changes are like so:

  • Alkaloses lowers ionized Ca and increases protein-bound calcium vs Acidosis rasises Ionized Calcium and lowers protein-bound calcium

CC: Hyperventilation causes respiratory alkalosis and reduces ionized calcium giving people the tingling sensation!

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2
Q

How do you measure ionized calcium? How do you estimate ionized calcium from total calcium?

A

Measuring ionized calcium is hard….samples taken careully and directly to freezer - finicky test and sucks to do…..SO INSTEAD….

Estimate Ionized Ca from Total Calcium and Albumin concentration!

CORRECTION FACTOR = (4-Albumin) x 0.8

Add correction factor to Total Calcium to get corrected calcium

*Corrected for low albumin

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3
Q

What are the most important organs and hormones in calcium regulation?

A

Organs - intestines, bones, kidneys

Hormones - PTH and Calcitriol

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4
Q

What is the relationship between PTH secretion and Calcium levels? What regulates this? Describe the relationship graphically.

A

Calcium sensing receptors on the Parathyroid cells act as the Calciostat and sense Ca in serum and either raise or lower PTH levels accordingly

More Calcium then PTH down

Less Calcium PTH up

(see graph picture)

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5
Q

Walk through the process of Vitamin D production and regulation.

A

1) 7-dehydrocholesterol in skin + UBV sunlight –> Vitamin D3

2) Vitamin D3 to the liver –> 25-OHD3

3) 25-OHD3 to the kidney –> 1,25OH-D3 aka Calcitriol which is the active form

Vitamin D2 from exogenous plant sources undergoes same 25 and 1-hydroxylation as D3

Regulation:

  • 7-dehydrocholesterol in skin decreases w/ age so need more sun and Melanin absorbs UVB more so darker pigments need more sunlight
  • 25-OD D is what you measure to Dx Vitamin D deficiency
  • 1-Hydroxylation in kdiney regulated and INCREASED by PTH but that ability decreases w/ age and renal insufficiency
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6
Q

How does PTH act on it’s target organs?

A

Bone:

  • Acute exposure stimulates bone formation by osteoblasts BUT prolonged exposure stimulates bone breakdown by osteoclasts (*can use synthetic PTH for osteoporosis)

GI Tract: no direct effect

Kidney

  • PTH promotes Ca absorption and P excretion in the proximal tubule
  • stimulates 1-hydroxylase production
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7
Q

What is the difference in renal effects from PTH vs 1,25D?

A

PTH tells kidney to lose P and hold onto Ca

1,25 D tells kidney to hold onto BOTH Ca and P!!!

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8
Q

What is the mechanism of different actions of PTH on bone cells? (RANK-RANKL expression pathway)

A

PTH binds receptors on OB acutely to stimulate them –> bone formation AND expression of RANKL cell surface receptors

then OC Precursors w/ RANK on their surface bind w/ RANKL and causes them to differentiate and activate into mature OC and get bone destruction

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9
Q

Vitamin D 1,25 actions on Target Organs?

A

Bone:

  • stimulates bone breakdown at high levels and maintains serum Ca and P for bone formation

GI:

Ca and P absorption increased

PTH Glands:

  • inhibits PTH release - feedback control!
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10
Q

What is Calcitonin? Actions? Where does it come from?

A

Calcitonin releaased and made by Thyroid C Cells

does NOT play a role in NORMAL physiology

pharmacologic doses inhibit bone resporption

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11
Q

What is PTHrP? What is the physiologic role and pathologic role?

A

Parathyroid Hormone Related Peptide (aa2-13) bids to the same receptor as PTH

Physiologic Role:

Made in Fetal parathyroid, cartilage, keratinocytes, placenta and in adult breast

Used for mobilization of Ca in pregnancy to make baby bones and for lactation

Pathologic Role:

causes Hypercalcemia in Solid tumors!!!!!!

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12
Q

Where is phosphorous found? REgulated by? Too much causes? relation to 1,25 D?

A

Phosphorous is a major component of Hydroxyapatite and cell membranes and ATP etc

Too much phosphorous can cause Vascular Calcification and therefore is tightly controlled

PTH and FGF23 (made by Osteocytes) stimulated by increased P and leads to Phosphaturia

*PTH stimulates 125D and FGF23 inhibits it!

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13
Q

What is the most common cause of Outpatient Hypercalcemia?

A

Primary Hyperparathyroidism

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14
Q

What are the causes of Primary Hyperparathyroidism?

A

85% Single adenoma

10% hyperplasia - sporadic or MEN1/2, or hereditary jaw tumor hyperparathyroidism sundrome

5% Ectopic - neck/mediastinum

1% cancer

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15
Q

Signs and Symptoms of Hyperparathyroidism?

A

Range from none to life-threatening depending on Degree of elevation of Ionized CA (>12 mg/dl; normal 8.5-10.5)

Bones - osteoporosis and fracture and pain

Stones - polyuria, azotemia, stones

Moans - NM weakness, fatigue and joint pain

Groans - GI constipation, anorexia, vomiting

Psychological Overtones - CNS - depression to obtundation

Other - e_ye Band Keratopathy_

NARROW QT –> how people die from cancer from high PTrP

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16
Q

What causes Autosomal Dominant Primary Hyperparathyroidism? What are the different types/forms of disease (MEN)? Which one causes Hypercalcemia?

A

Multiple Endocrine Neuromas!!!

MEN1: Parathyroid, Pituitary, Pancreas

  • Increased Calcium!!!!!!
  • Menin gene inactivation (tumor suppressor)

MEN2a: C Cells, Adrenal, Parathyroid

  • Thyroid tumor
  • ret gene activation (proto-oncogene)

MEN2b: C cells, Adrenal, Nerves, Parathyroid

  • Thyroid tumor
  • Ret gene activation
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17
Q

What are markers / how do you diagnose Primary Hyperparathyroidism? What else can also be associated with this?

A

Elevated Serum Ca

Elevated or inappropriately normal iPTH (should be suppressed)

Elevated or normal Urine Calcium (not low)

Associated:

  • elevated Calcitriol
  • low normal/low serum phosphorous
  • Mild hyperchloremic Metabolic Acidosis
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18
Q

How do you treat Primary Hyperparathyroidism? Surgical or Medical?

A

Asymptomatic - observation

Symptomatic = Surgery w/ Sestamibi scan

if US+ - minimally invasive

if US- then 4 gland exploration

If poor surgical candidate treat medically w/ Cinacalcet which is Calcium Sensing Receptor Antagonist and tells Parathyroid gland to not release PTH

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19
Q

What is Familial Hypocalciuric Hypercalcemia?

A

AD mutation that’s rare

Inactivating mutation on the Calcium sensing receptor so always thinks not enough Ca/PTH and so keeps releasing PTH

Shifts PTH / Ca Curve to the Right

Kidney effects - Uca low and increase reabsorption of Ca

Diagnosed by low Ca/Cr clearance ratio

does NOT require treatment

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20
Q

What are potential causes of non-PTH mediated hypercalcemia? What lab values would you see?

A

Here, PTH suppressed in response to High Calcium indicating normal Parathyroid feedback response

3 types of causes:

1) 1,25 OH D mediated: Vitamin D intoxication, Granulomatous diseases, Lymphomas
2) PTHrP Mediated - Cancer
3) Other - Milk Alkali syndrome or Multiple Myeloma

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21
Q

What is the most common cause of inpatient (symptomatic) Hypercalcemia?

A

CANCER - PTHRP MEDIATED!!!

22
Q

How do you treat Hypercalcemia overall? Acutely?

A

Overall: Treat Underlying cause:

  • Primary hyperparathyroid - surgery
  • cancer - surgery, CTX/RTX
  • granulomatous disease - glucocorticoids

ACUTE TREATMENT WHILE WAITING FOR DX:

  • Saline and Loop Diuretics (Furosemide)
  • IV Bisphosphonates - best is Zoledronic Acid (also used in osteoporosis)
  • Calcitonin - minimally effective
23
Q

How do IV bisphosphonates work?

A

Used for Acute tx of Hypercalcemia and for Osteoporosis

They have a phosphate moiety that is P-O-P and so binds to bone and OC can not break bone down –> REDUCE TURNOVER so can’t get more Ca out of bones

24
Q

What is the presentation and what are the causes for secondary Hyperparathyroidism?

A

Nothing wrong w/ Parathyroid glands but they are reacting properly to something else

DX: Normal or Low Calcium and Elevated PTH

Cuases:

  • Whole body deficiency of Ca or Excess P

Most common Cuase is CKD!!!!

  • Hypercalcuria - renal tubular leak
25
What are complications of Secondary Hyperparathyroidism?
Bone loss from PTH breakdown If associated w/ increased serum P like in CKD then Vascular Calfications
26
How does Tertiary Hyperparathyroidism arise? How do you diagnose it?
**_Diagnosis_** - elevated Ca and Elevated PTH or inappropriately normal PTH (same as Primary) Follows previous secondary hyperparathyroidism - CKD Pathology cahgnes from Hyperplasia to development of Monoclonal Tumor (adenoma) w/ Autonomy
27
What are the markers / how do you diagnose Hypoparathyroidism?
Low serum Ca High P LOW PTH or inappropriatly normal PTH (should be high)
28
What are the etiologies of Hypoparathyroidism?
Post-operative - Thyroidectomy, Head/Neck surgery MOST COMMON! Autoimmune - Polyglandular failure syndrome - AIRE gene Autosomal Dominant - CASR Mutation - 50% (vs FHH where inactivating mutation here it is the opposite and overly stimulated so stop releasing PTH and shift curve LEft)
29
What are the signs and symptoms of Hypocalcemia?
**TETANY!!!! HALLMARK -** paresthesias, cramps, laryngospasm **Chvostek Sign and Trousseau Sign** Mental status - fatigue, anxiety, depression --\> Psychosis Head - Calfication of basal ganglia and papilledema CV - **Prolonged QT** and Heart failure **_Cataracts_** in Eyes Fetal - dental hypoplasia *Kidney - stones and nephrocalcinosis - from small group - can get these in both hypo and hyper*
30
What is Chvostek sign? What is Trousseau Sign?
Chvostek - tap along facial nerve and see ipsilateral twitching Trousseau - elevated BP cuff over systolic for 2 minutes and see carpal spasm
31
What is Pseudohypoparathyroidism? What is the clinical Presentation?
Resistance to PTH **Albright's Hereditary Osteodystrophy** End organ resistance to PTH **See Low serum Ca, Elevated P and PTH** _Clinical_: - short stature - short pinky and ring fingers - Wide spaced nipples (teee hee) - MR
32
How do you diagnose and what are some causes of Vitamin D Deficiency? Cutoff for deficiency?
Diagnose: **Normal Calcium and Phosphorous but LOW 25-OH-D** TEst 25 OHD!!!! _Causes_: - **inadequate sun** (+old age) or malabsorption like in IBD - Anticonvulsants increase Vit D catabolis - **Obesity** - D sequestered in fat **CUTOFF: 25-OH-D \< 30!!!**
33
What are symptoms of Vitamin D deficiency in kids and adults?
**Childhood** - bones are soft --\> **_Rickets_** - **Bowed long bones** - Rachitic Rosary - splaying **Adults** - Softening of bones --\> **Pseudofracture** **"looser's Zones"** = indentation where arteries course over bones
34
What can cause / what do you see in Vitamin D resistance?
Hereditary Vit D Dependent Rickets: **HVDDR Type 1 - Lack of 1-Alpha Hydroxylase** Responds to Tx w/ 1,25 OHD2 **HVDDR Type 2 - mutations in Vit D receptor and TRUE RESISTANCE** -associated w/ ALOPECIA!!! NO HAIR ANYWHERE!
35
Treatment of hypocalcemia? both mild and crisis?
Mild Hypocalcemia - oral calcium and Vitamin D **_Crisis -_** symptoms include tetany, laryngospasm, seizures _Treatment_ - IV Ca infusion and Calcitriol
36
Describe releationship between bone mass and strength and age. How can you get Osteoporosis?
Bone Mass is proportional to bone strength and fracture risk Peak Bone mass in early 20s (F) and mid 20s (M) \>80% controlled by genes (SEE GRAPH) Osteoporosis - from failure to attain normal Peak bone mass or from bone loss or both!
37
What are the 2 Monogenic (developmental) Bone disorders?
**_Osteoporosis Pseudoglioma Syndrome (OPPG) f_**rom lack of signal transduction - Inactivating mutation in L***RP5 (LDL-Receptor-like-protein-5)*** so less bone is produced - Childhood Osteoporosis and Congenital Blindness **_Osteogenesis Imperfecta_** - defect in Excracellular proteins - mutations in ***Type 1 Collagen gene***s - Osteoporosis +/- Blue Sclerae
38
What are RF for osteoporosis?
Age Female Family History White or Asian Low body weight - especially post-menopausal women Smoking Alcohol use (EtOH toxic to osteoblsats) Hypogonadism (up to 1/3 men) Inactivity POor calcium intake
39
What are some secondary causes of Osteoporosis to be aware of?
**_Medications_**: - Glucocorticoids like prednison - Aromatase Inhibitors - Chronic Anticoagulants - Antidepressants and Anti-convulsants **_Diseases_** - Cushings - Hyperhtyroidism - DM 1 and 2 - GI problems - Celiac's Crohns, UC - Chronic illness - COPD, CHF - Muscle weakness
40
How do you diagnose Osteoporosis? Osteopenia vs osteoporosis?
**HIP FRACTURE OR SPINE COMPRESSION FRACTURE** _OR_ by **DXA which measure Bone mineral density** _Use T score for post-menopausal women and men \>50 yo:_ Osteopenia - T score -1.0 to -2.5 Osteoporosis \<-2.5 For every -1 on T score, RR of fracture increases 2-3 fold _Use Z score for children and young adults:_ SD from age matched controls **_and_** Fragility Fracture
41
Who gets treated in osteoporosis?
EVERYONE GETS TREATED!!!! who has osteoporosis Osteopenia - calculate absoulte 10 year risk of fracture w/ FRAX tool and treat those w/ \>20% risk for fracture and/or anyone w/ fracture of hip or \>3% risk fracture of hip
42
What are the different types of treatments for OSteoporosis?
**_Anti-resorptive --\> Interfere w/ OC function_** - **Bisphoshphonates**: Alendronate, Risendronate, Zolendronc Acid, or Ibandronate (Ibandronate does not reduce hip fracture) RANKL Inhibitor- Denosumab SERM - Reloxifene Calcitonin - Treat Hypercalcemi **_Anabolic --\> Get OB to build bone_** - **Teriparatide** PTH 1-34 SubQ injections **_Non-Pharmacologic Treatment:_** - CA and Vit D (best to give 25OHD really high doses) - exercise and weight bearing improved BMD
43
What is PAget Disease of Bone? Who gets it? How does it work?
Osteoporosis is global whereas Paget Disease is F***ocal disorder of bone metabolism*** See areas of enlarged but weakened bones and can cause bone pain and neurological complications 2-3% 40 yo but \>80 yo 10% prevalence Male:Female 4:3 **Autosomal Dominant!!!!** **_Pathophysiology_**: Increased rate of bone turnover via increased # OB, OC, and vasculature leading to new, immature, fragile woven bone that is prone to fracture
44
What are the clinical features of PAget Disease?
95% Asymptomatic!!! _Symptoms include:_ - PAIN!!!! - Increased warmth over bone bc more vasculature - fracture bone deformity - HF and/ or neurological - Rare - OSTEOSARCOMA!
45
What bones are affected in PAget's Disease?
2/3 polyostotoic and 1/3 monostotic ANY bone can be affected - doesn't spread to new bones over time!!! Most common bones: 72% Pelvis, then Spine, Skull, Tibia
46
What are Lab markers of bone formation? Bone Resporption? Turnover? What do you see in PAgets?
**Bone Formation = Alkaline Phosphatase (osteocalcin)** **Bone Resorption Marker = N-Telopeptide** (morning urine) or serum C-Telopeptide, Urine Pyridinium crosslinks, Hydroxyproine Markers of bone Turnover - correlate w/ eachother and disease severity **In PAgets -- BOTH ELEVATED!!!**
47
What do you see on RAdiographic evaluation of Paget's Disease?
can get nuclear bone scan or XR and see areas up uptake use MRI or CT to rule out tumor (+/-Biopsy) _Findings_: **Coarsening Trabeculae** **Osteoporosis Circumscirpta** - one little punched out area **Picture Frame Sign** - vertebrae getting bigger but more luscent inside **Pelvic Brim sign** - coarsening trabeculae **Cotton Wool Spots** - snowstorm appearance
48
Treatment for PAget's Disease?
Treat ALL patients w/ Bisphosphonates to reduce bone turnover bc natural history of disease is progression and want to prevent fractures
49
What is Renal Osteodystrophy? Who gets it and why? What are the types?
Present in ALL pts w/ CKD by the time that they reach dialysis due to 1) **Phosphate Retention 2) Excess PTH and 3) reduced Production of 1,25 OH-D** (SEE PICTURE) _Types Include:_ Hyperparathyroid Bone Disease - **Osteitis Fibrosa cYstica - HIGH PTH!!!!** Adynamic Bone disease - lower than expected PTH Mixed - Osteomalacia and Hyperparathyroid
50
What are Hereditary Rickets Diseases? Name them - 3 - and their presentation/features?
**_Rickets and Osteomalacia due to Hypophosphatemia_**: ***Renal Phosphate Wasting:*** **XLH: X-linked Hypophosphatemic Rickets** **Fanconi Syndrome** - renal wasting of P, glucose, AA, and associated w/ renal failure - Phosphate and glucose and AA wasted **Oncogenic Osteomalacia (FGF23) -** benign mesenchymal tumor produces FGF23 - Phosphaturia --\> Osteomalacia and fractures

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