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Endocrinology > Pathophysiology 3 > Flashcards

Pathophysiology 3 Flashcards

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1
Q

Major Cellular Level Players of Calcium Regulation?

A
  • Ca
  • Phosphorous
  • PTH
  • Vit D
  • FGF23
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2
Q

Minor Cellular level players of Ca regulation?

A
  • calcitonin
  • magnesium
  • acid/base (pH)
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3
Q

Major Tissue Level Players of Calcium Regulation?

A
  • parathyroid glands
  • gut
  • kidney
  • bone
  • liver
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4
Q

Minor Tissue level players of Ca regulation?

A

-skin

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5
Q

Total Body Calcium

A

~1kg

  • 99% in bone (hydrocyapatite)
  • 1% extracellular and soft tissues
  • 0.1% intracellular
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6
Q

Serum Calcium

A
  • 40% protein bound
  • 10% complexed (citrate or phosphate ions)
  • 50% ionized - free Ca that is bioavailable
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7
Q

What does low Ca do?

A

-stimulates release from parathyroid glands
Bone: increase Ca immobilization from bone
Kidney: Increase Calcium reabsorption from DCT
Intestines: with vit D, increase calcium absorption

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8
Q

What does Parathyroid Hormone do?

A

1) activates 1alpha-hydroxylase
2) stimulates reabsorption of Ca (distal nephron)
3) inactivates phosphate transporter (PCT)
- decrease type II Na*Pi transporter (inhibits phosphate reabsorption)

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9
Q

PTH

A

-84 aa peptide

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10
Q

Calcium-Sensing Receptor (CaSR)

A
  • senses Ca2+ level
  • found in parathyroid, kidney, C cells thyroid, bone
  • a member of GPCR family
  • stimulating the receptor results in a intra-cellular cascade to reduce PTH secretion
    inc. Ca - calcimimetics - dec. PTH
    dec. Ca - calcilytics - inc. PTH
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11
Q

PTH Dependent Hypercalcemia

A
  • Hyperparathyroidism (primary/tertiary)
  • Familial hypocalciuric hypercalcemia
  • Medication-induced (Li or HCTZ-mediated)
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12
Q

PTH Independent Hypercalcemia

A
  • Tumor induced (PTHrP or bone metastases)
  • Granulomatous diseases (TB), sarcoidosis, lymphoma inc. 1,25 vit D
  • Multiple myeloma
  • Hyperthyroidism/adrenal failure
  • Immobilization
  • Medication-induced: vit D toxicity, vit A, milk-alkali)
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13
Q

Primary Hyperparathyroidism

A

-80-85% adenoma
-15% hyperplasia (MEN1, MEN2A, HPT-Jaw Tumor Syndrome, familial HPT)
-W>H), sex (F>M)
Unknown Etiology
Serendipity Stones Moans Groans Bones
abdominals psychic

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14
Q

Symptoms in Primary Hyperparathyroidism

A

Majority Asymptomatic

  • fatigue/weakness
  • musculoskeletal pain
  • polydipsia/polyuria
  • constipation
  • anorexia/nausea/dyspepsia
  • pruritus
  • depression/memory loss
  • renal failure/kidney stones
  • osteoporosis/fracture
  • HTN
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15
Q

Primary HPT Work up

A

Biochemical: Ca, Albumin (ionized Ca), PTH, 25-OH Vit D, 24 hr urine Ca (to differentiate from FHH)
Imaging: Thyroid US & 99Tc-sestamibi scan-local
DXA

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16
Q

Management of Primary HPT

A

parathyroidectomy

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17
Q

Management of Primary HPT

A

Conservative

  • adequate hydration
  • use of bisphosphonates in patients with osteoporosis
  • maintenance of Vit D status (20-30ng/mL)
  • cinacalcet has been approved by FDA for those who do not qualify for surgery and have moderate hypercalcemia (Ca>12.5)
  • annual follow up: Ca/PTH, renal function, DXA
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18
Q

Familial Hypocalciuric Hypercalcemia

A

1) inactivating mutation of CaSR, 100% penetrance
2) Mildly inc. serum Ca, high-normal/mildly inc. PTH, hypocalciuria
3) asymptomatic
4) Work up: Serum Ca, PTH, 24 hr. urine calcium (<50-100 mg/24hr) Can also ask relatives to check serum Ca, genetic testing
5) no treatment is indicated

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19
Q

Tertiary Hyperparathyroidism

A
  • occurs in the face of long standing secondary hyperparathyroidism
  • parathyroid glands develop hyperplasia due to chronic low Ca and/or high Phosphorous levels
  • at 1 point, these glands become autonomous in the setting of end-stage renal disease or post-kidney transplant
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20
Q

Hypercalcemia of malignancy

A

-Clinical Presentation: consistent with signs and symptoms of hypercalcemia and potential diagnosis of malignancy
-polyuria, dehydration, confusion, abdominal and musculoskeletal pains, fatigue, nausea/vomiting
-weight loss, pulmonary symptoms, lymphadenopathy, history of cancer, Anemia, abnormal chest X-ray
Etiology: breast, lung, lymphoma, thyroid, kidney, prostate, multiple myeloma, pancreas
-breast and squamous cell carcinoma more common
-PTH level will be suppressed

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21
Q

Hypercalcemia can occur in malignancy without increase in PTHrP

Study These Flashcards
A
  • bony metastases can increase Ca levels
  • humoral factors (cytokines, TNFa) can activate osteoclasts
  • multiple myeloma can cause significant bone destruction resulting in hypercalcemia
22
Q

Initial Treatment of Acute Hypercalcemia

Study These Flashcards
A
  • address volume status
  • saline diuresis +/- furosemide (only after corrected volume)
  • calcitonin IM/SC (4-6 IU/kg q6-12 hrs) 3-4 days
  • Bisphosphonates (Pamidronate IV over 4hrs for 2-3 weeks) or Zoledronic acid IV over 15min
  • Glucocorticoids (useful in myeloma, granulomatous disease, Vit D toxicity)
  • Phosphate (rarely used, caution elevated Ca X Phos product)
  • Dialysis
23
Q

Major Causes of Secondary PTH Elevation

Study These Flashcards
A

1) Hypocalcemia
2) Hyperphosphatemia
3) Vit D Deficiency

24
Q

Approach to patient with Secondary Hyperparathyroidism

Study These Flashcards
A

1) Symptoms are non-specific and likely related to underlying disease causing elevated PTH but not due to PTH itself
2) Evaluate key elements of the Ca axis: serum PTH, Calcium (with albumin), Phosphorous, Creatinine, Vit D (do not collect 24-hr urine for Ca)
3) No indications for imaging studies if calcium is normal
4) Treat underlying reason (make sure vit. D is always replete)

25
Vitamine D Deficiency
1) Severe vit D deficiency is rare 2) Presenting complains in mild/moderate vit. D deficiency are very non-specific: musculoskeletal pains, fatigue 3) 50% of patients with osetoporosis have vit. D deficiency 4) Vit. D replacement (>800 units/day) showed ~20% reduction in risk or fractures -benefits of vit D replacement for prevention of cancer, diabetes mellitus, infections, hypertension are controversial -J-shaped association between mortality and vit D levels
26
Clinical Signs of Hypoclacemia
- agitation - hyperreflexia - convulsions - hypertension - long QT
27
Hypoparathyroidism (low PTH)
-primary process as low PTH decreases Ca post-thyroidectomy idiopathic-antibodies to PTH autoimmune parathyroid agenesis eg: DiGeorge syndrome hypomagnesaemia, hypermagnesemia, hyperphosphatemia
28
Hyperparathyrodism (high PTH)
-secondary process or when PTH increases due to low calcium from other resons renal failure vit D deficiency vit D or PTH resistance syndromes
29
Acute Pancreatitis
-free fatty acids chelate Ca
30
Massive Transfusion
-infusion of citrate will complex with Ca leading to decreased ionized Ca
31
Tumor Lysis Syndrome or Rhabdomyolysis
-phosphate release binds to ionized Ca
32
Severe Sepsis
Cytokines mediated | -hypocalcemia
33
Medications that cause hypocalcemia?
- phosphate | - bisphosphonates
34
Hungry Bone Syndrome
-hypocalcemia
35
Work up of Hypocalcemia
``` PTH is low -Hypoparathyroidism -Magnesium Deficiency -Phosphate Excess PTH is high -severe vit D deficiency -renal failure -vit D resistance or PTH resistance ```
36
Pseudohypoparathyroidism
- idiopathic inherited forms of PTH resistance - elevated PTH (1000s), hypocalcaemia, hyperphosphatemia - short stature, rounded face, foreshortened 4th metacarpals, obesity (albright's hereditary osetodystrophy) - variability in AHO or PTH renal resistance, subclassified
37
Pseudohypoparathyroidism Molecular Defect
inability of PTH to stimulate intracellular signaling events (cAMP pathway) due to mutation in Gsalpha subunit or elements downstream to cAMP signaling
38
Hypocalcaemia Treatment
``` Acute: always correct Mg if low -Ca gluconate (93mg elemental Ca/10ml) -1-2ampules over ~10-20min -0.5-2.0mg/kg/hr of elemental Ca IV Long Term: -oral Ca salts (3g a day) -Vit D (ergocalciferol/cholecalcirerol) -effective only if PTH is present -Calcitroil 0.5-1.0mcg/day ``` -Hydrochlorothiazide - increases reabsorption of Ca in distal tubule
39
MEN (multiple endocrine neoplasia)
1) AD - germline or sporadic mutations (2nd hit) 2) Different Penetrance (varying phenotype) 3) Benign & Malignant 4) Functionally Active and Inactive
40
Tumors in MEN
1) Parathyroid (primary HPT) 80-95% 2) Pancreas (insulinoma, gastrinoma, VIPoma) 50% 3) Pituitary (prolactinoma, Cushing's disease, acromegaly) 25%
41
Epidemelogy of MEN
-hypercalcemia due to HPT by age 40 -Pituitary tumors age 38 -Pancreatic tumors: Insulinoma age 25 Gastrinoma age 35
42
Parathyrooidectomy in patients with PHPT and Gastrinoma
-improves hypercalcemia and decreases gastrin
43
MEN2A
- 1/30,000, any age, more adults, 80% of all MEN2 1) medullary thyroid carcinoma - almost 100% 2) Pheochromocytoma - 40% 3) Primary HPT - 25%
44
MEN2AB
- 1/30,000, early onset, 5% of all MEN2 1) MEdullary thyroid carcinoma - 100% more malignant 2) Mucosal Neuromas - 100% 3) Marfanoid habitus - 50% 4) Pheochromocytoma - 50%
45
Clinical Features of MEN2B
- Mucosal neuromas | - marfanoid habitus
46
Screening of MEN2B: Biochemical
- index patient, complete screening by testing function of other endocrine glands of MEN - in first deg. relative initiate screening to identify hyperfunction of an endocrine gland known to be a part of MEN
47
Screening of MEN2B: Genetic
- index pat. screen for most prevalent genetic mutation for this type of MEN (genetic counseling) - in first degree relatives, genetic screening once mutation is confirmed in index patient - children are most vulnerable group
48
Clinical Features of MEN2B
- Mucosal neuromas | - marfanoid habitus
49
Screening of MEN2B: Biochemical
- index patient, complete screening by testing function of other endocrine glands of MEN - in first deg. relative initiate screening to identify hyperfunction of an endocrine gland known to be a part of MEN
50
Screening of MEN2B: Genetic
- index pat. screen for most prevalent genetic mutation for this type of MEN (genetic counseling) - in first degree relatives, genetic screening once mutation is confirmed in index patient - children are most vulnerable group

Endocrinology (15 decks)

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