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95 Cards in this Set
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there is a great variation in:
|
PT gland location AND number
- though POSTERIOR of thyroid and 4 is most common - develops from 3rd and 4th pharyngeal pouches |
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**PT glands that migrate with the thymus can be mistaken for:**
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mediastinal tumors
|
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PT gland is composed of:
(3) |
1. chief cells (38%)
2. oxyphil cells (38%) 3. lipid (25%) |
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chief cells secrete:
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PTH
|
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histo difference between chief cells and oxyphil cells:
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chief cells have less cytoplasm/more nuclear density
|
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hypoPTH is most commonly:
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IATROGENIC
following surgical resection of thyroid gland \ - though DiGeorge syndrome (22q11.2 deletion) is rare but important cause |
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3 causes of primary hyperPTH:
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1. PT gland adenoma (85%)
2. hyperplasia (15%) 3. carcinoma |
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3 features of PT gland adenoma:
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1. **involves only ONE gland**
2. majority of cases sporadic 3. though some associated with MEN1 or MEN 2A |
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4 features of PT gland hyperplasia:
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1. benign proliferation => heterogeneous
(unlike homogenous of adenoma) 2. **involves ALL glands** 3. majority of cases are sporadic 4. few are associated with MEN 1, 2A |
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classic MEN 1 =>
(3) |
1. tumors of Pituitary
2. tumors of PT gland 3. tumors of Pancreas |
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3 features of MEN 1:
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1. nearly all will develop PT gland tumor => hyperPTH
2. ~~loss of MEN1 tumor suppressor => loss of function => tumors 3. YOUNG people (same with MEN 2A) |
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classic MEN 2A =>
(3) |
1. Medullary Carcinoma
2. Phea 3. PT gland hyperplasia/adenoma |
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MEN 2A, 2B, and FMTC are caused by:
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RET proto- oncogene mutations
=> oncogene |
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classic MEN 2B =>
(4) |
1. Medullary Carcinoma
2. Pheo 3. marfanoid body type 4. mucosal neuromas => hyperPTH NOT present |
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Familial Medullary Thyroid Carcinoma (FMTC) =>
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Medullary Carcinoma WITHOUT other features of MEN2A or 2B
|
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PT gland adenoma ~~ LACK of:
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LIPIDS
- instead, inc. homogenous cells - usually chief cells - hyperplasia will show predominant cell type, such that it LOOKS like it's homogenous, but you'll see enough of the other cell and some lipids too |
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5 features of PT gland Carcinoma:
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1. RARE
2. PTH and Ca2+ levels marked elevated 3. invasion 4. recurrences are common 5. M/M due to hypercalcemia |
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***cytologic atypia is NOT:***
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used in the diagnosis of PT Carcinoma
- adenomas will have it too |
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Osteitis Fibrosa Cystica =
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complication of hyperPTH
- also called brown tumor, but not a true tumor |
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3 symps of Osteitis Fibrosa Cystica are all PTH-driven:
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1. bone pain
2. bone swelling/cysts 3. pathologic fractures (~~osteopenia, decreased density of bone) |
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4 pathology of bone changes in Osteitis Fibrosa Cystica:
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1. increased osteoclast activity
2. fibrosis 3. hemorrhage 4. cyst formation |
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Osteitis Fibrosa can mimic:
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true bone neoplasms, radiologically
|
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osteoclasts are:
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multi-nucleated
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nl bone on histo:
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purple
|
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Paget’s Dz =
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episode of excessive bone resorption followed by disorganized and thickened bone
- NOT driven by PTH |
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3 m.c. sites of Paget's Dz =
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1. spine
2. skull 3. pelvis - solitary OR multiple sites - Paget's increases with age |
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even though Paget's Dz bone sites are THICKER, they are:
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WEAKER
- will see more but disorganized lammelli on histo |
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calcium salts ~~
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structural integrity of the skeleton
|
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3 functions of calcium ions:
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1. Neuromuscular excitability
2. Blood coagulation 3. Hormonal secretion |
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99% of the body's calcium is found in:
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bones
|
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2 functions of PTH:
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1. **increase serum Ca2+**
2. dec. Phosphorus |
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PTH acts at 3 sites to increase Ca2+
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1. directly, releases Ca2+ from bones into blood
2. directly, reabsorbs Ca2+ from kidney tubules - indirectly, by activating Vit. D 3. indirectly, increases gut absorption of Ca2+, via Vit. D |
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how does PTH release Ca2+ from bone?
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ultimately activates osteoclasts => breakdown of bone => inc. blood Ca2+
|
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CaSR =
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Calcium Sensitive Receptor
- when Ca2+ gets high enough in the blood, it binds CaSR's on the PT gland, => dec. release of PTH - **when CaSR's are UNbound, PTH is released** |
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where is P regulated?
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in the kidney’s proximal tubular cells
|
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what does PTH do to P?
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**decreases it,**
by taking away NPT2 transporters away from the tubule lumen - PTH = phosphaturic hormone |
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functions of calcitonin:
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directly inhibits everything that PTH does
- NOT NEARLY as potent as PTH |
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7 signs and symptoms of HYPERcalcemia:
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1. serendipitous - ***most pts are asymp***
2. stones (kidney) 3. bone (pain) 4. groans (abd. pain, n/v, constipation, anorexia) 5. psychiatric overtones (lethargy, depression, anxiety) 6. neuromuscular HYPOexcitability 7. brady |
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dv
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HTN
extra part 4 HYPOcalcemia |
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5 symps of acute crisis of hypercalcemia:
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1. anorexia
2. polyuria 3. dehydration 4. impaired mentation 5. immobilization |
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acute crisis of hypercalcemia occurs in:
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in the hospital
|
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the first question to ask when you see hypercalcemia =
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is it PTH-mediated?
|
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hypercalcemia SHOULD cause _______ PTH
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LOW
- therefore a nl level of PTH in the setting of hypercalcemia is actually ABNORMAL |
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treatment for hypercalcemia of malignancy =
(4) |
1. hydration
2. diuretics 3. bisP 4. treat malignancy |
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treatment for Vit. D intoxication =
(4) |
1. stop Vit D
2. Hydration 3. low-Ca diet 4. steroids |
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treatment for granulomatous or lymphoproliferative disorders =
(4) |
1. hydration
2. low-Ca2+ diet 3. steroids 4. treat UC |
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misc. causes of hypercalcemia:
(4) |
1. milk-alkalosis
2. hyperthy 3. Pheo 4. VIPoma |
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***4 features of Primary HyperPTH:***
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1. elderly, women
2. mostly asymp 3. **m.c.c. of hypercalcemia in OUTPATIENTs** 4. HIGH 24hr urine Ca2+ |
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treatment of Primary HyperPTH =
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surgery
|
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key difference between Primary HyperPTH and FHH =
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LOW 24hr urine Ca2+ (hypocalciuria) in FHH
|
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secondary hyperPTH ~~
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HYPOcalcemia
|
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pathophys of tertiary hyperPTH:
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CKD + low 1,25-D and low calcium
=> inc. PTH => secondary hyperparathyroidism => autonomous overproduction of PTH => “tertiary hyperparathyroidism” which may result in hypercalcemia |
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4 types of familial hyperPTH:
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1. FHH
2. FHPTH 3. MEN 1 4. MEN 2A |
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4 features of FHPTH:
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1. = tumor jaw syndrome
2. ~~muts in HRPT2 tumor suppressor 3. => jaw fibromas 4. hyperPTH via adenoma |
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McCune Albright syndrome =
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constitutively-active GNAS protein (downstream of PTH r') that makes body think you have excess PTH
=> hypercalcemia, but low PTH |
|
signs/symps of McCune-Albright Syndrome =
(5) |
1. cafe-au-lait spots
2. coast-of-Maine border that respects the midline 3. fibrous dysplasia 4. precocious puberty 5. hyperthy (due to GNAS too) |
|
labs of McCune-Albright Syndrome:
(4) |
1. inc. Ca2+
2. inc. 1,25-D 3. inc. AP 4. NORMAL PTH |
|
4 endocrine causes of mild hypercalcemia:
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1. Hyperthyroidism
–direct effect of T3 on bone? 2. adrenal insufficiency – volume contraction, change in PTH set point 3. Pheo – volume contraction, change in PTH set points 4. VIPoma – volume contraction |
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4 meds/supplements that cause hypercalcemia:
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1. Vit. D
2. excess Ca2+ intake (milk-alkalosis/>3g per day) 3. Li2+ 4. **thiazide diuretics** |
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signs/symps of HYPOcalcemia:
(5) |
1. agitation
2. hyperreflexia (Trousseau's BP cuff, Chvostek's face) 3. convulsions 4. hypotension 5. long QT ~~ANY hyperexcitability |
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***m.c.c.'s of hypocalcemia = ***
(3) |
1. post-thyroidectomy
2. AI dz, esp. against CaSR's 3. Vit. D. deficiency |
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**labs of hypoPTH:**
(3) |
1. low PTH
2. low Ca2+ 3. high P |
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why is it called pseudohypoPTH?
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b/c PTH levels are actually HIGH,
but PTH can't do anything b/c cells are R to it |
|
features of pseudohypoPTH:
(4) |
1. aka Albright's Hereditary Osteodystrophy
2. GNAS mutation 3. skeletal phenotype 4. ~~hypocalcemia due to **PTH-RESISTANT** obesity |
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skeletal phenotype of pseudohypoPTH =
(2) |
1. PTH-R obesity
2. shortened 4th metatarsal |
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labs of pseudohypoPTH:
(3) |
1. LOW Ca2+
2. HIGH PTH 3. high P |
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difference between paternal and maternal forms of pseudohypoPTH:
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paternal inheritance = pseudo-pseudohypoPTH
**skeletal phenotype but NORMAL labs** |
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pathway of Vit D activation: Vit D is converted to 25-OH D in the:
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liver
=> then 1,25-D via 1alpha in the kidneys = active form |
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Rickets =
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skeletal deformities due to severe Vit. D deficiency **in children**
|
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features of RIcket's:
(5) |
1. curved leg bones
2. pigeon chest 3. enlarged skull 4. kyphosis 5. protruding abd |
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osteomalacia =
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Vit. D. deficiency in adults
|
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2 main forms of Ca2+ in the blood:
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1. albumin-bound
2. ionized - **bioactive** |
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BOTH albumin-bound and ionized Ca2+ are:
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*pH-dependent*
- occurs **in the vial** as well as in the body - can't tarry with blood sample if measuring Ca2+ |
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***relationship of albumin-bound Ca2+ to pH:***
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as pH increases, albumin-bound Ca2+ INCREASES
- i.e. INCREASES with alkalemia - ionized = red = opposite; decreases with alkalemia - total Ca2+ doesn't change |
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**m.c.c. of apparent or pseudo-hypocalcemia = **
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**hypoalbuminemia**
|
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4 causes of low albumin:
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1. poor nutrition
2. liver dz 3. renal 4. CHF |
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Phosphate is _____________ by Vit. D
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INCREASED
(via absorption from the gut) |
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Phosphate is HIGH in:
(3) |
1. renal failure
(since it's nly excreted by the kidneys) 2. hypoPTH 3. Vit. D toxicity |
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even though Vit. D. increase P absorption from the gut,
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PTH's effect of decreasing P at the kidneys prevails over Vit D's increase
|
|
when do you want to know 25-OH-D levels?
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**for overall Vit. D status**
|
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in which specific cases would you want to get 1,25-D levels instead of 25-OH-D?
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1. granulomatous dz's (increased)
2. hyperPTH (increased) 3. Rickett's differentiation - decreased in Type 1 - increased in Type 2 |
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25-OH-D levels will be decreased with:
(4) |
1. exposure to sun
2. Vit. D intake 3. malabsorption 4. liver dz |
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order of lab tests when faced with hypercalcemia:
(4) |
1. verify hyperCa2+
(includes P) 2. urine Ca2+ 3. PTH 4. Vit. D metabolites if PO4 is elevated |
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for an INPATIENT with hypercalcemia, always think:
|
MALIGNANCY
=> Ca2+ rises RAPIDLY |
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Vit. D. toxicity increases:
(2) |
Ca2+ levels,
Phosphate levels |
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Vit. D toxicity most often presents with:
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kidney stones
|
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always get _____ levels for patients in the:
|
ICU
|
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***m.c.c. of secondary hyperPTH = ***
|
CRF
- renal insufficiency => decreased excretion of P => inc. serum P => dec. free Ca2+ (as it binds to P) => all PTH glands are stimulated => inc. serum PTH |
|
chronic renal failure =>
(3) |
1. hypoproteinemia
2. hyperPhos 3. dec. synth. of 1,25-D => low Ca2+ => secondary hyperPTH |
|
m.c. presentation of primary hyperPTH =
|
ASYMP
|
|
hypercalcemia can cause:
|
acute pancreatitis,
as it activates pancreatic enzymes |
|
treatment of primary hyperPTH =
|
surgery
- if it's a one-gland adenoma, remove that one gland only |
|
pseudohypoPTH =
|
organ RESISTANCE to PTH
|
|
cause of primary hypoPTH =
|
lack/destruction/removal of PT gland
|
|
D2 and D3 =
|
25-OH
- NOT active 1,25-D |