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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
**PT glands that migrate with the thymus can be mistaken for:**
mediastinal tumors
PT gland is composed of:

(3)
1. chief cells (38%)

2. oxyphil cells (38%)

3. lipid (25%)
chief cells secrete:
PTH
histo difference between chief cells and oxyphil cells:
chief cells have less cytoplasm/more nuclear density
hypoPTH is most commonly:
IATROGENIC

following surgical resection of thyroid gland \

- though DiGeorge syndrome (22q11.2 deletion) is rare but important cause
3 causes of primary hyperPTH:
1. PT gland adenoma (85%)

2. hyperplasia (15%)

3. carcinoma
3 features of PT gland adenoma:
1. **involves only ONE gland**

2. majority of cases sporadic

3. though some associated with MEN1 or MEN 2A
4 features of PT gland hyperplasia:
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
classic MEN 1 =>

(3)
1. tumors of Pituitary

2. tumors of PT gland

3. tumors of Pancreas
3 features of MEN 1:
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)
classic MEN 2A =>

(3)
1. Medullary Carcinoma

2. Phea

3. PT gland hyperplasia/adenoma
MEN 2A, 2B, and FMTC are caused by:
RET proto- oncogene mutations

=> oncogene
classic MEN 2B =>

(4)
1. Medullary Carcinoma

2. Pheo

3. marfanoid body type

4. mucosal neuromas

=> hyperPTH NOT present
Familial Medullary Thyroid Carcinoma (FMTC) =>
Medullary Carcinoma WITHOUT other features of MEN2A or 2B
PT gland adenoma ~~ LACK of:
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
5 features of PT gland Carcinoma:
1. RARE

2. PTH and Ca2+ levels marked elevated

3. invasion

4. recurrences are common

5. M/M due to hypercalcemia
***cytologic atypia is NOT:***
used in the diagnosis of PT Carcinoma

- adenomas will have it too
Osteitis Fibrosa Cystica =
complication of hyperPTH

- also called brown tumor, but not a true tumor
3 symps of Osteitis Fibrosa Cystica are all PTH-driven:
1. bone pain

2. bone swelling/cysts

3. pathologic fractures
(~~osteopenia, decreased density of bone)
4 pathology of bone changes in Osteitis Fibrosa Cystica:
1. increased osteoclast activity

2. fibrosis

3. hemorrhage

4. cyst formation
Osteitis Fibrosa can mimic:
true bone neoplasms, radiologically
osteoclasts are:
multi-nucleated
nl bone on histo:
purple
Paget’s Dz =
episode of excessive bone resorption followed by disorganized and thickened bone

- NOT driven by PTH
3 m.c. sites of Paget's Dz =
1. spine

2. skull

3. pelvis

- solitary OR multiple sites

- Paget's increases with age
even though Paget's Dz bone sites are THICKER, they are:
WEAKER

- will see more but disorganized lammelli on histo
calcium salts ~~
structural integrity of the skeleton
3 functions of calcium ions:
1. Neuromuscular excitability

2. Blood coagulation

3. Hormonal secretion
99% of the body's calcium is found in:
bones
2 functions of PTH:
1. **increase serum Ca2+**

2. dec. Phosphorus
PTH acts at 3 sites to increase Ca2+
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
how does PTH release Ca2+ from bone?
ultimately activates osteoclasts => breakdown of bone => inc. blood Ca2+
CaSR =
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**
where is P regulated?
in the kidney’s proximal tubular cells
what does PTH do to P?
**decreases it,**

by taking away NPT2 transporters away from the tubule lumen

- PTH = phosphaturic hormone
functions of calcitonin:
directly inhibits everything that PTH does

- NOT NEARLY as potent as PTH
7 signs and symptoms of HYPERcalcemia:
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
dv
HTN

extra part 4

HYPOcalcemia
5 symps of acute crisis of hypercalcemia:
1. anorexia

2. polyuria

3. dehydration

4. impaired mentation

5. immobilization
acute crisis of hypercalcemia occurs in:
in the hospital
the first question to ask when you see hypercalcemia =
is it PTH-mediated?
hypercalcemia SHOULD cause _______ PTH
LOW

- therefore a nl level of PTH in the setting of hypercalcemia is actually ABNORMAL
treatment for hypercalcemia of malignancy =

(4)
1. hydration

2. diuretics

3. bisP

4. treat malignancy
treatment for Vit. D intoxication =

(4)
1. stop Vit D

2. Hydration

3. low-Ca diet

4. steroids
treatment for granulomatous or lymphoproliferative disorders =

(4)
1. hydration

2. low-Ca2+ diet

3. steroids

4. treat UC
misc. causes of hypercalcemia:

(4)
1. milk-alkalosis

2. hyperthy

3. Pheo

4. VIPoma
***4 features of Primary HyperPTH:***
1. elderly, women

2. mostly asymp

3. **m.c.c. of hypercalcemia in OUTPATIENTs**

4. HIGH 24hr urine Ca2+
treatment of Primary HyperPTH =
surgery
key difference between Primary HyperPTH and FHH =
LOW 24hr urine Ca2+ (hypocalciuria) in FHH
secondary hyperPTH ~~
HYPOcalcemia
pathophys of tertiary hyperPTH:
CKD + low 1,25-D and low calcium

=> inc. PTH

=> secondary hyperparathyroidism

=> autonomous overproduction of PTH

=> “tertiary hyperparathyroidism” which may result in hypercalcemia
4 types of familial hyperPTH:
1. FHH

2. FHPTH

3. MEN 1

4. MEN 2A
4 features of FHPTH:
1. = tumor jaw syndrome

2. ~~muts in HRPT2 tumor suppressor

3. => jaw fibromas

4. hyperPTH via adenoma
McCune Albright syndrome =
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:
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
4 meds/supplements that cause hypercalcemia:
1. Vit. D

2. excess Ca2+ intake
(milk-alkalosis/>3g per day)

3. Li2+

4. **thiazide diuretics**
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
***m.c.c.'s of hypocalcemia = ***

(3)
1. post-thyroidectomy

2. AI dz, esp. against CaSR's

3. Vit. D. deficiency
**labs of hypoPTH:**

(3)
1. low PTH

2. low Ca2+

3. high P
why is it called pseudohypoPTH?
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
skeletal phenotype of pseudohypoPTH =

(2)
1. PTH-R obesity

2. shortened 4th metatarsal
labs of pseudohypoPTH:

(3)
1. LOW Ca2+

2. HIGH PTH

3. high P
difference between paternal and maternal forms of pseudohypoPTH:
paternal inheritance = pseudo-pseudohypoPTH

**skeletal phenotype but NORMAL labs**
pathway of Vit D activation: Vit D is converted to 25-OH D in the:
liver

=> then 1,25-D via 1alpha in the kidneys

= active form
Rickets =
skeletal deformities due to severe Vit. D deficiency **in children**
features of RIcket's:

(5)
1. curved leg bones

2. pigeon chest

3. enlarged skull

4. kyphosis

5. protruding abd
osteomalacia =
Vit. D. deficiency in adults
2 main forms of Ca2+ in the blood:
1. albumin-bound

2. ionized
- **bioactive**
BOTH albumin-bound and ionized Ca2+ are:
*pH-dependent*

- occurs **in the vial** as well as in the body

- can't tarry with blood sample if measuring Ca2+
***relationship of albumin-bound Ca2+ to pH:***
as pH increases, albumin-bound Ca2+ INCREASES

- i.e. INCREASES with alkalemia

- ionized = red = opposite; decreases with alkalemia

- total Ca2+ doesn't change
**m.c.c. of apparent or pseudo-hypocalcemia = **
**hypoalbuminemia**
4 causes of low albumin:
1. poor nutrition

2. liver dz

3. renal

4. CHF
Phosphate is _____________ by Vit. D
INCREASED

(via absorption from the gut)
Phosphate is HIGH in:

(3)
1. renal failure
(since it's nly excreted by the kidneys)

2. hypoPTH

3. Vit. D toxicity
even though Vit. D. increase P absorption from the gut,
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?
**for overall Vit. D status**
in which specific cases would you want to get 1,25-D levels instead of 25-OH-D?
1. granulomatous dz's (increased)

2. hyperPTH (increased)

3. Rickett's differentiation
- decreased in Type 1
- increased in Type 2
25-OH-D levels will be decreased with:

(4)
1. exposure to sun

2. Vit. D intake

3. malabsorption

4. liver dz
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
for an INPATIENT with hypercalcemia, always think:
MALIGNANCY

=> Ca2+ rises RAPIDLY
Vit. D. toxicity increases:

(2)
Ca2+ levels,

Phosphate levels
Vit. D toxicity most often presents with:
kidney stones
always get _____ levels for patients in the:
ICU
***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