Parathyroid Pathology Dr. Singh Flashcards
3 types of cells in parathyroid
- Chief cell ( secreting PTH)
- Oxyphil cell
- Adipocytes
PTH causes
Release CA+ to be released from bone
Kidney (STOP excrete CA, maintain P)
Covert Vit D to make for CA
Hyperparathyroidism primary vs secondary
- Primary : high PTH + high Ca
2. Secondary : low PTH + high Ca
3 causes of Primary Hyperparathyroidism
- Adenoma
- Primary hyperplasia
- Parathyroid Carcinoma
Primary Hyperparathyroidism SX
- Bone pain (osteoporosis)
- Renal stones (Nephrolithiasis) , heart valve calcification
- ABD groans (C, gallstones)
- Psych moans (Depression…)
Bones, stones, groans, moans
Osteitis Fibrosis Cystica
- Looks like what
- Cause
- Can be mistake or look like
Brown tumors*, bone destruction that makes a hemorrhagic lesion , not neoplastic (from osteoclasts)
= can look like Metastatic disease
Primary Hyperparathyroidism in real world sx
None, just see high CA
Parathyroid adenoma
- How to know where it is
- H. Levels
- Which cells are involved
- What ends up happening as a result
- Technetium Scan : radioactive gland lights up at adenoma
- High PTH , high CA
- Chief cells, or oxyphil cells (large CA in blood)
- Large CA in blood causes normal parathyroid to involute/shrink
MEN 1 and parathyroid adenoma
1. Germline vs sporadic more common
- Somatic mutation (sporadic) = more common , germline (familial)
- Have to remove thyroid completely and parathyroid
Primary hyperplasia Parathyroid
- Can happen how
- Primary vs Secondary
- Histo
- TX
- Usually all 4 hyperproliferate
- Primary (all 4 just decide to proliferate), Secondary (low CA in body causes proliferation)
- No fat cells seen, entire gland if full of endocrine cells
- Parathryoidectomy (PTH lowers within minutes)
Parathyroid Carcioma parathyroid
- M/B
- Histo
- Another DX way to see this it happening
- Metastatic when dx
- Invasion of adjacent tissue + vascular invasion
- Adenoma was removed or parathyroids removed and PTH does not go down
Most common cause of hypercalcemia** (when PTH is low)**
Malignancy causing high CA
Other causes, high VITD, excess CA injection, Thiazides diuretics
hypercalcemia with PTH low
- Hormone levels
- SX
- High CA, low PTH
2. More symptoms then high CA from hyperparathyroidism (Mental status changes, N/V, Short QT)
- Asymptomatic hypercalcemia
- Symptomatic hypercalcemia
What do you think
- Primary Hyperparathyroidism
2. Malignant Hypercalcemia
Malignant Hypercalcemia
3 MOA If happens and what types of cancer it involves
- PTHrP secretary (PTH like protein) = usually SCC lung, breast, other, = biphosphatase treated
- Vit D excess (sarcoidosis, lymphomas) = steroid treated
- Local Osteolytic Hypercalcemia = malignancy in bone (breast cancer and myeloma) = increases osteoclasts
Hypocalcemia SX
- Tetany (Chvosteks sign + Trousseau sign)
- Prolonged QT
- Muscle cramps
- Numbness paresthesia
High PTH and low CA
Is called what and cause
- Secondary Hyperparathyroidism (reactive hyperplasia)
2. Renal disease causing dumping of CA + P resorption
Renal Osteodystrophy
1 .can happen from
2. Can lead to
- Secondary Hyperparathyroidism** (usually) , can in primary Hyperparathyroidism
- Rugger jersey sign (bone eroding) vertebral bodies in middle hollowing out
Calciphylaxis
- Consequence of what
- What happens
- Secondary hyperparathyroidism (usually due to renal disease)
- Extensive calcification and occlusion of BVs = ischemia, gangrene = die from infection/sepsis
2 highs that happen in secondary hyperparathyroidism
- Calciphylaxis
2. Renal Osteodystrophy
Tertiary hyperparathyroidism
After prolonged hypoglycemia = the parathyroids hyperplasia cant shut down, even when CA is back to normal PTH is still screamed a lot like before
= same lab values as in primary hyperparathyroidism (only has secondary hyperparathyroidism first)
Primary Hypoparathyroidism :
- Labs
- 5 causes
LOW CA, LOW PTH
- Surgery ** MOST COMMON**
- Autoimmune
- DiGeorges syndrome ( absent or not developed parathyroids, 3rd + 4th pharyngeal punch prob)
- CASR Germline mutation (AD, hypersensitive CA receptors)
- Familial Isolated Hypoparathyroidism : PTH can be made to functional state
DiGeorges syndrome
- Chr problem
- What happens in this
- Chr 22q11.2
- Immune deficiency (thymic hypoplasia) (Parathyroid hypoplasia/ aplasia = HYPOCALCEMIA) = arched back in child from tetany
- Heart outflow defects (Tetrology of fallot, Truncus arteriosus) = blue fingers and toes and lips
- Face : wide face, broad nose, low set ears, long upper lip, heavy eyelid)
Inactivated CASR (loss of function mutation)
- What happens
- Casing
- Contain it is called
- CA receptors in parathyroid think there is never enough CA
- Hypercalcemia from excess PTH secretary and low renal excretion
- Familial hypocaciuric hypercalcemia