Parathyroid Flashcards
(97 cards)
1
Q
The parathyroids are two pairs of small, oval shaped glands on the _
A
The parathyroids are two pairs of small, oval shaped glands on the posterior thyroid
2
Q
The superior parathyroids are derived from the _
A
The superior parathyroids are derived from the fourth pharyngeal pouch
3
Q
The inferior parathyroids are derived from the _
A
The inferior parathyroids are derived from the third pharyngeal pouch
4
Q
The consequences of hypercalcemia include _
A
The consequences of hypercalcemia include stones, bones, thrones, and psychiatric overtones
* Calcium oxalate stones
* Constipation
* Bone pain
* Psychosis
* Arrhythmias
5
Q
Consequences of hypocalcemia
A
Consequences of hypocalcemia:
* Tetany
* Prolonged QT interval
* Seizures
6
Q
Chvostek sign is indicative of _
A
Chvostek sign is indicative of hypocalcemia
7
Q
Trousseau’s sign is indicative of _
A
Trousseau’s sign is indicative of hypocalcemia
8
Q
QT prolongation is a sign of _ calcemia
A
QT prolongation is a sign of hypocalcemia
9
Q
PTH is a _ type of hormone
A
PTH is a peptide hormone
10
Q
PTH is made by _ cells
A
PTH is made by chief cells
11
Q
PTH acts on the bones to increase the release of _ and _
A
PTH acts on the bones to increase the release of calcium and phosphorus
12
Q
PTH increases the activity of _ type cells which then activate _
A
PTH increases the activity of osteoblasts which then activate osteoclasts
13
Q
PTH has three important effects on the kidney, _ , _ , _
A
PTH has three important effects on the kidney, increase Ca2+ absorption , increase phosphate excretion , increase 1alpha-hydroxylase activity
14
Q
1a-hydroxylase forms _
A
1a-hydroxylase forms 1,25-dihydroxyvitamin D (aka calcitriol)
15
Q
Calcitriol is _
A
Calcitriol is activated vitamin D also known as:
* 1,25-Dihydroxyvitamin D
* D3
16
Q
Increased calcitriol will have _ and _ effects on the GI system
A
Increased calcitriol will cause increased Ca2+ absorption and increased PO3- absorption in the gut
17
Q
Calcitriol is made in the _
A
Calcitriol is made in the proximal tubular cells of the kidney
18
Q
Although, the effect of 1,25(OH)2D is to (increase/decrease) phosphorous at the bone and gut, the net effect of the kidney is _
A
Although, the effect of 1,25(OH)2D is to increase phosphorous at the bone and gut, the net effect of the kidney is phosphorous excretion (net decrease)
19
Q
Fibroblast growth factor 23 (FGF23) is mostly concerned with _ homeostasis
A
Fibroblast growth factor 23 (FGF23) is mostly concerned with phosphorus homeostasis
20
Q
FGF23 is secreted by _ cells
A
FGF23 is secreted by osteocytes and osteoblasts
21
Q
What is the effect of elevated FGF23?
A
High FGF23 –>
* Decreases calcitriol
* Increases PO4 excretion
* Decreases PTH
22
Q
Calcitonin is secreted by _
A
Calcitonin is secreted by parafollicular C cells
23
Q
What is the function of calcitonin?
A
Calcitonin opposes PTH –> decreases osteoclast activity and decreases renal Ca2+ resorption
24
Q
PTH directly stimulates (osteoblasts/osteoclasts)
A
PTH directly stimulates osteoblasts –> make RANK ligand –> binds receptors on osteoclasts –> osteoclasts are activated
25
Name four causes of vitamin D deficiency
Name four causes of vitamin D deficiency:
1. **Poor dietary intake**
2. **Decreased sun exposure**
3. **Malabsorption** (IBD, gastric bypass)
4. **Fat-soluble vitamin deficiency** (celiac, CF)
26
_ is caused by vitamin D deficiency in children
**Rickets** is caused by vitamin D deficiency in children
27
_ is caused by vitamin D deficiency in adults
**Osteomalacia** is caused by vitamin D deficiency in adults
28
A deficiency in vitamin D causes PTH to (increase/decrease)
A deficiency in vitamin D causes PTH to **increase**
29
Rickets involves _ at the epiphyseal growth plates as a result of deficient vitamin D
Rickets involves **defective cartilage mineralization** at the epiphyseal growth plates as a result of deficient vitamin D
30
_ is a disorder of "bone softening" in adults whereby osteoid mineralization is abnormal from deficient vitamin D
**Osteomalacia** is a disorder of "bone softening" in adults whereby osteoid mineralization is abnormal from deficient vitamin D
31
What are the consequences of rickets/ vitamin D deficiency in children?
Consequences of rickets include:
* Bowed legs
* Kyphosis
* Scoliosis
* Fractures
* Poor growth
* Bone tenderness to palpation
32
Vitamin D deficiency (rickets or osteomalacia) is diagnosed via:
_ 1,25(OH)2D
_ PTH
_ alkaline phosphatase
_ Calcium
_ Phosphate
Vitamin D deficiency (rickets or osteomalacia) is diagnosed via:
**Low** 1,25(OH)2D
**High** PTH
**High** alkaline phosphatase
**Low-Normal** Calcium
**Low-Normal** Phosphate
33
Causes of hypoparathyroidism:
Causes of hypoparathyroidism:
* Surgical damage
* Damage to blood supply
* DiGeorge
* Autoimmune destruction
* Hypomagnesemia
34
Causes of hyperparathyroidism:
Causes of hyperparathyroidism:
* Parathyroid adenoma
* Hyperplasia
35
The downstream effect of hypoparthyroidism will be a dysregulation of calcium and phosphate levels resulting in (high/low) calcium and (high/low) phosphate
The downstream effect of hypoparthyroidism will be a dysregulation of calcium and phosphate levels resulting in **low calcium** and **high phosphate**
36
The clinical presentation of hypoparathyroidism may include _
The clinical presentation of hypoparathyroidism may include **Chvostek sign, Trousseau sign, hyperphosphatemia, tetany**
* Signs of low calcium and high phosphate
37
Management for hypoparathyroidism includes _
Management for hypoparathyroidism includes **oral calcium, vitamin D, magnesium, thiazides, PTH replacement**
38
_ is a decreased end organ sensitivity of PTH
**Pseudohypoparathyroidism** is a decreased end organ sensitivity of PTH
* It is a "pseudo" hypoparathyroidism because PTH will actually be high, sensitivity is just low
39
Pseudohypoparathyrodism is caused by an (AD/AR) mutation in the _ gene that leads to decreased end organ sensitivity to PTH
Pseudohypoparathyrodism is caused by an **autosomal dominant** mutation in the ***GNAS1*** gene that leads to decreased end organ sensitivity to PTH
40
GNAS1 is a gene that encodes a _ G protein subunit
GNAS1 is a gene that encodes a **Gs alpha subunit**
41
Pseudohypoparathyrodism will involve:
_ calcium
_ phosphate
_ PTH
Pseudohypoparathyrodism will involve:
**low** calcium
**high** phosphate
**high** PTH
42
Hyperparathyroidism will cause _ calcium and _ phosphate levels
Hyperparathyroidism will cause **high calcium** and **low phosphate** levels
43
Bone pain and bone fractures are associated with (hypo/hyper) parathyroidism
Bone pain and bone fractures are associated with **hyperparathyroidism**
44
High alkaline phosphatase (ALT) may be indicative of (hypo/hyper) parathyroidism
High alkaline phosphatase (ALT) may be indicative of **hyperparathyroidism**
45
We can treat hyperparathyroidism with calcimimetics like _ , bisphosphonates such as _ , or parathyroidectomy
We can treat hyperparathyroidism with calcimimetics like **cinacalcet** , bisphosphonates such as **alendronate** , or parathyroidectomy
46
Secondary hyperparathyroidism (hyperplasia of the glands) can be caused by _ or _
Secondary hyperparathyroidism (hyperplasia of the glands) can be caused by **decreased phosphate excretion** or **decreased vitamin D**
* These things signal that the PTH aren't working properly and we should proliferate
47
_ is a very common cause of secondary hyperparathyroidism due to the impaired 1alpha-hydroxylase activity and increased phosphate retention
**Chronic kidney disease (CKD)** is a very common cause of secondary hyperparathyroidism due to the *impaired 1alpha-hydroxylase activity* and *increased phosphate retention*
48
Why does PTH fail to correct hypocalcemia in the case of secondary hyperparathyroidism from CKD?
PTH fails to correct hypocalcemia because in CKD we have **diminished 1a-hydroxylase activity** and the **retained phosphate will bind up the calcium**
49
Secondary hyperparathyroidism (CKD) is associated with
_ calcium
_ phoshate
_ PTH
_ ALT
Secondary hyperparathyroidism (CKD) is associated with
**Low** calcium
**High** phoshate
**High** PTH
**High** ALT
50
Management options for secondary hyperparathyroidism (due to CKD):
Management options for secondary hyperparathyroidism (due to CKD):
* **Phosphate binder** (Sevelamer)
* **Calcimimetics** (Cinacalcet)
* **Bisphosphonates** (Alendronate)
* **Calcitriol**
* **Parathyroidectomy**
51
_ is a phosphate binder that can be used for secondary hyperPTH
**Sevelamer** is a phosphate binder that can be used for secondary hyperPTH
52
_ is a calcimimetic which is used in hyperparathyroidism treatment
**Cinacalcet** is a calcimimetic which is used in hyperparathyroidism treatment
53
_ is a bisphosphonate drug used to treat hyperparathyroidism
**Alendronate** is a bisphosphonate drug used to treat hyperparathyroidism
54
Tertiary hyperparathyroidism is most common in _
Tertiary hyperparathyroidism is most common in **post-transplant CKD patients**; it involves *autonomous hyperparathyroidism*
* Long periods of hyperphosphatemia in CKD lead to continued stimulation of PT --> desensitization --> autonomous activity
55
Tertiary hyperparathyroidism presents with _ and should be treated via _
Tertiary hyperparathyroidism presents with **high calcium, low phosphate, high PTH, sx of hypercalcemia** and should be treated via **parathyroidectomy**
56
_ is a condition that usually occurs from primary parathyroidism and involves "brown tumors" and bone pain due to increased osteoclast activity
**Osteitis fibrosa cystica** is a condition that usually occurs from primary parathyroidism and involves "brown tumors" and bone pain due to increased osteoclast activity
57
Explain the pathogenesis of osteitis fibrosa cystica
Explain the pathogenesis of osteitis fibrosa cystica:
1. High PTH
2. Increased osteoclast activity
3. Cystic bone spaces --> **hemosiderin deposition**
4. Creates "brown tumor" and bone pain
58
Pseudogout, pancreatitis, and polyuria may be clinical findings of (hyper/hypo) parathyroidism
Pseudogout, pancreatitis, and polyuria may be clinical findings of **hyperparathyroidism**
59
_ is a bone disorder due to CKD; associated with secondary hyperparathyroidism; it involves decreased active vitamin D, increased phosphate, increasted PTH, increased bone turnover and weak bones
**Renal osteodystrophy** is a bone disorder due to CKD; associated with secondary hyperparathyroidism; it involves decreased active vitamin D, increased phosphate, increasted PTH, increased bone turnover and weak bones
60
_ is an inherited mutation in the calcium sensing receptor gene that requires additional calcium to suppress PTH
**Familial hypocalciuric hypercalcemia** is an inherited mutation in the calcium sensing receptor gene that requires additional calcium to suppress PTH
61
FHH is an autosomal dominant mutation in the _ gene
FHH is an autosomal dominant mutation in the ***CaSR*** gene
62
FHH involves defective G-coupled calcium receptors in the _ and _
FHH involves defective G-coupled calcium receptors in the **kidney** and **parathyroids**
* Higher amounts of calcium needed to suppress PTH
63
What diagnostics are needed to diagnose FHH?
FHH will show
* High PTH
* High Ca2+
* Low 24 hour urine Ca2+
64
Only about _ % of calcium is circulating in the blood
Only about **1%** of calcium is circulating in the blood
* About 99% is stored in the bones
65
The majority of elemental calcium and phosphorus in the human body are found in the _
The majority of elemental calcium and phosphorus in the human body are found in the **bones**
66
About _ % of serum calcium is biologically active
About **50%** of serum calcium is biologically active
* Of the calcium that is in the blood, only 50% is free or ionized
67
The parathyroid glands have _ which help in the regulation of PTH release
The parathyroid glands have **calcium sensing receptors** which help in the regulation of PTH release
68
What is the action of PTH on the kidneys?
1. Increased phosphate secretion
2. Increased calcium reabsorption
3. Increased active vitamin D
69
What is the action of PTH on the bone?
PTH activates osteoblasts --> osteoclasts; we ge an increase in calcium and phosphorus release
70
What is the effect of PTH on the small intestine?
PTH increases calcium reabsorption via the effects of *calcitriol*
71
_ mediates the increase in small intestine's absorption of calcium and phosphate
***Calcitriol*** mediates the increase in small intestine's absorption of calcium and phosphate
72
Calcitonin _ calcium
Calcitonin **decreases** calcium
73
Hyperalbuminemia _ total calcium
Hyperalbuminemia **increases** total calcium
74
Hypoalbuminemia _ total calcium
Hypoalbuminemia **decreases** total calcium
75
Equation for corrected serum calcium
Corrected calcium = 0.8 (normal albumin - measured albumin) + serum calcium
* We usually use 4 g/dL for normal
76
(Acidemia/Alkalemia) increases the ionized calcium level
**Acidemia** increases the ionized calcium level
77
Labs expected with *primary* hyperparathyroidism
Labs expected with *primary* hyperparathyroidism:
PTH high
Calcium high
Phosphorus low
1,25D high
78
Secondary hyperparathyroidism from CKD will have the following labs:
PTH
Calcium
Phosphorus
Creatinine
1,25D
Secondary hyperparathyroidism from CKD will have the following labs:
**High** PTH
**Low** Calcium
**High** Phosphorus
**High** Creatinine
**Low** 1,25D
79
Secondary hyperparathyroidism from vitamin D deficiency will have the following labs:
PTH
Calcium
Phosphorus
Creatinine
1,25D
Secondary hyperparathyroidism from vitamin D deficiency will have the following labs:
PTH- high
Calcium- low
Phosphorus- low
Creatinine- normal
1,25D- low
80
Tertiary hyperparathyroidism will have the following labs:
PTH
Calcium
Phosphorus
Creatinine
1,25D
Tertiary hyperparathyroidism will have the following labs:
PTH- high
Calcium- high
Phosphorus- high
Creatinine- high
1,25D- low
**This happens when the calcium sensing receptors on parathyroid have a new set point
81
Causes of hypocalcemia
Causes of hypocalcemia:
* Hypoparathyroidism
* CKD
* Vitamin D deficiency
* Low magnesium
* Malabsorption
* Blood transfusion
* Pancreatitis
* Medications (loops, bisphosphonates)
82
Causes of hyperparathyroidism
Causes of hyperparathyroidism:
* PTHrp from cancer
* Hyperparathyroidism
* Calcitriol secreting tumors
* Granulomatous disease
* Medications (thiazides)
* FHH
83
Hypercalcemia is associated with _ QT interval
Hypercalcemia is associated with **shortened** QT interval
* Due to increased threshold potential
84
PTHrp secreting malignancy labs:
Calcium
PTH
Phosphorus
Calcitriol
PTHrp secreting malignancy labs:
Calcium- high
PTH- low **negative feedback from PTH**
Phosphorus- low
Calcitriol- normal
85
Granulomatous disease labs:
Calcium
PTH
Phosphorus
Calcitriol
Granulomatous disease labs:
Calcium- high
PTH- low
Phosphorus- high
Calcitriol- high
86
Malignancy metastasized to bone labs:
Calcium
PTH
Phosphorus
Calcitriol
Malignancy metastasized to bone labs:
Calcium- high
PTH- decreased
Phosphorus- increased
Calcitriol- normal
87
FHH labs:
Calcium
PTH
Phosphorus
Calcitriol
FHH labs:
Calcium- high
PTH- high
Phosphorus- low
Calcitriol- high
88
Sx of hypercalcemia
89
Osteoporosis, brown tumors, and nephrolithiasis are all complications of _
Osteoporosis, brown tumors, and nephrolithiasis are all complications of **primary hyperparathyroidism**
90
The two treatment options for primary hyperPTH are _ and _
The two treatment options for primary hyperPTH are **surgery** and **cinacalcet**
* Can treat hypercalcemia with IV fluids, bisphosphonates, calcitonin, loops
91
Brown tumor- primary hyperparathyroidism
92
Parasthesias, muscle twitching, and hyperreflexia are associated with (hypercalcemia/hypocalcemia)
Parasthesias, muscle twitching, and hyperreflexia are associated with **hypocalcemia**
93
Two important PE findings associated with hypocalcemia are _ and _
Two important PE findings associated with hypocalcemia are **Chvostek's sign** and **Trousseau's sign**
94
Two important arrythmias associated with hypocalcemia are _ and _
Two important arrythmias associated with hypocalcemia are **prolonged QT** and **Torsades**
95
Three causes of hypoparathyroidism in adults
Three causes of hypoparathyroidism in adults
1. Thyroidectomy
2. Autoimmune
3. Hypomagnesemia
96
The major problem in pseudohypoparathyroidism is _
The major problem in pseudohypoparathyroidism is **PTH resistance**
97
We treat pseudohypoparathyroidism with _ and _
We treat pseudohypoparathyroidism with **calcitriol** and **ca2+ supplementation** or with synthetic PTH
