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Clinical Chemistry 3 > Lecture 3: Parathyroid hormone > Flashcards

Lecture 3: Parathyroid hormone Flashcards

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1
Q

Parathyroid anatomy

A

The parathyroids consist of 4 glands located adjacent to the thyroid gland

Each gland weighs approximately 40 mg

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2
Q

Information about how the PTH is formed

A
  1. PTH gene is in chromosome 11
  2. PTH is synthesized as a 110 amino acid polypeptide called pre-pro-PTH
  3. It is cleaved to pro-PTH (90 amino acids) and then PTH (84 amino acids)

4.PTH is secreted in active form of the hormone.
Ca regulates synthesis, release and degradation of PTH

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3
Q

Targets sites for PTH

A

Bones, kidneys and GI

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4
Q

Cousin of PTH

A

Another hormone, parathyroid hormone-related protein, binds to the same receptor as parathyroid hormone

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5
Q

PTH and PHRP function

A

Parathyroid hormoneand its cousinparathyroid hormone-related protein(PTHrP) are critical controllers of calcium and phosphorus balance.

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6
Q

Two receptors have been identified that bind parathyroid hormone and PTHrP:

A

Type 1 parathyroid hormone receptor:
Binds both parathyroid hormone and amino-terminal peptides of PTHrP.

Type 2 parathyroid hormone receptor:
Binds parathyroid hormone but shows very low affinity for PTHrP.

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7
Q

Where is Type 1 parathyroid hormone receptor located and purpose

What happens if the receptor is mutated, affects?

A

Highly expressed in bone and kidney and mediates in these tissues the PTH-dependent regulation of mineral ion homeostasis.

The PTH1R also mediates the paracrine actions of PTHrP, which play a particularly vital role in the process of endochondral bone formation.

These important functions, the likely involvement of the PTH1R in certain genetic diseases affecting skeletal development and calcium homeostasis,

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8
Q

Function of Type 2 receptor and where is it found

A

Particularly abundant in brain and pancreas.

The PTH2R suggest involvement in regulation of fear, anxiety, reproductive behaviours.

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9
Q

PTH role on bones

A

Stimulates the release of calcium in anindirect processthrough osteoclasts which ultimately lead to resorptionof the bones.

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10
Q

PTH role on KIDNEYS

A

Targets the distal convoluted tubule and collecting duct, directlyincreasing calcium reabsorption.

Parathyroid hormone decreases phosphate reabsorption at the proximal convoluted tubule.

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11
Q

PTH role on Small intestine

A

Activate Vitamin D

Plays a role in calcium reabsorption in the distal convoluted tubule via calbindin-D, a cytosolic vitamin D dependent calcium binding protein.In the small intestine, vitamin D allows the absorption of calcium

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12
Q

Calcium-PTH: How does PTH respond in hypcalcemia?

Seconds to minutes
Minutes to 1 hour
Hours to days
Days to weeks

A

Seconds to minutes- exocytosis of PTH

Minutes to 1 hour- reduction in intracellular PTH degradation

Hours to days- increase in PTH gene expression

Days to weeks- proliferation of parathyroid cells

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13
Q

where is the Calcium sensing receptor expressed

A

predominantly expressed in the parathyroids and kidney.

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14
Q

Purpose of Calcium sensing receptor

A

allows regulation of PTH secretion and renal tubular calcium re-absorption in response to alterations in extracellular calcium concentrations.

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15
Q

Activation of the calcium sensor has two major signal-transducing effects:

A

Activation of phospholipase C :

Leads to generation of the second messenger’s diacylglycerol and inositol trisphosphate.

Inhibition of adenylate cyclase:- which suppresses intracellular concentration of cyclic AMP.

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16
Q

Draw the interaction of CaSR and CAMP

A

Lecture Slide

Increase in serum calcium leads to calcium receptor complex acting via one or more guanine nucleotide binding protein and second messengers leading to inhibition of PTH

Decreased serum ionized calcium leads to deactivation of receptors, which leads to stimulation of PTH

17
Q

Purpose fo PTH and Calcitriol

A

PTH and calcitriol are the major hormones modulating calcium and phosphate homeostasis

18
Q

Draw the homeostasis diagram of PTH regulation

A

Lecture Slide

19
Q

RANKL and IL expression in bone formation and resorption

AND diagram explanation

A

Bone formation
Performed by stimulating osteoblasts andinhibiting osteoclasts

Bone resorption
Performed by active osteoclast

Stimulated byRANKL in normal process
Stimulated byPTH in pathologic process(metastatic disease)

Interleukin 1 (IL-1)stimulates osteoclast differentiation and thus bone resorption

*upon PTH stimaution on osteoblasts, they secrete RANKL which binds to the RANK receptor on precusor osteoclasts causing them to be active

20
Q

What is Hyperparathyroidism

A

↑ PTH

PTH induced bone resorption and hypercalcemia

21
Q

Primary hyperparathyroidism is caused by…

A

DUE TO disorder of parathyroid gland

parathyroid adenoma

parathyroid hyperplasia

parathyroid carcinoma

It can occur as part of at least three familial endocrinopathies

Multiple endocrine neoplasia type 1 or type 2

isolated familial hyperparathyroidism

22
Q

Primary hyperparathyroidism pathogenesis

A

Overproduction ofPTHbyparathyroid chief cells

Effect ofPTHonbone→increased boneresorption =↑ releaseof calciumphosphate= ↑ calcium levels

InducesRANKLexpressioninosteoblasts→binding ofRANKLtoRANKonosteoclasts→activation ofosteoclasts

InducesIL-1expressioninosteoblasts→activation ofosteoclasts

Effect ofPTHon thekidneys=↑phosphateexcretion(phosphaturia)

23
Q

Primary hyperparathyroidism Symptoms and signs

A
  1. Renal – hypercalciuria
    - nephrolithiasis
    - nephrocalcinosis
    - polyuria and polydipsia
    - renal insufficiency

2.Neuromuscular – weakness
myalgia

3.Neurologic and psychiatric
- Memory loss Confusion
Depression
Lethargy
Psychosis

4.Skeletal
Bone pain
Osteoporosis

24
Q

Primary hyperparathyroidism Lab findings

A

Hypercalcemia

Serum phosphorus is low normal (<3.5 mg/dl) or low (<2.5 mg/dl)

Mild hyperchloremic metabolic acidosis (low Ph, PCO2, HCO3)

PTH is elevated or high normal

Alkaline phosphatase may be increased

25
Q

Secondary hyperparathyroidism information

A

Occurs most commonly in advancedchronic kidney diseasewhen decreased formation of active vitamin D in the kidneys and other factors leads to hypocalcemia and chronic stimulation of PTH secretion.

Hyperphosphatemiathat develops in response to chronic kidney disease also contributes.

Once the hyperparathyroidism is established, hypercalcemia or normocalcemia may occur.

26
Q

Secondary hyperparathyroidism Pathogenesis

A

↓calciumand/or↑phosphatebloodlevels leads to=reactivehyperplasiaof the parathyroidglands=↑PTHsecretion

Chronic kidney disease= impaired renalphosphateexcretion
=↑phosphatebloodlevels=↑PTHsecretion

In addition,CKD=↓ biosynthesisof activevitamin D=↓ intestinalcalciumresorption+↓ renalcalciumreabsorption= hypocalcemia=↑PTHsecretion

27
Q

Tertiary Hyperparathyroidism Description

A

Hypercalcemia and parathyroid overactivity in the presence of a condition that would be expected to cause secondary hyperparathyroidism (SHPT)

Occurs when prolongedparathyroidstimulation from a secondary cause results in autonomousparathyroid hyperfunction.

This almost exclusively occurs after the chronic stimulation from uremic SHPT, as well as in SHPT patients who undergorenal transplantation.

28
Q

Tertiary Hyperparathyroidism Pathogenesis

A

Chronic renal disease→ refractory and autonomous secretion ofPTH→hypercalcemia

Renal disease → secondary ortertiary hyperparathyroidism→renal osteodystrophy→ bone lesions

Familial hypocalciuric hypercalcemiabenign condition that causes chronically elevated serum calcium and reduced calcium excretion.

29
Q

PTH and Ca levels for primary, secondary and tertiary hyperparathyroidism

A

Primary
PTH: Normal/ High
Ca: High

Secondary
PTH High
Ca: low or normal

Tertiary
PTH: HIGH HIGH
Ca: HIGH

30
Q

Primary HPT, PTHrP Malig and NON PTHrP Malig PTH, PTHrP, Calcitriol and Ca levels

A 
Primary HPT
PTH High
PTHrp Low 
Calcitriol High
Ca High
Primary HPT
PTH Low
PTHrp High
Calcitriol  Low 
Ca High
Non Primary HPT
PTH Low
PTHrp Low
Calcitriol Low
Ca High
31
Q

What causes hypoparathyroidism

and the 3 types

A

occurs because of damage to or removal ofparathyroid glandsat the time of parathyroid or thyroid surgery.

  1. Deficient parathyroid hormone secretion
  2. Inability to Make Active Parathyroid Hormone.
  3. Resistance to Parathyroid Hormone (pseudo-hypoparathyroidism).
32
Q

Pathophysiology of hypoparathyroidism

A

Due to etiological cause

Decrease in gland function

Resistance to PTH

Inadequate PTH secretion and increased re-absorption of Ca in GI tract

Blood Ca falls too low

Muscular hyperirriability.

Uncontrolled spasm, hypocalcemic tetany

33
Q

Symptoms of hypoparathyroidism

A

Mild symptoms:
tingling in hands, fingers and mouth which progresses to severe muscle cramps and then to severe muscle cramps all over body and convulsions

34
Q

Deficient Parathyroid Hormone Secretion
 effects and symptoms

A

Lack of PTH leads to decreased blood levels of calcium (hypocalcemia) and increased levels of blood phosphorus (hyperphosphatemia).

There are no symptoms of too little parathyroid hormone other than the symptoms due to having a blood calcium that is too low.

35
Q

Inability to Make Active Parathyroid Hormone.
 effects and transmission

A

Deficient PTH secretion without a defined cause (e.g. surgical injury) is termed Idiopathic hypoparathyroidism.

This disease is rare and can be congenital or acquired later in life.

Congenital: Patients in this category are born without parathyroid tissues.

Acquired: Arises because the immune system has developed antibodies against parathyroid tissues

36
Q

Resistance to Parathyroid Hormone (pseudo-hypoparathyroidism). description

A

Characterised by hypocalcemia (too low blood calcium levels) and hyperphosphatemia (too high blood phosphorus levels)

But they are distinguished by the fact that they DO produce NORMAL parathyroid hormone.

The problem is that their bones and kidneys do not respond to the parathyroid hormone.

37
Q

Ca, P, PTH, Vit D and calcitriol levels for hypoparathyroidism, resistance to PTH, Liver disease and renal disease

A

Lecture Slide

Clinical Chemistry 3 (11 decks)

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