Parathyroid & Calcium 1

7/23/2019 Parathyroid & Calcium 1

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DISORDERS OF

CALCIUM HOMEOSTASISBY

UNIT III

PROFESSOR :Dr. K.B.R.SASTRYASST PROF :Dr. P. ANURADHA

Dr. SUNEEL KUMAR

PGs :Dr. MUJEEB AFZAL

Dr. P.PRIYADARSHINI

Dr. ABDUL SAMAD

Dr. SURESH


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Approx 1000 to 1200 g calciumpresent in adult

99.3 % in bone & teeth ashydroxyapatite crystals


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Corrected calcium

For eery 1!g"d# drop in serumalbumin belo$ g"d# measuredserum calcium decreases by 0.'

mg"d#.

Corrected calcium ( measured Ca)*0.'x+!measured albumin,- +Calcium

in mg"dl albumin in g"dl,


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FUNCTIONS

/one

Coagulation cascade

eurotransmitter release Contraction o cardiac seletal and

smooth muscle

ndocrine and exocrine secretions 4ntracellular signalling


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Why is the stringent

control of extracellularcalcium concentrationimportant ????


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PARATHYROID HORMONE

Pre pro PTH ( ! ""#

Pro PTH ( $% "" #

PTH ( &' "" #


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PARATHYROID HORMONE

ACTION ON BONE 5elease o interstitial calcium and phosphate

6timulates osteoblasts $hich releasecytoines lie 4#!7 $hich actiate osteoclasts

8steoclasts cause release o

hydroxyproline calcium phosphate


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ACTION ON KIDNEY Calcium and phosphate are reely ltered in

the glomeruli

:hosphate is absorbed rom :C; throughsodium!phosphate co!transporter


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CA#C4 ?0 % ! :C;

20 % ! ;hicascending limb o

loop o henle

@ > 10 % ! C; C;


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4;6;4A# BA#4 8F CA#C4 '0 % o ingested calcium isabsorbed

=ainly in duodenum & DeDunum.

Absorption is both passie and actie

:assie E paracellular route nonsaturable @ % ingested Ca absorbedby this route.

ActieE transcellularE receptormediated 2@% ingested Caabsorbed.


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ROLE OF ITAMIN D

. Promotes intestinal calcium

absorption

/ 1. Formation o calcium bindingprotein

+calbindin, 2. Formation o calcium stimulated

A;:ase

3. Formation o alaline phosphatase


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CA#C4;84

:roduced by the paraollicular cells " C cells othyroid gland.

5emnants o ultimobrachial body

6;4=


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HYPERCALCEMIA

6erum calcium I 10.@ mg"dl +I2.@ mmol"l,

4oniJed calcium I @.3 mg"dl +1.3 mmol"#,

=ild E;otal ca 10.@!11.9 mg"dl +2.@!3

mmol"l, +i @.7!' mg"dl 1.!2 mmol"l, =oderate E ;otal ca 12!13.9 mg"dl +3!

3.@mmol"l,

i ca '!10 mg"dl +2!2.@ mmol"l,

6eereE ;otal ca 1!17 mg"dl +3.@! mmol"l,

i ca 10!12 mg"dl +2.@!3 mmol"l,


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EPIDEMIOLOGY

4ncidence 1!2 case per 1000 adults.

Bigher incidence in 6outh Arica and6candinaia.

=ales I emalesE diKerencediminishes $ith increasing age.

Bypercalcemia rom all causeincrease $ith adancing age.


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)HEN TO SUSPECT

HYPERCALCEMIA***

=any are asymptomatic

;he mnemonic LstonesL LbonesMNthronesM Labdominal groansL andLpsychic oertonesL describes theconstellation o symptoms and signs

o hypercalcemia


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Bypercalcemia can result in atiguedepression mental conusionanorexia nausea omiting

constipation reersible renal tubulareKects increased urination short O;interal arrhythmias


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Phen calcium I13mg"dl >calcication inidneyssinesselslungsheartsto

mach and renal insuQciency

Phen calcium 1@!1'mg"dl > coma

and cardiac arrest can occur


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CAUSES OFHYPERCALCEMIA

:A5A;B584 > 5#A; :rimary hyperparathyroidism

#ithium therapy

Familial hypocalciuric hypercalcemia

6olid tumor $ith metastases

6olid tumor $ith humoral hypercalcemia

Bematological malignancies

=A#4AC ! 5#A;


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R4;A=4 > 5#A; Ritamin intoxication

6arcoidosis

4diopathic hypercalcemia o inancy

A668C4A; P4;B B4B /8;


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A668C4A; P4;B 5A# FA4# alali syndrome


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:roximal muscle $asting easyatiguibility atrophy o muscles

uodenal ulcer

:ancreatitis

Asymptomatic primaryhyperparathyroidism

Bypercalcemic parathyroid crisis


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LABORATORY TESTS Bypercalcemia

Bypophosphatemia

5aised :;B

5aised alaline phosphatase


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LITHIUM THERAPY

4t shits the :;B cure to right inresponse to calciumi.e. highercalcium leels are reSuired to lo$er

:;B secretions probably acting atthe calcium sensor

;here is complete reersal ohypercalcemia $hen lithium isstopped


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FAMILIAL HYPOCALCIURICHYPERCALCEMIA

Autosomal dominant trait

Caused by inactiating mutation in asingle allele o the calcium sensingreceptor

Abnormal sensing o the bloodcalcium by the parathyroid gland and

renal tubule causing inappropriatesecretion o :;B and excessie renalreabsorption o calcium


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JANSEN+S DISEASE

Autosomal dominant

Actiating mutation in the :;B":;Br:receptor

6hort limbed d$arsm

Bypercalcemia andhypophosphatemia $ithundetectable or lo$ :;B leels


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MALIGNANCY RELATED

HYPERCALCEMIA

Bistological character o tumor ismore important than extent ometastases

=CBA46=6 Bumoral hypercalcemia o malignancy

irect bone marro$ inasion 6eletal metastases


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ITAMIN D INTO,ICATION

Chronic ingestion o 0!100 times thenormal physiological reSuirement oitamin

Bypercalcemia is due to increasedactiity in the intestine and bone

4t is the conseSuence o increased

leels o 2@ +8B , iagnosis is by documenting

eleated leels o 2@+8B,

I100mg"ml


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Gr"-/o0"1os 23se"ses

4n granulomatous diseases liesarcoidosis tuberculosis and ungalinections excess 12@+8B, is

synthesiJed in macrophages andother cells

;here is a positie correlation

bet$een 2@+8B, and 12@+8B, :;B leels are lo$


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)ILLIAM+S SYNDROME

Autosomal dominant

CharacteriJed by supraalular aorticstenosis mental retardation elnacies

4t is due to abnormal sensitiity toitamin due to microdeletions at

the elastic locus and other genes onchromosome ?

#eels o 12@+8B, are eleated


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HYPERTHYROIDISM

About 20% o hyperthyroid patientshae high!normal or mildly eleatedserum calcium

4t is due to increased bone turnoer$ith bone resorption exceeding bone

ormation

;6B itsel has a bone protectie

eKect


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IMMOBILIZATION

4t is a rare cause o hypercalcemia inadults in the absence o anassociated diseasebut may cause

hypercalcemia in children andadolescents

Pith resumption o ambulation

hypercalcemia returns to normal ;here is a disproportion bet$een

bone ormation and bone resorption


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THIAZIDE DIURETICS

4ncrease calcium reabsorption.

=echanismE 2 hypothesis proposed.

First hypothesis E

6econd hypothesisE increased aCaexchanger in /# membrane o C;

CFdepletio

n

ecreased calciumltrate

4ncreased $ater & a absortion in:C; driing increased Ca absorption

in :C;


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ITAMIN A INTO,ICATION

Calcium leels may be eleated aterthe ingestion o @0000 to 100000units o itamin A daily

4t is presumed to increase boneresorption

Pithdra$al o the itamin is usually

associated $ith promptdisappearance o hypercalcemia


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SECONDARY

HYPERPARATHYROIDISM

;P8 =CBA46=6 4mpaired phosphate excretion

5aised leels o FF23 leads to reduction o

calcitriol leels

;5A;=; :hosphate excretion

6eelamer

calcitriol

ALUMINIUM


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ALUMINIUMINTO,ICATION

4t is characteriJed by acutedementia unresponsie and seereosteomalcia

Bypercalcemia deelops $hen thesepatients are treated $ith itamin

Aluminium is present at the site o

osteoid mineraliJation and calciumincorporation into the seleton isimpaired

MILK ALKALI


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MILK 4 ALKALISYNDROME

4t is due to excessie ingestion ocalcium and absorbable antacidssuch as mil or calcium carbonate

CharacteriJed by hypercalcemiaalalosis renal ailure

Chronic orm o the disease is termed

as /urnettTs syndrome

MILK ALKALI


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MILK 4 ALKALISYNDROME

A cycle o mild hypercalcemiaalalosis

seere hypercalcemia renalCa retention

C C


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B::5CA#C=4A

CA5F


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;BAH 8< VVVV

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Parathyroid & Calcium 1

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