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PARATHYROID Vendar

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Awais Arshad
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0% found this document useful (0 votes)
34 views5 pages

PARATHYROID Vendar

Uploaded by

Awais Arshad
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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INTRODUCTION

Normal value: 9-10.6 mg/dl

Hormone Stimulus Effect on Effect on Effect on Target: -


intestine: bone: kidneys:

Parathyroid ↓calcium Through vit ↑ resorption Ca  ↓PO4 ↑Ca2+


↑phospate D3 reabsorb
(phosphate activation PO4 
stronger =INDIRECT excrete
stimulus
than
calcium)
Calcitonin ↑calcium Bone Ca & PO4 ↓ PO4 ↓Ca2+
(from Gastrin mineralization excretion
parafollicular
cells in
thyroid)
Vit D3 ↓calcium ↑ absorption Moderate ↑ absorption of ↑ PO4 ↑Ca2+
ingested or ↑PTH of both levels  both
synthesized formation
in skin then High levels 
resorption
activated by
liver then
kidneys
under PTH
influence
HYPERPARATHYROIDISM

TYPES: -
Primary:- problem in the gland itself =
adenoma, why?  Mostly: sporadic (single
adenoma) ; less commonly :- familial MEN
syndrome (multiple adenomas)

Secondary: - secondary to something else: -


↓calcium ↑phosphate. When?  at 1) CKD (can’t
excrete phosphate nor activate vit D3); 2) Vit D3
deficiency.

Tertiary: - prolonged stimulation of gland makes it insensitive to negative


feedback = AUTONOMOUS. When?  At prolonged secondary

CLINICAL PICTURE
 Asymptomatic (= 50%)
 Renal (20%): Ca precipitates  stones, nephrocalcinosis; osmotic effect 
polyuria
 Skeletal (<5%): resorption  cystic lesions and easy fractures e.g. osteitis
fibrosa cystica, resorptions in fingers, bones, or teeth, brown tumor, etc.
 GIT: on stomach  PUD (Ca stimulates HCI secretion); on pancreas  Acute
pancreatitis (duct stones); on intestines  Constipation (Ca cause spasm of
intestine); general  pain, anorexia, nausea, vomiting.
 Neurological: Fatigue, depression of CNS fx,
 Cardiovascular: heart Short QT interval ; blood vessels Hypertension

INVESTIGATIONS

• Lab: - PTH, Ca, PO4, bone markers (ALP, cAMP)


• Imaging: - Sestamibi scan , others:- US, CT, MRI, Xray on bones
TREATMENT

Surgery  When? @symtomatic OR @asymptomatic PLUS any of:-

1. Age < 50.


2. Serum calcium (>11.5)
3. Kidney: - creatinine clearance <60 ml/min;
4. Bone: (1) Low mineral density, or previous fragility of bone
fracture. (2) T score < -2.5

1ry neck exploration: single adenoma: remove involved gland, multiple adenomata: remove
31/2 gland & implant remaining in brachioradialis (because superficial hence accessible).

Successful @ ↓PTH 50% after 10 minutes of surgical excision (intraoperative) not measured
by Ca, why because of Hungry Bone Syndrome. Rebound hunger of bones for Ca after being
suppressed for so long =↓Ca giving a false impression of postoperative hypoPTH.

Medical  Calcimimetic agents: Cinacalcet (Sensipar), Estrogen, Raloxifen,


Bisphosphonates, non calcemic vit D analogue (Paricalcitol).

DIFFERENTIAL DIAGNOSIS
Things that cause osteolytic bone lesions, like

 multiple myeloma
 metasteses

Hypercalcemia due to malignancy


• Lymphoma: production and activation of Vit D
• Bone cancer, metastasis, and multiple myeloma: bone resorption
• Paraneoplastic syndrome: - pheochromocytoma/ breast lung/
Kidney/ ovarian cancer secrete PTH like peptide. (high Ca2+, Low
P with normal or even low PTH)
• VIPoma leading to high VIP that stimulates PTH.
• All malignancies can lead -> Prolonged immobilization.

EMERGENCY : Malignant hypercalcemia


Treatment 
• Forced diuresis OR Dialysis.
• Glucocorticoids/ ketoconazole: inhibit vit D.
• Calcitonin, Bisphosphonate -* (inhibit osteoclast)
HYPOPARATHYROIDISM

 LOW PTH :-
1) Iatrogenic (Most Common):- post thyroidectomy or neck dissection
2) Autoimmune
3) Agenesis of gland = Di George syndrome
 HIGH PTH but resistance, why? 
1) Mg deficiency
2) Pseudo-hypoparathyroidism  hereditary defect in receptor (=resistance)
associated with other dysmorphic features including:- short stature, neck,
4th and 5th fingers. NB: Pseudo-pseudohypoparathyroidism: has same
dysmorphic features as previous one but with Normal PTH level and action.
(No resistance), while pseudo- Hypohyperparathyroidism: PTH resistance
at all tissues except: Bone.

Other causes of Hypocalcemia: Vitamin D deficiency: (Most Common cause)

CLINICAL PICTURE

Acute manifested: - (at low Ca nerves are hyperexcitable)


• Carpopedal spasm
• Bronchospasm and laryngospasm
• Prolonged QT interval and ventricular arrythmias (the silent killer)

Acute latent (milder and needs provocation)


• Chvostek: tapping facial nerve  face twitching
• Trousseau: cuff inflation at arm  carpal spasm
• Erb’s sign: stimulate nerve by electric current  needs 5 mAMp instead of
10

Chronic: abnormal teeth dentition, metastatic calcifications

INVESTIGATIONS

 Lab: PTH, ↓Ca, ↑PO4, ALP. @true hypo  ↓PTH; @pseudohypo


↑PTH &dystrophic features
 Imaging: US neck at absent gland due to surgery or hereditary
Digeorge; CT brain if basal ganglia calcifications
TREATMENT No PTH replacement so you try to replace its role: -

1) Ca substitute: - Ca carbonate (2-6g/day)


2) Vit D3 high doses: - (because normally PTH would have activated
it)  calcitriol, cholecalciferol.

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