Parathyroid, Ca, VitD: Hyperparathyroidism, Hypoparathyroidism, Milk-alkali syndrome, Vitamin D intoxication Flashcards
Parathyroid gland
-location
-function
How does Ca enter and leave our body
How does it exist in our body?
4 pea sized parathyroid glands behind thyroid
-increases free Ca levels
-acts on a negative feedback loop
Enters
-GI
Leaves
-urine, feces
Bone - CaPO4 crystals
Blood - free, albumin-bound, anion-complex
How does PTH work
If lowCa => PTH released
Bone
-osteoclastic activity increased => release Ca, PO4
Kidney
-hydroxylate and activate VitD in PCT => increase Ca uptake in gut
-increase Ca uptake in DCT
Primary parathyroidism
-pathophysiology, causes
-risk factors
-presentation
-mimics
-diagnosis
Overactive PTG - most common cause of high Ca
-adenoma most common
-hyperplasia, malignancy
-MEN
Older women
Bones - pain, osteopenia/porosis
Stones - kidney
Low muscle tone
Abdo groans - pain, N+V, polyuria
Psychiatric moans - fatigue, depression, memory impaired
Mimics
-dementia, depression
Serum adjusted Ca and PTH
-high Ca and PTH => parathyroid dependent high Ca
Xray - pepperpot skull
Definitive - total parathyroidectomy
If not suitable for surgery
-calcitonin - inhibits bone and kidney Ca release
-cinacalcet - reduce Ca without affecting bone density/urinary Ca
-denosumab, bisphosphonates
Relation of hyperparathyroidism to malignancy
-how does it differ from primary hyperparathyroidism
PTHrP secreting tumours - lung, breast, kidney
Osteolytic lesions - bone mets, MM
Assess for signs of malignancy
-fatigue, weight loss, pain, unexplained masses
Faster increase in Ca, more severe
PTH is low
Secondary hyperparathyroidism
-pathophysiology
-presentation
-diagnosis
-management
Another condition lowers Ca => PTG overworks, hyperplasia
Almost always in CKF
-PO4 excretion and VitD activation impaired => so uptake and increase of free Ca reduced
(PO4 binds to Ca => reducing free Ca)
High PTH => higher bone turnover so osteopenia/porosis risk, presentation similar as primary
Ca - low/normal
PO4 - high
VitD - low
Vitamin D and cinacelcet
Reduce dietary PO4, PO4 binders (CaCO3)
Surgery if needed
Tertiary hyperparathyroidism
-pathophysiology
-presentation
-management
PTG constantly releasing PTH, irrespective of Ca
-long term 2ndary hyperparathyroidism (from CKD)
High PTH => higher bone turnover so osteopenia/porosis risk, presentation similar as primary
Ca - normal/high
PO4 - high
VitD - low
Vitamin D and cinacelcet
Reduce dietary PO4, PO4 binders (CaCO3)
Surgery if needed
Milk-alkali syndrome
-pathophysiology
-presentation
-management
Caused by excess intake of Ca and absorbable alkali (CaCO3)
-dietary supplements for osteoporosis/hyperparathyroidism
-antacids
Triad
-hypercalcemia => met alk => AKI
Fluids and stop Ca supplements
Vitamin D toxicity
-pathophysiology
-presentation
-management
VitD => increases Ca uptake in DCT and gut
OD on VitD => hypercalcemia
-only possible from supplement OD
Painful bones
Abdo groans
Kidney stones
Low muscle tone
Psychiatric overtones
Vitamin D toxicity
-pathophysiology
-presentation
-management
VitD => increases Ca uptake in DCT and gut
OD on VitD => hypercalcemia
-only possible from supplement OD
Painful bones
Abdo groans
Kidney stones
Low muscle tone
Psychiatric overtones
Fluids
Stop VitD, reduce Ca intake
Bisphosphonates
Milk-alkali syndrome
-pathophysiology
-presentation
-management
Caused by excess intake of Ca and absorbable alkali (CaCO3)
-dietary supplements for osteoporosis/hyperparathyroidism
-antacids
Triad
-hypercalcemia => met alk => AKI
Fluids
Stop Ca supplements
Vitamin D toxicity
-pathophysiology
-presentation
-management
VitD => increases Ca uptake in DCT and gut
OD on VitD => hypercalcemia
-only possible from supplement OD
Painful bones
Abdo groans
Kidney stones
Low muscle tone
Psychiatric overtones
Fluids
Stop VitD, reduce Ca intake
Bisphosphonates
Hypoparathyroidism
-pathophysiology
-presentation
-management
Deficient PTH => abnormally low Ca, high PO4
Often caused by
-accidental damage during thyroid/neck surgery
-AI, DiGeorge
Hypocalcemia - Neuromusclar irritability
-numb, cramps, tingling, fatigue, spasm
Chvostek - twitching facial muscles when tapping CN7
Trousseau - curling of hand with BP cuff
Low PTH, Ca
High PO4
Ca supplements
VitD analogues - calcitriol
High Ca, low PO4 diet
Osteomalacia
-pathophysiology
-risk factors
-presentation
-diagnosis
-management
VitD deficiency => soft, weak bones
Older adults in both sexes
-malabsorption/lack in diet or sunlight
-CKD
Bone pain
Muscle weakness, proximal myopathy
Fractures
Bowing of long bones
Vertebral compression => kyphoscoliosis
Hypocalcemia symptoms
Low VitD, Ca, PO4
High ALP
Xray - translucent bones
VitD, Ca supplements
Sun exposure, dietary modifications
Rickets
-pathophysiology
-risk factors
-presentation
-diagnosis
-management
VitD, Ca, PO4 deficiency => weak bones, deformities
Children in both sexes
-dietary/sunlight deficiency
-prolonged breastfeeding/unsupplemented cow milk formula
Aching bones, joints
Lower limb abnormalities
-genu varum (toddlers)
-genu valgum (children)
-rickety rosary
-kyphoscoliosis
-craniotabes
-Harrison’s sulcus (depression of 6th rib)
Low VitD, Ca
High ALP
PO VitD
