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Medicine year 4 CDM > Block 6: DKA, Hypoparathyroidism, Hyperparathyroidism, bones > Flashcards

Block 6: DKA, Hypoparathyroidism, Hyperparathyroidism, bones Flashcards

1
Q

Further points for DKA management

A
  • Both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist
  • If the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin
  • The patient should be reviewed by the diabetes specialist nurse prior to discharge
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2
Q

DKA complications

A
  • Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • Iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
  • Acute respiratory distress syndrome
  • Acute kidney injury
  • Gastric stasis
  • Thromboembolism
  • Cerebral oedema
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3
Q

Primary hyperparathyroidism

A

High Ca+ levels due to high circulating PTH. Causes bone breakdown to release Ca+ and excess reabsorption in the kidney

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4
Q

Symptoms of Hypercalcaemia

A
  • Thirst, polyuria, renal stones
  • Weakness, myalgia, bone pain
  • Anorexia, vomiting, constipation
  • Mood change, depression, confusion
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5
Q

Causes of Hypercalcaemia

A
  • High PTH is primary or Tertiary Hyperparathyroidism, low PTH is cancer or other PTH independent causes
  • If cancer its majority Humoral hypercalcaemia and sometimes osteolytic metastasis
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6
Q

Investigations for Hypercalcaemia 1

A
  • Diagnosed by measuring serum adjusted calcium and parathyroid hormone (PTH) levels at same time
  • 24-hour urinary calcium to exclude familial hypocalciuric hypercalcaemia where its low
  • CT/MRI to identify lesion if suspected
  • Estimated glomerular filtration rate (eGFR) and creatinine to assess hydration status, risk of acute kidney injury and presence of chronic kidney disease
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7
Q

Investigations for Hypercalcaemia 2

A
  • Serum and urine protein electrophoresis, including testing for urine Bence-Jones protein to exclude myeloma
  • Full blood count (FBC) to exclude haematological malignancy
  • Liver function tests (LFTs) to exclude liver metastasis and some systematic diseases
  • Dual energy x-ray absorptiometry (DEXA) to assess bone health and risk of osteopenia/osteoporosis
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8
Q

Primary Hyperparathyroidism epidemiology

A
  • More female, peaks 50-70yrs
  • Family history
  • Benign solitary parathyroid adenoma-85%
  • ‘4-gland’ parathyroid hyperplasia-15%
  • Parathyroid carcinoma <1%: majority is benign
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9
Q

Inherited forms of primary Hyperparathyroidism- accounts for 15%

A
  • Multiple endocrine neoplasia (MEN)
  • Hyperparathyroidism jaw tumour syndrome
  • Familial isolated primary hyperparathyroidism
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10
Q

Biochemistry of primary Hyperparathyroidism

A
  • Hypercalcaemia with low serum PO43-
  • Raised or high-normal PTH
  • Elevated Bony alkaline phosphatase
  • Urinary calcium elevated or high normal
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11
Q

Complications of primary Hyperparathyroidism

A
  • Kidney stones, renal impairment
  • Osteoporosis at Wrist and Hip
  • Osteitis fibrosa cystica: periosteum of fingers and long bones is eroded
  • Brown tumours of bone: accumulation of osteoclasts
  • Corneal calcification: calcium deposited on the cornea, on the lateral and medial position. Appears white
  • ?Hypertension
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12
Q

Management of primary Hyperparathyroidism

A
  • Surgical neck exploration: If patient has symptoms or Complications (renal stones) of hypercalcaemia
  • Conservative management with regular monitoring: Only if asymptomatic (majority)
  • Calcimimetic drugs (calcium receptor agonists): Cinacalcet, reduces renal stimulation- excrete more in the kidneys
  • Bisphosphonates (anti-resorption therapy): Preserve bone density (monotherapy if conservative risk)
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13
Q

Malignant Hypercalcaemia

A
  • Median life expectancy of 6 weeks
  • Humoral hypercalcaemia of malignancy (80%): PTHrP related release from tumour- normally released when a baby
  • Bone erosion (20%): Diffuse bony disease, Focal osteolytic metastasis
  • Rare causes: cancer which release 1,25(OH)2D3 and ectopic PTH
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14
Q

Humoral hypercalcaemia of malignancy (HHM)

A
  • Squamous cell carcinomas: Lung, Breast, Oesophagus, Cervix, Skin, Renal, Bladder, Ovary, Vulva
  • Clinically obvious tumour mass
  • Excess production of PTHrP from tumour cells which acts on PTH receptors
  • Suppressed PTH and 1,25(OH)2D3
  • Patients not at high risk of pathological fracture: not one a specific bony lesion that might fracture
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15
Q

Myeloma

A
  • 30% of myeloma patients get hypercalcaemic
  • Myeloma sits in bone marrow causes osteolyses by cytokine release
  • Diffuse osteolysis due to local cytokines (IL6)
  • Causes renal impairement
  • Typical biochemical features: Phosphate may be elevated, Alkaline Phosphatase- normal
  • Hypercalcaemia is steroid responsive
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16
Q

Hyperparathyroidism: focal osteolytic metastasis

A
  • Lung, breast, prostate
  • Direct invasion of the bone by malignancy: seen on plain X-ray
  • Local pain
  • High risk of pathological fracture
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17
Q

Other causes of Hypercalcaemia

A
  • Drugs (thiazide diuretics, lithium): High PTH
  • Vitamin D intoxication: low PTH
  • Milk-Alkali Syndrome: increased calcium ingestion and reduced excretion. Normally due to PPI or anti-indigestion meds: low PTH
  • Sarcoidosis- increased hydroxylation of vitamin D
  • Renal failure: high PTH
  • Familial Benign Hypocalciuric Hypercalcaemia: mutation in Ca+2 receptor: High PTH
  • Immobility with high bone turnover (astronauts- or teenagers who break their leg): Low PTH
  • Endocrine Probs: Hyperthyroidism, Addison’s disease, Phaeochromocytoma
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18
Q

Management of severe hypercalcaemia

A
  • Baseline PTH if first presentation
  • Surgery: Parathyroidectomy with primary hyperparathyroidism
  • Ca+2 causes nephrogenic DI: Treat dehydration with IV N/Saline (6L/24hrs)
  • Specific treatments (next day): IV bisphosphonates (zolendronic acid) if primary hyperparathyroidism. If myeloma give steroids
  • Takes 72hrs to normalise calcium:
  • SC denosumab if renal impairment
  • Calcitonin: reduced calcium concentration by inhibiting kidney and bone reabsorption
  • Cinacalcet: reduces serum calcium without affecting bone density or urinary calcium
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19
Q

Parathyroidectomy is indicated:

A
  • Symptomatic disease: Symptoms ofhypercalcaemia, Osteoporosis and/or fragility fractures, Renal stones or nephrocalcinosis
  • Age <50 years
  • Serum adjusted calcium of 2.85 mmol/L or above
  • Estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m
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20
Q

Complications of Hyperparathyroidism

A
  • Osteoporosis and fragility fractures
  • Kidney stones and kidney injury
  • Hypertension and heart disease
  • Numerous gastrointestinal disorders including peptic ulcer disease, pancreatitis and gall stones
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21
Q

Hypopituitarism

A

Deficiency of one or more hormones produced by the anterior pituitary or released from the posterior pituitary. Clinical manifestation depends on the hormone affected

22
Q

Posterior pituitary

A

Produces oxytocin and ADH. Released neuronally by nerve signals from the Hypothalamus

23
Q

Hypopituitarism: most common causes

A
  • Pituitary adenoma and other tumours
  • Previous surgery/radiotherapy
  • Trauma
  • Apoplexy
  • Hypophysitis: inflammation
  • Infiltrative: hemochromatosis, lymphoma
24
Q

Hypopituitarism effects and mechanism

A
  • Adrenal: Central adrenal insufficiency (CAI), lack of ACTH release.
  • Thyroid
  • Prolactin
  • Gonadal
  • Somatotropic
  • DI

Hypopituitarism mechanism: Normal progression of symptoms GH -> FSH/LH -> TSH -> ACTH +/- DI

25
Q

Diagnosing CAI

A
  • Basal cortisol <100nmol/L: AI
  • Basal cortisol 100-400nmol/L: Do Corticotropin (Synathen test), if cortisol <500nmol/L at 30 or 60 minutes indicates AI
  • Basal cortisol >400 nmol/L: excludes AI
  • ACTH: low can be inappropriately normal (if low cortisol you expect ACTH to be high)
  • Other stimulation tests: Insulin tolerance test, Glucagon stimulation test, Short syncathen (corticotropin) test.
26
Q

CAI treatment

A

Hydrocortisone in divide doses, more in the morning. Fludrocortisone is not required

27
Q

Central Hypothyroidism

A
  • Reduced TSH.
  • Bloods: low T4/T3 and high TRH, low/inappropriately normal TSH
  • Treatment: thyroxine- adjust dose with T4/T3 levels (not TSH)
  • If concerned they have low cortisol start them on steroids before thyroid replacement
28
Q

Hypopituitarism: prolactin

A
  • Increased prolactin: Pituitary stalk compression (stops dopamine inhibition by tumour). Prolactinoma (pituitary adenoma with over production of prolactin). Can cause hypogonadism (low FSH/LH)
  • Prolactin deficiency: Marker of severe pituitary hypofunction
  • Deficit: Dopamine/prolactin
  • Treat only if prolactinoma (tumour that is over producing prolactin): Dopamine agonists
  • Dopamine from the Hypothalamus inhibits prolactin release
29
Q

Symptoms of Hypogonadism

A

Oligo/amenorrhea, erectile dysfunction, low libido, hot flashes, infertility, vaginal dryness, fatigue, weakness.

30
Q

Diagnosing Hypopituitarism (Hypogonadism): men

A
  • Low or inappropriately normal FSH and LH
  • Low total testosterone
  • Low free testosterone- available one (calculated using SHBG)
31
Q

Treating Hypogonadism men

A
  • Testosterone replacement (sc or topical): improved CV health, prostate and Hb
  • Fertility treatment when required
32
Q

Diagnosing Hypogonadism men

A
  • Low or innapropiately normal FSH and LH
  • Low estrogens
  • Rule out other causes of amenorrea including pregnancy and hyperprolactinemia
33
Q

Treating Hypogonadism women

A
  • Estrogen replacement in premenopausal
  • Fertility treatment when required
34
Q

GH pathophysiology

A

GH is released from the pituitary and travels to the liver where its metabolised to IGF-1 which is the active form

35
Q

Hypopituitarism (GH deficiency): diagnosis

A
  • GH release in pulses therefore single sample does not reflect GH activity. Test IGF-1 and GH stimulation test.
  • Stimulation test: administer insulin and sample blood at-30, 0, 30, 60, 120 min for GH and glucose
  • Glucose should drop to 2.2mmol/L, otherwise not valid.
  • GH deficiency: <3-5. cut offs for GH response are BMI related
  • Indications: previous GH deficiency during childhood, evidence of pituitary damage. Don’t do if elderly
  • GH increases in stress, gives energy, helps with growth
36
Q

Hypopituitarism (GH deficiency): monitoring and treatment

A
  • Monitor every 6 months: IGF-1, BMI, Metabolic profile (glucose and lipids), QoL, other deficits
  • Diagnosis: low IGF-1 and low GH after stimulation test
  • Treatment: GH injection
37
Q

Hypocalcaemia causes

A
  • Vitamin D deficiency: most common cause
  • Hypoparathyroidism
  • Drugs, Gd contrast (MRI)
  • Renal failure
  • PTH or vitamin D resistance syndromes
  • Severe illness: Acute pancreatitis, Acute rhabdomyolysis
  • Psuedohypoarathyroidism: resistance to PTH
38
Q

Symptoms of Hypocalcaemia

A
  • Paraesthesia of mouth & fingers: symmetrical numbness or tingling
  • Muscular twitching and leg cramps: evening and night
  • Laryngeal stridor
  • Carpopedal spasm (tetany)
  • Seizures
  • Papilloedema
  • Prolonged QTc
  • Chvostek’s sign: tap on parotid gland get involuntary twitching
  • Trousseau’s sign: inflate BP cuff for 1 min above systolic BP hands spasm
  • Hyperreflexia
  • Long term: extrapyramidal symptoms, cataracts and calcification of the basal ganglia
39
Q

Hypoparathyroidism causes

A
  • Post-surgical (thyroidectomy)
  • Congenital absence of parathyroid gland: DiGeorge syndrome, GCMB mutation
  • Autoimmune (with candidiasis & Addison’s)
  • Reset PTH setpoint (calcium receptor)
  • Tissue resistance to PTH: pseudohypoparathyroidism
  • Infiltration of parathyroid gland
  • Defective PTH molecule
40
Q

Biochemistry of Hypoparathyroidism

A
  • Low serum calcium
  • High serum PO43-
  • Low- undetectable circulating PTH (can be inappropriately normal)
  • Normal renal function
  • Low Urine calcium excretion
41
Q

Pathophysiology of Hypoparathyroidism

A

Calcidiol cant be converted to calcitriol in the liver because 1 alpha hydroxylation is PTH dependent. Therefore active vitamin D isnt produced

42
Q

Treatment of Hypoparathyroidism

A
  • Activated vitamin D: 1-Alfa calcidol (1 – 2.5 mcg daily), Calcitriol
  • Calcium (1–3 g daily): Effervescent solution “Sandocal”, Chalky tablets Adcal or Calcichew
  • Give both activated vitamin D and Calcium
  • In rare cases IV calcium
43
Q

Other causes of Hypocalcaemia

A
  • Drug induced hypocalcaemia: PO4, Bisphosphonates, Chemotherapy
  • Hypomagnesaemia: induced hypocalcaemia by inhibiting PTH release and peripheral action
  • Renal failure: Hypocalcaemia due to phosphate retention due to tubule damage. And failure of 1a hydroxylation of Vit D as it occurs in the kidneys. State of secondary hyperparathyroidism
44
Q

Parathyroid hormone acts to raise blood calcium levels by

A
  • Increasingosteoclastactivity in bones (reabsorbing calcium from bones)
  • Increasingcalcium reabsorptionin the kidneys (less calcium is lost in urine)
  • Increasingvitamin Dactivity, resulting in increasedcalcium absorptionin theintestines
45
Q

Calcium homeostasis

A
  • Drop in calcium is sensed by a calcium sensing receptor on the parathyroid cell and in the distal tubule
  • The Parathyroid cell releases more PTH
  • Acts on PTH receptor in renal tubule, bones and Duodenal lumen. Causes activation of vitamin D. Increased calcium absorption in the renal tubule, release of calcium from bone
46
Q

Vitamin D metabolism

A
  • Synthesised by sunlight: 7-dehydrocholesterol turns into previtamin D. Then turns to vitamin D3
  • Vitamin D3 turns into calcidol in the liver and into calcitrol in the kidney
  • Calcitriol is the active vitamin D hormone and effects calcium and skeletal homeostasis
47
Q

Sources of vitamin D

A
  • 90% from sunlight UVB exposure (April-October in the UK): 15 mins outside at midday
  • Coleocalciferol from oily fish (egg yoke, meat)
  • Ergocalciferol from yeast/mushrooms
  • UK has profound vitamin D deficiency
48
Q

Bone structure

A
  • Inert mineral (chalky): hydroxyapatite-Ca10(PO4)6(OH)2)
  • Osteoid (flexible): Type 1 collagen (fibres), Chondroitin (matrix)
  • Cellular component (5%): Osteoblasts: bone forming cells. Osteoclasts (from monocytes): bone resorbing cells. Osteocytes & haematopoetic tissue
49
Q

Osteoporosis vs osteomalacia

A
  • Osteoporosis: proportional reduction in solid components (osteoid)- increase in living cellular component of bone. Causes fractures
  • Osteomalacia: reduction in mineralised component (increased osteoid). Causes Bend
50
Q

Bone remodelling cycle

A
  • Resorption: multinucleated osteoclasts adheres to bone and secretes acid reabsorbing the bone
  • Osteoid formation: Osteoblasts are signalled to reform eroded bone, form osteoid which is mineralised
  • Lining cells lie on the top of the bone protecting it from osteoclasts

Medicine year 4 CDM (44 decks)

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