AMK 2 Flashcards
What are the parathyroid glands?- Action
4 glands on the posterior aspect of the thyroid gland.
- Release Parathyroid Hormone (Chief cells- CC) in response to Hypocalcaemia
- (LOW CA, CA SENSITIVE RECEPTOR ON CC STIMULATED LESS SO LESS INTRACELLULAR PATHWAYS INHIBIT PTH RELEASE. high CA detected by CSR and activated sending signals inside the cell to inhibit PTH release)
- Release Calcitonin (parafollicular cells )
(OPPOSING EFFECT OF PTH- RELEASED IN RESPONSE TO HYPERCALCEMIA DETECTED BY CSR.)
How does Parathyroid hormone work?
Increased activity of osteoclast - increased bone resorption (release CA , Pr etc from bone into blood)
- PTH binds to PTH receptor on osteoblast. Osteoblast releases rank ligand which binds to rank receptor on osteoclast and increases its activity)
—(g protein coupled receptor activation by PTH , causes calcium channel proteins to be embedded in the DCT membrane - CA reabsorbed from filtrate)
-Absorption of CA From GI tract into bloodstream.
(Vitamin D binds to receptor inside enterocyte causing gene expression and production of CA CHANNELS - embedded into membrane)
Increases expression of 1- alpha hydroxylase in kidney
Action of PTH?
- Increased activity of osteoclast - increased bone resorption
- `increased expression of 1 - alpha- hydroxylase in kidney involved in vitamin D synthesis.
- Increased absorption of CA from GI TRACT and DCT of kidney tubule
-
What is Hypocalemia and causes?
Serum below 8.8mg/dl (2.2mmol/L)
-Alkalosis - COOH in albumin become ionised - lose H+. So Ca2+ binds with the h+ group (complexed no longer free ionised- FREE IONISED TAKES PART IN CELLULAR PROCESSES.)
- Hypoparathyroidism - (can be caused by surgery(PTH gland accidentally damage or removed) or Autoimmune destruction - Less PTH release less CA2+ released into the blood)
- MAG Deficiency - Mg needed to produce PTH. - Acute pancreatitis - Free Fatty acids released and complexes with CA2+ forming insoluble product.
- Kidney failure - too much CA2+excreted in the urine.
- Tissue injury - Burns,
- Rhabdomyolysis -breakdown of muscle fibres - releases it’s products into bloodstream - myoglobin. Kidney breaks this down and its breakdown products damage kidney leading to kidney failure.
- Tissue lysis syndrome - large cell death - release p043- which complexes wit CA2+ to form calcium phosphate which is insoluble. - Vitamin D deficiency
- Too many blood transfusions
• Mild hypocalcemia may be asymptomatic or cause muscle cramps.
Consequences of Hypocalcaemia ?
Tetany - involuntary muscle contraction
- Chvostek’s - involuntary twitching of facial muscles.
Trousseau’s signs - carpal spasm - blood supply reduced to hand when cuff inflated to 20mmhg. Ocuurs in alkalosis, HYPO - calcaemic, kalemia, magnesia.
muscle cramps.
• Severe hypocalcemia (serum calcium
Treatment of hypocalcemia?
• Give IVcalcium gluconateto patients with tetany; treat others with oral calcium supplements. Vitamin D supplementation if needed.
(chronic hypocalcaemia - oral calcium supplements + vitamin D supplements if needed.)
If tetany occurs - do continuous potassium - calcium monitoring & ECG monitoring
0 if associated with hypomagnesia give magnesium gluconate.
What is Hypercalcemia ?
Causes
serum calcium above 10.4 mg/DL (2.6 mmHG)
-Acidosis - COOH groups in Albumin. Lots of H+ so COOH in this form and positively charged so CA2+ is repelled. Less bound CA and more Free ionized CA.
-Too much PTH - Abnormally high activity of osteoclast - too much bone resorption
CA2+ released into blood.
- Excess Vitamin D (from diet or supplements)
- Malignancy - tumour releases PTH related protein that mimics its action leading to increased activity of osteoclast and bon resorption.
- Medication - e.g. Thiazide diuretics - increase reabsorption - DCT
Consequences/ symptoms of Hypercalcemia?
High CA - NA channels less likely to open —- harder to depolarize , less excitable.
Slower / absent reflexes
- Slower muscle contraction -
- muscle weakness
- constipation - In the brain - hallucinations. confusion and Stupor ( altered consciousness only brought around by vigorous physical stimulation)
- Hypercalciuria (too much CA in urine )- draws water along with it - DEHYDRATION.
- Hypercalcemia + hypercalciuria cause kidney stones (calcium oxalate).
From capsule
The classic presentation of hypercalcaemia is ‘bones, stones, (abdominal) groans, and psychic moans’. Effects on the heart include arrhythmias and a short QT interval. Always consider hypercalcaemia in cancer patients with non specific symptoms.
Renal stones would be associated with a longstanding hypercalcaemia – so likely to be primary hyperparathyroidism rather than cancer
Treatment of Hypercalcemia ?8
Mild Hypercal - confirm diagnosis before treatment
Moderate - Saline
- Loop diuretic - makes the kidney past out more urine - CA excreted. .
- Bisphosphonate - Zoledronate , Pamidronate (They prevent bone resorption (osteoclast)- same as calcitonin )
Severe - Oral phosphate (CA binds forms CA phosphate - insoluble )
or saline + loop diuretic
Emergency
Rehydration - saline 0.9%
Watch for fluid overload in elderly and renal impairment patients
Loop diuretic rarely used - usually only in fluid overload patients
- Then intravenous biphosphonate (single dose)
E.g zolendronic acid
2ND LINE TREATMENTS
Glucocorticoids (inhibit 1,25OHD production)
• In lymphoma, other granulomatous diseases or
25OHD poisoning
• Prednisolone 40mg daily
• Usually effective in 2 to 4 days
Calcitonin
• Can be considered if poor response to
bisphosphonates
Calcimimetics e.g cinacalet
• Licensed for hypercalcaemia due to primary
hyperparathyroidism, parathyroid carcinoma or renal
failure
Parathyroidectomy
• Can be considered in acute presentation of primary
hyperparathyroidism if severe hypercalcaemia and
poor response to other measurements
Criteria to surgery for Primary Hyperparathyroidism?
SURGERY THE ONLY WAY TO Completely SOLVE PRIMARY HPTHism
Refer people with a confirmed diagnosis of primary hyperparathyroidism to a surgeon with expertise in parathyroid surgery if they have:
0 symptoms of hypercalcaemia such as thirst, frequent or excessive urination, or constipation or
0 end-organ disease (renal stones, fragility fractures or osteoporosis) or
0 an albumin-adjusted serum calcium level of 2.85 mmol/litre or above.
1.3.2Consider referral to a surgeon with expertise in parathyroid surgery for people with a confirmed diagnosis of primary hyperparathyroidism even if they do not have the features listed in recommendation 1.3.1.
What is Hyperparathyroidism ?
Types?
Hyperparathyroidism - excessive secretion of PTH.
0 Primary - One or more PTH glands produces excess PTH
0 Secondary - PTH secretion in response to decreased CA. (caused by liver and bowel disease, Vitamin D deficiency . )
0 Tertiary - long-standing secondary hyperparathyroidism that starts to behave like primary hyperparathyroidism.
What should be avoided when a person has hyperparathyroidism?
Thiazide diuretics - BP medication - can cause dehydration and raise serum CA2+.
Non - surgical treatment of Pruimary Hyperparathyrodism ?
If surgery unsuccessful , , unsuitable or declined and albumin adjusted serum calcium is :
- >2.85mmol(with symptoms of hypercalcemia)
- > 3mmol/L (no symptoms)
- Cinacalcet (stimulates body to produce less PTH)
Indications :
secondary hyperparathyroidism- end stage renal disease.
Hypercalcemia in parathyroid carcinoma. Primary hyperparathyroidism - Consider Bisphosphonate - in patients who have increased fracture risk - short term . (don't offer for chronic hypercalcemia of Hyperparathyroidism )
What is Hypoparathyroidism ? Consequences , treatements?
Too little production of PTH
Hypocalcaemia, Hypophosphatemia (< 2.5 mg/dL (0.81 mmol/L).)
Symptoms of hypocalcaemia etc.
TREATMENTS - Restore CA (calcium gluconate - IV (for severe- urgent management, us ) and phosphorus levels (Oral sodium phosphate or potassium phosphate)
0 Parenteral phosphate is usually given IV. It should be administered in any of the following circumstances:
When serum phosphate is < 1 mg/dL (< 0.32 mmol/L)
Rhabdomyolysis, hemolysis, or central nervous system symptoms are present
Oral replacement is not feasible due to underlying disorder
diet should be rich in CA and phosphorus
0 Vitamin should be given if needed.
What is Addison’s Disease ( primary , chronic , adrenocortical disease)?
Hypoadrenalism /adrenal insuffcinecy
- Not enough cortisol and aldosterone , andogens (sex hormone) produced
- Can be caused by autoimmune attack on adrenal cells leading to atrophy.
- iatrogenic - removal of adrenal gland
- Maligancy
- Adrenal hemorrage
- infection
- cushing sydrome medication
- secondary - insufficient ATCH secretion.
Need to prevent adrenal crisis - medical emergency.
Decreased androgens affects females more than males as the testes produce most of androgens in males.
Symptoms of Addison’s Disease?
0 lack of energy or motivation (fatigue)
0 muscle weakness
0 low mood - CORTISOL EFFECTS THE BRAIN
0 loss of appetite and unintentional weight loss - CORTISOL INCREASES GLUCOSE LEVELS (INCREAES INSULIN WHICH CAUSES ADIPOCYTES TO ACCUMULATE FAT)
0 increased thirst
0 Over time, these problems may become more severe and you may experience further symptoms, such as dizziness, fainting, cramps and exhaustion.
Addisonian pigmentation - hyper-pigmentation - You may also develop small areas of darkened skin, or darkened lips or gums ( low cortisol —-> increased MHC - melanocyte- stimulating hormone —–> Hyperpigmentation )
- reduced Blood pressure- ALDOSTERONE RETAIN NA (SALT) AND WATER WHICH INCREASES BP. Cortisol causes vasoconstriction increasing BP
- decreased Libido - Androgens
Find May last wait together By Lewisham high F,M,L,W,T, B F-fatigue M- muscle weakness L - low mood W - weight loss/loss of appetite B - decreased BP L - libido H - hyperpigmentation
- abdominal pain - sometimes it can be mistaken for pancreatitis
