endo bottom tier Flashcards
is hypo or hypercalcaemia more common
hypercalcaemia
hypocalcaemia risk factors
Low vit D -- Low intake ---- Dark skin ---- Reduced UV exposure: Live in an area with little sun/ work job inside etc ---- Malabosrption ---- Anti-epileptic drugs : induce enzymes that increase vit D metabolism ---- Vitamin D resistance (rare) -- Low active vit D ---- kidney/ liver issue (eg CKD) Genetic - hypoparathyroidism Radiation Mg deficiency Lactose intolerance In hospital / ICU
causes of hypocalcaemia
secondary hyperparathyroidism (vit d deficiency)
- Low vit D intake
- Chronic kidney disease - no active vit D
- Liver issue - no active vit D
hypoparathyroidism
- Genetic eg Di George syndrome
- Surgical (of thyroid, lymph- damaged parathyroid)
- Radiation
- Autoimmune
- Mg deficiency
- High phosphate - from chronic kindey disease
- Primary - failure of parathyroid gland, underactive
- Secondary - resulting from parathyroidectomy/thyroidectomy surgery/ radiation/ hypomagnesemia (magnesium needed for PTH secretion)
pseudohypoparathyroidism (PTH resistance)
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in secondary hyperparathyroidism
secondary hyperparathyroidism (vit D def)
- high PTH
- low Ca
- low phosphate
- PTH appropriate
- Low vitamin D levels mean low calcium absorption in the gut
- In response, PTH levels increase
- Vit D also needed for phosphate absorption. High PTH also decreases phosphate levels
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in hypoparathyroidism
- Underactive parathyroid- not much PTH produced
- So low Ca absorption (gut), reabsorption (kidney) and resorption (bone)
- low PTH
- low Ca
- high phosphate
- PTH inappropriate
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in pseudohypoparathyroidism
- high PTH
- low Ca
- high phosphate
- PTH appropriate
- PTH resistance so PTH is ineffective at increasing calcium levels
- In response to low calcium, PTH goes up. But this does not increase calcium levels
- High phosphate as PTH is ineffective
- Associated with short stature, short metacarpals, esp 4th, and sometimes intellectual impairment
calcitonin effect on Ca / phosphate
decreases Ca2+ and phosphate
bisphosphontes effect on Ca
reduces osteoclast activity, resulting in reduced Ca2+ (treatment for hypercalcaemia)
causes of tetany
ca deficiency K+ deficiency, Mg2+ deficiency Hyperventilation Alkalosis
hypoalbumineamia / calcium
presents as hypocalcaemia - Artefact of hypoalbuminemia (calcium binds to albumin)
hypocalcaemia presentation
increased muscle and nerve excitability
- cramps, spasm, tetany (similar terms, involantary contraction)
- convulsions, seizures
- paraesthesia - numbness around mouth/ extremeties
- cataracts, sight loss
- basal ganglia calcification
- fractures - undermineralised bone (vit D def secondary hyperparathyroidism)
- Trousseaus sign (inflate BP cuff- brachial artery occluded, this exacerbates low calcium causing spasm in hand/forearm –> salt bae shape)
- Chcostek’s sign (tap on facial nerves, face muscles twitch)
- dermatitis
- orientation impaired, confused
- anxious irritable irrationsal
- wheeze (muscle tone increases in smooth muscle)
- weak brittle nails
Hypocalcaemia investigations
- ECG - long QT interval if severe
- bloods - low Ca, vitD, phosphate, PTH, Mg (need to produce PTH)
- eGFR - look for CKD (cause of secondary hyperparathyroidism)
- x rat - pseudohypoparathyroidism has short metacarpals (esp 4th)
chvosteks sign
- when
tap on facial nerves, face muscles twitch
hypocalcaemia
trousseaus sign
- when
inflate BP cuff- brachial artery occluded, this exacerbates low calcium causing spasm in hand/forearm –> salt bae shape - straight fingers, bent at knuckle, wrist flexion
hypocalcaemia
hypocalcaemia management
Acute
- IV calcium (calcium gluconate)
- Monitor ECG
Chronic
- vit D supplements (vit d3 colecalciferol- still needs conversion/activation)
- Alfacalcidol = vitamin D analogue
- Calcitriol = active vitamin D
- Calcium supplements : calcium carbonate/citrate/phosphate
- Adcal = calcium + vit D3
- MgCl if hypomagnesia
hypocalcaemia complications
Bone weakness/ fractures/ difficulty walking /osteoporosis Convulsions/ seizures Death if untreated Abnormal heart rhythm Parkinsonism Eye damage
hypercalcaemia risk factors
Post menopausal women
Renal disease
Family history of overactive parathyroid
causes of hypercalcaemia
- high vitamin D (increased Ca absorption)
- malignancy- cancer/tumour in BONE (myeloma/ secondary metastases in bone)
serum calcium high (due to bone remodelling/resorption) so low PTH (neg feedback) - primary hyperparathyroidism benign adenoma - can be ant pit/ squamous cell lung cancer, breast and renal carcinomas– produce PTH (-like substance)
- tertiary hyperparathyroidism (= renal failure)- so cannot activate vit D, so Ca cannot be absorbed
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in high vit D
- low PTH
- high Ca
- low phosphate (or high acc??)
- PTH appropriate
- high vit D –> high Ca absoprtion –> low PTH
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in malignancy
- low PTH
- high Ca
- variable phosphate
- PTH appropriate
- bone remodelling/resorption –> high calcium –> so low PTH (neg feedback)
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in primary hyperparathyroidism
- high PTH
- high Ca
- low phosphate
- PTH inappropriate
- benign adenoma (lung, breast, renal, pituitary)–> PTH (-like) –> high Ca, low phosphate
state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in tertiary hyperparathyroidism
- high PTH
- high Ca
- high phosphate
- PTH inappropriate
- renal failure–> cannot activate vit D –> Ca not absorbed –> low Ca–> high PTH –> PTH stimulates gut and kidney but these sources don’t allow Ca increase here and bone resorption is only a temporary fix –> So PTH rises and gets STUCK on FULL blast –> Eventually Ca increases (he didn’t say how )
Phosphate levels high as kidneys can’t excrete it
if a patient presents to outpatient clinic with hypercalcaemia, is it more likely to be primary hyperparathyroidism or malignancy? and why?
primary hyperparathyroidism
malignancy is likely to present in other ways than sole hypercalcaemia
what must you be careful with when measuring serum calcium
false positive for hypercalcaemia if tourniquet left on too long or old serum sample
hypercalcaemia presentation
- Stones (kidney/ billiary - due to Ca2+ excess)
- moans (psychic) - confusion, coma, cognitive dysfunction, Depression, anxiety , insomnia
- groans (Abdominal)- nausea, constipation, abdominal pain, malaise
- bones - breaking down - Pain, Fractures, Osteopenia / osteomalacia. Osteoporosis
thirst and polyuria (excrete all Ca2+ in urine so thirsty and thus wee
hypercalcaemia investigations
- ECG - short QT interval
- bloods
- – Serum calcium high (False positive if tourniquet on too long or old serum sample)
- – PTH
- – phsophate
- – alkaline phosphate - hyperparathyroidism
- – TSH (to exclude hyperparathyroidism)
(Urine calcium- high - to exclude this rare condition where your kidneys reabsorb calcium despite hypercalcaemia )
Renal function
- If low, may indicate tertiary hyperparathyroidism
bones
- Xray/CT/MRI - looking for malignancies
- DXA bone scan - do see effects on bone, detect osteoporosis
hypercalcaemia management
- Rehydrate with saline 0.9% (polyuria) - IV
- Bisphosphonates as they prevent bone resorption (reduce osteoclasts activity) (also treat osteoporosis). Eg pamidronate
- Loop diuretics to excrete some calcium
- Surgical removal if primary or tertiary hyperparathyroidism
- Chemo may help for malignancy
- Monitor Ca in serum and urine
- Steroids if malignancy or vit D excess
- Cinacalcet - inhibits PTH
hypercalcaemia complications
Arrhythmia
Kidney stones
Kidney failure
Osteoporosis
primary hyperPTH causes
Benign adenoma on parathyroid
Parathyroid gland disease
Hyperplasia of all glands
A few due to parathyroid carcinoma
secondary hyperPTH causes
Vitamin D deficiency
Chronic kidney disease
GI disease- malabsorption
tertiary hyperPTH causes
Renal failure/ chronic kidney disease
Develops from secondary hyperparathyroidism
treatment for 1/2/3 hyperPTH
Primary (hyperCa)
- Surgical removal of tumour (underlying cause)/ parathyroid (if hyperplasia)
- Bisphosphonates - prevent bone resorption
- When surgery contrindicated: Cinacalecet – reduces sensitivity of parathyroid cells to Ca2+ so less PTH secretion
- Exercise
- Avoid diuretics
- Avoid high Ca2+/ vit D intake
Secondary (hypoCa)
- Calcium correction
- Supplements given for calcium and for vit D (alfacalcidol)
Tertiary (hyperCa)
- Surgical parathyroidectomy
- Cinacalcet - reduces PTH
hypoPTH risk factors
Anterior neck surgery Genetic - syndromes such as Di George syndrome Radiation Mg deficiency Chronic kidney disease
primary hypoPTH causes
Primary : low PTH due to parathyroid gland failure
- Genetic - syndromes such as Di George syndrome
- Autoimmune
secondary hypoPTH causes
Anterior neck surgery
Radiation
Mg deficiency
pseudohypoPTH causes
- PTH resistance, so PTH is ineffective at increasing calcium levels
- In response to low calcium, PTH goes up. But this does not increase calcium levels
- High phosphate as PTH is ineffective
- Associated with short stature, short metacarpals, esp 4th, and sometimes intellectual impairment
pseudopseudohypoPTH causes
- Same phenotypes (short stature, metacarpals…()
- But no issue with Ca2+ metabolism – all good
- Inherited from father
- Very rare
carcinoid tumour
- gender
- age
- causes
women
old
genestics /fam history
non hodgekin lymphoma
carcinoid tumour pathophysiology - what - where - secretes
- Carcinoid tumour = malignant Tumour secreting serotonin
- originates from enterochromaffin cells
- Tumour can be in fore/mid/hind gut - could also be gallbladder, kidney, liver, pancreas, lung etc
carcinoid syndrome-
when neuroendocrine tumour metastasis to liver (then products drain in to the hepatic vein)
carcinoid crisis
When a tumour outgrows its blood supply or is handled too much during surgery - mediators flow out
Life threatening…
- Vasodilation, caused by bradykinin
- Bronchoconstriction, caused by bradykinin
- Hypotension, caused by ACTH → increased cortisol
- Hyperglycaemia, caused by ACTH → increased cortisol
- Tachycardia , caused by sertotonin
But most tumours do not secrete hormones or compounds
serotonin effects
Bowel function - diar Mood Clotting Nausea Bone density Vasoconstriction Increases force of contraction and heart rate (ionotropic, chonotropic)
carcinoid tumour symptoms
Often asymptomatic Pain Weight loss Tiredness Weakness Cough inc blood Sob Wheeze Chest pain palpable mass appendicitis/ obstruction - due to GI tumours
carcinoid syndrome symtpoms
Bronchospasm Fast heart rate Diarrhea /const Skin flushing- red face/neck R sided heart lesions RUQ pain
why might cardiac failure be associated with carcinoid tumour
congestive
Due to tricuspid incompetence and pulmonary stenosis
carcinoid tumour investigations
Urine
- High levels of hydroxy indoleacetic acid (breakdown of serotonin)
imaging
- CXR/MRI/CT - To locate primary tumours
- Liver ultrasound - Confirm metastases
Octreoscan
- Octreotide is a somatostatin analogue
- Tumour has somatostatin receptors on it
- Octreotide is radiolabelled
- It attaches to receptors on tumour
carcnioid tumour management
Somatostatin analogues eg octreotide, lanreotide Slow growth of tumour Block release of tumour hormones Surgery radio/chemotherapy Manage symptoms / organ damage
prolactinoma
- gender
- cause
- f>m
- benign tumour of lactotroph cells in anterior pituitary
- Could also be because of antidopimnergic drug (so suspend treatment for a few days to see if due to drug or tumour)
prolactinoma pathophysiology
- benign tumour of lactotroph cells in anterior pituitary
- produces prolactin
- high levels of dopamine (in order to try to inhibit it)
micro and macro types based on size. micro is more common
prolactinoma symptoms
Hypogonadism (inhibits FSH/LH) inc Infertility, decreased libido, Menstrual irregularity, amenorrhea Galactorrhea (mammary gland) Headaches Visual - bitemp hemianop
prolactinoma investigations
bloods - prolactin, gonad hormones, dopamine
imaging pituitary
prolactinoma management
dopamine analogue/agonist → more inhibition of release
= cabergoline
prolactinoma complications
Infertility Decreased libido Visual loss Bone loss Pregnancy complications
pheochromocytoma causes /types and pathophysiology
Tumour of chromaffin cells in the adrenal medulla → secretes catecholamine
Familial : more noradrenaline
Sporadic: more adrenaline
pheochromocytoma presentation
Episodic Headaches Palpitations, tachy Sweating Tremor Anxiety Weight loss palor
pheochromocytoma investigations
ecg/HR
BP high
urine - catecholamines and metabolites high
bloods - catecholamines (less sensitive)
pheochromocytoma management
- Surgery
- alpha( and beta )blocker- to reduce adrenaline
- control complication = effects of HTN (MI, stroke, renal damage etc)
