endo bottom tier Flashcards

1
Q

is hypo or hypercalcaemia more common

A

hypercalcaemia

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2
Q

hypocalcaemia risk factors

A
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
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3
Q

causes of hypocalcaemia

A

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)

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4
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in secondary hyperparathyroidism

A

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
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5
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in hypoparathyroidism

A
  • Underactive parathyroid- not much PTH produced
  • So low Ca absorption (gut), reabsorption (kidney) and resorption (bone)
  • low PTH
  • low Ca
  • high phosphate
  • PTH inappropriate
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6
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in pseudohypoparathyroidism

A
  • 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
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7
Q

calcitonin effect on Ca / phosphate

A

decreases Ca2+ and phosphate

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8
Q

bisphosphontes effect on Ca

A

reduces osteoclast activity, resulting in reduced Ca2+ (treatment for hypercalcaemia)

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9
Q

causes of tetany

A
ca deficiency
K+ deficiency, 
Mg2+ deficiency
Hyperventilation
Alkalosis
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10
Q

hypoalbumineamia / calcium

A

presents as hypocalcaemia - Artefact of hypoalbuminemia (calcium binds to albumin)

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11
Q

hypocalcaemia presentation

A

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
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12
Q

Hypocalcaemia investigations

A
  • 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)
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13
Q

chvosteks sign

- when

A

tap on facial nerves, face muscles twitch

hypocalcaemia

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14
Q

trousseaus sign

- when

A

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

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15
Q

hypocalcaemia management

A

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
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16
Q

hypocalcaemia complications

A
Bone weakness/ fractures/ difficulty walking /osteoporosis
Convulsions/ seizures
Death if untreated
Abnormal heart rhythm
Parkinsonism 
Eye damage
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17
Q

hypercalcaemia risk factors

A

Post menopausal women
Renal disease
Family history of overactive parathyroid

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18
Q

causes of hypercalcaemia

A
  • 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
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19
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in high vit D

A
  • low PTH
  • high Ca
  • low phosphate (or high acc??)
  • PTH appropriate
  • high vit D –> high Ca absoprtion –> low PTH
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20
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in malignancy

A
  • low PTH
  • high Ca
  • variable phosphate
  • PTH appropriate
  • bone remodelling/resorption –> high calcium –> so low PTH (neg feedback)
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21
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in primary hyperparathyroidism

A
  • high PTH
  • high Ca
  • low phosphate
  • PTH inappropriate
  • benign adenoma (lung, breast, renal, pituitary)–> PTH (-like) –> high Ca, low phosphate
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22
Q

state whether the PTH, Ca, Phosphate is low/high and if the PTH is in/appropriate in tertiary hyperparathyroidism

A
  • 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

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23
Q

if a patient presents to outpatient clinic with hypercalcaemia, is it more likely to be primary hyperparathyroidism or malignancy? and why?

A

primary hyperparathyroidism

malignancy is likely to present in other ways than sole hypercalcaemia

24
Q

what must you be careful with when measuring serum calcium

A

false positive for hypercalcaemia if tourniquet left on too long or old serum sample

25
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
26
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
27
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
28
hypercalcaemia complications
Arrhythmia Kidney stones Kidney failure Osteoporosis
29
primary hyperPTH causes
Benign adenoma on parathyroid Parathyroid gland disease Hyperplasia of all glands A few due to parathyroid carcinoma
30
secondary hyperPTH causes
Vitamin D deficiency Chronic kidney disease GI disease- malabsorption
31
tertiary hyperPTH causes
Renal failure/ chronic kidney disease | Develops from secondary hyperparathyroidism
32
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
33
hypoPTH risk factors
``` Anterior neck surgery Genetic - syndromes such as Di George syndrome Radiation Mg deficiency Chronic kidney disease ```
34
primary hypoPTH causes
Primary : low PTH due to parathyroid gland failure - Genetic - syndromes such as Di George syndrome - Autoimmune
35
secondary hypoPTH causes
Anterior neck surgery Radiation Mg deficiency
36
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
37
pseudopseudohypoPTH causes
- Same phenotypes (short stature, metacarpals...() - But no issue with Ca2+ metabolism -- all good - Inherited from father - Very rare
38
carcinoid tumour - gender - age - causes
women old genestics /fam history non hodgekin lymphoma
39
``` 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
40
carcinoid syndrome-
when neuroendocrine tumour metastasis to liver (then products drain in to the hepatic vein)
41
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
42
serotonin effects
``` Bowel function - diar Mood Clotting Nausea Bone density Vasoconstriction Increases force of contraction and heart rate (ionotropic, chonotropic) ```
43
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 ```
44
carcinoid syndrome symtpoms
``` Bronchospasm Fast heart rate Diarrhea /const Skin flushing- red face/neck R sided heart lesions RUQ pain ```
45
why might cardiac failure be associated with carcinoid tumour
congestive | Due to tricuspid incompetence and pulmonary stenosis
46
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
47
carcnioid tumour management
``` Somatostatin analogues eg octreotide, lanreotide Slow growth of tumour Block release of tumour hormones Surgery radio/chemotherapy Manage symptoms / organ damage ```
48
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)
49
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
50
prolactinoma symptoms
``` Hypogonadism (inhibits FSH/LH) inc Infertility, decreased libido, Menstrual irregularity, amenorrhea Galactorrhea (mammary gland) Headaches Visual - bitemp hemianop ```
51
prolactinoma investigations
bloods - prolactin, gonad hormones, dopamine imaging pituitary
52
prolactinoma management
dopamine analogue/agonist → more inhibition of release | = cabergoline
53
prolactinoma complications
``` Infertility Decreased libido Visual loss Bone loss Pregnancy complications ```
54
pheochromocytoma causes /types and pathophysiology
Tumour of chromaffin cells in the adrenal medulla → secretes catecholamine Familial : more noradrenaline Sporadic: more adrenaline
55
pheochromocytoma presentation
``` Episodic Headaches Palpitations, tachy Sweating Tremor Anxiety Weight loss palor ```
56
pheochromocytoma investigations
ecg/HR BP high urine - catecholamines and metabolites high bloods - catecholamines (less sensitive)
57
pheochromocytoma management
- Surgery - alpha( and beta )blocker- to reduce adrenaline - control complication = effects of HTN (MI, stroke, renal damage etc)