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phase 2a mine > endo bottom tier > Flashcards

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
Q

hypercalcaemia presentation

A
  • 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
Q

hypercalcaemia investigations

A
  • 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
Q

hypercalcaemia management

A
  • 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
Q

hypercalcaemia complications

A

Arrhythmia
Kidney stones
Kidney failure
Osteoporosis

29
Q

primary hyperPTH causes

A

Benign adenoma on parathyroid
Parathyroid gland disease
Hyperplasia of all glands
A few due to parathyroid carcinoma

30
Q

secondary hyperPTH causes

A

Vitamin D deficiency
Chronic kidney disease
GI disease- malabsorption

31
Q

tertiary hyperPTH causes

A

Renal failure/ chronic kidney disease

Develops from secondary hyperparathyroidism

32
Q

treatment for 1/2/3 hyperPTH

A

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
Q

hypoPTH risk factors

A 
Anterior neck surgery
Genetic - syndromes such as Di George syndrome
Radiation
Mg deficiency
Chronic kidney disease
34
Q

primary hypoPTH causes

A

Primary : low PTH due to parathyroid gland failure

  • Genetic - syndromes such as Di George syndrome
  • Autoimmune
35
Q

secondary hypoPTH causes

A

Anterior neck surgery
Radiation
Mg deficiency

36
Q

pseudohypoPTH causes

A
  • 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
Q

pseudopseudohypoPTH causes

A
  • Same phenotypes (short stature, metacarpals…()
  • But no issue with Ca2+ metabolism – all good
  • Inherited from father
  • Very rare
38
Q

carcinoid tumour

  • gender
  • age
  • causes
A

women
old
genestics /fam history
non hodgekin lymphoma

39
Q 
carcinoid tumour 
pathophysiology
- what
- where
- secretes
A
  • 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
Q

carcinoid syndrome-

A

when neuroendocrine tumour metastasis to liver (then products drain in to the hepatic vein)

41
Q

carcinoid crisis

A

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
Q

serotonin effects

A 
Bowel function - diar
Mood 
Clotting 
Nausea
Bone density
Vasoconstriction
Increases force of contraction and heart rate (ionotropic, chonotropic)
43
Q

carcinoid tumour symptoms

A 
Often asymptomatic
Pain 
Weight loss
Tiredness
Weakness
Cough inc blood
Sob
Wheeze
Chest pain
palpable mass
appendicitis/ obstruction - due to GI tumours
44
Q

carcinoid syndrome symtpoms

A 
Bronchospasm
Fast heart rate
Diarrhea /const
Skin flushing- red face/neck 
R sided heart lesions 
RUQ pain
45
Q

why might cardiac failure be associated with carcinoid tumour

A

congestive

Due to tricuspid incompetence and pulmonary stenosis

46
Q

carcinoid tumour investigations

A

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
Q

carcnioid tumour management

A 
Somatostatin analogues eg octreotide, lanreotide
Slow growth of tumour
Block release of tumour hormones
Surgery
radio/chemotherapy
Manage symptoms / organ damage
48
Q

prolactinoma

  • gender
  • cause
A
  • 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
Q

prolactinoma pathophysiology

A
  • 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
Q

prolactinoma symptoms

A 
Hypogonadism (inhibits FSH/LH) inc Infertility, decreased libido,
Menstrual irregularity, amenorrhea
Galactorrhea (mammary gland)
Headaches 
Visual - bitemp hemianop
51
Q

prolactinoma investigations

A

bloods - prolactin, gonad hormones, dopamine

imaging pituitary

52
Q

prolactinoma management

A

dopamine analogue/agonist → more inhibition of release

= cabergoline

53
Q

prolactinoma complications

A 
Infertility
Decreased libido
Visual loss
Bone loss
Pregnancy complications
54
Q

pheochromocytoma causes /types and pathophysiology

A

Tumour of chromaffin cells in the adrenal medulla → secretes catecholamine

Familial : more noradrenaline
Sporadic: more adrenaline

55
Q

pheochromocytoma presentation

A 
Episodic
Headaches
Palpitations, tachy
Sweating
Tremor
Anxiety
Weight loss
palor
56
Q

pheochromocytoma investigations

A

ecg/HR
BP high
urine - catecholamines and metabolites high
bloods - catecholamines (less sensitive)

57
Q

pheochromocytoma management

A
  • Surgery
  • alpha( and beta )blocker- to reduce adrenaline
  • control complication = effects of HTN (MI, stroke, renal damage etc)

phase 2a mine (38 decks)

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