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Clinical Practice > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is the function of insulin?

A

reduces hepatic glucose production
increases skeletal muscle and adipose tissue glucose uptake
reduces glycogenolysis and gluconeogenesis
direct inhibition of glucagon secretion
inhibition of glucagon gene in pancreatic alpha cells

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2
Q

what are the most serious complications of diabetes?

A

diabetic ketoacidosis

hyperosmolar hyperglycaemic syndrome

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3
Q

what are the investigations and results required to diagnose DKA?

A

existing diabetes
or
new presentation with BM >11.1mmol/L

urinary ketones >++
or
capillary ketones >3.0mmol/L

venous pH <7.30
and/or
bicarbonate <15mmol/L

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4
Q

name some hyperglycaemic states

A

DM
HHS
stress hyperglycaemia
impaired glucose tolerance

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5
Q

name some ketotic states

A

ketotic hyperglycaemia
alcoholic ketosis
starvation ketosis

(not always harmful)

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6
Q

name some metabolic acidotic states

A 
lactic acidosis
hyperchloraemic acidosis
salicylism
uraemic acidosis
drug-induced acidosis
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7
Q

what are the signs of insulin reduction?

A 
total body K depletion
PO4 decrease
Cr increase
renal failure
ketoacidosis
hyperlipidaemia
glycogenolysis
gluconeogenesis
hyperglycaemia
hyperosmolarity
glucosuria
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8
Q

what is the pathogenesis of DKA?

A 
absolute insulin deficiency
gluconeogenesis, glucogenolysis and hyperglycaemia
->
osmotic diuresis
electrolyte abnormalities
dehydration
hormone sensitive lipase production
increased FFA to liver
increased ketogenesis
acidosis
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9
Q

what is the pathogenesis of HHS?

A 
relative insulin deficiency
gluconeogenesis, glucogenolysis and hyperglycaemia
->
osmotic diuresis
electrolyte abnormalities
dehydration
hyperosmolarity
increased hormone sensitive lipase
absent or minimal ketogenesis
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10
Q

what are the precipitants of a DKA?

A 
newly diagnosed diabetes
non-compliance
omission
pump failure
infection
inflammation
iatrogenic
infarction
intoxication
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11
Q

what are the symptoms of DKA?

A 
deep, rapid breathing (dyspnoea)
fruity-smelling breath
dry mouth
nausea
vomiting
abdominal pain
lethargy
polyuria
polydipsia
new diagnosis/symptoms of T1DM
develops over <1 day
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12
Q

what are the symptoms of HHS?

A 
polyuria +/-
polydipsia
weight loss
confusion
lethargy
develops over >1 day
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13
Q

what is the management of DKA?

A 
ABC
IV fluids (1L 0.9% NaCl over 1 hour)
insulin
potassium
treat cause
reassess
prevention of future DKA
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14
Q

what are the differences in managing DKA <18yrs?

A

fluid prescription based on estimated weight and estimated deficit
insulin not started until IV fluids running for 1 hour
use 0.9% NaCl with 5% glucose

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15
Q

describe the insulin infusion in a DKA

A

0.1 units/kg/hour (7 units in 70kg)
draw up 50 units Actrapid
add to 49.5ml 0.9% NaCl in a 50ml syringe
concentration 1 unit/ml
continue long-acting insulin (lantis, levemir)

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16
Q

what is the management of hyper/hypokalaemia post DKA?

A

> 5.5mmol/L nil
3.5-5.5mmol/L requires 40mmol/L replacement of infusion solution
<3.5mmol/L requires senior review

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17
Q

what are the causes of a DKA?

A 
gastroenteritis
UTI
pneumonia
MI
stroke
pancreatitis
non-compliance
cocaine
first presentation
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18
Q

what is involved in the reassessment of a DKA?

A

GCS
clinical observations
hourly CBG and ketones
once CBG <14mmol/L start 10% dextrose alongside 0.9% NaCl
high rate insulin infusion until ketones are clear
once ketones <0.6mmol/L, resume s/c insulin if able to eat and drink, fasting protocol with variable rate insulin if not

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19
Q

what are the complications of DKA?

A 
infection
shock
vascular thrombosis
pulmonary oedema
cerebral oedema (mannitol)
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20
Q

what is the treatment of HHS?

A 
hydration
treat underlying cause
insulin drip after aggressive hydration
switch to s/c regimen once glucose <11mmol/L and patient eating
K replacement
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21
Q

describe the effects of SGLT2 inhibitors

A 
glucosuria
free fatty acid release
pancreatic glucagon secretion
hepatic glucose production and ketogenesis
renal ketone resorption
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22
Q

what is the definition and causes of gluconeogenesis?

A

delivery of precursors to liver from breakdown of fat and muscle

insulin deficiency
glucagon excess

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23
Q

define hypoglycaemia

A

blood glucose <3.9mmol/L

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24
Q

what are the symptoms of hypoglycaemia?

A 
sweating
palpitations
agitation
shaking
hunger
confusion
drowsiness
speech difficulty
odd behaviour
incoordination
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25
Q

what are the risk factors for hypoglycaemia?

A 
intensive treatment
missed meal
PMHx severe hypo
hypo unawareness
duration of diabetes
increased age
exercise
pregnancy
lipoatrophy/hypertrophy
reduced clearance (renal failure, SUs, ACEis, ARBs)
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26
Q

what is the management of mild hypoglycaemia?

A

15-20g quick-acting carbohydrate
or
150-200ml pure fruit juice
test glucose level 15 minutes later and if <4.0mmol/L repeat up to 3 times

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27
Q

what is the management of moderate hypoglycaemia?

A

1.5-2 tubes of 40% glucose gel
or
1mg glucagon IM
test glucose level 15 minutes later and if <4.0mmol/L repeat up to 3 times

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28
Q

what is the management of severe hypoglycaemia?

A 
ABC
stop IV insulin
75ml 20% IV glucose over 15 minutes
or
1mg glucagon IM
check glucose after 10 minutes and repeat if <4.0mmol/L
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29
Q

in what conditions will glucagon not be effective?

A

malnourishment
severe liver disease
repeated hypoglycaemia

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30
Q

describe the hypothalamic-pituitary-thyroid axis

A

hypothalamus produces TRH which acts on the pituitary
pituitary produces TSH which acts on the thyroid
thyroid produces T3 and T4 which acts on the heart, liver, bone and CNS

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31
Q

what are the TFT results for primary hypo/hyperthyroidism?

A

hypo - FT4 low, TSH high

hyper - FT4 high, TSH low

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32
Q

what are the TFT results for secondary hypo/hyperthyroidism?

A

hypo - FT4 low, TSH low/normal

hyper - FT4 high, TSH high/normal

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33
Q

what are the symptoms and signs of hypothyroidism?

A 
tiredness
weight gain
cold intolerance, cold peripheries, hypothermia
goitre (deep voice)
depression
poor memory
dry hair and skin
myalgia, myotonia
constipation
periorbital oedema
deafness
hypertension
HF
bradycardia
pericardial effusion
anaemia
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34
Q

what are the causes of hypothyroidism?

A 
agenesis
Hashimoto's disease (autoimmune)
thyroiditis
iodine deficiency
antithyroid drugs
lithium
amiodarone
monoclonal antibody therapy
pituitary adenoma
following pituitary surgery
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35
Q

what is the treatment of hypothyroidism and what adjustments does this require in special situations?

A

thyroxine
1.6 mcg/kg
reduced dose with cardiac history, elderly
assess response after 6-8 weeks

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36
Q

what are the symptoms and signs of hyperthyroidism?

A 
weight loss
irritability
itching
heat intolerance
tremor
thirst
vomiting
diarrhoea
oligomenorrhoea
hyperkinese
tachycardia or AF
full pulse
warm vasodilated peripheries
exophthalmos
lid lag
goitre
bruit
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37
Q

what are the causes of hyperthyroidism?

A 
grave's disease (autoimmune)
toxic multi nodular goitre
toxic nodule (solitary)
thyroiditis (viral, autoimmune, postpartum)
gestational thyrotoxicosis
exogenous iodine
amiodarone
monoclonal antibody therapy
excess T4
TSH secreting pituitary adenoma
HCG producing tumours
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38
Q

describe the pathology and symptoms of Grave’s disease

A

autoimmune
presence of stimulating TSH receptor antibodies

thyroid eye disease (specific to Grave’s)
swelling and inflammation of retro-orbital tissues and extra ocular muscles; proptosis
gritty sensation in eye
lid lag
periorbital oedema
optic nerve compression (severe disease)

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39
Q

what is the treatment of hyperthyroidism?

A

anti-thyroid drugs (carbimazole)
radioactive iodine therapy
surgery

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40
Q

what are the side effects of carbimazole and prophythiouracil (PTU)?

A

rash
agranulocytosis (stop if develop a sore throat or fever and require surgery WCC measurement)
liver dysfunction (PTU)

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41
Q

describe the 2 regimens of anti-thyroid treatment and why/when they are used

A

titration - high dose anti-thyroid and titrate down as TFT improve, used in women planning pregnancy
block and replace - high dose carbimazole and replace with thyroxine, requires less monitoring

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42
Q

what are the causes of goitres/nodules?

A 
puberty
pregnancy
grave's
hashimoto's
thyroiditis
iodine deficiency
multi nodular goitre
solitary nodular
cysts
tumours
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43
Q

what are the types of thyroid cancer?

A 
papillary
follicular
medullary cell
anaplastic
lymphoma
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44
Q

what investigations should be performed on a thyroid lump?

A 
TFT
thyroid antibodies
US thyroid
FNA
CT thoracic inlet
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45
Q

what is the treatment of thyroid cancer?

A 
surgery (lobectomy or total thyroidectomy)
ablative radioactive iodine
high dose thyroxine (suppress TSH)
radiotherapy
chemotherapy
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46
Q

what hormones are produced by the different regions of the adrenal cortex and medulla?

A

zona glomerulosa - aldosterone
zona fasciculata - cortisol
zona reticularis - adrenal androgens
medulla - catecholamines

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47
Q

how do ACTH and RAAS affect the adrenal cortex?

A

cause the production of cortisol and aldosterone (glucocorticoids and mineralocorticoids)

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48
Q

what are the symptoms and signs of Cushing’s syndrome?

A 
weight gain
slow healing of cuts
increased infection risk
fatigue
glucose intolerance
sweating
moon face
buffalo hump
skin thinning
depression, irritability
hypertension
oligomenorrhoea/erectile dysfunction
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49
Q

what are the causes of Cushing’s syndrome?

A

ACTH dependent;
pituitary adenoma
ectopic ACTH

ACTH independent;
exogenous steroids
adrenal adenoma/hyperplasia

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50
Q

what investigations are required to diagnose Cushing’s syndrome?

A

24hr urinary free cortisol

48hr low dose dexamethasone suppression test

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51
Q

what is the treatment of Cushing’s syndrome?

A

treat the cause
transsphenoidal resection of pituitary tumour
surgical resection of adrenal tumour
weaning and discontinuation of exogenous steroid

in pituitary or adrenal surgery require steroid cover (IM then oral)

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52
Q

define Addison’s disease

A

an absolute or relative lack of adrenal (endocrine) function

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53
Q

what are the symptoms and signs of Addison’s disease?

A 
fatigue
weakness
weight loss
nausea
vomiting
abdominal pain
diarrhoea
constipation
myalgia
decreased libido
amenorrhoea
hyperpigmentation
hypotension
axillary and pubic hair thinning
vitiligo
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54
Q

what are the causes of primary adrenal insufficiency?

A 
autoimmune
TB
metastatic disease
trauma
opportunistic infection
bilateral adrenal haemorrhage/infarction
anticoagulant therapy
coagulopathy
postoperative state
severe sepsis
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55
Q

what are the causes of secondary/tertiary adrenal insufficiency?

A

panhypopituitarism
isolated ACTH deficiency
traumatic brain injury
high dose glucocorticoids

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56
Q

what is the treatment of adrenal insufficiency?

A

hydrocortisone 15mg morning and 5mg afternoon (glucocorticoid)
rarely prednisolone 5mg or dexamethasone 0.5mg
fludrocortisone 100mcg daily (mineralocorticoid), only required in primary disease

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57
Q

what are the rules for taking steroids?

A

double dose on sick days
never stop steroid replacement
attend GP/ED if vomiting/diarrhoea as hydrocortisone absorption will be impaired, will require IV or IM

58
Q

what are the symptoms and signs of an adrenal crisis?

A 
hypotension/shock
hypoglycaemia
hyperkalaemia
hyponatraemia
extreme fatigue
abdominal pain
nausea
vomiting
diarrhoea
59
Q

what is the treatment of an adrenal crisis?

A

fluid replacement
hydrocortisone 100mg IV stat then 6hrly
glucose replacement occasionally
treatment of underlying cause

60
Q

define primary aldosteronism

A

a group of disorders in which aldosterone production is
inappropriately high
relatively independent from RAAS
non-suppressible by sodium loading

61
Q

what are the causes of primary aldosteronism/Conn’s syndrome?

A 
aldosterone producing adenoma
bilateral adrenal hyperplasia
unilateral adrenal hyperplasia
aldosterone producing adrenocortical carcinoma
FH
62
Q

what are the signs and investigations required to diagnose primary aldosteronism?

A 
(resistant) hypertension
hypokalaemia
adrenal nodule
FHx of HTN or CVD <40yr
FHx of primary aldosteronism in first degree relative

aldosterone:renin ratio
saline suppression test
CT adrenals
adrenal venous sampling

63
Q

what is the management of unilateral and bilateral primary aldosteronism?

A

adrenalectomy

spironolactone
eplerenone
amiloride

64
Q

define a pheochromocytoma

A

a tumour arising from adrenomedullary chromaffin cells that commonly produces one or more catecholamines

65
Q

what are the symptoms and signs of a pheochromocytoma?

A 
headache
sweating
palpitations
postural hypotension
cardiomyopathy
end organ damage
hyperglycaemia
retinal haemangioblastoma
cutaneous neurofibromata
cafe-au-lait spots
66
Q

what investigations are required for the diagnosis of a pheochromocytoma?

A 
24hr urinary metanephrines
plasma metanephrines
clonidine suppression test
CT abdomen
MIBG
67
Q

what is the treatment of a pheochromocytoma?

A 
phenoxybenzamine (alpha-1 adrenoceptor blocker, controls BP, expands plasma volume and avoid a hypertensive crisis)
once alpha blockade is complete
beta blockade
laparoscopic adrenalectomy
genetic testing
68
Q

how does insulin dosing correct for hyperglycaemic episodes?

A

1 unit of insulin to reduce blood glucose by 2-3 mmol/L

69
Q

what are the considerations when prescribing insulin?

A

what insulin is the patient taking
what is the usual home dose of insulin
what is control usually like and why has it changed
what is the pattern of glucose monitoring
are adjustments needed
which insulin needs adjusted
how much does insulin need adjusted

70
Q

what rules must be adhered to in insulin adjustment?

A

10% adjustment - on regular insulin (basal bolus or BD mixed insulin)
correction for hyperglycaemia - on diet alone, oral agents or OD insulin

71
Q

what are the general principles of peri-operative diabetes care

A

continue long-acting insulin
take rapid and mixed insulin and oral hypoglycaemic agents the day before surgery and hold on day of surgery
IV variable insulin infusion started on day of surgery

ensure patient does not become dehydrated; 0.45% NaCl with 5% glucose and 10mmol/L K

72
Q

what structures are adjacent to the pituitary?

A

superior; optic chiasm
lateral; cavernous sinus (CN III, IV, VI, V1)
inferior; sphenoidal sinus

73
Q

what is the function of the pituitary?

A

anterior produces GH, prolactin, LH, FSH, ACTH, TSH

posterior produces ADH, oxytocin

74
Q

describe dynamic tests

A

in overproductive diseases we do a “suppression” test to try and suppress it to normal and vice versa
if a patient has the disease the hormones will not suppress/stimulate with dynamic testing

75
Q

what investigation results will confirm pituitary acromegaly?

A

elevated IGF1 and GH

oral glucose tolerance test; GH will remain high despite glucose load

76
Q

what is the treatment of pituitary acromegaly?

A

transsphenoidal surgery to resect tumour
risk of hypopituitarism so given cortisol until confirmed normal in post-op
radiotherapy
prolactinoma - dopamine agonists (bromocriptine/cabergoline)
acromegaly - dopamine agonists, somatostatin analogues, GH receptor antagonists

77
Q

what are the direct complications of hyperglycaemia?

A 
blood flow abnormalities
vascular permeability
angiogenesis
capillary occlusion
vascular occlusion
pro-inflammatory gene expression
78
Q

describe the findings of non-proliferative retinopathy

A

lipid deposits
haemorrhage
cotton wool spot due to ischaemia

79
Q

describe the findings of proliferative retinopathy

A

new vessel formation which can result in haemorrhage or retinal detachment

80
Q

define normal, micro and macroalbuminuria

A

normal <3
microalbuminuria ACR 3-30
macroabluminuria ACR>30

81
Q

what are the 3 ways of managing diabetic eye disease?

A

prevention (good blood sugar control)
early detection (eye screening)
treatment (laser, anti-VEGF)

82
Q

what are the 3 ways of managing diabetic renal disease?

A

prevention (good blood sugar and pressure control)
early detection (urinary ACR monitoring)
treatment (ACEi/ARBs)

83
Q

describe how ulcers occurs in diabetic patients

A

neuropathy increases injury risk

PVD impedes healing

84
Q

what are the 3 ways of managing diabetic neuropathy?

A 
prevention (good blood sugar control)
early detection (monofilament)
treatment (good foot care, podiatry)
85
Q

how is macrovascular disease (stroke) prevented in diabetes?

A

A1c 7%
blood pressure 130/80
LDL <2

86
Q

describe the immunological defects associated with diabetes

A

neutrophil function impaired
lymphocyte response impaired
production of IL-2 impaired
manifest as delayed/impaired response to injury and increased wound infections

87
Q

what are the aspects of diabetes that play a significant role in the impairment of healing?

A

peripheral vascular disease (ischaemia)
immunological defects
neuropathy (decreased pain and proprioception, dry skin, small muscle wasting)

88
Q

what are the risk factors for a neuropathic foot?

A 
age
poor blood sugar control
diabetes duration
HTN
renal failure (proteinuria, microalbuminuria)
neuropathy
ischaemia
inappropriate footwear
limited joint mobility
Hx of amputation or foot ulceration
dry skin
infection
89
Q

what are the signs of a neuropathic foot?

A 
well perfused
bounding pulses (absence of pulses doubles amputation risk)
distended dorsal veins
high arch
plantar callus, ulceration
lacks protective pain sensation
does not perceive trauma or infection

neuroischaemic - cool, pulseless, hairless

90
Q

what are the complications of a neuropathic foot?

A

plantar ulceration
gangrene
Charcot’s osteoarthropathy
neuropathic oedema

91
Q

define ankle brachial pressure index (ABPI)

A

highest pedal pulse pressure / highest brachial pulse

normal range 0.8-1.2

92
Q

describe the neurological assessment of a diabetic foot

A

autonomic and motor - observation
sensory - pressure, sharp touch, vibration
sensory - neurotip, 10g monofilament, neurothesiometer

93
Q

what are the reasons for debridement of a callous?

A

reduced plantar pressure
discover true dimensions of the ulcer
establish drainage
granulation of wound edge

94
Q

what is the treatment methods of a diabetic foot ulcer?

A

wound control (debridement, dressings, larvae therapy)
mechanical control (appropriate footwear, casts)
microbiological control
lifestyle (smoking cessation, exercise, alcohol, eating habits)
education

95
Q

what is the diabetic foot triad?

A

neuropathy
ischaemia
infection

96
Q

describe the rapid-acting insulins

A

novorapid/aspart, humalog/lispro, apidra
onset at 5-10 minutes
peak at 1-2 hours
duration of 3-5 hours

97
Q

describe the quick-acting insulins

A

actrapid, humulin S
onset at 30 minutes
peak at 3 hours
duration of 6 hours

98
Q

describe the intermediate-acting insulins

A

insulatard, humulin I
onset at 2 hours
peak at 5-8 hours
duration of 20 hours

99
Q

describe the long-acting insulins

A

levemir/detemir, lantus/glargine
immediate onset
duration of 20-24 hours

100
Q

what is the target blood sugar?

A

5-9 mmol

101
Q

describe insulin regimens

A

4x daily - greater flexibility, better control
2/3x daily - more common and suitable to lifestyle
1x daily - commonly in combination with OHAs

102
Q

what are the essential components of a regular diabetes check-up?

A 
any new health problems
BP
peripheral pulses
sensation in feet
foot ulceration
urinalysis (ACR)
visual acuity
glycemic control
lipid profile
103
Q

describe glomerular hypertension in diabetes

A

thickened by leaky GBM

filtrate includes a small amount of albumin

104
Q

which hormones are produced by the anterior pituitary and on which organs do they act?

A 
GH; bones, muscles, organs
prolactin; breast
LH and FSH; ovaries and testes
ACTH; adrenal cortex
TSH; thyroid gland
105
Q

which hormones are produced by the posterior pituitary and on which organs do they act?

A

ADH; kidneys

oxytocin; breasts and uterus

106
Q

what are the local signs and symptoms of pituitary problems?

A

headache

visual acuity, fields, movement

107
Q

what are the signs and symptoms of pituitary under function?

A

fatigue
reduced sexual function; gonadotrophin loss
delayed growth
thirst/polyuria; DI due to loss of ADH

108
Q

what are the signs and symptoms of pituitary over function?

A 
prolactin;
galactorrhea
amenorrhoea
reduced sexual function
reduced facial hair growth
gynaecomastia

GH;
overgrowth
metabolic features
gigantism in children (long bone growth)

ACTH;
Cushing’s disease

109
Q

what are the signs and symptoms of acromegaly?

A 
interdental separation
hirsutism
thick greasy skin
spade-like hands and feet
weight gain
headaches
visual deterioration
deep voice
carpal tunnel syndrome
prognathism
frontal bossing
large tonsils and tongue
GI and gallbladder polyps
hepatosplenomegaly
goitre
hypogonadism
hypothyroidism
hypoadrenalism
110
Q

what are the signs of prolactinoma?

A 
galactorrhoea
amenorrhoea
hypogonadism
erectile dysfunction
infertility
gynaecomastia
111
Q

what investigations are required to diagnose pituitary disease?

A 
prolactin
GH
IGF1; marker of GH production, screening test for acromegaly
cortisol/synacthen test
TFT
FSH
LH
oestrogen/testosterone
U&E
dynamic tests
MRI
genetic testing
112
Q

describe the dynamic tests used in pituitary disease

A

overproduction;
dexamethasone suppression test
oral glucose tolerance test

underproduction;
water deprivation test
insulin tolerance test

113
Q

what is the medical treatment of prolactinoma?

A 
1st line (not surgery)
dopamine agonists; bromocriptine, cabergoline
114
Q

what is the medical treatment of acromegaly?

A

dopamine agonists
somatostatin analogues
GH receptor antagonists
used in residual disease following surgery

115
Q

what is the medical treatment of Cushing’s disease?

A

dopamine agonists; metyrapone mitotane

somatostatin analogues

116
Q

what are the features of SIADH?

A 
hyponatraemia
hypotonic plasma
inappropriate urine osmolality
excessive renal Na loss
normal renal, adrenal and thyroid function
117
Q

what are the causes of SIADH?

A

tumours; small cell lung ca, thymoma, lymphoma, mesothelioma
respiratory; pneumonia, TB, aspergillosis, pulmonary abscess
CNS; meningitis, encephalitis, abscess, injury, Guillain barre, SAH, stroke
drugs; chemotherapy, antidepressants, antipsychotics, carbamazepine, PPIs, opiates
metabolic; hypothyroidism, glucocorticoid deficiency
idiopathic

118
Q

what are the actions of PTH?

A

bone; releases calcium and phosphorus

kidney; increases calcitriol formation, decreases calcium excretion, increases phosphorus excretion

119
Q

what are the actions of calcitriol?

A

bone; releases calcium and phosphorus

small intestines; increases absorption of dietary calcium and phosphorus

120
Q

what are the symptoms of hypercalcaemia?

A

renal; polyuria, polydipsia
GI; abdominal pain, vomiting, constipation, anorexia
CNS; depression, fatigue, weakness, confusion

121
Q

what are the causes of hypercalcaemia?

A 
hyperparathyroidism; primary or tertiary
malignancy; multiple myeloma, bone metastases
vitamin D or A intoxication
sarcoidosis
familial hypocalciuric hypercalcaemia (FHH)
thiazide diuretics
lithium
immobilisation
thyrotoxicosis
renal disease
Addisons disease
122
Q

describe the presentation of chronic hypercalcaemia

A

mild-moderate
often asymptomatic
mostly caused by primary hyperparathyroidism
surgical vs conservative management

123
Q

describe the presentation of acute hypercalcaemia

A 
severe
symptomatic
mostly caused by malignancy
treatment hypercalcaemia
find and treat cause
124
Q

define corrected calcium

A

measured Ca + 0.02 x (40 - albumin)

normal range 2.10-2.60 mmol/L

125
Q

how do you determine the mechanism of hypercalcaemia?

A

PTH elevated; primary or tertiary hyperparathyroidism

PTH suppressed; non-parathyroid cause

126
Q

what investigations should be performed to diagnose hypercalcaemia?

A 
history and examination
CXR
Bence-jones protein
plasma protein electrophoresis
biochemical profile; U&E, LFTs, TFTs, FBC, ESR
vitamin D
serum cortisol/short synacthen test
serum ACE
127
Q

what are the signs and causes of primary hyperparathyroidism?

A

raised Ca, raised/normal PTH
adenoma (90%)
multiple gland enlargement; MEN1, MEN2A, familial hyperparathyroidism
parathyroid carcinoma

128
Q

what are the signs and causes of secondary hyperparathyroidism?

A

low Ca, raised PTH

vitamin D deficiency

129
Q

what are the signs and causes of tertiary hyperparathyroidism?

A

raised Ca, very raised PTH

renal failure

130
Q

what are the clinical features of primary hyperparathyroidism?

A 
f>m
usually >50yrs
asymptomatic
renal stones
decreased bone density
hypercalcaemia symptoms
131
Q

what is the management of primary hyperparathyroidism?

A 
ensure adequate hydration
review medications; Ca and vitamin D supplements, thiazide diuretics
conservative management
medical; bisphosphonates, cinacalcet
surgical; parathyroidectomy
referral to genetics
132
Q

what are the indications for a parathyroidectomy?

A 
symptomatic hypercalcaemia
renal calculi/impairment
osteoporosis
correct calcium >2.85mmol/L
age <50
pancreatitis
133
Q

describe hypercalcaemia of malignancy

A 
late manifestation
poor prognostic sign
untreatable tumour
raised Ca, suppressed PTH
acute onset
very symptomatic
134
Q

which tumours metastasise to bone?

A 
kidney
prostate
breast
lung
thyroid
colon
ovary
135
Q

what is the treatment of hypercalcaemia?

A 
rehydration;
4-6L IVF / 24hrs
monitor for fluid overload
caution in elderly
loop diuretics if required

IV bisphosphonate therapy;
4mg zolendronic acid or 30-90mg pamidronate
can take up to 72hrs to reach full effect

2nd line; steroids, calcitonin

136
Q

what are the causes of hypocalcaemia?

A

vitamin D deficiency resulting in osteomalacia
hypoparathyroidism; surgical/radiation, autoimmune, Mg deficiency
renal failure
tumour lysis syndrome
pancreatitis
PPIs

137
Q

what are the signs and symptoms of hypocalcaemia?

A 
perioral parasthesia
cramps
depression
tetany
carpo-pedal spasm; trousseau's sign
chovstek's sign
prolonged QT interval
cardiac arrhythmia
seizures
138
Q

what are the signs of pseudohypoparathyroidism?

A

Albright’s hereditary osteodystrophy
short metacarpals
short stature
round face

139
Q

what investigations are required to diagnose hypocalcaemia?

A 
corrected Ca
PTH
vitamin C
magnesium
phosphate
ALP
140
Q

what is the treatment of mild, asymptomatic hypocalcaemia?

A

Ca >1.90mmol/L
oral Ca supplements; sandocal, adcal, calcichew
caused by vitamin D deficiency; cholecalciferol
caused by hypomagnesaemia; stop offending drugs, replace with IV magnesium

141
Q

what is the treatment of severe, symptomatic hypocalcaemia?

A

Ca <1.90mmol/L
medical emergency
10-20ml calcium gluconate / 10-20mins with cardiac monitoring
100ml calcium gluconate infused / 10hrs
treat underlying cause
consider vitamin D analogues; alfacalcidol or calcitriol

Clinical Practice (14 decks)

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