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4 CSIM2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what is diabetes insipidus

A

insufficiency or failure to respond to ADH

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2
Q

features of diabetes insipidus

A

polydipsia, polyuria, thirst

hypernatraemia, dilute urine

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3
Q

treatment of primary diabetes insipidus?

A

desmopression - ADH analogue

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4
Q

what does primary organ dsyfunction mean?

A

abnormality in target organ

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5
Q

what is secreted in the anterior pituitary gland?

A 
TSH
ACTH
GH
Prolactin
LH + FSH
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6
Q

what is secreted in the posterior pituitary gland?

A

stores ADH

produces oxytocin

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7
Q

describe the anatomy of the adrenal gland

A

adrenal cortex and adrenal medulla

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8
Q

describe the anatomy and function of the adrenal cortex

A

glucocorticoids - zona fasicularis
mineralcorticoids - zona glomerulosa
androgens - zona reticularis

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9
Q

what is the function of glucocorticoids

A

stress response, immune response, metabolism and other life functions

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10
Q

function of mineralcorticoids

A

electrolyte regulation
blood pressure
vascular volume

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11
Q

what is made in the adrenal medulla?

A

catecholamines like epinephrine, norepinephrine and dopamine

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12
Q

what happens in congenital adrenal hyperplasia?

A

group of conditions, causing either over or under production of mineralcorticoids or androgens, most commonly due to faulty gene for 21 hydroxylase

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13
Q

symptoms in over production of androgens in congenital adrenal hyperplasia?

A

clitoral megaly, shallow vagina, menstrual irregularity,

precocious puberty, infertility, excessive facial/pubic hair, rapid childhood growth

males - normal penis but aspermia

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14
Q

what is Conn’s syndrome?

A

hyperaldosteronism - hypernatraemia and hypokalaemia

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15
Q

what is phaeochromocytoma?

A

tumour producing too much catecholamines

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16
Q

which of the thyroid gland is the active hormone?

A

T3

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17
Q

why does sick euthyroidism happen?

A

enzyme that converts T4 to T3 is found in tissue throughout the body, when the body is under stress, it stops producing the enzyme causing increase in T4 but normal or reduced T3

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18
Q

what happens in Graves disease

A

antibodies made that bind to TSH receptors in thyroid gland, producing excess T4/T3

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19
Q

what happens in complete androgen insensitivity syndrome?

A

46XY male that has a defect in testosterone receptors, thus causing failure of male sexual characteristics to develop

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20
Q

what happens in turners syndrome?

A

45X chromosome defect, causing deficiency estrogen which results in a host of symptoms

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21
Q

what must be considered when measuring hormone levels?

A

time of day and the natural diurnal variations of hormones

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22
Q

how is calcium regulated?

A

drop in ca2+ is sensed by parathyroid, releasing PTH in response.

rise in ca2+ is sensed by thyroid gland releasing calcitonin in response

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23
Q

what functions does PTH have

A

increase osteoclast activity, increasing bone resorption

stimulating renal activation of vitamin D which leads to increased gut absorption of calcium

increase renal absorption of calcium from urine

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24
Q

how is vitamin D made

A

through sunlight in the skin it is converted from precursors and sent to the liver and finally the kidney where it is activated into calcitriol which increases gut absorption of calcium

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25
Q

what is bone made of?

A

non-organic hydroxyapatite, osteoid made of collagen and chondroitin, living cells like osteoblasts, osteoclasts, osteocytes and others

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26
Q

2 most common causes of hypercalcaemia

A

hyperparathyroidism

cancer

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27
Q

symptoms of hypercalcemia

A

thirst, polyuria, kidney pains, abdominal pains

bone pain, myalgia, weakness

constipation, vomiting, anorexia

mood change, depression, confusion

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28
Q

why do you get polyuria and thirst from hypercalcaemia?

A

high calcium in tubules impair resorption

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29
Q

common age/gender for primary hyperparathyroidism

A

elderly women, 1:1000 in population

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30
Q

most common cause of primary hyperparathyroidism?

A

benign solitary parathyroid adenoma

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31
Q

biochemistry in primary hyperparathyroidism?

Calcium	
Phosphate	
PTH	
Alk Phos	
Urinary calcium
A 
calcium high
phosphate low
PTH high
alk phos high
urinary calcium high
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32
Q

why is alk phos raised in primary hyperparathyroidism?

A

due to increased bone turnover

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33
Q

complications of primary hyperparathyroidism?

A

kidney stones, renal impairment

osteoporosis at peripheral bones (wrists, hips)

erosion of periosteium

osteoclastomas

corneal calcification

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34
Q

management of primary hyperparathyroidism?

A

usually surgical if symptomatic

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35
Q

T or F, if primary hyperparathyroidism is asymptomatic, surgery is not indicated

A

T

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36
Q

what medical management can be used in primary hyperparathyroidism?

A

calcium receptor agonist - cinacalcet

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37
Q

when is malignant hypercalcaemia usually seen?

A

late stage of cancer

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38
Q

3 common causes of malignant hypercalcaemia

A

humoral hypercalcaemia of malignancy

boney erosions due to metastasis

myeloma

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39
Q

pathophysiology of HHM?

A

abnormal activation of PTHrP gene producing PTHrP proteion causing bone resorption

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40
Q

common cancers that cause HHM?

A

lung, breast, oseophagus, cervix, skin, renal, bladder, ovary, vulva

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41
Q

HHM patients are at an increased risk of pathological fractures due to thinning of bone - T or F?

A

F

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42
Q

myeloma commonly presents with hypocalcaemia - T or F?

A

F, usually hypercalcaemia

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43
Q

why does myeloma cause chances in calcium?

A

diffuse osteolysis due to overproduction of local cytokines e.g. IL-6, causes erosion of bones

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44
Q

typical biochemistry of myeloma caused hypercalcaemia - Ca2+, Phos, alk phos

A

ca2+ raised, phos high, alk phos normal

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45
Q

why is phosphate raised in myeloma associated hypercalcaemia

A

myeloma produces lots of immunoglobulins causing renal damage which causes phosphate to rise

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46
Q

steroids are effective against treating hypercalcaemia due to myeloma - t or f

A

T

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47
Q

is phosphate usually high or low in hypercalcaemia?

A

usually low if PTH driven

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48
Q

why do focal osteolytic mets cause an increased risk of pathological fractures?

A

cancer invasion erodes bones and mineral structure, weakening it

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49
Q

pathological fractures due to boney mets usually heal with treatment - T or F

A

F, they are very difficult to heal due to cancer invasion

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50
Q

management for acute hypercalcaemia?

A

hydration - 6L saline over 24 hours

bisphonates once hydrated

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51
Q

what is the bisphosphonate of choice in hypercalcaemia?

A

zolendronic acid

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52
Q

acute rhabdomyolysis causes hypercalcaemia - T or F?

A

F, it causes hypocalcaemia

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53
Q

symptoms of hypocalcaemia?

A

paraesthesia of mouth and fingers

muscle twitching and leg cramps

laryngeal stridor - vocal cord cramping

seizures, hyperreflexia

chosteks sign, prolonged QTc

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54
Q

what is chvosteks sign

A

in hypocalcaemia, if u inflate a BP calf, and tap the patients parotid glands, it will cause twitching in the eye and face

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55
Q

common causes of hypocalcaemia?

A 
vit D deficiency
hypoparathyroidism
renal failure
drugs
acute rhabdomyolysis
acute pancreatitis
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56
Q

causes of hypoparathyroidism ?

A

iatrogenic post thyroidectomy
congenital absence of parathyroids
genetic/chromosomal abnormality
autoimmune conditions - autoimmune polyendocrinopathy

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57
Q

biochemistry of hypoparathyroidism?

calcium, phosphate, PTH, urinary calcium

A

cal - Low
phos - high
PTH - low
urinary cal - low

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58
Q

what is renal function like normally in primary hypoparathyroidism?

A

normal

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59
Q

why does serum magnesium affect calcium?

A

hypomagenisum inhibits PTH release and peripheral action of PTH

if patient is hypomagenesium, calcium will not correct until magnesium is corrected

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60
Q

what is secondary hyperparathyroidism?

A

when renal impairment causes hypocalcaemia and consequently hyperphosphataemia, stimulating PTH to be released

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61
Q

how is osteoporosis diagnosed?

A

clinically after osteoporotic fracture OR radiologically from DEXA

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62
Q

what is the DEXA diagnosis of osteporosis?

A

-2.5 SD of BMD

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63
Q

what are DEXA scans usually done of

A

wrist, femur, lumbar

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64
Q

risk factors for osteoporotic fractures

A 
low BMI, tall stature
smoking and alcohol
medication - steroids
prem menopause
calcium intake
fam hx
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65
Q

treatment for osteoporosis

A

calcium and vitamin D
lifestyle changes
bisphosphonates
HRT

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66
Q

what is osteomalacia?

A

vit D def causing bone abnormalities

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67
Q

what is different in bones in osteomalacia?

A

reduced mineral content - hydroxyapatite

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68
Q

symptoms of osteomalacia

A

in children - genu valrum/valgus

weakness, myalgia, bone pain, tetany

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69
Q

treatment of osteomalacia

A

vitamin D, colecalciferol, ergocalciferol

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70
Q

causes of osteomalacia

A

lack of sunlight/vitamin D
drugs - anticonvulsants
renal or hepatic disease
dietary def of calcium/phosphate

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71
Q

how to diagnose diabetes mellitus?

A

if asymptomatic, 2x random BM >=11.1

if symptomatic, one random BM over 11.1

or fasting BM over 7.0 or 2 hour after OGTT BM over 11.1

or Hba1c >= 48 mmol/mol

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72
Q

when should hba1c not be used for diagnosis of DM?

A

in children and young adults
for GDM
during pregnancy and 2 months after birth
if acutely unwell - hba1c takes 3 months to change
if on steroids or other glucose affecting drugs
renal failure
HIV

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73
Q

what is MODY?

A

maturity onset diabetes of the young - hereditary monogenic forms of DM affecting insuling production, that usually present between 20-50 years old

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74
Q

describe how insulin is secreted

A

rise in blood glucose causes influx of glucose into beta islet cells through channels, these are phosphorylated by glucokinase which is then used to produce ATP. ATP inhibits K-atp pumps which stops efflux of K from the cell. this causes depolarisation of the cell causing influx of Ca2+ ions, stimulating insulin release

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75
Q

clinical features of MODY

A 
usually asymptomatic, incidental finding. 
or misdiagnosis of t1dm or t2dm
low insulin requirement
family history if DM
lack of metabolic symptoms found in T2DM
76
Q

describe glucokinase MODY

A

functional insulin production but raised set point to trigger insulin secretion. persistently raised BM, no complications associated, no treatment needed

77
Q

describe hnf1a and hnf4a mody

A

similar symptoms
normoglycaemic in childhood, but progressively gets worse till 30s.
may be misdiagnosed as t1dm. usually notobese, poor control leads to complications. responds to sulphonylureas. do not use insulin

78
Q

describe MODY 5

A

AKA HNF-1b. causes renal complications - cysts and impaired function. associated with pancreatic and genitourinary abnormalities. require insulin

79
Q

where (within healthcare) is MODY commonly diagnsed

A

incidental finding
OGTT during pregnancy
renal clinic
after hypoglycaemia

80
Q

T1DM is not possible before 6 months old - t or F

A

True, called neonatal diabetes mellitus before 6 months

81
Q

what is c peptide

A

part of proinsulin that is cleaved off to form active insulin. used to measure insulin production, more reliable than measuring insulin because c peptide is not broken down by the liver

82
Q

when should hba1c not be used for diabetes

A 
young people
if pregnant or ?GDM
if acute onset of symptoms
anyone on glycemic affecting drugs
HIV
renal failure
83
Q

what is neonatal diabetes?

A

diabetes presenting before 6 months of age

84
Q

how does neonatal diabetes present

A

hyperglycaemia or DKA
low birth weight
low c peptide

85
Q

is c peptide high low or normal in neonatal diabetes

A

low

86
Q

neonatal diabetes is usually life long - t or f

A

false, can be transient or permanent

87
Q

what medication is used in neonatal diabetes

A

sulphonylurea

88
Q

what are some endocrinopathies that can cause secondary diabetes?

A 
cushings
acromegaly
phaeochromocytoma
hyperthyroidism
glucoagonoma
89
Q

Down’s syndrome is associated with diabetes - t or F

A

T

90
Q

what is lipodystrophy

A

condition where body is unable to produce and maintain fat tissue due to lack of leptin. associated with insulin resistance and other metabolic syndromes

91
Q

what are some drugs that can cause diabetes

A 
long term steroid use
HIV HAART
antipsychotics
beta blockers
statins
92
Q

name the hormones secreted or regulated by the anterior and posterior pituitary

A

anterior - GHRH, TRH, ACTH, LH/FSH, prolactin,

posterior: oxytocin, adh

93
Q

what is pituitary apoplexy

A

infarction/haemorrhage of the pituitary

94
Q

describe the adrenal-pituitary axis

A

CRH produced by hypothalamus stimulates pituitary to produce ACTH which stimulates adrenal glands to make cortisol/steroids

95
Q

symptoms of hypoadrenalism

A

fatigue, weight loss, nausea and vomiting, abdominal pain, postural hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, acidosis

96
Q

what is primary hypoadrenalism called and caused by

A

failure of adrenal glands to produce steroids, addison’s disease

97
Q

difference between primary and secondary hypoadrenalism

A

pri - adrenal glands not working, low glucocorticoids, mineralcorticoids, and sex steroids

secondary - pituitary not making acth, low glucocorticoids, but normal mineralcorticoids

98
Q

clinical features of addison’s disease

A

same as those of hypoadrenalism, but also pigmentation due to high ACTH, and salt craving due to low mineralcorticoids

99
Q

investigations in someone suspected of primary hypoadrenalism

A

pituitary panel test to find out extent of hormone deficiency
ACTH test - synacthen test

100
Q

what is the ACTH test

A

measure baseline cortisol and give acth, measure after 30 mins and 60 mins and see if cortison goes up. differentiates primary from secondary.

101
Q

management in hypoadrenalism

A

cortisol replacement, hydrocrotison, prednisolone, or dexamethasone, and fludrocrotisone.

102
Q

what to monitor in someone treated for hypoadrenalism

A

weight, postural bp, signs of excess, renin.

103
Q

biochemical markers of someone with primary hypoadrenalism

ACTH: 
cortisol: 
renin: 
sodium: 
potassium:
A

ACTH: high

cortisol: low
renin: high
sodium: low
potassium: high

104
Q

biochemical markers of someone with secondary hypoadrenalism

ACTH: 
cortisol: 
renin: 
sodium: 
potassium:
A

acth: low
cortisol: low
renin: normal
aldosterone: normal
sodium and potassium: normal

105
Q

causes of addison’s crisis

A

illness, injury, missed medication
surgery, burns, MI, pregnancy

usually in someone with known addison’s or hypoadrenalism

106
Q

clinical features of addison’s crisis

A 
abdominal pains
fatigue
n&v
low grade fever
muscle pains/cramps
dehydration
107
Q

signs of addison’s crisis (electrolytes, biochemical markers)

A 
hyponatraemia
hyperkalaemia
hypoglycaemia
hypotension
dehydration
108
Q

management of someone with addison’s crisis - dose and route, monitoring,

A

hydrocortisone 100mg IM/IV
IV fluids - 0.9% nacl
treat underlying cause
cardiac and electrolyte monitoring

109
Q

what is cushing’s syndrome

A

hypercortisolism

110
Q

causes of cushing’s syndrome

A

exogenous cortisol
cortisol producing adrenal tumour
pituitary tumour producing acth
ectopic tumour producing acth

111
Q

what is a pituitary tumour producing acth called?

A

cushing’s disease

112
Q

symptoms of cushings syndrome

A 
truncal obesity - buffalo hump, weight gain
facial fullness/moon face
proximal muscle wasting
diabetes/impaired glucose tolerance
gondal dysfunction
hypertension
kidney stones
skin/hair changes - acne, hirsutism, striae, pigmentation
psychological changes
osteoporosis
irregular periods
thirst/polydipsia,polyuria
impaired immune function
113
Q

how to investigate cushings syndrome

A

midnight cortisol
overnight dexamethasone suppression
low dose dexamethasone suppresion
high dose dexamethasone suppresion

114
Q

what do the dexamethasone suppresion tests tell you

A

low dose dex - if cortisol unsuppresed, diagnosis of cushings syndrome

high dose dex - measure ACTH and cortisol

if acth is low and cortisol high - adrenal tumour producing cortisol

if acth is low and cortisol is low - pituitary tumour producing acth

if acth is high and cortisol is high - ectopic tumour producing acth

115
Q

do you get metabolic acidosis or alkalosis in addisons disease?

A

acidosis - due to lack of aldosterone and failure of Na/H+ pumps to work, causing sodium to be secreted and h+ to be retained

116
Q

what further investigations to do after dexamethasone suppresion tests

A

imaging to find source of tumour

117
Q

what time of the day should ACTH be measured?

A

8-9am as they would be the highest.

118
Q

what an ACTH test, what levels of cortisol is considered normal??

A

> 580nmol/L

119
Q

what is the drug used in ACTH test, dose and route

A

250microgram tetracosactide IM or IV

120
Q

antibodies found in gRaves disease

A

TRAb

121
Q

what is the antibody found in autoimmune hypothyroidism

A

anti TPO

122
Q

when is goitre ultrasound indicated?

A

when the goitre is non-functional

123
Q

what is usually done to confirm after a thyroid ultrasound

A

FNA +/- histology

124
Q

what can be used to investigate a functional goitre?

A

radioisotope uptake scan

125
Q

clinical features of hypothyroidism

A 
tiredness
weight gain
depression
dry skin and brittle hair
constipation
menorrhagia
126
Q

dose of levothyroxine given to patients with hypothyroidism?

A

75-100mcg, if old start at 25-50mcg

127
Q

what blood markers are used to monitor in hypothyroidism management

A

if primary - TSH

if secondary - t4/t3

128
Q

causes of hyperthyroidism

A

graves disease

toxic nodule +/- multi

129
Q

management of primary hyperthyroidism

A

antithyroid medication
surgery
radioiodine ablation

130
Q

2 medical regimes used in hyperthyroidism

A

block and replace - carbimazole or PTU, then levothyroxine

or dose titration of carbimazole or PTU

131
Q

what usually causes 2ndary hyperthyroidism

A

TSHoma

132
Q

symptoms of hyperthyroidism

A 
anxiety
sleeplessness
weight loss
heat intolerance
tremors
diarrhea
graves -> exopthalmos, tibial myxodema, thyroid acropatchy
133
Q

physiology of gonado-pituitary axis

A

hypothalamus makes GNRH which stimulates pituitary to make fsh/lh, whcih stimulates gonads to make testosterone or estrogen

134
Q

causes of primary hypogonadism

A

congenital, chromosomal or genetic abnormality

acquired - infection, autoimmune, iatrogennic, drugs

135
Q

drug that can cause hypognoadism

A

ketoconazole

136
Q

what kind of hypogonadism would anabolic steroid use exhibit

A

secondary

137
Q

what would hyperprolactinaemia cause in terms of gondotrophic hormone balance

A

secondary hypogonadism, prolactin inhibits GnRH from hypothalamus

138
Q

investigations in suspected hypogonadism

A

male - testosterone, sperm count
female - ovary ultrasound, estrogen, progesterone
both - basal lh/fsh

139
Q

male features of hypogonadism

A 
loss of hair
acne, hirsutism
loss of muscle mass
loss of libido
osteoporosis
central obesity
low sperm count
shrunen testes
erectile dysfunction
140
Q

female features of hypogonadism

A

none/irregular periods
osteoporosis
infertility
loss of libido

141
Q

treatment for hypogonadism

A

testosterone replacement - gel patch or IM

estrogen/progesterone replacement (HRT)

142
Q

what is treatment in secondary hypogonadism?

A

fsh/lh replacement

143
Q

what controls prolactin production

A

TRH from hypothalamus stimulates prolactin, dopamine inhibits, extrogen also stimulates

144
Q

pathological causes of hyperprolactinaemia

A

drugs - antidopamine/antipsychotics

prolactin secreting adenomas
hypothyroidism (primary)

145
Q

why does hypothyroidism cause hyperprolactinaemia?

A

primary hypothyroidism causes TRH levels to rise, thus stimulating prolactin as well

146
Q

male features of hyperprolactinaemia

A 
galactorrhea
erectile dysfunction
headaches
osteoporosis
visual field defects
147
Q

why does hyperprolactinaemia cause erectile dysfunction

A

prolactin inhibits fsh/lh production

148
Q

features of acromegaly

A 
large hands, face organs, soft tissue overgrowth, increase interdental space
carpal tunnel syndrome
hypertension
cardiovascular disease
diabetes
149
Q

investigations for acromegaly

A

IGF-1 levels (elevated)

imaging

150
Q

management for acromegaly

A

transphenoidal surgery to remove tumour

or medical options

151
Q

what are 2 possible endocrine causes of hypertension?

A

hyperaldosteronism

phaeochromocytoma

152
Q

difference between primary and secondary hyperaldosteronism

A

primary produces excess aldosterone

secondary is triggered by underperfusion to stimulate increased aldosterone secretion

153
Q

how to tell if primary or secondary hyperaldosteronism

A

aldosterone:renin ratio

primary will have more aldosterone than renin, secondary will have high renin as well

154
Q

clinical features and biochemical markers of primary hyperaldosteronism

A 
hypertension
hypernatraemia
hypokalaemia
alkalosis
low renin
high aldosterone
155
Q

causes of secondary hyperaldosteronism

A

things that cause RAAS activation/renal underpfusion

cardiac failure
renal stenosis
nephrotic syndrome
liver failure
diuretics
156
Q

treatment of primary hyperaldosteronism

A

spironolactone then surgery

157
Q

reference range for serum sodium

A

135-144 mmol/L

158
Q

causes of hypernatraemia

A

low volume - not drinking water, excess urinary loss, extreme sweating or diarrhea

normal volume - diabetes insipidus

high volume - conn’s syndrome, too much hypertonic intake

159
Q

management of hypernatraemia

A

careful fluid resuscitation, avoid too rapid due to cerebral edema risk

160
Q

broad causes of hyponatraemia?

A

gaining too much water, loosing too much salt, or retaining too much water

161
Q

what is pseudohypontraemia

A

when other solutes in the serum decrease the relative concentration of sodium and water e.g. hypertriglyceridaemia, hyperglycaemia,

162
Q

causes of sodium depletion causing hyponatraemia?

A

renal loss - diuretics, salt wasting, nephropathy

gut sodium loss

163
Q

causes of reduced renal free water clearance (not excreting enough urine)

A

drugs, renail failure, portal hypotension and ascites, sepsis,

cardiac failure, nephrotic syndrome, siadh, hypoadrenalism

164
Q

symptoms of hypontraemia

A

often asymptomatic

headache, n&v, muscle cramps, lethargy

165
Q

signs of severe hyponatraemia

A

disorientation, seizures, coma, cerebral edema

166
Q

investigations in hyponatraemia?

A

urine tests - osomolality, sodium
plasma tests - lfts, bone panel, tfts, cortisol
radiology

167
Q

in hyponatraemia, what does low urine osmolality indicate ?

A

too much water intake - dipsogenic polydipsia, IVT

168
Q

in hyponatraemia, what does high urine osmolality indicate ?

A

not enough free water clearance, proceed to test urine sodium

169
Q

in hyponatraemia, what does high urine osmolality and low urine sodium indicate?

A

body is retaining sodium and fluids, e,g, heart failure, nephrotic syndrome, hypotensive shock

170
Q

in hyponatraemia, what does high urine osmolality and high urine sodium indicate?

A

body is concentrating urine inappropriately - SIADH, hypoadrenalism

171
Q

management of hyponatraemia

A

if acute and severe - hypertonic saline infusion

if chronic or mild, reduce non-essential fluids and treat cause, stop interacting medications

172
Q

where is potassium stored in the body

A

mostly intracellularly

173
Q

what affects serum potassium

A

potassium influx into cells caused by alkalosis, insulin and beta adrenergic agonist

potassium efflux caused by acidosis, a-adrenergic agonist and strenuous exercise

174
Q

where in the kidney is potassium regulated

A

DCT - 10%

175
Q

ECG changes in hypokalaemia

A 
flattened T waves and inversion
prolonged PR interval
ST depression
U waves
SVT
torsade de pointes
176
Q

neuromuscular clinical features of hypokalaemia

A

neuromuscular symptoms - tetany, cramps, weakness, constipation, paralysis

177
Q

ECG features of hyperkalaemia

A 
peaked T waves
lengthening PR segment
disappearing P waves
wide QRS
sinus bradycardia or slow AF
sine wave
178
Q

causes of hyperkalaemia

A 
hypoaldosternoism
ACEI, ARBS
renal failure
acidosis
tissue damage
increased intake
179
Q

management of hyperkalaemia

A 
urgent ECG
calcium gluconate
insuline, dextrose
salbutamol 
dialysis
180
Q

what is SIADH

A

syndrome of inappropriate antidiuretic hormone secretion

181
Q

how to diagnose siadh

A

hyponatraemia, low serum osmolality, high urine osmolality and sodium. with no other possible causes

182
Q

causes of SIADH

A

drug induced
CNS infection/inflammation/tumour
neoplasms
pulmonary disease

183
Q

drugs that can cause SIADH

A

na valproate, carbamazepine,
clofibrate, chlorpropamide
SSRIs
morphine, oxytocin

184
Q

what are some broad categories of strong cyp3a4 inhibitors

A

antibiotics - clarythromycin
antifungals - ketoconazole
antivirals - ritonavir

185
Q

clinical features of phaeochromocytoma

A

anxiety, tremors, palpitations, tachycardia, hypertension, headaches, weight loss, hyperglycaemia,

4 CSIM2 (11 decks)

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