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Zero to Finals: Medicine A.S. > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is cushing’s syndrome?

A

the signs and symptoms of prolonged abnormal elevated cortisol levels

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2
Q

what is cushing’s disease?

A
  • where a pituitary adenoma is producing excess ACTH

- a cause of cushing’s syndrome

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3
Q

presentation of cushing’s syndrome? (hint: there’s a LOT)

A
  • “lemon on matchsticks” (truncal obesity with proximal limb muscle wasting)
  • abdo striae
  • “moon face” (rounded)
  • “buffalo hump” (fat pad on back)
  • HTN
  • T2DM or hyperglycaemia
  • depression
  • insomnia
  • osteoporosis
  • easy bruising
  • poor skin healing
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4
Q

causes of cushing’s syndrome?

A
  • exogenous steroids
  • cushing’s disease
  • adrenal adenoma
  • paraneoplastic cushing’s
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5
Q

what is paraneoplastic cushing’s? commonest cause of this?

A
  • when a tumour releases ACTH but it is NOT in the pituitary
  • SCLC is commonest cause
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6
Q

what is ectopic ACTH?

A

ACTH released from anywhere other than the pituitary

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7
Q

diagnostic investigation for cushing’s syndrome?

A

dexamethasone suppression test

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8
Q

how is a dexamethasone suppression test carried out?

A
  • patient takes a dose of dexamethasone at night

- cortisol and ACTH measured in the morning

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9
Q

how is the result of a dexamethasone suppression test interpreted?

A
  • normal cortisol and ACTH suggest cushing’s syndrome

- if result is abnormal for a low dose test, do a high dose test next

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10
Q

results of dexamethasone suppression testing in adrenal adenoma?

A
  • ACTH suppressed but cortisol NOT supressed

- this is independent of the pituitary (which produces cortisol)

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11
Q

results of dexamethasone suppression testing in pituitary adenoma?

A
  • cortisol and ACTH both suppressed
  • pituitary still functioning somewhat normally
  • this is cushing’s disease
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12
Q

results of dexamethasone suppression testing in ectopic ACTH production?

A
  • neither cortisol nor ACTH suppressed

- it’s from an external source

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13
Q

investigations in cushing’s syndrome? hint: don’t forget ectopic causes

A
  • dex suppression test
  • 24h urinary free cortisol (high)
  • FBC (raised WCC)
  • UEs (K+ low if aldosterone also being secreted)
  • MRI brain (pit adenoma)
  • CT chest (SCLC)
  • CT abdo (adrenal adenomas)
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14
Q

management of cushing’s syndrome? hint: underlying cause

A
  • trans-sphenoidal removal of pituitary adenoma
  • surgery for adrenal tumour
  • surgery for source of ectopic ACTH
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15
Q

what can be done about adrenal tumours which cannot be removed?

A

remove both adrenal glands and give lifelong replacement steroid hormones instead

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16
Q

which 2 steroids are deficient in adrenal insufficiency?

A
  • cortisol

- aldosterone

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17
Q

what is addison’s disease? commonest cause?

A
  • primary adrenal insufficiency

- autoimmune is commonest cause

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18
Q

what is tertiary adrenal insufficiency? commonest cause?

A
  • reduced CRH release from the hypothalamus

- long-term steroid use

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19
Q

how can tertiary adrenal insufficiency be prevented?

A

taper down long-term steroids slowly

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20
Q

presentation of adrenal insufficiency?

A
  • fatigue and weakness (most common)
  • nausea
  • cramps
  • abdo pain
  • reduced libido
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21
Q

signs O/E of adrenal insufficiency?

A
  • bronze hyperpigmentation (addison’s), seen especially in palmar creases
  • (postural) hypotension
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22
Q

what causes bronze skin in addison’s disease?

A
  • increased circulating ACTH
  • ACTH stimulates melanocytes
  • increased melanin production
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23
Q

investigations and findings in adrenal insufficiency? hint: most are on bloods

A
  • UEs (low Na+, high K+)
  • early morning cortisol
  • short synacthen test (diagnostic)
  • ACTH levels (high in addison’s, low in secondary insufficiency)
  • adrenal cortex antibodies (autoimmune)
  • 21-hydroxylase antibodies (autoimmune)
  • CT / MRI adrenals
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24
Q

diagnostic test for adrenal insufficiency?

A

short synacthen test

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25
Q

what is synacthen?

A

synthetic ACTH

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26
Q

how is the short synacthen test carried out?

A
  • give synacthen at 8am
  • measure cortisol at baseline
  • then after 30 mins
  • then after 60 mins
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27
Q

what is the result of the short synacthen test in a healthy person?

A

cortisol should at least double

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28
Q

if cortisol fails to double on the short synacthen test, what does this indicate?

A

primary adrenal insufficiency (addison’s)

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29
Q

management of adrenal insufficiency?

A
  • steroid replacements
  • hydrocortisone for cortisol
  • fludrocortisone for aldosterone
  • double doses in acute illness
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30
Q

signs of addisonian crisis?

A

everything low but K+ high

  • reduced consciousness
  • hypotension
  • hypoglycaemia
  • hyponatraemia
  • hyperkalaemia
  • patient looks very unwell
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31
Q

triggers of addisonian crisis?

A
  • could be first presentation of addison’s disease
  • infection
  • trauma
  • other acute illness
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32
Q

management of addisonian crisis?

A
  • IV hydrocortisone 100mg stat
  • repeat 6 hourly
  • IV fluid resus
  • correct hypoglycaemia
  • monitor electrolytes and fluid closely
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33
Q

TFT findings in hyperthyroidism? hint: different if pituitary source

A
  • low TSH, high if pituitary adenoma

- high T3 and T4

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34
Q

TFT findings in hypothyroidism? hint: different if pituitary / hypothalamic source

A
  • high TSH
  • low TSH if pituitary / hypothalamic cause (secondary hypothyroidism)
  • low T3 and T4
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35
Q

in which conditions are anti-TPO antibodies present?

A
  • grave’s disease

- hashimoto’s thyroiditis

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36
Q

in which conditions are antithyroglobulin antibodies present?

A
  • grave’s disease
  • hashimoto’s thyroiditis
  • thyroid cancer
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37
Q

in which conditions are TSH receptor antibodies present?

A

grave’s disease

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38
Q

what is the difference between hyperthyroidism and thyrotoxicosis?

A
  • hyperthyroidism describes excessive thyroid hormone production by the thyroid
  • thyrotoxicosis means excess of thyroid hormone in the body
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39
Q

what is grave’s disease? describe the pathophysiology

A
  • autoimmune primary hyperthyroidism

- TSH receptor antibodies mimic TSH and stimulate the thyroid TSH receptors

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40
Q

commonest cause of hyperthyroidism?

A

grave’s disease

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41
Q

describe toxic multinodular goitre

A

nodules develop on the thyroid which keep producing thyroid hormone, independent to the feedback loop

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42
Q

what is exophthalmos? which condition is it seen in? what causes it?

A
  • eyeball bulging from socket
  • seen in grave’s disease
  • is a direct reaction to TSH receptor antibodies
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43
Q

describe pretibial myxoedema. which condition is it seen in? what causes it?

A
  • discoloured, waxy oedematous skin over shins
  • grave’s disease
  • is a direct reaction to TSH receptor antibodies
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44
Q

presentation of hyperthyroidism?

A
  • anxious, irritable
  • heat intol, sweating
  • tachycardia
  • weight loss
  • fatigue
  • diarrhoea
  • sexual dysfunction
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45
Q

which features in presentation are unique to grave’s disease?

A
  • diffuse goitre without nodules
  • bilateral exophthalmos
  • pretibial myxoedema
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46
Q

which features in presentation are suggestive of toxic mulitnodular goitre?

A
  • goitre with firm nodules felt in neck

- usually aged 50+

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47
Q

describe the presentation in de quervain’s thyroiditis?

A
  • viral infection with fever
  • neck pain / tenderness
  • dysphagia
  • hyperthyroidism followed by hypothyroidism
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48
Q

prognosis and management of de quervain’s thyroiditis?

A
  • self-limiting condition

- supportive treatment, e.g. NSAIDs, BBs

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49
Q

what is the other name for a thyroid storm? describe the presentation of this

A
  • thyrotoxic crisis
  • pyrexia
  • tachycardia
  • delirium
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50
Q

management of a thyrotoxic storm?

A
  • fluid resus if needed
  • BBs
  • propylthiouracil
  • hydrocortisone
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51
Q

management of hyperthyroidism?

A
  • 1st line: carbimazole
  • 2nd: propylthiouracil
  • radioactive iodine (drink)
  • BB (e.g. propanolol)
  • surgery
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52
Q

causes of hypothyroidism?

A
  • hashimoto’s thyroiditis
  • iodine deficiency
  • overtreatment of hyperthyroidism
  • drugs
  • tumours
  • infections
  • sheehan syndrome
  • radiation
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53
Q

presentation of hypothyroidism?

A
  • depressed
  • weight gain
  • fatigue
  • dry skin
  • coarse hair, hair loss
  • fluid retention (oedema, pleural effusions, ascites)
  • amenorrhoea
  • constipation
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54
Q

TFT findings in primary hypothyroidism?

A
  • TSH high

- T3 and T4 low

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55
Q

TFT findings in secondary hypothyroidism?

A
  • TSH low

- T3 and T4 low

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56
Q

management of hypothyroidism?

A

PO levothyroxine

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57
Q

how is levothyroxine treatment monitored?

A
  • measure TSH levels monthly until stable
  • if TSH is high, increase levothyroxine dose
  • if TSH is low, decrease levothyroxine dose
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58
Q

what does “diffuse high uptake” on a radioisotope scan of the thyroid suggest?

A

grave’s disease

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59
Q

what does “focal high uptake” on a radioisotope scan of the thyroid suggest?

A
  • toxic multinodular goitre

- adenoma

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60
Q

what do “cold areas” on a radioisotope scan of the thyroid suggest?

A

thyroid cancer

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61
Q

which cells produce glucagon? where are these found?

A
  • alpha cells

- islets of langerhans in pancreas

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62
Q

which cells produce insulin? where are these found?

A
  • beta cells

- islets of langerhans in pancreas

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63
Q

how does insulin reduce blood glucose levels? hint: 2 ways

A
  • causes body cells to absorb glucose to use

- causes muscle and liver cells to absorb glucose and store it as glycogen

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64
Q

what is ketogenesis? when is it done?

A
  • liver converting fatty acids into ketones

- done when both glucose and glycogen supplies are low

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65
Q

what is the normal blood glucose range?

A

4.4 - 6.1 mmol/L

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66
Q

pathophysiology of T1DM?

A
  • pancreas unable to produce enough insulin
  • no glucose gets absorbed out of the blood
  • causes hyperglycaemia
  • autoimmune
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67
Q

what is the body’s initial response to rising blood ketone levels?

A

kidneys produce bicarbonate to counteract the acidity

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68
Q

how does insulin affect potassium? what happens in DKA? what can happen when DKA is treated?

A
  • insulin causes cells to absorb potassium
  • in DKA, serum potassium is high or normal because there’s not enough insulin so none of it is being absorbed, but the kidneys carry on excreting it
  • however, total body potassium is low
  • treating with insulin can cause a severe hypokalaemia
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69
Q

overall effects of DKA on body?

A
  • hyperglycaemia
  • dehydration
  • ketosis
  • metabolic acidosis (with low bicarbonate)
  • potassium imbalance
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70
Q

presentation of DKA?

A
  • polyuria
  • polydipsia
  • N+V
  • acetone smell on breath (peardrops)
  • kussmaul breathing (deep, laboured breaths)
  • dehydration
  • hypotension (caused by dehydration)
  • altered consciousness
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71
Q

diagnostic criteria for DKA?

A
  • blood glucose >11mmol/L
  • blood ketones >3mmol/L
  • pH <7.3
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72
Q

FIG PICK: management of DKA?

A
  • Fluids (IV fluid resus)
  • Insulin infusion
  • Glucose (monitor closely, consider dextrose)
  • Potassium (monitor 4-hourly and correct)
  • Infection (treat underlying triggers)
  • Chart (check fluid balance)
  • Ketones (monitor them)
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73
Q

what is the max rate at which potassium can be infused?

A

10mmol/L

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74
Q

patient advice given in long term management of T1DM?

A
  • explain subcut insulin regimes
  • monitor carb intake and glucose
  • monitor complications
  • advice on changing injection site
75
Q

when should blood glucose be checked in T1DM?

A
  • on waking
  • after a meal
  • before bed
76
Q

what is a typical insulin regime in T1DM?

A
  • background insulin once daily (long-acting)

- short acting insulin 30 mins before each meal

77
Q

why does the injection site for insulin need to be changed regularly?

A

risk of lipodystrophy

78
Q

what is lipodystrophy?

A

the subcut fat hardens from being injected in so much

79
Q

symptoms of hypoglycaemia?

A
  • tremor
  • sweating
  • irritability
  • dizziness
  • pallor
80
Q

management of hypoglycaemia in T1DM? if severe?

A
  • first rapid acting glucose (e.g. lucozade)
  • then slower acting carbs (e.g. biscuits, toast)
  • if severe: IV dextrose and IM glucagon
81
Q

how could a patient in DKA end up hypoglycaemic?

A

overtreatment with insulin

82
Q

short term complications in T1DM?

A
  • hypoglycaemia
  • hyperglycaemia
  • DKA
83
Q

macrovascular complications in diabetes?

A
  • CAD
  • peripheral ischaemia (diabetic foot)
  • stroke
  • HTN
84
Q

microvascular complications in diabetes?

A
  • peripheral neuropathy
  • retinopathy
  • glomerulosclerosis (kidney)
85
Q

nature of neuropathy in diabetes?

A
  • peripheral

- “glove and stocking” distribution

86
Q

infection-related complications in diabetes?

A
  • UTIs
  • pneumonia
  • skin infections, esp in feet
  • oral / vaginal candida
87
Q

what 3 things are used to monitor T1DM?

A
  • HbA1c
  • capillary blood glucose
  • flash glucose monitoring (e.g. freestyle libra)
88
Q

what does HbA1c tell us? how often is it checked?

A
  • average blood glucose levels over last 3 months

- every 3-6 months

89
Q

non-modifiable risk factors for T2DM?

A
  • older age
  • non-white ethnicity
  • FHx
90
Q

modifiable risk factors for T2DM?

A
  • obesity
  • sedentary lifestyle
  • high carb diet
91
Q

how might T2DM present?

A
  • fatigue
  • polydipsia
  • polyuria
  • unintentional weight loss
  • opportunistic infections
  • slow healing
  • glucose in urine (on dipstick)
92
Q

when is an oral glucose tolerance test (OGTT) performed?

A

first thing in the morning, before breakfast

93
Q

what does an OGTT involve?

A
  • take a fasting glucose reading
  • then give 75g glucose drink
  • then measure glucose again 2 hours later
94
Q

diagnostic criteria for pre-diabetes?

A
  • HbA1c 42 - 47 mmol/L
  • fasting glucose 6.1 - 6.9 mmol/L (impaired)
  • OGTT 7.8 - 11 mmol/L (impaired)
95
Q

diagnostic criteria for diabetes?

A
  • HbA1c >48mmol/L
  • random glucose >11mmol/L
  • fasting glucose >7mmol/L
  • OGTT >11mmol/L
96
Q

diet advice in T2DM?

A
  • more veg and oily fish
  • fewer sugary foods including carbs
  • high fibre
97
Q

lifestyle advice given in T2DM?

A
  • diet changes
  • exercise and weight loss
  • stop smoking
  • optimise comorbid conditions (e.g. HTN)
98
Q

3 main complications to monitor for in T2DM?

A
  • diabetic retinopathy
  • kidney disease
  • diabetic foot
99
Q

what is the target HbA1c for type 2 diabetics on metformin alone?

A

48mmol/L

100
Q

what is the target HbA1c for type 2 diabetics on more than just metformin?

A

53mmol/L

101
Q

medical management of T2DM?

A
  • 1st line: metformin
  • 2nd: add add sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
  • 3rd: metformin + sulfonylurea + GLP-1 mimetic
  • 4th: metformin + insulin
102
Q

actions of metformin?

A
  • increases insulin sensitivity

- decreases liver production of glucose

103
Q

notable side effects of metformin?

A
  • diarrhoea
  • abdo pain
  • lactic acidosis
104
Q

example of sulfonylurea?

A

gliclazide

105
Q

MOA of gliclazide?

A

increases insulin production in pancreas

106
Q

notable side effects of gliclazide?

A
  • weight gain
  • hypoglycaemia
  • increases CVD risk
107
Q

notable side effects of pioglitazone?

A
  • weight gain
  • fluid retention
  • anaemia
  • HF
  • bladder cancer
108
Q

example of DPP-4 inhibitor?

A

sitagliptin

109
Q

notable side effects of sitagliptin?

A
  • GI upset
  • URTI
  • pancreatitis
110
Q

notable side effects of GLP-1 inhibitors?

A
  • GI upset
  • weight loss
  • dizziness
  • hypoglycaemia (less common)
111
Q

what are the 5 types of insulin? give an example for each

A
  • rapid-acting (novorapid)
  • short-acting (actrapid)
  • intermediate-acting (insulatard)
  • long-acting (levemir)
  • combination (humalog 25, 25:75)
112
Q

what causes acromegaly?

A

an excess of GH

113
Q

where is GH produced in the body?

A

anterior pituitary gland

114
Q

commonest cause of acromegaly?

A

pituitary adenoma

115
Q

what visual field defect is seen in pituitary adenoma? why?

A
  • bitemporal hemianopia

- it compresses the optic chiasm

116
Q

presentation of acromegaly?

A
  • headaches
  • bitemporal hemianopia
  • frontal bossing
  • large nose
  • macroglossia
  • large hands and feet
  • prognathism
  • arthritis
117
Q

describe frontal bossing

A

prominent forehead and brow bone

118
Q

describe prognathism

A

large, protruding jaw

119
Q

organ dysfunction caused by GH?

A
  • hypertrophic heart
  • HTN
  • T2DM
  • colorectal cancer
120
Q

management of acromegaly?

A
  • trans-sphenoidal removal of pituitary adenoma
  • removal of any tumour producing ectopic GH
  • meds which block GH
121
Q

which drugs can block GH?

A
  • pegvisomant
  • ocreotide (somatostatin analogue)
  • bromocriptine (DA agonist)
122
Q

which 2 hormones can inhibit GH?

A
  • somatostatin

- dopamine

123
Q

which cells produce PTH? where are these found?

A

chief cells on the parathyroid glands

124
Q

when is PTH secreted?

A

in response to hypocalcaemia

125
Q

how does PTH increase blood Ca levels? hint: think bone, gut and kidney

A
  • increases osteoclast activity (reabsorbs Ca from bones)
  • increases Ca absorption in gut
  • increases Ca reabsorption in kidney
  • increases vit D activity
126
Q

what causes primary hyperparathyroidism?

A

excessive PTH being secreted by a tumour on the parathyroid glands

127
Q

management of primary hyperparathyroidism?

A

surgical tumour removal

128
Q

PTH and calcium levels in primary hyperparathyroidism?

A
  • PTH is high

- serum calcium is high

129
Q

what causes secondary hyperparathyroidism?

A

2 main ways:

  • vit D deficiency
  • chronic renal / liver / failure (mostly CKD)
  • bowel disease
130
Q

PTH and calcium levels in secondary hyperparathyroidism?

A
  • PTH is high

- serum calcium is low

131
Q

what causes tertiary hyperparathyroidism?

A

prolonged secondary hyperparathyroidism, resulting in parathyroid hyperplasia

132
Q

PTH and calcium levels in tertiary hyperparathyroidism?

A
  • PTH is high

- serum calcium is high

133
Q

management of tertiary hyperparathyroidism?

A

surgical removal of some of the excess parathyroid gland

134
Q

main effects of primary hyperparathyroidism? how do these present?

A
  • excessive Ca resorption from bone (osteopenia, fractures)
  • excessive Ca excretion by kidneys (renal calculi)
  • hypercalcaemia (lots of features)
135
Q

where are juxtaglomerular cells found? what do they do?

A
  • afferent arteriole of glomerulus of nephron
  • sense BP
  • release renin in response to low BP
136
Q

what is the role of renin?

A

converts angiotensinogen into angiotensin I

137
Q

where is ACE found in the body? what does it do?

A
  • lungs

- converts angiotensin I to angiotensin II

138
Q

what is the role of angiotensin II?

A

stimulates adrenal glands to secrete aldosterone

139
Q

actions of aldosterone?

A
  • increases Na resorption in distal tubules
  • increases K secretion in distal tubules
  • increases H secretion from collecting ducts
140
Q

what is conn’s syndrome?

A

primary hyperaldosteronism

141
Q

causes of conn’s syndrome?

A
  • adrenal adenoma secreting aldosterone (commonest)
  • bilateral adrenal hyperplasia
  • familial hyperaldosteronism
  • adrenal carcinoma (rare)
142
Q

what causes secondary hyperaldosteronism? key finding?

A
  • excess renin, resulting in excess aldosterone

- high serum renin

143
Q

causes of secondary hyperaldosteronism? hint: renin goes up when kidneys get less blood

A
  • renal artery stenosis

- renal artery obstruction HF

144
Q

investigations for renal artery stenosis?

A
  • doppler USS
  • CT angiogram
  • MRA (angiography)
145
Q

how is hyperaldosteronism screened for?

A

work out renin:aldosterone ratio from bloods:

  • low:high = primary
  • high:high = secondary
146
Q

investigations for hyperaldosteronism?

A
  • bloods (renin, aldosterone)
  • BP (HTN)
  • electrolytes (hypokalaemia)
  • blood gas (alkalosis)
  • CT / MRI (adrenal tumour)
  • renal doppler USS (renal artery stenosis)
147
Q

management of hyperaldosteronism?

A
  • treat underlying cause (tumour removal)
  • percutaneous renal artery angioplasty (if RAS found)
  • aldosterone antagonists (eplerenone, spironolactone)
148
Q

types of hyperaldosteronism?

A
  • primary (conn’s syndrome)

- secondary

149
Q

commonest cause of secondary hypertension?

A

hyperaldosteronism

150
Q

where is ADH produced?

A

hypothalamus

151
Q

where is ADH secreted?

A

posterior pituitary

152
Q

actions of ADH?

A

water reabsorption in collecting ducts of nephron

153
Q

how much SIADH occur?

A
  • posterior pituitary secreting too much ADH

- ectopic ADH from a tumour (e.g. SCLC)

154
Q

how does SIADH affect sodium?

A
  • hyponatraemia

- the excess water dilutes it down

155
Q

how does SIADH affect urine osmolality (and therefore sodium too)?

A
  • high urine osmolality because less water is being excreted (so more concentrated urine)
  • high urine sodium because less water in it
156
Q

symptoms of SIADH? hint: non-specific

A
  • headache
  • fatigue
  • muscle aches
  • cramps
  • confusion
  • severe hyponatraemia (seizures, reduced consciousness)
157
Q

causes of SIADH?

A
  • Small cell lung cancer
  • Infection
  • Abscess
  • Drugs (carbamazepine, SSRIs)
  • Head injury
158
Q

drug causes of SIADH?

A
  • thiazide diuretics
  • carbamazepine
  • antipsychotics
  • SSRIs
  • NSAIDs
159
Q

how is SIADH diagnosed?

A
  • cannot test specifically for ADH
  • euvolaemic O/E
  • urine sodium high
  • urine osmolality high
  • rule out other causes of hyponatraemia
  • establish underlying cause
160
Q

causes of hyponatraemia?

A
  • adrenal insufficiency
  • diuretic use
  • D + V
  • burns, fistulas
  • excessive sweating
  • CKD, AKI
161
Q

investigations in SIADH?

A
  • UEs
  • CXR (?pneumonia, lung abscess, cancer)
  • CT thorax, abdo, pelvis + MRI brain if suspected cancer
162
Q

management of SIADH?

A
  • treat underlying cause
  • commonly drug cause - stop the drug
  • fluid restriction 500ml-1L (correct Na)
  • tolvaptan (ADH receptor blocker)
  • demeclocycline (ABx which inhibits ADH)
163
Q

major complication of SIADH? how can it happen?

A

persistent severe hyponatraemia can lead to central pontine myelinolysis

164
Q

pathophysiology of nephrogenic diabetes insipidus?

A

collecting duct of nephron not responsive to ADH

165
Q

causes of nephrogenic diabetes insipidus?

A
  • drugs, esp lithium
  • gene mutation
  • intrinsic kidney disease
  • hypokalaemia
  • hypercalcaemia
166
Q

pathophysiology of cranial diabetes insipidus?

A

hypothalamus not producing ADH for pituitary to secrete

167
Q

causes of cranial diabetes insipidus?

A
  • idiopathic
  • brain tumour
  • head injury
  • brain malformation
  • infection (meningitis, encephalitis, TB)
  • iatrogenic (brain surgery, radiotherapy)
168
Q

presentation of diabetes insipidus? hint: low fluid

A
  • polyuria
  • polydipsia
  • dehydration
  • postural hypotension
  • hypernatraemia
169
Q

investigations? hint: findings opp to SIADH

A
  • low urine osmolality
  • high serum osmolality
  • water deprivation test
170
Q

explain the water deprivation test

A
  • no fluid intake for 8 hours
  • measure urine osmolality
  • give desmopressin (ADH)
  • measure urine osmolality again
171
Q

what are the results for the water deprivation test if DI is nephrogenic? what about cranial?

A
  • nephrogenic: urine osmolality initially low and stays low (kidneys not responding to ADH)
  • cranial: UO initially low, then high (kidneys can respond to ADH)
172
Q

findings in water deprivation test if the patient has primary polydipsia / is normal?

A

urine osmolality is normal before even giving desmopressin

173
Q

management of diabetes insipidus?

A
  • treat underlying cause
  • desmopressin (synthetic ADH)
  • give higher dose if nephrogenic and monitor closely
174
Q

what is a phaeochromocytoma? what does it secrete?

A
  • tumour of chromaffin cells in or out of the adrenal gland

- secretes adrenaline

175
Q

main association of phaeochromocytoma?

A

25% are associated with multiple endocrine neoplasia 2 (MEN2)

176
Q

3 x 10% rule of phaeochromocytoma tumours?

A
  • 10% bilateral
  • 10% cancerous
  • 10% not in the adrenal gland
177
Q

diagnostic investigations for phaeochromocytoma?

A
  • 24h urinary catecholamines

- plasma free metanephrines

178
Q

why are urinary catecholamines checked in phaeochromocytoma instead of blood levels?

A
  • the adrenaline secretion is in bursts
  • blood levels will fluctuate
  • 24h urinary ones will give a better idea of total secretion
179
Q

why are plasma metanephrines checked in phaeochromocytoma?

A
  • breakdown product of adrenaline

- it has a longer half life so less likely to fluctuate than adrenaline

180
Q

presentation of phaeochromocytoma?

A
  • anxiety
  • sweating
  • headache
  • HTN
  • tremor
  • palpitations
  • tachycardia
  • paroxysmal AF
181
Q

management of phaeochromocytoma?

A
  • phenoxybenzamine (alpha blocker)
  • BBs once established on alpha blocker
  • adrenalectomy for tumour removal
182
Q

TFT results in sick euthyroid syndrome? where is this commonly seen?

A
  • low TSH
  • low T4
  • common in hospital inpatients
183
Q

TFT results in subclinical hypothyroidism?

A
  • high TSH

- NORMAL T4

184
Q

TFT results in pt with poor thyroxine compliance?

A
  • high TSH

- normal T4

Zero to Finals: Medicine A.S. (11 decks)

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