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Finals Revision > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is adrenal insufficiency?

A

the adrenal glands do not produce enough steroid hormones, particularly cortisol and aldosterone.

Steroids are essential for life = life-threatening unless the hormones are replaced.

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2
Q

What is Addison’s disease?

A

PRIMARY ADRENAL INSUFFICIENCY

specific condition where the adrenal glands have been damaged, resulting in a reduction in the secretion of cortisol and aldosterone

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3
Q

Most common cause of Addison’s disease

A

autoimmune

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4
Q

what is secondary adrenal insufficiency?

A

inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release

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5
Q

What is ACTH

A

Adrenocorticotrophic hormone

secreted by the pituitary gland

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6
Q

causes of secondary adrenal insufficiency

A

damage to pituitary gland:

  • pituitary tumour
  • infection
  • loss of blood flow
  • radiotherapy
  • Sheehan’s syndrome = massive blood loss in childbirth that leads to necrosis of the pituitary gland
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7
Q

what is tertiary adrenal insufficiency?

A

inadequate CRH release by the hypothalamus

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8
Q

what is CRH

A

Corticotrophin releasing hormone, released by the hypothalamus

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9
Q

Describe the HPA axis

A

hypothalamic-pituitary-adrenal axis:

  1. hypothalamus releases corticotrophin releasing hormone
  2. causing anterior pituitary to release adrenocorticotrophic hormone
  3. causing the adrenal cortex in the adrenal glands to release cortisol
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10
Q

causes of tertiary adrenal insufficiency

A

long term oral steroids - suppress the hypothalamus

This is why you shouldn’t suddenly withdraw exogenous steroids - hypothalamus is suppressed so no endogenous steroids will be produced

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11
Q

symptoms of adrenal insufficiency

A 
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
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12
Q

Signs of adrenal insufficiency

A

Bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)

Hypotension (particularly postural hypotension)

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13
Q

Ix for adrenal insufficiency

A

Hyponatraemia
Hyperkalaemia
Early morning cortisol - often falsely normal

Short synacthen test = FOR DIAGNOSIS

ACTH

  • High in primary adrenal insufficiency
  • low in secondary adrenal insufficiency

Adrenal cortex antibodies & 21-hydroxylase antibodies - in autoimmune adrenal insufficiency

CT/MRI adrenals
MRI pituitary

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14
Q

What is the short synacthen test?

A

For diagnosing adrenal insufficiency

Give synacthen (synthetic ACTH)
blood cortisol measured at baseline, 30 mins and 60 mins 
Synthetic ATCH wil stimulate healthy adrenal glands & the cortisol should at least double

Failure of cortisol to at least double = primary adrenal insufficiency (Addison’s)

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15
Q

tx of adrenal insuffiency

A

hydrocortisone to replace cortisol

fludrocortisone to replace adolesterone

Patients need: steroid card & double doses on sick days (don’t STOP)

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16
Q

What is an addisonian crisis?

A

Adrenal crisis

Acute presentation of severe Addison’s disease
The absence of steroid hormones leads to a life threatening presentation

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17
Q

Symptoms of addisonian crisis

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkaemia
Patients can be very unwell

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18
Q

what triggers an addisonian crisis

A

infection
trauma
other acute illness
sudden steroid withdrawal

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19
Q

mx of addisonian crisis

A 
Intensive monitoring 
IV hydrocortisone
IV fluid resuscitation 
Correct hypoglycaemia
Careful monitoring of electrolytes
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20
Q

What is cushings syndrome?

A

the signs and symptoms that develop after prolonged abnormal elevation of cortisol.

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21
Q

What is Cushings disease?

A

the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH.

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22
Q

Difference between cushings syndrome and cushings disease

A

Cushings disease causes cushings syndrome

but cushings syndrome isn’t always caused by cushings disease

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23
Q

symptoms of cushings syndrome

A 
round 'moon' face
central obesity
abdo striae
buffalo hump - fat pad on upper back
proximal limb muscle wasting
HTN
cardiac hypertrophy
hyperglycaemia (T2DM)
depression
insomnia

osteoporosis
easy bruising
poor skin healing

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24
Q

causes of cushings syndrome

A

exogenous steroids
cushings disease = pituitary adenoma releasing excessive ACTH
adrenal adenoma
paraneoplastic cushings - ACTH released from small cell lung cancer

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25
Q

ix for cushings syndrome

A 
dexamtheasone suppression test
24 hour urinary free cortisol
FBC - raised WCC 
U&E - hypokalaemia if aldosterone also secreted by adrenal adenoma
MRI brain - pituitary adenoma
chest CT - SCLC
Abdo CT - adrenal tumour
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26
Q

Tx for cushings syndrome

A

remove underlying cause

  1. trans-sphenoidal removal of pituitary adenoma (cushings disease)
  2. surgical removal of adrenal tumour
  3. surgical removal of tumours producing ectopic ACTH

If you can’t remove the cause - remove the adrenal glands and give replacement steroids for life

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27
Q

what is the dexamethasone suppression test used for?

A

used to diagnose cushings syndrome and find the cause

  1. Give dexamethasone at 10pm at night, measure cortisol and ACTH in the morning
  2. do low dose test first - give 1mg of dexamethasone = used to see if they have a normal HPA axis or if they have cushings syndrome
  3. do high dose test second if they have an abnormal low dose test to look for the cause of cushings syndrome
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28
Q

how does the low dose dexamethasone test work and what is a normal result/a result showing cushings syndrome?

A

Give 1mg dexamethasone at 10pm
In the morning measure cortisol and ACTH

In a normal person, the addition of steroids causes negative feedback on the hypothalamus and pituitary = low cortisol and ACTH in the morning

In someone with cushings syndrome, the addition of a small amount of steroids makes no difference as they already have high levels of cortisol. Therefore cortisol will be high/normal in the morning

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29
Q

how does the high dose dexamethasone test work and what do the results show?

A

high dose test is performed following an abnormal result on the low dose test

give 8mg of dexamethasone at 10pm, measure the cortisol and ACTH the next morning

In cushings disease (pituitary adenoma) = pituitary shows some response to negative feedback. 8mg of dex is enough to suppress cortisol & ACTH

In adrenal adenoma = cortisol production is independent on the pituitary. So cortisol is not suppressed but ACTH is

Ectopic ACTH production (SCLC) = cortisol and ACTh won’t be suppressed because ACTH production is independent of the hypothalamus and pituitary gland

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30
Q

What is diabetes insipidus?

A

a lack of ADH or lack of response to ADH = prevents the kidneys from concentrating the urine so there’s polyuria and polydipsia

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31
Q

how can diabetes insipidus be classified?

A

nephrogenic

cranial

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32
Q

what is nephrogenic diabetes insipidus?

A

when the collecting ducts of the kidneys do not respond to ADH

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33
Q

causes of nephrogenic diabetes insipidus

A
  • lithium
  • mutations in AVPR2 gene on X chromsome
  • Intrinsic kidney disease
  • Hypokalaemia
  • Hypercalcaemia
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34
Q

what is cranial diabetes insipidus?

A

when the hypothalamus does not produce ADH for the pituitary gland to secrete

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35
Q

Causes of cranial diabetes insipidus

A 
idiopathic
brain tumours
head injury
brain malformations
brain infections - meningitis, encephalitis, TB
Brain surgery/chemotherapy
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36
Q

presentation of diabetes insipidus

A 
Polyuria
polydipsia 
dehydration
postural hypotension 
HYPERNATRAEMIA
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37
Q

ix for diabetes insipidus

A

low urine osmolality
high serum osmolality
water deprivation test

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38
Q

what is the water deprivation test and how is it done?

A

used to diagnose diabetes insipidus

1) no fluids for 8 hours = fluid deprivation
2) measure urine osmolality
3) give synthetic ADH (desmopressin)
4) 8 hours later measure urine osmolality again

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39
Q

What do the results of the water deprivation test show?

A

For cranial diabetes insipidus = urine osmolality starts low as the brain isn’t producing any ADH, then after giving desmopressin the usine osmolality is high because the kidneys can still respond to ADH

For nephrogenic diabetes insipidus = the urine osmolality is low to start and stays low after desmopressin is given as the kidneys can’t respond to ADH

for primary polydipsia = the 8 hours of water deprivation will cause a high urine osmolality even before desmopressin is given

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40
Q

whats another name for the water deprivation test?

A

desmopressin stimulation test

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41
Q

management of diabetes insipidus

A

desmopressin in cranial DI

High doses of desmopressin in nephrogenic DI under close monitoring

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42
Q

what are the short synacthen test, dexamethasone suppression test and water deprivation test/desmopressin stimulation test each used for?

A

short synacthen test = low cortisol/adrenal insufficiency ie Addisons disease

dexamethasone suppression test = high cortisol ie cushings syndrome/disease

water deprivation test = diabetes insipidus (nephrogenic/cranial)

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43
Q

Symptoms/signs of Hypercalcaemia

A

‘bones, stones, groans and psychic moans’

  • abnormal bone remodelling/fracture risk
  • kidney stones
  • abdo cramps/nausea/ileus/constipation
  • lethargy, depression, psychosis

corneal calcification

shortened QT interval on ECG

hypertension

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44
Q

causes of Hypercalcaemia

A

1) primary hyperparathyroidism (most common in the community)
2) malignancy (most common in hospital) = SCLC, bone mets, myeloma

Other causes:
sarcoidosis
vitamin D intoxication
acromegaly
thyrotoxicosis
thiazides
dehydration
Addisons disease
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45
Q

mx for Hypercalcaemia

A

rehydration with NaCl - 3-4L /day
after rehydration = bisphosphonates (take 2-3 days to work)
calcitonin is quicker than bisphosphonates
steroids in sarcoidosis

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46
Q

symptoms of hypocalcaemia

A

NEUROMUSCULAR EXCITABILITY

tetany - muscle twitching, cramping and spasm
perioral paraesthesia
chronic hypocalcaemia = depression, cataracts
ECG = prolonged QT interval

Trousseau’s sign
Chvosteks sign

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47
Q

what is trousseau’s sign?

A

seen in hypocalcaemia

carpal spasm if the brachial artery occulded by inflating BP cuff to a pressure above their systolic BP

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48
Q

what is chvostek’s sign?

A

seen in hypocalcaemia

tapping over parotid causes facial muscles to twitch

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49
Q

causes of hypocalcaemia

A 
vitamin D deficiency (osteomalacia)
CKD
hypoparathyroidism 
pseudohypoparathyroidism
rhabdomyolysis 
magnesium deficiency 
massive blood transfusion
acute pancreatitis

contamination of blood samples with EDTA = falsely low calcium

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50
Q

mx of hypocalcaemia

A

IV replacement for severe hypocalcaemia - IV calcium gluconate 10ml of 10% solution over 10 mins

ECG monitoring

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51
Q

ECG changes seen in hyperkalaemia

A

Tall tented T waves
Small/loss of P waves
Widened QRS complex - leads to sinusoidal pattern
Asystole

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52
Q

Causes of hyperkalaemia

A 
AKI
Potassium sparing diuretics
ACEi
ARBs
Spironolactone 
Ciclosporin 
Heparin 
Metabolic acidosis
Addison's disease (primary adrenal insufficiency)
Rhabdomyolysis
Massive blood transfusion
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53
Q

Mx of hyperkalaemia

A

Stabilise cardiac membrane = IV CALCIUM GLUCONATE (this doesn’t lower serum K)

Short term shift of K from extracellular to intracellular space = INSULIN/DEXTROSE INFUSION & NEB SALBUTAMOL

Removal of K from body = CALCIUM RESONIUM (oral/enema), LOOP DIURETICS, DIALYSIS (haemofiltration/haemodialysis for patients with AKI & persistent hyperkalaemia)

Stop any exacerbating drugs
Treat underlying cause

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54
Q

classification of hyperkalaemia

A 
mild = 5.5 to 5.9
moderate = 6.0 to 6.4
severe = >6.5
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55
Q

how should you classify hypokalaemia?

A

with or without hypertension

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56
Q

causes of hypokalaemia with hypertension

A

cushings syndrome
conn’s syndrome (primary hyperaldosteronism)
liddle’s syndrome
11-beta hydroxyls deficiency - congenital adrenal hyperplasia

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57
Q

causes of hypokalaemia without hypertension

A 
diuretics
GI loss - diarrhoea and vomiting
renal tubular acidosis
bartter's syndrome - inherited cause of severe hypokalaemia
gitelman syndrome
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58
Q

symptoms of hypokalaemia

A

muscle weakness
hypotonia
predisposes to digoxin toxicity

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59
Q

ECG changes in hypokalaemia

A

U waves
small/absent t waves
prolonged PR interval
ST depression

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60
Q

causes of hypokalaemia with alkalosis

A

vomiting
thiazide and loop diuretics
cushings syndrome
conn’s syndrome (primary hyperaldosteronism)

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61
Q

causes of hypokalaemia with acidosis

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated DKA

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62
Q

mx of hypokalaemia

A

Check and replete Magnesium
Treat underlying cause

mild = oral KCl if no acidosis or ora potassium bicarbonate if there’s acidosis

moderate = oral KCl unless can’t have PO or there’s ECG changes

Severe = IV KCl. Do not give more than 20mmol/hr. concentration should not exceed 40mmol/L. Faster transfusion than 20mmol/hr through a central line in ICU. Need continuous cardiac monitoring and check K levels every 2-4 hrs

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63
Q

what are the causes of hyponatraemia?

A

URINARY SODIUM >20 MMOL/L

  • thiazide / loop diuretics
  • addison’s disease
  • diuretic stage of renal failure
  • SIADH
  • hypothyroidism

URINARY SODIUM <20 MMOL/L

  • diarrhoea
  • vomiting
  • sweating
  • burns
  • adenoma of rectum
  • HF
  • liver cirrhosis
  • nephrotic syndrome
  • IV dextrose
  • psychogenic polydipsia
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64
Q

complication of untreated hyponatraemia

A

cerebral oedema = brain herniation

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65
Q

symptoms of hyponatraemia

A

early = headache, lethargy, nausea, vomiting, dizziness, confusion, muscle cramps

late = seizures, coma, respiratory arrest

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66
Q

causes of hyponatraemia by volume status

A

hypovolemic hyponatraemia/clinically dehydrated: diuretic stage of renal failure, diuretics, Addisonian crisis

euvolemic hyponatraemia: SIADH

heart failure, liver failure, nephrotic syndrome

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67
Q

mx of hyponatraemia

A

hypovolaemic cause:
- 0.9% NaCl

euvolemic cause:
fluid restrict to 500-1000ml/day.
consider demeclocycline / vaptans

hypervolemic cause:
fluid restrict to 500-1000ml/day.
consider loop diuretic/vaptans

severe hyponatraemia with symptoms (<120mmol/L): HDU & give hypertonic saline (3% NaCl)

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68
Q

complications of mx of hyponatraemia

A

central pontine myelinolysis (osmotic demyelination syndrome)

don’t correct Na by more than 6-12 mmol/l in a 24 hour period

symptoms = dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma
(locked in syndrome)

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69
Q

causes of hypernatraemia

A

dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline

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70
Q

mx of hypernatraemia

A

a rate of no greater than 0.5 mmol/hour correction is appropriate = helps avoid cerebral oedema (seizures, coma and death)

IV 5% dextrose

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71
Q

causes of hyperlipidaemia

A 
Predominantly hypertriglyceridaemia =
diabetes mellitus (types 1 and 2)
obesity
alcohol
chronic renal failure
drugs: thiazides, non-selective beta-blockers, unopposed oestrogen
liver disease
predominantly hypercholesterolaemia =
nephrotic syndrome
cholestasis
hypothyroidism
familial hypercholesterolaemia
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72
Q

mx of hyperlipidaemia

A

for primary prevention:
- give to people with 10 year cardiovascular risk of >10% OR T1DM OR eGFR <60
ATROVASTATIN 20MG OD
(titrate up to 80mg if reduction in non-HDL cholesterol hasn’t fallen by at least 40%)

for secondary prevention:
- give if known IHD OR CVA OR PAD
ATROVASTATIN 80MG OD

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73
Q

How to assess 10 year cardiovascular risk

A

QRISK2

  • age
  • gender
  • ethnicity
  • postcode
  • BMI
  • smoker
  • family hx CAD
  • HTN, ?treated
  • total cholesterol:HDL cholesterol
  • DM
  • AF
  • Renal disease
  • RA
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74
Q

lifestyle advice for hyperlipidaemia

A

cardioprotective diet - reduce fats, wholegrain starches, 5 portion fruit/veg, 2 portions fish per week, 4-5 portions unsalted nuts/seeds/legumes per week

physical activity - 150 mins cardio per week

weight management

alcohol intake to <14 units per week

smoking cessation

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75
Q

what secretes parathyroid hormone and what is it secreted in response to?

A

chief cells in the parathyroid glands

PTH secreted in response to hypoclacaemia

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76
Q

What does PTH do?

A

Increases serum calcium by -

  • increasing osteoclast activity
  • increasing calcium absorption from gut
  • increasing calcium absorption from kidneys
  • increasing vitamin D activity = increases calcium absorption from intestines
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77
Q

symptoms of hyperparathyroidism

A

symptoms of hypercalcaemia = painful bones, kidney stones, abdominal groans and psychiatric moans

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78
Q

causes of primary hyperparathyroidism

A

tumour of the parathyroid glands = releases uncontrolled amounts of PTH

High PTH & high calcium

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79
Q

causes of secondary hyperparathyroidism

A

parathyroid gland hyperplasia in response to hypocalcaemia from low vitamin D/chronic renal failure

High PTH & low/normal calcium

80
Q

causes of tertiary hyperparathyroidism

A

cause of secondary hyperparathyroidism is treated but the enlarged parathyroid gland continues to produce large amounts of PTH

High PTH and high calcium

81
Q

mx of primary hyperparathyroidism

A

surgical removal of parathyroid gland tumour

82
Q

mx of secondary hyperparathyroidism

A

correct vitamin D deficiency or renal transplant for renal failure

83
Q

mx of tertiary hyperparathyroidism

A

surgically remove part of the parathyroid tissue

84
Q

cause of hyperthermia

A

malignant hyperthermia

85
Q

what is malignant hyperthermia?

A

condition often seen following administration of anaesthetic agents
characterised by hyperpyrexia and muscle rigidity
cause by excessive release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

86
Q

genetics associated with malignant hyperthermia

A

autosomal dominant inheritance

defects in a gene on chromosome 19 encoding the ryanodine receptor, which controls Ca2+ release from the sarcoplasmic reticulum

87
Q

causative agents of malignant hyperthermia

A

halothane
suxamethonium
antipsychotics - neuroleptic malignant syndrome

88
Q

ix for malignant hyperthermia

A

CK raised

contracture tests with halothane and caffeine

89
Q

mx of malignant hyperthermia

A

dantrolene - prevents Ca2+ release from the sarcoplasmic reticulum

90
Q

what classifies as hypothermia?

A

Mild hypothermia: 32-35°C

Moderate or severe hypothermia: < 32°C

91
Q

causes of hypothermia

A

Exposure to cold in the environment is the major cause
Inadequate insulation in the operating room
Cardiopulmonary bypass
Newborn babies.

92
Q

risk factors for hypothermia

A 
General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age
93
Q

symptoms of hypothermia

A

shivering
cold and pale skin. Frostbite occurs when the skin and subcutaneous tissue freeze, causing damage to cells.
slurred speech
tachypnoea, tachycardia and hypertension (if mild)
respiratory depression, bradycardia and hypothermia (if moderate)
confusion/ impaired mental state

94
Q

ix in hypothermia

A 
temperature
ECG
FBC & U&Es - high hb and haematocrit, platelets & WCC low due to sequestration in the spleen, can be hypokalaemic
BMs
Arterial blood gas
Coagulation factors
CXR
95
Q

ECG changes seen in hypothermia

A 
bradycardia
'J' wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
96
Q

what not to do when someone if hypothermic

A

Don’t put the person into a hot bath.
Don’t massage their limbs.
Don’t use heating lamps.
Don’t give them alcohol to drink.

97
Q

what causes primary hypoparathyroidism?

A

primary hypoparathyroidism:

- secondary to thyroid surgery

98
Q

symptoms of hypoparathyroidism and ECG changes

A

the symptoms of hypocalcaemia

  • tetany
  • perioral paraesthesia
  • Trousseau’s sign
  • Chvostek’s sign

ECG - prolonged QT interval

99
Q

ix for primary hypoparathyroidism

A

hypocalcaemia
high phosphate
low PTH

100
Q

mx for primary hypoparathyroidism

A

alfacalcidol

101
Q

what is pseudohypoparathyroidism?

A

the target cells are insensitive to PTH due to abnormality in a G protein

102
Q

what is pseudohypoparathyroidism associated with?

A

associated with low IQ, short stature, shortened 4th and 5th metacarpals

103
Q

ix for pseudohypoparathyroidism

A

low calcium
high phosphate
high PTH

measure urinary cAMP and phosphate following an infusion of PTH - in hypoparathyroidism this causes an increase in cAMP and phosphate levels, in pseudohypoparathyroidism type I cAMP and phosphate don’t increase, pseudohypoparathyroidism type II cAMP increases but phosphate doesn’t

104
Q

causes of hypothyroidism

A

Hashimoto’s thyroiditis - autoimmune

Iodine deficiency

carbimazole
propylthiouracil
radioactive iodine
thyroid surgery

Lithium
Amiodarone

secondary hypothyroidism:

  • tumours in pituitary gland
  • infection in pituitary gland
  • vascular e.g. sheehan syndrome
  • radiation to pituitary gland
105
Q

symptoms of hypothyroidism

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions, ascites)
Heavy or irregular periods
Constipation
106
Q

symptoms of hypothyroidism

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions, ascites)
Heavy or irregular periods
Constipation
Decreased deep tendon reflexes
carpal tunnel syndrome
occasionally - hoarse voice
107
Q

Ix for hypothyroidism

A

primary hypothyroidism = low T3 and T4, high TSH

secondary hypothyroidism = low T3, T4, TSH

108
Q

mx of hypothyroidism

A

levothyroxine (synthetic T4 that metabolises to T3 in the body)

titrate up dose until TSH level normal

measure TSH monthly until stable then less frequently

check TSH 8-12 weeks after dose change

109
Q

when should patients get a lower dose of levothyroxine?

A

elderly patients

IHD

110
Q

when should you increase a patients dose of levothyroxine?

A

in women who get pregnant

111
Q

SEs of levothyroxine

A

hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation

112
Q

interactions of levothyroxine

A

iron
calcium carbonate

(they reduce the absorption of levothyroxine so give at least 4 hours apart)

113
Q

mx of obesity

A

1 diet / exercise
2 medical:
- orlistat = pancreatic lipase inhibitor (causes faecal urgency/incontinence and flatulence)
3 surgical:
- laparoscopic adjustable gastric banding
- sleeve gastrectomy
- intragastric balloon
- biliopancreatic diversion with duodenal switch
- roux-en-Y gastric bypass surgery

114
Q

what are the effects of a pituitary tumour?

A
  • large ones can compress the optic chiasm = bitemporal hemianopia (loss of outer half of vision)
  • acromegaly (excessive GH)
  • hyperprolactinaemia
  • cushings disease (high cortisol)
  • thyrotoxicosis
115
Q

Causes of hyperthyroidism

A

primary hyperthyroidism -

  • Grave’s disease (autoimmune condition) - most common cause
  • toxic multi nodular goitre
  • solitary toxic thyroid nodule
  • thyroiditis - e.g. de quervains, hashimotos, postpartum and drug induced

secondary hyperthyroidism -
- TSH secreting pituitary tumour

amiodarone
over treatment with levothyroxine

116
Q

what is grave’s disease?

A

Autoimmune condition
TSH receptor antibodies cause a primary hyperthyroidism

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

most common cause of hyperthyroidism

117
Q

What is toxic multinodular goitre?

A

Also known as Plummer’s disease

Nodules develop on the thyroid gland - act independently of the normal feedback mechanism & continuously produce excessive thyroid hormone

118
Q

symptom specific to graves disease

A

Exophthalmos = bulging of eyeball

Pretibial myxoedema = deposits of mucin on anterior of leg - waxy discoloured oedematous appearance of skin (is a reaction to the TSH antibodies)

Diffuse goitre (without nodules)

119
Q

symptom specific to graves disease

A

Exophthalmos = bulging of eyeball

ophthalmoplegia

Pretibial myxoedema = deposits of mucin on anterior of leg - waxy discoloured oedematous appearance of skin (is a reaction to the TSH antibodies)

Diffuse goitre (without nodules)

digital clubbing

120
Q

symptoms specific to toxic multi nodular goitre

A

Goitre with firm nodules
Most patients are aged over 50
Second most common cause of thyrotoxicosis (after Grave’s)

121
Q

what is de quervain’s thyroiditis?

A

a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism

hyperthyroid phase followed by hypothyroid phase

122
Q

mx of de quervain’s thyroiditis?

A

self limiting condition
NSAIDs
beta-blockers for symptomatic relief of hyperthyroid

123
Q

what is thyrotoxic crisis/thyroid storm?

A

a more severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium

124
Q

what is Thyrotoxicosis

A

an abnormal and excessive quantity of thyroid hormone in the body.

125
Q

mx of thyrotoxic crisis

A

admit to hospital
monitoring
fluid resuscitation
anti-arrhythmic medication beta blockers

126
Q

mx of hyperthyroidism

A

1st = Carbimazole - can do titration block or block and replace (give levothyroxine too)

2nd = propylthiouracil

3rd = radioactive iodine

beta blockers for heart palpitations

thyroidectomy + levothyroxine

127
Q

how is Carbimazole used?

A

used in the management of thyrotoxicosis.

It is typically given in high doses for 6 weeks until the patient becomes euthyroid before being reduced.

blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

128
Q

side effects of Carbimazole

A

agranulocytosis

crosses the placenta, but may be used in low doses during pregnancy

129
Q

risks associated with propylthiouracil

A

severe hepatic reaction - including death

130
Q

strict rules when using radioactive iodine to treat hyperthyroidism

A

Must not be pregnant and are not allowed to get pregnant within 6 months

Must avoid close contact with children and pregnant women for 3 weeks (depending on the dose)

Limit contact with anyone for several days after receiving the dose

131
Q

how does radioactive iodine work in hyperthyroidism?

A

Treatment with radioactive iodine involves drinking a single dose of radioactive iodine.

This is taken up by the thyroid gland and the emitted radiation destroys a proportion of the thyroid cells.

This reduction in functioning cells results in a decrease of thyroid hormone production and thus remission from the hyperthyroidism.

Remission can take 6 months and patients can be left hypothyroid afterwards and require levothyroxine replacement.

132
Q

what autoantibodies are present in graves disease?

A

TSH receptor stimulating antibodies (90%)

anti-thyroid peroxidase antibodies (75%)

133
Q

what is acromegaly?

A

++ growth hormone

GH is produced by the anterior pituitary gland

134
Q

cause of acromegaly

A

pituitary adenoma that secretes unregulated amounts of GH

rarely caused by lung or pancreatic cancers that secrete GH

135
Q

presentation of acromegaly

A

Space Occupying Lesion:

  • Headaches
  • Visual field defect (“bitemporal hemianopia”)

Overgrowth of tissues:

  • Prominent forehead and brow (“frontal bossing”)
  • Large nose
  • Large tongue (“macroglossia”)
  • Large hands and feet
  • Large protruding jaw (”prognathism”)
  • Arthritis from imbalanced growth of joints

GH can cause organ dysfunction:

  • Hypertrophic heart
  • Hypertension
  • Type 2 diabetes
  • Colorectal cancer

Symptoms suggesting active raised growth hormone:

  • Development of new skin tags
  • Profuse sweating
136
Q

Ix for acromegaly

A

Insulin like growth factor 1 (IGF-1)

Oral glucose tolerance test while measuring GH - high glucose normally suppress GH

MRI brain - pituitary tumour

Ophthalmology referral for visual field testing

137
Q

Tx of acromegaly

A

trans-sphenoidal removal of the pituitary tumour

medications used to block GH:

  • pegvisomant
  • somatostatin analogues e.g. ocreotide
  • dopamine agonist e.g. bromocriptine
138
Q

how does the renin-angiotensin system work?

A

juxtaglomerular cells in the afferent arterioles in the kidney sense the BP
if there’s low BP, the kidney secrete renin
the liver then secretes angiotensinogen
renin converts angiotensinogen to angiotensin I
angiotensin I is converted to angiotensin II in the lungs with the help of angiotensin converting enzyme (ACE)
angiotensin II stimulates the release of aldosterone from the adrenal glands

139
Q

what does aldosterone do?

A

it is released by the adrenal glands

acts on the kidney to:

  • increase Na reabsorption from the distal tubule
  • increase potassium secretion from the distal tubule
  • increase hydrogen secretion from the collecting ducts
140
Q

what is primary hyperaldosteronism?

A

Conn’s syndrome

Adrenal glands are directly responsible for producing too much aldosterone
Low serum renin

141
Q

causes of primary hyperaldosteronism

A 
Adrenal adenoma - that secretes aldosterone
Bilateral adrenal hyperplasia 
Familial hyperaldosteronism 
Adrenal carcinoma (rare)
142
Q

what is secondary hyperaldosteronism

A

excessive renin stimulates the adrenal glands to produce more aldosterone

serum renin is high

143
Q

causes of secondary hyperaldosteronism

A

high renin happens when blood pressure to the kidneys is disproportionately lower than blood pressure to the rest of the body

renal artery stenosis
renal artery occlusion
heart failure

144
Q

Ix for hyperaldosteronism

A

do a renin / aldosterone ratio

Low renin and high aldosteronism = conn’s syndrome (primary hyperaldosteronism)

High renin and high aldosterone = secondary hyperaldosteronism

Blood pressure - HTN
Hypokalaemia
Blood gas - alkalosis
CT/MRI for adrenal tumour
Renal doppler US, CT angiogram or MRA for renal artery stenosis or obstruction
145
Q

Mx of hyperaldosteronism

A

Aldosterone antagonists:

  • Eplerenone
  • spironolactone

Treat underlying cause:

  • surgical removal of adenoma
  • Percutaneous renal artery angioplasty via the femoral artery
146
Q

what is the most common cause of secondary hypertension

A

hyperaldosteronism

if a patients HTN isn’t responding to antihypertensives, do a renin:aldosterone ratio

147
Q

what is a pheochromocytoma?

A

a tumour of chromatin cells in the adrenal medulla that secrete an unregulated amount of adrenaline

the adrenaline tends to be secreted in bursts, giving periods of worse symptoms followed by settled periods

148
Q

what is the cause of 25% of pheochromocytomas?

A

multiple endocrine neoplasia type 2 (MEN 2)

149
Q

what is the 10% rule used to describe pheochromocytoma?

A

10% bilateral
10% cancerous
10% outside the adrenal gland

150
Q

how is a pheochromocytoma diagnosed

A

24 hour urine catecholamines

plasma free metanephrines

151
Q

why are 24 hour urine catecholamines measured for pheochromocytoma?

A

adrenaline is a catecholamine

serum catecholamines will naturally fluctuate throughout the day so instead measure them in the urine over 24 hours

can see how much adrenaline the tumour is secreting over the 24 hours

152
Q

Why are plasma free metanephrines measured for pheochromocytomas?

A

adrenaline has a short half life in the blood

metanephrines are the breakdown products of adrenaline - have a longer half life

the levels of metanephrines are less prone to dramatic fluctuations

153
Q

symptoms of pheochromocytoma

A 
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal atrial fibrillation
154
Q

Mx of pheochromocytoma

A 
Alpha blockers (i.e. phenoxybenzamine)
Beta blockers once established on alpha blockers
Adrenalectomy to remove tumour is the definitive management - need to have symptoms medically controlled before surgery to reduce anaesthetic risk
155
Q

What is SiADH

A

there’s inappropriately large amounts of ADH

156
Q

What does ADH do and where is it secreted from?

A

secreted by posterior pituitary gland

stimulates water reabsorption from the collecting ducts in the kidneys

157
Q

Electrolyte disturbances and urine changes caused by SiADH

A

hyponatraemia due to excessive ADH causing lots of water reabsorption in the collecting ducts

get a euvolemic hyponatraemia - because the reabsorption is not significant enough to cause fluid overload

urine gets more concentrated by kidneys as more water is reabsorbed - high urine osmolality and high urine sodium

158
Q

symptoms of SiADH

A 
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia can cause seizures and reduced consciousness
159
Q

causes of SiADH

A

Post-operative from major surgery
Infection, particularly atypical pneumonia and lung abscesses
Head injury
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
Malignancy, particularly small cell lung cancer
Meningitis

160
Q

Diagnosis of SiADH

A

Diagnosis of exclusion (can’t measure ADH directly)

Euvolaemia on examination
U&Es = hyponatraemia
Urine sodium and osmolality high

Do CXR to look for lung abscess/cancer/pneumonia

Exclude other causes:

  • short synacthen test
  • no diuretic use
  • no diarrhoea, vomiting, burns, fistula, excessive sweating
  • no excessive water intake
  • no CKD or AKI
161
Q

Mx of SiADH

A

treat underlying cause or stop medications causing it

correct sodium slowly by no more than 10mmol/l increase in sodium in 24 hours (reduces risk of central pontine myelinolysis)

162
Q

Mx of SiADH

A

treat underlying cause or stop medications causing it

correct sodium slowly by no more than 10mmol/l increase in sodium in 24 hours (reduces risk of central pontine myelinolysis)

fluid restriction (500-1l)

Tolvaptan (a vaptan) - ADH receptor blockers

Demeclocycline - tetracycline abx that inhibits ADH

163
Q

Where is insulin produced?

A

beta cells in the islets of langerhans in the pancreas

164
Q

what is T1DM?

A

a disease where the pancreas stops being able to produce insulin.
When there is no insulin being produced, the cells of the body cannot take glucose from the blood and use it for fuel. Therefore the cells think the body is being fasted and has no glucose supply. Meanwhile the level of glucose in the blood keeps rising, causing hyperglycaemia.

165
Q

Causes of T1DM

A

Unknown cause
Some theories:
- Genetic component
- triggered by a virus: coxsackie B / enterovirus

166
Q

presentation of DKA

A 
Hyperglycaemia
Dehydration
Ketosis
Metabolic acidosis (with a low bicarbonate)
Potassium imbalance

The patient will therefore present with symptoms of these abnormalities:

Polyuria
Polydipsia
Nausea and vomiting
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered Consciousness
They may have symptoms of an underlying trigger (i.e. sepsis)
167
Q

Pathology of DKA

A
  1. Ketoacidosis - ketogenesis to make fuel
  2. dehydration - hyperglycaemia causes glucose to be filtered into urine so water is drawn into urine too
  3. potassium imbalance - hyperkalaemia as insulin draws K into cells, when insulin tx starts: sudden hypokalaemia
168
Q

Diagnosis of DKA

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

169
Q

Mx of DKA

A

FIG PICK

F - IV fluids with NaCl
I - INsulin - fixed rate insulin infusion (act rapid 0.1 unit/kg/hour)
G - glucose - add dextrose when BM <14

P - potassium (closely monitor)
I - infection (treat)
C - chart fluid balance
K - ketones (monitor blood ketones / bicarbonate)

Establish patient on normal subcut insulin regime prior to stopping insulin and fluid infusion

Don’t infuse K faster than 10 mmol/hr

170
Q

Long term management of T1DM

A

Patient education about:

  • Subcutaneous insulin regimes
  • Monitoring daily carbohydrate intake
  • Monitoring BMs - waking, before each meal and before bed
  • Monitoring & managing complications

Insulin:

  • Background, long acting insulin once daily + short acting insulin 30 mins before a meal
  • rotate injection sites to avoid lipodystrophy
171
Q

short term complications of T1DM

A

Hypoglycaemia

Hyperglycaemia (DKA)

172
Q

Typical symptoms of hypoglycaemia

A 
tremor
sweating 
irritability 
dizziness
pallor

severe: reduced LOC, coma and death

173
Q

Tx of hypoglycaemia

A

Rapid acting glucose (10-20g in liquid, gel or tablet form) / glycogen + slow acting carbohydrate if able to swallow

Reduced GCS = IM glucagon / IV dextrose (20% 125ml)

174
Q

Long term complications of T1DM

A

Macrovascular Complications:

  • Coronary artery disease is a major cause of death in diabetics
  • Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
  • Stroke
  • Hypertension

Microvascular Complications:

  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis

Infection Related Complications:

  • UTIs
  • Pneumonia
  • Skin and soft tissue infections, particularly in the feet
  • Fungal infections, particularly oral and vaginal candidiasis
175
Q

Monitoring of T1DM

A

HbA1C (to count glycerinated Hb) - check every 3-6 months

Capillary BMs

Flash glucose monitoring e.g. free style libre

176
Q

What happens in T2DM?

A

Repeated exposure to glucose and insulin makes the cells in the body become resistant to the effects of insulin.

It requires more insulin to produce a response from the cells and get them to take up and use glucose. 
The pancreas (beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less.

A continued onslaught of glucose on the body in light of insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia.

177
Q

Risk factors for T2DM

A

Non-Modifiable

Older age
Ethnicity (Black, Chinese, South Asian)
Family history

Modifiable

Obesity
Sedentary lifestyles
High carbohydrate (particularly refined carbohydrate) diet

178
Q

Presentation of T2DM

A 
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine (on dipstick)
179
Q

Ix for T2DM

A

HbA1C
Oral glucose tolerance test - test fasting plasma glucose have a 75mg glucose drink then measure plasma glucose 2 hrs later

180
Q

What is pre-diabetes?

A

An indication the patient is heading towards diabetes, need education on lifestyle + no medications.

HbA1c – 42-47 mmol/mol

Impaired fasting glucose – fasting glucose 6.1 – 6.9 mmol/l

Impaired glucose tolerance – plasma glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT

181
Q

What are the criteria for the diagnosis of T2DM?

A

HbA1c > 48 mmol/mol

Random Glucose > 11 mmol/l

Fasting Glucose > 7 mmol/l

OGTT 2 hour result > 11 mmol/l

182
Q

Mx for T2DM

A 
Patient education 
Diet modification 
Exercise weight loss
stop smoking 
treat HTN/lipids

Medical mx:
- 1st line = metformin
- 2nd line = add sulfonylura / pioglitazone / DPP-4 inhibitor / SGLT-2 inhibitor
- 3rd line = triple therapy with metformin and 2 of the second line drugs
OR metformin + insulin

183
Q

Treatment targets for T2DM

A

48 mmol/mol for new type 2 diabetics

53 mmol/mol for diabetics that have moved beyond metformin alone

184
Q

What is metformin, how does it work and what are its side effects?

A

A biguanide

Increases insulin sensitivity and decreases liver production of glucose

Side effects:
diarrhoea and abdo pain
lactic acidosis

DOES NOT CAUSE hypoglycaemia

185
Q

What is pioglitazone, how does it work and what are its side effects?

A

A thiazolidinedione

Increases insulin sensitivity and decreases liver production of glucose

Side effects:
weight gain
fluid retention 
anaemia
HF
Increased risk of bladder ca

DOES NOT CAUSE hypoglycaemia

186
Q

Give an example Sulfonylurea, how it works and the side effects

A

Gliclazide

stimulates insulin release from the pancreas

Side effects
Weight gain
HYPOGLYCAEMIA
increased risk of CVD and MI

187
Q

Give an example DPP-4 inhibitor, how it works and the side effects

A

Sitagliptin

Works by increasing GLP-1 activity

Side effects
GI upset
Symptoms of URTI
Pancreatitis

188
Q

Give an example GLP-1 mimetic, how it works and the side effects

A

Exenatide (subcutaneous injection)

Increase insulin secretions, inhibit glucagon production and slow absorption in GI tract

Side effects
GI upset
Weight loss
Dizziness
Low risk of hypoglycaemia
189
Q

What are example SGLT-2 inhibitors, how do they work and what are their side effects?

A

empagliflozin, dapagliflozin

cause glucose to be excreted in the urine

Side effects
Glucoseuria 
Increased UTIs
Weight loss
DKA
190
Q

What is a hyperosmolar hyperglycaemic state?

A

Medical emergency

Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies.

191
Q

Pathology of HHS

A

Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium

Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.

Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.

192
Q

Who gets HHS?

A

elderly with T2DM

ncidence in younger adults is increasing

can be the initial presentation of T2DM.

193
Q

Symptoms of HHS

A

General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia

194
Q

Criteria for diagnosing HHS

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)
195
Q

Mx for HHS

A
  1. Normalise the osmolality (gradually with NaCl)
    the serum osmolality is the key parameter to monitor
    if not available it can be estimated by 2 * Na+ + glucose + urea
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)

Finals Revision (18 decks)

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