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FCM Matrix > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Signs of diabetes mellitus

A

Polyuria
Polydipsia
weight loss

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2
Q

What are the types of diabetes?

A

T1DM = an absolute insulin deficiency causes persistent hyperglycaemia. (autoimmune)

T2DM = a combination of insulin resistance/insensitivity and insulin deficiency

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3
Q

Diagnostic criteria for diabetes

A

Symptomatic:
1. fasting glucose > 7.0 mmol/l

  1. random glucose > 11.1 mmol/l (or after 75g oral glucose tolerance test)

HbA1c > 48 mmol/mol

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4
Q

4 main ways to check blood glucose

A
  1. a finger-prick bedside glucose monitor
  2. a one-off blood glucose.
  3. a HbA1c.
  4. a glucose tolerance test.
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5
Q

Management of T1DM

A

Insulin

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6
Q

Management of T2DM

A
  1. Metformin
  2. Sulfonylureas, gliptins + pioglitazone
  3. Insulin
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7
Q

Signs and symptoms of DKA

A

Common in new diagnosis T1DM:

  1. abdominal pain
  2. polyuria, polydipsia, dehydration
  3. deep hyperventilation
  4. acetone-smelling breath (‘pear drops’ smell)
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8
Q

When should HbA1c be monitoried for T1DM?

A

Every 3-6 months

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9
Q

What is the HbA1C targets for T2DM?

A

Lifestyle = 48
Lifestyle + metformin = 48
Lifestyle + any drug cause hypoglycaemia (sulfonylurea) = 53

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10
Q

Diabetes Mellitus sick day rules

A
  1. Increase frequency of blood glucose monitoring to four hourly or more frequently
  2. Encourage fluid intake aiming for at least 3 litres in 24hrs
  3. If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
  4. It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
  5. Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
  6. Continue taking medication
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11
Q

What is Hashimoto’s thyroiditis

A

autoimmune disorder of the thyroid gland

typically associated with hypothyroidism although there may be a transient thyrotoxicosis in the acute phase

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12
Q

Clinical features of Hashimoto’s thyroiditis

A
  • hypo sx
  • goitre
  • anti-TPO and anti-thyroglobulin antibodies
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13
Q

What may trigger thyroid storm

A
  • surgery
  • trauma
  • infection
  • iodine load e.g CT Contrast
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14
Q

Management of thyroid storm

A

symptomatic tx (paracetemol), treat underlying, beta blockers

  • anti-thyroid drugs: e.g. propylthiouracil
  • Lugol’s iodine
  • dexamethasone (blocks conversion of T3 to T4)
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15
Q

What is Subacute (De Quervain’s) thyroiditis

A

thought to occur following viral infection and typically presents with hyperthyroidism

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16
Q

Investigations for Subacute (De Quervain’s) thyroiditis

A

thyroid scintigraphy: globally reduced uptake of iodine-131

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17
Q

Management of Subacute (De Quervain’s) thyroiditis

A

analgesia, self-limiting

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18
Q

Diagnostic critieria for DKA

A
  1. glucose > 11 mmol/l or known diabetes mellitus
  2. pH < 7.3
  3. bicarbonate < 15 mmol/l
  4. ketones > 3 mmol/l or
  5. urine ketones ++ on dipstick
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19
Q

Management of DKA

A
  1. Fluid replacement
  2. Insulin
  3. Correction of electrolyte disturbance
  4. Long-acting insulin
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20
Q

What is hypoglycaemia

A

blood glucose concentrations <3.3 mmol/L

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21
Q

Symptoms of hypoglycaemia

A
  • Sweating
  • Shaking
  • Hunger
  • Anxiety
  • Nausea
  • weakness
  • vision change
  • confusion
  • dizziness
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22
Q

Symptoms of severe hypoglycaemia

A
  • convulsion

- coma

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23
Q

Management of hypoglycaemia

A
  1. in the community:
    - oral glucose 10-20g should be given in liquid, gel or tablet form
    - Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
    - A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
  2. in a hospital setting:
    - If the patient is alert, a quick-acting carbohydrate may be given (as above)
    - If the patient is unconscious or unable to swallow, subcut or IM glucagon
    - Alternatively, IV 20% glucose solution through a large vein
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24
Q

Define hypercholesterolaemia

A

Total cholesterol > 7.5 mmol

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25
Q

Management of hypercholesterolaemia

A

Familial = high dose statin

Atorvastatin 80 mg

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26
Q

Management of hypertriglyceridaemia

A
  • Statins (e.g atorvastatin 10mg)/Fenofibrates (initially 200mg OD).
  • Qrisk score would also be done to determine risk of 10 years cardiac related mortality.
  • Weight loss/dietary advice
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27
Q

What is Addison’s disease?

A

Reduced cortisol + aldosterone produced

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28
Q

Features of Addison’s disease

A
  1. lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
  2. hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension,
  3. hypoglycaemia
    hyponatraemia and hyperkalaemia may be seen
  4. crisis: collapse, shock, pyrexia
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29
Q

Definitive investigation for Addison’s disease

A

ACTH Test (Short synacthen test)

Other:
9 am Serum Cortisol
1. > 500 nmol/l = Addison’s very unlikely
2. < 100 nmol/l = abnormal
3. 100-500 nmol/l = ACTH stimulation indicated

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30
Q

Management of Addison’s Disease

A

Combination of:

  1. hydrocortisone
  2. fludrocortisone
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31
Q

What is Addison’s crisis?

A

Acute exacerbation of chronic insufficiency

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32
Q

Causes of Addisonian crisis

A
  1. Sepsis or surgery
  2. adrenal haemorrhage
  3. steroid withdrawal
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33
Q

Management of Addisonian Crisis

A
  1. hydrocortisone 100 mg im or iv
  2. 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
  3. continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
  4. oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
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34
Q

Clinical features of hypothyroidism

A
  • Weight gain
  • Lethargy
  • Cold intolerance
  • dry skin, brittle hair
  • constipation
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35
Q

What is the most common cause of hypothyroidism

A

Hashimoto’s thyroiditis

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36
Q

What are the expected TFT results in primary hypothyroidism

A

High TSH, Low T4

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37
Q

What are the expected TFT results in Secondary hypothyroidism

A

Low TSH, Low T4

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38
Q

How is hypothyroidism classified

A

Primary = problem with thyroid gland itself

Secondary = disorder with pituitary gland

Congenital

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39
Q

Management of hypothyroidism

A

Levothyroxine

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40
Q

How long after levothyroxine dose change should TFT be repeated?

A

8-12 weeks

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41
Q

What is the most common cause of thyrotoxicosis

A

Graves’ disease

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42
Q

Epidemiology of Graves Disease

A

women 30-50 yo

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43
Q

Clinical signs of Graves disease

A
  • exophthalmos

- pretibial myxoedema

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44
Q

Which antibodies can help distinguish Graves disease from other forms of hyperthryoidism?

A

TSH Receptor stimulating antibodies

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45
Q

Management of Graves disease

A

propanolol to control symptoms

carbimazole is uncontrolled with propanolol

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46
Q

What is Graves Disease

A

autoimmune condition leading to overactive thyroid glands

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47
Q

What is the typical description of a patient with hyperparathyroidism in exam questions?

A

elderly females with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level

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48
Q

How do most patients with hyperparathyroidism present?

A

80% are asymptomatic

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49
Q

Mnemonic used to remember symptomatic features of primary hyperparathyroidism

A

bones, stones, abdominal groans and psychic moans

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50
Q

What are the expected blood results in primary hyperparathyroidism?

A

normal or raised PTH

raised Ca , low Phosphate

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51
Q

Characteristic Xray finding of hyperparathyroidism

A

pepperpot skull

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52
Q

Definitive management of primary hyperparathyroidism

A

total parathyroidectomy

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53
Q

What may be given to patients with hyperparathyroidism who are not suitable for surgical management

A

cinacalcet

- a calcimimetic which ‘mimics’ the action of calcium on tissues

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54
Q

What is hyperparathyroidism

A

condition in which one or more of the parathyroid glands makes too much PTH leading to excess calcium production

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55
Q

Most common cause of hyperparathyroidism

A

solitary adenoma

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56
Q

What are the expected blood results in secondary hyperparathyroidism?

A

High PTH

Low/normal Ca, High Phosphate

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57
Q

Cause of secondary hyperparathyroidism

A

CKD = low calcium = PTH Hyperplasia

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58
Q

What is hypoparathyroidism?

A

inadequate PTH activity = low calcium, high phosphate

59
Q

What is Tertiary hyperparathyroidism?

A

High PTH = normal or high Ca = normal of low Phosphate

HIGH ALP

60
Q

What is the cause of Tertiary hyperparathyroidism?

A

ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder

61
Q

Treatment for Tertiary hyperparathyroidism?

A

Allow 12 months to elapse following transplant as many cases will resolve

otherwise parathyroidectomy or excision of affected gland

62
Q

Main sx of hypoparathyroidism

A

secondary to hypocalcaemia

  • Tetany: muscle twitching, cramping, spasm
  • perioral paraesthesia
63
Q

Tx hypoparathyroidism

A

alfacalcidol

64
Q

Symptoms of thyroid cancer

A
  • a painless lump in neck
  • lymphadenopathy
  • unexplained hoarseness that does not get better after a few weeks.
  • persistent sore throat
  • difficulty swallowing
65
Q

What is Cushing’s?

A

Glucocorticoid excess –> increased cortisol

66
Q

What tests confirm Cushing’s?

A

1st line = overnight dexamethasone suppression test
In Cushing’s syndrome - you do not have their morning cortisol spike suppressed

24 hr urinary free cortisol

67
Q

Symptoms of Cushing’s syndrome

A
  1. Moon Face”, “buffalo hump”, truncal obesity
  2. Weight gain
  3. Gonadal dysfunction (Oligomenorrhea and infertility, decreased libido, hirsutism, erectile dysfunction)
  4. Mood change - emotional lability, anxiety, depression
  5. Proximal muscle weakness
  6. Thirst and polyuria (due to hyperglycaemia)
68
Q

Interpretation of high-dose dexamethasone test

A
  1. Normal Cortisol + Supressed ACTH = Adrenal cause
  2. Low Cortisol + Low ACTH = Cushing’s disease
  3. Normal Cortisol + high ACTH = Ectopic ACTH
69
Q

Management of Cushing’s disease

A

Depends on underlying cause:

  1. Cushing’s Disease
    - -> surgical removal of pituitary adenoma +/- bilateral adrenalectomy, radiotherapy
    - -> exogenous medication (steroids)
  2. Adrenal Adenoma
    - -> bilateral adrenalectomy
  3. Adrenal Carcinoma
    - -> Adrenalectomy, radiotherapy, chemotherapy
  4. Ectopic ACTH
    - -> Surgical removal if tumour located, radiotherapy, chemotherapy
70
Q

What is Gynaecomastia?

A

Abnormal amount of breast tissue in males

-> caused by an increased oestrogen: androgen ratio.

71
Q

Management of Gynaecomastia

A
  1. Refer if red flags (unilateral, hard/irregular tissue, fixed mass, pain, axillary LAD)
  2. Treat underlying cause
  3. Tamoxifen = pain in acute gynaecomastia
    - -> Has anti-oestrogen effect
  4. Possible surgical removal of breast tissue
72
Q

Causes of hyponatraemia

A

Sodium depletion

  • diuretics
  • Addisons disease
  • renal failure
  • diarrhoea
  • vomiting
  • burns

Water excess

  • secondary hyperaldosteronism
  • nephrotic syndrome
73
Q

Complication of severe hyponatraemia if left untreated

A

cerebral oedema

74
Q

What is used to treat acute hyponatraemia with severe symptoms?

A

Hypertonic saline (NaCl)

75
Q

Euvolaemic causes of hyponatraemia

A
  • SIADH (impaired water excretion caused by the inability to suppress ADH secretion)
  • Hypothyroidism (decreased rate of free water excretion)
76
Q

Tx of chronic hyponatraemia if hypovolaemic cause

A

Hypertonic saline (NaCl)

77
Q

Tx of chronic hyponatraemia if euvolaemic cause

A

fluid restrict (500-1000ml/day)

  • consider demeclocycline
  • consider Vasopressin receptor antagonists (Vaptans))
78
Q

Tx of chronic hyponatraemia if hypervolaemic cause

A

fluid restrict to 500–1000 mL/day

  • consider loop diuretics
  • consider Vasopressin receptor antagonists (Vaptans)
79
Q

When should Vaptans be avoided

A

hypovolaemic hyponatraemia

- may precipitate hypotension and renal failure

80
Q

Causes of hypernatraemia

A

dehydration
osmotic diuresis e.g.
diabetes insipidus
excess IV saline

81
Q

Complication of rapidly correcting hypernatraemia

A

cerebral oedema = coma, seizure, death

82
Q

Treatment of hypovolaemic hypernatraemia

A

IV Saline

83
Q

Treatment of hypervolaemic hypernatraemia

A

diuretics and 5% dextrose

84
Q

Investigations in hypo/hypernatraemia

A
  • serum osmolality

- serum electrolytes, urea, creatinine, and glucose

85
Q

Causes of hypomagnasaemia

A 
drugs
diuretics
PPIs
total parenteral nutrition
diarrhoea
alcohol
hypokalaemia
hypercalcaemia
metabolic disorders
86
Q

Signs and sx of hypomagnasaemia

A

similar to hypercalcaemia

  • tetany
  • seizures
  • arrhythmias
87
Q

Tx of hypomagnasaemia

A

IV Magnesium

Oral Mg salts if <0.4

88
Q

Features of hypocalcaemia

A

tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts

89
Q

ECG finding in hypocalcaemia

A

prolonged QT interval

90
Q

What is Trousseau’s sign

A

sign of hypocalcaemia where carpal spasm occurs if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic

91
Q

Causes of hypocalcaemia

A
  • vitamin D deficiency (osteomalacia)
  • CKD
  • hypoparathyroidism
  • Acute pancreatitis
92
Q

What might cause falsely low Ca levels

A

contamination of blood samples with EDTA

93
Q

Management of acute, severe hypocalcaemia

A

IV calcium gluconate

94
Q

ECG finding in hypercalcaemia

A

shortened QT interval

95
Q

Sx of hypercalcaemia

A

‘bones, stones, groans and psychic moans’

96
Q

2 main causes of hypercalcaemia

A

Primary hyperparathyroidism

Malignancy

97
Q

Initial tx of hypercalcaemia

A

rehydration with normal saline

98
Q

Which drugs may be used to treat hypercalcaemia

A
  • bisphosphonates
  • calcitonin
  • Loop diuretics (CAUTION as may worsen electrolyte derangement)
99
Q

What is Galactorrhoea?

A

Milky secretion from the breasts , not due to breastfeeding.

100
Q

Cause of Galactorrhoea

A

Excess prolactin due to drugs or physiological factors:

  • prolactinoma
  • pregnancy
  • acromegaly
  • primary hypothyroidism
  • PCOS
101
Q

Features of excess prolactin

A
  1. men: impotence, loss of libido, galactorrhoea

2. women: amenorrhoea, galactorrhoea

102
Q

Investigations for Galactorrhoea

A
  • Prolactin, TFTs, U&Es, LFTs

+/- hCG

  • MRI (prolactinoma)
103
Q

Management of Galactorrhoea

A
  • Rule out serious pathology – breast cancer
  • Treat underlying cause: hypothyroidism, prolactinomas
  • If the causes cannot be addressed:
    1. Dopamine agonist – bromocriptine or cabergoline
    2. Hormone treatment:
  • -> men = testosterone
  • -> women = oestrogen
104
Q

What is lactose intolerance?

A

An enzyme deficiency, rather than lactose allergy, which is an IgE-mediated reaction

105
Q

Symptoms of lactose intolerance

A

Gas build-up:

  • Bloating
  • flatulence
  • Abdominal discomfort

Acidic and osmotic effects of undigested lactose:

  • Loose watery stool
  • Perianal itching due to acidic stools
106
Q

Diagnosis of lactose intolerance

A

Can be made on clinical features alone

Trial of 2-week period of strict lactose -free diet

No single diagnostic test:

  • A lactose tolerance test
  • Breath hydrogen test
107
Q

Management of lactose intolerance

A

Avoid milk and dairy products

108
Q

What is Phaeochromocytoma?

A

Catecholamine-secreting tumour formed by chromaffin cell within the adrenal medulla
–> Catecholamine = norepinephrine epinephrine

109
Q

Symptoms of Phaeochromocytoma

A

Triad:

  1. headaches
  2. palpitations and tachycardia
  3. sweating

Other:

  • hypertension
  • anxiety
110
Q

Investigations for Phaeochromocytoma

A

24 hr urinary collection of metanephrines (sensitivity 97%*)

111
Q

Management of Phaeochromocytoma

A

Surgery is the definitive management.

Stabilise pt first with:

  1. alpha-blocker (e.g. phenoxybenzamine), given before a
  2. beta-blocker (e.g. propranolol)
112
Q

What is Acromegaly?

A

Excessive secretion of growth hormone due to pituitary adenoma.

Acromegaly causes an overgrowth of all organ systems, bones, joints and soft tissues.

113
Q

Features of Acromegaly

A
  1. coarse facial appearance, spade-like hands, increase in shoe size
  2. large tongue, prognathism, interdental spaces
  3. excessive sweating and oily skin: caused by sweat gland hypertrophy
  4. features of pituitary tumour = hypopituitarism, headaches, bitemporal hemianopia
  5. raised prolactin in 1/3 of cases → galactorrhoea
114
Q

1st line investigation for Acromegaly

A

Serum IGF-1 levels

115
Q

Other investigation for Acromegaly

A

Oral glucose tolerance test:
1. in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia

  1. in acromegaly there is no suppression of GH
  2. may also demonstrate impaired glucose tolerance which is associated with acromegaly

Pituitary MRI = pituitary tumour.

116
Q

1st line treatment for Acromegaly

A

Trans-sphenoidal surgery

117
Q

What is Diabetes insipidus?

A

Either:
1. a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI)

or

  1. an insensitivity to antidiuretic hormone (nephrogenic DI)
118
Q

Symptoms of Diabetes insipidus

A
  1. Polyuria (dilute urine)
  2. polydipsia (thirst)
  3. dehydration
119
Q

Investigation for Diabetes insipidus

A
  1. U&Es (hypernatremia, hyperuricemia)
  2. Plasma & urine osmolality
    - -> high plasma osmolality, low urine osmolality
    - -> a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
  3. Water deprivation test - urine abnormally dilute
120
Q

Management of Diabetes Insipidus

A
  1. Find & treat cause (pituitary tumour, metastases, head injury, meningitis, sarcoidosis, inherited)
  2. Cranial: Desmopressin (synthetic analogue of ADH)
  3. Nephrogenic: Bendroflumethiazide, low protein, low salt
121
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

122
Q

Features of Conn’s syndrome

A
  1. hypertension
  2. hypokalaemia
    - -> muscle weakness
123
Q

1st line investigation in suspected Conn’s syndrome

A

Plasma aldosterone/renin ratio

- High aldosterone + low renin

124
Q

Next step after 1st line investigation in Conn’s syndrome

A

High-resolution CT abdomen + adrenal vein sampling

125
Q

Management of Conn’s syndrome

A
  1. adrenal adenoma: surgery

2. bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

126
Q

Most common cause of Addison’s

A

Autoimmune

127
Q

Causes of hyperkalaemia

A
  • AKI
  • Addisons disease
  • Rhabdomyolysis
  • Drugs
128
Q

Which drugs cause hyperkalaemia

A

ACEi, ARB, spironolactone, heparin

129
Q

ECG changes seen in hyperkalaemia

A

tall-tented T waves, small P waves, widened QRS

130
Q

What does untreated hyperkalaemia lead to?

A

life-threatening arrhythmias

131
Q

Emergency treatment of severe hyperkalaemia

A
  • IV calcium gluconate: to stabilise the myocardium

- insulin/dextrose infusion: short-term shift in potassium from ECF to ICF

132
Q

Sx of hyperkalaemia

A
  • muscle weakness
  • numbness
  • palpitations
  • sob
  • n&v
133
Q

Sx of hypokalaemia

A
  • muscle weakness

- hypotonia

134
Q

What does hypokalaemia predispose patients to?

A

digoxin toxicity

135
Q

ECG features of hypokalaemia

A

U waves, long PR, long QT

136
Q

Causes of hypokalaemia

A
  • diuretics
  • diarrhoea
  • vomiting
  • excess alcohol
  • DKA
  • CKD
137
Q

Management of hypokalaemia

A

IV Potassium

138
Q

What is metabolic alkalosis

A

loss of hydrogen ions or gain of bicarbonate

139
Q

Main causes of metabolic alkalosis

A
  • vomiting
  • diuretics
  • hypokalaemia
  • primary hyperaldosteronism
  • Cushing’s syndrome
140
Q

What is the normal anion gap

A

10-18mmol/L

141
Q

Causes of metabolic acidosis

A

normal anion gap

  • GI (diarrhoea)
  • Addisons

raised anion gap

  • lactate (shock, sepsis, hypoxia)
  • ketone (DKA, alcohol)
  • renal failure
142
Q

Common causes of resp alkalosis

A
  • anxiety = hyperventilation
  • PE
  • pregnancy
  • altitude
  • salicylate poisoning
  • stroke
  • subarrachnoid haemorrhgae
143
Q

Common causes of resp acidosis

A
  • COPD
  • Decompensation in other resp conditions
  • sedative drug OD
  • neuromuscular disease
144
Q

What acid-base imbalance is associated with cushing’s syndrome?

A

Hypokalaemic metabolic alkalosis

FCM Matrix (17 decks)

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