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Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Which hormones are released by the anterior pituitary

A

TSH

ACTH

FSH

LH

GH

Prolactin

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2
Q

Which hormones are released by the posterior pituitary

A

Oxytocin

ADH

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3
Q

Give an overview of the thyroid axis

A

Hypothalamus releases TRH (thyrotropin releasing hormone)

Anterior pituitary releases TSH

Thyroid gland releases T3 and T4

T3 and T4 suppress release of TRH and TSH

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4
Q

Give an overview of the adrenal axis

A

Hypothalamus releases CRH (corticotrophin releasing hormone)

Anterior pituitary releases ACTH

Cortisol released (pulsatile) by both adrenal glands

Controlled by negative feedback

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5
Q

What are the actions of cortisol

A

Inhibition of immune system

Inhibition of bone formation

Raised blood glucose

Increased metabolism

Increased alertness

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6
Q

Give an overview of the growth hormone axis

A

Hypothalamus releases GHRH (growth hormone releasing hormone)

Anterior pituitary releases GH

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7
Q

What are the actions of growth hormone

A

Releases insulin-like growth factor 1 (IGF-1) from liver

Stimulates muscle growth

Increases bone density and strength

Stimulates cell regeneration and reproduction

Stimulates growth of internal organs

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8
Q

Give an overview of the parathyroid axis

A

PTH released from all 4 parathyroid glands in response to: low calcium, low magnesium, high phosphate

Controlled by negative feedback

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9
Q

What are the actions of PTH

A

Increases serum calcium

Increases number and activity of osteoclasts

Increases calcium reabsorption from kidneys

Stimulates kidneys to convert vit D3 to calcitriol

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10
Q

Give an overview of the renin-angiotensin-aldosterone system

A

Renin released by juxtaglomerular cells in afferent arterioles (more renin in response to lower blood pressure)

Renin converts angiotensinogen to angiotensin 1

Angiotensin 1 converted to angiotensin 2 by ACE (in lungs)

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11
Q

What are the actions of angiotensin 2

A

Vasodilation

Aldosterone release:
Increases sodium reabsorption from distal tubule
Increases potassium secretion from distal tubule
Increases hydrogen secretion from collecting ducts

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12
Q

What is Cushing’s syndrome

A

Signs and symptoms that develop following prolonged abnormally elevated cortisol levels

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13
Q

What are the clinical features of Cushing’s syndrome

A

Round middle with thin limbs: moon face, central obesity, abdominal striae, buffalo hump, proximal limb muscle weakness

High levels of stress hormone: hypertension, cardiac hypertrophy, hyperglycaemia, depression, insomnia

Other: osteoporosis, easy bruising, poor skin healing

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14
Q

What are the causes of Cushing’s syndrome

A

Long term steroid use

Cushing’s disease (pituitary adenoma releasing excess ACTH)

Adrenal adenoma

Paraneoplastic Cushing’s (excess ACTH from cancer)

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15
Q

What investigations are needed for Cushing’s syndrome

A

Dexamethasone suppression test

24 hour urine free cortisol

FBC, U&Es

MRI brain (pituitary adenoma)

CT chest/abdo (lung/adrenal cancer)

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16
Q

Explain the dexamethasone suppression test

A

Give dexamethasone at night, measure ACTH and cortisol in morning

Low dose:
- Cortisol level not suppressed

High dose (if low dose positive, do high dose to find cause):
- Low cortisol: Cushing’s disease
- Normal/high cortisol and low ACTH: Adrenal Cushing’s
- Normal/high cortisol and high ACTH: ectopic ACTH

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17
Q

What is the management for Cushing’s syndrome

A

Remove tumour

Remove adrenal glands (give replacement steroids for life)

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18
Q

What is adrenal insufficiency

A

Not enough cortisol or aldosterone produced

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19
Q

What is primary adrenal insufficiency

A

Addison’s disease

Adrenal glands damaged

Mostly autoimmune

All 3 zones affected

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20
Q

What is secondary adrenal insufficiency

A

Inadequate stimulation of ACTH by adrenal glands

Loss/damage of pituitary gland (surgery, infection, radiotherapy, Sheehan’s syndrome)

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21
Q

What is tertiary adrenal insufficiency

A

Inadequate CRH release from hypothalamus

Long term steroid use (> 3 weeks)

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22
Q

What are the clinical features of adrenal insufficiency

A

Fatigue

Nausea

Cramps

Abdominal pain

Reduced libido

Dizziness

Bronze hyperpigmentation of skin

Hypotension (especially postural)

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23
Q

What investigations are needed for adrenal insufficiency

A

U&Es

Early morning cortisol

Short synacthen test (gold standard)

ACTH (high in primary, low in secondary)

Antibodies (adrenal cortex antibody, 21-hydroxylase antibody)

CT/MRI adrenal

MRI pituitary

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24
Q

Explain the short synacthen test

A

For adrenal insufficiency

Give synthetic ACTH

Measure blood cortisol at 0, 30, 60 mins

Failure of cortisol to at leas double is Addison’s

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25
Q

What is the management for adrenal insufficiency

A

Steroid replacement (hydrocortisone for cortisol, fludrocortisone for aldosterone)

Give steroid cards and emergency ID tags

Double steroid dose during acute illness

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26
Q

What is an Addisonian crisis

A

Acute presentation of severe Addison’s

Absence of steroids can kill

Presentation: reduced consciousness, hypotension, hyperglycaemia, hyponatraemia, hyperkalaemia

Management: do not wait to confirm, intensive monitoring, parenteral steroids, IV fluids, correct hypoglycaemia, monitor electrolytes and fluid balance

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27
Q

What happens to TSH, T3 and T4 in hyperthyroidism

A

Low TSH

High T3 and T4

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28
Q

What happens to TSH, T3 and T4 in primary hypothyroidism

A

High TSH

Low T3 and T4

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29
Q

What happens to TSH, T3 and T4 in secondary hypothyroidism

A

Low TSH

Low T3 and T4

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30
Q

What are the antibodies that can affect thyroid function

A

Antithyroid peroxidase (anti-TPO) antibodies: against thyroid gland, found in Grave’s and Hashimoto’s

Antithyroglobulin antibodies: against thyroglobulin, can be found in normal thyroid/Grave’s/Hashimoto’s/thyroid cancer

TSH receptor antibodies: mimic TSH, found in Grave’s

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31
Q

What imaging is needed for thyroid pathology

A

Ultrasound

Radioisotope scan

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32
Q

What are the causes of hyperthyroidism

A

Garve’s disease

Toxic multinodular goitre

Solitary toxic thyroid nodule

Thyroiditis (viral infection, medications, post-partum)

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33
Q

What are the universal clinical features of hypothyroidism

A

Anxiety

Irritability

Sweating

Heat intolerance

Tachycardia

Weight loss

Fatigue

Frequent loose stools

Sexual dysfunction

Resting tremor

Hyper-reflexia

Lid lag

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34
Q

What are the clinical features of hyperthyroidism specific to Grave’s disease

A

Diffuse goitre

Grave’s eye disease

Bilateral exopthalmos

Pretibial myxoedema

Nail changes

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35
Q

What are solitary toxic thyroid nodules

A

Single nodule releasing thyroid hormone

Usually benign adenomas

Surgically remove

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36
Q

What is De Quervain’s thyroiditis

A

Viral infection presenting with: fever, neck pain, neck tenderness, dysphagia, features of hyperthyroidism

Get a hyperthyroid phase, then a hypothyroid phase

Self limiting: give NSAIDs and beta blockers for symptoms

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37
Q

What is thyroid storm

A

Rare presentation of hyperthyroidism

Presentation: hyperthyroidism, pyrexia, tachycardia, delirium

Admit for monitoring

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38
Q

What would the T3, T4 and TSH levels be in subclinical hyperthyroidism

A

Normal T3 and T4

Low TSH

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39
Q

What is the management for hyperthyroidism

A

Carbimazole

Propylthiouracil

Radioactive iodine

Beta blockers

Surgery (may need levothyroxine treatment for life)

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40
Q

What are the causes of hypothyroidism

A

Hashimoto’s

Iodine deficiency

Hyperthyroid treatment

Medications (lithium, amiodarone)

Secondary to tumour/infection/radiation/Sheehan’s

41
Q

Which antibodies are found in Hashimoto’s

A

Antithyroid peroxidase (anti-TPO) antibody

Antithyroglobulin antibody

42
Q

What are the clinical features of hypothyroidism

A

Weight gain

Fatigue

Dry skin

Coarse hair

Hair loss

Fluid retention

Heavy/irregular periods

Constipation

43
Q

What would the TSH, T3 and T4 levels be like in primary hypothyroidism

A

High TSH

Low T3 and T4

44
Q

What would the TSH, T3 and T4 levels be like in secondary hypothyroidism

A

Low TSH

Low T3 and T4

45
Q

What is the management for hypothyroidism

A

Replace with levothyroxine

Synthetic T4, metabolised into T3

46
Q

What is the normal range for blood glucose

A

4.4 - 6.1

47
Q

What is glucagon

A

Pancreatic hormone

Produced by alpha cells of islets of Langerhans

Released in response to low blood sugar and stress

48
Q

What are the main problems associated with diabetic ketoacidosis

A

Hyperglycaemia

Ketoacidosis

Dehydration

Potassium imbalance

49
Q

How might diabetic ketoacidosis present

A

Polyuria

Polydipsia

Nausea and vomiting

Acetone smell to breath

Dehydration

Hypotension

Altered consciousness

Symptoms of underlying trigger (eg sepsis)

50
Q

What is the diagnostic criteria for diabetic ketoacidosis

A

Hyperglycaemia: glucose > 11

Ketosis: ketones > 3

Acidosis

51
Q

What is the treatment for diabetic ketoacidosis

A

FIG-PICK

Fluids

Insulin

Glucose

Potassium

Infection (treat)

Chart (fluid balance)

Ketones (monitor)

52
Q

What is the long term management for type 1 diabetes

A

Patient education

Monitoring: carb intake, blood sugar levels, for complications

Insulin

53
Q

What are the short term complications of type 1 diabetes

A

Hypoglycaemia:
- Symptoms: tremor, sweating, irritability, dizziness, pallor, reduced consciousness, coma, death
- Treatment: rapid acting glucose, slow acting carbs, IV dextrose, IM glucagon

Hyperglycaemia:
- If not DKA, increase insulin
- If DKA, admit

54
Q

What are the long term complications of type 1 diabetes

A

Macrovascular: coronary artery disease, peripheral ischaemia, stroke, hypertension

Microvascular complications: peripheral neuropathy, retinopathy, kidney disease

Infection-related: UTIs, pneumonia, skin/soft tissue infections, fungal infections

55
Q

How can type 1 diabetes be monitored

A

HbA1c

Capillary blood glucose

Flash glucose monitoring

56
Q

What are the risk factors for type 2 diabetes

A

Old age

Black, chinese, south asian

Family history

Obesity

Sedentary lifestyle

High carbohydrate diet

57
Q

How might type 2 diabetes present

A

Fatigue

Polydipsia

Polyuria

Unintentional weight loss

Opportunistic infections

Slow healing

Glucoseuria

58
Q

Explain the oral glucose tolerance test

A

Measure blood glucose in morning, before breakfast

Give 75g glucose drink

Measure plasma glucose at 2 hours

Tests ability of body to deal with carbohydrates

59
Q

What is pre-diabetes

A

HbA1c: 42 - 47

Impaired fasting glucose: 6.1 - 6.9

Impaired glucose tolerance: 7.8 - 11.1 on OGTT

Educate to stop progression to diabetes

60
Q

What is the diagnostic criteria for type 2 diabetes

A

HbA1c: > 48

Random glucose: > 11

Fasting glucose: > 7

OGTT: > 11 at 2 hours

61
Q

What are the treatment targets for type 2 diabetes

A

HbA1c

48 for newly diagnosed

53 for those on more than just metformin

62
Q

What is the first line medical management for type 2 diabetes

A

Metformin

A biguanide

Increases insulin sensitivity

Side effects: diarrhoea, abdominal pain, lactic acidosis

63
Q

What are the second line medical managements for type 2 diabetes

A

Gliclazide (a sulfonylurea)

Pioglitazone (a thiazolidinedione)

Sitagliptin (a DPP4 inhibitor)

Empagliflozin (an SGLT-2 inhibitor)

64
Q

What is the third line medical management for type 2 diabetes

A

Triple therapy

Metformin + a second line

Metformin + insulin

65
Q

Give an overview of rapid acting insulins

A

10 mins - 4 hrs

Novorapid, humalog, apidra

66
Q

Give an overview of short acting insulins

A

30 mins - 8 hrs

Actrapid, humulin S, insuman rapid

67
Q

Give an overview of intermediate acting insulins

A

1 hr - 16 hrs

Insulatard, humulin I, insuman basal

68
Q

Give an overview of long acting insulins

A

1 hr - 24 hrs

Lantus, levemir, degludec

69
Q

Give an overview of combination insulins

A

Mixture of rapid and intermediate

Humalog 25, humalog 75, novomix

70
Q

What is acromegaly

A

Excess growth hormone

Mostly due to pituitary adenomas (often cause bitemporal hemianopia)

May be due to cancer secreting GHRH/GH

Complications: premature death (cardiovascular disease, bowel cancer)

71
Q

How might acromegaly present

A

Space occupying lesion: headache, visual disturbance

Overgrowth of tissue: frontal bossing, large nose, large tongue, large hands and feet, large protruding jaw, arthritis

Organ dysfunction: hypertrophic heart, hypertension, type 2 diabetes, colorectal cancer

Symptoms of excess growth hormone: new skin tags, profuse sweating

72
Q

What are the investigations for acromegaly

A

Do not use random GH measurement (fluctuates)

Insulin-like growth factor 1

OGTT whilst measuring GH (high glucose suppresses GH)

MRI brain (pituitary tumours)

Refer to ophthalmology

73
Q

What is the management for acromegaly

A

Trans-sphenoidal surgical removal of pituitary

Remove cancers

Medications to block GH: pegvisomant (GH antagonist), somatostatin analogues (inhibits GH release), dopamine antagonists (inhibit GH release)

Gamma knife radiotherapy

74
Q

What are the symptoms of hypercalcaemia

A

Renal stones

Painful bones

Abdominal groans (constipation, nausea, vomiting)

Psychiatric moans (fatigue, depression, psychosis)

75
Q

Give an overview of primary hyperparathyroidism

A

Uncontrolled PTH production by parathyroid cells

Get hypercalcaemia

Treat by surgically removing tumour

76
Q

Give an overview of secondary hyperparathyroidism

A

Vit D deficiency/chronic renal failure lead to low calcium absorption from gut, kidneys, and bones

Get hypocalcaemia

Parathyroid gland releases more PTH

Get hyperplasia of parathyroid cells

Treat underlying cause

77
Q

Give an overview of tertiary hyperparathyroidism

A

When secondary hyperparathyroidism continues for a long time

Get hyperplasia of parathyroid

Baseline PTH increases

When cause of secondary hyperparathyroidism treated, PTH stays high

High levels of calcium absorption from intestines, kidneys, and bones

Get hypercalcaemia

Treat by surgically removing parathyroid tissue

78
Q

Give an overview of primary hyperaldosteronism

A

Conn’s syndrome

Adrenal glands produce too much aldosterone

Serum renin levels low (suppressed by high blood pressure)

Causes: adrenal adenoma, bilateral adrenal hyperplasia, familial hyperaldosteronism, adrenal carcinoma

79
Q

Give an overview of secondary hyperaldosteronism

A

Excess renin stimulates adrenal glands to produce more aldosterone

Causes: renal artery stenosis, renal artery obstruction, heart failure

80
Q

What investigations are needed for hyperaldosteronism

A

Calculate renin:aldosterone

Blood pressure

Electrolytes

Blood gas (alkalosis)

81
Q

What is the management for hyperaldosteronism

A

Aldosterone antagonists (eplerenone, spironolactone)

Treat underlying cause (remove adenoma, renal artery angioplasty…)

82
Q

What is SIADH

A

Excess ADH

Due to: posterior pituitary producing too much ADH, ADH production by a cancer

Get hyponatraemia

Very concentrated urine (high urine osmolality and sodium)

83
Q

What are the symptoms of SIADH

A

Headache

Fatigue

Muscle aches and cramps

Confusion

Severe hyponatraemia

84
Q

How is SIADH diagnosed

A

Diagnosis of exclusion

Rule out other causes of hyponatraemia

85
Q

What is the management for SIADH

A

Stop causative medications

Correct sodium slowly (prevent central pontine myelinolysis)

Fluid restriction

ADH receptor blockers (tolvaptan)

Demeclocycline (antibiotic, inhibits ADH)

86
Q

What is central pontine myelinolysis

A

Complication of severe hyponatraemia being treated too quickly

As sodium falls, water crosses blood-brain barrier, brain swells

Phase 1 symptoms: due to electrolyte imbalance, encephalopathy, confusion, headaches, nausea and vomiting

Phase 2 symptoms: due to demyelination of neurones, a few days after sodium correction, spastic quadriparesis, pseudobulbar palsy, cognitive behavioural changes, significant risk of death

87
Q

What is diabetes insipidus

A

Lack of ADH/lack of response to ADH

Kidneys not able to concentrate urine

Can be nephrogenic or cranial

88
Q

What are the causes of nephrogenic diabetes insipidus

A

(Collecting ducts not responding to ADH)

Drugs: lithium

Genetic mutations

Intrinsic kidney disease

Electrolyte disturbances (hypokalaemia, hypercalcaemia)

89
Q

What are the causes of cranial diabetes insipidus

A

(Hypothalamus does not produce ADH)

Idiopathic

Brain tumour

Head injury

Brain malformation

Meningitis, encephalitis

Brain surgery

Brain radiotherapy

90
Q

How might diabetes insipidus present

A

Polyuria

Polydipsia

Dehydration

Postural hypotension

Hypernatraemia

91
Q

What investigations are needed for diabetes insipidus

A

Low urine osmolality

High serum osmolality

Desmopressin stimulation test

92
Q

Explain the desmopressin stimulation test

A

Aka water depletion test

Avoid fluid for 8 hours, measure urine osmolality, give synthetic ADH, measure urine osmolality at 8 hrs

Cranial diabetes insipidus: after deprivation is low, after ADH is high

Nephrogenic diabetes insipidus: after deprivation is low, after ADH is low

93
Q

What is the management for diabetes insipidus

A

Treat underlying cause

Desmopressin (synthetic ADH)

94
Q

What is phaeochromocytoma

A

Tumour of chromaffin cells

Get unregulated and excessive secretion of adrenaline

25% familial (MEN2 gene)

95
Q

How is phaeochromocytoma diagnosed

A

24 hr catecholamines

Plasma free metanephrines

CT/MRI abdomen

96
Q

How might phaeochromocytoma present

A

Anxiety

Sweating

Headache

Hypertension

Palpitations

Tachycardia

Paroxysmal atrial fibrillation

97
Q

What is the management for phaeochromocytoma

A

Alpha blockers

Beta blockers

Adrenalectomy

98
Q

What are the causes of hyperprolactinaemia

A

Firstly, exclude pregnancy

Severe hypothyroidism

PCOS

Pituitary tumours

Renal failure

Antipsychotics

Stress

99
Q

What is the management for hyperprolactinaemia

A

Dopamine agonists

Cabergoline, bromocriptine

Side effects: nausea, postural hypotension, psychiatric disturbance

Medicine (9 decks)

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