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Endocrinology Flashcards

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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
What is the management for adrenal insufficiency
Steroid replacement (hydrocortisone for cortisol, fludrocortisone for aldosterone) Give steroid cards and emergency ID tags Double steroid dose during acute illness
26
What is an Addisonian crisis
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
27
What happens to TSH, T3 and T4 in hyperthyroidism
Low TSH High T3 and T4
28
What happens to TSH, T3 and T4 in primary hypothyroidism
High TSH Low T3 and T4
29
What happens to TSH, T3 and T4 in secondary hypothyroidism
Low TSH Low T3 and T4
30
What are the antibodies that can affect thyroid function
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
31
What imaging is needed for thyroid pathology
Ultrasound Radioisotope scan
32
What are the causes of hyperthyroidism
Garve's disease Toxic multinodular goitre Solitary toxic thyroid nodule Thyroiditis (viral infection, medications, post-partum)
33
What are the universal clinical features of hypothyroidism
Anxiety Irritability Sweating Heat intolerance Tachycardia Weight loss Fatigue Frequent loose stools Sexual dysfunction Resting tremor Hyper-reflexia Lid lag
34
What are the clinical features of hyperthyroidism specific to Grave's disease
Diffuse goitre Grave's eye disease Bilateral exopthalmos Pretibial myxoedema Nail changes
35
What are solitary toxic thyroid nodules
Single nodule releasing thyroid hormone Usually benign adenomas Surgically remove
36
What is De Quervain's thyroiditis
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
37
What is thyroid storm
Rare presentation of hyperthyroidism Presentation: hyperthyroidism, pyrexia, tachycardia, delirium Admit for monitoring
38
What would the T3, T4 and TSH levels be in subclinical hyperthyroidism
Normal T3 and T4 Low TSH
39
What is the management for hyperthyroidism
Carbimazole Propylthiouracil Radioactive iodine Beta blockers Surgery (may need levothyroxine treatment for life)
40
What are the causes of hypothyroidism
Hashimoto's Iodine deficiency Hyperthyroid treatment Medications (lithium, amiodarone) Secondary to tumour/infection/radiation/Sheehan's
41
Which antibodies are found in Hashimoto's
Antithyroid peroxidase (anti-TPO) antibody Antithyroglobulin antibody
42
What are the clinical features of hypothyroidism
Weight gain Fatigue Dry skin Coarse hair Hair loss Fluid retention Heavy/irregular periods Constipation
43
What would the TSH, T3 and T4 levels be like in primary hypothyroidism
High TSH Low T3 and T4
44
What would the TSH, T3 and T4 levels be like in secondary hypothyroidism
Low TSH Low T3 and T4
45
What is the management for hypothyroidism
Replace with levothyroxine Synthetic T4, metabolised into T3
46
What is the normal range for blood glucose
4.4 - 6.1
47
What is glucagon
Pancreatic hormone Produced by alpha cells of islets of Langerhans Released in response to low blood sugar and stress
48
What are the main problems associated with diabetic ketoacidosis
Hyperglycaemia Ketoacidosis Dehydration Potassium imbalance
49
How might diabetic ketoacidosis present
Polyuria Polydipsia Nausea and vomiting Acetone smell to breath Dehydration Hypotension Altered consciousness Symptoms of underlying trigger (eg sepsis)
50
What is the diagnostic criteria for diabetic ketoacidosis
Hyperglycaemia: glucose > 11 Ketosis: ketones > 3 Acidosis
51
What is the treatment for diabetic ketoacidosis
FIG-PICK Fluids Insulin Glucose Potassium Infection (treat) Chart (fluid balance) Ketones (monitor)
52
What is the long term management for type 1 diabetes
Patient education Monitoring: carb intake, blood sugar levels, for complications Insulin
53
What are the short term complications of type 1 diabetes
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
What are the long term complications of type 1 diabetes
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
How can type 1 diabetes be monitored
HbA1c Capillary blood glucose Flash glucose monitoring
56
What are the risk factors for type 2 diabetes
Old age Black, chinese, south asian Family history Obesity Sedentary lifestyle High carbohydrate diet
57
How might type 2 diabetes present
Fatigue Polydipsia Polyuria Unintentional weight loss Opportunistic infections Slow healing Glucoseuria
58
Explain the oral glucose tolerance test
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
What is pre-diabetes
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
What is the diagnostic criteria for type 2 diabetes
HbA1c: > 48 Random glucose: > 11 Fasting glucose: > 7 OGTT: > 11 at 2 hours
61
What are the treatment targets for type 2 diabetes
HbA1c 48 for newly diagnosed 53 for those on more than just metformin
62
What is the first line medical management for type 2 diabetes
Metformin A biguanide Increases insulin sensitivity Side effects: diarrhoea, abdominal pain, lactic acidosis
63
What are the second line medical managements for type 2 diabetes
Gliclazide (a sulfonylurea) Pioglitazone (a thiazolidinedione) Sitagliptin (a DPP4 inhibitor) Empagliflozin (an SGLT-2 inhibitor)
64
What is the third line medical management for type 2 diabetes
Triple therapy Metformin + a second line Metformin + insulin
65
Give an overview of rapid acting insulins
10 mins - 4 hrs Novorapid, humalog, apidra
66
Give an overview of short acting insulins
30 mins - 8 hrs Actrapid, humulin S, insuman rapid
67
Give an overview of intermediate acting insulins
1 hr - 16 hrs Insulatard, humulin I, insuman basal
68
Give an overview of long acting insulins
1 hr - 24 hrs Lantus, levemir, degludec
69
Give an overview of combination insulins
Mixture of rapid and intermediate Humalog 25, humalog 75, novomix
70
What is acromegaly
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
How might acromegaly present
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
What are the investigations for acromegaly
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
What is the management for acromegaly
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
What are the symptoms of hypercalcaemia
Renal stones Painful bones Abdominal groans (constipation, nausea, vomiting) Psychiatric moans (fatigue, depression, psychosis)
75
Give an overview of primary hyperparathyroidism
Uncontrolled PTH production by parathyroid cells Get hypercalcaemia Treat by surgically removing tumour
76
Give an overview of secondary hyperparathyroidism
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
Give an overview of tertiary hyperparathyroidism
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
Give an overview of primary hyperaldosteronism
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
Give an overview of secondary hyperaldosteronism
Excess renin stimulates adrenal glands to produce more aldosterone Causes: renal artery stenosis, renal artery obstruction, heart failure
80
What investigations are needed for hyperaldosteronism
Calculate renin:aldosterone Blood pressure Electrolytes Blood gas (alkalosis)
81
What is the management for hyperaldosteronism
Aldosterone antagonists (eplerenone, spironolactone) Treat underlying cause (remove adenoma, renal artery angioplasty...)
82
What is SIADH
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
What are the symptoms of SIADH
Headache Fatigue Muscle aches and cramps Confusion Severe hyponatraemia
84
How is SIADH diagnosed
Diagnosis of exclusion Rule out other causes of hyponatraemia
85
What is the management for SIADH
Stop causative medications Correct sodium slowly (prevent central pontine myelinolysis) Fluid restriction ADH receptor blockers (tolvaptan) Demeclocycline (antibiotic, inhibits ADH)
86
What is central pontine myelinolysis
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
What is diabetes insipidus
Lack of ADH/lack of response to ADH Kidneys not able to concentrate urine Can be nephrogenic or cranial
88
What are the causes of nephrogenic diabetes insipidus
(Collecting ducts not responding to ADH) Drugs: lithium Genetic mutations Intrinsic kidney disease Electrolyte disturbances (hypokalaemia, hypercalcaemia)
89
What are the causes of cranial diabetes insipidus
(Hypothalamus does not produce ADH) Idiopathic Brain tumour Head injury Brain malformation Meningitis, encephalitis Brain surgery Brain radiotherapy
90
How might diabetes insipidus present
Polyuria Polydipsia Dehydration Postural hypotension Hypernatraemia
91
What investigations are needed for diabetes insipidus
Low urine osmolality High serum osmolality Desmopressin stimulation test
92
Explain the desmopressin stimulation test
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
What is the management for diabetes insipidus
Treat underlying cause Desmopressin (synthetic ADH)
94
What is phaeochromocytoma
Tumour of chromaffin cells Get unregulated and excessive secretion of adrenaline 25% familial (MEN2 gene)
95
How is phaeochromocytoma diagnosed
24 hr catecholamines Plasma free metanephrines CT/MRI abdomen
96
How might phaeochromocytoma present
Anxiety Sweating Headache Hypertension Palpitations Tachycardia Paroxysmal atrial fibrillation
97
What is the management for phaeochromocytoma
Alpha blockers Beta blockers Adrenalectomy
98
What are the causes of hyperprolactinaemia
Firstly, exclude pregnancy Severe hypothyroidism PCOS Pituitary tumours Renal failure Antipsychotics Stress
99
What is the management for hyperprolactinaemia
Dopamine agonists Cabergoline, bromocriptine Side effects: nausea, postural hypotension, psychiatric disturbance

Medicine (9 decks)

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