Endocrine Flashcards

1
Q

What hormones are produced by the anterior pituitary

A

TSH
ACTH
FSH
LH
GH
Prolactin

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2
Q

What hormones are produced by the posterior pituitary

A

Oxytocin
ADH

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3
Q

Describe hypothalamic pituitary thyroid axis

A

Hypothalamus - thyrotropin-releasing hormone
Pituitary - Thyroid stimulating hormone
Thyroid - T3 + T4
Negative feed back

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4
Q

Actions of cotrisol

A

Inhibit immune system
Inhibit bone formation
Raises blood glucose
Increases metabolism
Increases alertness

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5
Q

Actions of growth hormone

A

Stimulate muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

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6
Q

Actions of PTH

A

Increases serum calcium
Increases the activity and number of osteoclasts - causing bone reabsorption
Increases calcium reabsorption in kidneys
Activeates vitamin D in the kidneys - promotes calcium absorption from the small intestine.

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7
Q

Actions of aldosterone

A

Increases intravascular volume
Increase sodium reabsorption from the distal tubule
Increases potassium secretion from distal
Increase hydrogen secretion from collecting

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8
Q

Define Cushing’s Syndrome

A

Refers to the signs and aymptoms that develop after prolonged abnormal elevation of cortisol

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9
Q

Define Cushing’s Disease

A

Refers to specific pituitary adenoma that secretes excess ACTH.

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10
Q

Features of Cushing’s syndrome

A

Round moon face
Central obesity
Abdominal striae
Buffalo hump
Proximal limb muscle wasting

Hypertension
Cardiac hypertrophy
Hyperglycaemia
Depression
Insomnia

Osteoporosis
East bruising

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11
Q

Common causes of Cushing’s syndrome

A

Exogenous steroids
Cushing’s disease
Adrenal adenoma
Paraneoplastic - SCLC

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12
Q

Investigations in Cushing’s Syndrome

A

Overnight dexamethasone suppression test

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13
Q

Define adrenal insufficiency

A

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

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14
Q

Define Addison’s disease

A

Primary adrenal insufficiency
Autoimmune condition resulting in damage to the adrenal gland.

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15
Q

Define secondary adrenal insufficiency

A

Inadequate ACTH stimulating the adrenal gland
Pituitary dysfunction removal, infection, loss of blood supply in radiotherapy.
Sheehan’s - Blood loss in child birth causes pituitary necrosis

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16
Q

Define tertiary adrenal insufficiency

A

Inadequate CRH release by hypothalamus
Long term oral steroids

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17
Q

History of adrenal insufficiency

A

Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido

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18
Q

Clinical signs of adrenal insufficiency

A

Bronze hyperpigmentation - ACT stimulates melanocytes, particularly in skin creases
Hypotension - particularly postural

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19
Q

Investigations in adrenal insufficiency

A

Short synacthen test!
UE - hyponatraemia, hyperkalaemia
Early morning cortisol
ACTH leve
Auto antibodies
CT/MRI
MRI pituitary

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20
Q

Management of adrenal insufficiency

A

Steroid replacement
Hydrocortisone - glucocorticoid replacing cortisol
Fludrocortisone - mineralocorticoid replacing aldosterone

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21
Q

Define Addisonian crisis

A

Term used to describe the acute presentation of severe addisons, absence of steroid hormones leads to life threatening presentation

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22
Q

History of Addisonian crisis

A

Reduced conscious
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
Very sick
First presentation of Addison’s, or infection, trauma.

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23
Q

Management of Addisonian crisis

A

Parenteral steroids
IV fluid resuscitation
Correct electrolytes and glucose

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24
Q

Thyroid function test in hyperthyroidis,

A

TSH - Low
T3+4 - High

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25
Q

Thyroid function test in hypothyroidism

A

Primary
TSH - High
T3+4 - Low

Secondary
TSH - Low
T3+4 - Low

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26
Q

What antibodies are present in Grave’s disease

A

anti-TPO Antibodies
Antithyroid perocidase

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27
Q

Define hyperthyroidism

A

Where there is overproduction of thyroid hormone

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28
Q

Define thyrotoxicosis

A

Refers to abnormal and excessive quantity of thyroid hormone in the body

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29
Q

Define primary hyperthyroidism

A

Hyperthyroidism due to thyroid pathology

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30
Q

Define secondary hyperthyroidism

A

Thyroid producing too much hormone as a result of overstimulation
Pathology in the hypothalamus or pituitary

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31
Q

Most common cause of hyperthyroidism

A

Graves disease

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32
Q

Define graves disease

A

Autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism.

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33
Q

Clinical signs of Grave’s disease

A

Exophthalmos - bulging eyes
Pretibial myxoedema
Grave’s eye disease
Diffuse goitre - not nodular

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34
Q

History of hyperthyroidism

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss increased appetite
Fatigue
Frequent loose stool
Sexual dysfunction

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35
Q

Unique features of toxic multinodular goitre

A

Goitre with firm nodules
Over 50
Not graves

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36
Q

Define De Quervain’s thyroiditis

A

Describes the presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism
Hyperthyroid followed by hypo due to negative feed back.

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37
Q

Management of De Quervain’s thyroiditis

A

Self limiting
NSAIDs and beta blockers

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38
Q

Presentation fo thyrotoxicosis

A

Pyrexia
Tachycardia
Deliriu,

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39
Q

Management of thyrotoxicosis

A

As hyperthyroidism
Fluid resuscitation
Anti-arrhythmics and beta blockers

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40
Q

Management of hyperthyroidism

A

Carbimazole carful titration to normal levels or to block and replace
Radioactive iodine - taken up by thyroid and radiation destroys it
Levothyroxine replacement
Propranolol for symptoms
Surgery - remove nodules

41
Q

Common causes of hypothyroidism

A

Hashimoto’s thyroiditis - anti-TPO antibodies
Iodine deficiency
Iatrogenic
Medication - lithium, amiodarone
Hypopituitarism - tumours, infection, vascular, radiation

42
Q

Features of hypothyroidism

A

Weight gain
Appetite reduction
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention
Heavy or irregular periods
Constipation

43
Q

Investigations in hypothyroidism

A

TSH and T3+4
CT

44
Q

Management of hypothyroidism

A

Levothyroxine

45
Q

Define type 1 diabetes mellitus

A

A disease where the pancreas stops being able to produce insulin. May be genetic, linked to Viruses (coxsackie B + enterovirus).
As a result of no insulin being produced there is a constant state of hyperglycaemia.

46
Q

Define diabetic ketoacidosis

A

A state of hyperglycaemia with ketosis and acidosis.
As cells have no fuel they undergo ketogenesis, this leads to acidosis.
So hyperglycaemic that glucoses is excreted in urine, taking with it a lot of water resulting in dehydration.
Insulin drives potassium into cells - common complication of starting treatment

47
Q

History of DKA

A

Polyuria
Polydipsia
Nausea and vomiting
Acetone breath - pear drops
Dehydration
Altered consciousness

48
Q

Diagnosis of DKA

A

Hyperglycaemia - >11
Ketosis - Blood >3
Acidosis - pH <7.3

49
Q

Management of DKA

A

FIG-PICK
Fluids!!!
Insulin
Glucose - monitor and add when below roughly 14
Potassium - monitor and replace
Infection - treat underlying cause
Chart - fluid balance
Ketones

50
Q

Management of T1DM

A

Sub cu insulin
Monitoring glucose intake and BMs

51
Q

History of hypoglycaemia

A

Tremor
Sweating
Irritable
Dizziness
Pallor
Reduced consciousness

52
Q

Management of hypoglycaemia

A

100ml of 20% glucose over 5 minutes

53
Q

Macrovascular complications of T1DM

A

Coronary artery disease
Peripheral ischaemia - ulcers
Stroke
HTN

54
Q

Microvascular complications of T1DM

A

Peripheral neuropathy
Retinopathy
Kidney disease - glomerulosclerosis

55
Q

Define type two diabetes mellitus

A

Repeat exposure to glucose and insulin leads to resistance, requiring progressively more insulin putting strain on the pancreas. This leads to chronic hyperglycaemia

56
Q

Risk factors for TIIDM

A

Age
Black, Chinese, south Asian
FH
Obesity
Sedentary lifestyle
High carbohydrate

57
Q

History of TIIDM

A

Fatigue
Polydipsia and polyuria
Unintentional weight loss
Opportunistic infection
Slow healing
Glucose in urine

58
Q

Investigations in TIIDM

A

OGTT
HbA1c
Random glucose
Fasting glucose

59
Q

Numbers for diabetes diagnosis on OGTT, HbA1c, Random and fasting glucose

A

OGTT >11
Random glucose >11
Fasting glucose >7
HbA1c >48 (>42 for prediabetes)

60
Q

Management of TIIDM

A

Lifestyle - exercise and weightless
Metformin
Then pioglitazone

61
Q

Define acromegaly

A

Clinical manifestation of excessive growth hormone, most often caused by pituitary adenoma.

62
Q

What visual defect is often seen in acromegaly

A

Bitemporal hemianopia

63
Q

History of acromegaly

A

Headaches + visual field defects - space occupying
Arthritis
Largeness
Sweating

64
Q

Clinical signs of acromegaly

A

Frontal bossing - forehead and brow
Large nose
Macroglossia - tongue
Large hands and fee
Prognathism- protruding jaw
Hypertrophic heart
Hypertension
TIIDM
Colorectal cancer
Skin tags

65
Q

Investigations in acromegaly

A

Insulin-like growth factor
Oral glucose tollerance test
MRI head
Opthamology

66
Q

Management of acromegaly

A

Trans-sphenoidal removal of pituitary tumour
Somatostatin analogues to block GH release,

67
Q

Define hyperparathyridism

A

Overproduction of parathyroid hormone.

68
Q

Actions of parathyroid hormone

A

Raise blood calcium
Increase osteoclast activity - broken down and reabsorbed
Increase absorption in gut
Increase reabsorption
Activate vit D

69
Q

Presentation of hypercalcaemia

A

Renal stones, painful bone, abdominal groans and psychiatric moans.
Nausea and vomiting
Fatigue
Depression
Psychosis

70
Q

Causes of primary hyperparathyroidism

A

Tumour of the parathyroid gland.

71
Q

Causes of secondary hyperparathyroidism

A

Insufficient vit D
Chronic renal failure
Something causing hypocalcaemia - more parathyroid created in feed back

72
Q

Define Conn’s syndrome

A

Adrenal adenoma secreting aldosterone

73
Q

Define primary hyperaldosteronism

A

Adrenal glands secrete too much aldosterone, also causing low renin

74
Q

Causes of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia
Conn’s syndrome
Familial - type 1 and 2
Adrenal carcinoma

75
Q

Define secondary hyperaldosteronism

A

Excessive renin stimulates the adrenal glands to produce more aldosterone

76
Q

Causes of secondary hyperaldosteronism

A

Renal artery stenosis
Renal artery obstruction
Heart failure

77
Q

Investigations in hyperaldosteronism

A

Renin aldosterone ration
Blood pressure
UEs - hypokalaemia
Gas - alkalosis
CT/MRI - tumour
Renal doppler

78
Q

Management of hyperaldosteronism

A

Aldosterone antagonists = eplerenone, spironolactone
Remove tumour
Renal artery angioplasty

79
Q

Define syndrome of inappropriate Anti-Diuretic hormone

A

A condition where the is inappropriately high amounts of ADH

80
Q

Action of ADH

A

Secreted by the posterior pituitary glad and cause reabsorption of water in the collecting ducts - causing increase in blood volume and pressure

81
Q

History of SIADH

A

Headache
Fatigue
Muscle aches and cramps
Confusion`
?seizures and reduced consciousness

82
Q

Causes of SIADH

A

Posterior pituitary secretes too much
Post operative
Infection - lung abscess and atypical pneumonia
Head injury
Medication - thiazides, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs
Malignancy - Small cell lung cancer
Meningitis

83
Q

Investigations of SIADH

A

Diagnosis of exclusion
Euvolemic with hyponatraemia
Urine osmolality will be high - lots of salt very concentrated
CXR
CT TAP
MRI head

Negative short synacthen test - rule out adrenal insufficiency
No diuretic use
No diarrhoea
No excessive water intake
No kidney disease or AKI

84
Q

Management of SIADH

A

Correct sodium slowly to prevent central pontine myelinolysis
Less than 10mmol/L per 24hours

85
Q

Define diabetes insipidus

A

Lack of ADH or response to ADH
Prevents the kidneys from being able to concentrate urine, leading to polyuria and polydipsia.

86
Q

Define nephrogenic diabetes insipidus

A

When the collecting ducts do not respond to ADH

87
Q

Causes of nephrogenic diabetes insipidus

A

Drugs - lithium
Mutations in AVPR2 gene - X linked
Intrinsic kidney disease
Electrolyte disturbance

88
Q

Define cranial diabetes insipidus

A

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

89
Q

Causes of cranial diabetes insipidus

A

Brain tumours
Head injury
Brain malformation
Brain infections - meningitis, encephalitis, TB
Brain surgery or radiotherapy

90
Q

History of diabetes insipidus

A

Polyuria and polydipsia
Dehydration
Postural hypotension
Hyponatraemia

91
Q

Investigations in diabetes insipidus

A

Low urine osmolality - low salt concentration high water
High serum osmolality - lots of salt
Water deprivation test - desmopressin

92
Q

Fluid deprivation test results

A

No fluids 8 hours urine osmolality, desmopressin then urine osmolality again in 8 hours
Cranial - initialy low osmolality and then high
Nephrogenic - low before and after
Primary polydipsia - high initially

93
Q

Management of diabetes insipidus

A

Treat causes
Desmopressin if cranial

94
Q

Define phaeochromocytoma

A

A tumour of the chromaffin cells (adrenalin producing cells), that secretes unregulated amounts of adrenaline. Adrenaline is a catecholamine that stimulates the sympathetic nervous system.

95
Q

Causes of pheochromocytoma

A

25 % familial and associated with MEN 2
Patterns of tumour
10% bilateral
10% cancerous
10% outside adrenal gland.

96
Q

Investigations of phaeochromacytoma

A

24 hour catecholamines
Plasma free metanephrines (breakdown product of adrenaline - longer half life)

97
Q

History of phaeochromocytoma

A

Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardias
Paroxysmal AF

98
Q

Management of pheochromocytoma

A

Alpha blockers - phenoxybenzamine
Beta blockers
Adrenalectomy