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Zero to Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is Cushing’s syndrome?

A
  • refers to signs and symptoms

- after prolonged abnormal elevation of cortisol

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2
Q

What is Cushing’s disease?

A
  • refers to specific condition
  • where pituitary adenoma
  • secretes excessive ACTH
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3
Q

5 things that high levels of stress hormone can cause?

A
  1. hypertension
  2. cardiac hypertrophy
  3. hyperglycaemia (t2dm)
  4. depression
  5. Insomnia
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4
Q

5 key characteristics of a patient with Cushing’s disease?

A
  1. round moon face
  2. central obesity
  3. abdominal striae
  4. buffalo hump
  5. proximal limb muscle wasting
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5
Q

state 4 causes of Cushing’s syndrome?

A
  1. patients on long term high dose steroids
  2. Pituitary adenoma releasing excessive ACTH (Cushing’s disease)
  3. Adrenal adenoma (hormone secreting adrenal tumour)
  4. paraneoplastic Cushing’s
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6
Q

What is paraneoplastic Cushing’s?

A
  • excess ACTH
  • released from a cancer (not of the pituitary)
  • stimulates excessive cortisol release
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7
Q

What is the most common cause of paraneoplastic Cushing’s?

A

Small cell lung cancer

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8
Q

What tests might you do to test for Cushing’s?

A

Dexamethasone suppression test

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9
Q

What is a normal response for a low dose dexamethasone suppression test?

1mg

A
  • dexamethasone to suppress
  • release of cortisol
  • through negative feedback on hypothalamus and pituitary
  • hypothalamus responds by reducing CRH
  • pituitary responds by reducing ACTH

When the cortisol level is not suppressed, this is the abnormal result seen in Cushing’s Syndrome.

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10
Q

When is the high dose dexamethasone suppression test performed?

8mg

A

after abnormal result on the low dose test

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11
Q

Describe high dose dexamethasone suppression test in Cushing’s disease?

A

In Cushing’s disease

  • pituitary still shows some response to negative feedback
  • 8mg d.methasone enough to suppress cortisol
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12
Q

Describe high dose dexamethasone test in presence of adrenal adenoma?

A

In Adrenal adenoma

  • cortisol production independent from pituitary
  • cortisol not suppressed
  • ACTH suppressed due to negative feedback
  • on hypothalamus and pituitary gland
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13
Q

Where there is ectopic ACTH, describe result of high dose dexamethasone test?

A

In Ectopic ACTH (e.g. from small cell lung cancer)

  • neither cortisol nor ACTH suppressed
  • ACTH production independent of hypothalamus of pituitary
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14
Q

Describe 6 other investigations for Cushing’s?

Give an example of what might be found in these 6 investigations

A
  1. 24 hr urinary free cortisol
  2. FBC (raised white cells)
  3. U&Es (K+ low if aldosterone also secreted by adrenal adenoma)
  4. MRI (pituitary adenoma)
  5. Chest CT (small cell lung cancer)
  6. Abdominal CT (adrenal tumours)
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15
Q

3 main treatment options for Cushings?

A

Surgically remove tumour
- Tran sphenoidal (removal of pituitary adenoma)

  • surgical removal of adrenal tumour
  • surgical removal of tumour producing ectopic ACTH
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16
Q

If surgical removal of the underlying cause of Cushing’s is not possible, what else might be done?

A
  • remove adrenals

- give patient steroid hormone replacement for life

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17
Q

What is Adrenal Insufficiency?

A
  • where adrenal glands don’t produce enough steroid hormones
  • mainly cortisol and aldosterone
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18
Q

What is Addison’s disease?

A
  • adrenals damaged
  • reduction in secretion of cortisol and aldosterone
  • aka primary adrenal insufficiency
  • autoimmune
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19
Q

Addisons disease is also called…

A

primary adrenal insufficiency

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20
Q

Secondary adrenal insufficiency results from:

A
  • inadequate ACTH stimulating adrenals
  • results in low cortisol release
  • aar of loss of damage to pituitary
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21
Q

Sheehan’s syndrome

A
  • massive blood loss during child birth

- leads to pituitary gland necrosis

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22
Q

What is tertiary adrenal insufficiency?

A
  • result of inadequate CRH by hypothalamus
  • aar of patients being on long term oral steroids
  • causing suppression of hypothalamus
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23
Q

5 main symptoms of adrenal insufficiency

A
  1. fatigue
  2. nausea
  3. cramps
  4. abdominal pain
  5. reduced libido
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24
Q

2 main signs of adrenal insufficiency

A
  1. bronze hyperpigmentation

2. hypotension (particularly postural hypotension)

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25
Q

Why does bronze hyperpigmentation occur in adrenal insufficiency?

A

ACTH stimulates melanocytes

to produce melanin

hyperpigmentation found particularly in skin creases

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26
Q

Describe ACTH levels in primary adrenal failure?

A
  1. primary adrenal failure
    - ACTH level is high
    - pituitary trying to stimulate adrenals without any negative feedback
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27
Q

Describe ACTH levels in secondary adrenal failure?

A
  • ACTH low
  • adrenal glands not stimulated by ACTH
  • thus not producing cortisol
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28
Q

Test of choice for adrenal insufficiency?

A
  • short synacthen test
  • synthetic acth
  • blood cortisol measured at baseline, 30 min then 60 mins post administration
  • failure of cortisol to rise, less than double, indicates primary adrenal insufficiency
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29
Q

Treatment of adrenal insufficiency?

A
  • steroid replacement
  • hydrocortisone (glucocorticoid, used to replace cortisol)
  • fludrocortisone (mineralocorticoid, used to replace aldosterone(
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30
Q

During acute illness in a patient with adrenal insufficiency what happens to steroid dose?

A
  • steroid dose doubled
  • until patient has recovered
  • to match normal steroid response to illness
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31
Q

4 main presentations of patient in an Addisonian Crisis?

A
  1. reduced consciousness
  2. hypotension
  3. hypoglycaemia, hyponatraemia, hyperkalaemia
  4. VERY UNWELL
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32
Q

management of Addisonian Crisis

A
  1. Parenteral steroids (IV hydrocortisone 100mg stat, then 100mg every 6hrs)
  2. IV fluid resus
  3. correct hypoglycaemia
  4. monitor electrolytes and fluid balance
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33
Q

Low TSH

High T3 & T4

A

Hyperthyroidism

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34
Q

High TSH

Low T3 & T4

A

Primary hypothyroidism

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35
Q

Low TSH

Low T3 and T4

A

Secondary hypothyroidism

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36
Q

In which two conditions are antithyroid peroxidase antibodies found?

A

anti-TPO

  • usually present in Grave’s disease
  • and Hashimoto’s thyroiditis
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37
Q

In which three conditions are anti-thyroglobulin antibodies present?

A
  1. graves disease
  2. hashimoto’s thyroiditis
  3. thyroid cancer
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38
Q

in which condition are TSH receptor antibodies found?

A
  • autoantibodies
  • mimic TSH
  • bind to TSH receptor
  • stimulate thyroid hormone release
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39
Q

Diffuse high uptake in radioisotope scan is found in which condition?

A

Grave’s disease

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40
Q

Focal, high uptake in radioisotope scans are found in which two conditions?

A
  1. toxic multinodular goitre

2. adenomas

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41
Q

cold areas on radioisotope scan may indicate

A
  • low uptake

- thyroid cancer

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42
Q

Describe primary hyperthyroidism

A
  • due to thyroid pathology
  • thyroid itself is misbehaving
  • and producing excess thyroid hormone
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43
Q

What is secondary hyperthyroidism

A
  • thyroid produces excess thyroid hormone
  • as a result of overstimulation by thyroid stimulating hormone
  • pathology either hypothalamus or pituitary
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44
Q

Condition where nodules develop on thyroid gland that act independently of the normal feedback system

and continuously produce excessive thyroid hormone

A

toxic multinodular goitre

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45
Q

What is key features are caused by Grave’s disease?

A

Exophthalmos

Pretibial myxoedema

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46
Q

What causes pretibial myoxoedema?

A
  • deposits of mucin under skin
  • of anterior leg
  • gives discoloured, waxy, oedematous appearance to skin
  • due to reaction to the TSH receptor antibodies
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47
Q

Summarise four main causes of hyperthyroidism?

A
  1. Grave’s disease
  2. Toxic multinodular goitre
  3. Solitary toxic thyroid nodule
  4. Thyroiditis
48
Q

7 universal features of hyperthyroidism

A
  1. anxiety and irritability
  2. sweating and heat intolerance
  3. tachycardia
  4. weight loss
  5. fatigue
  6. frequent loose stools
  7. sexual dysfunction
49
Q

what is De Quervain’s thyroiditis?

A
  • presentation of a viral infection
  • fever, neck pain, tenderness, dysphagia
  • and features f hyperthyroidism
50
Q

Treatment for De Quervain’s thyroiditis

A

supportive

NSAIDS for pain and inflammation

beta blockers for symptomatic relief of hyperthyroidism

51
Q

Describe presentation of patient with a thyrotoxic crisis

A
  • pyrexia
  • tachycardia
  • delerium
52
Q

Management of a thyrotoxic crisis?

A
  • admission for monitoring
  • fluid resus
  • anti-arrhytmic medicatication
  • beta blockers
53
Q

first line treatment for hyperthyroidism management

A
  1. carbimazole
54
Q

second line treatment for hyperthyroidism

A

propylthiouracil

55
Q

summarise 5 management options for hyperthyroidism

A
  1. caribimazole
  2. propylthiouracil
  3. radioactive iodine
  4. beta blockers to block adrenalin symptoms
  5. thyroid surgery
56
Q

Four main causes of Hypothyroidism?

A
  1. Hashimoto’s thyroiditis
  2. iodine deficiency
  3. secondary to treatment of hyperthyroidism
  4. medications: lithium, amiodarone
57
Q

Two medications with may cause hypothyroidism?

A
  1. lithium
    - inhibits thyroid hormone production
  2. amiodarone
    - interferes with thyroid hormone production
58
Q

Describe secondary hypothyroidism?

A
  • where pituitary gland failing to produce enough TSH
59
Q

What four things may cause secondary hypothyroidism?

A
  1. tumours
  2. infection
  3. vascular (Sheehan syndrome)
  4. radiation
60
Q

Presentation and features of hypothyroidism

7

A
  • weight gain
  • fatigue
  • dry skin
  • coarse hair and hair loss
  • fluid retention
  • heavy or irregular periods
  • constipation
61
Q

management of hypothyroidism

A
  • levothyroxine

- dose titrated until TSH levels become normal

62
Q

what may trigger T1DM

A
  • certain viruses such as Coxsackie B virus and enterovirus
63
Q

describe why potassium imbalance occurs in DKA

A
  1. insulin normally drives potassium into cells
    - serum potassium can be high or normal as kidneys continue to balance K+ through urinary excretion
    - total body potassium will be low
    - as no potassium is stored incells
64
Q

5 main presentations of patient with DKA

A
  1. hyperglycaemia
  2. dehydration
  3. ketosis
  4. metabolic acidosis with low bicarb
  5. potassium imbalance
65
Q

Treating DKA

A

FIG PICK

  • IV fluid
  • Insulin
  • glucose
  • potassium
  • infection (treat)
  • check fluid balance
  • monitor ketones
66
Q

Injecting into the same spot can cause a condition where the subcutaneous fat hardens and patients do not absorb insulin properly from further injections into this spot.

this is known as

A

lipodystrophy

67
Q

long term macrovascular complications of type 1 diabetes

A
  • coronary artery disease
  • peripheral ischaemic causes poor healing, ulcers and diabetic foot
  • stroke
  • hypertension
68
Q

microvascular complications of type 1 diabetes include

A
  • peripheral neuropathy
  • retinopathy
  • kidney disease: glomerulosclerosis
69
Q

infection related complications of T1DM

A
  • UTI
  • pneumonia
  • skin and soft tissue infections
  • fungal infections, particularly oral and vaginal candidiasis
70
Q

Dietary management for T2DM

A
  • vegetables and oily fish
  • low carb diet
  • low glycaemic, high fibre diet
71
Q

HbA1c targets for

  1. new type 2 diabetics
  2. patients on metformin alone
A

48 mmol/mol for new type 2 diabetics

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

72
Q

Summarise medical management of T2DM

A

1st line : metformin

2nd line: add, sulfonylurea, pioglitazone, DPP-4 inhibitor, SGLT-2 inhibitor

3rd line: triple therapy, metformin + two second line drugs; or metformin and insulin

73
Q

Describe action of metformin

A
  • increases insulin sensitivity
  • decreases liver production of glucose
  • weight neural
74
Q

notable side effects of metformin

A
  • diarrhoea
  • abdominal pain
  • lactic acidosis
75
Q

action of pioglitazone

A
  • increases insulin sensitivity

- decreases liver production of glucose

76
Q

action of sulfonylureas

A
  • stimulate insulin release from pancreas
77
Q

notable side effects of sulfonylurea’s

A
  • weight gain
  • hypoglycaemia
  • increased CVD and MI risk
78
Q

what are incretins?

A
  • hormones produced by GI tract
  • secreted in response to large meals
  • reduce blood sugar
79
Q

how to incretins reduce blood sugar?

A
  • increase insulin secretions
  • inhibit glucagon production
  • slow absorption by GI tract
80
Q

main incretin is

A

glucagon-like-peptide-1

81
Q

incretins are inhibited by what enzyme

A

dipeptidylpeptidase-4

DPP4

82
Q

action of DPP-4 inhibitors

A
  • inhibits DPP-4 enzyme

- thus increases GLP-1 activity

83
Q

notable side effects of DPP-4 inhibitors

A

GI tract upset

symptoms of upper respiratory tract infection

pancreatitis

84
Q

SGLT-2 inhibitors end with the suffix

A

-glifoxin

85
Q

describe action of sglt-2 inhibitors?

A

sglt-2 protein responsible for reabsorbing glucose from urine into the blood in PCT

SGLT-2 blocks this

causes glucose excretion

86
Q

acromegaly caused by:

A

excessive growth hormone

87
Q

what may cause bitemporal hemianopia?

A
  • optic chiasm lies above pituitary gland
  • pressure on optic chiasm
  • will lead to stereotypical ‘bitemporal hemianopia’
88
Q

Investigations for Acromegaly

A
  1. insulin-like-growth-factor-1
  2. oral glucose tolerance test
  3. MRI brain for pituitary tumour
  4. ophthalmology for visual field testing
89
Q

three types of medications to block growth hormone in management of acromegaly

A
  1. GH antagonist: pegvisomant, subcut daily
  2. block GH release, somatostatin analogue, ocreotide
  3. dopamine agonist to block GH release
90
Q

four ways parathyroid hormone acts to raise blood calcium

A
  1. increase osteoclastic activity in bones
  2. increase calcium absorption from gut
  3. increasing calcium absorption from kidneys
  4. increasing vitamin D activity
91
Q

symptoms of hypercalcaemia

A

renal stones, painful bones, abdominal groans and pyschic moans

abdominal groans: constipation, nausea, vomiting

psychiatric moans: fatigue, depression and psychosis

92
Q

primary hyperparathyroidism

A
  • uncontrolled pth release
  • aar of tumour of pt glands
  • hypercalcaemia!
93
Q

secondary hyperparathyroidism

A
  • insufficient vitamin D or chronic renal failure
  • leads to low absorption of calcium
  • from intestines, idneys and bones
  • hypocalcaemia
94
Q

tertiary hyperparathyroidism

A
  • aar of longterm secondary hyperparathyroidism
  • leads to hyperplasia of glands
  • high levels of pth
  • high absorption of calcium in intestines, kidneys and bones
  • causes hypercalcaemia
95
Q

which cells in the afferent arteriole of the kidney sense blood pressure?

A

juxtaglomerular cells

96
Q

aldosterone acts of kidney to

A
  • increase sodium reabsorption from distal tubule
  • increase potassium secretion from distal tubule
  • increase hydrogen secretion from collecting ducts
97
Q

primary hyperaldosteronism

A
  • adrenal glands

- producing too much aldosterone

98
Q

secondary hyperaldosteronism

A
  • excessive renin
  • stimulating adrenal glands
  • to produce more aldosterone
99
Q

investigation for hyperaldosteronism

A
  • renin/ aldosterone ratio

High aldosterone and low renin indicates primary hyperaldosteronism

High aldosterone and high renin indicates secondary hyperaldosteronism

100
Q

management of hyperaldosteronism

A

Aldosterone antagonists

  • eplerenone
  • spironolactone
101
Q

management of SIADH

A
  • fluid restriction

- ADH receptor blockers

102
Q

What is central pontine myelinolysis?

A
  • osmotic demyelination syndrome

- complication of long term severe hyponatraemia

103
Q

What occurs in central pontine myelinolysis?

A
  • blood sodium levels fall
  • water will move via osmosis across BBB
  • brain swell
  • brain reduces solutes to brain to prevent it becoming oedematous
  • when blood sodium levels begin to rise, water rapidly shifts out of brain cells into blood
104
Q

describe the two phases of symptoms in central pontine myelinolysis?

A

1st phase

  • aar electrolyte imbalance
  • patient presents as encephalopathic and confused

2nd phase

  • due to demyelination of neurones
  • occurs few days after rapid correction of sodium
105
Q

Diabetes insipidus is a …

A
  • lack of or response to ADH
  • prevents kidneys from being able to concentrate urine
  • leading to polyuria and polydipsia
106
Q

two classifications of diabetes mellitus

A

nephrogenic

cranial

107
Q

what is nephrogenic diabetes insipidus?

A
  • collecting ducts of kidney
  • don’t respond to ADH
  • can be caused by, lithium, intrinsic kidney disease, electrolyte disturbance
108
Q

cranial diabetes insipidus?

A
  • when hypothalamus does not produce ADH
  • for pituitary to secrete
  • can be caused by brain tumours, head injury. brain malformations, brain infections
109
Q

investigations for diabetes insipidus?

A
  • low urine osmolality
  • high serum osmolality
  • water deprivation test
110
Q

method of water deprivation test?

A

Initially the patient should avoid taking in any fluids for 8 hours.

This is referred to as fluid deprivation.

Then, urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again.

111
Q

management of diabetes insipidus

A
  • desmopression (synthetic ADH)

Cranial DI to replace ADH

Nephrogenic DI higher doses under close monitoring

112
Q

adrenaline is produced where

A
  • adrenal medulla

- by chromaffin cells

113
Q

pheochromocytoma

A
  • tumour of chromaffin cells

- secretes unregulated and excessive amounts of adrenaline

114
Q

diagnosis of pheochromocytoma made with

A
  1. 24 hr urine catecholamines

2. plasma free metanephrines

115
Q

what are metanephrines ??

A

breakdown product of catecholamines

116
Q

five typical signs and symptoms of a patient presenting with pheochromocytoma?

A
  1. anxiety
  2. sweating
  3. headache
  4. hypertension
  5. palpitations, tachycardia and paroxysmal atrial fibrillation
117
Q

management of pheochromocytomas?

A
  • alpha blockers (i.e. phenoxybenzamine)
  • beta blockers once established on alpha blockers
  • adrenalectomy to remove tumour = definitive management

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