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Phase 3B > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the difference between primary and secondary adrenal insufficiency?

A

Primary: destruction of adrenal cortex and reduction in adrenal hormone output

Secondary: inadequate pituitary or hypothalamic stimulation of the adrenal glands

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2
Q

Which parts of the adrenal gland produce aldosterone, catecholamines, and glucocorticoids?

A

Aldosterone: zona glomerulosa
Catecholamines: Medulla
Glucocorticoids: zona fasciculata

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3
Q

Other than autoimmune destruction of the adrenal gland (Addison’s disease), give three other causes of primary adrenal insufficiency.

A

Invasion (neoplastic, sarcoidosis)
Trauma/infarction
CAH

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4
Q

What are three causes of secondary adrenal insufficiency?

A

Exogenous steroids and antipsychotics suppress the hypothalamic-pituitary axis
Cranial irradiation

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5
Q

How does Addison’s disease present in its chronic form?

A

Tall, tanned, tired, lean

Fatigue and weight loss
Nausea and vomiting
Craving for salt
Brown hyperpigmentation
Muscle cramps and dizziness (hypotension)
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6
Q

What is the biochemistry seen in a patient with Addison’s disease?

A

Low sodium
High potassium
High calcium

Low cortisol, high ACTH, high renin, low aldosterone

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7
Q

How is Addison’s disease diagnosed?

A 
ACTH stimulation (Synacthen) test
Adrenal autoantibodies
CT adrenals
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8
Q

What is the treatment of Addison’s disease?

A

Hydrocortisone TD
Fludrocortisone OD

Monitor symptoms, BP, Na, K, and signs of over-replacement

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9
Q

What occurs in treatment of primary adrenal insufficiency if hypothyroidism is present?

A

Precipitation of adrenal crisis if glucocorticoid is replaced before treatment of hypothyroidism

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10
Q

What is the most common presentation of Addison’s disease in children?

A

Hypogylcaemia

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11
Q

What are three precipitants of adrenal crises?

A

Stress inc pregnancy
Illness
Abrupt withdrawal of steroids

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12
Q

How does adrenal crisis present?

A

Dehydration
Hypovolaemic shock
Confusion
Abdo pain, fever, n+v

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13
Q

What is the management of an adrenal crisis?

A

Immediate IV/IM hydrocortisone at a stress dose (100mg adult)

0.9% saline
IV hydrocortisone in 5% glucose
Continuous cardiac and electrolyte monitoring

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14
Q

Cushing’s Syndrome can be ACTH dependent, or ACTH independent - give a few examples of each.

A

ACTH dependent: Cushing’s disease, ectopic ACTH-producing tumours

ACTH-independent: unilateral adrenal adenoma, adrenal carcinoma, McCune Albright syndrome, Excess glucocorticoid administration

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15
Q

What is the cause of Cushing’s disease?

A

Excessive ACTH released from pituitary

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16
Q

What are the most important signs of Cushing’s disease?

A 
Truncal obesity and buffalo hump
Proximal muscle wasting
Moon facies
Reduced libido
Hypertension
Osteoporosis
Skin: atrophy, purple striae, easy bruising, hirsuitism, acne, pigmentation
Oligomenorrhoea
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17
Q

How is Cushing’s syndrome and the cause diagnosed?

A

Syndrome: 24h urinary free cortisol, overnight dexamethasone suppression test, 48h low dose dexamethasone suppression test, sleeping midnight serum cortisol

The cause: raised plasma ACTH, serum K and bicarb, high dose dexamethasone suppression test, Corticotropin-releasing hormone (CRH) test, bilateral inferior petrosal sinus sampling, MRI pituitary/CT adrenals after it has been proved biochemically

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18
Q

How is a pituitary tumour removed?

A

Trans-sphenoidal microsurgeyr

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19
Q

Which drugs can normalise cortisol levels in patients who are waiting or unfit for surgery?

A

Ketoconazole and metryrapone

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20
Q

What is the pathophysiology of primary hyperaldosteronism?

A

Excessive aldosterone acts on the distal renal tubule, promoting sodium retention, which results in water retention, and volume expansion.

Excretion of potassium, resulting in hypokalaemia

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21
Q

What are three causes of primary hyperaldosteronism?

A 
Adrenal adenoma (Conn's syndrome)
Bilateral adrenal hyperplasia
Familial hyperaldosteronism GRA
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22
Q

What are three causes of secondary hyperaldosteronism?

A

Excessive renin in the circulation stimulates adrenals to produce aldosterone

Diuretics, CCF, hepatic failure, renal artery stenosis

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23
Q

How may hyperaldosteronism present?

A

Routine - hypertension
Polyuria and polydipsia
Headaches and lethargy

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24
Q

How is hyperaldosteronism diagnosed?

A
  1. Uncontrolled hypertension, hypokalaemia, and hypernatraemia
  2. Low renin
  3. High aldosterone
  4. Refer to specialists - selective adrenal venous sampling
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25
Q

What is the treatment of Conn’s syndrome?

A

Spironalactone prior to laparoscopic adrenalectomy

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26
Q

Define hypoglycaemia.

A

Blood glucose<3.0mmol/L

Hospitalised patients <4.0mmol/L

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27
Q

What are three risk factors for hypoglycaemia?

A

Tight glycaemic control
Impaired awareness
Injection into lipohypertrophy sites

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28
Q

How does hypoglycaemia present?

A

Sweating, shakiness, dizziness, nausea

Coma

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29
Q

What is the management of hypoglycaemia in the conscious adult?

A

Glucose 10-20g PO (can be glucogel)

Can repeat 1-3 times

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30
Q

What is the management of hypoglycaemia in the unconscious adult?

A

IV 75-80ml 20% glucose

If at home, 1mg IM/SC glucagon

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31
Q

Why is a longer acting carbohydrate given after glucose in hypoglycaemic patients?

A

Restores liver glycogen

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32
Q

What is the management of hypoglycaemic coma?

A

IV mannitol and dexamethasone

IV glucose

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33
Q

What is a side effect of glucagon for hypoglycaemia?

A

Causes more insulin to be released - potential for secondary rebound hypoglycaemia.

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34
Q

Which tumours are seen in MEN Type 1 syndrome?

A

Pituitary prolactinomas/adenomas
Parathyroid tumours
Endocrine gastroenteropancreatic tract tumours
Cutaneous tumours

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35
Q

Which tumours are seen in MEN Type 2 syndrome?

A

Medullary thyroid cancer
Hyperparathyroidism
Phaechromocytoma

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36
Q

What are three risk factors for phaechromocytoma?

A

MEN Type 2 (bilateral)
VHL disease
NFT Type 1

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37
Q

How do phaechromocytomas present?

A

Headache, profuse sweating, palpitations, tremor

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38
Q

How is phaechromocytoma diagnosed?

A

24 hour urinary metanephrines

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39
Q

What molecule do non-functional pancreatic endocrine tumours secrete?

A

Pancreatic polypeptide

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40
Q

Name three pancreatic endocrine tumours.

A

Insulinoma
Gastrinoma
Glucagonoma

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41
Q

What is secondary hyperparathyroidism?

A

Hyperplastic PTH glands and increased secretion of parathyroid hormone in response to chronic hypocalcaemia, which is from kidney, liver, or bowel disease.

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42
Q

What are the causes of primary hyperparathyroidism?

A

Single parathyroid adenoma (85%)
4-gland hyperplasia
Parathyroid carcinoma
MEN syndromes

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43
Q

How does hyperparathyroidism present?

A

Asymptomatic, incidental finding
Osteoporosis and pathological fractures
Hypercalcaemia

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44
Q

What is seen on bloods in hyperparathyroidism?

A

High corrected calcium
High PTH
Low phosphate
Low vitamin D

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45
Q

What is the management of mild, asymptomatic hyperparathyroidism?

A

Surveillance
Check creatinine and calcium bi-annually
3-site DEXA every 1-2 years

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46
Q

What is the treatment of symptomatic hyperparathyroidism?

A

Parathyroidectomy

OR

HRT and raloxifene

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47
Q

What are three complications of parathyroidectomy?

A

Recurrent laryngeal nerve injury
Hypocalcaemia
Haematoma

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48
Q

What is seen on bloods in secondary hyperparathyroidism?

A

Calcium: low/normal
PTH: high
Phosphate: high in renal disease, low in vitamin D deficiency

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49
Q

What is the management of CKD-related secondary hyperparathyroidism?

A

Calcium supplementation
Phosphate restriction/phosphate binders
Parathyroidectomy

50
Q

What is the pathophysiology of tertiary hyperparathyroidism?

A

The PTH glands become autonomous, producing excessive PTH even after the cause of hypocalcaemia has been corrected. This results in hypercalcaemia and hyperphosphataemia.

51
Q

What are the causes of hypoparathyroidism?

A

Anterior neck surgery
DiGeorge syndrome
Transient in the neonatal period

52
Q

How is hypoparathyroidism diagnosed?

A

S+S of hypocalcaemia

Bloods:
Low calcium, high phosphate, low PTH, normal ALP

53
Q

How does acute pituitary failure present?

A

Severe headache from stretching of the dura mater in the sella
Vomiting
Diplopia, bitemporal superior quadrantic field defect
Thermal dysregulation

54
Q

How is acute pituitary failure managed?

A

Deficiency of all hormones, urgent MRI

Resuscitation and stabilisation
IV hydrocortisone
Urgent transsphenoidal decompression

55
Q

Where do pituitary tumours invade?

A

Dura mater
Cranial bone
Sphenoid sinus

56
Q

What are the presentations of:

1) ACTH-secreting tumours
2) GH-secreting tumours
3) Prolactinomas
4) Non-secreting tumours
5) Thyrotropinoma

A

1) Cushing’s disease
2) Gigantism in children, acromegaly in adults
3) Women - galactorrhoea, infertility, oligomenorrhoea. Men - hypogonadism, infertility, erectile dysfunction
4) Visual loss
5) Hyperthyroidism

57
Q

How are pituitary tumours diagnosed?

A

Pituitary function tests
Lateral skull X-Ray
MRI

58
Q

Detail pituitary function tests.

A

Anterior: GnRH stimulation, TRH stimulation, insulin tolerance test for GH and ACTH

Posterior: prolactin levels

59
Q

In response to TSH, the thyroid produces thyroxine (T4) and triiodothyronine (T3). What happens to T4?

A

It is inactive, so needs to be converted to T3 in the liver and kidney

60
Q

Apart from Graves’ disease, give three other causes of hyperthyroidism.

A

Toxic multinodular goitre
Toxic adenoma
Thyroid carcinoma

61
Q

What are three risk factors for hyperthyroidism?

A

Smoking
Family history
High iodine intake

62
Q

What are the symptoms of hyperthyroidism?

A

SWEATING

Sweating
Weight loss
Emotionally labile
Appetite increase
Tremor/tachycardia/AF
Intolerance to heat/irregular periods
Nervousness
Goitre/GI problems (diarrhoea)

Patients also have proximal myopathy, eye disease, and brisk reflexes

63
Q

What are the symptoms of thyrotoxicosis?

A

Severe hyperthyroid symptoms
Hyperthermia
Mental disturbance
Arrhythmias

64
Q

What extra signs are seen in Graves’ disease?

A

Pretibial myxedema
Thyroid acropachy
Exophthalmos, opthalmoplegia

65
Q

How is Graves’ disease diagnosed?

A

Low TSH
High T4; if normal then High T3
anti-TPO antibodies or anti-thyroglobulin antibodies
131-I labelled thyroid scan

66
Q

What is the treatment of Graves’ disease?

A 
Carbimazole
Propanolol
Nitrazepam night sedation
Subtotal thyroidectomy once euthyroid
Radioactive iodine is CI in young adults as it leads to hypothyroidism after some time
67
Q

Which hyperthyroid treatments are contraindicated in pregnancy and breastfeeding?

A

Carbimazole (use propylthiuracil)

Radio-iodine (subtotal thyroidectomy)

68
Q

What is seen in secondary hyperthyroidism?

A

Pituitary releases too much TSH

High TSH, high T3, high T4

69
Q

What are three causes of hypothyroidism?

A

Iodine deficiency
Hashimoto’s/atrophic thyroiditis
Amiodarone/lithium

70
Q

What are the symptoms of hypothyroidism?

A

MOM’S SO TIRED

Memory loss and poor concentration
Obesity
Malar flush/menorrhagia
Slowness inc. constipation
Skin and hair dryness
Onset gradual
Tiredness
Intolerance to cold
Raised BP
Energy levels fall
Depression/delayed relaxation of reflexes
71
Q

How is control of hypothyroidism monitored long term?

A

TSH

72
Q

Why can gastroparesis occur in diabetics?

A

Neuropathy of the vagus nerve

73
Q

What is the initial management of prolactinomas?

A

Dopamine agonists e.g. bromocriptine

74
Q

What are the causes of raised prolactin?

A

The Ps:

Pregnancy
Prolactinoma
Physiological
PCOS
Primary hypothyroidism
Phenothiazines, metoclopramide, domperidone
75
Q

When is C-peptide used?

A

To distinguish type 1 diabetes from other types of diabetes:

Low in type 1
Normal or high in type

76
Q

Name five symptoms of hypothyroid myxedema.

A 
Expressionless dull face
Pale cool doughy skin
Cardiomegaly
Megacolon
Encephalopathy
77
Q

How is type 2 diabetes controlled?

A

HbA1c>48mmol/L or 6.5%
OR
Fasting blood glucose>7mmol/L or random>11.1mmol/L

One sample needed if symptomatic, two if not.

78
Q

What are the indications of self monitoring of blood glucose in type 2 diabetes?

A

Pregnancy
Patient on insulin
Hypoglycaemic episodes

79
Q

What is the management of type 2 diabetes?

A
  1. Metformin
  2. Metformin AND [DPP-4 inhibitor, pioglitazone, or sulfonylurea]
  3. Metformin AND sulfonylurea AND [DPP-4 inhibitor or pioglitazone]
    OR insulin
  4. Metformin AND sulfonylurea AND GLP-1
    OR insulin
80
Q

How does metformin work?

A

Opposes insulin resistance, decreases lipids and CV risk

81
Q

What are the side effects and contraindications of metformin?

A

Lactic acidosis, diarrhoea (try modified release)

CI: raised creatinine/eGFR<45

82
Q

Name two sulfonylureas.

A

Gliclazide

Glibenclamide

83
Q

How do sulfonylureas work?

A

Stimulate insulin release by binding to beta cell receptors

Stimulate the glycolytic pathway in the liver and inhibit the production of glucose

84
Q

What are the main side effects of sulfonylureas?

A

Weight gain

Prolonged/severe hypoglycaemia

85
Q

What type of drug is pioglitazone?

A

Thiazolidinediones

86
Q

How do DPP-4 inhibitors such as sitagliptin work?

A

Increase insulin secretion and lower glucagon secretion

87
Q

How do GLP-1 mimetics such as exenatide and liraglutide work?

A

Increase insulin secretion, lower glucagon secretion, slow gastric emptying
Prevent weight gain

88
Q

Define hyperosmolar hyperglycaemic state (HHS)

A

Hypovolaemia
Hyperglycaemia >30mmol/L
Without significant hyperketonaemia (<3mmol/L) or acidosis (pH.7.3)

89
Q

What may precipitate HHS?

A

Infection
Stroke/MI
Poor diabetic control

90
Q

How does HHS present?

A

Weakness, cramps, confusion
Focal neurological features
N+V may occur

91
Q

What osmolality is seen in HHS and how is it calculated??

A

> 320mosmol/kg

2Na + glucose + urea

92
Q

What other investigations are important in HHS?

A 
High Na+ and K+
U&amp;Es for pre-renal AKI
Glycosuria and normal ketonuria
Blood and urine cultures
CK and troponins
93
Q

How is HHS managed?

A

IV 0.9% saline

IV insulin 0.05IU/kg/hour

94
Q

What is type 1 diabetes?

A

Autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency.

95
Q

How does type 1 diabetes present?

A

Weight loss
Polydipsia and polyuria
Dehydration
Ketonuria and hyperventilation

96
Q

How is type 1 diabetes diagnosed, in terms of abnormal plasma glucoses, OGTT, and HbA1c?

A

Random >11.1mmol/L
Fasting >7mmol/L
OGTT >11.1mmol/L
HbA1c >48mmol/mol or >6.5%

97
Q

What is some general advice given to type 1 diabetic new diagnoses?

A

Carry a source of glucose
Train a parent on administering glucagon
Sick day supply box
Do not stop insulin if ill

98
Q

What levels of plasma glucose should be aimed for in type 1 diabetics?

A

On waking: 5-7mmol/L

Before meals: 4-7mmol/L

99
Q

Describe the basal bolus insulin regimen given to type 1 diabetic patients.

A

Bedtime: long acting insulin
Mealtimes: rapid or short acting insulin

100
Q

What is continuous subcutaneous insulin infusion?

A

Insulin pump

Indwelling catheter worn underneath patient’s clothing
Patient activates pre-meal boluses

101
Q

In which patients is an insulin pump useful for?

A

Poor glycaemic control
Recurrent hypoglycaemia
Young people

102
Q

Name three rapid acting insulins and why they are more useful than short acting insulins (Humulin).

A

Insulin aspart, glulisine, and lispro

Even faster onset of action so can be injected very shortly before or even after a meal

103
Q

Name two long acting insulins.

A 
Insulin glargine (Lantus)
Insulin determir
104
Q

Name three things that may precipitate DKA.

A

Infection
Steroid treatment
Discontinuation of insulin

105
Q

Name three signs of DKA.

A

Acetone smell to breath
Kussmaul respiration (respiratory compensation of acidosis)
Dehydration

106
Q

What is the criteria for DKA?

A

Ketonaemia >3mmol/L OR ketonuria >2+

Blood glucose >11mmol/L OR known DM

Venous pH <7.3, OR bicarbonate <15mmol/L

107
Q

What plasma osmolality and anion gap is seen in DKA?

A

> 290mOsm/kg

Anion gap >13mmol/L

108
Q

What is the management of DKA?

A

Resuscitation with ABCDE approach, obtain large bore IV access

IV 0.9% normal saline bolus followed by maintenance
watch potassium

Fixed rate IV insulin at 0.1IU/kg/hour

109
Q

In DKA, once plasma glucose <12mmol/L, replace normal saline with what and why?

A

5% dextrose

Prevents rapid-over correction and hypoglycaemia

110
Q

Name three complications of DKA.

A

Cerebral oedema
Iatrogenic hypokalaemia and hypoglycaemia
Cardiac dysrhythmia

111
Q

Give a cause of a non-tender and a tender goitre and what they present with.

A

Tender: De Quervain’s thyroiditis. Hyperthyroidism

Non-tender: Hashimoto’s thyroiditis: hypothyroidism

112
Q

Which autoantibodies are seen in Graves’ disease?

A

TSH receptor stimulating antibodies

113
Q

What is seen on blood tests in sick euthyroid syndrome?

A

Normal-low TSH, low T3, low T4

114
Q

What is the most common type of MODY (maturity onset diabetes of the young), and what are the characteristics?

A

MODY 3 - Hepatic nuclear factor 1-alpha (HNF 1-a)

Strong FH, misdiagnosed as type 1, but negative autoantibodies at diagnosis

Hepatic neoplasms

115
Q

What is the 2nd most common type of MODY and what are the characteristics?

A

MODY 2 - glucokinase

Blood glucose levels are reset higher e.g. 6-8mmol/L. Usually diet managed except in pregnancy

116
Q

What is the treatment of a thyroid storm?

A

Propylthiouracil
Iodine
Hydrocortisone (inhibits T3–>T4)
Propanolol

117
Q

What is the acid base balance seen in DKA?

A

Metabolic acidosis

Respiratory alkalosis to compensate

118
Q

What is the cause of acromegaly?

A

Growth hormone secreting pituitary adenoma

119
Q

How is acromegaly diagnosed?

A

Measure IGF-1 levels

If high, give oral glucose load and GH will fail to suppress

120
Q

Give eight symptoms of acromegaly.

A 
Headache
Sweating
Macroglossia
Increased size of hands and feet
Hypertension
Diabetes
Carpal tunnel
Bitemporal hemianopia
121
Q

How is acromegaly treated?

A

Transsphenoidal hypophysectomy
Pituitary radiotherapy
Somatostatin analogue e.g. octreotide
Dopamine agonist e.g. cabergoline

Phase 3B (20 decks)

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