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Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Suggest some tests that should be done for acromegaly?

A

CXR -cardiomegaly
ECG
Urine dip - glucosuria

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2
Q

List two complications of acromegaly

A

Cardiomegaly
and colonic polyps

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3
Q

How is adrenal insufficiency managed?

A

Patient education on ‘sick day’ rules, carrying a steroid card, and wearing a medical alert bracelet
Doubling the regular steroid medication dose during any intercurrent illness
Replacement of both glucocorticoids (typically with hydrocortisone) and mineralocorticoids (typically with fludrocortisone)
Regular screening for complications including an adrenal crisis and osteoporosis

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4
Q

What are the investigations for adrenal insufficiency?

A

U and E’s for hyponatremia
ACTH
Short synthacten test
Adrenal MRI
CT head

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5
Q

What are the causes of primary adrenal insufficiency?

A

Auto-immune destruction (most common)
Surgical removal of the adrenal glands
Trauma to the adrenal glands
Infectious diseases, such as tuberculosis (more common in developing countries)
Haemorrhage (e.g., Waterhouse-Friderichsen syndrome)
Infarction
Less commonly, neoplasms, sarcoidosis, or amyloidosis

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6
Q

What are the causes of secondary adrenal insufficiency?

A

Congenital disorders
Fracture of the base of the skull
Pituitary or hypothalamic surgery or Neoplasms in the pituitary or hypothalamus
Infiltration or infection of the brain
Deficiency of corticotropin-releasing hormone (CRH)

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7
Q

What are the side effects of steroid use?

A
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8
Q

What is the effect of amiodarone on the thyroid?

A

Type 1 (AIT 1): Primarily observed in patients with underlying thyroid nodules, amiodarone increases thyroid hormone production due to its high iodine content. This is more common in iodine-deficient areas. JOD BASEDOW

Type 2 (AIT 2): This is triggered by amiodarone in patients with a normally functioning thyroid gland, leading to a destructive thyroiditis. This type is more common in iodine-sufficient areas. WOLF-CHAIKOFF

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9
Q

List a key side effect for each of the anti-diabetes medications.

A

Metformin - lactic acidosis - avoid in kidney disease
DPP4 inhibitor i.e. sitagliptin - pancreatitis
Pioglitazone - weight gain, fluid retention, risk of bladder cancer
GLP-1/ exenatide - pancreatitis risk
Dapagliflozin - UTI risk

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10
Q

Outline the key aspects of carcinoid syndrome.

A

Symptoms: flushing, hypotension, diarrhoea, wheeze
Investigations: CT/ MRI, 5HIAA
Treatment: ocreotide and surgery

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11
Q

Outline some changes seen in Cushing’s syndrome

A
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12
Q

Outline the causes of Cushing’s?

A

ACTH dependent - pituitary tumour + ectopic
ACTH independent - adrenal tumours

disease = pituitary (d=p)

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13
Q

Discuss the tests for Cushing’s

A

Urinary cortisol
Low dose dexamethasone suppression - if suppressed then physiological
High dose dexamethasone suppression - pituiatry adenoma
Not suppressed - ectopic

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14
Q

Discuss the order of tests for Cushing’s

A

If ACTH is low likely an adrenal tumour
if high pituitary or ectopic

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15
Q

Discuss how the high dexamethsone test and low dexamethasone suppression tests vary.

A
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16
Q

Suggest the treatments for adrenal tumours.

A

Medication: Pasireotide (please), Metryrapone (Meet), Mifepristone (My), Ketoconazole (king)
Adrenalectomy

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17
Q

What is Nelson’s syndrome?

A

Nelson syndrome - enlarging of an adrenocorticotropic hormone-producing tumor in the pituitary gland.

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18
Q

Suggest Cushing’s disease management

A

Resection of the pituitary tumor or radiotherapy

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19
Q

What needs to be considered when managing Cushing’s patients?

A

Cortisol replacement

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20
Q

What is classed as delayed puberty?

A

> 14 in girls and >15 in boys
Causes are SHACKEN

Structural
Hypogodotropic hypogonadism/ hypergonadotropic hypogonadism
AID
CAH
Kallmans and Klinefelters
Exercise
No known cause

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21
Q

How is puberty investigated?

A

History and exam
BMI, height and weight
Bloods: TFTs, TTG-IgA,
Hormones: GH, FSH and LH, oestrogen and progesterone
Genetic testing
Wrist imaging

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22
Q

Discuss diabetes insipidus.

A

Deficiency in ADH.
Cranial or nephrogenic.
Cranial = head trauma, tumour, infection, sarcoidosis
Nephrogenic = Wolfram’s or offending drug like lithium, or CKD
Investigations: U and Es, water deprivation test
Treatments:
Cranial: desmopressin
Nephrogenic: correct electrolyte imbalance, stop offending drug. Trial high dose desmopressin (controversial) and trial NSAID and thiazide (even more controversial)

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23
Q

List three causes of cranial DI.

A

Head trauma
Sarcoidosis
Infection

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24
Q

List three causes of nephrogenic DI.

A

Wolfram’s
Lithium
CKD

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25
Q

What is the most common type of MODY?

A

MODY 3 is the commonest cause, occurring due to a mutation in HNF1A. It is characterised by a very high blood sugar (10-20), and is very sensitive to sulphonylureas (e.g. gliclazide.) Insulin is the next line of treatment if it doesn’t respond.

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26
Q

Discuss the tests for diabetes type 1.

A

Random blood glucose ≥ 11.1mmol/l or Fasting plasma glucose ≥ 7mmol/l
2-hour glucose tolerance ≥ 11.1mmol/l
HbA1C ≥ 48mmol/mol (6.5%)

Autoantibody testing: Identification of specific antibodies (e.g. anti-GAD, ICA, IAA) contributes to confirming the autoimmune nature of T1DM.
C-peptide levels: Evaluation of C-peptide production helps assess endogenous insulin secretion.
Urine ketone testing: Presence of ketones may suggest concurrent DKA.

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27
Q

What are the sick day rules for diabetes?

A

4 - check blood glucose and ketones every 3-4 h
3 - drink at least 3l
2 - 2 call if needing help
1 - continue medication

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28
Q

What is the treatment for DKA?

A
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29
Q

What are the values that signify DKA?

A

Diabetes >11
Ketones >3
Acidosis <7.3 AND bicarbonate <15
VBG needed

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30
Q

List 5 key concepts in managing DKA

A

British Journal of Diabetes

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31
Q

Suggest what signifies DKA resolution

A

<0.6 ketones
7.3 pH and >15 bicarbonate

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32
Q

What causes euglycaemic ketocacidosis?

A

SGLT2 inhibitors and pregnancy

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33
Q

What determines whether potassium is added to sodium chloride?

A

<3.5 senior review
3.5-5.5 add 40mmol
>5.5 do not add potassium

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34
Q

How is hypoglycaemia managed?

A
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35
Q

What is DKA?

A
36
Q

What are the normal thresholds for type 2 diabetes?

A

Random blood glucose ≥ 11.1mmol/l
Fasting plasma glucose ≥ 7mmol/l
2-hour glucose tolerance ≥ 11.1mmol/l
HbA1C ≥ 48mmol/mol (6.5%)

37
Q

When is dextrose added for DKA?

A

Diabetic ketoacidosis: once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the saline regime

38
Q

What is subclinical hyperthyroidism associated with?

A

Subclinical hyperthyroidism is associated with atrial fibrillation, osteoporosis and possibly dementia

39
Q

What is an impaired fasting glucose?

A

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

40
Q

What is GIF and GIT

A

GIF = Impaired fasting glucose = Between 6.1-7.0
GIT = impaired glucose tolerance = fasting <7, OGTT 7.8-11.1
Two occassions

41
Q

When do patients with diabetes need to surrender their driving licence?

A

After 2 hypoglycaemic events

42
Q

What is the most common cause of primary hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia is the most common cause of primary hyperaldosteronism (two better than one)

43
Q

Suggest a cause of falsely raised HbA1C

A

Splenectomy can give a falsely high HbA1c level due to the increased lifespan of RBCs

44
Q

What is acanthosis a sign of?

A

Acanthosis nigricans is a sign of insulin resistance,

45
Q

What gas abnormality is associated with Cushings?

A

hypokalaemic metabolic alkalosis

46
Q

How is glucogel management delivered?

A

he is conscious and able to swallow, he should be given oral glucose gel. This can be repeated after 15 minutes if blood glucose levels do not improve, for up to 3 treatments in total.

47
Q

T or F, canaligliflozin may be linked with foot ulcers

A

T - Closely monitor legs and feet of patients taking canagliflozin for ulcers or infection - possible increased risk of amputation

48
Q

What is the classification of diabetic retinopathy?

A

Dots, blots…cotton wool spots and exudates

49
Q

How is HHS managed?

A
50
Q

What is gastroparesis?

A

Erratic blood glucose control, bloating and vomiting think gastroparesis

51
Q

What is pre-diabetes defined as?

A

42-47 HbA1C

52
Q

What % of cases is eye disease worsened when radiotherapy is conducted?

A

Radioiodine treatment may lead to the development / worsening of thyroid eye disease in up to 15% of patients with Grave’s disease

53
Q

What can thyrotoxicosis cause to the heart?

A

Thyrotoxicosis can lead to high output cardiac failure

54
Q

When is a GLP-1 agonists considered?

A

When the BMI exceeds 35, it is recommended to substitute an existing antidiabetic medication with a GLP-1 receptor agonist such as liraglutide.

55
Q

Suggest some U and E changes linked with Addisons disease?

A

Hypoglycaemia, hyponatremia and hyperkalemia

56
Q

What is the optimum treatment for MODY?

A

GLICLAZIDE The patient has been diagnosed with maturity onset diabetes of the young (MODY) - type Hepatic Nuclear Factor 1 Alpha (HNF1A). HNF1A accounts for 70% of MODY cases. Sulfonylureas (e.g. gliclazide) are the optimal treatment in HNF1A-MODY.

57
Q

Outline some causes of hypoglycaemia.

A

Medications - bisoprolol, beta blockers
Diet
Addison’s
Insulinoma

58
Q

What is Whipple’s triad?

A
59
Q

What are the symptoms of prolactinoma?

A
60
Q

When should diabetics surrender their driving licence?

A

2 hypoglycaemic episodes

61
Q

What is sick euthyroid and how is it managed?

A

Sick euthyroid is common in unwell, elderly patients and often needs no treatment
EVERYTHING LOW (TSH can be normal)

62
Q

How is subclinical hypothyrodism managed?

A

Repeat TFTs in 6 months and treat with levothyroxine if not improved

63
Q

T or F, HbA1C must be repeated before diagnosis?

A

T

64
Q

T or F, haemodialysis gives a falsely low HbA1c

A

T

65
Q

What are the symptoms of hypoglycaemia?

A
66
Q

How is the normal patient’s regime managed in DKA?

A

In the acute management of DKA, insulin should be fixed rate whilst continuing regular injected long-acting insulin but stopping short actin injected insulin

67
Q

How many units of insulin are in 1ml

A

100 units

68
Q

How is thyrotoxicosis managed?

A

Radioiodine
Anti-thyroid drugs
Surgery

Thionamides
Propanolol

69
Q

How is thyrotoxic storm managed?

A
70
Q

What are the symptoms of myxoedema coma?

A
71
Q

What is the treatment for a myxoedema coma?

A
72
Q

What are the features of De Quervains

A

De Quervain’s thyroiditis: initial hyperthyroidism, painful goitre and globally reduced uptake of iodine-131

73
Q

What is the water deprivation test for?

A

Water deprivation test: primary polydipsia
urine osmolality after fluid deprivation: high
urine osmolality after desmopressin: high

74
Q

How is hypercalcemia manged?

A
75
Q

How is hypocalcemia managed?

A
76
Q

What is an affect of gliclazide?

A

Hypoglycaemia
Hyperinsulinemia
Weight gain

77
Q

What is first line in patients with raised BP, diabetes and of African ethnicity

A

An angiotensin II receptor blocker should be used first-line for black TD2M patients who are diagnosed with hypertension

78
Q

What are the investigations for primary aldosteronism?

A

Aldosterone renin ratio
CT scan
Sampling of adrenals veins

79
Q

Who should not be treated with sulphonylureas?

A

Lorry drivers due to hypoglycaemia

80
Q

What are the different MEN?

A

MEN 1 = gastrinoma and insulinoma as well, Zollinger
Easy
1 stomach, 1 parathyroid, 1 pancreas, 1 pituitary

phaeochromacytoma = 2

81
Q

What is shown here?

A

Thyroid acropachy

82
Q

What is shown here?

A

2nd and 3rd resorption in hyperparathyroidism

83
Q

What are the classes of BMI

A

Underweight < 18.49
Normal 18.5 - 25
Overweight 25 - 30
Obese class 1 30 - 35
Obese class 2 35 - 40
Obese class 3 > 4

84
Q

Suggest how MODY is inherited?

A

Autosomal dominant

85
Q

How is sick euthyroid managed?

A

No treatment necessary

Finals (24 decks)

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