Endocrinology Flashcards

1
Q

What levels of HbA1c and glucose are diagnostic for diabetes?

A

HbA1c >48
Random glucose >11
Fasting glucose >7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Medical management of type II diabetes

A

1st line - metformin
2nd line (if HbAa1c >58) - add 2nd drug from other diabetes drugs
3rd line - (if HbA1c remains above 58) - consider insulin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the most common sulphonylurea medication and it’s mechanism of action

A

Gliclazide

Increases insulin release from pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name the common thiazolidinedione and its MOA

A

Pioglitazone

Increases insulin sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name the common SGLT2-inhibitors

A

Empagliflozin, canagliflozin, dapagliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name the common DDP4 inhibitor and it’s MOA

A

Sitagliptin

Inhibits breakdown of GLP-1 (which in turn stimulates insulin release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name the common GLP-1 Mimetic

A

Exenatide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which diabetes medication class increases the risk of bladder cancer

A

Thiazolidinediones e.g, pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which diabetes medication is contraindicated in patients with heart failure?

A

Thiazolidinediones e.g, pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which diabetes medication class increase the risk of fournier’s gangrene?

A

SGLT-2 inhibitors e.g, empagliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which diabetes medication is preferable in patients who are overweight

A

DPP4 inhibitors e.g, sitagliptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathophysiology of hyperosmolar hyperglycaemic state (HHS)

A

Hyperglycaemia leads to osmotic diuresis with associated loss of sodium and potassium
Severe volume depletion leads to raised serum osmolarity
Hyperviscosity of blood can lead to vascular complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical features of Hyperosmolar hyperglycaemic state (HHS)

A

Nausea, vomiting
Polydipsia
Neurological symptoms e.g, reduced GSC, headaches, weakness
Cardiovascular symptoms - hypotension, tachycardia
Significantly raised serum osmolarity
Hypovolemic
Hyperglycaemic (>30)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Management of HHS

A

Admit
Normalise osmolality (gradually) - isotonic solution (normal saline)
IV fluid and electrolyte replacement
Normalise blood glucose (Gradually)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Medical management of diabetic neuropathy

A
Amitriptyline 
Duloxetine 
Gabapentin 
Pregabalin 
Topical capsaicin - may be used for localised neuropathic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of gastrointestinal autonomic neuropathy in type II diabetes

A

Metoclopramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the diabetes sick day rules

A

Continue meds are normal
Increase frequency of BM monitoring
Encourage fluid intake
May need sugary drinks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Presentation of diabetic ketoacidosis

A
Abdominal pain 
Polyuria/polydipsia 
Dehydration 
Kussmaul respiration 
Acetone smelling breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of diabetic ketoacidosis

A

IV Fluid replacement - isotonic saline
Fixed rate IV insulin replacement: 0.1 units/kg/hour
Correction of hypokalaemia
- if 3.5-5.5 give 40mmol/L in infusion
- if <3.5 seek senior review for additional K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What should happen in regular insulin medication during diabetic ketoacidosis

A

Stop short acting

Continue long acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the risks of diabetic ketoacidosis managemetnt

A

Arrthymias - secondary to hyperkalaemia
Cerebral oedema - secondary to fluid infusion, more common in children and needs to be closely monitored
Acute respiratory distress syndroem
AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is maturity onset diabetes of the young (MODY)?

A

Development of type II diabetes in patients <25 years old

Typically autosomal dominant condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Medical management of MODY

A

Sulfonylureas e.g, gliclizide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Features of insulinoma

A

Hypoglycaemia
Rapid weight gain
Raised insulin
Raised C-peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Clinical Features of Hyperthyroidism

A
Weight loss 
Restlessness 
Heat intolerance 
Palpatiations 
Diarrhoea 
Oligomenorrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Signs specific to Graves’ disease

A

Exophthalmos
Pretibial myxoedema
Digital clubbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Medical management of Graves Disease

A

Propanolol - for symptom relief

Carbimazole - titration or block and replace

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Main side effect to consider when starting carbimazole

A

Agranulocytosis
Need to monitor FBCs
Need to warn patient what to do if they get sore throat etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Alternative management of Graves’ disease if medical management is unsuccessful

A

Radioactive idodine

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a thyroid storm?

A

Life threatening complication of thyroidtoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Risk factors for thyroid storm

A

Thyroid surgery
Trauma
Infection
Acute iodine load e.g, CT contrast media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical Features of Thyroid Storm

A
Fever 
Tachycardia 
Confusion 
Nausea/vomiting 
Hypertension 
Abnormal LFTs - jaundice may be seen clinically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of thyroid storm

A

Beta blockers - IV Propanolol
Propylthiouricil
IV hydrocortisone - blocks conversation of T4 to T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Antibodies in Graves’ disease

A

Anti-TSH

35
Q

Antibodies in Hashimotos

A

Anti-TPO

36
Q

Drug causes of hypothyroidism

A

Lithium

Amiodarone

37
Q

Clinical features of hypothyroidism

A
Weight gain 
Lethargy 
Cold intolerance 
Dry skin 
Oedema 
Constipation 
Menorrhagia 
Decreased reflexes
38
Q

Cause of secondary hypothyroidism

A

Pituitary insufficiency

39
Q

Management of hypothyroidism

A

Levothyroxine

40
Q

What is myxoedema coma

A

Complication of longstanding untreated hypothyroidism

41
Q

Presentation of myxoedema coma

A
Confusion 
Hypothermia 
Odema 
Reduced respiratory drive 
Seizures
42
Q

Management of myxoedema coma

A

IV thyroid replacement
IV fluids
IV corticosteroids

43
Q

What is subclinical hypothyroidism

A

TSH raised

T3/T4 normal

44
Q

When would you treat subclinical hypothyroidism

A

TSH between 4-10
<65 years and symptomatic - trial levothyroxine
If asymptomatic - no treatment

TSH >10
<70 years - start treatment even if asymptomatic
>80 - no treatment

45
Q

What is de Quevain’s thyroiditis

A

Hyperthyroidism following viral infection
May present with painful goitre and raised ESR
Period of hypothyroidism following a few months of hyperthyroidism
No treatment needed

46
Q

Types of thyroid cancer and age groups typically found in

A

Papillary (65%) - seen in young females
Follicular (20%) - seen in women >50 years
Medullary
Anaplastic (Rare) - occurs in elderly patients

47
Q

Thyroid tumour markers for different cancers

A

Papillary and follicular - thyroglobulin

Medullary - calcitonin (originates from parafollicular cells)

48
Q

Management of hyperthyroidism in pregnancy

A

1st trimester - replace carbimazole with propylthiouracil as increased risk of congenital abnormalities
2nd trimester - switch back to carbimazole

Monitor thyroixine levels throughout pregnancy - should be kept in upper 1/3rd of normal limit to avoid fetal hypothyroidism

49
Q

Management of Hypothyroidism in pregnancy

A

Levothyroxine should be increased in pregnancy - 50% increase in dose as early as 4-6 weeks of pregnancy

50
Q

What is sick euthyroid syndrome

A

Deranged thyroid levels during infection or viral illness
Low/normal TSH
Low T3
Low T4

51
Q

Clinical features of primary hyperparathyroidism

A

Hypercalcemia
Low phosphate
Polyuria/Polydipsia - due to raised calcium
PTH may be raised or inappropriately normal due to raised calcium
Kidney stones

52
Q

What would an X-ray head show in primary hyperparathyroidism

A

Pepper pot skull

53
Q

Management of primary hyperparathyroidism

A

Surgery - total parathyroidectomy

Conservative management may be considered if patient is older and has no end organ damage
Cinacalcet considered in patients unsuitable for surgery

54
Q

Blood results on secondary hyperparathyroidism

A

PTH - high
Calcium - Low or normal
Phosphate - High

55
Q

Blood results in tertiary hyperparathyroidism

A

PTH - very high
Calcium - normal or high
Phosphate - normal or low

56
Q

Blood results in primary hyperparathyroidism

A

PTH - normal or high
Calcium - high
Phosphate - low

57
Q

Causes of primary hyperaldosteronism

A

Idiopathic bilateral adrenal hyperplasia
Conns syndrome
Adrenal carcinoma

58
Q

Features of primary hyperaldosteronism

A

Hypertension
Hypokalaemia - due to increased aldosterone
Alkalaosis - due to raised bicarbonate associated with increased aldosterone

59
Q

Diagnostic test in primary hyperaldosteronism

A

Plasma aldosterone/renin ratio - shows high aldosterone and low renin ratio

60
Q

Management of primary hyperaldosteronism

A

Bilateral adrenocortical hyperplasia - spironolactone

Adrenal adenoma - surgery

61
Q

What is Addison’s disease

A

Autoimmune destruction of adrenal glands

Leads to reduction in cortisol and aldosterone production

62
Q

Clinical features of Addison’s

A

Lethargy, weakness, anorexia
Hyperpigmentation - especially in palmer creases
Hypotension
Salt craving
Increased thirst - as sodium and water is being lost due to reduced aldosterone

63
Q

Blood results in Addison’s

A

Hyponatraemia
Hyperkalamia
Hypoglycaemia

64
Q

Diagnostic test for Addison’s

A

Short synacthen test

  • ACTH is given which would usually increase cortisol
  • in Addison’s cortisol will not rise in response due to defective adrenal gland
65
Q

Medical management of Addison’s

A

Glucocorticoid replacement - hydrocortisone

Mineralcorticoid replacement - fludrocortisone

66
Q

Advise on medication changes for Addison’s patients when they have intercurrent illness

A

Double glucocorticoid dose (double hydrocortisone)

67
Q

Management of Addisonian crisis

A

IV hydrocortisone

IV saline with dextrose

68
Q

What is Cushing’s syndrome

A

Symptoms due to excess cortisol

69
Q

Common causes of Cushing’s syndrome

A

Cushings disease - pituitary secreting ACTH
Ectopic ACTH production e.g, small cell lung cancer
Adrenal adenoma
Iatrogenic - excess steroids

70
Q

Differentiating between causes of cushings

A

Dexamethasone suppression test
Low dose - will not suppress pituitary tumour OR other causes
High dose - will suppress pituitary tumour releasing ACTH
High dose - will NOT suppress ectopic ACTH production or adrenal adenoma

Measuring ACTH to help differentiate - this will be low in adrenal adenoma

71
Q

What is a phaeochromocytoma?

A

Catecholamine secreting tumour of the adrenal glands

72
Q

Symptoms of phaeochromocytoma

A
Hypertension 
Headache 
Palpitations 
Sweating 
Anxiety
73
Q

Diagnosis of phaeochromocytoma

A

24hr collection of urinary meranephrines

74
Q

Management of phaeochromocytoma

A

Surgery

Pt must be stabilised with alpha blocker first e.g, phenoxybenzamine

75
Q

MEN type 1

A

Parathyroid hyperplasia
Pituitary hyperplasia
Pancreas - e.g, insulinoma, gastrinoma

76
Q

MEN Type IIa

A

Parathyroid hyperplasia

Phaeochromocytoma

77
Q

MEN type IIb

A

Thyroid cancer

Phaeochromocytoma

78
Q

What is kallman’s syndrome

A

Hypogonadotrophic hypogondism
X linked recessive trait
Leads to delayed puberty in boys

79
Q

Hormone levels in Kallmann syndrome

A

Low testosterone

Low LH and FSH

80
Q

Clinical presentation of kallman’s syndrome

A

Delayed puberty
Anosmia
Reduced sex hormones
Normal or above average height

81
Q

What is Klinefelter syndrome

A

Genetic disease causing XXY in men

82
Q

Hormone levels in Klinefelter syndrome

A

Low testosterone

Increase LH and FSH

83
Q

Clinical features of Klinefelter syndrome

A
Taller than average 
Lack of secondary sexual characteristics 
Small, firm testes 
Infertility 
Gynaecomastia