MSRA > Endocrine > Flashcards

Endocrine Flashcards

(74 cards)

Start Studying
1
Q

At what HbA1c should you add in another agent to treat diabetes?

What is the target range? And what is the target range if you’re on a drug which can cause hypos (e.g sulphonylureas?)

A

HbA1c >58

Or add an SLGT2 inhibitor to metformin if there are established cardiovascular risk factors

Note HbA1c 48 is the target
53 if you’re on a drug that can cause hypos

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

What are the criteria for pre diabetes?

A

HbA1c 42-47
Fasting glucose 6.1-6.9

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

What’s the criteria for impaired fasting glucose?

A

6.1-7

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

What’s the criteria for impaired glucose tolerance?

A

Fasting glucose <7

2 hour tolerance 7.8-11.1

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

What is the most likely adverse effect from radioiodine therapy?

A

Hypothyroidism

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

What is the mainstay of treatment for Addison’s?

A

Hydrocortisone (glucocorticoid replacement) and fludrocortisone (mineralocorticoid)

In intercurrent illness > double the hydrocortisone but leave the fludrocortisone the same

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

What conditions can give a falsely low HbA1c reading and why?

A

Sickle cell anaemia and haemoglobinopathies

Due to decreased FBC lifespan

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

What condition can cause a falsely high HbA1c reading and why?

A

Splenectomy - increased RBC lifespan

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

What test is used to diagnose Addison’s?

A

Short synacthen test

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

How do you manage De Quervain’s thyroiditis?

A

Conservative management with ibuprofen, sometimes steroids in more severe cases

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

What are the causes of primary hyperaldosteronism?

A

Adrenal adenoma in 20-30% of cases
Bilateral adrenal hyperplasia in 60-70% of cases

Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

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

How does primary hyperaldosteronism present?

A

Hypertension

Hypokalaemia

Metabolic alkalosis

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

What would the aldosterone/ renin ratio show in primary hyperaldosteronism?

A

High aldosterone levels
Low renin levels

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

How is primary hyperaldosteronism managed?

A

Adrenal adenoma > surgery
Bilateral hyperplasia > spironolactone (aldosterone antagonist)

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

What are the TFT results in sick euthyroid syndrome?

A

Low T3/4, normal TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is toxic multinodular goitre and how is it investigated and treated?

A

Thyroid gland contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.

Nuclear scintigraphy reveals patchy uptake.

Treatment is with radioiodine.

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

How does phaeochromocytoma present and how is it investigated?

A

Headache, sweating, palpitations, hypertension

Urinary metanephrines

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

How are prolactinomas treated?

A

Dopamine agonists - bromocriptine. Surgery if it doesn’t respond > trans sphenoidal approach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What blood gas pattern do you see in cushings?

A

Hypokalaemic metabolic alkaosis

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

What is the main serious adverse effect of carbimazole to be aware of?

A

Agranulocytosis

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

What is the difference between cushing’s disease and cushing’s syndrome?

What is cushing’s triad?

A

Cushing’s disease - increased ACTH production from the pituitary, usually due to an adenoma

Cushing’s syndrome - due to prolonged exposure to cortisol. E.g steroids or adrenal causes.

Cushing’s triad - irregular respirations, bradycardia and systolic hypertension resulting from raised intracranial pressure.

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

When should you start thyroxine when TFT results show a picture of subclinical hypothyroidism?

A

TSH high on 2 occasions 3 months apart and they are symptomatic
- Do a 6 mnonth trial of thyroxine

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

How do you interpret C-peptide levels?

A

Low - T1DM
Normal/ high - T2DM

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

What are the causes of a raised prolactin?

A

pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metoclopramide, domperidone, prochlorperazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What medications can reduce hypoglycaemic awareness in diabetics?
B-blockers
26
How does primary hyperaldosteronism present?
High BP Low potassium, high sodium Causes: Bilateral idiopathic adrenal hyperplasia Or conn's if there is an adrenal adenoma
27
Which condition is associated with a tender goitre?
De Quervain's thyroiditis aka subacute thyroiditis Can present with either hyper or hypothyroidism (hyper initially before developing into hypo)
28
What heart condition is acromegaly associated with?
Cardiomyopathy, hypertension, arrhythmias and LVH
29
How is acromegaly treated?
Ocreotide (somatostatin analogue) or trans-sphenoidal surgery
30
Hypercalcaemia is a side effect of which drug class?
Thiazide diuretics
31
What are the investigations for acromegaly?
IGF-1 levels, OGTT, serial GH measurements
32
How do you treat phaeochromocytoma?
Alpha blocker eg phenoxybenzamine 1st line, b-blocker 2nd line
33
What are the diagnostic criteria for diabetes?
Fasting glucose >7 Random glucose >11.1 HbA1c >48 2 hr glucose OGTT >11.1 Repeat testing or in combination with positive symptoms
34
Describe LADA?
Positive auto-antiodies May not require insulin at time of diagnosis Occurs in adults
35
Describe MODY?
Negative autoantibodies =
36
Describe the principle of carbohydrate counting?
1 unit of insulin per 10g of carbohydrate
37
What is the mechanism of action of metformin?
Decreases hepatic gluconeogenesis and increases peripheral glucose uptake
38
What is the mechanism of action of the sulphonylureas? Gliclazide, glimepiride
Increases insulin secretion By blocking B cell kATP channels So needs functioning B cells to be effective
39
What is the mechanism of action of the SGLT2 inhibitors?
Blocks SGLT2 in the proximal tubules - reducing glucose reabsortpion
40
What is the mechanism of action of the thiazidenides? Pioglitazone
PPARy agonists - enhance the action of insulin (but don't affect its secretion)
41
What is the mechanism of action of the DPP-IV inhibitors (aka gliptins)?
Prolong the action of GLP-1 (incretin) / reduce its breakdown This promotes insulin secretion
42
What is the mechanism of action of the GLP receptor agonists (dulaglutide, semaglutide, exenatide)?
Stimulate insulin secretion, delay gastric emptying, decrease appetite and suppress glucagon
43
Which diabetic drugs cause: weight loss/ weight gain or are weight neutral?
Weight gain: Sulphonylureas - gliclazide, glimeprimide TZDs - related to fluid retention and weight gain is subcut not visceral Weight loss: SGLT2 inhibitors - the flozins GLP receptor agonists - dulaglutide, emaglutide, exenatide Weight neutral: Metformin/ maybe slight weight loss DPP-IV inhibitors - the gliptins
44
Which diabetic drugs can cause hypos?
Sulphonylureas - gliclazide, glimepiride
45
Which diabetic drugs are good and bad in renal disease?
Sulphonylureas (gliclazide, glimepiride)- BAD SGLT2 inhibitors - GOOD
46
Which class of diabetes drugs is linked to increased risk of fractures (therefore avoid in the elderly), hepatotoxicity, fluid retention (avoid in HF) and bladder cancer?
TZDs - pioglitazone
47
Which class of diabetes drugs has a link to pancreatitis?
GLP receptor agonists - dulaglutide, semaglutide, exenatide
48
What are the biochemical diagnostic criteria for DKA?
Ketones > 3 BG > 11 Bicarb <15 / pH <7.3
49
What biochemical resutls would you expect in HHS?
Very high glucose Hyperosmolar (>320) Significant renal impairment Na may be raised Less acidotic/ ketotic than in DKA
50
Papillary thyroid cancer is the most common type. How does it spread?
Mostly lymphatic spread, also haematogenous Usually spreads to the lungs Reasonable survival rate
51
How does follicular carcinoma spread?
Haematogenous spread to bones, liver, lung
52
What syndrome / group of disorders is medullary thyroid carcinoma associated with?
Familial MEN
53
Which type of thyroid cancer is very aggressive?
Anaplastic carcinoma
54
What is the surgery of choice for thyroid cancers and why?
Subtotal thyroidectomy - total thyroidectomy risks damage to adjacent structures fc
55
What biochemical results would you expect in cushing's?
High ACTH (pituitary or ectopic causes) Low ACTH in adrenal causes High cortisol
56
What investigations are used in cushing's?
Dexamethasone suppression test 24hr urine cortisol Pituitary MRI Pituitary surgery
57
What are the treatment options for cushing's?
Metyrapone Surgery
58
How do prolactinomas present, what are the investigation and treatment options?
Amenorrhoea, infertility, impotence Headaches Abnormal visual fields Pituitary MRI Pituitary hormones Cabergoline - dopamine agonist
59
Acromegaly is usually caused by a macroadenoma. How is it investigated and treated?
Glucose tolerance test - Elevated IGF1 and hyperglycaemia CT/ MRI pituitary Pituitary hormones Treated with surgery Radiotherapy Ocreotide - somatostain analogue Carbegoline - dopamine agonist Pegvisomant - GH antagonist
60
What is the difference between cranial and nephrogenic DI?
In cranial DI there is not enough ADH (often idiopathic) In nephrogenic DI there is enough ADH but the kidneys are resistant to it Both cause polyuria and polydipsia
60
What are the investigation and treatment options for DI?
Water deprivation test (urine will remain dilute due to lack of ADH)
61
How do you treat DI?
Desmopressin ( only in cranial DI - in nephrogenic DI in the kidneys are resistant so no use)
62
What is conn's syndrome? What biochemical results do you see?
Primary hyperaldosteronism due to an adrenal adenoma or carcinoma Increased cortisol High sodium, Low potassium Alkalosis
63
Investigation and management of primary hyperaldosteronism (conn's)?
Raised aldosterone to renin ratio Adrenal CT Adrenal vein sampling Management - adrenalectomy or spironolactone if bilateral
64
What is addison's, what biochemical results do you see?
Primary adrenal deficiency Low cortisol Low sodium, High potassium Low glucose Anti-adrenal autoantibodies
65
What are the investigation and management options of addison's?
Synacthen test Raised renin to aldosterone ratio (opposite to conn's) Management - hydrocortisone and fludrocortisone
66
What is congenital adrenal hyperplasia?
Primary adrenal deficiency Autosomal recessive inheritance Low cortisol, high testosterone Managed with glucocorticoid and mineralocorticoid replacement
67
What is phaeochromocytoma?
Catecholamine secreting tumour in the adrenal medulla
68
What biochemical results do you see in phaeochromocytoma and how do you investigate for it? How is it treated?
High glucose High calcium Lactic acidosis 24 hour catecholamines and metanephrins MRI PET scan Alpha blockers then b-blockers
69
What are the zones of the adrenal gland and what is secreted form each?
Zona glomerulosa - Mineralocorticoids (aldosterone) Zona fasciculata - Glucocorticoids (cortisol) Zone reticularis - Androgens Medulla - Catecholamines (epinephrine/ norepinephrine)
70
What biochemical results do you see in the different types of hyperparathyroidism?
Primary hyperparathyroidism (adenomas/ carcinomas) High PTH, high calcium, low phosphate Secondary hyperparathyroidism (most commonly due to renal failure - parathyroid gland hyperplasia develops) High PTH, low calcium, high phosphate Tertiary hyperparathyroidism (occurs after many years of secondary High PTH, high calcium, low or normal phosphate
71
What is osteomalacia/ Ricketts?
Vitamin D deficiency See a picture of secondary hyperparathyroidism with raised PTH to try and compensate for poor calcium absorption
72
What is paget's disease?
Increased bone turnover Raised ALP Managed wit bisphosphonantes
73
What is osteogenesis imperfecta?
Genetic disorder with mutations in collagen genes Fractures and blue sclera

MSRA (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions