Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSRA > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Acromegaly
Features (7)

A
  1. Frontal bossing
  2. Spade like hands
  3. Macroglossia (large tongue)
  4. Prognathism (large jaw)
  5. Excessive sweating + oily skin
  6. Pituitary tumour features: headaches/ bitemporal hemianopia
  7. Raised prolactin in 1/3 of cases - galactorrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acromegaly
Complication (4)

A
  1. HTN
  2. DM
  3. cardiomyopathy
  4. bowel ca
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acromegaly
Management
Surgical (2)
Medical (3)

A

For pituitary adenomas:
1. Trans sphenoidal surgery
2. Removal of ectopics

Medical
1. Pegvisomant (GH antag)
2. Somatostatin analogues - octreotide
(Somatostatin is known as growth hormone inhibiting hormone)
3. Dopamine agonists

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

Acromegaly
What is it?
Causes (2)

A

Excess growth hormone production, produced in anterior pituitary gland, usually secondary to pituitary tumour
1. Pituitary adenoma
2. Ectopic GnRH - lung/ pancreatic ca

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

Explain the hypothalamic pituitary axis

A

Hypothalamus releases hormones than impact both anterior and posterior pituitary as follows

Hypothalamus –> Anterior pituitary
CRH –> stimulates ACTH production
TRH –> stimulates TSH production
TRH –> stimulates prolactin
GnRH –> stimulates FSH/ LH production
Somatostatin –> inhibits GH production
Dopamine –> inhibits prolactin production

Posterior pituitary
Oxytocin
ADH

ACTH –> adrenals –> cortisol on many tissues
TSH –> thyroid –> thyroxine
FSH/LH –> gonads –> androgen or oestrogen production
GH –> liver –> insulin growth factor release (IGF) on many tissues
Prolactin –> breast –> lactation

Oxytocin –> uterine muscle
ADH –> distal convoluting tubules –> water reabsorption

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

Acromegaly
Investigations (3)

A
  1. Insulin growth factor measurements
    IGF-1
  2. MRI for pituitary tumour
  3. OGTT - nil response to GH in acromegaly therefore raised glucose levels, pts without acromegaly, when given OGTT their glucose levels falls to <2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Addisons
What is it?

A

Also known as primary adrenal insufficiency
80% of cases –> autoantibodies against adrenal cortex
Therefore reduced production of aldosterone, cortisol and androgens

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

Addisons
Features

A
  1. Low BP
  2. Hair thinning
  3. Weight loss
  4. Increased fractures
  5. Palmer creases hyperpigmentation
  6. Loss of pubic hair
  7. Hypoglycaemia
  8. Collapse/ shock/ pyrexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Addisons
Investigations (2)

A
  1. short synACTHen/ ACTH stimulation test
    Baseline cortisol measured, given synachthen and expect cortisol to double when measured at 30 minutes and 60minutes. If still low then Addison’s
  2. 9am cortisol levels
    > 500 nmol/l Addison’s very unlikely
    < 100 nmol/l is definitely abnormal
    100-500 nmol/l for ACTH stimulation test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Addisons
Management

A
  1. Hydrocortisone (20-30mg/day) (double if sick)
  2. Fludrocortiose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does the adrenal gland work? Include hypothalamus-pituitary axis.

A

Hypothalamus produces CRH
CRH acts on ant. pituitary causing ACTH release
ACTH acts on adrenal gland
Adrenal gland split into medulla (inside) and cortex (outer).
ACTH acts on cortex.
Production of three hormones:
1. Mineralocorticoids e.g aldosterone
2. Glucoscorticoids e.g cortisol
3. Androgens (females mainly)

Mineralocorticoid release increase sodium reabsorption and water retention
Glucocorticoids causes:
1. Immunosuppression/ anti-inflammatory –> increased infection
2. Skin - thinning
3. Bone - increased osteoclasts, increases breakdown therefore increased risk of osteoporosis and fractures
4. Metabolic - weight gain, insulin resistance

Androgens –> increases libido

Increased mineralo/glucocorticoids and androgens has negative feedback on hypothalamus

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

Addisons
Primary causes (7)

A
  1. Autoimmune
  2. TB
  3. HIV
  4. Antiphospholipid syndrome
  5. Meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
  6. Metastases/ primary ca
  7. Congenital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Addisons
Secondary causes (1)
Secondary causes do not have which feature?

A

Pituitary disorders: tumours/ infiltration/ irradiation
(Secondary causes not associated with hyperpigmentation)

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

Electrolyte impact of Addison’s
K+
Na+
Gluc
Metabolic acidosis or alkalosis?

A

High K+, as reduced aldosterone leads to reduced Na reabsorption and therefore increased potassium retention
hyponatraemia
hypoglycaemia
Hyperkalaemic metabolic acidosis

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

Mx of thyrotoxicosis
MOA

A

Carbimazole high dose for 6 weeks/ until euthyroid then taper
Thyroid peroxidase inhibitor

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

anti-21-hydroxylase autoantibodies in which condition

A

Addisons

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

Thyroid hormones sythnthesis

A

Thyroid made up of lobules.
Lobules made up of follicles and colloid
T3 T4 synthesised in the colloid.
Iodide from the blood stream moves into follicle.
Iodide transported to colloid
Iodide uses peroxidase to create iodine

Follicle makes thyroglobulin and moves into colloid.
Thyroglobulin is made up of tyrosine

In the colide we now have tyrosine and iodine.
x1 iodine binding to tyrosine = MIT
x2 iodine binding to tyrosine = DIT

MIT+DIT = T3
DIT+DIT = T4

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

Name five corticosteroids in order of minimum to maximum glucocorticoid strength

A

Fludrocortisone
Hydrocortisone
Prednisolone
Dexamethasone + Betamethasone

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

Mineralocorticoid SE

A

Fluid retention
HTN

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

Cushings syndrome
Causes
ACTH dependent
ACTH independent
Pseudo

A

ACTH dependent
1. Pituitary adenoma = Cushing’s disease
2. Ectopic ACTH production e.g lung cancer

ACTH independent
1. Iatrogenic (steroids given to pt)
2. Adrenal carcinoma/ adenoma
3. Carney complex

Pseudo-Cushings
1. ETOH excess
2. Depression

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

Cushings
Metabolic acidosis or alkalosis

A

Hypokalaemic metabolic alkalosis

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

Cushings
Investigations (3)

A
  1. Overnight dexamethasone suppression test
  2. 24 hr urinary free cortisol
  3. CRH stimulation test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cushings
Features

A

Truncal obesity
Moon faces
Abdominal striae
Muscle wasting
Amenorrhea
Easy bruising
Buffalo hump
Fractures
DM

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

Cushings
Explained what the overnight dexamethasone test is
Explain its results

A

Split into low dose and high dose dexamethasone test
10pm give 1mg dexamethasone, 9am measure cortisol and ACTH

In a pt without any issues
Give 1mg dexamethasone, this acts on hypothalamus (negative feedback) and pituitary and adrenals –> therefore in the morning, you should have a low cortisol.

If you have Cushing’s syndrome (pituitary adenoma causing high cortisol)
As pt is used to having lots of cortisol, having 1mg dexamethasone will not cause negative feedback system. Therefore cortisol level will be normal or raised.

If low dose test is suggestive of Cushing’s you will then move on to high dose.

Give 8mg of dexamethasone at 10pm
Morning measure cortisol and ACTH

If you have Cushing’s disease (pituitary adenoma), 8mg is enough to trigger negative feedback system. Therefore ACTH will decrease and cortisol will fall.

If you have an adrenal gland tumour. The adrenal gland tumour cells will produce cortisol independent of ACTH. Therefore dexamethasone will work on pituitary through negative feedback system which leads to low ACTH. However as cortisol is independent of ACTH. Cortisol levels will be raised.

If you have ectopic ACTH production. Then dexamethasone will cause reduction in CRH and therefore ACTH. However as ectopic ACTH production still going on. ACTH will be raised and thus cortisol will be raised.

To summarise
Low dose test
Low cortisol = normal
High cortisol = cushing’s syndrome

High dose test
Low ACTH and low cortisol = Cushing’s syndrome
Low ACTH and high cortisol = Adrenal carcinoma/ adenoma
High ACTH and high cortisol = ectopic

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

Explain CRH stimulation test

A

This is to determine between pituitary source or ectopic source

In a pituitary source - CRH stimulation = increased ACTH = increased cortisol

In an ectopic source - CRH stimulation = ACTH remains the same and cortisol stays the same as the ectopic ACTH acts as negative feedback to the hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Mx Cushings

A

Pituitary source - surgery
Exogenous source - taper
Ectopic source - ketoconazole or metyrapone (adrenal steroid inhibitors)

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

T2DM
Diagnosis

A

Symptomatic can be done based on x1 result
1. Fasting glucose >=7
2. Random glucose/ OGTT >11 .1
3. HbA1C >=48

If asymptomatic needs x2 results

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

Values for diabetes
Pre diabetes/ impaired glucose tolerance
Normal

A

HbA1c >=48, 42-47, <=41,
Fasting glucose <=6, >=7
Impaired OGTT 2-hour value >= 7.8 but < 11.1
Impaired fasting glucose = fasting gluc 6.1-7.0

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

When can HbA1c not be used? (7)

A
  1. Suspected GDM
  2. Children
  3. HIV
  4. CKD
  5. Haemaglobinopathies
  6. Iron deficiency anaemia untreated
  7. Haemolytic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T2DM treatment
Given two examples of GLP-1 mimetics
Explain how they work and how often they are given

A

GLP-1 mimetics e.g exenatide (BD)/ liraglutide (OD)
- works by increasing incretins
- increases insulin
- reduced glucagon
- reduced appetite and gastric emptying
- leads to weight loss
- must be given within 1 hr to morning and evening meal SC

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

T2DM treatment
Give an example of DPP-4 inhibitors
Explain how they work

A

DPP-4 inhibitors e.g gliptins
DPP4 inhibits GLP-1, therefore inhibitors lead to increased GLP-1

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

HbA1c targets
How often do you check HbA1c?

A

Lifestyle + one medication not causing hypoglycaemia
Target = 48

Taking drugs causing hypoglycaemia
Target = 53

Every 3-6 months until stable, then 6 monthly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When do you add a second diabetic medication?

A

If HbA1c >=58

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

Medications T2DM groups (6)

A
  1. Biguanides –> metformin
  2. DPP4-inhibitorrs –> sitagliptin
  3. Sulfonylureas –> gliclazide
  4. Thiazolidinediones –> pioglitazone
  5. SGLT-2 –> canagliflozin
  6. GLP-1 mimetics –> exanatide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Sulfonylureas
MOA
Adverse effects (2)
Other SE (4)

A

Increase pancreas insulin production

  1. Hypoglycaemia
  2. Weight gain
  3. Low Na
  4. Bone marrow suppression
  5. Hepatotoxicity
  6. Peripheral neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

T2DM management
If metformin tolerated

A

1st line
1. Metformin

If HbA1c >58
Add
2. gliptin/ sulfonylurea/ pioglitazone/ SGLT-2

If HbA1c >58
Then combo of:
metformin+sulfonylurea+ gliptin
meformin+ sulfonylurea+SGLT2
metformin + sulfonylurea+ pioglitazone
metformin + pioglitazone + SGLT2
insulin + metformin

If triple therapy not effective
metformin + sulfonylurea + GLP-1 mimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

T2DM management
If metformin not tolerated (3)

A

1st line
1. Gliptin/ sulfonylurea/ pioglitazone

If HbA1c >58
2. Combo of any of the above two

If HbA1c >58
3. Insulin + metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When would you give GLP-1 mimetics?

A

BMI >=35 European and high weight OR
BMI <35 and unable to use insulin or weight loss would benefit other comorbidities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

T1DM
Target HbA1c
How often should it be checked
How often should they check their glucose level?
What should the levels be?

A

Target 48
Check every 3-6 months
Check four times a day, before every meal, before bed

4-7 before meals
5-7 fasting glucose/ on waking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Sick day rules for T1DM

A

Do not omit insulin
Check glucose levels every 1-2 hours including the night

41
Q

T1DM insulin regime of choice
When would you add metformin?

A

Multiple basal-bolus regimens over mixed insulins

1st line
BD insulin detemir

2nd line
OD insulin glargine or detemir

BMI >25 add metformin

42
Q

What is Charcot’s arthropathy?

A

Joint dislocations secondary to peripheral neuropathy

43
Q

How often should patient’s be screened for diabetic foot disease?
How is it done?

How often should diabetic patients be checked for retinopathy?

A

Annual basis
To screen for ischaemia:
1. Palpate dorsalis pedis and post tibial artery
To screen for neuropathy:
2. 10g monofilament on various parts of the sole of the foot

At diagnosis and annually thereafter

44
Q

What is metabolic syndrome?

A

Central obesity AND
At least x2 of:
- raised BP
- impaired glucose tolerance
- high cholesterol

45
Q

DKA
Features

A
  1. AP
  2. polyuria, polydipsia, dehydration
  3. Kussmaul respiration (deep hyperventilation)
  4. Acetone-smelling breath (‘pear drops’ smell)
46
Q

DKA
Diagnostic criteria

A
  1. glucose > 11 or known DM
  2. pH < 7.3
  3. bicarb < 15
  4. ketones > 3 or urine ketones ++ on dipstick
47
Q

DKA Mx

A
  1. Isotonic saline
  2. IV insulin infusion 0.1unit/kg/hour, once glucose <15 start 5% dex
  3. Correct hypokalaemia secondary to insulin
  4. Continue long acting insulin, stop short acting insulin

(0.9% normal saline over 1 hr for first bag, second + third bag over 2 hours NaCl with potassium chloride, fourth + fifth bag over 4 hours NaCl with potassium chloride)

48
Q

At what value of K+ do you need to replace it?

A

3.5-5.5 give 40mmols

49
Q

What are young adults/ children at risk of developing if we give fluids at too fast a rate during a DKA

A

Cerebral oedema - headache, irritability, visual disturbance –> usually occurs 4-12 hrs post rx

50
Q

HHS
Features

A

Occurs over a few days
1. Dehydration + hyperviscosity of blood
2. Polyuria
3. Fatigue/ lethargy/ N&V
4. Altered conscious level

51
Q

HHS
Diagnostic criteria

A
  1. Hypovolaemia
  2. High glucose >30 without significant ketonaemia or acidosis
  3. Raised serum osmolarity > 320
52
Q

HHS
Mx
How often do you need to check osmolality?

Estimated fluid loss

A
  1. NaCl 0.9%
    If not bringing down osmolality switch to NaCl 0.45%
    Check osmolality hourly

Estimated loss 100 - 220 ml/kg
Replace 50% of fluid loss in 12 hours, then further 50% in next 12 hours.

53
Q

HHS
Target glucose level

A

10-15

54
Q

When would you start insulin in HHS?
What rate?

A

Do not start insulin in T2DM unless ketones are present
Dose would be fixed rate 0.05 units/kg/hr

55
Q

What is Grave’s disease?
Name the antibodies (2)

A

Autoimmune antibodies leading to hyperthyroidism
1. TSH receptor stimulating antibodies
2. anti-TPO autoantibodies

56
Q

Grave’s disease
Features (4)

A
  1. exophthalmos
  2. ophthalmoplegia
  3. pretibial myxoedema
  4. thyroid acropachy (clubbing, soft tissue swelling of hands and feet and periosteal new bone formation)
57
Q

Grave’s disease
Mx

A
  1. Carbimazole until euthyroid 40mg - 12-18 months
    OR
  2. Carbimazole until euthyroid, then add thyroxine - 6-9 months
58
Q

Hashimoto’s
What is it?
Antibodies (2)

A

Autoimmune condition causing hypothyroidism
1. anti-thyroid peroxidase (TPO)
2. anti-thyroglobulin (Tg) antibodies

59
Q

Hypothyroidism is associated with which cancer?

A

MALT lymphoma

60
Q

Physiology of parathyroid gland
Role of PTH
How does it do this? (3)
What is the purpose of vit D?

A

Low calcium leads to increase in PTH
Role of PTH is to increase calcium levels
PTH causes:
1. Increased gut absorption
2. Increased reabsorption of calcium from the kidneys
3. Increased osteoclast activity, to break down bone to increase calcium levels

Vit D does the same as PTH, increase PTH leads to increase conversion of vit D into active form so it can help with above effects.

61
Q

Explain primary hyperparathyroidism
Causes (1)

A

High PTH
High calcium
Low phosphate

Caused by parathyroid gland tumour

62
Q

Explain secondary hyperparathyroidism
Causes (2)

A

High PTH
Low calcium
High phosphate

Caused by vit D deficiency or CKD

63
Q

Explain tertiary hyperparathyroidism

A

High PTH
High calcium
Low phosphate

Secondary to hyperplasia of parathyroid gland due to secondary hyperparathyroidism after it has been corrected

64
Q

Hypoparathyroid disease
What is it?
Usually caused by?
Mx

A

Low PTH and therefore low calcium and high phosphate
Usually secondary to thyroidectomy
Mx alfacalcidol

65
Q

Hypoparathyroidism symptoms
(Hint: same as hypocalcaemia)

A
  1. Trousseau’s sign
  2. Chvostek’s sign
  3. Muscle spasm
  4. Perioral paraesthesia
    ECG prolonged QT
66
Q

What is pseudohypoparathyroidism?

A

Low calcium, high PTH, high phosphate
Secondary to target cells being insensitive to PTH

67
Q
  1. Short stature
  2. Low IQ
  3. Short 4th and 5th metacarpals
    are features of which condition?
A

pseudohypoparathyroidism

68
Q

Lack of smell (anosmia) in a boy with delayed puberty =?
Hypogonadotropic hypogonadism
X linked recessive

A

Kallman’s syndrome

69
Q

When would meglitinides be used?
How do they work?
SE (2)

A

Used in pt’s with DM with erratic lifestyles
Increased pancreatic insulin secretions
Similar to sulfonylureas
Cause weight gain and hypoglycaemia (but less so than sulfonylureas)

70
Q

MEN Type I
Features
Which gene?

A

3Ps
1. Pituitary
2. Parathyroid gland
3. Pancreas
MEN 1 gene on chrm 11

Features
Hypercalcaemia
Moans boans abdominal groan and psychic moans

71
Q

MEN Type IIa

A

2Ps
Medullary thyroid cancer
1. Parathyroid gland
2. Phaeo

RET oncogene

72
Q

MEN Type IIb

A

1P (+1N)
Medullary thyroid cancer
Marfanoid body habitus
1. Phaeo
2. Neuromas

RET oncogene

73
Q

Phaeochromocytoma
What is it?
Name three associated conditions

A

Catecholamine secreting tumour

  1. MEN Type 2
  2. Neurofibromatosis
  3. von Hippel-Lindau syndrome
74
Q

Phaeochromocytoma
Investigation
Mx

A
  1. 24 hr urinary collection of metanephrines

Mx
1. Stabilise HTN with:
- first line: alpha blocker e.g phenoxybenzamine
- second line: beta blocker e.g propranolol

  1. Surgery
75
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism secondary to adrenal adenoma
Causes increased water and sodium reabsorption
Leading to HTN and hypokalaemia and an alkalosis

76
Q

Most common cause of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia
Leading to increase aldosterone production
Leading to increased water and sodium reabsorption
Leading to HTN and hypokalaemia and an alkalosis

77
Q

Features of primary hyperaldosteronism
K+ high or low
Acidosis or alkalosis

A
  1. HTN
    2 Hypokalaemia
  2. Alkalosis
78
Q

Primary hyperaldosteronism
Ix (3)

A
  1. Plasma aldosterone/renin ratio - high ald, low ren
  2. High-resolution CT abdomen
  3. Adrenal vein sampling
79
Q

Why is a high-resolution CT abdomen used primary hyperaldosteronism?

A

Used to differentiate between unilateral and bilateral sources of aldosterone excess

80
Q

Why is adrenal vein sampling used in primary hyperaldosteronism?

A

To identify the gland secreting excess hormone in primary hyperaldosteronism

81
Q

Mx
Adrenal adenoma (1)
Bilateral adrenocortical hyperplasia (1)

A
  1. Surgery
  2. Aldosterone antagonists (spiro)
82
Q

Primary hyperparathyroidism
Features (6)
(Hint: same as hypercalcaemia)

A
  1. Osteoporosis/ osteomalacia/ fracture
  2. Renal stones and diabetes insipidus (polyuria and polydipsia)
  3. Constipation/ N&V/ peptic ulceration/ pancreatitis
  4. Psychosis/ memory issues/ depression
  5. Corneal calcification
  6. HTN
83
Q

Primary hyperparathyroidism
Ix

A
  1. High calcium, low phosphate, high PTH
  2. technetium-MIBI subtraction scan
84
Q

Primary hyperparathyroidism
Mx

A

Mx
1. parathyroidectomy

If >50yo and calcium level less than 0.25 above normal level and no organ end damage:
1. Conservative management such as cinacalcet

85
Q

Cause of raised prolactin (5)

A
  1. Acromegaly
  2. Pregnancy
  3. Prolactinoma
  4. Stress
  5. Primary hypothyroidism (as TRH stimulates prolactin)
  6. PCOS
86
Q

Pepperpot skull on xray is characteristic of which condition?

A

Primary hyperparathyroidism

87
Q

What is the classification of pituitary adenomas
Micro and macro

A

Micro <1cm
Macro >1cm

88
Q

What is the most common form of pituitary adenoma?

A

Prolactinomas

89
Q

Diagnostic investigation for prolactinoma
Mx

A
  1. MRI

Mx
1. DA e.g cabergoline/ bromocriptine
2. Surgery if fails to respond to medical therapy

90
Q

What is Riedel’s thyroiditis?
What is it associated with?

A

Dense fibrous tissue replaces normal thyroid tissue causing hypothyroidism
Retroperitoneal fibrosis
1. hard, fixed, painless goitre

91
Q

What is sick euthyroid syndrome?
What will you find on bloods?
Mx

A

AKA non thyroidal illness
TSH, thyroxine and T3 are all low
Sometimes TSH can be normal (inappropriately normal given low thyroxine and T3)
Mx - nil, normally recovers post ilness

92
Q

Subacute (De Quervain’s) thyroiditis
By what week will it return to normal?

A

Presents with hyperthyroidism following a viral infection but is actually hypothyroidism.
Week 4

93
Q

Subacute (De Quervain’s) thyroiditis
Ix
Mx

A

thyroid scintigraphy: globally reduced uptake of iodine-131

Mx
1. Self limiting
2. NSAIDs/ aspirin for pain
3. Steroids in severe cases

94
Q

Subclinical hypothyroidism
Bloods
Mx

A

TSH raised but T3, T4 normal
Mx
TSH is between 4 - 10
If asymptomatic - repeat bloods 6 months
<65yo and symptomatic –> trial levothyroxine
If older - watch and wait approach

TSH>10
=<70yo = start rx
Otherwise watch and wait

95
Q

Toxic multinodular goitre
What is it?

A

benign thyroid nodules that secrete excess thyroid hormones

96
Q

What is the Ferriman-Gallwey scoring system used in?

A

Gold standard scoring system for assessment of hirsutism

97
Q

Mx of hirsutism (2)
Mx of facial hirsutism (1)

A
  1. Weight loss
  2. COCP
    Facial hirsutism
  3. Topical eflornithine (should start seeing results 6-8 weeks)
    - if no improvement after 4 months, refer to endocrine
98
Q

Hypothyroidism Mx
In pregnancy Mx

A

If >50yo or IHD or severe hypothyroidism start with a low dose e.g 25mcg

Otherwise start on 50-100mcg

Recheck TFTs 2-3 months and titrate until TSH normalised.

Pregnancy - increase dose by 25-50mcg

99
Q

Papillary thyroid cancer - bloods

A

Nil changed to TFTs as they do not secrete thyroxine

MSRA (22 decks)

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