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Flashcards in Endocrinology Deck (115)
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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
2
Q

Acromegaly

Complication (4)

A
  1. HTN
  2. DM
  3. cardiomyopathy
  4. bowel ca
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
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
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

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
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

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
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
10
Q

Addisons

Management

A
  1. Hydrocortisone (20-30mg/day) (double if sick)

2. Fludrocortiose

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

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
13
Q

Addisons

Secondary causes

A

Pituitary disorders: tumours/ infiltration/ irradiation

Secondary causes not associated with hyperpigmentation

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

15
Q

Mx of thyrotoxicosis

MOA

A

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

16
Q

Name of autoantibodies in Addison’s

A

anti-21-hydroxylase

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
18
Q

Name five corticosteroids in order of minimum to maximum glucocorticoid strength

A

Fludrocortisone
Hydrocortisone
Prednisolone
Dexamethasone + Betamethasone

19
Q

Mineralocorticoid SE

A

Fluid retention

HTN

20
Q

When do you need to taper steroids?

A
  1. > 40mg OD for 1 week
  2. > 3 weeks treatment
  3. Recently received repeat courses
21
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
22
Q

Cushings

Metabolic acidosis or alkalosis

A

Hypokalaemic etabolic alkalosis

23
Q

Cushings

Investigations (3)

A
  1. Overnight dexamethasone suppression test
  2. 24 hr urinary free cortisol
  3. CRH stimulation test
24
Q

Cushings

Features

A
Truncal obesity 
Moon faces 
Abdominal striae
Muscle wasting
Amenorrhea 
Easy bruising
Buffalo hump
Fractures 
DM
25
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 (high cortisol)
As pt is used to having lots of cortisol, haveing 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 summaries
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

26
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

27
Q

Mx Cushings

A

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

28
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

29
Q

T2DM

Diagnosis

A

Symptomatic can be done based on x1 result

  1. Fasting glucose >=7
  2. Random glucose/ OGTT at 2 hours >=11 .1
  3. HbA1C >=48

If asymptomatic needs x2 results

30
Q

Values for diabetes
Pre diabetes
Normal

A

HbA1C <=41, >=48

Fasting glucose <=6, >=7

31
Q

Values for diabetes
Pre diabetes/ impaired glucose tolerance
Normal

A

HbA1c <=41, >=48
Fasting glucose <=6, >=7
Impaired OGTT 2-hour value >= 7.8 but < 11.1

32
Q

When can HbA1c not be used?

A
  1. Suspected GDM
  2. Children
  3. HIV
  4. CKD
  5. Haemaglobinopathies
  6. Iron deficiency anaemia untreated
  7. Haemolytic anaemia
33
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 glucoagon
  • reduced appetite and gastric emptying
  • leads to weight loss
  • must be given within 1 hr to morning and evening meal SC
34
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

35
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

36
Q

When do you add a second diabetic medication?

A

If HbA1c >=58

37
Q

Medications T2DM groups (6)

A
  1. Biguanides –> metformin
  2. DPP4-inhibitorrs –> sitagliptin
  3. Sulfonylureas –> tolbutamide
  4. Thiazolidinediones –> pioglitazone
  5. SGLT-2 –> canagliflozin
  6. GLP-1 mimetics –> exanatide
38
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
39
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

40
Q

T2DM management

If metformin not toelrated (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

41
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

42
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

43
Q

Sick day rules for T1DM

A

Do not omit insulin

Check glucose levels every 1-2 hours including the night

44
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

45
Q

What is Charcot’s arthropathy?

A

Joint dislocations secondary to peripheral neuropathy

46
Q

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

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

47
Q

Diabetic foot disease
Low risk
Moderate risk
High risk

A

Low risk: No RF, just a callus

Mod risk: deformity/ neuropathy/ non-critical limb ischaemia

High risk: prev amputation/ ulceration on RRT/ combination of above two RF

48
Q

What is metabolic syndrome?

A
Central obesity AND 
At least x2 of: 
- raised BP
- impaired glucose tolerance
- high cholesterol
49
Q

How often should diabetic patients be checked for retinopathy?

A

At diagnosis and annually thereafter

50
Q

What are the most common precipitating factors for DKA? (2)

A
  1. MI

2. Missed insulin doses

51
Q

DKA

Features

A
  1. AP
  2. polyuria, polydipsia, dehydration
  3. Kussmaul respiration (deep hyperventilation)
  4. Acetone-smelling breath (‘pear drops’ smell)
52
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
53
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)

54
Q

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

A

3.5-5.5 give 40mmols

55
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

56
Q

What can cause a falsely low HbA1c?

A

Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis

57
Q

What can cause a falsely high HbA1c?

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

58
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
59
Q

HHS

Diagnostic criteria

A
  1. Hypovolaemia
  2. High glucose >30 without significant ketonaemia or acidosis
  3. Raised serum osmolarity > 320
60
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.

61
Q

HHS

Target glucose level

A

10-15

62
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

63
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
64
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)
65
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
66
Q

Contraindications for Grave’s

A
  1. Pregnancy

2. <16 yo

67
Q

Causes of gynaecomastia

A
  1. Kallman’s + Klinefelters
  2. Mumps
  3. Liver disease
  4. Testicular cancer (seminoma secreting HCG)
  5. hyperthyroidism
  6. haemodialysis
68
Q

Hashimoto’s
What is it?
Antibodies (2)

A

Autoimmune condition causing hypothyroidism

  1. anti-thyroid peroxidase (TPO)
  2. anti-thyroglobulin (Tg) antibodies
69
Q

Hypothyroidism
Primary causes: (6)
Secondary causes:

A
  1. Hashimoto’s
  2. Subacute thryroiditis (de Quervain’s)
  3. Riedel thyroiditis
  4. Iodine deficiency
  5. Drugs e.g carbimazole, amiodarone, lithium
  6. Post thyroidectomy
70
Q

Hypothyroidism is associated with which four conditions?

A
  1. T1DM
  2. MALT lymphoma
  3. Pernicious anaemia
  4. Addison’s
71
Q

Causes of hyperthyroidism (2)

A
  1. Grave’s

2. Toxic multinodular goitre

72
Q

Physiology of parathyroid gland

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.

73
Q

Explain primary hyperparathyroidism

A

High PTH
High calcium
Low phosphate

Caused by parathyroid glad tumour

74
Q

Explain secondary hyperparathyroidism

A

High PTH
Low calcium
High phosphate

Caused by vit D deficiency or CKD

75
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

76
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

77
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
78
Q

What is pseudohypoparathyroidism?

A

Low calcium, high PTH, high phosphate
Secondary to target cells being insensitive to PTH
Abnormality in a G protein

79
Q

Features of pseudohypoparathyroidism

A
  1. Short stature
  2. Low IQ
  3. Short 4th and 5th metacarpals
80
Q

Lack of smell (anosmia) in a boy with delayed puberty = ?

A

Kallman’s syndrome

81
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)

82
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

83
Q

MEN Type IIa

Which gene?

A

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

RET oncogene

84
Q

MEN Type IIb

Which gene?

A
1P
Medullary thyroid cancer
Marfanoid body habitus
1. Phaeo
\+ Neuromas

RET oncogene

85
Q

Phaeochromocytoma
What is it?
Name three associated conditions

A

Catecholamine secreting tumour

  1. MEN Type 2
  2. Neurofibromatosis
  3. von Hippel-Lindau syndrome
86
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
  2. Surgery
87
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

88
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

89
Q

Features of primary hyperaldosteronism

A
  1. HTN
    2 Hypokalaemia
  2. Alkalosis
90
Q

Primary hyperaldosteronism

Ix (3)

A
  1. Plasma aldosterone/renin ratio
  2. High-resolution CT abdomen
  3. Adrenal vein sampling
91
Q

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

A

High aldosterone levels alongside low renin levels (due to negative feedback)

92
Q

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

A

Used to differentiate between unilateral and bilateral sources of aldosterone excess

93
Q

Why is adrenal vein sampling used in primary hyperaldosteronism?

A

To identify the gland secreting excess hormone in primary hyperaldosteronism

94
Q

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

A
  1. Surgery

2. Aldosterone antagonists (spiro)

95
Q

Primary hyperparathyroidism
Features
(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
96
Q

Primary hyperparathyroidism

Ix

A
  1. High calcium, low phosphate, high PTH

2. technetium-MIBI subtraction scan

97
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

98
Q

Features of excess prolactin in

  1. Men (3)
  2. Women (4)
A

M: reduced libido, galactorrhea, impotence
F: amenorrhea, galactorrhea, infertility, osteoporosis

99
Q

Cause of raised prolactin (5)

A
  1. Acromegaly
  2. Pregnancy
  3. Prolactinoma
  4. Stress
  5. Primary hypothyroidism (as TRH stimulates prolactin)
  6. PCOS
100
Q

Pepperpot skull on xray is characteristic of which condition?

A

Primary hyperparathyroidism

101
Q

What is the classification of pituitary adenomas

A
Micro <1cm
Macro >1cm
OR
Secretory - produces hormones to excess
Non secretory - does not produce hormones to excess
102
Q

What is the most common form of pituitary adenoma?

A

Prolactinomas

103
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
104
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

105
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

106
Q

Subacute (De Quervain’s) thyroiditis

A

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

107
Q

Subacute (De Quervain’s) thyroiditis

Explain the four phases

A
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal
108
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
109
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

110
Q

Toxic multinodular goitre

What is it?

A

thyroid nodules that secrete excess thyroid hormones

111
Q

What is the Ferriman-Gallwey scoring system used in?

A

Gold standard scoring system for assessment of hirsutism

112
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
113
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

114
Q

Impaired glucose tolerance definition

Impaired fasting glucose =

A

fasting glucose <7
OGTT/ random 7.8-11.1

Impaired fasting glucose = fasting gluc 6.1-7.0

115
Q

Papillary thyroid cancer - bloods

A

Nil changed to TFTs as they do not secrete thyroxine