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Endocrinology Flashcards

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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
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2
Q

Acromegaly
Complication (4)

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

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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

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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

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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
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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

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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
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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
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10
Q

Addisons
Management

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

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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
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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)

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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

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15
Q

Mx of thyrotoxicosis
MOA

A

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

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16
Q

anti-21-hydroxylase autoantibodies in which condition

A

Addisons

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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

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18
Q

Name five corticosteroids in order of minimum to maximum glucocorticoid strength

A

Fludrocortisone
Hydrocortisone
Prednisolone
Dexamethasone + Betamethasone

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19
Q

Mineralocorticoid SE

A

Fluid retention
HTN

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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

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21
Q

Cushings
Metabolic acidosis or alkalosis

A

Hypokalaemic metabolic alkalosis

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22
Q

Cushings
Investigations (3)

A
  1. Overnight dexamethasone suppression test
  2. 24 hr urinary free cortisol
  3. CRH stimulation test
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23
Q

Cushings
Features

A

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

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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

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25
Explain CRH stimulation test
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.
26
Mx Cushings
Pituitary source - surgery Exogenous source - taper Ectopic source - ketoconazole or metyrapone (adrenal steroid inhibitors)
27
T2DM Diagnosis
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
28
Values for diabetes Pre diabetes/ impaired glucose tolerance Normal
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
29
When can HbA1c not be used? (7)
1. Suspected GDM 2. Children 3. HIV 4. CKD 5. Haemaglobinopathies 6. Iron deficiency anaemia untreated 7. Haemolytic anaemia
30
T2DM treatment Given two examples of GLP-1 mimetics Explain how they work and how often they are given
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
31
T2DM treatment Give an example of DPP-4 inhibitors Explain how they work
DPP-4 inhibitors e.g gliptins DPP4 inhibits GLP-1, therefore inhibitors lead to increased GLP-1
32
HbA1c targets How often do you check HbA1c?
Lifestyle + one medication not causing hypoglycaemia Target = 48 Taking drugs causing hypoglycaemia Target = 53 Every 3-6 months until stable, then 6 monthly
33
When do you add a second diabetic medication?
If HbA1c >=58
34
Medications T2DM groups (6)
1. Biguanides --> metformin 2. DPP4-inhibitorrs --> sitagliptin 3. Sulfonylureas --> gliclazide 4. Thiazolidinediones --> pioglitazone 5. SGLT-2 --> canagliflozin 6. GLP-1 mimetics --> exanatide
35
Sulfonylureas MOA Adverse effects (2) Other SE (4)
Increase pancreas insulin production 1. Hypoglycaemia 2. Weight gain 1. Low Na 2. Bone marrow suppression 3. Hepatotoxicity 4. Peripheral neuropathy
36
T2DM management If metformin tolerated
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
37
T2DM management If metformin not tolerated (3)
1st line 1. Gliptin/ sulfonylurea/ pioglitazone If HbA1c >58 2. Combo of any of the above two If HbA1c >58 3. Insulin + metformin
38
When would you give GLP-1 mimetics?
BMI >=35 European and high weight OR BMI <35 and unable to use insulin or weight loss would benefit other comorbidities
39
T1DM Target HbA1c How often should it be checked How often should they check their glucose level? What should the levels be?
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
40
Sick day rules for T1DM
Do not omit insulin Check glucose levels every 1-2 hours including the night
41
T1DM insulin regime of choice When would you add metformin?
Multiple basal-bolus regimens over mixed insulins 1st line BD insulin detemir 2nd line OD insulin glargine or detemir BMI >25 add metformin
42
What is Charcot's arthropathy?
Joint dislocations secondary to peripheral neuropathy
43
How often should patient's be screened for diabetic foot disease? How is it done? How often should diabetic patients be checked for retinopathy?
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
What is metabolic syndrome?
Central obesity AND At least x2 of: - raised BP - impaired glucose tolerance - high cholesterol
45
DKA Features
1. AP 2. polyuria, polydipsia, dehydration 3. Kussmaul respiration (deep hyperventilation) 4. Acetone-smelling breath ('pear drops' smell)
46
DKA Diagnostic criteria
1. glucose > 11 or known DM 2. pH < 7.3 3. bicarb < 15 4. ketones > 3 or urine ketones ++ on dipstick
47
DKA Mx
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
At what value of K+ do you need to replace it?
3.5-5.5 give 40mmols
49
What are young adults/ children at risk of developing if we give fluids at too fast a rate during a DKA
Cerebral oedema - headache, irritability, visual disturbance --> usually occurs 4-12 hrs post rx
50
HHS Features
Occurs over a few days 1. Dehydration + hyperviscosity of blood 2. Polyuria 3. Fatigue/ lethargy/ N&V 4. Altered conscious level
51
HHS Diagnostic criteria
1. Hypovolaemia 2. High glucose >30 without significant ketonaemia or acidosis 3. Raised serum osmolarity > 320
52
HHS Mx How often do you need to check osmolality? Estimated fluid loss
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
HHS Target glucose level
10-15
54
When would you start insulin in HHS? What rate?
Do not start insulin in T2DM unless ketones are present Dose would be fixed rate 0.05 units/kg/hr
55
What is Grave's disease? Name the antibodies (2)
Autoimmune antibodies leading to hyperthyroidism 1. TSH receptor stimulating antibodies 2. anti-TPO autoantibodies
56
Grave's disease Features (4)
1. exophthalmos 2. ophthalmoplegia 3. pretibial myxoedema 4. thyroid acropachy (clubbing, soft tissue swelling of hands and feet and periosteal new bone formation)
57
Grave's disease Mx
1. Carbimazole until euthyroid 40mg - 12-18 months OR 2. Carbimazole until euthyroid, then add thyroxine - 6-9 months
58
Hashimoto's What is it? Antibodies (2)
Autoimmune condition causing hypothyroidism 1. anti-thyroid peroxidase (TPO) 2. anti-thyroglobulin (Tg) antibodies
59
Hypothyroidism is associated with which cancer?
MALT lymphoma
60
Physiology of parathyroid gland Role of PTH How does it do this? (3) What is the purpose of vit D?
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
Explain primary hyperparathyroidism Causes (1)
High PTH High calcium Low phosphate Caused by parathyroid gland tumour
62
Explain secondary hyperparathyroidism Causes (2)
High PTH Low calcium High phosphate Caused by vit D deficiency or CKD
63
Explain tertiary hyperparathyroidism
High PTH High calcium Low phosphate Secondary to hyperplasia of parathyroid gland due to secondary hyperparathyroidism after it has been corrected
64
Hypoparathyroid disease What is it? Usually caused by? Mx
Low PTH and therefore low calcium and high phosphate Usually secondary to thyroidectomy Mx alfacalcidol
65
Hypoparathyroidism symptoms (Hint: same as hypocalcaemia)
1. Trousseau's sign 2. Chvostek's sign 3. Muscle spasm 4. Perioral paraesthesia ECG prolonged QT
66
What is pseudohypoparathyroidism?
Low calcium, high PTH, high phosphate Secondary to target cells being insensitive to PTH
67
1. Short stature 2. Low IQ 3. Short 4th and 5th metacarpals are features of which condition?
pseudohypoparathyroidism
68
Lack of smell (anosmia) in a boy with delayed puberty =? Hypogonadotropic hypogonadism X linked recessive
Kallman's syndrome
69
When would meglitinides be used? How do they work? SE (2)
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
MEN Type I Features Which gene?
3Ps 1. Pituitary 2. Parathyroid gland 3. Pancreas MEN 1 gene on chrm 11 Features Hypercalcaemia Moans boans abdominal groan and psychic moans
71
MEN Type IIa
2Ps Medullary thyroid cancer 1. Parathyroid gland 2. Phaeo RET oncogene
72
MEN Type IIb
1P (+1N) Medullary thyroid cancer Marfanoid body habitus 1. Phaeo 2. Neuromas RET oncogene
73
Phaeochromocytoma What is it? Name three associated conditions
Catecholamine secreting tumour 1. MEN Type 2 2. Neurofibromatosis 3. von Hippel-Lindau syndrome
74
Phaeochromocytoma Investigation Mx
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
75
What is Conn's syndrome?
Primary hyperaldosteronism secondary to adrenal adenoma Causes increased water and sodium reabsorption Leading to HTN and hypokalaemia and an alkalosis
76
Most common cause of primary hyperaldosteronism?
Bilateral adrenal hyperplasia Leading to increase aldosterone production Leading to increased water and sodium reabsorption Leading to HTN and hypokalaemia and an alkalosis
77
Features of primary hyperaldosteronism K+ high or low Acidosis or alkalosis
1. HTN 2 Hypokalaemia 3. Alkalosis
78
Primary hyperaldosteronism Ix (3)
1. Plasma aldosterone/renin ratio - high ald, low ren 2. High-resolution CT abdomen 3. Adrenal vein sampling
79
Why is a high-resolution CT abdomen used primary hyperaldosteronism?
Used to differentiate between unilateral and bilateral sources of aldosterone excess
80
Why is adrenal vein sampling used in primary hyperaldosteronism?
To identify the gland secreting excess hormone in primary hyperaldosteronism
81
Mx Adrenal adenoma (1) Bilateral adrenocortical hyperplasia (1)
1. Surgery 2. Aldosterone antagonists (spiro)
82
Primary hyperparathyroidism Features (6) (Hint: same as hypercalcaemia)
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
Primary hyperparathyroidism Ix
1. High calcium, low phosphate, high PTH 2. technetium-MIBI subtraction scan
84
Primary hyperparathyroidism Mx
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
Cause of raised prolactin (5)
1. Acromegaly 2. Pregnancy 3. Prolactinoma 4. Stress 5. Primary hypothyroidism (as TRH stimulates prolactin) 6. PCOS
86
Pepperpot skull on xray is characteristic of which condition?
Primary hyperparathyroidism
87
What is the classification of pituitary adenomas Micro and macro
Micro <1cm Macro >1cm
88
What is the most common form of pituitary adenoma?
Prolactinomas
89
Diagnostic investigation for prolactinoma Mx
1. MRI Mx 1. DA e.g cabergoline/ bromocriptine 2. Surgery if fails to respond to medical therapy
90
What is Riedel's thyroiditis? What is it associated with?
Dense fibrous tissue replaces normal thyroid tissue causing hypothyroidism Retroperitoneal fibrosis 1. hard, fixed, painless goitre
91
What is sick euthyroid syndrome? What will you find on bloods? Mx
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
Subacute (De Quervain's) thyroiditis By what week will it return to normal?
Presents with hyperthyroidism following a viral infection but is actually hypothyroidism. Week 4
93
Subacute (De Quervain's) thyroiditis Ix Mx
thyroid scintigraphy: globally reduced uptake of iodine-131 Mx 1. Self limiting 2. NSAIDs/ aspirin for pain 3. Steroids in severe cases
94
Subclinical hypothyroidism Bloods Mx
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
Toxic multinodular goitre What is it?
benign thyroid nodules that secrete excess thyroid hormones
96
What is the Ferriman-Gallwey scoring system used in?
Gold standard scoring system for assessment of hirsutism
97
Mx of hirsutism (2) Mx of facial hirsutism (1)
1. Weight loss 2. COCP Facial hirsutism 2. Topical eflornithine (should start seeing results 6-8 weeks) - if no improvement after 4 months, refer to endocrine
98
Hypothyroidism Mx In pregnancy Mx
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
Papillary thyroid cancer - bloods
Nil changed to TFTs as they do not secrete thyroxine

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