Endocrinology 1 Flashcards
What is acromegaly most commonly caused by?
Other causes:
Excess GH secondary to pituitary adenoma
ectopic GHRH or GH production by tumours e.g pancreatic
Features acromegaly (6)
Coarse facial appearance
Spade like hands
Increased shoe size
Large tongue
Prognathism (bulging of jaw)
Excessive sweating
Features of pituitary tumour (3)
Hypopituitarism
Headaches
Bitemporal hemianopia
Other features of acromegaly (2)
Hint 1. MEN 2. increased in 1/3 of cases
MEN 1
Raised prolactin in 1/3 of cases
Complications of acromegaly (4)
HTN
Diabetes
Cardiomyopathy
Colorectal ca
What is Addison’s disease?
Leads to a change in which two hormones?
autoimmune destruction of adrenal glands leading to hypoadrenalism.
Leads to a reduction in cortisol and aldosterone.
Features of Addison’s (8)
lethargy
anorexia
N&V
weight loss
hyperpigmentation (palmar creases) (only in Addison’s)
vitiligo
loss of pubic hair
hypotension
Electrolyte changes in Addison’s (4) (na k+ glucose gas)
Hyponatramia and hyperkalaemia
Hypoglycaemia
Metabolic acidosis
Addison’s crisis symptoms (3)
Collapse
Shock
Pyrexia
Primary causes of hypoadrenalism (6)
TB
Metastases
Adrenal haemorrhage
Meningococcal
HIV
Antiphospholipid syndrome
Secondary causes of hypoadrenalism (3)
Tumours
Irradiation
Exogenous glucocorticoid therapy
Addison’s Ix
Definite investigation:
ACTH stimulation test (short synACTHen test)
What is an ACTH stimulation test (short synACTHen test)?
Measure cortisol before and 30 minutes after giving synACTHen 250ug IM
Baseline cortisol measured, given synachthen and expect cortisol to double when measured at 30 minutes and 60minutes. If still low then Addison’s
Addison’s - what can you do if an ACTH stimulation test is not possible?
Measure 9am cortisol
Results for a 9am cortisol
> 500 - unlikely Addison’s
<100 - abnormal
100-500 = do a ACTH stimulation test
Explain the hypothalamic pituitary axis
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
Addison’s Mx (2)
- Hydrocortisone (20-30mg/day) (double if sick) - majority given in the first half of the day in 2-3 divided doses.
- Fludrocortiose (stays the same when sick)
What is Bartter’s syndrome?
What is the effect on BP
Autosomal recessive disease causing severe hypokalaemia
(defective chloride absorption at the NaKCl cotransporter in the ascending loop of Henle)
Associated with normotension
Features of Bartter’s (5)
Age group
Presents in childhood
FTT
Polyuria and polydipsia
Hypokalaemia
Normotension
Weakness
Mx of thyrotoxicosis
Carbimazole high dose for 6 weeks until pt becomes euthyroid before being reduced
MOA carbimazole
blocks thyroid peroxidase from coupling and iodinating thus reducing thyroid hormone production
Most common cause of thyrotoxicosis
Grave’s
Other causes of thyrotoxicosis (5)
Graves
Toxic nodular goitre
Acute phase of subacte thyroiditis
Acute phase of post partum thyroiditis
Amiodarone
DVLA rules for diabetics on insulin/ other hypoglycaemic inducing drugs such as sulfonylureas
Group 2
(5)
- no severe hypoglycaemia event in last 12 months
- full hypoglycaemic awareness
- show adequate control by regular blood glucose monitoring (BD monitoring and at times relevant to driving) (for 3 months before applying)
- driver must understand risks of hypoglycaemia
- no other debarring complications of diabetes
Group 2 versus Group 1 in the context of DVLA
HGV = Group 2
Car = Group 1
Car driver and on insulin or other hypoglycaemic inducing drugs such as sulfonylureas
Group 1
Hypoglyaemic awareness
No more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months
No visual impairment
Drivers are contacted by DVLA
If on tablets of exanatide or diet controlled do the DVLA need to be informed?
No
SE mineralocorticoids (2)
Fluid retention
HTN
When to have a gradual withdrawal of systemic corticosteroids? (3)
40mg OD for more than 1 week
Or if they have received any dose for more than 3 weeks
Recently received repeated courses
SE glucocorticoids psychiatric (3)
GI (2)
Eyes (2)
insomnia
depression
psychosis
Peptic ulcers
Pancreatitis
Glaucoma
Cataracts
Cushings
Metabolic acidosis or alkalosis
Hypokalaemic metabolic alkalosis
Cushings syndrome
Causes
ACTH dependent (2)
ACTH independent (3)
Pseudo (2)
ACTH dependent
1. Pituitary adenoma = Cushing’s disease
2. Ectopic ACTH production e.g small cell lung cancer
ACTH independent
1. Iatrogenic (steroids given to pt)
2. Adrenal carcinoma/ adenoma
3. Carney complex
Pseudo-Cushings
1. ETOH excess
2. Depression
Cushings
Investigations (3)
- Overnight dexamethasone suppression test
- 24 hr urinary free cortisol
- CRH stimulation test
Cushings
Explain what the overnight dexamethasone test is
Explain its results
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 disease (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
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.
TFTS interpretation
What would you expect the TSH to look like in steroid therapy and secondary hypothyroidism
Steroid Low TSH, normal T4
Secondary hypothyroidism low and low
Sick euthyroid TFTs
low and low although sometimes TSH can be normal
How to prevent thyroid related eye disease?
What medication can reduce the risk?
smoking cessation
prednisolone
Mx thyroid eye disease (4)
Topical lubricants
Steroids
Radiotherapy
Surgery
What is the classification of thyroid disorders?
Primary - problem with the thyroid gland
Secondary - usually due to pituitary (pituitary apoplexy)
Congenital - hypothyroidism
Name the thyroid condition:
Painful goitre and raised ESR
= subacute thyroiditis (hypothyroiditis)
Subacute (De Quervain’s) thyroiditis - hypo or hyper
By what week will it return to normal?
Presents with hyperthyroidism following a viral infection but is actually hypothyroidism.
Week 4
Name the thyroid condition:
Fibrous tissue replacing the normal thyroid parenchyma
Painless or painful goitre?
Hypo or hyper
Riedel thyroiditis
Painless
Hypothyroiditis
Toxic multinodular goitre
What is it?
benign thyroid nodules that secrete excess thyroid hormones
Postpartum thyroiditis
Hypo or hyper?
Hyper initially then hypo
Most common cause of low thyroid in the developing world?
Iodine deficiency
Name two drugs that can cause hypo thyroid and one that can cause hyper
Lithium hypo
Amiodarone both
Name a skin condition caused by hyperthyroidism
Pretibial myxoedema
Name three autoantibodies that can be tested for?
anti-TPO (Hashimotos)
TSH receptor antibodies (Grave’s)
Thyroglobulin antibodies
Mx hyperthyroidism (3)
- propranolol
- carbimazole
- radioiodine tx
When do you tx subclincial hypothyroidism? (figures)
TSH >10 and <= 70yo start rx if asymptomatic with levothyroxine
If >80 watch and wait
When do you tx subclinical hypothyroidism?
65yo
TSH 4-10 and T4 normal = subclinical hypothyroidism
<65 and symptomatic - trial levothyroxine for 6 months, if no improvement then stop
Subclinical hypothyroidism Mx
Older people (>80)
Asymptomatic people
Watch and wait, observe and repeat TFTs in 6 months
What are the main cause of subclinical hyperthyroidism?
Particularly in which group of patients? (sex and age)
Mx
Multinodular goitre - particularly in elderly females
If persistently low TSH then low dose carbimazole for 6 months
Describe Riedel’s thyroiditis
Describe the goitre
Age group and sex
Associated with which condition?
Hypothyroid characterised by dense fibrous tissue replacing the normal thyroid parenchyma
hard, fixed, painless goitre
middle aged women
associated with retroperitoneal fibrosis
Describe the 4 phases of subacute thyroiditis (De Quervain’s)
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
subacute thyroiditis (De Quervain’s)
Ix
thyroid scintigraphy: globally reduced uptake of iodine-131
subacute thyroiditis (De Quervain’s) mx (3)
self limiting
pain can be tx with NSAIDs or aspirin
if severe then steroids (especially if hypothyroidism develops)
Examples of meflitinides
When will they be used?
Similar to
SE (2)
Repaglinide
Erratic lifestyle
Similar to sulfonylureas
Weight gain and hypoglycamia
MODY mx (2)
Most common type
Gene defect
Increased risk of?
sensitive to sulfonylureas, insulin is not necessary
MODY 3
HNF alpha 1 gene defect
Increased risk of HCC
Metabolic syndrome criteria (5)
Atleast 3 of the following:
Raised BM
Raised BP
Raised waist circumference
Raised triglycerides
Reduced HDL
