Endo Flashcards
Important questions for thyroid eye disease
Whats bothering them most eg vision / discomfort
Swelling / redness / puffy
-Previous hayfever
Issues with eye movements
Any visual loss/ ability to focus / double vision
Unable to close eyelids
Thyroid history - what would warrant same day / very urgent opthal review
Visual loss / symptoms
Neck lump history key points
Is this new
- goitre often very long standing
- New is more concerning
issues with swallowing or speaking
Pain
Thyroid status
Questions for thyroid status?
Other key parts of history?
Head and general
Anxiety and mood
Energy levels
Weight
Eye symptoms
neck lump / pain
Chest
Palps
chest pain
Bowel
Bowel habit changes
Periods
tremors
Social
- SMOKING - big risk for eye disease. Must council on this
- Pregnancy especially post partum
- Seaweed - lots of iodine
DH
-Amiodarone (often long time lag)
-Lithium
-Biologics (sometimes years leater)
Surgical history
How thyroitoxic do you need to be to have thyroid eye disease
You can have it and be euthyroid / without thyrotoxicosis
Thyroid exam
Eyes
- look from side
- Any redness / Swelling
- Lid retraction
- Eye movements
Vision
Snellen chart
Fundoscopy
Neck
- Throidectomy scar
- feel for lump
- feel when swallows / sticks tongue out
-Any tenderness
- Auscultate for bruis
Hands
- warm
- sweat
- tremor
- Pulse / Atrial fibrillation
Shins
- Pre tibial myoxdema (often like orange peel)
- Deep tendon reflexes
Throid exam and this
Conjunctival injection
When doing snellen chart what should you ask to speed things up
Whats the lowest line you can read
Someone with thyroidectomy scar but signs of thyrotoxicosis
May have been partial thyroidectomy
Multinodular goitre may grow back again if some tissue left
Why thyrotoxicosis get bruis in neck
Increased blood flow from metabolically active thyroid
pre tibial myxodema
Post partum thyroiditis painful?
Can be often not.
Thyroiditis not always painful - DONT get side tracked by absence of pain
Differentials of thyroid neck lump
Short time period
- Need to rule out Cancer
Longer
- Cyst
- Nodule / multi nodular goitre
- Adenoma sometimes
Investigations in neck lump / thyrotoxicosis
Bloods
- TFTs - TSH / T3/T4
- TSH receptor antibody (graves)
US
Thyroid uptake scan
Ophthalmology review if any concern
Who has raised TSH receptor antibody
- Graves
- Thyroid eye disease
- Sometimes amiodarone (induces the antibodies)
[Usually negative in multi nodular goitre]
Why can you get thyroid eye disease without thyrotoxicosis
Eye disease is caused by the TSH receptor antibodies
Do you treat sub clinical thyrotoxicosis
Yes
- They have high risk of developing osteoporosis / AF if not
Most important red flags thyroid what would you do?
Visal loss including acuity
compelx opthalmoplegia
High dose steroids
Mild thyroid eye disease treatment
Stop smoking
Lubricating eye drops
Treat hyperthyroid
Thyroid eye disease steroids not working - whats next
Immunomodulators
Eg rituximab
Radiotherapy of orbits
Orbital decompression - last line
Hypothyroid patients often have what else on thier bloods? what do you do?
Raised cholesterol
Often improves with throxine replacement
When and how should you take thyroxine
on an empty stomach
Calcium eg milk reduces absorption significantly
Treatment for graves?
When for each?
Symptoms
- Propranolol 40mg TDS
Carbimazole
Propylthiouracil
- Used for women who are pregnant or breast feeding
Why propranolol specifically in thyrotoxicosis
Reduces conversion to t4 in peripheries
2 Main options style of thyrotoxicosis management
Titration
Block and replace
- Eg high dose carbimazole with thyroxine replacement
(Use if significant thyroid eye disease and want very close control)
Key thing to council patients when treating with antithyroid meds
Agranulocytosis
“If you get a severe sore throat you must stop taking this medication and present to hospital”
When would you use radio iodine?
Toxic multinodular goitre
- Good 1st line treatment
Graves
-Usually get a 12-18 month course of carbimazole then stop
-In 2/3 will get relapse and then its worth thinking of more definitive treatment
Key issues with radio iodine
2 weeks isolation at home
Especially avoid young children
Not if planning pregnancy -> fetal hypothyroidism
May end up with underactive thyroid.
Who must NOT get radioactive iodine
people with ongoing thyroid eye disease -> Makes it worse
Pregnant / planning
Acromegaly focused history
Brain
- Headaches
- Visual field loss
- Deafness
Snoring / OSA
Cardio
- Hypertension
- Diabetes - polyuria / dypsia
- Worse control
Sweating
Pituitary symptoms
- Libido
- Menstrual history
- Tired
- Dizzy
Bone changes
- Shape of face / jaw
- Hands and feet eg rings not fitting
- Carpal tunnel
- Dentition - Widening teeth gaps
Calcium
- Polyuria
- Bone pain
Family history
- Acromegally
- Endocrine - MEN1 / carney complex
Social history
- How affects function
- Smoking / alcohol CV health
Acromegaly exam
Hands
- Size, sweat, coarse skin
- Pulse
- Pain on joints
Carpal tunnel exam
- Tinnels / phalens
BP
Neck
- Acanthosis nigrans in neck
- Goitre + palpate thyroid with swallow
- Inspect face and teeth
Eyes
Fundoscopy
RAPD / accomdation
Visual field testing
Eye mocements
- I would like to complete a full cardiovascular assessment
- BP
- ECG (LVH)
- Epsworth sleep score
- Capillary blood glucose
How to present acromegaly
This patient has prominent supaorbital ridges and a large lower jaw, ears and nose.
His hands are large doughy and spade like and his skin is coarse and sweaty
There is evidence of bilateral carpal tunnel syndrome with thenar eminence wasting bilaterally and impaired sensation in the distrobution of the median nerve
There is increased interdental spacing and macroglosia.
There is evidecne of acanthosis nigrans.
He has a bitemporal hemaniopia
I would like to check a blood sugar and blood pressure
Acromegaly investigations
Make the diagnosis
- IGF - 1
- Glucose tolerance test with GH response
-> If positive refer to endocrine and book a MRI pituitary
Then assess complications
- ECG +/- Echo
- HBA1C, lipid profile
- Pituitary profile: 9am cortisol, T4 and TSH, Prolactin, Testosterone, LSH / FH
- Renal profile - Especially for hypoNa
- Calcium - Parathyroid adenomas in MEN1
- Visual field testing
- If OSA -> Sleep studies
- If carpal tunnel -> nerve studies
Why dont you measure GH in acromegaly
Anterior pit produces growth hormone in pulses
-> stimulates liver to produce Igf-1 continuously
ie GH levels vary through day
Acromegaly treatment
Education
Optomise CV health
Diabetes management
Surgery
- May have some medical management pre op Eg carbegoline
Acromegaly medical management
Dopamine agonists
- Bromocriptine / carbegoline
Somatostatin analouges
- All injectable
- Ocretide
Complications of pit surgery
- Meningitis
- Haemorrhage
- Tumours close to optic chiasm - optic ischemia (often if been stretched by tumour and then sags down post op.)
- Transient diabetes insipidus / hypopituitary
Pit hormone replacement in post op transient hypopit post op
Desmopressin
Levothyroxine
Hydrocortisone
What happens in oral glucose tolerance test acromegally
Growth hormone levels dont reduce and sometimes a paradoxically elevated
[usually supressed)
Extra blood test to rule out syndrome which may be cause of acromegaly
Ca - MEN 1
(Parathyroid hyperplasia)
What is MEN1
autosomal dominant
Pit tumours
Parathyroid hyperplasia
Pancreas tumours
Complications
acromegally
Untreated - >
- diabetes
- hypertension and CV disease
- colonic polyps + malignancy
Conditions which cause macroglosia
Downs
Acromegaly
Amyloid
Hypothyroid
DAAH
Acanthosis nigricans found in
Acromegaly
T2DM
Malignancy
Normal in indian subcontinent
MEN 2 gene? Features ? Seen in MEN2b
RET gene
Primary hyperparathyroid (MEN1 is hyperplasia)
Thyroid Ca
Phaeochromocytoma
MEN2B - marfanoid appwarance and mucosal neuromas
Present examination findings in a patient with Addisons. To complete?
Slim middle aged person there is slight bown pigmentation more prominently in skin folds.
There are well demarkated areas of depigmentation (vitiligo)
There is some superficial bruising on the abdominal wall suggesting possible T1DM
I would like to check L/S BP and check a capilliary blood glucose level
Addisons differenential diagnosis
(hypoadrenalism)
Primary hypoadrenalism (addisons)
TB
Surgical removal of Ca
Infiltration - malignancy / amyloid
What is addisons? Most common defect
Autoimmune distruction of adrenal cortex
21-hydroxylase is the most common antigen.
Lack of glucocorticoid and mineral corticoid hormones
Requires >90% destruction of gland to become clinically / biochemically symptomatic
Addisons symptoms
Non specific
Weight loss
Anorexia
Nausea and vomiting
Malaise
Weakness
Bowel habit change
Ammenorrhea
Syncope
Myalgia
Addisons signs on exam
- Hyperpigmentation (maximally in skin creases, scars and buccal mucosa)
- Muscle wasting
- Body hair loss
- Dehydration and postural hypotension
Why hyperpigmentation in addisons
Increased ACTH production in pituitary (due to lack of cortisol)
ACTH stimulates melanocytes
What characterises an addisons crisis? Key investigations? treatment?
Hypotension and dehydration
Often precipitated by illness / operation
Bedside
- Glucose
- BP
- ECG
- VBG
Bloods
Inflamm markers
Na and K+
TFTs
LFTs
Management
Venous gas - looking at K+ and Glucose
IV fluids (saline)
IV hydrocortisone 100mg 6hrly
Addisons diagnosis
Measure cortisol level (<100 suggestive, >550 unlikely)
The ACTH stimulation test
(basline cortisol then 250ngm synacthen then cortisol in 30 mins)
Stays low in addisons
Presents with hypoadrenalism and calcificaion of adrenals on imaging
Previous TB
Addisons associations
Autoimmune
Vitiligo
T1DM
Hypoparathyroid
Autoimmune thyroid
Pernicious anaemia
Hepatitis
Allopecia
Why dont you need to give fludrocortisone in acute hypoadrenal crisis
Hydrocortisone gives enough mineralcorticoid activity
Long term management of addisons
Conservative
- Educate espec sick day steroid rules
- Medic alert bracelet
- Often carry IM hydrocortisone in emergencies
Medical
- Gluco/mineral coriticoid replacement
- Approx 20-30mg hydrocortisone
- 50-100mcg fludrocortisone
- Managment of diabetes / thyroid disease
Secondary adrenalcortioid deficiency causes? Sign not found?
Lack of ACTH from Pituitary
- Exongenous steroids from resp/autoimmune diseases
- Panhypopituitarism eg in adenoma / Shehan syndrome
Dont get hyperpigmentation as this is secondary to the ACTH itseld
Present cushings
This middle aged lady has cushingoid features
There is an elevated BMI with central adiposity
Her skin is thin and brused and there is striae over the abdomen
There is a proximal myopathy and hypertension.
To complete my exam I would like to dip the urine, and check a blood glucose as well as assessing for a bitemporal hemaniopia
How to diagnose cushings location
Focused history for exogenous steroid use
1 Dexamethasone suppression test to confirm cushings syndrome
2 Check ACTH
- ACTH high will be raised in pituitary / ectopic ‘ACTH producing tumour
- ACTH low in Adrenal
a) If ACTH low (adrenal) -> CT/MRI adrenals
3 If ACTH high -> high dose dexamethasone supression
a) Cortisol supressed -> pituitary -> MRI
b) Cortisol unaffected -> CTCAP
Name features of cushings
- Hypertension
- Cardiac hypertrophy
- Type 2 diabetes
- Dyslipidaemia (raised cholesterol and triglycerides)
- Osteoporosis
- Adverse mental health (e.g., anxiety, depression, insomnia and rarely psychosis)
On inspection
- Round face (known as a “moon face”)
Central obesity
- Abdominal striae (stretch marks)
- Enlarged fat pad on the upper back (known as a “buffalo hump”)
- Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
- Male pattern facial hair in women (hirsutism)
- Easy bruising and poor skin healing
- Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
What features on exam make you think it could be an ACTH dependent cushings syndrome (pit / ectopic Eg small cell lung Ca)
Cough / haemoptysis / weight loss / smoking history
Bitemporal hemaniopia
Skin pigmentation
A high level of ACTH causes skin pigmentation by stimulating melanocytes in the skin to produce melanin. Excess ACTH, either from Cushing’s disease (pit adenoma) or ectopic ACTH.
Basics of cortisol production
Corticotrophin releasing hormone in hypothalamus
-> ACTH from pituitary
-> Cortisol production in zona fasiculata of adrenals
[With negative feedback on pituitary]
Blood test to determine pituitary vs ectopic ACTH.
Inferior petrosal sinus sampling
- Small catheters are inserted into the femoral veins
- The catheters are guided to the inferior petrosal sinuses
- Blood samples are taken from the catheters and the main vein of the abdomen
- The ACTH levels in the samples are compared to the ACTH levels in the peripheral blood
Causes of pseudocushings
Alcohol exess
Depression
Liver enzyme inducers
- Eg Phenytoin, rifampicin
Drug which can be used in those not fit for surgery in cushings
Metyrapone - reduces the production of cortisol in the adrenals
Surgical removal of both adrenal glands -> bitemporal hemaniopia?
Nelson’s syndrome
- development of an ACTH-producing pituitary tumour \
- due to a lack of cortisol and negative feedback.
-It causes skin pigmentation (high ACTH), bitemporal hemianopia and a lack of other pituitary hormones.
Thyroid mass differential
Single nodule
- Benign adenoma
- Cyst
- Abscess
- Carcinoma
Diffuse smooth goitre
- Iodine deficiency
- Puberty
- Graves
- Hashimotos
- Throiditis - eg post viral / pregnancy
Multinodular
- Toxic and non toxic depndent on thyroid status
Thyroid mass Ix?
- Bloods including TFTs and Ca
- Consider isotope uptake scan to look for inactive vs hyperactive tissue within the thyroid
If Hypothyroidism or cold nodule on isotope scan
- Fine needle aspiration and US to rule out thyroid Ca (as majority are non functioning)
If concerns of tracheal compression
- CT neck and Lung function tests
Either way shold have refereral to endocrinologist / ENT
What would make you think a thyroid mass was malignant
If <16 or >65
PMH thyroid Ca
Exposed to carcinogens eg radiation
Rapidly enlarging or very painful
Associated with cervical lymphadenoathy
Types of thyroid cancers? which is part of a syndrome
- Papillary most common (80%)
- Follicular - often in elderly
- Medullary - MEN2a eg family history (PTH hyperplasia and phaeochomocytoma) (secrete ACTH and calcitonin)
- Anaplastic - aggressive with compressive symtoms
- Lymphoma - often seen in hashimotos thyroiditis
[Squamous cell carcinoma]
Symptopms of large goitre
- Stridor
- Dysphagia
- Horse voice - Recurrent laryngeal palsy
- Occationally horners
What does a thyroid bruis suggest?
Graves
-> look for further evidence
Hyperthyroid signs
- General
Weight loss - Hands
Tremor
Thyroid acropachy - Head / Face
Mood disturbance - eg agitation
Flushing
Exopthalmous / opthalmoplegia
Hair loss
Goitre - Heart
AF / tachycardia - Abdo
Diarrhoea
Ammenorrhea
Loss of libido - Legs
Proximal myopathy
Pretibial myxodema
Thyroid acropachy - swellling and clubbing of hand
Define graves disease
Autoimmune disorder caused by thyroid stimulating antiboodies which activate TSH receptors
-> Hyperthyroidism
Management of hyperthyroid
Conservative
- Patient education inc patient.co.uk website
- Discuss treatmnent options
Medical
- Symptoms - B blocker eg propranolol
- Block Propylthyrouricil / carbimazole
- Consider thyroxine
Radioiodine can be used for permanent option
Surgical
If suspected malignancy
Those with compressive symptoms
Occationally cosmetic
Management of thyroid storm
Investigate for cause
Eg septic screen / medications / surgery
T3/4/TSH
FBC U&Es and BCs
- 40mg propranolol TDS for symptoms of palpitations and anxiety
- 100mg IV hydrocortisone 6hrly
- Replace fluids / electrolytes
- DW endocrine re carbamizole
Steroids - inhibit peripheral conversion of T4 into T3
Features of thyroid eye disease
Conjunctival oedema Oedema
Exopthalmous
Lid retraction
Lid lag
Reduced acuity
Complex opthalmoplegia
Causes of hypothroidism
Primary
- Iodine deficiency
- Hasimotos thyroiditis
- Iatrogenic
Too much cabrimazole / propythyouricil Thyroidectomy / radioiodine
- Drugs Eg Amiodarone / lithium
Secondary
- Hypothalmus / pituitary failure
What is hashimotos? Associated
Autoimmune disorder caused by anti-thyroglobulin / anti-thyroid peroxidase antibodies
- Causes gradulal destruction of thyroid -> hpothyroid
- Assoc - Autoimmune Addisons, T1DM
Untreated hypothyroid in pregnancy?
Growth restriction
Cognitive impairment
Large tongue
[cretinism]
Thyroiditis causes
Post infection
Post pregnancy
Post radioiodine for graves
During bacterial infection with thyroid abscess
Why OSA in acromegally
Causes soft tissue swelling in face and throat
OSA scoring systems
Epsworth sleepiness score >11
STOPBANG questionaire
Present hypothyroid
- This woman is overweight with coarse facial features. She has pale yellow dry skin.
- Her hair is dry and thin
- There is a loss of the outer 1/3 of her eyebrows
- There is generalised non pitting swelling of the tissues
- She is brady cardic
- There is a firm, smyetrical goitre
IF HYPOthyroid and graves -> hypothyroidism secondary to previously treated graves disease eg thyroidectomy
New diagnosis hypothyroid on throxine - what would a persistent raised TSH indicate
Compliane issues
Taking tablets with milk
Lack of absobtion other bowel issues
Addisons (get raised TSH if left untreated)
Pernicious anaemia
Complication of t4 replacement in elderly
Rapid correction can lead to IHD / MI
Present hyperthyroid
- This middle aged woman is thin and restless
- Her palms are warm and sweaty
- There is a fine tremor and an irregularly ireregular pulse indicating AF
- On examination of the eyes there is proptosis, lid retraction and lid lag
- There is evidence of proximal myopathy
- There is a warm swelling over the thyroid with a bruis
What eye signs might there be in graves
- Exopthalmus -> exposure keratitis and corneal ulceration
- Lid retraction
- Lid lag
- Optic nerve damage
- complex opthalmoplegia
Causes of exopthalmous
Bilateral - Graves / Cavernous sinus thrombosis
Unilateral - obrital tumour / cellulitis
Causes of hyperthryoid
Primary
- Graves
- Toxic nodule
- Multinodular goitre
- Iodine
- Over treatment
- Post partum thyroiditis
Secondary
- Pituitary function
- Amiodarone
Main side effects of carbimazole
Rash
Bone marrow supression / agranulocytosis -> seek medical advice if develop sore throat / infection
3 main aspects to Investigation of multinodular goitre
- TSH / T3 / T4
- US - solid / cystic
- Isotope uptake scan - Hot (with uptake) or cold
Cold, solid nodules -> Needle aspiraition as may be malignant
Types of familal dyslipidaemia [3 basic ones so you a least have an answer]?
Raised cholesterol. / trigycleride leads to? management?
Familial hypercholesterolaemia
Familial hypertriglyceridaemia
Familial combined hyperlipidaemia - most common [polygenic cause]
Issues
- Cholesterol -> accelerated astherosclerosis - coronaries nad peripheral
- Triglyceride -> pancreatitis and retinal vein thrombosis
Management
Conservative
- Weight loss / good exercise / diet
- Smoking and alcohol
- [Avoid B blockers / thiazide diruetics]
Medical
- Treatment of Diabetes / hypothyroid
- Statins
- ezetimbe - stop cholesterol absrobtion
- PKS9 inhibitors eg Evolocumab
- Fibrates - eg fenofibrate
- Cholestryramine - stop bile acid resorbtion -> circulating cholesterol used to make
