Endo5 Flashcards

(43 cards)

1
Q
A
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2
Q

What are the trimester by trimester TSH target ranges in pregnancy?

A

first trimester 0.1–2.5 mIU/L

second trimester 0.2–3.0 mIU/L

third trimester 0.3–3.0 mIU/L

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3
Q

How would you manage overt hypothyroid or a very elevated TSH in pregnancy?

A
Overt hypothyroidism (OH)
TSH \>2.5 with low T4

or TSH >10 irrespective of T4 level

Treatment of OH with levothyroxine is recommended. The goal is to normalise maternal serum TSH values within the trimester specific pregnancy reference range. Commencement of thyroxine while awaiting specialist review is generally appropriate (eg. 50–100 µg/day)

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4
Q

What is subclinical hypothyroidism in pregnancy? How would you manage it?

A

TSH between 2.5–10 with normal T4 levels

Evidence is variable as to the effect of SCH on pregnancy and the fetus<br></br>At this stage, the associated risk of obstetric complications has been more clearly demonstrated than the risk of neurocognitive deficits in the fetus. In addition, TPO Ab positivity may in itself be associated with fetal miscarriage and levothyroxone intervention in TPO antibody positive women with SCH may be beneficial

Options include treatment with levothyroxine to normalise maternal serum TSH or 4 weekly monitoring of TSH
Obtain TPO Ab levels while awaiting specialist review

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5
Q

How would you manage a patient with KNOWN (pre-existing) hypothyroidism in pregnancy?

A

Levothyroxine adjustment should be made as soon as pregnancy is confirmed
Aim to normalise TSH levels (ie. TSH <2.5) by increasing levothyroxine by two additional tablets weekly or by 25–30% and monitor thyroid function test
4 weekly
This adjustment can also be made preconception in women planning pregnancy

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6
Q

How do you rate severity of Vitamin D deficiency?

A

mild

30 to 49 nanomol/L

moderate

12.5 to 29 nanomol/L

severe

lower than 12.5 nanomol/L

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7
Q

Who should have their Vitamin D measured?

A

people at increased risk of vitamin D deficiency, such as those who:

are institutionalised or housebound (eg chronic illness, disability)

wear _clothing that covers most of the skin (_eg for cultural or occupational reasons)

have dark skin (Fitzpatrick skin types V and VI [Note 2])

have a medical condition (eg end-stage liver disease, kidney disease, hyperparathyroidism) or take a drug (eg r_ifampicin, antiepileptics_) that affects vitamin D metabolism and storage in the liver

have fat malabsorption (eg due to cystic fibrosis, coeliac disease or inflammatory bowel disease) or gastrectomy.

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8
Q

Who should be treated with Vitamin D?

A

Vitamin D supplementation is recommended for people who:

  • have uncomplicated moderate or severe vitamin D deficiency (serum 25-hydroxyvitamin D concentration lower than 30 nanomol/L), particularly if symptomatic
  • are starting drug therapy for osteoporosis and have a serum 25-hydroxyvitamin D concentration lower than 50 nanomol/L (see also Vitamin D and osteoporosis)
  • have osteomalacia or rickets.
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9
Q

Treatment of adult with mild vitamin D deficiency?

A
  1. consider lifestyle measures to increase exposure to sunlight first line.

If supplementation is preferred, use:

colecalciferol 25 to 50 micrograms (1000 to 2000 international units) orally, daily

Ensure anyone taking vitamin D also has 1300mg of Calcium in their diet.

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10
Q

Treatment of moderate to severe vitamin D deficiency?

A

colecalciferol 75 to 125 micrograms (3000 to 5000 international units) orally, daily for 6 to 12 weeks,

followed by 25 to 50 micrograms (1000 to 2000 international units) orally, daily.

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11
Q

What are three distinct forms of Diabetic retinopathy?

A
  1. Macular oedema - which includes diffuse or focal vascular leakage within the macula
  2. DR - caused by microvascular changes
  3. Retinal capillary non perfusion

DR - non proliferative - micro anuerysms, retinal haemorrhages, malformation and tortuous vessels - may be asymptomatic

proliferative - abnormal vessel growth on the optci disc or retina

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12
Q

What methods can be used to screen for diabetic retinopathy?

A

Colour fundus photography with interpretation by trained reader

Digital fundus photograpy

Direct opthalmoscopy or indirect slit lamp funduscopy through a dilated pupil.

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13
Q

What should you assess when looking at a diabetics vision?

A
  1. Visual acuity changes - due to refractory errors, (can use pinhole test to determine if there is a refractory error (blurring purely due to Ref Error is corrected by the pinhole).
  2. Cataracts (mainly with poor diabetic control and ketones) acute cataracts can have a snowflake appearance
  3. Fundoscopy through a dilated pupil (+/- retinal photography) - signs of DR, optic disc - eg glaucoma and ischaemic optic neuropathy
  4. Maculopathy - fundoscopy, retinal photography and surrogate markers eg fluroscein angiography
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14
Q

How would you describe the evolution of Diabetic retinopathy?

A
  1. Thickening of retinal basement membrane leads to a)microaneurysm formation and b) microvascular haemorrhages (dot and blot haemorrhages)
  2. Macrophages mop up the blood and the residual lipids showing up as hard exudates (defined border)
  3. Microinfarcts occur in occluded vessels - cotton wool spots (contain axoplasmic debris)
  4. Worsening retinal perfusion leads to neovascularisation
  5. These new vessels can burst causing vitreous haemorrhage or they can cause traction on the retinal pigment epithelium and lead to retinal detachment.
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15
Q

How is diabetic retinopathy managed?

A
  1. Photocoagulation
  2. For Macular oedema Anti VEGF and/or intravitreal steroids ar
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16
Q

What impact would newly diagnosed diabetic retinopathy have on your choice of lipid lowering therapies?

A

Fibrates should be considered in established diabetic retinopathy as they can slow deterioration (vs statins).

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17
Q

Which patients need urgent referral to an opthalmologist?

A

Patients with Sight threatening DR

- Macular oedema, proliferative DR, or severe non proliferative DR

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18
Q

How often should patients with Diabetic retinopathy be screened?

A

Most adults - EVERY 2 YEARS

Children from age of 9 - every 5 years

Certain high risk groups - yearly

  • ATSI*
  • Non english Speaking*
  • Poor control (HBA1c over 8%)*
  • Systemic disease - COMPLICATIONS micro/macro*
  • Established disease - over 15 years!*
19
Q

What are the minimum Medicare cycle of care requirements for a diabetic patient

A

Minimum

HbA1c Every year

Comprehensive eye examination Every 2 years

Weight, height, body mass index Every 6 months

Blood pressure Every 6 months

Foot examination Every 6 months

Total cholesterol, TG, HDL, cholesterol Every year Microalbuminuria Every year

Self care education Diet review Physical activity review Smoking status review Medication review

20
Q

Specific examination of the diabetic foot should include?

A

• palpate pulses • assess level of sensation (eg neuropathy/signs of ischaemia)• assess for presence of foot deformity • assess for presence of nail deformity • assess for presence of active lesion.

21
Q

How would you manage a patient with a diabetic foot ulcer?

A

M Metabolic/Medication

Optimise associated medical conditions, such as hyperglycaemia, hyperlipidaemia and hypertension.

A Assessment Examine diabetic foot ulcer and grade according to PEDIS classification (perfusion, extent [size], depth, infection and sensation).

D Debridement Surgically debride diabetic foot ulcer with necrotic or unhealthy tissue.

A Antibiotics Treat patient with diabetic foot ulcer with appropriate antibiotics on the basis of the severity of the infection.

D Dressing Perform frequent wound care with adequate dressings.

O Offloading Advise patient with diabetic foot ulcer to wear appropriate offloading shoes to reduce plantar pressure.

R Referral Facilitate early referral to a multidisciplinary diabetic foot team for optimal management of diabetic foot ulcer.

E Education Education on foot self-care should be provided to patients with diabetic foot ulcer or associated risk factors.

22
Q

How often should diabetic neuropathy be assessed?

A

Yearly in all adults.

Kids - 5 years after diagnosis and then yearly

23
Q

Common Complications of diabetic neuropathy?

24
Q

Management of hypopituitarism?

A

Involves replace of Glucorticoids, Thyroid hormone, Gonadal hormones, GH and arginine vasopressin

NB: Do not start thyroxine before replacing glucocorticoids – or you could induce an adrenal crisis

25
What is diabetes insipidius?
Reduced reabsorption of water from kidneys back into the circulation Leads to polyuria and polydipsia Electrolyte imbalance (esp hypernatraemia) Severe dehydration and seizures Diabetes insipidus can be central – reduced ADH from hypopituitarism Nephrogenic DI – reduced sensitivity of kidneys to ADH
26
What is the most common cause of central diabetes insipidus?
Usually a transient complication of pituitary surgery If no surgery – could be a malignancy (not adenoma) Refer patients with new onset DI (without obvious precipitant) for urgent endo review and WATER DEPRIVATION TEST (confirmatory test) (new onset DI with an obvious precipitant like head surgery does not require water deprivation test).
27
What is the management of chronic Diabetes insipidius?
If mild polyuria (up to 3 L/day) – can be left untreated as long as patient has access to water Mild – severe polyuria can cause hypernatraemia – initially treat with increased water intake. Ongoing management of polyuria – desmopressin (synthetic vasopressin analogue) 100micrograms orally twice a day. Adjust dose to response. Increase dose during pregnancy
28
What is the management of acute Diabetes insipidus?
Acute with a known cause – eg surgery or head injury If high urine output measure serum sodium conc and urine and plasma osmolality before commencement of treatment. Use parenteral desmopressin after confirmation of diagnosis Desmopressin 1-2mcg IM or IV. Repeat 12 hourly. Be careful of iatrogenic hyponatraemia Argipressin can be used that has a shorter half life.
29
What are presenting features of acute hypopituitarism?
Altered mental state Orthostatic hypotension Fever Hyponatraemia Hypoglycaemia
30
Management of acute hypopituitarism?
Urgent transfer to ED Check BSL, UEC, Adults: Hydrocortisone 100mg IV, then 50mg every six hours until stable and tolerating intake
31
What is pituitary apoplexy?
A syndrome of severe headache, neck stiffness, visual field defect, diplopia from cranial nerve palsies, hypopituiatirism (ACTH deficiency is most commn) Refer to a tertiary centre for endocrinology and neurosurgical review If caused visual loss then surg decompression is required
32
What kinds of pituitary adenomas are there?
Non functioning – can cause hypopituitarism Fucntioning include: prolactinoma, GH secreting adenoma, ACTH secreting adenoma
33
What genetic mutations can play a role in pituitary adenomas?
MEN1 – multiple endocrine neoplasia type 1 (consider if coexisting hyperparathyroid, pancreatic neuroendocrine tumours)
34
What is the most common type of pituitary adenoma?
Prolactinoma
35
What are the key symptoms of prolactinoma?
**Mass effects** in all (for macroadenomas) leading to a) Headache and b) Visual field defect (eg bitemporal hemianopia) and then blocking of GnRH Women – menstural disturbance, infertility, galactorrhea Men – erectile dysfunction, diminished libido Children – pubertal delay
36
What is the diff between microprolactinoma and macroprolactinoma?
Most are less than 10mm (micro) Macro is 10mm or more – can cause pressure effects – eg **headache,** visual impairment **(eg visual field defect - bitemporal hemianopia),** in addition to hyperprolactinaemia. (Tend to be bigger and more agro in men)
37
What are the symptoms of hyperprolactinaemia?
1. Of mass lesion - headache - visual field defect 2. Secretion of milk from breasts (galactorrhea - in women only) 3. Prolactin is an inhibitor if GnRH - therefore blocks LH receptor - Loss of libido in men - Erectile dysfunction in men - Irregular menstruation in females - Breast development in males - due to hypogonadism 4. Delay in Puberty 5. Infertility 6. Osteoporosis in later life Approach: If identified - look for cause and treat - Bromocriptine/Cabergoline 1st line Surgery 2nd line (if adenoma) RadioTx 3rd line
38
How do you treat prolactinoma?
Dopamine agonist therapy – goals are normalise serum prolactin concentration, restore normal gonadal function, reduce or stabalise prolactinoma Cabergoline 0.5mg orally, weekly in one or two doses, increase according to response by 0.5mg in montly intervals (max of 3mg) Or bromocriptine, or quinagolide Can take several months to restore gonadal function.
39
How is a diagnosis of primary adrenal insufficiency confirmed?
1. Positive short synathcen test. 2. Elevated ACTH level 3. Elevated plasma renin
40
What investigations should be ordered in suspected adrenal insufficiency?
Random cortisol (if \> 550 can exclude, if less than 50 - highly suggestive) 9AM ACTH level - a high level with low cortisol is diagnostic Short synathcen test - (an absent or severely blunted serum cortisol response to tetracosactrin 30 to 60 minutes after injection). (This doesn't differentiate between primary and secondary adrenal insufficiency) Plasma renin activity - HIGH in adrenal insufficiency UEC - low sodium and high potassium (due to aldosterone def) BLood glucose - can be hypoglycaemic (Due to gluconeogenic effects of cortisol) Adrenal antibodies
41
What are the causes of secondary adrenal insufficiency? How would you identify and treat Secondary adrenal insufficiency?
Causes: 1. Hypothalamic pituitary disease (Pan Hypopituitarism - check TSH) 2. Long term steroid therapy. Mx If the cause is pan hypopituitarism - MUST replace cortisone BEFORE thyroxine otherwise can precipitate an adrenal crisis If the cause is long term steroid therapy - very slow wean of steroids - may need to consider lifelong steroid therapy
42
If screening for cushings syndrome is positive - what further investigations would you consider?
1. 48 hour Dexamethasone suppression test 90% of pituitary dependent disease will suppress cortisone. IF not suppressed: - 10% still pituitary dependent disease - Ectopic ACTH secretion - Benign adrenal hyperplasia - Adrenal nodular hyperplasia - Adrenal Carcinoma - Adrenal Ca - Iatrogenic 2. Measure serum ACTH level 3. MRI brain for pituitary tumour 4. UEC - low potassium and high sodium - common in ectopic ACTH 5. CT imaging of adrenals - adrenal ca - large size and irregular outline - Adrenal adenoma - always detectable Bilateral adrenal hyperplasia - IN ACTH dependent disease this can be seen Bilateral adrenal nodular hyperplasia - Non ACTH dependent 6. CXR Then Check for complications: UEC Fasting glucose BP Bone Mass Densitometry Cataract Check FBE - high neutrophils, low lympocytes, low eosinophils Assess for proximal muscle weakness
43
What are the causes of hyperprolactinaemia?
A prolactinoma Distruption of pituitary stalk (trauma, surg, tumour) Pregnancy Hypothalamic disorder – tumour (glioma), infitltration (sarcoidosis), radiotherapy Drugs – including antipsychotics, methyldopa, metoclopramide, domperidone, opioids, SSRI, TCAs, Cannabis, OCP Systemic disorder including hypothyroid, kidney failure, liver failure, epileptic seizures, Neurogenic cause – breast stimulation and lactation, chest wall trauma or lesion, stress Pseudohyperprolactinaemia