Endocrine

Question 1

Pituitary Gland basics:
A-Location, Sections & corresponding hormones secreted?

B-Disorders of the hormone axis?

Answer 1

• Pituitary Gland
o Location:
 Below hypothalamus, near optic chiasm
• Significance: Pituitary tumours can cause bitemporal hemianopia

o	Sections:
	Anterior
•	TSH
•	ACTH
•	GH
•	FSH
•	LH
•	Prolactin
	Posterior
•	ADH
•	Oxytocin

o Disorders of the hormone axis:
 Primary: End organ (e.g. thyroid, adrenals)
 Secondary: Pituitary
 Tertiary: Hypothalamus

Question 2

Hyperprolactinaemia:
Physiology of prolactin?

Causes?

Answer 2

• Physiology of prolactin:
o TRH inhibits dopamine (therefore, stimulate prolactin release)
o Dopamine inhibits prolactin
o Prolactin inhibits GnRH

• Cause
o Physiological
 Pregnancy (sometimes), post-pregnancy/breast feeding (always)
 Stress

o	Endocrine causes:
	Prolactinoma
	Hypothyroidism: causes elevation in TRH= inc. in prolactin.
	Cushing’s (↑stress)
PCOS

o Drugs:
 Gut motility (metoclopramide, domperidone) – dopamine antagonists
 Typical antipsychotics (Haloperidol)

phenothiazines

Question 3

Hyperprolactinaemia:

Presentation, Ix & Mx?

Answer 3

• Presentation:

o Men: Erectile dysfunction, Hypogonadism

o Women: Amenorrhea/oligomenorrhea, galactorrhea

o Bitemporal hemianopia

• Ix:
o First:
 TFTs, Prolactin level

 MRI Pituitary (look for prolactinoma) <1cm=Microadenoma, if >1cm= macroadenoma.
*prolactinomas can be secretory or non-secretory.

• Rx for prolactinoma:
o First: Dopamine agonists (bromocriptine, cabergoline) usually x3yr

o If refractory: Surgery (Trans- sphenoidal surgery)

Question 4

Adenoma
disorders:
Acromegaly:
Terminology associated, physiology & causes?

Answer 4

• Terminology:
o Gigantism  ↑GH affecting children PRIOR to fusion of epiphysis; giants (>7ft tall)
o Acromegaly  ↑GH affecting adults, no growth of height (other changes though)

• Physiology: GH stimulates IGF-1 (produced in liver; stimulates growth)

• Cause:
o Functioning/ secretory Macroadenoma (75%; >1cm)

Question 5

Acromegaly:

Features, Ix & Mx?

Answer 5

• Features: ABCDEF of GH (arthralgia/arthritis, ↑BP, CarpTun, DM, Enlarged organs, Field defects)
• Ix:

o Initial test: Insulin-like Growth Factors (IGFs) (↑↑ in acromegaly)

o Best test/gold standard: OGTT w/ GH measurements

o Further Rx: MRI Pituitary

• Rx:

o First line: Surgery

Question 6

Diabetes Insipidus:

What is it? Causes?

Answer 6

Diabetes Insipidus: ADH deficiency (neurogenic/central) or unresponsiveness (nephrogenic)

• Cause:
o Cranial/Neurogenic (partial or complete lack of ADH) – any pathological process in brain

o Nephrogenic (lack of response from renal tubules)  lithium, ↑Ca, ↓K+, idiopathic

Question 7

Diabetes Insipidus: Symptoms, Diagnosis & Mx?

Answer 7

• Symptoms: Polyuria (dilute), polydipsia, nocturia

• Diagnosis:
o Step 1 – Water deprivation test
 Still pees lots = DI (+dilute)

o Step 2 – Vasopressin challenge
 Steps:
• Give vasopressin
o If urine concentrates (↑50% conc)  Neurogenic/Central
o If urine does not concentrate (<50%)  Nephrogenic

• Treat:
o Neurogenic/Central DI: Desmopressin (intranasally)

o Nephrogenic DI: High dose desmopressin

Question 8

Thyroid gland basics:

Function & Ix’s of all thyroid diseases:

Answer 8

• Thyroid gland
o 99% of iodine in body goes to thyroid gland  Produces T4 (mainly), some T3

INVESTIGATING ALL THYROID DISEASE
• STEP 1  TFTs:

o TSH low, T4 high: Primary hyperthyroidism

o TSH high, T4 low: Primary hypothyroidism

o TSH high/norm, T4 high : Secondary hyperthyroid

o TSH low/norm, T4 low: Secondary hypothyroidism (NB: normal TSH is INAPPROPRIATE)

• STEP 2  Autoantibodies – Anti-TSH Receptor (Graves’), Anti-Thyroid Peroxidase (Hashimoto’s)
• STEP 3  Radioactive Iodine Test (for hyperthyroidism)

Question 9

Hyperthyroidism: Features?

Answer 9

•	Features: THYRODISM
o	Tremor
o	Hair loss, heart rate up
o	Yawning
o	Restlessness
o	Oligomenorrhea/amenorrhea
o	Intolerance to heat
o	Diarrhoea
o	Increased appetite
o	Sweating
o	Muscle wasting/weight loss

Question 10

Hyperthyroidism: causes?

Answer 10

o Grave’s (most common)  30-50yr old
 Symptoms: ↑thyroid symptoms, small goitre, eye disease (specific to Grave’s; 40%)

 Graves eye disease  Only present in 40%
• Exophthalmos (very important sign)

• Ophthalmoplegia (very important sign)
• Lig lag (poor sign)  When patients moves eye from up to down, can temporarily see sclera above the iris (NOT down to up)
• Lid retraction
• Conjunctival oedema/chemosis
• Multinodular goitre (2nd most common overall, most common in >50 [NB: Graves <50]
• Single/hot nodule (single hot nodule on RIU)

• Subacute/De Quervain’s thyroiditis  ↓Radioiodine uptake, resolves on own in 2wks
o Cause: Recent viral infection
o Stages: 1) Hyperthyroid, 2) Hypothyroid, 3) Euthyroid (recovery)
o Features: Hyperthyroid symptoms, Thyroid pain + fever, NO eye symptoms

• Drugs (amiodarone, Li+)

Question 11

Ix of hyperthyroidism?

Answer 11

Diagnose:
 First:
• TFTs  ↓TSH, ↑FT4/FT3
• Anti-TSH receptor antibody (95% sens. graves)

 Second: Radioiodine Uptake (only need if atypical)  Diffuse excess uptake

Question 12

Mx of hyperthyroidism?

Answer 12

TREATING HYPERTHYROIDISM

• First: Treat symptoms (e.g. in hyperthyroid – give propanalol)

• Second – anti-thyroid therapy:
o Carbimazole, methimazole, propylthiouracil

• Third – definitive therapy:
o Radio-iodine ablation (I131 – radioactive form)
o Surgery

Question 13

Hypothyroidism features & causes?

Answer 13

Hypothyroidism
• Features:
o Tired, cold intolerance, weight gain, constipation, hoarse voice, menorrhagia, slowing/depression

• Causes:
o Hashimoto’s thyroiditis (most common in North America)
 Definition: Thyroid destruction via autoantibodies
 Epidemiology: Women 90%, men 10%

o Iatrogenic

o Drugs  Lithium, Amiodorone

o Subacute thyroiditis
 De Quervain’s (viral, not autoimmune)  Hypothyroid phase – give steroids

o Iodine deficiency (uncommon w/ iodine supplement, but most common worldwide)

Question 14

Hypothyroidism: Dx & Mx?

Answer 14

• Diagnosis:
o First: TFTs

o Second:
 Anti-thyroid peroxidase (TPO) (95% Hashimoto’s)

• Treat: Lifelong Thyroxine (T4)

Question 15

Hyperparathyroidism
• Epidemiology &
Types?

Answer 15

Hyperparathyroidism
• Epidemiology: 3rd most common endocrine disorder

•	Types:
o	Primary:
	Single adenoma (80%)
	15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

Question 16

Hyperparathyroidism: features, Dx & Mx?

Answer 16

• Features:
Polyuria, polydipsia, HTN.

o “Stones, Bones, Abdo groans, Thrones, Psych moans + Malignant undertones”
 Renal stones
 Pathological fractures & bone pain
 Abdo pain, N&V
Polyuria
 Depression, anxiety , confusion, coma, insomnia

• Diagnosis:
o Primary: ↑PTH + ↑Calcium + ↓Phosphate

o Then: Sestamibi/technitium scan  Hot PTH nodule(s) – 90% = single

• Treat:
o First: Treat hypercalcaemia (see below), or

o Second: Surgery – parathyroidectomy

calcimimetic agents such as cinacalcet- for secondary hyperparathyroidism.

Question 17

Hypercalcemia Mx?

Answer 17

•	 Any calcium >3 is an EMERGENCY
o	Acutely: 
	First: 
•	IV Fluids
•	Furosemide
o	NB: evidence does not support, but USEFUL if volume overloaded as can continue to give saline!

 If refractory after 24hr: IV Bisphosphonates

Question 18

Cushing’s disease: features

Answer 18

o Features:
 Fat  Moon face, Buffalo hump (+ supraclavicular fat pads), Central obesity, Striae
 Blood  Hyperglycaemia (30%), HTN (50%)
 Bone  Osteoporosis (inevitable if untreated)

METABOLIC SYNDROME (central obesity, raised triglyc, reduced HDL, raised BP, raised fasting plasma glucose) + OSTEOPOROSIS – big subsequent co-morbidity

Question 19

Cushing’s causes?

Answer 19

o Causes:
 Cushing’s Disease: Pituitary adenoma – NB: Cushing’s disease is the most common cause of high cortisol!

	Cushing’s Syndrome:
•	Iatrogenic/exogenous
•	Adrenal adenoma (10%)
•	Adrenal carcinoma (10%)
•	Adrenal hyperplasia w/o pituitary tumour (E.g. CAH; very rare)

Question 20

Cushing’s Dx?

Answer 20

o Diagnose:
 Is it Cushing’s (i.e. disease or syndrome)?
• First: Overnight Dexamethasone Suppression Test (Low Dose) 48hr

A condition of high cortisol (Cushing’s disease OR syndrome) has now been diagnosed, but must determine the source (pituitary, adrenal, ectopic)

• Where is it coming from?
o First: ACTH Level (at 9am and midnight)

 If low: Adrenal neoplasia/hyperplasia (or exogenous)

• CT/MRI adrenals
• Rx: Adrenalectomy

 If high: Pituitary adenoma

• MRI pituitary
• Rx: Trans-sphenoidal surgery

Question 21

Adrenal Insufficiency: Definition & causes?

Answer 21

Definition: inability of the adrenal glands to produce Glucocorticoids +/- mineralocorticoids.

Primary Adrenal insufficiency (loss of the gland function):
1- Drugs which lower adrenal hormone: Long-term steroids (most common cause of adrenal insufficiency), ketoconazole, metyrapone

2- Autoimmune (Addison’s; common [>80% of non-drug adrenal insufficieny])
o Progressive destruction of adrenal gland due to cytotoxic T-lymphocytes.
o Biochemical deficiencies only occur once 90% of gland destroyed.

3-Other: Waterhouse-Friderichsen: acute primary insufficiency due to adrenal hemorrhage. TB: in developing countries.

Secondary-pituitary failure: It SPARES the mucosa/skin + NO hypokalaemia.

Tertiary: Hypothalamic failure. Similar to secondary.

*The above are all chronic, but acute adrenal insufficiency is called Adrenal/Addisonian crises! Its when people have the chronic causes but get triggered by surgery, illness, infection, massive haemorrhage.

Question 22

Adrenal insuffiency: Features? (chronic & acute)

Answer 22

o Features: Difficult to diagnose
 Fatigue, weakness, N+V, GI disturbances.
 Hypotension, Hypoglycemia
 Hyperpigmentation (from ↑ACTH, i.e. only in primary!)
• Look in buccal mucosa + palmar/digit creases.

Addison’s as above but also: vitiligo, pernicious anaemia, hashimoto thyroiditis.

*ACUTE crises: Hypoglycaemia, Hyponatraemia, hyperkalaemia, metabolic acidosis & signs of shock!

Question 23

Adrenal Insuffiency: Dx?

Answer 23

o Diagnosis:
 First: Low blood sugar, low BP

 Second: Urinalysis (↑Na, ↓K) Blood (↓Na, ↑K)

 Short SynACTHen Test
• Addison’s disease – Cortisol will NOT rise!!!

This tells us if there’s adrenal insuffiency. Then to find out if its primary, secondary or tertiary: perform plasma ACTH= high= Addison’s. Low=2/3 causes.

Other: screen for TFT, TB,Haemochromatosis.

Question 24

Adrenal Insuffiency: Mx?

Answer 24

o Hydrocortisone

o Fludrocortisone

Acute: high dose IV hydrocortisone.

Question 25

Pheochromocytoma: definition, features?

Answer 25

(phios – dusky, chromo – colour, cytoma – growth of cells)
• Definition: Adrenaline producing tumour

•	Features: 
o	EPISODIC Headache (80%)
o	Palpitations (70%)
o	Profuse sweating (60%)
o	Tremor
o	HTN (sustained in 60%, paroxysmal in 40%)

Might be associated with: MEN type II, neurofibromatosis and von Hippel-Lindau syndrome (10%)

Question 26

Pheochromocytoma: Dx & Mx?

Answer 26

o First: Urinary metanephrines (97% sens, more specific)

o Positive Urine: MRI adrenals

• Treat: A-blocker: PHaeochromocytoma - give PHenoxybenzamine before beta-blockers otherwise hypertensive crisis

lABetalol- blocks both alpha & beta receptors if not above regimen.

Surgery: 10 days after Medical Rx

Question 27

T1DM-background?

Answer 27

• Type 1
o Background:
 No insulin production
 Insulin autoantibodies can be detected as early as 6-12mo of age
 Initiates with precipitating event (e.g. infection)

Question 28

T1DM:

Dx & Follow up?

Answer 28

o Diagnosis: Use the American Diabetes Association (ADA) criteria
 DIAGNOSE: Random BG ≥11.1 OR fasting BG ≥7 OR HbA1C >6.5% (48)
• If BG 6-6.9 (impaired fasting glucose): 75g OGTT (test 2hr after)
o Diabetes: BG ≥11.1
o Impaired Glucose Tolerance (IGT): BG 7.8-11

Anti-Islet cell + Anti-GAD (75% each)

Question 29

T1DM: Mx?

Answer 29

•	Treat: 
o	First: Insulin S/C
	Types:
•	Short-acting (e.g. novorapid)
o	Ultra-short acting 
o	Rapid acting
•	Intermediate (e.g. isophane)
•	Long-act (e.g. glargine, levemir) 

 Best regimen: 1 Long-acting OD + 1 Ultra-short acting at meal time

o Second: Insulin pump

o Third: Islet cell transplant

• Follow-Up:
o HbA1C

o Diabetic log

Question 30

T2DM- Background & Dx?

Answer 30

• Background:
o Insulin resistance, but still producing insulin

• Diagnosis: Same as T1DM

Question 31

T2DM: Mx?

Answer 31

• Treat:

o First: Diet + Exercise + Educate if >6.5% or 48mmol/mol (target to reduce to 6.5% or 48mmol/mol.

o Second: Metformin (biguanide)
If patient has HbA1c of >6.5% or >48mmol/mol & wants to try metformin:
 Start people on lifestyle + metformin unless mild and patient NOT overweight
 Lactic acidosis
 Diarrhoea/N+V (reduce in severity as Rx goes on, worse at beginning of Rx)

 Contraindicated if poor renal function

 No risk of hypos, no risk of weight gain (in fact causes weight LOSS) 
 ONLY oral hypoglycaemic proven to reduce stroke + MI 
 Reduced mortality 

The modified release variant of metformin appears to have a better gastrointestinal side effect profile and is recommended in patients experiencing those side effects as a second-line treatment. It’s given once daily rather than the immediate release which can be given TDS.

o Third – HbA1c still >6.5%: after 6 months. Increase Metformin dose to maximum tolerated dose e.g. His HbA1c is 51 mmol/mol (6.8%). You increase his metformin from 500mg bd to 500mg tds and reinforce lifestyle factors

Fourth: already on on drug but HbA1c risen to >7.5% or >53mmol/mol= add Second drug either Sulfonylurea (e.g gliclazide), Gliptins, or SGLT2 inhibitors, pioglitazone. Each has pros/cons so chosen for the right patients needs.

Sulfonylurea (e.g. gliclazide)
 Weight gain
 Risk of hypo so e.g. can’t be given to lorry drivers

Gliptins- DPP4 inhib when BMI <35 but probably the least effective drug and should only be used if there is no better alternative.

Sodium-glucose transport protein 2 (SGLT2) inhibitor (the ‘gliflozins’)-improve cardiovascular outcomes and reduce the admission rates for patients with heart failure - an extra benefit in this case. They do carry a small hypoglycaemia risk, but much less so than gliclazide.

Glitazone/Thiazolidenidiones (pioglitazone) usually given as last resort e.g. third drug.
 Weight gain
 Abnormal LFTs
 Fluid retention  Contraindicated in heart failure
 Bladder cancer (RR 2.64)
 Pathological fractures
 No risk of hypos

Fifth: If this fails, NICE recommends triple therapy with either:
Metformin + gliclazide + gliptin/glifozin/pioglitazone or
Metformin + pioglitazone + glifozin or
Insulin +/- other drug (not if significantly overweight and has already struggled with hypos)

o Sixth: Incretins (GLP-1 analogue [Exenatide]

 GLP-1 when BMI >35

achieve an 11 mmol/mol (1%) reduction in HbA1c AND 3% weight loss in the first 6 months in order for it to be continued.

o Last: Insulini

Question 32

Complications of DM: DKA for T1DM- give definition, presentation & Diagnosis?

Answer 32

•	Diabetic Ketoacidosis/DKA (Type 1)
o	Definition (Amer Diab Assoc):
	BG >11-13.8 
	pH <7.3 
	Ketones +

o Presentation:
 Young (teens)
 Abdominal pain, Vomiting, Confusion/Low GCS, SOB (Kussmaul breathing)
 Polyuria

o Diagnose: Criteria as above
 Blood sugar
 Urine dip
 VBG

Question 33

DKA: Mx?

Answer 33

• Treat:
o First:

 Fluid

 Insulin

 Dextrose?

 Potassium?

The osmolar gradient caused by the high blood glucose in DKA results in water shift from the intracelluar fluid (ICF) to the extracellular fluid (ECF) space and contraction of cell volume. Correction with insulin and intravenous fluids can result in a rapid reduction in effective osmolarity, reversal of the fluid shift and the development of cerebral edema.“ Or simply: Insulin clears up glucose + fluid = low osmolality (ECF) = water moves from low to high osmolality in the brain (ICF) = cerebral edema

Young patients need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc.

It usually occurs 4-12 hours following commencement of treatment but can be present at any time.

If any suspicion, request a CT head and call senior immediately.

Question 34

T2DM complication: • Hyperosmolar Hyperglycaemic State (HHS):

Give Features, Dx & Mx?

Answer 34

o Features:
 Very high blood glucose (often >30-40)
 Normal ketones (or small amount only)
 Normal pH (>7.3 at least, unless combined with AKI)

 Dehydrated/polyuria (massive – biggest problem)

o	Diagnose: 
	High blood sugar
	Normal pH
	Normal ketones
	High serum osmolality

o Treat:

 IV Fluid (vigorous; 0.9% NS)

 Insulin

 ± K+

Question 35

Chronic complications of DM?

Answer 35

o Microvascular
 Neuropathy
 Nephropathy
 Retinopathy

o Macrovascular  MI, Stroke, PVD…

Question 36

Hypoglycaemia: Definition, causes?

Answer 36

Hypoglycaemia*** (<3.0… however <2.5 = pathological)
• Definition: Whipple’s Triad:
o ↓glu
o Symptoms of hypoglycaemia (tachycardia, confusion, sweating…)
o Reversal with sugars

• Cause:
o Fasting/starving

o Liver failure, adrenal failure (Addison’s)

o Endogenous insulin
 Insulinoma

o Exogenous insulin  Factitious/Drugs:
 Insulin
 Sulfonylureas

Question 37

Hypoglycaemia: Mx?

Answer 37

• Mx:

o First:

 Not unwell (conscious):
• Oral sugar x3 (10-20g)

• Complex carb to prevent subsequent hypo

 Unwell (unconscious): IV dextrose (100mL of 20%) – check BM 15min later, and continue as necessary
• If IV access not available: Glucagon 1mg IM/SC/IV

o Second – Ongoing Mx: 10% dextrose infusion + hourly glucose monitoring
 Particularly important in sulphonylurea overdose as effects may continue

Question 38

Hypoglycaemia: Features & complications?

Answer 38

• Features: Lethargy, confusion, seizures, stroke-like syndrome, coma

• Complication: Prolonged hypoglycemic coma
o Cause: Cerebral oedema

Question 39

Hyperaldosteronism: Definition & causes?

Answer 39

Definition: High aldosterone secretion.

Causes:
1-Primary (Conn’s):
high Aldosterone, low renin
due to- adrenal adenoma or bilateral adrenal hyperplasia.

Secondary: high aldosterone & high renin.
Due to-Renovascular hypertension, juxtaglomerular cell tumors, oedema (cirrhosis, HF, Nephrotic disease).

Question 40

Features of Hyperaldosteronism:

Answer 40

Hypernatraemia, Hypokalaemia, Hypertension, Metabolic alkalosis

-Lethargy, headaches, muscle cramps.

Question 41

Hyperaldosteronism: Ix & Mx?

Answer 41

1-U&E’s for electrolytes imbalances + any renal secondary causes.

2-Aldosterone:Renin ratio- high=p Conn’s
Normal= Secondary.

*stop spironolactone & diuretics 6w before.

3-ECG 4-CT adrenals + adrenal venous sampling.

Mx:
Conn’s-
1-Adrenalectomt if adrenal adenoma.
2-Aldosterone antagonists: Spironolactone, eplerenone or amiloride if bilateral hyperplasia.

Secondary: Treat underlying cause.

Question 42

T2DM: drugs, MOA, SE & CI:

Answer 42

Metformin (biguanide):
MOA:
increase insulin sensitivity, increase glucose uptake, reduce liver gluconeogenesis.
SE:
 Lactic acidosis
 Diarrhoea/N+V (reduce in severity as Rx goes on, worse at beginning of Rx)

 CI:
poor renal function

Positives:
 No risk of hypos, no risk of weight gain (in fact causes weight LOSS)
 ONLY oral hypoglycaemic proven to reduce stroke + MI
 Reduced mortality

Sulfonylurea (e.g. gliclazide)
MOA: Insulin secretors-
1- stimulate pancreas to secrete Insulin by blocking K-channel= release insulin.

SE:
 Weight gain
 Risk of hypo

CI:
Liver impairment

Glitazone/Thiazolidenidiones (pioglitazone) PPAR gamma agonists:
MOA: increases insulin sensitivity by reducing peripheral insulin resistance.

SE:
 Weight gain
 Abnormal LFTs
 Fluid retention

CI: heart failure
	Bladder cancer (RR 2.64)
	Pathological fractures
Positives: 
	No risk of hypos

Incretins (GLP-1 analogue [Exenatide]:
MOA: Inhibits glucagon production in pancreas which stimulates cells of pancreas to release insulin.

SE: headaches, weight loss, pancreatitis.

DPP-4 inhibitor [Sitagliptin])
MOA: Inc. levels of GLP-1.

SGLT-2 inhibitor (sodium glucose transport protein 2) e.g. Dapagliflozin, canagliflozin, empagliflozin.
MOA: Helps kidney lower blood glucose levels (stops reabsorption of glucose back to blood).

SE: normoglycaemic ketoacidosis (CI IN T1DM!!)

Increased risk of lower-limb amputation: feet should be closely monitored

CI: frequent UTI’s & thrush infections.

o Last: Insulin

Question 43

Non- hyperparathyroidism causes of hypercalcaemia

Answer 43

Two conditions account for 90% of cases of hypercalcaemia:

1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
2. Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including; bone metastases, myeloma, PTHrP from squamous cell lung cancer

Other:
sarcoidosis*
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs: thiazides, calcium containing antacids
dehydration
Addison's disease
Paget's disease of the bone**
TB
histoplasmosis

Question 44

Hashimoto’s Thyroiditis: What is the single most important blood test to assess her response to treatment (levothyroxine)?

Dose?

Answer 44

TSH- the therapeutic goal is ‘normalisation’ of the thyroid stimulating hormone (TSH) level.

Cardiac disease, severe hypothyroidism or patients over 50 years the initial dose = 25mcg od

Other patients initial
dose = 50-100mcg od

Hypothyroidism in pregnancy= dose increased ‘by at least 25-50 micrograms