Endocrine CBL

Question 1

Presentation of T1DM

Answer 1

Onset usually in childhood
Usually lean
Typically acute - polyuria, polydipsia, weight loss
Ketosis prone
Presence of auto antibodies - islet cells, insulin
C peptide low or undetectable

Question 2

Autoimmune polyendocrine syndrome type 2

Answer 2

Triad of addisons, Al thyroiditis and T1DM
Common in females
Presents in adulthood
Associated with - coeliac, pernicious anaemia, alopecia

Question 3

DKA triad

Answer 3

Hyperglycaemia
Acidosis
Ketonuria

Question 4

Clinical signs of DKA

Answer 4

Abdo pain
Kussmauls breathing
Smell of ketones in breath

Question 5

Diabetes fasting and random glucose cut diagnostic criteria?

Answer 5

Fasting >7
Random >11.1

HbA1c of 48mmol/mol (6.5%) recommended cut off

Question 6

How does insulin deficiency lead to DKA?

Answer 6

Insulin deficiency = excess mobilisation of FFAs from adipose tissue, providing substrate for ketone production from the liver.

Ketones are excreted by kidneys and buffered in blood but this system eventually fails and acidosis develops.

Hyperglycaemia also occurs as the liver produces glucose from lactate and alanine.

Osmotic diuresis causes hypovolaema

Question 7

Name 3 ketones

Answer 7

B hydroxyl butyrate, acetoacetate, acetone

Question 8

Possible causes of DKA not with new T1DM?

Answer 8

Non compliance with insulin
Infection
Pregnancy
MI

Question 9

How should DKA be managed?

Answer 9

Insulin and fluids - monitor electrolytes (particularly potassium)

Question 10

Name 5 elements to be considered when educating a newly diagnosed T1DM?

Answer 10

Never stop insulin
Sick day rules
Recognising signs of hypoglycaemia
Smoking
Driving regulations (inform DVLA)
Exercise 
Planning a pregnancy

Question 11

Typical features of T2DM

Answer 11

Over 30
Gradual onset
25-30% have retinopathy at presentation
Overweight/obese
Autoimmune markers tend to be negative

Question 12

Define type 2 DM

Answer 12

Chronic, progressive metabolic disorder characterised by insulin resistance and impaired secretion

Question 13

Mx of diabetic cardiovascular disease

Answer 13

Risk factor modification - smoking, dyslipidaemia, hypertension, hperglycaemia

Lower BP - ACE, calcium channel blocker or thiazide diuretic

Question 14

Multidisciplinary team members in diabetes?

Answer 14

Optician
Podiatrist
Diabetic nurse specialist
Dietician

Question 15

Risk factors for gestational diabetes mellitus?

Answer 15

BMI
Previous birth weight  (4.5kg or more)
Previous GDM
Family history of diabetes
Minority ethnic origin

Question 16

Diagnosis of GDM

Answer 16

Fasting plasma glucose >5.11 or

two hours after OGTT >8.5

Question 17

Symptoms of thyrotoxicosis

Answer 17

Weight loss
Increased appetite
Tremor
Polyuria
Weakness, fatigue
Insomnia
Anxiety
Change in heat preference - cold not hot

Question 18

Most sensitive indicator of thyroid dysfunction?

Answer 18

Thyroid stimulating hormone (TSH) - cant be used in px with pituitary disease as they don’t produce TSH

Question 19

Sick euthyroidism

Answer 19

Low TSH, low free T3 and sometimes low T4

Question 20

Amiodarone and its effects on TFTs

Answer 20

1) inhibits T4-T3 conversion = mild raise in TSH
2) can induce hypothyroidism
3) Can induce hyperthyroidism - e.g. destructive thyroiditis

Px on amiodarone have High normal T4, low normal T3 and initially high TSH

Question 21

Px presents with

Raised T4
Low T3
Initial high TSH

Diagnosis?

Answer 21

Amiodarone effects

Question 22

Define hyperthyroidism and thyrotoxicosis?

Answer 22

Thyrotoxicosis is the syndrome resulting from excessive free thyroxine (t4) and free tri-iodothyronine (t3)

Hyperthyroidism refers to thyroid overactivity resulting in thyrotoxicosis

Question 23

Causes of thyrotoxicosis

Answer 23

Primary -
Graves
Toxic multinodular goitre
Toxic adenoma

Secondary -
TSH secreting pituitary adenoma
Gestational thyrotoxicosis
Thyroid hormone resistance syndrome

Question 24

Investigations to diagnose cause of thyrotoxicosis?

Answer 24

Thyroid autoantibodies -
Anti TPO antibodies
Anti TSH receptor antibodies (most reliable test for graves)

Nuclear imaging

Question 25

Nuclear imaging in diagnosing thyrotoxicosis

Answer 25

Thryoid scintigraphy scanning is useful when antibody testing is negative, a nodule is palpable

Patterns -

Diffuse uptake with suppression of background activity (graves)

Irregular uptake - multinodal goitre

Hot nodule - toxic adenoma

Reduced uptake - thyroiditis

Question 26

Tx of graves disease

Answer 26

Antithyroid drugs -

B blockers

Carbimazol and propylthiorucal (PTU)

Radioactive iodine

Surgery

Question 27

Carbimazole and propylthiouracil (PTU) MOA

Answer 27

Inhibit iodide organification by thyroid peroxidase = reduces T3 and T4 levels

Carbimazole is usually used, PTU if pregnant.

2 regimens -

1) Reducing regimen started higher then reduced once px euthyroid
2) block and replace - commence carbimazole then when euthyroid add thyroxine

Question 28

Features specific to graves eye disease

Answer 28

Exophthalmos - Lid lag and lid retraction (NOT ONLY SPECIFIC TO GRAVES) 
Periorbital oedema
Proptosis 
Grittiness and redness
Opthalmoplegia

Question 29

Factors increasing risk of developing opthalmopathy

Answer 29

Smoking
Male sex
Radioactive iodine treatment

Question 30

What features would elicit an urgent opthalmological referral in thyroid disease?

Answer 30

Blurred vision
Poor vision
Severe conjunctival pain
Poor colour vision
Recent or rapid changes in vision

Question 31

Tx of graves opthalmology

Answer 31

Grittiness - artificial tears
Eyelid - tape eyelids at night to avoid corneal damage
Proptosis - steroids

Question 32

MODY

Answer 32

Maturity onset diabetes of the young

Genetic mutation, autosomal dominant, disrupts insulin production