Endocrinology

Question 1

Describe the WHO classification of diabetes mellitus, impaired glucose tolerance and impaired fasting glycaemia

Answer 1

Fasting:
Normal <6.1
Impaired fasting glycaemia >6.1
Impaired glucose tolerance 6.1-7
DM >7

2 hours after 75g of oral glucose
Normal <7.8
Impaired fasting glycaemia >7.8
Impaired glucose tolerance 7.8-11.1
DM >11.1

HbA1c >48mmol/L (but below doesn’t DM)

Question 2

Classify the major types of diabetes mellitus.

Answer 2

Type 1: Due to autoimmune destuction of beta cells in the islets of Langerhans in the pancreas. Latent Autoimmune diabetes of adults os a form which presents late.
Type 2: Due to decreased insulin secretion with or without insulin resistance. Maturity Onset Diabetes of the Young is a type of T2DM which affects younger people.

Question 3

Outline the secondary causes of diabetes.

Answer 3

Drugs: NSAIDs, newer anti-psychotic drugs, thiazides, anti-HIV drugs
Pancreas: Pancreatitis, carcinoma, trauma, surgery, destruction of cells (cystic fibrosis, haemochromatosis)
Others: Phaeochromocytoma, Cushings, acromegaly, hyperthyroid, pregnancy

Question 4

Compare and contrast the typical presentations of Type 1 and Type 2 diabetes

Answer 4

Type 1:
Young
Ketoacidosis
Weight loss
Polydipsia
Polyuria

Type 2:
Family history
Obese
Low activity level
May be fatigued but with few classic symptoms
May be an incidental finding

Question 5

Describe the principles of the dietary treatment of type 1 and type 2 diabetes

Answer 5

Protein <1g/Kg
Fat <35% of total intake. Sat + Trans fat <10%
Carbs 40-60%. Low GI
Salt <6g/day, <3g if hypertensive
Fruit, vegetables, fibre

Question 6

Describe the methods of evaluating diabetic control

Answer 6

Urine dipstick: Poor as:
urine glucose lags behind blood glucose
Mean renal threshold is 10mM but wide range
Hypos below this range cant be tracked

Home blood testing:
Better test, patients should get into regular habbit of tracking levels

Hb1Ac:
Can give a indication of glycaemic control over previous 6 months. May be misleading in Thallesemea, pregnancy, anaemia.

Question 7

List the two major hyperglycaemic complications of diabetes.

Answer 7

Diabetic ketoacidosis

Hyperosmolar hyperglycaemic state

Question 8

Outline the metabolic pathways that underlie diabetic ketoacidosis (DKA).

Answer 8

When circulating levels of insulin drop, FFAs become available for metabolism
They move to the liver where they are converted to Acetyl CoA.
This is polymerised to acetoacetate which may be converted to acetone or B-hydroxybutarate (all of which are ketones)
These ketones enter the blood, causing it to become acidotic.
This results in the movement of potassium form the cells into the blood, where it is excreted in the urine.

Question 9

Outline the common reasons for the development of DKA. 3

Answer 9

Undiagnosed diabetes
Poorly administered/no insulin
Stress of illness

Question 10

Describe the typical symptoms of hypoglycaemia and outline the difference between autonomic (3) and neuroglycopaenic symptoms (5).

Answer 10

Autonomic: Adrenergic effects as sympathetic NS attempts to raise glucose levels
Sweating
Tremor
Palpitations

Neuroglycopaenic symptoms:
Drowsiness
Coma
Clumsy behaviour
Inappropriate behaviour
Agression

Question 11

Outline the major counter-regulatory hormone responses to hypoglycaemia

Answer 11

Glucagon - Usually inadequate
Adrenaline - May be inadequate in patients with longstanding diabetes
Growth hormone and cortisol may increase glucose level slightly long term.

Question 12

Describe why a patient may develop hypoglycaemia.

Answer 12

Too much insulin before bed
Skipping meals
Fasting
Exercise
Excess alcohol consumption

Question 13

Describe the treatment of hypoglycaemia

Answer 13

Any administration of rapid acting glucose - wipe into cheeks
Intramuscular glucagon may be administered
If patient unconscious then administration of IV dextrose may be appropriate.

Question 14

Describe the microvascular complications of diabetes affecting the eyes

Answer 14

Diabetic retinopathy is preventable
Patients must be referred to opthalmologist and have yearly check ups.
Progresses from: background retinopathy, to pre-proliferative retinopathy, to proliferative retinopathy
Maculopathy, cataracts and rubeosis iridis are also associated wth DM.
Microanuerysms and cotton wool spots may be visible during opthalmoscopy.

Question 15

Describe the microvascular complications of diabetes affecting the kidneys

Answer 15

Nephropathy occurs in diabetic patients due to glomerular disease.
Afferent and efferent arterioles become hypertrophied.
Afferent more vasodilated than efferent, causing damage to glomerulus, leakage of protein and deposition of hyaline material.
Microalbuminuria may be the first sign but this may not be detected on regular dipsticks.

Question 16

Describe the microvascular complications of diabetes affecting the nerves

Answer 16

Symmetrical sensory polyneuropathy:
Vibration, pain and temperature sensation all lost - Glove and stocking loss
Claw toes and rocker bottom feet
Charcot foot
Mononeuropathy - Commonly affects CN VI and III.
Amytrophy_ Painful wasting of quadriceps and pelvifemoral muscles
Autonomic dysfunction - Rarely causes symptoms but may cause disabling postural hypotension and GI disturbances as well as erectile dysfunction.

Question 17

Describe the features of accelerated macrovascular disease in people with diabetes

Answer 17

Stroke is twice as likely to occur
MI is 3-5 times more likely
Amputation of a foot due to gangrene is 50x more likely.

Question 18

Describe the causes and consequences of diabetic foot disease.

Answer 18

10-15% of diabetics develop foot disease during their lives.
Due to a combination of:
Ischaemia
Neuropathy
Infection

Question 19

Describe the classical symptoms 7 of hyperthyroidism and clinical findings. 4.

Answer 19

Weight loss
Tremor
Anxiety
Palpitations
Sweating
Increased appetite
Irritability

Signs:
Tachycardia
Warm peripheries
Goitre
Lid lag

Exopthalmos, thyroid acropatchy and pretibial myxoedema are unique to Graves disease.

Question 20

List the common causes of hypothyroidism 9

Answer 20

Primary:
Autoimmune - Hashimoto's thyroiditis, thyroid atrophy
Surgical - Thyroidectomy
Post radioactive iodine
Infective - TB
Iodine deficiency
Congenital

Secondary:
Peripheral thyroid resistance
Hypopituitarism
Drug induced - Amiodarone, carbimazole, lithium

Question 21

Describe Hashimoto’s thyroiditis

Answer 21

Production of autoanitbodies against TPO and thyroglobulin in thyroid gland.
Produces firm rubbery goitre.
First results in hyperthyroidism before hypo occurs.

Question 22

Describe the morphology and pathological consequences of a nodular goitre.

Answer 22

A lack of thyroid hormones results in increased release of TSH which causes increased vascularisation and growth of the gland to extract more iodine from the blood.

Multinodular most common - May be hyperthyroid or euthyroid.

Solitary nodular goitres are suspect for cancer.

Question 23

Outline the treatment of hypothyroidism.

Answer 23

Lifetime administration of levothyroxane (T4)
Given until TSH levels reduce.
Complete suppression of TSH levels is not recommended to avoid AF and osteoporosis.

Question 24

What thyroid autoantibodies would be present in Grave’s disease?

Answer 24

TSH stimulating autoantibodies.

TPO and thyroglobulin antibodies may also be present

Question 25

Classify malignant tumours arising in the thyroid gland.

Answer 25

Papillary 70%
Follicular 20%
Medullary 5%
Lymphoma 5%
Anaplastic

Question 26

Outline the clinical presentation and diagnosis of malignant tumours of the thyroid

Answer 26

75% of women have goitre
May have cervical lymphadenopathy
May present with cerebral, bone, lung mets
Risk factors include: Family history, previous

Investigate using thyroid function test, thyroid autoantibody test, USS, radionuclide scan, fine needle aspiration

Question 27

Classify pituitary adenomas according to size and function.

Answer 27

Prolactinoma 40-50% <10mm in women, may be over in men. Galactorrhoea, amenorrhoea, hypogonadism, erectile dysfunction.

GH secreting 20% mm-cm. Acromegaly

ACTH secreting 10-15% <10mm Cushings disease

TSH secreting rare <10mm Hyperthyroidism

Non-secreting <10mm. Hypothyroidism

Question 28

Describe the local symptoms that result from a large pituitary adenoma.

Answer 28

Bitemporal hemianopia - optic tract
Pressure on CN 3,4,6 in cavernous sinus.
Bony structures and meninges - Headache
Hypothalamic causes of thirst, appetite, sleep/wake cycle
Hydrocephalus - ventricles
CSF rhinorrhoea - sphenoid sinus

Question 29

List the major clinical 8 and biochemical features of Cushing’s disease

Answer 29

Signs and symptoms:
Moon face
Thin skin
Bruising
Buffalo hump
Striae
plethora
Proximal myopathy
Hypertension

Biochemical features:
Elevated ACTH release.
High cortisol levels
Cushings disease iscaused by hypersecretion of ACTH by pituitary but syndrome may be caused by an adrenal adenoma or ectopic source of ACTH release.

Confirmed by DEXA suppression test. Low dose should suppress adrenal tumour output of cortisol
High dose will differentiate between pituitary and ectopic sources of ACTH.

Question 30

List the major clinical 4 and biochemical features of Addison’s disease

Answer 30

Primary hypoadrenocortiaclism:
Pigmentation of skin
Hypotension
Syncope
Fatigue, tiredness

Biochemical features:
High levels of ACTH and CRH, low levels of cortisol, sex hormones, and aldosterone.
Hyperkalemia as low aldosterone.
Causes: Autoimmune destruction of adrenal cortex, TB, surgery, cancer.
SynATCHen test should stimulate cortisol release but won’t occur in Addison’s.

Question 31

Discuss the normal control of serum calcium and outline the actions of PTH, vitamin D and calcitonin.

Answer 31

PTH is released from chief cells in parathyroid glands.
It acts to increase serum calcium by:
Causing increased osteoclast activity
Increasing intestinal absorption of calcium
Increasing renal reabsorption of calcium
Increasing vitamin D synthesis

Vitamin D:
7-dehydrocholesterol to cholecalcitriol by photoactivation.
Then converted to 25(OH)D3 in the liver then 1,25di(OH)D3 in the kidneys.
Vitamin D acts to increase intestinal absorption of calcium and increase bone calcification and resorption.

Calcitonin:
Released by C cells of the thyroid gland.
Act to decrease calcium by inhibiting osteoclast activity and increasing renal excretion of phosphate and calcium.

Question 32

What are the symptoms of hypercalcaemia?

Answer 32

Stones -Renal or biliary
Bones - Bone pain
Groans - Abdo pain, N+V
thrones - Polyuria
Psychic moans - Depression

Question 33

List the common causes of a raised serum calcium concentration.

Answer 33

Excess PTH: Primary hyperparathyroidism, adenoma, carcinoma, ectopic
Malignancy: Myeloma, bony mets, PTHrP, osteoclastic factor release
Excess vit D: Vit D supplements, lymphoma, granulomatous disease
Excess intake: Milk-alkali syndrome
Other endocrine disease: Thyrotoxicosis, Addison’s disease
Drugs: Thiazides, vitamin A, lithium

Question 34

List the common causes of hypocalcaemia.

Answer 34

Decreased PTH: post srugical, Congenital (DiGeorge syndrome), severe hypomegnesia
High phosphate levels: CKD or phosphate levels
Vitamin D deficiency: Osteomalacia, rickets
Resistance to PTH: Pseudohypoparathyroidism
Drugs: Calcitonin, bisphosphonates.