BIOS222 · PDF fileBIOS222 Pathology and Clinical Science 2 & 3 Session 14 Endocrine system disorders 1 Bioscience Department

BIOS222

Pathology and Clinical Science 2 & 3

www.endeavour.edu.au

Session 14

Endocrine system disorders

1

Bioscience Department

© Endeavour College of Natural Health www.endeavour.edu.au 3

Session Learning Outcomes

At the end of the session, you should be able to:

o Outline the classification of the endocrine diseases.

o Describe the key investigations useful for diagnosing

endocrine diseases.

o Describe and discuss the aetiology, signs and symptoms,

investigations and management of hypo- and

hyperthyroidism.

o Briefly discuss various thyroid tumours.

o Understand the relationship between the PTH and calcium.

o Describe and discuss the signs and symptoms,

investigations and management of hypo- and

hyperparathyroidism


Session Plan

o Overview of the endocrine system

o Presenting problems in endocrine diseases

o Investigations of endocrine diseases

o Thyroid disease

• Overview of the thyroid gland

• Thyroid dysfunction

• Hyperthyroidism

• Hypothyroidism

o Thyroid tumours

o Parathyroid disease

• Overview of the parathyroid gland

• Hypoparathyroidism

• Hyperparathyroidism


Overview of the Endocrine System


Endocrine SystemEndocrine gland Hormones produced

Hypothalamus GnRH, TRH, Dopamine, GHRH, Somatostatin, CRH, ADH, Oxytocin

Pituitary gland Growth hormone, FSH, LH, prolactin, thyrotrophic hormone,

adrenocorticotrophic hormone, melanocyte stimulating hormone

Pineal gland Melatonin

Thyroid gland T3, T4, calcitonin

Parathyroid glands Parathormone

Adrenal glands- Glucocorticoids, mineralocorticoids, adrenaline, noradrenaline

Ovaries Oestrogen, progesterone, relaxin & inhibin

Testes Testosterone

Thymus gland Thymosine

Pancreatic islet tissue Insulin, glucagon, gastrin


The Principal Endocrine Axes

Walker, BR, Colledge, NR, Ralston, SH, & Penman, ID (eds) 2014, Davidson’s principles and practice of

medicine, 22nd edn, Churchill Livingstone Elsevier, Edinburgh


The Regulation of Endocrine

system

o Regulation by negative

feedback and direct

control is shown, along

with the equilibrium

between active

circulating free hormone

and bound or

metabolised hormone




Classification of Endocrine disease

o Hormone Excess

• Primary gland over-

production

• Secondary to excess

trophic substance

o Hormone Deficiency

• Primary gland failure

• Secondary to deficient

trophic hormone

o Hormone Hypersensitivity

• Failure of inactivation of

hormone

• Target organ over-

active/hypersensitivity

o Hormone resistance

• Failure of activation of

hormone

• Target organ resistance

o Non-functioning Tumours


Classification of Endocrine disease




Non-specific signs and symptoms

of Endocrine disease




Investigations of Endocrine

Diseases

o Hormone Assay through Blood test

• Random measurement

• Sequential or Dynamic measurements

• Stimulation tests for suspected hormone deficit

• Suppression test for suspected hormone excess

o Biopsy

o Imaging such as CT scans, MRIs


Overview of the Thyroid Gland


Thyroid Gland

o Two lobed gland

o Regulated by thyroid

stimulating hormone (TSH)

o Secretes several hormones:

• Triiodothyronine (T3) –

metabolically active form

• Thyroxine (T4)

• Calcitonin

Tortora, GJ & Derrickson, B 2014, Principles of anatomy and

physiology, 14th edn, John Wiley & Sons, Hoboken, NJ.


Production of T3/T4

1. Iodide Trapping in follicular cells

2. Synthesis of Thyroglobulin(TGB)

3. Oxidation of Iodide to Iodine (colloid cells)

4. Iodination of tyrosine in TGB

5. Coupling of T1 and T2 to form T3 and T4

6. Pinocytosis of T3 & T4 into the follicular cells

7. Secretion of thyroid hormone

8. Transport in blood with help of Thyroxine binding globulinTBG




Functions of

Thyroid Hormones• Energy Metabolism

• Regulate basal and cellular metabolism

• Increase ATP production & Increase body heat

• Increase glucose and fatty acid catabolism

• Increase cholesterol excretion

• Body growth

• Protein synthesis

• Nervous tissue development

• Skeletal system calcium regulation

• Regulation

• T3 & T4 stimulate β receptors & therefore enhance adrenaline, noradrenaline adrenergic response

• BP, Body fluids and vascular resistance


Thyroid Dysfunction


Thyroid Diseases




Thyrotoxicosis/Hyperthyroidismo Definition: It describes a constellation of clinical features

arising from elevated circulating levels of thyroid

hormone.

o Aetiology:

• Graves disease

• Multinodular goitre

• Solitary thyroid adenoma

• Sub acute thyroiditis

• Post-partum thyroiditis

• Iodine induced – drugs like amiodarone

• TSH-secreting pituitary tumors

• Follicular carcinoma


Thyrotoxicosis/Hyperthyroidismo Clinical features:

Symptoms:

• Weight loss despite normal or

increased appetite

• Heat intolerance, sweating

• Palpitations, tremor

• Dyspnoea, fatigue

• Irritability, emotional lability

• Diarrhoea, steatorrhoea

• Amenorrhoea/oligomenorrhoea,

Infertility, spontaneous abortion

Grossman SC & Porth CM 2014, Porth’s Pathophysiology- Concepts of Altered Health

States, 9th edn. Wolters Kluwer Health - Lippincott, Williams & Wilkins


Thyrotoxicosis/Hyperthyroidismo Clinical features:

Signs:

• Tremor

• Palmar erythema

• Sinus tachycardia

• Lid retraction, lid lag

• Goitre with bruit

• Systolic hypertension,

Cardiac failure

• Fine hair, skin pigmentation




Thyrotoxicosis/Hyperthyroidism

o Management:

• Depends on the

underlying cause

– Anti-thyroid drugs

– Radioactive iodine

– Surgery

– Beta-blockers

(short term)

o Diagnosis:

• Serum T3, T4 and

TSH

• TSH receptor

antibodies

• Isotope scanning

• ECG

o Complications:

• Atrial fibrillation

• Thyrotoxic crisis


Graves Diseaseo Definition: It is the most common manifestation of

thyrotoxicosis with or without a diffuse goitre affecting

mainly women aged 30-50 years. It is sometime referred

to as toxic goitre.

.o Aetiology:

• Autoimmune attack: IgG antibodies ((Thyroid

Receptor antibodies TRAb) directed against the TSH

receptor

• Genetic predisposition

• Microbial trigger: Escherichia coli and Yersinia

enterocolitica


Graves Diseaseo Clinical features:

• Similar to Thyrotoxicosis

– Weight loss,

tachycardia,

Hypertension, Agitation,

Anxiety, Palmer

erythema

•Ophthalmopathy

– Exophthalmos

– Peri-orbital oedema

– Diplopia

• Pretibial myxoedema




Graves Disease

http://www.physio-pedia.com/Hyperthyroidism#cite_note-dermopathy-6


Graves Disease

o Management:

• Anti-thyroid drugs

• Subtotal thyroidectomy

• Radio-iodine 131I

o Diagnosis:

Simillar to thyrotoxicosis

• Serum T3, T4 and

TSH

• TSH receptor

antibodies


• ECG

o Complications:

• Hypothyroidism

following treatment


Hypothyroidismo Definition: Implies inadequate levels of hormones

secreted by the thyroid gland. In adults it is termed

myxoedema and in infants is termed cretinism.

o Aetiology:

• Autoimmune Thyroiditis (Hashimoto’s disease)

• Radiation

• Surgery

• Drugs/Iatrogenic

• Idiopathic


Hypothyroidismo Clinical features:

Symptoms:

• Weight gain

• Cold intolerance

• Fatigue, somnolence,

Depression

• Dry skin, Dry hair, Alopecia

• Menorrhagia, Infertility

• Constipation

• Hoarseness

• Carpal tunnel syndrome

• Aches and pains, Muscle

stiffness




Hypothyroidismo Clinical features:

Signs:

• Facial features:– Large tongue

– Purplish lips

– Malar flush

– Periorbital oedema

– Loss of lateral eyebrows

• Anaemia

• Carotenaemia

• Bradycardia hypertension

• Delayed relaxation of

reflexes

• Dermal myxoedema




Hypothyroidism

o Management:

• Thyroxine replacement

– Levothyroxine

• Regular monitoring of

thyroid hormones

o Diagnosis:

Simillar to thyrotoxicosis

• Serum T3, T4 and TSH

• ECG

• Thyroid peroxidase antibodies

o Complications:

• Artherosclerosis

• Anaemia

• Adrenal fatigue


Myxedema Comao Definition: It is a life-threatening, end-stage expression of

hypothyroidism.

o Clinical features:

• Coma

• Hypothermia

• Cardiovascular collapse

• Hypoventilation

• Hyponatremia

• Hypoglycemia

• Lactic acidosis

o Management:

• Medical emergency

• IV triiodothyronine

• Slow rewarming

• Cautious use of IV

fluids

• Broad-spectrum

antibiotics

• High-flow oxygen


Hashimoto’s ThyroiditisDefinition: It is characterised by destructive lymphoid

infiltration of the thyroid, ultimately leading to a varying

degree of fibrosis and thyroid enlargement. It is

predominantly a disease of women.

o Aetiology:

• Autoimmune attack:

– Anti-thyroid peroxidase

– Antithyroglobulin,

– TSH receptor-blocking antibodies


Hashimoto’s Thyroiditiso Clinical features:

• Small or moderate diffused goitre

• Myxedematous psychosis, Depression or mania

• Weight gain, fatigue and muscle weakness

• Alternating bradycardia and tachycardia

• Infertility, hair loss, constipation, hot and cold

sensitivity

o Differential diagnosis:

• Chronic fatigue

• Fibromyalgia

• PMS

• Depression/ anxiety disorder


Hashimoto’s Thyroiditis

o Management:

• Thyroxine replacement

– Levothyroxine

• Regular monitoring of thyroid hormones

o Diagnosis:

• Thyroid examination for goitre

• T4 and TSH levels

• Autoantibodies:

• Anti-thyroid peroxidase antibodies

• Antinuclear factor (ANF)


Cretinismo Definition: It is a congenital hypothyroidism due to lack of

the thyroid gland, endemic iodine deficiency or from

abnormal biosynthesis of thyroid hormone or deficient

TSH secretion.


o Poor and severely stunned growth

o Neurological impairment

o Cognitive impairment

o Reduced muscle tone and coordination to the point

that they cannot stand or walk

o Slow reflexes

o Thick skin

o Enlarged tongue, protruding tongue


Cretinism

o Management:

• Hormone replacement

• Maintain adequate levels of iodine

– Intramuscular injections

– Iodised salt for cooking

o Diagnosis:

• Neonatal screening tests for T4 and TSH


Goitreo Definition: It is an enlargement of the thyroid gland that

can occur with both hypo and hyper thyroidism

o Classification:

• Simple diffuse

– presents between the ages of 15-25 years. The goitre is soft,

and symmetrical and the thyroid is enlarged to two or three

times its normal size. There is no tenderness,

lymphadenopathy or overlying bruit

• Multinodular

– May progress from simple diffused form into the multinodular

form. It can be toxic or non-toxic goitre.


Goitreo Aetiology:

• Simple diffuse goitre:

– Often during pregnancy

– Iodine deficiency

– Impaired thyroid synthesis

– Ingestion of goitrogen

– Drugs like lithium

• Multinodular goitre

– Long standing simple

goitre

– Functional autonomy of

thyroid tissue

http://www.78stepshealth.us/human-physiology/diseases-of-the-thyroid.html

http://medicalpicturesinfo.com/goiter/


Thyroid Tumourso Toxic adenoma

• Secretes excess thyroid hormones and inhibits

TSH secretion

o Medullary carcinoma:

• Tumour of parafollicular C cells

• Secretes calcitonin, 5-HT (serotonin) , ACTH and

prostaglandins

o Papillary carcinoma

• Most common malignant tumour (90%)

o Follicular carcinoma

• Single encapsulated lesion


Thyroid Tumours

o Management:

• Radio-iodine

• Surgery

o Prognosis:

• Excellent, malignancy has 10-year 40%

o Diagnosis:



Parathyroid Disease


Parathyroid Gland

o Four glands embedded within the

posterior aspect of the thyroid

• Each the size of an apple seed

o Produce parathryoid hormone

• Regulate calcium resorption

• Increases calcium uptake in

gut via activated Vit D3

(calcitriol)

• Phosphate excretion




Parathyroid Gland




Presenting Problems in

Parathyroid Diseaseo Hypercalcaemia: Increase in Serum calcium level may

be due to primary or secondary hyperparathyroidism if

PTH is normal or elevated; or can be due to

thyrotoxicosis if PTH is low

o Hypocalcaemia: Derease in Serum calcium level is much

less common than hypercalcaemia. It mostly occurs due

to low serum albumin with normal ionized calcium

concentration Also may develop due to magnesium

depletion, diuretics therapy and excessive alcoholism


Primary Hyperparathyroidism

o Definition: is caused by autonomous secretion of PTH,

usually by a single parathyroid adenoma, which can

vary in diameter from a few millimetres to several

centimetres.


• Hypercalcaemia

• Depression,

somnolence, reduced

cognition

• Skeletal deformities

• Polyuria, polydipsia

• Renal colic, renal

calculi (50% of cases)

• Nausea, anorexia,

• Constipation

• Indigestion & peptic

ulceration



http://endocrinediseases.org/parathyroid/symptoms_summary.shtml



o Management:

• Surgery

• Vitamin D supplement

• Regular monitoring of

calcium biochemistry,

renal function and bone

density

• High oral fluid intake

• Intravenous fluids and

bisphosphonates

• Parathyroidectomy

o Diagnosis:

• Serum PTH and Calcium level

• Parathyroid scan/ultrasound


Primary Hypoparathyroidism

o Definition: A condition where parathyroid glands

produce too little PTH leading to blood calcium levels to

fall (hypocalcaemia) and blood phosphorus levels to rise

(hyperphosphataemia).

o Aetiology:

• Damage to the parathyroid glands (or their blood

supply) during thyroid surgery

• Infiltration of the glands with iron or copper

• Autoimmune or genetic mutation


Primary Hypoparathyroidismo Clinical features:

• Muscle spasms

• Carpopedal (hand & foot) spasms

• Tetany

• Parasthesia

• Fatigue, headaches & insomnia

Acute:

• Severe cardiac arrhythmia

• Seizures

• Bronchospasm may lead to respiratory failure


Primary Hypoparathyroidism

o Management:

• Oral calcium salts

• Vitamin D analogue

• Regular monitoring of calcium biochemistry, renal

function and bone density

• Recombinant PTH

o Diagnosis:

• Serum PTH, Calcium, phosphate, vitamin D, level


Reading and Resourceso Crowley LV, 2012, An Introduction to Human Diseases – Pathology and

Pathophysiology Correlations, 9th edn, Jones and Bartlett Learning

o Grossman SC & Porth CM 2014, Porth’s Pathophysiology- Concepts of

Altered Health States, 9th edn. Wolters Kluwer Health - Lippincott, Williams

& Wilkins

o Hinson, J, Raven, P & Chew, S 2010, The endocrine system: basic science

and clinical conditions, 2nd edn, Churchill Livingstone Elsevier, Edinburgh

o Jamison, JR 2006, Differential diagnosis for primary care: a handbook for

health care practitioners, 2nd edn, Churchill Livingstone Elsevier,

Edinburgh.

o Jarvis, C, 2012 Physical Examination & Health Assessment, 6th ed.,

Elsevier Saunders, Philadelphia.

o Kumar, P & Clark, M 2012, Kumar and Clark’s clinical medicine, 8th edn,

Saunders Elsevier, Edinburgh.

o Kumar, V, Abbas, AK & Aster, JC 2015, Robbins & Cotran pathologic basis

of disease, 9th edn, Elsevier Saunders, Philadelphia.


Reading and Resourceso Lee, G & Bishop, P 2009, Microbiology and infection control for health

professionals, 4th edn, Pearson Education, Frenchs Forest, NSW.

o McCance, KL, Heuther, SE, & Brashers, VL 2014, Pathophysiology: the

biologic basis for disease in adults and children, 7th edn, Elsevier.

o Michael-Titus, A, Revest, P & Shortland, P 2010, The nervous system: basic

science and clinical conditions, 2nd edn, Churchill Livingstone Elsevier,

Edinburgh

o Mosby’s dictionary of medicine, nursing and health professions 2013, 9th

edn, Elsevier, St. Louis, MO.

o Tortora, GJ & Derrickson, B 2014, Principles of anatomy and physiology,

14th edn, John Wiley & Sons, Hoboken, NJ.

o VanMeter, KC & Hubert, RJ 2014, Gould's pathophysiology for the health

professions, 5th edn, Elsevier, St Louis, MO.

o Walker, BR, Colledge, NR, Ralston, SH, & Penman, ID (eds) 2014,

Davidson’s principles and practice of medicine, 22nd edn, Churchill

Livingstone Elsevier, Edinburgh.


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