Hospital Based Practice – Swellings.

Lymphadenopathy & Splenomegaly.

• Differential diagnosis of lymphadenopathy.
○ Localised lymph swelling
 Consider what structures have lymphatic drainage to the affected nodes.
 Examine these structures carefully for.
• Local infection.
○ Otitis media
○ Viral infection
○ TB
• Malignancy
• Lymphoma.
○ Generalised lymph swelling
 Infection.
• Particularly.
○ EBV
○ CMV
○ HIV
○ Rubella
• Also.
○ TB
○ Syphilis
○ Brucellosis
○ Toxoplasmosis
 Lymphoproliferative disease.
• Hodgkin’s or Non – Hodgkin’s lymphoma.
• Chornic or acute lymphoblastic leukaemia
 Connective tissue disease.
• SLE
• RA
 Infiltration.
• Sarcoidosis
 Drugs.
• Phenytoin.
○ “pseudolymphoma”
 Endocirne.
• Thyrotoxicosis.
○ Rarely.
○ Splenomegaly.
 Massive.
• Chronic myeloid leukaemia
• Myelofibrosis
• Malaria
• Kala – azar.
○ Visceral Leishmaniasis
 Moderate.
• Early presentations of massive splenomegaly.
• Portal hypertension.
○ Normally with liver cirrhosis
• Lymphoproliferative disorders.
• Acute leukaemia
 Mild.
• Early presentation of massive and moderate splenomegaly.
• Infection.
○ Infectious mononucleosis
○ Infectious hepatitis
○ Infective endocarditis
○ TB
○ Brucellosis
○ Schistosomiasis
• Haemolytic anaemias
• Immune thrombocytopaenic purpura.
• Connective tissue disease.
○ SLE
○ RA
• Infiltration.
○ Amyloid
○ Sarcoid
• Storage disorders.
○ Gaucher’s disease.
• Myeloproliferative disorders.
○ Polycythaemia rubra vera
○ Essential thrombocythaemia
• Megaloblastic anaemia.
• History in patient with lymphadenopathy or splenomegaly.
○ History is not particularly helpful in lymphadenopathy, but can help focus clinical
examination and further investigations.
○ Localised lymphadenopathy.
 Pain and rate of node enlargement.
• Painful and rapid enlargement is normally due to infection.
• Painless and slower enlargement more suggests malignancy.
• Painful and fast growing nodes can be malignancy.
○ If node isn’t noticed until it starts rubbing against clothes.
○ Node may remain unnoticed until it causes deformity.
 Symptoms in local structures.
• In the structures that drain to the node, has the patient noticed any.
○ Pain
○ Erythema
○ Mass
• Eg. Cellulitis can cause inguinal lymphadenopathy.
• Breast mass can cause axillary lymMain differentialphadenopathy.
• Neurological signs can be caused by a mass compressing a nerve or plexus
that is distant from the deficit.
 Systemic symptoms.
• Lymphoma patients may have.
○ Pruritis
○ B symptoms.
 Fever > 38 oC
 Drenching night sweats
 Weight loss
○ B symptoms indicate more extensive disease and a worse
prognosis.
○ Generalised lymphadeopathy.
 Main differentials are.
• Infection
• Malignancy.
○ Lymphoma
○ Metasteses.
 Full systemic enquiry is vital in these patients.
• Most causes of generalised lymphadenopathy can affect multiple systems
and distant primary may require careful pursuit.
 Special attention should be paid to.
• Common, but non – specific signs.
○ Anorexia
○ Malaise
○ General debility
• B symptoms of haematological malignancy.
○ Fever > 38 oC
○ Drenching night sweats
○ Weight loss
• Skin rash.
 ○ Rubella
○ SLE
○ Sarcoidosis

• Arthralgia and arthropathy.

○ SLE
○ RA
○ Syphilis
 Charcot’s joints.
• Infectious contacts.
○ Rubella
○ TB
○ EBV
• Risk factors for HIV.
• Drug history.
○ Phenytoin.

○ Splenomegaly.
 Previous medical history.
• Chronic liver disease
• Connective tissue disease
• Thalassaemia/ haemolysis
• Gaucher’s disease
• Damaged cardiac valves.
○ Rheumatic fever
○ Prosthetic valves
○ Infective endocarditis.
 Recent travel or infective consciousness.
• Infective mononucleosis
• TB
• Schistosomiasis
• Kala – azar
• Malaria.
 Systemic symptoms.
• Arthralgia
• Rash
• B symptoms.
 Symptoms of haemological disturbances.
• Hypersplenism can affect all three cell lines.
• Anaemia can cause.
○ Malaise
○ Breathlessness
○ Lethargy
• Neutropaenia can cause.
○ Recurrent infection
• Thrombocytopaenia can cause.
○ New or mucosal petechial bleeding.
 • Examination.
○ Full examination of lymphatics should be performed.
 Cervical
 Occipital
 Supraclavicular
 Axillary
 Inguinal
○ Examination should then focus on possible underlying causes.
Heart. nodes:
Arms.
Hands:
Abdomen:
General:
Lymph
Scratch liver
Chronic
Splenomegaly
Anaemia
Site
Murmurs marksdis eas e
Needle marks
Rheumatoid
Hepatomegaly
Purpura
Size arthritis
○
Splinter
As
Jaundice
Cons
cites
is tency
. haemorrhages
Clubbing ras
Butterfly
Tendernes s h.
Fixation

Normally reactive nodes are generally.

 Less thean 1 cm in diameter
 Feel soft
 Not fixed
 Can be tender
○ Lymphomatous nodes are often.
 Larger
 Rubbery
 Not fixed
 ○ Lymph nodes infiltrated by cancer are often.
 Hard
 Fixed to surrounding tissue
○ If splenomegaly is present, record size from left costal margin.
○ Important to distinguish the left kidney from the spleen.
 Often asked in clinical exams.
Spleen Left kidney
No palpable upper border Palpable upper border
Not ballotable Ballotable
Notch on medial border No medial notch
Moves inferomedially on inspiration Moves inferiorly on inspiration
Dull to percussion Resonant to percussion (over lies bowel)

○ Presence of hepatomegaly is important in clinical practice.

 Even more important in exams.
 Hepatosplenomegaly is a very common clinical scenario for exams.

• `Is there evidence of underlying cause.

○ Anaemia and bleeding may simply be due to hypersplenism.
○ Jaundice may be due to.
 Chronic liver disease
 Haemolysis
 Infective hepatitis
○ Cachexia suggests underlying malignancy.
○ Needle marks should prompt examination for.
 HIV
 Hep B
 Hep C
 Infective endocarditis.

Disease Clinical features.

Portal hypertension
Infectious mononucleosis
Bacterial endocarditis
Amyloidosis
Gaucher’s disease
Caput Medusae, venous hum, ascites.
Palatal petechiae, tonisllar enlargement, jaundice, tender hepatomegaly, rash
Clubbing, splinter haemorrhages, Osler nodes, Janeway lesions, Roth spots,
heart murmurs, haematuria, pyrexia.
Hepatomegaly, renal involvement, nephritic syndrome, macroglossia.
Adult type: Hepatomegaly, pathological fractures, pigmentation

Childhood type: Mental retardation, spasticity.

○ If patients have isolated cervical lymphadenopathy, think of oropharyngeal cancer.

 Do formal ENT examination.

○ If patients have both splenomegaly and generalised lymphadenopathy, consider.

 Lymphoproliferative disorders.
 Infection
 Connective tissue disorders
 Sarcoidosis.

• Investigations.
○ Bloods
 FBC
 Blood film
 • Thick and thin if malaria possible.
 Bone marrow.
• Aspiration
• Trephine
• Cytogenetic analysis
 LFTs
 Lactate dehydrogenase
 Calcium
 Uric acid
 Thyroid function
 Monospot
 Serology
 Blood cultures.
 Autoantibodies.
○ Sputum.
 MC&S
 Gram stain
 Zeilhs – Neilson stain.
○ Imaging.
 CXR
 Abdominal US
 CT.
• Chest
• Abdomen
• Pelvis
○ Excision biopsy of enlarged node.
○ Lumbar puncture.
 Rarely.
 Asses intracerebral involvement with m,alignancy.

○ FBC may show.

 Anaemia
 Leucopaenia
 Thrombocytopaenia
○ Blood film can be diagnostic.
○ Bone marrow indicated if FBC or blood film suggests haematological abnormalities.
 Useful in diagnosing.
• Leukaemia
• Myeloproliferative disorders
• Immun thrombocytopaenia
• Pancytopaenia
• Storage disorders
• Lymphoma
• Carcinoma that has infiltrated the marrow.

○ LFTs may show.

 Raised transaminases in.
• Infective hepatitis
• EBV
• CMV
 ALP and GGT elevated when porta hepatis obstruction by enlarged lymph nodes.
  Unconjugated hypebilirubinaemia occurs in haemolysis.
○ Lactate dehydrogenase.
 Useful prognostic marker in lymphoma
○ Calcium.
 Raised in.
• Malignancy
• Sarcoidosis
• Lymphoma
○ Uric acid.
 Raised in rapid cell turnover.
 Eg. Malignancy.
○ Thyroid function.
 Looking for thyrotoxicosis.
○ Monospot.
 Positive in EBV

○ Serology.
 EBV
 CM|V
 HIV
 Rubella
 Viral hepatitis
 Toxoplasmosis
 Brucellosis
○ Blood cultures.
 Repeat regularly if infective endocardidits is suspected.
○ Autoantibodies.
 Useful in diagnosis of connective tissue disorders.
 Rheumatoid factor.
• Positive in 75% of RA
• Also positive in some patients with
○ SLE
○ Mixed connective tissue disease
○ Scleroderma
○ Sjogren’s syndrome
 Anti – nuclear antibodies.
• Positive in 30% of RA
• Positive in 80% of SLE
 Anti – double stranded DNA.
• High titres in SLE
 Sjogren’s syndrome.
• Anti – Ro
• Anti - La
 Scleroderma.
• Anti – Scl170
○ CXR.
 Bilateral hilar lymphadenopathy.
• Lymphoma
 • Sarcoidosis
• TB
 Abdominal ultrasound.
• Will confirm splenomegaly.
• Poor at imaging retroperitoneal lymph node chains.
 CT Chest/ Abdomen/ Pelvis.
• Clear staging of malignancy
• Particularly good at detecting lymphoma in retroperitoneal lymphadeopathy.

○ Blood film abnormalities associated with splenomegaly and lymphadenopathy.

 Many of these will also cause normochromic normocytic anaemia.
 Leucoerythroblastic film will be seen whenever there is heavy bone marrow
involvement.
 Autoimmune haemolytic anaemia may also arise in lymphoma and chronic
lymphocytic leukaemia.
Disease Blood film.
Acute leukaemia Circulating blasts

Auer rods in AML

Chronic lymphocytic leukaemia Lymphocytosis

Smear cells
Chronic myeloid leukaemia Leucocytosis due to spectrum of myeloid cells
Myelofibrosis Tear drop poikilocytes

Leucoerythroblastic blood film

Lymphoma Often normal

Sometimes eosinophilia in Hodgkin’s lymphoma

Haemolysis Reticulocytosis (polychromasia)

Microspherocytosis

Erythroblasts
EBV, infectious hepatitis, toxoplasmosis Atypical lymphocytes
Malaria Parasitaemia

Thrombocytopaenia

Haemolysis.

Lumps
• Examine regional lymph nodes as well as the lump.
• History.
○ How long has it been there
 ○ Pain or tenderness
○ Any other lumps
○ Is it getting bigger
○ Ever been abroad
○ General health?
• Examination.
○ Based on.
 Site
 Size
 Shape
 Smoothness
 Surface
 Srroundings.
○ Does it transilluminate?
 If yes
○ Is it fluctuant?
○ Is it pulsitile.
 Very important
 Assessment with Doppler scan can help.

• Skin lumps.
○ Intradermal
 Sebaceous cysts
 Abscess
 Dermoid cyst
 Granuloma
○ Subcutaneous
 Lipoma
 Ganglion
 Neuroma
 Lymph node.

• Lipoma.
○ Benign fatty lumps.
○ Occur whenever fat can expand.
 Ie. Not scalp or palms.
○ Smooth imprecise margins
○ Hint of fluctuance.
○ Cause symptoms due to pressure on other structures.
○ Malignant changes are very rare.
 Suspect if.
• Rapid growth
• Hardening
• Vasculization
○ Dercum’s disease.
 Multiple, scatterd lipomas
  May be painful
 Typically occur in post – menopausal women.

• Sebaceous cysts.
○ Intradermal.
 Can’t move skin over them.
○ Has characteristic punctum.
 Mark blocked sweat glands.
○ Infection is common.
 Foul pus can exit from the punctum.
○ Treatment.
 Shelling out.
 Can be difficult to whole.
 Get expert tuition.

• Cutaneous abscesses.
○ Staphlococci are the most common organism.
○ Haemolytic streptococci are common in hands.
○ Proteus is common cause of axillary abscesses.
 If recurrent, consider hidradenitis suppuritiva.
• Also can cause recurrent inguinal abscesses.
○ Below the waist faecal organisms are common.
 Aerobes
 Anaerobes.
○ Treatment.
 Excision and drainage is normally curative.

○ Boils
 Abscesses that involve a hair follicle and its associated glands.
○ Carbuncles
 Area of subcutaneous necrosis which discharges to the surface via multiple sinuses.

• Rheumatoid nodules.
○ Collagenous granulomas.
○ Appear in established RA
○ Found on extensor aspects of joints.
 Particularly the elbows.

• Ganglia.
○ Degenerative cysts from adjacent joint or synovial sheath.
○ Commonly seen on
  Dorsum of wrist or hand
 Dorsum of foot.
○ May transilluminate.
○ 50% will disappear spontaneously
○ Management.
 Aspiration often effective.
• Combined with instillation of steroid and hyaluronidase.
 Excision is next line therapy.
 Blow with a bible/ surgery textbook is rarely effective.

• Fibromas.
○ May occur anywhere in the body.
○ Most commonly occur under the skin.
○ Whitish benign tumours.
○ Contain.
 Collagen
 Fibroblasts
 Fibrocytes.

• Dermoid cysts.
○ Contian dermal structures.
○ Found at junction of embryonic cutaneous boundaries.
 Eg. Midline of torso
 Eg. Lateral to the eye.

• Malignant connective tissue tumours.

○ Include.
 Fibrosarcoma
 Liposarcoma
 Leiomyosarcoma
• Smooth muscle
 Rhabdomyosarcoma.
• Striated muscle.
○ Sarcomas are staged using a modified TNM system.
 Includes tumour grade.
○ Needle core biopsies should be used for diagnosis before excision.
○ Refer management to a specialist.
 Suspected sarcoma should not be simply enucleated.
 Needs invasive rather than conservative management.

Salivary gland pathology.

• Three pairs of major salivary glands.
○ Parotid
○ Submandibular
○ Sublingual.
• Numerous, less important, minor salivary glands.
• History.
○ Palpable lump.
○ Pain
○ Swelling related to food
 ○ Altered taste
○ Dry eyes.
• Examination.
○ Note external swelling.
○ Look for secretions
○ Bimanual palpation for stones
○ Examine Facial nerve
○ Examine regional lymph nodes.
• Cytology.
○ |Can be attained by FNA.

• Salivary gland stone

○ Commonest cause of recurrent unilateral pain and swelling.
○ 80% are submandibular
○ Classical story is.
 Pain and swelling on eating
 Red, tender but uninfected gland.
○ Stone may be seen on
 Plain X – ray
 Sialography.
○ Distal stones can be removed via the mouth.
○ Proximal stones may require excision of the gland.

• Chronic and bilateral salivary gland symptoms may be due to autoimmune disease.
○ Sjogren’s syndrome
○ Mikulicz’s syndrome.
• Autoimmune disease causing salivary gland symptoms often also causes.
○ Dry eyes
○ Dry mouth.

• Fixed salivary swellings may be.

○ Tumour
○ Sarcoidosis
○ Idiopathic.

• Salivary gland tumours.

○ 80% are in parotid glands.
 80% of these are pleomorphic adenomas
• 80% of these are in the superficial lobe
○ Any salivary gland swelling must be removed for analysis if present for > 1 month.
○ Facial nerve palsy signifies malignancy.
○ Types of tumour.
 Sometimes benign.
• Crystadenolymphoma
• Pleomorphic adenoma
 Always malignant.
• Mucoepidermoid
 • Acinic cell
• Squamous CA
• Adenocarcinoma
• Adenoid cystic CA

○ Pleomorphic adenoma.
 Often present in middle age.
 Grow slowly.
 Remove via superifical parotidectomy.
○ Adenolyphoma.
 Present in older men
 Soft to palpation.
 Treat with enucleation.
○ Carcinoma.
 Rapidly growing.
 Presents with.
• Hard, fixed mass
• Pain
• Facial palsy.
 Treatment.
• Surgery
• Radiotherapy.

○ Complications of salivary surgery.

 Facial palsy.
Use a facial nerve stimulation in theatre to aid identification.
 Salivary fistula.
• Often closes spontaneously.
 Frey’s syndrome.
• Gustatory sweating.
○ On eating a lemon wedge, one cheek sweats and flushes due to
aberrant parasympathetic cholingergic innervation of cutaneous
sympathetic receptors.
• Interpose a soft – tissue flap at surgery as preventative measure.
• Typanic neurectomy may also help.

Lumps in the neck.

• Don’t biopsy neck lumps until head and neck tumour has been ruled out by an ENT surgeon.
• Culture all biopsied lumps for TB.

• Diagnostic questions.
○ How long has the lump been there?
 If < 3 weeks, self limiting infection is most likely cause.
 Extensive investigation is unwise.
○ Where is the lump.
 If it is intradermal, it is probably a sebaceous cyst.
 ○ Is it a lipoma?

○ If it is not of recent onset, intradermal or a lipoma, it requires further investigation.

 Will be a difficult hunt over complicated terrain.

• Midline lumps.
○ If patient is < 20, the likely diagnosis is a dermoid cyst.
 If the lump moves upwards on protruding the tongue, and is below the hyoid.
• Likely diagnosis is thyroglossal cyst.
○ Commonest congenital cervical lump.
○ Fluctuant lump.
○ Develops in cell rest in thyroid migration pathway.
○ Managed with surgery.
○ If patient is > 20, likely diagnosis is a thyroid isthmus mass.
 If the lump is bony hard, it may be a chondroma.

• Submandibular triangle.
○ Below jaw.
○ Above anterior belly of digastric muscle

○ If < 20 years old.

 Node – like swelling is likely to be self – limiting lymphadenopathy
○ If > 20 years old.
 Node – like swellings need malignant lymphadeopathy to be excluded
 Also consider TB
○ If swelling is not a node, think of.
 Submandibular salivary stone
 Sialadenitis
 Tumour
• Anterior triangle.
○ Below digastric muscle
○ In front of sternocleidomastoid.

○ Examine areas where these nodes drain from, as lymphoma may be the diagnosis
 Skin
 Mouth
 Throat
 Thyroid
 Also examine for splenomegaly.
○ Branchial cysts.
 Present when aged < 20
 Emerge under anterior border of sternocleidomastoid, where upper third meets
middle third.
 Due to non – disappearance of cervical sinus.
• Where 2nd branchial arch grows down over 3rd and 4th branchial arches.
 Lined with squamous epithelium.
 Contains fluid containing cholesterol crystals.
 Treat with excision.
 May be communication with pharynx through a fistula.
○ Cystic hygroma.
 Arise from jugular lymph sac.
  Transilluminate brightly
 Treatment.
• Surgery.
• Hypertonic saline sclerosant injection.
 Can recur and be troublesome.
○ Parotid tumour.
 Suspect if.
• Lump is in superioposterior aspect of anterior triangle.
• Patient is aged > 40 years.
○ Laryngeocele.
 Uncommon cause of anterior triangle lumps.
 Painless.
 May be enlarged by blowing.
 Classified as.
• Internal
• External
• Mixed.
 Can be associated with laryngeal cancer.

○ Carotid body tumours.

 Chemodectoma.
 Very rare.
 Move from side to side, but not up or down.
 Splay out carotid bifurcation
 Usually causes a firm mass.
• Occasionally soft and pulsitile.
• Doesn’t usually cause bruits.
 May be.
• Bilateral
• Familial
• Malignant in 5% of cases.
 Should be suspected in masses that are just anterior to upper third of
sternocleidomastoid.
 Diagnosis.
• Duplex ultrasonography.
○ Look for splaying at carotid bifurcation.
• CT scan.
 Treatment.
• Extirpation by vascular surgeons.
 • Posterior triangle.
○ Behind sternocleidomastoid.
○ In front of trapezius
○ Above clavicle.

○ If there are many small lumps, think of nodes.

 TB
 HIV
 EBV
 Chronic infection
 If < 20 years.
• Lymphoma
• Metasteses from.
○ GI
○ Bronchial
○ Head and neck
○ Large, bony lumps could be cervical ribs.
○ If appears or enlarges on swallowing,
 Think of pharyngeal pouch.

• Investigations.
○ Virology
○ Mantoux test.
○ Ultrasound.
 Shows lump consistency.
• Cystic
• Solid
• Complex
• Vascular
○ CT.
 Defines masses in relation to their anatomical neighbours.
○ CXR.
 Malignancy
 Bilateral hilar lymphadenopathy.
• Consider sarcoidosis
○ FNA.
 Once you know that it is safe.

Thyroid lumps.
• Examination.
 ○ Watch the neck whilst the patient swallows water.
○ Palpate from behind for.
 Size
 Shape
 Smoothness
 Number of nodules
 Tenderness
 Mobility
 Lymph nodes
○ Ask patient to swallow again.
○ Percuss for retrosternal extension
○ Auscultate for bruits

○ If thyroid is enlarged (goitre) consider

 Is enlargement smooth or nodular.
 Is patient thyrotoxic, euthyroid or hypothyroid?

• Smooth, non – toxic goitre.

○ Iodine deficiency
○ Congenital
○ Goitrogens
○ Thyroditis
○ Physiological.
○ Hashimoto’s thyroiditis.
 Autoimmune disorder.
 Due to thyroid apoptosis due to lymphocytes bearing Fas ligand.
• Smooth toxic goitre.
○ Grave’s disease.
• Nodules > 4 cm suggest malignancy.

• Multinodular goitre.
○ Usually euthyroid
○ Can be hyperthyroid.
○ Rarely
 Hypothyroid
 Malignancy.

• Single thyroid lump.

○ Common problem
○ Causes.
 Cyst
 Adenoma
 Malignancy.
• 10%
 Discrete nodule in multinodular goitre.
○ Investigations
 Thyroid function tests.
 Ultrasound.
• Is lump solid or cystic
 • Is lump complex or part of a group of lumps.

• If US shows impalpable nodules, then they can be simply monitored if they

are.
○ < 1 cm across.
 US can detect nodules of diameter 2 mm
 About 46% of autopsies reveal incidental thyroid nodules.
○ Asymptomatic
○ No past history of radiotherapy or thyroid CA
○ No family history of medullary cancer.
 If there is a family history do US – guided FNA.
 Excise if cytology is malignant.
 Radionuclide scan.
• Malignant lesions
○ Hypofunctioning or cold spots.
• Adeomatous lesions
○ Hyperfunctioning or hot spots.
 Fine needle aspiration.
• Cytology on fluid.
• Cytology can’t rule out malignancy.
• Most patients are referred for surgery anyway.

• Thyroid cancer.
○ There are 5 types.
 Papillary
 Follicular
 Medullary
 Lymphoma
 Anaplastic.

○ Papillary.
 60% of cases.
 Often in the young.
 Spreads.
• To lymph nodes
• To lung
 Management with combination of
• Total thyroidectomy
• Node excision
• Radioiodine.
 • T4 to suppress TSH
 Prognosis improved if.
• Young
• Female.
○ Follicular.
 About 25% of cases.
 Middle aged
 Spreads early via the blood.
• Bone
• Lungs
 Well differentiated
 Treatment.
• Total thyroidectomy
• T4 suppression
• Radioiodine ablation.
○ Medullary.
 About 5% of cases.
• 80% are sporadic.
• 20% are part of MEN syndrome.
 May produce calcitonin
 They don’t concentrate iodine
 Perform a phaeochromocytoma screen pre – op.
 Treatment.
• Thyroidectomy
• Node clearance
• External beam radiotherapy to prevent regional recurrence.

○ Lymphoma.
 About 5% of cases.
 Female:Mael ratio of 3:1
 May present with.
• Stridor
• Dysphagia
 Do full staging pre – treatment.
 Assess histology for mucosa – associated lymphoid tissue (MALT) origin.
• Associated with good prognosis
 Management.
• Chemoradiotherapy.
○ Anaplastic.
 Rare
 Female: Male ratio of 3:1
 Tends to affect elderly patients.
 Poor response to all treatments.
 In absence of unresectable disease try
• Excision.
 • Radiotherapy.

• Thyroid surgery.
○ Indications.
 Pressure symptoms
 Hypethyroidism
 Carcinoma
 Cosmetic reasons
○ Check vocal cords via indirect larygoscopy pre and post – op.
○ Complications.
 Early.
• Recurrent laryngeal palsy
• Haemorrhage.
○ If haematoma compromises airway, instantly remove sutures and
evacuate clot.
• Hypoparathyroidism.
○ Do daily calcium levels
○ A transient drop post op is common, but it should recover soon.
• Thyroid storm.
○ Symptoms of severe hyperthyroidism .
○ Treat with
 Propranolol
 Antithyroid drugs
 Iodine
 Late.
• Hypothyroidism
• Recurrent hyperthyroidism.

Leg Oedema.
• History.
○ Is it both legs or just one?
○ Is she pregnant?
○ Is she mobile?
○ Any history of trauma?
○ Does the oedema pit?
○ Any PMHx or DHx?
○ Any pain?
○ Any skin changes?
○ Any oedema elsewhere?

• Bilateral oedema
○ Implies systemic disease.
○ Causes.
 Increased venous pressure.
• Right heart failure.
 • Failure of leg veins
• Pelvic mass
• Pregnancy
 Decreased intravascular oncotic pressure.
• Low albumin.
○ Cirrhosis
○ Nephorotic syndrome
○ Malnutrition
○ Protein – losing enteropathy
 Venous insufficiency.
• Prolonged sitting
• Chronic.
○ Haemosiderin – pigmented skin
○ Itchy
○ Eczematous skin
○ Ulcers
• Vasodilators.
○ Eg. Nifedipine.
○ Gravity dependent.
 Legs are affected first.
 Severe oedema can stretch beyond legs.
 Bed bound get sacral oedema
○ Oedema due to IVC obstruction.
 Doesn’t progress above the legs
 Doesn’t redistribute when laying down.

• Unilateral oedema
○ Leg is often painful and red.
 Cellulitis
 DVT
 Insect bites.
○ May be due to connective tissue pathology.
 Tumour
 Necrotising fasciitis
 Trauma
• Check.
○ Sensation
○ Pulses
○ Severe pain, especially on passive movement.
 Impaired motility suggests.
• Trauma
• Arthritis
 • Baker’s cyst.
○ Compartment syndrome.
 Causes ischemic necrosis
 Requires emergency fasciotomy.

○ Non – pitting oedema is almost always due to lymphoedema.

 Due to poor lymphatic drainage.
 Can be primary.
• Milroy’s syndrome.
○ AKA lymphoedema praecox.
○ Inherited malfunction of the lmphatics.
○ Causes asymmetric swelling of the legs.
○ Usually occurs in young girls
○ Management.
 Reassure.
• Benign condition
• 10% progress to other leg.
 Actively treat any cellulitis
 Maintain good foot hygiene
 Try support stockings
• If they don’t work, try Lymphapress device.
• Provides active compression at night.
 Surgery with skin grafts is very rarely needed.
 Can be secondary.
• Radiotherapy
• Malignant infiltration
• Infection
• Filariasis
 Mechanism is complex.
• Management.
○ Treat the cause.
○ Diuretics for everyone is not the answer.
○ Reduce gravity – dependent oedema by raising ankles above hips.
 Foot stools won’t fully solve the problem.
○ TED stockings may help.
 Contraindicated in peripheral vascular disease and other causes of ischemia.
Thyroid disease.
• Physiology.
○ Hypothalamus secretes thyrotrophin releasing hormone (TRH)
○ TRH stimulates anterior pituitary to release the glycoprotein thyroid stimulating hormone
(TSH)
○ TSH increases production and release of Thyroxine (T4) and triiodothyronine (T3) from the
thyroid.
○ T3 and T4 exert negative feedback on TSH production.
○ Thyroid mainly produces T4.
○ T3 is 5 times as active as T4.
 85% of T3 is produced fro peripheral conversion of T4.
○ Most T3 and T4 in the body is inactive due to being bound to Thyroid binding globulin.
○ T3 and T4 increase cell metabolism, via nuclear receptors, and are thus vital for growth and
mental development.
 ○ Also increase effect of catecholamines.

○ Thyroid hormone abnormalities are normally due to problems in the thyroid gland itself.
 Rarely due to hypothalamus or pituitary gland.

• Basic tests.
○ Measurement of free T3 and T4 is more useful than measuring total T3 and T4.
 Total levels are affected by levels of TBG.
• Free levels are not.
 Total thyroid hormone levels are increased when TBG is increased and vice versa.
 TBG is increased in.
• Pregnancy
• Oestrogen therapy.
○ HRT
○ COCP
• Hepatitis
 TBG is decreased in.
• Nephrotic syndrome
• Malnutrition/ protein loss
• Drugs.
○ Androgens
○ Corticosteroids
○ Phenytoin
• Chronic liver disease
• Acromegaly.

○ Hyperthyroidism will cause.

 Low TSH
• Unless there is a TSH – secreting pituitary adenoma.
• This is rare.
 Most have raised T4
 1% have normal T4 and raised T3
○ Hypothyroidism will cause.
 High TSH
 Low T4
 Don’t ask for T3 if hypothyroidism suspected.
• Will not add any more information.

○ Changes in thyroid hormones with different pathologies.

Changes Pathologies
High TSH, Low T4 Hypothyroidism
High TSH, normal T4 Treated hypothyroidism

Sub clinical hypothyroidism

High TSH, High T4 or T3 TSH – secreting tumour

Thyroid hormone resistance

Low TSH, normal T3 and T4 Hyperthyroidism
Low TSH, low T4 and low T3 Sick euthyroidism

Pituitary disease
Normal TSH, abnormal T4 Changes in thyroid – binding globulin.
 Assay interference

Amiodarone

Pituitary TSH tumour.

○ Sick euthyroidism.
 TFTs may become deranged in any systemic illness
 Typical pattern is for everything to be low
 Test should be repeated after recovery to check for genuine thyroid pathology.
○ Assay interference.
 Presence of antibodies in the sample will interfere with the test.

• Other tests.
○ Thyroid antibodies
 Hashimoto’s disease and Grave’s disease both raise.
• Anti – thyroid peroxidise antibodies.
• Anti – thyroglobulin antibodies.
 If antibody positive in Grave’s disease, there is an increase of developing
hypothyroidism later on.
○ TSH receptor antibodies.
 May be increased in
• Grave’s disease.
• Pregnancy
○ Serum thyroglobulin.
 Useful in
• Monitoring treatment of thyroid CA.
• Detecting facticious (self – medicated) hyperthyroidism.
○ Will be low.
○ US scan.
 Distinguishes cystic from solid nodules.
• Cystic usually benign
• Solid tends to be malignant.
 Solitary large nodules, or dominant nodules in multi – nodular goitre, should be
aspirated by FNA and investigated for thyroid CA.

○ Isotope scan.
 Iodine – 123 or Technetium – 99 pertechnetate.
 Useful for
• Determining cause of hyperthyroidism.
• Detecting
○ Retrosternal goitres
○ Ectopic thyroid tissue
○ Thyroid metasteses
  Combined with whole body CT scan.
 If isotope scan shows nodules, the question is whether they are hot, cold or normal.
• 20% of cold nodules are malignant
• Few normal nodules are malignant
• Almost no hot nodules are malignant
○ Normally toxic adenomas.

• Screening thyroid function.

○ Patients with conditions who should be screened for abnormalities in thyroid function include.
 AF
 Hyperlipidemia
• 4 – 14% have hypothyroidism
 Diabetes.
• On annual review.
 Women with DM Type I during first trimester and post – delivery.
• 3 – fold rise in post – partum thyroid dysfunction compared with non –
diabetics.
 Lithium of amiodarone therapy.
• Every 6 months.
 Down’s, Turner’s or Addison’s syndrome.
• Yearly.

Thyrotoxicosis.
• Symptoms.
○ Weight loss
 10 – 30% have paradoxical weight gain.
○ Increased appetite
○ Itch
○ Heat intolerance
○ Sweating
 ○ Diarrhoea
○ Oligomenorrhoea
 May cause infertility
○ Tremor
○ Irritability
○ Frenetic activity
○ Emotional lability
○ Psychosis
• Signs.
○ Tachycardia
○ AF
○ Warm peripheries
○ Fine tremor
○ Palmer erythema
○ Hiar thinning
○ Lid lag.
○ Lid retraction.
○ Depending on the cause, there may be:
 Goitre
 Thyroid nodules
 Thyroid bruit.

• Grave’s disease.
○ Female: Male ratio of about 9:1
○ Common between 30 – 50 years.
○ Autoimmune disease caused by stimulatory TSH – receptor antibodies.
 Also react with orbital autoantigens.
 Causes exopthalamos
○ There is diffuse thyroid enlargement.
○ Patients are often hyperthyroid.
 May become euthyroid or hypothyroid over time.
○ It is associated with other autoimmune disease.
 Vitiligo
 Type I DM
 Addison’s disease.

• Toxic multinodular goitre.

○ Seen in iodine deficiency.
 Elderly
 Iodine deficient areas of the world.
○ Nodules that secrete thyroid hormones are present.
○ Management.
 Control thyrotoxicosis.
• Medication
 • Radioiodine
• Surgery.
○ If compression symptoms due to large thyroid.
 Dysphagia
 Dyspnoea

• Toxic adenoma.
○ Solitary nodule that produces T3 and T4.
○ Nodule is hot on isotope scanning.
○ The remained of the gland is cold and suppressed.
○ Treatment.
 Radioiodine.

• De Quervain’s thyroiditis.
○ Causes Subacute thyroiditis
○ Due to self – limiting viral infection.
○ Clinical picture.
 Painful goitre
 Fever
 Raised ESR
 Low isotope uptake on scan.
○ Management.
 NSAIDs

• Drugs.
○ Amiodarone
○ Lithium.
 Hypothyroidism is more common.

• Thyroxine intoxication.
○ Raised T4
○ Low T3 and Thyroglobulin.
○ Rarely seen with iodine excess.
 Contrast media
 Food contamination

• Ectopic thyroid tissue.

○ Metastatic follicular thyroid cancer
○ Choriocarcinoma
○ Struma ovarii
○ Ovarian teratoma containing thyroid tissue.

• Thyroid storm.
○ Clinical picture.
 Fever
 Agitation
 Confusion
 Coma
 Tachycardia
  AF
 D&V|
 Goitre
 Thyroid bruit
 “Acute abdomen” picture.
○ Precipitants.
 Radioiodine therapy.
 Thyroid surgery
 Infection
 MI
 Trauma
○ Confirm diagnosis with technetium uptake scan if possible.
 Don’t wait for results before starting treatment.
○ Treatment.
 Enlist expert endocrinology help.
 Resuscitate.
• ABC
• Normal saline at 125 ml/h
• NG tube if vomiting
• Sedate with chlorpromazine if needed.
 Take bloods.
• T3 & T4
• Blood culture.
 Propranolol.
• If not contraindicated
• 40 mg/ 8hours PO or IV
 High dose digoxin
• Slows the heart
• 1 mg over 2 hours
 Antithyroid drugs.
• Carbimazole 15 – 25 mg/ 6 h PO/NG/IV
• After 4 hours
○ Give Lugol’s solution 0.3 mL TDS PO for 1 week.
 Steroids, either.
• Hydrocortisone 100 mg/6h IV
• Dexamethasone 4 mg QDS PO
 Treat any suspected infection.
• Ceruroxime 1.5 g/ 8 h IV infusion
 Adjust IV fluids as needed.
 Treat fever with paracetamol and tepid sponging
 After 5 days reduce carbimazole to 15 mg TDS
 After 10 days.
• Stop propranolol and iodine.
• Adjust carbimazole as required.
• Treatments.
○ Drugs.
 β – blockers.
• Give rapid relief of symptoms.
 Anti – thyroid drugs.
• Carbimazole
 • Propylthiouracil

• Two strategies.
○ Titration.
 Give 4 weeks of antithyroid drug.
 Gradually reduce dose every 1 – 2 months according to
TFTs.
○ Block – replace.
 Give anti – thyroid drug with thyroxine.
• Concurrent thyroxine reduces risk of iatrogenic
hypothyroidism.

• In Grave’s disease, give either regimen for 12 – 18 months, then withdraw.

○ 50% will relapse.
○ Relapsed patients require radioiodine or surgery.
• Carbimazole side effects include.
○ Agranulocytosis.
 Severe neutoropaenia
 Can lead to life – threatening sepsis.
 Rare side effect
• About 0.03% of cases.
 If signs of infection.
• Stop drug.
• Get urgent FBC.
 Radioiodine.
• Iodine – 131 is used.
• Most become hypothyroid post treatment
• Be careful in active hyperthyroidism due to risk of thyroid storm.

• No evidence to suggest.
○ Increased cancer risk
○ Birth defects
○ Female infertility
• Contraindicated if pregnant or lactation.
 Thyroidectomy.
• Risk of
○ Damage to recurrent laryngeal nerve.
 Hoarse voice
○ Hypoparathyroidism
• Patients may become hypo or hyperthyroid.

• Complictions.
○ Heart failure.
 Thyrotoxic cardiomyopathy.
 Increased in elderly
○ Angina
 ○ AF
 Seen in 10 – 25%
 Control hyperthyroidism and warfarinize if not contraindicated.
○ Osteoporosis
○ Opthalmopathy
○ Gynaecomastia
○ Thyroid storm.

• Thyroid eye disease.

○ Associated with Grave’s disease.
 25 – 50% of cases.
 May be first presenting sign.
○ Main risk factor is smoking.
○ Eye disease may not correlate with thyroid disease.
 Patient can be thyrotoxic, euthyroid or hypothyroid at presentation.
○ Thyroid eye disease can be worsened by treatment of hyperthyroidism.
 Particularly radioiodine
 Often transient effect.
○ Retro – orbital inflammation and lymphocyte infiltration results in swelling of the orbit.
○ Symptoms.
 Eye discomfort
 |Grittiness
 Excess tear production
 Photophobia
 Optic nerve compression may cause.
• Diplopia
• Decreased visual acuity
• Afferent pupil defects

• If nerve compression is suspected seek urgent advice about need for

decompression
• The ability of the eye to protrude will reduce the risk of nerve compression.
○ Be extra wary of patients with Grave’s disease who DON’T have
bulging eyes.
○ Signs.
 Exopthalmos.
• Appearance of protruding eye due to lid retraction
 Proptosis.
• Eyes protrude beyond orbit.
• Look from above along the line of the forehead.
 Conjunctival oedema
 Corneal ulceration
 Papilloedema
 Loss of colour vision
 Opthalmoplegia
• Especially of upwards gaze.
• Due to muscle swelling and fibrosis.
○ Investigations.
 Diagnosis is clinical.
 CT or MRI of the orbits may reveal enlarged eye muscles.
○ Management.
  Should be managed by a specialist.
 Treat underlying thyroid disease.
 Advice to stop smoking.
• Worsens prognosis
 Most have mild disease.
• Treat symptomatically
• Artificial tears
• Sunglasses
• Avoid dust
• Elevate head of bed.
○ Reduces periorbital oedema.
• Fresnel prism.
○ Used to treat diplopia
○ Stick to one lens of glasses
○ Allows easy changing and exopthalamos changes.
 Minority experience severe disease.
• Characterised by.
○ Opthalmoplegia
○ Gross oedema.
• High – dose steroids.
• Surgical decompression.
○ If sight is being threatened.
○ For cosmetic reasons once activity of eye disease is reduced.
○ Usually done by inferior orbital approach.
○ Decompress into ethmoidal, sphenoial and maxillary sinuses.
○ Eyelid surgery may improve cosmesis and function
• Orbital radiotherapy.
○ Good for opthalmoplegia
○ Little effect on proptosis.

Hypothyroidism.
• Common and easy to treat.
• Insidious onset.
 ○ Both patient and doctor may not notice anything is wrong.
○ Be alert to subtle and non – specific signs.
 Particularly in women over 40 years old.
• Symptoms.
○ Tiredness
○ Lethargy
○ Depression
○ Cold intolerance
○ Weight gain
○ Constipation
○ Mennorrhagia
○ Hoarse voice
○ Poor cognition/ dementia
○ Myalgia.
• Signs.
○ Bradycardia
○ Dry skin and hair
○ Non – pitting oedema
 Eyelids
 Hands
 Feet
○ Cerebellar ataxia
○ Slow relaxing reflexes
○ Peripheral neuropathy
○ “Toad – like” face
○ Depending on the cuase, there may be.
 Goitre
 Signs of CCF
 Pericardial effusion
• Diagnosis.
○ Normally
 Raised TSH
 Low T4
○ In hypothyroidism secondary to thyrotoxicosis treatment, there may be no pituitary
stimulation, therefore TSH will also be low.
○ Cholesterol and triglycerides may be high.
○ Occasionally there is a normochromic normocytic anaemia.

• Causes.
○ Autoimmune.
 Primary atrophic hypothyroidism.
 • Female: Male ratio of 6:1
• Common
• Diffuse lymphocytic infiltration of the thyroid.
○ Leads to atrophy.
○ Hence, no goitre.
 Hashimoto’s thyroidistis.
• Autoimmune disease as with primary atrophic hypothyroidism.
• Plus goitre due to lymphocytic and plasma cell infiltration.
• Commoner in women in their 60s.
• May be hypothyroid or euthyroid.
○ Occasionally a short proceeding period of thyrotoxicosis
(Hashitoxosis).
• Antibody titres are very high.
 Both Primary atrophic and Hashimoto’s thyroiditis are associated with.
• Type I DM
• Addison’s disease
• Pernicious anaemia.
○ Acquired.
 Iodine deficienty.
• Due to poor iodine intake.
• Commonest cause world – wide.
 Iatrogenic.
• Post – thyroidectomy/ radioiodine.
• Antithyroid drugs.
• Amiodarone
• Lithium
• Iodine
 Subacute thyroiditis.
• Temporary hypothyroidism after hyperthyroid phase.
○ Conditions causing hypothyroidism..
 Pituitary pathology.
• Very rare.
 Turner’s syndrome
 Down’s syndrome
 Cystic fibrosis
 Primary biliary cirrhosis
 POEMS syndrome.
• Polyneuropathy
• Organomegaly
• Endocrinopathy
• M – protein band froms plasmacytoma
• Skin pigmentation/ teathering.
 Genetic.
• Defects in hormone synthesis
• Mostly autosomal recessive.
• Eg. Pendred’s syndrome.
○ Also causes deafness
○ Increased uptake on isotope scan, but displaced by KCl4.
• Treatment.
○ If healthy and young.
 Levothyroixine
• Aim to normalise, not suppress, TSH.
• Thyroxine has a half life of 7 days, so any dosage change will take 4 – 6
weeks to have an effect on TFTs.
• Once TFTs normal, review yearly.
• Levothyroxine metabolism increased by enzyme inducers.
○ Phenytoin
○ Rifampicin
○ Carbemazepine
○ Omeprazole
○ Alcohol
○ St John’s wort.

○ Enzyme inhibitors include.

 SSRIs
 Ciprofloxacin
 Cimetidien
 Erythromycin
 Ketoconazole
 Grapefruit juice.
 If elderly, or PMHx of IHD.
• Start low – dose levothyroxine, and titrate up on a monthly basis.
○ Be careful when titrating as thryoxine can precipitate angina or MI.
 If diagnosis becomes uncertain, but thyroxine already given.
• Stop treatment.
• Check TFTs in 6 weeks.

• Effects of amiodarone.
○ Can cause either hypo or hyperthyroidism.
○ Effects are due to the drug itself, and the iodine contained within it.
○ Hypothyroidism is due to iodine excess.
 Inhibits thyroid hormone synthesis and release.
○ Thyrotoxicosis is caused either by.
 Iodine excess, causing increased hormone synthesis.
 Toxic effects, causing thyroiditis and release of hormones.
○ 2% of people on amiodarone have clinically detectable thyroid hormone abnormalities.
 Seek expert help.
○ Half life of amiodarone is 40 – 100 days, so effects can persist long after the drug is
withdrawn.
○ If on amiodarone, check TFTs every 6 months.
 • Why does thyroid disease cause so many varied symptoms.
○ Almost all cell nuclei have receptors that strongly respond to T3.
 TRα – 1 is abundant in muscle and fat.
 TRα – 2 is abundant in brain
 TRβ – 1 is abundant in brain, liver and kidney
○ These enzymes, via effects on various enzymes, affect the following processes.
 Metabolism of substrates, vitamins and minerals.
 Modulation of all other hormones, and their tissue responses
 Stimulation of oxygen consumption and generation of metabolic heat.
 Regulation of protein synthesis.
 Regulation of carbohydrate and lipid metabolism.
 Stimulation of demand for co – enzymes and related vitamins.

Subclinical thyroid disease.

• Subclinical hypothyroidism.
○ Suspect if
 High TSH
 Normal T3 and T4.
 Asymptomatic.
○ Common.
 10% of those > 55 years have raised TSH.
○ Risk of progression to frank hypothyroidism is 2%
 Increases as degree of raised TSH worsens.
 Risk doubles if thyroid autoantibodies are present.
 Risk increased in males.
○ Management.
 Confirm raised TSH is persistent.
• Recheck in 2 – 4 months.
 Recheck history for any non – specific symptoms that could indicate frank
hypothyroidism.
• If present, discuss pros and cons of treatment with the patient.
○ Risks of untreated sub – clinical hypothyroidism are small
○ Increased risk of AF and osteoporosis if overtreated.
• One approach is to treat anyone who has increased risk of progression to
clinical hypothyroidism
○ TSH > 10
○ Positive thyroid autoantibodies.
○ Previously treated Grave’s disease
○ Other organ specific auto – immunity.
○ Type I DM
○ Myasthenia gravis
○ Pernicious anaemia
○ Vitiligo
• If patient doesn’t want treatment, or is not at increased risk, monitor TSH
annually.
• Subclinical hyperthyroidism.
○ Occurs when
 Low TSH
 Normal T3 and T4.
○ No consensus on whether management prevents subsequent complications of
hyperthyroidism.
 Trials are particularly looking at risk of AF and osteoporosis.
○ Management.
 Confirm suppressed TSH is persistent.
• Recheck in 2 – 4 months.
 Check for non – thyroid cause.
• Illness
• Pregnancy
• Pituitary or hypothalamic insufficiency.
○ Suspect if T3 or T4 are at the low end of normal.
• Use of TSH suppressing drugs.
○ Thyroxine
○ Steroids
 If TSH < 0.1, treat if symptoms of thyrotoxicosis.
• AF
• Unexplained weight loss
• Osteoporosis
• Goitre
 Options for treatment are.
• Carbimazole
• Propylthiouracil
• Radioiodine.
 If asymptomatic, recheck TFTs in 6 months.
Tuberculosis.
• TB kills 2 million people per year.
• Most HIV deaths are due to TB.
• TB is the reason that the poor stay poor.
• If patient is HIV positive, they have an increased risk of TB infection if.
○ Low CD4 count
○ High viral load.
○ High ESR
○ Many co – infections
○ Poor nutrition
• UK incidence.
○ 7000 cases per year.
○ 350 deaths per year.

• Clinical presentation.
○ Fever
○ Lassitude
○ Anorexia
○ Weight loss
○ Cough
○ Haemoptysis
○ Erythema nodosum
○ Exertional dyspnoea
○ Tachycardia
○ Lymphadeopathy
○ Consolidation
○ Bronchial breath sounds in apices.
○ Sometimes.
 Pleuritic chest pain.
 Pleural effusion

○ History of.
 TB exposure
 Immunosuppresion
 Non – vaccination.
○ In postprimary TB there will be a precipitating immunosuppresion.
 Steroids
 HIV
 Increasing age
 Diabetes Mellitus
 Malignany
 Chemotherapy.
• Non – pulmonary TB.
○ Miliary.
 Haemoptological spread to all tissues.
 Symptoms due to failure of.
• Liver
• Spleen
• Lungs
• Bone marrow
○ Genitourinary.
 Requency
 Dysuria
 Loin pain
 Haematuria
○ Bone.
 Paraspinal abscess
 Causes collapse of adjacent vertebrae.
○ Skin.
 Jelly – like lesions.
 On face and neck.
○ Heart.
 Acute or chronic pericarditis.
 Sometimes, pericardial effusion.

• Investigations.
○ When suspected, collect samples of everything relevant.
 Sputum
 Pleural fluid
 Pleural biopsy
 Urine
 Pus
 Ascites
 Peritoneal biopsy
 CSF
○ Culture for diagnosis and drug sensitivities.
 If cultures and staining negative, take pleural biopsies and bronchial lavage.
• Histology classically shows caeating granulomas.
 Traditional TB cultures took 12 weeks.
 New liquid cultures take 1 – 2 weeks.
 Presence of AFB in sputum implies patient is infectious, and needs strict barrier
nursing with masks to be worn.
○ Get advice on contact tracing.
 Test all close contacts.
• CXR
• Tuberculin skin test
 In areas of high incidence, 80% of infections occur outside the home.
• Spread your net as wide as you can.
 ○ CXR.
 Consolidation.
• Often apical
 Caviation
 Fibrosis
 Calcification
 Hilar lymphadeopathy.
 Pleural effusion.
• Sometimes
○ Tuberculin skin test.
 Positive response indicates immunity.
 Strong positive response suggests active disease.
 Heaf test is used for screening, not for investigation.
○ Bloods
 For baseline values.
 FBC
 U&Es
 LFTs
○ Visual exam.
 For baseline values.
• Ethambutol can cuase reversible ocular toxicity.
 Colour vision
• Ishihara charts.
 Visual acuity

• Management.
○ Stress vital importance of compliance for duration of therapy to prevent resistant strains.
 Consider supervised dosing.
○ 8 weeks of quadruple therapy, depending on sensitivities.
 Rifampicin
 Isoniazid
 Pyrazinamide
 ghEthambutol or Streptomycin
○ 16 weeks of double therapy.
 Rifampicin
 Isonazide.
○ Give pyridoxine throughout treatment.
 Vitamin B6
 Reduces risk of iatrogenic neuropathy.
○ For meningeal or pericardial disease, also give steroids.
 ○ Side effects of Anti – TB drugs.
 Seek help in renal or hepatic failure, or pregnancy.
 Monitor U&Es and LFTs.
• If creatinine clearance = 10 – 50 mL/minute.
○ Halve rifampicin dose
○ Give normal dose of Ethambutanol every 36 hours rather than
every 24 hours.
○ No change in Isoniazide or ethionamide dose or timing.
 Rifampicin.
• Hepatitis.
○ Small rise in AST is acceptable.
○ Stop if bilirubin rises.
• Orange urine and tears.
○ Will stain contact lenses.
• Enzyme induction.
• Flu – like symptoms.
 Isoniazide.
• Hepatitis
• Neuropathy
• Vitamin B6 deficieincy
• Agranulocytosis
 Ethambutanol
• Optic neuritis
• Colour vision is first thing to deteriorate.
 Pyrazinamide.
• Hepatitis.
• Arthritis.
• Contraindicated in.
○ Acute gout
○ Porphyria.

• Treating asymptomatic TB.

○ Imigrant or contact screening may identify infected people who are symptomatic or have no
radiological changes.
○ Chemoprohylaxis may be useful to kill infective organisms and prevent disease progression.
○ Treat with either
 Three months of. Isoniazide + Rifampicin
 Six months of Isoniazide monotherapy.
○ Suitable patients for chemoprophylaxis include.
 Adults with documented recent tuberculin conversion
 Imigrants aged 16 – 34 with Mantoux +ve without prior BCG vaccination.
○ Seek expert advice or consult the British Thoracic Society website.
○ If symptoms develop, treat with conventional quadruple therapy.
• Anti – TB prophylaxis.
○ Primary prophylkaxis is indicated in some HIV +ve patients.
○ In sub – Saharan Africa.
 50% of HIV patients get TB
 80% of TB patients are HIV +ve
○ Most common drug used is Isoniazide, with pyridoxine.
○ 9 months of prophylaxis probably gives the best cover.
○ Lifelong prophylaxis is not particularly beneficial.
○ Indicated if.
 No BCG, with Mantoux test of > 5 mm
 BCG > 10 years ago, and Mantoux test > 10 mm
 Recent exposure to active TB.
○ If prophylaxis not used, carefully monitor.
 Clinical signs
 CXR.

• TB Meningitis.
○ `Prodrome.
 Develops over 1 – 3 weeks.
• Rarely, even longer
 Fever
 Headache
 Vomiting
 Drowsiness
 Meningism
 Delerium
 Seizures.
○ CNS signs.
 Tremor
 Papilloedema
 Cranial nerve palsies.
○ Diagnosis.
 Serial Lumbar puncture.
• First few punctures may be normal.
 TB PCR.
 FBC.
• Look for immunosuppression.
 CXR.
• To look for pulmonary TB.
 CT.
• Obstructive hydrocephalus
• Basal enhancement.
• CNS tuberculomas.
○ Differentials.
 Pyogenic meningitis.
 Histoplasmosis
 Glioma
 CNS lymphoma
 Abscess
 Toxoplasmosis
 Neurocysticercosis
 Sarcoidosis
 Hydatid infection
 Advanced neurosyphilis.
○ Management.
 12 month therapy with.
• Isoniazid + pyridoxine
 2 month therapy with.
• Pyrazinamide
• Streptomycin/ Ethambutanol/ Ethionamide.
 Consider dexamethosone for first month of therapy.
• Risk of promoting appearance of tuberculomas.
 Consider Mannitol if raised ICP.

 Although a very serious condition, be caustious about giving very high doses.
• Will not improve response.
• Risk of hepatotoxicity.
 Always check sensitivities for the causative organism and discuss probability of
multi – drug resistant TB with a microbiologist.
• TB meningitis resistant to isoniazide and rifampicin is likely to be fatal.
○ Complications.
 Hydrocephalus.
• May need surgery.
 Reduced cognition
 Salt – wasting states.
• Hyponatraemia with hypernaturic polyuria, even when dehydrated.
• Responds to Fludrocortisone.
Glandular fever.
• Common disease of the young.
• May be unnoticed, or cuase acute illness.
• Spread by saliva or droplet inhalation.
• Incubation period of about 4 weeks.
• Caused by.
○ EBV infection of B – lymphocytes.
○ Causes proliferation of T – lymphocytes.
 Appear a atypical mononucleocytes, hence the alternate name of mononucleosis.
○ B – Cells are immortalised by EBV infection.
 These cells can be indistinguishable from immunoblastic lymphoma in
immunodeficient individuals.
• Suppressor T cells fail to stop multiplication of these B – cell.

• The patient.
○ Sore throat.
○ Fever
○ Anorexia
○ Malaise
○ Lymphadeopathy
○ Palatal petichiae
○ Splenomegaly
○ Hepatitis
○ Haemolysis
• Complications.
○ Are rare.
○ CNS.
 Meningitis
 Encephalitis
 Ataxia
 Cranial nerve lesions.
• Eg. Facial nerve
• Bilateral in 40% of cases.
 Gullian _ Barre syndrome
 Neuropathy
 Depression or fatigue.
• May last months
• Severity depends on features present at onset.
○ Less fit pre – morbidly.
○ No delay in becoming Monospot +ve.
○ Need for bedrest.
 Fatigue may also appear as part of “severe chronic active EBV” infection, along
with.
• Anaemia
• Thrombocytopaenia
• Severe hepatosplenomegaly.
 ○ Others.
 Thrombocytopaenia
 Pancytopaenia with megablastic marrow.
 Ruptured spleen
 Splenic haemorrhage
 Upper airway obstruction.
• May need observation on ITU.
 Hepatitis.
• May result in fulminant hepatic failure.
 Secondary infection
 Myocarditis
 Pericarditis
 Pneumonitis/ fibrosis
 Renal failure
 Autoimmune haemolysis
 Erythema nodosum

• Blood film.
○ Lymphocytosis
 About 20% WBC.
○ Atypical lymphocytes.
 Large, irregular nuclei.
○ Similar blood film seen in.
 Lots of viral infections.
• CMV
• HIV
• Parvovirus
• Dengue.
 Toxoplasmosis
 Typhus
 Leukaemia
 Lymphoma
 Drug hypersensitivity
 Lead poisoning.

• Heterophil antibody test (Monospot).

○ Heterophil antibodies develop in 90% of patients by week 3.
○ Antibodies disappear by 3 – 12 months.
○ False positive.
 Hepatitis
 Parvovirus infection
 Lymphoma
 Leukaemia
 Rubella
 Malaria
 Pancreatic CA
 SLE
○ Older patients may have false negatives and few specific signs that suggest EBV infection.
  May result in overinvestigation unless EBV – specific IgM is requested.
• EBV – specific IgM implies current infection.
• EBV – specific IgG implies past infection.

• Differential diagnoses.
○ Streptococcal sore throat
○ CMV
○ Viral hepatitis
○ HIV seroconversion illness
○ Toxoplasmosis
○ Leukaemia
○ Diptheria.

• Treatment.
○ Normally self – limiting.
○ Traditionally told to avoid alcohol to protect the liver.
 No apparent evidence to support this.
○ Oral Prednisolone.
 Rarely recommended
 Severe symptoms
 Severe thrombocytopaenia.
○ Never give ampicillin or amoxicillin for sore throat.
 Will precipitate severe rash in those with acute EBV infection.

• EBV oncogenicity.
○ Lymphoma
○ Nasopharyngeal CA.
 Especially in Asia
○ Leiomyosarcoma
○ Oral hairy leucoplakia.
• Other EBV associated disease.
○ Crescenteric glomerulonephritis
○ Haemophagocytic syndrome.
 EBV over – activates T – Cells and macrophages.
 Causes over production of cytokines.
 Can cause fatal coagulopathy and cerebral pontine myelinolysis.
○ Gianotti – Crosti rash.
 Self – limiting papular acrodermatitis of childhood.
 Consists of.
• Pale or red monomorphous papules and plaques.
• Place symmetrically.
• Found on.
○ Extensor surfaces of limbs
○ Buttocks
○ Face.
 Also called by.
• Streptococci
• Hepatitis B
• HIV
• Echovirus
 • Coxsakie
• RSV.

Cancers.
•
• Common malignancies including
○ Benign breast lumps
○ Melanoma & non-melanoma skin cancer
○ Pancreas
○ Head and neck
○ Unknown primary