Analysis of Rash

Analysis of Rash



1. How long have you had the rash? (To determine if acute or chronic.)

2. Where is the rash and where did it start?

3. Contact with anyone that also has had a rash? ( e.g. may suggest scabies, chicken
pox, impetigo, meningococcal disease.)

4. Past history of skin disorders? (e.g. atopic dermatitis (eczema), hives, scabies,
dermatitis herpetiformis, asteatosis (dry skin).)

5. Have you worn any new clothing recently? (e.g. contact dermatitis.)

6. Have you used any new cosmetic products recently? (e.g. perfumes, hair sprays
etc may cause allergic contact dermatitis.)

7. Do you have an allergic tendency? (e.g. asthma, hayfever - increases the chance of
atopic dermatitis (eczema).)

8. Aggravating factors? (e.g. eczema may be aggravated by soap, frequent washing,
chlorinated water, bubbles baths, sweating (because it is drying), sand pits, winter months,
extremes of hot and cold weather, emotional stress, wool clothing or blankets, chemical
disinfectants, detergents, scratching or rubbing, pregnancy, menstruation and various food
stuffs.)

9. Past medical history? ( e.g. Celiac disease may be associated with dermatitis
herpetiformis; presence of other allergic type conditions such as asthma, hives and hay fever
increase the risk of atopic dermatitis; varicose veins may suggest varicose eczema (patches
of dry scaly skin that overlie leg varicose veins); Erythema nodosum may be associated with
sarcoidosis, inflammatory bowel disorders (Crohn's disease and ulcerative colitis) and some
infections (streptococcal, tuberculosis, leprosy and fungal infections); necrobiosis lipoidica is
often associated with diabetes mellitus.)

10. Medications? (Some medications may cause sensitivities such as aspirin, morphine and
codeine.)

11. Known allergies? (e.g. food allergies, insect allergies, drug allergy.)

12. Family history? (e.g. allergies, psoriasis, eczema.)

13. Occupational history? (e.g. exposure to fiberglass may cause a generalized sensitivity;
allergic contact dermatitis e.g. contact with resins, rubber, latex, dyes.)



Analysis of related symptoms

1. Fever? (May suggest chicken pox, serum sickness, eczema herpeticum, exfoliative
dermatitis, severe allergic contact dermatitis from poison ivy.)

2. Itch, and if so is the itch mild, moderate or severe? (e.g. a very itchy rash may
suggest hives, atopic dermatitis, scabies, skin lice, insect bites, chicken pox, dermatitis
herpetiformis; a mild to moderate itchy rash may suggest tinea, psoriasis, drug eruption,
pityriasis rosea, candida or lichen simplex.)

3. Nails affected? (May suggest psoriasis or tinea.)

4. Butterfly shaped facial rash? (Suggests systemic lupus erythematosus.)

5. Symptoms of atopic dermatitis (eczema)? (e.g. itchy, red, dry, scaling, cracked skin.
The typical distribution changes as the person grows older. In infants the rash is usually on
the cheeks of the face, the folds of the neck and scalp. It may then spread to the limbs and
groin. During childhood a drier ad thicker rash develops in front of the elbow, behind the
knees and on the hands and feet, which may be dry, itchy, cracked and painful. Rarely does
eczema have an adult onset.)

6. Symptoms of allergic contact dermatitis? (e.g. may range from faint redness to
severe swelling, symptoms are often worse in area around the eyes, genitals and on hairy
skin, symptoms are least on hairless skin such as palms and soles. Allergic contact
dermatitis is usually confined to the site of exposure to the allergen.)

7. Symptoms of psoriasis? ( e.g. red lesions that enlarge and develop a silvery scale. The
commonest sites are the backs of the elbows and knees, then the scalp, sacral areas,
genital and nails.)

8. Symptoms of meningococcal septicemia? ( e.g. may start with cough, headache,
sore throat, nausea, vomiting and then progress to spiking fevers, chills, aching joints and
muscles. Later drowsiness, hemorrhagic rash most commonly on trunk and extremities but
can be anywhere, and low blood pressure. May have stiff neck and dislike for light.)

9. Symptoms of lupus erythematosus? ( e.g. fever, malaise, tiredness, Raynaud's
syndrome, butterfly shaped facial rash. Systemic lupus erythematosus may be complicated
by protein in the urine.)

10. Symptoms of Rosacea? ( e.g. flushing of the face with increases in skin temperature,
acne-like rash over the face. May be complicated by blepharitis, conjunctivitis, episcleritis or
corneal ulcers.)

11. Symptoms of sarcoidosis? (e.g. shortness of breath, cough, tiredness, skin symptoms
occur in 10% of cases and may include purple or brown plaques or nodules on face, nose,
ears and neck in chronic sarcoidosis.)

12. Symptoms of dermatomyositis? ( e.g. muscle weakness, muscle tenderness, muscle
pain, purple colored rash on face (especially on the eyelids, upper cheeks and forehead),
swelling round the eyes, red rashes, pain in joints, Raynaud's phenomenon, difficulty
swallowing, fever, weight loss, tiredness.)

DD of coma

Diseases that cause no focal or lateralization neurologic signs, usually with normal brainstem functions, CT scan and cellular content of the CSF are normal:

1- Intoxication: alcohol, sedative drugs, opiates, etc

2- Metabolic disturbances: anoxia, hyponatremia, hypernatremia, hypercalcemia, diabetetic acidosis, non ketotic hyperosmolar hyperglycemia, hypoglycemia, uremia, hepatic coma, hypercarbia, addisonian crisis, hypo- and hyperthyroid states, profound nutritional deficiency

3- Sever systemic infections: pneumonia, septicemia, typhoid fever, malaria, water-Friderichsen syndrome

4- Shock from any cause

5- Postseizure states, status epilepticus, subclinical epilepsy

6- Hypertensive encephalopathy, eclampsia

7- Severe hyperthermia, hypothermia

8- Concussion

9- Acute hydrocephalus

Diseases that cause meningeal irritation with or without fever, and with an excess of RBCs or WBCs in the CSF, usually without focal or lateralizing cerebral or brainstem signs, CT or MRI shows no mass lesions:

1- Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, trauma

2- Acute bacterial meningitis

3- Viral encephalitis

4- Others: Fat embolism, Cholesterol embolism, carcinomatous and lymphomatous meningitis …. Etc

Diseases that cause focal brainstem or lateralizing cerebral signs, with or without changes in CSF, CT and MRI are normal:

1- Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large middle cerebral artery territory) with secondary brainstem compression

2- Brainstem infarction due to basilar artery thrombosis or embolism

3- Brain abscess, subdural empyema

4- Epidural and subdural hemorrhage, brain contusion

5- Brain tumor with surrounding edema

6- Cerebellar and pontine hemorrhage and infarction

7- Widespread traumatic brain injury

8- Metabolic coma (as above) with preexisting focal damage

9- Others: cortical vein thrombosis, herpes simplex encephalitis, multiple cerebral emboli due to bacterial endocarditis, acute hemorrhagic leukoencephalitis, acute disseminated (postinfectious) encephalomyelitis, thrombotic thrombocytopenic purpura, cerebral vasculitis, gliomatosis cerebri, pituitary apoplexy, intravascular lymphoma, etc

Sources:

1- Harrison’s manual of medicine

DD of coma 2:

1- Trauma:

- Diffuse axonal injury

- Extradural, Subdural memorrhage

- Cerebral contusion

2- Vascular:

- Stroke

- Subarachnoid, intracerebral hemorrhage

- Vasculitis

3- Metabolic:

- Hypothermia

- Hypo- or Hyperglycemia

- Hypo- or hypercalcemia

- Hypo- Hypernatremia

- DKA, hyperosmolar coma

4- Organ failure:

- Cardiac/circulatory failure, cardiac arrest, hypotension

- Respiratory failure with CO2 retention (cerebral hypoxia)

- Liver failure (encephalopathy)

- Renal failure (uremic coma

- Hypothyroidism

5- Toxin/drug induced

- Alcohol

- Overdose (opiates, tricyclics, benzodiazepines)

- Carbon monoxide poisoning

6- Infective:

- Septicemia

- Meningitis

- Encephalitis

- Cerebral malaria

7- Cerebral:

- Cerebral infarction

- Brain tumor

- Brain abscess

- Epilepsy

8- Brainstem lesions:

- Tunors

- Hemorrhage/infarction

- Demylnation (MS)

- Wernick-karsakoff syndrome

Respiratory Diseases In a Nutshell

I hope everyone finds Respiratory Diseases In a Nutshell useful as I did. It's great for quick reading. Please note that it's highly recommended to correlate these notes with your reference.

I) Pneumonia

*Definition:

Pneumonia is an acute lower respiratory tract illness causing radiological shadowing. It is associated with fever and symptoms/signs in the chest. Incidence: 1-3/1000 population. Mortality: 10%.

*Symptoms:

Fever, rigors, malaise, anorexia, cough, sputum, hemoptysis, chest pain, dyspnoea

*Signs:

Cyanosis, confusion (may be only sign in elderly), tachycardia, hypotension, consolidation, increased tactile vocal fremitus, bronchial breathing

*Tests aim to:

Confirm diagnosis—CXR

Define cause—gram staining, culture (sputum), diagnostic antigen

Identify complications—CXR, CT, bronchoscopy

Assess severity—‘CURB’ score; confusion (less than 8 in mental test), urea (more than 7mmol/L), respiratory rate (more than 30/min), BP (less than 90 systolic and/or 60 diastolic). Score more than one indicates severe pneumonia. Other markers; AF, bacteremia, multilobular involvement, underlying disease, arterial O2 (less than 8kPa), WBC (less than 4 or more than 20), Albumin (less than 35g/l), age (60 or more)...each feature increases mortality by 5x, two or more present increases to 21x.

Exclude Cancer—bronchoscopy to people who age 50 and above, smoke, and present with pneumonia

*Differential diagnosis:

Pulmonary infraction and pulmonary edema (absent fever), TB (CXR cavitation), intra-abdominal pathology (lower chest pain with normal CXR)

*Management:

Antibiotics (broad spectrum), IV fluids, analgesia, oxygen

*Complications:

Respiratory failure, hypotension, AF, plural effusion, empyema (pus in plural space), lung abscess, septicemia, cholestatic jaundice, pericarditis and myocarditis

*Main Classification:

It is classified into four main types: a) community-acquired, b) hospital-acquired, c) aspiration, d) immunocompromised patients.

a) Community-acquired pneumonia

Epidemiology—very common, male = female, tends to occur at extremes of age, important cause of morbidity and morality, may be primary or secondary to the underlying disease.

Pathophysiology—spreads via air droplets. If local defense mechanisms are overcome, pneumonia develops. Tobacco smoke impairs local defenses.

Most common causative organisms—pneumococcus (60-75%), H. influenzae (4-5%), and mycoplasma (5-18%)

Clinical Settings—Mild, severe, and atypical

~Mild previously fit adults—Pneumococcus, H. influenzae, viruses (15%, influenza alone has 5-8%), Staphylococcus (1-5%), Legionella (2-5%)

~Mild previous respiratory illness—Pneumococcus, H. influenzae, Mycoplasma pneumonaie

~Severe—Pneumococcus, H. influenzae, Mycoplasma pneumonaie

~Elderly and debilitated—pneumococcus, H. influenzae, mycoplasma, staphylococcus, klebsiella, and gram-negative organisms.

~Atypical—Legionella, Clamydia species, P. Carnii

b) Hospital-acquired pneumonia

Definition—pneumonia occurring 2 or more days after hospital admission…infection before this is classified as community-acquired

Epidemiology—more common in elderly people, 2-5% of all hospital admissions, and 10-15% of hospital acquired infections.

Predisposing factors—increased aspiration risk, reduced host defenses, lung/skin instrumentation

Most common causative organisms—gram-negative organisms (specifically enterobacteria) or staphylococcus aureus; also pseudomonas, klebsiella

c) Aspiration

Those with stroke, myasthenia, bulbar palsies, esophageal disease, or poor dental hygiene…risk aspirating oropharyngeal anaerobes.

d) Immunocompromised patient

Definition—pneumonia occurring in patients with deficiency of cellular or humoral immune mechanisms

Increasing incidence due to—use of immunosuppressive drugs, chemotherapy, and HIV infections

Pathophysiology—defects in any one of the following protective mechanisms lead to increased risk of infection:

~Mechanical mechanisms: epiglottis, cough, gag reflexes, mucociliary escalator

~Specific immunological mechanisms: macrophage/neutrophils, b-cell antibodies, t-cell immunity

Most common causative organisms:

~Neutropenia: gram-negative bacteria, Staph. aureus, fungi (Candida, Aspergillus spp.)

~Reduced immunoglobins: pneumococci, H. influenzae

~T-cell defects: all previously mentioned except g-negative group, plus viruses (herpes zoster, CMV, adenovirus), mycobacteria, and pneumocystis species (P. Carnii in HIV in particular).

*Specific classification:

Consists of details of each causative organism, basically divided into "typical" (1-7) and "atypical" (8-11)…refer to “main classification” for the general types the organisms belong to.

1) Streptococcus pneumoniae (pneumococcal):

Incidence—commonest bacterial pneumonaie, commonest in winter months

Clinical features—rapid onset with high fever and herpes libialis

Diagnosis—CXR shows lobar consolidation

Treatment—benzylpenicillin

2) Mycoplasma pneumonaie:

Incidence—mainly in autumn (4-year epidemics)

Clinical features—flu-like symptoms

Diagnosis—CXR shows bilateral patchy consolidation

Specific complications—myocarditis, meningio-encephalitis, rash, hemolytic anemia (cold agglutinins)

Treatment—tetracycline

3) Viral:

Incidence—influenza is the commonest cause and is epidemic

Clinical features—myalgia and severe prostration precede influenza

Other causative viruses—measles, CMV, and varicella-zoster

4) H. influenzae: causes bronchopneumonia, usually underlies lung disease.

5) Staphylococcal pneumonaie:

Incidence—may complicate influenza infection

Features—rapid progression and high mortality rate

Clinical features—causes bilateral cavitating bronchopneumonia, plural effusion, and pneumothorax;

Treatment—flucloxacillin.

6) Klebsiella: causes cavitating pneumonia; treated by cefuroxime.

7) Pseudomonas: common pathogen in bronchiesctasis and CF, causes post-surgical HAI; treated by anti-pseudomonal penicillin.

8) Legionella:

Incidence—commonest in autumn from contaminated air conditioning

Clincal features—flu-like symptoms

Diagnosis—CXR shows bi-basal consolidation; blood tests show hyponetremia, lymphopenia, deranged LFT; urinalysis may show hematurea;

Key extra-pulmonary complications—confusion, coma, hepatitis, and renal-impairment

9) Chlamydia pneumoniae:

Incidence—commonest chlamydial infection

Clinical features—person-to-person spread; biphasic illness: pharyngitis, hoarseness, otitis, followed by pneumonia

Diagnosis—Chlamydia serology

Treatment—tetracycline

10) Chlamydia psittaci:

Clinical features—causes psittacosis, an ornithosis acquired from infected birds

Key extra-pulmonary features—legion but rare, e.g. meningioencephalitis, infective endocarditis, hepatitis, nephritis, rash, splenomegaly

Diagnosis—CXR shows patchy consolidation; diagnosis and treatment as “10”

11) Pneumocystis Carnii pneumonia:

Diagnosis—CXR may be normal or shows bihilar shadowing

Diagnosis—sputum, lavage, or lung biopsy

Treatment—co-trimoxazole; prophylaxis in immunocompromised is indicated (HIV).

II) Lung Abscess

*Definition:

A lung abscess is cavitating area of localized, suppurative infection within the lung. It mainly occurs in the elderly.

*Causative organisms:

Staph. aureus, Klebsiella species, anerobes, TB (less acute presentation)

*Clinical features:

Swinging fever, cough, purulent foul-smelling sputum, hemoptysis, chest pain, malaise, weight loss, finger clubbing, anemia, crepitations

*Investigations:

CXR shows cavitations, CT scan to exclude obstruction, sputum diagnosis, bronchoscopy, blood tests.

*Treatment:

Antibiotics—prolonged (6 weeks); amoxicillin + metronidazole

Surgery—postural drainage, surgical excision

III) Tuberculosis

*Epidemiology:

TB kills 3 million per year world wide. When including HIV-related TB, then TB is the leading infectious cause of death worldwide despite being highly-treatable. Worldwide prevalence: 2 billion people.

*Pathogenesis:

1. It spreads via respiratory droplets; transmission from close proximity to an infected individual.

2. Following inhalation, multiplication occurs in terminal air spaces.

3. Bacteria ingested by alveolar macrophages survive and spread to the local lymph nodes.

4. Bloodstream spread occurs to the lung apices and other organs, where latent infection persists for many years.

5. Slow development of cellular immune response leads to TB granulomata and cutaneous hypersensitivity to mycobacterial antigens.

*General investigations:

Pulmonary TB—staining of acid-fast bacilli in sputum, culture of samples on selective media

Extra-pulmonary TB—culture from appropriate samples is recommended (fine needle aspiration, liver biopsy, etc) or by histology. CXR may be diagnostic.

*Treatment:

Chemotherapy (6 weeks)

Drugs—combinations, e.g. isoniazid and rifampicin (6 months), pyrazinamide ethanbutol/streptomycin (first 2 months), resistance to individual drugs is common so prolonged use 2^nd and 3^rd line treatments in this case.

Surgery—in case of chronic constructive pericarditis, Potts’ disease.

*Classification:

a) primary TB, b) post primary pulmonary TB, c) post primary extra-pulmonary TB

a) Primary TB:

Epidemiology—exposure occurs in childhood in endemic areas, but later in childhood in the West.

Description—initial infection is usually pulmonary…peripheral lesion forms (Ghon focus), and its draining nodes are infected (Ghon complex). Possible calcification may occur.

From Ghon focus—progressive lung involvement, LN spread, plural effusion, widespread hematogenous dissemination

Diagnosis—Ghon focus can be displayed in CXR due to calcification

Clinical features—limited systemic spread, self limiting, spontaneous healing usually brief and asymptomatic, but pneumonic illness (fever, sweats, cough, etc) may occur.

Immunological phenomena—erythema nodosum, red eyes (iritis).

b) Post-primary pulmonary TB:

Epidemiology—any form of immunocompromise may allow reactivation years after primary infection.

High-risk groups—developing world residents; poverty, overcrowding, malnutrition; young and old; alcoholic; HIV positive; diabetes; hematological, malignancies, steroids

Symptoms—cough, hmeoptysis, tiredness, weight loss, fever of unknown origin.

Risk stratification—eroding into a bronchus, rapid multiplication and highly contagious (open TB)

Relations—ilitary TB, dissemination of multiple tiny foci

NB Miliary TB: two clinical syndromes occur, both with malaise, weakness, weight loss.

The young—developing third world; rapid onset (fatal), high fever, very unwell

The elderly—developed world; insidious onset, chronic course (slow decline in health; low or no fever, but it is occasionally fever of unknown origin.

Diagnosis—bilateral upper zone shadowing, CXR shows military pattern often, extra-pulmonary organisms (bone, liver, GU tract)

Complications—cavitation w/aspergilloma, plural effusion, massive hemoptysis, empyema

c) Post-primary extra-pulmonary disease:

Miliary TB, meningial T (CSF, classic meningitis symptoms, neck stiffness, etc), GU TB (dysurea, loin pain), bone TB (Pott’s vertebra), skin TB (jelly-like nodules), peritoneal TB (AFB in ascitis)

IV) Bronchiectasis

*Definition:

Bronchiectasis is chronic infection of the bronchi and bronchioles leading to permanent dilatation of these airways. Main organisms: H. influenzae, strep. Pneumoniae, staph. Aureus, pseudomonas aeruginosa.

*Etiology and causes:

Localized bronchiectasis:

Post-infection—severe pneumonia, measles

Bronchial—endobronchial (foreign body or tumor), or extra-bronchial obstruction (Brock’s syndrome)

Generalized bronchiectasis:

Congenital—Young’s syndrome, Kartagener’s syndrome, primary ciliary dyskinesia

Immune defects—hypogammaglobinemia, chronic granulomatus disease, complement deficiency

Immune complexes—allergic aspergillosis, RA, inflammatory bowel syndrome

*Pathophysiology:

Retention of bronchial secretions occurs and lung infection results, which is not cleared so the lungs become colonized. Certain bacteria further reduce sputum clearance. A ‘vicious cycle’ is set up and the chronic inflammatory response in the airways leads to tissue damage and bronchial wall dilation.

*Clinical features: extremely variable, some have no symptoms or signs.

The classic symptoms—Chronic cough, large volumes of mucopurulent sputum, unpleasant breath, haemoptysis occurs in 50% of patients,30-40% of patients have associated chronic sinusitis.

Signs—Anaemia, polycythaemia, clubbing is found in severe disease, cyanosis and signs of cor pulmonale are present at a late stage, crackles are presenting affected areas – and airflow obstruction with wheeze

Symptoms relating to the underlying cause—e.g. sinusitis, infertility, bronchial carcinoma, dextrocardia in Kartagener’s syndrome

*Complications:

1. Airways obstruction, loss of lung → respiratory failure

2. Pneumonia

3. Pneumothorax

4. Cerebral abscess (rare)

5. Secondary amyloid (→ renal failure)

*Investigations:

CXR—cystic shadows, thickened bronchial walls (tramline and ring shadows)

Sputum culture

High resolution CT—confirms and assesses severity. ‘Signet ring’ is a common sign

Investigation of cause—immunoglobulins, asperigillus precipitins or skin-prick test, bronchoscopy

Lung function test—reveals airflow obstruction

Saccharin test

*Management and Treatment:

Physiotherapy and bronchodilators

Antibiotics

Oxygen

Surgery—resection useful in localized, lung transplantation in young and severe cases.

*Prognosis:

Few symptoms—normal life

Generalized disease—respiratory failure

V) Chronic Obstructive Pulmonary Disease (COPD):

*Definition:

COPD is a common progressive disorder of airway obstruction with little or no reversibility, unlike asthma which is reversible (patients have either COPD or asthma, NOT both).

*Etiology:

Cigarette smoking, atmospheric pollutants, alpha-1-antitrypsin deficiency

*Constituents:

1. Chronic bronchitis: clinically defined as cough & sputum production for 3 months per year for more than 2 years.

2. Emphysema: histologically defined as enlargement of air spaces distal to the terminal bronchioles, with destruction of the alveolar walls. Pathological subtypes include; centri-acinar, pan-acinar, and irregular.

*Pathology:

Smoking à hypertrophy of bronchial mucus gland (Reid index) à productive cough à early chronic bronchitis à emphysema à loss of elastic recoil, hyperinflation, gas trapping (moderate disease) à breathlessness à V/Q mismatch (↓PO2) à loss of diffusing surface (↑CO2)à hypoxemia à if corrected by oxygen, may cause respiratory failure (severe disease)

*Signs:

Wheeze, lip pursing, cyanosis, bounding pulse, warm hands, sharp twitches in hands, barrel chest, sleepiness

*Clinical Assessment:

Pink Puffer—thin, anxious, type 1 respiratory failure, low PCO2, ↑ alveolar ventilation, breathless but not cyanosed

Blue Bloater—large, quiet, type 2 respiratory failure, high PCO2, ↓ alveolar ventilation, cyanosed but not breathless

*Investigations:

Lung function tests + arterial blood gases

Assess degree of reversibility with B2 agonist

CXR to exclude other smoking-related pathology

CT scan

*Management:

Smoking cessation, pulmonary rehabilitation, bronchodilators, steroids, oxygen therapy, lung volume reduction therapy

VI) Bronchial Asthma:

*Definition:

There is no universally accepted definition. It is characterized by recurrent episodes of cough, wheeze, chest tightness or breathlessness caused by reversible airway obstruction.

*Pathology:

Three factors contribute to airway narrowing:

1. Bronchial muscle contraction—triggered by a variety of stimuli

2. Mucosal swelling—caused by mast cell and asophile degranulation resulting in chemical mediator release

3. Increased mucus production

*Epidemiology:

It is the single most important cause of respiratory disease morbidity, 2000 deaths per year affecting 5-8% of the population.

*Classification:

1. Extrinsic—childhood, associated with atopy (familiar allergic, e.g. hay fever), positive skin test, possible remission later in life.

2. Intrinsic—adulthood, less likely to be caused by allergy, more progressive, doesn’t respond to treatment.

3. Occupational—relating to industrial work place allergens.

*Etiology:

Genetic factors, environmental (cold air, exercise, emotion), allergens (pollen, dust), occupational, drugs (b-blockers, aspirin), viral infections.

*Clinical features:

Classic attack—audible wheeze, hyper-resonant percussion, hyper-inflated chest, increased respiratory and heart rates, diminished air entry, pulsus paradoxus 5-10 mm/Hg.

Severe attack—inability to complete sentences/talk, pulse above 110 bpm, respiratory rate above 25/min, decreased expiration rate (PEF 30-50% of predicted), PP 10-20 mm/Hg.

Life threatening attacks—cyanosis, clammy, sweating, confusion, feeble respiration, PEF less than 33% of predicted, deviated trachea, PP more than 20 mm/Hg.

*Investigations:

Lung function test—may show airflow obstructions, peak flow measurements are useful markers, CXR and ABG in severe asthma.

*Management:

Patient education, avoidance of environmental triggers, acute asthma—O2, corticosteroid, inhaled b-agonists, chronic cases—Leukotrine antagonists

VII) Primary Tumors of the Lung

*Epidemiology:

Almost all are malignant. Accounts for 19% of all cancers and 27% cancer deaths…incidence is increasing in women.

*Etiology:

Cigarette smoking is the major risk factor. Others include: passive smoking, asbestos, silica, iron oxide, radiation, genetic, pulmonary fibrosis.

*Clinical features:

1) Local effects: breathless (phrenic nerve palsy) hoarseness (recurrent laryngeal nerve palsy), local pain, Pancost tumor (invasion of brachial plexus), Horner’s syndrome

2) Primary effects: cough with or without hemoptysis, breathlessness from bronchial obstruction, possible pneumonia, lobar collapse and plural effusion

3) Finger clubbing.

*Clinical manifestations:

1) Brain metastases: fits, confusion, headache

2) Bone metastases: pathological fractures, pain, hypercalcemia

3) Liver metastases: Jaundice and weight loss

4) Non-metastatic: a) endocrine (10%, causes weight loss)—SIADH (especially small lung cancer), parathyroid-related hormone peptide (6% of squamous), ectopic ACTH secretion (30% of small cell tumors); b) neurologic (10%, causes confusion)—Lambart-Eaton syndrome (with small cell cancer)

*Investigations:

CXR—shows peripheral circular opacity, hilar enlargement, consolidation, lung collapse, plural effusion, bony secondaries.

Bronchoscopy

Lung function tests

FBC/U&E—diagnosis paraneoplastic syndromes

CT—TNM staging of tumor

Staging:

a) Primary tumor—T0 not evident, T1 small in lobar or distal airway, T2 plural involvement, obstruction extending to hilum, T3 involves the chest wall, mediastinal plura, pericardium, T4 heart, great vessels, trachea, esophagus, vertebrae;

b) Regional nodes—N0 none, N1 ipsilateral hilum, N2 ipsilateral mediastinum, N3 contralateral;

c) Distant metastasis; M0 none, M1 present.

*Treatment: surgery, radiotherapy, chemotherapy, endobronchial treatments.

VIII) Pneumothorax:

*Causes:

Often spontaneous due to rupture of the subplural bulla…other causes include: asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic fibrosis

*Symptoms:

Asymptomatic, or may be sudden onset of chest pain. Patients with asthma or COPD may present with sudden deterioration.

*Signs:

Reduced expansion, hyper-resonate percussion, diminished breath sounds on the affected side.

*Management:

Chest drain

IX) Plural effusion:

*Definition:

Fluid in the plural space...fluids include: transudates, exudates, blood (hemothorax), pus (empyema), lymph with fat (chylothorax).

*Causes:

Transudates—increased venous pressure, hypoproteinemia, hypothyroidism

Exudates—increased leakiness of plural capillaries secondary to infection, inflammation or malignancy...this is due to pneumonia, TB, RA, bronchogenic carcinoma, metastasis.

*Symptoms:

Asymptomatic, or may have chest pain.

*Signs:

Decreased expansion and breath sounds on affected side, tactile vocal ferementus, bronchial breathing, marks and signs of associated disease

*Tests:

CXR—small effusions and angles, horizontal upper boarder means pnemothorax

Ultrasound

Aspiration

Plural biopsy

*Management:

Tetracycline, drainage, surgery