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

Peripheral Signs of Endocarditis

Roth's spots: Oval- shaped, white- centered hemorrhages
present on the retina of some patients with
infective endocarditis.



Roth's spots are named for Swiss pathologist
Moritz Roth (1839-1914), who, in 1872, described
white- centered hemorrhages on the funduscopic examinations
of patients with sepsis.3 In 1878, the spots were
found to consist of "round or elongated white foci
occurring close to the nerve head . . . single or multiple
and occasionally surrounded by a hemorrhagic ring."4
In 1931, these hemorrhages were associated with bacterial
endocarditis and described as "pathognomonic
canoe- shaped linear hemorrhagic spot(s) with a light
central area."
Pathogenesis
The pathogenesis of Roth's spots is unclear but is
thought to involve several potential mechanisms. In his
original studies, Roth believed that the spots represented
embolic bacterial infiltrates producing localized
retinal abscesses.4,5 The emboli were presumed to have
originated from the endocardium. The currently
accepted explanation involves anoxia that causes a sudden
increase in venous pressure, which results in capillary
rupture in the inner retinal layers.5 This rupture
results in extravasation of blood and formation of a
fibrin-platelet plug.
Diagnosis and Differential Diagnosis
Although Roth's spots have been classically associated
with endocarditis, they have also been found in many
other conditions, including hematologic malignancies,
connective tissue diseases, vasculitides, anemia, hypertension,
diabetes mellitus, HIV disease, and intracranial
hemorrhage.5 In the patient who has an otherwise typical
presentation of endocarditis, Roth's spots may be
helpful in the diagnosis; however, when nonspecific
symptoms are present, Roth's spots should alert the
physician to other possible systemic diseases.
Osler's nodes: Painful, erythematous nodules most
commonly found on the pads of the fingers and toes
of some patients with infective endocarditis.

Osler's nodes are named for Canadian
physician and educator Sir William Osler (1849-1919),
who, in 1893, described painful, erythematous nodules
on the pads of the fingers and toes in patients with
endocarditis.6 Several other clinicians predated Osler
in the description of these nodules,7,8 but he placed thegreatest significance upon the nodules and was the first to acknowledge their utility in the diagnosis of endocarditis.

Pathogenesis
Like that of Roth's spots, the pathogenesis of Osler's
nodes is unclear. One theory contends that these nodules
are the result of septic microemboli originating
from an endocardial valvular lesion, and that pathogenic
organisms can sometimes be recovered from
aspiration of these lesions.6,7 Another theory holds that
the nodes are caused by an immunologically-mediated
vasculitis caused by circulating immune complex deposition
in the skin.7 A fair amount of evidence supports
both explanations, therefore, the actual pathogenesis
of Osler's nodes remains a mystery.
Diagnosis and Differential Diagnosis
Osler's nodes are usually associated with subacute
bacterial endocarditis and appear late in the disease
course. However, the sign may also be found in other
conditions, including bacteremia, septic endarteritis,
typhoid fever, gonococcemia, and systemic lupus erythematosus.
6,7 Osler's nodes appear suddenly, are quite
painful, and are sometimes heralded by premonitory
paresthesias. Although generally located on the fingers
and toes, the nodes may be present on the forearms,
mucous membranes, flank, or trunk. With appropriate
antibiotic therapy, Osler's nodes resolve within 1 to
3 days and leave no sequelae.
Janeway lesions: Nontender, erythematous and nodular
lesions most commonly found on the palms and
soles of some patients with infective endocarditis.

Janeway lesions are named for noted
American physician Edward G. Janeway (1841-1911),
who, in 1899, described "numerous small hemorrhages
with slight nodular character in the palms of the hand
and soles of the feet . . . in malignant endocarditis."9 In
1906, Emanuel Libman, a student of Janeway, coined
the term "Janeway lesion," and went on to further
study these lesions and affirm their association with
infective endocarditis.

Pathogenesis
The pathogenesis of Janeway lesions is also unclear.
Some authors believe that these lesions are necrotic
microabscesses with an inflammatory infiltrate that
involves the dermis but not the epidermis.9,10 Other
authors believe that the lesions are the result of septic
microemboli that originate from the endocardium, a
fact that has been substantiated by histopathologic
studies in the literature.10 -12
Janeway Lesions Compared with Osler's Nodes
Janeway lesions are usually associated with acute
bacterial endocarditis.11 They frequently have an irregular
outline, are erythematous and nodular, and sometimes
appear hemorrhagic. They have been confused
with Osler's nodes; however, two important distinctions
exist. First, Janeway lesions usually occur on the palms
and soles, not on the pads of the fingers. Second,Janeway lesions are not tender, whereas Osler's nodes
are often exquisitely tender, which is the most compelling
difference between these two signs.
Splinter hemorrhages: Small, linear hemorrhages
under the nails that are usually asymptomatic and
found in some patients with infective endocarditis.

Splinter hemorrhages were originally described in
1920 in patients with endocarditis as "minute petechiae,
in the form of a vivid linear splash of red at the side of
the bed of a fingernail."13 In 1926, this association was
affirmed by Blumer,14 and in recent years, various other
authors have described splinter hemorrhages in other
conditions, including trichinosis, mitral stenosis, psoriasis,
onychomycosis, vasculitis, meningococcemia, and
trauma.13,15,16 Splinter hemorrhages have also been described
in healthy individuals,16 patients on hemodialysis,
and individuals who perform manual labor.15
Splinter hemorrhages are usually less than 2 to
3 mm long and lie under the distal one third of the
nail, traveling outward as the nail grows.13 Early in development,
the hemorrhages are reddish-brown; but with
maturity, they become brown to black, a process that
takes 1 to 2 days. Splinter hemorrhages are usually
asymptomatic, but they may be painful or tender to palpation.
They are caused by engorgement of capillaries
under the nail, but the etiology of the hemorrhages is
unclear. Potential mechanisms include digital vasospasm,
embolic events, and local factors that promote
capillary engorgement.
DIAGNOSIS OF ENDOCARDITIS
Because the diagnosis of endocarditis is often difficult,
many researchers have sought to standardize the
process and simplify the task. In recent years, two sets
of criteria for the diagnosis of endocarditis have been
described. The guidelines offered by Von Reyn et al17
rely on strict clinical criteria, including positive blood
cultures, murmurs, fever, and peripheral manifestations,
and ignore the importance of echocardiographic
data and a history of intravenous drug use as a risk factor
for endocarditis. The more recent Duke criteria
rely on clinical manifestations as well, but these guidelines
also factor in echocardiographic data and history
of intravenous drug use in the diagnosis of endocarditis.
18 The Duke guidelines also incorporate a system of
major and minor criteria that make them more specific
and sensitive than the Von Reyn criteria. Interestingly,
whereas Janeway lesions, Osler's nodes, and Roth's
spots are considered minor elements in the Duke criteria,
splinter hemorrhages are not included within the
Duke guidelines. Another recent study19 has suggested
modifications to the Duke criteria, including adding
splinter hemorrhages to the list of minor elements
because they were found to be more common than the
other peripheral phenomena in patients with endocarditis.
Despite the criteria outlined above, the peripheral
signs are seen less frequently today in patients with
endocarditis.1 This decrease in frequency has been
attributed to several causes, including earlier diagnosis
of endocarditis, earlier institution of antibiotic therapy,
and possible physician inexperience in recognizing the
signs.6 A recent study examining 135 cases of endocarditis
over 9 years noted that the peripheral manifestations
were fairly uncommon, with Osler's nodes present
in 6.7% of cases, Janeway lesions present in 2.2% of
cases, Roth's spots present in 3% of cases, and splinter
hemorrhages present in 39% of cases.2 By contrast,
murmurs were found in 94% of these cases, and fever
was found in 87% of cases.
SUMMARY
The peripheral manifestations of endocarditis are
venerable signs that may be useful adjuncts to the diagnosis
of endocarditis. With advances in technology and
treatment, the signs have become less common, but they
nevertheless remain a subject for intense scrutiny.

CVS Diseases In a Nutshell

I hope everyone finds CVS 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) Hypertension

Definition:

You cannot absolutely define hypertension, since its incidence is related to blood pressure which has a skewed normal distribution throughout the population.

Incidence:

Increases with age. Mild hypertension is 2% in ages 25 or less, 25% for those in their 50s, and 50% in those in their 70s.

Types and Causes:

1) Essential hypertension:

Incidence—95% of cases.

Causes—Lifestyle factors: Obesity, physical inactivity, alcohol, dietary; genetic factors; other CV factors: diabetes, smoking, cholesterol, age.

2) Secondary hypertension:

Incidence—2% of cases.

Uncommon Causes include:

Renal disease—75% of intrinsic origin (e.g. glomerulonephritis, PAN, polycystic kidneys), and 25% of renovascular origin (e.g. atheromatous)

Endocrine Disease—Cushing's syndrome, Conn’s Syndrome, acromegaly, hyperparathyroidism

Others—Pregnancy, steroids

3) Malignant hypertension:

Definition—severe hypertension (over 200/130) with bilateral hemorrhages and exudates (retinal changes)

Symptoms—headaches and visual disturbances, hypertensive emergencies like renal failure, heart failure, or encephalopathy are common.

Pathological hallmark is fibrinoid necrosis.

Consequences of hypertension:

The long-term risk is end-organ damage. Others include; stroke, coronary artery Disease, left ventricular hypertrophy, renal failure.

Signs and Symptoms:

It’s usually asymptomatic (except for the malignant type). Symptoms start appearing when end-organ damage occurs. Fully examine CVS and look for; signs of renal disease, Cushing, radiofemoral delay, weak femoral pulse, palpable kidneys, retinopathy and proteinurea.

Investigations:

Basic: Urea and Electrolytes.

Specific: renal ultrasound and arteriography, urinary free cortisol, renin, and aldosterone, ECHO, and 24-hour BP monitering.

Treatment:

Overall approach and aim: address CV risk factors and aim for 140/85 BP. All patients with sustained pressure of 160/100 or malignant hypertension should be treated.

Non-pharmacological measures: lifestyle modification.

Drugs: the "ABCD rule". It is better to "mix and match" the following drugs for initial therapy; if one matching fails, switch to another. It takes 4-8 weeks to produce their maximum effect:

1. ACE Inhibitors—used as first line of treatment for asthmatic patients, e.g. Captopril.

2. B-blockers—usually used as initial treatment unless patient is asthmatic, e.g. Atenolol and Metoprolol.

3. Calcium channel antagonists—used with B-blocker as initial treatment, e.g. Nifedipine.

4. Diuretics—thiazide diuretics, e.g. bendrofluazide.

Malignant hypertension treatment: most patients are managed with oral therapy (preferably a loop diuretic—furosemide), except for critical patients with encephalopathy. These patients should be given intravenous agents (preferably sodium nitroprusside) and monitored constantly to avoid sudden BP drops. BP drops should be controlled over days not hours, since stroke can be a serious complication in rushed treatment.

II) Heart Failure

Definition:

Cardiac output and BP are inadequate for the body’s requirements.

Factors and General Causes:

Pump Failure:

Heart muscle disease—IHD, cardiomyopathy

Restricted filling—constrictive pericarditis, restrictive cardiomyopathy

Inadequate heart rate—b-blockers, post MI.

Negatively inotropic drugs—e.g. most antiarrhythmic agents

Excessive preload: e.g. mitral regurgitation and fluid overload.

Chronic excessive afterload: e.g. aortic stenosis, hypertension.

Types:

1. Acute heart failure (LVF)

2. Chronic heart failure (RVF): specific causes include pulmonary hypertension and atrial septal defect.

3. Congestive Heart Failure: left and right ventricular heart failure together.

4. Low-output cardiac failure: inadequate or is only adequate with high pressures. Specific causes include ischemia, hypertension, valve disorders, and alcohol usage.

5. High-output cardiac failure: This is a rare type of HF. Evidently; this will later turn into LVF. Here, cardiac output only increases when needs increase, and the failure occurs when the output fails to meet the body's demand. Specific causes include heart disease with anemia or pregnancy, beri beri, thyrotoxicosis, vessel malformation, and Paget's disease.

Symptoms:

LVF: dyspnoea, poor exercise tolerance, fatigue, weight loss, muscle wasting, orthopnoea, paroxysmal nocturnal dyspnoea, nocturnal coughing and wheezing, nocturia.

RVF: peripheral edema, ascites, nausea, anorexia, facial engorgement, tricuspid regurgitation.

Signs:

Patient looks ill and exhausted, cool peripheries, peripheral cyanosis, tachycardia, raised JVP, displaced apex, murmurs, respiratory crackles, plural effusion.

Investigations:

Key Investigation: echocardiography, since it can indicate the cause.

Basic: if ECG and BMP are normal, then heart failure is unlikely. If either abnormal, then echo is required.

Blood tests: FBC, U&E, BMP.

Chest X-ray: ABCDE—Alveolar edema, B lines Kerley, cardiomegaly, dilated upper lobe vessels, effusion (plural effusion).

Treatment:

Acute Heart Failure: medical emergency. Continuous monitoring and IV management is needed. Investigations are done after the initial treatment.

Chronic Heart Failure:

1. Treat exacerbating factors—e.g. anemia, thyroid disease, infection, elevated BP.

2. Avoid exacerbating factors—e.g. NSAID and verapamil.

3. Maintain lifestyle—eat less salt, avoid smoking, and maintain weight and nutrition.

4. Drugs—loop diuretics, ACE inhibitors, beta-blockers, digoxin, and vasodilators.

Intractable Heart Failure: reassess the cause and manage in hospital.

III) Infective Endocarditis

Classification

50% occurs on normal heart valves, following an acute course and presenting with acute heart failure.

On abnormal heart valves, it tends to run on a subacute course. Predisposing cardiac lesions; valvular heart disease, tricuspid valves in IV drug users, patent ductus arteriosus, VSD, prosthetic valves (early or late phase).

Causes:

Bacteria: Any cause of bacteraemia exposes valves to the risk of colonization, e.g. dental work, UTI, respiratory infection, skin disease, surgery, fractures, etc. Commonest organism is streptococcus viridans (30-50%). Others include; staphylococcus aureus/epidermis, enterococci, gram-negative organisms (HACEK group—rare).

Fungi: rare—Candida, Aspergillus, and Histoplasma.

Others: SLE and malignancy.

Clinical features:

Signs of infection: fever, rigors, night sweats, malaise, weight loss, etc.

Cardiac lesions: new murmurs, vegetations, severe regurgitation, valve obstruction.

Immune complex deposition: vasculitis, microscopic haematuria, glomerulonephritis and acute renal failure.

Pathognomonic signs: roth spots, splinter hemorrhages, Osler’s nodes, Janeway lesions.

Embolic: pulmonary abscesses may occur in right-sided endocarditis.

Diagnosis:

Use Duke Criteria—evidence of 2 major criteria, or 1 major and 3 minor, or all 5 minor.

1. Major criteria:

Positive blood culture: typical organism in 2 separate cultures or persistently positive blood cultures (hours apart).

Endocardium: positive echocardiogram or new valvular regurgitation.

2. Minor criteria:

Predisposition (cardiac lesion, IV drug abuse)

Fever over 30C

Vascular/immunological signs

Positive blood culture and echocardiogram which do not meet major criteria

Treatment:

Antibiotics: intravenous, continues for 4-6 weeks, drug combinations recommended.

Surgery: removal and replacement of infected valve. Consider if; severe valve obstruction, heart failure, abscess formation, persistent bacteraemia, prosthetic valve endocarditis.

Prophylaxis: for patients with known valvular disease or prosthetic valves.

IV) Rheumatic Fever

Definition:

It’s a systemic infection which is still common in the Third World but rare in the West. Pharyngeal infection with group A beta-haemolytic streptococci triggers this disease 2-4 weeks later. Antigenic mimicry mechanism between strep and valve tissue causes permanent damage. Incidence: 5-15 years. It tends to recur if not prevented.

Clinical Features and Diagnosis:

Revised Jones criteria—evidence of recent strep infection plus 2 major criteria, or 1 major + 2 minor.

1) Evidence of strep infection:

Recent strep infection

History of scarlet fever

Positive throat swab

Increase in AOST above 200U/mL

Increase in DNase B titer

2) Major criteria:

Carditis: conduction defects (45-70%), tachycardia, cardiomegaly, murmurs (Carey Coombs’ murmur).

Arthritis: ‘fitting’ polyarthritis usually affecting the larger joints (75%).

Subcutaneous nodules: small, mobile, painless, on extensor surfaces of joints and spine (2-20%).

Erythema marginatum: geographical-type rash. Reddish edges but clear in the center. The 'white' spreads all over. It occurs in the trunk, thighs and arms, NOT in face or below knees/elbow. (2-10%)

Chorea: unilateral or bilateral involuntary semi-purposeful movements (10%).

3) Minor criteria:

Fever

Raised ESR or CRP

Arthralgia

Prolonged P-R interval

Previous rheumatic fever

Treatment:

Bed rest until CRP is normal, benzylpenicillin IM then penicillin, aspirin doses with monitoring for carditis/arthritis, haloperidol for chorea, and steroids for symptom improvement.

V) Deep Vein Thrombosis

Incidence:

DVT occurs in 20% of surgical patients, and many non-surgical ones. 65% below-knee DVTs are asymptomatic; they rarely embolize to the lung.

Risk:

Factors include increased age, pregnancy, surgery, malignancy, obesity, immobility, past DVT, thrombophilia, and synthetic estrogen.

Signs:

Signs include calf warmth/tenderness/swelling, mild fever, pitting edema. Do NOT perform Homans’ sign.

Differential diagnosis:

Cellulitis or ruptured Baker’s cyst (both may coexist).

Tests:

a) Guidelines:

Use D-dimer blood tests and pretest clinical probability score.

If test is negative and score is low, exclude DVT.

If vice versa on both tests, do compression ultrasound.

If this is negative, then repeat ultrasound in a week just in case.

Do thrombophilia tests in recurrent DVT, positive family history DVT, and if there are no predisposing factors.

b) D-dimer blood tests: sensitive but not specific to DVT—raised in infection, pregnancy, malignancy and post-op.

c) Pretest clinical probability scoring:

In patients with symptoms in both legs, the more symptomatic one is used. Points are graded for each clinical feature; a total of 3 or more points has high probability, 1-2 points has intermediate probability, and 0 or less points has low probability:

Active Cancer—1 point

Paralysis or recent plaster immobilization of leg—1 point

Major surgery or bedridden for more than three days within the last 4 weeks—1 point

Local tenderness along leg—1 point

Entire leg swollen—1 point

Calf swelling more than 3 cm compared to normal leg (10 cm)—1 point

Pitting edema—1 point

Collateral superficial veins—1 point

Alternative diagnosis as or more likely than DVT—(-2) points

VI) Aortic Valve Disease (Aortic Stenosis and Regurgitation)

a) Aortic Stenosis

*Definition:

Impaired systolic flow of blood from left ventricle to aorta by narrowed aortic valve.

*Causes:

Senile calcification is the commonest (tricuspid from 60-100 years). Other causes congenital (bicuspid valve, William’s syndrome).

*Symptoms:

These include angina, dyspnoea, dizziness, faints, systemic emboli if infective endocarditis.

*Signs:

Slow rising pulse with narrow blood pressure, forceful displaced apex beat, ejection systolic murmur, soft or absent A2, ejection click if valve mobile.

*Investigations:

Cardiac ultrasonography is the key investigation, as it allows assessment of LV function, valve function, and severity of stenosis. Doppler echo estimates gradient across valves. Cardiac catheter and ECG are also useful tests.

*Differential diagnosis:

AS can be mistaken for hypertrophic obstructive cardiomyopathy.

*Treatment and Management:

Poor prognosis; 2-3 year survival if angina, 1-2 year survival with cardiac failure. Valve replacement is recommended.

b) Aortic Regurgitation:

*Causes:

Congenital valve disease: rheumatic fever, infective endocarditis, rheumatoid arthritis, SLE.

Aortic root disease: hypertension, trauma, aortic dissection, Marfan’s syndrome, syphilitic aortitis.

*Symptoms:

These include dyspnoea, palpitations, cardiac failure.

*Signs:

Collapsing pulse, wide pressure pulse, displaced hyperdynamic apex beat, high-pitched early diastolic murmur, Corrigan's sign, Duroziez's sign, de Musset's sign, Quincke's sign, Traube's sign.

*Investigations:

Cardiac ultrasonography is diagnostic. Cardiac catheterization is used to assess. X-ray may show cardiomegaly (unlike AS, CXR is NOT used). CT and MRI are used on thoracic aorta.

*Management:

ACE inhibitors and diuretics to maintain severe AR

AV replacement surgery is recommended, possibly with root replacement. Indications include increasing symptoms, enlarging heart, ECG deterioration.

VII) Mitral Valve Disease (Stenosis, Prolapse, Regurgitation)

a) Mitral Stenosis

*Definition:

Impaired diastolic flow of blood from left atrium into left ventricle through narrow mitral valve.

*Causes:

Rheumatic is the commonest cause (99%). Other causes include SLE, congenital, malignant carcinoid, and prosthetic valve.

*Symptoms:

These include dyspnoea, fatigue, palpitations, chest pain, haemoptysis, and chronic bronchitis-like picture.

*Signs:

These include malar flush, low-volume pulse, AF, tapping apex beat (palpable S1), low-pitched rumbling mid-diastolic murmur, and opening snap.

*Differential Diagnosis:

Atrial myxoma may cause similar signs.

*Tests/Investigations:

Cardiac ultrasonography confirms the diagnosis.

ECG for AF

CXR shows left atrial enlargement, pulmonary edema, and mitral valve calcification. Use chest catheterization if one of these is present: signs of other valve disease, angina, valve calcification, and severe pulmonary hypertension.

*Treatment:

Drugs: diuretics, beta-blockers, digoxin, warfrin.

Surgery: mitral valvotomy or mitral valve replacement.

Penicillin prophylaxis against RF.

b) Mitral Regurgitation

*Definition:

Abnormal systolic flow of blood from left ventricle back into left atrium from leaking valve.

Causes:

Mitral Valve Disease: MV prolapse, rheumatic valve disease, papillary muscle dysfunction/rupture, endocarditis.

Functional MR (secondary): LV dilatation from any cause

Connective Tissue Disorders: Ehlers-Danlos, Marfan’s Syndrome

Congenital: associated with other defects, e.g. ASD

Symptoms:

These include dyspnoea, fatigue, palpitations, and infective endocarditis.

Signs:

These include AF, hyperdynamic displaced apex, soft S1, split S2, loud P2, pansystolic murmur radiating to the axilla.

Tests/Investigations:

Cardiac ultrasonography to confirm MR and monitor LV function

Echocardiography to check severity (transthoracic or transesophageal)

CXR (shows big LA and LV), ECG, and cardiac catheterization as in MS

Treatment: as in MS but use antibiotics for prophylaxis against endocarditis.

c) Mitral Prolapse

Definition:

Mitral valve is larger than usual (possible congenital deformity, may occur with others). Because of that, part of the valve prolapses back into the left atrium during ventricular systole. It has 5% prevalence. It occurs alone or with MR.

Symptoms: WITHOUT MR it’s asymptomatic but may cause chest pain and palpitations.

Signs: WITHOUT MR there is a mid-systolic click and/or late systolic murmur.

Tests: Echocardiography is diagnostic. ECG may show inferior T-wave inversion.

Complications: MR, cerebral emboli, arrhythmias, sudden death, and endocarditis WITH MR.

Treatment: b-blockers prevent symptoms and endocarditis prophylaxis WITH MR.

VIII) Congenital Heart Disease

Definition:

Abnormal embryological cardiac development or persistence of some parts of the fetal circulation after birth resulting in structural cardiac defects.

Incidence:

Major defects account for 8/1000 live births. Minor defects more common.

Main Classification:

Four major categories: 1) shunt defects, 2) valvular defects, 3) complex lesions, 4) associated syndromes.

1) Shunt defects:

Three main defects: a) ventricular septal defect, b) atrial septal defect, c) patent ductus arteriosus.

a) Ventricular septal defect:

Incidence—25% of CHD

Definition—a defect in the interventricular septum allowing blood to shunt from left to right.

Types—small and large

Murmurs—smaller holes are haemodynamically less significant and give louder murmurs (Maladie de Roger)…classically, you can hear a harsh pansystolic murmur with systolic thrill and possible parasternal heave at the left sternal edge. Larger holes give quiet murmurs.

Complications—High risk endocarditis is especially present in smaller holes. Larger holes have more serious complications; can lead to pulmonary hypertension and Eisenmenger's syndrome if untreated.

b) Atrial septal defect:

Incidence—10% of CHD

Definition—a defect in the interatrial septum allowing blood to shunt from left to right.

Murmurs—ASD produces systolic pulmonary flow murmur and splitting of the 2^nd heart sound.

Types—Ostium secundum (70%) and ostium primum (30%)

Presentation—secundum is often asymptomatic until adulthood. Primum presents early.

Complications—primum is often associated with AV valve anomalies and other defects (like VSD).

c) Patent ductus arteriosus:

Incidence—15% of CHD

Definition—Ductus arteriosus fails to close after birth, resulting in left-to-right shunting from the aorta to pulmonary artery.

Murmur—Continuous (machinery) murmur can be heard.

Complications—large ducts with significant shunt leads to complications (refer to ‘general shunt pathophysiology’)

*Associations:

Down’s Syndrome and Klinefelter’s Syndrome.

*Investigations/tests for shunt defects:

Echocardiography is diagnostic.

ECG showings in ASD: primum defect—left axis deviation (LAD), RBBB, and prolonged P-R interval, secundum defect—right axis deviation. Both are associated with RVH.

ECG showings in VSD: normal (small VSD), LAD + LVH (moderate VSD), LVH + RVH (large VSD).

Cardiac catheterization: O2 saturation in the right atrium (ASD) or right ventricle (VSD).

CXR: heart size, pulmonary plethora, enlarged arteries…all which depend on the size of the shunt.

*Treatment for shunt defects:

Surgical closure of the shunts before complications develop, precutaneous dilatation as an alternative.

*General shunt pathophysiology:

Mild-to-moderate shunt defect à left-to-right shunting à increase pulmonary blood flow à possible right heart hypertrophy

Large shunts à Eisenmenger’s Syndrome (i.e. irreversible pulmonary hypertension + shunt reversal from ‘left-to-right’ to ‘right-to-left’) à severe pulmonary hypertension signs (i.e. cyanosis, clubbing) à severe complications may develop (LVH, HF)

*Common complications to shunt defects:

These include bacterial endocarditis, heart hypertrophy (right or left), Eisenmenger’s Syndrome, heart failure, pulmonary hypertension, respiratory infections.

2) Valvular defects:

Definition:

Abnormal valve development, usually resulting in stenosis or atresia of valves

Types:

Three main types: a) aortic stenosis, b) bicuspid aortic valve, c) tricuspid atresia.

Bicuspid aortic valve:

Description—functions well at birth and go undetected. Most cases develop into AS and/or AR.

Associations—coarctation of aorta: the congenital narrowing of the descending aorta.

Coarctation of aorta:

Compensation—blood flow is maintained by increased collateral flow via mammary and intercostal arteries.

Associations—bicuspid aortic valve and Turner’s syndrome.

Signs—weak femoral pulse, radiofemoral delay, palpable collaterals around the scapulae, systolic murmur

Tests—echocardiography, CT or MRI, CXR shows rib notching

Complications—heart failure, infective endocarditis

Treatment—surgical correction or precutaneous dilatation

3) Complex lesions:

Definition:

These consist of abnormal relationships between various individual defects, including great vessels, arteries, chamber development, septal/valvular defects.

Types:

Three main types: a) Fallot’s tetralogy, b) Ebstein’s anomaly, c) transposition of the great vessels.

Fallot’s tetralogy:

Incidence—10% of CHD, most common complex lesion

Definition—combination of VSD and ‘right-to-left’ shunt due to; pulmonary stenosis, RVH, and dextro-position of the aorta which in turn overrides the VSD.

Features—children have breathlessness, dizziness, growth retardation

Signs—cyanosis, clubbing, pulmonary systolic murmur

Treatment—surgery aims to correct the defects and increase pulmonary blood flow via systemic-to-pulmonary artery shunts. The three main surgical shunts are; Blalock-Taussig (subclavian-to-pulmonary artery), Waterston (ascending aorta-to-right pulmonary artery), and Potts (descending aorta-to-left pulmonary artery).

Ebstein’s anomaly:

Tricuspid valve is displaced into the right ventricle, resulting in a small RV cavity and a large right atrium. It is associated with ASD and Wolf-Parkinson-White syndrome.

Transposition of the great arteries:

Definition—aorta arises from the right ventricle and pulmonary artery from the left ventricle.

Fate—incompatible with life unless there’s an ASD (shunting)

Treatment—balloon septostomy, interartiral shunt, congenitally corrected transposition.

IX) Coronary Syndromes/Ischemic Heart Diseases

Classification:

Acute Coronary Syndrome—unstable angina and evolving myocardial infarction

Chronic Coronary Syndrome—chronic stable angina

1) Angina Pectoris

*Definition:

This is due to myocardial ischemia and presents as a central chest tightness or heaviness, brought by exertion and relieved by rest. It may radiate to the arms, the neck, jaw, or teeth. Other precipitants include: emotion, cold weather, heavy meals.

*Associated symptoms:

Dyspnoea, nausea, sweatiness, faintness

*Causes:

Atheroma is the commonest. Anemia, AS, and arteritis are rare causes.

*Types:

a) Stable angina:

Definition—pain induced by effort, relieved by rest.

Risk stratification—outlook of chronic stable angina is worsened by; increasing age, exercise intolerance, impaired LV function, severe coronary disease, peripheral vascular disease, diabetes, etc.

Tests—Bruce protocol on exercise testing, four stages descending to ascending, 10-16% gradient, 0-12 minutes. ECG changes on exercise include; planar or downsloping ST depression (compared to the normal upsloping ST depression)

Treatment—anti-ischemic therapy, revascularization, coronary angioplasty, coronary artery bypass surgery (CABS)

b) Unstable angina:

Definition—pain of increasing frequency or severity, occurs on minimal excretion or at rest, unpredictable symptoms.

Risk stratification—factors associated with high-risk include: recurrent chest pain, impaired LV function, heart failure.

Tests—ECG shows ST depression and/or T wave inversion. Elevated cardiac markers (e.g. troponin, creatine kinase, AST, LDH), cholesterol, glucose

Treatment—emergency...aspirin, analgesia, IV b-blocker, LMW heparin, anti-platelet drugs to high-risk patients and cardiac catheterization

c) Crescendo angina: amount of effort provoking symptoms decreases, do not occur at rest. It can result from unstable angina.

2) Myocardial Infraction

*Definition:

Ischemic necrosis of the mydocardium as a result of acute occlusion of a coronary artery

*Causes:

Most common cause is atheromatous coronary artery disease. Rare causes include; coronary artery embolism/spasm/thrombosis/aneurysm/dissection, arteritis.

*Types:

a) Acute MI: otherwise known as ‘acute coronary syndrome with ST-elevation’.

b) Severe MI: ACS without ST-elevation. ECG can show; t-wave inversion (minutes or hours), and q-waves (days or months)

*Pathogenesis:

Basically, it’s plague rupture, thrombosis, and inflammation.

*Regions involved in MI:

a) Anterior: LAD artery occluded

b) Inferior: right CA

c) Posterior: right or circumflex

d) Lateral: circumflex or diagonal branch of LAD

*Clinical presentation:

a) Classic presentation: crushing central chest pain for more than 20 minutes, associated with sweating, pallor, and nausea.

b) Other presentations: arrhythmia, cardiac arrest, or heart failure

c) Elderly: collapse or confusion. "Silent infract" may occur

d) Diabetic: metabolic worsens or heart failure. “Silent infract” may occur.

*Differential Diagnosis:

Aortic Dissection and pericarditis

*Treatment:

Monitering in CCU, aspirin (chewed), masked oxygen, analgesia, thrombolysis

*Complications:

a) immediate/hours: AF, failed reperfusion

b) hours/days: cardiac rupture, cardiac arrest, re-infarction is common after thrombolysis

c) days/weeks: thromboembolism, chronic heart failure, tachycardia, Dressler’s syndrome.

Clinical Notes

Admission Note for Pelvic Pain, PID, GU Sx
* Admission Note for DKA, ICU
* Admission Note for Dizziness
* Admission Note for CP, ICU
* Admission Note for Back Pain
* Admission Note for Abdominal Pain
* Admission Note for Septic Shock, ICU
* Admission Note for Infection
* Admission Note for CP
* Procedure Note
Y massss...............

http://note3.blogspot.com/

ERCP

Endoscopic retrograde cholangiopancreatography.

This is my first time really taking the time to look at a radiograph taken during ERCP.

Images DO NOT belong to me. I take no credits for them. I found them randomly over Google.

Try naming the parts… Answers below.

1. Common bile duct
2. Common hepatic duct
3. Cystic duct
4. Endoscope
5. Gall bladder
6. Ampulla of Vater
7. Left hepatic duct
8. Neck of gall bladder
9. Pancreatic duct
10. Right hepatic duct

Here’s a gall stone.

And another.

The Dormia basket. A method to remove stones through an endoscope.

Yes la… I feel smarter by an inch.