Solitary Pulmonary Nodule

Definition: a single, <3 cm discrete, well-marginated, rounded opacity, surrounded by normal lung, with no lymphadenopathy or pleural effusion.
It is often an incidental finding, especially with increased use of CT scan but still it could be an be early, curable malignancy.

Etiology:
1. Benign (70%): Granuloma, Hemartoma, Bronchogenic cyst, AV malformation, Rheumatoid nodule
2. Malignant (39%): Bronchogenic carcinoma, Metastases from breast, heard, neck , colon.

Initial evaluation
• History: h/o cancer, smoking, age (<30 years = 2% malignant)
• CT: size/shape, calcium deposits, Lymphadenopathy, effusions, bony destruction, compare with old studies.

• High-risk features for malignancy: 

• ≥2.3 cm diameter, 
• spiculated,
•  >60 years old, 
• >1 ppd current smoker, 
• no prior smoking cessation

Shock - A Brief Discussion

Shock is a condition of severe impairment of tissue perfusion leading to cellular injury and dysfunction. Rapid recognition and treatment are essential to prevent irreversible organ damage and death.

Different Causes And Categories Of Shock:

Hypovolemic shock

• Hemorrhage
• Intravascular volume depletion (e.g., vomiting, diarrhea, ketoacidosis)
• Internal sequestration (ascites, pancreatitis, intestinal obstruction)

Cardiogenic shock

• Myopathic (acute MI, fulminant myocarditis)
• Mechanical (e.g., acute mitral regurgitation, ventricular septal defect, severe aortic stenosis, aortic dissection with aortic insufficiency)
• Arrhythmic

Extracardiac obstructive shock

• Pericardial tamponade
• Massive pulmonary embolism
• Tension pneumothorax

Distributive shock (profound decrease in systemic vascular tone)

• Sepsis
• Toxic overdoses
• Anaphylaxis
• Neurogenic (e.g., spinal cord injury)
• Endocrinologic (Addison’s disease, myxedema)

Clinical Manifestations:

• Hypotension (mean arterial BP <60 mmHg), tachycardia, tachypnea, pallor, restlessness, and altered sensorium.

• Signs of intense peripheral vasoconstriction, with weak pulses and cold clammy extremities. In distributive (e.g., septic) shock, vasodilation predominates and extremities are warm.

• Oliguria (<20 mL/h) and metabolic acidosis common.

• Acute lung injury and acute respiratory distress syndrome with noncardiogenic pulmonary edema, hypoxemia, and diffuse pulmonary infiltrates.

Approach To The Patient: 

Obtain history for underlying causes, including 

• cardiac disease (coronary disease, heart failure, pericardial disease), 
• recent fever or infection leading to sepsis, 
• drug effects (e.g., excess diuretics or ), 
• conditions leading to pulmonary embolism and 
• potential sources of bleeding.

Approach To A Patient With Chronic Obstructive Pulmonary Disease (COPD)

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airflow limitation due to impedance to expiratory airflow, mucosal edema, infection, bronchospasm and bronchoconstriction due to decreased lung elasticity.

Smoking is the main cause, but others are chronic asthma, α-1 antitrypsin deficiency and chronic infection (eg bronchiectasis).

History
Exertional dyspnoea, cough, and sputum are usual complaints.
Ask about:
• Present treatment including inhalers, steroids, antibiotics, theophyllines, nebulizers, opiate analgesia, and home O 2 treatment.
• Past history: inquire about previous admissions and co-morbidity.
• Exercise tolerance: how far can they walk on the flat without stopping? How many stairs can they climb? Do they get out of the house?
• Recent history: ask about wheeze and dyspnoea, sputum volume and color. Chest injuries, abdominal problems and other infections may cause respiratory decompensation.
• Read the hospital notes: have there been prior ICU assessments? Has the respiratory consultant advised whether ICU would be appropriate?

Examination

• Examine for dyspnoea, tachypnoea, accessory muscle use, and lip-pursing.
• Look for hyperinflation (‘barrel chest’) and listen for wheeze or coarse crackles (large airway secretions). 
• Cyanosis, plethora (due to secondary polycythaemia) and right heart failure (cor pulmonale) suggest advanced disease. 
• Look for evidence of hypercarbia: tremor, bounding pulses, peripheral vasodilatation, drowsiness, or confusion.
• Check for evidence of other causes of acute dyspnoea, particularly: asthma, pulmonary edema, pneumothorax , Pulmonary embolism. Remember that these conditions may co-exist with COPD.

How Should Doctors Recognize and Treat their Own Metal Illness

Introduction
Doctors have a higher than average incidence of suicide and alcoholism, and so all doctors must be prepared to face (and try to prevent) these and other health risks in their professional and private lives. A doctor's  skill at looking after himself/herself has never been as good as their skill at looking after others, but when the healer is wounded, is it clear that his ability to help others will be correspondingly reduced.

Indicators of Affected Mental State
If the time comes when a doctor's mental state seriously reduces the ability to work, the doctor must be able to recognize this and take appropriate action. The following may indicate that this point is approaching:
• Drinking alcohol before ward rounds or surgeries.
• The minimizing of every contact with patients, so that the doctor does the bare minimum which will suffice.
• Inability to concentrate on the matter in hand. The thoughts are entirely taken up with the workload ahead.
• Irritability (defined as disagreeing with >1 nurse in 24 hours time period).
• Inability to take time off without feeling guilty.
• Feelings of excessive shame or anger when reviewing past mistakes.
• Emotional exhaustion—for example knowing that you should be feeling pleased or cross with yourself or others, but on consulting your heart you draw a blank.
• Prospective studies suggest that introversion, masochism, and isolation are important risk factors for doctors’ impairment.

Hypersensitivity - Different Types

Type I Anaphylactic

• antigen reacts with IgE bound to mast cells
• anaphylaxis, atopy (e.g. asthma, eczema and hayfever)

Type II Cell bound

• IgG or IgM binds to antigen on cell surface
• autoimmune haemolytic anaemia, ITP, Goodpasture's, pernicious anemia, acute hemolytic transfusion reactions, rheumatic fever, bullous pemphigoid, pemphigus vulgaris.

Type III Immune complex

• free antigen and antibody (IgG, IgA) combine
• serum sickness, systemic lupus erythematosus, poststreptococcal glomerulonephritis, extrinsic allergic alveolitis (especially acute phase)