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🔗Refer Asthma First Aid & Prevention tips on Page 2‼️
ASTHMA
Mild intermittent
💊 Short acting β2-agonists (e.g. Salbutamol, Terbutaline) inhalations when needed.
💊 Anticholinergics (e.g. Ipratropium, Tiotropium) inhalations when needed, alone or in addition to beta-2 agonists
💬 Patient is asymptomatic between the dyspnoea episodes, so no daily medication required!
ASTHMA
Mild persistent
💊 Short acting β2-agonists (e.g. Salbutamol, Terbutaline) inhalations ➕ Corticosteroid inhalation (low dose)
💊 Short acting β2-agonists ➕ Mast cell stabilizer or Leukotriene antagonist or Theophylline sustained release
💬 Beta-2 agonist inhalation is needed every day, so once daily corticosteroid inhalation if given for asthma control.
ASTHMA
Moderate persistent
💊 Long acting beta-2 agonists (e.g. Salmeterol, Formeterol) inhalations ➕ Corticosteroid inhalation (low to high dose)
💊 Long acting beta-2 agonist tablets or Theophylline sustained release ➕ Corticosteroid inhalation (medium dose)
💬 The dose of corticosteroid inhalations depends on the severity of symptoms.
ASTHMA
Severe persistent
💊 Long acting beta-2 agonists (e.g. Salmeterol, Formeterol) inhalations ➕ Corticosteroid inhalation (high dose) ➕ Corticosteroid tablets/syrup
💊 Long acting beta-2 agonist tablets or Theophylline sustained release ➕ Corticosteroid inhalation (high dose) ➕ Corticosteroid tablets/syrup
💬 Systemic corticosteroids have significant adverse effects, so after adequate asthma control, are gradually withdrawn.*
ASTHMA
Acute severe asthma
💊 Oxygen 60% ➕ Nebulized beta-2 agonists (e.g. Salbutamol) in high dose ➕ Systemic corticosteroids
💬 An emergency condition, earlier called as status asthmatics. Aminophylline is no longer recommended.
* After adequate control of severe persistent asthma, systemic corticosteroids are withdrawn, and the patient then would be managed as moderate persistent type. This is called "step down" approach of management. In this approach, it is considered better to manage patients assuming in the next higher type and then, after reviewing in 1-6 months, to step-down, instead of "step-up" after failure in asthma control.
Aspirin induced
asthma
💊 Leukotriene antagonists (e.g. Montelukast, Zafirlukast)
Exercise induced
asthma
For Prophylaxis: Mast cell stabilizers or beta-2 agonists or Leukotriene antagonists💊
COPD
Dry cough
💊 Cough suppressants (e.g. Dextromethorphan) + Treat the cause e.g. post nasal drip by antihistaminics and decongestants.
Productive cough
💊 Expectorants (e.g. Pot iodide) &/or Mucolytics (e.g. Acetylcysteine) ➕ Treat the cause e.g. allergy by antihistaminics and bacterial infection by antibiotics
References: CLASSIFICATION OF DRUGS WITH DRUGS OF CHOICE 3RD EDITION BY VIKAS SETH
source – Nancy 13th edition
– Large molecules (such as blood cells); blocked by capillary wall.
– Negatively charged molecules; blocked by basement membrane.
– Mid-sized molecules (such as proteins), blocked by visceral layer of Bowman’s capsule.
– Small molecules (water, glucose, amino acids, nitrogenous wastes); pass freely through filtration membrane to become part of ultrafiltrate.
Glomerulonephritis involves inflammation of the filtration membrane, which alters its permeability and inhibits proper filtration, which can be fatal. Signs include the presence of blood or proteins in the urine.
Kidneys
Ureters
Urinary bladder
Urethra
Small-cell lung cancer
Adenocarcinoma
Squamous cell carcinoma
Large cell lung cancer
Non-small cell lung cancers, as a group
Small and Non-Small lung cancers
Complications of lung cancer more broadly
– Pancoast tumors are also responsible for Horner syndrome, which is characterized by ptosis (eyelid drooping), miosis (pupil constriction), and facial anhidrosis (lack of sweating).
Lung cancer is broadly divided into small-cell lung cancer and non-small cell lung cancer.
Collectively account for approximately 85% of all lung cancers.
Review of flow of blood through the heart and lungs
The Groups are defined by hemodynamic profiles and causes. These groupings are important because proper treatment of pulmonary hypertension requires that we know its underlying pathobiology.
– Indicate that that venous return brings oxygenated blood from the lungs to the left side of the heart.
– Then, show that, when left ventricular end diastolic pressure is elevated, which occurs in left heart failure, that left atrial pressure also increases;
– And, as a result, passive increases in the pulmonary vasculature occur due to venous backflow.
– However, in some individuals, reactive pulmonary hypertension develops when heart disease leads to pulmonary arterial dysfunction and precapillary hypertension; thus, hypertension is “mixed” pre- and post-capillary.
In reactive pulmonary hypertension, we see increased transpulmonary gradients and pulmonary vascular resistance.
When pulmonary hypertension is suspected, we can perform a variety of tests to determine its presence, severity, and cause.