PBL #7 - COPD/Pneumonia Flashcards
What are the most probable causes of hemoptysis?
- Acute/Chronic Bronchitis
- Pneumonia
- TB
- Lung cancer
- PE
- Trauma
- Sarcoidosis
- Goodpasture’s syndrome
- Wegener’s (Granulomatosis with polyangiitis)
What is the mechanism behind hemoptysis in the setting of pneumonia?
Inflammatory mediators released by alveolar macrophages and newly recruited neutrophils create alveolar capillary leak → erythrocytes can cross the alveolar-capillary membrane → consequent hemoptysis
How would you go about evaluating a patient that you think has Chronic Obstructive Pulmonary Disease?
- Spirometry without Beta-2 agonist
- Spirometry after Beta-2 agonist
- compare FEV1:FVC ratio
- no change → supports COPD Dx
- Chest x-ray
- CBC
- ABG
What is your approach to the diagnosis and treatment of pneumonia?
- Diagnosis:
- H & P, symptoms
- CXR
- sputum gram stain and cultures
- blood cultures
- Urinary Antigen Tests: for streptococcus pneumoniae and Legionella pneumophila for patients with severe CAP
- Treatment:
- Start broad spectrum empiric treatment
- Use gram stain and cultures to assess susceptibility for definitive treatment
What are appropriate treatments for common pathogens causing pneumonia?
- Streptococcus Pneumoniae (CAP)
- Penicillin G (G=IV, IM)
- Haemophilus Influenzae Type B
- Cephalosporin (ceftriaxone)
- Moraxella Catarrhalis
- Amoxicillin-Clavulanate
- Cephalosporins
- TMP-SMX
- Respiratory Syncytial Virus (RSV)
- Supportive
- Ribavirin in severe cases
- Guanosine analog to stop vRNA synthesis (Nucleoside inhibitor)
- Mycoplasma Pneumoniae
- Erythromycin
- Tetracycline
- Staphylococcus Aureus
- Penicillinase-resistant penicillins
- Vancomycin
- Chlamydia Pneumoniae
- Doxycycline
- Streptococcus agalactiae (GROUP B STREP)
- Penicillin G
- Legionella pneumophila
- Erythromycin
- Nocardia Asteroides
- TMP-SMX
- Pneumocystis Jirovecii
- TMP-SMX
- Pentamidine
What is the difference in FEV-1/FVC ratios in obstructive vs. restrictive pulmonary diseases?
- FEV-1/FVC ratio ~ 80% = normal
- < 80% = obstructive
- > 80% = restrictive
How does chronic alcoholism influence drug and treatment choice?
- Disulfiram-like reaction drugs: metronidazole, some cephalosporins, griseofulvin, procarbazine, sulfonylureas
- Chronic Alcohol use → Cytochrome P-450 inducer (drug interactions)
- remember that P-450 is Phase I metabolism
- Phase II metabolism is less effect from chronic alcohol use.
- Use this to our advantage when treating Delirium tremens (DTs)/withdrawal
- Use lorazepam because it is inactivated by phase II metabolism, whereas diazepam is more phase I and will be less effective in DTs.
- Theophylline is metabolized by P-450
- Warfarin is metabolized by P-450
What does discharge planning include for a patient with COPD, tobacco use, and alcohol abuse who has limited means and is presently homeless?
- Establish health care goals (motivational interviewing)
- quality vs. quantity of life
- what is he willing to sacrifice
- Stop smoking! → Causes of Emphysema and Chronic Bronchitis (COPD)
- give resources for free cessation programs
- Stop drinking! → Suppresses cough and makes patient more susceptible to infection
- give resources for treatment programs and ‘wet houses’
- Encourage follow up
What is the COPDGene Study?
- Type of epidemiologic study → genetic epidemiology study
- Epidemiologic research = looks at a large population of individuals and tries to understand disease process within that population
- Genetic epidemiological study = looks for genes suspected to be involved in a disease process for a population
- Goal: identify genes that affect health and wellness of a population
What are the most recent genetic findings in COPD?
- Small but important fraction of COPD: alpha1-antitrypsin deficiency – most common in populations of Northern European ancestry, highly under-diagnosed
- Presents as lower-lobe predominant emphysema, bronchiectasis, liver disease, panniculitis, and vasculitis
- Treat severe AATD w/ IV AAT protein
- Discovery of AAT was major factor in developing Protease-Antiprotease Hypothesis
- GWAS → 3 novel genetic loci have been unequivocally associated with COPD susceptibility
- IREB2, HHIP, FAM13A
How do you pharmacologically treat patients with COPD?
- Smoking cessation (e.g. Chantix, etc.)
- Short-acting β-2 Agonists
- Long-acting β-2 Agonists
- Long-acting Muscarinic Antagonists
- Glucocorticoids
- Oxygen Therapy
What distinguishes an adrenocortical steroid from a mineralocorticoid?
-
Glucocorticoids: Hormones include cortisol, cortisone, and corticosterone
- secreted by zona fasciculata of adrenal cortex (mesoderm)
- Under control by ACTH of adenohypophysis
- control carbohydrate, fat, and protein metabolism, stimulate gluconeogenesis
- anti-inflammatory
- repairing injury and managing stress
- dull pain
-
Mineralocorticoids: most common aldosterone and deoxycorticosterone
- secreted by zona glomerulosa of adrenal cortex (mesoderm)
- Under control of RAAS
- control electrolyte and water balance, stimulate kidney (Steroid response element)
- they are NOT anti-inflammatory
- NOT helpful in repair or stress
- DO NOT manage pain
What receptors does albuterol interact with and why is it better to use for bronchodilation than propranolol or ephedrine or epinephrine?
- Albuterol = Beta-2 Agonist → bronchodilator
- Propanolol = beta-1 and beta-2 Antagonist → bronchoconstriction
- Ephedrine = ↑NE → Alpha-1 agonist (releases catecholamines) → vasoconstrictor
- Epinephrine = beta-1, beta-2, and alpha-1 agonist → bronchodilator, tachycardia, (short acting)
Why is it better to use ipratropium/tiotropium vs beta agonists or atropine in treatment of COPD?
- Ipratropium/Tiotropium = Muscarinic Antagonists → prevents parasympathetic bronchoconstriction and mucus secretions
- Beta-agonists = increase sympathetic bronchodilation → more effective in reversible bronchoconstriction in asthmatics
- Atropine = antimuscarinic/anticholinergic → inhibit salivary and mucus glands
What are the advantages of inhaled vs systemically administered drugs?
Inhaled drugs are localized to the target organ, which generally allows for a lower dose than is necessary with systemic delivery (oral or injection), and thus fewer and less severe adverse effects.
