Exam Flashcards
Describe COPD
Group of disorders which are associated w a progressive destruction of air flow in the lungs resulting in impaired gas exchange
Identify the different types of COPD
- Emphysema and chronic bronchitis
- Also asthma, cystic fibrosis and bronchiectasis
Describe the pathophysiology of each type of COPD and relate signs and symptoms
Symptoms: SOB, incr. work of breathing, dyspnoea, productive cough, wheezing/tight chest, and/or cyanosis
- Emphysema: enlargement of gas exchange airways and alveolar wall destruction.
Inflammation, oxidative stress and protease/antiprotease imbalance occurs causing destruction of alveolar septa (cauliflower –> balloon), breakdown of elastic fibres and decr. healthy tissue repair.
Results in decr. SA and trapped air. = difficult expiration, hyperinflation and hypoventilation leading to hypoxemia and hypercapnia
- Chronic bronchitis: inflammation of the airways
Impairs inhalation, incr. mucus glands, decr. cilia function leading to hypersecretion of thick mucus that cannot be cleared.
Airway blockage and resistance = less alveoli receiving air = airways collapse early in expiration = air trapping in distal lungs leading to hypercapnia and cyanosis
- Asthma: chronic inflammatory condition of the airways stimulated by triggers resulting in hyperresponsiveness and obstruction.
Inflammation leads to bronchoconstriction, mucosa oedema and mucus plugging, = incr. airway resistance and decr. airflow (in exhalation = air trapping). V/Q mismatch = decr. gas exchange leading hypoxemia, cyanosis, hypercapnia, tissue hypoxia.
Less air coming in and harder to get out.
- Cystic fibrosis: autosomal recessive condition affecting epithelial chloride secretion (in resp. and digestive system).
Mucus secretions are abnormally thick and sticky. Chronic inflammation and infections occur; mucus traps microorganisms, abscess and cyst formation, bronchiectasis and pneumonia.
Progressive decr. in lung function leads to death.
- Bronchiectasis: abnormal, permanent dilation of bronchi, usually as a result of previous chronic infection.
Infection and inflammation results in progressive destruction of bronchial walls, mucus becomes hard to clear. Decr. vital capacity and exp. flow rate occur w coughing, excessive purulent sputum production, haemoptysis and possible atelectasis.
Outline further implications of COPD
- Hypoxemia: decr. arterial O2
- Hypercapnia: incr. arterial CO2 (bc hypoventilation)
- Atelectasis: collapse of lung tissue/alveoli
- Acute resp. failure - decr. gas exchange: PaO2 < 50mmHg or PaCO2 > 50mmHg
- Pulmonary hypertension and cor pulmonale: alveolar hypoxia and/or destruction of pulmonary vasculature; chronic hypoxia leading to polycythemia (excess RBC) and pulmonary vasoconstriction. –> heart pumping harder to compensate for incr. resistance and lack of nutrients due to decr. gas exchange –> heart failure.
Describe the medications that may be used to treat asthma
- High flow O2
- Beta agonist drugs
- Anticholinergics
- Corticosteroids
- Adrenalin
- CPAP
- SaO2 and cardiac monitoring
Describe the medications that may be used to prevent asthma
- Hydrocortisone
- Methylprednisolone
- Prednisone/prednisolone
Understand how asthma medications are used and their possible side effects
- Oxygen: prevents hypoxia and helps aid bronchodilation, decr. dyspnoea, support the myocardium and decr. risk of arrhythmia.
- Sympathomimetics: agonists at B2 adrenergic receptors on bronchiole smooth muscle. Side effects are tachycardia, palpitations, tremor and anxiety (due to non-selectivity).
- Anticholinergic drugs: block mACh receptors on bronchiole smooth muscle causing bronchodilation. Blocks PNS activity which can cause dry mouth (saliva production), GI effects (bowel motility), urinary retention.
- Corticosteroids: switch on/off genes involved in the inflammatory process or its regulation. Minimal side effects of inhaled, but can be irritation of mouth/throat.
- CPAP: keeps airways open throughout breathing cycle
- Adrenalin: keeps the bronchi wall muscles relaxed and the airway wide, + blocks the release of histamines
Outline the pathophysiology of MI, incl. signs/symptoms and consequences
- Myocardial ischemia and oxygen deprivation is prolonged, leading to irreversible hypoxic injury causing myocyte necrosis. Necrotic tissue is eventually replaced by fibrous scar tissue resulting in a part of the heart that can no longer contract
- Signs/symptoms: severe, sudden onset of pain, sweating, pale peripheries and nausea/vomiting. Indicated by elevated cardiac enzymes and T wave inversion.
- Consequences: arrhythmias, valvular incompetence, left ventricle failure, pericarditis, left ventricular aneurysm
Identify the 4 main classes of drugs used to treat cardiac conditions
- Diuretics
- Antihypertensives
- Anticoagulants
- Statins
What is the equation for BP
BP = CO x TPR
where CO = SV x HR
Describe the general effects of antihypertensives.
Describe the 3 types.
- Decrease rate and force of contraction to decr. CO and thus BP.
1. Beta blockers (-olol): block B1 adrenergic receptors on the SA and AV nodes to decr. HR and contractility, thus decr. CO.
2. Anti-arrhythmic drugs (e.g. digoxin): incr. parasympathetic activity to decr. HR, thus decr. CO
3. Vasodilators (Ca+ channel blockers, -dipine): decr. force of contraction leading to vasodilation and decr. TPR.
Describe the general effects of angiotensin antagonists (e.g. ACE inhibitors)
- inhibit the activity of angiotensin to. decr. BP Ace inhibitors (-pril): inhibit angiotensin converting enzyme (ACE), decreasing angiotensin II levels to lower BP by decr. vasoconstriction (decr. TPR and afterload) and decreasing Na+ and water retention (decr. blood vol. and preload)
Describe the general effects of statins
- Reduce the effects of high cholesterol levels on blood vessels
- Inhibit the pathway of cholesterol formation
Describe the general effects of diuretics
- Decr. blood vol. by forcing the incr. secretion of ions in order to decr. CO and thus decr. BP
- Thiazides: inhibit reabsorption of Na+ and Cl- ions in the DCT –> incr. excretion water
- Loop diuretics: inhibit active transport of Na+ and Cl- ions in the Loop of Henle –> incr. urine output
- Potassium sparing: block aldosterone receptors in the DCT to decr. Na+ reabsorption and K+ excretion –> incr. urine (and Na+) output (and decr. K+ excretion)
Describe key aspects in the management of patients w diabetes
Achieving near normal glycaemia to prevent symptoms of hyper- and hypoglycaemia (short term) and prevent complications (long term)
