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)
Discuss sources, formulations and administration of available insulin preparations
Sources:
- Animal insulin: Bovine (beef pancreas) and porcine (pig pancreas) which differs from human insulin by 3 and 1 amino acid(s) respectively. Result in the formation of antibodies in the human host (moreso the former)
- Human insulin: synthetic w same AA sequence as human insulin. Produced via enzymatic modification of porcine insulin or recombinant DNA techniques
Formulations:
- Short acting regular insulins: soluble, human or animal, suitable for IV or subcut.
- Longer acting cloudy insulins: insoluble crystal form, suspended in solution. Slowed absorption. Suitable only for subcut administration.
- Biphasic insulins: combination of soluble and suspended insulins; dual action.
Discuss indications and actions of the oral hypoglycaemic agents
- Sulphonylurea drugs: should only be used if dietary and exercise management is unsuccessful. Stimulate basal insulin secretions by pancreas (must have functioning beta cells). Can cause hypoglycaemia.
- Biguanides (e.g. metformin): used when diet, exercise and sulphonylurea drugs have been insufficient. Only works if some residual beta cell function. Decrease liver gluconeogenesis, and increase glucose utilization by peripheral cells. Hypoglycaemia not usually a problem. Also decr. LDL and VLDL and incr. HDL.
Distinguish between ischemic and hemorrhagic stroke
- Ischemic stroke
- Most common (80-85%)
- Narrowing or blockage or cerebral arteries –> tissue ischemia
- 2 main types:
* thrombotic: thrombus formation within a cerebral artery (including the arteries entering the brain)
* embolic: thrombus formed elsewhere becomes dislodged and lodges within a cerebral vessel. Most commonly the embolus originates from within the heart or large arteries)
- Both can be due to atherosclerosis; Lacunar infarcts: small cerebral vessels affected leading to small infarcted “spots” –> “hollows” out leaving small spaces in the brain - Hemorrhagic stroke
- Rupture of cerebral blood vessels resulting in bleeding and haematoma formation. The blood directly damages neural tissue and results in a lack of blood flow beyond the rupture site, leading to ischemia. Also incr. ICP
- 2 main types:
* Intracerebral haemorrhage: rupture of a cerebral vessel within the brain; assoc. w hypertension and aneurysms
* Subarachnoid haemorrhage: rupture of blood vessel within the subarachnoid space; assoc. w injury
Outline the risk factors for stroke
- Over 60
- Hypertension
- T2D
Also - Atrial fibrillation or other cardiac atrial disorders or valvular dysfunction
- Smoking
- Poor diet and activity
- Genetics
- High cholesterol
- Obesity
- Ischemic heart disease
- Obstructive sleep apnoea
Describe the pathophysiology of stroke, including common signs and symptoms
- occurs when there is cerebral infarction due to a significant reduction in, or lack of, blood flow to a part of the brain.
- Signs and symptoms
1. Numbness or weakness in the face, arm or leg.
2. Confusion, incl. trouble speaking or understanding speech
3. Trouble seeing, from one or both eyes
4. Dizziness
5. Headache, esp. a severe one that comes on suddenly
F.A.S.T.
*Face (drooping)
*Arms (asymmetry, weakness in one side)
*Speech (slurred, difficulty)
*Time: if you notice any of these signs, call 111 right away
Main treatment for the 2 types of stroke
- Ischemic: rTPA (tissue plasminogen activator), anticoagulants, clot removal
- Hemorrhagic: stop bleeding, then treatments to prevent further bleeding (depends on case)
