Exam (specific) Flashcards
1
Q
Mary: Risk factors for COPD
A
- Smoking
- Environment: air pollutants and/or occupational irritants
- History of resp. infections during childhood and/or family history of COPD
- alpha1 antitrypsin deficiency
2
Q
Mary: Signs and symptoms of emphysema
A
- incr. residual vol.
- Incr. WOB/laboured breathing
- SOB/SOB on exertion
- Dyspnoea (nostril flaring, incr. use of accessory mm)
- productive cough
(barrel-shaped chest, hyperinflation of lungs) - Hyperventilation
- Incr. RR
- Finger clubbing
3
Q
Mary:
Patho of emphysema: initiation + development
A
- Enlargement of gas exchange airways + alveolar wall destruction
- due to exposure to irritants or a1-antitrypsine deficiency - Inflammation, oxidative stress, incr. proteases, and decr. antiproteases
- Incr. alveolar tissue destruction (alveolar walls, septa, capillaries), decr. tissue repair, breakdown of elastic fibers
- Alveolar space enlargement –> decr. SA for gas exchange
Decr. elastin –> decr. recoil/radial traction - Air trapping (related to collapse of the small bronchioles during early expiration and the lack of recoil) and decr. gas exchange
- Expiration becomes more difficult + hyperinflation occurs
–> pursed lip expiration, prolonged expiration
–> incr. ventilation rate - Eventually hypoventilation occurs
–> hypoxemia + hypercapnia
4
Q
Mary:
Patho of emphysema: systemic implications of air trapping/decr. gas exchange
A
- Hypoxemia –> incr. anaerobic respiration –> incr. lactic acid –> metabolic acidosis
Hypercapnia –> respiratory acidosis - Tissue ischemia and hypoxia
- Pulmonary hypoxia –> vasoconstriction –> pulmonary hypertension + incr. pulmonary vascular resistance (PVR)
- Right side heart failure - cor pulmonale (bc it has to work harder)
- Atelectasis (alveolar collapse)
5
Q
Mary: Differences in patho bw chronic bronchitis and emphysema and asthma
A
Emphysema:
- alveolar membrane (and capillary) destruction –> V/Q (ventilation/blood flow) matched initially –> decr. gas exchange
- loss of elastin
- Compromised exhalation; pursed lip breathing
Chronic bronchitis:
- inflammation of the bronchioles w mucus hypersecretion (acute is usually due to infection) –> incr. airway resistance –> V/Q mismatch bc not enough air coming into alveolar spaces –> decr. gas exchange
- clogging up of airways w mucus
- Chronic cough
Asthma:
- inflamed and narrow bronchiolar smooth muscle
6
Q
Mary: What drugs was Mary prescribed and what do they do?
A
- Supplementary oxygen: decr. dyspnoea, prevent hypoxia, aid brochodilation
- Sympathomimetics (beta agonists)(inhalers/relievers): e.g. salbutamol (short-acting), salmeterol (long acting). Dilation. Act on receptors on bronchiole smooth muscle to open the airways.
- Corticosteroids: e.g. hydrocortisone, prednisone. Decr. inflammatory response
- Anticholinergics: e.g. Ipratropium. block mACh receptors on bronchiole smooth muscle to cause broncodilation
7
Q
Mary: Describe the tests/evaluations used in COPD
A
- Peak expiratory flow (PEF): measures how quickly you can exhale
- Forced expiratory volume (FEV): tests how much air you can exhale in 1sec
Also - Arterial blood gases and pH: checks O2 status and acid balance
- Pulse oximetry: estimates O2 content in arterial blood
- Body plethysmography: measures thoracic vol. and airway resistance
- Diffusing capacity: tests O2 transfer from the alveoli to circulation
- Sputum sample: diagnoses bacterial lung infection
- Chest X-ray
8
Q
Mike: Signs and symptoms of MI
A
- Nausea/vomiting
- Severe, sudden onset of pain (prolonged, not responsive to rest or medications)
- Feeling of impending doom
- Tightness/restriction/discomfort in chest
- Pallor or cool peripheries
- Sweating
- ECG changes
- Elevated cardiac enzymes (CK or CPK, CK-MB, troponin I & T)
9
Q
Mike: Risk factors for Myocardial Infarction
A
- smoking
- Obesity
- Incr. age
- Diet (hypercholesteremia/hyperlipidemia)
- Family history
- Diabetes
- Physical inactivity
- Sex (male is incr.)
- Cardiovascular conditions
○ Atherosclerosis
○ Hypertension
10
Q
Mike
Pathophysiology of MI: initial cascade, tissues directly affected
A
- Blockage of coronary arteries
- Myocardial ischemia and hypoxia
- Myocardial necrosis
Subendocardial: only the myocardium just below the endocardium
Transmural: full thickness of myocardium (caused by permanent blockage) - Myocardial cells breakdown (sarcolemma) and coagulation
- Leakage of cardiac enzymes (contractile proteins) from the cells (particularly troponin, which is used to indicate MI by testing levels in the blood)
- Ventricular dysfunction –> inadequate supply to the body
11
Q
Mike:
Pathophysiology of MI: effects on surrounding tissue (i.e. not starved of O2)
A
- Myocardial stunning: myocytes temporarily lose contractility
- Myocardial hibernation: myocytes preserve themselves by stopping their contractility (decr. Energy needs) in the hopes to regain ability later on
- Myocardial remodeling: remodeled to not be able to contract in order to preserve themselves
12
Q
Mike: Complications of MI
A
Necrotic tissue replaced w fibrous tissue (not contractile) which causes: ○ Arrythmias ○ Ventricular fibrillation ○ Ventricular failure ○ Valvular incompetence ○ Aneurysm ○ Pericarditis
13
Q
Mike: Describe tests/evaluations for MI
A
- ECG
- Measures the electroactivity of the heart using voltage over time
- reflects origin of heartbeat and conduction of electrical impulse
- Must be performed during an episode of angina
- Transient ST segment depression and T wave inversion are characteristic signs of subendocardial ischemia; ST elevation indicates transmural ischemia
- Used to: detect abnormal heart rhythms; detect heart problems; monitor recovery from a heart attack - Angiogram
- assesses whether there is damage to the arteries that supply the heart since impaired blood flow to the heart muscles can be a primary cause of chest pain.
- inject a contrast agent into the bloodstream, which makes the blood vessels surrounding the heart visible on an x-ray. - GCS
- used to describe the level of consciousness in a person
- used to help gauge the severity of an acute brain injury. - Other tests:
- FBC, BG, electrolytes, cardiac enzymes (troponin T: contractile protein that is only released when myocardial necrosis occurs, measure 10-12hrs after onset of symptoms, ref range is 0-0.03; early marker = myoglobin), thyroid function tests
14
Q
Mike: Management of MI
immediate treatment + those prescribed upon discharge
A
Main goals:
- decr. heart workload
- Incr. O2
- Reperfusion
Immediate management:
- Oxygen (if O2% less than 92)
- Aspirin
- Nitroglycerine (resolves chest pain by relaxing vascular smooth-muscle beds. Works well on coronary arteries, improving blood flow to ischemic areas)
- Morphine (additional pain relief if GTN doesn’t work. Also a venodilator, reducing ventricular preload and cardiac oxygen requirements)
Discharge meds:
○ Aspirin (anticoagulant, prevents clots)
○ Statins (decrease cholesterol synthesis in the liver)
○ Beta blockers/metoprolol (decr. BP, CO, HR/hypertension)
○ GTN (vasodilation and reduces preload and afterload, resulting in decreased cardiac workload)
○ Clopidogrel (anticoagulant, platelet aggregate inhibitor)
15
Q
Barry: Risk factors for stroke
A
Hypertension Diabetes Incr. age smoking, alcohol and drugs poor diet (hyperlipidemia/hypercholesterolemia) obesity physical inactivity sex atherosclerosis thromboembolism family history/genetics
