Exam (specific)

Question 1

Mary: Risk factors for COPD

Answer 1

1. Smoking
2. Environment: air pollutants and/or occupational irritants
3. History of resp. infections during childhood and/or family history of COPD
4. alpha1 antitrypsin deficiency

Question 2

Mary: Signs and symptoms of emphysema

Answer 2

• 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

Question 3

Mary:

Patho of emphysema: initiation + development

Answer 3

1. Enlargement of gas exchange airways + alveolar wall destruction
   - due to exposure to irritants or a1-antitrypsine deficiency
2. Inflammation, oxidative stress, incr. proteases, and decr. antiproteases
3. Incr. alveolar tissue destruction (alveolar walls, septa, capillaries), decr. tissue repair, breakdown of elastic fibers
4. Alveolar space enlargement –> decr. SA for gas exchange
   Decr. elastin –> decr. recoil/radial traction
5. Air trapping (related to collapse of the small bronchioles during early expiration and the lack of recoil) and decr. gas exchange
6. Expiration becomes more difficult + hyperinflation occurs
   –> pursed lip expiration, prolonged expiration
   –> incr. ventilation rate
7. Eventually hypoventilation occurs
   –> hypoxemia + hypercapnia

Question 4

Mary:

Patho of emphysema: systemic implications of air trapping/decr. gas exchange

Answer 4

1. Hypoxemia –> incr. anaerobic respiration –> incr. lactic acid –> metabolic acidosis
   Hypercapnia –> respiratory acidosis
2. Tissue ischemia and hypoxia
3. Pulmonary hypoxia –> vasoconstriction –> pulmonary hypertension + incr. pulmonary vascular resistance (PVR)
4. Right side heart failure - cor pulmonale (bc it has to work harder)
5. Atelectasis (alveolar collapse)

Question 5

Mary: Differences in patho bw chronic bronchitis and emphysema and asthma

Answer 5

Emphysema:

1. alveolar membrane (and capillary) destruction –> V/Q (ventilation/blood flow) matched initially –> decr. gas exchange
2. loss of elastin
3. Compromised exhalation; pursed lip breathing

Chronic bronchitis:

1. 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
2. clogging up of airways w mucus
3. Chronic cough

Asthma:
- inflamed and narrow bronchiolar smooth muscle

Question 6

Mary: What drugs was Mary prescribed and what do they do?

Answer 6

• 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

Question 7

Mary: Describe the tests/evaluations used in COPD

Answer 7

1. Peak expiratory flow (PEF): measures how quickly you can exhale
2. Forced expiratory volume (FEV): tests how much air you can exhale in 1sec
   Also
3. Arterial blood gases and pH: checks O2 status and acid balance
4. Pulse oximetry: estimates O2 content in arterial blood
5. Body plethysmography: measures thoracic vol. and airway resistance
6. Diffusing capacity: tests O2 transfer from the alveoli to circulation
7. Sputum sample: diagnoses bacterial lung infection
8. Chest X-ray

Question 8

Mike: Signs and symptoms of MI

Answer 8

• 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)

Question 9

Mike: Risk factors for Myocardial Infarction

Answer 9

• smoking
• Obesity
• Incr. age
• Diet (hypercholesteremia/hyperlipidemia)
• Family history
• Diabetes
• Physical inactivity
• Sex (male is incr.)
• Cardiovascular conditions
  ○ Atherosclerosis
  ○ Hypertension

Question 10

Mike

Pathophysiology of MI: initial cascade, tissues directly affected

Answer 10

1. Blockage of coronary arteries
2. Myocardial ischemia and hypoxia
3. Myocardial necrosis
   Subendocardial: only the myocardium just below the endocardium
   Transmural: full thickness of myocardium (caused by permanent blockage)
4. Myocardial cells breakdown (sarcolemma) and coagulation
5. Leakage of cardiac enzymes (contractile proteins) from the cells (particularly troponin, which is used to indicate MI by testing levels in the blood)
6. Ventricular dysfunction –> inadequate supply to the body

Question 11

Mike:

Pathophysiology of MI: effects on surrounding tissue (i.e. not starved of O2)

Answer 11

• 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

Question 12

Mike: Complications of MI

Answer 12

Necrotic tissue replaced w fibrous tissue (not contractile) which causes:
○ Arrythmias 
○ Ventricular fibrillation
○ Ventricular failure 
○ Valvular incompetence
○ Aneurysm
○ Pericarditis

Question 13

Mike: Describe tests/evaluations for MI

Answer 13

1. 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
2. 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.
3. GCS
   - used to describe the level of consciousness in a person
   - used to help gauge the severity of an acute brain injury.
4. 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

Question 14

Mike: Management of MI

immediate treatment + those prescribed upon discharge

Answer 14

Main goals:

1. decr. heart workload
2. Incr. O2
3. Reperfusion

Immediate management:

1. Oxygen (if O2% less than 92)
2. Aspirin
3. Nitroglycerine (resolves chest pain by relaxing vascular smooth-muscle beds. Works well on coronary arteries, improving blood flow to ischemic areas)
4. 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)

Question 15

Barry: Risk factors for stroke

Answer 15

Hypertension
Diabetes
Incr. age
smoking, alcohol and drugs
poor diet (hyperlipidemia/hypercholesterolemia)
obesity
physical inactivity
sex
atherosclerosis
thromboembolism
family history/genetics

Question 16

Barry:

Signs and symptoms of stroke

Answer 16

Facial droop
Arm weakness
Slurred speech/difficulty

Question 17

Barry: Pathophysiology of ischemic stroke, incl. atherosclerosis

Answer 17

• blockage in a cerebral blood vessel, resulting in ischemia and hypoxia of a part of the brain –> neural tissue necrosis and dysfunction.
  2 types:
  1. Thrombotic
• thrombus formation within the cerebral artery/ies supplying blood to the brain. Usually due to plaque formation (most commonly atherosclerosis).
  2. Embolic
• thrombus formed elsewhere (usually heart), dislodges then becomes lodged in brain

Atherosclerosis:
1. Endothelial injury + inflammation
2. LDL enters endothelium (+ cytokine release)
3. Foam cell production (as macrophages engulf LDL molecules) + accumulation in endothelium
4. Fatty streak formation
5. Smooth muscle cell proliferation and migration into plaque
6. Collagen produced over plaque to form a fibrous plaque
7. Plaque either
(A) decreases BV diameter –> ischemia
(B) rupture, leaving underlying tissue exposed to lumen, causing platelet adhesion + coagulation initiation, forming thrombus which leads to occlusion (ischemia + infarction)

Question 18

Barry: Difference bw ischemic and hemorrhagic stroke

Answer 18

1. Ischemic
   - blocked cerebral artery –> ischemia
2. Hemorrhagic
   - breakage of cerebral blood vessel, resulting in bleeding.

Question 19

Barry: patho of plaque formation and atherosclerosis

Answer 19

1. Injured endothelium becomes inflamed
2. Cytokines further injure endothelium
3. Smooth muscles grows and cells migrate into plaque forming fibrous plaque over fatty streak
4. Growing plaque decr. blood vessel diameter –> ischemia/limited perfusion
5. Plaques may rupture, exposing underlying tissue to lumen of vessel –> platelet adhesion and coagulation –> thrombus formation
   - thrombus occludes artery –> ischemia and infarction

Question 20

Barry: describe the GCS

• 3 components
• how it’s scored
• what the score means in terms of injury

Answer 20

Score bw 3-15 (contextual)
○ Eye Opening
- Spontaneous (4)
- Verbal/sound (3)
- Pain/pressure (2)
- None (1)
○ Verbal response
- Orientated (5)
- Confused (4)
- Words (3)
- Sounds (2)
- None (1)
○ Motor response 
- Obeys command (6)
- Localized (5) e.g. in the general area of the stimulus
- Normal flexion (4) e.g. towards the stimulus
- Abnormal flexion (3) e.g. away from the stimulus
- Extension (2)
- None (1)

Severity of TBI
Mild: 13-15
Moderate: 9-12
Severe: 3-8

Question 21

Barry: Outline the other neurological exams (apart from the GCS) that were done for Barry

Answer 21

○ Visual field (peripheral vision): measuring when he could see the pen from his right side. Took a while, had to be in the center of his eye
○ Facial movement: significant weakness/limited movement on the right side of his face. Visible drooping
○ Facial sensation: limited sensation in the right side of his face
○ Corneal reflex: did NOT exhibit a corneal reflex with his right eye.
○ Leg movement: could lift both his right and left legs, though there was apparent weakness in his right leg.
○ Arm movement: significant weakness is his right arm and was unable to lift it.

Question 22

Barry: treatments for stroke

For rtPA:

• what it is
• what it does/MOA
• when it’s used
• risks
• contraindications

Answer 22

1. Anti-Coagulants (e.g. aspirin, heparin, warfarin)
2. Antihypertensives (e.g. metoprolol, cilazapril, Clonodine, Frusemide)
3. Reperfusion: rtPA - fibrinolytic
   ○ tissue plasminogen activator, an enzyme
   ○ turns plasminogen into plasmin, which breaks down fibrin (blood clots); reverses any coagulation
   ○ used asap to treat an acute ISCHEMIC stroke, NOT a hemorrhagic stroke
   ○ Uncontrollable bleeding and fatality
   ○ recent major surgery, myocardial infarction, stroke, or other internal injuries, pre-existing coagulation/bleeding disorder, significant hypertension, any other bleeding risks

Question 23

Ben: Type 1 vs type 2 diabetes

Answer 23

○ Type 1: no effective insulin production; autoimmune destruction of pancreatic beta cells
○ Type 2: insulin resistance + some decr. Insulin production

Question 24

Ben: risk factors for T2 diabetes

Answer 24

• Obesity!!
• Pancreatitis
• Smoking
• Family history
• Gestational diabetes mellitus
• Poor diet + inactivity
• Sedentary lifestyle
• hypercholesteremia or hyperlipidemia

Question 25

Ben: signs and symptoms of T2 diabetes

Answer 25

- Hyperglycaemia!! - Polyuria - Polydipsia - Glycosuria - Recurrent infections/incr. susceptibility to infections - Poor wound healing - (Any signs and symptoms of) visual disturbances - (Any signs and symptoms of) autonomic neuropathy - (Any signs and symptoms of) peripheral neuropathy

Question 26

Ben: patho of T2 diabetes (2 mechanisms)

Answer 26

Hyperglycemia: 1. Glycosylation: glucose deposited in basement membrane of (i) blood vessels: decr. vascular gas, nutrient and waste exchange --> localised hypoxia + tissue damage; altered inflammatory responses (decr. mvement WBCs) --> poor wound healing + incr. susceptibility to infections; damage to vessel walls --> retinopathy (ii) nerves: decreases efficient AP conduction --> autonomic and peripheral neuropathies 2. Excess glucose in blood filtered by kidneys: glucose transporters become saturated --> some glucose remains in filtrate --> glycosuria. Osmotic gradient draws water into filtrate --> polyuria. Incr. renal water loss incr. osmolarity (dehydration) --> polydipsia 3. Lack of cellular glucose availability (Decr. glucose into cells) --> cellular 'starvation' signals hunger center (polyphagia) --> Incr. gluconeogenesis (catabolism of proteins and fats for ATP generation) (weight loss) and increased lipolysis and reliance on fatty acids for ATP generation --> Incr. production of (acidic) ketone bodies (--> ketoacidosis) + incr. lipid levels in blood (--> incr. likelihood of atherosclerosis)

Question 27

Ben: Complications - patho and impact. 1. Retinopathy 2. Nephropathy 3. Autonomic neuropathy 4. Peripheral neuropathy 5. Diabetic feet

Answer 27

1. Retinopathy - Macular oedema: fluid leaks into the part of the retina responsible for sharp, straight-ahead vision causing swelling and blurred vision - can occur when blood vessels, particularly capillaries, in the eye are damaged, resulting in leakage which then leads to swelling of the macula - glycosylation of blood vessels decreases gas, nutrient and waste exchange leading to localised damage. The retinal blood vessels are very delicate and are therefore susceptible to damage. 2. Nephropathy - Microvascular damage to glomeruli of the kidneys, leading to kidney disease - Ben is not experiencing any symptoms of renal disease atm 3. Autonomic neuropathy - Glycosylation on the basement membrane of neurons disrupts normal AP conduction. Can affect a variety of functions. - E.g. GI problems (gastroparesis [--> bloating], diarrhoea, vomiting), erectile dysfunction (PNS), postural hypotension. 4. Peripheral neuropathy - glycosylation affects action potential conduction in somatosensory neurons in the hands and feet. - sensory loss, including increased susceptibility to tissue damage, decreased wound healing and infection through a lack of sensory awareness E.g. recurring cellulitis, loss of sensation, issues w feet. 5. Diabetic feet - related to neuropathy (main one for Ben) and/or vascular complications

Question 28

Ben: describe the tests/evaluations that would be done

Answer 28

1. HbA1C - Measures glycosylated haemoglobin. - Haemoglobin accumulates glucose over the lifetime of a RBC (2-3months) depending on how much glucose is in the blood. - So the HbA1C test gives an indication of the average plasma glucose concentration over the previous 3 months by measuring the amount of glucose accumulated on RBCs. - Normal range: 20-42mmol/L is ideal, but aim for mid 50s and below

Question 29

Ben: management/treatment

Answer 29

1. Lifestyle changes: healthy diet, weight loss, incr. exercise, eliminate/reduce other risk factors (e.g. smoking) If that fails: 2. Oral hypoglycaemic drugs (sulphonylurea class) - reduce blood glucose - stimulate basal insulin secretion by the pancreas, so must have functioning beta cells 3. Injectable insulin - Usually only if lifestyle changes and oral hypoglycemics not effective - Humalog (short acting), use as necessary - Humulin NPH (long acting)

Question 30

Aspirin Mechanism of action - specific, general effect, side effects some of the relevant pharmacokinetic parameters eg half-life, bioavailability.

Answer 30

aspirin has antiplatelet action by binding irreversibly to the COX1 and COX 2 enzymes. This results in the COX 1 pathway activation where the effects include antiplatelet aggregation. It also contributes to some unwanted effects on this pathway such as removal of GI protection which can result in the gastric side effects including ulcer ad GI bleeding. Half life of aspirin CR is ~3-4 hours. Main side effects are GI and bruising/bleeding.

Question 31

Barry: parts of brain affected and associated complications

Answer 31

occlusions of the: - left middle cerebral artery - left posterior cerebral artery - left posterior inferior cerebellar artery affecting: - left temporoparietal area (parietal: temperature, taste, touch and movement) - left occipital lobe (primarily responsible for vision) - bilateral cerebellar infarcts (cerebellum coordinates and adjusts movement, controls reflexes, balance, and certain aspects of movement and coordination, does not initiate movement) - part of the right midbrain (visual and auditory information, temperature regulation, wakefulness) 1. Dysphagia (swallowing) 2. Aphasia/dysarthia (speech disorders) - left side of the brain is involved in speech and language. // Cranial nerve damage to some/all of V, VII, IX, X and XII bc they control muscles of speech 3. R) sided hemiparesis - bc left hemisphere stroke 4. Visual disturbances: Homonymous hemianopia (loss of half of each eye’s visual field) - relates to the infarcts in Barry's left occipital lobe; and prior visual coordination and balance problems bc infarcts in Barry's cerebellum 5. Depression 6. Fatigue