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BIOL2200 Objectives
BIOL2200 Objectives
Pathophysiology
1) Define the following initial concepts: Pathophysiology, signs and symptoms, diagnosis, hypoxia,
ischemia, thrombus, thrombosis, embolus, thromboembolism, atherosclerosis, hypoxemia.
2) Describe the five main tissue responses to stress: Atrophy, hypertrophy, hyperplasia,
metaplasia and dysplasia.
3) List some of the common causes of cell injury by physical, biological, chemical agents and
nutritional imbalances.
4) Explain the causes and cellular effects of three common mechanisms of cellular injury:
a) Hypoxia.
b) Free radical formation.
c) Failure of calcium homeostasis.
5) Describe the development and pathophysiological effects of hypoxia on cell function and the
corresponding changes in cell appearance observed.
6) Describe key differences between the two types of cell death: necrosis and apoptosis.
7) Describe the causes, locations and appearance of the following types of necrosis: coagulative,
liquefactive, caseous, gangrene and fat necrosis.
8) Outline two main categories of theory for the aging process (not required in depth).
9) Describe the cellular and chemical interactions that produce acute inflammation and be able to:
a) List the inflammatory cells involved.
b) List key chemical mediators.
c) Describe the sequence of cellular-chemical interactions that produce the:
i) Vascular response.
ii) Cellular response.
d) Describe observable tissue changes and explain the underlying causes, i.e.,
i) Redness.
ii) Heat.
iii) Swelling.
iv) Pain.
10) Describe the following four types of exudate and explain how these relate to the severity of
inflammation, the presence of infection and the state of wound healing.
1. Serous exudate.
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2. Fibrinous exudate.
3. Purulent exudate.
4. Hemorrhagic exudate.
11) Define chronic inflammation and outline its main causes and characteristics.
12) Describe the two main patterns of chronic inflammation, general (non-granulomatous) and
granulomatous.
13) Describe the sequence of cellular and chemical events in the three phases of wound healing:
1. Inflammatory.
2. Proliferative.
3. Contraction and remodeling.
14) Describe what meant by open and closed types of wounds and explain the terms clean incision,
healing by primary intension and by secondary intension.
15) Describe local problems of healing due to ischemia, blood clots, excessive fibrin, excessive
collagen, excessive wound contraction and wound disruption.
16) Describe common systemic problems of healing resulting from in particular inadequate
nutrition, diabetes mellitus, medications and age.
17) A “starting list” of more terms useful to know in pathophysiology and medicine (see module 1
slides for definitions): syndrome, local, systemic, acute, chronic, remission, exacerbation,
etiology, pathogenesis, prognosis, communicable disease, degenerative disease, idiopathic,
congenital, genetic.
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Module 3: Neoplasms
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o rupture
o infarction
10) Describe common general and systemic manifestations of cancer, regarding:
• Pain
• Fatigue and cachexia
• Anemia
• Leukopenia and thrombocytopenia
• Infection
• Gastrointestinal symptoms
• Skin reactions and hair loss
• Para-neoplastic syndromes
11) Outline commonly used diagnostic measures - such as lab tests, imaging techniques and staging-
grading tumours - in cancer detection and evaluation, including why and when a particular test
is carried out and its significance regarding potential outcomes and treatment.
12) Define tumour markers and describe their value in the diagnosis and evaluation of cancer.
13) Define carcinoma in-situ.
14) Describe the genetic and molecular basis for cancer, regarding:
• Gene mutations
• Proto-oncogenes and tumour suppressor genes
• The multistep hypothesis of carcinogenesis
• Defects in damaged repair genes
• Epigenetic silencing
15) Describe the stages of carcinogenesis
16) Outline the causative factors of cancer, including:
• Demography
• Heredity
• Immunological mechanisms
• Age
• Chemical carcinogens
• Low strength (solar) radiation high strength (nuclear) radiation
• Viral and bacterial infections
• Inflammation
17) Describe and outline the rationale of commonly used cancer treatments: chemotherapy,
radiation therapy and surgery.
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6) Describe folate anemia and how this relates to the macrocytic, normochromic appearance
of erythrocytes. Include the underlying causes, individuals at risk and clinical manifestations,
and why this is a serious risk factor in pregnancy.
7) Define polycythemia and differentiate the two etiologies: relative and absolute. Describe
two causes of absolute polycythemia.
9) Define leukocytosis and leucopenia, and outline common causes for each.
10) Define neutrophilia, neutropenia and agranulocytosis and outline common causes for each.
12) Describe the infective agent, transmission, pathophysiology and clinical manifestations of
infectious mononucleosis.
16) Define the type of cells that have become malignant in ALL, AML, CLL, CML.
17) Describe the characteristics (clinical manifestations), the evaluation and treatment of acute
leukemias, in general.
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18) Describe the characteristics (clinical manifestations), evaluation and treatment of chronic
leukemias, in general.
19) Determine:
a. which of the leukemias tend to be manifested in children / older individuals.
b. which of the leukemias can be sufficiently slow such that an individual may die of an
unrelated disease.
20) Explain the significance of the Philadelphia chromosome.
21) Define thrombocytopenia and describe its clinical manifestations and common causes.
23) Define primary and secondary thrombocytosis, their causes and clinical manifestations.
24) Define impaired platelet function: Outline three important causes for the acquired variety
and one type of inherited disorder.
25) Differentiate between inherited and acquired disorders of coagulation and give an example
of each.
26) Describe two causes of inappropriate coagulation and explain why this may lead to
uncontrolled bleeding.
27) Define and describe DIC and two major problems that it can cause.
28) Describe the etiology and underlying pathophysiology of DIC and circumstances that can
precipitate it.
29) Outline the main clinical manifestations of DIC and how can it be treated?
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3) Define angina pectoris and differentiate between stable angina and unstable angina,
including:
a) the differences in underlying pathology of each condition
b) the distinctive diagnostic clinical features of each condition regarding:
• the effect of short acting vasodilators such as glycerol trinitrate (GTN) on the signs
and symptoms.
5) Describe the ECG changes related to myocardial infarction and be able to distinguish
between STEMI and Non-STEMI ECG traces.
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6) Describe the changes in serum cardiac biomarkers in relation to myocardial infarction and
how these are used to differentiate MI from unstable angina from less severe forms of ACS
(i.e., unstable angina).
7) Describe the more general manifestations of ACS [in addition to 4 .II] and explain the
meaning of the term “silent MI”.
8) Define the following normal types of ECG: Sinus rhythm, tachycardia, bradycardia, sinus
arrhythmia.
9) Define the following types of ECG arrhythmias: Atrial fibrillation, heart block, ventricular
fibrillation, ST segment elevation, T-wave inversion, asystole.
10) Describe the purpose of cardio-pulmonary resuscitation (CPR) and defibrillation and identify
the context in which is appropriate to use each in regards to the ECG trace.
11) Identify the three main causes of death through myocardial infarction.
12) Describe the key aspects of care and their rationale during the immediate management of
ACS.
13) Define heart failure and list its main causes and common risk factors.
14) Describe the immediate compensatory effects of moderate heart failure, as in the case of a
myocardial infarction, including:
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• Pericarditis.
• Cardiogenic
• Hypovolemic
• Obstructive
30) Outline the specific and general principles in the treatment of shock.
1) Define Chronic Obstructive Pulmonary Disease (COPD) and name the two main underlying
pathological conditions: chronic bronchitis and emphysema.
2) Describe the development and underlying pathophysiology of chronic bronchitis.
3) Describe the development and underlying pathophysiology of emphysema.
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4) Describe the clinical manifestations of chronic bronchitis and emphysema and how to
differentiate the two conditions in diagnosis.
5) Outline principal modes of treatment for COPD.
6) Define or describe common signs and symptoms associated with respiratory disorders,
including: dyspnea, cough, abnormal sputum, hemoptysis, hyperventilation,
hypoventilation, cyanosis, pain, clubbing.
7) Explain why hypercapnia is usually an indication of hypoventilation rather than decreased
pulmonary perfusion.
8) Define hypoxemia and describe three defective mechanisms of oxygenation from which it
may result.
9) Explain what is meant by a “V/Q mismatch” and how low V/Q and high V/Q differ in terms
of their physiological causation.
10) Explain the concept “physiologic right to left shunt” in the context of V/Q mismatch..
11) Explain the concept of anatomical right to left shunting and describe one possible etiology
for this condition.
12) Define acute respiratory failure.
13) Outline common causes of acute respiratory failure.
14) Describe the ways in which a failure of ventilation differs from a failure in gas exchange
across the respiratory membrane, in terms of alterations of blood gasses and the type of
clinical intervention (treatment) required.
15) Define the following disorders of the chest wall and pleura: Flail chest, pneumothorax,
pleural effusion, empyema.
16) Define the following restrictive lung disorders: Atelectasis, bronchiectasis, pulmonary
edema.
17) Describe how the underlying pathophysiology of pulmonary edema can lead to a reduction
in the rate of oxygen diffusion into the blood resulting in hypoxemia.
18) Define acute respiratory distress syndrome (ARDS) and list its common causes.
19) Describe the pathogenesis of ARDS and how this results in damage to alveoli leading to
hypoxemia, including:
• the role of inflammatory cells and chemical mediators in the early stages
• fibrosis of the alveoli as inflammation progresses
20) Describe the effect ARDS has on lung function and treatment goals in its early stage
management.
21) Define pulmonary embolism (PE) and outline the origin and progress of a thrombolytic
embolism from a deep vein.
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Pathophysiology
1) Define gastroesophageal reflux disease (GERD) and describe its underlying causes, signs and
symptoms.
2) Describe peptic ulcer disease, outline its risk factors, and differentiate between gastric ulcer
and duodenal ulcer regarding location and clinical manifestations.
3) Describe the pathophysiology of peptic ulcers, including the two most common causes:
NSAIDs (non-steroidal anti-inflammatory drugs) and Helicobacter pylori infection.
4) Outline the main treatment options for peptic ulcer.
5) Define inflammatory bowel disease and describe and differentiate between the two forms:
Crohn’s Disease and ulcerative colitis, including:
• regions of the bowel affected and the nature of the inflammatory process
• the gross and histological appearance of the inflamed tissues
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1) Define prediabetes and outline how insulin imbalances may arise that produce this
condition.
2) Define the three key clinical manifestations of diabetes mellitus – the “three Ps”.
3) Define type 1 diabetes and describe the pathogenesis of the disease.
4) Describe the clinical manifestations of type 1 diabetes, including laboratory tests used to
confirm the diagnosis.
5) Define type 2 diabetes, outline its risk factors and describe its pathogenesis.
6) Define insulin resistance, and explain the mechanisms related to obesity that underlie its
development.
7) Describe the clinical manifestations of type 2 diabetes, including diagnostic laboratory tests.
8) Define metabolic syndrome.
9) Describe the following five acute complications of diabetes mellitus, including underlying
causation, clinical manifestations and treatment (if appropriate).
• Hypoglycemia
• Diabetic ketoacidosis
• Somogii effect
• Dawn phenomenon
• Hyperosmolar hypoglycemic state
10) Describe the following chronic complications of diabetes mellitus, including the underlying
pathological effects of chronic hyperglycemia and its clinical manifestations:
• Diabetic retinopathy
• Diabetic nephropathy
• Diabetic neuropathy
• Infection
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15) Define SIADH (syndrome of inappropriate antidiuretic hormone secretion) and outline its
most common causes and clinical manifestations.
16) Describe hypopituitarism of the anterior pituitary, its general causes and common
manifestations.
17) Define hypothyroidism and describe its common primary and secondary pathophysiological
causes and typical clinical manifestations.
18) Define hyperthyroidism and describe its common primary and secondary pathophysiological
causes and typical clinical manifestations.
19) Define Grave’s disease and Hashimoto’s disease.
20) Define adrenal cortical insufficiency and describe its common primary and secondary
pathophysiological causes and typical clinical manifestations.
21) Define Addison’s disease.
22) Define hyperthyroidism and describe its common primary and secondary pathophysiological
causes and typical clinical manifestations.
23) Describe the three main forms of glucocorticoid hormone excess, its clinical manifestations,
and differentiate between Cushing’s disease and Cushing syndrome.
1) List the three main mechanisms of cerebrovascular disease and define the term “stroke” or
“brain attack”.
2) What immediate important effects does a stoke have on brain tissue.
3) Describe and differentiate between an ischemic stroke, a cardiogenic stroke and a
hemorrhagic stroke including:
• underlying pathophysiology
• clinical manifestations
4) Explain why hemorrhagic stokes may be especially serious, including effects resulting from
large bleeds on the brain as a whole.
5) List the most frequent sites of arterial and cardiac abnormalities causing ischemic strokes
and differentiate between large vessel and small vessel ischemic strokes in terms of the
regions of the brain usually affected and the clinical manifestations produces.
6) List the common risk factors and long term deficits of stroke.
7) Describe transient ischemic attack (TIA), including its typical diagnostic signs and symptoms
and what it may be a risk factor for.
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• how changes in ICP affects cerebral perfusion (blood flow in the brain)
• what is meant by “compensatory mechanisms”
• mental status: i.e., behavior and levels of consciousness
• blood pressure, heart rate, respiration and body temperature
• pupil size and response to light
• brain herniation
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25) Describe the three characteristics alterations in motor function that may arise from
disruptions in the nervous system:
1) Define urinary tract obstructions and outline the common causes and sites of obstruction.
2) State the two most damaging effects of urinary tract obstruction and outline their
pathogenesis.
3) Describe renal calculi, including the risk factors or conditions that may predispose to their
formation, their clinical manifestations, diagnosis and treatment.
4) Describe how lower urinary tract obstructions - neurogenic bladder, enlarged prostrate and
urethral scaring - may alter the storage and emptying of urine.
5) Define glomerulonephritis and describe the pathophysiology of two of its common causes:
acute post-infectious glomerulonephritis and Goodpasture syndrome.
6) Describe and contrast nephritic syndrome with nephrotic syndrome.
7) Describe the pathophysiology of nephrotic syndrome, in particular the reasons why this
typically manifests in systemic edema and hyperlipidemia.
8) Define acute renal failure (a.k.a. acute kidney failure) and how this may manifest clinically.
9) Explain the RIFLE classification of acute renal failure and be able to estimate the GFR and
urine output for risk or injury categories in a patient of known body weight.
10) Define plasma creatinine concentration and blood urea nitrogen (BUN) and how these
reflect alterations in kidney function.
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11) Define and describe the three categories of causes of acute renal failure, their common
causes and treatment goals.
12) Define chronic kidney disease (CKD) and what this represents in terms of kidney function
and the risk factors associated with its development.
13) Define the intact nephron hypothesis and explain why symptoms for CKD are not apparent
until only 25% or less functional nephrons remain.
14) Describe potential clinical manifestations of CKD and how each relates to alterations in
kidney function.
15) Describe the pathophysiological effects CKD has on the following body systems:
hematologic, cardiovascular, pulmonary, immune, neurologic, gastrointestinal, endocrine
and reproductive.
16) Outline the evaluation and treatment of CKD.
17) Describe the importance and regulation of sodium balance in the body.
18) Define hypernatremia and describe its causes, pathophysiological effects and clinical
manifestations.
19) Define hyponatremia and describe its causes, pathophysiological effects and clinical
manifestations.
20) Define hyperkalemia and describe its causes, pathophysiological effects and clinical
manifestations.
21) Describe the underlying mechanism where by metabolic acidosis may produce
hyperkalemia.
22) Define hypokalemia and describe its causes, pathophysiological effects and clinical
manifestations.
23) Define hypercalcemia and describe its pathophysiological effects and clinical manifestations.
24) Define hypocalcaemia and describe its pathophysiological effects and clinical
manifestations.
25) Explain the mechanism by which hypocalcaemia increases excitability in muscle and nerve.
26) Define hypermagnesemia and describe its pathophysiological effects and clinical
manifestations.
27) Define hypomagnesemia and describe its pathophysiological effects and clinical
manifestations.
28) Describe how the three compensatory mechanisms – chemical buffers, the pulmonary and
renal systems - manage changes in arterial blood pH in order to maintain homeostatic
equilibrium.
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29) Describe the four categories of acid-base disturbances, including their common causes and
clinical manifestations.
30) List the normal range values for arterial blood pH, PaCO2, HCO3-, PaO2 and O2 saturation.
31) Define the terms compensation, partial compensation, and fully compensated in relation to
acid-base disturbances.
32) Explain the concept of primary acid-base disturbance and how this is reflected by changes in
bicarbonate and carbon dioxide for metabolic vs. respiratory acidosis and alkalosis.
33) List the primary acid-base disturbances in terms of changes in PCO2 and bicarbonate.
34) Be able to interpret from arterial pH and blood gas results (PaCO2, HCO3-, PaO2) whether a
primary acid-base disturbance is: metabolic acidosis, metabolic alkalosis, respiratory
acidosis or respiratory alkalosis.
35) Explain how the concept of anion gap in metabolic acidosis is used determine the
underlying cause of the disturbance, i.e., increased metabolic acids vs. a pathological loss of
bicarbonate ions.
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• Exogenous osteomyelitis
• Hematogenous osteomyelitis
15) What is the primary causative organism for osteomyelitis?
16) Describe the pathogenesis of hematogenous osteomyelitis in children and how this
condition differs in adults.
17) Outline the clinical manifestations of osteomyelitis.
18) Define osteoarthritis, outline its primary and secondary causes, and describe where the
condition usually occurs in the body.
19) Describe the pathological changes that occur to joints during the development of
osteoarthritis.
20) Describe the clinical manifestations of osteoarthritis, including the causes of joint
enlargement and how this affects joint function.
21) Define rheumatoid arthritis and outline how it differs in etiology from osteoarthritis.
22) Describe the underlying pathogenesis of rheumatoid arthritis, the role played by the
immune system and the significance of rheumatoid factor.
23) Describe the pathogenesis of joint destruction in rheumatoid arthritis, including the
inflammatory processes involved.
24) Define pannus and describe its role in the process of joint destruction of rheumatoid
arthritis.
25) Outline the clinical manifestations of rheumatoid arthritis, and compare and contrast the
condition with that of osteoarthritis.
26) Define ankylosing spondylitis, including how it is manifested and probable underlying
pathogenesis.
27) Define equinovarus, including how it is manifested and probable causation.
28) Define dysplasia of the hip, including how it is manifested and probable causation.
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3) Define dysfunctional uttering bleeding (DUB) and describe its underlying causation and
manifestations in relation to anovulatory cycles.
4) Define retrograde mensuration.
5) Define endometriosis, including its possible etiology and manifestations.
6) Describe cervical cancer, including its cause, associated risk factors and detection.
7) Describe endometrial cancer, including its incidence and associated risk factors.
8) Describe ovarian cancer, including its incidence and prognosis, associated risk factors and
detection.
9) Define the following terms in relation to breast disorders: galactorrhoea, mastitis, ductal
disorders, intraductal papillomas.
10) Regarding benign breast tumours, outline the terms fibrodenoma and “fibrocystic changes”,
including appearance, age occurrence, and manifestation.
11) Outline the incidence, pathogenesis and initial manifestation breast cancer.
12) Describe six risk factors associated with breast cancer.
13) Regarding disorders of the male reproductive system, define the following terms:
cryptorchidism, hydrocele, varicocele.
14) Describe torsion of the testis, including its common causes, manifestation and treatment.
15) Describe “benign prostatic hyperplasia” (BPH) including its incidence and manifestation.
16) Describe cancer of the prostate gland, including risk factors, detection, location and
manifestations.
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