Final Flashcards
1
Q
Distinguish between the 3 names that a drug might have
A
- Chemical name (based on structure)
- Generic name (shortened chemical name)
- Brand/trade name (given by pharmaceutical companies)
2
Q
Define what is meant by drug ‘Dose’
A
the precise amount of active ingredient in the medication
3
Q
What are the 3 phases of drug action
A
- Pharmaceutical
- Pharmacokinetic
- Pharmacodynamic
4
Q
Describe the pharmaceutical phase
A
how the drug processes from the administered
- Enteral: Oral/sublingual/rectal
- Parenteral: injections/inhalation/transdermal
5
Q
Describe the Pharmacokinetic phase
A
what the body does to the drug
1. absorption: passive diffusion vs. active transport vs. pinocytosis (administered route: IV most effective/oral goes through GI tract)
2. distribution: factors include [] absorbed, blood flow to tissue, % drug bound to plasma
3. metabolism: in the liver (inactivation of enzymes and prep for excretion), determines 1/2 life of drug
4. elimination: in the kidneys, sweat, bile, urine, etc.
6
Q
describe the pharmacodynamic phase
A
what the drug does to the body
- therapeutic action: stimulation/inhibition of function (therapeutic index)
- indications: approved use (off-label use, contraindication, side effect, adverse effect)
- potency and efficacy
7
Q
types of therapeutic action
A
- indications: approved use
- off-label use: not primary use
- contraindication: when shouldn’t be taken
- side effects: unwanted actions
- adverse effects: serious side effects (ex. allergic reaction, interactions)
8
Q
define the therapeutic index
A
- ratio of toxic dose and minimum effective dose
9
Q
Draw a graph of drug concentration vs time, and explain how this reflects the pharmacokinetics of
the drug
A
the half life shows the time it takes for half the drug concentration to be metabolized
- allows us to maintain therapeutic effect safely without toxicity (therapeutic index)
10
Q
Draw a graph of drug effect vs dose, and explain how this reflects the pharmacodynamics of the
drug.
A
- potency (x axis): the strength of a drug at a particular dose (the concentration needed to produce 50% of maximum effect)
- efficacy (y axis): the maximum effect that can be achieved by a drug (reflects the effect of the drug on the receptor once bound)
11
Q
Define and compare the different sources of pain: Nociceptive (and types) vs. Neuropathic Pain
A
- nociceptive pain: comes from an identifiable issue causing tissue damage
- somatic pain: within skin or deeper (well localized), somatosensory nerves detect the pain
- visceral pain: within or around organs (poorly localized), SNS fibres detect pain - neuropathic pain: caused by dysfunction of the NS, no identifiable tissue damage (poor/well localized, pain perceived without stimulus)
12
Q
describe acute pain (rate of occurance, where it arises from, type of fibre, duration, repsonse, treatment)
A
- warning, fast and localized
- comes from injury, mechanical or thermal
- Fast A-delta myelinated fibres
- sudden and short term
- causes stress response
- easy to treat
13
Q
describe chronic pain (rate of occurance, where it arises from, type of fibre, duration, repsonse, treatment)
A
- slow, diffused, prolonged
- comes from existing or chemical response
- slow unmyelinated C fibres
- long term, disabling, fatigue
- difficult to treat
- lasts more than 3 months
- issue of nerve hypersensitivity
- localized within CNS
14
Q
Describe the multidisciplinary aspects of pain management (including pharmaceutical and non-
pharmaceutical treatment)
A
- Non pharmacological: The 4P’s
- prevention: healthy lifestyle (sleep, diet, etc)
- psychological: counselling, social support, self management treatments
- physical: exercise, PT, massage, acupuncture, chiropractor
- pharmaceutical: medicine - pharmacological:
- analgesics: opioid and non-opioid drugs
- anesthetics: loss of feeling/movement of muscle
15
Q
Describe the 5 cardinal signs of acute inflammation
A
- pain: pressure on nerves/chemical mediators (nociceptors)
- heat: incr blood flow to area (incr immune cells)
- redness: incr blood flow to area (incr immune cells)
- swelling: edema (incr capillary permeability)
- loss of function: pain or inflammation/injury its-self
16
Q
overview of acute inflammatory response
A
- initiation and amplification:
- chem mediators are released into blood at site of injury by resident immune cells
- more immune cells are recruited - destruction:
- neutralization of the injury and debris removal by chem mediators and immune cells - termination:
- cytokines and chemokines end inflammatory process
17
Q
Explain the local action of chemical mediators during an acute inflammatory response
A
- pain response: bind to nearby nociceptors
- vascular response: vasodilation and incr capillary permeability
- cellular response: attract immune cells to the site of injury (chemotaxis)
18
Q
Describe the 3 potential healing fates of damaged cells, following an acute inflammatory response
A
- resolution: damaged cells recover
- regeneration: damaged cells are a cell type that can divide by mitosis and can replace the initial cell
- replacement: damaged cells replaced by connect tissue, loss of function in area
19
Q
what are the cells involved in inflammatory response
A
- platelets: release blood clotting proteins at the wound site
- mast cells: secrete chemical mediators
- neutrophils: migrate to the site and secrete factors that kill pathogens and debris (phagocytosis)
- macrophages: secrete cytokines, phagocytosis to remove pathogens and debris
20
Q
types of exudate
A
- serous: classic edema (watery fluid and small amounts of protein)
- fibrinous: repair tissue damage (thick and sticky, high cell and fibrin content)
- purulent: yellow/green think, high white blood cells and debris (bacterial infection)
- hemorrhagic: damaged blood vessels
- abscess: pocket of purulent exudate in a solid tissue
21
Q
Compare acute vs chronic inflammation (onset, duration, response, immune cells, tissue damage, local signs)
A
22
Q
Define atherosclerosis
A
- an inflammatory response to endothelial cell injury
- characterized by build up of atherosclerotic plaque within blood vessels
23
Q
State and identify the location of the common arteries affected by atherosclerosis
A
Most common (1) to least (5)
1. abdominal aorta and iliac arteries
2. proximal coronary arteries
3. thoracic aorta, femoral, and popliteal arteries
4. internal carotid arteries
5. vertebral, basilar, and middle cerebral arteries
24
Q
Summarize the risk factors for atherosclerosis
A
- age
- family history
- hypertension
- diabetes mellitus
- dyslipidemia
- smoking, diet, sedentary life
25
what is dislipidemia
- an imbalance of lipid components in the blood
(high triglycerides, high cholesterol, high levels of LDL, low levels of HDL)
26
difference between HDL and LDL
HDL: (good)
- transport cholesterol from liver to cells
- remove cholesterol and reduces risk of heart disease and stroke
LDL: (bad)
- transport cholesterol away from the peripheral cells to liver
- can build up in arteries and increase heart disease
27
Describe in detail the pathogenesis of atherosclerosis
28
Describe in detail the progression and consequences of atherosclerosis
29
Explain how atherosclerosis is diagnosed
diagnosis:
1. screening tests to assess risk:
- cholesterol level (HDL,LDL)
- BP
- existing stress level
2. imaging:
- coronary angiography: visualize blood flow in coronary arteries
- ultrasound: visualize blood flow in peripheral vessels
30
Explain how atherosclerosis is treated
1. risk reduction:
- diet/ lifestyle intervention
- pharmaceutical measures
- maintenance of existing conditions (diabetes, hypertension)
2. surgical intervention
- angioplasty
- bypass
31
Describe angioplasty and the types
A stent may be inserted after to maintain opening
1.balloon angioplasty:
- catheter with inflatable balloon that flattens the atheroma when inflated
2. laser angioplasty:
- catheter with a laser: inserted into narrow parts of the artery, then disintegrates the plaque
32
Describe a coronary artery bypass graft
- open heart surgery
- heart is arrested and cooled
- circulation bypassed using a heart-lung machine
- artery with plaque physically removed
- replaced with a piece of saphenous vein from leg or mammary artery
33
Define Angina, including its etiology and treatment, and compare stable vs unstable pectoris
- chest pain due to myocardial ischemia
- due to vessel occlusion and or inability to vasodilate to meet perfusion
- can be stable (due to exertion) or unstable (prolonged pain at rest)
- treated with rest, lifestyle modifications, etc.
- warning sign for MI
34
Explain myocardial infarction in terms of the etiology, development
- coronary artery is completely blocked --> prolonged ischemia --> cell necrosis --> infarction
- developed by:
- atheroma progressed to be obstructive
- thrombus breaks away and lodges in small branch
- development:
- damage may be reversed if blood supply is restored within 1 hour
- enzymes are released from damaged/dead myocardial cells
35
Explain myocardial infarction signs & symptoms
1. pain: sudden, crushing, severe, substernal chest pain with left arm/shoulder/jaw/neck
2. pallor, sweating, nausea, dizziness, dyspnea
3. anxiety
4. hypotension (rapid/weak pulse due to decr CO)
36
Explain myocardial infarction diagnosis
1. ECG changes
2. Blood markers (released by necrotic cells)
- Myoglobin
- CPK-MB: Creatine Phosphokinase
- AST: Aspartate Aminotransferase
- LDH-1: Lactate dehydrogenase
- Cardiac-specific Troponin
37
Explain myocardial infarction complications
- Sudden Death due to fibrillation
- Cardiogenic shock (acute HF): severely low CO
- Heart Failure (acute or chronic)
38
Explain myocardial infarction treatments
- Antithrombotic therapy
- Defibrillation to restore normal heart rhythm
- Surgery (Angioplasty, Coronary Bypass Surgery)
- Cardiac Rehabilitation programs: exercise, diet, stress reduction
39
Compare Coronary and Peripheral Artery Disease in terms of cause, location, signs/symptoms and
treatment
40
Define and describe varicose veins (pathogenesis, risk factors, location, treatment)
- irregular, diluted, tortuous areas of superficial or deep veins
- risk factors: incr BMI, pregnancy, family history, weight lifting (heavy)
- most common in legs
- treatment: elevation, compression stockings, intermittent voluntary muscle contractions, can be surgically removed
41
Define thrombophlebitis
- inflammation of a vein that leads to clots
- thrombus development in vein where inflammation is present
42
Define phlebothrombosis
- no inflammation, slowed blood flow leads to clots
- thrombus forms spontaneously in an area without prior inflammation
43
factors for thrombus development
- endothelial injury
- stasis of blood or sluggish blood flow
- incr blood coagulability
44
Describe signs/symptoms for venous thrombosis
- Aching, burning, tenderness in affected area
- Warmth, redness
- Edema as blood pools distal to obstructed thrombus
- Homan’s Sign: pain in the calf muscle upon foot dorsiflexion
45
describe treatments for venous thrombosis
1. Prevention:
- Compression stockings
- Exercise to improve muscle tone, reduce stasis
2. Pharmaceuticals: Anticoagulants
3. Surgical intervention: Thrombectomy
46
Describe the potential consequences of uncontrolled
hypertension
1. Endothelial cell injury:
- Atherosclerosis
2. Cardiac consequences:
- Coronary Artery Disease
- Left Ventricular Hypertrophy (due to higher afterload)
- Heart Failure
3. Peripheral Artery Disease
4. Organ damage (kidneys, brain, eyes)
47
Define hypertension and describe
- sustained daytime BP of >135 mmHg systolic and/or >85 mmHg diastolic
- sometimes isolated systolic (sometimes diastolic)
- mostly idiopathic = primary
- if cause known = secondary
48
describe the risk factors of hypertension
- age
- family history
- obesity
- diet
- low PA
- excess alcohol, smoking, stress
49
describe the classification of different stages of hypertension with BP
50
preload
volume of blood in ventricle at end of diastole
51
afterload
resistance left ventricle must have to overcome to circulate blood
52
Use the equation for Mean Arterial Pressure to describe the mechanisms of blood pressure regulation
53
Explain the Renin-Angiotensin-Aldosterone pathway in response to a decrease in MAP
54
Use the MAP equation to help explain the pathophysiological bases for primary hypertension
1. incr in BV (due to deficit in Na+ handling) leads to incr in MAP
- leads to incr Na+ doe to excess Na+ intake and reabsorption
2. incr peripheral vascular resistance:
- endothelial cell dysfunction --> promotes vasoconstriction
- activation of RAAS
- incr activation of SNS --> incr CO and PR
55
Summarize common treatments (pharmacological and lifestyle) for hypertension
1. pharmaceuticals:
- vasodilators , diuretics (decr BV), cardioinhibitory drugs (decr SV x decr HR = Decr CO), diet
2. lifestyle modifications:
- incr PA
- stop smoking
- decr alcohol level
- decr stress
56
Define hypotension (shock) --> cold shock using the MAP equation
- decr CO
- compensation: vasoconstriction --> incr R --> incr MAP
-blood flow is redirected to vital organs
1. hypovolemic (decr BV):
- Hemorrhagic & non-hemorrhagic (diarrhea, vomiting)
- Decreased blood volume --> Decreased venous return --> Decreased CO
2. Cardiogenic
- Problem with heart function --> Decreased ability for heart to pump --> decr CO
57
Define hypotension (shock) --> warm shock using the MAP equation
- decr systemic vascular resistance due to peripheral vasodilation
- compensation: incr HR
1. Anaphylactic Shock: the most extreme reaction to an allergen
- Mast cells release histamine & bradykinin --> vasodilation, edema, bronchoconstriction
- Treatment: IM Epinephrine increased CO, smooth muscle relaxation (airways), vasoconstriction
2. Septic Shock e.g. due to an infection in the bloodstream
- Macrophage activation Cytokine release ++ vasodilation
- Treatment: IV fluids & antibiotics
58
Define and describe the causes, signs/symptoms and treatment of orthostatic hypotension
59
Define hypotension (shock) --> neurogenic shock using the MAP equation
- Autonomic balance tips toward PNS --> vasodilation and bradycardia
* Causes: spinal Cord Injury, Traumatic Brain Injury, Vasovagal reflex
60
Define and describe the causes of orthostatic hypotension
- sudden, sustained drop in BP caused by standing up from sitting/laying down
- SBP decreased by at least 20mmHg or DBP decreased by at least 10mmHg for the first 3 minutes in upright position
1. impaired baroreceptor reflex function, hypovolemia, blood pooling in legs
2. Most commonly due to medication (anti hypertensives, diuretics, vasodilators)
3. Increased risk in older adults
61
describe signs/symptoms and treatment of orthostatic hypotension
1. Signs & Symptoms
- Pallor, blurred vision, feeling faint, dizziness, nausea
2. Treatment
- Water intake, salt intake, compression stockings
- Sleep in a slightly inclined position
- Leg resistance exercise
62
sinus tachycardia
HR faster than normal (>100BPM)
- due to issue in automatacy
63
sinus bradycarida
HR is slower then normal (<60 BPM)
- due to issue in automatacy
64
automaticity (normal conditions)
- Sinoatrial node (SAN) automatically sets the pace of the heart (no input required from the NS)
Normal Modulation:
1. SNS:
- Epinephrine & Norepinephrine released onto SA node
cells & bind to Beta-adrenergic receptors --> Incr Phase 4 slope--> Incr SA Node AP frequency
2. PNS:
- Acetylcholine released onto SA node cells & binds to
‘muscarinic’ receptors --> decr Phase 4 slope --> decr SA Node AP frequency
65
abnormal (incr) automaticity
- due to incr SNS activity
66
abnormal (decr) automaticity
- due to:
1. incr PNS activity (vasovagal reflex --> decr HR)
2. decr metabolic activity of pacemaker cells (decr body temp, hyporodism --> decr met rate
3. electrolyte imbalance (decr excitability of SA node cells)
4. heart damage or disease (slowed electrical conduction of heart)
67
how does electrical conduction affect arrhythmias
1. Triggered activity: spontaneous AP fired outside of normal stimulus from conduction system
2. Re-entry circuits: Abnormal conduction pathway is formed either due to an additional ‘accessory’ path or a block in the normal path
68
common types of arrhythmias
1. premature ventricular contractions
2. paroxysmal supraventricular tachycardia
3. fibrillation:
- atrial fibrillation
- ventricular fibrillation
69
describe premature ventricular contractions
- An electrical signal is initiated by the Purkinje fibers instead of the SA node --> ventricles contract ‘prematurely’ --> a brief pause follows before normal rhythm returns
- no P wave
70
describe paroxysmal supraventricular tachycardia
- New conduction pathway that begins somewhere in the atria (outside of the normal conduction) --> new signal travels down to the ventricles --> ventricular tachycardia
- Begins and ends suddenly
71
describe atrial fibrillation
heart still functions as a pump (not contracting asynchronously)
- symptoms: palpitations, chest discomfort, shortness of breath, dizziness
72
describe Ventricular fibrillation
– heart does not function as an effective pump
- Collapse (electrical shock required to reset normal sinus rhythm
- can cause death
73
treatments for arrhythmias
1. Drugs that control heart rate and rhythm:
- Beta Blockers (block SNS effect)
- Na + , K+ or Ca 2+ channel blockers
2. Ablation therapy:
- Map out the electrical activity of the heart --> destroy
specific region of the heart tissue that is causing the issue
3. implantation:
- Pacemaker: Regulates the rhythm through low energy
electrical pulses
- ‘Implantable Cardio defibrillator’ (ICD): Senses a stopped heart and delivers a strong electrical shock to restart the heart
74
Describe the types of chronic heart failure (systolic dysfunction)
- ventricles can't pump hard enough during systole (contractility is impaired)
- due to weakened ventricle
- Result: lower EF and CO
- impaired contractility --> incr ESV --> decr SV --> decr CO
75
Describe the types of chronic heart failure (diastolic dysfunction)
- not enough blood fills into the ventricle during diastole
- due to impaired relaxation of the ventricle
- result: normal EF, lower CO
- decr EDV --> decr SV --> decr CO
76
Describe the initial physiological compensation for heart failure
77
Describe the consequence of eventual decompensation of congestive heart failure
- CO decr (decr myocardial tissue function)
- EF decr (decr EF = decr SV / incr EDV)
- incr EDV due to ventricle output is less than inflow of blood
- blood starts to build up into pulm or systemic circulation --> heart failure
78
types of ventricular hypertrophy
1. symmetric: proportionate incr in wall thickness and diameter
2. concentric: disproportionate incr in wall thickness
- myofibrils grow in parallel
3. eccentric: disproportionate incr in wall circumference
- myofibrils grow in series
79
left sided heart failure
80
right sided heart failure
81
types of strokes
- ischemic (85%)
- hemorrhagic (15%)
- transient ischemic attack (mini/silent stroke)
82
describe ischemic strokes
- blood flow is blocked off in an area of the brain
1. causes:
- Atherosclerotic plaque build up
- Blood clot that travels to the brain
2. Extent:
- Partial vs total occlusion
- ~ 5 minutes of ischemia --> irreversible damage to nerve cells --> Necrosis & Inflammation
* Acute treatment is thrombolytic therapy: eg. tPA plasminogen activator (a clot busting agent)
83
describe hemorrhagic stroke
- A burst blood vessel leads to bleeding in an area of the brain, causing local swelling and damage
- Most common cause: Severe hypertension
- Symptoms are severe – extreme headache, loss of
consciousness, coma, death
- Anti clotting treatment would be life threatening in this case.
84
describe transient ischemic attacks (TIA)
- temporary blockage of a cerebral artery that resolved
- Symptoms the same as a stroke but can be milder and will fully resolve within 24 hours without treatment.
- warning sign of impending stroke
85
Summarize the risk factors
- age
- atherosclerosis
- hypertension
- atrial fibrillation
86
Summarize the treatments and prevention of stroke
1. treatments:
- antithrombotic therapy
- OT/PT/speech therapy
2. prevention:
- reduce risk factors
- healthy lifestyle modification
- prophylactic treatments (blood thinners)
87
what is the stroke response
88
describe obstructive lung disease
- Airway obstruction causes an increased resistance to airflow
- Larger impact on expiration --> air gets trapped --> limited ventilation
- airway obstruction
89
describe restrictive lung disease
- Reduced lung compliance increased stiffness --> limited expansion --> Limited ventilation
- Near normal rates of inspiration and expiration
- loosing the compliance of the lungs
90
describe air flow on pressure gradient and resistance
91
compliance
how easily the lung can expand
- compliance = change in V/ change is P
(outward push of lung motion)
92
elastance
ability of the lung to spring back after being stretched
(inward pull of lung motion)
93
bronchodilation
94
bronchoconstriction
95
radial traction
- the lungs contains elastic fibres the pull on the airway of the bronchioles helping them open during inspiration
- helps prevent airway collapse
96
describe lung volumes in obstructive and restrictive lung diseases
97
sketch a graph of Volume expired vs time for normal compared to restrictive and obstructive lung
disease and use this to show and explain the differences in FEV1/FCV ratios
98
Use the flow-rate volume loop to describe the functional consequences of obstructive and
restrictive lung diseases and relate this to the structural impairment of each
99
list factors that can contribute to increased airway resistance in obstructive lung diseases
- BRONCHOCONSTRICTION
- INFLAMMATION
- EXCESS MUCUS PRODUCTION
- REDUCED ALVEOLAR ELASTIC RECOIL (reduced recoil leads to less radial traction)
100
Describe the etiology and the types of asthma
- Bronchial obstruction due to hypersensitive and/or hyper responsive immune response
* Allergic (extrinsic) or Non-Allergic (intrinsic)
101
describe the universal response to asthma
- inflammation & edema of mucosa
- Increased secretion of thick mucus within airways
- Bronchoconstriction
102
describe the symptoms of asthma
- Coughing, wheezing, shortness of breath
- Coughing up thick mucus
103
allergic (extrinsic) asthma
104
non allergic (intrinsic) asthma
105
summarize the pathophysiology of an allergic asthma attack
106
partial obstruction (asthma)
107
total obstruction (asthma)
108
asthma treatments
- Determine triggers and avoid them if possible
- Good ventilation is key
- Inhaler if needed or prophylactically
- Other meds: anti-inflammatories (corticosteroids), long-acting bronchodilators
- GOAL IS TO MINIMIZE THE NUMBER AND SEVERITY OF ACUTE ATTACKS
109
Define Chronic Obstructive Pulmonary Disease
- A group of chronic respiratory disorders that cause...
- Progressive tissue degeneration
- Airway obstruction
- Most often a combination of emphysema & chronic bronchitis
- Irreversible and progressive damage to lungs
110
Describe the pathogenesis of Emphysema
- destruction of alveolar walls
111
Describe the structural and functional consequences of Emphysema
STRUCTURAL:
1. Breakdown of alveolar walls:
- Decreased SA for gas exchange
- Loss of elastic fibers --> decr elastance / incr compliance
- decr radial traction --> collapse of small airways
2. Increased mucus production:
- Due to chronic inflammation and infection
- Leads to thickening and fibrosis of the bronchial walls
CONSEQUENCES:
1. Progressive difficulty with expiration:
- Air trapping and increased residual volume
- Over Inflation of lungs
- Ribs remain in inspiratory position and increased
anterior-posterior diameter of chest (barrel chest)
112
Describe the symptoms of Emphysema
- Dyspnea
- Hyperventilation with a prolonged expiratory phase
- Fatigue from hypoxia
113
Describe the diagnosis and treatment of Emphysema
1. diagnosis:
- increased residual volume and TLC, decreased vital capacity, and inspiratory & expiratory reserve volume
- FEV1 and FVC reduced
2. treatment:
- Avoid irritants and infection
- Pulmonary rehab and breathing techniques
- Bronchodilators
- High-flow nasal O2 therapy
114
describe chronic bronchitis
- Chronic irritation of the bronchi due to exposure to inhaled irritants
- mucus production
115
116
116
117
pulmonary fibrosis
- A result of long-term exposure to irritants
- Inflammation --> fibrotic tissue
- decr barrier permeability at alveoli
- decr compliance
- More effort for inspiration
- Dyspnea
- Cough
117
diagnosis and treatment and symptoms of chronic bronchitis
117
pathogenesis of chronic bronchitis
117
types of restricitve lung disease
118
pulmonary edema cause and symptoms
118
how does edema affect congestive heart failure
119
pulmonary embolus (risk factors and symptoms and pathophysiology)
120
define diabetes mellitus
A chronic disorder of metabolism characterized by elevated plasma glucose levels (hyperglycemia) resulting from defects in insulin production, insulin action, or both
121
actions of insulin
122
describe insulin uptake
123
signs and symptoms of DM
124
Use a flow chart to explain the physiological consequences of insulin deficit
125
Explain the pathophysiology of Ketoacidosis and explain how it can go hand-in-hand with dehydration and symptoms
ketone bodies are produced as a byproduct of fatty acid metabolism in the liver
- broken down into ketone bodies
SYMPTOMS:
- fruity breathe, dehydration, nausea, hyperventilation, confusion, coma
126
describe T1DM and the treatments
- characterized by autoimmune destruction of beta cells of the pancreatic islets leading to lack on insulin
TREATMENTS:
1. Need to replace insulin
- Injections
- Pump
- Islet cell transplant
2. Need to tightly monitor blood glucose levels
- Careful monitoring of food intake and activity level in
relation to insulin administration
127
describe T2DM
- Characterized by Insulin Deficit (due to impaired action & production)
- Insulin resistance & Beta cell destruction
- SYMPTOMS are usually subtle (if present at all) and often manifest later in disease progression
RISK FACTORS:
* Genetics
* Chronic Energy Imbalance
* Overnutrition
* Physical inactivity
* Obesity (Chronic Inflammation and high FFAs circulating in the blood)
128
describe the glucose tolerance test for T2DM
129
etiology and pathophysiology of T2DM
130
sites of insulin resistance and the consequences
131
treatment for T2DM
132
GLP-1 action and the relationship to T2DM
133
obesity etiology and risk factors
- imbalance between consumed calories and expanded calories
- BMI of 30kg/m2 or more
- RISK FACTORS: T2DM, CVD, osteoarthritis, cancer, kidney disease
134
factors that affect BMI
- FFM:FM ratio (DEXA, bioimpedance scale)
- WC (where we store adipose tissue)
- waist to hip ratio (visceral or sub q fat)
- triglyceride levels
- blood glucose levels
135
diagnosing obesity
136
how does adiposity (obesity) affect T2DM
137
obesity treatment
138
diagnosis of metabolic syndrome
139
progression of METs
140
neoplasm (tumor)
1. Cellular growth that no longer responds to normal genetic control
- Dividing outside of regular mitotic signals
2. Deprives other cells of nutrients & metabolism
3. Characteristics of each tumor depends on
- Type of cell from which tumor arose
- Unique structure and growth pattern
141
benign tumors
142
malignant tumor
143
types of cancerous cell growth (precancerous)
1. Hyperplasia – Cells are dividing at a rate faster than normal
2. Atypia – Cell are slightly abnormal
3. Metaplasia – change in cell type in a particular area
4. Dysplasia – cells are abnormal, they are growing faster than normal & not arranged like normal cells
144
cell growth (progressed to cancerous)
1. Carcinoma: epithelial origin
2. Sarcoma: supportive and connective tissue
origin
3. Melanoma: melanocytes (skin pigment cells)
4. Myeloma: plasma cells
5. Leukemia: white blood cells
6. Lymphoma: develop within the lymphatic
system
7. Mixed types
145
how is cancer classified
- based on location and type of tissue
146
etiology of carcinogenesis and risk factors
147
multistage model of carcinogenesis
148
Summarize the general pathophysiological characteristics of malignant tumors (i.e. how they create
their own microenvironment)
Tumors create their own ‘microenvironment’
* Cells lack mitotic control and normal homeostatic function/cell communication
* Altered cell membranes and surface antigens
* Cells do not properly adhere to each other--> They secrete enzymes that break down proteins of the extracellular matrix. Enables them to break off from the tissue mass and spread.
* Secrete growth factors that stimulate development of new capillaries (promoting angiogenesis)
149
local effects of malignant tumors
150
systemic effects of miglanat tumors
151
spread of malignant tumors
1. Tissue Invasion – local spread
- Tumor cells grow into adjacent tissue
2. Metastasis – Spread to distant sites
- via blood and/or lymphatic system
- Liver and lungs are common sites of metastasis
3. Seeding – Spread of tumor cells within body fluid or along membranes within a body cavity
152
diagnosis of cancer
- Warning signs
- Routing screening and self-examination
- Blood tests
- X-ray, ultrasound, CT, MRI
- Histologic and cytological exams (Biopsy)
153
grading and staging of cancer
154
cancer treatments
- surgery
- radiation
- chemotherapy
155
personalized oncogenomics (POG)
156
cancer prevention
157
how does exercise affect cancer
- Regular physical activity linked to reduced cancer recurrence and improved survival
- reduce side effects of cancer (fatigue, lymphedema, mental health, QoL, muscle mass, improve treatment tolerance)
