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HES 311 > POST MIDTERM 1: FINAL EXAM > Flashcards

POST MIDTERM 1: FINAL EXAM Flashcards

1
Q

cardiac common pathologies

A
  • angina pectoris
  • myocardial infarction
  • heart failure
  • valve dysfunction
  • arrhythmias
  • inflammation
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2
Q

Vascular common pathologies

A
  • atherosclerosis
  • peripheral artery disease
  • coronary artery disease
  • varicose veins
  • hypertension/hypotension
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3
Q

Blood vessels micro anatomy

A
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4
Q

arteriosclerosis

A
  • hardening and thickening of arterial wall
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5
Q

most common type of arteriosclerosis

A

atherosclerosis

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6
Q

atherosclerosis

A

inflammatory response to endothelial cell injury
- characterized by build up of atherosclerotic plaques (atheroma) within the vessel wall

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7
Q

what is atherosclerosis vessel wall made up of

A

lipids (mainly cholesterol), cell debris, fibrin, thrombus

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8
Q

most common arteries affected

A
  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
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9
Q

atherosclerosis risk factors

A

age, family history, hypertension, diabetes mellitus, dyslipidemia, smoking, diet high in animal fat, sedentary lifestyle

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10
Q

dyslipidemia

A

an imbalance of lipid components in the blood

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11
Q

What are the four ways dyslipidemia can be classified

A
  1. high triglycerides
  2. high cholesterol
  3. high levels of low-density lipoproteins (Chylomicrons, VLDL)
  4. low levels of high-density lipoproteins (HDL, LDL)
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12
Q

What are the functions of LDL and HDL

A

transport of lipoproteins in the blood

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13
Q

Lipids are transported in combination with…

A

proteins

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13
Q

LDL definition

A

Low density lipoprotein

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14
Q

LDL function

A

transports cholesterol from liver to cells
- major factor contributing to atheroma formation

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15
Q

LDL considered as the

A

Bad lipid (it contains most amount of cholesterol)

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16
Q

HDL definition

A

high-density lipoprotein

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17
Q

HDL function

A

transports cholesterol away from peripheral cells to liver
- breakdown in liver and excretion

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18
Q

HDL considered the

A

good lipid (contains mostly protein)

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19
Q

atherosclerosis pathogenesis

A
  1. damage to endothelial cells
  2. LDL enters into intimal layer and become oxidized
  3. macrophages eat up lipids-> foam cells-> fatty streak
  4. inflammatory response causes growth factors to be released
  5. smooth muscle cell proliferation and migration from the tunica media into the tunica intima, fibroblasts recruited
  6. growth of extracellular matrix: formation of a fibrous cap over a lipidcore= fibrous plaque
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20
Q

atherosclerosis - progression and consequences

A
  1. Foam cells within lipid core undergo necrosis
  2. release enzymes that eat up fibrous cap
  3. eventual rupture
  4. platelets activate and adhere to site
  5. thrombus forms at the site of rupture
  6. thrombus occludes the lumen of the artery and can detach and travel to occlude a distal artery
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21
Q

consequences of atherosclerosis progression

A
  • ischemia (at least 70% of lumen occluded)
  • total occlusion/plaque rupture
  • weekend vessel wall
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22
Q

ischemia

A

less than normal amount of blood flow to part of your body

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23
Q

ischemia can lead to what diseases

A
  • coronary artery disease : angina pectoris
  • peripheral artery disease : claudication
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24
Q

total occlusion / plaque rupture causes:

A
  • clot detachment
    -> myocardial infarction and ischemic stroke due to not enough oxygenated blood flow
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25
Q

weekend vessel wall causes

A

aneurism

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26
Q

atherosclerosis diagnosis

A
  • screening test to asses risk
  • imagining
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27
Q

what do atherosclerosis screening tests look at

A

blood cholesterol level, blood pressure, exercise stress testing

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28
Q

what type of imaging is done to diagnose atherosclerosis

A
  • coronary angiography : visualize blood glow in coronary arteries
  • ultrasounds: visualize blood flow in peripheral vessels
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29
Q

atherosclerosis treatments

A
  • risk reduction
  • surgical intervention
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30
Q

types of atherosclerosis risk reduction options

A
  • dietary lifestyle intervention
  • pharmaceutical measures: anti-hypertensives, cholesterol-lowering, anticoagulants
  • maintenance of existing conditions (diabetes, hypertension)
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31
Q

surgical intervention types for atherosclerosis

A
  • angioplasty
  • bypass
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32
Q

angioplasty types

A
  • ballon angioplasty
  • laser angioplasty
    *a stent may be inserted after the angioplasty to maintain the opening
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33
Q

ballon angioplasty

A

catheter with an inflatable balloon that flattens the atheroma when inflated

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34
Q

laser angioplasty

A

catheter with a laser: inserted into narrowed part of artery: laser disintegrates plaque

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35
Q

Coronary artery bypass graft procedure

A
  • open heart surgery
  • heart is arrested and cooled
  • circulation bypassed using a heart-lung machine
  • artery with plaque physically removed
  • replaced with piece of saphenous vein from leg or mammary artery
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36
Q

what is Angina pectoris

A

chest pain due to myocardial ischemia

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37
Q

how does angina pectoris occur

A
  • due to vessel occlusion and/or inability to vasodilator to meet perfusion demand
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38
Q

Angina pectoris can be

A

stable (transient due to exertion) or unstable (prolonged pain at rest)

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39
Q

angina can be treated with

A
  • rest
  • lifestyle modification
  • nitroglycerin
  • surgical intervention
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40
Q

angina pectoris can be a warning sign for

A

MI
(especially unstable angina)

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41
Q

MI pathophysiology steps

A
  • coronary artery is completely blocked
  • prolonged ischemia
  • cell necrosis
  • infarction
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42
Q

common ways to develop MI

A
  • atheroma progression, obstructing artery
  • thrombus breaks away and lodges in a small branch
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43
Q

what determines the severity of MI damage

A
  • size
  • location
  • duration
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44
Q

is MI damage reversible?

A

yes if blood supply is restored within 1 hour
* enzymes are released from damaged and dead myocardial cells, they are then released in the blood

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45
Q

MI signs and symptoms

A
  • pain : sudden, severe, crushing, chest pain
  • pallor, sweating, nausea, dizziness, dyspnea
  • anxiety
  • hypotension rapid and week pulse
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46
Q

myocardial infarction diagnosis

A
  • ecg changes
  • blood markers released by necrotic cells
  • myoglobin, CPK-MB, AST, LDH, cardiac specific troponin
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47
Q

MI complications

A
  • sudden death due to fibrillation
  • cariogenic shock : severely low cardiac output
  • heart failure (acute or chronic)
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48
Q

MI treatment options

A
  • antithrombotic therapy
  • defibrillation to restore normal heart rhythm
  • surgery
  • cardiac rehabilitation programs : exercise, diet, stress reduction
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49
Q

peripheral artery disease cause

A

due to atherosclerosis in peripheral arteries or inflammation that leads to narrowing of arteries

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50
Q

where does peripheral artery disease often occur

A

in the legs

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51
Q

signs and symptoms of peripheral artery disease

A
  • fatigue and weakness in legs
  • intermittent claudication
  • weak peripheral pulse
  • pale, hairless skin
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52
Q

peripheral artery disease

A
  • reduce risk factors
  • increased physical activity
  • peripheral vasodilators
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53
Q

venous disorders (varicose veins)

A
  • irregular dilated, tortuous areas of deep veins
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54
Q

varicose veins risk factors

A
  • increased BMI
  • pregnancy
  • family history
  • heavy lifting
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55
Q

where are varicose veins most common

A

in legs

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56
Q

treatment for varicose veins

A
  • elevation and compression stockings
  • intermittent voluntary muscle contractions when sitting for long periods
  • surgical removal
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57
Q

thrombophlebitis

A
  • thrombus development in vein where inflammation is present : platelets adhere to inflamed site, thrombus develops
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58
Q

phlebothrombosis

A

thrombus forms spontaneously in an area without prior inflammation

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59
Q

factors for thrombus development

A
  • endothelial injury
  • stasis of blood or sluggish blood flow
  • increased blood coagulability(clotting)
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60
Q

signs and symptoms of venous thrombosis

A
  • aching, burning, tenderness in affected area
  • warmth, readness
  • edna with pooling blood
  • pain in calf muscle upon dorsiflexion
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61
Q

hypertension clinical definiton

A

sustained daytime BP > 135mmHg systolic and/or > 85 mmHg diastolic
* sometimes isolated as systolic or diastolic

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62
Q

90% of hypertension cases are

A

idiopathic: primary hypertension

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63
Q

if hypertension cause is unknown it is

A

secondary hypertension

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64
Q

hypertension risk factors

A
  • age
  • family history
  • obesity
  • diet
  • low physical activity
  • excess alcohol, smoking, stress
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65
Q

systolic pressure of 130-139 classifies as

A

hypertension stage 1

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66
Q

diastolic pressure of 80-90 classifies as

A

hypertension stage 2

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67
Q

systolic pressure of greater than 140mmHg classifies as

A

hypertension stage 2

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68
Q

diastolic pressure greater than 90mmHg classifies as

A

hypertension stage 2

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69
Q

risk of cardiovascular disease doubles with increments of ___ above _____

A

20/10, 115/75

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70
Q

__ % of Canadians have hypertension or pre hypertension

A

39%

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71
Q

Developing hypertension is ___

A

silent. You dont know you have it

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72
Q

effects of uncontrolled hypertension

A
  • endothelial cell injury : atherosclerosis
  • cardiac consequences:
    coronary artery disease, hypertrophy, heart failure
  • peripheral artery disease
  • organ damage (kidneys, brain, eyes)
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73
Q

preload

A

volume of blood in ventricles at the end of diastole (end diastolic pressure)

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74
Q

afterload

A

resistance left ventricle must overcome to circulate blood

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75
Q

increased after load =

A

increased cardiac workload

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76
Q

MAP equation

A

MAP= cardiac output x peripheral resistance

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77
Q

neural mechanisms of blood pressure regulation

A

Baroreceptors

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78
Q

renal/hormonal mechanisms of BP regulation

A
  • filtration rate
  • renin release
  • ADH
  • H2O reabsorption and BV
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79
Q

vascular mechanisms of blood pressure regulation

A

endothelial cells
nitric oxide
vasodilation
endothenlin
vasoconstriction

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80
Q

Primary hypertension

A
  • Na+ defect causes elevation of blood volume
  • Increased peripheral vascular resistance
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81
Q

Hypertension treatment

A
  • pharmaceuticals: vasodilators, diuretics, cardioinhibitory drugs
  • diet: DASH, reduced Na+ intake, reduced caffeine intake (positive inotrope)
  • lifestyle modifications: increased PA levels, smoking cessation, decreased alcohol intake, decreased stress
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82
Q

how does exercise work as a treatment for hypertension

A
  • exercise lowers BP physiological response after exercise
  • moderate intensity 20-30minutes per session
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83
Q

acute hypotension is also known as

A

shock

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84
Q

acute hypotension

A

inadequate tissue perfusion: tissue ischemia, cellular damage

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85
Q

hypertension equation

A

MAP= Co x R

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86
Q

general signs and symptoms of shock

A
  • tachycardia
  • decreased urine output
  • dizziness, feeling faint, altered mental status
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87
Q

main classifications of shock

A
  • hypovolemic
  • cardiogenic
  • anaphylactic
  • septic
  • neuronic
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88
Q

cold shock happens from

A

decreased cardiac output
vasoconstriction, increased resistance, which increase mean arterial pressure

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89
Q

where does blood get redirected to in cold shock

A

blood flow redirected to vital organs

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90
Q

hypovolemic cold shock

A
  • hemorrhagic and non-hemorrhagic (diarrhea and vomitting)
  • decreased blood volume-> decreased venous return-> decreased CO
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91
Q

cariogenic cold shock

A
  • problems with heart function -> decreased ability for heart to pump, CO decreased
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92
Q

warm shock causes

A

decreased systemic vascular resistance due to peripheral vasodilation

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93
Q

warm shock compensation

A

increased heart rate

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94
Q

anaphylactic shock (warm shock)

A

the most extreme reaction to an allergen
- mast cells release histamine and bradykinin-> increased vasodilation edema, bronchoconstriction

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95
Q

anaphylactic shock treatment

A

epinephrine, increased CO, smooth muscle relaxation, vasoconstriction

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96
Q

septic shock caused by

A

infection in bloodstreams

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97
Q

septic shock results in

A

macrophage activation-> cytokine release, increased vasodilation

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98
Q

septic shock treatment

A

IV fluids and antibiotics

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99
Q

neurogenic shock

A

loss of sympathetic tone: autonomic balance tips towards parasympathetic nervous system-> vasodilation and Bradycardia q

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100
Q

neurogenic shock can happen from

A
  • spinal cord injury
  • traumatic brain injury
  • vasovagal reflex (overreaction of the vagus nerve due to an abnormal response to pain, fear, emotion, sight of blood, etc)
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101
Q

orthostatic hypotension

A
  • sudden sustained drop in blood pressure caused by standing up from a sitting, lying position
    ( SBP decreased by at least 20mmHg or DBP decreased by at least 10mmHg for the first 3 minutes in upright position)
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102
Q

how is orthostatic hypotension caused

A
  • impaired baroreceptor reflex function, hypovolemia, blood pooling in legs
  • most commonly due to medication (vasodilators)
  • increased risk in older adults
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103
Q

signs and symptoms of orthostatic hypotension

A

pallor, vertigo, blurred vision, feeling faint, dizziness, nausea

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104
Q

treatment of orthostatic hypotension

A
  • water intake, salt intake, compression stockings, sleep slightly inclinde
  • leg resistance exercise
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105
Q

what are the two determinants of blood pressure

A
  • cardiac output
  • resistance
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106
Q

cardiac output depends on

A
  • stroke volume: preload and contractility
  • heart rate: modulated by SNS (increase HR), PNS (decrease HR)
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107
Q

peripheral resistance depends on

A

radius of our small arteries
- vasoconstriction (increased vascular resistance)
- vasodilation (decreased vascular resistance)

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108
Q

Neural mechanisms of blood pressure regulation

A

baroreceptors send signals to the medulla to modify HR, SV, and Vascular resistance. via SNS/PNS output

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109
Q

renal/hormonal mechanisms of blood pressure regulation

A

regulation of blood volume:
through:
- filtration rate: (impacting Na+ and H2O absorption and excretion)
- renin release (RAAS)
- ADH release (H2O reabsorption)

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110
Q

vascular mechanisms of blood pressure regulation

A

endothelial cells release
- nitric oxide: vasodilation
- endothelia: vasoconstriction

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111
Q

RAAS renin angiotensin-aldosterone system purpose

A

to increase mean arterial pressure

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111
Q

RAAS steps explained

A

Triggered by
- decreased MAP
- decreased filtration into kidneys
Response:
- kidneys release RENIN
- RENIN triggers
angiotensinogen, angiotensin 1, ACE, angiotensin 2
this triggers:
- thirst
- aldosterone release
- vasoconstriction
- increased blood volume
- increased Na+ and H2O reabsorption from kidneys
- increased peripheral vascular resistance

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112
Q

normal heart sinus rhythm determined by

A

action potential frequency of sinoatrial node cells

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113
Q

normal sinus rhythm rate

A

60-100BPM

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114
Q

pathway of excitation through the heart.

A
  1. electrical signalling begins in the SA node
  2. signal is focused and routed through the AV node
  3. conduction is slowed for AV node delay to allow blood flow into the ventricles before they’re given the electrical signal to contract
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115
Q

what are cardiac arrhythmias

A

abnormalities in either rate or path of electrical conduction

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116
Q

consequence of cardiac arrhythmias

A

can lead to disorganized contractions -> impaired cardiac output

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117
Q

sinus tachycardia heart rate abnormalities

A

HR is faster than normal >100BPM

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118
Q

sinus bradycardia

A

HR is slower than normal <60BPM

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119
Q

what are abnormalities in heart rate due to

A

an issue with automaticity

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120
Q

automaticity

A

sinoatrial node (SAN) sets pace of heart (no input required from nervous system)

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121
Q

normal automaticity modulation

A

SNS:
- epinephrine and norepinephrine released onto SA node cells and bind to beta-ardenergic receptors
- increased phase 4 slope -> increased SA node AP frequency

PNS:
- acetylcholine released onto SA node cells and binds to muscarinic receptors
- decrease phase 4 slope-> decreased SA node AP frequency

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122
Q

abnormal automaticity results in

A

Increased automaticity due to increased sympathetic NS activity
- hypovolemia
- hypercapnia (high blood CO2) or Hypoxia (low blood O2)
- pain or anxiety
- increased metabolic activity of pacemaker cells
- drugs that act like NE or epinephrine

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123
Q

arrhythmias due to : altered electrical conduction happens from

A

triggered activity : irritable area somewhere in the atria or ventricles that tigger ectopic firing (spontaneous action potentials fired outside of normal stimulus from conduction system)

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124
Q

re-entry circuits

A

Abnormal conduction pathway formed either due to an additional accessory path or a block in the normal path

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125
Q

common arrhythmias: premature ventricular contractions:

A

triggered activity -> an electrical signal initiated by purkinje fibers instead of SA node!

  • ventricles contract prematurely, a brief pause follows before normal rhythm returns
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126
Q

common arrhythmias: paroxysmal supraventricular tachycardia

A

new conduction pathway begins somewhere in atria (outside of normal conduction)
- new signal travels down ventricles-> ventricular tachycardia
*begins and ends suddenly

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127
Q

types of common arrhythmias

A
  • premature ventricular contractions
  • paroxysmal supra ventricular tachycardia
  • fibrillation
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128
Q

common arrhythmias: fibrillation

A

electrical activity independent of SA node-> chaotic contractions

  • atrial fibrillation: heart still functions as a pump but symptoms like
  • palpitations, chest discomfort, shortness of breath, dizziness

*ventricular fibrillation: heart does not function as an effective pump
- collapse (electrical shock required to reset normal sinus rhythm)

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129
Q

treatment for arrhythmias

A
  • drugs that control heart rate and rhythm
    ie. beta blockers, Na+, K+, or Ca2+ channels
  • ablation therapy: map out electrical activity of heart and destroy region of tissue causing issue
  • pacemaker implantation
    pacemaker: regulated rhythm through low energy electrical pulses
  • implantablee cardio defibrillator (ICD): sense a stopped heart and delivers a strong electrical shock to restart the heart
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130
Q

heart failure definition

A

any functional or structural issue of the heart that causes low cardiac output

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131
Q

heart failure can be

A

left or right sided
acute or chronic

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132
Q

chronic heart failure:

A
  • a long term condition that can last months or years
  • the heart can eventually no longer keep up with demand as it as weekend and can no longer maintain the cardiac output required
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133
Q

in chronic heart failure, the ventricle undergoes

A

adaptive responses like hypertrophy and dilation

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134
Q

what are causes of chronic heart failure

A

any pathology that affects regular heart function
most common:
- coronary artery disease, previous myocardial infarction
- chronic uncontrolled high BP

others: incompetent or stenosed heart valves, infection/inflammation of the heart arrhythmias

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135
Q

Heart failure simplified definiton

A

heart is not pumping out enough content as it needs

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136
Q

determinants of cardiac output equations

A

CO=sv x hr
SV= edv(preload) -esv

137
Q

Cardiac output is modulated by our

A

heart rate and stroke volume

138
Q

HR is determined by our

A

SNS(pacemakers produce positive chronotropic increasing HR) and PNS (pacemakers produce negative chronotropic slowing HR)

139
Q

SV is determined by our

A

preload and contractility (which is dictated by SNS (epinephrine) which will cause more forceful contractions)

140
Q

the frank starling law

A

the length tension relationship of cardiac myocytes (heart muscles)

  • shows the relationship between preload (EDV) and stroke volume
    *preload determines stroke volume
  • the more we stretch the walls of the heart, the higher the stroke volume will be
141
Q

what can we use to measure heart function

A

ejection fraction

142
Q

ejection fraction =

A

how well the ventricle pumps blood with each beat

  • how much of the blood coming in has been ejected out
143
Q

ejection fraction equation

A

EF(%)= SV/EDV x 100

144
Q

Heart failure can be due to

A
  1. Systolic dysfunction, ventricles can’t pump hard enough during systole (contractility is impaired)
    - due to weekend ventricle

AND OR

  1. Diastolic dysfunction, not enough blood fills into ventricles during diastole, impaired relaxation of ventricle
    - normal ejection fraction but lower cardiac output
    - end diastolic volume is lower
145
Q

what is the result of systolic dsyfunction

A
  • lower ejection fraction
  • lower cardiac output
  • end systolic volume is higher
  • impaired contractility
  • ventricles can’t pump as much blood out
  • heart failure
146
Q

What are heart failures initial compensation mechanisms to attempt to restore and maintain CO and MAP to perf use tissues?

A

decreased cardiac output and decreased renal blood flow triggers

  • activate renin
  • activate ang 1,2
  • increase thirst
  • activate angitensinogien
  • activate the renin-angiotensin
    aldosterone system
  • increase Na+ and H2O reabsorption
  • increase vasoconstriction which triggers increase aldosterone

all to increase BV to increase MAP

can also be detected by the baroreceptor reflex to increase sympathetic nervous response to increase
- vasoconstriction
- contractility
- sv
- hr

147
Q

diastolic dysfunction results in

A
  • decreased end diastolic volume
  • decreased stroke volume
  • decreased cardiac output
    *ejection fraction DOES NOT decrease
148
Q

heart failure initial compensation attempts to restore CO will result in

A

ventricular hypertrophy

149
Q

3 different types of ventricular hypertrophy

A

A. physiological symmetric hypertrophy
B. pathologic concentric hypertrophy
C. pathologic eccentric hypertrophy

150
Q

physiological symmetric hypertrophy

A

proportionate increase in wall thickness and diameter
- healthy muscle fibre growth

151
Q

B pathologic concentric hypertrophy

A

disproportionate increase in wall thickness
- myofibrils grow in parallel to be thicker muscle fibers
*often due to pressure overload

152
Q

C pathologic eccentric hypertrophy

A

disproportionate increase in wall circumference
- myofibrils will grow in series to be longer muscle gibers
*often due to volume overload

153
Q

eventually the heart can no longer compensate to restore CO, what happens

A

leads to congestive heart failure
- CO eventually decreases (decreased myocardial tissue function)

  • ejection fraction is reduced: causing lower ejection fraction, lower systolic volume
  • **increase end diastolic volume because the ventricle output is less than inflow of blood
    -> the blood begins to back up into pulmonary or systemic circulation (depending on the side the heart that is failing)
154
Q

Left sided heart failure process steps

A
  1. left ventricle weakens (from trying to contract with more force and overcome overload) and cannot empty
  2. there is decreased cardiac output to the system
  3. there is also decreased renal blood flow (renin-angiotensin and aldosterone secretion is stimulated in response)
  4. there is a backup of blood into the pulmonary vein
  5. the high pressure in pulmonary capillaries which leads to congestion or edema
155
Q

Right sided heart failure process steps

A
  1. Right ventricle weakens and cannot empty in response to (the increased resistance in pulmonary capillaries that cause a workload the heart cannot overcome)
  2. decreased cardiac output to the system
  3. decreased renal blood flow (stimulates renin-angiotensin and aldosterone)
  4. blood backs up into systemic circulation in the veneer cavea
  5. increase venous pressure results in edema in legs and liver and abdominal organs
  6. very high venous pressure causes disteneded neck vein and cerebral edema
156
Q

stroke: cardiovascular disorder with neurological consequences : physiology explained BRIEFLY

A

an area of the brain is deprived of blood

157
Q

Stroke symptoms depend on

A

the area deprived of blood

158
Q

types of stroke

A
  • ischemic
  • hemorrhagic
  • transient ischemic attack
159
Q

most common type of stroke

160
Q

ischemic stroke definiton

A
  • blood flow to an area of brain is blocked off
161
Q

ischemic stroke causes

A
  • atherosclerotic plaque build up which leads to blockage
  • blood clot traveling to brain from another location (atherosclerotic progression)
162
Q

ischemic stroke extent of damage depends on

A

length and degree of blockage
- partial vs total occlusion
( 5 minutes of ischemia can cause irreversible damage to nerve cells such as necrosis & inflammation)

163
Q

ischemic stroke acute treatment

A
  • thrombolytic therapy
    tissue plasminogen activator= clot busting agent

*tight time window for effectiveness

164
Q

hemorrhagic stroke definiton

A

15% of strokes
- burst blood vessel that leads to bleeding in an area brain causing local swelling and damage

165
Q

most common cause of hemorrhagic strokes

A

severe hypertension

166
Q

hemorrhagic symptoms

A

severe
- extreme headache, loss of consciousness, coma, death

167
Q

hemorrhagic stroke life threatening treatment

A
  • anticlotting treatment
168
Q

transient ischemic attack (TIA)

A

“mini stroke” “silent stroke”
- temporary blockage of a cerebral artery that resolved

169
Q

transient ischemic attack symptoms

A

same as stroke but can be milder will fully resolve within 24 hours (even minutes in some cases) without treatment

170
Q

TIA can be a warning of

A

an impending stroke (40% of people who have a TIA will eventually go on to have a full stroke, usually within a few days after the TIA)

171
Q

stroke risk factors

A
  • age
  • atherosclerosis
  • hypertension
  • atrial fibrillation
172
Q

stroke treatment

A
  • antithrombotic therapy
  • OTs , PTs, Speech-language pathologist
173
Q

stroke prevention

A
  • reduce risk factors
  • healthy lifestyle modifications
  • prophylactic treatments
174
Q

BE FAST

A

balance
eyes
face
arms
speech
time

175
Q

respiratory system airflow pathway

A

upper respiratory tract
- nasal cavity
- larynx
lower respiratory tract
- trachea
- primary bronchi (R/L)
- many smaller bronchi
- bronchioles (site of variable resistance: bronchoconstriction and dilation)
- Alveoli (site of gas exchange)

176
Q

air flow depends on

A

pressure gradient and resistance

177
Q

Flow equation

178
Q

resistance equation

179
Q

pressure gradient will cause air flow to

A

flow down from higher to lower pressure

180
Q

in pressure gradient, resistance will

A

decrease with increase in CSA

181
Q

modulation of bronchiolar radius is done by

A
  • bronchodilaton
  • bronchoconstriction
182
Q

bronchodilation

A

decreased resistance to air flow
* paracrine response
increased PCO2-> relaxation of bronchiole smooth muscle
*SNS response
epinephrine binds to Beta - adrenergic receptors-> relaxation of bronchiole smooth muscle

183
Q

bronchoconstriction

A

increased resistance to air flow
*paracrine response
histamine released by local mast cells in an immune response

*PNS response
Ach binds to muscarinic receptors
-> causes constriction of bronchiole Smooth muscle
rest and digest response

184
Q

lung compliance definition and equation

A

how easily the lung can expand
compliance = (delta V/ delta P)

185
Q

elastance definition

A

ability of the lung to springback after being stretched, the inverse of compliance
- due to the presence of elastin fibers throughout the lung interstitial space

186
Q

radial traction

A

elastic fibers pull on the airways of bronchioles helping them open during inspiration

187
Q

radial traction is possible because

A

healthy lung tissue contains elastic fibers surrounding the alveoli

188
Q

why is radial traction helpful

A

prevents airway collapse during expiration

189
Q

factors that affect alveolar gas exchange

A
  • O2 reaching alveoli
  • composition of inspired air
  • alveolar ventilation
  • rate of depth and breathing
  • airway resistance
  • lung compliance
  • gas diffusion between alveoli and blood
  • surface area
  • barter thickness
190
Q

Factors that affect pulmonary ventilation and/or Gas exchange

A
  • obstructive lung disease
  • restrictive lung disease
  • cardiovascular disorders
191
Q

obstructive lung diseases

A
  • away obstruction causes increased resistance to airflow

larger impact on expiration -> air gets trapped-> limited ventilation
ex) asthma, bronchitis, emphysema, chronic obstructive pulmonary disease (COPD)

192
Q

Restrictive lung disease

A

reduced lung compliance-> increased stiffness -> limited expansion -> limited ventilation
- near normal rates of inspiration and expiration
ex) pulmonary fibrosis

193
Q

cardiovascular disorders

A
  • pulmonary edema
  • pulmonary embolism
194
Q

diffusion rate can be impacted by

A
  • surface area
  • pressure gradient
  • barrier thickness
195
Q

During left-sided heart failure, blood backs up into pulmonary circulation, raising the hydrostatic pressure and forcing fluid out into the interstitial space. This leads to pulmonary edema. This impacts diffusion rate of gases due to modification of which of the following:
Surface area for diffusion
Pressure gradient of gases
Barrier thickness

A

barter thickness, the

196
Q

In Asthma, bronchoconstriction along with overproduction of mucus in the airways reduces the amount of O2 that reaches the Alveoli. This impacts diffusion rate of O2 due to modification of which of the following:
Surface area for diffusion
Pressure gradient of gases
Barrier Thickness

A

pressure gradient

197
Q

Lung volumes in obstructive lung disease

A
  • increase residual volume due to air being trapped in lungs
  • decreased expiratory reserve volume
  • decreased inspiratory reserve volume
  • air is trapped in lungs: not enough air can leave or enter
198
Q

lung volumes in restrictive lung disease

A
  • decreased residual volume
  • decreased expiratory reserve volume
  • decreased inspiratory reserve volume

*flow rates normal, volumes decreased

speed of flow is fine there’s just less air to move out
In restrictive disease, both FEV1 and FVC are reduced, but they’re reduced proportionally, so the FEV1/FVC ratio is normal or even increased.

199
Q

FEV1/FVC ratio in obstructive lung disease

A

less than or equal to 0.7

200
Q

FEV1/FVC ratio in restrictive lung disease

A

greater than or equal to 0.8

201
Q

which leads to an increased residual volume due to air trapping

A

obstructive lung disease

202
Q

which displays a more normal flow rate but an inability to fully inflate lungs

A

restrictive disease

203
Q

Obstructive lung diseases can cause increased

A

resistance to airflow due to reduced airway radius

204
Q

reduced airway radius can cause

A
  • bronchoconstriction
  • inflammation
  • excess mucus production
  • reduced alveolar elastic recoil (lead to less radial traction)
205
Q

radial traction

A

elastic recoil of alveoli in lungs to pull in the airways and hold them open

206
Q

in obstructive lung diseases the problem is often with

A

expiration (airways collapse due to inward force which is imposed by exhalation)

207
Q

where does air get trapped in obstructive lung disease

A

in the alveoli

208
Q

asthma

A

bronchial obstruction- due to hypersensitive (allergic extrinsic) or hyperresponsive (non allergic, intrinsic) immune response

209
Q

universal asthma response

A
  • inflammation and edna of muscosa
  • increased secretion of thick muscus within airways
  • broncochonstriction
210
Q

symptoms of asthma

A
  • coughing, wheezing, shortness of breath
  • coughing up thick mucus
211
Q

allergic asthma

A

extrinsic
- commonly manifests in childhood
(often grow out of it)
- hypersensitivity reaction triggers immune response
- triggered by inhaled allergens

212
Q

non allergic asthma

A

intrinsic
- more commonly manifests in adulthood
- hyperresponsive reaction to stimuli
- triggered by factors such as anxiety,stress, exercise, cold air, etc

213
Q

Pathophysiology of an allergic asthma attack

A

First stage (immediate):
- memory immune cells within respiratory muscosa recognize antigen

  • they release chemical mediators (histamine) which causes inflammation, increased mucus secretions, immune cell recruitment
  • they also stimulate vagus nerve causing bronchoconstriction

Second stage (within a few hours):
- increased leukocyte infiltration
- increased release of chemical mediators
- prolonged inflammation, mucus, bronchoconstriction, epithelial cell damage (over time with chronic asthma, those cells can regenerate)

214
Q

partial obstruction asthma

A
  • some air is passed through area of obstruction
  • but have less ability to move air out which results in air trapping

*attempts to forcefully expire can lead to collapse of smaller airways

  • residual volume increases : less air inspired, harder to cough out mucus
215
Q

in partial obstruction asthma, air trapped over time can cause

A
  • air trapped and hyperinflation can stretch out alveoli and cause loss of elasticity
216
Q

total obstruction asthma

A

muscus plug completely blocks airflow through narrowed airway
- atelectasis (collapse) of whole section to distal block

217
Q

asthma treatment goal

A

to minimize number and severity of acute attacks

218
Q

asthma treatment process

A
  • determine triggers and avoid them if possible
  • good ventilation
  • inhaler (salbutamol, beta 2- adrenergic agonist to allow for bronchodilation)
  • other meds: corticosterois, long acting bronchodilators
219
Q

what does asthma medication do to treat

A

bronchodilate

220
Q

chronic obstructive pulmonary disease

A
  • a group of chronic respiratory disorders that cause
  • progressive tissue degeneration
    *airway obstruction

combination of : emphysema and chronic bronchitis
- irreversible and progressive damage to lungs
- 80-90% of causes caused by smoking

221
Q

emphysema definition

A

“the disappearing lung disease
- destruction of alveolar walls

222
Q

pathogenesis of emphysema

A

smoking or air pollutant and/or genetic predisposition cause

  • oxidative stress, increased apoptosis and senescence
  • inflammatory cells release of inflammatory mediators
  • protease antiprotease imbalance

which all cause alveolar wall destruction

223
Q

elastase

A

protease that promotes breakdown of elastic fibers

224
Q

alpha 1- antitrypsin

A

anti protease that inhibits elastase

225
Q

what can increase oxidative stress and inflammation in alveoli

A

increases the activity of elastase and decrease effect of alpha 1- anti trypsin

226
Q

two types of lung tissue changes in emphysema

A
  1. breakdown of alveolar walls
  2. increased mucus production
227
Q

breakdown of alveolar walls in emphysema

A
  • decreased SA for gas exchange
  • loss of elastic fibers (decreased elastance and increased compliance)
  • decreased radial traction (collapse of small airways, resulting in air trapping)
228
Q

increased mucus production in emphysema

A
  • due to chronic inflammation and infection
  • leads to thickening and fibrosis of bronchial walls
229
Q

functional consequences of lung tissue changes in emphysema

A
  • progressive difficulty with expiration
    air trapping, increase in residual volume
  • overinflation of lungs
  • ribs remain in inspiratory position and increased anterior-posterior diameter of chest (barrel chest)
230
Q

alveoli with emphysema have

A
  • overinflated alveolus
  • loss of septal capillaries ( decreased SA)
  • loss of elastic fibers (decreased recoil)
231
Q

consequences of advanced emphysema

A
  • frequent and more severe infections because secretions are more difficult to remove
  • pulmonary hypertension and cor pulmonale
  • lower ventilation which causes vasoconstriction to try to match ventilation nd perfusion
  • increase MAP in pulmonary circulation causing increased workload of RV
232
Q

emphysema symptoms

A

dyspnea
hyperventilation with prologoned expiratory phase
fatigue from hypoxia

233
Q

emphysema diagnosis

A

based on chest x-rays and pulmonary function tests that look for:
increased residual volume and TLC, decreased vital capacity and inspiratory and expiratory reserve volume
- FEV1 and FVC reduced

234
Q

emphysema treatment

A
  • avoid irritants and infection
  • pulmonary rehab and breathing techniques, bronchodilators
  • high flow nasal O2 therapy
235
Q

chronic bronchitis definiton

A
  • chronic irritation of bronchi due to exposure to inhaled irritants
  • results in chronically inflamed airways with increased mucus production
236
Q

pathogenesis of chronic bronchitis

A

chronic exposure to irritant causes inflammation within the bronchial wall
- chronic inflammatory response
- hyperplasia of mucous glands and other cell walls

-airways narrow, hypersecretion of mucus

  • airway obstruction and build up of secretions
  • lower ventilation, and alveolar hyper inflation
  • arterial vasoconstriction in lungs
  • pulmonary hypertensionR and L sided congestive heart failure
237
Q

chronic bronchitis symptoms

A
  • chronic cough
  • this and purulent secretions
  • dyspnea (shortness of breath)h
238
Q

chronic bronchitis diagnosis

A
  • symptoms
  • chest X ray
239
Q

chronic bronchitis treatment

A
  • avoid irritants and infection
  • medication
  • chest therapy to help with expelling mucus
  • bronchodiltors
  • high flow of nasal O2 therapy
240
Q

Restrictive lung disease cause

A

impaired lung expansion, all lung volumes reduced

241
Q

2 types of restrictive lung disease

A
  1. extra pulmonary issue : limits lung expansion
  2. lung disease that impairs compliance
242
Q

extra-pulmonary lung disease which limit lung expansion

A
  • spinal disorders: kyphosis, scoliosis
  • disorders of muscle weakness: ALS, muscular dystrophy
243
Q

lung disease that impairs compliance

A
  • chronic inflammation that causes irritation, fibrosis, and decreased lung compliance
244
Q

pulmonary fibrosis definiton

A

Decreased lung compliance as….

a result of long term exposure to irritants
- inflammation of fibrotic tissue

245
Q

what does pulmonary fibrosis result in

A
  • decreased barrier permeability. at alveoli
  • decreased compliance which results in:
  • more effort for inspiration
  • dyspnea
  • cough
246
Q

pulmonary fibrosis

A

treatment: remove exposure, treat infection

247
Q

two vascular issues that effect gas exchange:

A
  1. pulmonary edema
  2. pulmonary embolus
248
Q

pulmonary edema

A

fluid collects around and in alveoli

Caused byL

inflammation within lungs
increased capillary permeability
pulmonary hypertension
increased hydrostatic P in blood
- increased fluid out of capillaries and into interstitial space

249
Q

pulmonary edema signs and symptoms

A
  • cough, dyspnea, rales, increased effort to inspire as compliance decreases, hypercapnia and/or hypoxia
250
Q

pulmonary edema association with congestive heart failure

251
Q

pulmonary embolus

A
  • blood clot that blocks the flow of blood through the lung tissue
    most originate within deep leg veins
252
Q

pulmonary embolus risk factors

A
  • immobility
  • trauma, surgery
  • deep vein thrombosis
  • anything that increases risk of blood clots
253
Q

pulmonary edema symptoms

A
  • chest pain
  • dyspnea
    SNS response: tachycardia
254
Q

Diabetes Mellitus

A

a chronic disorder of metabolism characterized by elevated plasma glucose levels (hyperglycemias), resulting in defects in insulin production, action or both

255
Q

insulin

A

released from beta cells of endocrine pancreas in response to glucose

256
Q

main actions of insulin

A
  • stimulates glucose uptake into cells and glucose metabolism
  • stimulates anabolic/fed-state metabolism
  • glycogen synthesis
    *fatty acid uptake and lipogenesis
    *protein synthesis
  • inhibits catabolic/fasted state metabolism
    *fat and glycogen breakdown
    *gluconeogenesis
257
Q

mechanism of insulin induced glucose uptake

A

glucose enters through the GLUT-4 transporter in muscle cells and adipose tissue

258
Q

insulin is required for translocation of

A

GLUT-4, a glucose transporter to the cell surface

259
Q

liver and brain do not require

A

insulin for glucose uptake
- but insulin is still important for anabolic processes in tissues

260
Q

consequence of insulin deficit (impaired production and/or action)

A
  • decreased glucose uptake in cells for metabolic and anabolic processes can cause impaired liquid, protein, and carbohydrate metabolism
  • cells can’t take up glucose so homeostasis is impacted
261
Q

diabetes mellitus- type 1, 2 backgroudn

A
  • 10% of type 1
  • 90% of type 2 (1 undiagnosed in every 2-3 diagnosed)
262
Q

how many people are estimated in living with pre diabetes

A

1 in 3 people

263
Q

pre diabetes is :

A

a precursor to type 2 diabetes
- blood glucose levels higher than normal but not high enough for type 2 diabetes diagnosis

264
Q

gestational diabetes

A

type two diabetes develops during pregnancy but disappears after delivery
- 3-20% of pregnant individuals
- 5-10% with gestational diabetes will develop type 2 later in life

265
Q

diabetes mellitus signs and symptoms

A

polyuria (frequent urination)
polydipsia (thirst)
polyphasic (hunger)
weight loss (T1DM)
fatigue
additional acute symptoms: ketoacidosis- very rare but very serious (T2DM)

266
Q

T1DM

A

onset of symptoms usually acute and intense

267
Q

T2DM

A

symptoms are usually subtle and insidious
- often no symptoms for years or decade prior to diagnosis

268
Q

diabetes pathophysiology

A

Insulin deficit from decreased insulin secretion or increased insulin resistant cells

  • decreased glucose transport into cells
    leads to:
  • polyphagia (hunger)
  • hyperglycemia (high blood glucose)
  • glyconeolysis
  • gluconeogeneis
  • lypoliysis
  • ketacidocsis-> acidocsis
    -elecrolyte imbalance

*all leads to dehydration

269
Q

osmotic diuresis

A

increased urine production due to excess solute filtered into kidneys

270
Q

diabetic ketoacidosis

A

ketone bodies are produced as a byproduct of fatty acid metabolism in liver
- fatty acids are brought into mitochondria in live then broken down into ketone bodies -> sent out to be used as an alternate source of ATP production in cells around body

  • excess can be excreted in urine

*both of these pathways are rate-limiting
(if there are too many ketone bodies present in the blood at one time, metabolic acidosis happens)

271
Q

signs and symptoms of diabetic ketoacidosis

A
  • fruity breath, dehydration, nausea and vomiting, hyperventilation, lenthargy, confusion, coma
272
Q

Diabetic ketoacidosis and dyhydration

A
  1. liver produces glucose to feed body without insulin, but glucose accumulates in bloodstream
  2. body starts breaking down fat by producing ketones, ketones then build up in bloodstream
  3. ketones and glucose transferred into urine. the kidneys use water to clear the blood from excess glucose and ketones
  4. body attempt to get rid of KETONES and GLUCOSE, a lot of water is lost. (osmotic diuresis) Leads to dehydration and may worsen ketoacidosis
273
Q

complications of chronic hyperglycemia

A
  • macrovascular disease: athlerosclerosis
  • microvascular disease
    retinopathy and nephropathy: microvascular damage due to high blood glucose
  • peripheral neuropathy : nerve degeneration due to ischemia, and altered metabolism, tingling and numbness
274
Q

Tye 1 diabetes

A

characterized by autoimmune destruction of Beta cells of pancreatic islets leading to lack of insulin
- possible predisposing factors: gentics, ecironemtnt

275
Q

type 1 diabetes progressive loss of beta cell mass over time explained

A

immune attack on islet beta cells
1. antibodies present in blood

pre-diabetes
2. partial loss of insulin secretion

  1. critical low beta cell mass

dibetes

276
Q

type 1 diabetes treatment

A

need to replace insulin
- through injections, pump, islet cell transplantt

need to tightly monitor blood glucose levels ( food intake and activity level in relation to insulin administration )

277
Q

islet cell transplantation

A
  1. donor pancreas with insulin producing islet in pancreas
  2. put in Ricordi chamber to separate islets
  3. islets introduced into liver
  4. transplanted islet secreting insulin in liver
278
Q

type 2 diabetes mellitus

A
  • characterized by insulin deficit (due to impaired action and production)
  • insulin resistance and beta cell destruction
  • symptoms usually subtle, often manifest later in disease progression
279
Q

type two diabetes risk factors

A
  • genetics
  • chronic energy imbalance
  • over nutrition
  • physical inactivity
  • obesity (chronic inflammation and high FFAs circulating in blood)
280
Q

Type 2 diabetes diagnosis and monitoring: glucose tolerance test

A
  • fasting blood glucose
  • oral glucose tolerance test
    or
  • hemoglobin level = glycated hemoglobin
281
Q

ethology and pathogenesis of type two diabetes

A
  • genetic predisposition and a chronic energy imbalance trigger
  • insulin resistance occurs: (insulin released but action is impaired)
  • increased stress on Beta cells
    initially: beta cell compensation- increased insulin secretion
    –> near normal blood glucose levels

overtime: beta cell dysfunction resulting in decreased insulin secretion-> hyperglycemia

282
Q

incretins

A

hormones released from GI tract in presence of carbohydrate
- bind to receptors on beta cells to increase amount of insulin release by glucose stimulus

283
Q

what makes skeletal muscle cells insulin resistant

A

impaired intracellular signalling in response to insulin binding to its receptor
- problem with insulin receptor function or something further downstream the signalling pathway the leads to GLUT-4 translocation to cell surface

resulting in less GLUT-4 translocation to cell surface

284
Q

3 primary sites of insulin resistance and the consequences

A
  • skeletal muscle
  • impaired glucose uptake
    *impaired anabolic mechanisms (glycogenesis, protein synthesis) metabolism impaired
  • liver
  • overproduction of glucose by liver (gluconeogenesis)
  • overproduction of fatty acids from glucose (lipogenesis)
  • adipose tissue
    *increased lipolysis-> increased free fatty acids circulating in blood
  • contributes to further insulin resistance in cells and atherosclerosis risk
  • chronic hyperglycemia causes damage to vascular endothelial cells
285
Q

treatment options for Type two diabetes

A
  • education, behaviour change technique
  • insulin injections
  • oral drugs:
    *metformin- suppress glucose output and decreased insulin resistance at skeletal muscles
    *sulfonylures- stimulated insulin production in pancreatic beta cells
    *thiazolidinediones decrease insulin resistance at target tissues
  • incretin-based therapies: drugs that mimic or enhance the effect of incretin hormones to increase insulin released from beta cells
286
Q

how are incretin hormones useful in treatment to type two diabetes

A
  • hormones like GLP- 1 are released in response to carbohydrate in the intestine, increase amount of insulin released from beta cells
287
Q

GLP-1 drug action for type 2 diabetes

A
  • an incretin hormone that binds to receptor to increase the amount of insulin released (glucose must be present for this action)

can also..
- delay gastric emptying
- decrease food intake
- slow rate of gluconeogensis
- protect beta cells from apoptosis and stimulate their proliferation

288
Q

Obesity

A

complex multifactorial chronic disease, with complex aetiology
- cause is defined as long-term energy imbalance between consume calories and expended calories

  • traditionally characterized by BMI of at least 30kg/m2

*a risk factor for many chronic diseases

289
Q

Rising obesity prevalence- worldwide epidemic

A

driven mainly by changes in global food system combined with other local environmental factors
- variation within a population due to interactions between environment and individual factors

290
Q

diagnosing obesity

A
  • location of excess adipose tissue matters (visceral adiposity is associated with chronic disease risk)
  • metabolic health matters
    adipose tissue can impact metabolism and inflammatory status
    *look at blood glucose and lipid levels, blood pressure, and inflammatory blood markers
291
Q

pathophysiological feature of obesity

A
  • increased adiposity
  • causes a cascade increase in, lipid production, SNS, renin-agiotensin aldosterone system, mechanical stress etc
  • resulting in increased fatty acid release, lipotoxicity, dyslipidemia, hypertension
291
Q

increased adiposity (obesity) and its link to type 2 diabetes

A
  • adipose tissue has endocrine functions that produce adipose-derived cytokines (adipokines) and other cytokines

levels decrease in obesity

  • also has Leptin which is pro inflammatory. plays role as a hormone

levels increase in obesity

  • other cytokines secreted in obesityL TNF-alpha, IL-6, etc-> pro- inflammatory

results in
- chronic systemic inflammation
- increased circulating free fatty acids

insulin resistance-> type 2 diabetes

291
Q

obesity treatment

A

treatment goal= weight loss

modalities:
- multimodal lifestyle interventions

  • pharmacotherapy: drugs aim to reduce food intake
  • medical devices : intragastric ballons, vagus nerve blocker, suppresses neural communication between stomach and brain
  • bariatric surgery
292
Q

5 principles of obesity

A
  1. obesity is complex
  2. driven by biology not by choice
  3. many health effects of excessive weight can start early
  4. obesity is treatable
  5. weight bias, stigma, discrimination are harmful
293
Q

metabolic syndrome metabolic risk factors

A

*if you have 3 or more of the above you can be diagnosed
- lowHDL cholesterol
- visceral obesity
- high triglycerides
- insulin resistance
- hypertension

294
Q

how common is metabolic syndrome

A

1 in 5 canadians
- is asymptomatic

295
Q

typical progression of metabolic syndrome

A

1) genetic predisposition and behavioural factors
2) accumulated body fat
3) develop Mets
4) greatly increased risk for an progression to multiple chronic diseases (type 2 diabetes, CVD,etc)

296
Q

process and timeline of change program

A
  • baseline visit going over bloodwork, readiness, plan
  • meet weekly with kin and dietitian to monitor progress, support and adjust as needed
  • 3-12 meets monthly with kin and dietician + doc every 3 months to review blood work
297
Q

purpose of change program

A

help people with diabetes and metabolic syndrome

298
Q

Canadians developing cancer stats

A

2 in 5 Canadians will develop cancer in their lifetime

299
Q

Neoplasm

A

a tumor
- cellular growth that no longer responds to normal genetic control
- divinding outside of regular mitotic signals

this deprive other cells of nutrients and metabolism

300
Q

characteristics of a neoplasm depend on

A

the type of cell from which the tumor Arose and the unique structure and growth pattern

301
Q

benign tumors

A

typically differentiated cells
replicate at higher rate than normal
expands in capsule, no spread

302
Q

malignant tumor

A

more often cells are abnormal meaning: poorly differentiated, nonfunctional, disorganized

rapid uncontrolled replication

can infiltrate other tissues and blood vessels: break away and spread to distant regions ( metastasis )

303
Q

progression from precancerous = to cancer cell growth

A

abnormal cell growth may develop into cancer

hyperplasia (cells divide at rate faster than normal)
atypic (cells are slightly abnormal)
metaplasia (change in cell type in particular area)
dysplasia(cells are abnormal, they are growing faster than normal and are not arranged like normal)

abnormal cell growth that has progressed to cancer

carcinoma in situ- cells very abnormal but have not grown into nearby tissue

304
Q

cancer classification is based on

A

1) location where cancer is first developed

2) based on type of tissue
- carcinoma: epithelial origin (80-90% of cancers)

  • sarcoma (supportive and connective tissue origin, bones tendons cartilage muscle fat)
  • melanoma: melanocytes (skin pigment cells)
  • myeloma: plasma cells
  • leukaemia: abc
  • lymphoma: within lymphatic system
  • can also have mixed types
305
Q

carcinogenesis

A
  • process of normal cells transformed into cancer cells
306
Q

carcinogenesis risk factors

A
  • multifactorial : lead to changes in gene expression
  • genetics afe
  • environment
  • lifestyle
  • biological factors
307
Q

careinogenesis development stages

A

1) initiation
- exposure to one or multiple carcinogens causes first DNA change
*promotes risk of developement

2) promotion
- exposure to promoters leads to changes in cell that promote cancer phenotype -> malignant conversion
* with the right combination, progression to cancer

3) progression
- changes to regulation of growth leads to malignant tumor growth, invasiveness, and metastasis
*can’t detect until its well into progression phase

308
Q

hallmarks of cancer (everything done around tumor growth to promote cancer progression )

A

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 extracellular matrix: enables them to break off from tissue and mass spread

*secrete growth factors that stimulate development of new capillaries (promoting angiogenesis)

309
Q

local effect of malignant tumors

A

pain:
- often absent until later stages when tumor is well advanced
- depends on type and location of tumor
- can be due to ischemia, blood or fluid collecting in the area, inflammation, infection, physical compression

obstruction:
- due to tumor compression
- can be reason to maintain treatment during late stages (palliative treatment)

Inflammation and necrosis of surrounding healthy tissue:
- loss of normal function

310
Q

obstruction by tumors

A
  • tumor blocking airflow in bronchus
  • types of tumor growth obstructing colon

tumor can compress a passageway or duct from inside or due to growth around a structure

311
Q

systemic effects of malignant tumors

A
  • fatigue
    inflammatory process, stress, anemia
  • weight loss and cachexia
    due to lack of appetite, fatigue, pain, stress, increased metabolic demands due to cancer
  • edema
    inflammatory response which causes fluid buildup within body cavities
  • bleeding
    of tumor erodes blood vessels
  • paraneoplastic syndromes
    tumor cells can secrete substances (like hormones) that affect neurologic function, blood clotting, hormone levels
312
Q

spread of malignant tumors steps

A
  1. tissue invasion
    - local spread of tissues growing into adjacent tissue
  2. metastasis
    - spreading to distant sites (often liver and lungs) via blood or lymphatic system
  3. seeding
    - spread of tumor cells within body fluid or along membranes within body cavity
313
Q

detection and diagnosis of malignant tumor

A

detection:
- unusual bleeding or discharge
- bowel bladder changes
- wart or mole changes
- sore that does not heal
- unexplained weight loss
- persistent fatigue
- anemia
- persistent cough
- solid lump

diagnosis:
- warning signs
- routing, screening and self examination
- good tests
-x ray ultrasounds
- biopsy

314
Q

grading of cancer

A
  • describes the extent of disease and provides basis for treatment and prognosis
  • grading describes appearance and behaviour of cell

grade 1-4
1= atypical
4= aggressive

315
Q

staging of cancer

A

staging describes the size and extent of spread
stage 1-4
1= small, localized, easy to treat
4= distant spread, difficult to treat

316
Q

TNM staging system

A

size of primary tumor (T)
involvement of lymph nodes (N)
spread (metastasis) of tumor (M)

317
Q

cancer treatment can be

A

curative vs palliative

318
Q

cancer treatment options

A
  • surgery
  • radiation therapy
  • delivered externally or implanted within tumor tissue
    *causes mutations that kill tumor cells and damages surrounding blood vessels
  • chemotherapy
    *matched to specific cancer types
  • uses an optimal combination of drugs to effectively target different points in the tumor cell cycle
319
Q

POG

A

personalized oncogenomics
- analyze to the cancer genome in order to determine the best treatment for individual

320
Q

prognosis of cancer

A

varies depending on type and staging of cancer
- cure is defined as 5 years without recurrence after treatment

321
Q

cancer prevention

A
  • healthy choices
  • informed decisons
322
Q

exercise and cancer prevention

A
  • lots of research supporting regular physical activity as effective primary prevention
  • linked to exercise effect on immune function
323
Q

exercising with cancer

A
  • observational studies: regular physical activity linked to reduce cancer recurrence and improved survival
  • evidence supporting effectiveness in decreasing common side effects of cancer
  • both aerobic and resistance considered safe and effective
  • ok during active treatment
  • prescription within individual limits, modify as needed
324
Q

three names a drug could have

A
  • chemical name: chemical structure
  • generic name: official non proprietary name
  • brand name: commercial name given by company
325
Q

drug dose def

A

precise amount of active ingredient in medication
- dose is combined with inactive substances that help fill out medication and make it more convenient to use and improve its effectiveness at getting to its target in the body

326
Q

three phases of drug action

A
  1. pharmaceutical phase: how drug is formulated and dissolves
  2. pharmacokinetic phase (absorption, distribution, metabolism, excretion)
  3. pharmacodynamic phase : what the drug does to the body
327
Q

drug concentration vs Time graph represents

A

pharmacokinetics
- how long it takes for drug to be absorbed

328
Q

drug effect vs dose graph represents

A

pharmacodynamics
shows potency and efficacy
- how much drug is need for effect and the maximum effect a drug can produce

329
Q

potency

A

drug dose needed to reach certain effect

330
Q

efficacy

A

maximum effect of a drug

331
Q

therapeutic index

A

the amount of drug that can be administered to help then until it becomes toxic

332
Q

Types of pain

A

nociceptive: from tissue damage
neuropathic: from nerve damage, or dyfunction

333
Q

acute pain

A
  • sudden onset, short duration, linked to injury or surgery,
334
Q

chronic pain

A

lasts 3 months, can press after injury is healed

335
Q

pain management approaches

A

pharmaceutical: NSAIDs , opioids, antidepressants

non-pharmaceutical: physiotherapy, cat, acupuncture

336
Q

5 cardinal signs of acute inflammation

A
  1. redness
  2. heat
  3. swelling
  4. pain
  5. loss of function
337
Q

chemical mediators in inflammation

A
  • histamine
  • prostaglandins
  • bradykinin
  • cytokines
338
Q

three healing fates post acute inflammation

A
  1. resolution: full recovery
  2. regeneration: replacement
  3. fibrosis: scar tissue formation
339
Q

pharmacodynamics consider

A

what the drug does to the body
- potency and efficacy

340
Q

pharmacokinetics consider

A

what the body does to the drug
1. absorption
2. distribution
3. metabolism
4. excretion

HES 311 (2 decks)

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