POST MIDTERM 1: FINAL EXAM Flashcards
(344 cards)
1
Q
cardiac common pathologies
A
- angina pectoris
- myocardial infarction
- heart failure
- valve dysfunction
- arrhythmias
- inflammation
2
Q
Vascular common pathologies
A
- atherosclerosis
- peripheral artery disease
- coronary artery disease
- varicose veins
- hypertension/hypotension
3
Q
Blood vessels micro anatomy
A
4
Q
arteriosclerosis
A
- hardening and thickening of arterial wall
5
Q
most common type of arteriosclerosis
A
atherosclerosis
6
Q
atherosclerosis
A
inflammatory response to endothelial cell injury
- characterized by build up of atherosclerotic plaques (atheroma) within the vessel wall
7
Q
what is atherosclerosis vessel wall made up of
A
lipids (mainly cholesterol), cell debris, fibrin, thrombus
8
Q
most common arteries affected
A
- abdominal aorta and iliac arteries
- proximal coronary arteries
- thoracic aorta, femoral and popliteal arteries
- internal carotid arteries
- vertebral basilar and middle cerebral arteries
9
Q
atherosclerosis risk factors
A
age, family history, hypertension, diabetes mellitus, dyslipidemia, smoking, diet high in animal fat, sedentary lifestyle
10
Q
dyslipidemia
A
an imbalance of lipid components in the blood
11
Q
What are the four ways dyslipidemia can be classified
A
- high triglycerides
- high cholesterol
- high levels of low-density lipoproteins (Chylomicrons, VLDL)
- low levels of high-density lipoproteins (HDL, LDL)
12
Q
What are the functions of LDL and HDL
A
transport of lipoproteins in the blood
13
Q
Lipids are transported in combination with…
A
proteins
13
Q
LDL definition
A
Low density lipoprotein
14
Q
LDL function
A
transports cholesterol from liver to cells
- major factor contributing to atheroma formation
15
Q
LDL considered as the
A
Bad lipid (it contains most amount of cholesterol)
16
Q
HDL definition
A
high-density lipoprotein
17
Q
HDL function
A
transports cholesterol away from peripheral cells to liver
- breakdown in liver and excretion
18
Q
HDL considered the
A
good lipid (contains mostly protein)
19
Q
atherosclerosis pathogenesis
A
- damage to endothelial cells
- LDL enters into intimal layer and become oxidized
- macrophages eat up lipids-> foam cells-> fatty streak
- inflammatory response causes growth factors to be released
- smooth muscle cell proliferation and migration from the tunica media into the tunica intima, fibroblasts recruited
- growth of extracellular matrix: formation of a fibrous cap over a lipidcore= fibrous plaque
20
Q
atherosclerosis - progression and consequences
A
- Foam cells within lipid core undergo necrosis
- release enzymes that eat up fibrous cap
- eventual rupture
- platelets activate and adhere to site
- thrombus forms at the site of rupture
- thrombus occludes the lumen of the artery and can detach and travel to occlude a distal artery
21
Q
consequences of atherosclerosis progression
A
- ischemia (at least 70% of lumen occluded)
- total occlusion/plaque rupture
- weekend vessel wall
22
Q
ischemia
A
less than normal amount of blood flow to part of your body
23
Q
ischemia can lead to what diseases
A
- coronary artery disease : angina pectoris
- peripheral artery disease : claudication
24
total occlusion / plaque rupture causes:
- clot detachment
-> myocardial infarction and ischemic stroke due to not enough oxygenated blood flow
25
weekend vessel wall causes
aneurism
26
atherosclerosis diagnosis
- screening test to asses risk
- imagining
27
what do atherosclerosis screening tests look at
blood cholesterol level, blood pressure, exercise stress testing
28
what type of imaging is done to diagnose atherosclerosis
- coronary angiography : visualize blood glow in coronary arteries
- ultrasounds: visualize blood flow in peripheral vessels
29
atherosclerosis treatments
- risk reduction
- surgical intervention
30
types of atherosclerosis risk reduction options
- dietary lifestyle intervention
- pharmaceutical measures: anti-hypertensives, cholesterol-lowering, anticoagulants
- maintenance of existing conditions (diabetes, hypertension)
31
surgical intervention types for atherosclerosis
- angioplasty
- bypass
32
angioplasty types
- ballon angioplasty
- laser angioplasty
*a stent may be inserted after the angioplasty to maintain the opening
33
ballon angioplasty
catheter with an inflatable balloon that flattens the atheroma when inflated
34
laser angioplasty
catheter with a laser: inserted into narrowed part of artery: laser disintegrates plaque
35
Coronary artery bypass graft procedure
- 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
36
what is Angina pectoris
chest pain due to myocardial ischemia
37
how does angina pectoris occur
- due to vessel occlusion and/or inability to vasodilator to meet perfusion demand
38
Angina pectoris can be
stable (transient due to exertion) or unstable (prolonged pain at rest)
39
angina can be treated with
- rest
- lifestyle modification
- nitroglycerin
- surgical intervention
40
angina pectoris can be a warning sign for
MI
(especially unstable angina)
41
MI pathophysiology steps
- coronary artery is completely blocked
- prolonged ischemia
- cell necrosis
- infarction
42
common ways to develop MI
- atheroma progression, obstructing artery
- thrombus breaks away and lodges in a small branch
43
what determines the severity of MI damage
- size
- location
- duration
44
is MI damage reversible?
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
45
MI signs and symptoms
- pain : sudden, severe, crushing, chest pain
- pallor, sweating, nausea, dizziness, dyspnea
- anxiety
- hypotension rapid and week pulse
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myocardial infarction diagnosis
- ecg changes
- blood markers released by necrotic cells
* myoglobin, CPK-MB, AST, LDH, cardiac specific troponin
47
MI complications
- sudden death due to fibrillation
- cariogenic shock : severely low cardiac output
- heart failure (acute or chronic)
48
MI treatment options
- antithrombotic therapy
- defibrillation to restore normal heart rhythm
- surgery
- cardiac rehabilitation programs : exercise, diet, stress reduction
49
peripheral artery disease cause
due to atherosclerosis in peripheral arteries or inflammation that leads to narrowing of arteries
50
where does peripheral artery disease often occur
in the legs
51
signs and symptoms of peripheral artery disease
- fatigue and weakness in legs
- intermittent claudication
- weak peripheral pulse
- pale, hairless skin
52
peripheral artery disease
- reduce risk factors
- increased physical activity
- peripheral vasodilators
53
venous disorders (varicose veins)
- irregular dilated, tortuous areas of deep veins
54
varicose veins risk factors
- increased BMI
- pregnancy
- family history
- heavy lifting
55
where are varicose veins most common
in legs
56
treatment for varicose veins
- elevation and compression stockings
- intermittent voluntary muscle contractions when sitting for long periods
- surgical removal
57
thrombophlebitis
- thrombus development in vein where inflammation is present : platelets adhere to inflamed site, thrombus develops
58
phlebothrombosis
thrombus forms spontaneously in an area without prior inflammation
59
factors for thrombus development
- endothelial injury
- stasis of blood or sluggish blood flow
- increased blood coagulability(clotting)
60
signs and symptoms of venous thrombosis
- aching, burning, tenderness in affected area
- warmth, readness
- edna with pooling blood
- pain in calf muscle upon dorsiflexion
61
hypertension clinical definiton
sustained daytime BP > 135mmHg systolic and/or > 85 mmHg diastolic
* sometimes isolated as systolic or diastolic
62
90% of hypertension cases are
idiopathic: primary hypertension
63
if hypertension cause is unknown it is
secondary hypertension
64
hypertension risk factors
- age
- family history
- obesity
- diet
- low physical activity
- excess alcohol, smoking, stress
65
systolic pressure of 130-139 classifies as
hypertension stage 1
66
diastolic pressure of 80-90 classifies as
hypertension stage 2
67
systolic pressure of greater than 140mmHg classifies as
hypertension stage 2
68
diastolic pressure greater than 90mmHg classifies as
hypertension stage 2
69
risk of cardiovascular disease doubles with increments of ___ above _____
20/10, 115/75
70
__ % of Canadians have hypertension or pre hypertension
39%
71
Developing hypertension is ___
silent. You dont know you have it
72
effects of uncontrolled hypertension
- endothelial cell injury : atherosclerosis
- cardiac consequences:
coronary artery disease, hypertrophy, heart failure
- peripheral artery disease
- organ damage (kidneys, brain, eyes)
73
preload
volume of blood in ventricles at the end of diastole (end diastolic pressure)
74
afterload
resistance left ventricle must overcome to circulate blood
75
increased after load =
increased cardiac workload
76
MAP equation
MAP= cardiac output x peripheral resistance
77
neural mechanisms of blood pressure regulation
Baroreceptors
78
renal/hormonal mechanisms of BP regulation
- filtration rate
- renin release
- ADH
- H2O reabsorption and BV
79
vascular mechanisms of blood pressure regulation
endothelial cells
nitric oxide
vasodilation
endothenlin
vasoconstriction
80
Primary hypertension
- Na+ defect causes elevation of blood volume
- Increased peripheral vascular resistance
81
Hypertension treatment
- 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
82
how does exercise work as a treatment for hypertension
- exercise lowers BP physiological response after exercise
- moderate intensity 20-30minutes per session
83
acute hypotension is also known as
shock
84
acute hypotension
inadequate tissue perfusion: tissue ischemia, cellular damage
85
hypertension equation
MAP= Co x R
86
general signs and symptoms of shock
- tachycardia
- decreased urine output
- dizziness, feeling faint, altered mental status
87
main classifications of shock
- hypovolemic
- cardiogenic
- anaphylactic
- septic
- neuronic
88
cold shock happens from
decreased cardiac output
vasoconstriction, increased resistance, which increase mean arterial pressure
89
where does blood get redirected to in cold shock
blood flow redirected to vital organs
90
hypovolemic cold shock
- hemorrhagic and non-hemorrhagic (diarrhea and vomitting)
- decreased blood volume-> decreased venous return-> decreased CO
91
cariogenic cold shock
- problems with heart function -> decreased ability for heart to pump, CO decreased
92
warm shock causes
decreased systemic vascular resistance due to peripheral vasodilation
93
warm shock compensation
increased heart rate
94
anaphylactic shock (warm shock)
the most extreme reaction to an allergen
- mast cells release histamine and bradykinin-> increased vasodilation edema, bronchoconstriction
95
anaphylactic shock treatment
epinephrine, increased CO, smooth muscle relaxation, vasoconstriction
96
septic shock caused by
infection in bloodstreams
97
septic shock results in
macrophage activation-> cytokine release, increased vasodilation
98
septic shock treatment
IV fluids and antibiotics
99
neurogenic shock
loss of sympathetic tone: autonomic balance tips towards parasympathetic nervous system-> vasodilation and Bradycardia q
100
neurogenic shock can happen from
- 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)
101
orthostatic hypotension
- 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)
102
how is orthostatic hypotension caused
- impaired baroreceptor reflex function, hypovolemia, blood pooling in legs
- most commonly due to medication (vasodilators)
- increased risk in older adults
103
signs and symptoms of orthostatic hypotension
pallor, vertigo, blurred vision, feeling faint, dizziness, nausea
104
treatment of orthostatic hypotension
- water intake, salt intake, compression stockings, sleep slightly inclinde
- leg resistance exercise
105
what are the two determinants of blood pressure
- cardiac output
- resistance
106
cardiac output depends on
- stroke volume: preload and contractility
- heart rate: modulated by SNS (increase HR), PNS (decrease HR)
107
peripheral resistance depends on
radius of our small arteries
- vasoconstriction (increased vascular resistance)
- vasodilation (decreased vascular resistance)
108
Neural mechanisms of blood pressure regulation
baroreceptors send signals to the medulla to modify HR, SV, and Vascular resistance. via SNS/PNS output
109
renal/hormonal mechanisms of blood pressure regulation
regulation of blood volume:
through:
- filtration rate: (impacting Na+ and H2O absorption and excretion)
- renin release (RAAS)
- ADH release (H2O reabsorption)
110
vascular mechanisms of blood pressure regulation
endothelial cells release
- nitric oxide: vasodilation
- endothelia: vasoconstriction
111
RAAS renin angiotensin-aldosterone system purpose
to increase mean arterial pressure
111
RAAS steps explained
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
112
normal heart sinus rhythm determined by
action potential frequency of sinoatrial node cells
113
normal sinus rhythm rate
60-100BPM
114
pathway of excitation through the heart.
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
115
what are cardiac arrhythmias
abnormalities in either rate or path of electrical conduction
116
consequence of cardiac arrhythmias
can lead to disorganized contractions -> impaired cardiac output
117
sinus tachycardia heart rate abnormalities
HR is faster than normal >100BPM
118
sinus bradycardia
HR is slower than normal <60BPM
119
what are abnormalities in heart rate due to
an issue with automaticity
120
automaticity
sinoatrial node (SAN) sets pace of heart (no input required from nervous system)
121
normal automaticity modulation
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
122
abnormal automaticity results in
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
123
arrhythmias due to : altered electrical conduction happens from
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)
124
re-entry circuits
Abnormal conduction pathway formed either due to an additional accessory path or a block in the normal path
125
common arrhythmias: premature ventricular contractions:
triggered activity -> an electrical signal initiated by purkinje fibers instead of SA node!
- ventricles contract prematurely, a brief pause follows before normal rhythm returns
126
common arrhythmias: paroxysmal supraventricular tachycardia
new conduction pathway begins somewhere in atria (outside of normal conduction)
- new signal travels down ventricles-> ventricular tachycardia
*begins and ends suddenly
127
types of common arrhythmias
- premature ventricular contractions
- paroxysmal supra ventricular tachycardia
- fibrillation
128
common arrhythmias: fibrillation
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)
129
treatment for arrhythmias
- 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
130
heart failure definition
any functional or structural issue of the heart that causes low cardiac output
131
heart failure can be
left or right sided
acute or chronic
132
chronic heart failure:
- 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
133
in chronic heart failure, the ventricle undergoes
adaptive responses like hypertrophy and dilation
134
what are causes of chronic heart failure
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
135
Heart failure simplified definiton
heart is not pumping out enough content as it needs
136
determinants of cardiac output equations
CO=sv x hr
SV= edv(preload) -esv
137
Cardiac output is modulated by our
heart rate and stroke volume
138
HR is determined by our
SNS(pacemakers produce positive chronotropic increasing HR) and PNS (pacemakers produce negative chronotropic slowing HR)
139
SV is determined by our
preload and contractility (which is dictated by SNS (epinephrine) which will cause more forceful contractions)
140
the frank starling law
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
what can we use to measure heart function
ejection fraction
142
ejection fraction =
how well the ventricle pumps blood with each beat
- how much of the blood coming in has been ejected out
143
ejection fraction equation
EF(%)= SV/EDV x 100
144
Heart failure can be due to
1. Systolic dysfunction, ventricles can't pump hard enough during systole (contractility is impaired)
- due to weekend ventricle
AND OR
2. 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
what is the result of systolic dsyfunction
- lower ejection fraction
- lower cardiac output
- end systolic volume is higher
- impaired contractility
- ventricles can't pump as much blood out
- heart failure
146
What are heart failures initial compensation mechanisms to attempt to restore and maintain CO and MAP to perf use tissues?
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
diastolic dysfunction results in
- decreased end diastolic volume
- decreased stroke volume
- decreased cardiac output
*ejection fraction DOES NOT decrease
148
heart failure initial compensation attempts to restore CO will result in
ventricular hypertrophy
149
3 different types of ventricular hypertrophy
A. physiological symmetric hypertrophy
B. pathologic concentric hypertrophy
C. pathologic eccentric hypertrophy
150
physiological symmetric hypertrophy
proportionate increase in wall thickness and diameter
- healthy muscle fibre growth
151
B pathologic concentric hypertrophy
disproportionate increase in wall thickness
- myofibrils grow in parallel to be thicker muscle fibers
*often due to pressure overload
152
C pathologic eccentric hypertrophy
disproportionate increase in wall circumference
- myofibrils will grow in series to be longer muscle gibers
*often due to volume overload
153
eventually the heart can no longer compensate to restore CO, what happens
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
Left sided heart failure process steps
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
Right sided heart failure process steps
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
stroke: cardiovascular disorder with neurological consequences : physiology explained BRIEFLY
an area of the brain is deprived of blood
157
Stroke symptoms depend on
the area deprived of blood
158
types of stroke
- ischemic
- hemorrhagic
- transient ischemic attack
159
most common type of stroke
ischemic
160
ischemic stroke definiton
- blood flow to an area of brain is blocked off
161
ischemic stroke causes
- atherosclerotic plaque build up which leads to blockage
- blood clot traveling to brain from another location (atherosclerotic progression)
162
ischemic stroke extent of damage depends on
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
ischemic stroke acute treatment
- thrombolytic therapy
tissue plasminogen activator= clot busting agent
*tight time window for effectiveness
164
hemorrhagic stroke definiton
15% of strokes
- burst blood vessel that leads to bleeding in an area brain causing local swelling and damage
165
most common cause of hemorrhagic strokes
severe hypertension
166
hemorrhagic symptoms
severe
- extreme headache, loss of consciousness, coma, death
167
hemorrhagic stroke life threatening treatment
- anticlotting treatment
168
transient ischemic attack (TIA)
"mini stroke" "silent stroke"
- temporary blockage of a cerebral artery that resolved
169
transient ischemic attack symptoms
same as stroke but can be milder will fully resolve within 24 hours (even minutes in some cases) without treatment
170
TIA can be a warning of
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
stroke risk factors
- age
- atherosclerosis
- hypertension
- atrial fibrillation
172
stroke treatment
- antithrombotic therapy
- OTs , PTs, Speech-language pathologist
173
stroke prevention
- reduce risk factors
- healthy lifestyle modifications
- prophylactic treatments
174
BE FAST
balance
eyes
face
arms
speech
time
175
respiratory system airflow pathway
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
air flow depends on
pressure gradient and resistance
177
Flow equation
P/R
178
resistance equation
1/r4
179
pressure gradient will cause air flow to
flow down from higher to lower pressure
180
in pressure gradient, resistance will
decrease with increase in CSA
181
modulation of bronchiolar radius is done by
- bronchodilaton
- bronchoconstriction
182
bronchodilation
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
bronchoconstriction
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
lung compliance definition and equation
how easily the lung can expand
compliance = (delta V/ delta P)
185
elastance definition
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
radial traction
elastic fibers pull on the airways of bronchioles helping them open during inspiration
187
radial traction is possible because
healthy lung tissue contains elastic fibers surrounding the alveoli
188
why is radial traction helpful
prevents airway collapse during expiration
189
factors that affect alveolar gas exchange
- 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
Factors that affect pulmonary ventilation and/or Gas exchange
- obstructive lung disease
- restrictive lung disease
- cardiovascular disorders
191
obstructive lung diseases
- 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
Restrictive lung disease
reduced lung compliance-> increased stiffness -> limited expansion -> limited ventilation
- near normal rates of inspiration and expiration
ex) pulmonary fibrosis
193
cardiovascular disorders
- pulmonary edema
- pulmonary embolism
194
diffusion rate can be impacted by
- surface area
- pressure gradient
- barrier thickness
195
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
barter thickness, the
196
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
pressure gradient
197
Lung volumes in obstructive lung disease
- 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
lung volumes in restrictive lung disease
- 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
FEV1/FVC ratio in obstructive lung disease
less than or equal to 0.7
200
FEV1/FVC ratio in restrictive lung disease
greater than or equal to 0.8
201
which leads to an increased residual volume due to air trapping
obstructive lung disease
202
which displays a more normal flow rate but an inability to fully inflate lungs
restrictive disease
203
Obstructive lung diseases can cause increased
resistance to airflow due to reduced airway radius
204
reduced airway radius can cause
- bronchoconstriction
- inflammation
- excess mucus production
- reduced alveolar elastic recoil (lead to less radial traction)
205
radial traction
elastic recoil of alveoli in lungs to pull in the airways and hold them open
206
in obstructive lung diseases the problem is often with
expiration (airways collapse due to inward force which is imposed by exhalation)
207
where does air get trapped in obstructive lung disease
in the alveoli
208
asthma
bronchial obstruction- due to hypersensitive (allergic extrinsic) or hyperresponsive (non allergic, intrinsic) immune response
209
universal asthma response
- inflammation and edna of muscosa
- increased secretion of thick muscus within airways
- broncochonstriction
210
symptoms of asthma
- coughing, wheezing, shortness of breath
- coughing up thick mucus
211
allergic asthma
extrinsic
- commonly manifests in childhood
(often grow out of it)
- hypersensitivity reaction triggers immune response
- triggered by inhaled allergens
212
non allergic asthma
intrinsic
- more commonly manifests in adulthood
- hyperresponsive reaction to stimuli
- triggered by factors such as anxiety,stress, exercise, cold air, etc
213
Pathophysiology of an allergic asthma attack
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
partial obstruction asthma
- 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
in partial obstruction asthma, air trapped over time can cause
- air trapped and hyperinflation can stretch out alveoli and cause loss of elasticity
216
total obstruction asthma
muscus plug completely blocks airflow through narrowed airway
- atelectasis (collapse) of whole section to distal block
217
asthma treatment goal
to minimize number and severity of acute attacks
218
asthma treatment process
- 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
what does asthma medication do to treat
bronchodilate
220
chronic obstructive pulmonary disease
- 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
emphysema definition
"the disappearing lung disease
- destruction of alveolar walls
222
pathogenesis of emphysema
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
elastase
protease that promotes breakdown of elastic fibers
224
alpha 1- antitrypsin
anti protease that inhibits elastase
225
what can increase oxidative stress and inflammation in alveoli
increases the activity of elastase and decrease effect of alpha 1- anti trypsin
226
two types of lung tissue changes in emphysema
1. breakdown of alveolar walls
2. increased mucus production
227
breakdown of alveolar walls in emphysema
- 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
increased mucus production in emphysema
- due to chronic inflammation and infection
- leads to thickening and fibrosis of bronchial walls
229
functional consequences of lung tissue changes in emphysema
- 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
alveoli with emphysema have
- overinflated alveolus
- loss of septal capillaries ( decreased SA)
- loss of elastic fibers (decreased recoil)
231
consequences of advanced emphysema
- 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
emphysema symptoms
dyspnea
hyperventilation with prologoned expiratory phase
fatigue from hypoxia
233
emphysema diagnosis
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
emphysema treatment
- avoid irritants and infection
- pulmonary rehab and breathing techniques, bronchodilators
- high flow nasal O2 therapy
235
chronic bronchitis definiton
- chronic irritation of bronchi due to exposure to inhaled irritants
- results in chronically inflamed airways with increased mucus production
236
pathogenesis of chronic bronchitis
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
chronic bronchitis symptoms
- chronic cough
- this and purulent secretions
- dyspnea (shortness of breath)h
238
chronic bronchitis diagnosis
- symptoms
- chest X ray
239
chronic bronchitis treatment
- avoid irritants and infection
- medication
- chest therapy to help with expelling mucus
- bronchodiltors
- high flow of nasal O2 therapy
240
Restrictive lung disease cause
impaired lung expansion, all lung volumes reduced
241
2 types of restrictive lung disease
1. extra pulmonary issue : limits lung expansion
2. lung disease that impairs compliance
242
extra-pulmonary lung disease which limit lung expansion
- spinal disorders: kyphosis, scoliosis
- disorders of muscle weakness: ALS, muscular dystrophy
243
lung disease that impairs compliance
- chronic inflammation that causes irritation, fibrosis, and decreased lung compliance
244
pulmonary fibrosis definiton
Decreased lung compliance as....
a result of long term exposure to irritants
- inflammation of fibrotic tissue
245
what does pulmonary fibrosis result in
- decreased barrier permeability. at alveoli
- decreased compliance which results in:
- more effort for inspiration
- dyspnea
- cough
246
pulmonary fibrosis
treatment: remove exposure, treat infection
247
two vascular issues that effect gas exchange:
1. pulmonary edema
2. pulmonary embolus
248
pulmonary edema
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
pulmonary edema signs and symptoms
- cough, dyspnea, rales, increased effort to inspire as compliance decreases, hypercapnia and/or hypoxia
250
pulmonary edema association with congestive heart failure
v
251
pulmonary embolus
- blood clot that blocks the flow of blood through the lung tissue
most originate within deep leg veins
252
pulmonary embolus risk factors
- immobility
- trauma, surgery
- deep vein thrombosis
- anything that increases risk of blood clots
253
pulmonary edema symptoms
- chest pain
- dyspnea
SNS response: tachycardia
254
Diabetes Mellitus
a chronic disorder of metabolism characterized by elevated plasma glucose levels (hyperglycemias), resulting in defects in insulin production, action or both
255
insulin
released from beta cells of endocrine pancreas in response to glucose
256
main actions of insulin
- 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
mechanism of insulin induced glucose uptake
glucose enters through the GLUT-4 transporter in muscle cells and adipose tissue
258
insulin is required for translocation of
GLUT-4, a glucose transporter to the cell surface
259
liver and brain do not require
insulin for glucose uptake
- but insulin is still important for anabolic processes in tissues
260
consequence of insulin deficit (impaired production and/or action)
- 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
diabetes mellitus- type 1, 2 backgroudn
- 10% of type 1
- 90% of type 2 (1 undiagnosed in every 2-3 diagnosed)
262
how many people are estimated in living with pre diabetes
1 in 3 people
263
pre diabetes is :
a precursor to type 2 diabetes
- blood glucose levels higher than normal but not high enough for type 2 diabetes diagnosis
264
gestational diabetes
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
diabetes mellitus signs and symptoms
polyuria (frequent urination)
polydipsia (thirst)
polyphasic (hunger)
weight loss (T1DM)
fatigue
additional acute symptoms: ketoacidosis- very rare but very serious (T2DM)
266
T1DM
onset of symptoms usually acute and intense
267
T2DM
symptoms are usually subtle and insidious
- often no symptoms for years or decade prior to diagnosis
268
diabetes pathophysiology
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
osmotic diuresis
increased urine production due to excess solute filtered into kidneys
270
diabetic ketoacidosis
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
signs and symptoms of diabetic ketoacidosis
- fruity breath, dehydration, nausea and vomiting, hyperventilation, lenthargy, confusion, coma
272
Diabetic ketoacidosis and dyhydration
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
complications of chronic hyperglycemia
- 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
Tye 1 diabetes
characterized by autoimmune destruction of Beta cells of pancreatic islets leading to lack of insulin
- possible predisposing factors: gentics, ecironemtnt
275
type 1 diabetes progressive loss of beta cell mass over time explained
immune attack on islet beta cells
1. antibodies present in blood
pre-diabetes
2. partial loss of insulin secretion
3. critical low beta cell mass
dibetes
276
type 1 diabetes treatment
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
islet cell transplantation
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
type 2 diabetes mellitus
- 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
type two diabetes risk factors
- genetics
- chronic energy imbalance
- over nutrition
- physical inactivity
- obesity (chronic inflammation and high FFAs circulating in blood)
280
Type 2 diabetes diagnosis and monitoring: glucose tolerance test
- fasting blood glucose
- oral glucose tolerance test
or
- hemoglobin level = glycated hemoglobin
281
ethology and pathogenesis of type two diabetes
- 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
incretins
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
what makes skeletal muscle cells insulin resistant
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
3 primary sites of insulin resistance and the consequences
- 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
treatment options for Type two diabetes
- 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
how are incretin hormones useful in treatment to type two diabetes
- hormones like GLP- 1 are released in response to carbohydrate in the intestine, increase amount of insulin released from beta cells
287
GLP-1 drug action for type 2 diabetes
- 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
Obesity
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
Rising obesity prevalence- worldwide epidemic
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
diagnosing obesity
- 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
pathophysiological feature of obesity
- 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
increased adiposity (obesity) and its link to type 2 diabetes
- 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
obesity treatment
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
5 principles of obesity
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
metabolic syndrome metabolic risk factors
*if you have 3 or more of the above you can be diagnosed
- lowHDL cholesterol
- visceral obesity
- high triglycerides
- insulin resistance
- hypertension
294
how common is metabolic syndrome
1 in 5 canadians
- is asymptomatic
295
typical progression of metabolic syndrome
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
process and timeline of change program
- 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
purpose of change program
help people with diabetes and metabolic syndrome
298
Canadians developing cancer stats
2 in 5 Canadians will develop cancer in their lifetime
299
Neoplasm
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
characteristics of a neoplasm depend on
the type of cell from which the tumor Arose and the unique structure and growth pattern
301
benign tumors
typically differentiated cells
replicate at higher rate than normal
expands in capsule, no spread
302
malignant tumor
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
progression from precancerous = to cancer cell growth
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
cancer classification is based on
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
carcinogenesis
- process of normal cells transformed into cancer cells
306
carcinogenesis risk factors
- multifactorial : lead to changes in gene expression
- genetics afe
- environment
- lifestyle
- biological factors
307
careinogenesis development stages
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
hallmarks of cancer (everything done around tumor growth to promote cancer progression )
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
local effect of malignant tumors
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
obstruction by tumors
- 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
systemic effects of malignant tumors
- 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
spread of malignant tumors steps
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
detection and diagnosis of malignant tumor
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
grading of cancer
- 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
staging of cancer
staging describes the size and extent of spread
stage 1-4
1= small, localized, easy to treat
4= distant spread, difficult to treat
316
TNM staging system
size of primary tumor (T)
involvement of lymph nodes (N)
spread (metastasis) of tumor (M)
317
cancer treatment can be
curative vs palliative
318
cancer treatment options
- 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
POG
personalized oncogenomics
- analyze to the cancer genome in order to determine the best treatment for individual
320
prognosis of cancer
varies depending on type and staging of cancer
- cure is defined as 5 years without recurrence after treatment
321
cancer prevention
- healthy choices
- informed decisons
322
exercise and cancer prevention
- lots of research supporting regular physical activity as effective primary prevention
- linked to exercise effect on immune function
323
exercising with cancer
- 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
three names a drug could have
- chemical name: chemical structure
- generic name: official non proprietary name
- brand name: commercial name given by company
325
drug dose def
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
three phases of drug action
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
drug concentration vs Time graph represents
pharmacokinetics
- how long it takes for drug to be absorbed
328
drug effect vs dose graph represents
pharmacodynamics
shows potency and efficacy
- how much drug is need for effect and the maximum effect a drug can produce
329
potency
drug dose needed to reach certain effect
330
efficacy
maximum effect of a drug
331
therapeutic index
the amount of drug that can be administered to help then until it becomes toxic
332
Types of pain
nociceptive: from tissue damage
neuropathic: from nerve damage, or dyfunction
333
acute pain
- sudden onset, short duration, linked to injury or surgery,
334
chronic pain
lasts 3 months, can press after injury is healed
335
pain management approaches
pharmaceutical: NSAIDs , opioids, antidepressants
non-pharmaceutical: physiotherapy, cat, acupuncture
336
5 cardinal signs of acute inflammation
1. redness
2. heat
3. swelling
4. pain
5. loss of function
337
chemical mediators in inflammation
- histamine
- prostaglandins
- bradykinin
- cytokines
338
three healing fates post acute inflammation
1. resolution: full recovery
2. regeneration: replacement
3. fibrosis: scar tissue formation
339
pharmacodynamics consider
what the drug does to the body
- potency and efficacy
340
pharmacokinetics consider
what the body does to the drug
1. absorption
2. distribution
3. metabolism
4. excretion
