week 9 + 10 Flashcards
1
Q
heart failure s any fucnitonal.structureal issue that____
A
causes low cardiac output
2
Q
what are the 2 most common causes of chronic. heart failure?
A
CAD - previous MI
chronic uncontrolled BP
3
Q
hypokalemia would lead to ___ autoamticity.Why
A
decrease MAP – increase baroreceptors – icnrease SNS - increase in automaticitiy
4
Q
drugs like cocaine or meth would do what to eutomaticity. why
A
increase automaticity - act lie EP or NE - ramp up SNS activity
5
Q
pain or anxiety would do what to autmaticity and why
A
increase- fight/flight -increase SN ctivity
6
Q
hypercapnia (high blood co2) would do what to what to automaticity?
A
increase SNS - increase chemorecpetors
7
Q
heart damage/disease would do what to autmaticity
A
decrease - becuase it slows conduction system of ehart
8
Q
what does electrolyte imabalnce do to the automaticity of the hear
A
decrase excitability of SA node - decrsae autmaticity
9
Q
what would hypothermia do to autmaticicty?
A
decrease - decrease body temp - decrea met reate
10
Q
what would the vasovagal refelx do to automaticity of the heart and why?
A
vasovagal refelx - ovvveractivtiaon of vagus N and PNS
11
Q
SV is a function of ___. and __
A
EDV nd myocaridal cotnracitlity
12
Q
what is ejeciton fraction?
A
How wel the venticle pumps blood with each beat
13
Q
what is the difference between heart failure due to systolic and diastolic dysfunction o
A
systolic - ventricles cant pump hatd enough (contracitlity issue)
- weakened ventricle
diastoluc -not enough blood into venicles during diastole
- impaired relaxation
- result: normal ejectrion fraction, low
14
Q
what happens to ejection fraction and CO in systolic vs diastolic dysfunction?
A
systolic - lower EF and CO
diastolic - normal EF - lower CO
15
Q
systolic dysfunction is also refferred to as___
diastolic as ___
A
heat failure with reduced EF
Heart failrue with presevred EF
16
Q
what happens to EF and CO in systolic vs diatolic dysftunnion
A
systolic - decreased EF and CO
diastolic - decreased CO, preserved EF
17
Q
what does initial compensation of heart failure work to do?
A
mechanisms to maintain sufficient CO and MAP i. order to perus tissues
18
Q
what does evenual decomepnstaion of CO lead to?
A
congestive failure - blood begins to back up into pulmonary or sytemic circulation (epndig on side of heart)
19
Q
what ar ethe twi ways we initiall compesnate to restore CO in ehart failrue? what is teh resulr?
A
increase barorecptor refelex
renin-angiotensin-aldosteron system
increase MAP
result is venricular hyeprotphy
20
Q
what does left sided heart failure lead to?
A
pulmonary edema
21
Q
explain the pathogensis of left sided heart failure?
A
the left ventricle is weaker and must contact with more force to overcome afterload - LV hypertrophy - eventual failure: decreased CO, blood backs up into pulmonary circulation = pulmonary edema
22
Q
pulmonary edema is most likely caused by?
A
pulmonary edema most likely caused by left sided heart failure
23
Q
what is most common cause of left sided hear failure
A
hypertesnion
24
Q
what is the most common cause of right sided heart failure
A
COPD/pulmonsty ises
25
explain the pathogenesis of right-sided heart failure
icreased resitance in pulmonary capillaries - increased RV workload - RV hyeprophy + failure
blood backs ito sytemic system
26
left sided failure is congestion nito ____ and right side dis congestion into ___
left pulmoanary
right -sytemic - ankle edema
27
___ sided heart faiure can lead to ___ heart failrue
left sided can elad to right sided
28
what is a stroke
CV disorder wher earea of the brain is deprived of blood
29
what are the 2 types of strokes? what is most common?
ischemic and hemmoraic - ischemic is the most common
30
what is an ischemic stroke and what are 2 common causes
it is when blood flow to the brain is blocked off
1. atheroscleroitc plaque build up in carotid artery - leads to blockasfe
blood clot travels to brain. - atherslerotic progression
31
___ minutes of total ischemis in an ischemic stroke can lead to irreversible damage of nerve cells and necrosis and inflammation
5 minutes
32
what is treatment for ischmic stroke?
thrombolytic therapy (TPA) - tissue plasminogen activator - a clot-busting agent - tight time window for effectiveness
33
what is a hemmorhagic stroke?
a burst blood vessel leads to bleeding in an area of the brain - swelling and dammge
34
what is the most common cause of a hemmorhagic stroke?
sever hypertesnion
35
why must u be certain of the type of stroke before adminsitering treatment?
anti-clotting meds like TPA (tissue plasminogen activator) are very helpful for ischemic stoke however for a hemorrhagic stroke where blood vessels can be life-threatening so must be certain that it is an ischemic stroke
36
a mini/silent stroke is also known as and is a result of ?
Transient ischmic attakcke
a temporary block of the cerebral artery that resolved
37
How is a transient ischemic attack different from a n ishchemic stroke?
bloackage is only temporary and then resolved - it can be awarning sign for ischmic stroke
38
name 4 risk factors of stroke?
age, hypertension, atheroscleoris, atrial fibrillairon
39
name som treatment and prevnion measures for stroke
tratemeant 0 antithrombotic if ischmic
PT, OT, speech pathologist - if cuntions related to these are disturbed
pregbention - reduce risk factors, pa, healthy lifestyle, prophualctic traetements
40
airflow depends on ___ and ___
airflow and resistnace
41
SNS reponse leads t o broncho___
dilation
42
PNS resposne leads to broncho_____
constiction
43
what is lung compliance adn elastance
how easily the lung can expand versus the ability of the lung to spring back after being stretched
44
what is radial traction and what does it help prevent?
elastic fibres pull on bronchioles helping them open during inspiration - prevents airway collapse during expiration
45
what is obstructive lung disease simply
examples
airway obstruction increases resistance to airflow - a larger impact on expiration because air gets trapped and limited ventilation
bronchitis, emphysema, astma, COPD
46
waht is lung compliance and what issue is assocaited with it?
lung compliance is how easily the lung can expand - it is reduced in restirctive lung disease
47
what is the basic pathophys of resitrictive lung disease?
reduce dlung compliance --> increased stiffness --> limtied expansion 00> limtied ventilation
48
what happens to inspiration and expiration rates in restricitve lung disease
the7y are near normal
49
what is one example of resitictiev lung disease
pulmonary fibrosis
50
n 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:
a) Surface area for diffusion
b) Pressure gradient of gases
c) Barrier Thickness
surface areea for diffusion
51
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:
a) Surface area for diffusion
b) Pressure gradient of gases
c) Barrier thickness
Barrier thickness
52
what is the oxygen diffusion rate equation
suraface area x concentration gradient / barrier thickness
53
Which leads to an increased residual volume due to ‘air trapping’?
a) Obstructive Disease
b) Restrictive Diseas
obstructive
54
in obstructive lung disease what happens to flow rates? lung volumes
all flow rates decrease
Lung volumes: inreased Rv, decreased VC< IRV
55
in resitrictive lung disease what happens to flow rates and lung volujme
flow rates remain the saem - lung volumes all decreased
56
what are 4 factors that lead to increased resitance due to decreased airway readius in obsutrctive lung sidease
bronchoconstriction, inflammation, excess mucus priuciton, reduced alveolar elastic recoil (less radial traction)
57
in obstructive lung disease waht is the problem and why?
rpoblme usually withe xpriation bc the air gets trapped in teh alveoli
58
asthma is a ___obstuction due to ____ and or ____ immune response
bronchial due to hyperrresponsie or hypersensitive
allergic (extrinisc or non-allergic (intricnisc)
59
what is the universal resposnea dn symptoms of asthm
universal respone - inflammation and edema of muscoa
increased sectrion of thick mucus in airways
bronchocontriction
symptoms - coughing, wheezing, breath shrotness, coughin up thick mucus
60
what type of asthma most commonly manifests in childhood?
allergic (extrininsc) - often grow out of it
61
what type of asthma often manifests in adulthood?
intrinis - non-allergic
62
what is the diff between allergic and non allergic astham
triggers; inhaled allergen lik dust, mite, dander, pollen mol
allergic - hypersensitivty triggers immune response
riggers; inhaled allergen lik dust, mite, dander, pollen mol
non-allergic.- hyperresponsive raction to certain stimuli
trigger: anxiet, dry air, stress, hyperventialiton, virus smoke
63
true or false most people either of allergic or non-allergic athm?
false- most have a combo
64
explain the pathophys of an allergic asthma attack
first stage (immediate)
- memory immune recognize antigen + relase chemical mediators like histamine
- inflammation, increaed mucus + immune cell recuitments
- also stimualtes vagus nerve, bronchoconstriction
second stage
- increased leukocyte infialtrtioan
increaes chemical mediator relase - prolonged inflammation, mucus, bronchocnticiton and epithelial cell damage
65
what is the differnce between partial and total obstruction in asthma?
partial - some air passed thru
- air trapping, attempt to forcefully exprire can lead to collapse of smaller aiways
total - mcucus completle blocks - leads to atlectatisis (colapse of whole distal section
66
whatis atelectasis and what leads to it?
atelectasis - is collapse fo tehwhoel distal section in TOTAL OBSRUCTION asthma
67
why would you not advice someone with parital obstuction asthma to forecefully exprire?
can acause cikkapse in smaller aireways
68
what happens to residual volume in parital osbtruction asthma how does this effect coughin
increases - less fresh air isnpired, makes it harder to cough out mucus
69
what can air trapping cause over time - what condition can we see this in
can cause hyper inflation and stretching of the alveoli - losing elasticity - seen in partial obstrciton asthma
70
what is the goal of asthma treatment and name some common traetment
minimize numebr and severity of acute attacks
avoid triggers, inhaler, antiingalmmatories, long acting bronchodilator
71
what is the drug found in most inhalers and how does it work
salbutamol
- a beta 2 adergenic agonsit - incrases bronchodilation
72
Define Chronic Obstructive Pulmonary Disease
a group of chronic respiratory disorder that cause - tissue dgeneration and airway obstruction
often combo of emphysema and chronic ronchitis
73
waht is COPD most often caused by. Is it reverisble
usually irriveersible and most often caused by smoking
74
what is emphysema often refferred to as and why
dissappeairng lung disease - desturction of alveolar wall, decreases alveoli/combiens sacs
75
waht 2 things intiate the pathogensis of emphysema? what do these 2 things lead to/pathogensis ?
smoking/air polluitatn + genetics
leads to
1. oxidative stress + increase apoptosis
2. inflammatory cells, release chemcial meidators
3. protease-antiportease imabalcen
all lead to alveolar wall destruction
76
explain the protesase/antiprotease imablcne in emphysema and what smoking does in this case
too many proteases specically elastace which rbeaksdown elastic fibres (attack tissues) not enough antiprotease (alpha 1-antitrypisin) - elastic fibres are over attacked
77
what are the proteas eand antiprotease involved in emphysema and how does smokeing play a role in these
protease = elasetace - breakse down elastic ifbres
antiprotease - alapha 1 antitrypsin
smoking increases inflmattion, oxidative stress, ad elastace
decreases alpha 1 -antitrypsin
78
what are the 2 lung tissue changes (structural) in emphysema?
1, mucus production
- due to chronic inflmmation + infection
- thickening + fibrosis of bronchial walls
2. breakdown of alveolar walls
- decrase SA for gas exchange
- loss of elastic fibre = decreased elastance + icnreased compliacne
- decrease radial traction and collapse of small ariwats
79
what are the functional consequneces of emphysema
diffculty with expiration
- increased airtrapping + RV
- overinflation of lungs
- ribs remain in inspiratory position and icnrease ant-post diamtet sof chest (barrel chest)
80
what is a fucntional consequrence that happens to the ribs in emphysema
barrel chest - ribs remain in sinpiratory postiion
81
what are some advanced consequences of emphysema
pulmonary hypertsnion and cor pulmonale
82
what is cor pulmoanle and name a condition it can occur in
emphysema, COPD, pulmonary fibrosis
lower ventilation causes vasoconstriction to trya ndmatch ventilation and prefusion
- increased MAP in pulmonary cicrulation and icnreased wokr of RV - ride side CHF
83
Name 3 symptoms of emphysema
dyspnea
hyperventialtion with prolonged expriatory pahse
fatigue from hypoxia
84
how do u diagnose emphysema
chest x ray and pulm function tsts
85
what should pumonary functions test show if u have emphysema?
increase Residual volume, and total lung cpacity
decreade vital capcity and inspitarotry and expriatory reserve volume
86
why are FEv1 and FVC reduced in emphysema?
FeV1 - FOECED EXPIRAOTY COLUME IN ONE SECOND IS REDUCE
FVC - FORCEFULLT EXHALE AFTER REATH IN REDUCED
87
what is chronic bronchitis?
chronic inflammation of airways and increased mcuus production - due to exposure of inhalled irritatnts (cifarette/pollution)
88
what causes chronic bronchitis/intiates the pathogenesis?
chrnci exposure to an irritation leads to inflammtion fo the bronchial wall
89
describe the pathogensisi of chronic broncjitis?
inflammtion of bronchial wall
chronic inflmamtory reponse + hyeprplasia of mucuous glands
narrowing of hairways - increase mucus secresion
airway obstruction + build up of sectrions
low ventilation + hyperinflation (less than emphysema)
arteiral vasoconsticiton in lungs - pulmonary hypertension + right side congestive Heartfailure
90
symptoms of chronic bronchitis
diagnosis
treatnment
chronic productive cough - secretinons thick and purulent
dyspnea
diagnosis - sumptonms + x ray
treatmetn - avoid irritants and infection
mediaiton+chest therapy
bronchodialtors
high flow o2 therapy
91
what is resitrictive lung disease and what are the 2 tyes
impaire dlung epeansion - all lung volumes aer reduvce
d1) extra-pulmoary issue
- spinal disorders (change in spine = less efficient breathing)
- disorders of muscle weakness liek ALS or msucle dystroph
2) lung disease thae impairs compliance
- chronic inflammtion/irriation --> fibrosis --> decreased compliance
92
whats a main differnce between chronic bronchitis and emphyema?
mroe alebrolar wall breakdown in emphysema and more mcuus with bronchitis - combo elads to COPD
93
escribe the cause and structural and functional consequences of Pulmonary Fibrosis
cause: long term ecposure to irritants
stifness and decreased complaince decreased barreir permability
- more effort for inspiration, sydpnea, cough
94
what ispulmonary edema and what ar 2 causes - wht do these 2 ultiamtely lead to
fluid collect in and aroudn the alveoli
causes - inflammation of lungs increase cap permability
pulmoanry hypertension - --? increased hydrostaic P in blood - i
increased fluid of capillaries into the Intersitial itial space
95
what are some signs an symptoms of pulmonary edema ?
cough, dyspean ,rales (rattling/cracklin)
cinrased effort o incspire as decreasd complaince
hupercapnia/hypoxia (elebate dblood co2)
96
Explain how chronic obstructive diseases such as Emphysema and Chronic Bronchitis can lead to
Right-sided Congestive Heart Failure
low oygen levels -pulmonary vasoconstiction = pulmonary hypertension
right side work harder - tight sided heart failure
97
explain how pulmonary Edema Associated with Congestive Heart Failure
Fig 13-2
n left sided heart failrue blood bakc up into pulmonry ciruclation (lungs) and fluid accumilated in intersitial sapce causing edema - decrease oxygen diffusion as alvoli become filled with lfuid
98
what are the 2 cacular issues that affect gas exchange.
pulmonary embolus
pulmonary edema
99
what is pulmoanry embolus?
blood clot block blood flow throught hte lung tissue
100
whre does pumonary embolus most often originate?
deep leg veins
101
what are some risk facors and symtpoms of pulmonary embolus
risk fators- immobility, trauma sutgery, deep vein thrombosis
anything that inreases risk of bloodc lots
symptoms - chesst pain, dyseonea, SNS repsoen - tachycardia
102
what is the difnition of diabetes mellitus?
chronic disorder of matbolus with elvatd blood glucose levels (hyeprglyecmia) resulting from defcts in insulin production, action or both
103
where are insulin cells released from?
beta cells of endocrine pancrease in resposnet o glcuose
104
what are the 3 main actions of insuline?
1. icnrease glucose uptake into cells (skeeltal msucle and adipose) + gluvos metbalism
2. stijmulate anabloic/fed metbaolism
- glycogen snthesis
- fatty acid uptake +lipogneis
protein synthesis
3. inhibit catbolic glucose reasctions/fasted state metablism
- sotp fat and gltcogen breakdown
- stop gluconeogensis - glucose form non-carb sources
105
how does insulin induce glucose uptake
required for translocaition of GLUT 4 transporter to cell surface
without insulin = no transporer whcih is needed for gluose to enter muscle cells +adpos tissue
106
do the liver and brain need insuline for flucose uptake? Is it still important for these tissues and why?
no - inly adipose tissue and muscle cells
yes it is - it is imporant for anabolic processes in these tissues
107
what is the consequence of insulin defeict
decreased glucose uptake into cells for metbaolic/anabolic precoesses
imapried lipid, protein, carb metabolism
108
what type of diabetes is most common
type II
109
what is gestational diabtes
type II diabetes develop during pregancy but disseaspeara afte rdelivery
110
name symptoms of diabetes mellitus, 3 poly?
polyuria - frquent urintion
polydispia - thirst
polyphagia- hunger
faitgue
weight loss (T1DM)
ketoacidsosis (acute)
111
what is the differnce in symptoms betwen type I and II diabetes
type I - onset of symptoms is acute and intesne
type II - symptoms are subtle adn insidious - often none for eyr prior ot diagnosis
112
Use a flow chart to ezplain physiological consequences of insulin deficit
113
In the flow chart of insulin deficit - what are teh 4 initial consequences of decreaed glucose into cells
polyphagia (hunger )
hyoergycemia - high blood glucose
glycogenolysis and gluconeogensis (catabolism)
lipolysis
114
explain the term starvation in a sea of plenty in terms of
our cells ares starving becuase gluose cannot be uptaken into them due to insuline issue but there is so much glucose in our blood
115
how does hyperglycemia lead to polyuria?
hyperglycemia = excess blood glucose spills into urine (glucosuria) - leads to poluruia/dyspia - thirst and urination - dheudration
116
what is osmotic diuresis and how does it occur in diabetes
incraes solute in urine leads to increased urine production due to excess oslute filtered into kidneys - incase of diabetes it is glucose
117
what happens during lypolysis in diabetes
keton bodies form - leading to keotacidosis and acifosis and ketouria (ketones in uria)
118
Explain the pathophysiology of Ketoacidosis and explain how it can go hand-in-hand with
dehydration
fatty acids broguht into mitochodnira in liver and broken down into keton bodies - used as alternate soruce of ATP proudction in cells
the ecvess is excreted in teh urine
both these paths are rate-limting
- too many keton bodies i blood ca lead tometbaolic acidossi
119
what are some signs an dsymptoms of ketoacidisosis
fruity breath, aceton, dehydartion, nausea vomtitng, hyeprvnetialation, confusion, coma
kidneys use water to clear the excess ketones + glucose - lots of wter lost - can lead to dehydration + worsen ketoacidosis (ketones more concentrated due to lesss water 0
cycle
120
what is type I diabetes characterized as ?
autoimmune destruction of Beta cells of pancreatic islets elading tolack fo insulin
predicsposing factors: genetics, envrionemta
121
explain the progressive losof beta cell mass over time in type I diabetes
1) the antibodies are presen in blood - immune atack on B cells
2) partial loss of insulin secretion (pre-diabtes)
3) critical low beta cell mass + dianosis of type I diabetes - inense symptoms
122
in type I diabetes there is a long ___ peiors meaning...
long prodromal period - silent with no symptoms but could measure antibodies in blood if we looked
123
what is treatment fo type I diabetes ?
need to replace insulin with pump, injection, islet cell transplatn + carefull monior blood glucose level - food intake + activity level
isley cells introduce - new insuline producint bet acells
124
Type I diabtes imparis insuline ____ whereas type II impairs insuline ___
insulin priduction (destroys beta cells)
type II - insulin deficit ( action and prodiction) - insuline resistance +beta cell destruction
125
compare and conrate type I an diI dibatetes
type I
- insulit production impaired (beta destroyes)
- acute and intensy symptom onset
- predisposing: gentics +environemnt
- autoimmune
treatment: insulin adminstation/islet cell transpla nt
Type II
- insulin production + action impaired (beta destoryed + insulin resistnce)
- sulte and insidious symptoms - manifest later
- risk: gentics, enery imablce (pa/nturition)
- obesity
treatment: PA< nutrion, inslin injections (later)
- hypglycemic drugs, supress liver output + decrease insulin resistance
- decrase insulin resitance at target tissues
126
what ar ethe three ways to diagnose T2 Diabetes?
fasting blood glycose >7mm
oral glucose >11 (after 2 hrs)
OR
heoglobin AC1 (glycated he,oglobine > 6.5% (over 3 months)
127
why dose glycated hemoglobin get emaured over 3 months?
RBS live 3 months
more tajn 6.5% = higher glucose in blood = diagnosis
128
for diagnosis of TII diabtes
fasting blood glucose >
oral glucose >
hemoglobin AC1>
fasting = >7
pre = 6.1-6.9
oral = >11
pre = 7.8-11
hemoglobin AC = >6.5%
129
what 2 things lead to insuline resitanc (action impaired) ein Type II diabetes
gentic + energy imablace
130
in the pathogensis of T2DM what happens?
gentic predispostion + energy imabalnce leads ot insuline resitance
lead to increased stress on beta cells
intially beta cells compensate by increaing insulin secretion so normla blood glucose levels
but over tiem the cells dysifuctnion = decreased insulin secretion + hyperglycemia
131
what makes skelteal muscle cells insluin resistant (what is the mchanism)
impaire dintracellular singlaling in reposne to insulien binding to receptor
-
problem wiht insulin reeptor fucntion or soemthing further downsram signalling pathway
= less GLUT4 translocation to cell
132
what are 3 priamry sights of insulin resistance and the consequences
skeletal mucscle
- impaired glucose uptake
impaired anablov mechanism (protein synthesi + glycogenesis)
liver
- oveerpoduction of glucpse by liver - gluconeogensis s
- oveproduction of fatty acids from glucose (lipogensis)
adipose tissue
- increased lipolysis --? icnrease free fatty acids circualtin in blood
- contributed to insuline resistanc efurther and atherosclerosis risk
133
explain how type II diabetes can cause atherosclerosis
insulin resistance in adipose tissue leads to increase lipolysis + free fatty acids in blood + chronic hyperglycemia damges endothelial cells
134
what are some drug option for type II diabets?
oral hypoglycemic drugs
- decrase insulin resitane, inrease production,
incretin based therapy - enhance increitm hromones like GLP 1 which are released in reposne to carbs - increase insluin relase (eg Ozempic)
135
what does GLP 1 do in type II diabtetes - what type of hormone
incretin hromone - target beta cells and bind to receptor ro incrase amoutn of insuline released (glucose must be present)
also delays gasrtic emptyin, decreadse food intake, slow rate of gluconeogensis, protect beta cells form apoptosis + stiualte proliferation
136
what is cause of obesity simply defined as? How was it traditionally chracterized?
long term energy imabalnce betweneconsumed calories and ecpended
traditionall bmi>30
137
what is etiology of oebsity
gentics plus environemnt
- driven by procesed food + local environemtn factors
enviromemtn _ individual
138
waht lcoation of adipose tissue puts you at risk for obesity? + also condiser?
visceral adiposity
meatbolic health
- adipose tissu eimapct meatbolsima nd inflmamation
139
explain the pathophs of increased adiposity/obesity
adipose tissue has endocrinesignalling functions
- produced adipose dervied ctokines (adipokines) and other cytokines
- 2 main:
adiponectin - Decrase levels
leptin - increase elvels (leptin receptor resitanc eincrease)
+ others
Result - chronic system inomamtion + increase FFA --> insuline rsitance --> type II diabetes
140
what 2 adipokines are produed ed by adipose tissue? waht do each do and reac tin obesity?
1. adiponectin - protecive efffect, insulin senitizing, anti-inflmatory
DECREASE in obesity
2. Leptin - proinflammatory
- Increas in obesity
- hormone regualtion food intake, metabolic reate
- reduces leptin receptor resitance
141
tratment goal of oebsity? How
weight loss
lifesytle interventions - PA, diet, beahviour modicaiton
pharmacotherapy
drugs - decrase food intake:
medical devices
- intragastric balloosn
vagun nerve blocker - siu[ress nerual communcaition betweenstomach and brain
142
what si the machiam of action of ezempic
Stimulates insulin release form pancreas
Keeps fuller longer - less hungry - triggers satiety
We want more glut4 - to increase insuline sensitivit
143
what are the 5 metabolic rsk vactors of MEts
visceral obesity
Low HDL level
high triglyceride lvels
insuline resistance (high blood glucose)
hypertesnion
3/5 = MetS
144
treatment for metabolci ydnrome targets..
diet and exrcsie
145
waht si the typcial progresion of MEts
1. genetics + behaviour --> accumulate dbod fat - devlop mets
icnrease risk for profresion to chronic disease (type 2 diabetes, CVD etc.)
146
what si teh change rpogram for MetS - who is involved
12 month rpgiram with dietician, kin + GP
involves, goal setting, meeting with dietician and kinesiologist
147
what is a neoplasm tumour and what are its chracersits
abnormal grwoth of c ell that no longer repsosds to normal gentic control
- dividing otusid eof regualr mtotic signals
deprives other cells of nutrient and metabolism
148
How do neoplasms act on toehr cells
deprives them of nutrients and metabolism
149
hat are 2 charterists of a neoplasm/tumour
type of cel whichb tumour aros and the unique structure and growth pattern
150
compare and contrast benign and malignant tumours
BENIGN
typical diffferntion
replicate high rate
expand within capsule + dont spread
joins together in tight apsule (cant spread)
more conn tissue
MALIGNANT
- abnormal, poorly differantiated, non functional, disorganzied cells
-- rapid/unctrolled replication
- infiltrate otehr tissues and blood vessels, break away, spread to distnat region (metasits)
- joins together more loosly s can spress - less ocnn tissue
151
what ist he diffenrec ein conective tissue in bening and malignant cancer tumours
being - mroe connective tissue - ahrder to spread
malignant - easier to spread - loose/less connective tissue
152
what are 4 example of abnormla clel growth that MAY progress into cancer?
hyeprplasia - cells dividing at a rate faster htan norma
atypia - cells slightly abnormal
metaplasia - change in cell type in area
dysplasia - abnormal cells, growing faster than norma + not arranged like normal cells
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what is example of cell growth that HAS progressed to cancerc/what is an exanome
carcinoma in situ - cell very abnormal but not growin into nearby tissue
154
what ar teh 2 ways cancer is classified
1. location
2. type of tissue
155
Based on type waht are the diff classifcaigon of cancer
CSMMLL
carcinoma - epithelail (linin of an oragan)
sarcoma - tissue (msucle, fat, cartilage)
melanoma - skin
myeloma - plasma cells
leukemia - white blood cells
lumphoma - lumphatic system
miz
156
What is the most common tupe of cancer?
carcinomam - epthial lining organ
157
what is a sarcoma
supportive and conenctive tissue cancer - boens, tendon, cartilage, msucle fate
158
what is a myeloma?
plasma cell cancer
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waht si the etiology of cancer?
carcinogensis - nromal cells transformed to cnacer cells
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what ar some risk factors for carcinogensis ?
multifactoria l -leads to cahgnes in gene expression
genetics
environemnt - smoking, UV, radiation, chemcial exposure
lifestyle - diet , activity, stress
biologicl a - chrinicn inflammton, hromones, obesity
l
161
Outline and briefly describe the multistage model of carcinogenesis
1. initiation
- exposure to one or multiple cacingogen causes first dna damage
2. promotion
exposure to promotors elad to hanges in cell taht rpmot cancer phenotype
3. progression
- changes to rugationa growth leads tomalignant tumor growth, invaivenss and metastis
162
explain how tumors create their own microenvironemnt
tumor cells lose normal homeostasis/cll cmmunciation
membrane and antigens change- look differnent to other cells
tumor cells dont stick to eachother propery so break off and spread
the secrete enzymes and brakdwon the extraellular matrix so tehy an break off the tisse mass and spread
create their owncapillary entowerka nd blod supplu (angiogensis) - new blood vesselt o tumour
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what are three local effect of malignant tumours?
pain
- often absent until later stages - tumor advaced
- depdns on type + lcoation
- due to sischemia, blood fluid, inflmamton, infetion, physcial compression
obstruction
- due to tumoru comrpession
- reason to maintain treatment suring alt stges
inflammation + necrosis of healthy tissue -- >lose normal function
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what are some systemic effects of malignant tumors
fatigue - inflmmation, stress, anemia
weght loss
- lack of appetite, fatigue, pin, increased metabolic demands
edema
- inflammatory resposne causes fluid build up in bodies cavities
bleeding
- if tumor erodes blood vessel
paraneoplastic syndromes
- rumor cell secrete subsstance that alters neuro fuction, blood clotting, hormones
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what ar eparaneopalstic syndromes
tumor cells secrete subsntace stha taffect neruologica funtion, blood clotting, hormones
166
Describe the 3 basic mechanisms of cancer spread
1. tissue invasion/loal spread
- tumor cells grow into adjacent tissue (eg carcionam of cervix)
2. metastis - spread to distant sties
- via blood and or lymp systen
- liver + lungs are common site of metasitist
3. seeding - spread of tumor cells within body fluid along memrbanes of body cavity
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what does grading and stagin of cancer cells decrive
Describes extent of the cancer
grading describes appearance and behavioru of cacner cell
1= poorly diff
4 = agressive
stagin describes size and extent of spread
1 = small, localized,east to traet (hasnt spread yet)
4= distant spread, poor prognosis, difficult to treat
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what is TNM stagi system?
Size of primary tumor (T)
* Involvement of lymph nodes (N)
* Spread (metastasis) of tumor (M)
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what are 3 watys of cancer tratment?
Surgery
* Radiation Therapy
* Delivered externally or implanted
within tumor tissue (brachytherapy)
* Radiation causes mutations that kill the
tumor cells and damages the
surrounding blood vessels
* Chemotherapy
* Cancer types are matched to specific
drug treatment
* Use an optimal combination of drugs to
effectively target different points in the
tumor cell cycle
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how does radiation therapy treat cancer
killl tumor cells + damges srrounding blood vessel
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hwo deos chemo treat cancer?
ptimal combination of drugs to
effectively target different points in the
tumor cell cycle
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what is personalized oncogenomics?
analyze cancer genome and detrmine the best treatment for individual
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what is cure of cancer defined as
5 year without recurrence
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what are some things we cna do to rpevent cancer
soke free,sun safe, healthy body, eat well, move, limti alcohol
awate of fam hitory, vaccination, medicaiotn risks, work sfety informed
exercise - effectiv rpiamry rpevention
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what have observational studies shown in exerciseing with cancer?
Regular physical activity linked to reduced cancer recurrence and
improved survival
* Evidence supporting effectiveness in decreasing common side-effects of cancer
* Fatigue
* Lymphedema
* Mental Health (Anxiety, Depression)
* Health-related Quality of Life
* Preserve aerobic fitness, muscle mass
* May improve treatment tolerance
* Both Aerobic & Resistance exercise considered safe and effective
* Ok during active treatment
* Prescription within individual limits, modify as needed
Consultation
with medical
professional
always
important
