Week 4 - Jan 27-31 Flashcards
1
Q
what is differnce between innate and adptive immunity
A
innate - non-sepcidic - breaod range
adaptive specific -targets specific athogens
2
Q
our immuen system is design to protect us from what 3 threats
A
- prevent entryu
- prevent spread/sgrowth
- remove threat
3
Q
infecitous disease is cayse dby ____ which __
A
apthogens - invade, multiply + cause damafe
4
Q
what is a pathogen?
A
a microorganism that cna ause disease
5
Q
what is an ifneciton?
A
pathogen repoduced in hsots body
6
Q
xamples of pathogens?
A
bacteria virus, fungi, protzoa, prions
7
Q
for adpative immunity we need to have had previous expoure..tru or false?
A
true
8
Q
are bacteria single or multicelled and they contain DNA or NRA
A
single celled - contain both
9
Q
do bacteria need a host to survive
A
no can survive outside
10
Q
whats a prime differnce between bacteria and viruss
A
bacteria can live otuisde host, viruses requireliving host to replucate
11
Q
single cell fungi are called __ chains of ells called
A
yeast vs mold
12
Q
fungi can prouce ariborn ___ which do what?
A
spores - trigger allregic raction if inhalse s
13
Q
are all funghi pathogenic?
A
no - only certain ones
14
Q
what is an exmaple of a pthogenic protozoa?
A
parasites
- tape worm, pin worm, amoeba, mlaria
15
Q
are protozoa eukaryotic or prokaryuptic? uni or multicelullar.
A
eukarytoic - unicellular
16
Q
do priopns contain gentic material?
A
no
17
Q
symptoms of prion are often____
A
neurodegenerative - demntia, ataxia…
18
Q
waht is a resevoir in infection?
A
the soruce carrying the infeciton
19
Q
what are the three period of infection? eplain eah=xh briefly
A
Incubation Period: Time between exposure to the pathogen and the appearance of symptoms. The pathogen is multiplying, but symptoms are not yet noticeable.
Prodromal Period: Early, mild symptoms appear (e.g., fatigue, mild fever). The body’s immune response is beginning to react to the infection.
Acute Period: The peak of the infection, with intense symptoms (fever, pain, etc.). The body fights the infection actively, and symptoms are most severe.
20
Q
what organs and tissues are invo
A
21
Q
explain how infection/# of organisms changes ove ritme in infection strting fom pathogen entering
A
- pathogen ener
- colonizes to site
- repoduces rapidly
- prodromal signs
5, acute signs -
2 fates - overhwelming infceiton plus death OR - decreased reproductino + death of pathogen - recovery, chronic infection or total recovery
22
Q
what organs/tissues involved in immune syste
A
boen marrow, spleen, thymus gland, tonsil, lumph nodes/vessels
23
Q
what cells in immune response?
A
wehite blod cells (leukocytes)
24
Q
what molecules/chemical meditaors involved in immuen respisne?
A
Cytokines e.g. Interleukin-6, C-Reactive Peptide, etc
* Other chemical mediators: Histamine, Bradykinin, Prostaglandin,
Leukotrienes
* Complement system (group of small proteins in the blood that
‘complement’ the immune response)
* Antibodies (Immunoglobulins
25
compare and contrast the innate and adaptive immune rsposne in terms of defense mechnism?
in innate - it is physical and chemical barriers and involveds inflammatory response
in adaptive -kills the compromsied cell (ntibody tags the antigen)
26
compare and contrast the innate and adaptive immune resposne in terms of immune cells.
in inante - non-sepcific - distinguish what should and should not be in boyd
adaptive - specific foe each invader - certian cells have antigens - ID uniwue part of pathogen
27
compare and contrast the innate and adaptive immune resposne in terms of molecular components?
Innate: on -sepcific; chemcial meditaos +inflammatory repsonse
adaptive: antibodies + chemcial mediators
28
compare and contrast the innate and adaptive immune resposne in terms of memroy
innate - nomemroy
adpative - immunolgoic memory - stornger and faster repsonse each time apthogen is rpesent
29
wht is the link betwen the innate and adaptive immune response?
dendritic cells
30
all the cells differentiated form ____ are those involved in innnate immuen response and are found ___
myeloid progenitor -these cells are found ircualting in blood and tissues at all times
31
what 5 leukocytes differetntiate from myeloid progenitor?
neutophil, eosinophil, basophil, mast cell, monocyte (macrophage + dendirtic)
32
waht 2 cells differntiate form monocytes?
decnritic cell + macrophage
33
what is the cells that does not diffentiate from myoloid but is involved in innate immune repsone?
natural killer cells
34
what cells specifically target cancer + viruses. What do they do to thes cells
natural killer cells - trigger apoptosis
35
what cells do natural killler cells speicfically target?
virus + cancer infected cells
36
the types of leukocytes in innate resposen are?
myloid progenitors - neutrophils, basophils, eucosanoids, mast cells, monocytes (desnitti +macrophage)
natural killer
37
what cells are involved in both innate and adpative immuntity
dednritic cells
in innate the rrecognize pathogens and in adptive the present antigens to T cells
38
what are the atigen presenting cells in the adaptive immune respone?
dendritic cells
39
what 3 tpes of cells are involve din adaptive immune repsone?
what do each do
Antigen presenting cells - dendritic cells
B lymptocytes
- recognize antigens that have entere dbody bfore _ secrete antibodies (plasma cells)
T lymphcytes
- recognize antigens present by dendritic cells
40
which type of cells recognize the antigens prsented by denrititc?
T cells
41
what do t lymphocytes turn into?
Helper T cells
- secrete cytokine to help coordinate immuen rsonse
cytotoci T cells
- kill target cells that present a specific antigen
42
what do helper T cells do?
secrete cytokines - cooridnte immune rsponse
43
what to cytotoxic T cells do
kill taget cells presentign specific antigen
44
what cells are the first responders of the innate immune response and first notice that cells are not acting nromally?
macrophages + neutrophils
+ natural killer celsl (if virus or cancer)
45
explaine the innate immune response.
first macrophages + neutrophils engulf the pathgoen (phagocytosis)
Then secrete chemical mediators that
- trigger inflammatory
- release other chem mediators
- recruit more immune cells (basophils, eosinophils, neutophils, macrophages, dendritic cells)
46
cells funcitons
Basophils: Release histamine and other chemicals during allergic reactions and inflammation, helping to recruit other immune cells.
Eosinophils: Combat parasitic infections and play a role in allergic responses by releasing toxic proteins to kill parasites.
Neutrophils: The first responders to infection, they engulf and digest pathogens through phagocytosis.
Macrophages: Engulf and digest pathogens, dead cells, and debris, and also help activate the adaptive immune system by presenting antigens to T cells.
Dendritic Cells: Capture and process antigens from pathogens and present them to T cells, bridging innate and adaptive immunity.
47
explain the initiation of the adaptive immune respones?
1. dendritic cell phagocytizes pathhogen for first time
2. breaks pathogen into small peptide
3. D cell travels to lymph node and presents an antigen (fragment of pathogen) to T cell
4. T cell differntiate into specific mature T cell (helper or cyotonic) + repoduce + memory T cells for next time
5. antigen specific B cells deevlop + repoduce - target specific pathogen + turn into plasma cells when exposed to antigen
= plasma cell secrete antibdies specific to antigen
+ ,become memory B cells for nect time
Antibodies attache to pathogen + mark for destruction
48
what does denritic cell present to T cell in adpative immune respones?
antigen (fragemnt of pathogen)
49
differnce betwenpriamry and secondary adaptive immuen rspone?
in priamry.- first exposure - less antibodies
secondary - more santbodies
50
what are the 4 types of immune system pathologuies - summarize ach
Hypersensitivity
autoimmune
immunodeficencty
imunocompromised condition
51
what is a hypersensitivty reaciton
immune system ovveracts causeing damge instd of protection
allergic reactions - allergen is antigen that provokes allergic raciton
52
what is the main exmaple of a hypersensitivyt reaction
allergic asthma
53
what is allergic asthma/
a hupersensitivty racion - chronic inflmmation in the airways
54
explain the alleric asthma response
the imm
55
Use Allergic Asthma to explain the basis of a hypersensitivity reaction
it is an exaggerated immue rsposne to an allergen (pathogen which is harmeless)
immmune system mistakens it for harmful subsstanc treats it as a ahrmful substance
- dednritic cells present atnigen to T cells - cytokins - mast cells + eosinophils - mor cytokines and leukotrines
repeated exposure to allregen causes inflammation of ariways) local inflamamatory repsone) and other asthma related symtposm like bronchospams + mucus secretion
56
what are autoimmuen conditions?
when the immuen sytem can distinguish between self and non-self antigens
trigger causes ell dmage/death, immune sytem forms antibodies - inflmamation occurs
57
what is the etiologu for autoimunce conditionlups
likely unknwon - oculdbe UV, environemt
58
what are soe sumtoms of lupus
fever, rash, joint pain, inglmattion - soecific depdnig on the system affectedd
59
what ae the 2 causes of immunodefficiencyt?
priamry - inherited
secodaru - indiuced as consequnce of disease, treatment, malnutirtion
60
what can induce secondary immundodeificency?
HIV< immunsopressive drugs, chemo/radiation tharpy
61
what complication arise form HIV
AIDS - acequire dimmunodificency syndrom - complciations that aride form the virus
62
how does HIV work simply?
Targert CD4+ immune cells ( t-helper, dedritci +macrophages) and entres cells inseting RNA - whenevr immune cell replicated + activates more virus is produced and this infects more immue cells killint the T-helper, denritic and macrpharges
63
when does HIV becom Aids?
when CD4+ count in blood gets critically low = body becomes vulnerable to opportunistic infeitons
64
why is HIV an immunodeficieny?
it attacks and destorys CD4+ cells whichar ekey in protecting body form infections, decrease cells - so ability to fight infections and pathogens and have healthy immune system decreases
HIV/AIDS is a form of immunodeficiency because it drastically reduces the immune system's ability to protect the body from harmful pathogens.
65
Why are people with HIV/aids more suseceptible to pneumonia?
It is an autoimmune coniditon so they are more susceptible to opportunistic infections like pneumio, tuberculosis and cancers since their immuen system siweakned and CD4+ cells are low in the body to fight off apthogens.
66
what therapy for HIV
nti-retroviral therapy (a combination of pharmaceuticals) is very effective at keeping HIV
infection chronic, preventing manifestation of AIDS
67
what are ose exrcise considerations fo rhtose living with HIV
people often asymptomatic
exercise can improve CVD risk, body comp, msucle fucntion, psyh symptoms and other adverse otucomes of HIV
normal ex px - for indiiduals capbility
68
peak bone densiy i determined by what 4 factos?
physcial acitivy, nutirion, gentics, hromones
68
Is HIV easily transmitted?
no - use barrier parecautions
69
exaplin curcve of bone density for males and femlaes
increased rapidly until adulthood - plateaus in adulthood then decreases with odler age
70
explain some differnces in bone density acors s lfiespan betwen malkes and females
males haev greatere density + increase more during puberty
females rapidly decrease during menopause - males les
71
what are predicots of bone lsoe
Hormone changes
* Estrogen, Testosterone
* Physical Inactivity
* Chronic Inflammation
* Inadequate Nutrient Intake or
absorption
* Smoking
* High Alcohol Intake
72
what is osteoperosis ? what happens to trabelcular and cortical bones
citically. lwo bone mass/decnsity wth loss of bony matrix. mineralization
corticla bone - porous and thing - trabeular bone loss = htinning
73
what is bone mass +. density
Bone Mass: amount of bone tissue in the skeleton
Bone Density: mineral mass per unit volume of bone
74
what are the 2 forms of oesteoporsis and etiology for eahc
1. primary - age related (incrase w older adults, esp females
2. secondary - fomr other disorder or issue
- conditions assoc with bone loss
- drug like glucorticoid
- alcholism
75
waht are the risk factors?
gentics, age
sex
sedentry life
menopause
nutrition deficic or malbosorption
alcohol consump, smoking
prolonged glcuocricord (prednison)
76
osteoperosis is when _____ > ____
resorption > fomration
77
what is the direct and indirect imapct of estrogen decline in terms of osteoperosis
Direct - lack of estrogen means icnreased osteoclast +decreaseed osteoblast
- estrogen usually inhibites OC actiivty and stimualtes OV
indirect - increase activity of cytokine - sitmualtes OC
increased OC via RANK receptor pathway
78
5 pathophysiology considerations for osteprosis ?
estrogen decline
chronic inflammation
peak bone density factors
age realtd decline
modifiable factors
79
In the RANK receptor pathway what does RANKL do and what blocks this action?
what does estrogen do
RANKL binds to receptor and stimulates osteoclast differnection/ativation
OPG is.a decory receptir andblcoks action of RANKL so RANKL cannot bind to receptor
steogen inhibits rankL and sitmulates OPG - therfore inhibtion of osteolastss
80
waht does Estrogen do in the RANK pathwyas? what cells are esteogen relased from and where do they bind?
stimualtes OPG and inhibits RANKL
estrogen released from osteoblasts
and binds to osteoclast
81
what is the result of estrogen in the RANKL pathway
1. inhibts RANKL
2. stimuatles OPG
RESULT - inhibtion of osteoclast formation
82
how does chronic inflammation cause osteoperosis
proinflmmatoary cytokines increase OC activity
83
what are some age related declines that can cause osteporiss?
decline in stem cells taht prod OB
declin growth facotrs for bone formation
84
what are 4 etiologies of secondary osterperosis
disease, alc use, coticosteroid use, female athlete triad
85
how does cushin syndorm cause osteoperosis
high cortisol promtoes bones resorption
86
how does alc cause osteperosis
direct inhibiter of OB
inrased pro-inflammatory cytokines
impaired ca and vit D absorption
87
what does the female athlete triad consist of?
intenste traintin + poor nutrition + mentrual dysunction (low estrogen)
88
name 3 signs and symtptoms of osteoperosis
1. spontaneous fractures (fragility) - femur, writst..
2. back pain form comrepssion fracurs of vertebrea
3. abnormla curve in spine with loss of height
89
what is some treatement of osteoperosis
dietary supplemets (vitamind D , Ca2+)
pharmaceutical that promote formation and inhibit absopriton
estrogent replaemtn threrapy for post-menopausal
90
How does physical acitvity preven osteoperis
anti - inflammatory effects
stimulates osteoblasst + osteocyre sutvivals by. mechanicla bone laoding
91
what is therapeutic goal for exercsie prescription for osteoperosi
prevent bone loss, prevent falls, prevent fractuire s
92
what are chonfocytes?
maintain cartilage - balcnace old adnd ne cartilage
93
osteoarthritis is a disea of ___ AND___
degenration + inflammtion in a synvoial joint
94
waht type fo joint does osteoarthritis occur in?
synvoial joint
95
what is osteoarthritis a result of/
something that cause incresase relase of degradiative enxye,s by chondocyts - breaks down cartilage
96
what is released by chondrocyte and breaks down cartilage ?
degradative enzymes
97
risk factors of osetoarthritis?
age, obesity, genetics, joint injurt, inflmamation
98
osteoarthritis affects ___ in their life
1;3
99
explain the pathophys of osetoarthritis
1. somthing triggers chondrocytes to release degradative enzymes
2. breakdown of cartilage
3. small piecs of cartillage breajk off into joint space
4. cells of synovium try to remove debris - immune cells recruit - cytokine secretion - inflmmation of synovium
5. cracks in carillage - synovial fluid enters and widens cracks
6. no smooth articular surface + even load distrubtuion- rubs against articulating bone
7. bone eburnation (polished bone) - ostephytes + cysts devellop
reulst is narrowed joint space with decreased ROM + inflamttion in and arround tissues
100
the final step/result of osteoarthritis is bone ___ and ___ develop
boen eburnatio n(polished) = osteophytes + cysts develop
101
what could be visible on an osteoarthritc x ray
narrow joint spac, ostephytes, subchondral cytsts
102
name some signs and symptoms of osteoarthritis
asymmetic, less than 4 joints, weight bearing
reduce ROM
stifness begining + end of day - increase with actiivty
movemtn/eight bearing pain
local inflmattion
enlarged joint can harden as ostephytes dvelop
103
what is typical treatment for osteoarthritis
exerccise, physio
pharmacological - anti-inflammtory
analgesics
hyluronic acid or corticosteroid injection
surgery
104
what are analgesics
block pain signalrs
105
rheumatoid artheritis is characterisize dby___ and __- (progressiv ejoint damge)
exacrbations and remission
106
rhuematoid arthritis has a ___ osnet and __ joints afffected begining with___
slow osnet, bilatera (symmetirc) ,starts in joints in fingers
107
severity of rheumatoid arhtitis may depnds on
numebr ogf joint, degree of inflammtion ,rapidity of progresion
108
what are soem risk factros for rheumatoid arthrits
gentics
sex - female (3:1)
evniemnet hazards (cigaette)
infections
109
women are more at risk for __ arthitis tahn ___
rheumatoid than osteo
110
in osteoarthritis when cells of the synovium try to remvoe debris what else happens?
immuen cells recruited, cytokine sexretion, inflammation of shnovium
111
explain the steps of rheumatoid arthritis
1. autoimmune response
2. inflammation of synovial membrane - vasodilation, increase cap permeabilaty, immune cells recruited, cytokienr elease, exudate
4. cytokines trigger synovail cells to rpoiferate
5. forms pannus (thickened and inflamed synovial emrbeane with granualtion scar tissue)
6. pannus releases proteolytic enzymes + cytokines)
7. destruciton of cartilage
112
in rhematoid arthritis what happens when the synovial mebran becomes inflammed?
vasodilation, increase capillary permeability, immuen cells recruited, cytokine relase, exudate
113
what do cytokinees trigger in the rheumatoid arthitis reposne and hat does this from?
synovial cells to proliferate - forms a pannus (thickened an dinflamed synvoial membrean with scar tissue)
114
what is a pannus and when is it formed? what does it release
thickened and inflame synovial membrane with scar tissue
releases proteolytic enzymes and cytokines
115
wht is anylosis
abnormal fusion of bones in joint - fibrous tissue
116
articualting bones exposed lead to what?
erosiion, degradation, ostephytes, cysts
117
what is the autoimmune response associated with rheumatoid arthritis (briefly explain in 2 steps)
trigger modifies articualr proteins - immune cells fail to recognize self - produce autoantibodies
118
what may be visble on an ray of rheumatoid arthritis?
narrowing joint space
decreased bone desnity around joints
soft tissue sweeling around the join
bone erosiion
119
what are some sighn and symptoms of rheuamtoid arthritis
mroe than 3 joints affected, symmetrically
begins in fingers
chronic mornign stiffens more than an hour - imrpoves thoughout day
120
explain stiffness throuhgout the day for rhemau=toid vs osteo arhtitis
osteo - beg and end of day stiffnes
rheuamtoid - chronic morning >1 hr that gets better thouhout day
121
what are the blood markers for rheumatoid arthritis
elavted blood CRP (c reactive - repsosne to inflammation)
elevated rheumatoid factor
122
what treatment apprahc can be used for rheumatoid arthritis?
treat to target
- disease-modifying anti-theumatic drugs, immuhnosupresants
symptom management with analgesics +antiinflammtories
123
what meds to mang esymptoms of rehuematoid arhtirit?
analgesics and antiinflammatories
occupational/physio therapy fofr chronii apin
exercise - whole body dynamic
124
waht is the most effective exercise method for htose with rheumatoid athritis?
WHOEL BODY DYNAMIC EX
125
the beggining of osteoarhtirtis is because something tirggers ___ to release ___
which favorus breakdown of ____
chondrocytes to relase degradative enszymes
cartilage
126
Early stages inflammation of synovial membrane occurs in what type of arthritis
both
127
Cartilage break down occurs in waht type of arthritis
both
128
chondorxytes release enzyems that breakdown carilgae - rhuem or osteo?
osteroarthritis
129
what is
