Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophys Test 1 > JG Day 2- Immunity and Infection > Flashcards

JG Day 2- Immunity and Infection Flashcards

1
Q

What is the gram stain classifications?

A
  • Gram +
  • Gram-
  • other (acid fast, nothing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the shapes of bacteria?

A
  • Cocci- spherical
  • Bacillus- rods
  • other- spiral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do the oxygen requirements vary among bacteria?

A
  • Aerobic- exposed to air (skin, resp tract)
  • microaerobic- lil o2 needed (stomach)
  • facultative anaerobic- anaerobes that can use O2 if available
  • obligate anaerobic- O2 is toxic to them, live places deep in body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is toxin formation by bacteria?

A
  • Toxins produced by bacteria to kill other microbes
  • endotoxin- from gram - bacteria, release by bacterial cell death i.e. LPS)
  • Exotoxin - come from gram + bacteria, secreted from live bacteria, i.e. botulinum toxin)
  • or no toxin produced

these toxins are not intended to harm us. most abx are toxins from microbes but they are not toxic to us

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the spore formation by bacteria?

A
  • Spores are formed by bacteria when bacteria is in danger (think like an escape pod)
  • spores are VERY hard to get rid of
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Are bacteria extra or intracellular?

A

Most are extracellular

intracellular bacteria are harder to get rid of

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is staphylococcus?

A
  • Gram positive
  • Cocci
  • Aerobic
  • in clusters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is streptococcus?

A
  • Gram positive
  • cocci
  • aerobic
  • in chains/pairs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is clostridium?

A
  • Gram positive
  • Rods
  • Anaerobic
  • spore forming
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is bacillus?

A
  • Gram positive
  • bacilli
  • aerobic
  • spore forming

first bacteria named- bacillis antracis which causes anthrax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is listera?

A
  • Gram positive
  • Bacilli
  • aerobic
  • non-spore forming

Surgeon that discovered listera discovered that if you clean instruments between patients, patient outcomes are better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is bacteroides?

A
  • Gram negative
  • rod
  • anaerobic

most common cell in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is neisseria?

A
  • Gram negative
  • SPheres
  • Pairs

Causes gonnorhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What determines gram staining?

A
  • Gram positive bacterium has a thick peptidoglycan layer
  • gram negative bacterium has a thick peptidoglycan layer and an outer membrane
    • this prevents the staining (usually purple violet) from entering peptidoglycan layer

gram staining dermines whether or not bacteria has outer wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is bacteria DNA like?

A
  • one, single, circular, double stranded chromosome
  • contains all genes that bacteria needs to code for whatever it needs to do
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are plasmids?

A
  • Code for 1-6 genes
  • carry a “superpower” for the cell
  • the bacteria is able to share this superpower with other cells
    • this is how we produce insulin.
    • give DNA for producing insulin to bacteria. Bacteria share the plasmid by combining with other bacteria via a pillus
    • then we harvest all the insulin made and kill the bacteria
      • also make other peptide drugs via this method
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are viruses?

A
  • True parasites
    • needs to get INTO cell to do anything
      • all intracellular
  • virion binds to cell, gains entrance.
    • only gets into cell with that cell speicfic protein
      • species and cell speicfic
  • DNA of virus puts gene in our DNA and then replicates
  • new viruses then use our plasma membrane and go off to another cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are 2 interesting methods where we can utilize viruses?

A
  • gene therapy- can give cell a virus with copy of good gene, then virus will replicate good gene (i.e. for sickle cell to replicate good hemoglobin)
  • if virus has protein that’s useful, we keep it
    • 2% of genes come from viruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the medically relevant fungi?

A
  • Candida albicans
    • normal gut flora
    • cuases opportunistic infections- when you’re already not feeling good, yeast makes you feel worse”
  • Aspergillis
    • highly aerobic
    • respiratory infection
  • Tinea- not a speicifc fungus but gneeral term for skin fungus
    • tinea cpitis- head
    • tinea cruris- groin (jock itch)
    • tinea pedia- feet (athelt’s foot)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are megakaryocytes?

A
  • pieces bud off to become platelets
  • not immune cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3 families of WBC?

A
  • Mononuclea pagocytic system
  • Polymorphonuclear leukocytes
  • lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a mononuclear phagocytic system?

A
  • monocytes- when they leave blood they become macrophages
  • macrophages- named based on where they are located
    • kuppfer cell- liver
    • microglia- brain
    • dust cell-lungs
    • osteoclast-bone. not immune cells but a lot of macrophages together to eat the bone
    • multinuclear giant cell- kind of like osteoclasts but are immune cells
      • if fighting off big infection, amcrophages aren’t big enough to handle it. a bunch of macrophages will then get together and form multinuclear giant cells
  • Dendritic cell (NOT macrophages)
    • langerhans cell-skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What polymorphonuclear leukocytes?

A
  • Neutrophil- most plentiful
  • Basophil
  • Eosinophil
  • Mast cell

sausage shped nuclei which can squeeze through endothelial cells to get from blood to tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 3 types of lymphocytes?

A
  1. B-cells
  2. T-cells
  3. NK- natural killer cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Types of B cells?

A

Plasma cells

memory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Types of T-cells?

A
  • Tc- cytotoxic T cells- CD8
  • Th1-helper 2 cells- CD4
  • TH2- helper T cells CD4
  • Memory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Order of frequency of immune cells?

A
  • Neutrophil
  • Lymphocytes
  • monocytes
  • eosinophils
  • basophils

“Never let monkeys eat bannas”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which immune cells are in tissue, not blood?

A

macrophages, dendritic cell, mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is humoral vs cell-mediated immune system?

A
  • Humoral= fluid, in blood (Extracellular)
  • Cell-mediated= intracellular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is innate vs adaptive immunity?

A
  • innate- born with it, always on
  • adaptive- learns, but only happens when exposed. slower response time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which immune cells are humoral?

A
  • Innate: Myeloid cells- non-host epitopes
  • Adaptive: B-cells- antibodies (also Th cells, APCs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which immune cells are cell-mediate?

A
  • Innate: NK cells
    • MHC existence
    • Goes around asking cells if they’re virally infected. If infected, NK cells tell cell to kill themselves.
      • however, viruses can hijack cell and tell cell to shut up
  • Adaptive: Tc-Cell
    • MC1-TCR
      • will hunt you down and kill the cells if virally infected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do cells of innate immunity work?

A
  • Macrophages all over body, waiting for something to happen
    • detects bacteria from a skin cut (for example)
      • signals release of cytokines/chmokines- magic fairy dust that tell imune cells to leave blood and go to tissue
  • Cytokines and chemokines cause endothelial cell retraction to allow neutrophils to leave
    • also allow plasma protein to leave, losing oncotic pressure, causing fluid to leave and cause edema
  • Inflammatory cells migrate into tissue releasing infllammatory mediators that cause pain
    • also cause swelling around injured site.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the function of macrophages?

A
  • Phagocytosis and actiation of bactericidal mechanisms
  • antigen presentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Function of dendritic cells?

A
  • Antigen uptake in peripheral sites
  • antigen presentation in lymph nodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is function of neutrophil?

A
  • Phagocytosis and activation of bactericidal mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is funciton of eosinophil?

A

killing of antibody-caoted parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is function of mast cell?

A

release of granules containign histamine and other active agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is order of inflammatory reactions?

A
  • Edema (from endothelial retraction)
  • neutrophils- clean up damage
  • macrophages- repair damage
    • one lonely macrophage to begin with. this macrophage signals that injury has occured via cytokine/chemokine
    • thousands neutrophils come
    • then more macrophages join after in order to repair the tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the process of phagocytosis?

A
  • Diffusion of chemotactic factors from site of injury
  • adhesion molecules on endothelial cells and neutrophiles (pavementing)
  • retraction of endothelial cells (Vascular permeability)
  • movmeent of neutrophils through opened intercellular junctions into tissue
  • neutrophils move up cytokine concentration gradient (crawl) to get to injury location
  • neutrophils then pagocytose whatever they can
    • will initial look for non-host epitose
    • produce H2O2 (hydrogen peroxide) and dumps it into vesicle with bacteria to destory bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is a PAMP?

A
  • Pathogen associated molecular pattern. What antibodies look for to bind to
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Are phagocyte looking for bacteria?

A

No, looking for a antibody stuck to something

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is role of B cells?

A
  • Adaptive immunity
  • B cells from bone marrow and make antibodies
    • antibodies made from plasma cells (transformed b cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are Tcells?

A
  • Come from thymus
  • Adaptive immune system
  • 2 types
    • cytotoxic- investigate host cells to see if it has a virus and then kill host cells with virus
    • helper t cells
      • help b cells mature and function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the process of making B/T cells?

A
  • Lymphoid stem cell released form bone marrow
  • goes to thymus to become immunocompetent, naive T cell or bone marrow to become immunocompetent, naive B cell
  • Then migrate to secondary lymhoid organs (i.e. lymph node, tonsil, spleen) to find antigen
  • once activated by antigen, B cells mature to plasma cells and produce antibodies
  • T cells are activated by antigen exposure and then become Th cells or cytotoxic tcells and do their function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are central lymphoid tissue?

A

primary

  • thymus
  • bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are peripheral lymphoid tissues?

A
  • aka secondary
    • adenoid
    • tonsils
    • lymph nodes
    • spleen
    • peyer’s patches (ileum only)
      *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which 2 organs do not have lymph nodes?

A

Brain

Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is an epitope?

A

Some molecular pattern we can grab onto

(found on antigens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is an antibody?

A
  • binds to antigen
  • y-shaped
  • “hands” of Y are binding unit to epitope (location on antigen we bind to)
    • antigen-specific
  • has 2 light chain, 2 heavy chain
  • consists of areas of heavy chain and parts of light chain that are constant
  • part of light chain is variable, where antigen binding sites are
51
Q

What are the diff types of immunoglobulins?

A
  • IgM- first immunoglobulin then differentiates into other classes
  • IgA- secreted into GI tract
  • IgE- antibody of peripheral tissue
  • IgG- antibody of blood
  • (Ignore IgD for this class)
52
Q

What is the Fab?

A

binding site of antibody (part that is variable for each antibody)

53
Q

How do antibodies protect the organism?

A
  • bind to:
    • toxins- toxin then neutralized
    • bacteria- phagocytes now more aggresively eating bacteria
    • virus- virus is then unable to bind to receptor on host cell and is ineffective

antibodies make immune system more effective but we don’t want antibodies to bind to us!

54
Q

How are B cells made?

A
  • A single progenitor cell (from bone marrow) gives rise to a large number of lymphocytes, each with a different genetic specificity on the variable portion (making different locks)
  • Nurse cells present varying proteins (from out body) to the made B cells to see if any self-react
  • If any B-cells self react, those B cells are destroyed (called clonal deletion)
  • We now have a pool of mature lymphocytes that may, or may not work against any antigen BUT we know they aren’t self-reactive
  • If the b-cell created finds it’s antigen, then we know this is a useful B-cell and we should make more and more antibodies (immunoglobulins) are produced by mature, activated B-cell (clonal selection)
55
Q

What is the immune reaction to a parastitic worm?

A
  • Parasitic worm dead in interstitial space (this parasite has antigens)
  • B-cell comes along and the parastiic worm antigen matches to it
  • starts replicating and converts to plasma cell to start secreting antibodies
  • antibody binds the mast cell and if the parastie antigen binds to the antigen, then the mast cell will degranulate and release ECF-A (eosinophil chemotactic factor of anaphylaxis)
  • this goes to the vasculature and promots endothelium retraction to allow eosinophils to get through vasculature
  • eosinophils attach parasite. attack enhanced once antibodies bind to parasite’s surface
56
Q

What is the difference between a primary and secondary immune response?

A
  • In primary immune response, IgM is the first antibody to respond
    • IgG then peaks later (because of class switch from IgM to IgG)
  • On the second exposure (secodary immune response), we have memory cells, so IgG peaks first and rises very quickly. IgM has same response as before
57
Q

What is the secretory immune system?

A
  • IgA sit underneath mucosal lining in organs exposed to “outside” aka mucosal-associated lymphoid tissue (airways, esophagus, GI tract) so antigens can be found quickly
58
Q

What is a peyer’s patch?

A
  • Gut Associated Lymphoid Tissue
  • M cell takes things form lumen of GI tract (in ileum) and move it underneath, so any antigen will be transported under basal lamina so it can be exposed to B/T cells.
  • The B cells convert to IgA (with the help of helper T cells) and then gets secreted back into lumen of intestine
59
Q

What is the placental syncytiotrophoblast?

A

Cells forming placenta join together and form one large plasma membrane, which stop substances from getting through gap junctions in cells

  • we actually acquired this from a virus
60
Q

How are maternal IgG’s transported to the fetal circulation?

A
  • Fc receptors located on maternal circulation side that recognize the IgG antibody
  • The IgG antibody is then endocytosed and is protected from lysosomal digestion durign transport fo the vacuole across the cell (aka transcytosis)
  • on the fetal side of the syncytiotrophoblast, IgG is released by exocytosis
61
Q

What are the antibody levels in umbilical cord and neonatal circulation?

A
  • Maternal IgG is shared with the fetus and will almost reach adult levels by birth.
  • After birth, maternal IgG levels quickly fall and child’s IgG begins to increase
62
Q

How do T cells work?

A
  • T cell still makes binding site in a similar method as b cell (randomly arranging DNA)
  • however, a t-cell always has the binding site attached to the cell, it is never free floating (unlike b-cell and their antibodies)
  • t-cell only has one binding site
  • t-cell isn’t actively looking for an antigen, but has antigens presented to itself by an MHC (major histocompatibility complex)
  • In order to t-cell immunity to funciton, need same TCR, MHC and antigen in order to bind
63
Q

What are the 2 classes of MHC?

A

Class I and Class II

64
Q

What is class I MHC?

A
  • Has 3 subclass- HLA-A, HLA-B, HLA-C
  • reacts with CD8 on Tc (cytotoxic) cells
65
Q

What are class II MHC?

A
  • 3 different genes- HLA-DR, HLA-DP, HLA-DQ
  • Reacts with CD4 on Th (helper) cells
66
Q

How do class I MHC work?

A
  • Cell chops up protein that we just made and presents it as an antigen on an MHC
  • That MHC is transferred to the surface and presented at the cell surface
  • if a T-cell comes along and binds, then we know the antigen is foreign (because we got rid of all our self-reacting t-cells)
  • therefore, we know the cell is virally infected
  • therefore, the cell needs to die
67
Q

How does a class II MHC work?

A
  • Cell phagocytoses a substance, chops it up and then presents the antigen at the cell surface
  • if a t-cell responds to the antigen, then that means the antigen is foreign
  • we want this cell to continue phagocytosing and killing other bacteria/foreign substances
68
Q

What are APCs?

A
  • professional Antigen Presenting Cells
  • only 3 cells present MHC-II to helper cells
    1. dendritic cells
    2. macrophages
    3. b-lymphocyte
69
Q

What cells express class I MHCs?

A

every cell in the body that has a nucleus (RBC do not have nuclei)

70
Q

How are t-cells developed in the thymus?

A
  • Lymphoid stem cell comes into thymus, is differentiated into T-cell
  • T-cell is presented to self-antigens in same process as b-cells
    • ones that react to self are destroyed (this is called negative selection)
  • The t-cells then go on to be presented to MHC
    • t-cells that bind to MHCs are made (positive selection)
71
Q

What are immune privileged sites?

A
  • Placenta/fetus
  • testes and ovaries
  • eyes
  • brain
  • thymus
72
Q

How do lymph nodes drain lymph?

A

afferent–> lymph node–> efferent lymphatic vessel

73
Q

Why do lymph nodes swell during infection?

A
  • Lymph nodes have b/t cells waiting to find antigen
  • once they find an antigen, they replicate
  • copious amount of b cells replicating causes swelling of lymph nodes
  • lymph node nearest to infection will be most swollen
74
Q

What is dendritic cell role in capturing antigens?

A
  • immature dendritic cell will pick up antigen in tissue, e.g. skin and migrate to lymph node
    • dendritic cell become mature after picking up antigen
  • Naïve helper T-cell in lymph node interacts with mature dendritic, will find its antigen and signal reactions
  • Activation of a B-cell by a T-cell independent antigen

We usually need T-helper cell to activate B-cell but with presentation of a repetitive antigen can activate B cell without it

75
Q

What is hypersensitivity disorder?

A

Response of immune system is out of proportion to the effect

  • Four diff types: I, II, III, IV
    • I, II, III are antibody mediated
    • IV- t-cells
76
Q

What is Type I hypersensitivity?

A
  • Immune Reactant- IgE (in peripheral tissue)
  • Antigen- soluble antigen
  • effector mechanism- mast-cell activation (granulation)
  • example of hypersensitivity reaction- allergic rhinitis, asthma, systemic anaphylaxis

Ex- allergy to cat dander in house.

Very fast activation

77
Q

What is Type II hypersensitivity?

A
  • Immune reactant- blood
  • Antigen- cell or matrix associated antigen
  • Effector mechanism- FcR cells (phagocytes, NK cells)
  • Example of hypersensitivity reacion- some drug allergies (i.e. peniccillin). Blood transfusion reaction, hemolytic disease of newborn, graves’ disease, myasthenia gravis

IgG binding to our own ECF protein

  • immune system assumes that if antibody binds, then it’s foreign and needs to be destroyed
78
Q

What is Type III hypersensitivity?

A
  • Immune reactant- IgG
  • Antigen- Soluble antigen
  • Effector mechanism- FcR cells complement
    • form immune complex of antibody and antigen.
    • hyperreaction and clumping up blood vessels
    • get stuck to wall
    • then neutrophils, macrophages come to attack the antigens stuck to the blood vessel wall
    • now causing blood vessel damage
  • example- serum sickness, arthus reaction, lupus, necrotizing vasculities

Way too much antigen and IgG causing immune complexes to get stuck on blood vessel and damaging blood vessel in process

79
Q

What is Type IV hypersensitivity?

A
  • Immune reactant- T cells
  • soluble antigen or cell-associated antigen
  • examples- transplant rejection, hasimoto’s thyroiditis, type 1 diabetes, poison ivy

Standard transplant rejection, CD8 cells looking for foreign cells and neutrophils going to attack (also poison ivy)

80
Q

What is the soruce of antigen for Type I hypersensitivities?

A

environmental antigens

81
Q

What is autoimmunity?

A

self-antigens

82
Q

What is alloimmunity?

A

immune response to another “person’s” antigens (ie pregnancy)

83
Q

What are some examples of Type I allergy hypersensitivities?

A

allergic rhinitis

anaphylaxis

asthma

84
Q

What are some examples of type II hypersensitivities with environmental allergies as a source?

A

hemolysis with penicillin (didn’t talk about in class…)

(RARE)

85
Q

What is an example of type III environmental allergy hypersensitivity?

A

wheat gluten

also rare.

86
Q

What is example of type IV hypersensitivity caused by environmental allergen?

A

poison ivy

87
Q

What is an example of type II autoimmunity hypersensitivity?

A

graves disease

myasthenia gravis

(2/3 all autoimmune are type II)

88
Q

What is an example of Type III autoimmunity hypersenesitivity?

A

Lupus

necrotizing vasculitis

89
Q

What is an example of type IV autoimmunity?

A

Hasimoto’s thyroiditis

type I diabetes

90
Q

What is example of type II alloimmunity hypersensitivity?

A

bad blood transfusion

hemolytic dx of newborn

hyperacute graft rejection- happens intraop. incredibly rare

91
Q

What is example of Type III alloimmunity?

A

serum sickness

92
Q

Example of type IV alloimmunity hypersensitivity?

A

transplant rejection

93
Q

What is the mechanism of a type I, IgE mediated reaction?

A
  • First exposure to an allergen stimulates B lymphocytes to mature into plasma cells and produce IgE
  • IgE is absorbed to surface of mast cell by binding with IgE specific Fc receptors
    • when adequate of IgE is bound, causes mast cell sensitization
  • During 2nd exposure, allergen cross-links surface boudn IgE and causes degranulation of mast cell
  • Initial phase has
    • vasodilation
    • vascular leakage
    • smooth muscle spasm
    • glandular secretions within 5-30 min
  • Late phase occurs 2-8 hours later
    • results from infiltration of tissue with inflammatory cells
94
Q

What are some manifestations of a type I hypersensitivity reaction?

A
  • Itching
  • Angioedema
  • edema of larynx
  • urticaria
  • bronchospasm
  • hypotension
  • dysrhythmia
  • GI cramping
95
Q

What is mechanism for Type II hypersensitivity reactions?

A
  • Antibody (IgG) binds to antigens on cell surface and destroys or prevents cell from functioning by
    • complement mediated lysis (erythrocyte can be target)
    • phagocytosis by macrophages in tissue
    • neutrophil mediated destruction
    • antibody dependent cell mediated cytotoxicity
    • modulation or blocking the normal function of receptors
  • Ex-
    • Myasthenia gravis- Antibody binds to ACh receptor and blocks ACh from working
      • leads to progressive weakness/paralysis
    • Graves’ disease- antibody binds to TSH
      *
96
Q

What does O blood contain (antigen and anibodies)

A

Blood O group have core H antigenic carbohydrates

Have A and B antibody in serum

97
Q

What does A blood contain? (antigen and antibody)

A

A blood has H antigenic carb modified into A antigens

Antibody against B antigen

98
Q

What does type B blood contain (antigen and antibody)

A

Type B blood has core H antigen modified to B antigens

Blood also has antibody against A antigen

99
Q

What does type AB contain?

A

Antigen has A and B

No antibodies in blood

100
Q

What is mechanism for Type III hypersensitivity?

A
  • Immune complex disease
  • relatively uncommon- lupus and overadministration of albumin are examples
  • aggregates stick to side of vessel, end up damaging BL
  • big problem in lupus is kidneys
101
Q

What is mechanism for Type IV hypersensitivity?

A
  • T-cell is self reactive
    • helper T-cell- upregulate immune system out of proportion
    • cytotoxic t-cell- will go around killing everything
  • Usually auroimmune dx and transplant
    • with transplants- we match MHC (HLA)
102
Q

What is the pathogenesis of autoimmunity?

A
  • Arises from many common
    • inheritance of susceptibility genes that may interfere with self-tolerance
      • generally MHC linked
    • environmental triggers (inflammation, other inflammatory stimuli) that promote lymphocyte entry into tissues, activation of self-reactive lymphocytes and tissue injury
  • becoming more prominent and virulent
  • typically some trigger causes the self reactive cell to become activated
    • cell responds appropriately, and fights infection but then turns to own cells
103
Q

Examples of rheumatic autoimmune ddiseases?

A

Rheumatoid arthritis

Scleroderma

Sjogren’s Syndrome

Lupus

104
Q

What are some GI autoimmune diseases?

A

Chronic active hepatitis

Crohn’s disease

Primary biliary cirrhosis

Ulverative colities

105
Q

What is an example of endocrine autoimmune diseases?

A

Graves’ disease

Hashimoto’s thyroiditis

Type 1 DM

106
Q

What are some examples of neurologic autoimmune diseases

A

multiple sclerosis

myasthenia gravis

107
Q

Examples of hematologic autoimmune diseases?

A

Autoimmune hemolytic anemia

idiopathic thrombocytopenic purpura

pernicious anemia

108
Q

Examples of renal autoimmune diseases

A

goodpasture’s syndrome

109
Q

Mutli organ autoimmune diseases?

A

Ankylosing spondylitis

polymyositis

psoriasis

sarcoidosis

vasculitis

110
Q

What is systemic lupus erythematosus?

A
  • Inherited susceptibility genes
    • class II MHC
    • Complement
    • other
  • Environmental triggers
    • UV irradiation
  • Both susceptibility and environmental triggers and cause cellular necrosis, dumping intracellular contents into plasma
    • nuclear proteins become antigens to system (B-cells not exposed to the nuclear proteins since they should be intracellular)
  • Activation of helper T cells and B cells
    • IgG autoantibody production
  • Immune complex and autoantibody-mediated tissue injury
111
Q

Who tends to be more affected by autoimmune disease? When do they tend to be intiated?

A

Women more affected than men

Mainly occurs during times of hormonal fluctuation

112
Q

What are 2 types of immune deficiency?

A
  • Primary (genetic)
    • lymphoid
      • SCID- both B and T cell affected
        • ADA deficiency
        • txmt- bone marrow transplant
      • Agammaglobulinemia- only B cell affected
      • Di George syndrome- T cell affected
    • myeloid
      • chronic granulomatous disease
  • Secondary (acquired)
    • HIV
113
Q

Where’s the normal location for B and T cells in lymph nodes?

A

Outer cortex= b cells

Inner cortex= t cells

114
Q

What are some immune problems with phagocytes?

A
  • Leukocyte adhesion deficiencies- won’t be able to stop neutrophils that are rolling along inside blood vessels
  • Chornic granulomatous disease- lack catalase so can’t make H2O2 to kill pathogen
    • myeloid problem
115
Q

What is HIV?

A
  • Cell speicfic for T-helper cells (CD4)
  • Binds to helper cells, injects RNA
  • RNA–> DNA with reverse transcriptase
  • DNA inserted into our DNA
  • We make it’s mRNA
  • it’s mRNA used by our ribosomes to make protein
  • big protein is then cut up into little pieces
  • virus then uses our plasma membrane to go on to other cells
116
Q

What are some treatments for HIV?

A
  • Entrance inhibitors- prevent virus from entering cells. not very popular
  • Reverse transcriptase inhibitors- prevents RNA–> DNA process. We don’t do reverse transcriptase in any other cell of body
  • Integrase inhibitors- prevent Proviral DNA from being impelemented into out DNA
  • Protease inhibitors- prevent the viral protein from being chopped up and sent off to other clels
117
Q

What is the conversion of HIV–> AIDS?

A
  • T helper cells present antigen on MHC I- presenting foreign protein and cytotoxic cell kills the Thelper cell
  • Measure of HIV progression is T helper cell count
  • <400 = AIDS
118
Q

What is mycobacterium?

A
  • Tuberculosis- acid fast staining
  • intracellular (often macrophages)
  • waxy coating- leads to cseous necrosis in TB
  • Types:
    • m tuberculosis: TB
    • M. leprae: leprosy
    • M. avium- intracellular- TB like dx in immunodifienct pt
  • starting to come back where HIV rates are high
    • US TB rates are decreasing
    • Worldwide- tb rates are increasing

From picture:

  • Host response in absent T cell-mediated immunity. In both cases (pic shows example of myco. avium and M. leprae), no granulomatous response; intracellular bacteria persist and proliferate within macrophages, because there are inadequate T cells (in case of AIDS) or T cells don’t appropriately activate macrophages to kill intracellular pathogens (lepromatous leprosy)
119
Q

What is toxic shock syndrome?

A

superantigen induce inflammatory response

  • superantigen- (ie bacterial toxins) bind directly to TCR and MHC II molecules
  • superantigens activate Th cells independently of TCR antigen specificity
    • Superantigen binds very tightly and indiscriminately to TCR and MHC II
    • T cell activates helper cells and get SUPER activated
    • ramps up immunes system to crazy levels and causes anaphylaxis shock
  • causitive agent-
    • streptococcus pyogenes
      • staphylococcus aureus
120
Q

How does HIV affect CD4 cells?

A
  • Decreased lymphokine produciton
  • loss of stiumuls for T and B cell activation

leads to:

  • lymphopenia
  • decreased CD4/CD8 cell ratio
  • decreased delayed hypersensitivity

makes you more susceptible to opportunistic infections

121
Q

How does HIV affect CD8 cell?

A
  • Impaired cytotoxic activity
  • impaired feedback
122
Q

How does HIV affect macrophages?

A
  • Decreased chemotaxis and phagocytosis
  • diminished IL-1 production
  • impaired presentation of antigen to T cells
123
Q

How does HIV affect B cells?

A
  • Diminished antibody production in response to antigen
  • production of immunoglobin

Causes non sepcific increased serum immunoglobin

Pathophys Test 1 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions