Ch. 16 Flashcards
(80 cards)
1
Q
What is the other name for type II hypersenstivity?
A
antibody-mediated hypersensitivity
2
Q
describe type II hypersensitivity.
A
cytotoxic (kills cells)
IgG or IgM attack antigens on cell surfaces
– usually involves antigens on RBCs or WBCs
– transfusion reactions
– Rh disease
– drug reactions
THESE CAN BE AUTOIMMUNE DISEASE
ALSO TISSUE SPECIFIC
3
Q
What are the different mechanisms of anti-body mediated HS?
A
complement mediated phagocytosis
inflammation
cell injury or physiologic responses without cell injury
4
Q
How does type II HS work in a nutshell?
A
antibodies that our body has made attach to the surface atigens of cells
after this is done a couple of things can happen:
the cell can be directed lysed
the complement system can be activated (which leads to cell lysis or the attraction of WBCs to eat the cell.
5
Q
If you are blood type A what surface antigen and antibody would you have?
A
A surface antigen
anti-B antibody
6
Q
What type of blood can a type A- blood type recieve?
A
A- or O-
7
Q
What blood can A+ recieve?
A
A+, A-, or O-
8
Q
universal donor?
A
O-
9
Q
universal recipient?
A
AB+
10
Q
What is another name for type III hypersensitivity?
A
Immune complex mediated
11
Q
How does type III HS work?
A
A free-floating antigen and antibody form a circulating immune complex that are deposited on vessels walls or extravascular tissues
This activates the complement system
leads to the recruitment an activation of inflammatory cells that release tissue damaging products
causes damage to blood vessels (THIS IS KEY TO REMEMBER)
12
Q
are type III immune complexes soluble?
A
NO
13
Q
are the immune complexes in type III identified as self?
A
NO
14
Q
Can type III be local or systemic?
A
YES local - arthitic response (rheumatory arthritis)
systemic - lupus
15
Q
Does the amount of antigen-antibody complexes in our blood fluctuate with out type III HS?
A
Yes, this is why with a lot of our type III HS autoimmune diseases there are flare periods as well as periods of remission.
16
Q
Why is it key to remember that the blood vessels get damaged in type III HS?
A
the damage to the blood vessels causes an increase in the inflammatory response
this can also decrease blood flow in the area of action
17
Q
What are some disease that are associated with type III HS?
A
autoimmune vasculitis, glomerulonephritis, systemic lupus, rheumatoid arthritis
18
Q
What are some things that can cause type III HS?
A
antibiotics MOST COMMON
food
drugs
insect venom
19
Q
What is serum sickness?
A
a type III HS reaction to penicillin
20
Q
What are the types of type IV HS?
A
direct-cell mediated
– viral infections
delayed-type
- TB test
- Allergic contact dermatitis
- hypersensitivity pneumonitis
21
Q
What is another name for type IV HS?
A
cell mediated
22
Q
What happens during direct-cell mediated type IV HS?
A
The antigen is presented by the antigen presenting cell
a CD8 T cell directly lyses the cell
23
Q
What happens during the delayed-type response of type IV HS?
A
The antigen is presented by an antigen-presenting cell
CD4 cell is activated and releases cytokines
This is a delayed reaction that takes little bit to manifest.
POISIN IVY, OAK, TB TEST,
24
Q
What does type IV HS ultimately lead to?
A
sensitized T cells that cause cell and tissue injury
25
How does allergic contact dermatits work with initial contact and secondary contact?
With primary contact --- (takes 7-10 days) SHOWS NO DERMATITIS, our t cells differentiate into memory t cells
secondary contact: our t memory cells activate many cells (causes dermatits)
26
What happens when we touch poisin ivy?
our skin protein combines with catechol molecules.
27
What are the manifestations of allergic contact dermatits due to poison ivy or oak?
erythematous
swollen
warm
vesicular lesions (have exudate)
intense pruritus
28
(nothing to do with hypersensitivity anymore) what are the two types of solid organ rejection?
Solid organ rejection
Humoral rejection (2 forms)
- - hyperacute
- - develop antibodies
29
describe solid organ t-cell rejection
t-cells attack the endothelium, endothelial cell death leads to ischemia and triggers inflammation with increased vascular permeability
also leads to local accumulation of lymphocytes and macrophages
PLAYS A ROLE IN ACUTE AND CHRONIC REJECTIONS
30
describe humoral rejection. (2 forms)
hyperacute - circulating antibodies react with the graft ( this can be seen during the surgery), usually already have the antibodies, could have been a bad organ match, or the person could have had a previous transplant
develop antibodies - the destruction can be from antibodies developed, cell mediated, complement system, or inflammation BUT THE TARGET IS USUALLY BLOOD VESSELS THAT FEED THE NEW ORGAN, CAUSES ISCHEMIA AND THE ORGAN WILL END UP DYING
31
When does acute transplant rejection usually occur, what cells play a role?
First few months
| T CELLS PLAY A ROLE IN DESTROYING THE GRAFT CELLS (organ cells)
32
When does chronic transplant rejection usually occur, what cells are involved?
4-6 months
T or B CELLS
usually attacks the vessels (fibrosis of vessels causing them to fail)
33
Describe what graft-versus-host-disease (GVHD) is.
This is a case where instead of the hosts body attacking the donated tissue, the donated tissue begins attack the hosts cells.
34
Where do we most often see GVHD?
bone marrow transplants and in immunocompromised patients who recieve blood products.
35
What is happening during GVHD?
The donor T cells and NK cells are attacking the hosts HLA antigens
36
how does GVHD most often present?
with a pruritic skin rash that sloughs off
37
What has to be present for GVHD to develop?
transplant has functional cellular immune component (this is why bone marrow is often a case)
recipient tissue has foreign antigens to the donor
recipient immunity is compromised so it cant destroy the transplanted cells
38
Does gender tend to effect GVHD?
YES, we tend to see it more in men who get transplants from women
ALSO SAID THAT WOMEN AND CHILDRENS BONE MARROW IS MORE LIKELY TO CAUSE THIS REACTION
39
What is self tolerance?
This is the inability to mount an immune response against self. (GOOD)
40
What is central tolerance?
the elimination of self reactive T cells from the thymus and self reactive B cells form the bone marrow
41
What is peripheral tolerance?
The elimination of self reactive T and B cells that escaped detection in the central lymphoid organs.
42
What are the steps of central tolerance in the thymus?
pre-T cells are made in the bone marrow and are sent to the thymus
If the thymus detects that they are self-reactice it triggers apoptosis
43
What are the mechanisms of autoimmune disorders?
genetic predisposition + trigger event
estrogen (many autoimmune diseases are more common in women than men)
breakdown in t-cell anergy (unresponsiveness to an organism) (in this case its self)
release of sequestered antigens (stored antigens that were made when in fetal development, we dont need them normally) COMMON IN PROMATOZOA AND OCCULAR DISEASES
molecular mimicry - a foreign antigen that closely resembles a self-antigen = antibodies formed against the foreign antigen (these antibodies can attack self antigens too because the self are closely related to the foreign) COMMON WITH STREP THROAT, WHICH IS WHY WE TREAT IT, ARE SIMILAR TO HEART AND KIDNEY CELLS
superantigens - active immune response without processing or presentation, (DONT NEED AN INITIAL EXPOSURE TO CAUSE DRAMATIC RESPONSE)
44
Go more in depth about superantigens.
Family of substances that can short-circuit the immune system response and cause inappropriate activation of CD4 helper cells
processing and presentation is not required by APCs.
the superantigens bind directly to the MHC II complex molecules and cause a massive release of T-cell inflammatory cytokines (IL and TNF) and uncontrolled proliferation of T cells
45
What are some examples of disorders with superantigens?
adults: toxic shock syndrome
children: kawasakis disease
46
What are some examples of autoimmune type III diseases?
systemic lupus erythmatosus (SLE):
- - chronic multisystem disease
- - more common in females
rheumatoid arthritis
- - circulating immune complexes containing antibodies go into joint spaces and cause inflammation
- - more common in females
47
What are the manifestations of SLE?
```
arthralglias or arthritis (90% MOST COMMON)
vasculitis and rash (70-80% VERY COMMON)
renal disease (40-50%)
hematologic changes (50%)
cardiovascular disease (30-50%)
```
48
What are the manifestations of rheumatoid arthritis?
redness, swelling, and painful joints
49
How do we treat autoimmune disorders?
suppressing the immune system
50
What do the treatments for autoimmune disorders put people at risk for?
cancer, infections, ect...
51
With autoimmune disorders, do the patients have hypoactive or hyperactive immune systems?
HYPERACTIVE
52
What are the different types of immunodefciency?
Primary:
- - humoral (B-cell)
- - Cellular (T cell)
- - combined immunodeficiency
Acquired:
-- AIDS
53
What is a humoral (B cell) deficiency (primary)?
the body has an impaired ability to produce antibodies IgG IgM IgA
PRONE TO INFECTIONS FROM ENCAPSULATED ORGANISMS
IgA is in our mucous membranes (makes very prone for respiratory and GI infection)
54
What does a T-cell deficiency cause (primary)?
impair the bodies ability to orchestrate a proper immune response
PRONE TO CANCERS AND INTRACELLULAR INFECTIONS
55
How do people survive a combined B and T cell deficiency (primary)?
bone marrow or stem cell transplant
56
What are some warning signs of a primary immundeficiency?
8 or more infection/year
2 or more serious sinus infections/year
2 or more months on antibiotics with little effect
2 or more pneumonias/year
failure of infant to gain weight
recurrent deep skin infection or organ abcess
persistnat thrush in mouth or skin after 1 year of age
need for IV antibiotics
2 or more deep seated infections
Family history of primary immunodeficiency
57
What is the relationship between HIV and AIDS?
HIV is the virus that causes aids
58
At what point does HIV turn in to full blown AIDS?
CD4 count of less than 200
59
can HIV be transferred from mother to infant?
YES
60
How is HIV transmitted?
```
BODY FLUIDS:
sexual contact (semen and vaginal fluids)
```
breast milk
blood-to-blood contact
- -contaminated needles (0.3% with large bore needle in deep muscle, as opposed to 30% with hep B, 3% for hep 3%)
- - transfusions (screening make it very low risk now)
- - during pregnancy or birth
NOT IN URINE TEARS OR SWEAT
61
What are the 8 steps of HIV replication?
1. the virus binds to CD4 cell and attaches to surface molecules
2. fusion to the CD4 membrane and uncoating of the virus
3. DNA synthesis - changes from a single stranded RNA virus to double stranded DNA using the reverse transcriptase enzyme
4. integration - enters the nucleus of CD4 cell and becomes that cells DNA
5. transcription to mRNA
6. translation- rRNA uses message from mRNA to create protein chain
7. cleavage of chain into parts that will make up new virus
8. proteins and viral RNA reassemble to make new viruses
62
What happens during HIV replication?
the CD4 cell gets killed and releases the copies of HIV into the bloodstream where more CD4 cells will be invaded and killed to make more virions
63
Does HIV only have the receptors for CD4 cells?
YES, it is the only cell it can replicate in
64
What is the window period?
the time between infection and seroconversion where the person can still infect someone, but the labs will show a negative result if tested for the disease because they dont have any antibodies yet
no signs and symptoms yet
65
What are the different phases of HIV infection?
primary phase
latent period
overt AIDS
66
Describe the primary phase of the HIV virus.
The patient will have signs and symptoms of systemic infection
seroconversion will occur (body will produce antibodies against HIV)
USUALLY 1-6 MONTHS LONG
(this is why tests for HIV after possible exposure last 6 months usually)
67
Describe the latent period of HIV infection.
the virus is replicating, CD4 count is gradually falling
may last 10-11 years or even longer
SEVERE SIGNS AND SYMPTOMS USUALLY GONE
68
Describe the overt AIDS stage.
CD4 count of
69
Can people go through the primary phase of HIV without knowing it? What can happen with that?
YES, people can
what might happen is they could go into their latent period where they show no symptoms but their CD4 count is still dropping
They might not find anything out until they have overt AIDS or an AIDS defining illness
70
What are some AIDS-associated illnesses?
opportunistic infections
- -respiratory (bacterial pneumonia, or a severe pneumonia caused by P. jiroveci, TB is common cause of death)
- -GI
- -nervous system
salmonella, c diff, criptosporidium
ulcers
HANDS (HIV Associated Neuro-cognitive Disorders)
AIDS dementia complexe
cancers (kaposi sarcoma)
wasting syndrome (10% involuntary weight lose with diarrhea, weakness and fever)
metabolic disorders (diabetes,mitochondrial disorders ect..)
71
Is wasting syndrome present with infections?
NO, this syndrome is diagnosed when there is no presence of infections
72
What is the #1 cause of death in HIV patients?
TB
73
What are the common manifestations of uncontrolled HIV infection?
fevers (especially in evening)
night sweats
diarrhea
fatigue
weight loss
lymphadenopathy
VERY SIMILAR SYMPTOMS TO MONO, HAVE TO LOOK FOR RISK FACTORS AS WELL, OTHERWISE IT MIGHT GO UNNOTICED
74
Can people with HIV have a normal life span?
YES, 50% do
75
Where do many complications from diagnosed HIV come from?
the treatment itself
76
What are the goals of HIV treatment with antiretroviral therapy?
reduce HIV-RNA (viral load) below detectable levels
increase CD4 count
prevent emergence or viral resistance
improve quality of life
reduce HIV-associated morbidity and mortality
77
What did she say about HIV infection and pregnancy?
ALL PREGNANT WOMEN SHOULD BE TESTED
ALL PREGNANT HIV-INFECTED WOMEN SHOULD BE TREATED (2ND TRIMESTER TO DELIVERY) brings transmission rates down tremendously
C-SECTIONS REDUCES TRANSMISSION BUT NOT RECOMMENDED IF HIV RNA LEVEL SUPPRESSED (this may reduce transmission possibility a little, but puts the mother at a high risk for infection)
78
What is post-exposure prophylaxis?
This is a treatment to prevent HIV if you have been exposed, medication that attempts to stop the virus from replicating in you
no controlled trials have been done that demonstrate its efficacy
79
What are some risk factors for contracting HIV?
deep stick
hollow-bore needles
terminal illness in source, (high RNA)
needle in blood vessel
visible blood on needle
sexual exposure (higher from men to women than from women to men)
80
If you are stuck by a needle used on someone with HIV, should you be tested for hep B and C as well?
definately, the risk factors for the three diseases are the same
