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Pathophysiology > Ch. 16 > Flashcards

Ch. 16 Flashcards

1
Q

What is the other name for type II hypersenstivity?

A

antibody-mediated hypersensitivity

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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

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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

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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.

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5
Q

If you are blood type A what surface antigen and antibody would you have?

A

A surface antigen

anti-B antibody

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6
Q

What type of blood can a type A- blood type recieve?

A

A- or O-

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7
Q

What blood can A+ recieve?

A

A+, A-, or O-

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8
Q

universal donor?

A

O-

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9
Q

universal recipient?

A

AB+

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10
Q

What is another name for type III hypersensitivity?

A

Immune complex mediated

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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)

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12
Q

are type III immune complexes soluble?

A

NO

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13
Q

are the immune complexes in type III identified as self?

A

NO

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14
Q

Can type III be local or systemic?

A

YES local - arthitic response (rheumatory arthritis)

systemic - lupus

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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.

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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

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17
Q

What are some disease that are associated with type III HS?

A

autoimmune vasculitis, glomerulonephritis, systemic lupus, rheumatoid arthritis

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18
Q

What are some things that can cause type III HS?

A

antibiotics MOST COMMON

food

drugs

insect venom

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19
Q

What is serum sickness?

A

a type III HS reaction to penicillin

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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
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21
Q

What is another name for type IV HS?

A

cell mediated

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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

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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,

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24
Q

What does type IV HS ultimately lead to?

A

sensitized T cells that cause cell and tissue injury

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25
Q

How does allergic contact dermatits work with initial contact and secondary contact?

A

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)

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26
Q

What happens when we touch poisin ivy?

A

our skin protein combines with catechol molecules.

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27
Q

What are the manifestations of allergic contact dermatits due to poison ivy or oak?

A

erythematous

swollen

warm

vesicular lesions (have exudate)

intense pruritus

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28
Q

(nothing to do with hypersensitivity anymore) what are the two types of solid organ rejection?

A

Solid organ rejection

Humoral rejection (2 forms)

    • hyperacute
    • develop antibodies
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29
Q

describe solid organ t-cell rejection

A

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

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30
Q

describe humoral rejection. (2 forms)

A

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

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31
Q

When does acute transplant rejection usually occur, what cells play a role?

A

First few months

T CELLS PLAY A ROLE IN DESTROYING THE GRAFT CELLS (organ cells)

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32
Q

When does chronic transplant rejection usually occur, what cells are involved?

A

4-6 months

T or B CELLS

usually attacks the vessels (fibrosis of vessels causing them to fail)

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33
Q

Describe what graft-versus-host-disease (GVHD) is.

A

This is a case where instead of the hosts body attacking the donated tissue, the donated tissue begins attack the hosts cells.

34
Q

Where do we most often see GVHD?

A

bone marrow transplants and in immunocompromised patients who recieve blood products.

35
Q

What is happening during GVHD?

A

The donor T cells and NK cells are attacking the hosts HLA antigens

36
Q

how does GVHD most often present?

A

with a pruritic skin rash that sloughs off

37
Q

What has to be present for GVHD to develop?

A

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
Q

Does gender tend to effect GVHD?

A

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
Q

What is self tolerance?

A

This is the inability to mount an immune response against self. (GOOD)

40
Q

What is central tolerance?

A

the elimination of self reactive T cells from the thymus and self reactive B cells form the bone marrow

41
Q

What is peripheral tolerance?

A

The elimination of self reactive T and B cells that escaped detection in the central lymphoid organs.

42
Q

What are the steps of central tolerance in the thymus?

A

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
Q

What are the mechanisms of autoimmune disorders?

A

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
Q

Go more in depth about superantigens.

A

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
Q

What are some examples of disorders with superantigens?

A

adults: toxic shock syndrome
children: kawasakis disease

46
Q

What are some examples of autoimmune type III diseases?

A

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
Q

What are the manifestations of SLE?

A 
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
Q

What are the manifestations of rheumatoid arthritis?

A

redness, swelling, and painful joints

49
Q

How do we treat autoimmune disorders?

A

suppressing the immune system

50
Q

What do the treatments for autoimmune disorders put people at risk for?

A

cancer, infections, ect…

51
Q

With autoimmune disorders, do the patients have hypoactive or hyperactive immune systems?

A

HYPERACTIVE

52
Q

What are the different types of immunodefciency?

A

Primary:

    • humoral (B-cell)
    • Cellular (T cell)
    • combined immunodeficiency

Acquired:
– AIDS

53
Q

What is a humoral (B cell) deficiency (primary)?

A

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
Q

What does a T-cell deficiency cause (primary)?

A

impair the bodies ability to orchestrate a proper immune response

PRONE TO CANCERS AND INTRACELLULAR INFECTIONS

55
Q

How do people survive a combined B and T cell deficiency (primary)?

A

bone marrow or stem cell transplant

56
Q

What are some warning signs of a primary immundeficiency?

A

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
Q

What is the relationship between HIV and AIDS?

A

HIV is the virus that causes aids

58
Q

At what point does HIV turn in to full blown AIDS?

A

CD4 count of less than 200

59
Q

can HIV be transferred from mother to infant?

A

YES

60
Q

How is HIV transmitted?

A 
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
Q

What are the 8 steps of HIV replication?

A
  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
Q

What happens during HIV replication?

A

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
Q

Does HIV only have the receptors for CD4 cells?

A

YES, it is the only cell it can replicate in

64
Q

What is the window period?

A

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
Q

What are the different phases of HIV infection?

A

primary phase

latent period

overt AIDS

66
Q

Describe the primary phase of the HIV virus.

A

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
Q

Describe the latent period of HIV infection.

A

the virus is replicating, CD4 count is gradually falling

may last 10-11 years or even longer

SEVERE SIGNS AND SYMPTOMS USUALLY GONE

68
Q

Describe the overt AIDS stage.

A

CD4 count of

69
Q

Can people go through the primary phase of HIV without knowing it? What can happen with that?

A

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
Q

What are some AIDS-associated illnesses?

A

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
Q

Is wasting syndrome present with infections?

A

NO, this syndrome is diagnosed when there is no presence of infections

72
Q

What is the #1 cause of death in HIV patients?

A

TB

73
Q

What are the common manifestations of uncontrolled HIV infection?

A

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
Q

Can people with HIV have a normal life span?

A

YES, 50% do

75
Q

Where do many complications from diagnosed HIV come from?

A

the treatment itself

76
Q

What are the goals of HIV treatment with antiretroviral therapy?

A

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
Q

What did she say about HIV infection and pregnancy?

A

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
Q

What is post-exposure prophylaxis?

A

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
Q

What are some risk factors for contracting HIV?

A

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
Q

If you are stuck by a needle used on someone with HIV, should you be tested for hep B and C as well?

A

definately, the risk factors for the three diseases are the same

Pathophysiology (13 decks)

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