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NURA 662 Adv Pathophysiology > Immunity + Infection > Flashcards

Immunity + Infection Flashcards

1
Q

microaerobic

A

need some oxygen but a lot of oxygen will kill them

-find in GI tract

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2
Q

facultative anaerobic

A

can use oxygen if they have It, but can survive without it

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3
Q

obligate anaerobic

A

cannot tolerate oxygen

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4
Q

aerobic

A

need oxygen for oxidative phosphorylation
if they don’t have o2 they die
find on skin and lungs

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5
Q

endotoxin

A

from gram NEGATIVE bacteria

released by bacterial cell death

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6
Q

exotoxin

A

from gram POSITIVE bacteria

released from live bacteria

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7
Q

T or F: most bacteria make toxins.

A

False: most bacteria DO NOT make toxins

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8
Q

Gram negative vs gram positive

A

gram NEGATIVE has outer membrane prevents gram stain from entering during gram stain - stains pale - has thick peptidoglycan layer + outer membrane layer

gram POSITIVE - has peptidoglycan layer withOUT outer membrane - holds gram stain - stains purple

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9
Q

candida albicans

A

fungi

normal gut flora - lives in everyone and doesn’t usually cause problems

causes opportunistic infections

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10
Q

aspergillus

A

fungi

highly aerobic - going to cause problems where we have a lot of oxygen
I.e. skin, respiratory infections

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11
Q

tinea capitis

A

fungus

head

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12
Q

tinea pedis

A

fungus

athletes foot

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13
Q

tinea curis

A

fungus

groin - jock Itch

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14
Q

What is tinea?

A

general term for skin fungus - “dermatophyte”

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15
Q

Most common WBC

A

neutrophil - very short lived, about 4 days

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16
Q

What are memory cells?

A

both b cells and ts cell can become memory cells –> very long lived

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17
Q

Humoral

A

extracellular

INNATE:

  • myeloid cells (neutrophils, macrophages, mast cells, eosinophils)
  • does not change, immediate response

ADAPTIVE:

  • b cells (antibodies, also Th cells, APCs)
  • change over time based on specific threats body has encountered
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18
Q

Cell Mediated

A

intracellular - mostly viral infections

INNATE:
-NK cells (MHC existence)

ADAPTIVE:
-cytotoxic T cells (if cell is abnormal It kills It)

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19
Q

Cells always start with which immunoglobulins

A

IgM and IgD

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20
Q

Cells can make a class switch from IgM to which of IG types?

A

IgG, IgE, IgA

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21
Q

IgG

A

most common in blood

only one that crosses the placenta

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22
Q

IgE

A

allergies, found in tissues bound to mast cells

allergic rhinitis

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23
Q

IgA

A

secreted in GI tract, GU tract, respiratory tract

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24
Q

MHC 1: present self antigen to which type of T cell?

A

cytotoxic t cell (CD8) - useful for virally infected cell

in a cell, a piece of one of your proteins is presented on MHC - I

  • if t cell binds to this, then the cell is virally infected (It is producing foreign protein) - could also be mutated DNA
  • t cell kills this cell
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25
Q

MHC 2: present foreign antigen to which type of T cell?

A

helper T cells (CD4)

presentation at the cell surface of exogenous derived antigens via MHC 2 (macrophage ingested something that is foreign to us
-macrophage could have eaten one of our cells after necrosis but hopefully when present, t cell wont react

DON’T WANT T CELL TO KILL MACROPHAGE, t cell will sound alarm and set things into motion

26
Q

Endogenous protein is cut up and presented on _____ ?

A

MHC 1

27
Q

Exogenous protein is cut up and presented on _______ by ______?

A

MHC 2 by APCs (b cells, macrophages, dendritic cells)

28
Q

Type I hypersensitivity: mechanism, mediated by….

A

IgE mediated
mast cells have IgE receptors
degranulate when see antigen –> inflammation

29
Q

Type I hypersensitivity examples

A

allergic rhinitis
anaphylaxis
asthma

30
Q

Type II hypersensitivity: mechanism, mediated by…

A

IgG mediated against cellular or structural proteins
IgG - antibody of blood/circulation
antibodies bind to our cells and cause immune response (destruction of cells)

31
Q

Type II hypersensitivity examples

A

blood transfusion reactions - blood type mismatch
hemolytic disease of newborn
-rh factor incompatibility - Rh - mom with Rh + fetus
-mom makes IgG, binds to fetal Rh+ blood, newborn born with anemia because RBCs were destroyed by fetal immune system (also hyperbilirubinemia)
Grave’s disease - antibody binds to TSH receptors and activates them
Myasthenia Gravis - antibody binds to Ach receptor on muscle and destroys receptor

32
Q

Type III hypersensitivity: mechanism, mediated by…

A

IgG against blood born antigen

  • we always have stuff in blood that we want to clear out and body is able to do this when antigen is in small amounts
  • when we have too much antigen & antibody, they form immune complexes that are forming faster than phagocytes can take care of them
  • with a lot of antigen in blood and lots of antibodies, we get globs (immune complexes) quick than cells can phagocytize them

-start sticking on blood vessels –> cause vascular damage (neutrophils destroy immune complexes and chew right into blood vessels)

33
Q

Type III hypersensitivity examples

A

Lupus
necrotizing vasculitis
serum sickness

34
Q

Type IV hypersensitivity: mechanism, mediated by…

A

T cells (cytotoxic, H1 and H2)

35
Q

Type IV hypersensitivity examples

A

transplant rejection (body attacks as foreign tissue)
hashimotos thyroiditis
T1DM (kills pancreatic B cells that produce insulin)
poison IVY/contact dermatitis

36
Q

Type I (IgE mediated) - Allergy (environmental antigen)

A

COMMON

allergic rhinitis
anaphylaxis
allergic asthma
atopic eczema
food allergies
penicillin allergy
37
Q

Type II (tissue specific) - Allergy (environment antigen)

A

RARE

38
Q

Type III (immune complex) - Allergy (environment antigen)

A

RARE

Farmer’s lung
Post - streptococcal
glomerulonephritis

39
Q

Type IV (T cell mediated) - Allergy (environment antigen)

A

Poison Ivy

allergic contact dermatitis

40
Q

Type I (IgE mediated) - Autoimmunity (self - antigens)

A

RARE

41
Q

Type II (Tissue specific) - Autoimmunity (self - antigens)

A

COMMON

Grave's disease
Myasthenia Gravis
Autoimmune hemolytic anemia
Immune thrombocytopenic purpura
Rheumatic fever
GBS
Pernicious Anemia
42
Q

Type III (immune complex) - Autoimmunity (self - antigens)

A

Lupus
necrotizing vasculitis
rheumatoid arthritis

43
Q

Type IV (T cell mediated) - Autoimmunity (self - antigens)

A

COMMON

Hashimoto’s thyroiditis
T1DM
multiple sclerosis
celiac disease

44
Q

Type I (IgE mediated) - Alloimmunity (another “person’s” antigens)

A

RARE

45
Q

Type II (Tissue specific) - Alloimmunity (another “person’s” antigens)

A

bad blood transfusion
hemolytic disease of the newborn
hyperacute graft rejection

46
Q

Type III (Immune complex) - Alloimmunity (another “person’s” antigens)

A

serum sickness

47
Q

Type IV (T cell mediated) - Alloimmunity (another “person’s” antigens)

A

transplant rejection

48
Q

Additional autoimmune diseases or have components that are autoimmune diseases

A

scleroderma
chron’s disease
ulcerative colitis
primary biliary cirrhosis
ankylosing spondylitis - “autoinflammatory”
fibromyalgia - not officially declared autoimmune
polymyositis - not officially autoimmune
psoriasis - autoimmune and nonautoimmune varieties
sarcoidosis - autoimmune and nonautoimmune varieties

49
Q

SCID (severe combined immunodeficiency)

A

Primary (genetic) lymphoid immunodeficiency

ADA, adenosine deaminase, deficiency –> don’t produce B OR T cells - severely immunocompromised (think bubble boy)

no humoral reaction and no cellular reaction

lymph node - almost completely empty (only macrophages, dendritic cells, etc.)

50
Q

Agammaglobulinemia

A

Primary (genetic) lymphoid immunodeficiency

“no antibody in the blood”

no b cells - no IgG, no IgM, no IgA, etc.

(cellular reaction present and no humoral reaction)

lymph node - no germinal centers

51
Q

DiGeorge syndrome

A

Primary (genetic) lymphoid immunodeficiency

No thymus - no t cells

(humoral reaction present and no cellular reaction)

lymph node - t cells absent –> empty inner cortex

52
Q

Secondary (acquired) immunodeficiency

A

HIV (human immunodeficiency virus)

53
Q

Chronic granulomatous disease

A

Primary (genetic) MYELOID immunodeficiency

  • problem with not being able to make hydrogen peroxide (to kill bacteria once endocytosed)
  • phagocyte has bacteria in It that It cant kill, person will get lots of bacterial infections (no effect on viruses)
54
Q

Virus that infects helper t cells

A

HIV

55
Q

mycobacterium

A

acid fast staining
INTRACELLULAR (often macrophages)
waxy coating - leads to caseous necrosis in tuberculosis

56
Q

Lupus patho and S/S

A
  • antinuclear antibodies - produce antibody against double stranded DNA
  • wouldn’t attack cells: because DNA is inside cells and antibody can’t get to It
  • during necrosis: cells rupture and spill guts and DNA is floating around, antibodies bind to It and we get immune complexes and vasculitis
  • immune complexes that gather in blood –> T3 hypersensitivity
  • butterfly rash: UV damage of skin
  • kidney failure is tremendous risk because kidney has lots of capillaries
57
Q

sepsis

A

results from pathogens typically in the blood

endothelial cell retraction – plasma proteins leak out – water follows and leaves blood

58
Q

SIRS

A

like sepsis, but no pathogens

59
Q

toxic shock syndrome

A

superantigen induced inflammatory response

-bind directly to the TCR and the MHC class II molecules
-Superantigens activate Th cells independent of TCR antigens specifically
higher binding and higher binding affinity
going to bind a lot more helper t cells and for longer

60
Q

toxic shock syndrome

A

superantigen induced inflammatory response

  • bind directly to the TCR and the MHC class II molecules
  • Superantigens activate Th cells independent of TCR antigens specifically
  • higher binding and higher binding affinity
  • going to bind a lot more helper t cells and for longer

NURA 662 Adv Pathophysiology (7 decks)

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