Brainscape's Knowledge GenomeTM

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


See full index

Path EOY - POP > Immunity > Flashcards

Immunity Flashcards

1
Q

innate

A

non-specific, no memory

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

innate immunity - major components

A

epithelial barriers
phagocytic cells
innate lymphoid cells
plasma proteins - complement

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

innate immunity - cellular components

A

phagocytes -
monocytes/macrophages - fever and t cell and macrophage activation, lymphocyte activation, increased antibody prodcution, induce acute phase protein production
neutrophils
eosinophils
basophils
mast cells

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

innate immune system - secreted components

A

complement - increased vascular permeability, formation of ILs and TNF
cytokines - promote leukocyte cheomtaxis
lysozome
acute phase proteins

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

adaptive immunity

A

specific
remembers pathogens
cell mediated and humoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

adaptive immunity - cellular components

A

B cells/plasma cells - make antibodies and memory cells
T cells -
CD4 - helper cells - make cytokines, activate other immune cells, inhibit immune function
CD8 - cytotoxic

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

adaptive immunity - secreted components

A

antibodies
cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

immune recognition of pathogens

A

PAMPs/DAMPs –> activate pattern recognition receptors

PRRs classifications -
secreted - bind microbial surface - activate complement, enable phagocytosis
transmembrane - in cell membrane - macrophages, NK cells, dendritic cells
cytosolic - in cytoplasm of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

toll-like receptors

A

mediate inflammation in gut
bind bacterial lippolysaccharides
activate signal cascade that regulates inflammatory responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

dendritic cells

A

antigen presenting
phagocytic

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

T helper cells (CD4)

A

Th1 -
activated by IL-12 and IL-18
produce IL-2, IFN-gamma and TNF-beta
direct cell mediated response

Th2 -
activated by IL-4
produce IL-3-6,10, and 13
direct humoral response

also Th17 and T-regs

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

FIP - immunopathogenesis

A

antibody production counter productive - enhance uptake and replication in macrophages

–> type 3 hypersenstivity

vaccination makes it worse

effusive - failure to mount T cell immunity in face of vigorous B cell response
dry form - partially effective cell mediated response keeping virus to smaller number of macrophages

dry form always after brief spell of effusive disease

terminal stage - immunity collapses and disease reverts to effusive

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

failure of passive immunity

A

dam –> neonate in colostrum (IgG)

failure predisposes neonates to systemic infection - eg joint ill

measured -
indirect - serum total protein, zinc sulphate turbidity
direct - ELISA (foals)

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

antibodies

A

B cells –> plasma cells –> produce immunoglobulins

5 classes -
IgG - most abundant - bloodstream and colostrum - small so can go into interstitial spaces
IgM - large - mostly in bloodstream, more antigen binding ability than IgG
IgA - mucosal surfaces and milk
IgE - produced by plasma cells, high affinity for tissue mast cells, involved in allergy
IgD

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

primary lymphoid organs

A

antigen independent formation of lymphocytes

thymus
bursa of fabricus
bone marrow
peyers patches in ruminants
foetal liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

secondary lymphoid organs

A

antigen dependent formation of lymphcytes

spleen
tonsil
peyers patches in species other than ruminants
lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tertiary lymphoid organs

A

MALT/GALT/BALT
sampling of pathogens at epithelial surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

primary and secondary immunodeficiency

A

primary - genetic deficiency in a component of the immune system

secondary - exogenous causes of defective immunity - infectious, radiation, chemotherapy, nutritional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

severe combined immunodeficiency disease (SCID)

A

Different genetic defects - x-linked, autosomal recessive, sporadic

affects both cell mediated and humoral adaptive immunity

arabian horses - autosomal recessive –> lymphopenia and agammaglobulinemia –> death due to secondary infection
marked thymic response

20
Q

chediak higashi syndrom

A

defective ability to release intracellular granules and reduced ADP storage

affects all granulocytes, melanocytes and platelets

21
Q

leukocyte adhesion deficiency

A

dogs (irish setters) and cattle (holsteins)

CD18 deficiency

high numbers of circulating neutrophils but can’t penetrate endothelium

22
Q

fell pony syndrome

A

foal immunodeficiency
autosomal recessive

severe anemia and B cell lymphopenia

23
Q

grey collie syndrome

A

cyclic neutropenia
autosomal recessive
neutrophil count drops

24
Q

Parvovirus (canine parvo and feline panleukopenia)

A

destruction of gut/bloodstream barrier –> consumption of immune factors –> direct infection of immune cells –> lymphocytes destroyed

diarrhoaw
secondary bacterial infections
panleukopenia

25
Q

hypersensitivity

A

altered injurious immune reactivity to a specific antigen in a sensitised host

general features -
response elicited by antigens - endogenous, exogenous, or non-microbial
imbalance of effector and control mechanisms
associated with susceptibility genes
poorly controlled normal effector mechanisms cause tissue injury mechanisms
sensitisation and effector phases

26
Q

type 1 hypersensitivity - Allergic

A

previously sensitised individual
antigen binds to IgE antibody on mast cell surface
excessive Th2 response
promotes inflammation
systemic or local reaction

2 phase -
intermediate - vasodilation, vascular leakage, smooth muscle spasm, gland secretion
late - infiltration with leukocytes and destruction of mucosal epithelium

local immediate hypersensitivity reactions
systemic anaphylaxis - vascular shock, oedema, respiratory distress

mediators -
histamine
enzymes
proteoglycans
arachidonic acids
cytokines

diagnosis -
signs
mast cells tryptase
post mortem - acute cardiogenic failure, diffuse congestion of lungs, liver and intestines, marked diffuse alveolar oedema

degeneration of centrolobular hepatocytes, increased mast cells

27
Q

type 2 hypersensitivity - cytotoxic

A

antibodies react with antigens on cell surfaces or in ECM
destroy target cells - trigger inflammation or interfere with normal function

IgG and IgM

3 mechanisms -
opsonisation and phagocytosis - IMHA
inflammation - glomerular nephritis, vascular issues, organ rejection
dysfunction - myasthenia gravis

28
Q

hypersensitivity type 3 - immune complex

A

antigen-antibody complexes formed
inflammation at site of depostion

eg blue eye in canine adenovirus, FIP

29
Q

hypersensitivity type 4 - delayed

A

CD4 T cell mediated
organ specific disease, inflammation - activate macrophages
tuberculin skin reaction

30
Q

acute allergic reaction

A

local hypersensitivity
type 1

cutaneous only

erythema
pruritus
uricaria
angioedema

31
Q

generalised (systemic) reaction

A

mild - skin/mucosal tissue without other organ involvement

moderate - involving 2 or more organ systems

severe - evidence of neurological compromise

moderate and severe classified as anaphylaxis

32
Q

mast cells

A

innate
granulocytes
in connective tissue adjacent to blood vessles and lymphatics in skin and mucosa
degranulate to release histamine when exposed to inciting agent and IgE

33
Q

histamine

A

increased vasodilation and permeability of vessels

34
Q

eosinophils

A

only in GIT, secondary lymphoid tissues, adipose tissue, thymus, mammary gland, and uterus
acts with mast cells as allergic effector unit - regulate mast cells and vice versa
granule content can cause tissue damage

35
Q

self tolerance

A

lack of responsiveness to own antigen

4 mechanisms -
central -
T and B cells apoptosed
T cells pushed to becoming T regs
peripherally -
Y and B cells become unreactive
T regs locally repress immune system

36
Q

immunoprivileged tissues

A

tested, brain, eye

don’t communicate with blood/lymph so thymus doesn’t need to tell lymphocytes not to react to self

leakage into tissues –> exposure to immune response –> marked and chronic response

difficult to elicit immune response to antigens in these sites

37
Q

mechanisms of autoimmunity

A

defective tolerance -
breakdown of self tolerance mechanisms
genetic

increased expression of self antigens or changes to self antigens -
antigens undergo structural changes - cellular stress or injury
immune system not tolerant of new epitropes

inflammation/infection -
upregulation of costimulators on antigen presenting cells that present self antigens
infectious agents present antigens that look like self antigens
polyclonal b cell activation
tissue injury - self antigen release that may be altered
stimulates production of cytokines

38
Q

lupus

A

systemic or cutaneous - lesions in multiple tissues or just skin

systemic -
loss of B and T cell tolerance to self antigens
autoantibodies produced
type 3 hypersensitivity reaction
deposition of anti-antibody complexes - in glomerulus, blood vessels, skin, and joints

presentations -
renal disease
polyarthitis
hematologic disorders
respiratory or neurologic dysfunction

cutaneous -
often nose
ulcerative dermatitis, alopecia

signs -
fever
polyarteritis
glomerularnephritis
mucocutaneous lesions
skin lesions
lymph node and spleen enlargement

diagnosis -
IMHA, lymphopenia, increase CD4:CD8 ratio
antinuclear antibody titre - dogs

39
Q

pemphagus

A

group of autoimmune skin disease

immune reaction against anchoring collagens

pustules, vesicles, bullae, erosions, ulcers

histo - epidermal thickening, loss of adhesion between epithelial cells

40
Q

single gene disorders

A

of somatic cells, germs cells, or mitochondria

autosomal dominant - polycystic kidney disease
autosomal recessive - lysosomal storage disease
X-linked - duchenne’s muscular dystrophy

41
Q

chromosomal disorders

A

turner like syndrome -
x monosomy
horses and pigs
small body, poor comformation, angular, deformities
small and inactive ovaries
diagnosis by karotyping

42
Q

complex multigenic disorders

A

diabetes type 1
systemic lupus erythematous

43
Q

polycystic kidney disease

A

persian cats and bull terriers
mutated polycysin 1 or 2 gene

modified cilia function and cell proliferation and migration –> renal failure

PUPD
low USG
azotemia
bilaterally enlarged or shrunken kidneys
large cysts with firm pale areas (fibrosis) in between

cats - also cysts in liver and pancreas

44
Q

lysosomal storage disease

A

young animals
lack of protein for lysosomal degeneration pathways

signs depend on part of CNS affected - ataxia, head and limb tremors
typically no gross lesions
may see accumulated material in macrophages in blood of CSF
urinalysis - gags

45
Q

duchennes muscular dystrophy

A

lack of dystrophin gene
muscle fibres susceptible to repeated necrosis, regeneration and fibrosis

progressive muscle atrophy –> weakness in diaphragm –> impaired respiration and hiatal hernia

Path EOY - POP (7 decks)

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