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Pathology > Lecture 6: Dermatology > Flashcards

Lecture 6: Dermatology Flashcards

1
Q

What are the components of the immune system

A

Cells
recognition molecules
soluble factors

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2
Q

Describe nonspecific immunity

A

First line of defence, non specific

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3
Q

Describe the anatomic and physiologic portion of nonspecific immunity

A

skin, mucosa, cilia

stomach pH, Body Temperature

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4
Q

Describe the cellular portion of the nonspecific immunity

A

phagocytic cells, NK cells

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5
Q

describe the molecular portion of the nonspecific immunity

A

inflammation

complement system

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6
Q

Where do the cells from the nonspecific immunity come from

A

recruited by the molecules of inflammation

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7
Q

What is the function of the cells of the nonspecific immunity

A

ingest + destroy pathogens

neutralize toxins

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8
Q

Describe the self/nonself identification by neutrophils, monocytes, tissue macrophages, NK cells

A 
Express membrane receptors that innately recognize several pathogens (pathogen recognition receptors)
Recognizes PAMPs (pathogen-associated molecular patterns)
Also DAMPS (damage associated molecular patterns)
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9
Q

Describe the cell mediated specific immunity

A

T-Lymphocytes for intracellular pathogens

B-Lymphocytes for extracellular pathogens and toxins

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10
Q

Describe the characteristics of specific immunity

A 
Specificity
Diversity
Memory
Self/non-self recognition
MHC molecules
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11
Q

Describe T Lymphocytes

A

Contains T Cell Receptor
TCR can only recognize antigen in combination with a MHC molecule.
Each T Lymphocyte expresses a different TCR

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12
Q

What is the CD4 T Lymphocyte

A 
Helper T lymphocytes
Recognizes MHC class II: found on antigen presenting cells
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13
Q

What is the CD8 T Lymphocyte

A

Cytotoxic T Lymphocytes: Recognizes MHC class I: found on all nucleated cells

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14
Q

What is a signal 2 lymphocyte:

A

important for tolerance and auto-immunity

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15
Q

What do T-Lymphocytes do when activated

A

Expand clonal

differentiate into: Effector Cells or Memory cells

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16
Q

Describe the antigen receptor in B Lymphocytes

A

Membrane-bound immunoglobulin. The immunoglobulin gene can rearrange- antigen recognition diversity.

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17
Q

What happens to B Lymphocytes when activated

A 
Expand clonally
Differentiates into:
Effector cells plasma cell (antibody secreting)
Needs the action of T-helper lymphocyte
Memory cells
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18
Q

What is the function of a macrophage

A

Phagocytosis
Antigen presentation to T-Lymphocyte
MHC class II

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19
Q

What is the function of a dendritic cell

A

Very efficient antigen presenting cell

Capture antigens in circulation and present to T-Lymphocytes in lymph nodes

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20
Q

Describe a Type 1 hypersensitivity

A

Immediate hypersensitivity
Misdirected/innapropriate response
occurs within minutes of exposure

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21
Q

Describe the type 1’s immediate hypersensitivity

A

IgE mediated
Against:
Environmental antigens (allergens)
Parasite antigen

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22
Q

What does a type 1 hypersensitivity reaction require

A

Need to be previously SENSITIZED

Mediated by mast cells

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23
Q

What does mast-cell degranulation in a type 1 hypersensitivity reaction result in

A 
Vasodilation
Edema
Smooth muscle contraction
Mucus production
Inflammation
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24
Q

Describe the systemic reaction in a type 1 hypersensitivity

A

Anaphylaxis

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25
Q

Describe the localized type 1 hypersensitivity reaction

A

Skin, mucosa, GIT

Atopy, allergic rhinitis

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26
Q

What is allergic dermatitis

A

cutaneous manifestation of type I hypersensitivity

Inhalation, ingestion, percutaneous

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27
Q

What do you call an allergic dermatitis with a genetic predisposition

A

atopic dermatitis

28
Q

Describe a flea bite hypersensitivity

A

Most common hypersensitivity in cats & dogs

Very pruritic dermatitis (mostly on back)

29
Q

What is urticaria and angiodema

A

Most often in horses and dogs
Multifocal or localized areas of edema
Urticaria: superficial
Edema: deep dermis and subcutis

30
Q

What are the immunologic causes of Urticaria and Angioedema

A

food, drug, antisera, insect bites

31
Q

what are the non immunologic causes of urticaria and angiodema

A

heat, exercise, stress

32
Q

Describe a cytotoxic hypersensitivity

A

Development of antibodies against self cells or tissue

May be from self antigen or exogenous antigen adsorbed to self

33
Q

What does a cytotoxic hypersensitivity cause

A 
IMHA, ITP (cytotoxic)
Myasthenia gravis (altered function)
34
Q

What immune complexes are involved in a type 2 hypersensitivity

A

IgM and IgG

35
Q

What does a type 2 hypersensitivity reaction require

A

a sensitized host

36
Q

What enhanced phagocytosis of antigen by macrophages in type 2 hypersensitivity

A

opsonization by antibodies or complements

37
Q

How can an antibody activate the complement system and what happens when it does it

A

Antibody can activate the complement system, via the classical pathway, resulting in the elaboration of inflammatory mediators

38
Q

What can antibodies against cell receptors do

A

activate or inhibit cell function. ex: TSH

39
Q

What is immune mediated hemolytic anemia

A

Common, life-threatening acute anemia
Young middle-aged females, cocker spaniels
Usually idiopathic
Infection, drugs, neoplasia

40
Q

What is neonatal isoerythrolysis

A 
A form of IMHA
Colostrum derived maternal antibodies
Attacks newborn’s RBC
Common in horses
Immunosensitization of mother to incompatible blood type from stallion

8-10h after birth up to 4-5 days

41
Q

what is pemphigus (foliaceous)

A

Most common and milder form of pemphigus
Often adverse reaction to drugs
Autoantibodies against a protein in desmosomes
Pustules with acantholytic keratinocytes

42
Q

What are three different type 2 hypersensitives

A

Immune Mediated Hemolytic Anemia
Neonatal isoerythrolysis
Pemphigus

43
Q

Describe a type 3 hypersensitivity

A

Immune-complex hypersensitivity
Antigen-antibody complexes that activate complement and cause damage
Similar to type II
Type II: antigen directed against self
Type III: antigen just get “stuck” to tissue

44
Q

What happens when immune complexes are deposited into tissues

A

Activation of complement system

tissue DAmage

45
Q

Why do antibody antigen complexes go wrong

A

Improper atb/ag ratio
Weak, chronic atb response
Too many atb-ag complexes

46
Q

What is type 3 hypersensitivity caused by

A

chronic/persistant infection

foreign antigen inhalation

47
Q

Where do antibody-antigen complexes accumulate in

A

Blood vessels
Synovial membranes
Glomeruli
Choroid plexus (brain)

48
Q

What is systemic lupus erythematous

A 
Multiorgan disease (dogs; rarely cat & horse)
Defective T-Lymphocyte suppression results in B-Lymphocyte hyperactivity
49
Q

What are the predisposing factors for systemic lupus erythematous

A

Genetics
Viral infection
Hormones
UV light

50
Q

Describe how systemic lupus erythematous affects the body

A

Formation of autoantibodies to a variety of antigens, including nucleic acid
Organ specific antigens
Clotting factors
Cells (RBC, platelets, leukocytes)

Main damage: atb-ag complexes
Many tissue, notably skin (intensified by UV light)

51
Q

What are the skin symptoms of systemic lupus erythematous

A

Local or generalized

Erythema, depigmentation, alopecia, crusting

52
Q

What are the systemic signs of systemic lupus erythematous

A

Polyarthritis
Fever
Anemia, thrombocytopenia
Proteinuria

53
Q

What causes equine infectious anemia

A

caused by the lentivirus

54
Q

how does the lentivirus cause equine infectious anemia

A

infects monocytes and macrophages

55
Q

what does equine infectious anemia do to the body

A

Immune-mediated (atb-atg complexes deposition)

Decreased erythropoiesis

56
Q

how do you diagnose equine infectious anemia

A

coggins test for diagnostic

57
Q

describe a type 4 hypersensitivity

A

Delayed-type hypersensitivity
Cell mediated hypersensitivity

Interaction between T-lymphocytes and specific antigens
Sensitized T-lymphocytes
Response is 24-48h after exposure
Granuloma formation

Unlike type I, II & III:
NOT dependent on antibody

58
Q

describe tuberculosis

A

Caused by acid-fast bacilli of the genus Mycobacterium.
Chronic, debilitating disease
Occasional acute, rapidly progressive course.
Affects practically all species of vertebrates
Mycobacterium Tuberculosis and others
Often the body is unable to clear the infection
Chronic Granuloma formation

59
Q

Describe johne’s disease

A

Mycobacterium paratuberculosis.
Chronic, contagious granulomatous enteritis
Often in cattle
Persistent diarrhea, progressive weight loss, debilitation, and eventually death
Thickened and corrugated intestine with enlarged and edematous neighboring lymph nodes
Granulomas

60
Q

What is auto-immune thyroiditis

A

Chronic and progressive lymphocytic infiltration and subsequent destruction of the thyroid gland

61
Q

Who is predisposed to getting auto-immune thyroiditis

A

Doberman Pinschers, Beagles, Golden Retrievers, and Akitas

62
Q

What is special about auto-immune thyroiditis

A

Probably has both humoral (Type II - cytotoxic) and cell-mediated (Type IV - delayed) components
MHC probably involved

63
Q

What is bovine/canine leukocyte adhesion deficiency

A

Genetic, congenital anomaly of leukocytes
Prevents leucocytes from migrating from the blood in the tissues
Very high neutrophilia
Animals are highly susceptible to infection
Die very young

64
Q

Describe feline infectious peritonitis

A

Mutation of benign enteric coronavirus to FIP virus
Infects monocytes & macrophages and spreads through blood
Type III (immune complex)
Vasculitis
Type IV (delayed) also likely
Granulomas

65
Q

Describe keratitis sicca

A

Due to an aqueous tear deficiency
Usually results in persistent, mucopurulent conjunctivitis and corneal ulceration and scarring
Dogs, cats & horses
Dogs: often autoimmune dacryoadenitis of both the lacrimal and nictitans glands
Not well understood

Pathology (10 decks)

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