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ACVD Board Exams > Dermatopathology 7% > Flashcards

Dermatopathology 7% Flashcards

1
Q

What is the difference between apoptosis and necrosis?

A
  • Apoptotic keratinocytes are shrunken, brightly eosinophilic, angular to rounded contour and do not rupture; induced by viral, drug-induced or autoimmune
  • Necrosis is associated with cellular swelling and rupture; external stimuli including trauma or infection will induce this necrosis
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2
Q

Define Necrolysis

A

disintegration, separation or exfoliation occurring secondary to cell death

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3
Q

What is a grenz zone?

A

Marginal zone of collagen that separates the epidermis from an underlying dermal abnormality; characteristic of some tumors and granulomas

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4
Q

What is a flame follicle?

A

A hair follicle with large amounts of trichilemmal keratinization involving the outer root sheat; these hairs are in catagen or early telogen stage of hair cycle.

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5
Q

What is the dunstan blue line?

A

An area where the stratum corneum is lifted at the point of its attachment to the epidermis by degenerate nuclear debris and cocci; a feature of some epidermal collarettes caused by superficial staphylococcal infections.

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6
Q

What is desmoplasia?

A

What is desmoplasia?

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7
Q

What are civatte bodies (also referred to as Colloid bodies)?

A

Apoptotic keratinocytes in the stratum basale of the epidermis

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8
Q

How deep does formalin typically rapidly infiltrate when fixing specimens?

A

1 cm

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9
Q

What is the desired ratio of formalin to tissue when submitting biopsies?

A

10 parts formalin, 1 part tissue is necessary for rapid fixation.

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10
Q

What is the max dose of lidocaine to use in dog/cat for local anaesthesia?

A

5 mg/kg for dogs; 2.5 mg/kg for cats

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11
Q

What are clinical signs of lidocaine toxicity?

A

Myocardial depression, muscle twitching, neurotoxicity, seizures, death.

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12
Q

Does lidocaine have antimicrobial properties?

A

Lidocaine inhibits various gram-positive (including coagulase-positive Staphylococcus) and gram-negative (including Pseudomonas) bacteria, mycobacteria, and fungi; bicarbonate and epinephrine do the same. There are implications with performing tissue cultures using these injectables for local anaesthesia; preferrerable to use a ring block or regional/general anaesthesia to perform tissue cultures.

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13
Q

What stain is used to visuailize dermatophytic macroconidia obtained from a dermatophyte culture?

A

Lactophenol cotton blue

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14
Q

How long does a dermatophyte need to grow on dermatophyte test medium before it produces macroconidia?

A

7-10 days

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15
Q

What kind of an environment should DTM cultures be placed ?

A

Place in the dark at 30 degrees C with at least 30% humidity; desiccation and exposure to UV light hinder growth; a pan of water in the incubator usually provides enough humidity.

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16
Q

What pH indicator is in “enhanced sporulation agar” aka “rapid sporulating medium” and what color does it change at alkaline pH

A

Bromothymol; blue-green

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17
Q

What is enhanced sporulation agar (ESA) or rapid sproulating meida?

A

Contains dextrose agar, peptones, chloramphenicol, gentamicin and cycloheximide to inhibit the growth of contaminants and bromothymol as a pH indicator that turns the medium blue-green at an alkaline pH.

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18
Q

Which fungi are sensitivie to cycloheximide and, thus, cannot be isolated from DTM culture?

A

Cryptococcus neoformans, members of the Zygomycota phylym, some Candida, Aspergillus spp. Pseudallescheria boydii and many agents of the phaeohyphomycosis

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19
Q

Which fungi can cause a red color change in DTM?

A

Blastomyces dermatitidis, Sporothrix schenkii, Histoplasma capsulatum, Coccidioides immitis, Pseudallescheria boydii, and some Aspergillus spp.

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20
Q

Why is phenol red added to dermatophyte test medium?

A

Phenol red is a pH indicator; Dermatophytes first use protein in the medium and produce alkaline metabolites which turns the medium from yellow to red. When the protein is exhausted, dermatophytes then use carbohydrates giving off acid metabolites. This results in the medium changing from red back to yellow. Most other fungi use carbohydrates first and proteins only later on. They may also produce a change to red in DTM but only after a prolonged incubation (10-14 days or longer). DTM cultures should be examined daily for the first 10 days.

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21
Q

What is contained in dermatophyte test medium?

A

Sabouraud dextrose agar that contains: Gentamicin, cycloheximide, chlortetracycline. PHENOL RED: pH indicator

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22
Q

Do dermatophytes form macroconidia in tissue?

A

No; any macroconidia collected from the hair coat represents saprophytes or environmental contamination and have no known clinical significance.

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23
Q

In lieu of 10-20% Potassium hydroxide, “chlorphenolac” can be used to digest and clear keratin. What does chlorphenolac contain?

A

50 g chloral hydrate is added to 25 ml of liquid phenol and 25 ml of liquid lactic acid

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24
Q

What is the “Mackenzie” Method?

A

Obtaining a fungal culture using a sterile toothbrush

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25
Q

Aside from Microsporum canis, what other dermatophytes may fluoresce under wood’s lamp?

A

Microsporum distortum, Microsporum audouinii, Trichophyton schoenleinii; apple-green coloured hair shifts occur secondary to a tryptophan metabolite.

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26
Q

What is a Wood’s lamp? What spectrum of light does it emit and what is it filtered through?

A

A UV light with a wavelength of 353.7 nm that is filtered through a cobalt or nickel filter.

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27
Q

Cytologicaly, what is suggestive of a deep pyoderma?

A

Fewer bacteria present with the vast majority intracellular; deep infections have mixed cellular infiltrate with large numbers of histiocytes, macrophages, lymphocytes and plasma cells.

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28
Q

What are other names for the Diff Quik stain?

A

Modified Wright stain , a Romanovsky-type stain

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29
Q

What are other names for the Diff Quik stain?

A

Modified Wright stain , a Romanovsky-type stain

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30
Q

How can you differentian a louse knit from a cheyeletiella knit?

A

Louse knits are operculated and the majority are firmly adhered to the hair shaft; Cheyletiella knits are non-operculated and only attached to the hair at one end.

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31
Q

What is the most useful positioning for radiographic visualization of the bulla?

A

The rostroventral-caudodorsal open-mouth view; also the most challenging to perform.

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32
Q

What are clinical signs consistent with otitis interna?

A

Associated with damage to the vestibular and cochlear branches of cranial nerve 8; clinical signs include horizontal nystagmus, asymmetrical ataxia, head tilt, circling, falling or rolling toward the affected side.

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33
Q

What are clinical signs consistent with otitis media

A

Facial nerve paralysis: injury to the facial nerve as it courses near the middle. drooping of or inability to move the ear or lip, drooling of saliva, or decreased/absent palpebral reflex. Horner’s syndrome - due to injury of the sympathetic nerve fibers which course near the middle ear and characterized by ptosis, miosis, enophthalmos and protrusion of the nicitating membrane; KCS can occur if the parasympathetic nerve that course with the facial nerve are affected.

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34
Q

What is mammomonogamus auris?

A

A strongylid nematode identified as a cause of head shaking in domestic cats; nematode noted to reside in the middle ear.

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35
Q

What is in contained in the dorsolateral compartment of the feline dorsolateral tympanic compartment?

A

The auditory occsicles, the osteum of the auditory tube and the tympanic membrane

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36
Q

What is the stapes attached to?

A

The incus; the foot plate of the stapes is attached to the vestibular (oval) window which is in direct contact with the perilymph

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37
Q

What is the incus attached to?

A

The malleus and the stapes

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38
Q

What is malleus attached to?

A

The pars tensa, petrous temporal bone and the incus

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39
Q

What are the names of the three auditory ossicles?

A

Malleus, incus, stapes

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40
Q

How long do experimentally ruptured tympanic membranes take to a) regenerate and b) heal completely

A

a) 14 days b) 21-35 days

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41
Q

Where does the manubrium attach to the eardrum?

A

The medial aspect of the pars tensa

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42
Q

Using indirect immunofluorescence and salt-split skin, where does circulating IgA and IgG autoantibodies deposit in cases of LAD?

A

epidermal side

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43
Q

Where does a collagen IV-specific monoclonal antibody deposit in the bullae/vesicle/cleft seen in LAD?

A

Dermal side

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44
Q

What are clinical differential diagnoses for linear IgA disease?

A

mucous membrane pemphigoid, bullous pemphigoid, epidermolysis bullosa acquisita, vesicular cutaneous lupus erythematosus, severe erythema multiforme, toxic epidermal necrolysis, bullous drug eruptions, type I bullous systemic lupus erythematosus.

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45
Q

What are the clinical features of Linea IgA disease?

A

ulcers in the oral cavity, face, extremities, pawpads and the intertriginous regions of the axillae and groin, intact vesicles were not seen.

46
Q

What is linear IgA disease and what is the pathogenesis?

A

very rare vesiculobullous subepithelial blistering autoimmune disease; skin-fixed and circulating IgA autoantibodies target LAD-1, the processed extracellular segment of type XVII collagen. Intact lesions are usually minimally inflamed histologically.

47
Q

How is Canine Darier’s disease histologically different from pemphigus vulgaris?

A

In contrast to pemphigus vulgaris, canine Darier’s disease features cornification of dissociated keratinocytes as well as severe epidermal and follicular infundibular hyperplasia; immunofluorescence studies reveal antikeratinocyte autoantibodies in PV but not in canine Darier’s disease.

48
Q

What are key features of Canine Darier’s disease?

A

Loss of keratinocyte cohesion, or acantholysis, occurring throughout the epidermis and follicular infundibula gives a “crumbling brick wall” appearance; dermal inflammation is mild except in areas with secondary superficial pustulation.

49
Q

What is the specific pathomechanism behind Darier’s and Hailey Hailey disease?

A

Result from different, but similar, genetic mechanisms in Ca 2+ pumps. In Darier’s disease, the SERCA2 (ATP2A2) gene which codes for the SERCA2 pump located on the ER is mutated. In hailey hailey disease, the mutation affects the SPCA1 (ATP2C1) gene for the pump located in the golgi apparatus. Both pumps restore calcium stores within the ER and golgi apparatus after a transient increase in intracellular calcium.

50
Q

What is canine Darier’s disease?

A

A rare genodermatosis characterized by a defect of epithelial cohesion due to the formation of weak desmosomal connections. The defect leads to recurrent vesicles and bullae.

51
Q

Where does a collagen IV-specific monoclonal antibody deposit in the bullae/vesicle/cleft seen in EBA?

A

Epidermal side

52
Q

Where does a collagen IV-specific monoclonal antibody deposit in the bullae/vesicle/cleft seen in EBA?

A

Epidermal side

53
Q

Describe the histopathologic features of epidermolysis bullosa acquisita

A

Large, flat subepidermal bullae may be filled with blood; neutrophils accumulate along the base or within the cleft sometimes intensly; neutrophils often line up beneath the basement membrane and degenerate resulting in leukocytoclasia. Mild to moderate inflammation and dermal edema; ulceration is common.

54
Q

What other disease can be histologically and immunologically identical to epidermolysis bullosa acquisita?

A

Type I bullous systemic lupus erythematosus

55
Q

Using salt split skin, where are the autoantibodies of EBA deposited?

A

The dermal side

56
Q

How is EBA clinically different from BP and MMP?

A

EBA is more likely to have pawpad involvemebt

57
Q

What age / breed appears to be predisposed to EBA?

A

Young adult Great Danes.

58
Q

What clinical lesions can be seen within EBA?

A

erythematous macules and urticarial plaques and patches and eventuate into transient tense vesicles that evolve rapidly into widespread well-demarcated ulcers; epidermal sloughing occurs in the oral cavity, mucocutnaeous junctions and intertriginsous or frictional regions such as the face, axillae and abdomen; halitosis, hypersalivation and anorexia can be seen; the nasal planum and pawpads may be affected; dogs may be lethargic, depressed and febrile, lymphadenopathy may be seen.

59
Q

What is the pathogensis of epidermolysis bullosa acquisita?

A

Autoantibodies are directed against the aminoterminal, noncollagenous (NC1) domain of type VII collagen, a major component of dermal anchoring fibrils that bind to the basement membrane zone found within the lamina densa. Can be thought of the acquired version of dystrophic epidermolysis bullosa.

60
Q

Describe the histopathologic features of epidermolysis bullosa

A

The epidermis is cleanly separated from the underlying dermis to form a bulla or vesicle; inflammation is not present within early bullae and dermal inflammation is sparse.

61
Q

Where is collagen IV located?

A

It is a major component of the lamina densa

62
Q

What forms of inherited epidermolysis bullosa have been documented in animals?

A

Junctional and Dystrophic

63
Q

What forms of inherited epidermolysis bullosa have been documented in animals?

A

Junctional and Dystrophic

64
Q

How are skin lesions in dystrophic epidermolysis bullosa different from junctional epidermolysis bullosa?

A

Lesions in dystrophic epidermolysis bullosa are typically more severe and widespread; skin lesions can occur on the paw pads and claws may be sloughed, defective tooth enamel and growth retardation may be seen.

65
Q

What are the distribution of skin lesions seen in junctional epidermolysis bullosa?

A

Skin overlying bony prominences of the face and legs, pawpads, pinnae, intertriginous skin and other frictional sites, oral cavity, dystrophic claws may be seen,

66
Q

What are the skin lesions seen in junctional epidermolysis bullosa?

A

Multiple oral and cutaneous vesicles and bullae lead to ulceration; lesions typically present from birth

67
Q

What is the underlying mechanism of dystrophic epidermolysis bullosa?

A

Defects in anchoring fibrils that include diminished or absent expression of type VII collagen.

68
Q

What is the underlying mechanism of disease of junctional epidermolysis bullosa?

A

In humans: defective express ion hemidesmosome/anchoring filament proteins including collagen XVII (bullous pemphigoid antigens BPAG2, BP180), integrin alpha-6 and laminin-5; In dogs (specifically German Short Haired Pointers): an absence of collagen XVII due to a mutation in the gene encoding laminin-5

69
Q

What are the three forms of hereditary epidermolysis bullosa seen in humans and where does the cleavage occur?

A

1) Epidermolysis bullosa simplex (i.e. epidermolytic epidermolysis bullosa) - through the basal cell layer2) junctional epidermolysis bullosa - through the lamina lucida 3) dystrophic epidermolysis bullosa (dermolytic epidermolysis bullosa) - through the sublamina densa

70
Q

What is epidermolysis bullosa?

A

A group of mechanobullous diseases of variable etiology, recognized in dogs, cats and humans; in the hereditary form structural defects occur in the basal cell layer or at various levels of the basement membrane zone resulting in loss of epithelial integrity, blister formation and clinical disease of varying severity.

71
Q

What are the primary skin lesions seen in paraneoplastic pemphigus?

A

Severe ulceration of the oral cavity and mucocutaneous junctions of the planum nasal, vagina, anus, ulceration of the muzzle, pinnal margins, claw beds,

72
Q

What targests have been identified in paraneoplastic pemphigus?

A

Envoplakin, periplakin, bullous pemphigoid antigen 1 (BPAG1), desmoplakin I and II, extracellular segments of human desmoglein 3 and canine desmoglein I

73
Q

What are the underlying aetiologies of paraneoplastic pemphigus?

A

Thymic lymphoma, splenic sarcoma, possibly thymoma, drug reactions, other immunologic

74
Q

The histopathology of paraneoplastic pemphigus has histologic features of what three diseases?

A

1) Pemphigus vulgaris (suprabasilar clefting) 2) erythema multiforme (apoptosis +/- lymphocytic satellitosis) and 3) pemphigus foliaceus (intraepidermal pustulation with free keratinocytes)

75
Q

What is pemphigus vegetans?

A

A variant of pemphigus vulgaris

76
Q

Describe 6 histopathologic features of pemphigus vulgaris

A

1) Suprabasilar clefts forming bullae; often roof of bulla detaches from a specimen leaving a row of plump, rounded basal cells (i.e. tombstone cells) attached the basement membrane 2) Free acantholytic cells may be seen above the cleft and free acantholytic cells may be present within the lumen 3) bubble-like vacuoles may occur in basal and suprabasilar locations and delineate the sites of future clefts 4) inflammation is absent from intact bullae; neutrophils and acantholytic cells co-mingle on the surface of deroofed bullae 5) Ulceration and fibrinosuppurative exudation are common sequelae 6) Lesions frequently extend to superficial and sometimes deep hair follicles.

77
Q

How do the clinical lesions of bullous pemphigoid and pemphigus vulgaris differ?

A

The ulcers seen in PV coalesce and expand, leading to lesions that are substantially larger than previously existent intact bullae.

78
Q

What is the distribution of lesions seen in pemphigus vulgaris?

A

Oral cavity and mucocutaneous junctions; concave pinnae and auditory orifices; nasal planum; ip margins; genitalia; anus; periocular skin; perionyxis, paronychia; coalescing ulcers on the tongue, palate and gingiva which are not contiguous with the teeth should increase suspicion for PV; corneal ulcers and esophageal involvement may be present; haired skin lesions occur in areas of high friction and trauma (axillae, groin, limps, lateral pressure points of the limbs), pawpads slough in a minority of cases

79
Q

What is a positive Nikolsky sign?

A

The artificial extension of a blister or ulcer induced by digital pressure to adjacent mucous membrane or skin

80
Q

Describe the clinical lesions seen in pemphigus vulgaris?

A

Fragile, transient vesicles and bullae rapidly progress to form ulcers; partial bilateral symmetry can be striking; fragile, irregularly shaped vesicles and bullae develop in groups; erythema may precede vesicle formation; a positive Nikolsky sign may be elicited; baterial overgrowth is common; thick, ropy, tenacious, odorous saliva is an additional feature.

81
Q

Define “epitope spreading”

A

A primary autoimmune inflammatory process exposes previously sequestered antigens, resulting in a secondary autoimmune response

82
Q

1) What is the target of pemphigus vulgaris? 2) Where is it located?

A

a) Desmoglein-3; when lesions involve haired skin, sometimes desmoglein-1 can also be attacked. b) A 130 kDa, transmembrane desmosomal cadherin of keratinocytes that is more strongly expressed in the suprabasilar keratinocytes of the oral mucosa

83
Q

Histologically, how is mucous membrane pemphigoid different from epidermolysis bullosa acquisita and bullous pemphigoid?

A

Mucous membrane pemphigoid may feature a lichenoid dermatitis.

84
Q

How does inherited epidermolysis bullosa and linear IgA dermatosis histologically differ from bullous pemphigoid, mucous membrane pemphigoid and XX.

A

Inherited epidermolysis bullosa and linear IgA dermatosis are typically less inflamed.

85
Q

Using indirect immunofluorescence and salt-split skin, where does circulating IgG antibodies deposit in cases of mucous membrane pemphigoid?

A

Epidermal side

86
Q

Describe 5 histopathologic features of mucous membrane pemphigoid

A

1) Bull develops at the dermal-epidermal junction beneath an intact epiermis 2) Bullae are typically devoid of inflammatory cells but may contain erythrocytes, neutrophils and eosinophils 3) In dogs, superficial dermis typically contains neutrophils, eosinophils and often lymphocytes and plasma cells 4) Dermal inflammation is typically lichenoid 5) Ulceration may occur, which is oftentimes accompanied by more intense neutrophilic inflammation and fibrinosuppurative exudation.

87
Q

Clinically, how does bullous pemphigoid and mucous membrane pemphigoid differ?

A

Mucous membrane pemphigoid has a marked mucocutaneous predilection

88
Q

What are the most commonly affected sites in cases of mucous membrane pemphigoid (list in descending order)?

A

Oral cavity (most commonly affecting the gums, hard palate and tongue), lips, planum nasale, perinasal skin, periorbital region, concave pinnae, genitalia and anus. Bulbar conjunctiva is affected in a small number of dogs; pawpad lesions are very uncommon; esophageal lesions have been seen in the cat.

89
Q

What are the most commonly affected sites in cases of mucous membrane pemphigoid (list in descending order)?

A

Oral cavity (most commonly affecting the gums, hard palate and tongue), lips, planum nasale, perinasal skin, periorbital region, concave pinnae, genitalia and anus. Bulbar conjunctiva is affected in a small number of dogs; pawpad lesions are very uncommon; esophageal lesions have been seen in the cat.

90
Q

What are the common clinical skin lesions of mucous membrane pemphigoid?

A

Erosive - ulcerative lesions, intact flaccid or turgid vesicles may be present in protected areas; adherent crusts (especially when lesions are located on haired skin); scarring (when present) may be atrophic; hypopigmented macules seen periorbitally in a minority of dogs.

91
Q

What is the most common autoimmune disease of the basement membrane zone in the dog and cat?

A

Mucous membrane pemphigoid

92
Q

a) What is the target of mucous membrane pemphigoid? B) Where is the target located?

A

a) Several antigenic epitopes have been described: NC16a segment of collagen XVII; the 30 kDa carboxy-terminal segment of collagen XVII; three chains of purified laminin-5; alpha-3 chain of laminin 5 ( in one cat)

93
Q

When presented with an immune-mediate subepidermal blistering disease that demonstrated intense accumulations of neutrophils at the base of the bulla, or along the basement membrane, what disease is favoured?

A

Epidermolysis bullosa acquisita

94
Q

When presented with an immune-mediate subepidermal blistering disease that demonstrated intense accumulations of eosinophils at the base of the bulla, or along the basement membrane, what disease is favoured?

A

Bullous pemphigoid

95
Q

When presented with an immune-mediate subepidermal blistering disease that demonstrated intense accumulations of eosinophils at the base of the bulla, or along the basement membrane, what disease is favoured?

A

Bullous pemphigoid

96
Q

Where does a collagen IV-specific monoclonal antibody deposit in the bullae/vesicle/cleft seen in bullous pemphigoid?

A

Along the dermal side

97
Q

Using indirect immunofluorescence and salt-split skin, where does circulating IgG antibodies deposit in cases of bullous pemphifoid?

A

The epidermal side

98
Q

Where does the artificial split occur using “salt split skin”?

A

The lamina lucida

99
Q

Where does the artificial split occur using “salt split skin”?

A

The lamina lucida

100
Q

How can you identify degranulated eosinophils?

A

Luna stain

101
Q

Describe 4 histopathologic features of bullous pemphigoid

A

1) Small to large turgid vesicle-bullae develops at the derma-epidermal junction; cleft formation may extend to follicular infundibula 2) Within the base of the bullae, eosinophilis and neutrophils are often intermingled with fibrin; may be a lack of cells in the feline disease; 3) Dermis is minimally to mildly inflamed; characteristic eosinophils line up in rows in clusters just beneath the basement membrane of intact skin and below blisters 4) Roof of bulla/vesicle may ulcerate

102
Q

What is the distribution of skin lesions seen in bullous pemphigoid?

A

head, ears or trunk, back, axillae, abdomen, mucosal or mucocutaneous junctions, anus and claw beds; in CATS: lips, pinnae, hard and soft palate; Paw pads are RARELY affected; oral lesions less common in BP then pemphigus vulgaris

103
Q

What are the primary skin lesions seen in bullous pemphigoid?

A

Erythematous macules, patches or plaques progres into multifocal tense vesicles to variably sized bullae with irregular borders; these then rupture resulting in ulcers, which can be overlain by crusts; ulcers classically do NOT coalesce and spread and tend to remain the same size as the previous bullae; scarring is common;

104
Q

a) What is the target in Bullous pemphigoid? B) where is the target located?

A

a) Autoantibodies are directed against the 180 kDa bullous pemphigoid antigen (i.e. BP180, also known as BPAG2); this is a consituitve transmembrane glycoprotein present in basal keratinocytes; IgG target epitopes located in the NC 16A ectodomain of type VXII collagen. b) The lamina lucida

105
Q

What is solar elastosis?

A

Basophilic degeneration of elastic fibers that characterize aging human skin and seen in UVL damage in animals

106
Q

What are antimicrobial peptides and what are some examples?

A

Small cationic peptides that participate in innate immunty, beta-defensins and cathelicidins; present in stratum corneum, hair follicles and sebaceous glands of healthy dogs and cats. These peptides also appear to function in regulating cell proliferation, extracellular matrix production and cellular immune responses.

107
Q

What are the cardinal signs of inflammation?

A

rubor (redness), tumor (swelling), calor (heat), dolor (pain)

108
Q

List 8 factors that lead to autoimmunity

A

1) Failure of self-tolerance mechanisms 2) Polyclonal B cell activation by certain virsues/parasites stimulate certain autoreactive cells producing antibodies to DNA, IgG, phospholipids, erythrocytes and lymphocytes 3) Failure of regulatory T-cell function 4) Activation of T-cells by superantigens 5) Expression of class II MHC on normal cells following damage, allowing recognition by helper T cells 6) Exposure of previously hidden antigens such as the CNS, testes or lens 7) Molecular mimicry 8) Viruses or lymphoid neoplasia may interfere with normal immune function, allowing development of autoreactive cells

109
Q

What is molecular mimicry?

A

Cross-reactivity between microorganisms and self-antigens

110
Q

List 6 different ways antibodies can help deal with infectious agents

A

1) They can neutralize antigens, viruses, and toxins 2) They can opsonize organisms, bind to Fc receptors on phagocytic cells and initate phagocytosis, 3) They can form immune complexes that can actitve complement, leading to phagocytosis of C3b-coated bacteria, 4) By activating complement, they can initiate inflammatory cell infiltraion and lysis of bacterial cell wals 5) antibodies on the surface of B cells can activate the cell and cause it proliferate and start producing more antibody 6) Antibodies can present antigens to T cells and stimulate a helper response.

111
Q

What is isotype or class switching?

A

The way that B cells are stimulated to switch from secreting one antibody type (i.e. IgG) to another (i.e. IgE)

112
Q

What are four different ways B cells can become activated?

A

1) Direct contact between antigens and IgM and IgD on the surface of B cells 2) B cell acting as an antigen presenting cell with T lymphocyte by presenting antigens on cell-bound antibodies (i.e. b cell receptor) to T lymphocytes via an MHC II molecule. The antigen is internalized and needs to be processed by MHC II molecules on the surface of B cells before it can be presented to the T cell receptos; t cells then secrete cytokines that subsequently activate B cells. If B cell presents to Th2 cell, Th2 cell secretes IL-4 which promoted IgE production3) Some B cells are pre-programmed to produce IgM against common bacterial polysaccharies and lipds; these can produce antibody without needing T cells 4) B cell response to microbes are greatly enhanced if the antigens are recognized in association with complement.

ACVD Board Exams (11 decks)

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