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DVM 2 - 1 > HLI 5 > Flashcards

HLI 5 Flashcards

1
Q

List 8 hallmarks signs of immunodeficiency

A

1) disease affecting particular breed
2) disease occurring in young littermate animals with onset shortly after the expected time of loss of maternally derived immunity
3) Chronic recurrent infections
4) Infection of multiple body sites
5) Failure of infection to respond to antimicrobial therapy.
6) Infection with environmental saprophytes (e.g. Aspergillus, Pneumocystis) - most healthy animals don’t get sick from these
7) Persistent lymphopenia or hypogammaglobulinaemia.
8) Failure to respond to vaccination

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2
Q

Give an example of a inherited defect in innate immunity, what seen, clinical signs and breeds

A

Pelger Huёt Anomaly

  • Quite common in the breeds
  • Reduced segmentation of granulocyte nuclei
  • NO toxic change - well mature
  • No functional disorders identified, incidental finding - healthy animals
  • Australian shepherd dogs, American foxhound, other breeds and cats
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3
Q

Give an example of a inherited defect of the acquired immune system, what animals, what lead to and why

A

Severe Combined Immunodeficiency (SCID) -
- Arabian horses and Jack Russell terriers
- Autosomal recessive
- Mutation of gene coding DNA-protein kinase
- Can’t rearrange VDJ chains to form T and B cell receptor
○ Cannot detect many antigens
- Lymphopenia & lymphoid hypoplasia
- Foals die 2- 6 months despite care
- Lack of serum IgG and IgA

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4
Q

Selective Immunoglobulin Deficiencies, when see clinical signs what are the 3 main ones, what animals found in and how to diagnose

A

Clinical signs after decrease of maternal immunity
1) IgA deficiency- Dogs ((German shepherd) - increase mucosal infections
2) IgG deficiency
3) IgM deficiency - foals
Total globulin levels won’t be abnormal so to diagnose may need to do a serum electrophoresis

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5
Q

List 5 acquired or secondary defects of the immune system

A

1) Retroviruses - FIV and FeLV, Koala retrovirus
2) Drugs
a. Chemotherapy
b. Corticosteroids
c. Immunosuppressives – cyclosporin, azathioprine
3) Malnutrition
4) Irradiation
5) Ageing

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6
Q

Feline Immunodeficiency virus (FIV) what occurs, how transmitted and the 4 stages of the infection

A
  • Progressive decline in CD4+ T lymphocytes
  • Transmitted via bite wounds (blood/saliva)
    Acute phase
  • Mild illness, lymphadenopathy
  • CD4 levels reduce
    Asymptomatic Phase
  • Healthy but CD4 levels continue to decline over months to years
    Progressive or recurrent illness
  • lymphadenopathy, weight loss, leukopenia
    Terminal phase
  • Chronic multi-systemic disease
  • Neoplasia
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7
Q

List 3 main and factors within promoting autoimmune diseases

A

1) Genetics – MHC, IgA deficiency
2) Environmental factors
○ Infections
○ Drugs – e.g. TMS
○ Vaccines
○ Diet
3) Reduced function of natural T-reg cells permits activation of auto-reactive T cells and B cells - against self-antigens

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8
Q

Give an example of an autoimmune disease what occurs and clinical signs

A

ystemic Lupus Erythematosus (SLE)
- Failure of mechanisms that maintain immunological self-tolerance
- Production of autoantibodies against nuclear and cytoplasmic components of the cell -> Autoantigen-antibody complexes deposit throughout the body→ type III hypersensitivity reaction → inflammation of joints, skin, and kidney
Clinical signs
- variable, organs affected are unpredictable
- Lethargy, anorexia, fever of unknown origin
- Haemolytic anaemia, thrombocytopenia, bone marrow necrosis
dermatitis,

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9
Q

Type II Hypersensitivity Autoimmune Disorders what are the 3 steps

A
  • Antibody against self-antigens leads to the following:
    1. Complement-mediated destruction
    2. cytotoxicity from NK cells
      phagocytosis from macrophages
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10
Q

List 3 immune-mediated haematologic disorders

A

1) Immune mediated haemolytic anaemia
2) Immune mediated neutropenia
3) Immune mediated thrombocytopenia

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11
Q

In flea allergy dermatitis what are more effective corticosteroids, anti-histamines or NSAIDS and why

A

Coricosteroids are more effective
Antihistamine
- Prevent binding of histamine to the receptor
- Not stopping the production and action of other molecules
NSAIDS
- Inhibits prostaglandins - decrease vasodilation and sensitisation of nerves for itching
Not decreasing IgE production or T cell activation

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12
Q

List the 4 ways infectious agents enter the skin and skin examples

A

1) through epidermal barrier
- UV light, infections
2) through adexal barrier - rupture of follicles
3) through vessels (haematogenous)
4) through support structures - extension from muscles

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13
Q

Hyperkeratosis what diseases are typically associated with

A

1) Congenital ichthyosis*
2) Vitamin A deficiency
3) Zinc deficiency (Zinc-responsive dermatosis)
3) Seborrhea (primary and secondary)
4) Sarcoptic mange*
5) Superficial necrolytic dermatitis

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14
Q

Possible causes of acanthosis and is it reversible

A

internal factors (e.g. metabolic), or external injury (self trauma)is reversible

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15
Q

Actinic keratosis what is it, causes and macroscopical and histological changes

A

solar induced hyperplastic lesion

  • skin which becomes erythematous with comedones and crusts, and palpably thickened
  • It may progress to squamous cell carcinoma.
  • Histologically there is hyperkeratosis and parakeratosis, epidermal hyperplasia
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16
Q

what are the typical areas where callus occurs

A

generally forms over a pressure point

- elbow, hock, sternum are most commonly affected

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17
Q

List 3 general causes of skin necrosis

A

1) Physical injury(chemical, thermal burns, radiation)*
2) Chemical injury (irritant contact dermatitis, toxic epidermal necrosis)
3) Injury as a result of vasculitis, ichemia and infarction (vasculitis, thromboembolism).

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18
Q

Consequences of thermal injuries to the skin

A

Erosion and ulceration usually follow and vesicles may develop due to dermal-epidermal separation. In full-thickness necrosis the damaged skin becomes firm and dry due to avascular necrosis and eventually sloughs. Secondary bacterial infections are common and can develop into life-threatening sepsis.

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19
Q

What are the 2 main histological features of skin burns

A

1) coagulation necrosis

2) dermal-epidermal separation

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20
Q

is spongiosis more likely to occur in acute or chronic injuries

A

acute as generally occurs with inflammation

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21
Q

What 3 diseases are characterised by cutaneous vesicles and what can result

A

1) Viral infections (poxvirus, vesicular diseases)
2) Pemphigus foliaceus or vulgaris, bullous pemphigoid
3) Thermal burns
Result of acantholysis or epidermal oedema

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22
Q

what is the difference between a vesicle and a pustule

A

Vesicle -> fluid-filled raised lesion <10mm

Pustule -> discrete, puss-filled, raised lesion

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23
Q

What is the typical mechanism for the development of acantholysis

A

initiated by damage to adhesion molecules, leading to splitting of the desmosomes
- typically occurs in immune-mediated diseases.

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24
Q

What are the gross features of photosensitisation and the pathogenic mechanism

A

Lesions on area without hair and non-pigmented
Sheep -> face, nose, eyelids lesions - dacial eczema
long wavelength UV absorbed by a complex photodynamic molecule and a biological substrate, which results in release of energy that produces reactive oxygen molecules, including free radicals -> chemical burns of the skin

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25
Q

List 4 skin changes associated with endocrine diseases such as cushings

A

1) bilaterally symmetric alopecia
2) thinning of the skin (atrophy) that tears easily
3) atrophy of hair follicles (telogen)
4) dystrophic calcification of the dermis

26
Q

List 3 common causes of folliculitis and furuncolosis

A

1) bacteria (staph)
2) dermatophytes (microsporum)
3) parasites (demodex)

27
Q

Describe the pathogensis and gross changes in flea allergy dermatitis

A

Pathogenesis
- Type 1 and IV hypersensitivity reactions
Gross - pruitis, erythema, wheals, papules

28
Q

What are hte typical lesions of feline eosinophilic granulomas and the histological changes

A

Lesions

1) Indolent ulcer (upper lip)
2) eosinophilic plaque (raied, round, oozing)
3) eosinophilic granuloma (linear raised, nodules caudal medial thighs)

29
Q

What is pemphigus foliaceus what is the pathogenesis and typical lesions

A

Is an autoimmune disease
autoantibodies target desmosomal proteins in the epidermal layer -> leads to acanthylysis and formation of vesicles
lesions -> vesicles that evolves into pustules and crusts

30
Q

List the macroscopical features of acute vs chronic skin injury

A 
Acute 
- Vascular –sun burn- erythema – Allergy
- Pustules ,papules
- Blisters
- Oedema
- Haemorrhage, vasculitis
- Necrosis
Chronic 
- Hyperkeratosis
- Acanthosis
- Metaplasia
- Dysplasia
- Fibrosis
- Atrophy
31
Q

What are the 2 main defects in skin integrity

A

1) Draining tract = opening between sub-cutis and epidermis
2) Furunculosis: sinus tracts due to rupture of hair follicles beneath skin surface
Common around the anus, very painfull

32
Q

What are the 5 grades in the severity score for pruritis

A

Grade 0: dog does not itch
Grade 1: Occasional episodes of itching (more than previously)
Grade 2: More frequent episodes, but stops when sleeping and otherwise distracted
Grade 3: Regular episodes when dog is awake, but stops when distracted
Grade 4: Prolonged episodes of itching when dog is awake, and can also occur when sleeping or distracted
Grade 5: Almost continuous itching, needs to be physically restrained to stop

33
Q

What are the 3 processes that could lead to alopecia

A
  • is hair being pulled out due to over-grooming or scratching? (pruritic disease)
  • is hair is being lost normally but not being replaced (follicular shut down such as hypothyroidism, Cushing’s disease)?
  • is hair is being forced out or damaged (folliculitis bacterial, parasitic , fungal)
34
Q

List some further diagnosis techniques for skin disease

A
  • Skin scrapes
    • Tape preps
    • Impression smears
    • Cytology from swabs - especially from the ear
    • Coat brushings
    • Fungassays
    • Culture
    • Woods lamp examination
  • Biopsies
35
Q

Allergen testing 3 ways achieved

A

1) Food elimination trials are easily done in general practice- novel protein and carbohydrate source- needs to be done for 6-8 weeks.
2) Blood testing- Elisa- if only can’t refer for intradermal allergen testing as not as reliable and many false positives
3) Intradermal skin allergen testing- normally done by a referral specialist

36
Q

What are the 3 stages in wound healing

A

1) inflammation/debridement
2) repair/proliferation
3) remodelling/maturation

37
Q

List 3 wound configurations and describe them

A

1) Abrasion -> shear force (scraping), retain dermis
2) puncture - penetrating trauma, deep wound -> tip of the iceberg
3) laceration - long linear trauma, cutting.slicing
4) degloving - large regions of skin loss - caught and ripped

38
Q

List and describe 4 stages of wound contamination

A

1) Clean
- Aseptically created surgical wound
2) Clean-contaminated
- Appears grossly clean, but likely significant bacteria
- Haven’t prepared the skin before incision
3) Dirty/Contaminated
- Foreign material present in wound
4) Infected
- Inflamation, chronic, >10^5 bacteria per gram - official amount needed before considered infected

39
Q

What are the 3 wound chronicity and golden period

A

1) acute, fresh, clean (<6 hours = goldern period)
2) recent/actue (within last few days) - inflammation but granulation may be occurring
3) chronic - likely o be infected

40
Q

What is the 3 immediate responses of tissue to injury

A

1) blood flushes the wound, release vasoactive compounds -> vasoconstriction
2) platelet degranulation - Arachidonic acid cascade -> vasodilation, inflammation
3) blood clot - platelets, cytokines etc

41
Q

Stage 1 of wound healing what occurs, clinical signs, and cells involved, what is important about this step

A

Inflammatory and debridement
Clinical features: Inflammation, exudate, leukogram, necrotic material
Cellular level: neutrophils, macrophages
Cytokines: from platelets, endothelium, epithelium
Important
1) where infection can occur
2) most painful period (inflammation) -> anti-inflammatory prolong but need pain relief

42
Q

Stage 2 of wound healing clinical features, cellular and what occurs

A

Proliferation & Repair (Day 4-12)
Clinical features: Granulation tissue, contraction, epithelialisation
Cellular level: ECM breakdown, fibroblasts -> collagen synthesis, myofibroblasts, endothelial/epithelial migration, cytokine modulation
1) granulation tissue -> fibroblasts, mechanical and biological barrier (resistant to infection)
2) contraction -> myofibroblasts form, tension limited
3) reepithelialisation -> 1mm per week, epithelial cells loosen from basement membrane
REQUIRES - viable cells, moist environment, no infection

43
Q

Stage 3 of wound healing what occurs, does it get to 100% what can lead to

A
  • Randomly oriented type III collagen replaced gradually with type I collagen, crosslinked and aligned with tension
  • Never quite reach 100% original strength (only bone does)
    Percentage strength of normal tissue (generally normally overcompensated)
    •At 1 week – 3%
    •At 3 weeks – 30%
    •At 3 months – 80%
    Healing process can lead to contracture if near a joint
    Limited the movement of the joint
44
Q

List 8 local factors that affect wound healing

A

1) wound perusion (oxygen and nutrients)
2) tissue viability
3) foreign material
4) fluid accumulation
5) infection
6) mechanical forces
7) tension
8) motion

45
Q

What are the 7 Halstead’s principle

A

1) Gentle tissue handling
2) Accurate haemostasis
3) Preservation of blood supply
4) Aseptic technique
5) Lack of wound tension
6) Tissue layer approximation
7) Elimination of dead space

46
Q

Primary closure what occurs and what is needed

A
  • suture wound edges directly
  • eliminate dead-space
    1) healthy tissues
    2) minimise tension -
47
Q

Delayed Primary Closure when occurs and when secondary closure

A

Delayed primary
• If the wound can’t be immediately closed primarily
- Wound contaminated -> Debride surgically
- Patient requires stabilisation
• Some tension-relieving techniques require staged procedures
• If awaiting lab results (e.g. was tumour resected completely?)
•Secondary closure = waiting until after granulation

48
Q

Second intention healing what is needed and what use to ensure infection free

A

Moist, good oxygen supply, protection from contaminants
Bandaging
The aim of bandaging in secondary intention healing is to provide a suitable wound microenvironment to favour rapid healing

49
Q

Film vs foam dressing and when would use

A

Film - attached to thin absorbant layer, minimally exudative wounds with frequent bandage changes
Foam - similar, more absorbant, increase cost, less frequent change

50
Q

What is the most common skin tumour in dogs and cats

A

Dogs - Mast cell tumour

Cat - squamous cell carcinoma

51
Q

Describe the gross features and biological behaviour of canine benign cutaneous histiocytoma

A

Gross features - solitary, multiple, small, firm, raised, dome or button shaped, hairless mass
Biological behaviour - most undergo spontaneous regression within 3 months of development

52
Q

Describe the biological behavior and significance of histological grading of canine mast cell tumour

A

histologically graded in 2 or 3 grades (1 to 3 or
high and low); the higher the grade the poorer the prognosis. High grade MCT
commonly metastasise to lymph nodes

53
Q

What are the gross and histological features of canine epitheliotropic lymphoma

A

Grossly it presents with erythematous patches, exfoliative dermatitis and plaques; in
later stages it appears more nodular ( nodular and tumour stage).
Histo: neoplastic lymphocytes tend to accumulate in the epidermis and may obscure the dermo-epidermal junction

54
Q

Describe the features of benign and malignant forms of melanocytic tumours in dogs and horses

A

Dogs
Benign - solitary, circumscribed, brown to black, head and distal limbs
Malignant - heavily pigmented or no melanin, infiltrative growth may metastasise
Horse
Benign - horses born grey to black and lose pigment with age
Malignant - 80% of grey horses

55
Q

Transmissible Venereal Tumour gross features, typical location, histological, prognosis and cell of origin

A

Gross - appear as single or multiple nodular or multilobulated, califlower like
location - reproductive
histo - high amount of round cells
prognosis - spontaneous regression after 6 months generally
cell of origin - unknown believed to be histiocytic

56
Q

Soft tissue sarcomas what is their histological features and their behavior

A

Histo - composed of spindle cell in bundles, fascicles, abundant stroma, varies of cell of origin
behaviour - graded in to 3 groups (1 to 3) according
to malignancy (mitotic index, presence of necrosis and degree of pleomorphism).
These tumours can be highly infiltrative, frequently recur after excision but
metastasize infrequently.

57
Q

Describe the pathogenesis of vaccine-associated fibrosarcoma

A
  • usually of low-grade malignancy but in cats, a more aggressive type has been identified in association with vaccination
  • firms masses at vaccination site
  • very locally aggressive and high rate of metastasis (70%)
58
Q

What are the gross, histological features and biological behaviour of equine sarcoid

A

Grossly - 1) verrucous -> wart-like - horny, dry, cauliflower mass 2) fibroblastic -> proud flesh-like - fleshy, fibrous, variably sized nodules, often ulcerated
Histo - thickened epidermis overlying proliferating fibroblasts
Biological behaviour - vary greatly, locally aggressive, non-metastatic fibroblastic generally but unpredictable

59
Q

What is the main skin tumour involved with UV light exposure and features and where location in cats

A
  • extremely aggressive locally but slow to metastasise
  • grossly plaque-like firm, poor circumscribed masses, crust and ulceration
    Cat - eyelids, pinnae (ear), nasal planum
60
Q

Describe the cause, gross, histological and biological behaviour of papillomas

A

Cause - host specific papillomaviruses
Gross - 0.5-3cm, warty and may be inverted
histo - thickened epidermis with filiforme projections and covered by excess keratin
Bio - are benign, rarely undergo malignant transformation and do not metastasise

61
Q

What are the most common tumours of perianal glands and their expected behaviour

A

Adenomas or carcinomas

Behaviour - generally benign course, ulcerate and bleed, do not metastasise and rarely undergo malignant transformation

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