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HLI Flashcards

1
Q

What are some functions of the skin (9)?

A 
Physical protection
Radiation protection
Antimicrobial action 
Barrier function 
Thermoregulation
Sensory activity
Metabolic
Nutrition
Social
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2
Q

Skin appendages can be divided into two groups. What are these groups (give examples)?

A
  1. Glands (sebaceous, sweat, special)

2. Keratinised (hair, horn, hoof, claw, feather)

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3
Q

What are the layers of the epidermis from the top to the bottom?

A
  1. Stratum corneum
  2. Stratum lucidum (only present in some non-haired regions)
  3. Stratum granulosum
  4. Stratum spinosum
  5. Stratum basale
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4
Q

Where are melanocytes situated (what layer)?

They produce the pigment melanin by oxidation of tyrosine using what enzyme?

A

Stratum basale

Tyrosinase

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5
Q

What are the differences between the two distinct layers of the dermis?

A

The supfl layer (papillary) is more regular than the deeper reticular layer. It also has epidermal derivatives and conforms to the contour of the stratum basale

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6
Q

Vaccinations and microchips are injected where?

A

Hypodermis (subcutis)

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7
Q

By which mode do sebaceous glands secrete sebum? Where are they often located? In which species are they poorly developed?

A

Holocrine mode

Located next to hair follicles and empty their secretions directly into them.

Poorly developed in pigs

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8
Q

What is the difference between apocrine and merocrine sweat glands?

A

Apocrine are over most of the skin. They’re simple, tubular glands with a duct that opens into hair follicles.

Merocrine sweat glands release sweat via exocytosis and their ducts open directly onto the epidermis. Only located in special areas (dog/cat foot pads, equine frog, nasolabial plate, pig carpal glands).

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9
Q

Sudoriferous glands are least active in which domestic species?

A

Goats and cats

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10
Q

What are the four main structures of a hair follicle?

A
  1. Internal epithelial root sheath
  2. External epithelial root sheath
  3. Dermal papilla
  4. Hair matrix

(A dermal root sheath also encloses the follicle)

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11
Q

What is the arrector pili muscle?

A

Fascicle of smooth muscle cells attached to dermal sheath

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12
Q

What is different about hair produced in a secondary hair follicle?

A

It lacks a medulla

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13
Q

A compound hair follicle has several follicles grouped together. Which of the following is true?

a. Each follicle has its own glands and roots
b. Each follicle has its own root but not necessarily its own gland

A

B (own root but not necessarily own gland)

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14
Q

What is a distinguishing feature of tactile hairs?

A

They have their own blood filled sinus between the dermal root sheath layers

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15
Q

What are the three fibre types comprising the primary trio in sheep?

A 
Kemp
Heterotype hair
True wool (lacks a medulla like secondary hair follicle hairs)
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16
Q

What are the layers of the horn-producing epidermis?

A

Stratum basale
Stratum spinosum
Stratum corneum

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17
Q

Which layers are thickest in the walls of the claw plate?

A

Str. spinosum and corneum

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18
Q

What is hyperkeratosis? Distinguish between orthokeratotic and parakeratotic hyperkeratosis.

A

Increase in the thickness of the st. corneum

Orthokeratotic= anuclear
Parakeratotic= nuclear
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19
Q

Name three diseases in which you might see hyperkeratosis.

A

Sarcoptic mange
Zinc deficiency
Vitamin A deficiency
Congenital icthyosis

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20
Q

What is acanthosis? How is this different to acantholysis?

A

Increased thickness of the st. spinosum

Acantholysis is the disruption of intercellular junctions (desmosomes) between keratinocytes of the epidermis. It typically occurs in immune mediated diseases.

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21
Q

Name 2 situations in which you might see hyperplasia of the skin as a primary lesion.

A

Callus
Sarcoptic mange
Actinic keratosis

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22
Q

What is the difference between spongiosis and ballooning degeneration?

A

Spongiosis refers to intercellular oedema of the epidermis

Ballooning degen is deformation of the cells and them becoming spherical

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23
Q

What may cause epidermal spongiosis? How about ballooning degen?

A

Spongiosis: staphylococcus spp.; malassezia infection

Balloon: poxvirus, herpesvirus, trauma

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24
Q

What is hyperpigmentation?

A

Increased melanin or increased melanocytes (chronic infl diseases or endocrine dermatoses)

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25
Q

In which diseases of the skin might you see crusting/ulceration?

A

Sarcoptic mange
Dermatophilosis
Greasy pig disease
Pemphigus foliaceus

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26
Q

What is luminal folliculitis?

A

Leukocytes from the follicular wall migrate into the lumen (due to stimulus in follicular lumen such as bacteria).

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27
Q

What are some common diseases with folliculitis?

A

Demodectic mange
Dermatophytosis (ringworm)
Bacterial infections

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28
Q

What diseases may result in dermal atrophy?

A

Hyperadrenocorticism
Hypothyroidism
Congenital collagen defects

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29
Q

What is congenital icthyosis?

A

Hereditary disorder

Lamellar hyperkeratosis

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30
Q

What might you expect histologically with actinic keratosis?

A 
Hyperkeratosis
Parakeratosis
Epidermal hyperplasia
Apoptotic sunburn cells
Fibrosis of the dermis
Degen of dermal collagen
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31
Q

Describe the pathogenesis of primary and secondary photosensitization.

A

Ingestion of plant with photoreactive substances—> deposit in the skin—> sunburn

Genetic inability to metabolise heme pigments—> build up of photoreactive haematoporphyrin pigments

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32
Q

What is contagious ecthyma?

A

Localised infection of young sheep and goats caused by parapoxvirus.

Causes vesicles, pustules, crusts and scars

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33
Q

What are the two most important factors in the initiation of dermatophylosis?

A

Prolonged moisture and mechanical damage

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34
Q

What is greasy pig disease?

A

Acute fatal dermatitis caused by staphylococcus hyicus.

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35
Q

What is deep pyoderma?

A

Deep bacterial folliculitis/ furunculosis

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36
Q

Feline leprosy is a granulomatous disease caused by what agent??
Where do nodules typically occur?

A

Mycobacterium lepraemurium. Nodules typically occur on the head, neck and distal limbs.

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37
Q

What is dermatophytosis?

A

Ringworm. Fungal infection of skin hair and claws

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38
Q

What is malassezia?

A

Infection caused by lipophilic yeast (rare in cats; common in dogs)
Opportunistic secondary pathogen

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39
Q

How does hyperadrenocorticism affect the skin?

A

Bilaterally symmetric alopecia
Atrophy
Telegen
Dystrophic calcification of the dermis

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40
Q

What does eosinophilic granuloma in cats often involve?

A

Indolent ulcer (on upper lip)
Eosinophilic plaque
Eosinophilic granuloma

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41
Q

What does SLE stand for and what does it involve?

A

Systemic lupus erythematosus= multi organ disease of dogs (rarely cats and horses also)

Failure of immune system to maintain immunological self-tolerance

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42
Q

What is pemphigus foliaceus?

A

Autoimmune disease in dogs, cats, horses and goats. Results in acantholysis and vesicles

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43
Q

What wound configuration involves partial thickness damage caused by shear forces? (I.e dermis is still intact)

A

Abrasion

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44
Q

What is the difference between clean-contaminated and contaminated wounds?

A

Clean-contaminated: created acutely with no evidence of contamination and can usually be primarily sutured with a low risk of infection/breakdown. May require antibiotics.

Contaminated: foreign material, bacteria or other. Requires debridement or healing before closure

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45
Q

An infected wound has a bacterial burden over…?

A

10^5

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46
Q

How can wounds be classified?

A

According to their
▪️configuration (abrasion, puncture, laceration, degloving),
▪️contamination level ( clean, clean-contaminated, contaminated, infected)
▪️chronicity (acute, recent, chronic)

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47
Q

What are the three stages of wound healing and what are the major cell types associated with each stage?

A

(0: blood clotting)
1: inflammation/ debridement (neutrophils and macrophages and then monocytes after 48hrs)
2: proliferation and repair (fibroblasts, myofibroblasts, endothelial cells and epithelial cells)
3: remodelling/maturation (fibroblasts)

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48
Q

What are some systemic factors that might influence wound healing (6)?

What are some local factors (7)?

A 
Systemic:
Poor perfusion
Hyperadrenocorticism
Hypoproteinaemia
Diabetes mellitus
Exogenous corticosteroids 
Immunocompromise
Local:
Infection
Tension
Neoplasia
Poor vascularity
High motion/ shear stresses
Moisture level
Fluid accumulation
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49
Q

What are some tension relieving techniques that might be useful in wound management?

A 
Undermining
Mattress sutures
Subcut suture layers
Releasing incisions
Reconstruction techniques
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50
Q

What is the difference between a papule, nodule and a pustule?

A 
Papule= small solid elevation in skin less than 1cm diameter
Nodule= small solid elevation in skin greater than 1cm diameter
Pustule= small circumscribed elevation in skin filled with pus
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51
Q

What is an epidermal collarette?

How about a wheal?

A

Annular area of scale formed when a pustule ruptures

Wheal is a sharply circumscribed area of oedema

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52
Q

What is hypotrichosis?

What is leukotrichia?

A

Hair thinning

Loss of pigment in hair (leukoderma is loss of pigment from skin)

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53
Q

What is a comedone?

A

Dilated hair follicle

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54
Q

Briefly describe the severity scoring system for pruritus.

A

0: no itch
1: occasional
2: more frequent but stops when asleep or distracted
3: regular, stops when distracted
4: prolonged when awake. Occurs when sleeping/ distracted
5: almost always

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55
Q

What is the plasmalemma?

A

Cell membrane surrounding each myofibre

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56
Q

What is the most important component of the sarcolemma?

A

The basal lamina

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57
Q

Where are satellite cells located with regards to skeletal muscle? What is unique about these cells?

A

Between the basal lamina and the plasmalemma

They are the only muscle cells capable of mitotic division post-natally (each time they divide they contribute 1 myocyte nucleus to the myofibre and 1 daughter cell to the satellite cell pool)

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58
Q

What are the 4 major fibre types in mammalian skeletal muscle?

A

Type 1: slow twitch, red, oxidative
Type 2A: fast twitch, white, oxidative glycolytic
Type 2B: fast twitch, white, glycolytic
Type 2X: fast twitch, white, different myosin heavy chain

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59
Q

What are sensory muscle spindles and where are they found?

A

Lymph filled sacs with up to 20 small intrafusal fibres. They are especially numerous in muscles involved in fine precision movements and are anchored in the perimysium in association with a small sensory nerve branch

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60
Q

What are some congenital disorders of muscle? (We learnt about 8 specifically)

A 
▪️Arthrogryposis
▪️Congenital flexures
▪️Myofibrillary hypoplasia
▪️Myotonic syndromes
▪️Spastic syndromes
▪️Periodic paralysis
▪️Myasthenia gravis 
▪️Muscular dystrophy
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61
Q

What do most cases of arthrogryposis result from?

A

Defective innervation of muscles

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62
Q

What causes congenital myasthenia gravis and in which dog breeds is it typically seen?

A

Decreased density of Ach receptors in post synaptic muscle membranes.

JRT, Springer spaniels, smooth Fox terriers

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63
Q

What are some acquired muscle disorders?

A

Muscle atrophy
Muscle hypertrophy
Muscle pigmentation
Neoplasia

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64
Q

What are some causes of muscle atrophy?

A

Disuse
Denervation
Metabolic (cachexia, endocrinopathies)

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65
Q

Is denervation atrophy reversible? What muscle types does it typically involve?

A

Potentially (provided that the motor end-plate has survived, the nerve sheath has not been disrupted, and the original motor axons regenerate and contact the muscle fibres)

Type 1 and 2

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66
Q

What muscles are most severely affected in atrophy of cachexia?

A

Non-postural muscles

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67
Q

What are some causes of muscle hypertrophy?

A

Physiological (eg. Increased workload with training)
Compensatory
Congenital (double muscling)

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68
Q

If the sarcolemma tube is disrupted how does muscle repair occur?

A

Via budding or by fibrosis

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69
Q

What are some causes of muscle degeneration?

A 
Genetic
Circulatory 
Trauma
Nutritional
Exertional
Toxic
Inflammatory/ infectious
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70
Q

Duchenne type muscular dystrophy is what type of condition?

What dog breeds is it mostly seen in?

A

X-linked recessive
Golden retrievers and Irish terriers

(Affected animals may have defective or deficient dystrophin complex)

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71
Q

What is recurrent exertional rhabdomyolysis?

A

Autosomal dominant condition affecting 5-15% of TBs

Results in sudden hindlimb weakness, stiff gait, sweating, generalised muscle tremors

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72
Q

What is porcine stress syndrome?

A

Autosomal recessive condition affecting heavily muscled pigs.

Involves a defect in the ryanodine receptor gene which leads to increased calcium levels within sarcoplasmic and hypercontraction

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73
Q

What are some examples of circulatory muscle pathologies?

A

Compartment syndrome
Muscle crush syndrome (acute muscle trauma)
Downer syndrome

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74
Q

What are the sites in the body of leukopoiesis?

A

In the early embryo, the yolk sac
In the foetus, it’s the liver, spleen and bone marrow
In the neonate it’s the liver and bone marrow
In the adult it’s just the bone marrow in health (liver and spleen with disease)

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75
Q

Where does lymphopoiesis occur and how long do most lymphocytes live for?

A

It occurs in the thymus and bone marrow in the embryo and young animal. Then in secondary lymphoid tissues in the adult

Most live for about 2 weeks

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76
Q

Which leukocytes recirculate?

A

Monocytes and lymphocytes

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77
Q

What is myelopoiesis?

A

Production of granulocytes (including neutrophils, basophils and eosinophils) and monocytes

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78
Q

What regulates myelopoiesis?

A 
Stem Cell Factor (SCF)
Colony stimulating factor (CSF)
Cytokines 
▪️neutrophils: IL-6, complement C5a, TNF-alpha
▪️eosinophils: IL-5
▪️basophils: IL-3
▪️monocytes: IL-1, 3 and 6
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79
Q

In granulopoiesis, what cells make up the mitotic (proliferation) pool? What cells make up the maturation and storage pool?

A

Mitotic: myeloblasts, promyelocytes and myelocytes

Maturation and storage: metamyelocytes, bands and segmented

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80
Q

Approximately what percentage of cells comprises the mitotic pool in granulopoiesis? What is the transit time of the cells in this pool?

A

20%

2-3 days

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81
Q

What is the transit time of cells in the maturation pool of granulopoiesis?

A

2-3 days but can be less if demand is high

82
Q

When we collect blood, we collect leukocytes from what pool of cells?

A

Circulating pool

83
Q

What are some mechanisms for increased granulopoiesis?

A

▪️recruitment of more stem cells (takes 3-5 days)
▪️increased divisions in proliferation pool (takes 2-3 days)
▪️hastened maturation (toxic change)

84
Q

How long do neutrophils spend in the circulation and how long do they last in tissues?

A

10-12hrs in circ

24-48 hours in tissue

85
Q

How long do eosinophils spend in the circ. and in the tissues?

A

Circ: mins-hrs
Tissue: unknown

86
Q

How long do basophils spend in the circ and tissue?

A

Circ: 6 hrs
Tissue: 2 weeks

87
Q

How long does it take for monocytes to mature and how long do they circulate for?

A

24-36 hours maturation

Blood transit time=18-23 hrs

88
Q

What are the developmental steps of a monocyte?

A

Monoblast-> promonocyte-> monocyte (then tissue macrophages and activated macrophage)

89
Q

Platelet production is regulated by what hormone? How long do they live for?

A

Thrombopoietin

5-9 days

90
Q

What percentage of platelets are sequestered in the spleen?

91
Q

How do platelets form and how are they removed from the circulation?

A

Formation: fragmentation of megakaryocyte cytoplasm. They are anucleate (in mammals but not in birds 🦅 and reptiles 🦎)

They are removed through phagocytosis by macrophages in spleen and liver.

92
Q

What are some indications for bone marrow collection? (9)

A 
Persistent cytopenia
Persistent cytosis 
Atypical/ abnormal cells on smear
Persistent unexplained fever
Bone lytic lesions
Unexplained hyperglobinaemia
Unexplained hyperproteinaemia 
Unexplained hypercalcaemia
Infectious disease screening (leishmania)
93
Q

In what circumstances might you be hesitant to take a bone marrow biopsy?

A

When the patient has a coagulopathy or a marked thrombocytopenia

94
Q

What are common sites used for bone marrow biopsy/aspirate collection?

A

Pelvis (iliac crest)
Proximal humerus
Proximal femur (trochanteric fossa)
Sternum

95
Q

What is the difference between normocellular, hypercellular and and hypocellular bone marrow?

A 
Normocellular= haematopoeitic cells make up 25-75% marrow particles
Hypercellular=  >75% and rare fat
Hypocellular=   <25%
96
Q

What is a multiple myeloma? What are the diagnostic criteria for a multiple myeloma?

A

Plasma cell myeloma (neoplastic plasma cells)

Diagnostic criteria (2 or more of the following):
▪️neoplastic plasma cells in bone marrow
▪️monoclonal gammopathy
▪️osteolytic lesions
▪️light-chain proteinuria
97
Q

What are some causes for neutrophilia and neutropenia?

A 
Neutrophilia:
▪️Acute inflammation
▪️Chronic active inflammation
▪️Physiologic leucocytosis
▪️Stress leukogram
▪️Paraneoplastic syndrome
Neutropenia:
▪️Acute overwhelming infl (sepsis)
▪️Endotoxaemia 
▪️Bone marrow disease
▪️Immune mediated destruction
98
Q

What are some causes of lymphocytosis and lymphopenia?

A 
Lymphocytosis:
▪️Physiologic leucocytosis
▪️Lymphoproliferative disease
▪️Antigenic stimulation/ inflammation (mild)
▪️Hypoadrenocorticism (mild)

Lymphopenia:
▪️Corticosteroid/ stress response
▪️Loss of lymphatic fluid (eg intestinal lymphangiectasia)
▪️Acute inflammation?

99
Q

What are some causes of monocytosis?

A

▪️Acute or chronic infl
▪️Corticosteroid/ stress response in dogs 🐕
▪️Chronic myeloid leukaemia
▪️Paraneoplastic syndrome

100
Q

What might cause an increase in eosinophil numbers in the blood?

A 
Parasitic infections
Allergies
Paraneoplastic syndrome 
Hypereosinophilic syndrome
Eosinophilic leukaemia
101
Q

What cells types are present in the medullary cords of the lymph nodes?

A

Lymphocytes, plasma cells and macrophages

102
Q

What cell type predominates in the cortex of the thymus?

A

Lymphocytes

103
Q

Where can Hassall’s corpuscles be found?

What is their function?

A

In the medulla of the thymus
? They are degenerate epithelial cells that have formed clumps

(Reticular epithelial cells Direct differentiation of Tcells and produce thymic hormones including thymopoietin, thymosin and thymulin)

104
Q

What are the primary lymphoid organs of the body?

A

Bone marrow
Thymus
Bursa of Fabriscius
Ileal Peyer’s patches (ruminants, pigs, horses, dogs and humans)

105
Q

What are some secondary lymphoid organs?

A 
Lymph nodes 
Spleen
Tonsils
Mucosa-associated lymphoid tissues
Haemal nodes (ruminants)
Caecal tonsils
106
Q

What are some functions of the lymphatic system?

A

Capture fluid lost from the body
Control infection
Lymphocyte transport

107
Q

Describe the location of the thymus.

A

Dorsal to upper part of sternum (cranial to heart)

108
Q

Describe the circulation of blood through the spleen.

A

Enters via splenic artery ➡️ trabecular artery ➡️ central artery ➡️ pulp artery ➡️ arteriole ➡️ capillary ➡️ venous sinus and open sinus

109
Q

What are some cytological criteria for malignancy?

A 
Anisokaryosis
Anisocytosis
Macronucleoli
Atypical mitosis
Irregular nucleoli
Multinucletion
110
Q

What is the most common form of lymphoma in horses? What about dogs?

A

Multicentric in both

111
Q

Give an example of caseous (or necrotising) and suppurative lymphadenitis.

A

Caseous:
Corynebacterium pseudotuberculosis
Suppurative:
Streptococcus equi

112
Q

What are some common infectious diseases in which th lymph nodes are involved secondarily?

A
  • mycobacterium avium paratuberculosis (Johne’s)
  • mycobacterium bovine (tuberculosis) in cattle
  • FIP
113
Q

What is PARR used for?

A

PCR for antigen receptor rearrangement is used to distinguish reactive lymphoid hyperplasia from lymphoid neoplasia

114
Q

What is hypercalcaemia of malignancy? Why does it occur?

A

A paraneoplastic syndrome seen with canine and feline lymphoma.
May occur due to resorption of bone resulting from elaboration of parathyroid hormone-like peptides which increases calcium release from bone and absorption of calcium from intestine

115
Q

What is the most common haematopoietic neoplasm of dogs?

A

Lymphoma (most are multicentric)

116
Q

What are the two forms of bovine lymphoma?

A

Enzootic bovine lymphoma. Caused by bovine leukaemia virus. Often multicentric and seen in adults

Sporadic bovine lymphoma. Occurs in young cattle and has three forms.

  1. Calf form (<6mo). Multicentric. Involves BM, liver, kidneys, spleen
  2. Juvenile/ thymic form (<2yo). Mediastinal. Cranial thoracic/ lower cervical masses
  3. Cutaneous form (2-3yo). Skin. Raised skin lesions. Ulcerations.
117
Q

What are some degenerative diseases of the spleen? (5)

A
  1. Lymphoid necrosis
  2. Siderotic plaques
  3. Haemosiderosis
  4. Amyloidosis
  5. Senile atrophy
118
Q

What are some circulatory disease of the spleen? (7)

A
  1. Active acute hyperaemia
  2. Passive congestion
  3. Splenic infarcts
  4. Splenic haematomas (looks like haemangiosarcoma)
  5. Splenic rupture
  6. Splenic volvulus
  7. Splenic contraction
119
Q

What are some inflammatory diseases of the spleen? (4)

A
  1. Acute congestive splenitis (enlarged and dark red)
  2. Acute suppurative splenitis
  3. Chronic suppurative splenitis
  4. Chronic granulomatous splenitis
120
Q

What are some hyperplastic diseases of the spleen?

A
  1. Lymphoid hyperplasia (reactive)
  2. Nodular hyperplasia
  3. Extramedullary haematopoiesis
121
Q

What are some neoplastic diseases of the spleen?

A 
Haemangiosarcoma
Lymphoma
Mast cell tumour
Histiocytic neoplasia
Splenic sarcoma
Metastatic neoplasia
122
Q

What are thymomas? How do they differ to thymic lymphomas?

A

Benign proliferation of lymphocytes formed from the epithelial component of the thymus

Thymic lymphomas are a malignant proliferation of lymphocytes. Both occupy the mediastinum

123
Q

What are the 5 signs of toxic change in neutrophils? What are they indicative of?

A
  1. Basophilic cytoplasm
  2. Döhle bodies
  3. Foamy cytoplasm
  4. Toxic granulation
  5. Ring form neutrophils

Indicative of hastened maturation

124
Q

What is a Barr body?

A

Inactivated X chromosome seen as a “nuclear drumstick” (female animals)

125
Q

In what situations might we see hypersegmented neutrophils?

A

Normal in horses. Can also be seen in animals with chronic inflammation, hypercortisolaemia, myeloproliferative disease

126
Q

What is Pelger-Huët anomaly?

In what domestic species has it been found in?

A

Hereditary disorder associated with granulocyte nuclear hyposegmentation

Australian shepherds and American foxhounds

127
Q

What is unusual about neutrophils in Birman cats?

A

They have pink granulation

128
Q

What is Chediak-Higashi syndrome?

What domestic species has it been identified in?

A

Hereditary disorder in which there is fusion of granules and lysosomes-> dilute hair colour and atypical granulation of neutrophils

Brangus and wagyu cattle, blue smoke Persian cats and mink

129
Q

What are some causes of thrombocytopaenia and thrombocytosis?

A

Thrombocytopenia:

  • infl (endotoxaemia)
  • splenomegaly/ splenic masses
  • immune mediated thrombocytopaenia
  • DIC
  • artefact
  • marrow disease

Thrombocytosis:

  • inflammation
  • splenic contraction
  • Hypercortisolaemia
  • response to chronic haemorrhage
  • myeloproliferative disease
130
Q

What is important to remember in regards to the association between lipaemia and total solids?

A

Lipaemia can lead to false elevations in Hb, MCH, MCHC and refractometer protein

131
Q

An acute inflammatory leukogram is characterised by…? What about a severe acute inflammatory leukogram?

A

Acute infl: neutrophilia (+/- left shift, toxic change and monocytosis)

Severe acute: WBC >50x10^9/L (often with marked regenerative left shift)

132
Q

A physiologic leukocytosis leukogram is characterised by…?

What about a stress leukogram?

A

Lymphocytosis and neutrophilia (marginating-> circulating pool)

Stress: lymphopaenia (+/- neutrophilia, monocytosis and eosinophilia)

133
Q

How would you describe a leukogram with a persistent neutropenia with no left shift or toxic change and no identifiable focus of inflammation?
What might cause such a leukogram?

A

Granulocytic hypoplasia leukogram. May be caused by:

  • Cyclic neutropenia of grey collies
  • Immune mediated disease
  • Drug toxicity
  • Myelodysplastic syndrome
134
Q

What is the difference between alpha, beta and gamma globulins?

A

Alpha- produced by the liver and involved in transport of other molecules.
Beta- mostly produced by liver and B lymphocytes. Includes IgM and IgA and complement proteins plus clotting proteins.
Gamma- IgG. Synthesised by B lymphocytes

135
Q

What is the most common cause of hyperproteinaemia is…?

A

Dehydration!

136
Q

What are the main mechanisms that lead to hypoalbuminaemia?

A
  1. Increased albumin loss (eg. haemorrhage, protein-losing emteropathy)
  2. Decreased albumin production (liver failure, infl., malabsorption etc)
  3. Haemodilution (excessive administration of IV fluids)
  4. Sequestration (accumulation in body cavities)
137
Q

What are some causes for hypoglobulinaemia?

A
  1. Increased loss
  2. Decreased production
  3. Failure of passive transfer
  4. SCID
138
Q

What are acute phase proteins?

A

Proteins produced by the liver and involved in inflammation. Examples: C-reactive protein, serum amyloid A, haptoglobin

139
Q

How do positive and negative acute phase proteins levels change with inflammation?

A

Negative APPs DECREASE with infl., whilst positive APPs INCREASE with infl.

140
Q

What are some major and moderate APPs?

A

Major: C-reactive protein, serum amyloid A, haptoglobin
Moderate: fibrinogen (used as infl. indicator in horses and cattle)

141
Q

Briefly describe what a type II hypersensitivity reaction is.

A

Inappropriate immune response to cell-bound antigens (cytotoxic hypersensitivity). Leads to activation of complement and membrane attack complex.

Blood transfusions, penicillin reactions, neonatal isoerythrolyis

142
Q

Briefly describe what a type III hypersensitivity reaction is.

A

Inappropriate response to soluble antigens (immune complex mediated)

Involves complement activation

143
Q

Briefly describe what a type IV hypersensitivity reaction is.

How about a type V reaction?

A

=delayed type. T-cell mediated (CD8 cells through MHC pathway)

Type V is caused by agonist effects of Abs binding to endocrine receptors.

144
Q

What are type I hypersensitivity reactions?

A

Inappropriate immune responses mediated by IgE inducing mast cell activation.

145
Q

Generally speaking, where do lymphomas and leukaemia originate? How can they be distinguished cytologically?

A

Lymphomas in tissue, leukaemia in bone marrow

They can’t be distinguished from each other cytologically. The distinction is often clinical.

146
Q

How can acute lymphoid leukaemia and chronic lymphoid leukaemia be distinguished?

A

Cytology. Lymphocytes in ALL are intermediate to large and are blastic. Cytopenias are common, clinical progression is rapid and prognosis is poor. The opposite can be said for CLL

147
Q

What might we expect to see with chronic lymphoid leukaemia?

A

Firstly, it is often an incidental finding. We might see mild splenomegaly and/or lymphadenomegaly. A CBC is usually diagnostic with a marked increase in total white blood cells (majority being small mature lymphocytes)

Note: this disease likely originates in spleen rather than the bone marrow.

148
Q

Choose the correct option:

In general, large cell lymphoma is ?indolent/aggressive? and small cell lymphoma is ?indolent/aggressive?.

A

Large: aggressive 🦍
Small: indolent

149
Q

On physical examination, what finding is common in dogs with aggressive nodal lymphoma?

A

Hepatosplenomegaly

150
Q

In dogs, what are the general findings with gastrointestinal and splenic lymphoma?

A

GI: often large cell origin, aggressive, poor prognosis
Splenic: often indolent but can behave aggressively.

151
Q

What is Hodgkin’s like lymphoma in cats?

A

Lymphadenomegaly affecting the lymph nodes of the head and neck only

152
Q

What is the cell of origin for localised histiocytic sarcomas (and histiocytic sarcoma complexes)?
What about for haemophagocytic histiocytic sarcoma?
Feline progressive histiocytosis?

A

Interstitial dendritic cell
Macrophage
Dendritic cell

153
Q

What is canine cyclical haematopoesis?

A

Haematopoietic stem cells defect of collies causing trilineage cycling of blood cells (deficits more apparent in neutrophils)

154
Q

What is canine leukocyte adhesion deficiency (clad) and bovine leukocyte adhesion deficiency?

What animals is it seen in?

A

Mutation encoding for integrin CD11/ CD18 which mediates the firm adhesion of leukocytes to the vascular endothelium to allow leukocytes to exit blood vessels and enter tissue.

Irish setter dogs and Holstein fresians

155
Q

What is SCID?

A

Severe combined immunodeficiency virus. Congenital immunodeficiency in Arabian horses. Characterised by failure to produce functional T or B cells

156
Q

How is equine SCID different from canine SCID?

A

Canine SCID x-linked and is caused by a defect in T cell receptor ability to respond to interleukins (as opposed to a defect in the gene coding DNA protein kinase in horses which leads to an inability to rearrange receptors)

157
Q

What is lethal acrodermatitis?

What does it cause?

A

Autosomal recessive defect in zinc and copper metabolism, and T-cell function. Seen in bull terriers.
Stunted growth, skin/resp infections, parakeratosis, low IgA

158
Q

What is x-linked agammaglobulinaemia?

A

Rare disease of male foals characterised by a lack of B cells and low levels of Igs.

159
Q

What is one of the most common immunodeficiencies diagnosed in animals? What characterises it?

A

Common variable immunodeficiency.

Late onset, B cell lymphopenia and hypoglobulinaemia. Poor response to vaccination, recurrent fevers

160
Q

What are the most common forms of selective immunoglobulin deficiencies?

A

IgM def in foals
IgA def in GSD and shar peis
IgG def in Weimaraners and CKCS

161
Q

Explain the different phases in the pathogenesis of FIV.

A

Acute phase: mild illness, lymphadenopathy, ⬇️ CD4 T lymphs

Asymptomatic phase: healthy but CD4 cells continue to ⬇️

Progressive/ recurrent illness: stomatitis, lymphadenopathy, weight loss, leukopenia

Terminal phase: chronic multi-systemic disease

162
Q

What is autoimmunity?

A

Specific immune response to self-antigens

163
Q

What are some examples of autoimmune diseases?

A
  • Systemic lupus erythematosus
  • Discoid lupus erythematosus
  • Pemphigus foliaceus
  • Pemphigus vulgaris
  • Bullous pemphigoid
164
Q

What is systemic lupus erythematosus? What are the clinical signs?

A

Autoimmune disease characterised by the production of autoantibodies to self tissues, most notably nuclear antigens. Immune complexes are formed (type III hypersens.)

CS: polyarthritis, non erosive lesions, proteinuria (due to renal lesions)

165
Q

What are some clinical signs of DLE?

A

Lesions confined to the nasal planum, periocular skin and pinna.
Depigmentation, elopecia, erosion, ulceration, crusting and scarring

166
Q

What is bullous pemphigoid?

A

A vesiculobullous autoimmune skin and mucosal disease of horses, dogs and cats. Autoantibodies are directed against the bullous pemphigoid antigen which is a constitutive protein of basal keratinocytes

167
Q

What is Evan’s syndrome?

A

The occurrence of immune-mediated thrombocytopenia concurrently with IMHA

168
Q

What are the primary storage sites for histamine?

A

Lung, skin, stomach and basophils

169
Q

What are some biological effects of histamine?

A 
Vasodilation
Increased vascular permeability
Sensitisation of nerve endings to pain/ promotes itch
Increased HR and force of contraction
Increased gastric acid secretion
Bronchoconstriction
170
Q

What are eicosanoids?

How do they differ from other autocoids such as histamine?

A

Products of fatty acid oxygenation (mainly arachidonic acid) as a result of phospholipid membrane metabolism. They include prostaglandins, thromboxane and leukotrienes.

Unlike other autocoids, they are not found preformed in tissues or cells

171
Q

All eicosanoid receptors are what type?

A

G-protein coupled receptors

172
Q

What are prostanoids? Through what pathway are they synthesised?

A

Prostaglandins and thromboxane.

Cyclo-oxygenase pathway

173
Q

What are some clinical uses of prostanoids?

A

PGF(2alpha):
Used to decrease oestrus length and synchronise oestrus in mares and cows
Used to induce parturition in cows, mares and sows
Examples include dinoprost and cloprostenol

PGE:
Cytoprotection in gastric ulceration (misopristol)

174
Q

Which prostanoids cause vasodilation?

Which cause vasoconstriction?

A

PGI2, PGD2

Thromboxane

175
Q

What are the effects of glucocorticoids once they enter a cell and bind to a cytoplasmic receptor?

A

They either repress or induce certain genes. Repressioninvolves inhibition of transcription factors that normally switch on genes for COX-2. Induction involves formation of specific mRNAs which direct the synthesis of specific proteins involved in the inflammatory response

176
Q

What are the four major effect types of glucocorticoids?

A
  1. Metabolism, water and electrolyte balance
  2. Negative feedback effects on the anterior pituitary and hypothalamus
  3. Anti-inflammatory
  4. Immuno-suppressive effects
177
Q

How do GCs affect carbs, proteins and fats?

A

Carbs: decreased uptake and utilisation of glucose, increased gluconeogemesis
Proteins: increased catabolism
Fats: enhanced lipolysis, fat redistribution

May also cause an increased appetite

178
Q

What determines the anti-inflammatory potency and duration of action of GCs?

A

Structure of steroid base and ester it is complexed with.

179
Q

What are some side effects of glucocorticoids?

A

Some of the most common are:

  • PU/PD (inhibit ADH)
  • metabolic effects and polyphagia (stimulate appetite, lipogenesis, lipolysis
  • reduced collagen synthesis
  • increased bruising
  • alopecia
  • hepatomegaly
  • gastric ulceration
  • immonological effects
  • reproductive effects
180
Q

What are some contraindications for GC use?

A 
Immature animals
Bone healing
Post-surgery
Diabetes mellitus
Protein losing diseases
Liver disease
Pregnancy
Concurrent NSAID use
181
Q

Why should abrupt cessation of glucocorticoids therapy be avoided?

A

To reduce risk of iatrogenic hypoadrenocorticism as a result of failure of normal endogenous cortisol production secondary to ACTH suppression by administered glucocorticoids

182
Q

What are the three major effects of NSAIDs? How are these effects achieved?

A

Anti-inflammatory
Anti-pyrexic
Analgesic (decreased production of prostaglandins that sensitive nociceptors)

Inhibit COX pathway and therefore the formation of prostanoids.

183
Q

How do NSAIDs impair platelet activity?

A

Inhibit thromboxane formation

184
Q

What are disease modifying osteoarthritis drugs?

A

Polysulphated polysaccharide drugs which retard the degradation of articular cartilage and may have an effect on chondrocyte metabolism. Also stimulate hyaluronan synthesis.

185
Q

What are some examples of immunosuppressive drugs?

A

Azathioprine
Cyclosporin
Oclacitinibn(apoquel)

186
Q

What four characteristics distinguish cancer cells from normal cells?

A
  • uncontrolled proliferation
  • de-differentiation and loss of function
  • invasiveness
  • metastasis
187
Q

How does azathioprine work?

What are some side effects one might expect to see with it?

A

Azathioprine interferes with the synthesis of purine nucleotides causing inh8bitiom of DNA synthesis. It inhibits colonial proliferation during the induction phase of the immune response

Side effects: myelosuppression leading to neutropenia, thrombocytopenia, anaemia. Also GI and hepatotxicity.

188
Q

How does cyclosporin work? What is it used for?

A

Inhibits T-lymphocyte function by inhibiting cytokines production (IL-2 and IFN-gamma) so that helper T-cell activation is blocked (inhibits calcineurin).

Keratoconjunctivitis sicca (dry eye) and atopic skin disease

189
Q

How does apoquel (oclacitinib) work? What is it used for?

A

Inhibits cytokines that are dependent on Janus kinase enzyme activity.

Pruritis in allergic and atopic dermatitis in dogs

190
Q

What is p53 and why is it important?

A

p53 is a tumour suppressor gene which halts the progression of cells from G1 to S-phase. It is often non-functional in neoplastic cells

191
Q

What is the importance of the Rb gene?

A

It is another tumour suppressor gene (retinoblastoma). It controls progression of the cell from the G1 phase to the S-phase.

192
Q

Why are most chemotherapy drug doses based on body surface rather than body weight?

A

Because surface area is a measure of metabolic rate. It is also safer due to the narrow margin of safety of many chemotherapy drugs.

193
Q

What are some mechanism in which cancer cells may become resistant to anti-neoplastic drugs?

A
  1. Decrease cell permeability/ uptake of drugs
  2. Increased efflux of drugs
  3. Increased production of enzymes which degrade the drug
  4. Increased capacity to repair or bypass drug effects
  5. Decreased binding of drug to receptors or target enzymes
194
Q

What are some ways to overcome resistance to anti-neoplastic drugs?

A
  1. Use of multi-drug protocols
  2. Use drugs with different mechanisms of action
  3. Give drugs at a maximal dose if there are no or acceptable adverse effects
195
Q

What class of anti-neoplastic drug is cyclophosphamide? How does it work?

What are some side effects?

A

Alkylating agent.

Forms covalent bonds with DNA impeding replication and causing DNA damage, ultimately leading to cell death (apoptosis).

Myelosuppression, alopecia, sterile haemorrhagic cystitis.

196
Q

What class of anti-neoplastic drug is azathioprine? How does it work?

A

It’s an antimetabolite. It interferes with the synthesis of purine nucleotides and inhibits DNA synthesis.

197
Q

What class of anti-neoplastic drug is cisplatin? How does it work?

A

Produces inter- and intra- cross links in DNA by binding to guanine residues. It is used for carcinomas and sarcomas and can cause renal toxicity.

198
Q

What class of anti-neoplastic drug is vincristine? How does it work? What is it used for and what are some side effects?

A

Mitotic spindle inhibitor
Binds to tubulin in the mitotic spindle and prevents cell division (G2 phase and M phase of cell cycle).

Lymphoreticular neoplasms, carcinomas and sarcomas.

Side effects: peripheral neurotoxicity, constipation and myelosuppression

199
Q

What class of anti-neoplastic drug is doxorubicin? How does it work?

A

It’s a cytotoxic antibiotic.

Inhibits topoisomerase II which is an enzyme involved in DNA cleavage, unwinding and re-joining. It also intercalates DNA. Most active in S-phase.

Used for many neoplasms

200
Q

What class of anti-neoplastic drug do glucocorticoids belong to? How do they work? What are they used for?

A

Hormones!

Cause apoptosis of lymphocytes. Used typically for lymphoma and mast cell tumours

201
Q

What class of anti-neoplastic drug is toceranib? How does it work? What were they specifically developed for?

A

Tyrosine kinase inhibitor

Inhibits TK receptors involved in malignant transformation of cells. Developed especially for canine mast cell tumours.

DVM2 (13 decks)

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