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Pathology > Inflammation 2 (Exudate, Diagnosis) > Flashcards

Inflammation 2 (Exudate, Diagnosis) Flashcards

1
Q

Which exudate is formed from blood plasma

A

Serous

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2
Q

What do serous exudates indicate

A

Mild injury Or- serious exudate on the way!

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3
Q

Where are serous exudates normally found

A

Cavities lined by mesothelium (joints, pericardial, peritoneal) Skin, lungs, mucosa

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4
Q

The exudate you have is translucent, which the slightest red tinge

A

Serous

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5
Q

How can you differentiate serous exudate from edema

A

Serous has higher protein content, maybe some neutrophils and maybe some red tinge

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6
Q

Fate of serous exudate

A

Usually just reabsorbed

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7
Q

Microscopic appearance serous exudate

A

Homogenous, pink stained, few erythrocytes

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8
Q

Your patients exudate is on a tissue and looks granular and whitish-yellow. What is it

A

Fibrinous exudate

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9
Q

Whats a pseudomembrane

A

A layer of fibrinous exudate that can be pulled off Often on intestinal mucosa

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10
Q

Microscopic appearnace of fibrinous exudate

A

Strands of non-homogenous pink material Usually on membrane, filling cavities

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11
Q

Fate of fibrinous exudate

A

Mild: reabsorbed

Chronic: turned into fibrous adhesions, which can adhered viscera together and constrict visceral movement

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12
Q

Is fibrinous the same as fibrous

A

NO - fibrin is result of inflammation

Fibrous is result of chronc change

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13
Q

You have a mucous-y exudate. WHat is it

A

Catarrhal exudate

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14
Q

Gross appearance catarrhal exudate

A

Thick, snot-like

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15
Q

Microscopic appearance catarrhal exuate

A

Pale blue, attached to mucosal membrane surface (which is congested) Hyperplastic goblet cells

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16
Q

Fate of catarrhal exudate

A

Either flushed out or persists and becomes purulent

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17
Q

You have pus-like materieal oozing out. What is it

A

Purulent exudant

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18
Q

What is purulent exudate

A

Accumulation of dead neutrophils + liquefied tissue

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19
Q

Gross appearance purulent exudate

A

Liquefied, creamy Yellow to green to black

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20
Q

Microscopic appearance purulent exudate

A

Many neutrophils - intact and degenerative

Pyknosis, karyorrhexis (signs of liquefactive necrosis)

Cellular debris

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21
Q

Fate of purulent exudate

A

If inciting cause is killed: slowly cleaned up by macrophages and neutrophils

If it breaks lose and into body: septicemia!

Absorption of toxins in it can also cause toxemia and death

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22
Q

Cells in acute inflammation

A

Neutrophils

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23
Q

Cells in chronic inflammation

A

Lymphocytes, plasma cells, macrophages

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24
Q

Edema occurs in acute or chronic inflammation

A

Acute

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25
Q

Fibrosis occurs in acute or chronic inflammation

A

Chronic

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26
Q

Granulation tissue occurs in acute or chronic inflammation

A

Chronic

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27
Q

What is granulomatous exudate compose of

A

Mononuclear cells (macrophages, lymphocytes, plasma cells)

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28
Q

What type of macrophages become abundant in granulomatous exudate

A

Epithelioid macrophages (large cytoplasm, resemble epithelial cells)

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29
Q

Whats a granuloma

A

Focal discreet reaction of closely packed epitheliod macrophages

Can be encapsulated with central core of caseous necrosis

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30
Q

Gross appearance granulomatous exudate

A

Diffuse or as granulomas

Sheet of macrophages

Cut surface white, granuloma may have pus center with necrotic core

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31
Q

Microscopic appearance of granulomatous exudate

A

Sheets of macrophages

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32
Q

Which disease is poster child for granulomatous exudate

A

Johne’s disease Inflammatory bowel disease

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33
Q

Prognosis for granulomatous infection

A

Not very good :(

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34
Q

Whats an indication of chronic antigen stimulation

A

Presence of lymphocytes and plasma cells, but no macrophages (Lymphoplasmacytic infiltration)

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35
Q

When will you likely see chronic lymphoplasmacytic infiltration

A

Chronic bacterial and viral infections

Autoimmune disease

Drug reactions

Hypersensitivities

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36
Q

Gross appearance of lymphoplasmacytic infiltration

A

Difficult to see grossly!

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37
Q

Microscopic appearance of lymphoplasmacytic infiltration

A

Lymphocytes in lamina propria of intestine, portal triad of liver, interstitium of kidney and brochioles

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38
Q

What is perivascular cuffing

A

When lymphocytes surround blood vessels in tissues Chronic inflammation

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39
Q

What is peribronchial cuffing

A

When lymphocytes surround bronchi Chronic inflammation

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40
Q

Significance of lymphoplasmacytic infiltration

A

Not clear! If its severe, can limit function of organ (ie lots of lymphocytes in lamina propria of bowel inhibt absorption —> inflammatory bowel disease)

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41
Q

5 important categories when describing inflammation

A

Severity

Timeframe

Distribution

Exudate

Tissue

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42
Q

What is used to described severity

A

Mild Moderate Marked

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43
Q

What is used to describe timeframe of inflammation

A

Peracute - instantaneous with death (alive —> dead) Acute - hours to days Subacute: around 10 days Chronic: >10 days

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44
Q

Type of exudates you see in acute inflammaton

A

Serous Hemorrhagic Fibrinous Catarrhal Purulent

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45
Q

Type of exudates you see with chronic inflammation

A

Granulation

Much less pus, redness, heat

46
Q

Words to describe distribution of inflammation

A

Focal: one part of organ

Multifocal: several small parts of organ

Locally extensive: large part of organ

Diffuse: whole organ

47
Q

Type of hypersensitivities

A

Type 1 (IgE) –> Anaphylaxis, Atopy

Type 2 (cytotoxic antibodies) –> IMHA, Pemphigus foliaceus

Type 3 (immune complex) –> Glomerulonephritis, vasculitis

Type 4 (cell mediated) -> IBD, Rheumatoid arthritis

48
Q

Which pathway and chemical incites fever

A

Arachidonic Acid Pathway –> prostaglandin E2, acts on hypothalamus

49
Q

Which cytokines incite fever

A

PG-E2

IL-1

50
Q

2 ways body heals

A

Regeneration

Repair

51
Q

Which type of cells multiply throughout life

A

Labile cells

52
Q

Examples of labile cells

A

Epithelial cells

Lympho-hematopoietic cells of lymphoid organs and bones

53
Q

Which cells can multiply but need stimulation first

A

Stable cells

54
Q

Examples of stable cells

A

Liver

Kidney

Pancreas

Adrenal

Bone

Tendon

Peripheral nerves

Smooth muscle cells

55
Q

Which cells cant regenerate

A

Permanent cells

56
Q

Examples of permanent cells

A

Cardiac and skeletal muscle

CNS

Ocular tissues (except corneal epithelium)

57
Q

Healing by repair is mainly done by what? Why is this not idea;

A

Large scale deposition of fibrous CT

Can restrict movement of vital organs (ie myocardial contractility)

58
Q

Which factor is important for regeneration

A

TGF-beta

Stimulates fibroblasts to synthesize procallagen

59
Q

Mechanisms occuring in tissue repair

A

Deposition of fibrous CT

Granulation

Fibroblasts (TGF-beta)

Anigiogenesis

60
Q

What triggers angiogenesis

A

HIF-alpha

EGF

VEGV

61
Q

What are primary and secondary union

A

Occurs in healing by repair

Primary union: edges are apposing, minimal tissue loss (surgical wound)

Secondary union: edges arent opposing so a gap needs to be filled to close wound

62
Q

Steps of Primary union

A

(overlapping sequence)

1) Clot formation between apposing sides
2) Inflammatory response - to remove dead tissue
3) Fibroblast and endothelial response: at edge of lesion, divide and migrate up towards dermis (granulation tissue)
4) Continuity of blood flow: between two apposing margins
5) Epithelial regeneration: surface grows over newly formed granulation tissue
6) Collagen formation: proliferation of fibroblasts, deposition of collagen fibers to strengthen wound

63
Q

How long does primary union take in skin? Surgical wounds?

A

Skin: 3-5 days

Sutures are removed 10-14 days to ensure its complete

64
Q

Burns, infarction and abscesses will likely have what kind of healing union

A

Secondary — edges cant be directly apposed

65
Q
A
66
Q

Which exudate do you expect to see with mild damage to epithelium? How is it formed

A

Serous exudate

Formed by diapedesis through cells - which makes it different from hemorrhage

67
Q

Which exudate is formed with marked vascular damage, and consists of proteins that can impair organ function/stick organs together?

A

Fibrinous exudate

68
Q

Whats the term for an exudate that is tightly adhered to an area of necrosis? Removing this exudate will damage underlying tissue

A

Diptheric membrane (fibrinous exudate)

69
Q

An exudate is discharge in the shape of a tubular organ. What type of exudate?

A

Fibrin cast (fibrinous exudate)

70
Q

Purulent exudate in body cavities is called

A

Empyema

71
Q

What happens if purulent exudate gets loose in the body?

A

Can introduce bacteria to bloodstream - septicemia

Can absorb toxic elements - toxemia, death

72
Q

Two clear indications a lesion is chronic

A

Fibroplasia (proliferation of new collagen)

Vascularization

73
Q

Fibroplasia + Vascularization cause

A

Granulation tissue

74
Q

You’re sent a histological sample of an exudate. You see many lymphocytes, macrophages and plasma cells. You also see a multinucleate giant cell. What type of exudate?

A

Granulomatous

75
Q

Which nutrients are beneficial to wound repair

A

Vitamin C

Protein

76
Q

Which chemical factors play an important role in wound healing

A

Tissue growth factors (csf, egf etc)

Myeloid colony stimulating factor

Cytokines (interleukins, TNF, interferons)

77
Q

T/F body healing occurs faster in heat

A

True - colder bodies slow inflammation and healing

Important for reptile medicine

78
Q

A bearded dragon is brough in with a laceration to his hindleg. You clean the wound, but what is an important factor you are going to consider in wound management?

A

Wounds heal best in warmer temperatures. As reptiles are poikilothermic, its important to keep them warm to promote healing.

79
Q

What type of immune deficiency results from an inherited defect and may be associated with particular breeds?

A

Primary immunodeficiencies

80
Q

What type of immune deficiency is acquired (immunosuppressive toxin, virus)

A

Secondary immunodeficinecy

81
Q

What’s a primary immunodeficiency affecting Holstein calves

A

Bovine leukocyte adhesion deficiency (BLAD)

Autosomal recessive

82
Q

Genes for which protein are mutated in calves with BLAD

A

Integrin (CD18)

83
Q

Pathogenesis of BLAD

A
  • Lack of integrin
  • Neutrophils cant attach to vascular endothelium/emigrate from blood vessels
  • T-cells cant migrate to injury site –> delayed type 4 immune response
84
Q

C/S calves with BLAD

A
  • Oral ulcers
  • Servere peridontitis
  • Teeth loss
  • Chronic pneumonia
  • Recurrent/chronic diarrhea
85
Q

What do grey collies suffer from>

A

Canine cyclical neutropenia (Grey Collie Syndrome)

86
Q

Pathogenesis of Grey Collie Syndrome

A
  • Autosomal recessive immunodeficiency
  • Profound neutropenia
  • Cyclic lack of response of bone marrow to growth factors –> maturation defect in hematopoietic stem cells
    • Neutrophil maturation arrests at 11 and 14 days
    • Netruopenia for 3-4 days
    • Rebound neutrophilia
  • Usually fatal due to infection during neutropenic cycle
87
Q

Diagnosis of grey collie syndrome

A
  • Clinical signs
  • CBCs over 2 week period
  • DNA test for autosomal recessive gene
88
Q

T/F grey collie syndrome cant be treated

A

False. It can, with bone marrow transfer, but this is uncommon

89
Q

SCID foals are deficient in which leukocytes

A

B and T cells

90
Q

What’s pathagnomic for grey collie syndrom

A

Grey noses! (all collies have black noses except those with grey collie syndrome)

91
Q

SCID is caused by what type of mutation

A

5-base pair deletion –> frame shift (dysfunction protein)

92
Q

Clinical and CBC signs of SCID

A
  • Very low lymphocyte levels (<1,000 cells/ul (normal: 1,500-6,000)
  • Agammaglobinemia after maternal antibody catabolized
  • Thymic and splenic hypoplasia
  • Hypoplastic LNs –> lack lymphoid follicles and germinal centers
93
Q

Which animals are at risk of SCID

A
  • Arabian foals
  • Jack Russel Terriers
  • Basset Hounds
  • Welsh corgis
  • Mice
94
Q

SCID in bassett hounds and corgis affect which sex?

A

Males (females are carriers)

95
Q

Which cytokine is mutated in X-linked SCID (bassets, corgis)

A

IL-2 (stimulates T-cell development)

96
Q

T/F B-cells are present in X-linked SCID

A

Present, but not functional (due to lack of T-cell stimulation)

97
Q

Describe antibody levels in dogs with X-linked SCID

A
  • Low IgG
  • No IgA
  • Normal IgM
98
Q

T/F - live attenuated Distemper vaccines are preferred for dogs with X-linked SCID

A

FALSE!

Dogs can die after modified live vaccines (causes distemper)

99
Q

Which gene is deficient in hypotrichiosis cats and mice

A

FOXN1 gene –> premature stop codon

100
Q

What are effects of hypotrichiosis in cats and mice

A
  • Lack of hair growth
  • Lack of thymus growth —> NO T-cells!
101
Q

Which cat breeds are affected by hypotrichosis

A

Birmans

102
Q

Secondary immunodeficiencies are caused by which virus family? What do they target

A

Retroviruses

Targets: CD4+ T helper cells, follicular dendritic cells

103
Q

What does canine distemper virus target

A

Lymphocytes! (and epithelial and nervous tissue)

104
Q

One of the earliest clinical signs of canine distemper

A

Lymphopenia

105
Q

Which chemo drug inhibits DNA and RNA synthesis, causing severe bone marrow suppression

A

Lomustine

106
Q

Which chemo drug causes cross-linking and miscoding of DNA, leading to immunodepression

A

Cyclophosphamide

107
Q

Which chemo drug is a slow acting alkylating agent causing mild to moderate immunodepression

A

Chlorambucil

108
Q

Which fungal toxin causes bone marrow hipoplasia, decreased lympcyte and macrophage function

A

Trichothecene mycotoxins

109
Q

T/F heavy metals suppress synthesis and expression of inflammatory cytokines

A

True

110
Q

T/F - heavy metals have causd immune mediated disease

A

True

111
Q

Which cells are believed to decline with age

A

Mononuclear cells (lymphocytes, macrophages)

112
Q

Whats the most important immunodeficiency in foals

A

Failure of passive transfer (IgG)

Pathology (8 decks)

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