Inflammation 2 (Exudate, Diagnosis) Flashcards
Which exudate is formed from blood plasma
Serous
What do serous exudates indicate
Mild injury Or- serious exudate on the way!
Where are serous exudates normally found
Cavities lined by mesothelium (joints, pericardial, peritoneal) Skin, lungs, mucosa
The exudate you have is translucent, which the slightest red tinge
Serous
How can you differentiate serous exudate from edema
Serous has higher protein content, maybe some neutrophils and maybe some red tinge
Fate of serous exudate
Usually just reabsorbed
Microscopic appearance serous exudate
Homogenous, pink stained, few erythrocytes
Your patients exudate is on a tissue and looks granular and whitish-yellow. What is it
Fibrinous exudate
Whats a pseudomembrane
A layer of fibrinous exudate that can be pulled off Often on intestinal mucosa
Microscopic appearnace of fibrinous exudate
Strands of non-homogenous pink material Usually on membrane, filling cavities
Fate of fibrinous exudate
Mild: reabsorbed
Chronic: turned into fibrous adhesions, which can adhered viscera together and constrict visceral movement
Is fibrinous the same as fibrous
NO - fibrin is result of inflammation
Fibrous is result of chronc change
You have a mucous-y exudate. WHat is it
Catarrhal exudate
Gross appearance catarrhal exudate
Thick, snot-like
Microscopic appearance catarrhal exuate
Pale blue, attached to mucosal membrane surface (which is congested) Hyperplastic goblet cells
Fate of catarrhal exudate
Either flushed out or persists and becomes purulent
You have pus-like materieal oozing out. What is it
Purulent exudant
What is purulent exudate
Accumulation of dead neutrophils + liquefied tissue
Gross appearance purulent exudate
Liquefied, creamy Yellow to green to black
Microscopic appearance purulent exudate
Many neutrophils - intact and degenerative
Pyknosis, karyorrhexis (signs of liquefactive necrosis)
Cellular debris
Fate of purulent exudate
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
Cells in acute inflammation
Neutrophils
Cells in chronic inflammation
Lymphocytes, plasma cells, macrophages
Edema occurs in acute or chronic inflammation
Acute
Fibrosis occurs in acute or chronic inflammation
Chronic
Granulation tissue occurs in acute or chronic inflammation
Chronic
What is granulomatous exudate compose of
Mononuclear cells (macrophages, lymphocytes, plasma cells)
What type of macrophages become abundant in granulomatous exudate
Epithelioid macrophages (large cytoplasm, resemble epithelial cells)
Whats a granuloma
Focal discreet reaction of closely packed epitheliod macrophages
Can be encapsulated with central core of caseous necrosis
Gross appearance granulomatous exudate
Diffuse or as granulomas
Sheet of macrophages
Cut surface white, granuloma may have pus center with necrotic core
Microscopic appearance of granulomatous exudate
Sheets of macrophages
Which disease is poster child for granulomatous exudate
Johne’s disease Inflammatory bowel disease
Prognosis for granulomatous infection
Not very good :(
Whats an indication of chronic antigen stimulation
Presence of lymphocytes and plasma cells, but no macrophages (Lymphoplasmacytic infiltration)
When will you likely see chronic lymphoplasmacytic infiltration
Chronic bacterial and viral infections
Autoimmune disease
Drug reactions
Hypersensitivities
Gross appearance of lymphoplasmacytic infiltration
Difficult to see grossly!
Microscopic appearance of lymphoplasmacytic infiltration
Lymphocytes in lamina propria of intestine, portal triad of liver, interstitium of kidney and brochioles
What is perivascular cuffing
When lymphocytes surround blood vessels in tissues Chronic inflammation
What is peribronchial cuffing
When lymphocytes surround bronchi Chronic inflammation
Significance of lymphoplasmacytic infiltration
Not clear! If its severe, can limit function of organ (ie lots of lymphocytes in lamina propria of bowel inhibt absorption —> inflammatory bowel disease)
5 important categories when describing inflammation
Severity
Timeframe
Distribution
Exudate
Tissue
What is used to described severity
Mild Moderate Marked
What is used to describe timeframe of inflammation
Peracute - instantaneous with death (alive —> dead) Acute - hours to days Subacute: around 10 days Chronic: >10 days
Type of exudates you see in acute inflammaton
Serous Hemorrhagic Fibrinous Catarrhal Purulent
Type of exudates you see with chronic inflammation
Granulation
Much less pus, redness, heat
Words to describe distribution of inflammation
Focal: one part of organ
Multifocal: several small parts of organ
Locally extensive: large part of organ
Diffuse: whole organ
Type of hypersensitivities
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
Which pathway and chemical incites fever
Arachidonic Acid Pathway –> prostaglandin E2, acts on hypothalamus
Which cytokines incite fever
PG-E2
IL-1
2 ways body heals
Regeneration
Repair
Which type of cells multiply throughout life
Labile cells
Examples of labile cells
Epithelial cells
Lympho-hematopoietic cells of lymphoid organs and bones
Which cells can multiply but need stimulation first
Stable cells
Examples of stable cells
Liver
Kidney
Pancreas
Adrenal
Bone
Tendon
Peripheral nerves
Smooth muscle cells
Which cells cant regenerate
Permanent cells
Examples of permanent cells
Cardiac and skeletal muscle
CNS
Ocular tissues (except corneal epithelium)
Healing by repair is mainly done by what? Why is this not idea;
Large scale deposition of fibrous CT
Can restrict movement of vital organs (ie myocardial contractility)
Which factor is important for regeneration
TGF-beta
Stimulates fibroblasts to synthesize procallagen
Mechanisms occuring in tissue repair
Deposition of fibrous CT
Granulation
Fibroblasts (TGF-beta)
Anigiogenesis
What triggers angiogenesis
HIF-alpha
EGF
VEGV
What are primary and secondary union
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
Steps of Primary union
(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
How long does primary union take in skin? Surgical wounds?
Skin: 3-5 days
Sutures are removed 10-14 days to ensure its complete
Burns, infarction and abscesses will likely have what kind of healing union
Secondary — edges cant be directly apposed
Which exudate do you expect to see with mild damage to epithelium? How is it formed
Serous exudate
Formed by diapedesis through cells - which makes it different from hemorrhage
Which exudate is formed with marked vascular damage, and consists of proteins that can impair organ function/stick organs together?
Fibrinous exudate
Whats the term for an exudate that is tightly adhered to an area of necrosis? Removing this exudate will damage underlying tissue
Diptheric membrane (fibrinous exudate)
An exudate is discharge in the shape of a tubular organ. What type of exudate?
Fibrin cast (fibrinous exudate)
Purulent exudate in body cavities is called
Empyema
What happens if purulent exudate gets loose in the body?
Can introduce bacteria to bloodstream - septicemia
Can absorb toxic elements - toxemia, death
Two clear indications a lesion is chronic
Fibroplasia (proliferation of new collagen)
Vascularization
Fibroplasia + Vascularization cause
Granulation tissue
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?
Granulomatous
Which nutrients are beneficial to wound repair
Vitamin C
Protein
Which chemical factors play an important role in wound healing
Tissue growth factors (csf, egf etc)
Myeloid colony stimulating factor
Cytokines (interleukins, TNF, interferons)
T/F body healing occurs faster in heat
True - colder bodies slow inflammation and healing
Important for reptile medicine
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?
Wounds heal best in warmer temperatures. As reptiles are poikilothermic, its important to keep them warm to promote healing.
What type of immune deficiency results from an inherited defect and may be associated with particular breeds?
Primary immunodeficiencies
What type of immune deficiency is acquired (immunosuppressive toxin, virus)
Secondary immunodeficinecy
What’s a primary immunodeficiency affecting Holstein calves
Bovine leukocyte adhesion deficiency (BLAD)
Autosomal recessive
Genes for which protein are mutated in calves with BLAD
Integrin (CD18)
Pathogenesis of BLAD
- 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
C/S calves with BLAD
- Oral ulcers
- Servere peridontitis
- Teeth loss
- Chronic pneumonia
- Recurrent/chronic diarrhea
What do grey collies suffer from>
Canine cyclical neutropenia (Grey Collie Syndrome)
Pathogenesis of Grey Collie Syndrome
- 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
Diagnosis of grey collie syndrome
- Clinical signs
- CBCs over 2 week period
- DNA test for autosomal recessive gene
T/F grey collie syndrome cant be treated
False. It can, with bone marrow transfer, but this is uncommon
SCID foals are deficient in which leukocytes
B and T cells
What’s pathagnomic for grey collie syndrom
Grey noses! (all collies have black noses except those with grey collie syndrome)
SCID is caused by what type of mutation
5-base pair deletion –> frame shift (dysfunction protein)
Clinical and CBC signs of SCID
- 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
Which animals are at risk of SCID
- Arabian foals
- Jack Russel Terriers
- Basset Hounds
- Welsh corgis
- Mice
SCID in bassett hounds and corgis affect which sex?
Males (females are carriers)
Which cytokine is mutated in X-linked SCID (bassets, corgis)
IL-2 (stimulates T-cell development)
T/F B-cells are present in X-linked SCID
Present, but not functional (due to lack of T-cell stimulation)
Describe antibody levels in dogs with X-linked SCID
- Low IgG
- No IgA
- Normal IgM
T/F - live attenuated Distemper vaccines are preferred for dogs with X-linked SCID
FALSE!
Dogs can die after modified live vaccines (causes distemper)
Which gene is deficient in hypotrichiosis cats and mice
FOXN1 gene –> premature stop codon
What are effects of hypotrichiosis in cats and mice
- Lack of hair growth
- Lack of thymus growth —> NO T-cells!
Which cat breeds are affected by hypotrichosis
Birmans
Secondary immunodeficiencies are caused by which virus family? What do they target
Retroviruses
Targets: CD4+ T helper cells, follicular dendritic cells
What does canine distemper virus target
Lymphocytes! (and epithelial and nervous tissue)
One of the earliest clinical signs of canine distemper
Lymphopenia
Which chemo drug inhibits DNA and RNA synthesis, causing severe bone marrow suppression
Lomustine
Which chemo drug causes cross-linking and miscoding of DNA, leading to immunodepression
Cyclophosphamide
Which chemo drug is a slow acting alkylating agent causing mild to moderate immunodepression
Chlorambucil
Which fungal toxin causes bone marrow hipoplasia, decreased lympcyte and macrophage function
Trichothecene mycotoxins
T/F heavy metals suppress synthesis and expression of inflammatory cytokines
True
T/F - heavy metals have causd immune mediated disease
True
Which cells are believed to decline with age
Mononuclear cells (lymphocytes, macrophages)
Whats the most important immunodeficiency in foals
Failure of passive transfer (IgG)
