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147 Cards in this Set
- Front
- Back
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Innate Immunity (defense mechanisms + before infection) consist of:
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1) Barriers (Physical-static and kinetic, Biological, Chemical)
2) Acute phase response 3) Humural innate immunity 4) Cellular innate immunity |
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Adaptive immunity gone awry:
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1) immunologic defiency (too little immunity)
2) Hypersensitivity and autoimmunity (Too much immunity) |
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Type of Primary Immunodefiencies
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A) Chediak-Higashi syndrome (abnormal lysosomes and pigmentation)
B) Leukocyte adhesion defiency (defect in B2 intregrin, thus NO can't bind and exit BVs) C) SCIDs (defects in both humoral and cellular immune responses; gross lesion: small or absent thymus, and lesions associated with infection). |
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Type of Secondary Immunodefiences (More Common):
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1) Animal AIDS: SIV, FIV
2) Lymphotropich viruses: BVD (epithelio- and lymphotrophic), Canine parvovirus and feline panleukopenia 3) Passive transfer failure (most common type) 4) Steriod induced immunodefiency/immunosuppresion (Chronic stress, adrenal cortical tumur or prolonged steriod therapy) 5)other causes: malnutrition, chemotherapy, radiation therapy, age |
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Too much immunity: 4 basic immune reactions
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1=immediate hypersensitivity
2=cytotoxic hypersensitivity 3=immune-complex hypersensitivity 4=delayed hypersensitivity |
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Define Hypersensitivity:
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: is an exxagerated immunological reaction to a normally harmless antigenic stimulus resulting in injury to the host (prior sensitization to the antigen is required) (type 1 and 4)
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Define Autoimmune diseases:
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: develop when antibodies or T cells are reactive against self-antigens (tend to be type 2 or 3).(More than 1 mech. can be +)
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Innate immunity
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Barriers
-Physical barriers (static and kinetic) -Biological barriers -Chemical -Acute phase response (APP, fever, hypoferremia) -Humoral innate immunity -Microbicidal components (MAC of complement, defensins, lysozyme) -Microbiostatic components (transferrin, lactoferrin) -Opsonins (MBL, C3b, CRP) -Cellular innate immunity -Phagocytes (macrophages and neutrophils) -Natural killer (NK) cells |
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Adaptive (acquired) immunity
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Adaptive immunity develops after microbe exposure to + powerful infection combat
-Cellular immunity (T-lympho) defense against intracellular microbes -Humoral immunity (B lympho and Ab) defense against extracellular microbes and their toxins |
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Primary (inherited) immunodeficiencies
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Chediak-Higashi syndrome:
-hereford cattle, Persian cats etc MOA: abnormal lysosomes =defective killing of phagocytosed microorganisms + Abnormal pigmentation (melanocytes) |
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Primary (inherited) immunodeficiencies
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=Leukocyte adhesion deficiency
-Irish setters, Holsteins, Humans =Persistent neutrophilia Defect in ß2 integrin, thus circ. NO =no bind to endothelium => no exit BVs |
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Primary (inherited) immunodeficiencies
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Bovine: BLADS
=severe gingivitis, tooth loss, oral ulcers, enteric ulcers, cutaneous ulcers, abscesses without pus +pneumonia Histo:sparse NO infiltration of neutrophils into damagaed mucosa or pulmonary alveoli, despite neutrophilia |
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Primary (inherited) immunodeficiencies
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SCID
=Arabian foals, dogs and mice =Defects in both humoral and cell-mediated immune responses. -foals normal to 1-3 months(passive immunity)then=> fatal infections |
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Secondary (acquired) immunodeficiencies
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Animal AIDS
-Simian immunodeficiency virus (SIV);Feline immunodeficiency virus (FIV) -Progressive T-lympho loss Immunodeficiency => infections => death Bite = Main FIV transmission |
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Secondary (acquired) immunodeficiencies
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Lymphotropic viruses
-Bovine viral diarrhea =Epitheliotropic + Lymphotropic =oral, esophagus, and rumen erosion, dependant edema |
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Secondary (acquired) immunodeficiencies
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Feline +canine parvovirus
=Cryptal necrosis =panleukopenia |
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Secondary (acquired) immunodeficiencies
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Passive transfer failure (most NB)
Colostrum is NB for neonates of species with epitheliochorial placentation born hypogammaglobulinemic absorbed during the first 24-48 hours of life Failure results: septicemia, meningitis, polyarthritis and polyserositis |
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AUTOIMMUNE DISEASES
Acquired Myasthenia Gravis |
Systemic muscular disease caused by type II reaction
Auto-antibodies against acetylcholine receptors Receptors cannot interact with acetylcholine -Clinical signs: muscle weakness and fatigue exacerbated by exercise and resolves with rest -Megaesophagus +/- aspiration pneumonia |
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AUTOIMMUNE DISEASES
Iso-immune thrombocytopenia in piglets |
Sows are sensitized to platelet antigens of piglets
Develop anti-platelet antibodies and secrete them into colostrum Ingested colostral antibodies are absorbed by piglets Antibodies bind to platelets and platelets are subsequently destroyed This results in thrombocytopenia and widespread hemorrhages |
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Lesion
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A pathologic change in the tissues
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Hyperplasia
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is an increase in the number of cells in an organ or tissue, usually resulting in increased volume of the organ or tissue
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Hypertrophy
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refers to an increase in cells
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HYPERSENSITIVITY (ALLERGY)Atopy (atopic dermatitis)
Type I hypersensitivity reaction |
Allergen exposure is predominantly respiratory (Ca)
Inherited predisposition to Type I hypersensitivity reaction Excessive production of IgE which, together with a specific antigen, trigger degranulation of mast cells Lesions: erythema, urticaria, self-inflicted trauma (licking, rubbing due to pruritus) |
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HYPERSENSITIVITY (ALLERGY)
Food hypersensitivity dermatitis |
Non seasonal pruritic disease dogs
Type I and/or type IV reaction to food antigens Lesions: erythema, urticaria, self-inflicted trauma (licking, rubbing due to pruritus) |
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AUTOIMMUNE DISEASES
Pemphigus |
-Dermal disease caused by type II reaction.
-Pathogenesis: Development of antidesmosomal auto-antibodies which bind to desmosomal proteins (interepithelial attachment proteins) and, subsequently, disruption of cell-cell adhesion, resulting in formation of intraepithelial pustules. -Lesions: intraepithelial pustules (muzzle, periocular, pinnae, foot pads, around nails) or erosions following pustular ruptures. |
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AUTOIMMUNE DISEASES
Acquired Myasthenia Gravis |
Systemic muscular disease caused by type II reaction
Auto-antibodies against acetylcholine receptors Receptors cannot interact with acetylcholine -Clinical signs: muscle weakness and fatigue exacerbated by exercise and resolves with rest -Megaesophagus +/- aspiration pneumonia |
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Equine purpura haemorrhagica
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After Streptococcus equi infection
Some horses have high level of antigen antibody complexes in circulation Ag-Ab complexes are deposited in vessels with consequential vasculitis, generalized edema and purpura. |
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Feline infectious peritonitis
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Progressive often fatal immune-complex disease of cats
Caused by a coronavirus FIP virus is spread systemically by infected macrophages Immune complexes (virus+Ab or viral antigen+Ab) are deposited on venular walls and cause type III immune reaction. Based on experimental infections outcome of FIP infection depends on cell mediated immunity (CMI) Strong and rapid CMI virus contained and eradicated Weak CMI effusive form of FIP with marked fibrinous exudation Moderately strong CMI dry form with granulomatous inflammation |
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Amyloidosis
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Amyloid is a pathologic proteinaceous substance
Diagnosis morphologic identification in biopsy Amyloid is amorphous, eosinophilic, extracellular Congo red stain - pink or red and birefringent green Amuloid deposits have a uniform ß-pleated sheet |
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Define Inflammation
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: is the reaction of vascularized living tissues to local injury which comprises a series of changes in the terminal vascular bed, the blood and the CT that are designed to eliminate the offending irritant and to repair the the damage tissue
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5 Cardinal signs of inflammation?
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1)Warmth (calor)
2)Pain (dolor) 3)Redness (rubor) 4)swelling (tumor) 5)loss of function |
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What is a granuloma?
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A focus of chronic inflammation consisting of an aggregation of epitheliod macrophages often with giant cells surrounded by lymphocytes +/or plasma cell and intermingling fibroblasts
Macro: ~ looking to a neoplasm |
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Define the Acute Phase Response?
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An adaptive component of innate defense and consists of numerous predetermined and well-orchestrated local and systemic reactions to the acute phase stimuli.
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Define shock?
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is a circulatory dyshomestasis associated with the loss of circulating blood volume, reduced CO +/or inappropriate peripheral vascular resistance.
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Bacterimia
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Presence of bacteria in the blood
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Septicemia
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presence of bacteria in the blood that causes systemic disease
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Endotoxemia
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presence of endotoxin (LPS) in the blood that causes systemic disease
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Differentiate fibrin and fibrosis?
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An insoluble protein essential to clotting of blood. The Formation of fibrosis tissue (the common connective tissue of the body).
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Differentiate granulomatous inflammation and granulation tissue?
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Is a distinctive pattern of chronic inflammatory reaction characterized by a focal accumalation of activated MOs (epitheloid), surrounded by lymphocytes and/or plasma cells and fibroblasts. In contrast, is the new tissue formed in repair of soft tissue, characterized by angiogensis and fibroblasts.
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Inflammation
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is the rxn of vascularized living tissue to local injury=a series of changes in the terminal vascular bed, the blood, and the CT designed to eliminate the irritant and repair the damaged tissue.
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Cardinal signs of inflammation?
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Redness, heat, swelling, pain, and loss of function.
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Absess
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A localized collection of pus in a fibrous cavity.
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Exudate
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A protein rich fluid that has escaped from BVs into the extravascular tissue due to inflammatory processes.
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Transudate
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A fluid substance that has passed through a membrane or been extruded from a tissue. High fluidity, low protein and cell content
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Chemotaxis
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The directional movement of cells toward a chemical attractant along a [] gradient.
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Intregrins
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are transmembrane heterodimeric glycoproteins expressed on leukocytes that bind to ligands on endothelial cells (to mediate firm adhesion)
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Selectins
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are sugar binding protiens on endothelium, platelets that mediate the rolling phase of leukocytes exit from BV to ECF.
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Opsonin
Opsoninization |
is a protien that binds to antigens and enhances their phagocytosis.
Is the process of coating a particle (ex. microbe) to target it for phagocytosis. |
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Cytokines
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proteins made by many cells that modulate the functions of other cells
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Chemokines
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are a family of cytokines that fxn as leukocyte chemoacttractants.
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Leukocytosis
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is the increase in the number of leukocytes in the blood
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Bacterimia
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presence of bacteria in the blood
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Septicemia
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presence of bacteria in the blood causing systemic disease
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Endotoxemia
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presence of endotoxin in the blood causing systemic disease
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Endotoxin
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A heat stable protein present in bacterial cell. LPS of gram - bacteria. Pyogenic, septic shock...
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Acute phase response
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is an adaptive component of the innate defence and consists of numerous predetermined and co-ordinated local and systemic physiological rxns to an acute phase stimuli: fever, acute phase proteins, anorexia, somnolence, leukocytosis
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Acute phase proteins
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liver-produced plasma proteins whose composition changes due to infection or inflammation. + APP: proinflammatory or antimicrobial fxns; - APP: homeostasis maintainence
+APP: opsonins, proteinase inhibitors, metal binding proteins, coagulation and complement proteins |
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Regeneration
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structural and functional resistution of injured tissue
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Repair by scar formation and fibrosis
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repair of injured tissue by fibrous CT. Scarring/fibrosis restores structure/continuity, but not fxn of injured tissue.
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Autocrine signalling
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when a cell respond to signal molecules secreted that cell
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Paracrine signalling
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when a cell produces a ligand, which acts on adjacent targets cells that express the appropriate receptor (usually a different cell type).
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Endocrine Signalling
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endocrine organ cells systhesized hormones which carried by the blood act on target cells distant from the site of systhesis
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Hypersensitivity
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an exxaggerated immunological rxn to a normally harmless antigenic stimulus resulting in host injury. (Type 1+4)
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Autoimmune diseases
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develop when AB or Tcell react against self antigens. (Type 2+3).
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Atopy
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a type 1 hypersensitivity in skin. An inherited predisposition to produce excessive IgE which when coupled to certain antigen, triggers degranulation of dermal mast cells and circ. basophils. (antigens exposure=respiratory)
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Erythemia
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redness due to capilary dilation
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Urticaria
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eruption of itching wheals (=acute dermal edema and redness due to capilary dilation).
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Amyloid
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is a pathologic protieneous substance that deposits between cells in many tissues/organs in a wide variety of clinical settings.
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Dysplasia
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disorderly or atypical proliferative responses in the cellular context due to loss of regular differentiation and orderliness, accompanied by atypica
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Agenesis
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Complete failure of an organ/tissue to develop (associated with a lack of primoridium)
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Aplasia
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organ absence or rudimentary organ development due to a failure of development or failure of a tissue to renew itself
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Hypoplasia
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Failure of an organ to attain normal size
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Malformations
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intrinsic abnormalities or abnormalities during development (can be 1 or multiple system) and caused by genetic, enviro., multifact, or unknown
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Neoplasia
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the growth of an abnormal, purposelss, autonomous tissue mass, where the growth is uncoordinated and faster than that of normal tissues and persists in the same manner with removal of change evoking stimulus.
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Anisocyctosis
Anisokyaryosis Pleomorphism Macrocytosis |
cell size variation
nuclear size variation variation in cell size+shape larger than normal cell size |
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Benign vs malignant
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Benign: good differentiation, slow growing, expansile, functional, encapsulated
Malignant: poor differentiated (pleomorphic to anaplastic), rapidly growing, invasive, unlikely fxnal, recurs post incision, invades vascular, metastasizes |
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Factors determing speed of tumor growth?
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-rate of cell loss/apoptosis
-number of cells in mitosis -length of mitotic cycle |
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Metasis
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the spread of a tumour cells to and implantation @ sites discontous/ distant from original mass via lymphatics (carcinoms) or BVs (sarcomas) or exfoliation and direct implantation
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Initiation
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non-lethal genetic cellular event which creates neoplasia potential (regulatory genes changes can result in neoplasia)
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Promotion
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inducition of proliferation in initiated (tranformed)cell to consequently increase the likelihood of further mutatuion occurring.
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Paraneoplastic syndrome
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related to the production of biologically active substances that cause physiological changes not readily explained by tumour presence
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Cachexia
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Multifactorial paraneoplastic syndrome characterized by anorexia, body wt loss, adipose tissue and skeletal muscle loss due to cytokine excess (TNF, IL6, IFN Y) causing muscle proteolytic pathway hyperactivation, modified lipid and carb. metabolism
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Organ hypertropy
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an increase in the size of an organ due to an increase in cell size, not number
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Organ/tissue atropy
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decrease in the size of an organ/tissue (after it has reached normal size) caused by a loss of cells or decreased cell size
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Metaplasia
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is a reversible process in which one type of mature differentiated cell is replaced by a different mature differentiated cell (of same germ line and in an abnormal location).
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Osteoporosis
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reduction in the quantity of bone
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Hyperemia
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is an engorgement of a capillary bed due to inceased arteriolar blood flow into an area/organ
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Congestion
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is an engorgement of a capillary bed due to decreased venous outflow
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Hypostatic congestion
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congestion due to pooling of blood in a dependant part
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cyanosis
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dark blue-purple skin + mucous membrane discoloration due to defiecient blood oxygenation
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Ischemia
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local abscence of blood due to obstruction of blood supply or local stagnation/congestion of blood causing ichemic damage due to decreased blood drainage
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Hypoxia
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Decreased below normal levels of O2 in inspired gases, arterial blood or tissues
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Edema
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excessive accumalation of fluid in tissue or body cavity interstial spaces
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Anasarca
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generalized severe infiltrationof edema fluid into the subQ CT
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Dependant edema
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a clinically detectable increase in EC fluid volume localized in a dependant part characterized by pitting or swelling
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Pitting edema
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edematous tissue that remains indented for a few minutes after firm finger pressure is applied on it
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Deydration
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reduction in water content in body
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Hydropericardium
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a non-inflammmatory fluid in the pericardial sac.
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Ascities
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a non-inflammatory accumalation of fluid in the peritoneal cavity ~hydroperitoneum
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Effusion
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escape of fluid from BVs or lymphatics into the tissues/ cavity, usually non-inflammatory fluids.
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Lymphadema
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obstruction of lymphatic vessls or nodes to result in increased lymph accumulations in the affected region to cause edema
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Transdate
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low protein fluid which, due to increased hydrostatic pressure or osmotic force changes, crosses normal intact membranes
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Hemmorrhage
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escape of blood from the intravascular space
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anemia
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Less than normal amounts of RBCs #'s, blood Hb and/or packed RBCs manifested as pale skin +MM, breath shortness, lethargy, and fatigue
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Hematopoiesis
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process of formation and development of the various blood cells and other formed elements
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Petechiae
Ecchymosis Purpura |
-minute hemorrhagic spots
-larger than P., due to extravassation of blood into tissues -systemic, generalized, multifocal, random haemorrhages in many organs + tissues |
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Paintbrush haemorrhages
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linear haemorrhages (underlying structure is linear ex. myocardium)
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Suffusion
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Act of pouring blood over the body/tissue=large, flat, spreading haemorrhages
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Hematoma
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localized mass of extravascated blood that is relatively or completely confined w/in an organ or tissue or space or potential space
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Hemothorax
Hemopericardium Hemoperitioneum Hemoarthrosis |
Blood in the
-thorax -pericardium -peritoneum -joints |
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Melena
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dark colored tarry stools due to upper GT blood digestion
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Hematochezia
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bloody stool passage
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Epistasis
Hematopytsis |
-Nosebleed
-spitting of blood from lungs or bronchial tubes as a result of bronchial or pulmonary hemorhages |
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Hematuria
coagulation Hemostasis |
-blood in urine
-formation of a clot -arresting of blood |
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Thrombus
Embolus |
-clot in CV system from blood
-plug composed of thrombus, mass of bacteria or other material, that is carried by the blood and occludes the vessel |
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Infart
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is an area of ischemic necrosis in which all components of the affected tissues have undergone necrosis
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Necrosis
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is death of cells and tissues in the living animal
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Degeneration
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reversible deteriorating pathologice change in cells or tissues, to result in diminished or lost fxn
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Autolysis
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is self-digestion or degradation of cells and tissues by the hydrolytic enzymes normally present in the those tissues
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Apoptosis
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is a pathway of cell death tha is induced by a tightly regulated intracellular energy-dependant program in which cells destined to die activate enzymes that degrade the cell's own nuclear DNA and nuclear and cytoplasmic proteins. Cells pm intact, but altered to be target for phagocytosis.
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Thrombocytopenia
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where there is an abnormally small number of blood circulating platelets
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Autophagy
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segregation and disposal of damaged organelles w/in a cell
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Ubiquitin-proteosome pathway
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degragation of cytosolic and nuclear proteins, via conjugation to Ubiquitin->then degraded w/in a proteosome. Pathway induced by TNF, glucocorticoids, thyroids
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Heterophagy
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lysomal digestion of ingested material from ECF
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Reversible cell injury
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fxnal and morphologic changes that changes are reversible if damaged stimulus is removed.
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Cell swelling
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increase in cell size + volume because increase in H2o bcs. cell can't regulate H20 ingress and excretion due to membrane damage, energy production failure, or injuries to enzymes regulating ion channels
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Cloudy swelling
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influx of H20 dilutes cytoplasmic matrix
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Degeneration
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-hydropic: increase cell swelling
-vacuolar: increase in vacuoles in cytoplasm of various sizes -ballooning: cells greatly enlarged and cytoplasm basically a clear space |
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Hepatic lipidosis
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abnormal accumalation of lipids in cell due to increase in FFA into liver, decreased ketone body oxidation, TG accumalation due to dec. apoprotein synthesis, impaired lipoprotein sythesis or secretion.
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Steriod hepatopahty
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massive glycogen accumulations in hepatocytes due to high levels of corticosteroids
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Irreversible cell injury
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with continued damgage, cell injury becomes irreversible. Severe mitochondrial damage and loss of membrane fxnality. Undergoes neco or apop.
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Coagulation necrosis
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tissue preservation due to injury or subsequent acidosis denaturing proteolytic enzymes->characteristic of hypoxia cell death
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Sequestrum
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an area of coagulative focus where circulation ins impaired preventing leukocyte invasion and thus tissue can't be removed by scavenger leukocytes
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Liquifactive necrosis
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focal infection of pyogenic bacteria leads to accumulating leukocytes which release enzymes to cause tissue lysis and then pus
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Malacia
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liquifaction necrosis in CNS (which has very little fibrous CT therefore after NO release lytic enzymes ->area of lipid debris and fluid
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Caseous necrosis
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conversion of dead cells into a granular, friable mass-> necrotic focus composed of a coagulum of nuclear and cytoplasmic debris. Bacteria is encapsulated with a thin fibrous capsule, then bacteria proliferates and burst through capsule, new capsule formed...
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Gangrenous necrosis
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all initially represent coagulation necrosis
-dry: coag. necrosis 2ndary to extremities, tail or ear infarction with mummification -wet: coag. necrosis ->further degradation by saprophytic bacteria -Gas: anaerobic bacteria proliferate in area of necrotic tissue |
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Fat necrosis
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pancreatic fat necrosis results in activation of lipases w/in and around pancreas->split cell membrane into fatty acids wich combine with Ca+ to make soap
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Karyohexis
Pycnosis karyolysis |
-nucleus undergoing fragmentation
-nuclear shrinkage +increased basophilia -chromatin basophilia fades due to DNAase activity |
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Dystrophic calcification
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-occurs locally in necrotic tissue w/out high serum levels or chance in ca metabolism
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Metastatic calcification
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occurs in normal tissues when hypercalcemia (due to increased PTH, bone tissue destruction, Vit D toxicity, or renal failure).
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sequestrum
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an area of coagulation necrosis that persists for weeks due to impaired circulation preventing leukocyte invasion.
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Ischemia
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Local absence of blood due to blood supply obstruction or local stagnation/congestion causing ischemic damage due to decreased blood drainage
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Infarct
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is an area of ischemic necrosis in which all components of the affected tissues have undergone necrosis
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Thrombosis
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is coagulation within the cardiovascular system formed during life from the constituents of blood
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Embolus
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a plug, composed of detached thrombus, mass of bacteria, or other material, that is carried by the blood and occludes a vessel
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Thrombus
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a clot in the cardiovascular system formed during life from blood constituents
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