Frontline Defenses
Describe how mechanical, chemical, and physical defenses of epithelial surfaces prevent microbial entry.
They block, trap, or flush out pathogens before the immune system activates.
Explain what an acute inflammatory leukogram indicates/which cell changes characterize it.
Leukocytosis with neutrophilia and a regenerative left shift (bands < segs).
List the five cardinal signs of inflammation and the physiologic basis for each.
Redness, heat, swelling, pain, loss of function — all due to vascular and chemical mediators.
State the overall purpose of the complement system in immunity.
It amplifies innate defense by tagging, lysing, and recruiting immune cells against pathogens.
Define an antigen and explain what makes a molecule highly immunogenic.
Antigens are foreign molecular structures that trigger an adaptive immune response
strong immunogens are large, complex, stable, and foreign to the host.
Outline the four phases of phagocytosis and explain how phagocytes recognize microbes.
Chemotaxis → Adherence → Ingestion → Destruction. Recognition via PRRs and opsonins.
Define a degenerative left shift and describe its clinical significance.
(bands?segs?wbc count?prognosis?)
Bands > segs ± low WBC = inadequate marrow response and poor prognosis.
Describe the sequence of vascular events that occur immediately after tissue injury.
Vasodilation → ↑ permeability → stasis of blood flow → margination → rolling/adhesion → emigration.
Differentiate the classical and alternative pathways of complement activation.
Classical = triggered by antibody-antigen complexes
Alternative = triggered directly by pathogen surfaces.
Differentiate between antigen, epitope, and hapten.
Antigen = whole molecule
Epitope = specific binding site
Hapten = small molecule that becomes immunogenic only when bound to a carrier.
Explain how pattern-recognition receptors (PRRs) interact with pathogen-associated molecular patterns (PAMPs) to trigger innate immunity.
PRRs detect conserved microbial patterns and initiate cytokine-driven inflammation.
Describe the appearance and significance of toxic neutrophils.
Neutrophils show cytoplasmic basophilia, foamy cytoplasm, and Döhle bodies. sign of rapid production.
Explain how increased vascular permeability contributes to the development of exudate.
It allows plasma proteins and cells to leave vessels, forming protein-rich inflammatory fluid.
Explain the function of C3b in the complement system.
C3b acts as an opsonin, marking microbes for phagocytosis and amplifying the cascade.
Explain how cross-reacting antibodies can lead to false-positive tests or autoimmune disease.
Antibodies to one antigen may bind a different molecule with a similar epitope, causing cross-reactivity.
How do natural killer (NK) cells decide whether to destroy a host cell?
They target cells lacking or altering MHC-I or expressing stress or antibody signals.
Compare stress (cortisol) and catecholamine leukograms and when each occurs.
Stress = neutrophilia + lymphopenia ± monocytosis; Catecholamine = neutrophilia + lymphocytosis.
Differentiate serous, fibrinous, catarrhal, and purulent exudates by composition and clinical meaning.
Serous = plasma fluid
Fibrinous = fibrin protein
Catarrhal = mucus
Purulent = neutrophils + debris.
Describe the mechanism and outcome of the membrane attack complex (MAC).
Sequential C5b-C9 insertion forms a pore that lyses target cells.
Describe the role of modified-live vaccines in stimulating adaptive immunity against intracellular pathogens.
They replicate inside host cells, activating both cytotoxic T-cell and antibody responses for durable protection.
Explain how viral infections like FIV in cats affect the immune system through targeting of CD4⁺ T-cells.
Viruses such as FIV infect and destroy CD4⁺ T-helper lymphocytes, weakening both humoral and cell-mediated immunity.
Explain how acute, chronic, and overwhelming inflammatory leukograms differ
(neutrophils? type of shift?)
Acute = neutrophilia + left shift
Chronic = neutrophilia without left shift
Overwhelming = neutropenia + degenerative shift.
Explain fibrinous fibrosis relation, and the consequences of that transition.
Persistent inflammation organizes fibrin into fibrous scar tissue, causing adhesions or loss of function.
Describe how IgA prevents pathogen and explain why complement activation is limited in this environment.
IgA blocks microbial attachment to epithelial cells through immune exclusion, while complement is minimally active at mucosal sites to avoid tissue damage.
Explain how MHC-I and MHC-II molecules coordinate antigen presentation to CD8⁺ and CD4⁺ T-cells
MHC-I presents intracellular peptides to CD8⁺ CTLs
MHC-II presents extracellular peptides to CD4⁺ helper T-cells.