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WorksheetsPART 1: QUESTIONS 1-40
Total questions: 100
Worksheet time: 50mins
The process where cells decrease in size due to reduced workload is called:
Hypertrophy
Hyperplasia
Atrophy
Dysplasia
Metaplasia
The first immune cell to arrive at a site of acute inflammation is:
Neutrophils
Macrophages
Eosinophils
Basophils
NK cells
Which of the following are considered first-line defenses of innate immunity?
Intact skin
Mucous membranes
Stomach acid
Cytotoxic T-lymphocytes
Cough reflex
Liquefactive necrosis is most often seen in the brain following ischemia.
True
False
Which antibody is secreted in breast milk to protect infants’ mucosal surfaces?
IgG
IgM
IgA
IgE
IgD
The cardinal signs of acute inflammation include all EXCEPT:
Heat
Redness
Pain
Loss of function
Necrosis
The mediator that is primarily responsible for pain in acute inflammation is:
Histamine
Bradykinin
Complement C3b
Leukotriene C4
CRP
Which chemical mediator causes sustained vascular permeability and bronchoconstriction longer than histamine?
Leukotrienes
PAF
Prostaglandins
Bradykinin
C5a
What is the functional purpose of mucus production during inflammation?
Blocks lymph drainage
Traps pathogens & debris
Dilates vessels
Stimulates fibroblasts
Produces antibodies
The end-product of the clotting cascade that forms the insoluble mesh of a clot is:
Fibrinogen
Fibrin
Thrombin
Collagen
Factor X
Systemic manifestations of significant acute inflammation may include:
Fever
Leukocytosis
Malaise / fatigue
↑ plasma CRP
Decreased vascular permeability locally
The WBC type elevated in parasitic infections is:
Neutrophils
Macrophages
Eosinophils
Basophils
Cytotoxic T-cells
Which antibody class is first produced in a primary immune response and is most efficient at agglutination?
IgA
IgE
IgG
IgM
IgD
Which cells act as professional antigen-presenting cells (APCs) for helper T-cells?
B-lymphocytes
Macrophages
Dendritic cells
All of the above
Neutrophils
The Fab region of an antibody is the part that:
Binds to mast-cell Fc-receptors
Binds to the antigen’s epitope
Anchors antibody to B-cell membrane
Determines antibody class
Activates complement directly
Helper T-cells (CD4+) activate both humoral and cell-mediated immunity by releasing cytokines.
True
False
Which cell type directly kills virus-infected host cells by releasing perforin?
Cytotoxic T-cells (CD8+)
Helper T-cells (CD4+)
B-lymphocytes
Plasma cells
Eosinophils
Which mediator released by mast cells activates platelets during the inflammatory response?
Histamine
PAF (Platelet-Activating Factor)
Prostaglandins
Leukotrienes
TNF-α
Which type of necrosis is typically seen in solid-organ infarcts such as heart & kidney?
Coagulative
Liquefactive
Caseous
Fat
Fibrinoid
Which type of necrosis is typically seen in the brain after ischemia?
Coagulative
Liquefactive
Caseous
Fat
Wet gangrene
Which type of necrosis shows a “cheese-like” appearance in TB granulomas?
Coagulative
Liquefactive
Which cell type predominates in the proliferative phase of wound healing and lays down collagen?
Neutrophils
Macrophages
Fibroblasts
Endothelial cells
Basophils
Factors that can impair wound-healing include:
Diabetes mellitus
Vitamin C deficiency
Corticosteroid therapy
Ischemia / poor perfusion
Adequate oxygen supply
Granulation tissue contains proliferating capillaries, fibroblasts, and macrophages.
True
False
Which vitamin is essential for collagen synthesis during wound-healing?
Vitamin A
Vitamin B12
Vitamin C
Vitamin D
Vitamin K
Dry gangrene is characterized by which pattern of necrosis and what major cause?
Liquefactive – infection by bacteria
Coagulative – chronic arterial occlusion
Caseous – tuberculosis
Which mediator is most associated with swelling/edema due to ↑ vascular permeability?
Histamine
Leukotrienes
Bradykinin
Complement C5a
Thrombin
Wet gangrene differs from dry gangrene by the presence of:
A. A line of demarcation & mummified tissue
B. Anaerobic bacterial infection, foul smell, oozing fluid
C. Ischemic coagulative necrosis without infection
D. Calcification of vessels
E. Granulomatous caseous necrosis
Keloid formation after wound-healing is due to:
Vitamin C deficiency
Excess collagen deposition in scar tissue
Loss of granulation tissue
Low fibroblast activity
Insufficient angiogenesis
The ABO blood-group antigens are carried on:
RBC plasma membrane carbohydrates
WBC MHC-II molecules
Platelet glycoproteins
Serum antibodies
T-cell receptors
Which antibody crosses the placenta to protect the fetus?
IgA
IgE
IgG
Which antibody mediates Type I immediate allergic reactions by binding to mast-cell Fc-receptors?
IgA
IgE
IgG
IgM
IgD
MHC-I molecules present antigens from inside the cell (e.g., viral peptides) on all nucleated cells.
True
False
Helper T-cells (CD4+) are critical in adaptive immunity because they:
Directly lyse virus-infected cells
Produce antibodies themselves
Activate B-cells, cytotoxic T-cells & macrophages via cytokines
Are part of innate immunity only
Activate complement without antigen
Which class of antibody is mainly a B-cell receptor and not secreted in large amounts?
IgA
IgE
IgG
IgM
IgD
Which immune cells suppress B- and T-cell proliferation to help prevent hypersensitivity reactions?
Helper T-cells
Regulatory T-cells
Cytotoxic T-cells
The complement component most important for opsonization of bacteria is:
C1q
C3b
C5a
C9
C-reactive protein
Which cell type predominates later in chronic inflammation, surviving longer than neutrophils and cleaning up debris?
Macrophages
Fibroblasts
Basophils
NK-cells
Mast-cells
The immune-cell target that is progressively lost in HIV infection is:
CD8+ cytotoxic T-cells
CD4+ helper T-cells
B-lymphocytes
Neutrophils
NK-cells
AIDS-defining opportunistic infections often appear when CD4+ T-cell count drops below approximately:
500 cells/μL
350 cells/μL
200 cells/μL
100 cells/μL
50 cells/μL
Which complement component forms the Membrane Attack Complex (MAC) that lyses bacteria?
C1q
C3b
C5b-C9 complex
Factor B
Properdin
The mediator primarily responsible for fever in systemic inflammation is:
IL-1 / TNF-α acting on hypothalamus
Histamine
Bradykinin
Prostaglandin D2
PAF
The mediator that causes vasodilation, increases vascular permeability and attracts neutrophils & eosinophils is:
C3b
Leukotrienes
Histamine
C5a
Thrombin
The mediator primarily responsible for chemotaxis of neutrophils is:
C5a
Histamine
CRP
Bradykinin
IgG
Which WBC type is typically elevated in allergic reactions such as hay fever and asthma?
Neutrophils
Basophils
Eosinophils
Granulomas are collections of activated macrophages (epithelioid cells) often surrounded by lymphocytes.
True
False
Which disease is characterized by granulomatous inflammation with caseous necrosis?
Rheumatoid arthritis
Asthma
Tuberculosis
Lupus nephritis
Gout
The typical histological appearance of caseous necrosis is:
Clear fluid-filled cyst
Cheese-like soft granular center
Calcified scar
Fatty chalky deposits
Gel-like transparent matrix
Which cell type contracts the wound edges during healing?
Myofibroblasts
Macrophages
Fibroblasts
Smooth-muscle cells
Endothelial cells
The difference between regeneration and repair is that:
Regeneration replaces tissue with scar tissue
Repair restores tissue with identical original cells
Regeneration restores original architecture & function; repair uses collagen scar
Both involve fibroblast collagen only
Repair never involves fibroblasts
Local factors that can impair wound-healing include:
Infection at wound site
Poor local blood supply
Excessive movement of wound edges
Foreign bodies in wound
Adequate oxygenation
Dehiscence refers to:
Abnormal narrowing of scar
Separation of wound edges after they were closed
Excessive collagen formation in scar
Formation of purulent cavity
Overgrowth of granulation tissue
Hyperacute transplant rejection occurs because of:
Pre-formed anti-donor antibodies causing complement-mediated lysis
Gradual T-cell infiltration over weeks to months
Graft-versus-host donor T-cells attack recipient
Bacterial infection of graft
Lack of vascular anastomosis
Graft-versus-host disease after bone-marrow transplant is caused by:
Recipient cytotoxic T-cells attacking donor graft
Donor cytotoxic T-cells attacking recipient tissues
IgE-mediated mast-cell degranulation
Immune-complex deposition in joints
Neutrophil enzymes destroying vessels
The pathophysiological mechanism of rheumatic fever-induced carditis following strep throat is:
Immune-complex deposition in myocardium
Cross-reactive IgG antibodies bind to heart valves & activate complement
T-cell-mediated delayed response
Direct bacterial invasion of myocardium
IgE-mediated mast-cell histamine release
Type II hypersensitivity is mediated by IgG or IgM antibodies directed against antigens on cells or tissues.
True
False
An example of a Type II cytotoxic hypersensitivity reaction is:
Serum sickness
Hay-fever allergic rhinitis
Hemolytic transfusion reaction
Contact dermatitis from nickel
Arthus reaction
An example of a Type III immune-complex hypersensitivity is:
Post-streptococcal glomerulonephritis
Graft-versus-host disease
Hemolytic anemia
Asthma attack
TB skin test
An example of a Type IV delayed hypersensitivity reaction is:
Penicillin-induced hemolytic anemia
Serum sickness
Contact dermatitis from poison ivy
Anaphylaxis to peanuts
Pernicious anemia
The difference between acute and delayed hypersensitivity is primarily:
The organ affected
The time after exposure & immune mechanism involved
The dose of antigen
Whether complement participates
Whether fever occurs
The first-line epithelial defense of the respiratory tract is:
Acidic gastric juice
Mucociliary escalator
Salivary amylase
Lysozyme in tears
Normal skin flora
Chemotaxis is important in inflammation because it:
Stimulates fibroblasts to secrete collagen
Guides WBCs to migrate toward higher concentration of chemical attractants
Produces vasodilation to increase blood flow
Causes smooth-muscle contraction in vessels
Activates complement
Liquefactive necrosis commonly leads to abscess formation in bacterial infections.
True
False
Fat necrosis in acute pancreatitis is caused by:
Lipase-mediated digestion of fat and calcium saponification
Caseous degeneration of adipose cells
Coagulative ischemic death of fat lobules
Liquefactive conversion by neutrophils
Immune-complex deposition in adipose
Bilirubin accumulation in tissues most commonly leads to:
Cyanosis
Icterus / jaundice
Hyperpigmented brown skin
Pitting edema
Petechiae
Physiologic situations where apoptosis is normally required include:
A. Embryonic digit separation (fingers & toes)
B. Menstrual cycle endometrial shedding
Necrosis is often accompanied by malaise, fever, leukocytosis and tachycardia, but apoptosis generally is not.
True
False
Hypertrophy of the left ventricle due to chronic hypertension is best described as:
Pathologic increase in cell number
Physiologic enlargement of cell size due to pressure overload
Metaplasia from one cell type to another
Dysplasia from chronic irritation
Hyperplasia due to hormonal stimulus
Metaplasia in the bronchi of a chronic smoker typically involves:
Squamous epithelium → columnar epithelium
Columnar epithelium → stratified squamous epithelium
Fibroblast → adipocyte transformation
Cuboidal → columnar change
Epithelial → mesenchymal conversion
The key difference between dysplasia and metaplasia is that dysplasia:
Is an orderly, reversible change in cell type
Is always physiologic
Shows disordered cell growth with increased nuclear atypia, pre-cancerous
Occurs only in connective tissue
Involves necrosis
The latent period before measurable antibodies appear in a primary immune response is about:
1-2 days
3-5 days
7-10 days
In a secondary immune response after re-exposure, antibodies rise:
Slower and lower than primary response
Faster and to much higher levels than primary
Same as primary response
Only IgE is produced
Requires APCs each time
Most plasma cells survive after activation for about:
2-3 days
4-5 days
2 weeks
1 month
Years
The region of an antibody that binds to Fc-receptors on immune cells and complement proteins is the:
Fab region
Variable light-chain tip
Heavy-chain hinge
Fc region
Idiotype
The first complement component to bind to an antibody-antigen complex and start the classical pathway is:
C1q
C2
C3
C4
C5
Regulatory T-cells help suppress the immune response and prevent autoimmune disease.
True
False
NK-cells kill antibody-coated cells by:
Engulfing them by phagocytosis
Binding to Fc portion of antibody and releasing perforins & granzymes
Activating complement directly
Presenting antigen to CD4 cells
Switching IgM to IgG
The ABO blood-group incompatibility reaction at transfusion is an example of:
Type I hypersensitivity
Type II cytotoxic antibody-mediated hypersensitivity
Type III immune-complex hypersensitivity
Type IV delayed T-cell-mediated hypersensitivity
Innate NK-cell attack
The Arthus reaction and serum-sickness are examples of:
Type I hypersensitivity
Type II hypersensitivity
Type III immune-complex hypersensitivity
Type IV delayed hypersensitivity
Auto-inflammatory fever syndromes
The five cardinal signs of local acute inflammation include:
Redness
Heat
Swelling
Pain
Loss of function
Opsonization refers to:
Coating microbes with antibodies or complement to enhance phagocytosis
Direct lysis of bacteria by complement MAC
Fever induction via IL-1
Histamine-induced vasodilation
Killing by NK-cells without antibodies
The WBC that predominates in chronic inflammation and orchestrates tissue cleanup and repair is:
Neutrophils
Macrophages
Basophils
Eosinophils
NK-cells
Serous exudate is best described as:
Thick, pus-filled creamy fluid
Watery fluid with few cells (like blister fluid)
Thick fibrin-rich sticky mesh
Blood-tinged fluid from vessel rupture
Necrotic tissue debris
Fibrinous exudate is typical of:
Urticaria
Fibrin-rich sticky exudate seen on pericardial or pleural surfaces
Watery blister fluid
Caseous granuloma discharge
Fat necrosis
Purulent (suppurative) exudate is characterized by a high content of:
RBCs
Pus with neutrophils, bacteria & necrotic debris
Watery serum with few cells
Fibrin mesh and plasma proteins
Lymphocytes only
Hemorrhagic exudate contains mainly:
Lymphocytes
RBCs from damaged blood vessels
Dead neutrophils
Fibrin mesh
Eosinophils
Edema refers to excess fluid in interstitial tissue or body cavities.
True
False
Pus-filled cavity within a tissue is called:
Cyst
Granuloma
Abscess
Vesicle
Keloid
Granulomas help contain:
Persistent foreign bodies or pathogens that resist usual acute inflammation
RBC breakdown products like bilirubin
Histamine granules
Acute viral infections that resolve quickly
Edema due to allergy
C-reactive protein (CRP) is an acute-phase reactant whose level rises in:
Chronic stable disease only
Acute inflammation & tissue injury
Viral latency with no inflammation
Rouleaux formation of RBCs in lab tests occurs due to:
Increased plasma fibrinogen and globulins making RBCs stack together
Dehydration shrinking RBCs
Immune-complex coating of RBCs
Overproduction of hemoglobin
Clotting cascade activation
Systemic fever during inflammation decreases serum iron & zinc because:
The liver & spleen sequester them to limit microbial growth
Kidneys excrete them to reduce BP
Hypothalamus destroys them with heat
CRP binds them directly
Complement consumes them
Muscle catabolism during prolonged systemic inflammation occurs because:
Cytokines mobilize amino acids for liver acute-phase protein synthesis
Fever melts down muscle enzymes
Complement degrades myosin
Macrophages phagocytose myocytes
Neutrophils release collagenase
Chronic wounds often have impaired healing because:
Excess oxygen supply damages fibroblasts
Persistent infection, poor perfusion & prolonged inflammation prevent proliferation phase
Lack of platelets to form clot
Absence of macrophages in wound
Excess vitamin C
Vitamin C deficiency affects wound-healing because:
It inhibits complement activation
It is required for hydroxylation of collagen for tensile strength
It stimulates excess fibroblast proliferation
Systemic factors that can impair wound-healing include:
Malnutrition
Diabetes mellitus
Advanced age
Corticosteroid therapy
Peripheral vascular disease
First-intention healing best describes:
Clean surgical incision with minimal tissue loss and closely apposed edges
Large infected wound left open to heal by granulation
Bone fracture callus formation
Scar hypertrophy after trauma
Keloid removal scar
Second-intention healing best describes:
Minimal granulation tissue
Wound edges widely separated, requiring more granulation tissue & contraction
Rapid epithelial regeneration with little scar
Healing under sterile bandage without inflammation
Absence of collagen formation
The main function of clotting cascade in wound-healing is to:
Produce fever for better immunity
Recruit neutrophils by chemotaxis
Form fibrin mesh to stop bleeding & scaffold repair
Break down fibrin to remodel clot
Release histamine to increase permeability
Angiogenesis refers to growth of new capillaries into granulation tissue during repair.
True
False
