Final Bookmarks

Question 1

Trace the flow of blood in the systemic (body) circulation.

Hint: Lewd Angry Artists Always Create Very Very Vivid Realities

Answer 1

Lewd Angry Artists Always Create Very Very Vivid Realities:

Left ventricle → Aorta → Arteries → Arterioles → Capillaries (body) → Venules → Veins → Vena cavae → Right atrium

Systemic circulation: oxygenated blood goes to the body and returns deoxygenated to the right atrium.

Question 2

Trace the flow of blood in the pulmonary (lung) circulation

Hint: Rowdy Pirates Parade Carefully Past Peaceful Lagoons

Answer 2

Rowdy Pirates Parade Carefully Past Peaceful Lagoons:

Right ventricle → Pulmonary arteries → Pulmonary arterioles → Capillaries (lungs) → Pulmonary venules → Pulmonary veins → Left atrium

This is pulmonary circulation: deoxygenated blood goes to the lungs and returns oxygenated to the left atrium.

Question 3

EBV Mechanism of Disease

Answer 3

KISS BLaRS

•	KISS – spread by saliva; enters through mouth/tonsils
•	BLa – infects naïve B cells → becomes latent in memory B cells
•	R S – reactivation in some memory B cells → virus shed again in saliva

Question 4

What are the main second-line defenses? (Hint: “CIC + Inflammation + Fever)

Answer 4

Second-line defenses include molecular and cellular systems:

Molecular – CIC: Cytokines (inflammation, fever, recruit leukocytes, antiviral), Iron-binding proteins (hide iron from bacteria), Complement (inflammation, opsonization, cytolysis).

Maybe: Cellular – Lymph: the lymphatic system and lymphoid tissues (nodes, spleen, MALT, thymus, bone marrow) that filter fluid and screen for foreign agents.

Question 5

Antimicrobial peptides (AMPs) - what do they do, how do they do it, and where are they found?

Answer 5

Proteins that destroy a wide spectrum of viruses, parasites, bacteria, and fungi as part of first line defenses

Directly target pathogens by disrupting their plasma membrane and/or cell wall; can also target intracellular components and processes.

**Immune modulation: **AMPs can stimulate leukocytes, contributing to the overall immune response.

Neutrophils release potent antimicrobile peptides

Mast cells contain diverse enzymes & AMPs in their granules

Part of first line (chemical) defenses

*Also stored in granules of neutrophils and other leukocytes as part of second-line cellular defenses.

Question 6

What does each branch do (innate vs adaptive), and how do they interact?

Answer 6

Innate: barriers plus internal defenses like phagocytes, NK cells, inflammation, fever, complement, and interferons.

Adaptive: B cells, T cells, and antibodies that provide highly specific, long-lasting protection; together they form the 3rd line of defense. Interaction: innate responds first and helps activate/shape adaptive responses, while adaptive enhances and backs up innate defenses when needed.

Question 7

What is fever in terms of immunity, and why is it considered a protective innate response?

Answer 7

Fever is a systemic innate immune response in which the hypothalamus raises the body’s temperature set point. It is protective because it speeds up immune reactions and tissue repair and helps inhibit the growth of many temperature-sensitive pathogens.

Pathway: Pyrogens -> hypothalamus -> prostaglandins -> higher set point -> fever.

Question 8

Describe the basic process of inflammation and list its three main functions (Hint: ‘CER’).

Answer 8

Inflammation begins with vascular changes (vasodilation and increased permeability), followed by leukocyte recruitment (neutrophils then macrophages), and ends with resolution/repair as debris is cleared.

Three main functions: Containment of the injury or infection, Elimination of pathogens and dead cells, and initiation of Repair of damaged tissue.

Explanation: Remember the flow—vessels, leukocytes, repair—and the mnemonic CER: Contain, Eliminate, Repair.

Question 9

Granulocytes – list each type with its key appearance and main job (Hint: N-E-B-M).

Answer 9

Neutrophils – multi-lobed nucleus; highly phagocytic first responders against bacteria and viruses.

Eosinophils – bi-lobed nucleus with red-orange granules; attack parasites and participate in allergy/asthma.

Basophils – bi-lobed nucleus obscured by dark purple granules; release histamine in allergy and parasite responses.

Mast cells – round nucleus with dark granules, reside in tissues; mediate allergy, inflammation, and parasite defense.

Explanation: All four are granulocytes; remember the order with N-E-B-M (Never Eat Bad Meat).

Question 10

Agranulocytes – list each type with its key appearance and main job (Hint: M-D-L).

Answer 10

Monocytes → macrophages – large horseshoe-shaped nucleus; highly phagocytic, become macrophages that clean up and activate adaptive immunity.

Dendritic cells – ruffled membrane with long cytoplasmic extensions; highly phagocytic antigen-presenting cells that prime T cells.

Lymphocytes (NK, B, T) – small cells with large round nucleus; NK cells kill infected/tumor cells innately, B and T cells mediate adaptive immunity.

Explanation: M-D-L (My Dirty Lymphs) helps you recall Monocytes, Dendritic cells, and Lymphocytes as the agranulocytes.

Question 11

Briefly describe the overall roles of leukocytes (white blood cells) in immunity.

Answer 11

Patrol, eat, kill, and coordinate all arms of the immune response.

• Immune surveilliance
• Phagocytosis
• Release cytokines to coordinate inflammation and adaptive immunity.
• Include granulocytes and agranulocytes that together give rapid innate defense and help activate and sustain B- and T-cell responses.

Question 12

Use Table 11.2: Match each leukocytosis with the leukocyte increased and its typical noncancerous cause.

Answer 12

Neutrophilic leukocytosis – increased neutrophils; usually acute (sudden onset) bacterial infections.

Eosinophilia – increased eosinophils; allergy, asthma, or parasitic infections.

Basophilia – increased basophils; usually only seen with certain rare blood cancers (no common noncancer cause).

Monocytosis – increased monocytes; chronic infections or chronic inflammation.

Lymphocytosis – increased lymphocytes (often T or B cells); chronic infections/inflammation and viral infections.

Explanation: Remember N-E-B-M-L and link each cell type to its hallmark association: acute bacteria, allergy/parasite, blood cancers, chronic infection/inflammation, and viral/chronic conditions.

Question 13

What is the basic flow of fluid in the lymphatic system? (Hint: “PILB”)

Answer 13

Fluid moves

Plasma → Interstitial fluid → Lymph → Blood

Plasma = fluid inside blood vessels

Interstitial fluid = fluid in the interstitial space (the spaces around cells and vessels)

Lymph = interstitial fluid that has entered lymphatic vessels

Mnemonic: PILB – Plasma, Interstitial, Lymph, Blood.

Question 14

In a type I hypersensitivity reaction, what key events occur during post-sensitization exposure?

Answer 14

Same allergen comes back and binds to the IgE already on mast cells/basophils.

This cross-linking of IgE triggers the cells to degranulate.

Explanation: After sensitization, mast cells and basophils are pre-armed with IgE, so re-exposure rapidly cross-links IgE and activates these cells.

Question 15

In type I hypersensitivity, what is degranulation and why does it lead to rapid allergy symptoms?

Answer 15

Degranulation = release of pre-stored granules (e.g., histamine, other pro-inflammatory factors).

These mediators cause immediate allergy symptoms (vasodilation, leaky vessels, mucus, bronchospasm, itching, etc.).

Question 16

Sensitization (first exposure) vs. Post-Sensitization (Second Exposure)

Answer 16

First time: allergen → make IgE → IgE coats mast cells.

Next time: allergen grabs IgE on mast cells → cells explode their granules → fast allergy reaction.

Question 17

Which body systems are commonly involved in systemic anaphylaxis?

Answer 17

Skin, respiratory system, gastrointestinal system, cardiovascular system, and central nervous system.

Explanation: Systemic anaphylaxis is a body-wide type I reaction, so multiple organ systems show signs—especially skin plus respiratory and/or cardiovascular.

Question 18

How does the Rh factor change transfusion compatibility for a given ABO type?

Answer 18

Rh+ blood has the Rh antigen and can receive both Rh+ and Rh− of a compatible ABO type. Rh− blood lacks the Rh antigen and should receive only Rh− of a compatible ABO type.

Explanation: People who are Rh− can form anti-Rh antibodies, so giving them Rh+ red cells can cause a hemolytic transfusion reaction.

Question 19

Transfusion Compatibility and Reactions; incompatible transfused red blood cells cause a ___

Answer 19

Hemolytic transfusion reaction

– Lyses red blood cells
– Could kill the patient
– Signs and symptoms occur within hours
 Fever, chills, lower back pain, chest pain, tachycardia, reduced blood pressure
– No therapy to reverse a transfusion reaction or block it
once it starts
– Supportive care to reduce kidney failure

Question 20

ACID mnemonic

Answer 20

Mnemonic: ACID
*
A = Allergy (Type I)
*
C = Cytotoxic (Type II)
*
I = Immune Complex (Type III)
*
D = Delayed (Type IV)

Question 21

Summarize the 4 types of hypersensitivity (I–IV) in terms of main mediator, antigen type, timing, and typical examples. (Hint: “ACID”)

Answer 21

Type I – Allergy: IgE; soluble allergens; immediate (minutes); mast cell/basophil degranulation. Examples: food/drug allergy, atopic asthma, seasonal allergy, atopic dermatitis, insect-sting anaphylaxis.

Type II – Cytotoxic: IgG or IgM vs cell-surface or basement-membrane antigens; minutes–hours; causes cell lysis or dysfunction. Examples: hemolytic transfusion reaction, Rh incompatibility, autoimmune hemolytic anemia, Goodpasture syndrome, Graves’ disease, myasthenia gravis.

Type III – Immune complex: IgG or IgM + soluble antigens → immune complexes deposit in tissues; hours–days; complement activation and intense inflammation. Examples: serum sickness, lupus, some vasculitides, post-strep glomerulonephritis.

Type IV – Delayed: T cell–mediated (no antibodies); delayed onset (24–72 h); Th1 cells, macrophages, or cytotoxic T cells cause tissue damage. Examples: contact dermatitis (latex, nickel, poison ivy), TB skin test, chronic transplant rejection, celiac disease.

Explanation: Mnemonic ACID—Type I: Allergy; Type II: Cytotoxic; Type III: Immune complex; Type IV: Delayed (T cell).

Question 22

How do type II and type III hypersensitivity reactions differ in the antigens they target and where the damage occurs?

Answer 22

Think Type II = antigens on the cell surface; Type III = immune complexes stuck in tissues after they settle out of the blood.

Type II: antibodies (IgG/IgM) bind fixed antigens on specific cells or basement membranes → targeted cells are directly lysed or their function is altered (e.g., RBC destruction, receptor stimulation/blockade).

Type III: antibodies bind soluble antigens in the circulation → immune complexes form, become insoluble, and deposit in vessel walls and tissues, where they activate complement and attract neutrophils, causing inflammation (e.g., vasculitis, glomerulonephritis, serum sickness).

Question 23

What are the key features and classic examples of type IV (delayed) hypersensitivity?

Answer 23

Type IV is T cell–mediated (no antibodies), has a delayed onset (typically 24–72 hours after exposure), and involves Th1 cells, macrophages, and/or cytotoxic T cells causing localized tissue damage and inflammation.

Classic examples include contact dermatitis (latex, nickel, poison ivy), a positive TB skin test, some forms of transplant rejection, and celiac disease.

Explanation: When a question emphasizes delayed rash after contact or a delayed skin-test reaction requiring T cells and macrophages, it is pointing to type IV delayed hypersensitivity.

Question 24

What is human T lymphotropic virus (HTLV)

Answer 24

HTLV is an **oncogenic retrovirus spread by body fluids **and frequently goes unnoticed until blood screening or malignancy appears.

Question 25

Which bacterial species is one of the most common agents causing infective endocarditis, and why is it clinically important?

Answer 25

Staphylococcus aureus is one of the most common causes of infective endocarditis and is clinically important because it can rapidly damage heart valves and cause severe, acute disease. Explanation: S. aureus frequently enters the bloodstream from skin or devices and has a strong tendency to adhere to and destruct cardiac valves.

Question 26

For Lyme disease, what are the pathogen, typical transmission, classic early sign, and key long-term complications if the infection is not treated?

Answer 26

Lyme disease is a tick-borne spirochetal infection (Borrelia burgdorferi) recognized by the bull’s-eye rash and flu-like symptoms, and can progress to joint, heart, and nervous system involvement. Details: Pathogen: Borrelia burgdorferi (a spirochete bacterium); Transmission: bite of an infected Ixodes (deer) tick, especially in the Northeastern United States; Classic early sign: erythema migrans “bull’s-eye” rash with fever, headache, and fatigue; Complications: chronic arthritis, neurologic problems, irregular heartbeat, and myocarditis if untreated.

Question 27

Describe Invasive Candidiasis. Think: Is it opportunistic? Is it common? How does it present? Is it deadly?

Answer 27

* Invasive candidiasis = candidemia = Candida yeast in the bloodstream. * Typically opportunistic in immunocompromised or critically ill. * Most common systemic fungal infection in immunocompromised patients and 4th most common healthcare-associated bloodstream infection. * Presents like sepsis; untreated mortality ~25–40%.

Question 28

Which factors should you remember as true risk factors for sepsis, and which one from the homework question should you treat as not a typical risk factor?

Answer 28

Risk factors: chronic illnesses such as cancer, diabetes, AIDS, and cardiovascular disease; wounds; significant infections including nervous system infections; and recent surgery or invasive procedures. Not a typical risk factor: blunt force trauma without associated infection. Explanation: Sepsis arises from dysregulated responses to infection, so underlying disease, invasive procedures, and existing infections increase risk, whereas isolated blunt trauma does not by itself.

Question 29

Which clinical signs and associated findings should you associate with possible sepsis for this course?

Answer 29

**Diarrhea and vomiting; pale or mottled skin; sleepiness or extreme fatigue; confusion or delirium; lymphangitis (red streaking from an infection site);** and leukopenia or other abnormal white blood cell counts (to be confirmed with the professor for exam wording).

Question 30

How are the lymphatic and cardiovascular systems connected in terms of fluid movement and return to circulation?

Answer 30

The lymphatic system functions as a drainage and return pathway, collecting excess interstitial fluid derived from plasma and delivering it back into the cardiovascular system while also filtering it through immune tissues. Details: Plasma leaks from blood capillaries into interstitial spaces, where excess fluid enters lymphatic capillaries as lymph; lymphatic vessels then carry lymph through lymph nodes and MALT and ultimately return it to the venous blood near the large veins (e.g., subclavian veins).

Question 31

Define myocarditis, endocarditis, and pericarditis and link each term to the heart structure involved.

Answer 31

Myocarditis is inflammation of the myocardium (heart muscle); endocarditis is inflammation or infection of the endocardium, especially the heart valves; pericarditis is inflammation of the pericardium, the sac surrounding the heart. Explanation: The suffix -itis means inflammation, and the root tells you the layer: myo- (muscle), endo- (inner lining/valves), peri- (around the heart in the pericardial sac). ## Footnote Order: Peri, Epi, Myo, Endo

Question 32

Briefly define: MALT, and the spleen, focusing on what each filters or carries.

Answer 32

MALT (mucosa-associated lymphoid tissue) samples and protects mucosal surfaces such as the gut and respiratory tract; Spleen filters blood (not lymph), removing old red blood cells and screening blood for pathogens.

Question 33

Provide an overview of the roles of Lymph and lymphatic vessels, lymph nodes and MALT, and the spleen.

Answer 33

Lymph and lymphatic vessels handle excess interstitial fluid and return it to circulation; Lymph nodes and MALT filter lymph or mucosal drainage, while; The spleen uniquely filters blood directly.

Question 34

Which major arthropod vectors in this chapter are linked to which key systemic cardiovascular or lymphatic infections?

Answer 34

Mosquitoes: Zika, yellow fever, dengue, chikungunya, malaria (and others); Ticks: Lyme disease (Borrelia burgdorferi), tularemia, Rocky Mountain spotted fever (Rickettsia rickettsii); Fleas: Plague (Yersinia pestis).

Question 35

For Rocky Mountain spotted fever, what are the pathogen, main transmission route, and characteristic sign to remember?

Answer 35

RMSF is a tickborne rickettsial disease and a systemic infection of the cardiovascular and lymphatic systems.

Question 36

Which viruses in this chapter are classic systemic viral hemorrhagic fevers, and what two high-yield points should you remember about them?

Answer 36

Ebola, Marburg, and Lassa viruses cause hemorrhagic fevers with high mortality rates, and most cases occur in Africa.

Question 37

Name two common retrovirus cells, how are they transmitted, and the major diseases are they associated with.

Answer 37

HIV and HTLV are T cell–targeting viruses, both spread by body fluids, with HIV linked to AIDS and Kaposi sarcoma and HTLV linked to T cell leukemia and neurologic disease.

Question 38

How do normal microbiota foster health?

Answer 38

Colonization resistance & immune modulation They compete for nutrients/space and tune host immunity, limiting pathogen establishment.

Question 39

Which of the following outcomes is NOT a direct result of complement activation? A) Opsonization of pathogens B) Enhancement of the inflammatory response C) Direct lysis of pathogens D) Release of histamines by mast cells

Answer 39

Release of histamines by mast cells Explanation: **Complement mainly causes opsonization, inflammation, and lysis;** histamine release is classically from mast cells and IgE.

Question 40

What is the primary outcome of precipitation reactions involving soluble antigens and IgG or IgM antibodies?

Answer 40

Formation of immune complexes. Explanation: Precipitation reactions form antigen–antibody complexes that can then be cleared.

Question 41

Which of the following is NOT a function of IgG antibodies? A) Enhancing phagocytosis B) Triggering the complement system C) Promoting allergic reactions D) Neutralizing bacterial toxins

Answer 41

Promoting allergic reactions Explanation: IgG does opsonization, complement activation, and toxin neutralization; IgE drives most allergic reactions.

Question 42

Antibodies increase phagocytosis. They accomplish this by:

Answer 42

PAO Precipitating small, soluble antigens to make them readily detectible by phagocytes Causing agglutination of large antigens, such as bacterial cells Serving as opsonins, factors that bind a target antigen to tag it for phagocytosis.

Question 43

Compare IgG, IgA, IgM, and IgE in terms of their main location and 'job.' (Hint: 'GAMe of locations')

Answer 43

IgG: **G**estation,in blood/tissues and placenta; IgA: **A**irways, in mucosal surfaces and secretions; IgM: Ly**Mph**, blood, first made; IgE: Allergi**E**s -- bound to mast cells/basophils for allergy and parasites. IgD: Blood <1%, not much known

Question 44

High levels of IgG antibodies in a patient’s blood usually indicate what about the timing of infection or exposure?

Answer 44

That the patient is in the late stages of an infection or has had previous exposure to that antigen. Explanation: IgG dominates later and in secondary responses, reflecting past or ongoing but established exposure. First exposure (primary response): Always starts with IgM. Then class-switches mainly to IgG (systemic), or to IgA at mucosal surfaces, or IgE in allergy/parasites. So: IgM → IgG/IgA/IgE (depending on the situation). Later exposures (secondary response): IgG (or IgA/IgE) comes up fast and high, IgM is still made but is smaller and not the main player. Exam hook: “Order” is really IgM first, then switched isotypes (usually IgG, sometimes IgA or IgE) depending on the type/site of response.

Question 45

What is a primary immune response, and what are its key features?

Answer 45

Immune system’s first response to a new antigen. APCs activate T helper cells, which help activate B and T cells. B cells first make IgM, then IgG, and both B and T cells form memory cells for faster responses later.

Question 46

Compare Mast cells and Basophils (include locationa and role)

Answer 46

Both are involved in allergic reactions and parasite defense, releasing histamine and other mediators. Mast cells: Reside in tissues (especially skin, mucosa, near blood vessels); Act as tissue scouts (first responders in tissues). Basophils: Circulate in the blood—granulocytes that can enter tissues during inflammation.

Question 47

Complement

Answer 47

blood proteins that amplify immunity—bridge innate ↔ adaptive via a protease cascade. Key outcomes (IOC): Opsonization — C3b/C4b coat bugs for phagocytes. Inflammation/chemotaxis — C3a, C5a recruit/activate cells. Cytolysis — MAC forms pores and kills microbes.

Question 48

Compare a primary vs secondary response

Answer 48

Exam hook: primary = first time, slower, IgM-heavy; secondary = repeat, faster, stronger, IgG-heavy.

Question 49

How do normal microbiota help limit pathogens and shape immune responses? (Hint: “C-C-E-T”)

Answer 49

Normal microbiota: Crowd out pathogens by competing for space and nutrients. Make Chemicals (acids, bacteriocins) that inhibit or kill invaders. Modify the Environment (pH, O₂, nutrients) to favor friendly microbes. Train the immune system, helping it respond to real pathogens and maintain tolerance to harmless antigens. Explanation: Remember C-C-E-T: Crowd, Chemicals, Environment, Train—how microbiota act as a built-in barrier and immune “coach.”

Question 50

Describe normal, acute inflammation, which is essential for healing

Answer 50

Vessels dilate and get leaky → more blood, plasma, and leukocytes to the area. Mediators/chemical signals like histamine, kinins, eicosanoids, cytokines → turn on the response Neutrophils and macrophages contain and eliminate the problem, clearing microbes and debris → signals fade and tissue repair begins

Question 51

What happens when inflammation is unregulated or becomes chronic?

Answer 51

If chemical signals (histamine, kinins, eicosanoids, cytokines) of inflammation don't shut off → Blood vessels stay leaky, more fluid and cells keep entering → persistent swelling and irritation. Recruited leukocytes keep releasing enzymes and inflammatory mediators → nearby healthy tissue gets caught in the crossfire. Over time, this can lead to tissue damage, scarring/fibrosis, and loss of normal function in that organ + chronic diseases e.g., atherosclerosis, some autoimmune diseases

Question 52

When are endotoxins (Lipid A of LPS) mainly released from Gram-negative bacteria?

Answer 52

When the bacterial cell dies (lysis) LPS is part of the outer membrane and is liberated on lysis, provoking cytokine release → fever and possible shock.

Question 53

What early clinical sign commonly indicates endotoxin (LPS) exposure?

Answer 53

Endotoxin-induced fever LPS triggers macrophage cytokines (IL-1, TNF-α) that act on the hypothalamus to raise body temperature.

Question 54

Which bacterial component can trigger hypotension and septic shock when released?

Answer 54

Endotoxin (Lipid A of LPS) On Gram-negative lysis, lipid A drives cytokine release and vasodilation leading to endotoxic shock.

Question 55

What role do T helper cells play in antibody class switching?

Answer 55

They provide signals (cytokines and costimulation) to B cells that direct antibody class switching. Explanation: T helper cells 'coach' B cells with cytokines and costimulatory signals so they switch to the appropriate antibody class.

Question 56

What is fever and how does it work? (Hint: “PC-HBS”)

Answer 56

Fever is a systemic rise in body temperature **triggered by Pyrogens that cause Cytokine release **(IL-1, TNF, IFN-α). These **signal the Hypothalamus to raise the set point,** and the body responds with** Boosted metabolism, Shivering, and vasoconstriction**—changes that generally enhance immune defenses.

Question 57

What is the function of cytokines in the immune response (molecular second-line defense)?

Answer 57

Cytokines are signaling molecules that call in and regulate immune cells, specifically: * Stimulate inflammation * Stimulate tissue and blood vessel repair * Generate fever * Recruit leukocytes to fight infection * Promote leukocyte and lymphatic tissue development * Antiviral effects (interferons) * Immune system regulation/activation

Question 58

What are proinflammatory cytokines?

Answer 58

Proinflammatory cytokines are cytokines whose main function is to induce and amplify inflammation.

Question 59

What is a cytokine storm, and why is it dangerous?

Answer 59

A cytokine storm is an exaggerated cytokine response in which excessive cytokine levels trigger a self-destructive immune reaction, causing severe, sometimes irreversible tissue damage and a poorer prognosis (as in some severe COVID-19 cases). Explanation: When cytokine levels become excessive, a normally protective response turns into harmful systemic inflammation and organ injury.

Question 60

Which branch of the immune system produces antibodies?

Answer 60

Adaptive humoral response. Explanation: B cells differentiate into plasma cells that secrete antibodies as part of the humoral branch.

Question 61

Summarize third-line defenses (adaptive immunity) and their main stages. (Hint: “A-L-P-M”)

Answer 61

A – Antigen presentation: APCs (like dendritic cells) display antigen with MHC I or II. L – Lymphocyte activation: Specific T cytotoxic (CD8), T helper (CD4), and B cells are activated by the presented antigen plus signals. P – Proliferation & differentiation: Activated cells clonally expand into effector cells and memory T and B cells; B cells become plasma cells. M – Antigen elimination & memory: Effector Tc cells kill infected/cancer/transplant cells, Th cells release factors that help Tc and B cells, plasma cells secrete antibodies, and memory cells provide faster, stronger responses on re-exposure. Explanation: Remember A-L-P-M to walk through adaptive immunity: Antigen is shown, Lymphocytes are turned on, they Proliferate, then eliminate the antigen and leave Memory.

Question 62

Define: Helper T Cells (CD4+) Cytotoxic T Cells (CD8+) Memory T Cells

Answer 62

Helper T Cells (CD4+): Activate macrophages, B cells, cytotoxic T cells via cytokines; regulate immunity. Cytotoxic T Cells (CD8+): Kill virus-infected, cancerous, or damaged cells (perforin/granzyme). Memory T Cells: Persist for long-term protection; faster response on re-encounter.

Question 63

Name the three lines of defenses, subtypes, and general process

Answer 63

Question 64

What are the main features and functions of IgD?

Answer 64

IgD is a monomer found mainly on the surface of naïve B cells as a B-cell receptor (BCR). It helps B cells recognize antigen and start activation; only a small amount is found free in blood.

Question 65

Name and define the four categories of adaptive (humoral) immunity (natural vs artificial; passive vs active).

Answer 65

Naturally acquired active immunity: Infection naturally triggers the patient's own immune response; memory cells and antibodies form and provide long-term protection. Artificially acquired active immunity: Vaccination triggers an immune response; memory cells and antibodies form and provide long-term protection. Naturally acquired passive immunity: Patient receives antibodies by nonmedical means (e.g., maternal IgG across placenta, IgA in breast milk); no memory cells form; protection is temporary. Artificially acquired passive immunity: Patient receives protective antibodies as a medical treatment (e.g., antiserum, antivenom, immune globulin); no memory cells form; protection is temporary.

Question 66

Which categories of adaptive immunity give long-term protection, and which give only temporary protection? Why?

Answer 66

Long-term protection: Naturally acquired active and artificially acquired active immunity, because the patient's own immune system makes antibodies and memory cells. Temporary protection: Naturally acquired passive and artificially acquired passive immunity, because borrowed antibodies are cleared and no memory cells are made.

Question 67

Howo to remember Natural vs Artificial, Active vs Passive Immunity

Answer 67

**_Active vs Passive_** **Active = you act**: your own immune system makes antibodies and memory → long-term protection. **Passive = pre-made**: you receive antibodies made elsewhere → temporary protection. **_Natural vs artificial = how do you get them?_** **Natural = no needle** (everyday life, no medical procedure). **Artificial = assisted** (given on purpose by healthcare). -- **Quick phrase to remember all 4:** "Infections and Immunizations are Active; Moms and Meds are Passive." - Infections → naturally acquired active - Immunizations (vaccines) → artificially acquired active - Moms (placenta, breast milk) → naturally acquired passive - Meds (antiserum, antivenom, IVIG) → artificially acquired passive

Question 68

What is an "inappropriate" immune response (e.g. hypersensitivity)

Answer 68

Inappropriate immune reactions include those that are misdirected against intrinsic body components (self), leading to autoimmune disorders.

Question 69

Summarize the key points about Rh factor incompatibility and hemolytic disease of the newborn (HDN).

Answer 69

**HDN is a type II hypersensitivity where maternal IgG against Rh destroys fetal Rh⁺ RBCs; RhoGAM works by blocking sensitization after fetal blood leaks into maternal circulation.** Rh⁻ mother + Rh⁺ fetus → fetal RBCs may enter mom’s blood during first pregnancy/birth → mom becomes sensitized and makes IgG anti-Rh antibodies. In a later Rh⁺ pregnancy, maternal IgG anti-Rh crosses the placenta, attacks fetal Rh⁺ RBCs → hemolysis, severe fetal anemia, HDN. If a mother is already sensitized, HDN can’t be fully prevented; pregnancy is closely monitored and fetal transfusions may be needed. Prevention: give Rh(D) immunoglobulin (RhoGAM) to Rh⁻ women so they never become sensitized to Rh antigen.

Question 70

Provide examples of nonautoimmune type III hypersensitivities

Answer 70

antitoxins against toxins (e.g., botulism, anthrax, tetanus).

Question 71

Name the disease and microorganism for each of the following: Lassa fever, Ebola, Marburg virus disease, Rocky Mountain spotted fever, Lyme disease, Staphylococcal scalded skin syndrome, and tularemia.

Answer 71

Lassa fever: Lassa virus Ebola: Ebola virus Marburg virus disease (hemorrhagic fever): Marburg virus Rocky Mountain spotted fever (RMSF): Rickettsia rickettsii (a Rickettsia species) Lyme disease: Borrelia burgdorferi Staphylococcal scalded skin syndrome: Staphylococcus aureus Tularemia: Francisella tularensis Explanation: These are classic disease–agent pairs you are expected to recognize, especially the viral hemorrhagic fevers (Lassa, Ebola, Marburg) and the bacterial zoonoses (RMSF, Lyme, SSSS, tularemia).

Question 72

The 4 main leukocytes of the innate defense system are neutrophils, basophils, eosinophils, and mast cells. What are their main roles in our defense?

Answer 72

Neutrophils: Highly phagocytic, most abundant granulocytes; rapid first responders that primarily target bacteria and viruses. Eosinophils: Moderately phagocytic; important for fighting parasites and also involved in allergy/asthma. Basophils: Rare granulocytes that release histamine and other mediators, promoting inflammation and allergic responses. Mast cells: Tissue-resident granulocytes near body openings that act as sentinels; release histamine and other factors in allergy, inflammation, and parasite defense. Explanation: These granulocytes are key innate leukocytes—neutrophils and eosinophils focus on killing invaders (especially bacteria and parasites), while basophils and mast cells orchestrate inflammation and allergic responses at blood and tissue sites.

Question 73

Which of the following is an example of an autoimmune disorder? 1) Your patient is born with X-linked agammaglobulinemia. 2) After infection with, Campylobacter jejuni, your patient develops Guillain-Barré syndrome. 3) Following an untreated case of strep throat, your patient develops rheumatic heart disease. 4) Your juvenile patient develops Type I diabetes mellitus.

Answer 73

2) After infection with, Campylobacter jejuni, your patient develops Guillain-Barré syndrome. 3) Following an untreated case of strep throat, your patient develops rheumatic heart disease. 4) Your juvenile patient develops Type I diabetes mellitus.

Question 74

# Four Classes of Hypersensitivity Reactions:

Answer 74

Question 75

In a local type I allergic reaction (for example, a bee sting), what causes the redness and swelling at the site?

Answer 75

Redness and swelling are due to the release of histamine during degranulation of mast cells and basophils. Explanation: Histamine from degranulated mast cells and basophils causes vasodilation and increased vascular permeability, leading to redness and edema.

Question 76

Choose the false statement. In desensitization immune therapy, TH1 cells encourage specific B cells to make IgG against the allergen. Degranulation occurs when allergens bind IgE that is on the surface of mast cells or basophils. During sensitization, allergens trigger IgE production. IgG binds to the surface of mast cells and basophils.

Answer 76

IgG binds to the surface of mast cells and basophils. Explanation: It is IgE—not IgG—that binds mast cells and basophils in type I hypersensitivity.

Question 77

Which of the following is an example of a non-autoimmune type IV hypersensitivity? Graft-versus-host disease Hashimoto thyroiditis Guillain-Barré syndrome Celiac disease

Answer 77

Graft-versus-host disease. Explanation: GVHD is a T cell–mediated (type IV) reaction where donor T cells attack host tissues; the other listed conditions are autoimmune type IV diseases.

Question 78

In IgE-mediated allergy, which cells make IgE, which cells does it bind, and what drug class treats the histamine effects?

Answer 78

B cells make IgE; it binds mast cells and basophils; symptoms are treated with antihistamines. Explanation: IgE from B cells arms mast cells/basophils for degranulation, and antihistamines block the downstream histamine receptors.

Question 79

Dengue fever is a ___________ viral ______ infection.

Answer 79

Dengue fever is a vector-borne viral systemic infection.

Question 80

Trace the full flow of blood, starting and ending at the vena cavae.

Answer 80

Vena cavae → right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary arteries → lungs → pulmonary veins → left atrium → mitral/bicuspid valve → left ventricle → aortic valve → aorta → systemic circulation → back to vena cavae.

Question 81

Why is the left ventricle more muscular than the right ventricle?

Answer 81

Left ventricle: pumps at high pressure to the whole body → thicker wall. Right ventricle: only pumps to low-pressure lungs → thinner wall.

Question 82

How is the cardiovascular system “closed” and the lymphatic system “open”?

Answer 82

Cardiovascular: closed loop of vessels; blood stays inside unless trauma. Lymphatic: open-ended lymph capillaries start in tissues and collect excess interstitial fluid as lymph.

Question 83

What is a retrovirus, and which 2 do you need to know?

Answer 83

RNA virus that uses reverse transcriptase to make DNA and integrate into host genome. Key examples: HIV and HTLV (both infect T cells).

Question 84

List the 3 main clinical stages of HIV infection.

Answer 84

1) Acute HIV: high viral load, flu-like illness, antibodies not yet detectable. 2) Chronic/latent (clinically asymptomatic): low-level replication; person often feels well. 3) AIDS: very low CD4 T helper cells; opportunistic infections and cancers.