1
Q
Trace the flow of blood in the systemic (body) circulation.
Hint: Lewd Angry Artists Always Create Very Very Vivid Realities
A
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.
2
Q
Trace the flow of blood in the pulmonary (lung) circulation
Hint: Rowdy Pirates Parade Carefully Past Peaceful Lagoons
A
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.
3
Q
Kissing Disease:
1) Common name
2) Etyilogical Agent and Family
3) What diseases does it lead to?
4) Transmission
5) Signs and symptoms
6) At-risk groups
A
1) Mononucleosis
2) Epstein-Barr virus (E B V); Herpesviridae family
3) → Mononucleosis (and possibly Burkitt’s Lymphoma)
4) Bodily fluids (e.g., saliva), sharing personal items (e.g., toothbrushes, eating utensils, drinks)
5) Asymptomatic or mild (e.g., fever, sore throat)
Mononucleosis is a more severe form of infection: Extreme fatigue, swollen lymph nodes in neck and armpit, severe sore throat, headache, splenomegaly, and rash
6) Teens and young adults at highest risk of having EBV infection progress to mono
90% of U.S. population experiences an EBV infection at some point
4
Q
EBV Mechanism of Disease
A
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
5
Q
High levels of IgM antibodies in a patient’s blood usually indicate what about infection timing?
A
Recent exposure to a pathogen or antigen (early stages of infection).
Explanation: IgM rises early in a primary response, so high IgM suggests recent or current new exposure.
6
Q
In two words provide the structure and function for neutrophils, eosinophils, basophils, mast cells, monocytes, macrophages, and dendritic cells.
A
Neutro: “multi-lobed / first phagocyte”
Eosino: “red granules / parasites”
Baso (bilobed) /Mast: “dark granules / histamine”
Mono: “kidney nucleus / precursor”
Macro: “large / phagocyte + cytokines”
Dendritic: “branched / APC”
7
Q
What is lysozyme, and how does it help protect the body?
A
Antimicrobial enzyme that breaks down peptidoglycan in bacterial cell walls, causing bacterial lysis.
It’s part of innate immunity and is found in secretions like mucus, saliva, sweat, and tears, where it helps protect surfaces from infection.
8
Q
Name the three lines of defenses, subtypes, and general process
A
9
Q
Describe the first line defenses (innate immunity) and provide examples
A
**Physical barriers – actual structures
**- Intact skin (epidermis)
- Mucous membranes lining respiratory, GI, GU tracts
**Mechanical barriers – movement/flow that physically removes microbes
**- Mucociliary escalator in the respiratory tract (cilia + mucus)
- Flushing action of tears, saliva, urine
- Peristalsis in the intestines
**Chemical barriers – substances that inhibit or kill microbes
**- Lysozyme in tears, saliva, mucus
- Stomach acid (low pH), vaginal acidity
- Sebum, fatty acids, salt in sweat
10
Q
What are the main second-line defenses? (Hint: “CIC + Inflammation + Fever)
A
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.
11
Q
Opsonization
A
the process by which a pathogen, a damaged cell, or a foreign particle is coated with specific proteins, called opsonins, to enhance its recognition and elimination by immune cells (phagocytes).
12
Q
Summarize third-line defenses (adaptive immunity) and their main stages. (Hint: “A-L-P-M”)
A
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.
13
Q
Antimicrobial peptides (AMPs) - what do they do, how do they do it, and where are they found?
A
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.
14
Q
On which day does the production of IgG occur in the secondary response?
A
Day 5
15
Q
What does “non-specific” mean in innate immunity?
A
What “non-specific” means in this context
Innate (2nd line) cells and molecules:
Recognize patterns that are shared by many microbes (PAMPs like LPS, peptidoglycan) or by damaged host cells (DAMPs).
Use fixed receptors you were born with (pattern-recognition receptors, PRRs).
Respond the same way to a wide range of invaders once activated: inflammation, phagocytosis, complement activation, fever, etc.
So yes, inflammation is very local (redness, heat, swelling exactly where the cut is), but the type of response is the same whether that cut has Staph, Strep, or E. coli. It’s targeted to the site, but not customized to the exact microbe’s antigen.
16
Q
What are the first-line defenses, with examples? (Hint: “MCP”)
A
First-line defenses are MCP:
Mechanical – flushing/trapping (tears, mucus + cilia, urine)
Chemical – hostile substances (lysozyme, stomach acid, AMPs)
Physical – skin as a barrier.
17
Q
What are the general features of innate immunity?
A
Fast, first line of defense you’re born with.
Immediate and nonspecific, recognizes many pathogens without prior exposure, eliminates invaders, and maintains self-tolerance (distinguishes self from non-self).
18
Q
Specificity: Describe differences in innate vs adaptive immunity
A
Innate 2nd line = “local and focused, but pattern-based and the same playbook for many microbes” → non-specific.
Adaptive 3rd line = “designed for this exact antigen and better/faster next time” → specific.
You can think of it like this:
Innate = firefighters going to any burning building and using the same hoses and foam.
Adaptive = a locksmith making a custom key for one specific lock.
19
Q
Compare innate vs adaptive immunity (big picture) — origin, speed, specificity, memory, and which line of defense each branch represents
A
Innate: inborn, fast, non-specific, no memory; present in all eukaryotes; 1st and 2nd lines of defense.
Adaptive: acquired over time, slower on first exposure (about 4–7 days), antigen-specific, has memory; only in vertebrates; 3rd line of defense.
20
Q
What does each branch do (innate vs adaptive), and how do they interact?
A
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.
21
Q
Which cells are directly responsible for the rapid, stronger secondary antibody (humoral) response to a previously encountered antigen?
A) Memory B cells and plasma cells
B) Plasma cells
C) Memory B cells
D) T cells
A
Memory B cells and plasma cells
Explanation: In a secondary antibody response, memory B cells quickly recognize the antigen and proliferate, differentiating into plasma cells that secrete large amounts of high-affinity antibodies.
T cells also form memory cells, but they do not produce antibodies, so they are not the best answer here.
22
Q
What is fever in terms of immunity, and why is it considered a protective innate response?
A
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.
23
Q
Outline the basic activation pathway of fever (from pyrogens to raised body temperature).
A
Pyrogens -> hypothalamus -> prostaglandins -> higher set point -> fever.
Pyrogens such as bacterial toxins and cytokines from macrophages stimulate the hypothalamus to produce prostaglandins, which reset the body’s thermostat to a higher set point so the body generates and conserves heat until core temperature reaches the new set point.
24
Q
Describe the basic process of inflammation and list its three main functions (Hint: ‘CER’).
A
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.
25
What are the cardinal signs of inflammation, and what happens if inflammation is unregulated or chronic?
The cardinal signs of inflammation are redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).
If inflammation is unregulated or becomes chronic, the same processes that protect and heal can cause ongoing tissue damage and contribute to chronic disease.
Explanation: This card ties the classic signs you must memorize to the concept that uncontrolled inflammation harms host tissues.
26
Granulocytes – list each type with its key appearance and main job (Hint: N-E-B-M).
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).
27
Agranulocytes – list each type with its key appearance and main job (Hint: M-D-L).
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.
28
Briefly describe the overall roles of leukocytes (white blood cells) in immunity.
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.
29
What is leukocytosis?
Leukocytosis is an elevated white blood cell count in the blood, usually due to an increase in one specific type of leukocyte in response to infection, inflammation, stress, or less commonly blood cancers.
Explanation: The suffix -cytosis means too many cells; here it signals that WBCs are abnormally high, often indicating an active disease process.
30
Use Table 11.2: Match each leukocytosis with the leukocyte increased and its typical noncancerous cause.
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.
31
What is the basic flow of fluid in the lymphatic system? (Hint: "PILB")
Core flow to memorize (names change):
Plasma → Interstitial fluid → Lymph → Blood
In words (high yield):
Blood plasma in blood capillaries is filtered → becomes interstitial fluid in the tissues → some of that enters lymphatic capillaries and is now called lymph → lymph flows through lymphatic vessels → lymph nodes → lymphatic ducts (thoracic / right lymphatic) → empties into subclavian veins → back to blood (plasma).
You can remember: PILB = Plasma → Interstitial → Lymph → Blood, with “vessels, nodes, ducts, veins” in the middle.
32
Differentiate between localized and systemic anaphylaxis
Localized anaphylaxis
- Isolated symptoms (e.g., watery eyes, runny nose, confined rash)
Systemic anaphylaxis
- System-wide response
- Anaphylactic shock
- Potentially life-threatening response
- Treatment usually involves administration of epinephrine
33
What are the four main clinical categories of type I hypersensitivity reactions? (Hint: "FASt AD")
Food and drug allergies; atopic asthma; seasonal allergies; atopic dermatitis (also stings, local or systemic)
Explanation: These are the main IgE-mediated allergy presentations to recognize; mnemonic—FASt AD: Food/drug, Atopic asthma, Seasonal, Atopic Dermatitis.
34
What are the key signs and symptoms of type I food and drug allergies?
Hives/rash/skin swelling; diarrhea or stomach pain; odd taste or feeling in the mouth; tingling or itchy throat; itchy, watery, red eyes; sneezing; cough or congestion.
Explanation: Food and drug allergies often affect the skin, gastrointestinal tract, eyes, and upper respiratory tract shortly after exposure.
35
What are the key signs and symptoms of atopic asthma as a type I hypersensitivity?
Cough; shortness of breath (dyspnea); chest tightness; wheezing.
Explanation: Atopic asthma is mainly a lower-respiratory manifestation of type I hypersensitivity, causing bronchoconstriction and airflow limitation.
36
What are the key signs and symptoms of seasonal allergies (allergic rhinitis) as a type I hypersensitivity?
Cold-like symptoms -- usually upper respiratory (sneezing, cough, congestion, runny nose, postnasal drip); itchy, watery, red eyes; itchy sinuses; itchy or sore throat; ear congestion -- p
37
What is the characteristic presentation of atopic dermatitis as a type I hypersensitivity?
Persistent, dry, itchy, scaly skin rash.
Explanation: Atopic dermatitis (eczema) is a chronic, pruritic, scaly rash often associated with other atopic conditions such as asthma and allergies.
38
In a type I hypersensitivity reaction, what key events occur during post-sensitization exposure?
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.
39
In type I hypersensitivity, what is degranulation and why does it lead to rapid allergy symptoms?
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.).
40
Sensitization (first exposure) vs. Post-Sensitization (Second Exposure)
First time: allergen → make IgE → IgE coats mast cells.
Next time: allergen grabs IgE on mast cells → cells explode their granules → fast allergy reaction.
41
Which body systems are commonly involved in systemic anaphylaxis?
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.
42
What are the key skin signs of systemic anaphylaxis?
**Hives (urticaria); itching (pruritus); flushing; swelling (angioedema).**
Explanation: **Skin findings are the most common and often appear first**, making them an important early clue to anaphylaxis.
43
What are the key respiratory signs of systemic anaphylaxis?
Swollen or itchy throat; hoarseness; shortness of breath (dyspnea); wheezing or bronchospasm.
Explanation: Airway swelling and bronchospasm can quickly become life-threatening and are a major reason anaphylaxis is an emergency.
44
What are the key gastrointestinal signs of systemic anaphylaxis?
Nausea; vomiting; cramping or abdominal pain; diarrhea.
Explanation: Gastrointestinal symptoms often accompany food-triggered anaphylaxis and help distinguish it from a simple localized allergy.
45
What are the key cardiovascular signs of systemic anaphylaxis?
Chest pain; decreased blood pressure; rapid heart rate (tachycardia); weak pulse.
Explanation: Profound vasodilation and fluid leakage from vessels cause hypotension and tachycardia, which can progress to shock.
46
What are the key central nervous system symptoms that can appear in systemic anaphylaxis?
Uneasiness or anxiety; dizziness; fainting (syncope); confusion; intense headache.
Explanation: CNS symptoms often result from low blood pressure and poor perfusion and signal that anaphylaxis is affecting circulation and the brain.
47
For the ABO system (ignoring Rh), which antigens does each blood type have, and which types can each receive from?
Type A: A antigen; can receive A, O. Type B: B antigen; can receive B, O. Type AB: A and B antigens; can receive A, B, AB, O. Type O: no A or B antigens; can receive only O.
Explanation: A recipient can receive only red cells that do not introduce a new A or B antigen they lack, or they will mount an antibody-mediated reaction.
48
How does the Rh factor change transfusion compatibility for a given ABO type?
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.
49
Which blood type is the universal donor and which is the universal recipient, and why?
O− is the universal donor because its red cells have no A, B, or Rh antigens. AB+ is the universal recipient because its red cells have A, B, and Rh antigens and therefore the person lacks antibodies against any of them.
Explanation: Transfusion reactions occur when donor cells have antigens the recipient does not have; O− introduces no new antigens, while AB+ already expresses all three major antigens.
50
# Transfusion compatibility table review
51
Summarize the key points about Rh factor incompatibility and hemolytic disease of the newborn (HDN).
**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.
52
Urticaria
Hives: The raised, itchy, red wheals seen after an allergic reaction
53
Redness and swelling at a bee sting site are primarily caused by which mediator and which cells... What type of reaction is this?
Histamine released during mast cell/basophil degranulation.
Type I (IgE-mediated, immediate) hypersensitivity.
54
Which OTC medication is most appropriate to relieve itching and swelling from a bee sting
antihistamines — first-line for mile local reactions
55
Transfusion Compatibility and Reactions; incompatible transfused red blood cells cause a ___
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
56
List and describe the steps in a transfusion reaction
“Antibodies Connect, Hemoglobin Kills.”
1. Antibodies bind antigen
2. Connect with complement (Antigen–antibody complex binds complement)
3. Hemolysis releases hemoglobin
4. Free hemoglobin Kills (damages) kidneys.
Explanation: Recipient antibodies first bind donor RBC antigens, then activate complement, which lyses the RBCs (hemolysis) and releases hemoglobin that can precipitate in renal tubules and injure the kidneys.
57
Define hypersensitivity.
Discuss whether it localized or systemic.
Inappropriate immune responses
(e.g., allergy, cytotoxic, immune complex, delayed)
– Can be localized and therefore restricted to a given tissue, or;
– Can be systemic and spread through the body , affecting multiple tissues and organ systems
58
# Which of the following is an example of a hypersensitivity reaction?
1) Two days following administration of a tuberculin skin test, the patient has a large induration.
2) Upon receiving type B blood, a patient with type A blood has disseminated intravascular coagulation.
3) Your patient has allergic rhinitis, prompted by exposure to pollen.
4) Following an influenza vaccination, a patient is exposed to the flu virus and makes high titers of IgG antibody.
1) Two days following administration of a tuberculin skin test, the patient has a large induration.
2) Upon receiving type B blood, a patient with type A blood has disseminated intravascular coagulation.
3) Your patient has allergic rhinitis, prompted by exposure to pollen.
59
What is an "inappropriate" immune response (e.g. hypersensitivity)
Inappropriate immune reactions include those that are misdirected against intrinsic body components (self), leading to autoimmune disorders.
60
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.
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.
61
ACID mnemonic
Mnemonic: ACID
*
A = Allergy (Type I)
*
C = Cytotoxic (Type II)
*
I = Immune Complex (Type III)
*
D = Delayed (Type IV)
62
# Four Classes of Hypersensitivity Reactions:
63
Which types of hypersensitivities include autoimmune responses?
Types II, III, and IV include autoimmune responses. Type I does not.
64
Characteristics and Mechanism of Type I Hypersensitivity (Allergies)
Characteristics
* Mediated by: IgE (Immunoglobulin E)
* Not autoimmune
* Triggered by allergens (antigens that trigger IgE production)
* Can be localized or systemic
Mechanism
1. Sensitization stage: Allergen exposure triggers IgE production by plasma cells
2. IgE binding: IgE binds to surface of mast cells or basophils
3. Post-sensitization exposure: Allergen binds to IgE anchored to mast cells/basophils
4. Degranulation: Triggers release of proinflammatory factors (histamine, leukotrienes, prostaglandins)
65
Give several examples of autoimmune type II hypersensitivities and briefly state what is targeted in each.
Autoimmune hemolytic anemia – RBCs
Rheumatic heart disease – heart valves
Goodpasture syndrome – basement membrane in kidney and lung
Graves’ disease – TSH receptor
Myasthenia gravis – ACh receptors at neuromuscular junction
66
What are the key characteristics of type II (cytotoxic) hypersensitivity?
Mediated by IgG or IgM antibodies; targets nonsoluble antigens on cell surfaces or extracellular matrix; often involves autoimmune responses; main outcome is cell lysis (destruction).
Explanation: In type II reactions, IgG or IgM antibodies bind nonsoluble/fixed antigens on cells or tissues, marking them for destruction and causing cytotoxic damage.
67
Describe the basic mechanism of type II (cytotoxic) hypersensitivity.
Host antibodies recognize and tag target cells with antigens.
Cytotoxic destruction then occurs via (1) complement-dependent cytolysis, where complement forms a membrane attack complex (MAC) and lyses the cell, and/or (2) complement-independent cytolysis, where leukocytes such as NK cells bind the antibody-tagged cell and trigger its lysis.
68
What are the key features of type III hypersensitivities, and give a nonautoimmune example.
IgG or IgM bind soluble antigens; excess immune complexes form; complexes become insoluble and deposit in tissues; deposits activate complement and cause strong inflammation; n
Nonautoimmune example: antitoxins against toxins (e.g., botulism, anthrax, tetanus).
Explanation: Type III reactions are driven by deposited immune complexes that trigger complement activation and inflammation; antitoxin therapies illustrate antibodies binding soluble targets outside of autoimmunity.
69
Provide examples of nonautoimmune type III hypersensitivities
antitoxins against toxins (e.g., botulism, anthrax, tetanus).
70
Which type of hypersensitivity does this describe:
IgG or IgM bind self antigens on specific cells or basement membranes, leading to cell damage or altered function in the targeted tissues.
Autoimmune type II hypersensitivity
71
Summarize the 4 types of hypersensitivity (I–IV) in terms of main mediator, antigen type, timing, and typical examples. (Hint: "ACID")
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).
72
How do type II and type III hypersensitivity reactions differ in the antigens they target and where the damage occurs?
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).
73
What are the key features and classic examples of type IV (delayed) hypersensitivity?
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.**
74
Anaphylaxis
Anaphylaxis is a severe, potentially life-threatening allergic reaction that can be caused by triggers like certain foods, medications, insect stings, or exercise.
Symptoms appear rapidly and can include hives, swelling of the lips or tongue, wheezing, difficulty breathing, low blood pressure, dizziness, and confusion. Immediate medical attention is critical; the first step is to use an epinephrine auto-injector if available, followed by calling emergency services.
75
**LOW PRIORITY** For yellow fever, what are the pathogen type, main vector, characteristic sign that gives the disease its name, and main prevention strategy?
Pathogen type: yellow fever virus (a viral hemorrhagic fever);
Vector: Aedes aegypti mosquito;
Key sign: jaundice (yellowing of skin/eyes) with high fever;
Prevention: mosquito control (drain standing water, nets, avoid bites).
Explanation: Yellow fever is a mosquito-borne viral infection where jaundice creates the classic “yellow” appearance; controlling Aedes mosquitoes is the main way to prevent transmission.
76
For Zika virus, how long should a couple wait to try to conceive if both partners had symptomatic Zika after travel, and why?
Six months, because the male partner must wait at least 6 months after infection to ensure viral clearance and prevent vertical transmission.
Explanation: Lecture guidance says women wait ≥8 weeks, but men wait 6 months; when both are infected, the longer 6-month male waiting period controls the risk of congenital Zika syndrome.
77
For Zika, what is the caustive agent, the pathogen type, main routes of transmission, typical symptoms, and key complication to remember?
Causative agent: Zika virus, a single-stranded, RNA genome
Pathogen: Zika virus (a Flavivirus);
Transmission: Aedes mosquitoes, sexual contact, blood/bodily fluids, and vertical (mother to fetus);
Symptoms: often mild fever, rash, conjunctivitis, joint pain, or asymptomatic;
Key complication: **congenital microcephaly and other birth defects.**
Explanation: Zika is usually mild in adults but dangerous in pregnancy because transplacental infection can cause severe fetal brain and developmental abnormalities.
78
What is human T lymphotropic virus (HTLV)
HTLV is an **oncogenic retrovirus spread by body fluids **and frequently goes unnoticed until blood screening or malignancy appears.
79
In acute HIV infection, what is the key laboratory testing issue that characterizes the early “window period”?
The virus is present with a high viral load, but HIV antibodies are not yet detectable in the patient’s serum.
Explanation: During acute infection, standard antibody tests can be negative despite active infection and high infectivity because the immune system has not produced enough detectable antibody.
80
Which bacterial species is one of the most common agents causing infective endocarditis, and why is it clinically important?
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.
81
Which clinical or device-related sources commonly lead to bacteremia that can seed endocarditis in at-risk patients, and which source from your homework was not considered typical?
Common sources: venous catheters, urinary tract infections, skin abscesses, and infected gums;
| Non-typical source in the homework question: pneumonia.
82
Dental procedures that traumatize gums can introduce bacteria into the blood, which then adhere to abnormal or prosthetic valves and cause
Bacterial endocarditis.
83
For Lyme disease, what are the pathogen, typical transmission, classic early sign, and key long-term complications if the infection is not treated?
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.
84
For invasive candidiasis (candidemia), which hospital-related procedures or devices are important ways the infection can be contracted?
Surgery, central venous catheters, kidney dialysis, and intravenous lines are all important ways invasive candidiasis can be contracted.
| especially in immunocompromised patients
85
Describe Invasive Candidiasis.
Think: Is it opportunistic? Is it common? How does it present? Is it deadly?
* 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%.
86
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?
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.
87
Which clinical signs and associated findings should you associate with possible sepsis for this course?
**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).
88
How are the lymphatic and cardiovascular systems connected in terms of fluid movement and return to circulation?
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).
89
What is sepsis, and how does it differ from septic shock in big-picture exam terms?
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response (systemic response) to infection;
Septic shock is a severe form of sepsis with dangerously low blood pressure and circulatory failure despite fluids, often leading to multi-organ failure.
90
Define myocarditis, endocarditis, and pericarditis and link each term to the heart structure involved.
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
91
List the layers of the heart from outermost to innermost and give a brief function for each.
Pericardium: outer protective sac around the heart;
epicardium: outer surface layer of the heart wall;
myocardium: thick muscle layer that contracts to pump blood; endocardium: smooth inner lining of chambers and valves in contact with blood.
Explanation: From outside in, remember Pericardium (sac), Epicardium (surface), Myocardium (muscle), Endocardium (end/inside lining).
92
Briefly define: MALT, and the spleen, focusing on what each filters or carries.
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.
93
Provide an overview of the roles of Lymph and lymphatic vessels, lymph nodes and MALT, and the spleen.
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.
94
Which major arthropod vectors in this chapter are linked to which key systemic cardiovascular or lymphatic infections?
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).
95
**LOW PRIORITY**Which pathogens cause plague and tularemia, and how are they broadly classified in this chapter?
Plague is caused by Yersinia pestis and tularemia is caused by Francisella tularensis; both are zoonotic systemic bacterial infections.
Both are rare zoonotic bacteria that can cause systemic cardiovascular or lymphatic disease.
96
For Rocky Mountain spotted fever, what are the pathogen, main transmission route, and characteristic sign to remember?
RMSF is a tickborne rickettsial disease and a systemic infection of the cardiovascular and lymphatic systems.
97
Name the mosquito-borne, systemic viral infection emphasized in this chapter what key feature or complication is linked to it.
Zika virus: usually mild but can cause microcephaly when vertically transmitted.
| Transmitted by mosquitoues
98
Dengue fever is a ___________ viral ______ infection.
Dengue fever is a vector-borne viral systemic infection.
99
Which viruses in this chapter are classic systemic viral hemorrhagic fevers, and what two high-yield points should you remember about them?
Ebola, Marburg, and Lassa viruses cause hemorrhagic fevers with high mortality rates, and most cases occur in Africa.
100
Name two common retrovirus cells, how are they transmitted, and the major diseases are they associated with.
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.
101
True/False:
Adaptive immunity is specific and tailored to each pathogen; innate responses are general and consistent.
True: Adaptive immunity is specific and tailored to each pathogen; innate responses are general and consistent.
102
How do normal microbiota foster health?
Colonization resistance & immune modulation
They compete for nutrients/space and tune host immunity, limiting pathogen establishment.
103
All of the cardinal signs of inflammation can essentially be linked to ______
Vascular changes.
Explanation: Vasodilation and increased permeability cause redness, heat, swelling, and pain at the inflamed site.
104
How do some viruses evade the host’s antibody-mediated immune response?
Antigenic variation (e.g., antigenic drift/shift) changes viral surface epitopes so existing antibodies can’t bind/neutralize
105
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
Release of histamines by mast cells
Explanation: **Complement mainly causes opsonization, inflammation, and lysis;** histamine release is classically from mast cells and IgE.
106
What is the primary outcome of precipitation reactions involving soluble antigens and IgG or IgM antibodies?
Formation of immune complexes.
Explanation: Precipitation reactions form antigen–antibody complexes that can then be cleared.
107
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
Promoting allergic reactions
Explanation: IgG does opsonization, complement activation, and toxin neutralization; IgE drives most allergic reactions.
108
Immunoglobulins
Another name for antibodies;
Glycoprotein molecules made by plasma cells (activated B cells);
They are essential participants in the humoral immune response.
109
Antibodies increase phagocytosis. They accomplish this by:
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.
110
Describe antibody production during a primary response
IgM is first antibody produced in the course of infection and is characterized by its large pentamer structure, which limits its migration
111
Are MHC (Major Histocompatibility Complex) II molecules part of the Y-shaped antibody structure? If not, what main components are?
No. A typical antibody is a Y-shaped protein built from two heavy and two light chains;
MHC II is a separate antigen-presenting molecule on some immune cells.
112
What is antibody isotype (class) switching and what is the benefit?
Changing the antibody isotype that is made while keeping the same antigen specificity.
Benefit: It expands the operational capacity of antibodies without changing their antigen specificity.
Explanation: Class switching alters the constant region (e.g., IgM to IgG/IgA/IgE), giving new effector functions but preserving which antigen is recognized.
113
Describe the main features and functions of IgG.
Features: Monomer; most abundant in blood/tissues; crosses placenta; dominates secondary response.
Functions: Neutralization, opsonization, complement activation; long-term and fetal immunity.
114
Describe the main features and functions of IgA.
Features: Dimer in secretions (mucus, tears, saliva, breast milk); mucosal antibody.
Functions: Neutralizes and blocks pathogen adhesion on mucosal surfaces.
115
Describe the main features and functions of IgM.
Features: Pentamer in blood; first made in primary response.
Functions: Strong complement activation and agglutination; marker of recent infection.
116
Describe the main features and functions of IgE.
IgE = "AllergEEs" → allergies + anaphylaxis
Features: Monomer bound to mast cells/basophils.
Functions: Triggers allergy (histamine release) and defends against helminths
Desensitization therapy used for IgE
117
Compare IgG, IgA, IgM, and IgE in terms of their main location and 'job.' (Hint: 'GAMe of locations')
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
118
High levels of IgG antibodies in a patient’s blood usually indicate what about the timing of infection or exposure?
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.
119
What is a primary immune response, and what are its key features?
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.
120
Briefly compare a primary response to immunological memory
The primary response is slower and less effective, while immunological memory allows for a faster and more robust response upon re-exposure to the same antigen.
121
Immunological Memory
Long-lasting presence of memory B and T cells after an infection that, that, on re-exposure to the same antigen, trigger a faster, stronger IgG-dominant response that often prevents symptoms.
122
Describe the functions of each leukocyte:
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
| Hint: “Phagocytes Produce Mighty Defensive Responses.”
“Phagocytes Produce Mighty Defensive Responses.”
(builds off "Never Let Monkeys Eat Bananas")
Each word cues the action:
Phagocytes → Neutrophils (phagocytize bacteria)
Produce → Lymphocytes (produce antibodies)
Mighty → Monocytes (macrophages) (long-lived eaters)
Defensive → Eosinophils (defend against worms)
Responses → Basophils (release histamine/inflammatory response)
123
Compare Mast cells and Basophils (include locationa and role)
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.
124
Complement
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.
125
Compare a primary vs secondary response
Exam hook: primary = first time, slower, IgM-heavy;
secondary = repeat, faster, stronger, IgG-heavy.
126
Primary response
Triggered by first exposure to an antigen.
Slow: long lag phase (days) before antibodies appear.
Lower peak antibody level, mostly IgM first, then some IgG.
Naïve B and T cells are being activated and memory cells are being made.
127
Secondary (memory) response
Triggered by subsequent exposure to the same antigen.
Fast: very short lag phase, antibodies appear quickly.
Much higher peak, longer-lasting response, mostly IgG (or IgA/IgE depending on antigen).
Uses memory B and T cells, so it’s stronger, faster, and more specific.
128
How do normal microbiota help limit pathogens and shape immune responses? (Hint: “C-C-E-T”)
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.”
129
Describe normal, acute inflammation, which is essential for healing
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
130
What happens when inflammation is unregulated or becomes chronic?
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
131
Exam hook: Good vs. Bad Inflammation
Short, well-controlled inflammation = protective.
Long-lasting or poorly regulated inflammation = your own cells become “bystander casualties,” leading to tissue damage and disease.
132
When are endotoxins (Lipid A of LPS) mainly released from Gram-negative bacteria?
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.
133
What early clinical sign commonly indicates endotoxin (LPS) exposure?
Endotoxin-induced fever
LPS triggers macrophage cytokines (IL-1, TNF-α) that act on the hypothalamus to raise body temperature.
134
Which bacterial component can trigger hypotension and septic shock when released?
Endotoxin (Lipid A of LPS)
On Gram-negative lysis, lipid A drives cytokine release and vasodilation leading to endotoxic shock.
135
Which toxin type triggers massive, nonspecific T-cell activation and cytokine storm?
Superantigen
136
Choose which statement is correct about cancer:
A) Cancer cells release cytokines that can confuse immune cells
B) Cancer cells are immortal cells
C) Cancer is a disease that can be both genetic and acquired
D) All of the above
All of the above
137
What role do T helper cells play in antibody class switching?
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.
138
What molecules act as key signaling proteins that allow immune cells to communicate with one another?
Cytokines.
Explanation: Cytokines are soluble signaling proteins used for immune cell communication and coordination.
139
What is fever and how does it work? (Hint: “PC-HBS”)
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.
140
What is the function of cytokines in the immune response (molecular second-line defense)?
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
141
What are proinflammatory cytokines?
Proinflammatory cytokines are cytokines whose main function is to induce and amplify inflammation.
142
What is a cytokine storm, and why is it dangerous?
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.
143
Why are cytokines important in clinical practice?
Cytokines are key immune mediators that can serve as diagnostic and prognostic markers and as therapeutic targets; for example, drugs that block cytokine actions (such as anti–IL-6 therapy like tocilizumab) can be used to treat cytokine storms in severe disease.
Explanation: Because cytokine levels both reflect and drive disease activity, they can be measured and pharmacologically modulated to guide and improve patient care.
144
Which branch of the immune system produces antibodies?
Adaptive humoral response.
Explanation: B cells differentiate into plasma cells that secrete antibodies as part of the humoral branch.
145
Which cell type is primarily responsible for phagocytosing bacteria and releasing enzymes to combat infection?
Neutrophils.
Explanation: Neutrophils are fast-responding phagocytes that ingest bacteria and release killing enzymes.
146
Which cell types are considered classic antigen-presenting cells (APCs)?
Dendritic cells, macrophages, and B cells.
Explanation: These cells process and present antigen on MHC to T cells
T cells use T-cell receptors (TCRs) and must see antigen presented by an APC to be activated
| *neutrophils are not classic APCs
147
Describe the humoral branch of adaptive immunity (third line defense), including the primary role, stages, key facts, and end result.
Humoral Immunity (B Cells)
Primary Role: Become plasma cells that make antibodies, protecting against extracellular pathogens/antigens.
Activated by direct antigen binding ± T Helper cells (via cytokine signals)
Differentiation:
Plasma Cells: Secrete large amounts of specific antibodies (neutralize, opsonize, activate complement).
Memory B Cells: Long-lived; enable rapid, stronger response on re-exposure.
Key Fact: Independent of MHC for initial recognition; T-dependent (most) vs T-independent (some polysaccharides).
148
Describe the Cellular Immunity (T Cells) branch of adaptive immunity (third line defense), including the primary role, stages, key facts, and end result.
Cellular Immunity (T Cells)
Primary Role: Kill infected/abnormal cells; coordinate immune response.
Activation: By APCs presenting antigen via MHC (Class I or II).
Subtypes:
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.
Key Fact: MHC-restricted no antibody production.
Key Interactions
Helper T cells bridge humoral & cellular: Provide signals for B cell activation & class switching.
149
Name the site of maturation for T and B Cells
T cells → thymus
B cells → bone marrow
150
Fill in the blanks:
B cells use____________ and can bind _______ directly (no ___ presentation required), then become ______ cells that secrete _______________.
B cells use B-cell receptors (BCRs) and can bind antigen directly (no MHC presentation required), then become plasma cells that secrete antibodies.
151
Define:
Helper T Cells (CD4+)
Cytotoxic T Cells (CD8+)
Memory T Cells
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.
152
What are the main features and functions of IgD?
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.
153
Name and define the four categories of adaptive (humoral) immunity (natural vs artificial; passive vs active).
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.
154
Howo to remember Natural vs Artificial, Active vs Passive Immunity
**_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
155
Which categories of adaptive immunity give long-term protection, and which give only temporary protection? Why?
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.
156
A patient receives an inactivated tetanus vaccine and develops their own antibodies and memory cells. This is an example of:
A) Naturally acquired active immunity
B) Naturally acquired passive immunity
C) Artificially acquired active immunity
D) Artificially acquired passive immunity
C) Artificially acquired active immunity
157
Why can attenuated live vaccines be risky for certain patients?
Live-attenuated strains can still replicate and may cause disease (or rarely revert) in immunodeficient patients.
158
What is attenuation and how is it used?
Attenuation (weakened but infectious)
Loss of virulence during lab passage without immune pressures yields weakened strains used in some live vaccines.
Infectious, but weakened to the point that they do not cause disease in an immune-competent host; seen in pathogens grown in petri-dishes — they aren’t fighting host’s immune response so they lose their virulence
159
Why are strict aseptic/depyrogenation practices essential for parenteral drugs and devices regarding endotoxin?
Endotoxin control: **Lipid A cannot be neutralized** in patients and **there are no vaccines**;
prevention of contamination is the only effective control.
160
True/False: Lipid endotoxins can be neutralized
False: Lipid endotoxins cannot be neutralized; no vaccines or effective treatments exist.
Strict aseptic and decontamination practices prevent endotoxin contamination in drugs and medical devices.
161
What are adhesins (second step to infection) and why are they important?
Adhesins are surface virulence factors that let microbes (bacteria, fungi, protists, viruses) stick to host cells—often using pili, fimbriae, capsules, or cell wall components.
Some bind multiple tissues.
Because they’re surface exposed, adhesins are key targets for vaccine development.
162
Distinguish between live attenuated vs inactivated vaccines (full compare/contrast)
Live Attenuated Vaccines:
Composition: Made from weakened pathogens that do not cause disease in healthy individuals.
Advantages: They closely mimic natural infections, leading to strong and long-lasting immune responses.
Drawbacks: Can cause disease in immune-compromised individuals and may mutate back to a pathogenic form. They require refrigeration, complicating transport and storage in areas with unreliable electricity.
Inactivated Vaccines:
Composition: Contain killed pathogens or parts of pathogens, such as proteins or polysaccharides.
Advantages: Safe for immune-compromised individuals and stable at room temperature, making them easier to store and transport.
Drawbacks: They are noninfectious, so they are quickly cleared from the body, often requiring booster doses to maintain immunity.
Both types of vaccines play crucial roles in public health by contributing to herd immunity, which helps protect at-risk populations and limits the spread of diseases.
163
What is the purpose of vaccination, and how do vaccines work in terms of the immune response?
Vaccines provide artificially acquired active immunity by exposing the immune system to a killed or weakened form of a pathogen (or its antigens). This does not give immediate protection; over about two weeks the body mounts a primary response, makes antibodies, and forms memory B and T cells, so later exposure to the real pathogen triggers a fast, strong secondary response that often prevents disease.
164
Define herd immunity and explain how it can be achieved naturally and artificially.
Herd immunity occurs when enough people in a population are immune to an infection that transmission is greatly reduced, protecting even those who are not immune. It can develop naturally after widespread infection in the community, or artificially through high vaccination coverage (for many diseases around 85%, and for measles or pertussis closer to 95%).
165
In general, which vaccine types should be avoided and which are preferred in immunocompromised patients?
Live attenuated vaccines should generally be avoided because the weakened microbe can still replicate and may cause disease or rarely revert. Inactivated, subunit, toxoid, and other non-live vaccines are preferred because they cannot replicate and are safer for immunocompromised patients.
166
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.
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).
167
The 4 main leukocytes of the innate defense system are neutrophils, basophils, eosinophils, and mast cells. What are their main roles in our defense?
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.
168
In a local type I allergic reaction (for example, a bee sting), what causes the redness and swelling at the site?
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.
169
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.
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.
170
Which of the following is an example of a type I hypersensitivity reaction?
Serum sickness
Atopic eczema
Anaphylactic shock following injection of bee venom
Atopic asthma after exposure to pet dander
Atopic eczema; Anaphylactic shock following injection of bee venom; Atopic asthma after exposure to pet dander.
Explanation: These are IgE-mediated type I reactions; serum sickness is a type III immune-complex reaction.
171
Which of the following is an example of a type III hypersensitivity?
Scleroderma
Hemolytic disease of the newborn
Graft-versus-host disease
Rheumatoid arthritis
Scleroderma; Rheumatoid arthritis.
Explanation: Scleroderma and rheumatoid arthritis involve immune-complex (type III) mechanisms; hemolytic disease of the newborn is type II, and graft-versus-host disease is type IV.
172
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
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.
173
In IgE-mediated allergy, which cells make IgE, which cells does it bind, and what drug class treats the histamine effects?
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.
174
# Define:
- Intubation
- Analgesia
- Malaise
* Intubation = placing a tube in the airway to support breathing.
* Analgesia = pain relief/pain control.
* Malaise = general sense of feeling unwell.
175
Trace the full flow of blood, starting and ending at the vena cavae.
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.
176
Why is the left ventricle more muscular than the right ventricle?
Left ventricle: pumps at high pressure to the whole body → thicker wall. Right ventricle: only pumps to low-pressure lungs → thinner wall.
177
How is the cardiovascular system “closed” and the lymphatic system “open”?
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.
178
What is an arbovirus?
Arthropod-borne virus. Transmitted by mosquitoes, ticks, sandflies, fleas, etc. (e.g., Zika, dengue, yellow fever, chikungunya).
179
What is a retrovirus, and which 2 do you need to know?
RNA virus that uses reverse transcriptase to make DNA and integrate into host genome. Key examples: HIV and HTLV (both infect T cells).
180
List the 3 main clinical stages of HIV infection.
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.
181
Describe the relationship between HIV viral load and T helper cell count over time.
Acute: viral load spikes ↑, T helper cells drop ↓. Chronic: viral load at lower “set point”; T helper cells slowly decline. AIDS: viral load rises again ↑; T helper cells fall below critical level ↓.
182
What key points should you remember about ticks and Lyme disease?
Vector: Ixodes (deer) ticks transmit Borrelia burgdorferi. Need ~24–48 hours of attachment to transmit. Prevention: tick checks, protective clothing, prompt removal after woods/high grass.
