Test 2 - Questions Flashcards
Describe the phases of acute inflammation and explain how they relate to the clinical manifestations of the condition.
- Vascular Phase – Vasodilation and increased permeability; leads to redness, heat, and swelling.
- Cellular Phase – Migration of leukocytes (mainly neutrophils) to the injury site.
- Phagocytosis – Removal of pathogens/debris.
- Resolution or progression – Tissue repair or chronic inflammation if unresolved.
Consider the chemical mediators of acute inflammation. Where do they come from?
They come from cells (e.g., mast cells, basophils, platelets, damaged tissues) and plasma proteins (e.g., complement system, kinins).
Consider the chemical mediators of acute inflammation. Explain the roles of histamine, prostaglandins, leukotrienes and bradykinin in the inflammatory response.
Histamine: Causes vasodilation and increases vascular permeability.
Prostaglandins: Cause pain, fever, and enhance effects of other mediators.
Leukotrienes: Cause increased vascular permeability, chemotaxis, and bronchoconstriction.
Bradykinin: Pain and vasodilation.
Consequences of acute inflammation
Abscess formation, scarring, or complete resolution.
Regeneration vs. repair
Regeneration: Replacement by identical cells—restores normal function.
Repair: Replacement by scar tissue (fibrosis)—may lose function.
Healing by 1st vs 2nd intention
1st Intention: Clean, surgical wound with minimal tissue loss.
2nd Intention: Larger wounds, greater tissue loss; longer healing time and more scarring.
Factors influencing wound healing
Infection, blood supply, medications (like steroids), diabetes.
Complications of wound healing
Infection
Dehiscence (wound reopening)
Hypertrophic scars or keloids
Chronic wounds
Contractures (in joints)
What is Ribonucleic acid (RNA)?
A single-stranded molecule involved in protein synthesis; it carries genetic instructions from DNA to the ribosomes.
What is Deoxyribonucleic acid (DNA)?
A double-stranded molecule that stores genetic information. It is composed of nucleotides and forms the genetic instructions used in growth, development, functioning, and reproduction.
Describe the basic structure and function of DNA
double helix composed of two strands of nucleotides with a sugar-phosphate backbone and nitrogenous bases (A, T, C, G). It stores genetic information.
Describe the basic structure and function of RNA.
single-stranded and contains the bases A, U (instead of T), C, and G. It helps in protein synthesis by carrying the genetic code from DNA to the ribosome.
Describe the relationship between DNA and RNA.
RNA is synthesized from DNA through a process called transcription.
DNA serves as the template for RNA, which then travels out of the nucleus and is used in translation to assemble proteins.
Describe the relationship between genes and chromosomes.
Genes are specific sequences of DNA located on chromosomes. Each chromosome carries hundreds to thousands of genes.
Explain why mutations occur? Describe their possible effects.
Mutations can occur due to errors during DNA replication, exposure to radiation, chemicals, or viruses.
Effects: They can be harmless, beneficial (e.g., increased resistance to disease), or harmful (e.g., cancer or genetic disorders).
Name the 3 types of genetic disorders.
- Chromosomal disorders (e.g., Down syndrome)
- Single-gene (Mendelian) disorders (e.g., cystic fibrosis)
- Multifactorial inheritance disorders (e.g., heart disease, diabetes)
What is meant by multifactorial inheritance disorders? Name examples
Conditions caused by a combination of multiple genes and environmental factors.
Examples include type 2 diabetes, heart disease, asthma, and some cancers.
How is self-tolerance developed?
We develop central tolerance during fetal development in the thymus (T cells) and bone marrow (B cells), where self-reactive lymphocytes are eliminated.
Peripheral tolerance occurs after birth, where additional mechanisms (like regulatory T cells) suppress any self-reactive immune cells that escaped initial deletion.
Explain how our genetic make-up can contribute to the development of autoimmune diseases.
Certain genes—especially those related to immune regulation—can increase the risk of autoimmune diseases. For example, specific HLA (human leukocyte antigen) alleles are linked to diseases like Type 1 diabetes and rheumatoid arthritis.
Under what circumstances could an individual be predisposed to an autoimmune disease?
An individual may be predisposed to autoimmune disease due to:
- Genetic factors (e.g., certain HLA types)
- Family history of autoimmune conditions
- Environmental triggers (e.g., infections, toxins)
- Hormonal influences (more common in females)
- Dysregulation of immune tolerance mechanisms
Explain the relationship between infection and autoimmune diseases.
Infections can trigger autoimmune diseases through a process called molecular mimicry, where parts of the pathogen resemble the body’s own tissues.
This can confuse the immune system, leading it to attack self-tissues after the infection is gone.
- NO - Type O has anti-A antibodies that will attack A antigens on recipient’s cells.
- NO - Recipient’s anti-A antibodies will attack the donor RBCs.
- YES - AB has no anti-B antibodies, safe to receive B plasma.
- NO - AB RBCs have A and B antigens, which O will attack.
- YES - O RBCs have no antigens; universal RBC donor.
- NO - AB RBCs have A antigens, which Type B recipient’s anti-A antibodies will attack.
- NO - B antigens on RBCs would be attacked by Type A’s anti-B antibodies.
- YES
Type 1 Reactions (Allergic Reactions)
a. Explain the mechanism.
When you first meet an allergen (like pollen), your body doesn’t attack it right away. Instead, it makes IgE antibodies against it.
These IgE antibodies stick to mast cells (cells loaded with chemicals).
Next time you meet the allergen, it sticks to the IgE, mast cells explode and release stuff like histamine, which causes sneezing, itching, swelling, etc.
Type 1 Reactions (Allergic Reactions)
b. Why is there no reaction the first time, but there is the second time?
The first time, your body is just getting ready — making those IgE antibodies.
You don’t feel anything.
The second time, your body is ready to attack, so the mast cells explode and you get the reaction.
Why can Type 1 reactions be fatal?
Because sometimes the reaction is so strong, your throat can swell up, your blood pressure can drop, and you can’t breathe.
That’s called anaphylaxis, and it can be life-threatening.
Type 2 Reactions (Cytotoxic Reactions) Mechanism?
In Type 2, the body makes antibodies that attack your own cells (like red blood cells).
These antibodies stick to cells and then the immune system comes in and destroys those cells.
Type 2 Reactions (Cytotoxic Reactions) Examples?
Blood transfusion mismatch
Hemolytic disease of the newborn
Graves’ disease
Myasthenia gravis
Type 3 Reactions (Immune Complex) mechanism?
In Type 3, antibodies and antigens stick together and form little clumps (called immune complexes).
These clumps get stuck in places like your joints, skin, and kidneys.
The body freaks out and sends immune cells, which causes inflammation and damage.
Type 3 Reactions (Immune Complex) examples?
Lupus (SLE)
Rheumatoid arthritis
Post-strep glomerulonephritis
Type 4 Reactions (Delayed Hypersensitivity) mechanism?
Unlike the others, Type 4 doesn’t use antibodies.
Instead, T-cells (white blood cells) react to something (like metal or a TB test).
It takes time (1–3 days) to show up — that’s why it’s “delayed.”
Type 4 Reactions (Delayed Hypersensitivity) examples?
Allergic contact dermatitis (poison ivy, nickel)
TB skin test (Mantoux)
Type 1 diabetes
Multiple sclerosis
Hypersensitivity vs autoimmunity
Hypersensitivity = too much immune response.
Autoimmunity = wrong target — your immune system attacks your own body.
So autoimmunity is a type of hypersensitivity, but not all hypersensitivities are autoimmune.
Name the type of hypersensitivity reaction that fits each of the following characteristics:
a. Examples include allergic contact dermatitis and the Mantoux test reaction.
b. IgE antibodies are most important
c. Examples include acute poststreptococcal glomerulonephritis, rheumatoid arthritis and SLE
d. Involves Th1, Th17 and Tc cells
e. Involves antibodies attaching to an cell specific antigen, then causing tissue damage via one or more of the following: complement activation, phagocytosis, neutrophil activation
f. Mast cells and basophils involved
g. An example is Graves disease
h. Examples include asthma, hayfever, reactions to some foods or drugs, reaction to a bee sting etc
a. Type 4
b. Type 1
c. Type 3
d. Type 4
e. Type 2
f. Type 1
g. Type 2
h. Type 1
What type of hypersensitivity reaction(s) are involved in:
a. Hyperacute graft rejection
b. Acute graft rejection
c. Chronic graft rejection
a. 2
b. 4
c. 2 & 4
