Disease process & Immunity Test 2

When does adaptive immunity activate?

• When innate immunity has failed to prevent infection

• Both systems work together to eliminate the pathogens

What are the characteristics of adaptive immunity?

• Highly specific

• Memory - can provide long-lasting protection

• Able to distinguish self-antigen from pathogens

What are the immune cells involved in adaptive immunity?

• Lymphocytes

• T cells

• B cells

What are the two types of responses for adaptive immunity?

• Cell mediated immune responses

• Antibody responses

What are the APC (Antigen presenting cells)?

• Dendritic cells

• Macrophages

• B cells

What are the types of T cells? What MHC class do the effector T cells have?

• Effector T cells

  • CD⁴⁺ Helper T Cells - MHC II

  • CD⁸⁺ Cytotoxic T Cells - MHC I

• Memory T Cells

• Naive T Cells

What immune cell activates naive T cells

Dendritic cells

How do APC present antigen fragments?

1. Ingest microbe antigen

2. ingested antigens are broken down

3. A fragment of the broken down antigen is presented with MHC molecule on the cell surface

How does T Cells fight against pathogen?

1. An APC presents the antigen to the CD⁴⁺ Helper T Cell

2. CD⁴⁺ Helper T Cell releases cytokines

3. Cytokines activate CD⁸⁺ cytotoxic T cells and cytotoxic T cells duplicate

4. Cytotoxic T cells bind to infected cell body and causes cell lysis by release of perforins.

How does antibody mediated immunity work?

• Activated B cells produce antibodies that bind to free antigens in body fluids

• Some B cells become memory cells which become active in future encounters of this same antigen and confer immunity to that antigen

What are the 2 ways B cells are activated?

• T Cell dependent

• T Cell independent

How does T-cell independent B cell activation happen?

• B cell receptors (BCRs) interact with the antigen

• BCRs for naive B cells are membrane-bound

  • An antigen binds to the BCR on only one type of B cell

  • B cell then produces clones of itself

  • Clones of B cells becomes plasma cells → produce antibodies that are specific to the same type of antigen

• The response is short lived and does not result in the production of memory B cells

How does T cell dependent B cell activation happen?

1. Antigen binds to BCR on naive B cell and stimulates an internalization of the antigen.

2. After internalization, antigen is processed and presented with MHC II to CD⁴⁺ Helper T.

3. Presented antigen is recognised by CD⁴⁺ Helper T cell

4. CD⁴⁺ Helper T produce and secrete cytokines that activate B cell

5. B cell proliferates → plasma cell → antibodies

6. B cell clones also proliferate into memory B cells

   • Quickly responds to subsequent exposures to same antigen.

What does MHC stand for, and what is its primary function?

Major Histocompatibility Complex

It presents antigens to T cells to trigger an immune response

Why is antigen presentation necessary for adaptive immunity?

T cells cannot recognize whole viruses; they need antigen fragments presented on MHC molecules.

What types of cells express MHC molecules?

All nucleated cells express MHC I APCs (Dendritic cells, macrophages, B cells) express MHC II.

What type of antigens are presented by MHC Class I?

Endogenous antigens — viral proteins made inside infected cells.

Which T cell recognizes MHC Class I?

CD⁸⁺ cytotoxic T cells.

What immune response is triggered by MHC I presentation?

CD⁸⁺ cytotoxic T cells kill infected cells to stop viral replication.

Which cells express MHC Class II molecules?

Antigen presenting cell (APC): Dendritic cells, macrophages, and B cells.

What type of antigens are presented by MHC Class II?

Exogenous antigens — viral particles taken up by APCs.

Compare MHC Class I and II molecules

Feature	MHC Class I	MHC Class II
Expressed on	All Nucleated cells	Professional APCs only
Presents	Endogenous (intracellular) antigens	Exogenous (extracellular) antigens
Recognized by	CD8+ Cytotoxic T cells	CD4+ Helper T cells
Immune Response	Kills infected cells	·  Activate B cells, macrophages ·  Support activation of CD8+ T cell - CD4+ T cells release cytokines which promote the proliferation and differentiation of CD8+ T cells into effector cytotoxic T cells

Describe the immune response triggered by MHC I antigen presentation?

MHC I-antigen complex is transported to the surface of the cell. CD⁸⁺ cytotoxic TCR (T-cell receptor) recognises a foreign peptide presented by MHC 1 and activates. The CD⁸⁺ cytotoxic T cells release perforins and granzymes. Which induce apoptosis in the infected cell. Afterwards some CD⁸⁺ cytotoxic T cells differentiate into memory T cells to provide long-term immunity by enabling a faster stringer response if the same antigen is encountered again

Name an example of PAMPS (Pathogen-Associated Molecular Patterns)

• Flagellin

• LPS (lipopolysaccharide)

• Double stranded RNA

• Unmethylated CpG motifs

How are T cells activated?

CD⁴⁺ T cells recognize the MHC II–antigen complex via their TCR and become activated.

What happens when CD⁴⁺ Helper T cells release cytokines?

• Stimulate B cells

• Enhance activity to phagocytose and kill bacteria.

  macrophages

• Recruit other to the site of infection.

  immune cells

What cell activates Naive CD⁴⁺ T cells?

Dendritic cells

How do antibodies help eliminate the bacteria from the body? (Name the mechanisms)

• Neutralization: Antibodies bind to bacterial toxins or surface proteins, blocking their ability to infect host cells.

• Opsonisation: Antibodies coat the bacteria, making them easier for phagocytes like to recognize and engulf.

• Complement Activation: Antibodies trigger the complement system, leading to bacterial lysis.

Table for hypersensitivity

Type	Name	Immune Mechanism	Onset	Examples	Key Cells Involved	Clinical Relevance / Feature
I	Immediate (Allergic)	IgE-mediated activation of mast cells	Seconds to minutes	Asthma, anaphylaxis, hay fever	Mast cells, basophils, IgE	Can be life-threatening; rapid onset; allergy-related
II	Antibody-mediated Cytotoxic	IgG/IgM antibodies bind to cell surface antigens	Minutes to hours	Hemolytic anemia, blood transfusion reactions	IgG, IgM, complement, NK cells	Targets specific cells; often involves blood cells
III	Immune Complex-mediated	Antigen-antibody complexes deposit in tissues	Hours to days	Serum sickness, lupus, rheumatoid arthritis	Neutrophils, complement	Causes inflammation in tissues; systemic effects
IV	Delayed-type (Cell-mediated)	T-cell mediated response	48–72 hours	Contact dermatitis, TB skin test, graft rejection	T cells (CD4+, CD8+)	No antibodies involved; delayed response

What does IgE bind to?

• Mast cells

• Basophils

What antigen is involved in Type I Hypersensitivity?

IgE

Define Type I hypersensitivity

Type I hypersensitivity is an immediate allergic reaction mediated by IgE.

What is the immunological mechanism involved in Type I Hypersensitivity.

• IgE-mediated activation of Mast cells and Basophils

• Releases Histamine

Why do type I hypersensitivity symptoms appear so rapidly upon re-exposure to allergen?

• Body was already sensitised to allergen

• IgE antibodies specific allergen protein were previously produced.

• IgE antigens were already bound to mast cells

• Upon re-exposure, the allergen cross-linking, causing immediate degranulation and release of histamine, leading to rapid onset of symptoms

What are the two emergency treatments And it's commonly used for anaphylaxis?

• Epinephrine

• Anti-histamines

How does epinephrine help with Anaphylaxis?

• Reverses airway constriction

• Reduces swelling

• Raises blood pressure

How does antihistamines help with anaphylaxis?

• Blocks histamine receptors

• Reducing symptoms like hives and itching

What are the key cells involved in Type II Hypersensitivity?

• IgG

• IgM

• Complement

• NK Cells

Define Type II hypersensitivity

Type II hypersensitivity is Antibody-mediated Cytotoxic with IgG or IgM antibodies binding to cell surface

What is the immunological mechanism involved in Type II Hypersensitivity.

• IgG/IgM antibodies bind to cell surface antigens

• binding activates the complement system or attracts phagocytic cells, leading to the destruction of the red blood cells.

What is the onset of type I hypersensitivity?

Seconds to minutes

What is the onset of type II hypersensitivity?

Minutes to hours

What is the onset of type III hypersensitivity?

Hours to days

What is the onset of type IV hypersensitivity?

48–72 hours

What are the key cells involved in Type III Hypersensitivity?

• Neutrophils

• Complement

What are the key cells involved in Type IV Hypersensitivity?

T cells (CD4+, CD8+)

What is the immunological mechanism involved in Type III Hypersensitivity.

• Antigen-antibody complexes deposit in tissues

• Immune complexes can deposit in small blood vessels → Activate complement system → inflammation and tissue damage

• Organs that have dense capillary networks and high filtration networks make them prone to immune complex deposition

What is the immunological mechanism involved in Type IV Hypersensitivity.

• T-cell mediated response

• CD⁴⁺ helper T cells and CD⁸⁺ cytotoxic T cells recognize antigens presented by APC → release cytokines that recruit macrophages and cause tissue inflammation

What are the symptoms of Type I hypersensitivity?

• Asthma

• anaphylaxis

• hay fever

What are the symptoms of Type II hypersensitivity?

• Hemolytic anemia

• Blood transfusion reactions

What is the clinical relevance of Type I Hypersensitivity?

• Can be life threatening

• rapid onset

• allergy related

What is the clinical relevance of type II hypersensitivity?

• target specific cells

• often involve blood cells

What is the clinical relevance of type III hypersensitivity?

• cause this inflammation in tissues

• systemic side effects

What is the clinical relevance all type IV hypersensitivity?

• No antibodies involved

• delayed response

What are the symptoms for type III hypersensitivity?

• Serum sickness

• lupus

• rheumatoid arthritis

What are the symptoms for type IV hypersensitivity?

• Contact Dermatitis

• TB skin test

• graft rejection

Why are type IV hypersensitivity reactions delayed?

• Involve cell mediated immunity

• takes time for T cells to recognize antigen become activated and recruit other immune cells to the site

• unlike antibody mediated reactions which occur within minutes

Why are complement levels often low in patients experiencing type III hypersensitivity reactions like lupus?

• Complement system is continuously activated by immune complexes deposited in tissues

• Persistent activation leads to consumption of complement proteins

• Low complement levels are a marker of ongoing immune complex mediated inflammation

Why is it important to perform blood typing and cross matching before transfusions?

• Ensure donor blood is compatible with recipient's immune system

• If incompatible blood is transfused recipient's antibodies may recognize the donor red cells as foreign and attack them

• leading to type II hypersensitivity reaction like hemolysis

What is myocardial infraction?

• Sudden and complete interruption of blood supply to a portion of the heart

• An area of tissue death due to a lack of oxygen

What can cause myocardial Ischemia or infraction?

• Partial obstruction of artery

  • Atherosclerotic plaques can cause partial or complete narrowing (stenosis)

• Coronary vasospasm (vasoconstriction)

  • Acute Coronary vasospasm can be relieved by nitrates \

  • Restoring normal coronary blood flow

• Thrombus (stationary clot)

  • plaques occasionally rupture

  • induces platelet activity and coagulation cascade to form clot or thrombus

• Embolus (floating clot)

  • thrombus detached from vessel wall

  • carried in bloodstream as embolus

What are the complications arising from uncontrolled hypertension?

• Renal complications

  • End stage Renal Disease

• Cerebral complications

  • Hemorrhagic stroke

  • Ischemic stroke

• Left ventricular hyperhtrophy

• Coronary artery disease (CAD)

  • Myocardial infraction, angina

• Left ventricularsystolic failure

  • heart failure

• Peripheral vessel damage

  • Leads to peripheral vascular disease stiffening of blood vessel

  • accelerates atherosclerosis

State the formula for defining blood pressure and explain its individual component.

• BP = CO (Cardiac Output) x PVR (Peripheral Vascular Resistance)

• Cardiac output is a measurement of blood flow through the heart to the systemic and pulmonary circulation per min (ml/minute)

What is the difference between myocardial ischemia and myocardial infarction?

myocardial ischemia

• When the lumen is significantly blocked (not complete) , oxygen supply to heart muscle is diminished

Myocardial infraction

• When there is a sudden and complete interruption of blood supply to a portion of the heart

What is the difference between Atherosclerosis and Arteriosclerosis?

• Atherosclerosis: formation of intimal lesions that protrude into and obstruct vascular lumina

• Arteriosclerosis: Hardening of the arteries resulting in thickening and loss of elasticity

What are the invasive methods used to assess atherosclerosis?

• Intravascular ultrasound

• Coronary Angiography

What are the clinical manifestations of atherosclerosis?

• Coronary heart disease

  • Angina pectoris, myocardial infraction, sudden cardiac death, congestive heart failure (CHF) and arrhythmias

• Cerebrovascular disease

  • Transient ischemic attack, stroke

• Peripheral vascular disease

  • Intermittent claudication, gangrene, cold feet, painful feet, impotence

What are the different types of stroke?

• Transient Ischemic attack

• Ischemic stroke

• Hemorrhagic stroke

State 3 symptoms of stroke?

• Slurred speech

• Weakness or numbness in face, arm and leg on one side of the body

• Double vision

Describe the role of kidney in blood pressure regulation.

• Renin-angiotensin system (RAS)

• restore normal blood pressure and fluid balance by

  • regulating sodium and water retention

  • vascular tone

  • systemic vascular resistance

State 3 consequences of myocardial infarction.

• Sudden cardiac death

• cardiac arrythmia

• vascular remodeling

• deep vein thrombosis

• recurrent myocardial infraction

Explain why edema(redness) is a common symptom of Heart Failure.

• Presence of edema suggests congestive heart failure

• failure to properly eject blood from LV cause back flow of blood to lungs. This results in pulmornary edema

• When the right side of the heart fails, it cause blood to be back up in the venous system and cause edema in the periphery i.e legs

What are the 2 categories of heart failure?

Systolic dysfunction

• Reduced contractility (left ventricular) is the principal mechanism of heart failure in coronary heart failure in coronary heart disease and dilated cardiomyopathy

Diastolic dysfunction

• Disorders in which the filling of the ventricle is impaired either by inflow obstruction or by reductions in ventricular compliance

What are the 3 types of angina and define each type.

1. Stable symptoms that occur during physical exertion and are relieved by rest or medication

2. unstable angina - angina at rest well as with minimal exertion

3. Vasospastic or Prinzmetal’s angina resulting from vasospasm of coronary artery, occurs most commonly at rest and is not precipitated by exertion of stress.

If premature beat occurs in the ventricular, it will affect ____?

Ventricular

If premature beat occurs in the atrial, it will affect _____?

Atria and Ventricular

Explain why ventricular fibrillation has higher mortality as compared to atrial fibrillation.

Ventricular Fibritillation	Atrial fibrilation
• Life threatening/emergency, required immediate defibrillation	• Can be managed chronically with medication
• Signal is pass from atrial to ventricular; ventricular is the end stage of contraction • If fibrillation occurs at ventricular, blood circulation will cease completely	• If fibrillation occurs at atrial, atrial will beat irregularly & inefficiently • Ventricular still able to pump to supply blood to rest of body
◦ Sudden death	• Risk of stroke & heart failure • Palpitation/fatigue/dizziness

Explain how the following influences the firing rate of myocyte causing arrhythmia.

• Circulating hormone (thyroid hormone/ adrenaline)

  • Thyroid hormone/ adrenaline: increase heart rate

• Serum ion concentration

  • Electrolytes maintain action potential

  • Na/K: influence depolarisation & repolarization

• Cellular hypoxia

  • Ocygen is essential for the normal electrical activity of cardiac muscle cells

  • Hypoxia reduces ATP production; failure of ATP- dependent ion pump (Na/K-ATPase pump)

  • causing partial depolarisation

• Drugs

  • Affecting ion channels, altering electrolyte balance, increasing sympathetic or slowing electrical condition in the heart

  • eg. digoxin/bronchodilators/ anti psychotics

What is the pathology of Erectile Dysfunction?

• Nerve impulses in the brain,spinal column and area around the penis

• response in muscles, fibrous tissues, veins and arteries in and near the corpora cavernosa

• ED occurs when any of the events are disrupted

What diseases contribute to Erectile dysfunction?

• Diabetes (Thicker blood)

• High blood pressure

• nerve disease or nerve damage

• multiple sclerosis

• atherosclerosis

• heart disease

• affect nerves, arteries, smooth muscles and fibrous tissues

What lifestyle factors contribute to erectile dysfunction?

• Smoking

• Drinking alcohol

• Obesity

• Not exercising

Contributes to heart disease and vascular problems

What types of surgeries contribute to erectile dysfunction?

• Prostate and bladder surgery for cancer

• Can injure nerves and arteries near the penis → could result in ED

Wh

What are the side effects of medication that can contribute to erectile dysfunction?

• Blood pressure drugs

• Anti histamines

• Anti depressants

• Appetite suppressants

• Cimetidine

• Ulcer drug

W

What are the psychological factors that can contribute to erectile dysfunction?

• Stress

• anxiety

• depression

• low self esteem

• fear of sexual failure

What hormonal abnormality contributes to erectile dysfunction?

Low levels of testosterone