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IB Biology HL > Topic 6.3 Disease Defenses > Flashcards

Topic 6.3 Disease Defenses Flashcards

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1
Q

First line of defense

A

Surface barriers that prevent the entry of pathogens into the body, including intact skin and mucus membranes.

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2
Q

Characteristics of skin as a line of defense

A
  • Protects external structures when intact
  • Consists of a dry, thick and tough region composed predominantly of dead surface cells
  • Contains biochemical defense agents (ex. sebaceous glands secrete chemicals, enzymes which inhibit microbial growth on skin)
  • Secretes lactic acid and fatty acids to lower skin pH (~5.6 – 6.4 )
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3
Q

Characteristics of mucus membranes as a line of defense

A
  • Protects internal structures (ex. cavities and tubes such as the trachea and urethra)
  • Consists of a thin region of living surface cells that release fluids to wash away pathogens (mucus, saliva, tears, etc.)
  • Contains biochemical defense agents (ex. secretions contain lysozyme which can destroy cell walls and cause cell lysis)
  • May be ciliated to aid in the removal of pathogens
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4
Q

Clotting (haemostasis)

A

The mechanism by which broken blood vessels are repaired when damaged, functioning to prevent blood loss from the body and limit pathogenic access to the bloodstream when skin is broken.

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5
Q

Key components of a blood clot

A
  • Platelets (primary haemostasis): undergo a structural change when activated to form a sticky plug at the damaged region
  • Fibrin strands (secondary haemostasis): form an insoluble mesh of fibers trapping blood cells at the site of damage
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6
Q

Coagulation cascade

A

A complex set of reactions contributing to the process by which blood clots are formed.
- Stimulated by clotting factors released from damaged cells (extrinsic pathway) and platelets (intrinsic pathway)

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7
Q

Principle events of a coagulation cascade

A
  • Clotting factors cause platelets to become sticky and adhere to the damaged region to form a solid plug
  • Clotting factors also initiate localized vasoconstriction to reduce blood flow through the damaged region
  • Clotting factors then trigger the conversion of prothrombin (inactive) into enzyme thrombin (active)
  • Thrombin catalyzes the conversion of plasma protein fibrinogen (soluble) into fibrous form fibrin (insoluble)
  • Fibrin strands form a mesh of fibers around the platelet plug and traps blood cells to form a temporary clot
  • When the damaged region is completely repaired, an enzyme (plasmin) is activated to dissolve the clot
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8
Q

Coronary thrombosis

A

The formation of a clot within the blood vessels that supply and sustain coronary arteries
- The closing of an artery by a blood clot can lead to a heart attack

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9
Q

Atherosclerosis

A

Blood clots form in coronary arteries when the vessels are damaged as a result of the deposition of cholesterol.

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10
Q

Formation of atherosclerosis

A
  • Fatty deposits develop in the arteries and significantly reduce the diameter of the lumen
  • Restricted blood flow increases pressure in the artery, leading to damage to the arterial wall
  • Damaged region is repaired with fibrous tissue, which significantly reduces the elasticity of the vessel wall
  • As the smooth lining of the artery is progressively degraded, lesions form called atherosclerotic plaques
  • If plaque ruptures, blood clotting is triggered, forming a thrombus that restricts blood flow
  • If the thrombus is dislodged it becomes an embolus and can cause a blockage in a smaller arteriole
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11
Q

Second line of defense

A

The innate immune system, which is non-specific and non-adaptive in its response.

  • Non-specific: does not differentiate between different types of pathogens
  • Non-adaptive: responds to an infection the same way every time
  • Includes phagocytosis, inflammation, fevers, and antimicrobial chemicals
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12
Q

Phagocytosis

A

The process by which solid materials (ex. pathogens) are ingested by a cell via endocytosis

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13
Q

Process of phagocytosis

A
  • Phagocytic leukocytes circulate in the blood and move into the body tissue (extravasation) in response to infection
  • Damaged tissues release chemicals (ex. histamine) that draw white blood cells to the site of infection via chemotaxis
  • Pathogens are engulfed when cellular extensions surround the pathogen and then fuse to form an internal vesicle
  • The vesicle is fused to a lysosome to form a phagolysosome, and the pathogen is digested
  • Pathogen fragments (antigens) can be presented on the surface of the phagocyte in order to stimulate the third line of defense
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14
Q

Third line of defense

A

The adaptive immune system, which is specific in its response.

  • Specific: can differentiate between particular pathogens and target a response that is specific to a given pathogen
  • Immunological memory: can respond rapidly upon re-exposure to a specific pathogen, preventing symptoms from developing
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15
Q

Lymphocytes

A

A class of leukocyte coordinating the adaptive immune system, resulting in the production of antibodies

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16
Q

Types of lymphocytes

A
  • B lymphocytes (B cells): antibody-producing cells that recognize and target an antigen
  • Helper T lymphocytes (T(small H) cells): regulator cells that release chemicals (cytokines) to activate specific B lymphocytes
  • Cytotoxic “killer” T cells (T (small C) cell): kills cancerous, infected, or damaged cells in the body
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17
Q

Activation of the adaptive immune system

A
  • following phagocytosis, dendritic cells present digested fragments of pathogens (antigens) on their surface
  • Dendritic cells then migrate to lymph nodes and activate specific helper T cells
  • Helper T cells release cytokines to activate specific B cells capable of producing antibodies specific to the antigen
  • Activated B cells will divide and differentiate to form short-lived plasma cells that produce high amounts of specific antibodies
  • Antibodies will target their specific antigen, enhancing the capacity of the immune system to recognize and destroy the pathogen
  • A small proportion of activated B cells (and activated TH cell) will develop into memory cells to provide long-lasting immunity
18
Q

Antigen

A

A substance that the body recognizes as foreign, eliciting an immune response.

19
Q

Antibody

A

A protein produced by B cells and plasma cells that is specific to a given antigen.

20
Q

Structure of an antibody enabling antigen-antibody specificity

A
  • Antibodies are Y-shaped, made of 4 polypeptide chains that are joined together by disulphide bonds
  • The ends of antibody arms are where antigens bind – variable regions that differ between antibodies
  • The rest of the molecule is constant across all antibodies and serves as a recognition site for the immune system (opsonization)
  • Each type of antibody recognizes a unique antigen, making antigen-antibody interactions specific
21
Q

Antibiotics

A

Compounds that kill or inhibit the growth of microbes (bacteria) by targeting prokaryotic metabolism.

  • Narrow spectrum: effective against specific bacteria
  • Broad spectrum: effective against many bacteria
22
Q

How do antibiotics target bacteria?

A
  • Antibodies can target metabolic features including key enzymes, 70s ribosomes, and components of the cell wall – features that eukaryotic cells do not possess
  • Can kill invading bacterial (bactericidal) or suppress its reproduction (bacteriostatic)
23
Q

Viruses vs. antibiotics

A

Viruses do not possess a metabolism (are not alive), and instead take over the cellular machinery of infected hosts
- Thus, cannot be treated with antibiotics – instead treated with specific antiviral agents

24
Q

Antibiotic resistance

A
  • Genes may confer resistance by encoding traits that degrade the antibiotic, block its entry, increase its removal, or alter the target
  • Bacteria reproduce at a rapid rate, so resistant strains of bacteria can proliferate very quickly following the initial mutation
  • Resistant strains can pass resistance genes to susceptible strains via bacterial conjugation (horizontal gene transfer)
25
Q

Reasons of antibiotic resistance prevalence

A
  • Antibiotics are often over-prescribed or misused
  • Many antibiotics are freely available without prescription
  • Certain antibiotics are commonly included in livestock feed
  • Multi-drug resistant bacteria can be common in hospitals, where antibiotic use is high
  • Example: the Golden Staph
26
Q

The discovery of penicillin

A
  • Identified by Alexander Fleming in 1928
  • Discovery was a fortuitous accident, resulting from the unintended contamination of a dish with S. aureus
  • Penicillium mold began to grow on the dish, and a halo of inhibited bacterial growth was observed
  • Fleming concluded that the mold was releasing a substance (penicillin) that was killing nearby bacteria
27
Q

Medical applications of penicillin

A

Demonstrated by Florey and Chain in 1940, whereby penicillin was tested on infected mice.

  • 8 mice injected with hemolytic streptococci, 4 of them injected with doses of penicillin subsequently
  • Untreated mice died of bacterial infection, while those treated survived
  • Florey, Chain, and Fleming awarded the Nobel Prize as a result
  • Synthetic derivatives of penicillin have been created for more stability and tolerance as medical treatments
  • However, such experiments on lab mice would be considered unethical now
28
Q

Human Immunodeficiency Virus (HIV)

A

A retrovirus that infects helper T cells, disabling the body’s adaptive immune system.

29
Q

Acquired Immuno-Deficiency Syndrome (AIDS)

A

A variety of symptoms and infections caused by HIV.

30
Q

Effects of HIV on the human body

A
  • HIV specifically targets the helper T lymphocytes that regulate the adaptive immune system
  • Following infection, the virus undergoes a period of inactivity (clinical latency), during which infected helper T cells reproduce
  • Eventually, the virus becomes active again and begins to spread, destroying T lymphocytes in the process (lysogenic cycle)
  • With a reduction in the number of helper T cells, antibodies are unable to be produced, resulting in a lowered immunity
  • The body becomes susceptible to opportunistic infections, eventually resulting in death if the condition is not managed
31
Q

Transmission of HIV

A

HIV is transmitted through the exchange of bodily fluids.
- Unprotected sexual contact (protection method: condoms)
- Blood transfusions or organ transplant
- Injections (drug use)
- Occupational exposure
- Pregnancy, childbirth, and breastfeeding
A global issue more commonly associated with less-developed countries.

32
Q

Immunity to HIV

A

A small minority people are genetically immune to HIV.

- They lack a receptor on helper T cells that HIV requires for docking

33
Q

Pathogen

A

A disease-causing agent that disrupts the normal physiology of the infected organism.

  • Cellular (living) pathogens: parasites, protozoa, fungi, prokaryote
  • Acellular (nonliving) pathogens: virus, prion
34
Q

Inflammation

A

A non-specific way in which the body responds when a pathogen damages body tissue.
- Can be short-term (acute) or long-term (chronic)

35
Q

Inflammatory response process

A
  • Mast cells (localized) and basophils (circulating) release histamine when tissue damage occurs
  • Histamine causes local vasodilation and increases capillary permeability to improve the recruitment of leukocytes to the region
  • Damaged cells release chemotactic factors, which attract leukocytes to the site of infection
36
Q

Side effects of inflammation

A
  • Increased blood flow causes redness and heat

- Increased permeability releases fluids and causes swelling and tenderness

37
Q

Fever

A

An abnormally high temperature associated with infection, triggered by the release of prostaglandins.

  • Combats infection by reducing growth rate of microbes
  • Can increase metabolic activity in cells to strengthen immune response
38
Q

Mechanism of fevers

A
  • Activated leukocytes release pro-inflammatory chemicals called cytokines
  • Cytokines stimulate the anterior hypothalamus to produce prostaglandins
  • Prostaglandins lead to an increase in body temperature
  • Up to a certain point a fever may be beneficial, but beyond a tolerable limit it can cause damage to the body’s own enzymes
39
Q

Classes of leukocytes

A
  • Neutrophils: unable to renew lysosomes, dying after engulfing few pathogens and forming the majority of pus
  • Eosinophils: release chemical products that perforate cell membranes
  • Basophils: responsible for initiating inflammatory responses by releasing histamine and heparin
  • Monocytes: similar function to neutrophils but are able to renew lysosomes; also differentiates into macrophages or dendritic cells
  • Lymphocytes: responsible for the production of antibodies (B and helper T cells) and the killing of unneeded cells (cytotoxic T cells)
40
Q

Haemophilia

A

An X-linked recessive condition that impairs the body’s ability to control blood clotting.

  • Hemophiliacs have lower levels of functional clotting factors in their blood plasma (fibrin formation does not occur)
  • Lasting blood clots cannot form, so hemophiliacs can die from minor injuries

IB Biology HL (32 decks)

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