Patho - Term Test III (Immunity)

Question 1

Define innate (natural or native) immunity.

Answer 1

defense mechanisms that are present at birth and provide the initial response to invasion and injruy

Question 2

What are the first, second, and third lines of defence? What are their respective functions

Answer 2

1) physical, mechanical, and biochemical barriers (prevent damage from environment or infection by pathogenic microorganism)
2) inflammatory response (activated to protect body from further injury, fight infection, and promote healing - there is already tissue injury/infection at this point)
3) adaptive (acquired/specific) immunity (long term protection against specific invaders)

Question 3

Define adaptive (acquired or specific) immunity.

Answer 3

refers to immuntiy that develops over someone’s lifetime and provides long-term protection against specific invaders

Question 4

Adaptive immunity involves “memory” which serves what purpose?

Answer 4

allows for rapid response for future exposures to the same invader because the body already has a memory of this invader

Question 5

What is the timing of defense of the following:

1) Barriers
2) Inflammatory Reponse
3) Adaptive immunity

Answer 5

1) constant
2) immediate response
3) there is delay between 1st exposure to antigen and max response; immediate response against 2’s exposure to the same antigen

Question 6

What is the specificity of defense of the following:

1) barriers
2) inflammatory response
3) adaptive immunity

Answer 6

1) broadly specific
2) broadly specific
3) very specific towards target

Question 7

What cells are involved with barriers?

Answer 7

1) epithelial cells

Question 8

What cells are involved with inflammatory response?

Answer 8

1) mast cells
2) granulocytes (neutrophils, basophils, eosinophils)
3) monocytes/macrophages
4) NK cells
5) platelets
6) Endothelial cells

Question 9

What cells are involved with adaptive immunity?

Answer 9

1) T lymphocytes
2) B lymphocytes
3) Macrophages
4) Dendritic cells

Question 10

Memory is involved with which of the following lines of defense?

1) Barriers
2) Inflammatory response
3) adaptive immunity
4) all of the above

Answer 10

adaptive immunity (specific immunologic memory by T and B lymphocytes)

Question 11

What molecules are active in innate barriers?

Answer 11

• Defensins
• Collectins
• Lactoferrin
• Bacterial toxins

Question 12

What molecules are active in inflammatory response?

Answer 12

• Complement activation
• Clotting factors
• Kinins
• Cytokines

Question 13

What molecules are active in adaptive immunity?

Answer 13

• antibodies
• complement
• cytokines

Question 14

Innate barriers have what kind of protective functions? (3)

Answer 14

1) anatomical barriers (skin, mucous membranes)
2) cells and secretory molecules (lysozymes, low pH of stomach and urine)
3) ciliary activity

Question 15

Inflammatory responses have what kind of protective functions? (4)

Answer 15

1) vascular responses
2) cellular components (mast cells, neutrophils, macrophages)
3) secretory molecules of cytokines
4) activation of plasma protein systems

Question 16

Adaptive immunity has what kind of protective functions?

Answer 16

1) activated T and B lymphocytes
2) cytokines
3) antibodies

Question 17

How does the following remove infectious microorganisms:

1) skin
2) respiratory tract
3) GI tract
4) urinary tract

Answer 17

1) skin: microorganisms being sloughed off with dead skin cells
2) resp tract: epithelial cells producing mucus to trap microorganisms + cilia (coughing, sneezing it out)
3) GI tract: vomiting, defecation
4) urinary tract: urination

Question 18

Low temperature on skin and low pH in stomach (activate/inhibit) growth of pathogenic microorganisms.

Answer 18

inhibit

Question 19

How do epithelial cells trap & destroy invaders?

Answer 19

secrete mucus, saliva, sweat, tears, and earwax & have lethal substances (ex. lyosozymes that attack cell walls of gram+ve bacteria)

Question 20

How do sebaceous glands kill bacteria/fungi?

Answer 20

• secrete fatty acids and lactic acid
• create acidic environment (pH 3 -5 on skin)

Question 21

What are antimicrobial peptides? Provide an example.

Answer 21

Host defense peptides that are secreted by epithelial cells and kills/inhibits growth of disease-causing microorganisms

ex. (any one of the following):
- Cathelicidins
- Defensins
- collectins
- mannose-binding lectin

Question 22

What are defensins?

Answer 22

antimicrobial peptides produced by neutrophils and epithelial cells (disrupts bacterial membranes)

Question 23

What are collectins?

Answer 23

soluble glycoproteins that facilitate ability of macrophages to recognize and kill pathogenic microorganism, can also activate lectin pathway of complement system

Question 24

Surfactant is a type of ____________.

Answer 24

collectin

Question 25

I am cool with manna and mustafa using my flashcards. True or false.

Answer 25

False (just kidding :))

Question 26

How many racoons can you shove up your butthole?

Answer 26

almost 2

Question 27

Normal microbiome has a _______ and ________ relationship with the body (parasitic/commensal/opportunistic/etc).

Answer 27

commensal (benefitting microorganism without affecting the body) mutualistic (benefitting both microorganism and body)

Question 28

What are 6 functions of normal microbiome?

Answer 28

1) produces enzymes that facilitate digestion of fatty acids and large polysaccharides 2) synthesizes essential metabolites 3) releases antibacterial substances that are toxic to invaders 4) competes with pathogens for nutrients and blocks attachment of pathogens to the epithelium 5) fosters adaptive immunity by inducing growth of gut-associated lymphoid tissue (needed for local and adaptive immunity) 6) contributes to bidirectional communication between brain and GI tract

Question 29

True or False. Prolonged treatment of broad-spectrum antibiotics can decrease normal microbiome protective activity and lead to overgrowth of pathogenic microorganisms.

Answer 29

True (because broad-spectrum antibiotics target wide range of bacteria so it kills good and bad bacteria)

Question 30

What are opportunistic pathogens?

Answer 30

pathogens that are part of normal microbiome that are harmless under normal conditions but then can cause disease in immunocompromised individuals who lack usual defense mechanisms

Question 31

Define inflammation.

Answer 31

Dynamic process programmed to respond to cellular or tissue damage irrespective of location or condition of tissue; it is non-specific

Question 32

What is the process of acute inflammatory response?

Answer 32

1) cell/tissue damage 2) release of inflammatory mediators (from mast cell degranulation, activation of plasma protein systems) 3) changes in microcirculation 4) migration of leukocytes, plasma proteins, biochemical mediators from circulation into damaged tissue 5) destroy invaders in tissue, limit tissue injury, promote healing

Question 33

Which of the following is false in regards to inflammatory response? 1) process can occur in vascularized and avascularized tissues 2) activation is rapid 3) response includes cellular and chemical components 4) response is non-specific

Answer 33

1) process can occur in vascularized and avascularized tissues process can only occur in vacularized tissues because a blood supply is needed for cells and chemical components to go to injury site

Question 34

What are the cardinal signs of acute inflammation?

Answer 34

Rubor (redness, erythema) Calor (heat) Tumor (swelling) Dolor (pain) Loss of function

Question 35

In inflammatory response, what sort of changes occur in the microcirculation (capillaries, venules, arterioles)?

Answer 35

1) hemostasis (coagulation) - clotting cascade and activates platelets (clotting slows blood flow, walls off injury, and provides a meshwork for healing) 2) vasodilation - increases blood volume delivered to injured site and slows velocity of blood flow which allows more time for fluid, cells, chemical movement into surrounding tissues which results in erythema/warmth in injury site 3) increased vascular permeability - endothelial cells contract which cause blood vessels to become porous ==\> leads to exudation and edema surrounding injury site 4) WBC adhesion - adhere to inner walls of vessels where they migrate through the enlarged spaces between endothelial cells and into surrounding tissue (influx in phagocytes - neutrophils, macrophages)

Question 36

Exudation vs edema

Answer 36

exudation - fluid leaking from vessels edema - tissue swelling from fluid leaking

Question 37

Lymphangitis vs lymphadenitis

Answer 37

Lymphangitis: inflammation of lymph vessels Lymphadenitis: inflammation of lymph nodes

Question 38

What are the 3 key systems for an effective inflammatory response?

Answer 38

1) complement system 2) clotting system 3) kinin system

Question 39

True or False: Plasma protein systems have multiple proteins/enzymes that are usually inactive (proeznymes) in the blood and get activated when there is tissue damage

Answer 39

True

Question 40

Purpose of complement system

Answer 40

intensifies/complements capacity of antibiotics/phagocytes to clear pathogens and damaged cells and activate inflammation (so they either destroy pathogens directly or can eradicate pathogens through enhancing activity of other components of the immune response)

Question 41

Activation of C3 and C4 within the complement system lead to what molecules being produced that are critical to immune response? What are their functions?

Answer 41

1) C3b - serve as opsonins (coats surface of bacteria to increase their susceptibility tto phagocytosis by inflammatory cells) - getting it ready for ingestion 2) C5a - functions as chemotactic factor (stimulates movement of leukocytes and attracts them to injury site) 3) C3a, C5a - anaphylatoxins; induces rapid degranulation of mast cells to release histamine (which induces vasodilation and increased capillary permeability)

Question 42

What is the membrane attack complex (MAC)?

Answer 42

Component of complement system that is composed of C6-C9 that lead to bacterial destruction and tissue injury by creating pores in outer membranes of cells/bacteria (water infusion occurs, leads to cell death)

Question 43

What are the 3 major pathways/cascades that control complement activation?

Answer 43

1) classical 2) alternative 3) lectin

Question 44

How is the classical pathway activated which controls complement activation?

Answer 44

classical pathway is activated by antibodies when they bind to antigens, which then activates complement cascade and triggers infection

Question 45

How does alternative pathway get activated control complement activation?

Answer 45

activated directly by substances found on surfaces of infectious microorganisms --\> forms a complex that then causes activation of complement cascades and triggers infection

Question 46

How does lectin pathway control complement activation?

Answer 46

does not require antibodies for activation, activated by several plasma proteins (particularly mannose-binding lectin MBL) that bind to the bacteria and activate complement cascade

Question 47

What is the purpose of the clotting/coagulation system?

Answer 47

A group of plasma proteins that form a blood clot when cascade is activated

Question 48

What is a blood clot composed of?

Answer 48

meshwork of fibrin strands and platelets

Question 49

How is the clotting system activated?

Answer 49

By a variety of substanes (collagen, enzymes, bacterial toxins) released during tissue injury/infection

Question 50

Functions of Clotting/coagulation system include what?

Answer 50

1) plug damaged vessels to stop bleeding (hemostasis) 2) trap microorganisms (localizing them) 3) prevent spread of microorganisms to adjacent tissues 4) provide framework for future repairing and healing

Question 51

What are the two converging pathways that lead to clot formation? How are these two pathways activated?

Answer 51

extrinsic and intrinsic pathways Extrinsic (tissue factor) pathway activated by tissue factor/tissue thromboplastin which is released by damaged endothelial cells of blood vessels + reacts with activated factor VII Intrinsic (contact activation) pathway activated by exposed endothelium and negatively charged substances (resulting from vessel wall damage) coming in contact with factor XII/Hageman factor

Question 52

Where do the intrinsic and extrinsic pathways of the clotting system converge, and after they converge what is the end product?

Answer 52

They coverge at factor X and form a common pathway that leads to activation of fibrin to eventually form a fibrin clot Fibrinogen also makes fibrinopeptides that are chemotactic and attract neutrophils and increased vascular permeability

Question 53

What is the kinin system's function?

Answer 53

To activate and assist inflammatory cells

Question 54

How is the Kinin System activated and what is the end product?

Answer 54

Activated by Hageman factor (Factor XII) End product: bradykinin

Question 55

What does bradykinin do, as part of the inflammatory response?

Answer 55

Causes dilation of blood vessels and acts with prostaglandins to induce pain, trigger smooth muscle cell contraction (bronchoconstriction) and increase vascular permeability

Question 56

All the plasma protein systems are tightly regulated and highly interactive. What are two reasons as to why this would be beneficial for the human body?

Answer 56

1) inflammatory process is critical for survival so interaction of these systems allows for efficient activation regardless of cause of tissue injury 2) biochemical mediators released during inflammatory response are potent and can be harmful to the person so they have to be controlled and confined to injured tissues

Question 57

Which of the following do not down-regulate or inactive plasma protein systems? 1) protease inhibitors 2) Hageman factor 3) Carboxypeptidase 4) Kininase 5) Histaminase

Answer 57

2) Hageman factor

Question 58

Formation of clots activates fibrinolytic system. What is the function of this system and how does it work?

Answer 58

The fibrinolytic system functions to limit clot size (works oppositely to clotting system) and degrade clot after bleeding has ceased How it works: Thrombin (which is made in the clotting system) activates plasminogen which is converted to plasmin which then degrades fibrin polymers in clots

Question 59

What types of cells/components are involved with inflammation?

Answer 59

1) mast cells 2) endothelial cells 3) platelets 4) phagocytes (neutrophils. macrophages) 5) lymphocytes

Question 60

Which cells are the most important mediators of inflammation?

Answer 60

Mast cells

Question 61

Precursors of macrophages are also known as:

Answer 61

monocytes

Question 62

What lymphocytes are involved with the following? 1) innate immunity 2) adaptive immunity

Answer 62

1) innate: NK cells 2) adaptive: B and T lymphocytes

Question 63

What are pattern recognition receptors (PRRs)?

Answer 63

set of receptors on cells that are involved in initiating innate immune response and recognize antigens

Question 64

Where are pattern recognition receptors generally expressed on?

Answer 64

cells in tissues near body's surface (skin, resp tract, GI tract, genitourinary tract) so they can monitor environment for cell damage/infectious microorganisms

Question 65

What are the two types of molecular patterns that PRRs recognize?

Answer 65

1) pathogen-associated molecular patterns (PAMPs) 2) damage-associated molecular patterns (DAMPs)

Question 66

PAMPs vs DAMPs

Answer 66

PAMPs: molecules expressed by infectious agents found either on surface or released as soluble molecules DAMPs: products of cellular damage

Question 67

Toll-like receptors: what do they recognize and where are they found?

Answer 67

Recognize PAMPs located on cell wall/surface of microorganisms Found on outer membrane of phagocytic cells with early contact with infectious microorganisms (i.e. dendritic cells, macrophages)

Question 68

C-type lectin receptors: what do they recognize and where are they found?

Answer 68

Recognize PAMPs (especially fungal antigens) and DAMPs Found on outer membrane of phagocytic cells

Question 69

Nucleotide-binding-like receptors (NLRs) and NOD-like receptors: what do they recognize, what is their function, and where are they found?

Answer 69

Recognize PAMPs and DAMPs Function: initiate production of proinflammatory mediators and help control inflammatory response Found in cytoplasm of innate immune cells (lymphocytes, macrophages, and dendritic cells)

Question 70

Complement receptors: what do they recognize and where are they found? what is their function?

Answer 70

Recognize components of complement system Found on many cells involved with immune response, platelets, epithelial cells, vascular smooth muscle Function: result in chemotaxis and activation of innate immune cells

Question 71

Scavenger receptors: what do they recognize and where are they found? What is their function?

Answer 71

Recognize bacterial pathogens, damaged cells, and soluble lipoproteins (HDL, LDLs, etc.) They are found on surfaces of macrophages Functoin: remove old RBcs and cells undergoing apoptosis

Question 72

What are cytokines?

Answer 72

Small signaling proteins that bind to specific cell membrane receptors to regulate innate/adaptive immunity and are responsible for activating other cells; mediators of inflammation

Question 73

True or false. Cytokines can be proinflammatory or anti-inflammatory

Answer 73

True - depends on whether they tend to induce or inhibit inflammatory response

Question 74

Which of the following are not cytokines? 1) interleukins 2) lymphokines & monokines 3) chemokines 4) TNF-a 5) bradykines 6) interferon

Answer 74

bradykines

Question 75

What are lymphokines, monokines?

Answer 75

cytokines that are secreted from lymphocytes and monocytes (respectively)

Question 76

What are chemokines?

Answer 76

cytokines that are chemotactic and are typically synthesized in response to proinflammatory cytokines

Question 77

What are interleukins?

Answer 77

cytokines that are produced primarily by WBCs (macrophages, neutrophils) in response to stimulation of PRRs/other cytokines and serve to alter behaviour of cells; can be proinflammatory or anti-inflammatory

Question 78

Four functions of interleukins include what?

Answer 78

1) chemotaxis (attracting leukocytes) 2) regulating cell adhesion molecules (CAMs) which are proteins that facilitate binding of cells or with ECM 3) induction, proliferation, and maturation of leukocytes in bone marrow 4) general enhancement/suppression of inflammation and adaptive immune response

Question 79

Which of the following is not an proinflammatory cytokine? 1) IL-1 2) TNF-a 3) IL-6 4) IL-10

Answer 79

IL-10

Question 80

What is tumor necrosis factor-alpha (TNF-a)? What is its role in inflammation?

Answer 80

A proinflammatory cytokine that is primarily secreted by macrophages in response to PAMP and toll-like receptor recognition Function: contributes to damaging effects of chronic inflammation and causes fever, synthesis of other inflammation-related proteins (acute phase proteins), muscle wasting (cachexia), and intravascular thrombosis

Question 81

What is interleukin-1 (IL-1)?

Answer 81

A proinflammatory cytokine mainly produced by macrophages and is an endogenous pyrogen (causing fever); also acts as a growth factor for many cells

Question 82

What is interleukin-6 (IL-6)?

Answer 82

A proinflammatory cytokine produced by macrophages, lymphocytes, fibroblasts and other cells Function: directly induces hepatocytes in the liver to produce acute phase proteins (proteins needed for inflammation), stimulates growth and differentiation of red blood cells in bone marrow, and growth of fibroblasts for wound healing

Question 83

Proinflammatory vs anti-inflammatory

Answer 83

Proinflammatory: up-regulate infection with goal of eradicating pathogens (causes fever, further inflammation, tissue death) Anti-inflammatory: diminish and control inflammatory response

Question 84

Two important anti-inflammatory cytokines include:

Answer 84

IL-10 TGF-b (transforming growth factor-beta)

Question 85

What is interleukin-10 (IL) and its function?

Answer 85

Anti-inflammatory cytokine primarily produced by lymphocytes function: - suppress activation and proliferation of other lymphoctes - limit production of proinflammatory cytokines - results in downregulation of inflammatory and adaptive immune responses

Question 86

What is transforming growth factor-beta (TGF-b) and its function?

Answer 86

anti-inflammatory cytokine that is produced in response to inflammation Function: suppress activity of lymphocytes and downregulate production of proinflammatory cytokines by macrophages

Question 87

What are interferons (IFNs) and its subclasses?

Answer 87

cytokines that protect against viral infections Type I interferons (IFN-a, IFN-b): produced and released by virally infected cells in response to viral dsDNA; do not kill viruses directly but induces antiviral proteins Type II inferferons (IGN-y): produced primarily by lymphocytes and increase bactericidal activity of macrophages

Question 88

List the immunoreactive cells.

Answer 88

1) mast cells 2) endothelial cells 3) platelets 4) neutrophils 5) eosinophils 6) basophils 7) monocytes/macrophages 8) lymphocytes and NK cells

Question 89

What are mast cells?

Answer 89

Significant, potent activators of inflammatory response with granules containing mediators that are released in tissue injury

Question 90

What are the two mechanisms in which mast cells release their mediators?

Answer 90

1) degranulation: release of contents of mast cell granules (histamine, chemotactic factors, cytokines) 2) synthesis: production and release of mediators in response to a stimulus

Question 91

What sort of vascular changes does histamine cause?

Answer 91

- constriction of large blood vessels/smooth muscle and dilation of postcapillary venules (net result: increased blood flow within microcirculation) - also causes increased vascular permeability secondary to retraction of endothelial cells

Question 92

Histamine H1 vs H2 receptors?

Answer 92

H1 receptors: causes bronchoconstriction (smooth muscle contraction) when activated - is proinflammatory when histamine binds to it H2 receptors: when activated, supresses leukocyte function (so function is anti-inflammatory) and induces secretion of gastric acid

Question 93

Antihistamines and H2 blockers are used against histamine function. What do each of these classes of drugs do?

Answer 93

Antihistamines: drugs block binding of histamine to H1/H2 receptors resulting in decreased vascular effects H2 blockers: medications that reduce gastric acidity in individuals prone to peptic ulcers/GERD

Question 94

Mast cells initiate synthesis of other mediators of inflammation. These mediators include what?

Answer 94

1) leukotrienes 2) prostaglandins 3) platelet-activating factor

Question 95

What are leukotrienes and its functions?

Answer 95

Leukotrienes are lipids that induce smooth muscle contraction (especially bronchoconstriction) and increase vascular permeability ; made from arachidonic acid from mast cell membranes function: stimulate slower and more prolonged inflammatory response (similar effects to histamine in later stages of inflammatory response)

Question 96

What are prostaglandins and its functions?

Answer 96

long-chained unsaturated fatty acids that cause increased vascular permeabiity, neutrophil chemotaxis, and pain they are produced by the action of cyclooxygenase (COX)

Question 97

What are the two forms of cyclooxygenase (COX)? If inhibited via inhibitor drugs, what will happen?

Answer 97

COX-1: activates platelets and protects stomach lining - if inhibited, GI tract bleeding and ulcers (think aspirin and NSAIDs suppressing inflammation but causing GI bleeds) COX-2: associated with inflammation - if inhibited, increased risk of CV disease due to effects on blood vessels and clotting

Question 98

What are platelet-activating factors?

Answer 98

- mediators that are produced by neutrophils, monocytes, endothelial cells, mast cells, and platelets - has similar activity as leukotrienes - causes endothelial retraction, platelet activation, mast cell activation

Question 99

Where are endothelial cells found and what do they do?

Answer 99

They are found lining blood vessels and regulate circulation (controlling water and solute movement between blood and tissues)

Question 100

What happens to endothelial cells when there is tissue injury?

Answer 100

endothelial cells contraction leading to increased capillary membrane permeability (allows for plasma and nutrients to move out of capillaries and into injured tissue)

Question 101

Platelets have no nucleus and are formed from \_\_\_\_\_\_\_.

Answer 101

megakaryocytes

Question 102

What do platelets do during inflammation/vascular injury?

Answer 102

- blood clotting - degranulate and release mediators like serotonin that have similar effects to histamine to accelerate inflammation - synthesizes thromboxane that vasoconstricts and induce platelet aggregation - recognizes and kills pathogens - release growth factors that promote wound healing

Question 103

What are the three granulocytes?

Answer 103

neutrophils, basophils, eosinophils

Question 104

The earliest phagocytes at site of inflammation are what?

Answer 104

neutrophils

Question 105

What is the primary function of neutrophils? How are they removed?

Answer 105

Function: phagocytize pathogenic microbes and remove cellualr debris and dead cells from lesions Short-lived so removed with purulent exudate (pus) through epithelium or drained through lymphatic system

Question 106

What are the functions of eosinophils?

Answer 106

primary defence against parasites and regulate vascular mediators released from mast cells (have lysosome enzymes that degrade vasoactive substances to limit vascular effects of inflammation)

Question 107

What are the functions of basophils?

Answer 107

- release histamine - also has heparin (anticoagulant) - important source of cytokines involved in adaptive immune response especially with allergies and asthma

Question 108

What are monocytes?

Answer 108

The largest WBCs that are produced in bone marrow and migrate to site of inflammation where they transform into macrophages

Question 109

What is the primary function of macrophages?

Answer 109

prolonged phagocytosis (can survive acidic environment of inflammatory site) so removes debris and promote healing and repair M1 macrophages: greater bactericidal activity M2 macrophages: primarily involved in tissue healing and repair

Question 110

What do dendritic cells do?

Answer 110

Antigen-presenting cells: they recognize invaders via PRRs and internalize invaders, then migrate through lymphatic vessels to lymph nodes where they present the invaders to T lymphocytes

Question 111

Difference between: B lymphocytes T lymphocyes NK cells

Answer 111

B lymphocytes - produces antibodies T lymphocytes - directly kills virus/cancer cells NK cells: part of innate immunity; recognizes and eliminates cells infected with virus/cancerous cells

Question 112

The two most important phagocytes for ingesting pathogens/damaged cells are:

Answer 112

neutrophils, macrophages

Question 113

Margination/pavementing is defined as what?

Answer 113

increased adhesion of neutrophils to endothelial cell wall of capillaries and venules (adhesion molecules increase stickiness of the cells)

Question 114

The emigration of cells through interendothelial junctions is known as:

Answer 114

diapedesis

Question 115

What are the 5 stages of phagocytosis?

Answer 115

1) Adherence - of phagocyte to its target through PRRs and opsonization 2) engulfment - bind to surface of phagocyte and engulfed into a phagosome 3) Phagosome formation 4) Fusion with lyososomal granules = phagolysosome 5) target destruction - lysosomal enzymes kill and digest microorganisms

Question 116

What are opsonins?

Answer 116

proteins that coat the target bacteria and act like glue tightening the affinity between phagocyte and target (makes phagocytosis more effective) ex. the most efficienct opsonins: C3b (from complement) and antibodies

Question 117

Within the phagolysosome, there are oxygen-dependent and -independent mechanisms that kill the pathogens. Describe how these mechanisms kill the pathogens.

Answer 117

Oxygen-dependent mechanisms: result from production of toxic oxygen species Oxygen-independent mechanisms: acidic pH, proteins binding to and damaging target cell membrane, enzyme attack on pathogen cell wall, inhibition of bacterial growth

Question 118

Phagocytes may die at inflammation sites. What occurs as a result of this?

Answer 118

Causes inflammation-associated tissue destruction due to releasing its enzyme contents (but this is minimized with natural inhibitors found in blood)

Question 119

Define acute inflammation.

Answer 119

Inflammation that is rapid onset and continues only until threat to body is eliminated (self-limiting, usually lasts 8-10 days from injury onset)

Question 120

Local manifestations of acute inflammation include what?

Answer 120

heat swelling redness pain potential loss of function exudate

Question 121

How do exudative fluids occur?

Answer 121

from increased vascular permeability and leakage of fluid into tissues

Question 122

Exudate that is water with few plasma proteins and leukocytes (Ex. fluid in blister), and indicates early or mild inflammations is known as what?

Answer 122

Serous exudate

Question 123

Describe fibrinous exudate and where you would find such?

Answer 123

thick and clotted exudate (indicates more advanced inflammation) ex. in lungs with pneumonia

Question 124

Accumulation of large number of leukocytes which occur in persistent bacterial infection (abscesses, pus) is known as what kind of exudate?

Answer 124

Purulent/suppurative exudate

Question 125

Exudate that is filled with RBCs and indicates bleeding is known as?

Answer 125

hemorrhagic exudate

Question 126

What are the 3 systemic manifestations of acute inflammation?

Answer 126

fever leukocytosis increased plasma protein levels

Question 127

What causes fever?

Answer 127

endogenous and exogenous pyrogens (specific cytokines release from neutrophils and macrophages) - act directly on hypothalamus which control's body's thermostat

Question 128

Treatment for febrile seizures?

Answer 128

tylenol, removing clothing "(to avoid exacerbation of problem)

Question 129

What is leukocytosis?

Answer 129

increased in number of circulating WBCs beyond upper limit of normal (11000 ml^3 in adults) - may also notice "left shift" (i.e. increase in ratio of immature to mature neutrophils)

Question 130

What is produced by the liver during acute inflammation?

Answer 130

acute phase reactants/proteins - C-reactive protein - Fibrinogen - Haptoglobin - Amyloid - Ceruloplasmin

Question 131

Someone with inflammatory process going on in the body would show _______ (increased/decreased) ESR and _______ (increased/decreased) c-reactive protein.

Answer 131

Increased; increased

Question 132

True or false. Chronic inflammation lasts at least 2 weeks and is always preceded by an unsuccessful acute inflammatory response

Answer 132

False. What's true is that it lasts at least 2 weeks but this statement is false because chronic inflammation can follow acute inflammation that was inadequate BUT can also be a distinct process on its own

Question 133

Chronic inflammation is characterized by:

Answer 133

- pus formation - suppuration (purulent discharge) - incomplete wound healing

Question 134

What are granulomas?

Answer 134

A walled-off/isolated infected area full of macrophages (epithelioid cells and giant cells), lymphoctytes, collagen - may calcify

Question 135

Epithelioid cell formation vs Giant cell formation

Answer 135

Epithelioid: differentiated macrophages that specialize in taking up debris and small particles giant cell: multinucleated active phagocytes that take up larger cells

Question 136

Regeneration is the process of what?

Answer 136

damaged tissue is replaced with healthy tissue of the original type (occurs in wounds that are minor damage with no complications)

Question 137

Define resolution/maturation in the context of wound healing

Answer 137

returning of injured tissue to its original structure and function (may take up to 2 years)

Question 138

Resolution may not occur in what wound situations?

Answer 138

1) extensive damage 2) injury site is where original tissue cannot regenerate 3) areas where infection has resulted in abscesses or granuloma formation 4) where fibrin persists in the lesion

Question 139

Define repair in the context of wound healing

Answer 139

replacement of destroyed tissue with scar tissue

Question 140

What is scar tissue?

Answer 140

collagen that mostly fills in the lesion to restore tissue integrity and strength but has no physiologic functions of tissue

Question 141

What are the 4 overlapping stages in wound healing?

Answer 141

1) hemostasis (coagulation) 2) inflammation 3) proliferation with new tissue formation 4) remodeling and maturation

Question 142

Wounds healing by primary intention are wounds that can be described to have\_\_\_\_\_\_\_.

Answer 142

minimal tissue loss

Question 143

Surgical incisions and paper cuts are examples of wounds that will heal by \_\_\_\_\_\_\_\_\_.

Answer 143

primary intention

Question 144

Wounds healing by secondary intention are wounds that can be describe as\_\_\_\_\_\_\_\_\_\_.

Answer 144

needing more tissue replacement; more time and care required as well

Question 145

Open wounds such as pressure ulcers and burns can be described to heal by \_\_\_\_\_\_\_\_\_\_\_\_.

Answer 145

secondary intention

Question 146

At best, repaired tissue that heals by secondary intention regains \_\_\_% of its original tensile strength

Answer 146

80

Question 147

What are the three regions/areas of the body in which normal tissue can regenerate without scarring ? This type of healing is known as \_\_\_\_\_\_\_\_\_\_\_\_\_.

Answer 147

- liver - bones - epithelium - known as compensatory hyperplasia

Question 148

A patient is recovering from an MI. He asks you whether or not his heart and cardiac function can return to normal. What do you say to him?

Answer 148

- MI heals with fibrous scar tissue rather than with cardiac muscle so cardiac function is not restored completely

Question 149

Phase I of wound healing is known as \_\_\_\_\_\_\_. What happens during this phase?

Answer 149

Hemostasis/coagulation - vascular injury causes immediate vasoconstriction and then vasodilation, and initiates clotting cascade and platelet activation to form a blood clot - platelets also degranulate and release factors that cause increased permeability and promote growth factors that initiate proliferation in undamaged cells

Question 150

Phase II of wound healing is known as \_\_\_\_\_\_\_. What happens during this phase?

Answer 150

Inflammation - begins within minutes; macrophages and mast cells release cytokines that increase blood flow to wound and bring needed cells and proteins to injury site (neutrophils to clear wound of debris and bacteria; lymphocytes to initiate immune response)

Question 151

Phase III of wound healing is known as \_\_\_\_\_\_\_. What happens during this phase?

Answer 151

Proliferation and New Tissue Formation - begins 3-4 days after injury and continues up to 2 weeks - wound is sealed and fibrin clot is replaced with normal/scar tissue (debridement) - angiogenesis - granulation tissue formation - epithelization occurs: epithelial cells growing into wound (can be sped up with moist wound to prevent it from becoming a scab) - fibroblast proliferation, collagen formation, wound contraction

Question 152

What is wound contraction?

Answer 152

a process of wound healing where fibroblasts turn into myofibroblasts and anchor themselves to wound bed to contract their fibers and exert tension on neighbouring cells (needed for closure of all wounds, noticeable 6-12 days after injury)

Question 153

Phase IV of wound healing is known as \_\_\_\_\_\_\_. What happens during this phase?

Answer 153

Remodeling and Maturation - begins several weeks after injury and is normally completed within 2 years - tissue regeneration and wound contraction continue in this phase - cellular differentiation, scar formation/remodeling (scar tissue becomes avascular)

Question 154

What factors can contribute to dysfunctional wound healing?

Answer 154

1) ischemia 2) excessive bleeding 3) excessive fibrin deposition 4) predisposing factors/disorders (diabetes, obesity, wound infection, inadequate nutrients, drugs, tobacco smoke)

Question 155

How does ischemia cause dysfunctional wound healing?

Answer 155

ischemia leads to cell death and infection which prolongs inflammation/delays healing - also reduces energy production and impairs collagen synthesis & tensile strength of regenerating tissue

Question 156

How does excessive bleeding cause dysfunctional wound healing?

Answer 156

- delays healing because large clots increase amount of space that granulation tissue must fill - clots also serve as mechanical barriers to oxygen diffusion - accumulation of blood is also a great place for bacterial growth leading to infection and inflammation

Question 157

How does excessive fibrin deposition cause dysfunctional wound healing?

Answer 157

- fibrin can eventually turn into fibrous adhesions which turn into bands that distort/impinge and strangulate organs --\> leads to pain and organ dysfunction

Question 158

How does diabetes cause increased risk of dysfunctional wound healing?

Answer 158

- persistent hyperglycemia leads to wounds being ischemic (small-vessel diseases and impaired blood flow) - suppresses macrophage function - hyperglycemia also increases a type of oxygen that does not allow oxygen to be readily realeased into tissues

Question 159

How does obesity cause increased risk of dysfunctional wound healing?

Answer 159

- impaired leukocyte function predisposes wound to infection - decrease growth factor production - increased proinflammatory cytokines - dysregulation of collagen synthesis - decrease in angiogenesis

Question 160

How does wound infection cause increased risk of dysfunctional wound healing?

Answer 160

- continued pathogen invasion into injured area means continuous need for body to fight off infection, uses nutrients, release of inflammatory mediators = delays wound healing

Question 161

How does inadequate nutrients cause increased risk of dysfunctional wound healing?

Answer 161

- your tissues at the wound already have increased metabolic demands so lacking nutrients is no good - vitamin A and C are requrred for collagen synthesis so lack of this leads to poorly formed connective tissue and significantly impaired healing - others include iron, zinc, manganese, and copper

Question 162

How does tobacco smoke cause increased risk of dysfunctional wound healing?

Answer 162

- toxic agents (CO, hydrogen cyanide) delay wound healing - nicotine also vasoconstricts which predisposes the tissue to ischemia and infection, thus compromising wound healing

Question 163

How do various drugs (antineoplastic/anticancer agents, NSAIDs, steroids) cause increased risk of dysfunctional wound healing?

Answer 163

- antineoplastic agents: slow cell division and inhibit angiogenesis - NSAIDs suppress acute inflammation and inhibit prostaglandin production which delays wound healing + associated with excessive scarring - steroids: disrupt wound healing by preventing macrophages from migrating to injruy site

Question 164

Which scars are likely to recur despite surgical removal?

Answer 164

keloids

Question 165

Which demographics have been shown to have a higher incidence of keloids with wound healing?

Answer 165

darker skin pigmentation familial tendency

Question 166

Define dehiscence. How does this happen and what is the treatment for it?

Answer 166

Complication where wound pulls apart at suture line (generally occuring 5-12 days after suturing) Happens due to excessive strain; increase risk in obese people because adipose tissue is difficult to suture Tx: prompt surgical attention

Question 167

What is a contracture?

Answer 167

excessive wound contraction that leads to anatomic deformity

Question 168

Where can contractures occurs and what is the management/treatment for this?

Answer 168

- Can occur with burns, particularly at joints - internal contractures can occur in duodenum (from improper healing of peptic ulcers); esophagus (from chemical burns like lye ingestion); abdomen from surgery/infection/radiation Treatment/prevention: - proper positioning - ROM exercises - compression - surgery for internal contractures

Question 169

Newborn innate immunity is limited. Where do they get their immunity from?

Answer 169

At the beginning as their own immunity is building, their immuntiy is acquired from their mother through placenta and breast milk

Question 170

Describe how the following affect/present in an infant's innate immunity/healing ability (relative to an adult's): 1) inflammatory response/inflammatory cytokine production 2) complement levels 3) monocyte/macrophage levels 4) Susceptibility to chemotactic defects 5) severity of sepsis and meningitis if infected 6) newborns via C-section 7) ability to fight off infection in utero

Answer 170

1) depressed inflammatory response, limited production of cytokine production 2) diminished complement levels 3) normal monocyte/macrophage numbers but delayed chemotaxis of monocytes 4) Predisposition to infections associated with chemotactic defects (especially cutaneous abscesses caused by Staph or Candidiasis) 5) predisposition to overwhelming sepsis and meningitis when infected by bacteria with no circulating maternal antibodies 6) reduced gut microbial diversity in newborns delivered via C-section 7) weak ability to fight off in utero infectio becaused infants have compromised oxidative and bactericidal response

Question 171

Describe how the following factors affect/present in an elderly's innate immunity/healing ability (relative to an adult's): 1) number of cells associated with innate immunity & cell function 2) risk of chronic inflammation 3) Ability to heal and repair 4) subcutaneous fat 5) epidermal changes 6) efficacy of vaccines

Answer 171

1) normal number of cells associated with innate immunity, diminished cell function (decreased phagocytic activity, antibody protection, and altered cytokine synthesis) 2) increased risk 3) risk of decreased/impaired healing and increased infection associated with chronic diseases 4) less subQ fat which diminishes layers of protection against injury 5) atrophied epidermis & underlying capillaries so decreased perfusion and increased risk of hypoxia in wound beds 6) diminished effectiveness due to normal aging process

Question 172

How may ASA interfere with wound healing?

Answer 172

ASA is an antiplatelet which prevents blood clotting so if there is excessive bleeding froma cut, it may lead to hemorrhagic stroke

Question 173

What are the two effectors for adaptive immunity?

Answer 173

lymphocytes and antibodies

Question 174

When does adaptive immunity kick in?

Answer 174

When external barriers have been compromised and innate immuntiy activated

Question 175

What are the main purposes of adaptive immunity?

Answer 175

- slowly ehance the first responder's job (inflammation) & promote processes against reinfection - destroy infectious invaders that are resistant to inflammation - long term protection against future exposure to same invaders

Question 176

What are the 4 characterists of adaptive immunity? Describe each briefly.

Answer 176

1) inducible - effectors (lymphocytes and antibodies) do not pre-exist in large numbers but are produced in response to infection 2) specific - to the infecting microbe 3) long-lived: here for a good time and a long time (different than inflammatory mediators that need to be cleared out quickly before they cause more harm than good) 4) memory: if re-infected by the same microbe, lymphocytes and antibodies are produced immediately

Question 177

What are antigens?

Answer 177

molecular targets of antibodies and lymphocytes (recognized by antibodies)

Question 178

How do lymphocytes become T and B cells?

Answer 178

lymphocytes go through extensive differentiation in the fetus before any exposures and then further differentiate when they go to primary lymphoid organs (thymus - turn into T cells; bone marrow - B cells) and they develop origin specific cell surface proteins and antigen receptors that allow you to differentiate between the two

Question 179

True or False: one individual lymphocyte is programmed to recognize only one specific antigen

Answer 179

True

Question 180

Before birth, each individual has produced enough B and T lymphocyes to recognize at least _____ different antigens. This is know as \_\_\_\_\_\_.

Answer 180

10^8 Generation of clonal diversity

Question 181

Define clonal diversity

Answer 181

the process by which extensive diversity of antigen receptors on B and T cells is established/produced

Question 182

True or false. Only a small selection of B and T cells undergo clonal selection at a given time.

Answer 182

True - because not every B and T cells have the same receptors for the antigen so some are chosen while others are just chilling (think like they are the chosen ones because they have certain characteristics)

Question 183

B and T lymphocytes leaving the primary lymphoid organs are immunocompetent. What does this mean?

Answer 183

Immunocompetent means they are able to respond to antigens but have not had any exposure to antigens yet and are thus naive

Question 184

Where do immunocompetent B and T cells go once leaving primary lymphoid organs?

Answer 184

enter blood and lymphatic vessels and migrate to secondary lymphoid organs (lymph nodes, spleen, tonsils, adenoid, peyer patches)

Question 185

How is clonal selection activated and what happens during this process?

Answer 185

- Initiated when there is an actual exposure to an antigen - antigens are processed and presented on the surface of phagocytes to lymphocytes (Th cells) - B and T cells that recognize that antigen are then chosen and differentiated into even more specialized cells (B cells into plasma cells that produces antibodies; T cells into Tc cells that identify and kill target cell) - also differentiate into memory cells

Question 186

Cellular immunity is mediated by what cells?

Answer 186

effector T cells that kill target cells (Tc cells) OR regulate immune response (Treg cells) + memory T cells that respond more quickly to re-exposure to antigen

Question 187

Humoral immunity is mediated by what cells/molecules?

Answer 187

soluble proteins produced by plasma cells + memory B cells that can produce more antibody rapidly to re-exposure

Question 188

Antibodies are also known as:

Answer 188

immunoglobulins

Question 189

What are antibodies

Answer 189

proteins used by the immune system to identify and neutralize foreign objects like bacteria and viruses

Question 190

Antibodies binding to antigens on bacteria and viruses are known as what sort of immune response?

Answer 190

humoral immune response

Question 191

Cell-mediated immune response involves what?

Answer 191

Effector T cells that circulate in the blood and tissues and defend against invaders/abnormal cells by killing targets directly and stimulating other leukocytes

Question 192

Active immunity vs passive immunity

Answer 192

Active: develops in response to exposure to an antigen (so now you are actively immune to this antigen by developing antibodies) --\> long lived Passive: receiving preformed antibodies/lymphocytes; they eventually get killed off by your own body so these are short-lived and not as strong

Question 193

A child acquiring immunity through her mother's breast milk/placenta at birth is known as:

Answer 193

passive immuity (or passive acquired immunity)

Question 194

A patient receiving an injection of antibodies to a disease is known as what type of immunity?

Answer 194

passive immunity

Question 195

If the antigen source is infectious agents, how are you protected through: a) your body b) vaccines Also indicate dx and tx of infectious agents.

Answer 195

a) body has antibody response against pathogenic microorganisms b) vaccines induce a safe and protective immune response (like childhood vaccines) Dx: measure circulating antigen or antibody Treatment: passive tx with antibody to treat/prevent infection (i.e. administering antibodies into patient)

Question 196

Your patient asks you how your body and vaccines works to protect you from cancerous antigens. They also ask you how cancers are diagnosed and treated against cancerous antigens. What do you say?

Answer 196

- body has immune surveillance to prevent early cancers and tumor growth/spread - vaccines with cancer antigens induce immunity to prevent tumor/growth and spread Dx: measuring circulating antigens Tx: immunotherapy (treatment with antibodies that are against cancer antigens)

Question 197

If the antigen source was from environmental substances, how are you protected through your body? Also indicate dx and tx against environmental substances.

Answer 197

a) your body tries to prevent them from coming in (secretory IgA are in bodily secretions and limits systemic exposure to potential allergens) Dx: measure circulating antigen or antibody (Ex. dx of allergy measured by circulating IgE) Tx: immunotherapy (administration of antigen for desensitization of individuals with severe allergies)

Question 198

If the antigen source is self-antigens, how are you protected through: a) your body b) vaccines Also indicate potential diagnosis and treatment related to self-antigens?

Answer 198

a) your body's immune system is tolerant to self-antigens (but can be altered by an infectious agent leading to autoimmune disease) b) typically don't need vaccines to protect against self-antigens; but some vaccines may alter tolerance to self-antigens (autoimmune disease) Dx: measuring circulating levels of antibody against self-antigen for dx of autoimmune disease Tx: no clear example

Question 199

Antigens vs. immunogens

Answer 199

Antigens: molecules that can bind with antibodies or antigen receptors on B/T cells Immunogens: molecules that bind to receptors and will induce an immune response (therefore all immunogens are antigens but not all antigens are immunogens)

Question 200

Most immunogenic antigens are (large/small) molecules

Answer 200

large (ability of an antigen to induce immune response is frequently relate to the size of antigen)

Question 201

What are haptens?

Answer 201

super small molecules that are too small to induce an immune response by themselves but become immunogenic after combining with large molecules that function as carriers

Question 202

Poison ivy contains a hapten known as _______ that chemically changes upon skin contact and binds to larger proteins in the skin to become immunogenic. This leads to T-cell response and the onset of ______ symptoms.

Answer 202

urushiol poison ivy rash

Question 203

When does the following occur? 1) generation of clonal diversity 2) clonal selection

Answer 203

1) primarily in fetus 2) primarily after birth and throughout life

Question 204

B cells in bone marrow develop a variety of necessary surface markers as it matures in order to allow for further differentiation and proliferation of B cells. These receptors are known as what?

Answer 204

B cell receptors (antibody complex; it's basically an antigen receptor)

Question 205

B cell receptors (BCRs) in incompetent B cells are made up of what?

Answer 205

membrane-associated IgM with or without IgD antibodies that have identical specificities for antigens

Question 206

Somatic recombination can occur in B and T cells. What does this mean and what is the significance of this?

Answer 206

Somatic recombination is the rearrangement of existing DNA in B/T cell development while in their primary lymphoid organs which allow for specificities of BCR/TCR HOWEVER: for this can cause the BCR/TCR to recognize and attack self-antigens which leads to autoimmune diseases (this is controlled by clonal deletion/central tolerance which is apoptosis)

Question 207

Clonal deletion/central deletion occurs in \_\_\_\_% of B cells, and \_\_\_% of T cells

Answer 207

\>90%; \>95%

Question 208

T cell receptors (TCRs) in incompetent T cells are made up of what?

Answer 208

two protein chains: alpha and beta chains

Question 209

During T cell differentiation, surface molecules CD4 and CD8 also develop during development. What happens to these happens as T cells mature?

Answer 209

as T cells mature, either CD4 or CD8 is retained (one or the other) - CD4-retaining cells become Th cells (60% of immunocompetent T cells) - CD8-retaining cells become Tc cells (40% of immunocompetent cells)

Question 210

What are antigen-presenting cells (APCs)?

Answer 210

cells that process and present the antigens to the immune cells - dendritic cells, macrophages, B cells

Question 211

Major Histocompabitility complex (MHC): What are they and where are they found?

Answer 211

glycoproteins that present antigens on APC surfaces for recognition by appropriate T cells; found on all cell surfaces of humans cells except RBC

Question 212

MHC are also called?

Answer 212

HLA - human leukocyte antigens

Question 213

What are the two classes of MHC molecules

Answer 213

MHC Class I - found on all nucleated cells and present endogenous antigens that are recognized by Tc cells MHC Class II - found only on APCs and present exogenous antigens which are recognized by Th cells

Question 214

What cells have both MHC class I and II molecules on their cell surface?

Answer 214

APCs - meaning they can present both endogenous and exogenous antigens to Tc and Th cells respectively

Question 215

What are the two steps in clonal selection?

Answer 215

1) antigen processing and presentation 2) cellular interactions in immune response

Question 216

Any cell that actively response to a stimulus and effects from change is known as:

Answer 216

an effector cell

Question 217

In clonal selection, three signaling events are required to produce a protective immune response (producting effector and memory cells for adaptive immunity). What are the three signaling events?

Answer 217

1) antigen-specific recognition through TCR/BCR complex 2) activation of intercellular communication 3) response to specific groups of cytokines

Question 218

What are Th (T-helper) cells?

Answer 218

cells that help the antigen-driven maturation of B and T cells (they are the ones that APCs present antigens to)

Question 219

What are the 6 steps of activating Th cells?

Answer 219

1. APC presents antigen which is recognized and binds on Th cell 2. antigen binding is strengthened by binding CD4 on Th cells with MHC class II molecule (on APC) 3. intracellular signaling pathways activated (by CD3 and CD4) 4. intercellular communication occurs and further activates Th cell 5. IL-1 secreted by APC and provides an additional signal through IL-1 receptor on Th cell 6. IL-2 secreted by Th cell and acts as an autocrine (self-stimulating) to induce further maturaiton and proliferation of Th cell

Question 220

Activated Th cells undergo differentiation into what 4 cells?

Answer 220

Th1 Th2 Th17 Treg

Question 221

Describe the function of the following cells: 1) Th1 cells 2) Th2 cells 3) Th17 cells 4) Treg cells

Answer 221

Th1: provides help in developing Tc cells (so is part of cell-mediated immunity) & defends against pathogens Th2: provides help in developing B cells (so involved wih humoral immunity) Th17: secrete lymphokines that activate macrophages to site of inflammation Treg: limit immune response by suppressing response and maintaining tolerance against self-antigens

Question 222

What are superantigens (SAGs)?

Answer 222

A group of molecules produced by bacteria viruses that bind to portion of the TCR/MHC that is outside of the normal binding site causing the APC to not be able to process and present it to an immune cell

Question 223

What effect does superantigens have on the body?

Answer 223

leads to excessive systemic inflammatory response (fever, low BP, potentially fatal toxic shock)

Question 224

Two examples of superantigens include:

Answer 224

Staphylococcus aureus Streptococcus pyogenes

Question 225

Tcytotoxic cells (Tc cells) do what?

Answer 225

starts off as immunocompetent Tc cell that can react with antigen but cannot kill target cells their TCR recognizes antigens presented by MHC Class I molecules and on virus/cancerous cells and then signals happen which then allow Tc to turn into effector Tc cells that are able to kill the bad cells (via apoptosis)

Question 226

How do B cells turn into plasma cells?

Answer 226

- B cell binds with antigen - B cell gets activated to process and present antigen on MHC class II molecules to TCR on Th cell - Th cells activated - intercellular communication induces Th2 cell differentiation and secretion of cytokines - B cell proliferation initiated and maturation into plasma cells

Question 227

What do plasma cells do?

Answer 227

make antibodies (that recognize the identical antigen as the BCR)

Question 228

What are T-cell independent antigens?

Answer 228

large bacterial products that bypass cellular interactions of B cells and Th cells leading to direct stimulation of B cell maturation and proliferation

Question 229

Class switch is a major component of B cell maturation. What is class switch?

Answer 229

the process that results in change in antibody production from one class to anotehr

Question 230

What are memory cells?

Answer 230

B and T cells that have differentiated and now remain inactive until there is another exposure to the same antigen - these cells will rapidly become plasma cells/effector T cells without cell interactions and go do their things

Question 231

The most abundant Ig and accounts for most of the protective activity against infections is:

Answer 231

IgG (80-85%)

Question 232

True or false: during pregnancy, maternal IgG is transported across placenta and protects newborn child during first 6 months of life

Answer 232

true

Question 233

How many subclasses does IgG have?

Answer 233

4 (IgG-1 to IgG-4)

Question 234

The Ig that is found predominantly in blood is

Answer 234

IgA

Question 235

The Ig that is found predominantly in bodily secretions is:

Answer 235

secretory IgA (or IgA-2)

Question 236

What is the benefit/important role of secretory IgA?

Answer 236

the secretory component of it protects the Ig from being degraded by proteolytic enzymes (meaning it can survive harsh GI environments and protect against microbes that multiple in body secretions)

Question 237

The largest antibody and the first one to be produced during primary response to an antigen is:

Answer 237

IgM

Question 238

IgE presence and function in the body:

Answer 238

The antibody that is normally low in circulation and has specialized functions as a mediator of many common allergic responses and defense against parasitic infections

Question 239

What is IgD's function?

Answer 239

part of BCR antigen receptor on surface of early B cells

Question 240

Before exposure to antigens and Th2 cells, B cells produce what two Ig that are used as cell membrane receptors?

Answer 240

IgM, IgD

Question 241

TRUE OR FALSE - During clonal selection, B cell proliferates and developes into plasma cells. at this point, B cells have the option of becoming secretor of IgM or changing class to secreted form of IgG, IgA, IgE

Answer 241

True

Question 242

What are the 3 structural parts of an antibody?

Answer 242

think of a Y two identical fragments bind antigen (antigen-binding fragments or Fab) third fragment: Fc or crystalline fragment that is responsible for functions of antibodies

Question 243

Antibody has how many polypeptide chains in its structure?

Answer 243

4 (2 light chains, 2 heavy chains)

Question 244

Epitope vs paratope

Answer 244

epitope: antigenic determinant (the precise area of the antigen that is recognized by antibody) paratope: antigen-binding site (the matching portion on the antibody)

Question 245

Antibodies can function to protect against infection through direct or indirect mechanisms. What are the direct mechanisms (through action of antibody alone)?

Answer 245

1) neutralization: inactivating or blocking antigens from binding to receptors (ex. using antitoxins to bind to toxin and prevent interaction with host cell) 2) agglutination: clumping insoluble particules that are in suspension 3) precipitation: making a soluble antigen into an insoluble precipitate

Question 246

Antibodies can function to protect against infection through direct or indirect mechanisms. What are the indirect mechanisms (i.e. done through activating other components of innate immune response)?

Answer 246

can be done through Fc portion of antibody, activating complement and phagocytes 1) inflammation (inducing this) 2) phagocytosis: antibodies acting as opsonin to facilitate phagocytosis of bacteria (usually IgG) 3: complement activation: to produce factors that destroy pathogens or increase activity of other components of inflammatory/adaptive immune response (IgM is the best for this one)

Question 247

What are monoclonal antibodies?

Answer 247

antibodies that are produced in the lab from B cells that has been cloned so entire antibody is of the same class, specificity, and function (can be used for immunotherapies that is resistant to standard chemotherapy tx)

Question 248

How does IgE protect from parasitic infections?

Answer 248

IgE is designed to specifically initiate an inflammatory response to attract eosinophils, this is done by: 1) parasitic antigens causing B cells to produce IgE 2) IgE binds to mast cell which degranulates and releases factors that attract eosinophil 3) eosinophil attaches to surface of parasite and releases potent lysosomal enzymes

Question 249

What happens when IgE is produced against innocuous environmental antigens?

Answer 249

causes common allergies (this is the primary cause)

Question 250

Systemic vs. secretory immune system

Answer 250

Systemic: made up of immunocompetent lymphocytes that migrate among secondary lymphoid organs and tissue Secretory: immune system that protects external surfaces of the body through lacrimal and salivary glands and various lymphoid tissues (plasma cells in these sites secrete antibodies into bodily secretions to prevent them from infecting body's surface and eventually causing systemic disease)

Question 251

Immune responses to antigen has two phases. These are known as what?

Answer 251

primary and secondary immune response

Question 252

How does primary immune response differ from secondary immune response?

Answer 252

primary: - single initial exposure that leads to latent period/lag phase (this is where clonal selection is happening) - IgM antibody is detected first followed by IgG, both against same antigen - if no further exposure to antigen, antibodies catabolized but immune system is primed Secondary: - more rapid production of lots of antibodies because memory cells are all ready to go - IgM transiently produced but IgG production is increased by lots making it dominant class of Ig during this phase

Question 253

Endogenous antigens are recognized by:

Answer 253

Tc cells (adheres to antigen, induces target cell to undergo apoptosis)

Question 254

What are NK cells?

Answer 254

group of lymphocytes that lack antigen-specific receptors but has other cell surface activation receptors to identify protein changes on cell surface when infected with virus/cancer

Question 255

Antibody-dependent cellular cytotoxicity (ADCC) is known as what?

Answer 255

an immune mechanisms where Fc receptors on the antibodies allow for antigen to attach, followed by NK cells to attach and activate normal killing mechanisms

Question 256

Newborns cannot produce all classes of antibodies. What antibodies are produced before and after birth?

Answer 256

- In utero: IgM (if utero infections are present) & lots of IgG but from mother - After birth: newborn's own IgG production begins and rises steadily through 1st year of life while maternal IgG is destroyed

Question 257

What happens to our immune function and thymus as we age?

Answer 257

decreased immune function, T cell function, and reduced antibody responses to antigens thymus also reaches max size at sexual maturity and then starts to shrink so less T cell function (there is also decrease in thymic hormone production and organ's ability to mediate T-cell differentiation)

Question 258

Inappropriate responses or hypersensitivity reactions may include which of the following? 1) allergies 2) alloimmunity 3) autoimmunity 4) immune deficiency 5) all of the above

Answer 258

all of the above

Question 259

What are hypersensitivity reactions?

Answer 259

altered immunologic responses to an antigen that results in disease or damage to the individual

Question 260

How are hypersensitivity reactions classified?

Answer 260

Two ways: 1) by immunologic mechanism that causes disease (Types I-IV) 2) by source of antigen that immune system is attacking (allergy, autoimmunity, alloimmunity)

Question 261

True or False. The mechanism that initiates onset of hypersensitivity reactions is unknown however likely a combination of genetic, infectious, and environmental agents

Answer 261

True

Question 262

Type I hypersensitivity reaction is also known as \_\_\_\_\_\_. Describe the following for this reaction: 1) rate of development 2) class of antibody involved 3) principal effector cells involved 4) is complement involved? 5) example of this type of reaction

Answer 262

IgE-mediated reaction 1) immediate development 2) IgE 3) Mast cells 4) No 5) seasonal allergies, asthma

Question 263

Type II hypersensitivity reaction is also known as \_\_\_\_\_\_. Describe the following for this reaction: 1) rate of development 2) class of antibody involved 3) principal effector cells involved 4) is complement involved? 5) example of this type of reaction

Answer 263

Tissue-specific reaction 1) immediate development 2) IgG, IgM 3) NK cells, macrophages, neutrophils 4) Frequently 5) Graves disease

Question 264

Type III hypersensitivity reaction is also known as \_\_\_\_\_\_. Describe the following for this reaction: 1) rate of development 2) class of antibody involved 3) principal effector cells involved 4) is complement involved? 5) example of this type of reaction

Answer 264

Immune complex-mediated reaction 1) immediate development 2) IgG, IgM 3) neutrophils 4) Yes 5) SLE

Question 265

Type IV hypersensitivity reaction is also known as \_\_\_\_\_\_. Describe the following for this reaction: 1) rate of development 2) class of antibody involved 3) principal effector cells involved 4) is complement involved? 5) example of this type of reaction

Answer 265

Cell-mediated reaction 1) delayed 2) none 3) lymphocytes, macrophages 4) no 5) contact sensitivity to poison ivy, metals (jewelry), latex

Question 266

Immediate vs delayed hypersensitivity reactions

Answer 266

Immediate: occurs within minutes to few hours after exposure to antigen, generally caused by antibody delayed: hours to appear (and max severity days after exposure), caused by cells (T cells, NK cells, macrophages

Question 267

The most severe and immediate hypersensitivity reaction is:

Answer 267

anaphylaxis

Question 268

Most common allergic reactions are which type of hypersensitivity reaction?

Answer 268

Type I (against environmental antigens)

Question 269

What does sensitization mean? And what is the mechanism behind it?

Answer 269

Sensitization means your body recognizes what you're allergic to During first exposure: 1) APCs present antigen to B cells under direction of Th2 2) causes B cells to turn into plasma cells and secrete IgE 3) IgE binds to mast cell and when enough is bound, mast cell is sensitized

Question 270

After sensitization occurs, what happens during re-exposure to an allergen (in type I hypersensitivity reactions)?

Answer 270

allergen connects with IgE and causes mast cell degranulation --\> histamine is released causing local edema, smooth muscle contraction, mucous secretion, and other sx of acute inflammatory reaction

Question 271

what happens when histamine binds to H1 receptors in the body?

Answer 271

bronchioconstriction edema (increased vascular permeability) vasodilation (increased blood flow)

Question 272

what happens when histamine binds to H2 receptors in the body?

Answer 272

increased gastric acid secretion

Question 273

Allergic reactions caused by food allergies (due to type I hypersensitivity) present with what symptoms?

Answer 273

nausea/vomiting diarrehea abdo pain

Question 274

Most common food allergy in adults

Answer 274

shellfish

Question 275

What happens to the skin during allergic reactions by type I hypersensitivity?

Answer 275

- urticaria (localized release of histamine and increased vascular permeability resulting in edema) - wheal and flare reaction: wheals (white fluid blisters) and flares (redness) + pruritus

Question 276

What happens to the mucous membranes in response to allergic reactions?

Answer 276

- conjunctivitis (inflammation of membrane lining eyelids) - rhinitis (inflammation of mucous membranes of nose) - asthma (bronchoconstriction)

Question 277

What happens in the lungs in response to allergic reactions?

Answer 277

- bronchospasm (airways constrict) - edema - thick secretions - leads to breathing insufficiencies/difficulties, wheezing

Question 278

An individual is described as atopic, what does this mean?

Answer 278

those who are genetically predisposed to develop allergies (tend to have higher quantities of IgE and more Fc receptors for IgE on mast cells)

Question 279

What tests/evaluations can be done to determine IgE hypersensitivity? How about treatment?

Answer 279

Dx: - food challenges - skin tests - lab tests for total IgE and allergen-specific IgE Tx: - antihistamines to block histamine receptors - block mediators to stop them from functioning (corticosteroids, leukotriene receptor inhibitor, PAF inhibitor)

Question 280

What are type II hypersensitivity reactions?

Answer 280

aka tissue-specific hypersensitvity reactions and are generally immune reactions against a specific cell or tissue

Question 281

what are tissue specific antigens?

Answer 281

antigens that are expressed on plasma membranes of only certain cells

Question 282

There are 5 general mechanisms by which type II hypersensitivity reactions can affect cells. What are they?

Answer 282

1) antibodies activate complement which destroys cells 2) antibodies cause cell destruction via phagocytosis by macrophages (complement is activated by antibodies, an opsonin from complement is deposited on target cell -\> increased phagocytosis) 3) neutrophil-mediated damage (molecules are released and bind to antibody, activates complement which makes chemotactic factors for neutrophils = tissue destroyed) 4) antibody-dependent cell-mediated cytotoxicity (ADCC) - antibodies on target cells are recognized by Fc receptors on NK cells, macrophages, or neutrophils and toxic substances are released that kill cell 5) target cell malfunction (Does not destory target cell but causes it to malfunction; antibodies change the function of the receptor on cell surface by blocking, stimulating, or destroying receptor)

Question 283

What are type III hypersensitivity reactions?

Answer 283

aka immune complex-mediated hypersensitivity reactions disease reactions caused by antigen-antibody (immune) complexes that are formed in circulation and deposited in vessel walls/other tissues

Question 284

How do type III hypersensitivity reactions lead to tissue damage?

Answer 284

complement is activated, and neutrophils are trying to destroy the immune complexes but this means lots of lysosomal enzymes are released into inflammatory site instead of into phagolysosomes leading to tissue damage

Question 285

What is the primary difference between Type II and III mechanisms for hypersensitivity reactions?

Answer 285

Type II: antibody binds to antigen on cell's surface Type III: antibody binds to soluble antigen that was released into blood or body fluids

Question 286

Immune complex-mediated hypersensitivity reactions most commonly result in what disorders/symptoms?

Answer 286

vasculitis in skin, kidneys, and lungs

Question 287

There are two model types/mechanisms that can describe various type III hypersensitivities. What are they?

Answer 287

Serum sickness Arthus reaction

Question 288

What happens in serum sickness?

Answer 288

reaction that happens due to immune complexes are formed in the blood and then depositied in target tissues

Question 289

An example of serum sickness is Raynaud phenomenon. What is this?

Answer 289

condition caused by temperature-dependent deposition of immune complexes (cryoglobulins) in capillary beds of peripheral circulation - precipitates at temps below normal body temp particularly in tips of fingers, toes, and nose - ends up blocking circulation and cause localized pallor and numbness followed by cyanosis (can become gangrenous if circulation is not restored)

Question 290

What happens in arthus reaction?

Answer 290

- reactions are cutaneous/localized - deposition of immune complexes mainly in the vascular walls leading to vasculitis - lesions are similar to typical inflammatory reaction (increased vascular permeability, accumulation of neutrophils, edema, hemorrhage, clotting, tissue damage)

Question 291

What are type IV hypersensitivity reactions?

Answer 291

cell-mediated hypersensitivity reactions reactions that are mediated by T lymphocytes and do not involve antibodies - antigens stimulate T cells to attack cell target directly or recruit phagocytes to do it

Question 292

Graft rejections, TB skin reactions, and allergic reactions from poison ivy and metals are what type of hypersensitivity reactions?

Answer 292

Type IV

Question 293

What is the delayed hypersensitivity skin test?

Answer 293

testing for TB exposure - slow onset - TB antigen is injected into the dermis of someone who has latent/active TB - if there is a reaction (induration - clear hard center that is indicated of macrophages and lymphocytes) and erythema, it is a +ve skin test result for TB infection

Question 294

For type IV hypersensitivity reactions, what happens during first exposure vs re-exposure?

Answer 294

first contact: sensitization (produces reactive T-cells) but symptoms-wise, no rash/dermatitis re-exposure: type IV cell-mediated reaction activated - dermatitis is present

Question 295

Allergy (atopy) is defined as:

Answer 295

hypersensitivity to environmental antigens (medicines, natural products, infectious agents, and others that are not naturally found in the individual)

Question 296

Define allergens

Answer 296

antigens that cause allergic responses

Question 297

Bee stings cause type ___ hypersensitivity reaction.

Answer 297

I

Question 298

A patient comes in with GI issues and throat tightness. On further evaluation, you obtain a low BP. What could this patient be suffering from and what is the treatment for such?

Answer 298

anaphylaxis tx: 1) epinephrine - reverses bronchodilation effects (antihistamines are NOT effective here because they're already bound) 2) potential clinical desensitization to allergens (small incremental doses over prolonged period)

Question 299

Define autoimmunity

Answer 299

disturbance in the immunologic tolerance of self-antigens

Question 300

True or false. everyone has autoantibodies (antibodies that are against our own antigens).

Answer 300

true. in small quantities that do not develop into autoimmune diseases

Question 301

Autoimmune disease are more common in (men/women).

Answer 301

women

Question 302

Define tolerance (in the context of immune control) and its relevance to autoimmune diseases.

Answer 302

Tolerance is the state of immunologic control so that individual does not make a detrimental immune response against his/her own cells and tissues - in autoimmune diseases, there is a breakdown of tolerance

Question 303

Symptoms of SLE result from a type III hypersensitivity reaction. What does this mean?

Answer 303

means that autoantibodies react with antigens and form immune complexes that are then deposited in the kidneys causing severe kidney inflammation

Question 304

SLE tends to occur more in which individuals?

Answer 304

- women, especially 20-40 age group - black individuals more than white individuals - genetic predisposition (increased incidence in twins, familial hx with SLE)

Question 305

What are the 11 most common clinical findings of individuals with SLE (i.e. symptoms)?

Answer 305

1) rash (on face/cheeks) 2) discoid rash (raised patches, scaling) 3) photosensitivity (skin rash from light) 4) oral/naso ulcers 5) non-erosive arthritis 6) serositis 7) renal dysfunction 8) neuro disorders 9) hematologic manifestations (anemia, leukopenia) 10) immunologic disorders 11) present of antinuclear antibodies (ANA)

Question 306

Dx and Tx of lupus includes?

Answer 306

Dx: lab testing to show positive ANA screening on test and medical history Tx: no cure but prevention/management of sx include: - NSAIDs (for pain and inflammation) - corticosteroids for active disease - immunosuppressants - antimalarial meds - protection from sun exposure

Question 307

What is alloimmunity?

Answer 307

immune response to non-self antigens from members of the same species (alloantigens/isoantigens) occurs when immune system of one individual produces an immunologic reaction against tissues of another individual

Question 308

Provide 3 examples of when alloimmune responses can occur.

Answer 308

1) transfusions 2) transplanted tissue 3) fetus during pregnancy

Question 309

What are the two types of alloantigens?

Answer 309

1) blood group antigens 2) histocompatibility antigens (HLAs)

Question 310

A and B blood group antigens are co-dominant. True or False.

Answer 310

True - both can be expressed at the same time

Question 311

Universal donor is blood type \_\_\_\_. Universal recipient is blood type \_\_\_.

Answer 311

donor: O recipient: AB

Question 312

The natural occuring blood group antibodies (i.e. anti-A antibodies, anti-B antibodies) are also known as:

Answer 312

isohemagglutinins

Question 313

If blood types were inappropriate mixed, what would happen?

Answer 313

severe transfusion reaction - agglutination or complement-mediated lysis

Question 314

The most important antigen of the Rh blood group is?

Answer 314

D antigen

Question 315

Most people in North America are Rh (positive/negative).

Answer 315

positive (85%)

Question 316

People who have D antigen are Rh\_\_\_\_\_.

Answer 316

positive

Question 317

What is hemolytic disease of the newborn? What is the treatment?

Answer 317

disease caused by IgG anti-D alloantibody produced by Rh-negative mothers against RBCs of Rh positive fetuses (mom's antibody crosses the placenta and destroys baby's RBCs) tx: RhoGAM shot

Question 318

Why does transplant rejection occur?

Answer 318

because HLA antigens are different between donor and recipient, and the recipient is having an immune response against foreign HLA antigens on donor tissue leading to rejection

Question 319

What occurs prior to any transplantation procedures to minimize tissue rejection?

Answer 319

tissue typing to identify differences in HLA antigens

Question 320

Transplantation rejection can be classified as:

Answer 320

Hyperacute Acute Chronic

Question 321

What is a hyperacute transplantation rejection? How do you avoid this?

Answer 321

Hyperacute: immediate and rare, rejection occurs due to presence of pre-existing antibodies (type II reaction) to HLA antigens on vascular endothelial cells in graft tissue - usually found in those with previous hx of multiple blood transfusions/transplants - white graft appears - HOW TO AVOID: testing the recipient for pre-existing antibodies prior to transplant

Question 322

What is an acute transplantation rejection? What is the tx for this?

Answer 322

cell-mediated immune response that occurs days to months after transplant & occurs when recipient develops an immune response against unmatched HLA antigens after transplantation (type IV reaction) treatment: combo of corticosteroids and antirejection drugs that block adaptive immune function

Question 323

What is a chronic transplantation rejection? What is the treatment for this?

Answer 323

occurs after months/years of normal function and characterized by slow, progressive organ failure - usually from chronic inflammation and weak cell-mediated reaction (type IV) against minor histocompatability antigens on grafted tissue - occurs in those who were poorly matched, have comorbidities, who received a damaged graft, or have required multiple acute rejection episodes - treatment: few; possible graft replacement with new transplant

Question 324

Define immune deficiency:

Answer 324

failure of immune or inflammatory response to function normally resulting in increased susceptibility to infections

Question 325

primary/congenital vs secondary/acquired immune deficiency?

Answer 325

primary: caused by genetic defect secondary: caused by another condition (cancer, infection, aging)

Question 326

True or false. Primary/congenital immune deficiencies are far more common than acquired forms.

Answer 326

False. Acquired forms are far more common

Question 327

What is the clinical hallmark sign of immune deficiency?

Answer 327

tendency to develop unusual/recurrent severe infections

Question 328

In children, how do severe primary immune deficiencies present?

Answer 328

failure to thrive

Question 329

If a patient indicates that they are experiencing reccurent infections with microorganisms that require opsonization, what deficiencies may be contributing to his immune deficiency?

Answer 329

B-cell/phagocyte deficiencies

Question 330

Primary immune deficiencies are mostly a result of:

Answer 330

single gene defects (sporadic mutations, not inherited)

Question 331

The three most commonly diagnosed primary immune deficiencies are:

Answer 331

1) common variable immune deficiency 2) selective IgA deficiency 3) IgG subclass deficiency

Question 332

Combined deficiencies are resulting from defects of what part of the immune system?

Answer 332

development of both B and T lymphocytes

Question 333

Severe combined immunodeficiencies (SCIDs) are the most severe kind of the combined deficiencies. It is characterized by what?

Answer 333

1) few detectable lymphocytes in circulation and 2' lymphoid organs 2) underdeveloped thymus (due to absence of T cells) 3) absent or reduced IgM and IgA levels

Question 334

Adenosine deaminase (ADA) deficiency is due to:

Answer 334

accumulation of toxic purines (classified under SCIDs)

Question 335

What happens in Bare Lymphocyte Syndome?

Answer 335

- adequate B and T cells but defective cooperation - lymphocytes and macrophages unable to produce MHC therefore antigen presenting and intercellular cooperation are not effectively occuring - can result in life-threatening infections in children, usually die before 5 yo

Question 336

What is Wiskott-Aldrich syndrome (WAS)?

Answer 336

X-linked recessive disorder (gene mutation) where IgM antibody production is ++depressed + major defect in platelet function Clinically: bleeding secondary to thrombocytopenia (low blood platelet count), eczema, recurrent infections

Question 337

What is DiGeorge syndrome? Include S/S and Tx.

Answer 337

- disorder due to gene deletion leading to lack/parial lack of thymus (thymic aplasia/hypoplasia) and thus greatly decreased T cell numbers and function - parathyroid gland also absent so inability to regulate calcium concentration - S/Sx: abnormal development of facial features (low set ears, fish shaped mouth, wide set eyes, shortened upper lip, underdeveloped chin) - Tx: transplant of fetal thymus tissue or thymic epithelial cells but this is only temporary improvement.

Question 338

Which category of primary immune deficiencies is the most common?

Answer 338

Predominantly antibody deficiencies

Question 339

Predominantly antibody deficiencies result from what? It can lead to what conditions?

Answer 339

defects in B-cell maturaiton or function - can lead to hypogammaglobulinemia (low levels of circulating Ig) or agammaglobulinemia (totally or near absent Ig)

Question 340

Treatment for B-cell immune deficiencies that lead to hypo/agammaglobulinemia includes:

Answer 340

IV Ig administration (antibody-rich) which replaces individual's antibodies temporarily so continuous treatment is needed

Question 341

What is selective IgA deficiency? Include S/S.

Answer 341

when class switch to IgA does not occur - mostly asymptomatic but with recurring sinus, pulmonary, and GI infections; + chronic intestinal candidiasis - may lead to allergens/diseases worsening due to secretory IgAs not doing what they normally do in bodily secretions

Question 342

What is Bruton agammaglobulinemia? Include S/S

Answer 342

X-linked agammaglobulinemia caused by blocked development of mature B cells in bone marrow (so there are few/none circulating) - S/Sx: repeated bacterial infections (strep throat, septicemia, conjunctivitis, middle ear infection)

Question 343

What is chronic granulomatous disease (CGD)? Include S/S.

Answer 343

Severe defect in oxidant manufacturing system that is needed for bacterial destruction in phagocytic killing - S/S: recurrent pneumonias - tumour-like granulomata in lungs, skin, bones - infections with opportunistic microorganisms

Question 344

What is Chronic mucocutaneous candidiasis? What are S/S and Tx?

Answer 344

disease caused by ineffective interaction between Th17 lymphocytes and macrophages so macrophages cannot be activated S/S: recurrent candida infections in mucous membranes and skin Tx: transplant of fetal thymus tissue/thymic epithelial cells (only temp improvement)

Question 345

What is C3 deficiency?

Answer 345

A complement immune deficiency leading to complement cascade not being activated Results in life-threatening infections with encapsulated bacteria (influenza, pneumonia)

Question 346

What is mannose-binding lectin (MBL) deficiency?

Answer 346

A complement immune deficiency with primary defect in lectin pathway of complement activation - results in increased risk of infection with microorganisms that have mannose-rich capsules

Question 347

Evaluation of Primary Immune Deficiencies include:

Answer 347

- complete blood count (CBC) with differential - quantitative determination of Ig (IgG, IgM, IgA) - assay of total complement

Question 348

Treatment for primary immune deficiencies include:

Answer 348

- replacement therapy (i.e. replacing the missing component of the immune system) - gene therapy (long term replacement of specific immune factors) - bone marrow transplant (for SCID)

Question 349

Treatment for SCID presents a risk of graft-versus-host disease (GVHD). What does this mean?

Answer 349

complication to transplant. occurs when T cells in transplanted graft are mature and therefore capable of cell-mediated immunity against recipient's HLA - this can be diminished by removing mature T cells from tissue used to treat individuals with immune deficiences

Question 350

Three of the more severe secondary/acquired immune deficiencies include:

Answer 350

1) malignancies 2) immunosupressive treatment 3) AIDS

Question 351

How are malignancies related to immune deficiency?

Answer 351

- disease itself or tx of malignancies can cause immunosuppression - cancer cells are also able to protect themselves by suppressing T lymphocytes

Question 352

What is acquired immunodeficiency syndrome (AIDS)?

Answer 352

acquired immunodeficiency that develops in response to viral infection (HIV) - it is the most advanced stage of HIV infection

Question 353

How does HIV affect immune system?

Answer 353

HIV infects and destroys CD4+ Th cells which are needed for development of B cells and T cells which means it destroys the cells that regulate normal immune response

Question 354

How can HIV be transmitted?

Answer 354

blood borne so via blood products, IV drug use, sex, maternal-child transmission

Question 355

The most common route to be affected by HIV is _______ and (women/men) make up majority of those with HIV/AIDS.

Answer 355

heterosexual activity; women

Question 356

The primary target cell of HIV is:

Answer 356

helper T cells

Question 357

What are the viral enzymes involved in HIV infecting host cell?

Answer 357

1) reverse transcriptase - converts RNA into DNA 2) integrase - helps new DNA insert into infected cells' genetic material 3) protease: processes the genetic material to make a new virion core

Question 358

When a new virion is released from host cell, how does it make itself less vulnerable to adaptive immune attack?

Answer 358

takes some of the host cell membrane with it

Question 359

Treatment for HIV/AIDS?

Answer 359

Antiretroviral therapy

Question 360

At time of dx of AIDS/HIV infection, how may the patient present?

Answer 360

1) serologically negative (no detectable antibody) 2) serologically positive (positive for antibody against HIV proteins) 3) early stages of HIV disease 4) AIDS

Question 361

What is the window period?

Answer 361

The period between infection and appearance of antibody against HIV proteins

Question 362

Acute HIV syndrome occurs when?

Answer 362

weeks after infection (virus at this time is progressively infecting T cells and other cells and spreads to lymphoid organs) - sharp decrease in number of circulating CD4+ T cells

Question 363

When does clinical latency of HIV infection/AIDS occur? What is happening during this time period

Answer 363

between ~9 weeks to 7/8 years - person is asymptomatic but virus replicates and T cell destruction continues

Question 364

Average time between HIV infection and development of AIDS is:

Answer 364

just over 10 years

Question 365

Who is recommended to be screened for HIV infection?

Answer 365

- ages 13-64 who have been informed to do so - men x men - pregnant women - those with STDs or TB

Question 366

Early stages of HIV disease mimic those of:

Answer 366

influenza (headaches, fever, fatigue)

Question 367

How does HIV infection differ in children compared to adults?

Answer 367

- more aggressive infection - neuro invovlement (failure to obtain developmental milestones, loss of intellectual ability, motor deficits, impaired brain growth, brain atrophy)

Question 368

Define endemic disease

Answer 368

A disease that is consistently present in a certain geographical location (high but constant rates of infection in a particular population)

Question 369

Define: Symbiosis

Answer 369

benefits only human, no harm to microorganism

Question 370

Define mutualism

Answer 370

benefits both human and microorganism

Question 371

Define commensalism

Answer 371

benefits only microorganisms, no harm to human

Question 372

Define pathogenic relationship

Answer 372

benefits microorganisms, harms human

Question 373

Define opportunism

Answer 373

where benign microorganisms become pathogenic because of decreased human host resistance

Question 374

Direct transmission of infection can include:

Answer 374

1) vertical transmission (ex. mother to child) 2) horizontal transmission (one person to another through blood/bodily fluids) 3) zoonotic infections: from animals

Question 375

Indirect transmission of infection can include:

Answer 375

1) coming in contact with infected materials 2) inhalation/droplet infection 3) ingestion/contamination of food/water 4) vaccination

Question 376

Define colonization

Answer 376

ability of pathogenic microorganism to survive and multiply on/within human environment - chances increase with making biofilms and increased adherence

Question 377

Define dissemination

Answer 377

spread of infection by direction extension through surrounding tissue or through blood/lymphatic vessels

Question 378

Define communicability

Answer 378

ability to spread from one individual to another and cause disease

Question 379

Define immunogenicity

Answer 379

ability to induce an immune response

Question 380

Define infectivity:

Answer 380

ability to invade and multiply in host

Question 381

Define pathogenicity

Answer 381

ability to produce disease (depends on communicability, infectivity, extent of tissue damage, and virulence)

Question 382

Define toxigenicity

Answer 382

ability to produce soluble toxins/endotoxins (toxic byproducts) - greatly influences degree of virulence

Question 383

Define virulence

Answer 383

capacity to cause severe disease

Question 384

Define epidemic

Answer 384

number of new infections in a particular population greatly exceeds the number usually observed

Question 385

Define pandemic:

Answer 385

epidemic that spreads over large area (continent/worldwide)

Question 386

What are the four stages of infection?

Answer 386

1) incubation period: between initial exposure and onset of first symptoms 2) prodromal stage: when first sx occur (often mild, general malaise) 3) invasion/acute illness period: rapid multiplying of pathogens here, patient is symptomatic and immune/inflammatory responses are triggered 4) convalescence: immune system does its job to remove infectious agents; sx decline, may be fatal, or enter latency phase

Question 387

Describe structure/composition of bacteria

Answer 387

- prokaryotes (no nucleus) - small - aerobic or anaerobic - motile or immotile

Question 388

Three types of bacteria, categorized by structure

Answer 388

cocci - spherical bacteria bacilli - rod-like forms spirochetes - spiral forms

Question 389

Gram-negative vs. gram-positive bacteria

Answer 389

difference is in structure of their bacterial cell wall (both have inner cell membrane but gram- negative has outer memebrane as well that stops antibiotics from penetrating the cell)

Question 390

What are the 5 virulence factors that help bacteria cause infection?

Answer 390

1) pili (fimbria) - hair like projections that increase attachment and adhesion to cells and invade tissue 2) flagella: mobility and expresses adhesion molecules 3) capsules: outer covering resists host immunity and prevents phagocytosis 4) enzymes: promote tissue invasion 5) toxins

Question 391

What effect does botulinum toxin have?

Answer 391

neurotoxic protein produced by bacteria Clostridium botulinum that prevents release of neurotransmitter acetylcholine from axon endings at the NMJ and thus causes flaccid paralysis

Question 392

Bacteremia vs septicemia

Answer 392

Bacteremia: occurs when bacteria are present in the blood Sepsis/Septicemia: occurs when bacteria are growing in blood and release large amounts of toxins (growth)

Question 393

what bacteria is the major cause of nosocomial infection?

Answer 393

Staphylococcus aureus (opportunistic)

Question 394

What are viruses?

Answer 394

obligatory intracellualr microbes that have nucleic acid protected by capsid

Question 395

What are the 5 modes of transmission for viruses?

Answer 395

1) aerosal (respiratory tract fluids) 2) infected blood 3) sexual contact 4) vector 5) zoonotic infection

Question 396

What is the viral life cycle?

Answer 396

1) attachement - to target cell 2) penetration - entrance via endocytosis/membrane fusion 3) uncoating - release of viral nucleid acid 4) replication - synthesis of viral proteins and mRNA (injected material into host) 5) assembly - new virions formed 6) release - existing of new virions by lysis or budding of cell

Question 397

Define antigenic variation

Answer 397

viruses making small changes to genes that produce viral surface antigens to escape immune defenses

Question 398

antigenic drift vs antigenic shift

Answer 398

antigenic drift: minor changes where it results in combination of two different strains of a virus making a new virus (but we have partial protection) antigenic shift: major changes where two or more different viruses combine to form a new strain

Question 399

Influenza is transmitted by what routes?

Answer 399

aerosols, body fluids (highly infectious)

Question 400

Symptoms between ____ days after infection and include what?

Answer 400

1-4 days - chills, fever, sore throat, muscle aches, severe headaches, coughing, weakness, generalized discomfort, nausea, comiting, potential pneumonia

Question 401

Describe the structure of fungi

Answer 401

- relatively large eurkaryotes (have nucleus) with thick, multilayered walls of polysaccharides - reproduction by simple division or budding

Question 402

What are the two basic structures of fungi?

Answer 402

1) single celled yeasts (spheres) 2) multicellualr molds (filaments, hyphae) dimorphic fungi ar those that can exist in either form^

Question 403

Infections cause by fungi are known as

Answer 403

mycoses

Question 404

Fungi that invade skin, hair, and nails to digest keratin are known as

Answer 404

dematophytes

Question 405

The most common fungal infection in humans is

Answer 405

C albicans

Question 406

What are parasitic microorganisms?

Answer 406

microorganisms that establish a relationship in which parasites benefit at the expense of other species

Question 407

What are the modes of transmission for parasitic infections?

Answer 407

human to human via vectors and ingestion

Question 408

Most common parasite worldwide?

Answer 408

malaria

Question 409

Some antibiotics are bactericidal while others are bacteriostatic. What do these terms mean?

Answer 409

bactericidal: kill microorganisms bacteriostatic: inhibit growth until microorganism is destroyed by individual's own protective mechanism)

Question 410

What are the 4 main mechanisms of action of most antibiotics?

Answer 410

1) inhibition of function or production of cell wall/membrane 2) prevention of protein synthesis 3) blockage of DNA replication 4) interference with folic acid metabolism

Question 411

How can microbes resist/inactivate antibiotics?

Answer 411

- make resistance genes and spread them to to other generations of microbes - degrade or alter antibiotics - eject antibiotics from the cell - modify cell wall to prevent antibiotic binding or uptake - modification of cellular target of antibiotic

Question 412

What species cause septic shock and multiple organ failure?

Answer 412

- endotoxins (aka lipopolysaccharide or LPS) from gram-ve bacteria - exotoxins from gram+ve bacteria (because they activate complement and clotting systems which lead to overproduction of various cytokines that cause fever platelet activation, intravascular coagulation and increased vascular permeability = hypotension, shock, organ failure)

Question 413

What happens during gram-ve sepsis/septicemia?

Answer 413

when bacteria are growing in the blood and release large amounts of endotoxins leading to endotoxic shock

Question 414

Staphylococcus aureus are (gram-ve/gram+ve) bacteria that are (cocci/bacilli/spirochetes).

Answer 414

gram+ve cocci

Question 415

How can Staphylococcus aureus be transmitted?

Answer 415

- direct skin contact - indirect contact with shared items/contaminated surfaces \*it is a common inhabitant on normal skin and nasal passages, is opportunistic, secretes exotoxins

Question 416

Staphylococcus aureus is known to be antibiotic resistant (penicillin). How does this occur?

Answer 416

production of beta-lactamase which is an enzyme that destroys peniciilin

Question 417

Staphylococcus aureus resistance of methicillin leads to what?

Answer 417

MRSA (superbug that leads to resistance)

Question 418

The ability of pathogens to cross surface barriers is known as:

Answer 418

invasion/penetration

Question 419

Which microorganism is involved with urinary tract infection?

Answer 419

Neisseria gonorrhoea

Question 420

How does bacteria survive in extracellular environments?

Answer 420

use virulence mechanisms to proliferate in body fluids (induces formation of humoral antibodies due to extracellular bacterial antigens)

Question 421

How does bacteria survive in intracellular environments?

Answer 421

can enter and survie in cells where they evade humoral antibodies and can disrupt cell structure and function; can only be eliminated by a cellular immune response

Question 422

Function of exotoxins

Answer 422

directly injure cells by damaging cell membranes or by entering cells and changing their function - causes production of antitoxins (antibodies)

Question 423

The most poisonous exotoxin is

Answer 423

botulinum neurotoxin (from Clostridium botulinum) whih is used in botox

Question 424

H1N1 swine flu is an example of an antigenic \_\_\_\_\_\_.

Answer 424

shift

Question 425

Influenza virus expresses two surface proteins that are essential to virulence. What are they?

Answer 425

HA - hemagglutinin (glycoprotein necessary for entrance into ell receptors on respiratory tract epithelium) NA - neuraminidase (enyme that releases new virions from infected cells)

Question 426

Without a major shift occurring, influenza is usually considered (epidemic/endemic/pandemic).

Answer 426

epidemic

Question 427

Please identify the following conditions: 1) dermatophytes affecting the scalp 2) dermatophytes affecting the feet 3) dermatophytes affecting the grown

Answer 427

1) tinea capitis 2) tinea pedis (athlete's foot) 3) tinea cruris (jock itch)

Question 428

A patient has an infection caused by his indewlling catheter and IV lines. The microorganism most responsible for this infection is: a) Toxoplasma gondil b) Candida albicans c) Plasmodium falciparum d) none of the above

Answer 428

b) Candida albicans - fungal infection (easy access straight ito the bloodstream(

Question 429

What can disseminated candidiasis look like in a patient

Answer 429

* abscesses in organs (because deep infections of internal organs) * persistent/recurrent fever * gram-ve like symptoms (hypotension, tachycardia) * disseminated intravascular coagulation (DIC) - blood clotting disorder

Question 430

The most common parasitic infections in the US are:

Answer 430

* Toxoplasma gondil (lifelong infection that may cause blindness, miscarriage, and CNS abscesses) * Trichomonas vaginalis (common sexually transmitted infection)

Question 431

What are antibiotics?

Answer 431

natural products of fungi, bacteria, and related microorganisms that affect growth of other microorganisms (used to prevent spread of infection)

Question 432

How can overuse of antibiotics lead to Superbugs?

Answer 432

Overuse of antibiotics lead to destruction of normal microbiome which lead to selective overgrowth of antibiotic-resistant strains/pathogens can occur (aka Superbugs)

Question 433

What method results in the strongest resistance against future infections from the same microbe?

Answer 433

Recovery from infection (so actually getting it and then recovering from it)

Question 434

What are vaccines?

Answer 434

biological preparations of antigens that stimulate production of protective antibodies or cellular immunity against a specific pathogen without causing potentially life-threatening disease

Question 435

What is the purpose of booster vaccines?

Answer 435

Primary immune response to a vaccine is usually short lived so booster shots help push the immune system through multiple secondary responses that result in large numbers of memory cells and sustained protective levels of antibody/T cells

Question 436

What are toxoids? What is their clinical significance?

Answer 436

* purified exotoxins that have been chemically detoxified without loss of immunogenicity * Clinical significance: Vaccination against systemic exotoxins (i.e. diphtheria, tetanus, pertussis) has been achieved using toxoids

Question 437

Vaccines for rabies, hep A and hep B are examples of (passive/active) immunity

Answer 437

passive \*with rabies, you get one shot of Ig (passive immunity) and then multiple shots of active immunization (killed viral vaccine)