Infection, fever and inflammation

Question 1

Host defense systems:

Answer 1

Skin mucous membranes: primary defense

Inflammation:

Non specific response occurs after any injury or infection
Immediate and general protection against any pathogen
Involved phagocytic WBS antimicrobial substance, natural killer cells

Immune response:

SPECIFIC form of response
Antigen-antibody
Recognizes and elimates altered host cells
Particular pathogen
Takes time to develop

Question 2

first line of defense :

Non specific resistance to disease

Answer 2

Mechanical: mucous membrane, skin, hair, cilia, saliva, urine, vomiting

Chemical: acid ph of skin, gastric juice

Question 3

second line of defense: Non specific resistance to

Answer 3

Antimicrobial proteins: Interferons, and the Complement system (MHC1)

Natural killer cells: Phagocytes
inflammation and
Fever

Question 4

structure of the immune system: organs and tissues

Answer 4

Lymph nodes:
Distribute our lymphatic vessels, Filter lymph and remove bacteria and toxins from circulation, Proliferation of immune cells (where T and B cells encounter antigens and initiate immune response)

Thymus: Located in mediastinum, Produces t lymphocytes
Mostly Inactive after puberty (T cells)

Spleen: largest lymph organ
Reservoir for blood, Macrophages clear cellular debris and process hemoglobin,

Tonsils:
Produce lymphocytes
Guard against airborne and ingested pathogens

Red bone marrow:
Houses stem cell that develop in lymphocytes (houses hematopoietic stem cells that can differentiate into various WBC, granular and a granular)

Question 5

What 3 factors comprise the Epidemiologic triangle

Answer 5

Pathogen:
-Any Agent that causes disease

Host
-Resistance: ability to ward off disease
-Susceptibility: vulnerability or lack of resistance to disease
-Host factors :how likely someone is to contract a disease
-Age, immunity, genetics, nutrition, underlying or pre existing diseases, health habits, stress, psychological factors

Environment:
-Humidity poor sanitation, migration status, pollution, standard of living

Question 6

Types of agents of disease

Answer 6

-Biologic: allergens, infectious organisms
-Physical: kinetic, radiation, thermal, noise
-Social and psychological: stress
-Chemical: toxins, dusts fire

Question 7

What does (emia) mean?

Answer 7

emia: its in the blood

Septicemia: infection; in the blood

bacteremia: presence of bacteria in the blood

Viremia
Presence of virus particles in the blood

Question 8

Viruses

Answer 8

Viruses contain a protein coat encapsulating them with their cores being RNA or DNA

No metabolic ability: cannot replicate outside the body. But some can

Can remain dormant for long periods and replicate/ produce symptoms for months to years

Question 9

Bacteria

Answer 9

Reproduce by cell division, no true nucleus, single celled
Pathogenic bacteria
Endotoxins: released when the cell wall decomposes. Can cause fever and damage
Exotoxins: produced by the alive intact bacteria

Question 10

MYCOPLASMAS AND RICKETTSIA

Answer 10

mycoplasma ⅓ size of bacteria, can reproduce on thei own. Do not have a vell wall thus they do not gram stain

Rickettsia
a diverse collection of obligately intracellular Gram-negative bacteria found in ticks, lice, fleas, mites, chiggers, and mammals.

Question 11

Fungi

Answer 11

Reproduce aesexualy

Relatively large microbes

Contain a true nucleus

Yeast or mold

Mycotic infections
Fungi that release mycotoxins

Question 12

parasites

Answer 12

Protozoa

Unicellular animals
Malaria, amebic dysentery

Helminths
Worm like parasites
Contact with eggs or larva getting in the skin

Arthropods
Ticks, biting flies

Ectoparasites
Outside the body
Transmitted through contact with clothing, begging, grooming
Lice, mites, bed bugs, chiggers

Question 13

Chain of infection

Answer 13

Trace the transmission of a disease from its source to

Pathogen (disease causing agent)

Reservoir (where pathogen lives and grows)

Portal of pathogen exit (exiting host)

Transmission (how they are passed: droplets, airborne (smallest size of droplet)

Portal of entry (how they enter host)

New host

Question 14

Normal Body Flora

Answer 14

Harmless microorganisms that reside in or on the body

Found on skin and in the nose, mouth, pharynx, distal intestine, colon, distal urethra & vagina

provide many useful function:

help prevent colonization of pathogens

intestine flora help create vitamine K

Question 15

Peripheral smear: cellular elements

Answer 15

Peripheral smear : cellular elements: know functions, roles, what elevated counts of each mean

GRANULOCYTES: granules in cytoplasm
Neutrophils (bands when
immature one are released from exhaustion of red bone marrow)

Phagocytosis “pyogenic” less amount of neutrophils→ increases the number of bands created (when immune response is activated for 24-48 hours)

Basophils
Allergy and inflammatory response

Eosinophils
Release heparin and histamine. Delayed allergic response and parasitic infection response.

Agranulocytes: no granules in cytoplasm
Lymphocytes
B and T cells
B: mature into plasma cells and release antibodies
T: regulate cell mediated immunity

Monocytes:
Phagocytosis, severe infections

Red blood cells

Platelets

Question 16

Macrophages

Answer 16

Lack surface receptors for specific antigens

Have receptors for Fc region and for complement

Ingest and process antigen and deposit it on its surface in association with MHC II complex. It presents the antigen MHC complex to T lymphocytes which active these T cells.

Secrete cytokines: Tumor necrosis factor and interleukin which produce fever

Both humoral and cell mediated responses

Question 17

MHC 1 and MHC 2

Answer 17

MHC Class I: endogenous antigen presentation ( self from not self)

Location: Found on the surface of all nucleated cells in the body.

Function: Presents endogenous antigens (from within the cell) to cytotoxic T-cells (also known as CD8+ T-cells), which are responsible for eliminating infected or tumor cells.

Example: Presents peptides derived from viral proteins or cellular proteins to cytotoxic T-cells.

MHC class II: exogenous antigens (foreign pathogens)

Location:
Expressed on antigen-presenting cells (APCs), such as macrophages, dendritic cells, and B cells.

Function:
Presents exogenous antigens (from outside the cell) to helper T-cells (also known as CD4+ T-cells), which help orchestrate other immune responses.

Example:
Presents peptides derived from pathogens or other extracellular sources to helper T-cells.

Question 18

Dendritic cells

Answer 18

Monneuclar

Activate naive T cells that have not been subjected to an antigen

Question 19

Reticuloendothelial system: tissue macrophages

Answer 19

Lung: alveolar macrophages
Liver: Kupffer’s cells
Spleen
Lymph nodes
Intestine: Peyer’s patches
CNS: microglial cells
Skin: Langerhans’ cells
Connective tissue: histiocytes

Question 20

WBC differential (types of leukocyte and function)

Answer 20

Question 21

WBC differential count

Answer 21

Relative count % percentage must add up to 100%

Absolute count # of each cell totaled

Absolute count total (total # of all WBC) X Relative count % of a type of WBC = absolute count of that specific type

the sum of absolute count of specific types should = Absolute total count

The sum of relative count % of all types of WBC should = 100%

Make sure to include neutrophil bands in the count

Important: Absolute count changes (of specific types of WBC) are very important in assessing stage infection/injury and type

i.e an increase in # of neutrophil bands means prolonged infection

Question 22

Osis vs enia

Answer 22

osis ex: leukocytosis means increased WBC count above normal

enia: leukopenia means decreased WBC count below normal

Question 23

Significance of WBC count

Answer 23

type of injury: Infection, inflammation, tissue necrosis, allergies

Critical values: <2500 cells/mm^3 or > 30,000 cells/mm^3 are the normal absolute total count #
(10,000 to 15,000) are common in critcal wounds

Age: infants tend to have higher WBC and elderly may not develop increased WBC count even in the presence of severe bacterial infection

Monocytes: increase in severe infection, Bands also increase (36-40a0 hours

Question 24

ESR and CRP

Answer 24

non specific markers, its an exclusive test (ex: if WBC is normal and ESR and CRP is normal than the patient is prob not having an infection, or at least not yet) elevation in either may mean trauma, infection, necrosis

ESR: rate at which RBC settle out of anti coagulated blood in one hour
in acute infections ESR doesn’t elevate for 4-24 hours and peaks after several days. Fibrinogen and immunoglobins increase infection making RBC stick together (Rouleaux formation)

CRP: protein made by the liver in response to (IL-1, IL-6, AND TNF-alpha) acute damage, levels increase up to 1000x times normal then rapidly declines when the inflammatory response goes away. good indicator of healing response. 18-24 hours and starts to decrease earlier as well.

Question 25

culture and sensitivity

Answer 25

specimen sample placed in culture media and allowed to grow antimicrobial agents are used to test effectiveness (note that in vitro tests do not reflect attainable concentrations at infection site or other factors like ph that can change activity of a drug) ex: Kirby bauer

Question 26

serial solution

Answer 26

logarithmic fashion of diluting a sample used to dilute specimen from patient to get a countable number of separate colonies TNC: too numerous to count

Question 27

Gram stain

Answer 27

Positive: purple, bacteria have thick cell wall of peptidoglycan negative: stain red

Question 28

Urinalysis

Answer 28

Appearance and color: cloudy, (pus, necrotic WBC) or RBC’s or bacteri Oder Foul may be indicator of infection Ph Bacteria can increase pH Urea splitting bacteria (alkaline) Leukocyte esterase Screening test used to detect WBCs in urine Nitrites Screening tests for UTI’s Bacteria produce enzyme called reductase which can reduce nitrites (50% accuracy) False positive if contaminated with vaginal secretions

Question 29

stool culture

Answer 29

Normal flora bacteria and fungi, can be pathogenic if immunocompromised Pathogens: salmonella, shigella, campylobacter yersinia Presence of urine can inhibit bacterial growth for false negative do samples need to be seperate Diarrhea good indicator to use this test

Question 30

Acute inflammatory response

Answer 30

Response Rapid and non specific Protective response to cellular injury from any cause Only occurs in vascularized tissue Results in accumulation of fluid and cells at the site Itis = inflammation signs: rubor, swelling, tumor, heat (calor), pain (dolor), loss of function

Question 31

Inflammation

Answer 31

Vascularized tissue experiencing a injury (blood supply) Active, aggressive, and non specific You can have inflammation and not infection, but have infection and there will be inflammation Colonization (presence of microbes does not along produce inflammation) Infection is the only activity that can cause cell injury and inflammation Cellular injury will produce non specific inflammatory response

Question 32

Hypoxic Mechanisms of cellular injury

Answer 32

Hypoxia: Lack of sufficient oxygen Decreased oxygen in the air, loss of hemoglobin function, decreased red blood cells, diseases of respiratory or cardiovascular systems Ischemia: Reduced blood supply (gradual vs sudden acture) Ex: gradually narrowing of the arteries, thrombosis: complete blockage of an artery by blood clot, embolus (traveling blood clot from distant cite now blocking blood flow) Anoxia: Total lack of oxygen 3 minutes without oxygen: risk of brain damage Infarction (heart attack) Cell death Hypoxia does not produce ischemia, but ischemia can certainly produce hypoxia. Both can make infarction occur

Question 33

Vascular response: to damage

Answer 33

Arteriolar vasoconstriction → vasodilation → swelling→ erythema (redness) → hyperemia Increased capillary permeability→ allows fluid to escape into tissue → swelling edema (fluid dilutes toxins) Pain and impaired function, tissue swelling and release of chemical mediators

Question 34

cellular response

Answer 34

WBC move toward damaged cells → phagocytosis of dead cells and microbes (particularly neutrophils)→ platelets move toward damage cells and control any excess bleeding in area Mast cells→ release heparin to maintain blood flow to the area Heparin makes platelets less effective (stop bleeding but enough to perfuse the area and let WBC arrive) Granulocytes: Neutrophils, basophils, eosinophils Mononuclear phagocytes Margination and emigration of leukocytes Chemotaxis Phagocytosis

Question 35

More on granulocytes:

Answer 35

More on granulocytes: Neutrophil-primary phagocyte: -Arrive early -Polymorphonuclear (PMN or polys) segmented neutrophils -Bands are immature neutrophils Eosinophils -Allergic and parasitic infections -Release chemical mediators for inflammation Basophils: (mast cells in tissues) -Inflammation and allergic reaction -Contain histamine and is a mediator of inflammation Leukocytosis = an increase in WBCs

Question 36

Mononuclear phagocytes

Answer 36

largest WBC (3-8%) 3-4X LONGER LIFESPAN; and stay longer in tissues Mature into macrophages w/ in 48 hours monocytes and macrophages are predominant cell type Can phagocytize larger material than neutrophils. But cannot do so for smaller items Migrate to local lymph and play a role in specific immunity Role in chronic inflammation, wall off material that cannot be digested Ex: copd, nodules are walled off debris that could not be destroyed monocytes can differentiate to macrophages

Question 37

Margination and emigration of leukocytes:

Answer 37

Fluid leaves capillaries, increasing blood viscosity Release of chemical mediators (histamine, leukotrienes, and kinins) and cytokines affect endothelial cells of capillaries This increases expression of adhesion molecules Leukocytes marginate Emigration- diapedesis through capillary walls

Question 38

Chemotaxis:

Answer 38

how leukocytes travel through tissue and find the damaged area Guided by secreted cytokines (chemokine, Interleukin-8) from damaged tissue, bacterial and cellular debris, complement fragments (C3a and C5a) Migration is response to chemical signals increases chance of sufficiently localized cellular response Once WBC get there how do they identify self and not self (MHC1)

Question 39

Phagocytosis

Answer 39

Once migration is complete neutrophils and macrophages engulf and degrade bacteria and cellular debris 4 steps Chemotaxis Attraction of WBC to area Adherence: Opsonization Coats the antigen with antibody (Fc) or complement (C3a) (tagging pathogens), this tagging makes them more visible to phagocytes Engulfment Surround and enclose the particle in phagocytic vesicle (phagosome), which then merges with lysosome, and antibacterial molecules and enzymes which digest the microbe Intracellular killing Via enzymes, defensins, toxic products

Question 40

steps of leukocyte recruitment to site of injury or infection

Answer 40

Margination: injury occurs, chemical mediators released, then selectin proteins released from endothelial cells to recruit leukocytes emigration: WBCs move through blood vessel wall and into the surround tissue migration: WBCs find their way to the cite of damgage via chemotaxis phagocytosis: the engulfment of pathogen or debris, destruction of that debris via merging it with lysosome vesicle internally of phagocyte cells

Question 41

Inflammatory mediators (6)

Answer 41

Histamine plasma proteases prostaglandins leukotrienes platelet activating factor cytokines

Question 42

Histamine

Answer 42

main chemical inflammatory mediator, by released basophils, platelets and mast cells. Causes vasodilation and increased blood flow (more WBC margination) and increases capillary permeability Stimulates Bronchoconstriction (H1 receptors) Gastric acid secretion (H2 receptors) (must take anti protons med to stop acid production in hospital)

Question 43

Plasma proteases

Answer 43

Kinins: by activated complement proteins, and clotting factors Bradykinin: increases capillary permeability and causes pain Contributes to vascular phase of inflammation through fibrinopeptides formed during final step of blood clotting process

Question 44

Prostaglandins

Answer 44

Produced from arachidonic acid found in the cell membranes via cyclooxygenase PGE and PGE2 especially important They increase blood flow and capillary permeability Potentiate effects of histamine, cause fever in response to infection. Stimulate pain receptors Block by NSAID’s

Question 45

Leukotrienes

Answer 45

increase vascular permeability Affects adhesion of WBC to capillary during injury or infection Act as chemoattractant SRSA = slow reacting substance of anaphylaxis→ role in bronchoconstriction in asthma

Question 46

Platelet activating factor

Answer 46

Generating from a complex lipid in cell membranes Affects a variety of cell types Induces PLT aggregation Activated neutrophils Potent eosinophil chemoattractant

Question 47

Cytokines (interlukins)

Answer 47

Cytokines: (don't memorize each interleukin but what they do) Peptides produced by a variety of immune and inflammatory cells: Macrophages, monocytes, neutrophils, lymphocytes Also found in non inflammatory cells Fibroblasts and endothelial cells Referred to by specific name or numbered Interleukin Function as local hormones that affect host response to injury or infection Multiple effects serve as a communication links between immune and IL-1, IL-6: Promote fever, tiredness Released from macrophages and monocytes, or activated T cells Activate B cells→ plasma cells and secrete antibodies IL-2 Secreted by activated helper T cell IL-2→ stimulates cytotoxic T cells Alert macrophages to increase phagocytosis Noninflammatory cytokines: IL-10 Decease activation of B cells

Question 48

Inflammatory Exudates:

Answer 48

Fluid, plasma protein, cell contents Types: Serous: watery, low protein plasma Fibrinous: fibrinogen, thick sticky meshwork like a clot Membranous: develop on mucous membrane surface, necrotic cells enmeshed in fibrino-purulent exudate Purulent or suppurative: contains pus (WBCs, neutrophils and macrophages, proteins and tissue debris_ Hemorrhagic: leakage of RBC’s

Question 49

Abscesses and ulcers

Answer 49

Abscess: Typically have a central necrotic core containing purulent exudate surrounded by a layer of neutrophils Ulceration: Site of inflammation where an epithelial surface has become necrotic or eroded. associated with subendothelial inflammation Injury or vascular compromise In chronic lesions, the area surrounding the ulceration develops fibroblastic proliferation with scarring and accumulation of chronic inflammatory cells

Question 50

Granuloma formation:

Answer 50

If acute response is failed then chronic ensues 1-2 mm lesion of macrophages surround by lymphocytes Associated with foreign bodies Formed with giant cells Outside: encased by a collagen new Inside:debris decays and forms a liquid that may diffuse out leaving the thick wall casing (created by macrophages

Question 51

Acute phase response: systemic responses

Answer 51

Changes in concentration of plasma proteins Liver increases synthesis of acute phase proteins as fibrinogen and c reactive protein Increased erythrocyte sedimentation rate Fever In bacterial infections: Increased number of leukocytes Increased number of circulating WBC;s by stimulating production in bone marrow (neutrophilia and shift to the left) In parasitic infection and allergic reactions ( Eosinophilia) Viral infections: neutropenia and lymphocytosis In overwhelming infections and presence of other debilitating disease such as cancer (leukopenia) Skeletal muscle catabolism and negative nitrogen blance Amino acids are used for immune response and tissue repair Lethargy( effects of interleukins and TNF)

Question 52

Lymphadenopathy

Answer 52

characterized by a localized or generalized enlargement of the lymph vessels

Question 53

Lymphadenitis

Answer 53

Inflammatory condition of the lymph noes Nodes may be enlarged, hard, smooth or irregular, and may be red, feel hot or tender to the touch Location of the node is indicative of the site of origin of disease-affected node are proximally located along the lymphatic drainage pathway painful nodes area associated with inflammation non painful nodes are associated with neoplasms (benign, or malignant cancer)

Question 54

Fever aka pyrexia

Answer 54

Elevation in body temperature Cardinal manifestation of disease Do not minimize it or ignoe it Following major surgery or mI, low grad temp for 1st 48-72 hours is normal Body thermostat is in the hypothalamus Raised by toxins released during inflammatory process

Question 56

stages of fever and patterns

Answer 56

prodromal General malaise, fleeting aches and pains Stage 1: cold shaking and chill stage 10-40 min with rapid steady rise in temperature, increase cellular metabolism and vasoconstriction and cessation of sweating Stage 2: flush Thermostat reset, cutaneous vasodilation, skin warm and flushed, dehydration Stage 3: defervescence Initiation of sweating patterns: Intermittent Returns to normal at least every 24 hours Remittent Varies a few degrees in either direction Sustained or continuous Temperature increases with minimal variation Recurrent or relapsing One or more episodes of fever each lasting several days with one ore more days of normal T between episodes

Question 57

Manifestations of fever:

Answer 57

Anorexia Myalgia (muscle pain) Arthralgia (joint pain) Fatigue Increase in RR Diaphoresis Dehydration Metabolic acidosis Headache Delirium and confusion Incoordination and agitation Febrile convulsions Herpetic lesion or blisters

Question 58

treatment of fever

Answer 58

Modification of external environment Tepid baths and cooling blanket Treatment of underlying cause Fluid replacement and simple carbs Antipyretics: Acetaminophen, NSAIDS, ASA (aspirin) Children: most common Elderly: 20-30 % present with absent or blunted febrile response due to metabolism slowing down with age