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chapter 2 Flashcards

1
Q

Causes of antibiotic resistance

A

 Antibiotic Overuse – creation of ‘superbugs’ – antibiotic-resistant organisms
 Methicillin-resistant Staphylococcus aureus (MRSA)
 Multi-drug resistant Mycobacterium tuberculosis
 Vancomycin-resistant Enterococci
 Multi-drug resistant Pseudomonas aeruginosa
 Fluoroquinolone-resistant Clostridium difficile
Antibiotic Resistance – Other Factors
 Increased travel/exposure – with globalization
 TB on the rise; 2nd leading cause of death due to infectious disease worldwide  Susceptible sub-populations:
 Kids in daycare
 Aging
 Hospital populations
 3 rd world poverty – stress, poor nutrition, close quarters (easy spread), lack of medical care
-use in agriculture

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2
Q

Some bacteria, all viruses, and all parasites cause illness via infection.
– Bacteria: Salmonella spp., Listeria monocytogenes, Campylobacter jejuni, Vibrio parahaemolyticus, Vibrio vulnificus, and Yersinia enterocolitica.
– Viruses: Hepatitis A, norovirus, and rotavirus.
– Parasites: Trichinella spiralis, Giardia duodenalis

A

Infection

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3
Q

results when a person eats food containing toxins that cause illness.
Toxins are produced by harmful microorganisms, the result of a chemical contamination, or are naturally part of a plant or seafood.

A

Intoxication: Some bacteria cause an intoxication.
Viruses and parasites do not cause foodborne intoxication.
– Bacteria: Clostridium botulinum, Staphylococcus aureus, Clostridium perfringens, and Bacillus cereus

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4
Q

Signs and symptoms – know what they are

Signs and Symptoms of Infectious Diseases

A 
 Many and varied
  Can be systemic (fever) or local (pus) 
 Depends on: 
– Etiologic agent
 – type and virulence 
– System affected 
– Health of the individual
Common Systemic Signs & Symptoms
  Fever  Chills  Sweat  Malaise  Nausea  Vomiting  Change in leukocyte type and/or number  Enlarged lymph nodes  Possible cognitive changes in the elderly
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5
Q

– pathogenesis (pyrogen affect hypothalamus), causes, over 37 C

A

− Fever

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6
Q

many types and variety of causes of rash

A

FYI Common Rashes with Infections
 Maculopapular eruptions: – Measles, Rubella, Fifth Disease, Roseola
 Nodular lesions: – Streptococcus, Pseudomonas
 Diffuse erythema: – Scarlet Fever, Toxic Shock Syndrome
 Vesiculobullous eruptions: – Varicella, Herpes zoster
 Petechial purpuric eruptions: – Epstein Barr Virus

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7
Q

-Can be associated with many infectious diseases, not just sepsis  Easily palpated – Cervical – Inguinal – Axillary  Other reasons for inflamed lymph nodes: – Cancer – Rheumatoid Arthritis – Medications

A

− Lymphangitis

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8
Q

local infection spreading into the lymphatic system – Lymphangitis – Moves towards local lymph node

A

red streak

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9
Q

−- Secondary to an infection  Usually from: – Hemolytic Streptococcus and/or Staphylococcus
 Lymph nodes most often affected: – Submandibular – Cervical – Inguinal – Axillary

A

Sepsis

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10
Q

Aging We become more susceptible to infectious disease as we age:
 Immunosenescence – changes in the immune system as we age
 Decreased circulation and poor wound healing
 Decreased function of natural barriers: – Skin; pH less acidic; fewer natural secretions to help with flushing (i.e. tears
– Decreased cough/gag reflexes · decreased ability to clear secretions
– Decreased bronchiolar elasticity and mucociliary activity · increased risk of pneumonia

A

 Decreased T-cells formed, but increased memory cells
– Slower to respond/require a stronger stimulus
– Increased likelihood of reactivation of dormant infections (i.e. TB, shingles)
 Co-morbidities – incidence of chronic disease rises with age
 Medications – can also mask symptoms/signs
 Increased risk for falls/fractures – Increased risk for infections (hospitals?)
 Surgical-related infections
 Dentures
 Exposure higher – old age homes

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11
Q

why no fever with aging?

A 
– Impaired thermoregulatory system 
– Masking effects of drugs 
 1 st symptoms of infection in elderly may be: 
– Confusion 
– Memory loss 
– Delirium
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12
Q

· Organism establishes parasitic relationship with host
· Invasion + multiplication of organism = immune response
· Damage to host:
– Microorganism’s toxins, replication, or indirectly by competing for nutrient
– By our own immune system

A

Infectious Disease

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13
Q 
An organism that elicits a pathologic response in the host
 · Depends on:
 · Site of invasion ·
 Number of pathogens, and virulence ·
 How well they disseminate in host
 · IMMUNE STATUS OF THE HOST
A

pathogen

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14
Q

pathogens that cause disease in people with apparently intact immune systems ·

A

Principal pathogens

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15
Q

pathogens that don’t cause disease in people with intact immune systems, but can cause devastating disease in hospitalized or immunocompromised people ·

A

Opportunistic pathogens

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16
Q

the ability of the organism to induce disease

A

Pathogenicity

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17
Q

refers to the potency of the pathogen in producing sever disease and is measured in case fatality rate

A

Virulence

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18
Q

An environment in which an organism can live and multiply
 Animal, plant, soil, food, organic substance
 Humans
 Human and animal reservoirs can be symptomatic or asymptomatic

A

A reservoir

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19
Q

-where the organism leaves the reservoir  Corresponds to entry point on next host 

A

– A portal of exit

Examples: – Respiratory droplets, blood, vaginal secretions, semen, tears – Urine, feces – Open lesions, pus

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20
Q

Contact – directly or indirectly.
– Direct = physical contact
Indirect= via an inanimate intermediate object, called a fomite.

A

– Ex. Intercourse - HIV vs. touching a handrail – enteric pathogens

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21
Q

disease-causing organisms float on air currents in the room. Often propelled from respiratory tract through coughing/sneezing.

A

Airborne –– Ex. TB, Chickenpox

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22
Q

different then airborne because they do not remain suspended in air but fall within 3ft of course. Produced by coughing/sneezing.

A

·Droplet – Ex. Influenza ·

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23
Q

occurs when infectious organisms are transmitted through a common source to many potential susceptible hosts. – Ex. Salmonella in contaminated food

A

Vehicle

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24
Q

–involves insects and/or animals that act as intermediaries between 2 or more hosts

A

·Vector

– Ex. Lyme disease via Black-legged or Deer Ticks

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25
Q

Where the pathogen invades/enters:  Ingestion  Inhalation  Bites  Contact with mucous membranes  Percutaneous  Transplacental
– A susceptible host · This sequence is called the “chain of transmission

A

A portal of entry

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26
Q

factors of host susceptibility

A

FACTORS:
 Age, sex, ethnicity  Health & nutrition  Hormonal balance  Co-morbidities  Living conditions  Personal behaviours (drug use, hygiene, diet, sexual practices)
· Medications – i.e. corticosteroids, chemo · Environment – i.e. daycare, hospitals · Use of invasive equipment – i.e. catheters, i.v. lines, chest tubes · Stress · Underlying medical disorders that specifically decrease T-cell and B-cell medicated immunity – i.e. HIV, Diabetes, Malignant cancers

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27
Q

Time between entering the host, and “infection” – Hours (GI bugs) to months (Lyme dz) – Symptoms = end of incubation – ‘latency’ = dormant

A

Incubation

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28
Q

– Clinical symptoms – Host-parasite interaction causes injury – Mild Fatal – Communicability: ability to spread to another host

A

Infection

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29
Q

smallest, RNA or DNA covered with proteins – Antibiotics don’t help – Antiviral meds only moderately effective · Entirely dependent on host · Some anti-viral meds are specific – Acyclovir - ’s DNA replication

A

Virus

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30
Q

Very small self-replicating bacteria with no cell wall, dependant on host for nutrition ·

A

Mycoplasmas

Eg. M.hominis; M.pneumoniae

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31
Q

Single celled organisms with cell wall; independent · Replicate by growing and dividing in half – they can do this in any tissue · Classified by shape (spherical-cocci, rod-shaped - bacilli, spiral-shaped - spirochetes), staining (Gram positive/negative), motility, spores, O2 /nonO

A

bacteria

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32
Q

types of bacteria

A

aerobic and anaerobic
example-normal gut flora-anaerobic
– Staphlococcus aureus is aerobic (lungs, skin)

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33
Q

Small obligate intracellular parasites – non-motile gram negative bacteria · Primarily animal pathogens that produce disease in humans · Transmitted via insect bites (tick, flea, louse, mite) · Require host for replication · i.e. Q Fever (Coxiella); “Trench Fever” carried by lice (Rochalimaea)

A

Rickettsiae

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34
Q

Smaller than bacteria but larger than viruses – Obligate intracellular - Dependent on host for replication – Always contain both RNA and DNA (unlike viruses) – Susceptible to antibiotics – curative - Most common STD - Leading cause of P.I.D. - Leading cause of preventable blindness in neonates

A

Chlamydiae

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35
Q

Unicellular organism that produce hyphae (filamentous outgrowths) · Contain nuclei (eukaryotic) · Cell walls · Yeasts or molds · Reproduce by budding off · Eg. Candida albicans

A

Fungi (yeast/mold)

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36
Q

-large, multicellular organisms that are generally visible to the naked eye in their adult stages. · can be either free-living or parasitic in nature. · In their adult form, helminths cannot multiply in humans. There are three main groups of helminths: – Flatworms (platyhelminths) – these include the trematodes (flukes) and cestodes (tapeworms). – Thorny-headed worms (acanthocephalins) – Roundworms (nematodes) – the adult forms of these worms can reside in the gastrointestinal tract, blood, lymphatic system or subcutaneous tissues.

A

Helminths (worms)

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37
Q

Single cells or groups of cells · Motile, free living in moist environments · Cell membrane, no cell wall · Divide similar to bacteria · Eg. Giardia

A

protozoa

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38
Q

Most common bacterial pathogens on the skin

· Over 30 spp. – only a few relevant ones ·

A

Staphylococcus

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39
Q

· Transmission: – Direct contact – nasal passages most common; also skin, axilla, perineum, vagina, oropharynx · Risks: – Insulin-dependant Diabetics; HIV+; hemodialysis; IV drugs; chronic skin lesions; corticosteroid use; surgery; burns · Pathogenesis: – Secretes membrane-damaging enzymes & toxins – Stimulate a strong host immune response

A

S.aureus
S. aureus is the most virulent
· Leading cause of nosocomial and community acquired infections · 13% of all hospital infections = 2 million/year leading to 60,000-80,000 deaths per year · All ages · Blood,skin, lung, soft tissue, joints, bones · Gram +

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40
Q

· Clinical Manifestations of s.aureaus

A

– suppuration (pus) and abscess formation
– eg. Boils, pus filled vesicles – respiratory tract infection (esp. in newborns), osteomyelitis, infections of burns and surgical wounds, septicemia, Toxic Shock Syndrome, bacterial arthritis, bacterial endocarditis, impetigo – Consumption of S.aureus toxins in contaminated food is common cause of food poisoning – Fever, chills, and diffuse erythema, pain, swelling
S. aureus · Diagnosis: culture from infected site, blood, or other fluids · Must test for antibiotic resistance · Prognosis: good with tx, unless MRSA – if untreated systemic (e.g. endocarditis) – MRSA

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41
Q

· one of most common bacterial pathogens of humans · Causes many diseases: · Skin infection, pharyngitis (“Strep Throat”), rheumatic fever, » suppurative - invasion of site with necrosis and pus acute inflammation » non-suppurative - away from site of invasion, immune related and triggered by previous strep infection (Eg. rheumatic fever) · S/Sx: fever, chills, sore throat, enlarged lymph nodes, skin inflammation · Usually transmitted via respiratory droplets

A

· Group A Streptococcus (S. pyogenes)

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42
Q

“Strep Throat” · Most common in children, 5-10 y. old · Incubation: 1-5 days · Clinical Manifestations: · sore throat with pain on swallowing, · beefy red pharynx, · tonsillar exudates, · swollen tonsils and uvula, · swollen regional lymph nodes, · malaise and weakness, · anorexia · Can also colonize with no symptoms · Complications: otitis media, sinusitis, or rarely arthritis, endocarditis, meningitis, etc

A

Streptococcal Pharyngitis ·

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43
Q

 Usually follows untreated Strep throat – pyogenic exotoxin is released  Kids ages 2-10  Clinical Manifestations: – Sore throat, – fever, – strawberry tongue, – Rash which starts on upper chest, spares palms/soles  Desquamation of palms and soles later on

A

Scarlet fever-strawberry tongue

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44
Q

 Serious infection that progresses rapidly along fascial planes  Usually in legs  Causes severe tissue damage  Used to be called Streptococcal gangrene  Edema, tenderness, pain, fever

A

Necrotizing Fasciitis

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45
Q

– Most common cause of neonatal pneumonia, meningitis, sepsis – Fatal in 3-4% of neonates
– Normal vaginal flora in 30% females · may be passed on to baby as it passes through birth canal – Only 1% of these babies develop infection – Infection in baby: hypotension, pneumonia, bacteremia, meningitis – This is the reason moms are put on antibiotics just before delivery due date

A

 Streptococcus agalactiae

(group B strep

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46
Q

is a very important gram + organism because it is a major cause of bacterial pneumonia and meningitis in adults, and otitis media in children
 Etiology & Risk Factors – post-influenza or viral URTI, chronic disease, immunosuppression, alcohol abuse
 Clinical Features of Strep Pneumoniae pneumonia: – acute fever, chills – pleuritis w/ pleuritic chest pain – Dyspnea – productive cough or purulent sputum - possibly blood-streaked

A

streptococcus pneumococcus(group b strep)

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47
Q

·· Etiology: severe trauma, wartime injury, septic abortion · Pathogenesis: – death of tissue with loss of vasculature, bacterial invasion, fermentation gas and putrefaction (decomposition) · Clinical Features: <3 days after injury-sudden severe pain- dishcahrge with foul-odour- prognosis-possimbly amputation, extremities better better than visceral or trunk

A

Clostridium Perfringes – Gram + – gas gangrene

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48
Q

 Gram positive bacteria  Spread through aerosol or skin shedding’s  Range from asymptomatic carriage to life-threatening syndrome that includes pharyngitis and toxin-mediated damage to heart, nerves, and other organs.

A

Corynebacterium Diphtheria

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49
Q

– aerobic gram negative  opportunistic pathogen, spread by contact  Most common nosocomial pathogens
 Uncommon in healthy populations
 Thrives in pools, tubs (moist environ.)
 Pneumonia, wound infections esp. burns, sepsis, UTIs, osteochondritis  Inherently antibiotic-resistant

A

Pseudomonas

 P. aeruginosa

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50
Q

· Gram-negative coffee bean-shaped diplococci aerobic bacteria · Neisseria gonorrhoeae (gonococcus) - responsible for the sexually transmitted infection gonorrhea · Neisseria meningitides (meningococcus) – significant cause of bacterial meningitis

A

Neisserial Infections

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51
Q

is a Gram-negative, rodshaped coccobacillus, a facultative anaerobic bacterium that can infect humans and animals.  It causes the deadly disease named plague

A

 Yersinia pestis

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52
Q

most common · Hepatitis

A

· Hep B, C and HIV

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53
Q

spread through sex, blood or placenta – Vaccine available ·

A

hep b( viral infection

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54
Q
  • spread through blood – No vaccine available ; ·
A

hep C -viral infection

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55
Q

– retrovirus that causes HIV infection and Acquired Immunodeficiency Syndrome – infects CD4+ T cells · Bodily fluid transfer

A

Human Immunodeficiency Virus

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56
Q

 Mucosal contact = initial transmission  After first outbreak, becomes latent in sensory ganglia  Periodic lifetime outbreaks with certain triggers (a bad cold, high stress, decreased immune function, etc.)

A

Herpesviruses (HSV)

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57
Q

herpes simplex virus type

A 
· Type 1 (HSV 1) – cold sores – 70% population ·
 Type 2 (HSV 2) – Genital – 20% population – birth canal infection ·
type 3- · 1 o form: – highly contagious 1-2 days before vesicular rash · 2 o form: Herpes Zoster – 10- 20% reactivated dermatome pattern
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58
Q

– mucosal contact, lymph/blood spread – 95% between 35-40years of age have been infected · Fever, rash, fatigue, lymphadenopathy, spleen enlargement · Possibly involved in later development of FM, CFS, and MS

A

Type 4 – EBV (Epstein Barr virus)

Infectious Mononucleosis - “the kissing disease”

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59
Q

· 80% pop’n are carriers, esp. with AIDS · transmission: all fluid except saliva, spread via lymphocytes · usually asymptomatic/self-limiting · In immunocompromised - fever, splenomegaly, hepatitis, blindness, peripheral neuropathy

A

Type 5 · Cytomegalovirus (CMV)

Type 6 & 7 – B & T-cell viruses associated with roseola (or 6 th disease) – Rash – Fever – Runny nose

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60
Q

– associated with Karposi’s sarcoma in AIDS

A

Type 8

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61
Q

– Outbreaks common in winter & spring
– Large droplet transmission or direct contact
– Sxs: high fever, chills, malaise, myalgia, HA, sore throat, congestion, nonproductive cough

A

influenza(respiratory virus)

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62
Q

– Leading cause of lower resp. infections in children worldwide – Mild in older children/adults – “common cold”

A

Respiratory Syncitial Virus (RSV)

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63
Q

– Many strains – some cause · cervical cancer · Genital warts

A

Human Papilloma virus – DNA viruses

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64
Q

– almost eradicated · Rarely causes poliomyelitis

A

Poliovirus

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65
Q

bacteria Borelia burgdorferi – Vector - deer, bear or black-legged tick
· Stage I – 1 st 2 weeks; localized; “bull’s-eye” rash flu-like Sx ·
Stage 2 – early disseminated, rash resolved, Lyme arthritis unilateral swelling large joints, fatigue, loss of appetite
· Stage 3- (50% of untreated) intermittent arthritis, profound fatigue, chronic neuropathy, bone erosion · Tx: prevention, antibiotics

A

lyme disease

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66
Q

transmission: sex, sharing needles, vaginal birth ·

A

STI’s ·

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67
Q

– the cause of 99.9% of cervical cancer; also genital warts common in men · Chlamydia – most common

A

HPV – Human Papilloma Virus

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68
Q

can lead to neo-natal blindness and P.I.D. ·
Syphilis – 3 stages: · Painless chancre · Warty lesion · Very bad complications [granulomas, CVD, neuropathologies, CNS infection, insanity]

A

STI

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69
Q

– painful urination; pus discharge from urethra, P.I.D. in female partner, sterility/ectopic pregnancy – cured with antibiotic, but serious Antibiotic resistance now

A

Gonorrhea

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70
Q

– (Tinea corporis): the fungi spread, forming a ring shape with a red, raised border. This expanding raised red border represents areas of active inflammation with a healing center.

A

· Ringworm

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71
Q
  • Superficial fungal infection which leads to hypopigmented or hyperpigmented patches on the skin.
A

Tinea Versicolor

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72
Q

Can infect the mouth, groin or vagina. Also an opportunistic infection. ·

A

Candidiasis

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73
Q

– opportunistic fungal infection causing pneumonia

A

Pneumocystis carnii

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74
Q

-Develops embryologically from the venous system · It’s main job: take up extra fluid · Physiological functions in the body: – Maintain fluid level – Fight infections – Remove cellular waste/debris from extracellular spaces

A

Lymphatic System

75
Q

Inflammation of a lymph vessel

A

Lymphangitis

76
Q
  • Inflammation of one or more lymph nodes
A

Lymphadenitis

77
Q

Increased lymph fluid in the tissues

A

Lymphedema

78
Q

Accumulation of lymphatic fluid in tissue chronic inflammation progressive tissue fibrosis decreased tissue oxygenation and increased risk of infection (decreased activity of macrophages) · exacerbated by further infection (cellulitis or lymphangitis) or inflammation · Sequelae: – Delayed wound healing, possible necrosis

A

Pathogenesis of lymphedema

79
Q

swelling, pain, paraesthesia (tingling), ROM, loss of function · Stemmer’s sign – thick skinfold over 2nd toe

A

Clinical Manifestations of lymphedema

80
Q

Enlargement of the lymph nodes

A

Lymphadenopathy

81
Q

· The complement cascade has multiple pathways that converge to form:

A

Membrane attack complex

82
Q

Pathology is:

A

the study of disease

83
Q

Natural Killer cells are a part of which immune system?

A

Innate

84
Q

Which of the following describes lymphedema?

A

Increased lymph fluid in the tissues

85
Q

Your patient come to you complaining that their child has a sore throat, fever, really red tongue that looks almost like a strawberry and a rash everywhere but there palms/sole. She most likely has caused by .

A

Scarlet fever; Group A strep (Strep pyogenes)

86
Q

An increase in the size of the tissue caused by an increase in the number of cells, is called:

A

Hyperplasia

87
Q

, white blood cells, called B lymphocytes (B cells), make antibodies
that attack pathogens in the blood.

A

In humoral immunity

88
Q

In white blood cells, called T lymphocytes (cytotoxic and helper T
cells), mobilize other immune cells and find and destroy abnormal or infected cells

A

cell-mediated immunity

89
Q

The response is the body’s response to specific invader

A

adaptive/acquired

90
Q

A substance that triggers the immune response is known as a (n)

A

antigen .

91
Q

The main role of antibodies

A

is to tag antigens/microbes for destruction by immunesystem cells

92
Q

The main working cells of the immune system are two types of

A

lymphocytes

93
Q

___________ can recognize these hidden organisms and destroy the cells

A

T-lymphocytes

94
Q

differentiate into Memory cells or plasma cells.

A

b-lymphocytes

95
Q

What type of B cell is produced that acts immediately against antigens once contact with a Thelper cell has occurred. How do these cells stop antigens from infecting other cells?

A

Plasma cells – create antibodies that mark them for destruction

96
Q
  1. Considering adaptive immunity, why is the secondary response to a previously identified
    pathogen so much faster than the primary response?
A

Memory cells

97
Q

What is a major histocompatibility complexes?

A

Cells fingerprint – identifies self from non-self

98
Q

Discuss specificity as it relates to acquired immunity. How can this system be so specific in
response? Where does the basis for the specificity come from?

A

Each antigen has a specific B cell or T cell that will responds to it. Identifying different
epitopes of different antigens.

99
Q

an increase in body temperature which slows or stops

pathogens

A

fever

100
Q

a secretion of the nose and throat that stops pathogens

A

mucus

101
Q

c. an enzyme found in the tears and saliva that breaks down bacteria cell walls

A

. lysozyme

102
Q

chemicals that increase blood flow to tissues

A

. histamines

103
Q

combination of physical and chemical barriers that defend

against pathogens

A

exterior defenses

104
Q

redness, swelling and pain at the site of an injury

A

inflammatory response

105
Q

proteins that fight viral growth

A

interferons

106
Q

. the body’s most important nonspecific defense

A

skin

107
Q

. the body’s most important nonspecific defense

A

skin

108
Q

Series of interconnected events & a dynamic process
-Acute (sudden and stats for a brief period of time) vs. Chronic (stays for a long time)
Occurs only in multicellular organisms – must be able to mount a neurovascular and cellular response

Protective and usually beneficial

Occurs only in living tissue

A

Inflammation

109
Q

Nonspecific, predictable response of tissue or entire body to injury. Causes:

A

Chemical agents

Physical force

Microbes

Any other stimuli that disturbs normal steady state

110
Q

Signs of Inflammation

A

Four cardinal signs of inflammation (Celsus 30 BC-38 AD) must know!

Heat (calor)

Redness (rubor)

Swelling (tumor)

Pain (dolor)

Loss of function (function laesa - added later in 1900)

111
Q

Five classical signs of inflammation

A 
(Acronym – SHARP or PRISH) 
Swelling 
Heat 
Altered Function/Immobility 
Redness 
Pain
112
Q

Inflammatory Process

A

Inflammation is a complex process that includes:

  1. Changes in circulation of blood
  2. Changes in vessel wall permeability
  3. White blood cell response
  4. Release of soluble mediators
113
Q

A. Vasoconstriction of arterioles – last only seconds
B. Vasodilation (muscle release histamine)

A mechanical stimulus stimulates nerves to relax the smooth muscle cells on precapillary arterioles → blood rushes into capillaries → redness, swelling, warm tissue

Hyperemia (increase redness)

C. Edema – fluid leaks out of blood vessels
D. Pain

Direct trauma

Pressure from edema

Chemical mediators

Swelling of nerve endings

A
  1. Circulatory Changes – first response to injury
114
Q

Changes in permeability of capillary and post capillary venule walls occurs because of:

A. Increased pressure inside congested blood vessels

B. Slowing of circulation → reduces oxygen and nutrient supply

C. Adhesion of platelets → Release of soluble mediators of inflammation

D. Adhesions of leukocytes (white blood cells) to endothelial cells – pavementing

A
  1. Vessel Wall Changes

D. Adhesions of leukocytes (white blood cells) to endothelial cells – pavementing

115
Q

-the act or process of forming a margin specifically : the adhesion of white blood cells to the walls of damaged blood vessels.

A

1 Margination

116
Q

-A condition occurring during inflammation in which leukocytes adhere to the linings of capillaries.

A

2 Pavementing
Attach to endothelium = pavementing

Protrusions from cytoplasm stick to endothelial cells (especially postcapillary venules)

117
Q

movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.

A

4 Chemotaxis

118
Q

-a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.

A

5 Exudate

119
Q

is extravascular fluid with low protein content and a low specific gravity (< 1.012). It has low nucleated cell counts (less than 500 to 1000 /microliter) and the primary cell types are mononuclear cells: macrophages, lymphocytes and mesothelial cells.

A

6 Transudate-

120
Q

invasion of site with necrosis and pus acute inflammation

A

7 Suppurative-

121
Q

(from Ancient Greek φαγεῖν (phagein) , meaning ‘to eat’, and κύτος, (kytos) , meaning ‘cell’) is the process by which a cell uses its plasma membrane to engulf a large particle (≥ 0.5 μm), giving rise to an internal compartment called the phagosome. It is one type of endocytosis.

A

8 Phagocytosis-

122
Q

is the process of forming grains or granules from a powdery or solid substance, producing a granular material. It is applied in several technological processes in the chemical and pharmaceutical industries.

A

9 Granulation tissue

123
Q

a type of raised scar. They occur where the skin has healed after an injury. They can grow to be much larger than the original injury that caused the scar. Anything that can cause a scar can cause akeloid. This includes being burned, cut, or having severe acne

A

10 Keloid-

124
Q

is when a surgicalincisionreopens either internally or externally. Although this complication can occur after any surgery, it tends to happen most often within two weeks of surgery and following abdominal or cardiothoracic procedures.

A

11 Wound Dehiscence-

125
Q

-is the capability of multicellular organisms to resist harmful microorganisms from entering it.Immunityinvolves both specific and nonspecific components. The nonspecific components act as barriers or eliminators of a wide range of pathogens irrespective of their antigenic make-up

A

12 Immunity

126
Q

the branch of medicine and biology concerned with immunity.

A

13 Immunology-

127
Q

having a normal immune response.

A

14 immunocompetence-

128
Q

-a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies.

A

15 antigen

129
Q

-a blood protein produced in response to and counteracting a specific antigen. Antibodies combine chemically with substances which the body recognizes as alien, such as bacteria, viruses, and foreign substances in the blood.

A

16 antibodies

130
Q

, group of genes that code for proteins found on the surfaces of cells that help the immune system recognize foreign substances. MHC proteins are found in all higher vertebrates. In human beings the complex is also called the human leukocyte antigen (HLA) system.

A

17 MHC-Major histocompatibility complex(MHC)

131
Q

the part of an antigen molecule to which an antibody attaches itself.

A

18 Epitope -

132
Q

-refers to the gradual deterioration of the immune system brought on by natural age advancement. The adaptive immune system is affected more than the innate immune system.

A

19 Immunosenescence

133
Q

· Organism establishes parasitic relationship with host · Invasion + multiplication of organism = immune response

A

20 Infection-

134
Q

Microorganisms can be present, but not cause symptoms · “colonization of organisms” · You could be carrier – can transmit to other people and be ‘infectious’ while also non-symptomatic

A

21 Carrier-

135
Q

pathogens that cause disease in people with apparently intact immune systems

A

22 Principal Pathogen-

136
Q

-pathogens that don’t cause disease in people with intact immune systems, but can cause devastating disease in hospitalized or immunocompromised people

A

23 Opportunistic Pathogen

137
Q

– refers to the potency of the pathogen in producing sever disease and is measured in case fatality rate

A

24 Virulence e

138
Q

– the ability of the organism to induce disease

A

25 Pathogenicity -

139
Q

Also know which are examples of diseases that HAIs  Nosocomial infections – Originating or taking place in a hospital, acquired in a hospital, especially in reference to an infection. – A.k.a. Hospital acquired infections (HAI) – Most common are UTIs (from catheters or urologic procedures), blood infections (from IV catheters or surgical wounds), and GI infections

A

26 Nosocomial (HAIs)

140
Q

– occurs when infectious organisms are transmitted through a common source to many potential susceptible hosts. – Ex. Salmonella in contaminated food

A

27 Vehicle

141
Q

(leukocyte rolling across endothelium)

Move through the blood vessel wall to inflamed tissue

Phagocytosis → swelling and pain

A

D. Emmegration (aka transmigration)
Emigration leads to exudate

Exudate – fluid containing more protein than transudate and also polymophonuclear leukocytes or polymophonuclear neutrophils (PMNs) (the first WBC to reach the problem area)
Within first 48 hours of inflammation
Exudate contains a high concentration of PMNs, monocytes, eosinophils
Lifespan of only 2-4 days

142
Q

Chemical mediators – Histamine,

A 
Histamine 
Released by mast cells and platelets 
Causes contraction of endothelial cells of venules → gaps → increased blood vessel 
permeability 
Vasodilator and bronchoconstrictor 
Lasts less than 30 minutes
143
Q

Bradykinin,

A

Plasma protein formed by Hageman factor (Coagulation factor XII)

Same effects as histamine but at a slower pace

Causes pain

144
Q

– several proteins that are activated in a cascade acting on one another Numbered 1-9 (C1, C5..)
All pathways converge to form the Membrane Attack Complex (MAC) (key to destruction of foreign agent)
Bores holes into membranes of microbes or body’s owncells
Fill with fluid → cell death

A

Complement System
3 pathways that activate the complement cascade
1. Classical pathway – activated by antigen-antibody complexes.
2. Alternative pathway – activated by bacterial endotoxins, fungi, snake venom
3. Lectin pathway – activated by binding of lectin to bacteria

145
Q

Derived from phospholipids of cell membranes
Form leukotrienes and prostaglandins
Polyunsaturated fatty-acid found in brain, muscle and liver

A

Arachidonic Acid Derivatives

146
Q

increase vascular permeability and promote chemotaxis
Formed through the LOX pathway (lipoxygenase pathway)
Bronchospasm – contract smooth muscles in bronchi

Anaphylactic shock

A

Leukotrienes –

147
Q
  • Stimulate vasodilation, increase vascular permeability

Formed through the COX pathway (cyclooxygenase pathway)

Pain and fever

A

Prostaglandins

148
Q

WHITE BLOOD CELLS (AKA. LEUKOCYTES)

Neutrophils (Most abundant)

Eosinophils

Basophils → Mast Cells

Monocytes → Macrophages (macrophages form monocyte) (macrophages found in tissues)

Lymphocytes → Plasma Cells (not all lymphocytes will form plasma cells)

A

Cells of Inflammation

149
Q

2-3% of circulating WBCs
Appear 2-3 days After PMNs in area of inflammation
Longer lifespan – chronic inflammation
Like PMNs they are mobile, phagocytic and bactericidal
nteract with basophils
Allergic reactions – hay fever, asthma
Respond to parasitic infection (Mainly hellmas parasite, round worm, hook work and tape worm)

A

Eosinophils

150
Q

Less than 1% of circulating WBCs
Most prominent in allergic reactions (IgE)
Cytoplasmic granules contain histamine
Precursors to Mast Cells
Basically basophils outside of the blood vessel

A

Basophils

151
Q 
Derived from monocytes in blood 
Large 
Appear at site of inflammation 3-4 days after onset of infection or injury 
Long-lived 
Chronic inflammation 
Phagocytosis and release cytokines
A

Macrophages MUST KNOW

152
Q

**two main phagocytic cells =

A

Monocytes/Macrophages and Neutrophils”

153
Q

Released from megakaryocytes in bone marrow
No nucleus
Cytoplasm contains vacuoles and granules
Histamine, coagulation proteins, cytokines, growth factors
Release histamine in early stages of inflammation

A

Platelets (not cells, they are cellular fragments)

154
Q

Classification of Inflammation

A

Acute
Sudden onset
Hours to days
Eg. Common cold, ankle sprain

Chronic 
Weeks to months to years 
May be result of: 
Recurrent acute inflammation 
Prolonged healing of acute inflammation 
Persistence of causes of inflammation 
Due to prolonged duration it produces more extensive tissue destruction, heals less 
readily, and is associated with more functional deficiencies. 
155
Q

Etiology – what caused the inflammation

A 
Infectious 
Bacterial, viral, protozoal, fungal, helminthic 
Chemical – organic or inorganic 
Physical 
Heat, trauma, foreign body 
Immune – to be discussed shortly  
Location 
Localized or Systemic 
Boil – local vs Sepsis (= bacteremia or septicemia)  - systemic
156
Q

Produce extracellular matrix

Fibronectin – provides the glue to hold cells together in wound healing

A

Fibroblasts

Collagen – from fibrils in interstitial spaces

157
Q

Properties of smooth muscle cells and fibroblasts
Contract like muscle cells and secrete cell matrix substances like fibroblasts
Holds edges of damaged tissue together

A

myofibroblasts

158
Q

Precursors of blood vessels
Proliferate from small blood vessels at the edges of damaged tissue
Appear 2-3 days after injury. By day 6 new blood vessels are formed
Provide a route for scavenger cells to remove tissue debris and scabs
Allow oxygen and nutrients to flow to injured site

A

Angioblasts (angio = vessels)

159
Q

Vascularized tissue filled with macrophages, myofibroblasts, angioblasts, fibroblasts
Turns into a scar 

A

Granulation tissue

160
Q 
Site of wound 
Mechanical factors 
Size of wound 
Presence or absence of infection 
Circulation issues 
Nutritional and metabolic factors 
Age
A

Wound Healing

Depends on:

161
Q

Deficient scar formation – poor formation of granulation tissue

Inadequate collagen production can lead to wound dehiscence

A

Complications of Wound Healing

Excess scar formation

Keloid scar – hypertrophic scars

Can lead to disfigurement and loss of function

162
Q

Immune Response
Innate Immunity (born with)
Nonspecific, protective
No memory

A

Acquired Immunity
Specific
Has memory

163
Q

1st line of defence

A

Physical Barriers – Exterior Defenses
Skin – best defense we have
Shown when significant burns occur –infection is a major problem

Mucosa – body openings have their own
defences

Tears – lysozymes protect the eyes, wash away
foreign substances

Ears – ciliated, ear wax

Stomach and duodenal - low pH values (acidic)

Vagina – acidic

Urine – acidic

164
Q

Innate Immunity

2nd line of defence – cells and inflammation

A

Phagocytes

  1. Neutrophils
  2. Monocytes
  3. Macrophages
Cells that release inflammatory mediators 
1.Basophils 
2.Eosinophils 
3.Mast cells 
4,Complement system

Natural Killer Cells

Interferons

165
Q

Large granular lymphocytes that are neither T or B lymphocytes

Function is to kill viruses, infected cells, and tumor cells

Bind to potential target cells – release cytotoxic granules, and cytokines

Natural killer cells burst forth from the tonsils, lymph nodes and spleen, and destroy infected and cancerous cells while the immune system’s T and B cells are still mobilizing

Without natural killer cells, threatening conditions can get a strong foothold before the adaptive immune response kicks in

A

Natural Killer cells

166
Q

Act as messengers, within the immune system and between the immune system and
 other systems of the body
- are produced by virally infected cells early in infection to limit the spread of infection by protecting surrounding (noninfected) cells

-once a cell is infected by a virus, certain genes are turned on in the cell that will produce these interferons that coat the surrounding cells to make them viral resistant

Inhibit tumor growth

A

Interferons

167
Q

Acquired Immunity

Based on specific responses elicited by Antigens
Antigen – any chemical substance that can induce a specific immune response

Specific
Antigen specific – remembers the Antigens to an immune response can be mounted faster and more effectively

A

Has memory
Our bodies create immunologic memory to distinguishes self from non-self
Immunocompetence – ability to mount an appropriate immune reaction

168
Q

Immunity acquired by introduction of an antigen into the host
environmental exposure
Vaccination

A

Active Immunity

169
Q

Immunity acquired when antibodies produced by one person are transferred to another
trans placental transfer, breast milk, antibody inoculation

A

Passive Immunity

Does not form memory cells; therefore, is only temporary immunity (lasting a few weeks to months)

170
Q

Very small cells, round nucleus, very little cytoplasm
Derived from bone marrow stem cells and turn into one of two different lineages
Bone marrow stem cells → migrate to the thymus →T lymphocytes
Bone marrow stem cells → remain and mature in bone marrow → colonize lymphoid tissues as B lymphocytes

 

A

Lymphocytes
Primary lymphoid organs – bone marrow and thymus

T and B lymphocytes enter blood circulation and colonize secondary lymphoid organs
Lymph nodes
spleen

Also form mucoca-associated lymphoid tissue (MALT)
Gastrointestinal mucosa
Bronchial mucosa

171
Q

 Mature in thymus
 Part of Cell-Mediated Immunity
 2/3rds of all lymphocytes in the blood, lymph nodes and spleen
 All express protein CD3 on their membrane
 Linked to T-cell receptor
Used to recognize antigens

A 
T Lymphocytes 
 Several sub-types of T lymphocytes 
 T Helper cells 
 T Suppressor cells 
 Cytotoxic cells
172
Q

Express protein CD4 (aka CD4 cells)
75% of all T-cells
Assist B-cells to mature and produce antibody secreting protein mediators called lymphokines (ie. IL-1 and interferons)
Activate macrophages – help to destroy bacteria
Help other T-cells recognize and destroy virally infected cells (CD8 = cytotoxic T-cells)
Help NK cells kill infected cells

HIV destroys or inactivates helper T-cells, leaving the body at risk for infections

A

T helper cells (“master regulator”)

173
Q

Suppress activation of the immune system and prevent pathologic self-reactivity (auto-immune disease)

A

T suppressor cells

174
Q

Express CD8 antigen on their surface

Mediate the killing of virus infected cells or tumor cells

A

Cytotoxic T cells

175
Q

Differentiate into immunoglobulin producing plasma cells or memory B Cells
Part of Humoral Immunity

A

B Lymphocytes
Memory B-cells
circulate among the blood, lymphoid system, and tissues for 1 year or longer
-responsible for more rapid and sustained immune response that occurs with repeated exposure to the same antigen

Plasma cells
Fully differentiated B lymphocytes
Produce immunoglobulins (antibodies) (Ig)
Surface of plasma cell is coated with Ig
5 types of antibodies produced

176
Q

Major anti-bacterial and anti-viral antibody
most abundant type in blood
Only antibody to cross placenta
Responsible for the protection of the newborn for the first 6 months of life

A

IgG

177
Q

primary or initial immune response
Largest antibody
stays in blood vessels

A

IgM

178
Q 
Defends external body surface 
Found on mucous membranes 
Found in secretions 
Saliva 
Breast milk 
Urine 
Seminal fluid 
Tears 
Nasal fluid
A

IgA

179
Q

Controls lymphocyte activation or suppression

Found exclusively on B-cells

A

IgD

180
Q

Primary factor in eliminating parasitic infections
Functions during allergic reactions
Activates mast cells to release histamine
Associated with anaphylaxis, hives, allergen induced asthma

A

IgE

181
Q

Two Types of Acquired Immunity

A

)

182
Q

Mediated by Antibodies (Ab) present in body fluids or secretions
Humoral = body fluids
Blood, Lymph, Interstitial Fluid
Aka. Antibody-Mediated Immunity

B Lymphocytes
Formed in bone marrow
Mature in bone marrow
Differentiate into Memory B-cells or plasma cells
Plasma cells secrete Immunoglobulins (Antibodies) to mount an immune response
Bind Antigen to display it for destruction
Memory B-cells
‘remember’ Antigen after first exposure

A

Acquired Immunity - Humoral
1. Humoral - B Lymphocytes (B-cells)

Protects against extracellular microbes and their toxins (eg. bacteria

183
Q

All viruses and some bacteria hide inside cells where antibodies cannot reach them
T-lymphocytes can recognize these hidden organisms and destroy the cells
Also implicated in transplant rejection, hypersensitivity reactions, and some autoimmune diseases

Interaction with antigen→ activates T-lymphocyte to produce specialized Tcells (or sensitized T-cells): 
Helper T-cells (75% of all T-cells) 
Cytotoxic T-cells 
Suppressor T-cells 
Memory cells
A
  1. Cell Mediated – T Lymphocytes (T-cells)

Defense against intracellular microbes (eg. viruses)

184
Q

Lines of Defense

A

1st line of defense- skin, mucosal, hair, pH barriers

INNATE

2nd line of defense – inflammation

INNATE

3rd line of defense - immune system cells

ACQUIRED

gen path (5 decks)

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