Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho 2 > Chap 8- Infectious diseases > Flashcards

Chap 8- Infectious diseases Flashcards

1
Q

types of physical barriers

A
  • skin defenses
  • GI tract defenses
  • respiratory tract defenses
  • urogenital tract defenses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

skin barriers

A
  • keratinized outer layer
  • low pH
  • fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

GI tract defenses

A
  • gastric acid
  • pancreatic enzymes
  • bile detergents
  • peyer patches
  • defensins
  • peristalsis
  • protective flora
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

respiratory tract defenses

A
  • bronchial epithelium ciliary activity
  • mucous layer
  • defensins
  • IgA
  • alveolar macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

urogenital tract defenses

A
  • frequent bladder flushing with urine
  • low vaginal pH
  • intact epidermal/ epithelial barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what factors influence consequences of infectious disease?

A
  • virulence of organism
  • magnitude of infection
  • pattern of seeding
  • host factorts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how are most pathogens transmitted?

A
  • respiratory
  • fecal oral
  • sexual
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

stages of infection

A
  • host encounter
  • gain entry
  • multiply and spread
  • direct or indirect tissue inury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are possible outcomes of infection

A
  • resolution
  • chronic active infection
  • prolonged asymptomatic excretion of agent
  • latency
  • host death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are some mechanisms of immune evasion?

A
  • antigenic variation
  • resistance to antimicrobial peptides
  • resistance to phagocytes
  • evasion of apoptosis and maniupation of host cell metabolism
  • resistance to cytokine and complement sys
  • evasion of recognition by CD4 and CD8 cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

viral mechanism of injury

A
  • prevent synthesis of macromolecules in host
  • production of degradative enzymes and toxic proteins
  • antiviral immune responses
  • transformation of infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

tropism

A
  • ability for virus to infect certain cells only

- match for receptors on the body human body and the virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

mechanisms of bacterial injury

A
  • bacterial virulence
  • bacterial adherence to host cells via adhesions and pili
  • toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what factors impact bacterial virulence

A
  • ability to adhere to host cells
  • ability to invade cells/ tissues
  • ability to deliver toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are adhesins

A
  • bacterial surface proteins

- allow bacteria to bind to host cells or ECM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pili

A
  • proteins in surface of bacteria

- act as adhesins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are bacterial endotoxins

A
  • lipopolysaccharide in outer membrane

- stimulates host immune response and injuries of host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what type of bacteria produce endotoxins

A

gram-negative bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are exotoxins

A
  • produced during normal growth and metabolism of bacteria

- secreted or released following lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what type of bacteria produce exotoxins

A

gram positive bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

examples of acute viral infections

A
  • measles
  • mumps
  • poliovirus
  • viral hemorrhagic fevers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

examples of chronic productive viral infections

A
  • HBV

- HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

examples of chronic latent viral infections

A
  • HSV
  • VZV
  • CMV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

examples of transforming viral infections

A
  • EBV

- produce cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

measles

A
  • affects multiple organs
  • severity ranges from self limited to severe
  • leading cause of vaccine preventable death and illness worldwide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how is measles transmitted?

A

respiratory droplets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

pathogenesis of measles

A
  • replication of virus in respiratory tract/ lymphatic tissue
  • viremia and systemic dissemination
  • T cell mediated
  • antibody mediated immunity to protect against reinfection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is responsible for the measles rash

A

T cell mediated response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is another name for measles

A

rubeola

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

mumps

A
  • acute systemic viral infection
  • pain and swelling of salivary glands
  • vaccine has reduced incidence greatly in US
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are clinical symptoms of mumps

A
  • pain and swelling of salivary glands
  • aseptic meningitis
  • orchitis
  • pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what type of virus are the measles and mumps viruses

A

paramyxovirus family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

pathogenesis of mumps

A
  • upper respiratory tract infection
  • lymph node infection and dissemination into blood stream
  • salivary gland swelling and pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how is polio transmitted

A

fecal oral route (enterovirus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

poliovirus pathogenesis

A
  • ingested
  • replicates in mucosa of pharynx and gut
  • moves through lymphatics to lymph nodes then blood
  • causes viremia and fever
  • antibodies control disease in most cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

poliovirus symptoms

A
  • mostly asymptomatic
  • 1% of pts it invades CNS and replicates in motor neurons
  • can cause spinal polioyelitis or bulbar poliomyelitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

spinal poliomyelitis

A
  • paralysis of limb muscles

- especially affects kids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what disease does polio mimc

A

guillian barre syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

viral hemorrhagic fever pathogenesis

A
  • life threatening multisystem syndrome -> vascular dysregulation and damage -> shock
  • infect endothelial cells, macrophages and dendritic cells -> cytokine released
  • reduced ability of dendritic cells to present antigen
  • damage to BV -> hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how are viral hemorrhagic fevers transmitted?

A

through infected insects or animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what viruses cause viral hemorrhagic fevers

A
  • enveloped RNA viruses
  • arenavirus
  • filovirus
  • bunyavirus
  • flavivirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

mild symptoms of viral hemorrhagic fevers

A
  • fever
  • HA
  • rash
  • myalgia
  • neutropenia
  • thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

severe sx of viral hemorrhagic fevers

A
  • life threatening hemodynamic deterioration

- shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what type of virus is the herpes virus

A
  • dna virus

- establishes latent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

classifications of HSV

A
  • alpha herpesvirinae
  • beta herpesvirinae
  • gamma herpesvirinae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are examples of alpha herpesvirinae

A
  • HSV type 1
  • HSV type 2
  • varicella zoster
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are examples of beta herpesvirinae

A
  • cytomegalovirus
  • human herpes virus type 6
  • hyman herpes virus type 7
48
Q

what are examples of gamma herpesvirinae

A

epstein barr virus

49
Q

HSV pathogenesis

A
  • replicate in skin and mucosa membrane
  • viral multiplication
  • lysis of epithelial cells -> ulcers
50
Q

where do HSV and varicella reside

A
  • usually trigeminal nerve
51
Q

where does cytomegalovirus usually reside

A

monocytes

52
Q

where does EBV usually reside

A

b cells

53
Q

HSV 1

A
  • cold sores
  • gingivostomatitis
  • major cause of corneal blindness and fatal encephalitis
54
Q

HSV 2

A
  • genital sores

- can lead to life threatening disseminated visceral infections and encephalitis

55
Q

how is varicella zoster virus transmitted

A
  • respiratory aerosols

- gets into blood and causes skin lesions

56
Q

acute infection of VZV

A

chickenpox

57
Q

reactivation of VZV

A
  • shingles
  • innervated by trigeminal ganglia
  • see blisters in specific dermatomes
58
Q

other manifestations of VZV

A
  • interstitial pneumonia
  • encephalitis
  • transverse myelitis
  • necrotizing visceral lesions
59
Q

cytomegalovirus

A
  • infects monocytes and bone marrow progenitors
  • in healthy typically asymptomatic
  • in neonates and immunocompromised can cause serious systemic infection
  • most common opportunistic viral pathogen in AIDS
60
Q

how is cytomegalovirus transmitted

A
  • saliva
  • sexually
  • transplacentally from pregnant mother to unborn baby
  • blood transfusions or organ transplants
  • during childbirth
61
Q

typical symptoms of CMV in infants

A
  • deafness and mental retardation
62
Q

typical symptoms of CMV in immunosuppressed

A
  • pneumonitis
  • hepatitis
  • choriorentitis
  • meningoencephalitis
63
Q

cytomegalic inclusinon disease

A
  • caused by CMV
  • IUGR
  • hemolytic anemia
  • jaundice
  • encephalitis
64
Q

oncogene viruses

A
  • EBV
  • HPV
  • HBV
  • HTLV-1
65
Q

EBV infection outcomes

A
  • infectious
  • lymphadenopathy and splenomegaly
  • lymphomas
  • infect B cells -> proliferate -> thrombocytopenia
  • nasopharyngeal carcinomas
  • resolves in most pts with in 4-6 weeks
66
Q

lymphomas associated with EBV

A
  • burkitt

- hodgkin

67
Q

s. aureus infections

A
  • skin lesions
  • abscesses
  • sepsis
  • osteomyelitis
  • pneumonia
  • endocarditis
  • food poisoning
  • toxic shock syndrome
68
Q

what type of bacteria is staphylococcus

A

gram positive cocci

69
Q

why can staphylococcus result in toxic shock syndrome

A
  • contains superantigens

- superantigens cause inappropriate and excessive stimulation of T cells

70
Q

ways staphylococcus evades infection

A
  • surface receptors binding to endothelial cells
  • superantigens
  • surface A protein
  • bacterial toxins
  • capsule and biofilm
71
Q

types of streptococcus

A
  • alpha hemolytic

- beta hemolytic

72
Q

types of alpha hemolytic streptococcus

A
  • s. pneumoniae

- viridans streptococci

73
Q

types of beta hemolytic streptococcus

A
  • s. pyogenes

- s. agalactiae

74
Q

s. pneumoniae

A
  • alpha hemolytic streptococcus
  • common cause of community acquired pneumonia in elderly
  • causes meningitis in kids and adults
75
Q

viridans streptococci

A
  • alpha hemolytic streptococcus
  • found in normal oral flora
  • common cause of endocarditis
76
Q

s. pyogenes

A
  • beta hemolytic streptococcus
  • pharyngitis
  • scarlet fever
  • erysipelas
  • impetigo
  • rheumatic fever
  • toxic shock syndrome
  • glomerulonephritis
77
Q

s. agalactiae

A
  • beta hemolytic streptococcus
  • colonizes in female genital tract
  • causes spesis and meningitis in neonates
  • chorioamnionitis in pregnancy
78
Q

ways that steptococcus evades immune response

A
  • m protein
  • protein F
  • streptokinase
  • pneumolysin
  • hyaluronic acid capsule
79
Q

m protein

A
  • prevents phagocytosis

- binds fibrinogen and complement proteins

80
Q

protein F

A
  • mediates adhesion to fibronectin

- fibronectin is ECM protein

81
Q

streptokinase

A
  • cleaves plasminogen to activate plasmin

- dissolves clot

82
Q

pneumolysin

A

inserts into host cell membrane and lyses cell

83
Q

diptheria

A
  • caused by corynebacterium diptheriae

- transmitted by respiratory droplets or skin exudate

84
Q

ways that diptheria evades immune response

A
  • AB toxin which blocks protein synthesis

- forms pseudomembrane

85
Q

pseudomembrane in diptheria

A
  • exotoxin
  • causes necrosis of epithelial cells
  • liberates serous and fibrinous material
86
Q

types on neisserial infections

A
  • n. meningitidis

- n. gonorrhoeae

87
Q

n. meningitidis

A
  • causes meningitis in adolescents and young adults
  • transmitted through respiratory route
  • most can eliminate infection
  • antigenic variation
88
Q

how does n. meningitidis evade immune response

A
  • covered in capsule

- capsule inhibits opsonization and destruction by complement system

89
Q

n. gonorrhoeae

A
  • 2nd most common STD
  • infection in urogenital tract by interacting with epithelial cells -> cellular invasion
  • causes PMN
  • arthritis, meningitis, and neonatal opthalmia
90
Q

who is more likely to become infected by nisseria

A
  • people who lack complement proteins that form MAC
91
Q

pertussis

A
  • gram negative coccobacillus
  • highly communicable
  • produces AB toxin
  • inhibit neutrophils and macrophages
  • paralyzes cilia
92
Q

what is another name for pertussis

A

whooping cough

93
Q

what are possible outcomes of severe bordetella infection

A
  • laryngotracheobronchitis causing:
  • bronchial mucosal erosion
  • hyperemia
  • copious mucopurulent exudate
  • lymphadenopathy
94
Q

p. aeruginosa

A
  • gram negative bacillus
  • deadly in people with CF, severe burns, neutropenia
  • very resistant to antibiotics
  • common hospital acquired infection
95
Q

possible clinical outcomes of p. aeruginosa

A
  • corneal keratitis in contact lens wearers
  • endocarditis and osteomyelitis in IV drug users
  • external otitis
96
Q

how does p. aeruginosa evade immune response

A
  • excrete exotoxin A -> inhibits protein synthesis
  • elastase
  • leukocidin
  • hemolysins- destroys cell membranes
97
Q

what is the evidence of infection in Tb

A
  • fibrocalcific pulmonary nodule at site of infection

- can lay dormant for years

98
Q

what affects outcome of Tb

A
  • T cell mediated immunity

- causes pathologic lesions like caeseating granulomas and cavitation

99
Q

where does Tb infection reside/ replicate

A

macrophages

100
Q

what is the ghon complex

A
  • parenchymal lung lesion

- nodal involvement

101
Q

pathogenesis of Tb

A
  • 3 weeks post infection IL12 released by dendritic cells
  • Th1 response
  • release IFN gamma
  • macrophages activated
  • granuloma and caseous necrosis
102
Q

primary Tb

A

develops in previously unexposed person

103
Q

secondary Tb

A
  • develops in previously sensitized host

- usually involves apex of upper lobes of one or both lungs with cavitation

104
Q

systemic symptoms of Tb

A
  • related to cytokine released by activated macrophages
  • malaise
  • anorexia
  • weight loss
  • low grade fever
  • night sweats
105
Q

late stages of Tb

A
  • increasing amounts of sputum, hemoptysis, pleuritic pain
106
Q

dx of Tb

A
  • history
  • xrays
  • gold standard= sputum culture
107
Q

syphilis

A
  • chronic STD
  • varied clinical sx
  • caused by spirochete tryponema pallidium
108
Q

primary syphilis

A
  • 3 weeks after contact
  • chancre on penis, cervix, vaginal walls, or anus
  • heals without therapy
109
Q

secondary syphilis

A
  • 2-10 weeks post exposure
  • widespread mucocutaneous lesions in oral cavity, palms of hands, soles of feet
  • lymphadenopathy
  • mild fever
  • malaise
  • weight loss
110
Q

tertiary syphilis

A
  • long latent period (5 years)
  • CV syphilis
  • neurosyphilis
  • benign tertiary syphilis
111
Q

CV syphilis

A
  • aortitis

- aortic valve insufficiency

112
Q

neurosyphilis

A
  • meningovascular disease
  • diffuse brain parenchymal disease
  • CSF abnormalities
  • increased protein
  • decreased glucose
113
Q

benign tertiary syphilis

A
  • gummas in bone, skin, and mucous memrbanes

- gummas are bumps/ elevations

114
Q

what causes lyme disease

A
  • borrelia burgdorferi

- can be persistent or severe

115
Q

how does lyme disease evade immune response

A

antigenic variation

116
Q

what causes damage from lyme disease

A
  • host immune response
  • does NOT produce toxin
  • T cell and cytokine release mediates immune response
  • antibodies made 2-4 weeks post infection
  • direct complement mediated phagocytosis and killing of bacteria

Patho 2 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions