Brainscape's Knowledge GenomeTM

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


See full index

CRRAB 2 > 3: Resp ID 1 Handout > Flashcards

3: Resp ID 1 Handout Flashcards

1
Q

Most common cause of URIs (general)

A

Viral

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

What is noteworthy re: the ideal environment for Rhinovirus replication?

A

Preferentially replicate at 33C (upper airways), not 37

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

After rhinovirus, other frequent causes of common cold (6)

A

parainfluenza, coronavirus, Influenza C, Coxsackie A&B, Adenoviruses

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

Common cold symptoms (4)

A

Nasal discharge/ congestion, mild sore throat, cough, afebrile (except kids may be)

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

Treatment of common cold. How long does it last?

A

Symptomatic. ~1 week or less, self-limiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Etiology of sinusitis

A

Usually bacterial infec secondary to viral URI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Presentation of sinusitis (3)

A

fever, purulent nasal discharge, sinus tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 most common microorganisms in sinusitis

A

Strep pneumoniae, Haemophilus influenzae -each ~35% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common cause of pharyngitis in children <3 and adults

A

Viral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Most common cause of pharyngitis age 5-15

A

Strep pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pharyngitis presentation (4)

A

Fever, sore throat, edema, hyperemia of tonsils and pharyngeal walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What illnesses are collectively called croup?

A

Acute laryngitis, laryngotracheobronchitis (viral croup), and epiglottitis (bacterial croup)

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

Why is croup more concerning in young children?

A

Narrower airway -> obstruction with inflammation is of concern.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Croup usually resolves within ___

A

about a week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rhinovirus is most likely to present as ___. How does it spread and attach?

A

Rhinitis. Spread by contact or aerosol. Binds ICAM-1 of URT epithelial cells

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

What causes tissue damage/ destruction in rhinitis?

A

Immune response. Virus itself does not kill its host cells.

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

What other problems does the immune system create for itself in rhinitis (2)

A

Local infection -> inc ICAM-1 expression -> facilitates viral spread. Exudate blocks airways, can -> sinusitis or otitis media

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

Despite downsides of the immune response, the pro is ____

A

IgA immunity to the serotype down the road!

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

What effect does parainfluenza virus have on infected cells?

A

Utilizes fusion (F) surface proteins. Infected cells -> multinucleate giant cells

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

Clinical presentation of parainfluenza virus

A

Children: croup and pneumonia. Adults: moderately severe rhinitis

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

Parainfluenza virus virulence factors allowing establishment of infection

A

Aerosols. Viral hemagglutinin (HA) envelop proteins interacts w sialic acid on cell surfaces -> endocytosis. Viral neuraminidase env protein cleaves HA-SA bond -> viral spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does parainfluenza virus -> clinical presentation of croup

A

Progress down tracheal and bronchial epithelium -> inflam & swelling of mucus membranes -> narrowing of lumen (insp stridor) and barking cough

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

How is parainfluenzavirus diagnosed?

A

Symptoms, possible lab hemaglutination activity in resp secretions + serology for anti-HA antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment of parainfluenza virus

A

Supportive: cool mist, O2 if severe. Corticosteroids.

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

Second most common causative agent of rhinitis

A

Coronavirus (usually indistinguishable from rhinovirus infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is SARS

A

rapidly progressive viral pneumonia (+fever, dyspnea, cough), can -> resp failure, death

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

Spread of coronavirus

A

Inhalation through respiratory aerosols

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Timing of coronavirus symptom manifestation

A

3 day incubation period + 6-7d of cold symptoms

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

Treatment for coronavirus

A

Supportive care

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

Influenza genome

A

A & B: 8 segments

C: 7 segments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Is influenza A or C more virulent?

A

A. C often -> asymptomatic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

With which type(s) of influenza do we not see antigenic shifts? Why?

A

B & C. No animal reservoir.

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

What is happening microscopically during the initiation of influenza C infection?

A

Like parainfluenza: utilizes hemagglutinin (envelope) + sialic acid on host cell surface. NA cleavage -> spread.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Does influenza C kill its host cells? What is the result?

A

It can -> tissue damage + immune response (IL-1 & IFN-gamma)

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

Diagnosis of influenza C

A

Nasopharyngeal swab rapid antigen test. Can culture & detect HA type via RBC agglutination test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Treatment for influenza C. Is there a vaccine?

A

Supportive: acetaminophen, hydration, rest. No vaccine available.

37
Q

Most common infections with Coxsackie A

A

herpangia (mucosal epithel infec -> red vesicles, fever, sore throat) & hand-foot-and-mouth disease

38
Q

Most common manifestation of Coxsackie B infection

A

Pleurodynia, myocarditis (50% of cases), pericarditis

39
Q

Both Coxsackie A & B can cause ___ (3)

A

URI. Infection of anterior horn motor neurons or meninges -> aseptic meningitis or paralysis

40
Q

Typical season for coxsackie virus. Transmission.

A

Summer and fall. Fecal to oral or aerosol.

41
Q

Diagnosis of coxsackie virus

A

Isolate virus, serology

42
Q

Treatment for coxsackie infection

A

Supportive. Anti-inflammatory agents for symptomatic infections.

43
Q

Where is latent adenovirus often found following infection?

A

Tonsillar adenoids

44
Q

How is it that adenovirus can be given as a live vaccine without causing infection?

A

Serotypes have a specific site of infection and assoc disease. Immunize away from favored site.

45
Q

Possible presentations of adenovirus infection (4)

A

Resp infec (rhinitis) w ability to progress to atypical pneumonia, conjunctivitis, hemorrhagic cystitis (presents w hematuria and dysuria), gastroenteritis

46
Q

Virulence factor for adenovirus

A

Binds to cells utilizing hemagglutinin

47
Q

Treatment of adenovirus

A

live virus vaccine of specific serotype - only used in military

48
Q

Possible clinical presentations of strep pyogenes (4)

A

pharyngitis, impetigo, erysipelas (type of superficial cellulitis w dermal lymphatic involvement), cellulitis

49
Q

Virulence factors of strep pyogenes and what they do (4)

A

Streptokinase (plasminogen to plasmin -> fibrinolysis), M protein resists phagocytosis, hayluronidase breaks down CT, DNase

50
Q

Strep pyogenes releasing toxin can result in (2)

A

scarlet fever or streptococcus toxic shock syndrome

51
Q

Treatment of strep pyogenes

A

Penicillin G (IV or IM)

52
Q

What antibodies are present in someone who has had a strep pyogenes infection?

A

anti-streptolysin O

53
Q

Top 2 causes of bacterial pneumonia in COPD

A
  1. nontypeable H flu

2. Moraxella catarrhalis

54
Q

Moraxella catarrhalis virulence factors (4)

A

pili for attachment to mucosa, antigenic variation, endotoxin, capsule

55
Q

Possible clinical presentations of moraxella catarrhalis (3)

A

Otitis media, sinusitis, pneumonia

56
Q

Where does Moraxella catarrhalis generally colonize initially?

A

Nasopharynx, then spread to mucosal surfaces -> endotoxin (OM, sinusitis, pneumonia)

57
Q

What are the biochemical features of Moraxella Catarrhalis that can aid in diagnosis (4)

A

Hydrolyzes tributyrin, produces DNase, reduces nitrite and nitrate, no ferm. of sucrose, glucose, maltose, or lactose

58
Q

Treatment of moraxella catarrhalis

A

Amoxicillin-Clavulanate, 2 or 3 gen cephalosporins, TMP-SMX

59
Q

Why is it that only lysogenic corynebacterium diphtheriae cause systemic disease?

A

Toxin is carried by a phage

60
Q

Clinical presentation of corynebacterium diphtheriae infection

A

local -> pseudomembrane + airway obstruction. Systemic -> arrhythmia, myocarditis and polyneuritis - cranial and periph nerve palsy

61
Q

What is the pseudomembrane of c. diphtheriae composed of? (3)

A

Bacterial cells, WBCs and necrotic mucosa

62
Q

What is diphtheria toxin, and what does it do?

A

AB toxin ADP ribosylates eukaryotic elongation factor-2 (eEF2), inactivating this protein -> no translation

63
Q

Characteristics of c. diphtheria allowing for identification

A

Gram + rod, looks like chinese letters under micro, forms black colonies on potassium tellurite

64
Q

C. diphtheria treatment

A

Antitoxin, penicillin, or erythromycin.

65
Q

1 cause of community acquired pneumonia

A

Strep pneumoniae

66
Q

Local (2) and systemic (3) infections caused by strep pneumo

A

Local: lobar pneumonia, OM. Systemic: osteomyelitis, septic arthritis, endocarditis

67
Q

Why are asplenic individuals at increased risk of strep pneumo infection?

A

Capsule, unable to clear antibody-coated organisms

68
Q

What is the Quellung reaction

A

Combining antibody with organism with specific polysaccharide capsule antigen -> swelling and opaque

69
Q

What organisms is the Quellung reaction positive for?

A

Strep pneumo, e. coli, h. flu, klebsiella pneumo, n. meningitides, salmonella

70
Q

What patient factors might help strep pneumo establish an infection (3)

A

Viral infection, allergy, or smoking hinder clearance of strep

71
Q

How can strep pneumo seed infection in meninges?

A

Pt lacks anti-capsular IgG, allowing invasive strain to enter lung lymphatics -> bloodstream -> meninges

72
Q

Strep pneumo classification for ID - inc __-hemolytic, catalase, and optochin sensitivity

A

Gram + diplococci, alpha hemoytic, catalase neg, susceptible to optochin. Quellung +

73
Q

Treatment of strep pneumo

A

Penicillin or cephalosporins for most but Vanco for meningitis.

74
Q

What makes up the pneumovax vaccine?

A

Capsular polysaccharides

75
Q

What type of h. flu is encapsulated and which is not? Which c olonize locally vs more invasive?

A

Hib: encapsulated, more invasive. Non-typeable: no capsule, colonizes locally.

76
Q

Local clinical presentations of Hib (3)

A

epiglottitis, OM, pneumonia

77
Q

Systemic presentations of Hib (3)

A

Meningitis, septic arthritis, cellulitis

78
Q

How does Hib evade the immune response? (2)

A

IgA protease to evade sec IgA, capsule to avoid phagocytosis

79
Q

How does Hib spread in the body?

A

Resp droplets -> invades submucosa -> spreads via bloodstream -> CNS, soft tissue, large joints

80
Q

Hib laboratory identification

A

Gram neg, requires hemin (X factor) and NAD (V factor) on chocolate agar. Immunofluorescence and + Quellung

81
Q

Treatment of Hib

A

3rd gen cephalosporin e.g. ceftriaxone

82
Q

What may be given to close contacts of Hib infected individuals?

A

Rifampin for prophylaxis

83
Q

Common clinical presentation of RSV

A

Children: bronchiolitis, pneumonia. Adults: rhinitis

84
Q

Virulence factors of RSV

A

G surface protein: attachment, F surf prot: fusion of host cells.

85
Q

Transmission of RSV

A

hand to hand or aerosol

86
Q

Pathogenesis of bronchiolitis with RSV

A

Attaches to bronchiolar epithel w protein G -> lower resp infec -> necrosis and inflamm of bronchioles -> mucus obstrx airway -> bronchiolitis and wheezing

87
Q

How does RSV cause pneumonia?

A

Same as bronchiolitis but in alveoli.

88
Q

Treatment of RSV

A

Supportive. Albuterol, aerosolized ribavirin

89
Q

What prevention of RSV is available? Who gets it?

A

Synagis, a F antigen vaccine. High risk infants: premies, lung or heart disease.

CRRAB 2 (12 decks)

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