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x. ID > 4/17 URI: iBook Ch 9 > Flashcards

4/17 URI: iBook Ch 9 Flashcards

1
Q

Define Pharyngitis

What agents cause it?

What is the most important distinction to make in diagnosing Pharyngitis?

A

An inflammatory syndrome of the pharynx caused by several types of organisms.

Predominant causes are viral but can also be due to bacterial and atypicals.

Most impt distinction: Group A Strep (bacteria) vs all other causes (primarily viral)

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2
Q

Common cold: cardinal symptoms?

A
  • Nasal discharge and obstruction
  • Sneezing
  • Sore/scratchy throat
  • Nonproductive cough with sensation of postnasal drip
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3
Q

Common cold: physical findings?

Avg duration of illness?

A
  • Red nares with clear discharge, “glassy” nasal membranes
  • Throad injected wiht mucus on posterior pharyngeal wall; no exudate
  • No or mild fever (<1’ elevation)
  • Duration ~1 week, will last 3d longer in smokers
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4
Q

Common cold: most common cause? next most common?

Seasons most prevalent?

A
  • Rhinovirus (HRV) is most common followed by coronavirus
  • Rhinovirus prevalent in fall/spring; coronavirus and RSV in winter
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5
Q

Common cold: incubation period? at what point is maximal viral excretion?

A

Incubation is 48-72 h

Max viral excretion coincides with peak of clinical illness, but begins 1 day before, and may persist over a week.

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6
Q

Common cold: most effective transmission?

A
  • hand to hand transmission more efficient than droplet spread for rhinovirus. may persist on fomites (contaminated object or surface) for several hours.
  • influenza, parainfluenza, adenovirus, coxsackievirus transmit via aerosol
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7
Q

Common cold: where does replication of rhinovirus occur?

-What are the major mediators of symptoms?

A

Rhinovirus replicates in nasal epithelium, but does not cause much destruction.

-Symptoms are mainly due to immune response of host: mainly kinins

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8
Q

Common cold: diagnosis?

A

Clinical diagnosis (viral cultures not readily avail)

-Challenge is to distinguish bacterial conditions (infrequent; treatable) from viral illness (more common; self-limited)

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9
Q

Common cold: treatment?

A

Symptomatic treatment!

  • Rhinorrhea: intranasal ipratropium bromide or cromolyn sodium to reduce volume and severity
  • Sore throat: ibuprofen, warm saline gargles
  • couth: antitussives
  • systemic sx: rest, ibuprofen
  • Decongestants
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10
Q

Common cold: treatments that are NOT effective?

A

antibiotics, Vit C, echinacea, antihistamines, expectorants, glucocorticoids, zinc

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11
Q

Common cold in kids: what should I avoid giving them? why?

A

Avoid aspirin use in children with URI

May cause Reye’s Syndrome

[potentially fatal; affects many organs, especially the brain and liver. Also –> hypoglycemia. Classic features: rash, vomiting, liver damage.

Exact cause unknown. Has been associated with aspirin consumption by children with viral illness; also occurs in the absence of aspirin use.]

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12
Q

Common cold: 3 possible complications?

Frequency of these complications?

A
  • Sinusitis. occurs in 40% of adults w cold sx.
  • Acute Otitis media. Primarily occurs in kids; 50-80% of adults develop Eustachian tube dysfunction.
  • Lower resp tract disease. In adults, up to 40% of acute asthma attacks are secondary to colds.
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13
Q

Group A ß-hemolytic streptococcal pharyngitis (GABHS): symptoms?

A
  • Abrupt onset
  • Sore throat, pain w swallowing
  • Systemic illness: fever, malaise
  • Nasal congestion/cough in 50% (not prominent)
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14
Q

Group A ß-hemolytic streptococcal pharyngitis (GABHS): Physical findings?

A
  • temps of 100-104
  • Diffuse redness of pharynx and tonsils (may be bright red)
  • Tonsillar exudate in 50-80% (patchy or confluent)
  • Enlarged, tender anterior cervical lymph nodes
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15
Q

Group A ß-hemolytic streptococcal pharyngitis (GABHS): what are the factors leading to infection?

Group A ß-hemolytic strep causes what % of sore throats in adults? kids?

A

Exact factors leading to infection are unknown: may be altered host immunity, bacterial interference, elaboration of enzymes (streptokinase, hyaluronidase, proteinase) by virulent strains.

Group A ß-hemolytic strep: 10% of sore throats in adults & 25% in kids.

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16
Q

Group A ß-hemolytic strep: diagnosis?

A

Two methods:

  • Culture: throat swab –> agar. look for beta-bemolysis. Type with a latex agglutination assay. (false neg 5%)
  • Rapid enzyme immunoassay. Preferred for clinical diagnosis; allows prompt treatment.
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17
Q

Group A ß-hemolytic strep: why is it impt to accurately identify the Group A strep?

A
  • prevent the immune-medient sequela of rheumatic fever (potential –> heart disease)
  • prevent suppurative complications (peritonsillar abscess)
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18
Q

Group A ß-hemolytic strep: how can we estimate the probability of Group A strep infection?

A

Three clinical clues: tonsillar exudates, enlarged tender cervical LNs, temp > 100.

If all three sx present, probability of Group A strep infection = 42%.

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19
Q

How can we decrease the occurence of acute rheumatic fever in suspected Group A strep?

A

Can decrease rheumatic fever 10x by starting antibiotics within 9d of onset of sx. Continue for 10d of treatment overall.

Antibiotics can also reduce symptoms, suppurative complications, and infectious spread.

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20
Q

Group A ß-hemolytic strep: what antibiotics to use?

A
  • Oral penicillin V
  • Benzathine penicillin via single IM injection if compliance is problematic
  • If PCN allergy, Erythromycin, clarithroymycin, azithromycin
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21
Q

Group A ß-hemolytic strep: meds for symptoms?

A
  • For sore throat, fever & systemic sx: acetominophen
  • Severe sore throat: acetaminophen w Codeine or viscous Xylocaine
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22
Q

Mononucleosis: symptoms?

Onset?

A

Pharyngitis/laryngitis

Fever, headache, malaise, fatigue

Abrupt onset or several day prodrome

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23
Q

Mononucleosis: Physical findings?

A

Fever

Adenopathy: both cervical and generalized

-Splenomegaly (50%)

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24
Q

Mononucleosis: Etiology?

A

Majority: EBV.

Also: CMV, HIV

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25
Q

EBV: how is it spread?

A

(remember this is the main cause of mono)

spread by intimate contact with oropharyngeal secretions.

Can persist up to 18m after clinical recovery.

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26
Q

EBV: what are peak periods of seroconversion?

severity of clinical illness increases w what?

A

Peak periods of seroconversion are 0-5 yrs and in the 20s

Severity of clinical illness increases with age.

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27
Q

Mononucleosis: Diagnosis?

A
  • Clinical syndrome
  • Hematologic findings: Lymphotycosis; Atypical lymphocytosis = hallmark; thrombocytopenia
  • Heterophile antibodies (antibodies that agglutinate sheep erythrocytes). Commercial test “Monospot” available.
  • EBV antibodies
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28
Q

Mononucleosis: Treatment?

A

Treatment = symptomatic

Occasionally give steroids for airway obstruction, severe thrombocytopenia, hemolytic anemia

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29
Q

define acute bronchitis.

how does it contrast with chronic bronchitis?

A

acute inflammatory condition of the tracheobronchial tree that does not involve the pulmonary parenchyma

contrast w chronic: chronic has significant sputum production on most days during at least 3 months each of 2 consecutive years (who comes up this stuff??!!). also contrasts with acute exacerbation of chronic bronchitis (AECB)

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30
Q

Acute Bronchitis: Cardinal Symptoms?

A
  • Persistent cough (days to weeks)
  • Possible sputum production
  • Possible fevers
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31
Q

Acute Bronchitis: Physical Findings?

A
  • Cough
  • Possible fevers (most likely with Influenza, Adenovirus, Mycoplasma)
  • Lung exam: crackles or wheezes, no consolidation
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32
Q

Acute Bronchitis: Etiology? (what pathogens?)

Which pathogens are most important/treatable? (2)

A

Majority of cases are viral.

Most important (and treatable) are Mycoplasma pneumoniae and Chlamydia pneumoniae

Bordetella pertussis should be considered with appropriate epidemiology

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33
Q

Acute Bronchitis: What changes may be found in the airway following URI? what is evidence for this?

A

Changes in airway dynamics: bronchoconstriction and bronchial hyper-reactivity.

Evidence = prolonged non-productive cough.

34
Q

Acute Bronchitis: Rhinovirus infection causes production of what mediators?

What individuals are particularly prone to this?

A

Rhinovirus infection increases production of leukotriene C4 and IgE mediated histamine release –> bronchoconstriction, bronchial hyper-reactivity.

Atopic pts are particularly susceptible.

35
Q

Acute Bronchitis: Mycoplasma’s incubation period is how long? what is its rate of spread among close contacts?

A

Mycoplasma: long incubation (21 days)

High rate of spread among close contacts (60%)

36
Q

Mycoplasma “bronchitis” Cardinal symptoms?

A

Cough! Dry hacking cough initially, then production of mucoid sputum, then purulent (yellow or green) sputum

Cough lasts 2 weeks - 1 month

37
Q

Mycoplasma “bronchitis”: Physical findings?

A
  • Lung exam: Rhonchi and coarse rales. May be a loose-sounding cough like pneumonia
  • Low grade fever (associated with bacterial infections)
  • Wheezes, especially in asthmatic and atopic pts.
38
Q

Acute Bronchitis: what is most important diagnostic task?

A

Distingush bronchitis from pneumonia.

39
Q

What are the main distinctions between bronchitis and pneumonia?

A

“typical” pneumonia: patients are usually more ill than w bronchitis, abrupt onset of sx, higher fever, stronger cough, more sputum

“atypical” pneumonia: subacute onset, dx made based on pulmonary exam (crackles, consolidation) or CXR (infiltrate). symptoms last longer than w bronchitis.

40
Q

CXR findings with acute bronchitis v pneumonia?

A

Acute bronchitis: CXR may be normal, may have peribronchial cuffing.

Pneumonia: there will be an infiltrate.

41
Q

Distinguish acute bronchitis from a common cold.

what is the nature of the sx?

duration?

A

acute bronchitis: cough is severe and is the primary symptom. may persist for weeks

Cold: cough is only one of several sx and is less severe. usually resolves in 7-10d.

42
Q

what is the distinction between acute bronchitis and chronic bronchitis or acute exacerbation of chronic bronchitis (AECB)?

A

Chronic bronchitis defined as productive cough on majority of days during at least 3 months out of two years.

AECB = increased sputum production, change in color/consistency of sputum. no signs of systemic infection (ie no fever)

43
Q

Acute bronchitis: treatment for cough and wheezing?

A

Cough and wheezing can be treated symptomatically

cough: dextromethorphan or codeine
wheezing: inhaled beta agonist bronchodilator (albuterol) or rapid taper of steroids (prednisone)

44
Q

Acute bronchitis: when would I use antibiotics?

Which ones?

A

Only use antibiotics when bacterial infection is documented or highly likely.

Erythromycin or another macrolide (clarithrymycin, azithromycin) since they treat both M pneumoniae and C. pneumoniae. Both also reduce bronchial hyper-reactivity

45
Q

Acute bronchitis: how would I document that I have a bacteria and therefore should use antibiotics?

A

Document with IgM serology for M pneumoniae or PCR or culture for B pertussis.

46
Q

Quick review: the 3 agents associated with Acute Bronchitis?

A
  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Bordetella pertussis
47
Q

Acute sinusitis: definition?

What are the possible types of pathogens?

A

Infection of one or more of the paranasal sinuses.

Pathogens may be viral (most common), bacterial (hardest to diagnose) or fungal (immunocompromised host).

48
Q

Acute sinusitis: what are the three types (not pathogens) of bacterial infections?

A
  • acute community-acquired bacterial sinusitis (ACABS)
  • community-acquired chronic
  • nosocomial (acquired in a health-care facility)
49
Q

Embryonic development of the sinuses: sinuses develop as outpouchings of what? at what point are they fully developed?

A

Outpouchings of the nasal airway into the body cranium during the second trimester

Not fully developed until adolescence!

50
Q

Top 3 bacteria causing acute sinusitis?

A

-Streptococcus pneumoniae (25-30%)

  • Haemophilus influenza (15-20%)
  • Moraxella catarrhalis (pediatric, 15-20%)
51
Q

What are the ostia, and why are they important?

A

They are tiny bony canals which converge at the ostio-meatal complex. Serve as conduits for drainage of the sinuses into the nasal cavity, and ventilation of the sinuses.

52
Q
A
53
Q

Symptomatic sinusitis follows obstruction of the ostia during a viral URI. what other factors can contribute to the sinusitis? (anatomic or other disease states)

A
  • allergic rhinitis
  • nasopharyngeal polyps, hypertrophied adenoids
  • impaired nasopharyngeal ciliary activity
  • cystic fibrosis (genetic; abnl transport of Cl and Na -> viscous secretions)
  • Wegener’s granulomatosis (vasculitis of small/med vessels; ANCA+)
  • Immunoglobin deficiencies
54
Q

Acute community acquired bacterial sinusitis (ACABS): how are the bacteria introduced into the sinuses?

A

Normally the sinuses are sterile: bacteria are introduced by coughing, sneezing, nose blowing.

Leads to acute bacterial sinusitis

(top 3 bacteria: Strep pneumo, Haemophilus influenza, Moraxella catarrhalis - peds)

55
Q

Chronic sinusitis: how is the pathophys different from acute?

what additional bacteria may be responsible?

A

Chronic = persistent infection due to permanent blockage of the ostia, or due to abnormal ciliary clearance.

-Bacteria: Staph aureus, anaerobic gram positives, gram negative bacilli

(also the 3 acute ones: Strep pneumo, Haemophilus influenza, Moraxella catarrhalis - peds)

56
Q

Is acute sinusitis prevalent in young kids?

A

No - generally not seen before 1y of age. Probably due to the underdevelopment of the sinus cavities

57
Q

ACABS: symptoms?

A

URI symptoms: rhinorrhea, nasal obstruction, facial pressure

PLUS persistent cough, purulent nasal discharge, headache, facial pain

58
Q

a severe temporal or retro-orbital headache may be associated with what type of sinusitis?

A

sphenoid sinusitis

59
Q

Acute sinusitis: physical exam findings?

A
  • nasal exam with otoscope may reveal purulent discharge from middle meatus
  • pain with palpation of maxillary or frontal sinuses
  • diminished transillumination
60
Q

Acute sinusitis: “gold standard” diagnosis?

A

aspiration and culture

61
Q

Acute sinusitis: basis for diagnosis typically used in practice?

what would differentiate allergic v. infectous sinusitis?

A

often based on history and physical findings.

Initial distinction is to differentiate allergic from infectious sinusitis. Allergic: sneezing, itchy eyes, history of prior episodes, lack of common cold symptoms.

62
Q

Acute sinusitis: how to differentiate VRS (viral rhinosinusitis) from ACABS (acute community acquired bacterial sinusitis)?

A

ACABS classic presentation: fever > 38’, unilateral facial pain/ tenderness/ erythema/ swelling

ACABS may also start out looking like VRS (viral sinusitis - common cold) but then symptoms do not resolve within one week as expected with VRS. At that point be suspicious for a bacterial infection.

63
Q

When would you use imaging to diagnose ACABS? what modality would you use?

A

Not typically used for diagnosis of ACABS but may be needed to work up chronic sinusitis.

CT is more sensitive than xray; CT = method of choice. An air fluid level with a flat meniscus is highly specific for ACABS.

64
Q

What is the general course of acute bacterial sinusitis?

If there are pyogenic complications, what would they be for each sinus?

A

Spontaneous recovery in 50%. Possible to develop chronic sinusitis.

Pyogenic complications:

Maxillary/frontal sinusitis –> subdural empyema, brain abscess, Pott’s puffy tumor, meningitis

Ethmoid sinusitis –> Subperiosteal orbital abscess, orbital cellulitis, meningitis

Sphenoid sinusitis –> cavernous sinus thrombosis, meningitis

65
Q

Acute sinusitis: when is it appropriate to prescribe antibiotics?

A

When pt presents with classic presentation (fever >38, unilateral facial pain, facial tenderness/erythema/swelling)

OR

> 10 days of URI symptoms

66
Q

Acute sinusitis: what antibiotics are best? what do they need to cover?

A
  • amoxicillin-clavulanate, cefuroxime, cefpodixime, new quinolones (moxifloxacin)
  • need to cover H influenza and S pneumoniae (produce B lactamase)
67
Q

Acute sinusitis: what is the role of antihistamines? NSAIDS? decongestants? steroids?

surgical drainage?

A
  • Antihistamines/NSAIDs: possible symptomatic relief
  • Decongestants are often used but not proven useful
  • Corticosteroids have no use
  • Surgical drainage may be needed for complications or for failure to respond to oral antibiotics
68
Q

Influenza: onset? symptoms?

A

Acute onset

Main symptoms are systemic: Fevers, headache, myalgia

Less severe symptoms are pharynitis, respiratory sx.

69
Q

Influenza: Physical findings?

A

Ill appearing

high fever

minimal pharyngitis

small, tender, cervical adenopathy

70
Q

Right now Jen has a malaise. Sx: Horrible rhinorrhea. Sneezing. headache. sore throat. fatigue.

No myalgia. no fever. no lymphadenopathy. no dyspnea.

onset was gradual.

What is the likely diagnosis? pathogen? treatment?

A

Probably just a common cold. Could be sinusitis.

Not group A strep: no fever.

Not mono: no lymphadenopathy

Not bronchitis: no wheezing, no dyspnea

Not pneumonia: no fever, no dyspnea

Not flu: no fever, no adenopathy

If common cold, pathogen is likely rhinovirus. Hand to hand transmission (those damn undergrads!!). Treatment is symptomatic.

If it lasts longer than a week, it is probably bacterial sinusitis rather than viral URI. Would be Strep pneumo or H influenza. At that point I should take amox-clavulanate, cefuroxime, cefpodoxime, or new quinolones. Or 50% chance it will just go away even if it is bacterial. Theoretically possible to be a fungal infection, but I’m not immunocompromised that I know of.

71
Q

Influenza: caused by which bugs?

how is it transmitted?

how long is someone infectious?

A

Influenza virus A and B (family Orthomyxidae)

Transmission via small particle aerosol

Viral shedding is from 1d prior to onset of symptoms to 5-10d after fevers resolve.

72
Q

Influenza: once a virus is deposited on the resp tract epithelium, how will it get into the body and cause problems?

A

Deposited on resp tract epithelium, then attaches to and penetrates columnar epithelial cells. Once adsorbed, the virus starts a replication cycle (4-6 h). Then infects adjacent cells.

73
Q

Influenza: what is the body’s response to the virus?

A

Interferon response (INF).

correlates with improvement of sx, and decreases viral titers.

INF may be active in recovery process between the 3rd and 6th day before any antibody can be detected.

Antibody develops by the second week after exposure.

74
Q

In relation to influenza, what is antigenic variation?

What glycoproteins are involved?

A

Influenza virus changes antigenicity frequently. allows it to cause major epidemics in humans.

Influenza A: variation is frequent: almost annual.

Influenza B: variation is less frequent

Influenza C: variation does not occur.

Principally happens with external glycoproteins HA and NA.

75
Q

What is antigenic drift? antigenic shift?

A

types of antigenic variation (influenza).

antigenic drift: relatively minor changes within an influenza subtype.

antigenic shift: more major changes within influenza subtypes

76
Q

Antigenic drifts and shifts: how are they identified?

A

New influenza subtypes are identified by external glycoproteins HA and NA

Antigenic drift (minor changes): subtypes identified by location and year of virus isolation. Ex: Influenza A/Texas/77/H3N2

Antigenic shift (major changes): “new” viruses identified by enumeration of H and N glycoproteins. Ex: H1N1, H2N2, H3N2

77
Q

Influenza: diagnosis?

A
  • Clinical diagnosis in setting of epidemic has high positive predictive value
  • Rapid assays (ELIZA) on nasopharyngeal aspirate are very specific and 90% sensitive
  • Culture from nose of throat: 2/3 will be positive in 3 days
78
Q

Influenza: treatment?

A
  • Supportive
  • Against Influenza A: Amantadine/rimantadine. Reduces duration of s/s by about 50%. A/E: CNS toxicity. Contraindicated if seizure disorder.
  • Oseltamivir and Zanamivir (neuraminidase inhibitors)
79
Q

Influenza vaccine: efficacy?

A

80-90%

80
Q

Influenza Vaccine: who is it recommended for?

A
  • healthy pts aged 65+
  • residents in nursing homes or other chronic care facilities
  • adults/kids with disorders of pulm of CV (incl kids with asthma)
  • adults/kids who have been hositalized with metabolic disorders (diabetes, renal dysfxn, immunosuppression)
  • kids 6m-18y who need long-term aspirin therapy and may develop Reye’s Sx after influenza infection
  • Health care workers who may transmit to high-risk patients
  • Home health care providers
  • HIV positive patients
81
Q

Influenza antivirals: what is efficacy rate?

A

75-90%

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