Brainscape's Knowledge GenomeTM

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


See full index

Emergency Med > Bioterrorism > Flashcards

Bioterrorism Flashcards

You may prefer our related Brainscape-certified flashcards:
Royal College: Emergency Medicine flashcards
1
Q

What are the three groups biologic agents are divided into?

A

Bacteria
Viruses
Toxins

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

What are the biologic agents that are considered to have the most severe potential?

A 
Bacillis anthracis (anthrax)
Yersinia pestis (plague)
Variola major (smallpox)
Francisella tularensis (tularemia)
Clostridium botulinum (botulism)
Filoviruses and arenaviruses (viral hemorrhagic fevers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Organism for anthrax

A

B. anthracis
Gram-positive spore-forming bacterium
Appears as long chains, resembling bamboo or boxcars

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

Where is anthrax found?

A

In grass-eating mammals that ingest or inhale the spores while feeding
Humans become infected by eating infected animals or through contact (skin or inhalation) with spores on the fur or hide of animals

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

What are the three forms of anthrax?

A 
Cutaneous
-Most common
Pharyngeal or gastrointestinal
Inhaled
-Most deadly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology of anthrax

A 
Exposure to spore via skin (or worse) inhalation
Spores germinate into bacilli
Transported to regional lymph nodes
Release toxins
Sx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prevention of anthrax

A

Vaccine available to military at risk only

Cipro or doxy prophylaxis for 30 days (with vaccination) or 60 days (no vaccination)

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

Sx/exam of anthrax

A 
Painless papules that become vesicular with significant edema
Progress to ulcerated black eschar in 1 wk
Constitutional sx (fevers, chills, myalgias) and lymphadenopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pharyngeal or GI anthrax

A

Ulcers and edema of pharynx followed in 5 days by abdominal pain, upper and lower GI bleeding

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

Inhaled anthrax

A

Mild flu-like sx that rapidly progress to respiratory distress and septic shock

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

Diagnosis of anthrax

A 
Primarily a clinical dx
CXR
Mediastinal lymphadenopathy (CT is more sensitive than CXR)
Possible pleural effusions
May be clear of infiltrates
Gram stain and culture of skin lesions
Tissue or pleural fluid evaluation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tx of anthrax

A

Supportive and symptomatic care
Simple cutaneous anthrax (nontoxic): Cipro, doxy, or amoxicillin
Toxic pts or inhalational dz; require triple antibiotic therapy
-Cipro or doxy plus two other abx (e.g., rifampin, clinda)
Antibiotic therapy must continue for 60 days

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

Plague organism and how it’s transmitted

A

Y. pestis, a Gram-neg bacillus

Normally a dz of rodents transmitted to humans by inhalation of flea feces or bite of infected flea

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

Forms of dz- plague

A

Bubonic (skin)
-Bacilli migrate to regional lymph nodes- bubo
Pneumonic (inhalational)
-MC: may be transmitted person to person
Septicemia (from secondary dissemination)

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

Bubonic plague

A

Two to three days incubation followed by:

  • Regional painful lymph node inflammation and necrosis (bubo)
  • Fevers, chills, malaise
  • Will disseminate over next week in 50% (if untreated)
  • Leads to septicemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pneumonic plague

A

Two to three days incubation followed by:

  • Abrupt onset of fevers, chills, and flulike illness
  • Severe pneumonia in 24 hrs
  • Pts may develop meningitis, liver injury, coagulation disturbances, and gangrene in extremities (black death)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Septicemic plague

A

Characterized by endotoxemia, shock, DIC, and coma

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

Dx of plague

A

Suspect in any healthy individual who develops overwhelming Gram-negative sepsis
Gram stain and culture all body fluids

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

Tx of plague

A 
Isolate pts
Do not incise and drain fluctuant lymph nodes (aspiration ok)
Abx: Multiple choices available
Mild bubonic may be treated at home
Prophylaxis: Same drugs for 7-day course
20
Q

Smallpox

A

Organism: V. major, a large DNA virus
Was successfully eradicated in 1980 with small pox vaccine, but US and Russia have viral repositories for research purposes
Threat to resurface d/t lack of vaccination

21
Q

Clinical forms of smallpox

A

Variola major and minor- 90% of cases
-The classic form of dz
Hemorrhagic
Malignant

22
Q

Sx/exam of smallpox- variola major and minor

A

Incubation period of 2 wks followed by:

  • Constitutional sx
  • Maculopapular rash
  • Begins in mouth
  • Predilection for face, then spreads distally involves palms and soles
  • Changes from vesicular to pustular with all lesions in same stage
23
Q

Sx/exam of smallpox- hemorrhagic

A

Quicker and more toxic course
Petechiae and hemorrhage
Ninety percent mortality rate

24
Q

Sx/exam of smallpox-malignant

A

Also quicker and more toxic course

Lesions are flatter and never progress to pustules

25
Q

Major criteria for smallpox

A

Febrile prodrome
Classic smallpox lesions
Lesions in some stage of development

26
Q

Minor criteria for smallpox

A 
Centrifugal distribution of pustules
Toxic appearance
First lesions in mouth, face or forearms
-Slow evolution of lesions
Pustules on the palms and soles
27
Q

Major and minor criteria- how they come into play for smallpox

A

Three major- presumed dz
Two major or one major and four minor- probable disease
Fever than four minor- dz not likely
Lab PCR identification of variola DNA in a clinical specimen

28
Q

Tx of smallpox

A

Isolate pt
Very contagious until all scabs fall off
Exposed persons- vaccinate within 3 days to prevent or attenuate dz. Vaccinia immunoglobulin is given simultaneously with vaccine and redosed as needed to limit complications of vaccination
Antivirals are being investigated as tx

29
Q

Tularemia

A

Organism: Francisella tularensis, a Gram-neg intracellular bacterium
Tularemia is transmitted primarily from ticks, lagomorphs, and rodents via direct contact or ingestion of infection water, soil, or fomites
Several forms exist depending on route of contact

30
Q

Localized dz with regional lymph node involvement- tularemia

A

Ulceroglandular: MC- ulcers with LAD
Glandular: 2nd MC LAD without skin lesions
Oculoglandular: Conjunctivitis with preauricular LAD
Oropharyngeal: Severe pharyngitis with cervical lymphadenitis

31
Q

Invasive and generalized dz- tularemia

A

Typhoidal
-Fevers, chills, GI sx, NO skin lesions
Pulmonary
-Fevers, chills, SOB, nonproductive cough

32
Q

Dx of tularemia

A

Based on clinical findings

Antibody titers, rapid PCR

33
Q

Tx of tularemia

A

Isolation is not required
Antibiotic: Streptomycin is drug of choice
Prophylaxis= doxycycline

34
Q

Organisms in viral hemorrhagic fevers

A

Filoviruses and grenaviruses

Normally transmitted via mosquitoes, rodents, or their parasites

35
Q

Sx/exam of viral hemorrhagic fevers

A

Incubation period from 4-21 days, followed by:

  • Fevers, myalgias, prostration
  • Petechial hemorrhage, DIC
  • Multisystem organ dysfunction, cardiovascular collapse
36
Q

Dx of viral hemorrhagic fevers

A

ELISA

PCR

37
Q

Tx of viral hemorrhagic fevers

A

Supportive care
Antiviral: Ribavirin
Prophylaxis: Ribavirin

38
Q

Nerve agents

A

Organophosphates

Include sarin, soman, VX (vesicant?)

39
Q

Vesicants

A

Agents that induce blistering via cellular damage, including mustard

40
Q

Pathophysiology of nerve agents

A

Inhibit acetylcholinesterase
Leads to accumulation of acetylcholine at muscarinic and nicotinic receptors
Leads to cholinergic toxidrome

41
Q

Sx/exam of nerve agents

A 
Cholinergic toxidrome
Salivation/sweating
Lacrimation
Urination
Defecation
Excretion?
GI distress
Emesis
Miotic pupils
Fasciculations
Muscle weakness
Apnea
AMS
Seizures
42
Q

Dx of nerve agents

A

Based on hx exposure and clinical presentation

43
Q

Tx of nerve agents

A

Supportive care
Atropine dosed to secretion control (may require 2-4 mg at frequent intervals)
Pralidoxime chloride (2-PAM) to reverse paralysis
Benzodiazepines for seizures

44
Q

Sx/exam of vesicants

A

Local skin effects: Severe pain, vesicle formation, and inflammation to site of contact
Skin injury resembles second-degree burn
Inhalation effects: Pharyngeal edema and pulmonary necrosis- varying degrees of respiratory distress
Systemic effects: Bone marrow suppression

45
Q

Tx for vesicants

A

Skin and mucus membrane decontamination with irrigation

Supportive care

Emergency Med (11 decks)

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