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Study Guide Flashcards

1
Q

kaffa

A

tartar troops flung bodies of plague via a catapult in 1346

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2
Q

French-Indian War

A

Smallpox blankets from hospitals to Natives in 1757

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3
Q

World War One

A

i. Chlorine gas in trench warfare in 1915

ii. German troops fired shells of phosgene in 1918

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4
Q

Georgi Markov

A

Bulgarian political exile assassinated with a ricin pellet in umbrella tip in 1978

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5
Q

Bhagwan Shree Rajneesh

A

Cult in Oregon that contaminated salad bars with Salmonella enteritides to disrupt elections in 1984

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6
Q

Aum Shinrikyo cult

A

i. Anthrax aerial release of spores in Tokyo in 1994

ii. Sarin gas release in 1995

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7
Q

Kim Jong-nam

A

Lethal nerve agent (VX) in 2017

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8
Q

organophosphates
pesiticides
warfare agents: G series & VX

A

nerve agents

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9
Q

What are the G series nerve agents (3)

A

sarin gas
soman
tabun

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10
Q

Toxicity occurs from inhibition of AChE at the NMJ resulting in constant exposure and production of ACh that stimulates the post-synaptic neuron

A

nerve agent MOA

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11
Q

neuromuscular synapses are effected by affects on the ___ type of receptors

A

nicotinic

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12
Q

neuroglandular synapses are effected by affects on the ___ type of receptors

A

muscarinic

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13
Q

organophosphate + AChE bind to form an irreversible inactivation of the phosphorylated AChE

A

aging process of nerve agents

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14
Q

DUMBBBELLS of nerve agents

_____ effects

A

MUSCARINIC effects

1) D: Diarrhea
2) U: Urination
3) M: Miosis –> dominates over mydriasis
4) B: Bradycardia
5) B: Bronchospasm
6) B: Bronchorrhea
7) E: Emesis
8) L:Lacrimation
9) L: Lethargy
10) S:Salivation

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15
Q

MTWHF of nerve agents

_____ effects

A

NICOTINIC effects

1) M: mydriasis
2) T: tachycardia –> dominates over bradycardia
3) W: weakness
4) H: HTN
5) F: fasciculations

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16
Q

Seizure treatment with nerve agents

A

midazolam - benzos

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17
Q

muscarinic treatment to prevent secretions with nerve agents

A

atropine

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18
Q

nicotinic treatment to prevent muscular paralysis

when is it most effective?

A

pralidoxime - most effective before aging process

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19
Q

examples of blistering agents (4)

A

i. Nitrogen Mustard
ii. Sulfur Mustard
iii. Lewisite
iv. Phosgene

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20
Q

toxicity of blistering agents:

Where does it damage the most?

What does the damage look like?

How long before sx are seen?

What agent damages the earliest?

A

i. Exerts damage on actively proliferating cells: basal epidermal cells, hematopoietic cells, mucosal lining of intestines

ii. Damages the skin causing blistering and irritation in a “string of pearls” distribution that overlies “normal” severely damaged skin
1) Most damaging to the eyes

iii. Mustards can take 4 - 12 hours to show
iv. Lewisite damages immediately

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21
Q

Garlic/horseradish odor

A

sulfur mustard

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22
Q

geraniums

A

lewisite

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23
Q

fruity odor/no odor/musty/fishy odor

A

nitrogen mustard

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24
Q

blood agents (2)

A

hydrogen cyanide

cyanogen chloride

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25
Q

How does cyanide effect the ETC?

What organs are effected the most?

A

i. Cyanide travels to the mitochondria of cells, binds ferric irons and inactivates the cytochrome oxidase of the electron transport chain to induce anaerobic respiration resulting in elevated levels of lactic acid & high anion gap metabolic acidosis
ii. Hits the heart and CNS the hardest

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26
Q

bitter almonds/peach kernels odor

A

hydrogen cyanide

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27
Q

pungent biting odor

A

cyanogen chloride

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28
Q

HA, N, vertigo, rapidly improve

A

small exposures to hydrogen cyanide (blood agent)

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29
Q

HA, N, vertigo, seizures/coma

A

moderate exposures to hydrogen cyanide (blood agent)

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30
Q

rapidly die due to rapid/deep breathing, convulsions, respiratory/cardiac failure

A

large exposures to hydrogen cyanide (blood agent)

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31
Q

Difference in manifestations between blood agents hydrogen cyanide and cyanogen chloride

A

Cyanogen chloride is the same as hydrogen cyanide except there is more respiratory damage

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32
Q

correcting metabolic acidosis utilizes what drug

A

sodium bicarb

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33
Q

what basic element is used to treat cyanide exposure, unlike in carbon monoxide poisoinings

A

oxygen

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34
Q

cyanide antidote kit: amyl nitrate and sodium nitroprusside

A

1) Inhale amyl nitrate and IV inject sodium nitroprusside

2) Binds to CN in the ETC to remove it from the ferric iron and is converted to methemoglobin

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35
Q

cyanide antidote kit: sodium thiosulfate

A

converts CN to thiocyanate to renally excrete

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36
Q

cyanide antidote kit: hydroxocobalamin

A

converts CN to cyanocobalamin to renally excrete

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37
Q

what are the choking agents? (2)

A
  • phosgene

- chlorine gas

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38
Q

phosgene odor

A

newly mown/musty hay

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39
Q

phosgene requires what unique care

A

refrigeration

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40
Q

hydrolysis of phosgene:

what’s the equation?

what element of the equation causes what damage?

What’s the edema you see with phosgene exposure?

A
  • > phosgene and water = HCl + CO
    a) Hydrochlorous acid causes epithelial damage and necrosis of airways
    b) Severe non-cardiogenic pulmonary edema
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41
Q

acylation of phosgene results in what clinical manifestations

A

more pulmonary damage –> acute lung injury

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42
Q

how doe chlorine affect the body

A

Chlorine and airway water causes hypochlorous acid and oxygen free radicals that’s highly damaging to the airway

43
Q

what makes biological agents appealing? (4)

A
  1. cheap
  2. require little knowledge
  3. allows evasion
  4. nonspecific onset that is hard to differentiate
44
Q

category A agents and microbes (6)

A
  1. anthrax (b. anthracis)
  2. plague (Y. pestis)
  3. botulinum (C. botulinus)
  4. smallpox (variola major)
  5. tularemia
  6. viral hemorrhagic fevers
45
Q

category B agents (4)

A
  1. ricin toxoalbumin from ricinus communis of castor beans
  2. brucellosis
  3. glanders
  4. Q fever
46
Q

category C agents - things that can become problems (4)

A
  1. hantavirus
  2. influenza, avian influenza
  3. SARS-CoV
  4. MERS
47
Q

anthrax is AKA

A

woolsorter’s disease

48
Q

spores of anthrax are highly resistant to ___, ___, ____, ____, and ____

A

Spores are highly resistant to drying, heat, gamma radiation, UV light, and many disinfectants

49
Q

what are the four ways to become infected with anthrax

A
  1. inhalation
  2. injection
  3. ingestion
  4. cutaneous
50
Q

virulence of anthrax is based on three distinct proteins:

A 
lethal factor (LF)
protective antigen (PA) 
edema factor (EF)
51
Q

how does anthrax get the edema toxin?

what does it do to the body?

A

edema factor and the protective antigen combine and give skin manifestations of anthrax, pulmonary edema, and peripheral edema

52
Q

how does anthrax get the lethal toxin?

what does it do to the body?

A

lethal toxin is a combo of the lethal factor and the protective agent that results in systemic reactions, hypovolemia, hypotension, and death

53
Q

what’s the dx factor of anthrax

A

nodes of the peribronchial tree from inhalation anthrax

54
Q

CXR of anthrax

A

widened mediastinum and pleural effusions

55
Q

ABX to treat anthrax and what’s the effect?

how long to treat?

A
  1. ciprofloxacin gives CNS penetration
  2. meropenem gives bactericidal effects
  3. linezolid inhibits protein synthesis and prevents production of factors, antigens, and toxins

give for 2 to 3 weeks

56
Q

how do you treat cutaneous anthrax

A

any FQ or doxycycline –> don’t need the CNS penetration so safe to use doxy

57
Q

what’s the most toxic substance known

A

botulinum toxin

58
Q

how is botulinum toxin deadly

A

toxin irreversibly binds peripheral cholinergic synapses in the NMJ to result in permanent muscle paralysis

59
Q

4 D’s of botulinum

A
  1. dyphonia
  2. dysphagia
  3. diplopia
  4. dysarthria
60
Q

clinical manifestations of the paralysis

A

progressive descending skeletal muscle paralysis and respiratory failure

61
Q

effects of ABX on botulinum toxin

A

no effect

62
Q

cannot give what to treat botulinum toxin as there is no ACh in the synapses

A

atropine

63
Q

so how do you treat botulinum

A

antitoxin and supprotive care

make sure to check for equine serum allergy to antitoxin via dermal injection first

64
Q

smallpox vs. chickenpox

A

smallpox: synchronous changes in lesions and centrifugal distribution
chickenpox: asynchronous changes in lesions and centripetal distribution

65
Q

how do you get ricin toxalbumin

A

easily extracted from castor beans

66
Q

what does the ricin toxin do to the cells?

to the body?

A

inhibits protein synthesis and DNA replication in cells

leads to DIC and micro-circulatory failure

67
Q

how do you treat ricin

A

no treatment –> supportive and aggressive airway control

68
Q

very light, charged particle that in large quantities can damage the basal statum of the skin

what sensitive body part is most affected by this particle?

A

beta particles

most damaging to the lens of the eyes

69
Q

what particle is similar to x-ray waves and can penetrate the whole body

A

gamma particles

70
Q

what particle causes 20x the damage of gamma rays

A

neutrons

71
Q

damage to what body part by radiation results in severe hemorrhage, severe fluid loss, and severe electrolyte loss

A

gastrointestinal damage as one of the most highly proliferative tissues in the body

72
Q

food irradiation plants

A

cobalt-60

73
Q

x-rays and cancer treatments

A

cesium-137

74
Q

nuclear batteries

A

strontium-90

75
Q

effects on the body from the explosion itself

A

primary blast effects

76
Q

effects of the materials blown outward and into the body

larger radius of effect than the explosion itself

A

secondary blast effects

77
Q

effects on the body from being a projectile

A

tertiary blast effects

78
Q

effects of the chemicals and resulting burns on the body

A

quaternary blast effects

79
Q

primary blast effects include what injuries

A

blast lung

aortic rupture

80
Q

what injuries result from blast lung

A

triad of apnea, bradycardia, hypotension

81
Q

what injuries result from aortic rupture

A

aorta is sandwiched between heart and spinal column

82
Q

what are three specific injuries that occur with primary blast effects

A
  1. shearing
  2. spalling
  3. imploding
83
Q

what’s spalling

A

more dense tissues turn into little “bullets” and move into the less dense tissues

84
Q

what’s imploding

A

pressure from the blast explosions forces and compresses gas into tissues that cause them to implode on themselves

85
Q

tertiary effects of picking up people and moving them as projectiles heavily effects

what are two other injuries common in teritary blast effects?

A

pediatrics as they weigh less

also includes crush injuries and coup-countercoup

86
Q

quaternary blast effect injuries include

A

thermal/chemical burns

inhalation exposures

87
Q

what five things occur in the hot/red zone of a mass casualty?

A
  1. manage airway (nasopharyngeal tube)
  2. give 2 rescue breaths in peds
  3. autoinjectors (antitoxin or epi)
  4. needle decompression of tension pneumothorax
  5. tourniquet use to control bleeds
88
Q

what does SALT stand for? what’s it used for?

A

triage method of Sort, Assess, Lifesaving interventions, Treatment/transport

89
Q

i. Require immediate care and will survive: things that complicate airway, circulation, or breathing
1) Mechanical airway obstruction
2) Sucking chest wound
3) Tension pneumo
4) Maxillofacial wounds with airway compromise
5) Unstable chest/abdominal wounds
6) Incomplete amputations
7) Exsanguinating hemorrhage
8) 2nd/3rd degree burns

A

red triage category

90
Q

Can delay care but will need attention: minor surgical repairs, minor crush injuries, minor cuts/wounds

A

yellow triage category

91
Q

Require minimal care - more than first aid, and need to be moved out of the triage area: superficial wounds, closed/uncomplicated fx, blast eardrum, psych/emotional disorders, small burns (1st/2nd)

A

green triage category

92
Q

Those that need to be comforted as they die: they need a lot of unavailable resources to survive

A

gray triage category

93
Q

Those that are deceased: not even alive when you get there/nothing to be done to save them

A

black triage category

94
Q

what does MARCH-H stand for

A 
Massive hemorrhage
Airway compromise
Respirations
Circulation
Head injuries 
Hypothermia
95
Q

eye opening stages of glasgow coma scale

A

1: no response
2: react to pain
3: open on command
4: open spontaneously

96
Q

verbal response of glasgow coma scale

A

1: no response
2: incomprehensible sounds
3: inappropriate words
4: confused
5: oriented to time/person/place

97
Q

motor response of glasgow coma scale

A

1: no response
2: abnormal extension (cerebrate posturing)
3: abnormal flexion (decorticated)
4: withdrawals from pain
5: moves towards pain
6: obeys commands

98
Q

spinal vs. neurogenic shock

A

spinal shock loses sensations

neurogenic shock loses hemodynamic stability - triad of hypotension, bradycardia, peripheral vasodilation

99
Q

stages of hypothermia:

i. Body compensates by bumping up metabolic rate:
Shivering, HTN, tachycardia, tachypnea, vasoconstriction

A

mild

100
Q

stages of hypothermia:

i. Freeze up:
Amnesia, difficulty speaking, unable to use hands, difficulty walking, crazy acting, lose pain reception, comatose

A

severe

101
Q

stages of hypothermia:

i. Body starts to slow:
1) Slow and labored movement, paradoxical undressing
2) Cyanotic lips, ears, fingers, toes
3) Really start acting weird

A

moderate

102
Q

stay away from STD’s:

A

Shielding
Time
Distance

103
Q

Distance of radiation exposure

A

1/x^2

MultiSystems (3 decks)

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