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Pathophysiology > Chap 29, 30, 42, 43 > Flashcards

Chap 29, 30, 42, 43 Flashcards

1
Q

Guillian-Bare Syndrom (GBS)

A

AUTOIMMUNE DISEASE

  • Causes an acute peripheral nervous system disorder results in a flaccid paralysis of the skeletal muscle and loss of muscle reflexes
  • Paralysis of the diaphragm and ventricular failure can develop= needing to be on mechanical vent.
  • “weak legs”
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2
Q

Polyneuropathy

A

Flaccid paralysis of the skeletal muscle and loss of muscle reflexes

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3
Q

Major Pathologic or structural changes of the lungs with GBS

A
  • Mucous accumulation
  • Airway obstruction
  • Alveolar Consolidation
  • Atelectasis
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4
Q

Development of GBS is unknown, but they do know that it is from an

A

immune response of foreign antigens that attack nerve tissue and lymphocytes
-Macrophages attack and strip off the myelin sheath of the peripheral nerves and leave swelling and frags of neural axons

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5
Q

Onset of GBS

A

1-4 weeks after a febrile episode caused by a mild resp. or gastrointestinal viral or bacterial infection

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6
Q

Clinical History of GBS

A
  1. Symmetric muscle weakness in distal extremities or dysesthesias (unpleasant, abnormal sense of touch), accompanied by paresthesia (tingling, burning, shockline sensation)
  2. Pain (especially lower back, butt, legs)
  3. Numbness
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7
Q

Dysesthesias

A

unpleasant, abnormal sense of touch

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8
Q

Paresthesia

A

tingling, burning, shockline sensation

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9
Q

Muscle paralysis in GBS

A

spreads upwards starting at the (g)round to (b)rain

-Ascending paralysis

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10
Q

GBS paralysis spreads in what time period

A

In single day or several days

  • peaks about 2 weeks
  • 90% full recovery, as long as 3 years
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11
Q

Diagnosis of GBS

A

Pts clinical hx
cerebrospinal fluid findings
EMG
Nerve conduction studies (NCS)= increase and protein

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12
Q

EMG and Nerve Conduction Studies (NCS) show what with GBS

A

Acute polyneuropathy with demyelinating antibodies- associated with axonal subtypes of GBS

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13
Q

Treat GBS with what

A

Corticosteroid

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14
Q

GBS common in

A

Higher chance in whites 50 years old and older

-Similar male and female

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15
Q

Acute Vent. Failure averages

A

Vital Capacity < 20ml/kg
NIF < -25cmH2O
pH < 7.32 or
PaCo2 > 45 mmHg

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16
Q

We measure vital capacity with

A

NIF

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17
Q

GBS potential medical emergency

A

30% -> acute vent. failure and require mechanical vent..

-Stabalize vitals and supportive care, frequent measurements FVC and MIP

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18
Q

GBS primary treatment

A
  1. Plasma pheresis

2. Intravenous immune globulin

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19
Q

Plasma pheresis

A

Removes antibodies from plasma that contributes to the immune system attack on peripheral nerves

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20
Q

Intravenous immune globulin

A

Blood product that contains IgG from donors

-Lasts 2weeks - 3 months

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21
Q

Added risk of thromboembolism increase=

A

patient receives anticoagulants , elastic stockings, and passive range of motion exercises (ev. 3-4 hours) turn patient frequently

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22
Q

Myasthenia Gravis

A

Most common chronic disorder of the neuromascular junction, only affects myoneural (motor) junction, sensory function not lost.
-Interferes with acetylcholine (AcH) between the axon terminal and receptor sites of voluntary muscles

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23
Q

Hallmark clinical features of Myasthenia Gravis

A

Fluctuating Skeletal muscle weakness usually improves following rest
-Fatigue and weakness usually improves as well with rest

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24
Q

2 clinical types of Myasthenia Gravis

A
  1. Ocular

2. Generalized

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25
Q

Ocular

A

Type of Myasthenia Gravis

-Muscle weakness limited to eyelids and extra ocular muscle

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26
Q

Generalized

A

Type of Myasthenia Gravis

  • Involves a variable combination of
    1. Muscles of mouth and throat respiratory for speech and swallowing (bulbar muscles)
    2. Limbs
    3. Respiratory Muscles
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27
Q

Dropped Head Syndrome

A

Neck extensor and flexor muscles affected

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28
Q

Myasthenia Crisis

A

When diaphragm goes-> mechanical vent. required

-Mucous accumulation with airway obstruction, Alveolar Consolidation, and Atelectasis may develop

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29
Q

Cause of Myasthenia Gravis

A

Related to AcH receptor (AcHR) antibodies (IgG) that blocks the nerve impulse transmissions and neuromuscular junction

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30
Q

Seropositive/ Seronegative Myasthenia Gravis

A

with or without AChR and MUSK

-90% Seropositive

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31
Q

Antibodies usually arise within

A

thymus or related tissue

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32
Q

Peak age of onset of Myasthenia Gravis

A

15-35 years old in females, and 40-70 years old in Males

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33
Q

Myasthenia Gravis provoked by

A

emotional upset, physical stress, exposure to increase temp changes, febrile illness, and pregnancy

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34
Q

Tests/ Diagnoses of Myasthenia

A
  1. Clinical presentation and history
  2. Bedside tests
  3. Immunologic studies
  4. Electrodiagnostic Studies
  5. Elevation of conditions associated with myathenia gravis
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35
Q

Signs and Symptoms of Myasthenia Gravis

A
  • Facial Muscle Weakness
  • Ptosis
  • Diplopia
  • Ophthalmoplegia
  • Difficulty breathing
  • Speaking
  • Chewing
  • Swallowing
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36
Q

Ptosis

A

Dropping of one or both eyelids

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37
Q

Diplopida

A

double vision

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38
Q

Opthalmoplegia

A

Paralysis or weakness of one or muscles for eye movement

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39
Q

Bedside Diagnostic test of Myasthenia Gravis

A
  • Ice pack test

- Edrophonium (Tensilon)

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40
Q

Ice pack test on myasthenia gravis

A

3-5 minutes when ptosis(dropping of one or both eyelids) is present

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41
Q

Edrophonium (tensilon)

A

Pt with ptosis or ophthalmoparesis

  • short acting drug, blocks cholinesterase from breaking down AcH (10 min)
  • Has false neg/ positives
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42
Q

1st diagnostic of Myasthenia Gravis

A

Serologic tests

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43
Q

Two types of Drowning

A 
DRY DROWING (10-15%)
-Laryngospasm keeps water out of lungs
-Normal lungs
WET DROWNING (85-90%)
-Glottis relaxes and patient inhales water
-Leads to pulmonary edema
44
Q

Wet drowning that leads to pulmonary edema

A

-Alveolar/ Capillary Edema
-Loss of surfactant
=
-Atelectasis
-Frothy White secretions-> hard for alveoli to open, so add PEEP

45
Q

Better the survival vs worse when drowning

A 
BETTER
-Colder the water
-The younger
-The cleaner
-Shorter time in water
-No other serious the better
-Good CPR start ASAP
WORSE
-Suicides tend to have a lower survival rate
46
Q

Drowning Sequence

A
  1. Panic and violent struggle to return to the surface
  2. Period of calmness and apnea
  3. Swallowing of large amounts of fluid-> vomiting
  4. Gasping inspirations and aspirations
  5. convulsions
  6. Coma
  7. Death
47
Q

Hypothermia while drowning=

A

shuts down body and cells arent eating up O2

-Common in kids less than 4 and teenagers

48
Q

Steps to treating drowning patients

A
  1. Remove wet clothing- Hypothermia lowers med responses
  2. Warm body up
    - Warm IVs
    - Warming blankets
    - Heated aerosol for inhalation
    - Lavage of warm solutions to gastric, bladder , rectum, etc
    - Rarely ECMO
  3. Oxygen
  4. Ventilation
    - May develop ards
49
Q

Cough and sputum production of drowning patients

A
  • Cough and sputum production= Frothy (blocking air), pink, stable bubbles
50
Q

Chest assessment in drowning patients

A

-Crackles (Popping alveoli open) and rhonchi

51
Q

Burn defined as

A

Denaturing and destruction of tissue proteins and bonecaused by thermal, electrical, or chem injury.
-20% suffer from inhalation injury as well

52
Q

Degrees of burn

A

1st degree- Sunburn
2nd degree- deeper in the tissue= blistering
3rd degree- Basal cells= scarring and need surg intervention

53
Q

Four Phases of Burn Care

A
  • Initial Evaluation and Resuscitation
  • Initial wound excision and biologic closure
  • Rehab, Reconstriction, and reintegration
54
Q

Initial Evaluation and resuscitation of burn

A

First 72 hours, achieve accurate fluis resuscitation and throrough evaluation.
-We make sure enough O2 and ABG

55
Q

Initial wound excision and biologic closure of burn

A

Day 1-7

-Identify and remove all full thickness wounds and optain biologic closure

56
Q

Rehab, reconstruct and reintegration of burn

A

Entire hospital stay

-Initially to maintain range of movement and reduce edema

57
Q

Evaluate what on a burn

A

Extent, depth, and circumferential components

58
Q

5 predicted events of burn

A

-Acute airway obstruction
-bronchospasm
-Infection
Leading cause of morbidity = Resp. Failure

59
Q

1st goal treating burn

A
  • Fluid resuscitation-IV

- Remove Eschar (burn tissue) and closure of open wounds-> avoid infection/ sepsis and multiple organ failure-> ARDS

60
Q

Inhalation definition

A

Damage to lungs by the inspiration of superheated gases (temp above 150*C), steam, or noxious of products of incomplete combustion

  • Hot gas
  • Steam
  • Noxious Products
61
Q

Diagnosing Inhalation injuries

A
  • Morbidity increases with smoke inhalation

- -History, Exam, CXR-Pulmonary Edema?, Bronchoscope, PaO2/ FiO2 ratio, Radioisotope scanning

62
Q

PaO2/ FiO2 ratio with ARDS

A

If below 100

63
Q

Interventions of Inhalation Injuries

A

Airway clearance

  • Suction on vent.
  • Heated wire circuit to provide humidity
64
Q

Phases of inhalation injury

A
  • Exudative
  • Degenerative
  • Proliferative
  • Reparative

+Leads to ARDS

65
Q

Management of Inhalation injuries

A
  • Intubate anyone with suspected airway injury
  • Edema comes on in first 4 hours and can be difficult to intubate if you wait
  • Can be difficult to tape due to burned tissue, use twill tape
  • Tracheostomy for severe cases
66
Q

Complications of inhalation injuries

A
  • Airway Obstruction
  • Tissue Swelling
  • Secretions
  • Bronchospasm
  • Tissue sloughing
  • Pulmonary infections
  • Resp Failure
67
Q

Steam is far worse with

A

H2O

68
Q

Carbon Monoxide Poisoning (CO) 1st intervention

A

Administer 100% O2 NRB- wide open

69
Q

Contraindicated of CO poisoning

A

Pulse Oximeters

  • Use co-oximeter to get actual HbCO
  • Affinity for hgb is 210 times of oxygen
70
Q

Carboxyhemoglobin results in

A
  • An acute physiolgic anemia
  • Anemic anemia= not enough O2 carried to cells-> Disruption to carrying
  • -Hydrogen cyanide (HCN)- Poisoning is produced by the combusion of nutrogen containing compounds in a low O2 atmosphere
  • HCN binds to cytochrome oxidase system and inhibits cellular
71
Q

Hydrogen Cyanide (HCN)

A

poisoning is produced by the combustion of nitrogen containing compounds in a low O2 atmosphere

72
Q

Patient is nice and pin but still hypoxic from CO poisoning why

A

Blood comes out very pink

73
Q

Co-oximeter measures both

A

CO and SaO2

-Subtract the CO from the SpO2 to find the real SaO2

74
Q

So any amount of CO that reduces the SaO2 to less than

A

90% causes hypoxemi

75
Q

normal people have what CO

A

0%

-Heavy smokers can have up to 7% CO

76
Q

SaO2=

A

SpO2-SaCO

77
Q

20% or more SaO2=

A

CO poisoning

78
Q

Treatment of CO poisoning

A
  • 100% oxygen (NRB or intubate)
  • Hyperbaric oxygenation
  • Changes the atmospheric pressure
  • So instead of 760mmHg for PAO2 , 2 atmospheres would be 1520mmHg
  • Increasing the PaO2
79
Q

The onset of the signs and symptoms of myasthenia gravis is / are

A
  1. Slow and insidious
  2. Sudden and rapid
  3. Intermittent
  4. Often Elusive
80
Q

Myasthenis gravis

  1. is more common in young men
  2. Has a peak age of onset in females of 15 to 35 years
  3. Is often provoked by emotional upset and physical stress
  4. Is associated with receptor-binding antibiodies
A
  1. Has a peak age of onset in females of 15 to 35 years
  2. Is often provoked by emotional upset and physical stress
  3. is associated with receptor binding antibodies
81
Q

Which of the following is associated with myasthenia gravis

  1. bronchospasm
  2. mucous accumulation
  3. Alveolar hyperinflation
  4. atelectasis
A

Mucous accumulation, atelectasis

82
Q

When monitoring the pt with myasthenia gravis, ALL of the following are indicators of acute ventilatory failure

A

pH 7.31
PaCO2 55 mmHg
MIP -15 cmH20

83
Q

Which antibodies is believed to block the nerve impulse transmission at the neuromuscular junction in myasthenia gravis

A

IgG

84
Q

In guillian barre syndrome, which of the following pathologic changes develop in the peripheral nerves

A

Inflammation, Demyelination, edema

85
Q

Which of the following is associated with guillain barre syndrome

A
  1. Alveolar consolidation
  2. Mucous accumulation
  3. Alveolar hypoinflation
  4. Atelectasis
86
Q

Guillain Barre syndrom is more common in

A

people older than 50 years of age, and white than in blacks

87
Q

Full recovery from guillain barre syndrom is expected in approx what percentage of cases

A

90%

88
Q

Which of the following are indicators for intubation and mech vent in pts with guillain barre syndrom

A

pH < 7.40
PaCO2 > 45
FVC < 20 mL/kg
MIP < -30cm H20

89
Q

In the US, drowning is the

A

third leading cause of accidental death

90
Q

according to the CDC and prevention, about how many people drown each year in the US

A

1500

91
Q

Which of the following are the major anatomic alterations of the lungs associated with near drowning victims?

A
  1. consolidation
  2. bronchospasm
  3. increased alveolar-capillary membrane thickness
  4. atelectasis
  5. excessive bronchial secretions
92
Q

Which of the following clinical manifestations are associated with near drowning victims?

  1. frothy, pink sputum
  2. crackles
  3. increased pH
  4. increases SvO2
A

Frothy pink sputum

Crackles

93
Q

Which of the following pulmonary function testing values are associated with near drowning victims?

  1. normal or decreased FEV1
  2. decreased FVC
  3. decreased RV
  4. normal or increased FEV1/FVC ratio
A

d. 1, 2, 3, and 4

94
Q

Near drowning refers to the situation in which a victim:

A

d. at least temporarily survives a liquid submersion

95
Q

What anatomic alterations happen during a wet drowning?

  1. the victim coughs out any water
  2. the glottis relaxes
  3. water enters the airways and alveoli
  4. inhaled water causes bronchial constriction
A

c. 2, 3, and 4 only

96
Q

The pulmonary effects of a near drowning victim inhaling water include:

  1. capillary fluid moves into alveoli
  2. surfactant production is increased
  3. pulmonary shunting is increased
  4. atelectasis develops
A

d. 1, 3, and 4 only

97
Q

Given the following options, which would occur last in a near drowning sequence?

a. convulsions
b. panic and violent struggle to return to the surface
c. swallowing then vomiting large amounts of fluid
d. gasping inspirations and aspiration

A

A

98
Q

An ambulance has just transported an apneic near drowning victim to the Emergency Department. The paramedic is performing bag-mask ventilations for the victim who has a pulse and blood pressure. As the respiratory therapist, what would you recommend be done?

  1. initiate mechanical ventilation
  2. continue bag-mask ventilations
  3. intubate the victim
  4. begin chest compressions
A

1 and 3

99
Q

percentage hospitalized patients with thermal injury have an acute upper airway obstruction

A

20-30%

100
Q

Except for the rare instance of steam inhalation, direct thermal injuries usually do not occur below the level of which of the following structures

A

Larynx

101
Q

When chest wall burns are present, the pts pulmonary condition may be further aggravated by which of the following

A
  1. Decreased lung and chest compliance
  2. Increased airway resistance
  3. Administration of narcotics
  4. Immobility
102
Q

Which of the following is/are the pulmonary related pathologic changes associated with smoke inhalation

  1. Pneumomediastinum
  2. Bronchospasm
  3. Pulmonary edema
  4. Pulmonary embolism
A

2, 3, 4

103
Q

Which of the following produce carbon monoxide when burned?

  1. Polyurethanes
  2. wood, cotton, paper
  3. Organic material
  4. Polyvinylchloride
A

Organic material, Polyvinylchloride

104
Q

Which of the following oxygenation indices is or are associated with smoke inhalation and burns during the early and intermediate stages

A

Increase VO2
Increase in C(a-v)O2
Decreased DO2
Decrease SvO2

105
Q

f an adult’s entire right arm, right leg, and anterior truck have been burned, approximately what percentage of the patient’s body surface area is burned?

A

45%

106
Q

healing time for a second degree

A

7-21days

107
Q

Breathing 100% oxygen at 1 atmosphere reduces the COHb half life to less than

A

1 hour

Pathophysiology (9 decks)

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