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N116 > Thermoregulation > Flashcards

Thermoregulation Flashcards

1
Q

Thermoregulation

A

The process of maintaining the core body temperature at a nearly constant value

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2
Q

What does body temperature below 36 C or above 40 C cause

A

Disorientation

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3
Q

Body temperature above 42 C causes?

A

Convulsions and permanent cell damage

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4
Q

Normothermia

A

Normal body temperature 36.5-37.2

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5
Q

Hypothermia

A

Body temperature below 36.2

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6
Q

Hyperthermia

A

Body temperature above 37.6

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7
Q

Hyperpyrexia

A

Extremely high body temperature above 41.5

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8
Q

Fever

A

Elevation in body temperature due to a change in the hypothetical set point
Temporary resetting of the hypothalamic thermostat

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9
Q

Temperature regulation varies in response to :

A 
Location
Activity
Environment
Circadian Rhythm
Gender
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10
Q

Heat production and conservation mechanisms

A
  • Chemical reactions of metabolism
  • Skeletal muscle contraction
  • Chemical thermogenesis
  • Vasoconstriction
  • Shivering
  • Voluntary mechanisms
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11
Q

Processes of heat transfer

A

Radiation
Convection
Conduction
Evaporation

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12
Q

Radiation

A

Objects warmer than environment lose heat as infrared radiation
Accounts for more than half of body’s heat loss

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13
Q

Conduction

A

Direct transfer of energy due to physical contact with cold object
Not very effective in gaining or losing heat

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14
Q

Convection

A

Heat loss to cooler air
Heat rises away from skin, cool air replaces it
Accounts for about 15% of body’s heat loss

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15
Q

Evaporation

A

Water changes from liquid to vapor as it evaporates
Absorbs energy and cools surface
Insensible perspiration from lungs and skins consistent
Accounts for about 20% of body’s heat loss
Sensible perspiration from sweat glands varies in rate

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16
Q

How is temperature regulation coordinated?

A

By the heat-loss centre and the heat gain centre

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17
Q

What pathways does the heat-loss centre use?

A

Parasympathetic pathways

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18
Q

Heat- gain centre uses which pathways

A

Sympathetic pathways

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19
Q

Populations at greatest risk for problems with thermoregulation are:

A

Very young persons
Very old persons
Poor persons
Persons living in very hot or cold climates

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20
Q

What damage can occur from hyperthermia

A

Nerve damage, coagulation of cell proteins and death

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21
Q

How can hyperthermia occur

A

Can be accidental, therapeutic or associated with stroke or head trauma

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22
Q

Thermoregulation Disorders - Hyperthermia

A

Fever
Heat stroke
Malignant Hyperthermia

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23
Q

Thermoregulation Disorders- Hypothermia

A

Frostbite

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24
Q

What happens when the Vasomotor centre is inhibited during hyperthermia?

A

Peripheral blood vessels dilate
Blood flows more to surface of the body
Increases heat loss by radiation and convection

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25
Q

What happens when the sweat glands are stimulated to increase secretions during hyperthermia?

A

Increases heat loss by evaporation

Limited capability in higher humidity environments

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26
Q

What happens when the respiratory system is stimulated during hyperthermia?

A

Increased respiratory depth and breathing more through mouth

Increased heat loss through evaporation from lungs

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27
Q

3 steps caused by hyperthermia

A
  1. Vasomotor center inhibited
  2. Sweat glands stimulated to increase secretions
  3. Respiratory centres stimulated
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28
Q

At what temperature does nerve damage produce convulsions in an adult?

A

41 degrees C

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29
Q

What temperature causes death

A

43 degrees C

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30
Q

What does fever activate?

A

Heat production and conservation measures to a new set point

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31
Q

What kind of pyrogens are associated with fever?

A

Exogenous and Endogenous

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32
Q

What is a central fever caused by

A

Trauma

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33
Q

What are the benefits of a fever?

A

Kills many micro-organisms
Decreases serum levels of iron, zinc and copper
Promotes lysosomal breakdown and auto destruction of cells
Increases lymphocytic transformation and phagocyte motility
Augments antiviral interferon production and phagocytosis

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34
Q

Pharmacotherapies for fever

A

Antipyretics
Acetaminophen
NSAIDS

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35
Q

What is the goal of pharmacotherapies used for fevers?

A

Lower body temperature, while treating the underlying cause of the infection

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36
Q

What is the drug of choice for treating fevers in children?

A

Acetaminophen

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37
Q

Action of Acetaminophen (Tylenol)

A

Inhibits synthesis of prostaglandins
Mild to moderate pain control
Antipyretic

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38
Q

Contraindications of Acetaminophen (Tylenol)

A 
Known allergy
Severe liver disease
Genetic disease enzyme deficiency
Chronic alcoholism
Renal disease
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39
Q

Toxicity Symptoms of Acetaminophen (Tylenol)

A 
Cyanosis
Anemia
Neutropenia
CNS Stimualtion
Delirium followed by vascular collapse
Seizures
Coma 
Death
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40
Q

Pharmacokinetics: Absorption of Acetaminophen (Tylenol)

A

Well absorbed after oral administration. Rectal absorption varies.

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41
Q

Pharmacokinetics: Distribution of Acetaminophen (Tylenol)

A

Widely distributed, crosses placenta and enters breast milk.

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42
Q

Pharmacokinetics: Metabolism of Acetaminophen (Tylenol)

A

By the liver, metabolites are excepted in the liver

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43
Q

Half life of Acetaminophen (Tylenol)

A

1-3 hours

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44
Q

Prostaglandins

A

Lipids that promote inflammation and are found in all tissues

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45
Q

Cyclooxygenase

A

Key enzymes in the biosynthesis of prostaglandins and have 2 forms

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46
Q

2 forms of cyclooxygenase

A

Cyclooxygenase-1

Cyclooxygenase-2

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47
Q

Cyclooxygenase-1 Location

A

Present in all tissues

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48
Q

Cyclooxygenase-1 Functions

A

Protects gastric mucosa, supports kidney function, promotes platelet aggregation

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49
Q

Cyclooxygenase-1 Inhibition by medications

A

Undesirable: increases risk for gastric bleeding and kidney failure

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50
Q

Cyclooxygenase-2 Location

A

Present at sites of tissue injury

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51
Q

Cyclooxygenase-2 Functions

A

Mediates inflammation
Sensitizes pain receptors
Mediates fever in the brain

52
Q

Cyclooxygenase-2 Inhibition by medications

A

Desireable: results in suppression of inflammation

53
Q

Misoprostol

A

A prostaglandin like substance that inhibits gastric acid secretions and stimulates the production of protective mucous

54
Q

When is misoprostol usually used

A

used mostly when taking NSAIDS and glucocorticoids to prevent ulcers

55
Q

What does misoprostol prevent

A

GI bleeds

56
Q

What does a synthetic prostaglandin E1 analogue do?

A

inhibits gastric acid secretion and has a cytoprotective component

57
Q

NSAIDS

A 
A large and chemically diverse group of drugs that have:
Analgesic activities
Anti-inflammatory activities
Antipyretic activities
Aspirin-platelet inhibition
58
Q

What are properties that all NSAIDS share?

A

Antipyretic properties
Analgesic properties
Anti-inflammatory properties

59
Q

NSAIDS are used to relief

A 
Mild to moderate headaches
Myalgia
Neuralgia
Arthralgia
Postoperative pain
treatment of gout and hyperuricemia
60
Q

NSAIDS help with pain that is associated with…

A

Arthritic disorders like rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis, and osteoarthritis

61
Q

NSAIDS mechanisms of action

A

Inhibit cyclooxygenase thus blocking inflammation

Blocking the chemical activity of the enzyme Cyclooxygenase

62
Q

NSAIDS inhibit which pathways?

A

Leukotriene pathway, prostaglandin pathway or both

63
Q

What is the drug of choice for mild to moderate pain, inflammation and fever

A

NSAIDS

64
Q

Ibuprofen (Advil, Motrin) Action

A

Inhibits cyclooxygenase-1 and cyclooxygenase-2 thus decreases inflammation

65
Q

Ibuprofen (Advil, Motrin) Dosage

A

Administered orally

200-400mg PO q6h

66
Q

Ibuprofen (Advil, Motrin) uses

A

Mild to moderate pain in acute or chronic disorder

67
Q

Ibuprofen (Advil, Motrin) Adverse effects

A

Headache
Dizziness
GI upset
Nephrotoxicity

68
Q

NSAIDS Contraindications

A 
Known drug allergy
Conditions that place the patient at risk for bleeding
Rhinitis
Vitamin K deficiency 
Peptic ulcer disease
69
Q

NSAIDS Adverse effects

A 
Heartburn to severe GI bleeding
Acute kidney injury
Noncardiogenic pulmonary edema
Altered hemostasis
hepatotoxicity
Skin eruption, sensitivity hearing
Tinnitus, hearing loss
70
Q

NSAIDS nursing considerations

A

Take with food or milk
Avoid alcohol
Assess for bleeding disorders/ GI bleed
Obtain baseline liver and renal function tests
Do not give to children
Consult with health care provider before taking herbal products

71
Q

Use NSAIDS with care in which clients

A

Clients with alcoholism, CHF, Renal disease, hypertension, and fluid retention

72
Q

How long does it take NSAIDS to reach optimal effects

A

1-3 weeks

73
Q

Heatstroke

A

Potentially lethal result of an overstressed thermoregulatory centre

74
Q

What temperatures can the brain not tolerate

A

40.5 degrees C and over

75
Q

What happens when the body’s temperature exceeds 40 degrees C?

A

Regulatory centre stops functioning and the body’s heat loss mechanism fails
Cardiovascular and thermoregulatory centres may stop functioning

76
Q

Causes of heatstroke

A

Exertion
Overexposure to heat
Impaired physiological mechanism for heat loss

77
Q

Heatstroke Symptoms

A 
High core temperature
Absence of sweating
Tachycardia
Confusion
Agitation
Coma
78
Q

Heatstroke Complications

A 
Cerebral edema
Degeneration of the CNS
Swollen dendrites
Renal tubular necrosis
Hepatic failure
Death
79
Q

Heat Cramps

A

Severe spasmodic cramps in the abdomen and extremities

Following prolonged sweating and associated sodium loss

80
Q

Who are heat cramps more common in

A

Individuals not accustomed to heat or those performing strenuous work in warm climates

81
Q

Symptoms of heat cramps

A

Fever
Rapid pulse
Increased BP

82
Q

Heat exhaustion

A

Result of prolonged high core temperatures

Profound vasodilation and profuse sweating

83
Q

Manifestations of Heat Exhaustion

A 
Dizziness
Weakness
Nausea
Confusion
Syncope
84
Q

Malignant Hyperthermia

A

A potentially lethal hypermetabolic complication of a rare inherited muscle disorder that may be triggered by inhaled anaesthetics & depolarizing muscle relaxants.

85
Q

What happens to the muscles in malignant hyperthermia

A

Muscle cells have an unregulated accumulation of calcium
Muscles contract and stiffen at the same time
Uncoordinated muscle contractions

86
Q

Symptoms of Malignant hyperthermia

A

Absent reflexes
Fixed pupils
Apnea
Flat ECG

87
Q

Risk factors for malignant hyperthermia

A

Genetic
History of heat stroke or hyperthermia after exercise
Muscle abnormalities that may be associated with malignant hyperthermia

88
Q

Diagnosis Malignant hyperthermia

A

Genetic testing

Muscle biopsy

89
Q

Expected duration of malignant hyperthermia

A

With timely treatment resolution of symptoms should occur within 12-24 hours

90
Q

Clinical manifestations of Malignant hyperthermia

A 
Altered calcium function in muscle cells with hyper metabolism
Hyperthermia
Uncoordinated muscle contractions
Increased muscle work
Increased oxygen consumption
Raised level of lactic acid production
Acidosis
Rapid or painful muscles, especially in jaw
Sweating
Tachycardia
Tachypnea
Brown coloured urine
Shock
91
Q

Malignant hyperthermia treatment

A 
Stop giving triggering medication
Administer Dantrolene (Dantrium)
Lower body temperature
Administer oxygen
Medicate to control heartbeat, BP and correct electrolyte imbalances
92
Q

Use of Dantrolene (Dantrium)

A

Relaxes muscles and stops the increase in muscle metabolism

Given IV until stability is achieved, then continued PO for 3 days

93
Q

Intervention strategies for hyperthermia

A 
Remove excess clothing and blankets
Provide external cool packs
Provide a cooling blanket
Hydrate with cool fluids
Lavage with cool fluids
Administer antipyretic drug therapy
94
Q

Hypothermia

A

When body temperature falls below acceptable levels

95
Q

How does the body prevent Hypothermia

A

heat-loss centre is inhibited and heat gain centre is activated

96
Q

Steps of heat gain centre

A
  1. Stimulate vasometer centre
  2. Shivering thermogenesis
  3. Nonshivering thermogenesis
97
Q

Stimulation of gasometer centre does what

A

Constricts peripheral blood vessels, reducing heat loss by radiation, convection and conduction

98
Q

Shivering thermogenesis does what

A

Activates brief contractions of skeletal muscles

99
Q

Nonshivering thermogenesis is stimulated how

A

Hormonally

Thyroid hormones and epinephrine increases metabolic activity of all tissues

100
Q

Hypothermia produces

A

Ice crystals, which form inside the cells, causing them to rupture and die

101
Q

Tissue hypothermia

A

Slows the rate of cellular metabolism
Increases blood viscosity and slows blood through the microcirculation
Facilitates blood coagulation and stimulates vasoconstriction

102
Q

Hypothermia Response Mechanisms

A

Peripheral vasoconstriction
Intermittent repurfusion of extremities
shivering
Stupor

103
Q

Peripheral Vasoconstriction

A

Shunts blood away from cooler skin to core to decrease heat loss and produces peripheral tissue ischemia

104
Q

Intermittent reperfusion of extremities (Lewis Phenomenon)

A

Helps preserve peripheral oxygenation until core temps drop dramatically

105
Q

Shivering

A

Induced by the hypothalamic centre
Thinking becomes sluggish
Coordination is depressed

106
Q

Stupor

A 
Heart & respiratory rate decline
Cardiac output diminishes
Metabolic rate falls
Acidosis
Eventually V fib & asystole occur at 30 degrees C
107
Q

Therapeutic Hypothermia

A

Used to slow metabolism and preserve ischemic tissue during surgery or limb re-implantation
May lead to ventricular fibrillation and cardiac arrest

108
Q

Accidental Hypothermia

A

Commonly the result of sudden immersion in cold water or prolonged exposure to cold

109
Q

Hypothermia Risk factors

A 
Hypothyroidism
Hypopitutarism
Malnutrition
Parkinson's Disease
Rheumatoid arthritis
Chronic increased vasodilation
Failure of thermoregulatory control resulting from cerebral injury, ketoacidosis, uremia, sepsis, and drug overdose
110
Q

Hypothermia treatment

A

Reversible with rewarming

111
Q

Hypothermic Injuries

A

Frost nip
Chilblains
Frostbite
Flash freeze

112
Q

Frostnip

A

Mild and completely reversible injury characterized by skin pallor and numbness

113
Q

Chilblains

A

More serious than frosting; violaceous skin colour with plaques or nodules, pain, and pruritus, but no ice crystal formation; chronic vasculitis can develop and is usually located on the face, anterior lower leg, hands, and feet

114
Q

Frostbite

A

Tissues freeze and form ice crystals at temperature less than -2 degrees C progresses from distal to proximal and potentially reversible

115
Q

Flash Freeze

A

Rapid cooling with intracellelular ice crystals associated with contact with cold metals or volatile liquids

116
Q

What happens to frozen skin?

A

Becomes white or yellowish, has a waxy texture

117
Q

What parts of the body does frostbite commonly affect

A

Fingers, toes, ears, nose and cheeks

118
Q

First degree frost bite

A

Partial skin freezing

119
Q

Second degree Frost bite

A

Full thickness skin freezing

120
Q

Third degree Frost bite

A

Full thickness & subcutaneous freezing

121
Q

Fourth degree frost bite

A

Deep tissue freezing

122
Q

Intervention strategies for hypothermia

A

Remove person from cold
Provide external warming measures
Provide internal warming measures

123
Q

Safety tip for core warming

A

Core rewarming must be done slowly to minimize the risk for dysthymias. Cardiac monitoring is required when the patient is recovering from severe hypothermia.

124
Q

CNS trauma leads to…

A

Central fever
Inflammation, increased ICP, inter cranial bleeding
Does not induce sweating
Resistant to antipyretic therapy

125
Q

Central fever

A 
Sustained noninfectious fever
Appears with or without bradycardia
Caused by major body trauma
Does not induce sweating
Resistant to antipyretic therapy

N116 (11 decks)

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