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Homeostasis 393 > Final > Flashcards

Final Flashcards

1
Q

Total body water for newborn/infant

A

70% - 80%

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2
Q

Total body water for adult

A

50% - 60%

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3
Q

Total body water for older adult

A

55%

Most concerning for dehydration and fluid balance

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4
Q

Total body water comprised of

A

1/3 Extracellular fluid: interstitial and plasma

2/3 Intracellular fluid

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5
Q

Osmotic pressure

A

Force that attempts to balance the concentration of solute and water between intracellular and extracellular fluids
Water follows higher concentration of solutes

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6
Q

Isotonic

A

Solute and water concentration is the same on both sides of cell

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7
Q

Hypertonic

A

Solute concentration higher outside of cell than inside

Cell will shrink due to water leaving

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8
Q

Hypotonic

A

Solute concentration is lower outside the cell than inside

Cell will swell due to water entering

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9
Q

Isotonic fluids (IV)

A 
Same osmolarity as body fluids
NS 0.9% NaCl
Lactated ringers
Used for fluid replacement
Monitor I and O; hydration status; electrolyte levels
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10
Q

Hypertonic fluids (IV)

A

Given for sodium and volume replacement
Monitor hydration: lung sounds
Monitor electrolytes, particularly sodium

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11
Q

Hypotonic fluids (IV)

A

D5W starts as isotonic until glucose is metabolized and becomes hypotonic
Glucose is needed but then must watch for adverse effects of hypotonic solution: edema

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12
Q

Normal serum concentration range for Calcium (Ca)

A

9 - 11 mg/dl

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13
Q

Normal serum concentration for Magnesium (Mg)

A

1.5 - 2.5 mEq/L

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14
Q

Normal serum concentration for Potassium (K)

A

3.5 -5 mEq/L

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15
Q

Normal serum concentration for Sodium (Na)

A

135 - 145 mEq/L

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16
Q

Sodium

A

Major extracellular cation
Regulates osmotic forces and water balance
Regulates acid-base balance
Facilitates nerve conduction and neuro-muscular function
Transport of substances across cellular membrane

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17
Q

Potassium

A 
Major intracellular cation
Maintains cell electrical neutrality
Cardiac muscle contraction
Transmission of nerve impulses
Maintains acid-base balance
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18
Q

Calcium

A

Major role in cardiac action potential

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19
Q

Magnesium

A

Important in women’s health

Suppresses release of acetylcholine (low Mg = too much movement; high Mg = too little movement)

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20
Q

Filtration

A

Movement of ECF from intravascular space to interstitial space

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21
Q

Reabsorption

A

Movement of ECF from interstitial space to intravascular

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22
Q

Oncotic pressure

A

Osmotic pressure exerted by proteins (albumin)

Pulling force

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23
Q

Hydrostatic pressure

A

Generated by pressure of fluids on capillary walls

Pushing force

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24
Q

What forces favor filtration?

A

Capillary hydrostatic pressure: pushes fluid out of capillary and into interstitial space
Interstitial osmotic pressure: pulls fluid into interstitial space from capillary

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25
Q

What forces favor reabsorption?

A

Interstitial hydrostatic pressure: pushes fluid out of interstitial space into capillary
Capillary osmotic pressure: pulls fluid into capillary

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26
Q

Normal pH

A

7.35 - 7.45

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27
Q

Acid - Base balance

A

1 Carbonic acid (H2CO3) acid side = 20 bicarbonate ions (HCO3 -) basic side

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28
Q

Acid

A

Donates Hydrogen ion

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29
Q

Base

A

Absorbs Hydrogen ion

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30
Q

Relationship between hydrogen ions and pH

A

Inverse relationship
More H+ = lower pH (acidosis)
Less H+ = higher pH (alkalosis)

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31
Q

Alkalosis

A

pH above 7.45

Lower H+ Kicks up the pH

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32
Q

Acidosis

A

pH below 7.35

Higher H+ sliDes down the pH

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33
Q

3 Chemical Acid-Base buffers

A 
Bicarbonate - Carbonic acid buffer (ECF)
Protein buffer (ICF): hemoglobin absorbs/releases H+
Phosphate buffer (ICF): sodium phosphate absorbs/releases H+
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34
Q

Carbonic acid/ bicarbonate Buffer

A

If pH is high (alkalosis/basic), carbonic acid contributes H+ -> H+ increases causing pH to decrease
If pH is low (acidosis/acidic), bicarbonate will absorb H+ -> H+ decreases, causing pH to increase

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35
Q

Respiratory system: 2nd line buffer

A 
Happens quickly
If acidic (low pH), breath is faster and deeper to remove carbon dioxide from blood -> lowers H+ and increase pH
If basic (high pH), breath is slower and shallower to add carbon dioxide to blood -> increases H+, causing pH to lower
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36
Q

Renal system: 2nd line buffer

A

Takes longer (hours to days)

  1. Secretes more or less H+ into renal tubule and out in urine: secreting more H+ lowers H+ in blood and increase pH; secreting less H+ increases H+ in blood and lowers pH
  2. Reabsorbs more or less bicarbonate: reabsorb more: more base = higher pH; reabsorb less: less base = lower pH
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37
Q

Range for pCO2

A

35 - 45 mmHg

Respiratory system

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38
Q

Range for HCO3-

A

22 - 26 mmHg

Kidney system

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39
Q

ROME

A

Respiratory Opposite
Lower pCO2 = Higher pH
Metabolic Equal
Lower HCO3- = Lower pH

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40
Q

Range for pO2

A

80 - 100 mmHg

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41
Q

First line of immune defense

A 
Physical barriers
Innate
Epithelial cells
E.g. skin, mucous membranes, cilia, normal flora
Not specific/ No memory
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42
Q

2nd line of innate immunity

A 
Inflammation
Not specific
In response to and proportional to degree of injury
Immediate
No memory
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43
Q

Adaptive immunity

A

3rd line: delayed response
Specific toward antigen
Memory

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44
Q

B cells

A

Humoral: from bone marrow

Antibodies

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45
Q

T cells

A

Crafted in lymphocytes

Cell mediated

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46
Q

Benefits of inflammation

A

Prevents infection and further damage
Self limiting
Prepares for healing: 1st step in wound healing

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47
Q

3 steps of inflammation

A
  1. Increased vascular permeability
  2. Recruitment and emigration of leukocytes
  3. Phagocytosis
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48
Q

What do mast cells release

A

Histamines: potent vasodilator; leads to itching, pain and swelling
Prostaglandins: vasodilator; chemotic factor, pain
Leukotrienes: chemotaxis

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49
Q

Chemotaxis

A

Calls other inflammatory cells to injury site
Leukotrienes
Prostaglandins

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50
Q

Vasodilation causes

A

Heat, redness and swelling

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51
Q

Leukotrienes

A

Chemotaxis: calls other inflammatory cells during phase 1 of inflammation
Antagonist drug: asthma reducer

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52
Q

Margination

A

Neutrophils stick to vessel wall

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53
Q

Emigration/ Diapedesis

A

Neutrophil exits blood vessel

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54
Q

4 steps of phagocytosis

A
  1. Recognition and adherence
  2. Engulfment and formation of phagosome
  3. Fusion with lysosome to form phagolysosome
  4. Destruction and digestion
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55
Q

Phagocytosis

A

Phase 3 of inflammation

Digestion of bacteria

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56
Q

By products of phagocytosis

A

Oxygen (free) radicals: can cause cell damage over long term

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57
Q

Three main hormones in pregnancy

A

Human chorionic gonadotropin (hCG), estrogen and progesterone

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58
Q

hCG

A

Produced by conceptus and placenta
Positive pregnancy test
Prevents involution of corpus luteum
Positive feedback loop: causes corpus luteum to secrete larger quantities of sex hormones (estrogen, progesterone)

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59
Q

Estrogen

A

Produced by corpus luteum and placenta
Helps with enlargement of uterus, breasts, external genitalia
Helps relax pelvic ligaments

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60
Q

Progesterone

A

Produced by corpus luteum
Role in nutrition of early embryo
Decreases uterine contractility so uterus can expand and not immediately contract back
Helps estrogen prepare breasts for lactation

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61
Q

Formation of placenta

A

Formed by trophoblastic cells around blastocyst

Fully formed by end of first trimester

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62
Q

Function of placenta

A

Provides nutrition to fetus and some immunity; excretes waste
All happens by diffusion

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63
Q

Flow of blood through placenta

A

Fetus has 1 umbilical vein and 2 umbilical arteries
Blood from placenta carried to fetus via umbilical vein to IVC and liver to right atrium to left atrium (bypass lungs) to left ventricle to aorta to body and out through umbilical arteries

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64
Q

Blood volume increase during pregnancy

A

30% by end of pregnancy

Hematocrit decreased by not anemia

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65
Q

Cardiac output increase during pregnancy

A

30 - 40 % by 27th week

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66
Q

Macrophages

A

Phagocyte

Clean up process in inflammation

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67
Q

Three inflammatory mediator cascades

A

Compliment System
Coagulation/ Clotting system
Kinin system

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68
Q

Complement system

A

Directs traffic

Destroys directly or indirectly by recruiting others

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69
Q

Activation of complement system

A

Classical pathway: antibodies
Alternate: infectious organisms
Lectin: other plasma proteins

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70
Q

Results of activation of complement system

A

Chemotaxis: calls phagocytes to area
Opsonization: Complement tags surfaces of bacteria to mark for phagocytes to destroy
Direct lysis of pathogens: destruction
Degranulation of mast cells: inflammatory mediators

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71
Q

Coagulation/ Clotting system activated by

A

Extrinsic: tissue injury
Intrinsic: Abnormal vessel wall
Components of kinin system

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72
Q

Coagulation/ Clotting system results in

A

Clot formation: fibrinogen
Migration of leukocytes
Chemotaxis
Increased permeability

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73
Q

Kinin system

A

Works closely with clotting system
Initiated by activation factors
Bradykinin (chemical)

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74
Q

Bradykinin

A

Vasodilation
Vascular permeability
Pain

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75
Q

Cytokines and Chemokins

A

Signaling molecules
Produced by macrophages and T helper cells
Involved in chemotaxis, recruitment, stimulation of leukocytes

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76
Q

Leukocytes

A

White blood cells

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77
Q

Which leukocytes are capable of phagocytosis

A

Neutrophils
Eosinophils
Basophils
Monocytes

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78
Q

Which leukocytes are not capable of phagocytosis

A

Lymphocytes

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79
Q

Neutrophils

A 
"Early responder"
Short lived
Phagocytosis
Release toxins
Destroy bacteria
Remove debris and dead cells
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80
Q

Eosinophils

A

“Fumigator”
Noted in allergic reactions and parasite infections
Regulate inflammatory response

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81
Q

Monocytes

A 
"Disaster response"
Macrophages
Longer living
Phagocytosis
Secrete cytokines: signaling molecules
Present antigens to activate T cells
Clean up
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82
Q

Basophils

A 
"Firefighters"
Mast cells
Allergic reactions
Acute and chronic inflammation
Wound healing
Tame inflammation
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83
Q

Lymphocytes

A 
"Special forces"
Adaptive and innate
Longest to mobilize
Trained for specific tasks
B-cells: able to produce antibodies
T-cells: T4 (helper), T8
Natural killer cells: non-specific (innate immunity)
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84
Q

Systemic manifestations of inflammation

A

Fever: cytokines that are pyrogens
Leukocytosis: increase in circulating WBCs
Lab changes

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85
Q

Lab changes during inflammation

A

Plasma proteins produced by liver increase
Erythrocyte sedimentation rate
C-reactive protein: opsonin (tagger) to phagocytosis

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86
Q

3 Phases of Wound Healing

A

Inflammation: filling
Proliferation/new tissue: sealing
Remodeling and maturation: shrinking

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87
Q

Inflammation stage of wound healing

A 
Coagulation
Bring cells needed
Fibrin mess of blood clot
Degranulation of platelets: growth factor
Macrophages: clear debris
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88
Q

Proliferation stage of wound healing

A

“Sealing”
3-4 days after injury, continues up to 2 weeks
Wound is sealed
Fibrin clot replaced by normal or scar tissue
Granulation tissue: new lymphatic vessels and new capillaries
Contraction begins

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89
Q

Remodeling/Maturation stage of wound healing

A 
Begins several weeks after injury
Normally complete within 2 years
Fibroblast: deposit collagen for strength
Tissue continues to regenerate
Wound continues to contract
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90
Q

What causes dysfunctional wound healing

A 
Ischemia: low blood supply
Obesity: impaired leukocyte function
Diabetes: impaired circulation
Malnutrition
Medications (steroids)
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91
Q

Gate control theory of pain

A

Only one impulse can make it through at a time

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92
Q

Neuromatrix theory of pain

A

Brain produces patterns of nerve impulses drawn from various inputs

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93
Q

Nocioceptors

A

Sensory nerve receptor that responds to pain

94
Q

Afferent pathways

95
Q

Efferent pathways

96
Q

Pathway of pain

A

Starts at PNS
travels on afferent pathways to dorsal horn spinal cord
To the CNS
Efferent pathways from CNS to dorsal horn to motor area

97
Q

Interpretive centers for pain

A

Brainstem, midbrain, diencephalon, cerebral cortex

98
Q

4 stages of nociception

A
  1. Transduction
  2. Transmission
  3. Perception
  4. Modulation
99
Q

Transduction stage of nociception

A

Tissue damage = exposure
Chemical mediators: histamine, bradykinins, prostaglandins (inflammation)
Nociceptors: A delta and C fibers; become excited

100
Q

Transmission stage of nociception

A

Impulses conducted to dorsal horn of spinal cord
Sensory fibers involved: A delta and C fibers
Continues to CNS

101
Q

A delta fibers

A

Medium sized
Thinly myelinated: fast
Well-localized, reflex withdrawal
Glutamate

102
Q

C fibers

A

Unmylenated: slow
Dull, aching pain that lasts longer
Substance P

103
Q

Perception stage of nociception

A

CNS
Conscious awareness of pain
Affective: emotional response
Cognitive: learning

104
Q

Pain threshold

A

Level of painful stimulation required to be perceived as pain
Similar in most people

105
Q

Pain tolerance

A

Degree of pain one is willing to bear before seeking relief

Varies

106
Q

Modulation stage of nociception

A

Change or inhibition of transmission of pain

Occurs at multiple sites along the pain pathway

107
Q

Excitatory neuromodulators

A

Substance P
Histamine
Glutamate
Increase sensation of pain

108
Q

Inhibitory neuromodulators

A 
GABA
Serotonin
Norepinephrine
Endogenous opioids
Decrease sensation of pain
109
Q

Two types of pain

A

Physiologic

Pathologic

110
Q

Types of physiologic pain

A

Acute
Ischemic
Referred
Beneficial

111
Q

Types of pathologic pain

A

Chronic
Neuropathic
Serve no purpose

112
Q

Acute pain

A

Resolves when injury heals
Usually less than 3 months
Therapy: short term; opioids and nonopioids

113
Q

Chronic pain

A

Longer than expected healing time
Usually more than 6 months
Example: fibromyalgia

114
Q

Periperhal sensitization

A

Reduction in pain threshold: less painful stimuli to register as pain
Causes chronic pain

115
Q

Central sensitization

A

Increased responsiveness and sensitivity to pain

Causes chronic pain

116
Q

Clinical manifestations of chronic pain

A

Sometimes similar as acute but usually looks different on assessment
Hard to describe
Psychosocial manifestations: irritability and depression

117
Q

Treatment for chronic pain

A

Multimodal

Pain clinic

118
Q

Neuropathic pain

A

Injury to nerves

119
Q

Causes of neuropathic pain

A

Chemo, surgery, radiation, trauma, diabetic neuropathy

120
Q

Clinical manifestations of neuropathic pain

A

Constant ache with intermittant sharp

121
Q

Treatment for neuropathic pain

A

Difficult to manage
Typical pain meds usually don’t work
Antidepressants and anticonvulsants can help

122
Q

Ischemic pain

A

No blood flow to tissue

123
Q

Referred pain

A

Perceived in an area other than injury

124
Q

3 Pain management strategies

A
  1. Interrupting peripheral transmission
  2. Modulating pain transmission at spinal cord level
  3. Altering perception and integration of nociceptive impulses in brain
125
Q

Interrupting peripheral transmission of pain

A

Non-pharm: heat/cold; splint; minimize use
Pharm: NSAIDS: inhibit prostaglandin production
Local anasthetics: block sodium channels; stop conduction impulses

126
Q

Modulating pain transmission at spinal cord level

A

Non-pharm: Cutaneous stimulation: therapeutic touch

Pharm: epidural; intrathecal anesthesia

127
Q

Altering perception and integration of nociceptive impulses in brain

A

Non-pharm: distraction, guided imagery, biofeedback, hypnosis
Pharm: opioids

128
Q

Signs and symptoms of acute pain

A 
Increased HR, BP, RR
Dilated pupils
Pallor and perspiration
N & V
Urine retention
129
Q

Physiologic response to acute pain

A 
Blood shunts from superficial vessels to muscles, heart, lungs and brain
Bronchioles dilate 
Decreased gastric secretions
Decreased GI motility
Increase in circulating blood glucose
Hypomotility of badder and ureters
130
Q

What hormone is produced by the developing conceptus and placenta?

131
Q

What is the clinical significance of HCG?

A

Basis of pregnancy test
Prevents involution of corpus luteum
Causes corpus luteum to secrete larger quantities of sex hormones

132
Q

How much does BMR increase during later half of pregnancy?

133
Q

Which hormones are involved in lactation?

A

Estrogen and progesterone stimulate tissue growth
Prolactin stimulates further production via baby suckling
Oxytocin responsible for let down/ milk getting out and contraction of uterus

134
Q

Drugs are prescribed to pregnant women based on what basis?

A

Risk vs. benefit

135
Q

Drugs taken in early pregnancy could cause what?

A

Death of the fetus

Conception through week 2

136
Q

Which weeks of pregnancy cause major morphologic malformations?

A

3- 8 weeks post conception

Embryonic period

137
Q

Which weeks of pregnancy cause most functional problems when exposed to teratogens?

A

9 weeks to term (38)

138
Q

During pregnancy, intestinal transit time is prolonged, how would this effect the PK of a drug?

A

Increased absorption

139
Q

By 3rd trimester, renal blood flow is doubled with large increase in glomerular filtration. How would this effect PK of a drug?

A

Increased excretion

140
Q

For some drugs, _____ metabolism also increases during pregnancy.

141
Q

During what weeks is a fetus not susceptible to teratogens? Why?

A

Weeks 1 and 2

Death or spontaneous abortion will result

142
Q

Pharmacological effects in a fetus can be toxic. Give example

A

Respiratory depression in opioid use

143
Q

What was thalidomide?

A

Fast-acting teratogen used in 1950’s and 60’s for morning sickness.
Caused phocomelia: short or missing limbs

144
Q

What does a category X drug for pregnancy mean?

A

Animal or human studies demonstrate definite risk of fetal abnormality. Should come with a contradiction statement on drug label.

145
Q

FDA approval for drugs used during pregnancy are based on what kind of testing?

146
Q

What three factors determine how readily a drug is excreted in breastmilk?

A

Drugs that are highly lipophilic, with small molecules, and remain non-ionized

147
Q

What is the recommended dose of folate for pregnant women?

A

400 - 800 mcg

148
Q

What is the recommended dose of folate for lactating women?

149
Q

What role does folic acid play in fetal development?

A

Role in cell division
Synthesis of DNA
Neuro-development

150
Q

When does neural tube closure occur?

A

18 to 26 days after conception

151
Q

Pregnant women need more _____ due to increase in blood volume.

152
Q

Two reasons pregnant women need iron

A

Due to increased RBC production

Due to loss of blood during birth

153
Q

Recommendation for iron for a pregnant woman

A

27 mg/ day

154
Q

What can you take with iron to increase absorption?

155
Q

Fetal skeletal development occurs mostly in what trimester?

156
Q

What is the calcium RDA for pregnant or lactatin women?

157
Q

Embryonic period lasts from…

A

Conception to 8 weeks

158
Q

Fetal period lasts from…

A

9 weeks to 40

159
Q

What week does a fetus start developing surfactant?

160
Q

How many days does it take a fertilized egg to reach uterus and implant?

161
Q

A blastocyst is made up of which two cell types

A

Inner cell mass

Trophoblast

162
Q

Inner cell mass forms the

163
Q

Trophoblast helps form the

164
Q

Inner cell mass divides into

A

Epiblast and hypoblast

165
Q

What is formed from the epiblast?

A

Amniotic sac

166
Q

What is formed from the hypoblast?

167
Q

What provides embryo with nutrition until placenta is formed?

168
Q

What are the three primary germ layers of the embryo?

A

Ectoderm, mesoderm and endoderm

169
Q

What germ layer is responsible for development of CNS?

170
Q

What germ layer is responsible for structure and organization such as the skeletal system?

171
Q

What germ layer is responsible for metabolism and homeostasis and forms the liver, GI tract, and pancreas?

172
Q

When during pregnancy have all gross characteristics of the organ systems already begun to develop?

A

First trimester

173
Q

By which month of pregnancy are all organs grossly the same as a neonate?

174
Q

Which systems are not fully developed at birth?

A

Nervous system
Kidneys
Liver

175
Q

During what trimester do fetal kidneys begin to excrete urine?

176
Q

By which month of pregnancy does fetal bone marrow produce most of RBC in fetus?

177
Q

Hemoglobin concentration of fetal blood is what % greater than that of the mother

178
Q

Babies born before which week need respiratory support because of underdeveloped alveoli

179
Q

Surfactant

A

A phospholipid in lungs which decreases surface tension of alveoli
Often given to babies born between 26 and 34 weeks

180
Q

What week does fetal circulation begin?

181
Q

What structure allows fetal blood to skip the liver?

A

Ductus venosus

182
Q

What structure shunts blood from pulmonary artery to aorta to skip the lungs?

A

Ductus arteriosus

183
Q

What structure allows blood to flow directly from right atria to left in a fetal heart?

A

Foramen ovale

184
Q

Head to toe growth and development is called

A

Cephalocaudal

185
Q

Core before fine motor development is called

A

Proximodistal

186
Q

What is a time dependent loss of structure and function?

187
Q

Three theories of aging

A

Molecular: gene regulation theory
Cellular: Cell senescence, telomeres, reactive oxygen species
Systemic: neuroendocrine

188
Q

Programmed senescence theory of aging

A

Limit to number of cell divisions that human cells can undergo

189
Q

Telomeres

A

Caps on the end of each chromosome
A little bit is lost after each cell division
Cell dies when telomere is gone

190
Q

Free radicals

A

Cause aging by causing damage to DNA, RNA, proteins and individual cell death

191
Q

Neuroendocrine theory

A

Aging is a decreased ability to survive stress

192
Q

GI factors affecting absorption rate in neonates and infants

A

Prolonged/irregular gastric emptying

Lower gastric acidity until 2

193
Q

Absorption and Distribution of IM meds in neonates and infants

A

Low blood flow through muscles: slow/erratic distribution of IM meds
Better absorption of IM meds than adults

194
Q

Topical meds for infants/ neonates

A

Thin skin so topical meds can result in toxicity

195
Q

What results from neonates having low serum levels of albumin?

A

Decrease in protein binding of drugs and therefore more free drug in blood

196
Q

When do infants reach normal PPB levels?

A

Between 10 - 12 months

197
Q

When does the blood brain barrier fully develop in infants?

198
Q

When do infants have adult liver capacity?

199
Q

PK parameters for a 1 year old

A

Equal to an adult except drug metabolism increases until 2 then declines

200
Q

Geriatric patients absorb drugs

A

More slowly than adults

201
Q

What is the most important cause of adverse drug reactions in the elderly?

A

Drug accumulation due to reduced renal excretion

202
Q

Why are adverse drug interactions and reactions 7 x more common in elderly?

A

Drug accumulation
Polypharmacy
Greater severity of illness
Multiple pathologies

203
Q

Three types of vaccines

A

Killed vaccine: whole killed microbe
Attenuated live vaccine
Cell parts: e.g. acellular pertussis

204
Q

Toxoid

A

Weakened bacterial toxin

E.g. tetanus toxoid and diptheria toxoid

205
Q

Active immunity

A

Via natural disease or vaccine
Antibodies and memory B cells
Cytotoxic and memory T cells

206
Q

Passive immunity

A

Administration of antibody
Immediate but short lived protection
Eg breastfeeding or Immunoglobulin admin

207
Q

What hormone is responsible for aiding the uterus in contracting back to normal size after birth?

208
Q

D5 1/2 NS IV fluid

A

Hypertonic: given for sodium and volume replacement
Monitor hydration: lung sounds
Monitor electrolytes: sodium in particular
Also monitor pulse, BP, and urine output

209
Q

Acetaminophen classification

A

Analgesic
Antipyretic
(Not anti-inflammatory)

210
Q

Nursing considerations for acetaminophen

A

No more than 4g/ day

Less for alcholic and malnourished patients

211
Q

MOA for acetaminophen

A

Slows production of prostaglandins in CNS

Selective COX inhibition

212
Q

Adverse reactions for acetaminophen

A

Acute toxicity results in liver damage

Early signs are N & V diarrhea, sweating, abdominal pain

213
Q

What inactivates the toxic metabolite NAPQI?

A

Glutathione

Otherwise will attack liver

214
Q

Prototype drug for nonsteroidal antinflammatory drug

215
Q

MOA for Ibuprofen

A

COX 1 inhibitor: decreased platelet aggregation and kidney damage
COX 2 inhibitor: decreased inflammation, fever and pain

216
Q

Adverse reactions for ibuprofen

A

Indigestion (dyspepsia), abdominal pain, heartburn, nausea
Chronic use can lead to ulcers
Impairs renal blood flow (particular problem for elderly)
General edema or swelling

217
Q

Nursing considerations for ibuprofen

A

Use cautiously with older adults and clients with heart failure

218
Q

COX I produces

A

Protective prostaglandins
Acid reduction in stomach mucosa
Clotting by increased platelet stickiness

219
Q

COX II produces

A

Inflammatory prostaglandins

Pain, fever and inflammation

220
Q

Two main types of opioid receptors

A

Mu and Kappa

221
Q

Mu receptors result in

A

Analgesia, respiratory depression, euphoria, sedation, decreased GI motility, physical dependence

222
Q

Kappa receptors result in

A

Analgesia and sedation, decreased GI motility

223
Q

Pure opioid agonists

A

Morphine, oxycodone, hydrocodone, fentanyl

Turns both Mu and Kappa receptors on

224
Q

Pure opioid antagonists

A

Blocks Mu and Kappa receptors
Naloxone
Reverses effects of opioid agonists: increases respiration, pain returns, diarrhea, agitation
Treats overdose

225
Q

Morphine sulfate

A

Opioid analgesic/ agonist

Pain relief, sedation, reduction of bowel motility

226
Q

Adverse reactions to morphine

A 
Respiratory depression
Constipation
Orthostatic hypotension
Urinary retention
Sedation
Biliary colic
N & V
Overdose
227
Q

Cardiac symptoms in a dying person

A 
Tachycardia
Hypotension
Peripheral cooling, mottling, cyanosis
Decreased pulses
Decreased O2 in blood
228
Q

Cheyne-Stokes pattern

A

Rapid breath followed by apnea

In a dying patient

229
Q

Pharmacologic interventions for “death rattle”

A

Scopolamine patch for secretions

Opioids to assist with dyspnea

230
Q

Dysphagia and decreased appetite in a dying person puts them at risk for?

A

Aspiration

Homeostasis 393 (1 decks)

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