Final Flashcards

(230 cards)

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
What forces favor reabsorption?
Interstitial hydrostatic pressure: pushes fluid out of interstitial space into capillary Capillary osmotic pressure: pulls fluid into capillary
26
Normal pH
7.35 - 7.45
27
Acid - Base balance
1 Carbonic acid (H2CO3) acid side = 20 bicarbonate ions (HCO3 -) basic side
28
Acid
Donates Hydrogen ion
29
Base
Absorbs Hydrogen ion
30
Relationship between hydrogen ions and pH
Inverse relationship More H+ = lower pH (acidosis) Less H+ = higher pH (alkalosis)
31
Alkalosis
pH above 7.45 | Lower H+ Kicks up the pH
32
Acidosis
pH below 7.35 | Higher H+ sliDes down the pH
33
3 Chemical Acid-Base buffers
``` Bicarbonate - Carbonic acid buffer (ECF) Protein buffer (ICF): hemoglobin absorbs/releases H+ Phosphate buffer (ICF): sodium phosphate absorbs/releases H+ ```
34
Carbonic acid/ bicarbonate Buffer
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
35
Respiratory system: 2nd line buffer
``` 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 ```
36
Renal system: 2nd line buffer
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
37
Range for pCO2
35 - 45 mmHg | Respiratory system
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Range for HCO3-
22 - 26 mmHg | Kidney system
39
ROME
Respiratory Opposite Lower pCO2 = Higher pH Metabolic Equal Lower HCO3- = Lower pH
40
Range for pO2
80 - 100 mmHg
41
First line of immune defense
``` Physical barriers Innate Epithelial cells E.g. skin, mucous membranes, cilia, normal flora Not specific/ No memory ```
42
2nd line of innate immunity
``` Inflammation Not specific In response to and proportional to degree of injury Immediate No memory ```
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Adaptive immunity
3rd line: delayed response Specific toward antigen Memory
44
B cells
Humoral: from bone marrow | Antibodies
45
T cells
Crafted in lymphocytes | Cell mediated
46
Benefits of inflammation
Prevents infection and further damage Self limiting Prepares for healing: 1st step in wound healing
47
3 steps of inflammation
1. Increased vascular permeability 2. Recruitment and emigration of leukocytes 3. Phagocytosis
48
What do mast cells release
Histamines: potent vasodilator; leads to itching, pain and swelling Prostaglandins: vasodilator; chemotic factor, pain Leukotrienes: chemotaxis
49
Chemotaxis
Calls other inflammatory cells to injury site Leukotrienes Prostaglandins
50
Vasodilation causes
Heat, redness and swelling
51
Leukotrienes
Chemotaxis: calls other inflammatory cells during phase 1 of inflammation Antagonist drug: asthma reducer
52
Margination
Neutrophils stick to vessel wall
53
Emigration/ Diapedesis
Neutrophil exits blood vessel
54
4 steps of phagocytosis
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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Phagocytosis
Phase 3 of inflammation | Digestion of bacteria
56
By products of phagocytosis
Oxygen (free) radicals: can cause cell damage over long term
57
Three main hormones in pregnancy
Human chorionic gonadotropin (hCG), estrogen and progesterone
58
hCG
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)
59
Estrogen
Produced by corpus luteum and placenta Helps with enlargement of uterus, breasts, external genitalia Helps relax pelvic ligaments
60
Progesterone
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
61
Formation of placenta
Formed by trophoblastic cells around blastocyst | Fully formed by end of first trimester
62
Function of placenta
Provides nutrition to fetus and some immunity; excretes waste All happens by diffusion
63
Flow of blood through placenta
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
64
Blood volume increase during pregnancy
30% by end of pregnancy | Hematocrit decreased by not anemia
65
Cardiac output increase during pregnancy
30 - 40 % by 27th week
66
Macrophages
Phagocyte | Clean up process in inflammation
67
Three inflammatory mediator cascades
Compliment System Coagulation/ Clotting system Kinin system
68
Complement system
Directs traffic | Destroys directly or indirectly by recruiting others
69
Activation of complement system
Classical pathway: antibodies Alternate: infectious organisms Lectin: other plasma proteins
70
Results of activation of complement system
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
71
Coagulation/ Clotting system activated by
Extrinsic: tissue injury Intrinsic: Abnormal vessel wall Components of kinin system
72
Coagulation/ Clotting system results in
Clot formation: fibrinogen Migration of leukocytes Chemotaxis Increased permeability
73
Kinin system
Works closely with clotting system Initiated by activation factors Bradykinin (chemical)
74
Bradykinin
Vasodilation Vascular permeability Pain
75
Cytokines and Chemokins
Signaling molecules Produced by macrophages and T helper cells Involved in chemotaxis, recruitment, stimulation of leukocytes
76
Leukocytes
White blood cells
77
Which leukocytes are capable of phagocytosis
Neutrophils Eosinophils Basophils Monocytes
78
Which leukocytes are not capable of phagocytosis
Lymphocytes
79
Neutrophils
``` "Early responder" Short lived Phagocytosis Release toxins Destroy bacteria Remove debris and dead cells ```
80
Eosinophils
"Fumigator" Noted in allergic reactions and parasite infections Regulate inflammatory response
81
Monocytes
``` "Disaster response" Macrophages Longer living Phagocytosis Secrete cytokines: signaling molecules Present antigens to activate T cells Clean up ```
82
Basophils
``` "Firefighters" Mast cells Allergic reactions Acute and chronic inflammation Wound healing Tame inflammation ```
83
Lymphocytes
``` "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) ```
84
Systemic manifestations of inflammation
Fever: cytokines that are pyrogens Leukocytosis: increase in circulating WBCs Lab changes
85
Lab changes during inflammation
Plasma proteins produced by liver increase Erythrocyte sedimentation rate C-reactive protein: opsonin (tagger) to phagocytosis
86
3 Phases of Wound Healing
Inflammation: filling Proliferation/new tissue: sealing Remodeling and maturation: shrinking
87
Inflammation stage of wound healing
``` Coagulation Bring cells needed Fibrin mess of blood clot Degranulation of platelets: growth factor Macrophages: clear debris ```
88
Proliferation stage of wound healing
"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
89
Remodeling/Maturation stage of wound healing
``` Begins several weeks after injury Normally complete within 2 years Fibroblast: deposit collagen for strength Tissue continues to regenerate Wound continues to contract ```
90
What causes dysfunctional wound healing
``` Ischemia: low blood supply Obesity: impaired leukocyte function Diabetes: impaired circulation Malnutrition Medications (steroids) ```
91
Gate control theory of pain
Only one impulse can make it through at a time
92
Neuromatrix theory of pain
Brain produces patterns of nerve impulses drawn from various inputs
93
Nocioceptors
Sensory nerve receptor that responds to pain
94
Afferent pathways
Sensory
95
Efferent pathways
Motor
96
Pathway of pain
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
Interpretive centers for pain
Brainstem, midbrain, diencephalon, cerebral cortex
98
4 stages of nociception
1. Transduction 2. Transmission 3. Perception 4. Modulation
99
Transduction stage of nociception
Tissue damage = exposure Chemical mediators: histamine, bradykinins, prostaglandins (inflammation) Nociceptors: A delta and C fibers; become excited
100
Transmission stage of nociception
Impulses conducted to dorsal horn of spinal cord Sensory fibers involved: A delta and C fibers Continues to CNS
101
A delta fibers
Medium sized Thinly myelinated: fast Well-localized, reflex withdrawal Glutamate
102
C fibers
Unmylenated: slow Dull, aching pain that lasts longer Substance P
103
Perception stage of nociception
CNS Conscious awareness of pain Affective: emotional response Cognitive: learning
104
Pain threshold
Level of painful stimulation required to be perceived as pain Similar in most people
105
Pain tolerance
Degree of pain one is willing to bear before seeking relief | Varies
106
Modulation stage of nociception
Change or inhibition of transmission of pain | Occurs at multiple sites along the pain pathway
107
Excitatory neuromodulators
Substance P Histamine Glutamate Increase sensation of pain
108
Inhibitory neuromodulators
``` GABA Serotonin Norepinephrine Endogenous opioids Decrease sensation of pain ```
109
Two types of pain
Physiologic | Pathologic
110
Types of physiologic pain
Acute Ischemic Referred Beneficial
111
Types of pathologic pain
Chronic Neuropathic Serve no purpose
112
Acute pain
Resolves when injury heals Usually less than 3 months Therapy: short term; opioids and nonopioids
113
Chronic pain
Longer than expected healing time Usually more than 6 months Example: fibromyalgia
114
Periperhal sensitization
Reduction in pain threshold: less painful stimuli to register as pain Causes chronic pain
115
Central sensitization
Increased responsiveness and sensitivity to pain | Causes chronic pain
116
Clinical manifestations of chronic pain
Sometimes similar as acute but usually looks different on assessment Hard to describe Psychosocial manifestations: irritability and depression
117
Treatment for chronic pain
Multimodal | Pain clinic
118
Neuropathic pain
Injury to nerves
119
Causes of neuropathic pain
Chemo, surgery, radiation, trauma, diabetic neuropathy
120
Clinical manifestations of neuropathic pain
Constant ache with intermittant sharp
121
Treatment for neuropathic pain
Difficult to manage Typical pain meds usually don't work Antidepressants and anticonvulsants can help
122
Ischemic pain
No blood flow to tissue
123
Referred pain
Perceived in an area other than injury
124
3 Pain management strategies
1. Interrupting peripheral transmission 2. Modulating pain transmission at spinal cord level 3. Altering perception and integration of nociceptive impulses in brain
125
Interrupting peripheral transmission of pain
Non-pharm: heat/cold; splint; minimize use Pharm: NSAIDS: inhibit prostaglandin production Local anasthetics: block sodium channels; stop conduction impulses
126
Modulating pain transmission at spinal cord level
Non-pharm: Cutaneous stimulation: therapeutic touch | Pharm: epidural; intrathecal anesthesia
127
Altering perception and integration of nociceptive impulses in brain
Non-pharm: distraction, guided imagery, biofeedback, hypnosis Pharm: opioids
128
Signs and symptoms of acute pain
``` Increased HR, BP, RR Dilated pupils Pallor and perspiration N & V Urine retention ```
129
Physiologic response to acute pain
``` 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
What hormone is produced by the developing conceptus and placenta?
HCG
131
What is the clinical significance of HCG?
Basis of pregnancy test Prevents involution of corpus luteum Causes corpus luteum to secrete larger quantities of sex hormones
132
How much does BMR increase during later half of pregnancy?
15%
133
Which hormones are involved in lactation?
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
Drugs are prescribed to pregnant women based on what basis?
Risk vs. benefit
135
Drugs taken in early pregnancy could cause what?
Death of the fetus | Conception through week 2
136
Which weeks of pregnancy cause major morphologic malformations?
3- 8 weeks post conception | Embryonic period
137
Which weeks of pregnancy cause most functional problems when exposed to teratogens?
9 weeks to term (38)
138
During pregnancy, intestinal transit time is prolonged, how would this effect the PK of a drug?
Increased absorption
139
By 3rd trimester, renal blood flow is doubled with large increase in glomerular filtration. How would this effect PK of a drug?
Increased excretion
140
For some drugs, _____ metabolism also increases during pregnancy.
Hepatic
141
During what weeks is a fetus not susceptible to teratogens? Why?
Weeks 1 and 2 | Death or spontaneous abortion will result
142
Pharmacological effects in a fetus can be toxic. Give example
Respiratory depression in opioid use
143
What was thalidomide?
Fast-acting teratogen used in 1950's and 60's for morning sickness. Caused phocomelia: short or missing limbs
144
What does a category X drug for pregnancy mean?
Animal or human studies demonstrate definite risk of fetal abnormality. Should come with a contradiction statement on drug label.
145
FDA approval for drugs used during pregnancy are based on what kind of testing?
Animal
146
What three factors determine how readily a drug is excreted in breastmilk?
Drugs that are highly lipophilic, with small molecules, and remain non-ionized
147
What is the recommended dose of folate for pregnant women?
400 - 800 mcg
148
What is the recommended dose of folate for lactating women?
500 mcg
149
What role does folic acid play in fetal development?
Role in cell division Synthesis of DNA Neuro-development
150
When does neural tube closure occur?
18 to 26 days after conception
151
Pregnant women need more _____ due to increase in blood volume.
Iron
152
Two reasons pregnant women need iron
Due to increased RBC production | Due to loss of blood during birth
153
Recommendation for iron for a pregnant woman
27 mg/ day
154
What can you take with iron to increase absorption?
Vitamin C
155
Fetal skeletal development occurs mostly in what trimester?
Third
156
What is the calcium RDA for pregnant or lactatin women?
1000 mg
157
Embryonic period lasts from...
Conception to 8 weeks
158
Fetal period lasts from...
9 weeks to 40
159
What week does a fetus start developing surfactant?
24
160
How many days does it take a fertilized egg to reach uterus and implant?
6
161
A blastocyst is made up of which two cell types
Inner cell mass | Trophoblast
162
Inner cell mass forms the
Embryo
163
Trophoblast helps form the
Placenta
164
Inner cell mass divides into
Epiblast and hypoblast
165
What is formed from the epiblast?
Amniotic sac
166
What is formed from the hypoblast?
Yolk sac
167
What provides embryo with nutrition until placenta is formed?
Yolk sac
168
What are the three primary germ layers of the embryo?
Ectoderm, mesoderm and endoderm
169
What germ layer is responsible for development of CNS?
Ectoderm
170
What germ layer is responsible for structure and organization such as the skeletal system?
Mesoderm
171
What germ layer is responsible for metabolism and homeostasis and forms the liver, GI tract, and pancreas?
Endoderm
172
When during pregnancy have all gross characteristics of the organ systems already begun to develop?
First trimester
173
By which month of pregnancy are all organs grossly the same as a neonate?
Fourth
174
Which systems are not fully developed at birth?
Nervous system Kidneys Liver
175
During what trimester do fetal kidneys begin to excrete urine?
Second
176
By which month of pregnancy does fetal bone marrow produce most of RBC in fetus?
Third
177
Hemoglobin concentration of fetal blood is what % greater than that of the mother
50%
178
Babies born before which week need respiratory support because of underdeveloped alveoli
36
179
Surfactant
A phospholipid in lungs which decreases surface tension of alveoli Often given to babies born between 26 and 34 weeks
180
What week does fetal circulation begin?
Week 3
181
What structure allows fetal blood to skip the liver?
Ductus venosus
182
What structure shunts blood from pulmonary artery to aorta to skip the lungs?
Ductus arteriosus
183
What structure allows blood to flow directly from right atria to left in a fetal heart?
Foramen ovale
184
Head to toe growth and development is called
Cephalocaudal
185
Core before fine motor development is called
Proximodistal
186
What is a time dependent loss of structure and function?
Aging
187
Three theories of aging
Molecular: gene regulation theory Cellular: Cell senescence, telomeres, reactive oxygen species Systemic: neuroendocrine
188
Programmed senescence theory of aging
Limit to number of cell divisions that human cells can undergo
189
Telomeres
Caps on the end of each chromosome A little bit is lost after each cell division Cell dies when telomere is gone
190
Free radicals
Cause aging by causing damage to DNA, RNA, proteins and individual cell death
191
Neuroendocrine theory
Aging is a decreased ability to survive stress
192
GI factors affecting absorption rate in neonates and infants
Prolonged/irregular gastric emptying | Lower gastric acidity until 2
193
Absorption and Distribution of IM meds in neonates and infants
Low blood flow through muscles: slow/erratic distribution of IM meds Better absorption of IM meds than adults
194
Topical meds for infants/ neonates
Thin skin so topical meds can result in toxicity
195
What results from neonates having low serum levels of albumin?
Decrease in protein binding of drugs and therefore more free drug in blood
196
When do infants reach normal PPB levels?
Between 10 - 12 months
197
When does the blood brain barrier fully develop in infants?
12 months
198
When do infants have adult liver capacity?
12 months
199
PK parameters for a 1 year old
Equal to an adult except drug metabolism increases until 2 then declines
200
Geriatric patients absorb drugs
More slowly than adults
201
What is the most important cause of adverse drug reactions in the elderly?
Drug accumulation due to reduced renal excretion
202
Why are adverse drug interactions and reactions 7 x more common in elderly?
Drug accumulation Polypharmacy Greater severity of illness Multiple pathologies
203
Three types of vaccines
Killed vaccine: whole killed microbe Attenuated live vaccine Cell parts: e.g. acellular pertussis
204
Toxoid
Weakened bacterial toxin | E.g. tetanus toxoid and diptheria toxoid
205
Active immunity
Via natural disease or vaccine Antibodies and memory B cells Cytotoxic and memory T cells
206
Passive immunity
Administration of antibody Immediate but short lived protection Eg breastfeeding or Immunoglobulin admin
207
What hormone is responsible for aiding the uterus in contracting back to normal size after birth?
Oxytocin
208
D5 1/2 NS IV fluid
Hypertonic: given for sodium and volume replacement Monitor hydration: lung sounds Monitor electrolytes: sodium in particular Also monitor pulse, BP, and urine output
209
Acetaminophen classification
Analgesic Antipyretic (Not anti-inflammatory)
210
Nursing considerations for acetaminophen
No more than 4g/ day | Less for alcholic and malnourished patients
211
MOA for acetaminophen
Slows production of prostaglandins in CNS | Selective COX inhibition
212
Adverse reactions for acetaminophen
Acute toxicity results in liver damage | Early signs are N & V diarrhea, sweating, abdominal pain
213
What inactivates the toxic metabolite NAPQI?
Glutathione | Otherwise will attack liver
214
Prototype drug for nonsteroidal antinflammatory drug
Ibuprofen
215
MOA for Ibuprofen
COX 1 inhibitor: decreased platelet aggregation and kidney damage COX 2 inhibitor: decreased inflammation, fever and pain
216
Adverse reactions for ibuprofen
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
Nursing considerations for ibuprofen
Use cautiously with older adults and clients with heart failure
218
COX I produces
Protective prostaglandins Acid reduction in stomach mucosa Clotting by increased platelet stickiness
219
COX II produces
Inflammatory prostaglandins | Pain, fever and inflammation
220
Two main types of opioid receptors
Mu and Kappa
221
Mu receptors result in
Analgesia, respiratory depression, euphoria, sedation, decreased GI motility, physical dependence
222
Kappa receptors result in
Analgesia and sedation, decreased GI motility
223
Pure opioid agonists
Morphine, oxycodone, hydrocodone, fentanyl | Turns both Mu and Kappa receptors on
224
Pure opioid antagonists
Blocks Mu and Kappa receptors Naloxone Reverses effects of opioid agonists: increases respiration, pain returns, diarrhea, agitation Treats overdose
225
Morphine sulfate
Opioid analgesic/ agonist | Pain relief, sedation, reduction of bowel motility
226
Adverse reactions to morphine
``` Respiratory depression Constipation Orthostatic hypotension Urinary retention Sedation Biliary colic N & V Overdose ```
227
Cardiac symptoms in a dying person
``` Tachycardia Hypotension Peripheral cooling, mottling, cyanosis Decreased pulses Decreased O2 in blood ```
228
Cheyne-Stokes pattern
Rapid breath followed by apnea | In a dying patient
229
Pharmacologic interventions for "death rattle"
Scopolamine patch for secretions | Opioids to assist with dyspnea
230
Dysphagia and decreased appetite in a dying person puts them at risk for?
Aspiration