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Sprinig 2018 > N393 Final > Flashcards

N393 Final Flashcards

1
Q

How do hormones change in pregnancy?

A

Every woman has cycle with variation; same hormones responsible play key role in maintaining pregnancies upon conception and fertilization

The corpus luteum is endocrine structure(produces hormones) or gland formed in ovary at site where egg is released

If egg not fertilized, the corpus luteum goes away

If egg is fertilized, the CL transforms into endocrine organ that helps maintain pregnancy

We think CL and hormones released is responsible for morning sickness

CL is responsible until placenta is large enough to take over

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2
Q

Hormones

A

HCG
Estrogen
Progesterone

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3
Q

HCG

A

(Human Chorionic Gonadotropin)
Produced by developing conceptus and placenta

Is a positive feedback mechanism; tells CL to release larger quantities of sex hormones (estrogen and testosterone)

Basis of many pregnancy tests and lab tests

Prevent involution of corpus luteum

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4
Q

Estrogen

A

Produced by CL and Placenta

Enlargement of uterus, breasts, and external genitalia

Relax pelvic ligaments so body can accommodate larger growing organ of uterus and baby inside

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5
Q

Progesterone

A

Produced by CL

Role in nutrition of early embryo

Decreases uterine contractility (tells body to “chill out”)

Helps estrogen prepare breasts for lactation

Shown in graph how it increases and then drops off completely to allow labor

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6
Q

Formation of placenta

A

Formed from trophoblast cells around the blastocyst (fetal development tissues)

Placenta thickness between mom and baby is about 1 layer of cells in some places - think about this small barrier with pharmacology

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7
Q

Function of placenta

A

Diffusion: Primary way placenta works

Higher concentration to lower

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8
Q

Flow of blood through placenta

A

Mom has uterine arteries and veins that empty into middle sides (maternal sinuses)

Baby side has umbilical vein and umbilical arteries, getting what they need from diffusion

Nutrients
Waste is exchanged
Gases (CO2 and O2)

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9
Q

Body’s response to pregnancy: weight

A 
Weight gain- average total: 24 lbs (by end of pregnancy)
Fetus: 7lbs
Placenta, amniotic fluid: 4 lbs
Uterus: 2 lbs
Breasts: 2 lbs
Plasma volume: 6 lbs
Fat: 3 lbs
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10
Q

Body’s response to pregnancy: Metabolism & Nutrition

A

Metabolism & Nutrition*
Basic metabolic rate increases 15% during later half of pregnancy
Providing nutrients to help baby grow
Placental stores of nutrients are needed to sustain fetal grown during the last months of pregnancy (a lot of moms worry about weight)

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11
Q

Body’s response to pregnancy: Breast Development

A

Starts in first few weeks of gestation; they are enlarging but not working or prepared to do milk portion of it

Hormones
estrogen, progesterone, prolactin oxytocin

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12
Q

Breast development Hormones

A

Estrogen: stimulates tissue to grow

Progesterone: stimulates tissue to grow; the ductules, lobes in breasts

Prolactin: stimulated production with baby eating/suckling (baby eats = prolactin levels rise = nipple stimulated = milk produced)

Oxytocin: responsible for let down or milk ejection and responsible for uterine contractions
Will help uterus return to size while breastfeeding

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13
Q

Body’s response to pregnancy: Kidney Function

A

Increased renal plasma flow and glomerular filtration rate

More fluid that all must go through kidneys

Very little is related to waste of fetus; babies would produce urine and would be in amniotic fluid, it is sterile

Majority of this is mom with increased plasma and fluid she needs to process

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14
Q

Body’s response to pregnancy: Circulatory

A

Mom’s cardiac output will increase 30-40% by 27th week of pregnancy; By end of pregnancy, 30% greater blood volume

Less RBCs in relation to blood volume may see resulting in dilutional anemia; not anemic, not decrease in hematocrit; in relation to everything going on, she will have/experience decrease in hematocrit

Moms will be monitored closely but in greater context it is just because mom has more plasma volume

Heart working harder to maintain the new volume

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15
Q

Body’s response to pregnancy: Respiratory

A

Respiratory- increased RR

20% increase in oxygen use by mother at term

May see higher RR taking vitals

Progesterone increases minute ventilation

Uterus presses abdominal content up against the diaphragm

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16
Q

Common complaints during pregnancy and anatomical reason why

A

Spine
Back pain, displaced center of gravity back pain

Intestines
Constipation, organ moved around

Bladder
Constant urination, bladder squished

Stomach
Gastric reflux/indigestion, change in pressure, no room to expand
Can’t eat as much, get full fast

Lungs
Can’t take deep breaths

Sleeping changes
Needing to pee
Needing to sleep on side
Edema
Extra fluid

Breast tenderness
Colostrum can be excreted for weeks

Falls
Increased risk for falls

Massive stretching
Heart should not enlarge

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17
Q

What to avoid during pregnancy (don’t need to know specifics)

A

Cigarettes, alcohol, illicit drugs, stimulants, Vitamin A at doses higher than 5,000 IU, Liver(?), herbal products, Dieting and skipping meals, Iodine, Limit certain fish, undercooked or raw fish, meat, etc.

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18
Q

Prenatal vitamins

A

Various products may not be equivalent/interchangeable; Content not standardized
Regulation as “supplement”
Potential compliance issues- health individuals may not appreciate need - Education!

Adverse effects
Nausea, vomiting, constipation (especially Fe- containing)
Take with food or in evening to
Constipation- hydration, fiber intake activity

Notes
Recommend reputable brand if OTC (may have prescription)
Stress on body - need supplement

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19
Q

Folic Acid Function

A

Cell division, DNA synthesis (makes DNA)
Neurodevelopment
FA goes through reduction with dihydrofolate reductase reduced to tetrahydrofolic acid and goes on to make amino acids

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20
Q

Folic Acid Use in Pregnancy

A 
Start preconception (preferably in months before)
Neural tube closure @ 18-26 days post conception
Populations at risk for deficient (e.g., epilepsy, family history neural tube defect, etc)
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21
Q

Folic Acid Dose

A 
Decreased neural tube defects
Preconception & 1st trimester
400-800 mcg daily
Different doses for certain increased risk groups
Adverse effects
Water soluble-few AE
May mask deficiency of Vitamin B12
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22
Q

Iron Function

A

HB (70-80% of total body Fe); myoglobin; iron-containing enzymes
Other
Transferrin
Ferritin (storage iron pool)
Fe from degraded RBCs recycles (120 days)
As you take iron in, some immediately stored, some go through life cycle, as RBC dies it releases iron again and it will keep going through cycle
Loss largely due to blood loss
Iron deficiency anemia
Fe requirements
Increased RBC production

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23
Q

Iron - Uses in pregnancy

A

Expansion of maternal RBC mass, blood volume

RBC production in fetus

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24
Q

Iron- Dose

A

Determined by Hb & iron status prior (highly variable)

General pregnancy RDA=27 mg/day (vs. 15-18 mb/d non-pregnant)

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25
Q

Iron- Adverse effects

A

GI
Nausea, bloating, constipation
Causes dark stools, be careful could be blood

Caution!! Overdose can be fatal; leading cause of death is poisonings

Want to make sure stored appropriately and not laying around (red tablets, yummy!)

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26
Q

Oral Iron

A

(ferrous is most easily absorbed/common)
With adequate stores, Fe absorption is decreased
Dietary- heme form best
Various (ferrous sulfate, gluconate, fumarate, etc.(solid or liquid)
~10% absorbed- body knows it doesn’t need it
Vitamin C increases absorption
Food decreased absorption (but may help with GI Distress initially… nausea and constipation)
Compare mg “elemental iron” in products

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27
Q

Iron- what to know

A

Different formulations
Different between salt and elemental
Ferrous sulfate (salt form) = 65 mg of elemental iron
When talking about how much iron is in something, focus on ELEMENTAL IRON
Same with calcium

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28
Q

Calcium

A 
Functions- need for everything
Bone
Neuronal excitability/NT release
Muscle contraction
Cardiac action potential, contraction
Blood coagulation

Pregnancy
Fetal skeletal development (mostly 3rd trimester)-Forming baby, need to supplement their development
Maternal skeletal

RDA- pregnancy /lactation
1000 mg elemental Ca++/day (19-50 years) this includes food intake

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29
Q

Calcium salts- oral

A

Forms vary & have differing Ca++ content
Calcium carbonate, citrate, etc.
Common adverse effects include (not many)
GI (especially constipation)

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30
Q

Drugs in pregnancy

A

~⅔ of pregnant females take ≥1 med
Both pregnancy & non-pregnancy related conditions
Drugs of abuse (e.g., alcohol, caffeine, etc.)
Safety testing cannot be done in pregnancy women- requires retrospective approach (registries)
Adverse consequences may occur with just 1 dose!
Effects are relative to period of pregnancy
Very early -death
3-8 weeks- major morphologic malformation
9-term -physiologic defect/minor morphologic
Risk vs. benefit approach to taking medication
Consequences of leaving condition untreated may be more harmful to embryo/fetus

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31
Q

Physiologic changes in pregnancy- GI

A

GI tract- impact on tone and motility of bowel (would impact absorption)

Prolongation of intestinal transit time– everything is moving through pretty slowly

Increased absorption potential- can’t predict how slow and may lead to continuous absorption

Potential impact on enterohepatic recirculation
Increased potential

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32
Q

Physiologic changes in pregnancy- Kidney

A

By 3rd trimester, renal blood flow is doubled
Results in large increase in glomerular filtration rate-
Excretion impacted- decreased drug concentration excreting out more

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33
Q

Physiologic changes in pregnancy- Liver

A

For some drugs, hepatic metabolism increase

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34
Q

Embryo/Fetal Development

A

1-2 week exposure to teratogens

3-8 week: Embryonic period
Organogenesis- making the organs
Exposure to teratogens during this time may cause malformation
I.e., cleft palate, neural tube defect,

9- 38 week: Fetal period
Exposure to teratogens during this time may impact function of the organs

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35
Q

Types of effects

A

Teratogenic

Behavioral- neurocognitive

Pharmacological or toxic effects in fetus

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36
Q

Teratogen

A

an agent/factor that causes a malformation of an embryo

Fetal structural malformation; or
Other- miscarriage, stillbirth, etc.
Exposure to medication within 1-2 weeks, pregnancy will terminate

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37
Q

Pharmacological or toxic effects in fetus

A

Pharmacologic effect: respiratory depression with opioid
Example: baby would have depressed breathing if it is taken right before delivery

Delayed toxicity
Example: Diethylstilbestrol (DES): estrogenic substance- causes vaginal cancer in female offspring 18 years or so after they were born
Physiologic dependence-infant

Prototype example: Thalidomide- treating morning sickness in 1950s-1960s, children born with “seal limbs”

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38
Q

New Labels for Pregnancy

A
  1. 1 Pregnancy: Includes labor and delivery
  2. 2: Lactation: Includes nursing mothers
  3. 3 Females and Males of Reproductive Potential (new)

Old Labeling

  1. 1 Pregnancy
  2. 2 Labor and Delivery
  3. 3 Nursing Mothers
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39
Q

FDA Pregnancy Categories

A

A:
Controlled human studies fail to demonstrate risk in 1st trimester; no evidence of risk in later trimesters
B:
Animal- failure to demonstrate risk (or do show risk, but controlled human studies do not)
Human- no controlled studies
C:
Animal- adverse effect on fetus - or - no studies done
Human- no controlled studies
D:
Human- proof of human fetal damage
“WARNING” statement on drug label
X:
Animal or human studies demonstrate definite risk of fetal abnormality
“CONTRADICTION” statement of drug label

Lack of teratogenic effect in animals ≉ safety in humans
FDA drug approvals are based on animal testing

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40
Q

Nursing agents to support safe drug use in pregnancy

A

Problematic Agents (not an all-inclusive list)
Considerations to minimize risks
Drug therapy during breastfeeding

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41
Q

Considerations to minimize risk of drug use during pregnancy

A

Educate women of childbearing age
Assume any drug will reach the embryo/fetus (some drugs won’t cross but don’t assume)
Weigh risk vs. benefit
Is a drug needed?
Eliminate unnecessary drugs
Avoid certain drugs, if drug therapy is necessary
If necessary, use drugs with better safety profile
Avoid substances of abuse (before & during)
For known teratogens (e.g., isotretinoin, Retin-A)
Written informed consent
Multiple forms of contraception
Pregnancy test just prior to initiation

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42
Q

Problematic agents

A 
Drugs with hormonal effects
Anticancer (Ex: cytotoxic)
Antiseizure
Drugs that affect thyroid
Ethanol
Drugs of abuse
Mercury
Drugs that affect cell development/differentiation (ex: Vitamin A derivatives-isotretinoin)
Antimicrobial
Drugs that affect RAAS
Warfarin (anticoagulant)
New: analgesics-insufficient data for FDA action
NSAID-miscarriage; opioids-birth defects; Tylenol- ADHD
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43
Q

Drug therapy during pregnancy

A

Large number of drugs can be excreted in breastmilk

Extent of excretion and infant exposure is based on medication absorption factors- think about factors that determine whether a drug can pass through a membrane

Factors determining if it will enter breast milk:
Lipophilic
Small in size
Ionized vs non
Is it compatible with breastfeeding? Look for diarrhea in infant
Don’t always have a lot of data to understand clinical effects
Always look it up
How would you counsel a patient?

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44
Q

Age related effects on PK processes

A

Immature organs, alterations in binding, alterations in # of receptors (increases and decreases)

May show greater variability patient to patient (vs.geriatrics and adults)

Lack of safety or efficacy data- not used in studies (patients excluded under 18 years of age typically, may not have data on younger people with medication)- may be dosing guesses early on

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45
Q

Neonates & Infants

A

Kinetic differences in kids- longer time above MEC

With appropriate weight based dose, adults decrease faster than children; we have a longer period of time above MEC

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46
Q

Neonates & Infants: Absorption

A

Not good predictability;

Prolonged & irregular gastric emptying time
Reach adult levels at 6-8 mo
Increase in absorption

Low gastric acidity
Reach adult levels at about 2 years
Ionization- GI absorption

Low blood flow through muscles in first days of life
Slower absorption in muscles (IM route)-(infants better than neonate/adults)
Slow and erratic in neonates
Give a lot this way for infants

Very thin stratum corneum and greater blood flow to skin
Topical is FAST; worried about toxicity
Very thin skin with a lot of blood flow

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47
Q

Neonates & Infants: Distribution

A

Protein bending
Low serum albumin levels
Increased free drug- risk of toxicity or increased clinical effect
Adult levels in 10-12 months
Endogenous compounds (bilirubin) compete with drugs for available binding sites

Blood brain barrier
May need decreased dosing if it has increased CNS potential or toxicities
Worry about stuff getting in there
Not fully developed at birth; it protects your brain so stuff doesn’t get in

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48
Q

Neonates & Infants: Metabolism

A

Low drug-metabolizing capacity
Increased risk of toxicity because not metabolizing like need to
Liver maturation at about 1 year

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49
Q

Neonates & Infants: Excretion

A

Low during infancy (below) resulting in increased drug levels…Decreased renal excretion means increased drug levels
Renal blood flow
Glomerular filtration
Active tubular secretion

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50
Q

Children 1 year & older: PK processes

A

By age 1, most PK parameters = adults
Exceptions:
Drug metabolism continues until about 2 year of age (then gradually declines)

Excretion of some drugs can increase tremendously

BBB is fully developed about a year or older

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51
Q

Factors Affecting Medication Complications in the Elderly

A

Alterations in pharmacokinetics
Multiple and severe illnesses

Multidrug therapy
Different prescriber

Poor adherence
Cost, forget to take, dementia, trouble swallowing, have to take a lot/can’t keep straight, don’t want to, etc.

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52
Q

How can we help geriatric patients?

A

Technological strategies, pill boxes, pill packs (send prescriptions and they send pill packs), community outreach programs, routes of administration, simplifying regimen, does every provider know everything the patient is on

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53
Q

Geriatric patients: Absorption

A 
Rate affected, not really sure how much; can lead to delayed response
Increased gastric
Decreased absorptive surface area
Decreased splanchnic blood flow
Decreased GI motility
Delayed gastric emptying
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54
Q

Geriatric patients: Distribution

A

Several things can happen:

Increased body fat
Lipophilic drugs will have increased distribution into fatty areas; can lead to decreased plasma concentration levels of these drugs because they are hanging out in the fat

Decreased lean body mass
Decreased muscle mass, not a lot going out to muscles

Decreased total body water
Increase concentration if drugs are water soluble (hydrophilic drugs)- smaller pool for them to play in
If same amount given as someone with normal water, it could increased risk of toxicity

Decreased serum albumin
Decreased protein binding = increase in free drug

Decreased cardiac output

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55
Q

Geriatric Patients: Metabolism

A

Decreased metabolism

Decreased hepatic blood flow
Decreased hepatic mass
Decreased activity of hepatic enzymes

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56
Q

Geriatric Patients: Excretion

A

MOST important part!! This will be the most concerning outcomes, biggest toxicity

Decreased renal blood flow
Decreased glomerular filtration rate
Decreased tubular secretion
Decreased number of nephrons

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57
Q

PK Geriatric Patients: Overall

A

A- increased, D- all over the place, M- won’t happen as good as it should

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58
Q

Geriatric Patients & Kidneys

A

Important to understand that how well kidneys work as geriatric patient we know what labs to look at

Lab to look at: Creatinine; Creatinine clearance is estimate of glomerular filtration rate

It is a protein> proteins come from muscle> geriatric patients have decrease in muscle mass
Ex: 80 year old with creatinine clearance may look good but doesn’t mean same as someone that is younger; if there albumin is 2.4, their muscle will look super small … the number doesn’t mean much

Normal creatinine is 120. Clearance calculation example: (140-age/serum creatinine) That would put an 80 year old 60 versus 20 year old would be at 120. This would tell a nurse how to adjust dosage for clearance

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59
Q

PD changes in elderly

A

May have significant alterations in receptor activity but is difficult to predict

Reduction in number of receptors

Reduction in receptor affinity

We know very little about how this actually applies to clinical practice

Can’t adjust for this

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60
Q

Adverse Drug Reactions: Geriatric Patients

A

7 times more common in the elderly vs. younger patients

Accounts for 16% of hospital admission in older patients and 50% of all medication related deaths

Why?
Drug accumulation -(poor D/M/E and erratic A)
Polypharmacy- all drugs and doctors and pharmacies don’t know
Greater severity illness
Multiple pathologies
Greater use of NTI drugs- effective/toxic concentration is narrow
Alterations in pharmacokinetics
Inadequate supervision of long-term therapy
Poor adherence

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61
Q

Basic events of embryology

A

Conception: fertilization of egg with sperm
Approximately two week difference between gestational age and conception
Conception
Occurs in fallopian tubes

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62
Q

Embryonic Period

A

First 8 weeks post conception *think malformations
All major organs are formed
Three primary germ layers
Basic body plan emerges
Week 1- travel
Week 2- implantation
*says embryo not susceptible to teratogens because there is no blood supply from mom supplying baby; doesn’t mean whatever mom is exposed to doesn’t change environment or make it optimal for implantation
It would be spontaneous abortion, women don’t even know they are pregnant

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63
Q

Blastocyst

A

Cleavage: Journey of 6 days to travel to uterus; cells are dividing and then implanting

Two distinct types of cells

Inner cell mass: forms the embryo

Trophoblast: layer of cells surrounding the cavity which helps form the placenta

Float for about 3 days

Implantation on about 6 days pays conception

Trophoblast erodes uterine wall

Takes 1 week to complete

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64
Q

Implantation

A

Adherence of the trophoblast to the uterine wall

Inner cell mass divides into epiblast and hypoblast

2 fluid filled sacs
Amniotic sac from epiblast
Yolk sac from hypoblast- nutrition, primitive digestive system

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65
Q

3 primary layers of tissue formation

A

Ectoderm
Mesoderm
Endoderm

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66
Q

Ectoderm

A

Interactions with external environment; CNS; External affairs

Nervous Tissue:
Epidermis

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67
Q

Nervous tissue

A 
Neural tube
CNS
Retina
Posterior pituitary
Pineal gland
Neural crest
Pigment cells
Adrenal medulla
Cranial and sensory nn
Cranial and sensory ganglia
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68
Q

Epidermis

A 
Hair
Nails
Mammary glands
Cutaneous glands
Anterior pituitary
Teeth enamel
Inner ear
Eye lens
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69
Q

Mesoderm

A

Structure & organization; Architect & engineers; skeletal system

Skeleton (head and body)
Muscle
Connective Tissue
Circulatory sys (Cardiovascular & Lymphatic)
Spleen
Adrenal cortex
Genital system: (Gonads, ducts, accessory glands)
Dermis
Dentine of teeth
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70
Q

Endoderm

A 
Metabolism & homeostasis; chemist
Epithelium of GI tract
Liver
Pancreas
Urachus
Urinary bladder
Epithelial portions
Pharynx
Thyroid
Trachea, bronchi, lungs
Tympanic cavity
Pharyngotympanic tube
Tonsils
Parathyroids
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71
Q

Fetal period

A

(weeks 9-40) including fetal lung & circulatory development

Remaining 30 weeks (+2 weeks of conception = 40 weeks) *think function

Organs grow larger and become more complex

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72
Q

Overview of organ development

A

By 1st month, gross characteristics of all different organ systems have already begun to develop
By 4th month, organs are grossly the same as neonate
By birth, nervous system, kidney, and liver are not fully developed

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73
Q

Organogenesis

A

up until week 16

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74
Q

Differentiation

A

week 16 > birth

Ex: jaundice, liver is not fully developed

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75
Q

Gastrointestinal development

A

Midpregancy- ingest and absorb large amounts of amniotic fluid

Last 2-3 months- small quantities of meconium formed

Shouldn’t have much or would be indication of distress in baby

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76
Q

Kidney development

A

Begin to excrete urine during second trimester
Fetal urine = most of amniotic fluid
If not developing properly, ultrasound will show less fluid

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77
Q

Fetal blood

A

By 3 months, bone marrow is producing most of RBC

Even at low PO levels, fetal hemoglobin can carry

20-50% more oxygen than maternal hemoglobin

Hemoglobin concentration of fetal blood is about 50% greater than that of the mother

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78
Q

Lung Development

A

Surfactant is detectable at about 24 weeks in amniotic fluid

Is a phospholipid, produced inside lungs

Decreases surface tension (alveoli sticking together)

It is important in lung development and alveoli

Makes work of breathing easier

Lung function is not fully formed until 36-38 weeks

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79
Q

Fetal Circulation

A

Heart begins to beat at week 4

3 major structures: don’t need liver or lungs
ductus venosus
Ductus Arteriosis
Foramen ovale

1 Factor
High Pulmonary Vascular resistance

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80
Q

Ductus Venosus

A

Shunts blood to skip liver

Liver isn’t fully functional until after birth (some blood gets in to make sure that it is developing) but mom and placenta do the work of the liver

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81
Q

Ductus Arteriosis

A

Shunts blood into aorta which takes out of body

Blood shunted due to high pressure in lungs

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82
Q

Foramen ovale

A

Shunt/hole between right and left atrium

83
Q

High Pulmonary Vascular Resistance

A

Lungs are high pressure, filled with fluid, blood doesn’t want to go there so two other structures are created to avoid

84
Q

Growth & Development

A

Growth:
Increase in physical size (height, weight, head circumference)

Development:
Continuous, orderly series
Increase in function and complexity
Increase in capabilities

85
Q

Patterns of G & D

A

Pace
Rapid from birth to 2 and puberty to ~15 years
Slower from 2 to puberty and 16-24 years

Cephalocaudal
Head to toe
Ex: Can sit up before walking

Proximodistal
Middle to outside
Ex: Sitting before fine motor

Simple to complex
Fine motor development

86
Q

Factors that influence G&D

A

*Always give ranges

Critical/sensitive period

Genetics

Environment
physical and psychosocial (prenatal exposure/SES/access)(toxins/lead/pollution/etc.)

\Culture

Health status
Family

87
Q

Response of the body to pregnancy

A 
Average weight gain 24 lbs
15% increase in basal metabolic rate
20% increase in respiratory rate
30-40% increase in cardiac output
30% increase in blood volume

Increased renal plasma flow and glomerular filtration rate

Breast development

88
Q

Pace

A

Rapid from birth to 2 and puberty to ~15 years

Slower from 2 to puberty and 16-24 years

89
Q

Cephalacaudal

A

Head to toe

Ex: Can sit up before walking

90
Q

Proximodistal

A

Middle to outside

Ex: Sitting before fine motor

91
Q

Simple to complex

A

Fine motor development

92
Q

Factors that influence pediatric development

A 
*Always give ranges
Critical/sensitive period
Genetics
Environment
physical and psychosocial (prenatal exposure/SES/access)(toxins/lead/pollution/etc.)
Culture
Health status
Family
93
Q

Aging

A

Is a normal physiologic process- universal and inevitable
Time dependent loss of structure and function
Cellular and molecular level
Not a disease

94
Q

Three theories of aging

A

Gene Regulation Theory
Programmed Senescence Theory
Neuorendocrine

95
Q

Programmed Senescence Theory

A

Cell senescence
Limits the number of cell divisions that humans can undergo
Genetically programmed (small amount of DNA is lost with each cell division)
Cell damage

Telomeres
Caps at the end of chormosones that protect, they shorten and eventually cell division stops

Reactive Oxygen Species
The formation of free radicals that triggers cell damage/DNA/RNA/Proteins/Cell death (UV light, metabolism, inflammation, ionizing radiation, smoking, air pollution)

96
Q

Systemic

A

Neuroendrine- decreasing ability to survive stress; diminished ability to coordinate communication, program physiological response, maintain optimal functional state

HPA axis forever overwhelmed

Immunity decreased

97
Q

TBW (Total Body of Water)

A

Newborn/Infant = 70-80%
Adult = 50-60%
Older/Aging Adult = 55%
Trends: decreasing over lifespan

in 2 compartments: extracellular (1/3) or intracellular (2/3)

Extracellular fluid is plasma and interstitial fluid

98
Q

4 forces move

A

Cell membrane is permeable to water but not electrolytes, those need active transports

Filtration, Reabsorption, Oncotic, Hydrostatic

99
Q

Osmosis vs. Filtration & Reabsoprtion

A

Osmosis- btw intracellular and extracellular

Filtration & Reabsorption - capillary membrane

100
Q

Extracellular

A

A lot of Na+ (sodium) & Cl- (chloride)

Less of K (Potassium), Mg (Magnesium), Ca (Calcium) and Protein

101
Q

Intracellular

A

A lot of K, Protein

Less of Na, Cl, Mg, Ca

102
Q

Osmotic pressure

A

is force that attempts to balance the concentration of solute and water between intracellular and extracellular fluids

Water follows higher concentration of solutes in an attempt to balance

103
Q

Isotonic

A

solute and water concentration is the same on both sides

104
Q

hypertonic

A

solute concentration is higher on outside than inside

ex: osmolality 300, water goes out, cell shrinks

105
Q

hypotonic

A

solute concentration is lower outside the cell than inside the cell

ex: osmolality: 200, water goes in, cell swells

106
Q

Osmolity

A

is the number that reflects amount of solutes per kilogram

107
Q

Top 5 fluids

A

Hypotonic: D5W
Hypertonic: D5 1/2 NS, D5NS
Isotonic: Lactated Ringers, NS .9% NaCl

108
Q

Hypertonic Fluids

A

when you need sodium and fluid volume replacement and monitoring hydration, lung sounds, electrolytes

D5 ½ NS: used for Na and volume replacement; CAUTION, go slow, monitor BP, pulse rate, and quality of lung sounds & serum Na and urine output

and

D5NS

109
Q

Hypotonic Fluids

A

D5W: isotonic until inside then body then metabolize glucose and become hypotonic; for when you need sugar, glucose

Don’t give to infants ore head injury patients! May cause cerebral edema

110
Q

Isotonic fluids

A

same osmolarity as body fluid, used for fluid replacement in safe way; monitoring I&O’s,, skin turgor, mucous membranes, electrolytes (secondary)

NS 0.9% NaCl: used to expand volume, dilute medications and keep vein open

Lactated Ringers: used for fluid resuscitation

111
Q

Normal Serum Electrolyte Concentrations

A

Calcium 9-11mg/dl
Magnesium 1.5-2.5 mEq/L
Potassium 3.5-5 mEq/L
Sodium 135-145 mEq/L

Labs drawn from extracellular space, it will show reflection of whats happening on inside

112
Q

Na

A

135-145 mEq/L
Major extracellular fluid cation
Regulates osmotic forces & water balance (pull water one way or another)
Regulates acid-base balance
Facilitates nerve conduction and neuromuscular function
Transport of substances across cellular membrane

113
Q

K

A

Range: 3.5-5.0 mEq/L
Major intracellular fluid cation
Maintains cell electrical neutrality
Facilitates cardiac muscle contraction and electrical conductivity
Facilitates neuromuscular transmission of nerve impulses
Maintains acid-base balance

114
Q

Ca

A

Range 9-11 mg/dL
Vital for cell permeability, bone and teeth formation, blood coagulation, nerve impulse transmission, and normal muscle contraction
Plays important role in cardiac action potential and is essential for cardiac pacemaker automaticity

115
Q

Mg

A

Range: 1.5-2.5 mEq/L
Role in smooth muscle contraction relaxation
Suppresses release of acetylcholine at neuromuscular junctions
Low Mg = increased acetylcholine = too much movement
High Mg = decreased acetylcholine = too little movement

116
Q

Filtration

A

movement of ECF from intravascular space to interstitial space

Forces that favor filtration:
Water moving from capillaries to interstitial
Capillary hydrostatic (push force)
Interstitial oncotic (pull force)
117
Q

reabsorption

A

movement of ECF from interstitial space to intravascular space

Forces that favor reabsorption:
Moving from interstitial to vascular
Capillary osmotic (pull force)
Interstitial hydrostatic (push force)
118
Q

Oncotic pressure

A

osmotic pressure exerted by proteins pulling

Capillary (plasma) oncotic pressure

Osmotically attracts water from the interstitial space back into the capillary

Pulls water back into vascular space
Interstitial oncotic pressure
Attracts water from capillary into the interstitial space

119
Q

Hydrostatic pressure

A

force generated by pressure of fluid on capillary walls pushing

Capillary hydrostatic pressure (blood pressure)
Facilitates the outward movement of water from the capillary to the interstitial space

Capillary hydrostatic pressure is primary force that pushes water out of vascular space

Interstitial hydrostatic pressure
Facilitates the inward movement water from the interstitial space into the capillary

120
Q

Acid-Base Balance

A

pH normal range = 7.35-7.45
Acid: contribute or donate H+
Base: absorb an H+ ion
Inverse relationship: increased H+ = decreased pH #, decreased H+ = increased pH #

121
Q

Acidosis

A

pH below 7.4 (↑H+)

122
Q

Alkalosis

A

pH above 7.4 (↓H+)

123
Q

1st line buffer: 3 chemicals

A

Bicarbonate-Carbonic Acid buffer (ECF)
H2CO3 (Carbonic acid) ⇄ H+ + HCO3 (Bicarbonate ion)

Protein buffer (ICF) - Hemoglobin absorbs/liberate H+

Phosphate buffer (CF) - Sodium Phosphate can absorb/liberate H

If the pH is alkalosis- carbonic acid will contribute its H+… end result is:
Increase H+ & decrease in the pH

If the pH is acidosis - H+ will wimbine with bicarbonate… end result is:
Decrease H+ & increase in the pH

124
Q

2nd line buffer: respiratory

A

If acidosis, breathe faster and deeper = removes CO2 gas from the blood = lower pCO2 of the blood … end result is:
Decrease in H+ = increase in pH

If alkalosis, breathe slower and shallower = adds more CO2 gas to the blood = Higher pCO2 of the blood
Increase H+ & decrease in the pH

125
Q

2nd line buffer: renal

A

Secrete more or less H+ into the renal tubule and take out in urine

Phosphate
Ammonia
Secrete more H+ → ↓H+ → ↑pH
Secrete less H+ → ↑H+ → ↓pH

126
Q

Respiratory acidosis/alkalosis

A

High or low pCO2 value

127
Q

Metabolic acidosis/alkalosis

A

High or low HC03 value

128
Q

Normal arterial values

A

pH: 7.35-7.45
pCO2: 35-45 mmHg
HC03: 22-26 mmHG
pO2: 80-100 mmHg

129
Q

compensation

A

With partial compensation = buffer system activated but pH still high
With full compensation = buffer system activated and pH is normal

130
Q

Hypoxemia

A

O2 values is off

131
Q

1st line of Immunity

A 
Physical barriers
Characteristics:
Innate
Constant presence
Epithelial cells
Not very specific response
No memory
Examples: skin and mucous membranes, cells and secretory molecules, cilia, normal flora
132
Q

2nd line of Immunity

A 
Innate immunity- inflammation
Characteristics:
Not specific
In response to (and usually in proportion to degree of) injury
Immediate response 
No memory
133
Q

3rd line of Immunity

A 
Adaptive
Characteristics:
Delayed response
Very specific toward “antigen’
Discriminatory & diverse
T & B lymphocytes, macrophages, dendrite cells
Specific memory
Examples
Antigens: infection diseases, environmental substances
Humoral (b cell): antibodies
Cell mediated (t cell): crafted cells in lymphocytes
Immunizations
Immunotherapy
134
Q

Benefits of Inflammation

A

Prevents infection and further damage by microorganisms
Self limiting through plasma protein systems
Interacts with components of adaptive immune system so a more specific response can occur
Prepares the area for healing
3 phases of wound healing: inflammation is first

135
Q

Components of Inflammation

A
  1. increased vascular permeability
  2. recruitment and emigration of leukocytes
  3. phagocytosis
136
Q

Inflammation part 1: increased vascular permeability

A

(Get extra blood and cells to that area of body)
Mast cells releases- 3 key players
Histamines: potent vasodilator
Ex: targeting effects of this histamine? Give antihistamine to down inflammation response
Prostaglandins: vasodilate, chemotic factor (cells), pain
Leukotrienes: chemotaxis calling), inflammation > asthma
Vasodilation
Greater blood volume & hydrostatic pressure
Pushes fluid into surrounding tissue, the more fluid in vessels create push out into surrounding tissue to get specific type of cells where they need to go

137
Q

Inflammation Part 2: recruitment and emigration of leukocytes

A

(Get from vascular to interstitial space)… 3 set stages:
Margination: neutrophils stick to the vessel wall, lining up; “pavementing”
Emigration/Diapedesis: neutrophils exits vessel
Chemotaxis (calling): tissues release chemotaxins (cells), migration toward higher concentration of chemotactic factors (prostaglandin, leukotrienes)

138
Q

Inflammation Part 3: phagocytosis

A

(Doing its job of phagocytosis- digestion of things that should not be there)
Digestion; Results in:
By products- oxygen radicals which can cause cell damage
Pus- collection of dead neutrophils, bacteria, and cellular debris
Macrophages - cleaning

139
Q

Kinins

A

Can activate itself
Works closely with clotting system
Initiated by activation of Factor XII to Factor XIIa
Results in: Bradykinin- chemical responsible
Pain
Vasodilation
Increased vascular permeability

140
Q

Coagulation

A 
at same time but different pathway to do some of same functions
Activated by:
Extrinsic- tissue injury
Intrinsic- abnormal vessel wall & Factor XII
Components of kinin system
Responsible for:
Clot formation
Migration of leukocytes
Chemotaxis
Increased permeability
141
Q

Compliment

A

“the one responsible for direction traffic”
Destroy pathogens direct or indirectly by recruiting others
Activated by:
Classical pathway- antibodies
Alternate- infectious organisms
Lectin- other plasma proteins
Results in:
Chemotaxis- calling, phagocytes attracted to area
Opsonization- tags/coats surface of bacteria; play come in & destroy
Direct lysis of pathogens- destroying pathogens
Degranulation of mast cells- inflammatory mediators (histmine, prostaglandin, leukotrienes, others)

142
Q

Cascade systems

A

compliment, kinins, coagulation

143
Q

Physical findings of inflammation

A 
Pain (prostaglandin)
Heat (vasodilation)
Redness (vasodilation)
Swelling (vasodilation)
May have loss of function depending on what is going on
144
Q

who is involved in the inflammatory process

A

Histamine, prostaglandin, leukotrienes
Bradykinin
Cytokinins
Leukocytes (WBCs)

145
Q

cytokines and chemokines

A

Signaling molecules
Other names: monokinens, lymphokines, interleukins, tumor necrosis factor
Produced primarily by macrophages and T helper cells
Involved in: chemotaxis, recruitment, stimulation of leukocytes

146
Q

Leukocytes

A

(*capable of phagocytosis)-formed in bone marrow with specific jobs to do

neutrophils*
eosinophils*
basophils*
monocyte*s
lymphocytes
147
Q

Neutrophils

A 
Early responder (6-12 hours)
Polymorphonuclear leukocytes PMN
Phagocytosis
Release toxins
Bands are immature neutrophils
Destroy bacteria, remote debris & dead cells, short lived
148
Q

eosinophils

A

Noted in allergic reactions and parasitic infections

Regulate inflammatory response “fumigation”

149
Q

basophils

A 
Mast cell
Pro Inflammatory chemicals
Allergic reactions
Acute and chronic inflammation
Wound healing
150
Q

monocytes

A 
Macrophages
Longer living
Phagocytosis
Secrete cytokines (signaling molecules)
Present antigens to activate T cells
Clean up (disaster response team)
(mononuclear)
151
Q

lymphocytes

A

B&T longest to mobilize, trained for specific things) (mononuclear)

B-Cells
Able to produce antibodies
Have antibody like receptors on their surfaces (immunoglobulins)

T-Cells
T-4 (CD4) cells
Helper cells
T-8 (CD8) cells
No antibody circulating in order to work

Natural Killer cells
Nonspecific- innate

152
Q

systemic manifestations of inflammation

A

Fever: cytokines released from neutrophils & macrophages that are pyrogens (fever causing)
Leukocytosis- increase in circulating WBCs
Lab changes- acute phase reactants (plasma proteins produced by liver, increased during inflammation)
Erythrocyte sedimentation rate- ESR = inc. sed = inc. inf
C-reactive protein

153
Q

3 phases of inflammation

A

inflammation, proliferation, remodeling and maturation

154
Q

inflammation

A

(Fill)
Coagulation/hemostasis
Bring cells that are needed to area
Fibrin mesh of blood clot = scaffold for healing
Degranulating platelets = growth factors
Macrophages = clear debris (can’t heal while old stuff there)

155
Q

proliferation

A

Begins 3-4 days after injury
Continues for up to 2 weeks
Wound is sealed, fibrin clot replace scaffold by normal or scar tissue
Granulation tissue - new lymphatic vessels & new capillaries
Contraction begins

156
Q

remodeling and maturation

A 
Begins several weeks after injury
Normally complete within 2 years
Fibroblast- deposit collagen
Tissue continues to regenerate
Wound continues to contract
157
Q

dysfunctional wound healing

A

Ischemia
Obesity- impaired leukocyte function, predisposition to infection
Diabetes- impaired circulation, increased risk for infection
Infection
Malnutrition- risk for infection, delayed healing, reduced tensile strength
Medications- delay healing, prevent macrophages from migrating inhibit fibroblasts

158
Q

goals of immunization

A

Short term: prevention in specific individual; population

Long term: disease eradication & eradicate in US (polio, smallpox, diphtheria)

159
Q

toxoid

A

Weakened bacterial toxin

160
Q

vaccine

A 
Killed vaccine (whole, killed microbe)
Attenuated, live vaccine (risk to immunocompromised)
Cell parts (mount response to part of cell)
161
Q

active immunity

A 
Via natural disease or vaccine
Biological response
Antibodies & Memory B cells
Cytotoxic & Memory T cells
Several weeks to full response
Boosters
162
Q

passive immunity

A 
Administration of antibody
Immediate protection
Duration: few weeks or months
Examples
Breastfeeding
Immunoglobulin administration (Hep B, Tetanus, Rabies)
163
Q

herd immunity

A

Non-immunized individual protected
High vaccination rates protect unvaccinated
If only some get vaccinated- illness spreads

164
Q

childhood immunization concerns

A 
Minor illness or local reaction
No OTC analgesics (dec immune response)
Febrile seizures
Autoimmune disease
Autism 
Thimerosal 
Aluminum as an adjuvant
165
Q

true contraindication

A

Anaphylactic reactions to specific vaccine: should not get further doses of THAT vaccine
Anaphylactic reaction to a vaccine component: should not get further vaccines with THAT component
Moderate or severe illnesses with or without a fever

166
Q

not contraindication

A

Mild to moderate local reaction following a dose
Mild acute illness w/ or w/o low grade fever
Diarrhea
Current antimicrobial therapy
Convalescent phase of illnesses
Prematurity
Recent exposure to an infectious disease
Personal or family history of penicillin allergy or nonspecific allergies

167
Q

regulation & logistics of immunizations

A

National Childhood Vaccine Injury Act- 1986
Details vaccine, vaccine information sheets

Reporting of Adverse Effects
VAERS VAE Reporting System

Storage & Handling
Storage, Reconstitution, Expiration Dates

Who can administer

168
Q

vaccine information sheets

A 
Requirement of National Childhood Vaccine Injury act
Sheets must be given to all vaccines
Produced by the CDC
Benefits and risk
Given before each dose
Available in >30 languages
169
Q

nocieptive pain

A

type of sensory nerve receptors that respond to pain (different receptors for different things)

170
Q

afferent pathways

A

sensory - PNS → Dorsal horn & spinal cord → CNS

171
Q

interpretive center

A

brainstem, midbrain, diencephalon, cerebral cortex

Location, ,characteristics, emotional response, meaning

172
Q

efferent pathways

A

motivation - CNS → dorsal horn → motor area

173
Q

4 stages of nociception

A

transduction, transmission, perception, modulation

174
Q

transduction

A

Tissue Damage from exposure>
Release of that area of Chemical Mediators > Histamine, bradykinin, prostaglandin → inflammation >
Nociceptors receptors excited- A delta, C fibers

175
Q

transmission

A

Impulses conducted centrally into the dorsal horn of spinal cord
Continue carrying impulse to CNS
Transmitting different types of sensations
Primary sensory fibers involved:
A delta fibers- medium sized, thinly myelinated (travels fast); well localized, reflex control; neurotransmitter: Glutamate
C fibers: unmyelinated, slow transmission; slow, dull, achy, burning pain; neurotransmitter substance P

176
Q

perception

A

Conscious awareness of pain
Sensory- presence, location, characteristics, intensity
Affective- emotional response
Cognitive- learning
Influenced by
Pain threshold: level of painful stimuli required to be perceived as pain- similar among people
Pain tolerance: degree of pain one is willing to bear before seeking relief

177
Q

modulation

A 
(change or inhibition of transmission of pain)
Occurs at multiple sites along the pain pathway
Excitatory neuromodulators(makes pain worse) or
Inhibitory neuromodulators (tone down pain
178
Q

excitatory neuromodulators

A

(makes pain worse)

Substance P, histamine, glutamate

179
Q

inhibitory neuromodulators

A

(tone down pain)

GABA, serotonin, norepinephrine, endogenous opioids

180
Q

physiologic pain

A

tissue injury

Acute, Ischemic, Referred

181
Q

chronic pain

A

long term changes within CNS/PNS; pain without purpose

Chronic, Neuropathic

182
Q

Acute

A 
Sympathetic Nervous System
Resolves when injury heals ~3 months
Signs & Symptoms:
Increased HR, BP, RR
Dilated pupils
Pallor and perspiration
Nausea and vomiting
Urine retention
Physiologic response
Blood shunts from superficial vessels to muscles, heart, lungs, and brain
Bronchioles dilate
Decreased gastric secretions, GI motility 
Increased blood glucose
Hypomotility of bladder and ureters
Therapy
Short term
Opioid & nonopioid 
Safe  short term, if better managed- no chronic
183
Q

Chronic

A

Longer then expected healing time; ~6mo<
Results from:
Peripheral sensitization: reduction pain threshold
Central sensitization: increased responsiveness & sensitivity
Clinical manifestations: some acute, usually psychosocial (irritability, depression)
Treatment: multimodal, pain clinic
Examples: Fibromyalgia

184
Q

Neuropathic

A

Results from injury to nerves themselves (chemo,surgery, radiation, trauma, diabetic hemopathy)
Clinical manifestations: constant ache wither intermittent sharp pain
Treatment: difficult to manage, doesn’t respond well to opioids/pharmacology; antidepressants/anticonvulsants do work well

185
Q

Ischemic

A

Results from no blood flow to tissue; inflammatory process → release chemicals
Clinical manifestations depends on the site (aching, burning, tingling)
Treatment: improve blood supply (nitroglycerin - powerful vasodilator, could increase BP, headache)

186
Q

Referred pain

A

Interrupting peripheral transmission of noception

Modulating pain transmission at the spinal cord level

Pain perceived in area other than injury
Consider signs and symptoms different between m/f

187
Q

Treatment Modalities

A

Altering the perception and integration of nociceptive impulses in the brain

188
Q

Altering the perception and integration of nociceptive impulses in the brain

A

Non-pharmacologic: distraction, imagery, hypnosis, biofeedback
Pharmacologic: opioids
Take home messages
As a nurse, working with a patient and their pain management needs to be both pharmacologic & non
You can do peripheral and spinal cord/brain and have multiple combinations for the most effective pain relief

189
Q

Modulating pain transmission at the spinal cord level

A

Non-pharmacologic: cutaneous stimuli (massage, therapeutic touch, nerve stimulation, acupuncture, heat & cold)
Best way for a nurse to help modulate pain at spinal cord level: therapeutic touch, massage, etc.
Pharmacologic: epidurals, intrathecal anesthesia

190
Q

Interrupting peripheral perception of nocicpetion

A

Non-pharmacologic (ice, heat vs cold, stabilize, splint, minimize use)
Pharmacologic (both should happen)
NSAIDS - inhibit prostaglandin production
Local anesthetics - block sodium channel (stop conduction of impulses)

191
Q

Oxycodone

A

Therapeutic uses = relief of pain
MOA: mimic action of endogenous opioid peptides primarily at mu receptor
Drug interactions: CNS depressants, anticholinergic drugs, hypotensive drugs
AE: respiratory depression, constipation, orthostatic hypotension, urinary retention, sedation, euphoria, cough suppression, biliary colic, emesis

192
Q

Morphine

A

Prototypical opioid analgesic
Therapeutic uses = relief of pain
MOA: mimic action of endogenous opioid peptides primarily at mu receptor
Drug interactions: CNS depressants, anticholinergic drugs, hypotensive drugs
Blocks muscarinic receptor = dry
AE: respiratory depression, constipation, orthostatic hypotension, urinary retention, sedation, euphoria, cough suppression, biliary colic, emesis

193
Q

Ibuprofen

A

Ibuprofen
MOA: inhibit Cox 1 and 2 enzymes
Therapeutic uses: analgesia, inflammation, antipyretic
Generally well tolerated
Upper GI complaints
Bleeding, ulcer formation and perforation, bowel obstruction
Use of >4 weeks increases risk of ulcer development
Renal injuries
Impairs renal blood flow
Can be a problem when in combination with exhaustive exercise
Can be problematic in the elderly
Acute liver injury
Unusual event
<5/100,000 cases per year)
More likely to occur in conjunction with hepatotoxic agents
General edema or swelling
Heart failure
Elderly with heart failure at risk
Can accelerate symptoms of the disease

194
Q

Acetaminophen

A

Don’t take more than 4 grams in 24 hours
Worry about potential for liver toxicity
Don’t take if consume alcohol
Be conscious of combination prescription and OTC medications
Combination products (cough and cold, headache products, sleep aids, prescription pain relievers)

195
Q

Opioid analgesics

A

Act on Opioid receptors Mu, Kappa, Delta
Mu: analgesia, sedation, decreased GI motility, AND respiratory depression, euphoria, physical dependence
Kappa: analgesia, sedation, decreased GI motility
Delta: learning more about this receptor, may be a novel target for pain and depression treatments

196
Q

Pure Opioid Agonists

A

(turns on receptors)
Mu: Agonist
Kappa: Agonist
Norpine, oxycodone, hydrocodone, fentanyl, etc

197
Q

Agonist-Antagonist Opioids

A

Mu: Antagonist & Kappa: Agonist
Pentazocine, malbuphine, butorphanol
Mu: Partial agonist (little Mu) & Kappa: Antagonist
Buprenorphine

198
Q

Pure Opioid Antagonists

A

Mu: antagonist
Kappa: antagonist
Naloxone, naltrexone
Reverses effects of opioids*

199
Q

How does acetominaphen work

A

Selective COX inhibition in the CNS - reduces fever and pain (not inflammation)
Metabolized in the liver (knocks it out)
CYP450 - drug interactions
NAPQI toxic metabolite becomes inactive by glutathione
Give glutathione in overdose situation
Do not exceed 4 grams in 24 hours
Pain relief similar to NSAID but no anti-inflammatory activity
Know if patient has multiple drugs with acetaminophen

200
Q

2nd generation NSAID

A

Celecoxib (Celebrex)
MOA: Cox 2 Inhibitors
Advantages: Less GI toxicity
Disadvantages: Expensive, Increased cardiovascular risks

201
Q

1st generation NSAID

A

Ibuprofen
MOA: inhibit Cox 1 and 2 enzymes
Therapeutic uses: analgesia, inflammation, antipyretic

202
Q

NSAID

A

Non-Steroidal Anti Inflammatory Drug

Indirect simulation of nociceptors (Cyclooxygenase pathways - COX 1 & 2)
Cox 1: protective prostaglandins (stomach mucosa, platelet stickiness)
Found in most tissues
Responsible for synthesizing the prostaglandins that maintain gastric mucosa and renal function
Cox 2: Inflammatory prostaglandins (pain, fever, inflammation)
Normally not present in healthy cells
Produced by presence of inflammation
NSAIDS will work by inhibiting Cox 1 & Cox 2

203
Q

Common AE with OTC analgesics

A

Analgesic: drug to reduce pain by acting in the CNS or on peripheral pain mechanisms; Generally well tolerated

Upper GI complaints
Bleeding, ulcer formation and perforation, bowel obstruction
Use of >4 weeks increases risk of ulcer development

Renal injuries
Impairs renal blood flow
Can be a problem when in combination with exhaustive exercise
Can be problematic in the elderly

Acute liver injury
Unusual event
<5/100,000 cases per year)
More likely to occur in conjunction with hepatotoxic agents

General edema or swelling

Heart failure
Elderly with heart failure at risk
Can accelerate symptoms of the disease

If someone was taking this for several weeks, we would worry about ulcer, we would ask about stomach pain, blood in stool, etc.

Sprinig 2018 (6 decks)

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