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NUR 325 Intro Pathophysio > WK 1: Infection/Immunity/Cellular Adaptation/Into to PathoPharm > Flashcards

WK 1: Infection/Immunity/Cellular Adaptation/Into to PathoPharm Flashcards

1
Q

Pharmacology

A

study of the biologic effects of drugs that are introduced into the body to cause some sort of change

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2
Q

Pharmacokinetic

A

what happens to drugs within the body

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3
Q

pharmacodynamics

A

-MOA
-what do drugs do in the body/how they work

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4
Q

Generic name of a drug

A

-the official name
-can only have ONE generic name
-usually more complicated name
-lowercase
for the tests, must know generic names
EX: generic name: acetaminophen

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5
Q

Chemical name of a drug

A

-long and complex
-used within research
EX: N-acetyl-para-aminophenol is the chemical name for Tylenol

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6
Q

Trade name of a drug

A

-brand name
-easier to remember
-uppercase
EX: Tylenol

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7
Q

What is a prototype of a drug

A

-typically the first drug that represents a group/class of medication

EX: Tylenol was the prototype for acetaminophen

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8
Q

Therapeutic effects of drugs

A

-intended effects of drug
-what we want to happen

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9
Q

Side Effects of drugs

A

-unintended effects
-unavoidable
EX: getting an upset stomach when taking Tylenol

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10
Q

Toxicities of drugs

A

harmful effects

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11
Q

Adverse Effects of drugs

A

-unexpected reaction
-dangerous reaction

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12
Q

Allergic reaction of a drug

A

-unexpected
-potential to be dangerous
-involves immune system response

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13
Q

What do you need to know with each medication?

A
  • generic name
    -drug classification
    -MOA
    -indications
    -common/serious adverse effects
    -nursing indications
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14
Q

What is a nursing indication?

A

-thinking about what the nurse needs to consider/ worry about with a certain medication.
-what needs to be assessed prior to giving med?
-any SERIOUS interactions?
-CYP drug?
-any condraindications?

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15
Q

What cooperation approves the use of new drugs?

A

FDA (food and drug administration)

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16
Q

phases of drug approval through the FDA

A
  1. Preclinical trials (animal testing)
  2. Phase I (human volunteers)
  3. Phase II (patients w/ intended Dz)
  4. Phase III (Vast clinical market)
  5. Phase IV (continued evaluation by FDA)
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17
Q

Schedule 1 controlled substance

A

NOT approve for medical use
EX: heroin, LSD

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18
Q

Schedule 2 controlled substance

A

used medically but HIGH POTENTIAL for abuse
-no Rx refills allowed
EX: narcotics, amphetamines

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19
Q

Schedule 3 controlled substance

A

have less potential for abuse
EX: non barbiturate sedatives, non-amphetamines, stimulants; i.e. lortab, vicodin

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20
Q

Schedule 4 controlled substance

A

Some potential for abuse
EX: primarily sedatives, anti-anxiety medications; i.e Xanax, valium, Ambien

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21
Q

Schedule 5 controlled substance

A

Low potential for abuse
medications with small amounts of certain narcotics or stimulants
Ex: cough suppressants with some codeine, ephedrine containing medications

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22
Q

Over the Counter Medications (OTC)

A

-consumers must be able to diagnose own condition and monitor effectiveness easily
-low risk side effects
-low abuse potential

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23
Q

Dietary and herbal Supplements can only claim affect on what?

A

body structure or function
NOT medical conditions

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24
Q

Why is it important to get a full health history in regards to medications and daily herbal intake?

A

Some herbals can increase the toxicity of prescription medications OR cause decreased therapeutic effects

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25
Q

What is a teratogen?

A

a substance that causes congenital malformations in developing fetuses

Ex: alcohol, weed, nicotine

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26
Q

Categories of Teratogens

A

A: safe for fetus
B: lack of studies to show benefit/ risk
C: No studies, talk to OB
D: possible risk to fetus, talk to OB
X: known risk that cannot be outweighed

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27
Q

What are some examples of category X tetragens?

A

-thalidomide
-chemotherapy agents
-Isotretinoin / Retin A (acne treatment)

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28
Q

Pharmacogenomics

A

study of how genes affect a persons response to drugs

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29
Q

Pathophysiology

A

study of disease and injury

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30
Q

Disease

A

disruption in homeostasis
-Physical: injury, HF
-Mental: depression, anxiety
-Social: Autism

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31
Q

Causes of Disease: intrinsic condition

A

genes
immunity
age
gener

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32
Q

Causes of Disease: extrinsic condition

A

bacteria
viruses
injury
behaviors
stressors
fungi

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33
Q

Process of Disease

A
  1. Identification: Signs (objective) and symptoms (subjective)
  2. Occurrence: How often, when?
  3. Diagnosis: identification
  4. Etiology: cause
  5. Prognosis: Likelihood of recovery
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34
Q

Stages of Disease

A
  1. Exposure: where did they get sick?
  2. Onset: sudden/insidious/latent/prodromal/manifestations
  3. Remission
  4. Convalescence
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35
Q

Types of disease causes:
1. Idiopathic
2. Latrogenic
3. Exacerbation

A
  1. unknown cause. Think “idiot”
  2. caused by some treatment they received/medical reason. think “lateral”
  3. worsening of a disease, acute decline of chronic disease
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36
Q

Hypo-

A

below, less than normal
Ex: hypokalemia = low potassium

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37
Q

Hyper-

A

above normal, excess
Ex: hyperkalemia = high potassium

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38
Q

-penia

A

decrease, deficiency
Ex: neutropenia: low white blood cells

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39
Q

-cytosis

A

referring to cells
Ex: phagocytosis= ingesting of old cells

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40
Q

-osis

A

-a condition, status, or process
-production or increase
-invasion or infection

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41
Q

-itis

A

disease or inflammation

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42
Q

-pathy

A

disease or suffering

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43
Q

Three Phases of Drug Action

A
  1. pharmaceutic phase
  2. pharmacokinetic phase
  3. Pharmacodynamic phase
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44
Q

Phase 1 of drug action: pharmaceutic phase

A

Dissolution phase, all oral drugs must go through dissolution in order to be absorbed

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45
Q

Phase 2 of drug action: pharmacokinetic phase

A

-what the body does to the drug
-has four processes:
1) absorption: through small intestines into blood
2) distribution: drug leaving blood, passing through cell membrane to site of action
3) metabolism/biotransformation: liver metabolizes drug
4) excretion: kidney excretion

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46
Q

Drugs crossing the cell membrane

A

-drugs must be lipid soluble to pass the phospholipid bilayer
-water soluble drugs require passage through channels or pores

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47
Q

First Pass Effect and Bioavailability

A

-percentage of drug broken down in liver
-bioavailability is the amount of drug left after first pass
-bioavailability of PO meds vary, bioavailability of IV meds are 100%

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48
Q

What are the three routes of absorption?

A
  1. Enteral: GI tract (EC/PO/SL/buccal/rectal)

2.Parenteral:
(SQ, IM, IV, Intrathecal, epidural)

  1. Topical/ Transdermal (eyes/ears/skin/nose/lungs)
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49
Q

why cant you give a patient a PO drug rectally?

A

they have a different bioavailability

50
Q

Where do enteric coated medications break down?

A

the small intestine

51
Q

Where do PO medications break down?

A

the stomach

52
Q

what are some disruptions in medication distribution?

A

-decreased blood flow
-PVD
-abscesses
-tumors

53
Q

What is the blood brain barrier (BBB)?

A

cells in capillary wall of brain with very tight junctions that prevent drug passage through

54
Q

what kind of drugs can cross the blood brain barrier?

What else can cross the BBB?

A

-drugs that have a transport system
-drugs that are lipid-soluble

-alcohol
-glucose
think of how they affect mental state

55
Q

what is the major organ/site for drug metabolism?

A

the liver

56
Q

what is the major site for excretion?

A

kidney

57
Q

kidney disease or dysfunction can cause decreased drug excretion, what does this lead to?

A

the drug can build up and cause toxicity

58
Q

serum half-life (T 1/2)

A

time required for the serum concentration of a drug to decrease by 50%

-this dictates how often a drug is given and how far apart the dosing is

59
Q

what is a “steady state”

A

when intake of a drug is equal to the amount of drug metabolized and excreted

-goal of elimination is having a steady state

60
Q

onset of a medication

A

time it takes for drug to elicit therapeutic response

61
Q

peak of a medication

A

time it takes for drug to reach its maximum therapeutic effect

62
Q

duration of medication

A

time drug concentration is sufficient to elicit a therapeutic response

63
Q

receptors

A

proteins that are located on cell surfaces

64
Q

Agonist vs. Antagonist

A

Agonist: stimulates / activates

Antagonist: inhibits / blocks
(produces action by preventing other natural substances from binding)

65
Q

Therapeutic Index

A

the measure of relative safety of drugs

66
Q

Black Box Warning

A

required by the FDA for dangerous drugs

-strongest safety warning a drug can have while still being on the market

67
Q

What are some high alert drugs?

A

Insulin
Heparin
Opioids
Injectable potassium chloride ( IV KCL)
Neuromuscular blocking agents
chemotherapy drugs

68
Q

how can the nurse minimize drug interactions?

A

-minimize # of drugs patient receives
-thorough drug history
-vigilant monitoring of patients taking drugs with a narrow therapeutic index

69
Q

Drug interactions that increase therapeutic effects

A
  1. Additive effects: 2 drugs w/ similar MOA
  2. synergism/potentiation: 2 drugs w/ different MOA but combined effect
  3. activation: decreases metabolism rate of drug
  4. displacement: displacement of one drug by second drug increases effect of displaced drug
70
Q

Antidote

A

drug given to ANTAGONIZE the toxic effects of another drug

71
Q

Older adults and pharmacokinetic consequences

A

-Hepatic Changes: drugs metabolize slower
-GI Changes: decreased absorption of oral drugs
-Cardiac/ Circulatory
-Renal Changes: drugs excreted less completely

72
Q

Inflammation

A

-d/t cell injury
-protective mechanism
“-itis”
-Acute (<2wks) vs. chronic

73
Q

Localized signs of inflammation

A

redness, swelling, heat, pain, loss of function

74
Q

Two causes of inflammation

A
  1. Exogenous: external -> surgery, burns
  2. Endogenous: Internally -> tissue ischemia
75
Q

chemotaxis

A

process by which neutrophils are attracted to inflamed tissue

76
Q

types of inflammatory exudates

A
  1. Serous: water, mild inflammation
  2. Serosanguineous: pink tinged
  3. Purulent: severe inflammation w/ bacterial infection
  4. Hemorrhagic: lots of RBC, most severe
77
Q

systemic manifestations of Cytokines IL-1, IL-6, and TNFa

*cytokines are responsible for systematic responses to inflammation

A

fever
increased neutrophils
lethargy
muscle catabolism

78
Q

B-cells

A

-Humoral immunity
-two kinds: Memory cells and plasma cells

79
Q

T-cells

A

-Cell-mediated (recognize antigens on surface of cells)
-part of adaptive defense mechanism

80
Q

What are the five classes of antibodies?

A
  1. IgG: most common. protect against bacterial/viral infections
  2. IgM: for cytotoxic functions
  3. IgA: Secretory functions (saliva, tears, etc..)
  4. IgD: “B-cell helpers”
  5. IgE: against allergic reactions/parasites
81
Q

Passive Immunity

A

-think breastfeeding
-transfer of plasma containing antibodies from immunized person to non-immunized person

82
Q

Active Immunity

A

-vaccines

83
Q

Types of vaccinations

A
  1. Traditional: inactive or killed organisms (flu shot)
  2. Attenuated: weakened but still live vax. (flu vax nasally) CANNOT give to people with weakn immune systems/underlying conditions
  3. Toxoids: inactive toxins (tetanus)
  4. Conjugate: H. Influenzae type B
  5. mRNA: newest
84
Q

What is an infection?

A

colonization of a host by a microbial species

-can be localized or systemic

85
Q

Virus caused infection

A

-cannot multiple without a host cell
-common
-DNA/RNA with protein shell

86
Q

Bacteria caused infection

A

-single celled
-can reproduce inside or outside cells
-common

87
Q

Fungal infection

A

-spore forming organism
-rare
Ex: yeast infection

88
Q

Protozoa infection

A

-rare
-live in water
Ex: maleria

89
Q

Helminths infection

A

-rare
-parasitic worms

90
Q

Prions infection

A

-rarest
-only composed on proteins

91
Q

Direct vs. Indirect transmission of infection

A

Direct: kissing, sex, direct contact from soil

Indirect: airborne, vehicle or vector borne

92
Q

Vector vs. Vehicle borne transmission

A

Vector: something else is carrying the Dz. Ex: mosquitos ad ticks

Vehicle: carried by water, blood, food
Ex: Hepatits ??

93
Q

Different portals of entry for organisms

A

1.Oropharynx and nasopharynx (airways, lungs, stomach, GI tract)
2. GU tract (UTI)
3. Skin (biggest vulnerability)
4. Translocation (movement of bacteria across intestinal lining)
5. Blood (needle-stick)
6.MAternal-Fetal Transmission

94
Q

Stages of Infection

A
  1. Incubation Period
    (organism entering body/multiplying)
  2. Prodromal Stage
    (pre-symptoms/not feeling well)
  3. Acute Stage
    (Full blown symptoms)
  4. Convalescent Stage
    (Dz getting better, feeling better)

5.Resolution Phase
(pathogen eliminated. Some never reach this phase, like chickenpox, why?)

95
Q

The Infectious Process Steps

A
  1. injury
  2. increased permeability
  3. immigration of leukocytes
    4.phagocytosis
  4. exudate
  5. systemic symptoms
96
Q

The Infectious Process: Injury

A

-initial insult to area occurs
-short period of vasoconstriction(why?)
-prolonged period of vasodilation (why?)

97
Q

The Infectious Process: Increased permeability

A

-fluid pulled into vascular space
-fluid moves out of vessel to the place of injury

98
Q

The Infectious Process: Immigration of Leukocytes

A

-neutrophils attracted to area of injury

99
Q

The Infectious Process: phagocytosis

A

WBC’s recognize, engulf, and destroy invading organisms

100
Q

The Infectious Process: Exudate

A

purpose of exudates are to transport the leukocytes to injured area, dilute toxins and transport nutrients for healing process

101
Q

The Infectious Process: systemic symptoms

A

-can occur if infectious process does not stay localized
-stimulates hypothalamic fever set point

102
Q

Colonization vs. Infection

A

-if an infection sticks around longer than a systemic infection it can turn into a colonization

-colonization: in a specific body site, no S/Sx present. Ex: staph Infection

-Infection: clinical S/Sx of illness/inflammation present, colonization can develop into infection

103
Q

Nosocomial

A

Infections that occur within a healthcare facility

104
Q

Drug resistant infections

A

-MRSA: METHICILLIN resistant staph aureus
-CRE: CARBAPENEM (class of Abx) resistant enterobacteriaceae
-MDRO: MULTI-DRUG resistant organism

105
Q

what is a superinfection?

A

an new infection that occurs during treatment for a different infection

-Abx killing normal/helpful flora, then drug resistant pathogens cause superinfection

Ex: C-Diff

106
Q

Cellular adaption

A

changes in the cells to permit survival & maintenance of cellular function

-cells can change size/form

107
Q

Abnormal cellular changes can occur due to…?

A

radiation, medication, lack of oxygen

108
Q

Atrophy of cells

A

-shrinking of cell size
-all atrophic cells have decreased function
-Physiologic: d/t developmental issue
-Pathologic: d/t environmental conditions

109
Q

Hypertrophy of cells

A

-increased size of cell
-can increase function
-can also occur with Dz processes/negative effect

110
Q

Hyperplasia of cells

A

-increase in # of cells d/t increased cellular devision usually in response to injury

-hyperplasia usually turns into dysplasia

111
Q

Normal hyperplasia examples versus abnormal

A

Normal: pregnancy related changes, wound healing

Abnormal: BPH, thyroid hyperplasia, endometrial hyperplasia

112
Q

Dysplasia cells

A

abnormal changes in size/shape/organization of mature cells.can be reversible

-can be precursor to cancer, BUT does not indicate cancer.

113
Q

Metaplasia cells

A

-most associated with cancer
-allows cells to survive better in hostile environment, IS reversible

114
Q

Neoplasm

A

irregular growth b/c of gene mutation

115
Q

Anaplasia

A

cancer cells

-neoplasia and anaplasia used interchangeably

116
Q

Cancer

A

uncontrolled cellular growth with rapid uncontrolled proliferation and loss of ability of cells to differentiation

117
Q

Neoplasms: Benign vs. Malignant

A

Benign: more mature, stay in one spot, usually do not cause issues, usually encapsulated

Malignant: not mature cells, often metastasize, no capsule

118
Q

Necrosis

A

cellular injury that can lead to cellular death d/t Dz, injury, or failure of blood supply.
-irreversible, can lead to gangrene

119
Q

Liquefactive necrosis

A

in tissues with lots of lipids.
release of proteolytic enzymes

120
Q

Dry Gangrene

A

-blackened/dry/wrinkled
-spreads slow
-has demarkation line

121
Q

Wet Gangrene

A

-foul smell, can be systemic, liquefaction
-extensive bacterial infection
-cold, pulseless, swollen
-NO line of demarkation

122
Q

Gas Gangrene

A

-anaerobic, spore forming
-destroys connective tissue
-gaseous bubbles
-w/ severe trauma / compound fractures

NUR 325 Intro Pathophysio (7 decks)

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