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Pathopharmacology Intro > Module 1 > Flashcards

Module 1 Flashcards

1
Q

Define pharmacology.

A

The study of biological effects of drugs that are introduced into the body to cause some sort of change.

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2
Q

Define pharmacokinetics.

A

What happens to the drugs in the body.

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3
Q

Define therapeutic effect.

A

The intended effects of the drug (what we want to happen.

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4
Q

What are side effects?

A

Unintended, sometimes unavoidable effects of a medication.

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5
Q

What kind of effects do toxicities have?

A

Harmful.

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6
Q

What type of response does an allergic reaction stimulate?

A

Immune response.

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7
Q

What name of medications is all lowercase? Which has an uppercase?

A

Lowercase = generic names, uppercase = trade names.

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8
Q

What is a prototype drug? What is typically done with those?

A

Typically the first drug that represents a group or class of medications. They are used for comparison when other manufactures like Walgreens or Kroger make the drug.

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9
Q

List and define each of the components YOU are responsible for knowing about medications for this class.

A

Names (trade and generic)
Classification
Mechanism of action (how the drugs work)
Indication (why they are being used, what do they treat)
Common and serious adverse events
Contraindications
Nursing indications (assessments to complete, serious interactions, what do i need to monitor with this)

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10
Q

How are new drugs approved?

A

Through strict scientific tests, approved by FDA.

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11
Q

What happens in preclinical trials?

A

Tested on lab animals for therapeutic and adverse events.

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12
Q

What happens in phase 1 clinical trials?

A

Healthy human volunteers are used to test the drugs.

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13
Q

What happens in phase 2 clinical trials?

A

Drug is tried on patients who have the disease the drug is designed to treat.

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14
Q

What happens in phase 3 clinical trials?

A

Drug is used in clinical market.
Prescribers informed of adverse effects and instructed to monitor patients.
Still can have new adverse events and be taken off market

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15
Q

What happens in phase 4 clinical trials?

A

Continued evaluation from FDA.

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16
Q

Define schedule 1 drugs.

A

Not approved for any medical use, no reason to prescribe.

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17
Q

Give two examples of a schedule 1 drug.

A

Heroin, LSD.

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18
Q

Define schedule 2 drugs.

A

Used medically but HIGH potential for abuse.

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19
Q

Give two examples of types of drugs that are schedule 2.

A

Narcotics and amphetamines.

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20
Q

Define schedule 3 drugs.

A

Have less potential for abuse than schedule 2.

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21
Q

Give two specific examples of schedule 3 drugs.

A

Lortab and vicodin.

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22
Q

Can schedule 2 drugs be have prescribed refills?

A

No.

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23
Q

Define schedule 4 drugs.

A

Have some potential for abuse.

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24
Q

What are two types of drugs that are classified as a schedule 4 drug.

A

Anti-anxiety and sedatives. (Xanax, Valium, Ambien)

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25
Q

Define schedule 5 drugs.

A

Low potential for abuse.

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26
Q

What is an example of a schedule 5 drug.

A

Cough syrup that has codeine in it.

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27
Q

Why are some OTC medications behind the counter?

A

Have increased risk of being abused (like sudafed).

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28
Q

Dietary and herbal supplements can only claim what?

A

Affect on body structure or function. Cannot “treat” a medical diagnosis, disease, or condition.

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29
Q

How can herbal supplements interact with drugs?

A

Some herbal supplements can increase the toxicity of prescription medication.
Some can cause decreased therapeutic effects.

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30
Q

Define teratogen.

A

Substances that can cause congenital malformations in developing fetus.

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31
Q

What is a category A teratogen?

A

Safe for fetus.

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32
Q

What is a category B teratogen?

A

Lack of studies to show benefits and risks.

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33
Q

What is a category C teratogen?

A

No studies in humans. Animal studies show possible risk. Patients should consult OB.

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34
Q

What is a category D teratogen?

A

Drugs that have a possible risk to the fetus. Patients should consult with OB about risks and benefits.

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35
Q

What is a category X teratogen?

A

Drugs that have a known risk that cannot be outweighed by possible benefits.

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36
Q

Define pathophysiology.

A

Study of disease and injury.

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37
Q

Define pathology.

A

Lab study of cells and tissues.

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38
Q

What are the two causes of diseases?

A

Intrinsic and extrinsic factors.

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39
Q

Define intrinsic factors that cause disease. Give examples.

A

Something that is going wrong inside the body.
EX: genes, age, immunity, age, gender.

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40
Q

Define extrinsic factors that cause disease. Give examples.

A

Something that has gotten you sick from the outside.
EX: bacteria, viruses, injury, behaviors, stressors, fungi.

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41
Q

What does etiology mean?

A

The cause of disease.

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42
Q

What are the 4 stages of disease?

A
  1. Exposure
  2. Onset
  3. Remission
  4. Convalescence
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43
Q

What are the types of onset for a disease?

A

Sudden, insidious (slow and gradual), latent, prodromal (onset symptoms before sickness), and manifestation.

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44
Q

What is convalescence?

A

Recovering from a disease.

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45
Q

Idiopathic vs. Iatrogenic diseases.

A

Idiopathic: We don’t know what caused it, although we may have some theories and ideas,
Iatrogenic: Caused by some type of medical treatment.

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46
Q

What is exacerbation?

A

Worsening or acute decline in a person’s condition or disease.

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47
Q

Hypo-

A

Under, below.

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48
Q

Hyper-

A

Above, over.

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49
Q

-penia

A

Lack of, deficiency.

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50
Q

-cytosis

A

Refers to cells, increase.

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51
Q

osis-

A

Process/condition, production/increase, infection.

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52
Q

-itis

A

Inflammaton.

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53
Q

-pathy

A

Disease or suffering.

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54
Q

Signs of localized inflammation:

A

Redness, swelling, heat, pain, loss of function.

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55
Q

What is the purpose of inflammation?

A

Acts as a protective mechanism to begin the healing process. Includes destroying invading/harmful agents, limits the spread of harmful agents, and prepares damaged tissue for repair.

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56
Q

Exogenous vs. Endogenous examples of causes of inflammation:

A

Exogenous: Falls, burns, surgery, trauma.
Endogenous: Tissue ischemia, internal damage.

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57
Q

Acute vs. Chronic inflammation:

A

Acute: Lasts less than two weeks.
Chronic: Extends over longer periods (can cause scar tissue)

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58
Q

What is chemotaxis?

A

Process by which neutrophils are attracted to inflamed tissue.

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59
Q

What is exudate?

A

Fluid that leaks out of blood vessels, neutrophils, and debris.

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60
Q

What is serous exudate?

A

Watery, low protein, mild inflammation.

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61
Q

What is serosanguineous exudate?

A

Pink-tinged fluid, small amount of RBC.

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62
Q

What is purulent exudate?

A

Severe inflammation with bacterial infection, neutrophils, protein, and debris.

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63
Q

What is hemorrhagic exudate?

A

Lots of RBC, most severe inflammation.

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64
Q

What do cytokines cause in the inflammatory response?

A

Fever, increased neutrophils, lethargy, muscle breakdown.

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65
Q

What is the major histocompatibility complex (MHC)?

A

Cluster of genes of chromosome 6 that are proteins on all cell surfaces that label cells as part of the self as opposed to an invader.

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66
Q

What are the two types of cells involved in adaptive immunity?

A

B and T cells.

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67
Q

What are the 2 types of B cells?

A

Memory B cells and plasma B cells.

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68
Q

What do memory B cells do?

A

Remember exposure to specific antigens (“name tags”).

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69
Q

What do plasma B cells do?

A

Secrete antibodies that are then circulated in the blood and bind to the antigen that triggered production.

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70
Q

What does IgG do?

A

Protect against bacterial and viral infections by remembering previous infections or vaccinations.

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71
Q

What is the most common type of immunoglobulin?

A

IgG.

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72
Q

What does IgM do?

A

Acts as the signaler for cytotoxic functions. This is the first to be produced after exposure or immunization.

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73
Q

What does IgA do? Where can this be found?

A

Protects against infection. Saliva, tears, secretions, GI/GU tract, breast milk.

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74
Q

What does IgD do?

A

Stimulates B cells to multiply and differentiate.

75
Q

What does IgE do?

A

Plays a role in immunity against parasites and allergic reactions.

76
Q

What is passive immunity?

A

Transfer of plasma antibodies from an immunized person to a non-immunized person.

77
Q

What are two examples of passive immunity?

A

Mother to fetus and injected antibodies.

78
Q

What is active immunity?

A

Protected state due to body’s response.

79
Q

What are two examples of when you would gain active immunity?

A

Immunizations and after an active infection.

80
Q

What is a traditional vaccine?

A

Inactivated or killed organism.

81
Q

What is an attenuated vaccine?

A

Weakened organism.

82
Q

Who cannot receive attenuated vaccines?

A

People who have weakened immune systems.

83
Q

What are the 3 phases of drug action?

A
  1. Pharmaceutic phase
  2. Pharmacokinetic phase
  3. Pharmacodynamic phase
84
Q

What happens in the pharmaceutic phase of drug action?

A

Drug begins to dissolve to be absorbed.

85
Q

In order to be absorbed, oral medications must be what?

A

Dissolved.

86
Q

What are the 4 processes of the pharmacokinetic phase of drug action.

A

Absorption, distribution, metabolism, and excretion.

87
Q

How can drugs make it through the phospholipid layer of cell membranes?

A

Must be lipid-soluble.

88
Q

How can water-soluble drugs get through the phospholipid layer?

A

Have to use channels or pores.

89
Q

What is the first-pass effect?

A

Metabolism of drug before systemic circulation.

90
Q

Where are drugs mainly metabolized?

A

The liver.

91
Q

What is bioavailability?

A

The amount of drug left after the first-pass.

92
Q

What is the bioavailability of IV medications? Why?

A

100%, because it by-passes the liver.

93
Q

Where are enteric coated medications broken down?

A

Intended to be broken down in the small intestines. The coating protects it from the stomach acid.

94
Q

What enteral route is not subject to first-pass effect? Why?

A

SL or buccal, because these are highly vascularized tissue areas and it bypasses the liver.

95
Q

What is included in the enteral route?

A

Anything that goes by way of the GI tract.

96
Q

What is included in the parenteral route?

A

IM, SQ, IV, epidural, and intrathecal.

97
Q

What is the fastest parenteral route? Is it subject to the first-pass effect? Why?

A

IV, it is not subject to first-pass effect because it goes straight into circulation.

98
Q

What areas are going to have the best distribution?

A

Areas that have high blood flow.

99
Q

What are some potential disruptions in distribution?

A

Decreased blood flow, PAD, abscesses, and tumors.

100
Q

Is binding to a protein reversible?

A

Yes.

101
Q

What is the goal of the protein-binding effect?

A

To maintain a steady state, maintaining a steady free drug concentration.

102
Q

Do bound drugs or unbound drugs exert effects?

A

Only unbound drugs “free” can exert effects.

103
Q

What is albumin?

A

Primary plasma protein that drugs bind to.

104
Q

What is the concern with hypoalbuminemia?

A

Not enough albumin to bind drugs to. There is the possibility of overdose or toxicity. There is more free drug available to exert effects.

105
Q

After a drug is metabolized what is the new structure called?

A

Metabolite.

106
Q

What does the liver do to metabolize drugs?

A

Converts lipid-soluble drugs into water-soluble metabolites to be excreted by kidneys. This is done through the use of cytochrome P-450 enzymes.

107
Q

What is a substrate?

A

If a drug uses CPY450 system for metabolism.

108
Q

What is a pro-drug?

A

Substance that uses CYP450 to convert into an active form.

109
Q

What is an inducer?

A

Speeds up metabolism of the CYP450, which reduces the amount of drug that is in the body and reduces therapeutic effect.

110
Q

What is an inhibitor?

A

Slows down the metabolism of CYP450 system, which increases the amount of drug in the body.

111
Q

What is the major site of excretion?

A

Kidneys.

112
Q

What is the concern with kidney disease or dysfunction?

A

Unable to excrete drug metabolite, which causes build up and causes toxicity.

113
Q

What is the best measure of kidney function?

A

Glomerular filtration rate.

114
Q

What is taken into account with GFR?

A

Creatinine level, age, body size, and gender.

115
Q

What is serum half life?

A

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

116
Q

How many half lives does it take to reach a steady-state?

A

4-5 half lives.

117
Q

Define onset.

A

Time it takes for drug to elicit therapeutic response.

118
Q

Define peak.

A

Time it takes for the drug to reach its max therapeutic response.

119
Q

Define duration.

A

Time drug concentration is sufficient to elicit a therapeutic response.

120
Q

What is the focus of the pharmacodynamic phase of drug action?

A

What the drug does to the body.

121
Q

What are receptors?

A

Proteins located on the cell surfaces.

122
Q

Agonists vs. antiagonists:

A

Agonist: a drug that has the ability to initiate a desired effect by binding to a receptor
Antagonist: A drug that produces its action by not stimulating receptors by preventing/blocking/inhibiting other natural substances from binding and causing an effect.

123
Q

When are black box warnings used?

A

Required by the FDA for drugs that are especially dangerous.

124
Q

Define high alert medication.

A

Have serious potential to harm if misgiven.

125
Q

What are some examples of high alert medications?

A

Insulin, heparin, opioids, chemotherapy, injectable potassium chloride.

126
Q

Define additive effect:

A

2 drugs taken with similar MOA. Drug effects add together.

127
Q

Define synergism/potentiation:

A

2 drugs with different MOA but result in a combined drug effect greater than that of either drug alone.

128
Q

Define antidote.

A

Drug given to antagonize the toxic effects of another drug.

129
Q

Why is decreased intestinal absorption a problem for drug absorption?

A

Drug may not get broken down so it won’t be absorbed.

130
Q

What are 2 common causes of infections?

A

Virus and bacterial.

131
Q

What is a virus?

A

Only has DNA or only has RNA, surrounded by a protein shell. But it has to have a host cell to replicate in.

132
Q

How many strands of DNA do bacteria have?

A

One.

133
Q

Can bacteria produce outside of the body?

A

Yes.

134
Q

List and define the 4 types of rare causes of infections.

A

Fungal - spore forming organisms
Protozoa - typically lives in water environment
Helminths - parasitic worms
Prions - mis-folded proteins that can attach to other proteins and cause disastrous effects.

135
Q

Give an example of fungal, protozoa, helminth, and prion infections.

A

Fungal - yeast infection
Protozoa - Malaria
Helminth - round worms
Prions - mad cow disease

136
Q

What are examples of reservoirs?

A

Water, animals, insects.

137
Q

What are examples of direct transmission?

A

Kissing, sec, coming into contact with contaminated soil, droplet spreads.

138
Q

What are examples of indirect transmission?

A

Airborne

139
Q

What is vehicle-borne transmission?

A

Indirect transmission through water, food, or blood.

140
Q

What is vector-borne transmission?

A

Something else carries disease or pathogen like mosquitos, fleas, or ticks.

141
Q

Common portals of entry:

A

Oropharynx, nasopharynx, genitourinary tract.

142
Q

What is the body’s biggest barrier to pathogens?

A

Skin.

143
Q

What is translocation?

A

Movement of bacteria across intestinal lining. This occirs frequently in peritoneal cavity.

144
Q

What are the stages of infection?

A

Incubation period, prodromal stage, acute stage, convalescent stage, resolution.

145
Q

What happens in the incubation period?

A

Time from when the organism gets into the body to when the first symptoms appears.

146
Q

What happens in the prodromal stage?

A

Onset of nonspecific symptoms, this happens before you actually get sick.

147
Q

What happens in the acute stage?

A

You are actually sick.

148
Q

What happens in the convalescent stage?

A

Symptoms starting to get better, illness is going away.

149
Q

What happens in the resolution stage?

A

Pathogen is out of the body.

150
Q

What are the components of the infectious process?

A

Injury, increased permeability, immigration of leukocytes, phagocytosis, exudate, systemic symptoms.

151
Q

What happens at the injury stage of the infectious process?

A

Initial injury occurs, followed by short period of vasoconstriction (to slow bleeding and prevent movement of invading pathogens), then prolonged period of vasodilation (allows blood to flow freely, brings immune cells to area, contributes to inflammation system).

152
Q

What happens at the increased permeability stage of the infectious process?

A

Fluids are pulled out of the vascular space and to the place of injury.

153
Q

What happens at the immigration of leukocytes stage of the infectious process?

A

Neutrophils are attracted to the area of injury, they attach to the endothelium of the injured cells, and move through into the surrounding injured tissues.

154
Q

What happens at the exudate stage of the infectious process?

A

Transports the leukocytes to injured area, dilute toxins that might be present, and transport nutrients for the healing process.

155
Q

What happens at the systemic symptom stage of the infectious process?

A

If the infection doesn’t stay localized, a total body response is initiated. This stimulates hypothalamic fever set point.

156
Q

What does increasing the fever set point do?

A

Conserve body heat, stimulate defense mechanisms to get rid of organisms, the heat can make bacteria less virulent and divide slower, improves neutrophil and macrophage function, and improves antibody release and T-cell activation.

157
Q

What vital signs indicate an infection?

A

Increased temperature, HR, and RR.

158
Q

What does a gram stain do?

A

Takes a stain of the bacteria and shows whether it is gram + or gram -. Shows shape and arrangement.

159
Q

How long does it take to get a gram stain back?

A

Few hours.

160
Q

How long does it take to get a culture back?

A

Takes up to 24 hours to get basic result, may take 72 hours for full identification and sensitivity pattern.

161
Q

Nitrites in urine should be _______. Why?

A

Negative. A positive indicates an infection. Bacteria changes nitrates into nitrites.

162
Q

Leukocyte esterase should be _________. Why?

A

Negative. A positive indicates an infection.

163
Q

What should the RBC count be in urine? Why?

A

<5, more than than = infection.

164
Q

What is a nosocomial infection?

A

Infection that occurs while in healthcare facilities that is usually more virulent and causes more damage.

165
Q

MRSA is resistant to what?

A

A specific drug.

166
Q

CRE is resistant to what?

A

An entire class of medications.

167
Q

What is a superinfection?

A

New infection that occurs during treatment for a different infection.

168
Q

Why does a superinfection happen?

A

The antimicrobial we use to treat initial/primary infection, inhibits/kills normal flora.

169
Q

Define cellular adaptation.

A

Changes that your cells go through to survival and ongoing maintenance.

170
Q

Define atrophy.

A

Decreased or shrinking in cell size.

171
Q

Physiologic vs pathologic atrophy:

A

Physiologic: related to development or development issues.
Pathologic: related to decreased workloads or changed environmental conditions.

172
Q

What are some examples of pathologic atrophy?

A

Nutritional deficiencies, decreased blood supply, hormonal changes, prolonged immobility, aging.

173
Q

Atrophied cells have decreased amounts of __________ and/or increased __________.

A

Protein synthesis
Protein catabolism.

174
Q

What is hypertrophy?

A

Increase in size of the cell.

175
Q

What organs are most prone to hypertrophy in a negative way?

A

Heart and kidney.

176
Q

What is hyperplasia?

A

Increased number of cells due to increased rate of cellular division.

177
Q

What can be considered normal physiologic hyperplasia?

A

Pregnancy related changes and wound healing.

178
Q

What is dysplasia?

A

Abnormal changes in size, shape, and/or organization of mature cells.

179
Q

What is dysplasia often associated with? What is the caveat?

A

Cancer, however dysplasia does not EQUAL cancer.

180
Q

Is dysplasia reversible?

A

Yes.

181
Q

What is metaplasia?

A

Reversible replacement of one type of mature cells to another, less differentiated, area.

182
Q

Is metaplasia reversible?

A

Yes.

183
Q

What is neoplasia?

A

Cellular growth nor responding to normal regulator processes, usually because of gene mutations.

184
Q

What is cancer?

A

Uncontrolled cellular growth with rapid uncontrolled proliferation and loss of the ability to differentiate.

Pathopharmacology Intro (6 decks)

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