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Internal Medicine Final > unit 1 stuff > Flashcards

unit 1 stuff Flashcards

1
Q

illness vs disease

A

deviation from healthy state physically or mentally (is based on PERCEPTION)
vs
biologic/psychologic alteration (has OBJECTIVE data)

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2
Q

the words “impairments”, “interventions”, “desired outcomes”, “functional limitations” are all part of what concept

A

ICF Framework

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3
Q

what does ICF framework shift healthcare focus to

A

focus to life and human functioning as a whole, rather than just pathology

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4
Q

depression, alcoholism, and schizophrenia are all examples of what type of diability

A

cognitive

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5
Q

psychoneuroimmunology

A

the study of interactions among behavior, neural, endocrine, enteric, and immune functions

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6
Q

the way people perceive reality is considered their ….

A

consciousness

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7
Q

noncommunicable diseases

A

lifestyle diseases that are largely preventable

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8
Q

primary, secondary, and tertiary medicine

A

primary = reducing risk factors
secondary = promotes early detection
tertiary = preventing severe disability (REHAB!!)

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9
Q

what are 4 genome variation mechanisms that can occur

A
  1. single base pair changes
  2. insertions of base pairs
  3. deletions of base pairs
  4. structural rearrangement of chromosomes
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10
Q

impairment vs disability vs handicap (and their levels)

A

functional loss (organ level)

activity limitations (person level)

social disadvantage (societal level)

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11
Q

the upregulation or downregulation of genes based on environmental factors

A

epigenetics

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12
Q

upregulation of DNA

A

adding methyl group and turning on gene expression

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13
Q

downregulation of DNA

A

subtracting methyl group and turning off gene expression

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14
Q

8 epigenetic factors that influence health

A

geographic
socioeconomic
health disparities/inequities
social
environmental
cultural
client variations
age

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15
Q

what epigenetic factor is most adverse on a patient’s health

A

socioeconomic status

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16
Q

cultural relativity

A

behavior is judges in relation to the context of the culture
(health = luck vs unhealth = punishment)

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17
Q

what characteristic was disproved from being an epigenetic causation

A

race/ethnicity

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18
Q

4 main client variations

A
  1. race/ethnicity
  2. gender
  3. sexual orientation
  4. generation
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19
Q

what is the most important factor in changing a person’s epigenetics

A

nutrition

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20
Q

enteric nervous system

A

basically how the gut is your second brain

microbiome!!

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21
Q

food must have _______ in it to be considered a prebiotic

A

nondigestible fiber

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22
Q

what vitamin reduces chronic pain

A

vitamin D

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23
Q

what are the 3 theories of aging

A
  1. programmed-based
  2. damaged-based
  3. telomerase theory
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24
Q

what are the 3 theories of programmed-based aging

A
  1. gene mutation theory
  2. genetic control theory
  3. planned obsolescence theory
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25
Q

what is the damage-based theory of aging

A

wear and tear over the years plus an accumulation of free radicals in the body

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26
Q

what is the telomerase theory of aging

A

telomeres are shortened with each cell division which leads to gradual damage to the chromosomes

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27
Q

where would a legion in the brain cause a decrease in executive function

A

the right hemisphere

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28
Q

who made the germ theory

A

louis pasteur

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29
Q

who discovered mitochondrial DNA

A

douglas wallace

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30
Q

when did the human genome project start and finish

A

1990-2003

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31
Q

supercenturians

A

people who live over 110 years old

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32
Q

pharmacotherapeutics

A

use of specific drugs to prevent, treat, or diagnose diseases

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33
Q

pharmacokinetics

A

how the body absorbs, distributes, and eliminates drugs

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34
Q

pharmacodynamics

A

the drug’s MECHANISM in the body

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35
Q

toxicology

A

harmful effects of chemicals

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36
Q

what must be taken into consideration when dealing with pharmocotherapeutics

A

toxicology

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37
Q

pharmacogenetics

A

different reactions can occur due to differences in genetic makeup

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38
Q

what drug name system is nonproprietary and the most effective to use when communicating with a patient

A

genetic names

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39
Q

preclinical trial

A

testing pharmacokinetic and pharmacodynamic properties on animals

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40
Q

phase I clinical trial PLUS how many subjects are involved

A

pharmacological actions and toxic effects on humans

10-100 healthy VOLUNTEERS

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41
Q

phase II clinical trial PLUS how many subjects are involved

A

dosage range and effectiveness
side effects

50-500 people

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42
Q

phase III clinical trial PLUS how many subjects are involved

A

safety and effectiveness

100s-1000s of people tested

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43
Q

phase IV clinical trial PLUS how many subjects are involved

A

post marketing surveillance
FDA approved and watches market for new symptoms

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44
Q

how long do FDA trials typically last

A

7-9 years

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45
Q

orphan drugs

A

drugs for patients with rare disease

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46
Q

off-label prescribing

A

drug treats conditions other than what drug was approved for

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47
Q

schedule I drug + 2 examples

A

highest potential for abuse
restricted to research ONLY

LSD, heroin

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48
Q

schedule II drug + 2 examples

A

high potential for abuse/addiction

morphine, fentanyl

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49
Q

schedule III drug + 2 examples

A

mild-mod physical dependence + strong psychological dependence

anabolic steroids, amphetamines

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50
Q

schedule IV drug + 2 examples

A

limited possibility of physical/psychological dependence

stimulants, depressants

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51
Q

schedule V drug + 2 examples

A

lowest relative abuse potential

cough meds, antidiarrheals

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52
Q

potency

A

specific amplitude a dose produces

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53
Q

what is the difference between maximal effect and potency

A

potency measures how much of the drug is needed to make a reaction

maximal effect measures the max effects a drug is able to produce before the ceiling effect

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54
Q

ceiling effect

A

the maximal effect a drug can have no matter how big the dosages get

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55
Q

cumulative dose response curve

A

% of population that exhibits a specific response (NOT MAGNITUDE)

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56
Q

median effective dose (ED)

A

dose where 50% people respond to drug well

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57
Q

what is the other term for median effective dose

A

beneficial effect dose

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58
Q

median toxic dose

A

50% people get toxic effect from drug

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59
Q

therapeutic index definition AND equation

A

TI = TD / ED

indicates the drug’s safety value

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60
Q

what does a high vs low therapeutic index mean

A

high = more safe
low = dangerous/toxic

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61
Q

3 enteral routes of drug administration

A

oral
sublingual/buccal
rectal

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62
Q

what drug administration route is most susceptible to the “first pass effect” and WHY

A

oral because the liver could filter the drug out of the system

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63
Q

4 parenteral routes of drug administration

A

inhalation
injection
topical
transdermal

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64
Q

how do local anesthesia, insulin, and hormones typically get administered

A

subcutaneous injection

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65
Q

what is the benefit of getting an intrathecal injection

A

the drug can bypass the blood/brain barrier + can get to the CNS

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66
Q

how do vaccines typically get administered?

A

intramuscular injection

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67
Q

what type of drug administration method does nasal spray, eyedrops, and eardrops fall under

A

topical

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68
Q

name 2 specific methods of transdermal administration

A

iontophoresis
phonophoresis

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69
Q

iontophoresis

A

electric current

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70
Q

phonophoresis

A

ultrasound waves

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71
Q

what are the 2 rules of transdermal administration categorization

A
  1. must be able to penetrate skin
  2. must not be degraded majorly by dermis enzymes
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72
Q

bioavalibility

A

% of drug that reaches bloodstream

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73
Q

are hydrophilic or hydrophobic molecules absorbed easier

A

hydrophobic

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74
Q

lipid rafts (what are they + what is the function)

A

lipid domains made of cholesterol + sphingolipids that move freely

cell signaling, endocytosis, ion channel functioning

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75
Q

a substance’s ability to pass through pores depends on 3 characteristics

A

size
shape
electrical charge

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76
Q

passive rate of diffusion depends on 4 things

A
  1. magnitude of gradient
  2. size of substance
  3. diffusion distance
  4. temperature
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77
Q

t/f: there has to be a gradient for passive diffusion to occur

A

TRUE

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78
Q

active transport

A

carrier mediated transportation fueled by ATP

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79
Q

facilitated diffusion

A

carrier mediated with NO energy spent

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80
Q

difference between active transport and facilitated diffusion

A

both are carrier mediated but…

ACTIVE has a gradient + goes from low to high concentrations

FACILITATED doesn’t have a gradient + goes from high to low like passive diffusion

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81
Q

what membrane transportation method (passive/active/facilitated) does glucose use to get into muscle cells

A

facilitated diffusion

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82
Q

what are the 4 ways molecules can transport through/across a membrane

A

passive diffusion
active transport
facilitated diffusion
endo/exocytosis

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83
Q

how does ionization impact diffusion

A

it decreased lipid solubility, making it harder to diffuse

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84
Q

what charge molecule (+ / - / 0) can diffuse the easiest

A

neutral (0)

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85
Q

weak acids can become __ charge in high pH environments

A

positively charged

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86
Q

what does it mean when drug volume distribution (Vd) is EQUAL to body water

A

uniform distribution of drug

(look for a normal, double digit number… 42 was the example given)

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87
Q

what does it mean when drug volume distribution (Vd) is GREATER THAN body water

A

drug is concentrated in tissues

(look for a HIGH NUMBER… 420 was the example given)

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88
Q

what does it mean when drug volume distribution (Vd) is LESS THAN body water

A

drug is in the plasma

(look for a LOW NUMBER… 8.4 was the example given)

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89
Q

bones store what 2 toxic agents from drugs

A

heavy metals (like lead) and tetracyclines

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90
Q

biotransformation

A

“drug metabolism”
chemical changes that take place after the drug is administered

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91
Q

metabolite

A

altered version of drug

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92
Q

oxidation

A

predominant biotransformation method

adds oxygen OR removes hydrogen

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93
Q

reduction

A

removes oxygen or adds hydrogen

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94
Q

hydrolysis

A

drug is broken into several parts

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95
Q

conjugation

A

body hormone/chemical is added to the drug

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96
Q

phase I and phase II of biotransformation mechanisms

A

phase I modifies molecule to make it more polar (oxidation/reduction/hydrolysis)

phase II involves SYNTHESIS (endogenous substance added–> conjugation)

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97
Q

cytochrome P450 monooxygenase is responsible for what biotransformation mechanism

A

oxidation

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98
Q

enzyme induction and what does it lead to

A

enzymes adapt to metabolize drugs quicker which leads to TOLERANCE

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99
Q

metabolites must be _(polar/nonpolar)__ to be excreted

A

POLAR

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100
Q

what is drug clearance + what is its equation

A

CL = Q x [(ci-co) / ci]

ability to eliminate drug either systematically or single organ/tissue level

101
Q

what does Q, ci, and co stand for in:
CL = Q x [(ci-co) / ci]

A

Q = blood flow to the organ
ci = drug entering
co = drug exiting

102
Q

how is systematic clearance calculated

A

by adding clearance of each organ up

103
Q

half-life

A

amount of time it takes for 50% of the drug to be eliminated

104
Q

genetic polymorphisms

A

small genetic variants between people

(these are why some people get varying sickness symptoms or reactions to drugs)

105
Q

acetylcholine receptor is an example of which kind of receptor

A

ion channel

106
Q

how do acetylcholine receptors work

A

Ach molecules bind and open the channel for sodium (Na+) to go through

107
Q

GABA receptor is an example of which kind of receptor

A

ion channel

108
Q

insulin system uses what receptor system

A

receptors that directly activate enzymes

  • insulin binding DIRECTLY INCREASES ACTIVATION which signals glucose uptake into the muscles
109
Q

explain the secondary messenger system using stimulatory G proteins + adenylate cyclase

A

substrate binds to the receptor
G protein sends a signal to the enzyme adenylate cyclase
enzyme creates SECONDARY MESSENGER cAMP
cAMP activates protein kinase

110
Q

what do regulator proteins do

A

change cell function

111
Q

tyrosine kinase protein uses which receptor mechanism

A

receptors that directly activate enzymes

substrate binding directly causes phosphorylation to increase kinase activity

112
Q

what is the largest group of surface receptors

A

G-proteins

113
Q

where does a beta-I selective drug target? why?

A

heart
it has more beta-1 receptors than any other organs in the body

114
Q

Agonist has both __________ and __________

A

affinity and efficacy

115
Q

competitive antagonists

A

agonists/antagonists have equal opportunity to bind
agonist can knock off antagonist

116
Q

noncompetitive antagonists

A

irreversible bonds

117
Q

mixed agonist/antagonist example

A

estrogen agonist in bone but antagonist in breast tissue

118
Q

desensitization

A

overstimulation of receptors cause decrease in function
negative feedback

119
Q

down regulation

A

overstimulation of receptors causes # of receptors to diminish
negative feedback

120
Q

super-sensitivity

A

prolonged periods without any receptor stimulation causes an increase in receptors
ex: parkinson’s

121
Q

chelating agents

A

binds to heavy metals to prevent toxicity

122
Q

ischemia + what 2 things can cause it

A

lack of blood flow that causes cells to swell

thrombus or atherosclerosis

123
Q

what is sepsis caused by

A

endotoxins

124
Q

direct cytopathic effect of a virus

A

RNA virus goes into cell and destroys contents directly

125
Q

indirect cytopathic effect of a virus

A

T lymphocytes detect foreign virus protein receptors on cell and destroy the cell
(uses the body’s cells to destroy each other)

126
Q

partial agonists

A

these do not evoke a maximal response EVEN IF all receptors are bound

127
Q

inverse agonists

A

bind to the same receptor as an agonist but produces the opposite reaction

128
Q

cross reactivity in immune reactions

A

foreign body + host antigen = attack on specialized cells

129
Q

what is a granuloma + what disease commonly has these

A

aggregate of macrophages surrounded by lymphocytes

common in TB

130
Q

example of direct and indirect chemical factors that cause cell injury

A

direct: heavy metals like mercury
indirect: metabolized into harmful substance like acetaminophen

131
Q

kwashiorkor

A

protein malnutrition

132
Q

marasmus

A

general malnutrition

133
Q

what are the #1 causes of death in impoverished countries

A
  1. marasmus
  2. kwashiorkor
134
Q

reactive oxygen species (ROS)

A

unstable molecules that “steal” electrons from healthy cells

135
Q

oxygen toxicity

A

Hydrogen binds to Oxygen and creates harmful compounds that kill cells

136
Q

positive uses of free radicals

A
  1. fights inflammation
  2. kills bacteria
  3. regulates autonomic nervous system
137
Q

oxidative stress leads to __% lifestyle-related diseases

138
Q

what is degenerated by free radicals in Parkinson’s disease?

A

substantia nigra

139
Q

antioxidants interaction with ROS

A

detoxify ROS and protects cells by giving electrons
can be endogenous and exogenous

140
Q

nitric oxide (NO)

A

helpful free radical that protects heart, GI, blood vessels, blood clotting, fights common cold

141
Q

how can you increase Nitric Oxide (NO) bioavailability

A

long-term aerobic training

142
Q

metaplasia

A

change from one cell type to another

143
Q

dysplasia

A

abnormal development or growth of cells, tissues, or organs

144
Q

cell injury by intracellular accumulation (plus an example)

A

increased storage of lipids, proteins, carbs, pigments (like fatty liver)

145
Q

leukopenia is a sign of

A

infection or sepsis

146
Q

leukocytosis is a sign of

A

active inflammation

147
Q

pyknosis

A

clumping of nucleus

148
Q

karyorrhexis

A

fragmentation of nucleus

149
Q

karyolysis

A

dissolution of nucleus

150
Q

blebs

A

membranous lobes created as the cell membrane breaks up in cell death

151
Q

5 types of necrosis

A
  1. coagulative
  2. caseous
  3. liquefactive
  4. fatty
  5. fibrinoid
152
Q

coagulative necrosis

A

Ischemia
nucleus phyknosis and karyolysis
Kidneys, heart, and adrenal glands
Protein denaturation

153
Q

caseous necrosis

A

cell membrane explodes and debris looks like cheese
granuloma forms

154
Q

liquefactive necrosis

A

neuron death causes liquification and abscess in brain

155
Q

fatty necrosis

A

pancreatic lipases create calcium soaps (white + chalky appearance)
acute pancreatitis from abdominal trauma

156
Q

fibrinoid necrosis

A

plasma proteins + cell debris accumulate from trauma to blood vessel wall

157
Q

4 signs of inflammation

A
  1. erythema (redness)
  2. heat
  3. edema (swelling)
  4. pain
158
Q

granulation

A

tiny red granules that are visible in the base of a healing wound

159
Q

what cells make granulation + how

A

made by macrophages releasing GF with endothelial cells and fibroblasts

160
Q

exudate

A

high protein + cellular debris that leaks due to vessel permeability

161
Q

transudate

A

low protein composition that leaks due to osmosis, not vessel permeability

162
Q

2 types of effusion

A

exudate
transudate

163
Q

4 chronic inflammation cells

A
  • granulation
  • macrophages
  • lymphocytes
  • plasma cells
164
Q

3 acute inflammation signs

A
  • increased blood flow
  • edema with leaking plasma proteins
  • neutrophil + WBC emigration
165
Q

6 mediators of blood flow

A
  1. histamine
  2. serotonin
  3. bradykinins
  4. anaphylatoxins
  5. leukotrienes
  6. prostaglandins
166
Q

what are the different cells in acute vs chromic inflammation

A

acute: platelets + neutrophils
chronic: plasma cells + lymphocytes

167
Q

5 inflammatory exudates

A
  1. hemorrhagic/sanguineous
  2. serosanguineous
  3. serous
  4. purulent
  5. catarrhal
168
Q

hemorrhagic (sanguineous) exudate

A

bright red and bloody

169
Q

serosanguineous exudate

A

blood-tinged yellow/pink fluid
48-72 hours after injury

170
Q

serous exudate

A

thin/watery exudate (think blisters)
indicates early inflammation
albumin and immunoglobulins

171
Q

purulent exudate

A

cloudy pus
indicates bacterial infection

172
Q

catarrhal exudate

A

thin, clear mucus
respiratory infection

173
Q

stasis

A

slowing or stopping of the normal flow of a fluid, such as blood

174
Q

margination

A

leukocytes accumulate in blood vessels

175
Q

diapedesis

A

migration of WBC to injury site

176
Q

chemotaxis

A

movement in response to chemical signals

177
Q

chemotactic agent

A

attracts cells to injury site

178
Q

how long do neutrophils live and what are they replaced by

A

24 hours
monocytic/macrophage

179
Q

histamine function

A

vasodilation and bronchoconstriction

180
Q

what cells produce histamine

A

mast cells, basophils, platelets (granuals)

181
Q

endothelial contraction importance

A

it increases the permeability of the blood vessels

182
Q

what does platelet activating factor (PAF) do

A

causes us to feel fever and pain

183
Q

arachidonic acid

A

produces prostaglandins and leukotrienes

184
Q

prostaglandins

A

a type of platelet activating factor that mediates pain and fever responses

185
Q

what do corticosteroids to

A

suppresses inflammation by stopping phospholipase A2

186
Q

what pathway does Aspirin stop

A

cyclooxygenase pathway

187
Q

2 important cytokines with overlapping functions

A

IL-1 and TNF

188
Q

what chemical mediator produces autocrine, paracrine, and hormonal inflammatory effects?

189
Q

IL-1

A

produces fever

190
Q

TNF

A

induces IL-1

191
Q

what are the phagocytic cells (3)

A

neutrophils, monocytes, macrophages

192
Q

kinin enzymatic system

A

produces bradykinin
- causes dilation, produces pain

193
Q

what are the 4 components of tissue healing

A
  1. fibronectin
  2. proteoglycan
  3. elastin
  4. collagen
194
Q

Fibronectin function

A

forms scaffold, tensile strength, and “glues” other substances/cells together

  • chemotactic for fibroblasts and macrophages
195
Q

what secretes fibronectin

A

plasma proteins

196
Q

proteoglycan function

A

stabilizes and hydrates the tissue

197
Q

elastin function

A

forms fibrils by cross-links

198
Q

what cell secretes proteoglycans

A

fibroblasts

199
Q

what is the main extracellular component of tendons

200
Q

type I collagen function

A

mature scarring
in all body tissues

(MOST COMMON TYPE)

201
Q

type II collagen function

A

cartilaginous tissue
growth pates (physis)
3 month half-life

202
Q

type III collagen function

A

thin filaments
disulfide bonds for bridges
found in babies
breakdown of this = wrinkles

203
Q

type IV collagen function

A

in basement membranes

204
Q

the glomeruli of kidney nephrons are made of what kind of collagen?

205
Q

what collagen type helps develop capillaries

206
Q

what inhibits collagen

A

free radicals

207
Q

what 4 cells produce growth factor

A
  1. platelets
  2. fibroblasts
  3. endothelial cells
  4. macrophages
208
Q

platelet growth factor function

A

speeds up healing through inflammation, repair, and remodeling

209
Q

fibroblast growth factor function

A

stimulates endothelial cells to form new blood vessels

210
Q

what are the 4 phases of healing

A
  1. hemostasis and degeneration
  2. inflammation
  3. proliferation and migration
  4. remodeling and maturation
211
Q

hemostasis and degeneration process

A

platelets release growth factor for inflammation

212
Q

inflammation goals (3)

A

to inactivate injurious agent
to remove dead cells
to heal the tissue

213
Q

what elements are needed for inflammation (5)

A

blood flow
circulating cells
connective tissue
chemical mediators
collagen

214
Q

proliferation and migration goals

A

angiogenesis/neovascularization (new blood vessels)
granulation tissue

215
Q

granulation tissue

A

endothelia and fibroblast cells make new blood vessels that look red and granular

216
Q

contracture

A

excessive shrinking that limits mobility and organ functioning (like skin on burn victim)

217
Q

anthrofibrosis

A

joint scarring caused by contracture

218
Q

tissue contraction in remodeling

A

myofibroblasts shrink healing tissue

219
Q

labile cells

A

divide constantly
GI/skin

220
Q

stable cells

A

not normally dividing but can when stimulated
muscle cells

221
Q

primary intention

A

wounds that heal under conditions of minimal tissue loss (surgery, small scar)

222
Q

secondary intention

A

Wound healing where edges can’t be easily approximated and wound fills with granulation (large scar)

223
Q

tertiary intention

A

A wound with a large gap of missing tissue that has been contaminated and needs a drainage tube while healing (suture closed later)

224
Q

can damaged lung cells fully regenerate?

A

yes, if the basement membrane stays normal

225
Q

how often does the digestive tract regenerate

A

every 5 days
full turnover in 3-4 weeks

226
Q

peripheral nerve healing

A

new axonal sprouts form withing 24 hours

227
Q

wallerian degeneration

A

degeneration of a nerve distal to an injury

228
Q

does a transection or contusion heal quicker in skeletal muscle

A

transection

229
Q

contusion of muscle healing

A

loss of strength
incomplete
high rate of reinjury

230
Q

what is the tissue structure of bone

A

80% cortical
20% cancellous

231
Q

bone fracture healing steps

A
  1. hematoma formation
  2. soft callus (fibrocartilage)
  3. bony callus (fibroosseous union)
  4. remodeling and complete restoration of medullary canal
232
Q

how long does the restoration of the medullary cannal take?

A

months to years

233
Q

factors that can impact bone healing (6)

A
  • type of bone
  • site
  • treatment
  • complications
  • comorbidities
  • soft-tissue injury
234
Q

what 2 cell types are needed for tendon/ligament healing

A
  1. tenoblasts
  2. fibroblast
235
Q

when does the proliferative phase occur in tendon/ligament healing

236
Q

prostaglandins mediate which tissue inflammation process

A

tendon/ligament

237
Q

why are cartilage injuries not regenerative? (3 reasons)

A

cartilage is aneural, avascular, and alymphatic

238
Q

4 types of cartilage

A
  1. articular (hyline)
  2. fibrocartilage
  3. elastic
  4. fibroelastic
239
Q

articular cartilage examples (4)

A

joint surfaces
costal cartilage
bone apophyses
epiphyseal plates

240
Q

fibrocartilage examples (4)

A

tendons
ligaments
meniscus
vertebral discs

241
Q

1 elastic cartilage example

242
Q

1 fibroelastic cartilage example

243
Q

synovial membrane

A

membrane lining the capsule of a joint

244
Q

intimal layer

A

inner layer of synovial membrane next to the joint space

245
Q

subintimal layer

A

outer layer of synovial membrane
supportive layer made of fibrous and adipose tissue

246
Q

what 2 elements have high concentration in reversible cell injury

A

sodium and calcium

247
Q

sequence (4) of WBC in inflammatory response

A
  1. margination
  2. adhesion
  3. diapedesis
  4. chemotaxis
248
Q

how do myofibroblasts remodel and mature tissue?

A

through tissue contraction to shrink the healing tissue together with contractile proteins

Internal Medicine Final (4 decks)

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