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Medical Conditions I > Exam #1 > Flashcards

Exam #1 Flashcards

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USMLE® Step 1 flashcards
1
Q

pathology

A

branch of medicine that investigates the nature of disease

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2
Q

clinical pathology

A

pathology applied to the solution of clinical problems

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3
Q

pathogenesis

A

development of unhealthy conditions

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4
Q

pathophysiology

A

study of altered body function due to disease

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5
Q

morphology

A

fundamental structure or form of cells or tissue

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6
Q

histology

A

study of cells and extracellular matrix of body tissues

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7
Q

etiology

A

cause of the disease

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8
Q

risk factors

A

conditions, events, or substances suspected of contributing to the development of the disease

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9
Q

epidemiology

A

study of the cause and distribution of disease in a population

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10
Q

incidence

A

number of new cases during a specified time

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11
Q

prevalence

A

number of existing cases in a population at a given point in time

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12
Q

morbidity

A

effect an illness has on a person’s life

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13
Q

mortality

A

rate of death (over a given time, for a given population or disease)

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14
Q

signs

A

observable phenomenon

EX: skin rash, cough, joint deformity, etc.

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15
Q

symptoms

A

subjective feelings expressed by the patient

EX: I feel pain/tired/dizzy, etc.

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16
Q

health

A

no universally accepted definition

  • ability to function normally in society
  • disease-free state
  • WHO: state of complete physical, mental, and social well-being
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17
Q

disease

A

dynamic process disrupting physiologic function that manifests itself with a set of signs and symptoms
-has an etiology, pathogenesis, morphologic changes, clinical manifestations, diagnosis and clinical course

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18
Q

illness

A

sickness or derivation from a healthy state

-perception and response of the person

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19
Q

clinical course of an illness

A

1) acute: rapid onset and short duration
2) subacute: between acute and chronic (days to months)
3) chronic: long-standing illness or disability; may involve exacerbations

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20
Q

patient/client management model

A 
examination
evaluation
diagnosis
prognosis
intervention
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21
Q

medical diagnosis

A

identification of pathology

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22
Q

PT diagnosis

A

-the label encompassing a cluster of signs/symptoms, syndromes, or categories
-the process of arriving at that label
EX: musculoskeletal, neuromuscular, etc.

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23
Q

differential diagnosis

A

determination of which one of several diseases may be producing symptoms

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24
Q

primary prevention

A

aimed towards removing or reducing disease risk factors

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25
Q

secondary prevention

A

promote early detection of disease and intervene to avoid further complications

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26
Q

tertiary prevention

A

aimed at limiting the impact of established disease

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27
Q

validity

A

how meaningful is the test

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28
Q

reliability

A

how consistent are the results

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29
Q

sensitivity

A

true positive

proportion of people with a positive test result who have the condition

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30
Q

specificity

A

true negative

proportion of people with a negative test who don’t have the condition

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31
Q

predicative value

A

degree of certainty that can be associated with a positive or negative finding obtained on a diagnostic test
-probability that a person does or does not have the condition given a particular test result

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32
Q

positive likelihood ratio

A

increase in odds for the condition to be present/proven

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33
Q

negative likelihood ratio

A

decrease in odds for the condition to be present/proven

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34
Q

likelihood ratio of 1

A

test neither proves or disproves the condition

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35
Q

snOUT

A

high Sensitivity, a Negative test rules OUT the diagnosis

  • majority of true non-fallers correctly identified
  • few false negatives
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36
Q

spIN

A

high Specificity, a Positive test rules IN the diagnosis

  • majority of true fallers correctly identified
  • few false positives
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37
Q

biomedical model of health

A

focus on disease process

biological state influences health

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38
Q

biopsychosocial model of health

A

psychological system and social factors interact with one’s biology to impact health

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39
Q

social-ecological model of health

A

considers intrapersonal factors in relationship to social and environmental factors
-emphasizes social and organizational factors impacting health

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40
Q

factors impacting health

A 
sociodemographics
health status
geography
race and ethnicity
age and aging
gender
lifestyle factors
behavioral factors
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41
Q

sociodemographics

A

populations shifts –> growing rural population

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42
Q

obesity: CNS-mediated endocrine dysfunction

A

hormonal problem that affects hypothalmic-pituitary-adrenal system
-stress –> cortisol secretion –> stimulates SNS –> hypothalamic arousal –> metabolic syndrome

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43
Q

obesity: problem of energy regulation

A

problem with the Na+/K+/ATP pump

-less ATPase pumps –> decreased energy

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44
Q

obesity: adipose cell theory

A

excessive number and size of fat cells

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45
Q

obesity: microbial theory

A

altered gut microbes alter energy intake, absorption and storage

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46
Q

geography

A

stress, nutrition, access to medical facilities and safety of the community, treatment variations

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47
Q

geographic pathology

A

infectious and parasitic diseases

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48
Q

environmental pathology

A

contaminants

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49
Q

cell membrane

A
  • lipid bilayer: provides structure, relatively impermeable
  • proteins: transmembrane, transportation
  • carbohydrates: form cell coat
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50
Q

nucleus

A

control center-stores heredity material

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51
Q

components of the nucleus

A
  • nucleolus: organelle that manufactures ribosomes
  • nuclear envelope/membrane: contains pores-allows passage of material between nucleus and cytoplasm
  • chromatin: DNA and proteins
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52
Q

DNA

A

protein synthesis, transmission of genetic material

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53
Q

RNA

A

copies and carries DNA instructions, site for protein synthesis, transports amino acids, production of protein

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54
Q

cytoplasm

A

surrounds nucleus

-contains water, electrolytes, suspend proteins, neutral fats, and glycogen molecules and organelles

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55
Q

ribosomes

A

small particles of nucleus proteins
free-floating or attached to endoplasmic reticulum
site of protein synthesis: attach to mRNA

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56
Q

endoplasmic reticulum

A

transport substances

  • rough ER: contains ribosomes, proteins synthesis, modification of protein structure
  • smooth ER: lipid synthesis, regulation of intracellular calcium (SER), metabolism and detoxification of hormones and drugs
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57
Q

golgi apparatus

A

modification of large proteins and lipids –> active form

-proteins synthesized in ER –> packaged in vesicles –> to golgi apparatus –> secreted

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58
Q

lysosomes

A

digestive

-vesicles containing enzymes that digest worn-out cell organelles, macromolecules, bacteria, or entire cells

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59
Q

peroxisomes

A

degrades peroxides, controls free radicals, breaks down large fatty acids

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60
Q

mitochondria

A

powerhouse

  • generates fuel for energy for cellular activity (O2, ATP)
  • regulate cell death (apoptosis), dysregulatory apoptosis –> disease
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61
Q

cytoskeleton

A

controls cell shape, transport and movement

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62
Q

microtubule specialization

A

cilia

flagella

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63
Q

catabolism

A

breaking down of nutrients and body tissues –> energy

  • complex molecules into simpler ones
  • used for energy production, recycling of molecular components, or excretion
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64
Q

anabolism

A

constructive process

  • builds healthy body tissues from dietary calories and protein
  • necessary for growth, maintenance and tissue repair
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65
Q

G-protein linked cell membrane metabolism

A

on-off switch for signal transmission

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66
Q

Enzyme (kinase)-linked cell membrane metabolism

A

mediate responses

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67
Q

ion-channel linked cell membrane metabolism

A

involved in electrical synaptic transmission

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68
Q

passive movement across cell membrane

A

without energy expenditure

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69
Q

chemical gradient

A

difference in number of particles on either side of membrane

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70
Q

electrical gradient

A

difference in charged particles or ions

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71
Q

simple diffusion

A

movement through membrane without carrier

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72
Q

facilitated diffusion

A

transport protein

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73
Q

ion channels and gates diffusion

A

open/close

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74
Q

osmosis diffusion

A

diffusion of water across membrane

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75
Q

endocytosis

A

incorporate material from outside the cell

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76
Q

exocytosis

A

enclosed vesicle first fuses with the plasma membrane

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77
Q

stress theories: general adaptation syndrome

A

1) alarm
2) resistance
3) exhaustion

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78
Q

stress theories: physiological responses and pathological states

A

stress –> problems with proteins

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79
Q

stress theories: personal factors

A

determine organ failure related to stress

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80
Q

reversible cell injuries

A 
atrophy
hypertrophy
pseudohypertrophy
hyperplasia
metaplasia
dysplasia
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81
Q

atrophy

A

reversible cell injury

  • decrease in cell size or number of cells
  • physiologic: shrinkage occurs in development; involves entire body
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82
Q

hypertrophy

A

reversible cell injury

  • increased size of cell/organ due to increased workload or hormones
  • physiologic: result of normal physiological conditions
  • pathologic: result of disease conditions; adaptive or compensatory
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83
Q

pseudohypertrophy

A

reversible cell injury
-increase in size of organ or body part BUT not due to increase in same cell type; RATHER infiltration of other cell types

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84
Q

hyperplasia

A

reversible cell injury

  • increase in number of cells resulting from an increased rate of cellular division
  • physiologic: due to hormonal stimulation; increased functional demands; compensatory mechanism
  • pathologic: abnormal proliferation of normal cells due to excessive hormonal stimulation or effects of growth factors
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85
Q

metaplasia

A

reversible cell injury

-reversible change in cell morphology –> one type of cell converts into another

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86
Q

dysplasia

A

reversible cell injury

-increased number of cells with altered morphology and loss of historical organization

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87
Q

irreversible cell injuries

A

cell death: apoptosis, necrosis, gangrene

pathologic calcifications: dystrophic, metastatic

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88
Q

apoptosis

A

irreversible cell injury

-controlled cell destruction; programmed cell death

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89
Q

necrosis

A

irreversible cell injury

-pathologic; unregulated; result of injury to cell integrity

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90
Q

gangrene

A

irreversible cell injury

  • variant of necrosis
  • dry: decreased arterial blood supply
  • wet: decreased venous return and bacterial infection
  • gas: infection of Clostridium bacteria dissolve cell membrane
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91
Q

dystrophic pathologic calcification

A

irreversible cell injury

-occurs in injured or dying tissue

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92
Q

metastatic pathologic calcification

A

irreversible cell injury

-occurs in normal tissue due to hypercalcemia

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93
Q

causes of cell injury

A 
ischemia/hypoxia
infections
immune responses
genetics
nutritional factors
physical factors
mechanical factors
chemical factors
free radicals
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94
Q

hypoxia

A

cause of cell injury

-lack of sufficient oxygen, reducing oxygen metabolism and generation of ATP

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95
Q

bacterial infection

A

cause of cell injury

  • invades tissue –> release toxins –> cell lysis and degradation of extracellular matrix
  • sepsis: blood infection interferes with blood volume/flow –>shock
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96
Q

viral infection

A

cause of cell injury

  • direct: RNA virus inserts itself into cell membrane receptor –> disturbs nucleus and/or cell membrane
  • indirect: virally encoded protein inserts self into membrane –> forms channel in protein –> alters permeability of cell –> cell swelling and death
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97
Q

immune responses

A

cause of cell injury

  • normal: provides a defense against foreign antigens
  • abnormal: becomes overzealous (i.e. allergy, etc.)
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98
Q

genetics

A

cause of cell injury

  • alter number or structure of chromosomes
  • produce single gene mutations –> alter proteins
  • cause multiple gene mutations –> multi-factor problems
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99
Q

contusion

A

bleeding into the skin or underlying tissues as consequence of a blow that squeezes or crushes soft tissue and ruptures blood vessels

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100
Q

abrasion

A

skin injury produced by shearing force

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101
Q

laceration

A

skin or soft tissue injury produced by sharp, incisional force

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102
Q

hematoma

A

collection of blood in soft tissue/enclose space

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103
Q

programmed change theory of cellular aging

A

aging is genetically programmed

activation of particular gene(s) after a number of cell divisions

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104
Q

error theory of cellular aging

A

accumulation of random events or damages to vital cell membranes

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105
Q

somatic mutation theory of cellular aging

A

mutations in DNA/deficit in repair mechanism

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106
Q

oxidative free radical theory of cellular aging

A

free radical damage

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107
Q

wear and tear theory of cellular aging

A

accumulated damage to vital parts of the cell

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108
Q

telomerase theory of cellular aging

A

in absence of telomerase, telomeres shorten –> decline in gene expression and inhibition of cell replication

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109
Q

rigor mortis

A

muscle stiffening occurs when the myosin cannot detach from the actin (due to deficient ATP) until lysosomal enzymes break down myofilaments

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110
Q

pharmacology

A

study of how chemical substances affect living tissue

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111
Q

pharmacotherapeutics

A

use of chemical agents to cure, prevent and diagnose medical disease
-goal is to deliver the appropriate amount of drug for a reasonable length of time to achieve desired beneficial effects while minimizing adverse effects

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112
Q

pharmacokinetics

A

how drugs get through the body and what happens to them in the body
-absorption –> distribution –> metabolism –> excretion

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113
Q

pharmacodynamics

A

potency and efficacy

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114
Q

pharmacogenomics

A

effect or influence of genetics on drugs

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115
Q

phases of human (clinical) testing

A

1) safety assessment
2) drug effectiveness -small patient sample
3) drug effectiveness -large patient sample
4) post-market surveillance

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116
Q

parts of a prescription

A

prescriber’s name and contact info
patient’s name and date
superscription: method of administration, treatment method
inscription: drug name, dose, quantity to dispense
signa: instructions to patient
refill instructions
prescriber’s signature

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117
Q

PO

A

by mouth

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118
Q

IV

A

intravenous

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119
Q

IM

A

intramuscular

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120
Q

QD

A

once a day (“daily”)

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121
Q

BID

A

twice a day

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122
Q

TID

A

three times a day

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123
Q

QID

A

four times a day

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124
Q

HS

A

at night

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125
Q

pharmacotherapeutic drug

A

drug’s action on a specific disease process

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126
Q

pharmacological drug

A

result of drug action on the body

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127
Q

“gated” ion channels

A

ligand and voltage-gated
quick opening and closing of channels
allows for ion transfer along concentration gradient

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128
Q

G-protein coupled receptors

A
  • G-proteins made of alpha, beta, gamma subunit
  • slower (more prolonged) opening of channels (seconds) than seen in ion channels and remain open longer
  • production of second messengers
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129
Q

kinase-linked receptors

A
  • transmembrane helical region with large extracellular space for ligand binding
  • size of extracellular space related to size of endogenous ligand
  • slower
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130
Q

DNA-coupled receptors

A

intracellular: in nucleus

stimulate gene transcription –> protein and enzyme synthesis

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131
Q

drug-receptor interaction: specificity

A

acting on only one type of receptor

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132
Q

drug-receptor interaction: selectivity

A

acting on one subtype of receptor

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133
Q

drug-receptor interaction: agonist

A

binds to receptor to create response

-when all receptors are occupied by agonist –> maximum response (not infinite)

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134
Q

drug-receptor interaction: antagonist

A

blocks receptor site; binds to receptor but doesn’t cause change

  • competitive: antagonist can be overcome with greater concentration of agonist
  • noncompetitive: antagonist blocks receptor site permanently; no effect with increased concentrations of agonist
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135
Q

graded dose-response curve: Emax

A

maximum response point

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136
Q

graded dose-response curve: Efficacy

A

strength of response

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137
Q

graded dose-response curve: Kd (ED50)

A

median effective dose

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138
Q

graded dose-response curve: Potency

A

concentration of drug needed to produce a given response

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139
Q

quantal dose-response curve: LD50

A

lethal to 1/2 of subjects

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140
Q

quantal dose-response curve: TD50

A

toxic/adverse effect in 1/2 of subjects

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141
Q

administration of drugs: oral

A

most convenient, most favored, most complex

first pass metabolism: liver metabolism

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142
Q

administration of drugs: sublingual and buccal

A

rapid absorption due to tissues and proximity to capillaries

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143
Q

administration of drugs: rectal

A

solutions, suspensions, or suppositories

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144
Q

administration of drugs: intravenous

A

requires injection

145
Q

administration of drugs: subcutaneous

A

given under skin into fat (usually stomach)

146
Q

administration of drugs: intramuscular

A

directly into skeletal muscle

147
Q

administration of drugs: epidural

A

drug delivered into spinal column, but outside dura mater

148
Q

administration of drugs: intrathecal

A

into spinal subarachnoid space

149
Q

distribution of drug depends on

A
  • blood flow (if IV administered)
  • lipid solubility: lipid soluble drugs pass blood-brain barrier quickly
  • plasma protein binding: some portion of drug bound to albumin, but need free drug for effects –> must increase overall dose –> prone to more drug-to-drug interaction
150
Q

metabolism of drugs

A

takes place primarily in the liver

-reduces lipid solubility

151
Q

phase one of metabolism of drugs: catabolic

A
  • mechanisms: inactivation of drug, various mechanisms
  • alterations in process: differences in enzymes around people, effect of diet and environment, competition for same enzyme slows metabolism
152
Q

phase two of metabolism of drugs: conjugation

A

hydrophilic groups attach to drug –> inactive compound –> less lipid soluble –> prepares for excretion

153
Q

first-order elimination

A

rate of elimination is directly proportional to concentration of drug

154
Q

half-life elimination

A

50% of drug is cleared per unit of time

-dependent on clearance and volume of distribution (Vd)

155
Q

steady state

A

amount of drug excreted during unit of time equals amount of drug administered

156
Q

classifying medication effects: A,B,C,D,E

A 
A: augmented = dose-related, predictable
B: bizarre = unrelated to dose; unpredictable
C: chronic = dose and time-related
D: delayed
E: end of treatment
157
Q

drug-drug interactions

A
  • diminished response (subtraction)
  • additive response (addition)
  • synergistic response (multiplication)
158
Q

pharmacokinetic basis: A,D,M,E

A

A: absorption
D: distribution
M: metabolism
E: excretion

159
Q

Type 1 drug allergy

A

anaphylactic reactions

  • degranulation of mast cells and/or basophils
  • histamine –> severe allergic reaction
  • cardiovascular and respiratory collapse within minutes to an hour
  • epinephrine = treatment of choice
160
Q

radiology

A

branch of medicine concerned with radiant energy and radioactive substances

161
Q

radiograph

A

production of an image of an anatomical part

162
Q

radiodensity

A

tissues produce various shades of gray, depending on their density
-thickness and composition

163
Q

attenuation

A

any mechanism by which photons (x-ray) are lost

-due to absorption or scattering

164
Q

radiolucent

A

lesser density = lesser absorption

165
Q

radiopaque

A

greater density = greater absorption

166
Q

systematic approach to film evaluation: A,A,B,C,C,S

A 
A: architecture
A: alignment
B: bone density
C: contour
C: cartilage
S: soft tissue
167
Q

computed tomography

A

vertebral column, sternum, ribs, etc.
excellent bone detail
radiation

168
Q

magnetic resonance imaging

A 
soft tissue
T1: anatomical detail
T2: pathology (tumor)
multi-planar
expensive
169
Q

scintigraphy

A

bone scans
identify bone metastases
poor spatial resolution

170
Q

ultrasonography

A

visualize structures
inexpensive
poor bone detail

171
Q

What does neoplastic mean?

A

cancer-related

172
Q

What does psychogenic mean?

A

a psychology problem manifests themselves as health problems

173
Q

What are free radicals?

A

atoms with unpaired electron –> react to

interrupt normal physiological activity

174
Q

What does idiopathic mean?

A

no known cause

175
Q

What does iatrogenic mean?

A

due to medical action/treatment

176
Q

The PT role in diagnosis, what should they do?

A

formulate PT diagnoses
recognize need to refer to another discipline
communicate & collaborate with other HCPs

177
Q

How are PTs being seen as primary care providers?

A

direct access

legislative, professional, and educational initiatives

178
Q

Why are PTs being viewed as primary care practitioners?

A
  • exploding patient population demanding quick & easy access
  • increasing # of patients
  • decreasing appointment times because increasing demand for profit
  • use of PTs as “physician extenders”
179
Q

What do PTs use laboratory tests for?

A
  • determine appropriateness for treatment
  • make necessary adjustments to plan of care
  • reference range
180
Q

What are the 6 criteria to evaluate diagnostic tests?

A
  • validity
  • reliability
  • sensitivity
  • specificity
  • predictive value
  • likelihood ratio
181
Q

What is the equation for sensitivity?

A

(true +) / (true + + false -)

182
Q

What is the equation for specificity?

A

(true -) / (true - + false +)

183
Q

What is a false negative?

A

a person who tests as negative but who is actually positive

184
Q

What is a false positive?

A

a person who tests as positive but who is actually negative

185
Q

What is the likelihood ratio equation?

A

sensitivity/ 1 - specificity

186
Q

How does race and ethnicity affect health care?

A
  • increase of individuals living in lower socioeconomic environment
  • less accessible for minorities and rural populations
  • routine healthcare more for affluent, better educated, & higher income people
  • African-Americans less likely to receive rehab services & less intense
187
Q

In the U.S. half of deaths are due from________ & _______.

A

behavioral & lifestyle factors

188
Q

How does being male affect health?

A
  • poorer health
  • decreased life expectancy
  • less likely to seek medical treatment
  • more likely to engage in risky behavior
  • considered the norm
189
Q

How does being female affect health?

A
  • more likely to seek medical help
  • more likely to practice preventative medicine
  • more likely to have a PCP
  • tend to use a “tend and befriend” approach to managing stress
190
Q

What is the self-efficacy?

A

ability or confidence of a person to implement an effective behavior

191
Q

What is a negative cellular response to stress includes?

A

when stress is overwhelming or adaption is ineffective, injury, maladaptive changes, & cell death occur

192
Q

What is a positive cellular response to stress includes?

A

stress to a body & tissues can be beneficial ex: hypertrophy

193
Q

What are cell injuries that are reversible?

A
  • sub-lethal
  • after removal of stressor–> cell recovers
  • can become chronic
  • examples: swelling, atrophy, hypertrophy
194
Q

What are cell injuries that are irreversible?

A
  • due to significant injury to cell, resulting in cell death
  • alterations in nucleus, mitochondria, & lysosomes
  • rupture of cell membrane
  • leads to necrosis
195
Q

What makes up the alarm phase of general adaptation syndrome theory?

A
  • fight, flight, freeze

- mobilize resources

196
Q

What makes up the resistance/adaptation phase in general adaptation syndrome theory?

A

how they cope with stressor

197
Q

What makes up the exhaustion phase of the general adaptation syndrome theory?

A

reserves depleted

198
Q

What is physiological atrophy?

A

shrinkage that occurs in development & involves entire body ex: aging related

199
Q

What is physiological hypertrophy?

A

result of normal physiological conditions

ex: increased muscle mass with exercise

200
Q

What is pathological hypertrophy?

A

results of disease conditions (adaptive or compensatory)

201
Q

What is adaptive hypertrophy?

A
  • pathologic hypertrophy

- myocardial hypertrophy from heart disease

202
Q

What is compensatory hypertrophy?

A
  • pathologic hypertrophy

- enlargement of remaining organ or tissue after portion removed (liver)

203
Q

What is physiologic hyperplasia?

A
  • due to hormonal stimulation, increased functional demands, compensatory mechanism
  • example: increased breast and increased liver
204
Q

What is pathologic hyperplasia?

A
  • abnormal proliferation of normal cells due to excessive hormonal stimulation or effects of growth factors
  • example: warts
205
Q

What physiologic processes is apoptosis involved in?

A

normal physiologic processes

  • embryonic development
  • control of immune cell numbers
  • regression of breast tissue after weaning from breast- feeding

Abnormal processes

  • cancer (failure of apoptosis)
  • viral infections (destruction of targeted cells)
206
Q

What are characteristics of dry gangrene?

A
  • caused by decreased arterial blood supply
  • tissue dry, dark brown/black
  • almost exclusively limited to the extremities
  • often complication of diabetes, frostbite, arteriosclerosis
  • loss of blood to cells
207
Q

What are characteristics of wet gangrene?

A
  • caused by decreased venous return & bacterial infection in an area of tissue
  • neutrophils invade the site, causing necrosis
  • wound is cold, swollen, black, & foul smelling
208
Q

What are characteristics of gas gangrene?

A
  • infection of Clostridium bacteria dissolve cell membranes
  • bubbles of hydrogen sulfide gas form
  • high mortality rate if not treated
209
Q

What are causes of hypoxia?

A
  • inadequate O2 in air
  • respiratory disease
  • ischemia-decreased blood flow
  • anemia
  • edema
  • inability of cells to use O2
210
Q

What are the results of hypoxia?

A
  • reliance on anaerobic metabolism
  • lactic acid builds up in cells from glycolysis
  • lowered pH damages cell structures & impairs cell function
211
Q

What causes an allergy?

A

caused by specific antibodies (IgE) on surface of specialized cells

212
Q

What is anaphylactic shock?

A

can result in circulatory collapse; kidney dysfunction

213
Q

What is hyperglycemia?

A

increased glucose causing obesity

214
Q

What is hyperlipidemia?

A

increased lipoproteins causing fat deposits in heart, liver, and muscle

215
Q

What are the effects of hyperthermia?

A

inactivates temperature-sensitive enzymes, damages vessels, accelerates cell metabolism

216
Q

What are the effects of hypothermia?

A
  • induces vasoconstriction & increases blood viscosity

- can rupture cell membrane

217
Q

What is ionizing radiation & how does it affect the cell?

A
  • causes radiolysis of water–>production of radicals–>kills cells, interrupts cell replication, or causes genetic mutation
  • swelling, disruption of mitochondria & other organelles, alterations in cell membrane–>can lead to gene mutations
  • rapidly-dividing cells more vulnerable
218
Q

What are characteristics of electrical injuries?

A

-tissue damage greatest in tissues with least resistance
-bone–>fat–>tendons–>skin–>muscle–>blood–>nerves
(greatest resistance-t—————————->least resistance)
-may interrupt brain function, respiration, and other vital functions

219
Q

What can a free radical injury cause?

A
  • can create reactions with cellular components
  • can cause chain reaction–>damage to cell membrane, changes in proteins, changes in DNA
  • cause of degenerative conditions (Parkinson’s)
  • defenses against:
    - anti-oxidants: neutralize free radicals
    - moderate exercise
220
Q

What are characteristics of cellular aging?

A
  • aging occurs at the cellular level
  • # of cell functions decline with age
    • DNA prime target
      - reduced ability to divide
      - reduced ability to withstand microorganisms
  • result–>reduced
    - functional reserve
    - ability to resist infection
    - pathological changes
221
Q

What is somatic death?

A

death of a person

222
Q

What is pharmacokinetics?

A

is what the body does to the drug

223
Q

What is pharmacodynamics?

A

what the drug does to the body

224
Q

What are the 2 steps of drug development before human testing?

A
  • 1st target a market (media/society)

- 2nd preclinical testing (animal studies)

225
Q

What is phase 1 of human testing in drug development?

A
  • safety assessment
  • healthy volunteers
  • about 2 years
226
Q

What is phase 2 of human testing in drug development?

A
  • drug effectiveness
  • small patient sample
  • 1-2 years
227
Q

What is phase 3 of human testing in drug development?

A
  • drug effectiveness
  • large patient sample
  • 3-6 years
228
Q

What is phase 4 of human testing in drug development?

A
  • post-market surveillance

- last for an infinite amount of time

229
Q

What are barriers to drug development?

A
  • lack of funding
  • clinical syndromes without specific markers
  • lack of animal model for screening
230
Q

What is a meta-analysis and what is it used for?

A
  • combines data from multiple small drug trials to assess patterns of effects
  • statistical technique
  • way to combat problem of small sample sizes
231
Q

What is treatment investigational new drugs (IND) status?

A
  • FDA mechanism for approving drugs for life-threatening conditions
  • special priority through approval process
232
Q

Research demonstrates that up to _____ of adverse drug events are preventable.

A

50%

233
Q

What are schedule 1 class of drugs?

A
  • research only
  • high abuse
  • no medical use
  • examples: LSD & coke
234
Q

What are schedule 2 class of drugs?

A
  • high abuse potential but accepted medical use
  • no refill w/o new prescription
  • DEA number required on prescription
  • example: Oxycontin
235
Q

What are schedule 3 class of drugs?

A
  • lower abuse potential
  • 5 refills in 6-month period
  • steriods
236
Q

What are schedule 4 class of drugs?

A
  • less abuse potential than above classes
  • 5 refills in a 6-month period
  • example: valium
237
Q

What are schedule 5 class of drugs?

A
  • lowest abuse potential
  • may be available without a prescription
  • example: cough syrup
238
Q

What is a chemical name?

A

specific molecular structure

239
Q

What is the generic name of a drug?

A
  • “official name”
  • may be similar to other drugs in same class
  • used in scientific documentation
240
Q

What is the trade/brand name of a drug?

A
  • copyrighted by pharmaceutical company

- usually easier for the public to recognize

241
Q

Pharmacotherapeutic classification is?

A

drug’s action on a specific disease process

242
Q

What is pharmacological action?

A

result of the drug action on the body

243
Q

What is the molecular action?

A

result of the drug action on the molecular target

244
Q

What is a ligand?

A

a substance that is able to bind to and form a complex with a biomolecule to serve a biological purpose

245
Q

What is an endogenous ligand?

A
  • formed within the body

- hormones

246
Q

What is an exogenous ligand?

A
  • formed outside the body

- medication

247
Q

What is a ligand-gated channel?

A

a ligand must bind to the receptor to open it

248
Q

What is a voltage-gated channel?

A
  • a change in voltage opens the channel

- example: Na/K pump

249
Q

what is the ideal drug-receptor interactions?

A

a drug would bind to only one type of receptor (doesn’t happen)

250
Q

What is a competitive antagonist?

A

can be overcome with greater concentration of the agonist

251
Q

What is a noncompetitive antagonist?

A

blocks receptor site permanently; no effect with increased concentrations of the agonist

252
Q

In a dose-response curve, the larger the dose, ______ the response.

A

larger (to a point)

253
Q

What is a partial agonist in a dose-response curve?

A

smaller response for more meds

254
Q

What is the therapeutic index?

A
  • ratio of LD50 to ED50

- the bigger/wider the safer the drug is

255
Q

What are the limitations of ED50, LD50, & TI?

A
  • do not take into account drug-drug interaction
  • patients & docs may not agree on what is “effective” outcome for drug
  • patients may not be compliant in drug usage
  • info on lethality/toxicity done mainly in animal studies
256
Q

What is absorption & what factors influence it?

A
  • drug transferred from administration site–>systemic circulation
  • factors
    • movement of drug through membrane
    • administration methods
    • dosage formula
    • physiochemical properties of drug
    • administration method
257
Q

What are absorption and irritation issues with oral intake of medication?

A
  • many medications cause GI upset
  • mechanisms to delay disintegration
    - coated (enteric) tablets slow-release agents
258
Q

What is the effect of food in the stomach and oral intake of medication?

A
  • increasing gastric mobility improves drug delivery to small intestine (but balance with malabsorption from excessive peristalsis)
  • food in GI tract usually delays absorption
259
Q

What is bioavailability?

A

denotes amount (percentage) of drug actually reaching the cardiovascular system

260
Q

What is first pass metabolism of oral intake?

A
  • liver metabolism = 1st pass & key location

- drug is partially dismantled here prior to entering circulation

261
Q

What are the pros and cons of rectal administration?

A

Pros:
-for children and those vomiting or unable to swallow
Cons:
-inconsistent absorption

262
Q

What are the pros and cons of IV administration?

A

Pros: multiple sites available
Cons: no margin for error

263
Q

What are the pros and cons of subcutaneous administration?

A 
Pros: ease of self-administration
Cons:
   -repeated injections -->lipoatrophy
   -variable absorption
   -impacted by immobilization, heat, exercise
264
Q

What are the pros and cons of intramuscular administration?

A

Pros: more rapid absorption than subcutaneous
Cons: painful, difficult to self-administer, effect of exercise

265
Q

What are the pros and cons of intrathecal administration?

A

Pros: lower dose effective
Cons: infection risk

266
Q

What effect does exercise have on absorption?

A
  • variable effect for orally administered drugs
  • may increase absorption of drugs administered via
    • intramuscular
    • subcutaneous
    • transdermal
    • inhalation
267
Q

If IV administered, distribution is based on _______.

A
  • blood flow
    • greatest in brain, heart, liver, and kidney
    • less in muscle, skin, & fat
268
Q

What is lipid solubility?

A
  • lipid soluble drugs pass blood-brain barrier quickly–> other lipid tissues–>diffuse out & back into brain
  • amount of body fat can impact dose required
269
Q

How does plasma protein binding work?

A

-some portion of drug bound to albumin
BUT
-need free drug for effects so must increase overall “dose” so, prone to more drug-to-drug interactions

270
Q

What are characteristics of the blood-brain barrier and the placenta?

A
  • blood-brain barrier
    • lipid soluble drugs pass easily into the brain
    • water soluble drugs don’t
  • placenta
    - less of a barrier to drugs, but….diffusion delayed
271
Q

What are the characteristics of the metabolic processes?

A
  • biotransformation
    • inactivation
    • preparation for elimination
  • Takes place primarily in the liver
    • decreases drug’s activity
    • reducing lipid solubility is key
272
Q

What are the different types of elimination?

A
  • renal excretion (glomerular filtration to enter tubules)
  • fecal excretion
    - drug uptake into hepatocytes leads to elimination in bile
    - better route for larger molecular-weight compounds
273
Q

What is half-life principle dependent on?

A

dependent on clearance & volume of distribution

274
Q

What are characteristics of first-order elimination and dosing?

A
  • because of 1st order elimination, it takes a long time for the drug to build up in the body
  • steady state: typically occurs within 4-5 half-lives
275
Q

What is zero-order elimination?

A

elimination not dependent on plasma concentration; constant amount lost per unit of time

276
Q

What are age-related factors affecting pharmacokinetics?

A
  • more drugs = more drug-drug interactions
  • more competition for P450 enzymes
  • decreased serum albumin concentration
  • lean body mass decreases
  • liver & renal finction decrease
  • changes in drug-receptor interactions
  • reduced blood flow in GI tract
277
Q

What are genetic factors affecting pharmacokinetics?

A
  • gene mutations tend to control production of enzymes

- can also see mutations in genes that code for drug transporters and drug receptors

278
Q

What are disease factors affecting pharmacokinetics?

A
  • most profound effects found with diseases of the liver & kidneys
  • some illnesses decrease function of P450 enzymes
  • effects of other drugs taken for disease processes (competing activity)
279
Q

Drug vs. Drug interactions

A
  • increasing incidence due to increasing number of medications that our patients are taking (polypharmacy)
  • often results in adverse effects/reactions
280
Q

Patients taking >/= _____ medications associated with higher risk of preventable adverse drug events.

A

7

281
Q

What are side effects?

A

minor, unintended effects

282
Q

What is an adverse drug reaction?

A

significant, unintended effect at therapeutic dosage

283
Q

What is an adverse drug event?

A

negative outcome not necessarily related to chemistry of drug

284
Q

What is the risk/benefit ratio?

A
  • present for every drug
  • ratio increases as patient ages
  • risks are present due to
    • drug-drug interactions
    • food-drug interactions
    • patient-related factors
    • allergic reactions
    • side effects
285
Q

According to WHO, adverse effects are?

A

any unintended or unwanted effects of a drug that may occur at acceptable dose levels

286
Q

What is the beneficial effect?

A

is why you’re taking the drug

287
Q

What is an adverse effect?

A

is anything else that occurs while you’re taking the drug

288
Q

What is augmented classifying medication effects?

A
  • dose-related, predictable

- example: warfarin (hemorrhage), insulin (hypoglycemia)

289
Q

What is bizarre classifying medication effects?

A
  • unrelated to dose, unpredictable

- example: penicillin (allergic reaction)

290
Q

What is chronic classifying medication effects?

A
  • dose & time related

- example: sinemet (dyskinesia)

291
Q

What is delayed classifying medication effects?

A

carcinogenic

292
Q

What is end of treatment classifying medication effects?

A

Oxycontin (opioid withdrawal)

293
Q

What is a drug allergy and drug-induced illness?

A
  • drug + protein = “foreign body”
  • body produces an antibody
  • next dose of drug= TROUBLE
294
Q

What is a Type II (cytotoxic reaction) drug allergy type?

A
  • cell death

- non-urticarial rashes

295
Q

What is a Type III (autoimmune reaction) drug allergy type?

A
  • inflammatory response

- urticaria rash

296
Q

What is a Type IV (cell-mediated hypersensitivity) drug allergy type?

A
  • contact dermatitis

- non-urticarial rashes

297
Q

What can we do to prevent/decrease the risk of ADEs?

A
  • clear communication

- gather accurate medication history

298
Q

What is the relevance of diagnostic imaging to PTs?

A
  • to assure a comprehensive PT exam
  • support, refute, or explain the PT exam
  • inform the plan of care
299
Q

What is reflective imaging & what is an example?

A
  • energy inserted into body–>captured–> converted into an image
  • example: MRI
300
Q

What is ionizing radiation and an example?

A
  • ionizing radiation penetrates matter–>detected

- examples: X-ray & CAT scans

301
Q

What is emission imaging and an example?

A
  • blood drawn–>tagged with radiopharmaceutical agent–> reintroduced–>picked up by scintillation camera
  • example: scanner
302
Q

What are the advantages of digital imaging?

A
  • decreased dose per study
  • image reproduction virtually instantaneous
  • no need to re-develop film
  • total portability
  • finer images produced
  • decreased cost of film & storage space
303
Q

What are the disadvantages of film imaging?

A
  • potential for increased radiation dose to patient
  • cost of film
  • repeat exposure
  • time for chemical development
  • inability to alter image
  • need to physically transport & store film
304
Q

What is the attenuation coefficient?

A

determines the average intensity of x-rays of a particular energy that transmitted

305
Q

Reading a plain film you need to understand…….

A
  • densities of tissues
  • anatomical planes of the body
  • general rules/guidelines/processes
  • orientation of radiograph
306
Q

What are the rules of positions & projections?

A
  • one view is no view

- films are typically AP except hand & chest

307
Q

The higher the mu (attenuation coefficient), the less x-ray is transmitted (less scattered) & the more _____ the tissue appears.

A

radiopaque

308
Q

What composes architecture of a image?

A

size & appearance

309
Q

What information does alignment offer?

A

stability & integrity (info from alignment of bone or joint)

310
Q

What is bone density?

A
  • texture of bone altered due to osteolytic changes

- local bone density may increase as a function of a repetitive process

311
Q

What is contour?

A

trace cortical line of bone for irregularities, smoothness, & continuous

312
Q

What is cartilage space?

A
  • difficult to see on radiograph

- better if you can see normal x-ray first

313
Q

What is soft tissue?

A

muscles are not viewed with distinction but gross bruising, edema, atrophy & hemorrhage can be viewed

314
Q

What are advantages of radiographs?

A
  • cheap
  • readily available
  • familiar
  • easy to read
  • cover large areas
  • good spatial resolution
  • reproducible
315
Q

What are the disadvantages of radiographs?

A
  • some limitations in early disease/fracture
  • limited soft tissue information
  • 2D image
  • storage/loss
  • operator error
316
Q

What is a fluoroscopy?

A
  • radiograph movie
  • contrast exam of GI tract to follow the course of the barium
  • guide in performing arterial & venous catheter insertion
  • joint observation
  • swallowing
317
Q

What is an angiography?

A

away to study blood vessels & organs

318
Q

What are the advantages of CT scans?

A
  • good for viewing: vertebral column, sternum, ribs & sella furcica
  • readily available
  • excellent bone detail
  • good for complex anatomy
  • soft tissue contrast
319
Q

What are the disadvantages of CT scans?

A
  • ionizing radiation
  • attention to technique
  • limited axial slice
  • limited effectiveness in assessment of soft tissue
320
Q

What are the advantages of a MRI?

A
  • excellent for viewing soft tissue, bone marrow, & joints
  • very good spatial resolution
  • best method for joint evaluation
321
Q

What are the disadvantages of a MRI?

A
  • expensive
  • risk of claustrophobia
  • poor cortical bone detail
  • metal artifact can’t go in
322
Q

What are the advantages of nuclear medicine?

A
  • fairly available
  • physiological information
  • effective in identifying bone metastases
  • entire body
  • vascular/soft tissue/bone
  • stress factor
323
Q

What are the disadvantage of nuclear medicine?

A
  • poor spatial resolution

- tracer activity depends on vascular supply & tissue

324
Q

What is a PET scan used for?

A
  • used in research to detect cognitive decline & early Alzheimer’s
  • In patients with cancer, used to detect disease & monitor treatment effectiveness
325
Q

What is sepsis?

A
  • bacterial infection

- blood infection–>interferes with blood volume/low–>shock

326
Q

What is toxicity?

A

adverse drug event at high dosage

327
Q

What is DNA?

A
  • genetic information found in the nucleus
  • composed of different combinations of nucleic acids–> contain instructions for assembling amino acids –> structural units of proteins
328
Q

What is a gene?

A
  • chemical messenger of heredity
  • composed of DNA molecules along a double helix
  • carry instructions for synthesizing proteins
329
Q

What are chromosomes?

A
  • organization & storage of genetic information
  • arranged in pairs (homologous chromosomes)
  • 46 singles or 23 pairs
  • 22 autosomes & 1 sex
330
Q

What is the genetic code?

A
  • a sequence of 3 bases form a triplet code=codon
  • 4 bases
  • molecular language
  • if there is a misspelling that alters the protein
331
Q

What is meiosis?

A
  • cell division of reproductive cells
  • shuffles genetic material from each parent into new form
  • 4 “daughter” cells
332
Q

What is mitosis?

A
  • cell division of somatic cells
  • exact reproduction of cells that normally die off
  • skin cells
  • 2 ‘daughter’ cells (exact copies)
333
Q

What is a mutation?

A
  • a change in the normal DNA pattern of a gene

- 2 types (somatic & gamete)

334
Q

What is a somatic mutation?

A
  • random mutations, not transmittable

- most are corrected by repair mechanisms

335
Q

What is a congenital defect?

A
  • an abnormality present at birth

- may or may not, be due to genetic factors

336
Q

What is a gamete mutation?

A

inherited mutation (or ability to be)

337
Q

What is a genetic disorder?

A
  • a discrete event that affects gene expression in a group of cells related to each other by gene linkage
  • may be apparent @ birth or may arise later in life
  • various causes, most due to DNA sequence issues
338
Q

What are single-gene disorders?

A
  • caused by a single defective or mutant gene involving autosome or x-chromosome (lead to abnormal proteins)
  • characterized by patterns of transmission (dom or res)
  • single mutant gene often expressed in multiple parts of the body
  • likelihood of developing disease based on probability
339
Q

What is an allele?

A

alternate forms of a gene, one from each parent

340
Q

What is a locus?

A

position of gene on the chromosome

341
Q

What is a genotype?

A
  • genetic info stored in the code

- example: BB, Bb, bb

342
Q

What is a phenotype?

A
  • associated recognizable traits

- example: hair color or eye color

343
Q

What is heterozygous pattern of inheritance?

A
  • person with different alleles

- example: Bb

344
Q

What is homozygous pattern of inheritance?

A
  • person with same alleles

- example: BB or bb

345
Q

What is an autosomal dominant?

A
  • trait expressed only in homozygous or heterozygous pairing
  • acts regardless of what else is present
  • example: BB or Bb
346
Q

What is an autosomal recessive?

A
  • trait expressed only in homozygous pairing
  • acts only if unopposed
  • example: bb
347
Q

What is autosomal dominant disorders?

A
  • 50% chance of inheritance
  • age of onset often delayed
  • variable gene penetrance & expression
  • commonly affects complex metabolic pathways or key components of structural proteins (e.g. collagen)
348
Q

What is an autosomal recessive disorders?

A
  • manifested only when both alleles are affected
  • age of onset frequently early & symptoms more uniform
  • characteristically caused by deficiencies in enzymes rather than structural proteins
349
Q

What are x-linked disorders?

A
  • almost always associated with X chromosome & typically are recessive (seen more in males b/c they only have 1 X chromosome)
  • mother usually carries 1 normal and mutant X, has 50% chance of passing on
  • females typically not affected & males are affected
350
Q

What are multifactorial inheritance disorders?

A
  • caused by multiple genes & often influenced by environment

- do not follow clear-cut pattern of inheritance

351
Q

What are the chromosomal disorders?

A
  • leading cause of mental retardation & miscarriage
  • 1 major mutation occurs in 1 to 12 conceptions
  • 50% result in “spontaneous abortions” in the 1st trimesters
  • usually develop during meiosis
  • various mechanisms lead to these disorders
352
Q

What is the deletion mechanism of chromosomal defects?

A

broken chromosomes & loss of DNA

353
Q

What is the duplication mechanism of chromosomal defects?

A

excessive DNA (generally less serious than deletions)

354
Q

What is the inversion mechanism of chromosomal defects?

A

breaking then reinserting in an inverted position

355
Q

What is the translocation mechanism of chromosomal defects?

A

interchanging of non-homologous chromosomes

356
Q

What is the unequal cross-over mechanism of chromosomal defects?

A

chromosomes crossover unequally

357
Q

What are uses of genes in medicine?

A
  • prenatal screening
  • gene testing
  • gene therapy
358
Q

What is gene testing?

A
  • a potential way to sure wide variety of hereditary & age-related conditions
  • may be able to be used to:
    - replace injured tissue
    - build new coronary blood vessels
    - alter drug sensitivity
  • obstacles/concerns
    - how to avoid immune response
    - ethics (designer babies)
359
Q

What is gene testing?

A
  • done to identify those with faulty gene that may or may not lead to disorder
  • concerns
    • psychological implications
    • uncertainty regarding who should be tested
    • safeguards & protocols may not be set
    • privacy

Medical Conditions I (3 decks)

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