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Pathophysiology > EXAM 1 General Concepts of Pathophysiology > Flashcards

EXAM 1 General Concepts of Pathophysiology Flashcards

1
Q

what reflects changes causing health to fall outside the normal range (loss of homeostasis)?

A

Disease

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2
Q

To treat disease effectively, we must understand what 3 things?

A
  1. Normal processes being disturbed
  2. Characteristics of the disturbance
  3. Secondary effects of the disturbances
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3
Q

Example of Secondary effects of the disturbances

A

comorbidity

complications

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4
Q

Factors Affecting “Normal”

A
  1. Genetic variations (e.g., Gilbert’s syndrome)
  2. Cultural variations (e.g., diet, literacy)
  3. Age differences (e.g., body composition)
  4. Gender differences (e.g., Hct, Hgb)
  5. Situational differences (e.g., altitude-Hct)
  6. Diurnal variations (e.g., serum cortisol)
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5
Q

what is Etiology?

A

the cause(s) or reason(s) for disease or functional alteration(s)

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6
Q

what is pathogenesis?

A

the sequence of events in response to injury or disease

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7
Q

what characteristic changes in the appearance of tissues or cells associated with disease

A

Morphologic changes

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8
Q

Functional alterations and clinical significance are determined by ____.

A

cellular changes:

which result in signs, symptoms, clinical course and expected outcome

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9
Q

what is natural history?

A

Natural history is the progression from initial change to recovery or death

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10
Q

what is a lesion?

A

Lesion is a tissue abnormality caused by disease or trauma

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11
Q

what is a sign?

A

is an objective finding, documentable (you can experience it)

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12
Q

What is a symptom

A

is a subjective feeling or complaint (what the patient says has happened)

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13
Q

what are Sequelae

A

Sequelae are conditions resulting from disease or trauma

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14
Q

what are complications?

A

Complication is a new problem resulting from the presence of a disease
(sinusitis from pneumonia)

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15
Q

_____ describes the disappearance of a disease and return of health

A

resolution

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16
Q

Alterations/mutations result in abnormal protein production (e.g., cystic fibrosis) is what Etiologic Classification of Disease?

A

Inherited (familial)

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17
Q

Prenatal (in utero) and neonatal (1st two months) disorders of development (e.g., atrial-septal defect) is what Etiologic Classification of Disease?

A

Congenital

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18
Q

Inherited or acquired deficiencies or abnormalities of metabolic systems or processes (e.g., phenylketonuria, diabetes) is what Etiologic Classification of Disease?

A

Metabolic

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19
Q

disorders that appear in utero or appear shortly after birth?

A

Congenital disease

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20
Q

Gradual breakdown of tissue and loss of function (e.g., osteoarthritis) is what Etiologic Classification of Disease?

A

Degenerative

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21
Q

Loss of growth control (e.g., lung cancer) is what Etiologic Classification of Disease?

A

Neoplastic

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22
Q

Over- or under-responsive immune system, against self (e.g., rheumatoid arthritis) or environmental antigens (e.g., poison ivy rash) is what Etiologic Classification of Disease?

A

Immunologic

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23
Q

poison ivy is what type of disorder?

A

Immunologic disease

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24
Q

Microorganisms, parasites, toxins, tissue destruction (e.g., influenza) are what Etiologic Classification of Disease?

A

Infectious

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25
Q

Trauma or toxicity (e.g., burn) are what Etiologic Classification of Disease?

A

Physical agent-induced

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26
Q

Deficiency and excess of nutrients (e.g., vitamin D deficiency, hypervitaminosis A) are what Etiologic Classification of Disease?

A

Nutritional

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27
Q

Caused by the health care system (e.g., errors, therapy, complication, misdiagnosis) is what Etiologic Classification of Disease?

A

Iatrogenic

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28
Q

Originating in the mind (e.g., somatoform disorders) is what Etiologic Classification of Disease?

A

Psychogenic

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29
Q

when Cause is unknown (e.g., idiopathic scoliosis) what is the Etiologic Classification of Disease?

A

Idiopathic

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30
Q

misdiagnosis is an example of what classification of disease?

A

Iatrogenic

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31
Q

Cell-cell communication occurs via secreted molecules (____) which interact with complementary cell-associated molecules (____)

A

ligands

receptors

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32
Q

your pt presents with a complaint of fatigue and cough. while listening to heart you hear murmur. when asked pt says she has palpitations. what finding is a sign?

A

murmur

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33
Q

Hormone binding to receptor communicates signal through cell membrane via ion channels, enzyme activation (e.g., insulin receptor) – primarily water soluble hormones

this is example of what type of receptors?

A

Cell surface receptors

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34
Q

Hormone crosses membrane and binds to intracellular receptors which communicate the signal to the nucleus (e.g., cortisol receptor) – primarily lipid soluble hormones

this is example of what type of receptors?

A

Intracellular receptors

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35
Q

type of receptor on cell membrane and are associated with water soluble hormones

A

Cell surface receptors

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36
Q

type of receptor that is associated with lipid soluble molecules

A

Intracellular receptors

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37
Q

examples of lipid soluble molecules

A

cortisol. estrogen, testosterone

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38
Q

Four types of cell-cell communication

A
  1. autocrine
  2. synaptic
  3. paracrine
  4. endocrine
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39
Q

Cells respond to signaling molecules that they secrete, providing feedback to themselves (e.g., T lymphocytes and IL-2) is what type of cell-cell communication?

A

autocrine

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40
Q

Rapid onset, short duration, very specific effect is what type of cell-cell communication?

A

autocrine

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41
Q 
Nervous system (e.g., neurotransmitters in synapse)
 is what type of cell-cell communication?
A

Synaptic

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42
Q

Rapid onset, short duration, very specific effect

is what type of cell-cell communication?

A

Synaptic

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43
Q

Chemicals secreted into local area, then rapidly destroyed so only local cells affected (e.g., histamine, eicosanoids)
is what type of cell-cell communication?

A

Paracrine

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44
Q

Slight delay in action, intermediate duration, several actions
is what type of cell-cell communication?

A

Paracrine

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45
Q

Mediators which travel via bloodstream, target cells widely distributed (e.g., protein and steroid hormones) is what type of cell-cell communication?

A

Endocrine

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46
Q

Delayed action, long duration, multiple significant actions is what type of cell-cell communication?

A

Endocrine

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47
Q

when hormone travels through bloodstream and is distributed everywhere is what type of cell communication?

A

Endocrine

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48
Q

Cell growth and division is strictly regulated to address needs of ________, ____, and ____..

A

tissue growth, development and maintenance

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49
Q

Somatic cell division where each daughter cell receives an identical and complete set of 46 chromosomes

A

Mitosis

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50
Q

Gamete (egg and sperm) cell division in which the number of chromosomes is reduced in half (diploid to haploid, 23 in humans)

A

Meiosis

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51
Q

Growth factors are hormones (autocrine, paracrine, endocrine) secreted by cells which affect _________.

A

the rate of division and path of differentiation of themselves or other cells

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52
Q

___ helps cells adapt to stress

A

Adaptation

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53
Q

____ occurs when cells are unable to adapt to stress

A

injury

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54
Q

2 types of cell injury

A

Reversible injury

Irreversible injury

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55
Q

___ is the end stage of irreversible cellular injury

A

death

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56
Q

2 types of cell death

A

necrosis and apoptosis

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57
Q

what changes start immediately upon injury?

A

biochemical

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58
Q

what changes occur after biochemical derangements?

A

morphologic

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59
Q

The response of the cell to injury depends on:

A
  1. Length of time of exposure to the injurious agent
  2. Dose of injurious agent
  3. Type of cell and its ability to adapt
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60
Q

_____ are less able to adapt to hypoxia than cardiac muscle cells

A

neurons

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61
Q

small dose causes what kind of changes?

A

minimal

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62
Q

Injurious agents interfere with membrane-bound calcium ATPase, allowing ______ to enter cytosol and accumulate in mitochondria and endoplasmic reticulum

A

calcium

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63
Q

Increased intracellular calcium activates (4 enzymes)

A
  1. Phospholipases
  2. Proteases
  3. ATPases
  4. Endonucleases
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64
Q

enzyme that destroys membrane phospholipids

A

Phospholipases

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65
Q

enzyme that destroys cell proteins, e.g., cytoskeleton

A

proteases

66
Q

enzyme that results in ATP depletion

A

ATPases

67
Q

enzyme that degrades nuclear DNA

A

Endonucleases

68
Q

Increased intracellular calcium activates enzymes which result in?

A

Results in biochemical changes, water influx, organelle and cell swelling and loss of function

69
Q

Decrease/loss of ATP within cell due to decrease in oxidative phosphorylation by mitochondria, leading to: (3 things)

A
  1. Failure of Na+/K+ co-transporters
  2. Increased anaerobic glycolysis, generating lactic acid
  3. Reduced intracellular pH, causing some morphologic changes of cell injury (e.g., denaturing proteins, affecting enzyme function)
70
Q

does lactic acid denature proteins?

A

yes

71
Q

does lactic acid affect acid base balance?

A

yes

72
Q

___ changes causes morphological changes

A

biochemical

73
Q

Morphologic features

of cell injury (5)

A
  1. Increase in cell size (swelling due to Na+/K+ co-transporter failure)
  2. Swelling of mitochondria and endoplasmic reticulum (water influx)
  3. Nuclear and chromosomal changes (decreased pH)
  4. Detachment of ribosomes from endoplasmic reticulum (ATP depletion)
  5. Small cytoplasmic blebs (cytoskeleton disruption)
74
Q

morphological changes in cell injury reflect _____ damage.

A

membrane

75
Q

while examining a ct scan you notice a calcium deposit in the pts coronary artery, this is an indicator of what?

A

necrotic cell death

76
Q

Critical biochemical events

2

A
  1. Inability to reverse mitochondrial dysfunction

2. Profound disturbances in plasma membrane function

77
Q

Progressive degradation of cell proteins and membrane phospholipids
Membrane ion pump disruption and water influx
Cytoskeletal abnormalities
Cell protein and lipid oxidation (oxygen radical injury)

these are all disturbances in ______.

A

plasma membrane function

78
Q

All cells die either by _______.

A

necrosis or apoptosis

79
Q

_____ is the type of cell death resulting from irreversible cell injury

A

Necrosis

80
Q

this type of cell death indicates a pathologic process

A

necrosis

81
Q

this type of cell death Involves injury to many cells within an area of tissue

A

necrosis

82
Q

Necrotic cells/tissues initiate an ________, which may further injure surrounding cells and tissues

A

inflammatory response

83
Q

in necrosis, Release of_____ dissolves affected tissue, may injure surrounding cells and tissues

A

lysosomal enzymes

84
Q

type of necrosis that results from denaturation of proteins (e.g., ischemic death)

A

Coagulative necrosis

85
Q

type of necrosis that results from autodigestion resulting in cells dissolving (e.g., bacterial tissue infections and abscess formation)

A

Liquefactive necrosis

86
Q

type of necrosis that occurs with chronic and granulomatous inflammation, looks “cheesy” (e.g., tuberculosis)

A

Caseous necrosis

87
Q

heart attack has what type of necrosis in cardiac muscle?

A

Coagulative necrosis

88
Q

type of necrosis that occurs when fat cells become nectotic, both liquefactive and coagulative necrosis occur (e.g., acute pancreatis)

A

Fat necrosis

89
Q

bacterial infections/ rapidly growing tumors/ abbesses are associated with what type of necrosis

A

Liquefactive necrosis

90
Q

granulomas/ tuberculosis are associated with what type of necrosis?

A

Caseous necrosis

91
Q

type of necrosis associated with adipose tissue

A

fat necrosis

92
Q

IM injections (corticosteroid shots) have to be in muscle not subcutaneous because it can cause what type of necrosis?

A

fat necrosis

93
Q

programmed cell death

A

Apoptosis

94
Q

calcium deposits occurs in areas of _______.

A

necrotic cell death

95
Q

______ is a distinctive pattern of cell death occurring in specific physiologic and pathologic circumstances
.

A

apoptosis

96
Q

Physiologic examples of apoptosis (2)

A
  1. Programmed cell death that occurs during embryogenesis and development
  2. Hormonal dependent changes in adult tissues
97
Q

Pathologic examples of apoptosis

A

Certain neurodegenerative diseases, gradual ischemic damage, autoimmune disorders, cancer

98
Q 
Morphologic characteristics
of apoptosis (3)
A
  1. Involves single cells or small groups of cells
  2. Characteristic nucleus and chromatin changes
  3. Pronounced cytoplasmic blebbing with formation of membrane-bound apoptotic bodies
99
Q

is apoptosis associated with inflammation?

A

NO

100
Q

are lysosomal enzymes released in apoptosis?

A

NO

101
Q

when T lymphocytes are killed in thymus gland, the thymus is not inflamed because it undergoes what kind of cell death?

A

apoptosis

102
Q

large number of cells are involved with what type of cell death?

A

necrosis

103
Q

single cells or small groups of cells are involved with what type of cell death?

A

apoptosis

104
Q

dead cells by apoptosis are removed by ______.

A

macrophages

105
Q

you identify an area of tissue death on right chest with an abscess and inflammation, what process is most likely responsible for the presentation?

A

necrosis

106
Q

what is atrophy?

A

Shrinkage in cell size by loss of cell substance

107
Q

If prolonged, atrophy may progress to cell death by _______.

A

apoptosis

108
Q

This term also used to describe reduction in organ size, usually resulting from disease

A

atrophy

109
Q

type of atrophy with Normal changes in cells and organs, generally related to developmental or hormonal changes

A

Physiologic atrophy

110
Q

Embryo development,
Decreased workload,
Change in degree of endocrine stimulation, and
Aging (i.e., reduced skeletal muscle mass)
all result in what type of atrophy?

A

physiologic

111
Q

type of atrophy with Changes in cells and organs related to some pathology

A

Pathologic atrophy

112
Q

Loss of innervation (e.g., carpal tunnel syndrome) is what type of atrophy?

A

Pathologic atrophy

113
Q

Diminished blood supply (e.g., vascular dementia) is what type of atrophy?

A

Pathologic atrophy

114
Q

Inadequate nutrition (e.g., muscle wasting) is what type of atrophy?

A

Pathologic atrophy

115
Q

Loss of endocrine stimulation (e.g., pituitary pathology) is what type of atrophy?

A

Pathologic atrophy

116
Q

hypothenar eminence will be atrophied in what syndrome?

A

carpel tunnel syndrome

117
Q

what is hypertrophy?

A

An increase in the size of cells with resulting increase in organ size

118
Q

in hypertrophy, Size is related to _______.

A

increased cellular components ( e.g., myofilaments)

119
Q

hypertrophy is Physiologic, or pathologic, or both

A

both

120
Q

______ related to increased functional demand or specific hormonal stimulation

A

Physiologic hypertrophy

121
Q

does Physiologic hypertrophy enhance function

A

yes

122
Q

hypertrophy type Physiologically related to increased functional demand or specific hormonal stimulation, causing pathology

A

Pathologic hypertrophy

123
Q

hypertrophy type that results in reduced function

A

Pathologic hypertrophy

124
Q

Acromegaly is an example of ______ hypertrophy, caused by growth hormone excess

A

Pathologic hypertrophy

125
Q

what is an increase in the number of cells in an organ or tissue, possibly resulting in increased volume

A

hyperplasia

126
Q

Requires DNA synthesis, only occurs in cells capable of proliferating

A

hyperplasia

127
Q

Stimulated by growth factors, some cytokines and hormones

A

hyperplasia

128
Q

is hyperplasia physiologic, pathologic, or both

A

both

129
Q

what is physiologic hyperplasia

A
  • hormonal
    i. e. menstrual cycle
  • compensatory
    i. e. wound healing
130
Q

what is pathologic hyperplasia

A
  • may predispose to neoplasm due to increased DNA synthesis

i. e. proliferation of cells of prostate gland causing benign prostatic hyperplasia

131
Q

A reversible change in which one adult cell type is replaced by another adult cell type in order to function under stress or other pathologic stimulus

A

metaplasia

132
Q

What is usually caused by chronic irritation and inflammation and may predispose to neoplasia

A

metaplasia

133
Q

example of metaplasia

A

Squamous to columnar epithelium change due to acid reflux in distal esophagus – Barrett’s metaplasia

134
Q

Is metaplasia ever normal?

A

NO - implied that some sort of stress is occurring

135
Q

Deranged cell growth within a tissue, with cells of varied shape, size, appearance, associated with genetic mutations

A

dysplasia

136
Q

Loses the morphological characteristics of mature, differentiated cells

A

dysplasia

137
Q

_______ cells may become _______ with continued exposure to offending agent

A

Metaplastic cells may become dysplastic with continued exposure to offending agent

138
Q
  • Related to chronic irritation, inflammation, other pathologic stimuli (e.g., human papilloma virus infection)
  • Considered premalignant
A

dysplasia

139
Q

stages of wound healing

A
  • Inflammatory
  • proliferative
  • remodeling
140
Q
  • immediate to 2-5 days
  • Hemostasis (vasoconstriction, platelet aggregation, thrombus formation)
  • Inflammation (vasodilation, diapedesis and phagocytosis)
A

inflammatory phase

141
Q
  • 2 days to 3 weeks
  • Granulation (plasma protein deposition, fibroblast ingrowth and collagen deposition, capillary ingrowth)
  • Contraction (wound edges begin to pull together)
  • Epithelialization (epithelial cells grow over new granulation tissue to 3 cm)
A

proliferative phase

142
Q
  • 3 weeks to 1-2 years
  • Reorganization of fibrotic tissue (scar), vasculature
  • Tissue tensile strength increases up to ~80% its original strength
A

remodeling phase

143
Q

Wound edges are approximated (brought together) by sutures or other mechanisms to enhance healing rate and outcome

A

Healing by first intention (primary union)

144
Q

Wound edges are not approximated, defect fills in over time

A

Healing by second intention (secondary union)

145
Q

results in a large tissue defect that must be filled by gradual expansion of granulation tissue

A

healing by second intention

146
Q
  • Granulation tissue must grow in from margins
  • More intense inflammation, much longer to heal
  • Increased likelihood for significant scarring and wound contracture
A

healing by second intention

147
Q

should you let wounds “air out”?

A

NO - don’t want them to dry out bc then will have to remake new capillaries and epithelial cells

148
Q

Repair of damaged tissue requires replacement of parenchymal cells AND stromal proteins

A

fibrosis

149
Q
  • Fibroblast migration (on plasma protein matrix) and proliferation
  • Collagen matrix deposition
  • Growth of new blood vessels (angiogenesis)
  • Remodeling
A

components of fibrosis

150
Q

what is the first type of tissue to be produced?

A

granulation tissue

151
Q
  • New connective tissue from fibroblasts and capillary networks that form at the base of a wound
  • Typically grows from the base of a wound and fills the wound slowly (may over-grow – “proud flesh”)
A

granulation tissue

152
Q

Result of site-specific changes in balance of collagen / matrix synthesis versus degradation by tissue metalloproteinases

A

tissue remodeling

153
Q

produced by many tissue cells, and they are rapidly inactivated by tissue inhibitors of metalloproteinase produced by many of the same tissues

A

metalloproteinases

154
Q

what are some modifiers of wound healing?

A 
Nutrition
Metabolic status
Circulatory status 
Glucocorticoids 
Infection 
Foreign bodies i
Size, location, type of wound 
Early stress on wound
155
Q

Tensile strength of wound increases slowly to ___% by __-__ months (its new maximum strength)

A

Tensile strength of wound increases slowly to 80% by 3-12 months (its new maximum strength)

156
Q

Increased ____ strength related to net collagen ____ and collagen _____ _______

A

Increased tensile strength related to net collagen deposition and collagen cross linking

157
Q

wound repair pathology

A

Dehiscence
Hypertrophic Scarring
Contracture

158
Q

opening of a previously closed wound and associated with poor wound closure

A

dehiscence

159
Q
  • Causes include excessive stress, poor suture technique
    Ie abdomen bc of viscera trying to push out against opening
  • Usually occurs between 7 and 10 days post operatively
A

dehiscence

160
Q
  • Should be assumed that the defect involves the entire wound (full length, full depth)
  • May also be associated with ulceration in areas of impaired vascularity (e.g., sutures too tight)
A

dehiscence

161
Q
  • Genetic predisposition, especially with darker skin
  • Excessive granulation tissue, blocks re-epithelialization
  • Often hyperpigmented
A

hypertrophic scarring (keloid)

162
Q
  • Increased collagen and matrix deposition occurs as wound edges approach each other, followed by collagen crosslinking and “contraction”
  • great with healing by second intention
A

wound contracture

Pathophysiology (4 decks)

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