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
2
Q
To treat disease effectively, we must understand what 3 things?
A
- Normal processes being disturbed
- Characteristics of the disturbance
- Secondary effects of the disturbances
3
Q
Example of Secondary effects of the disturbances
A
comorbidity
complications
4
Q
Factors Affecting “Normal”
A
- Genetic variations (e.g., Gilbert’s syndrome)
- Cultural variations (e.g., diet, literacy)
- Age differences (e.g., body composition)
- Gender differences (e.g., Hct, Hgb)
- Situational differences (e.g., altitude-Hct)
- Diurnal variations (e.g., serum cortisol)
5
Q
what is Etiology?
A
the cause(s) or reason(s) for disease or functional alteration(s)
6
Q
what is pathogenesis?
A
the sequence of events in response to injury or disease
7
Q
what characteristic changes in the appearance of tissues or cells associated with disease
A
Morphologic changes
8
Q
Functional alterations and clinical significance are determined by ____.
A
cellular changes:
which result in signs, symptoms, clinical course and expected outcome
9
Q
what is natural history?
A
Natural history is the progression from initial change to recovery or death
10
Q
what is a lesion?
A
Lesion is a tissue abnormality caused by disease or trauma
11
Q
what is a sign?
A
is an objective finding, documentable (you can experience it)
12
Q
What is a symptom
A
is a subjective feeling or complaint (what the patient says has happened)
13
Q
what are Sequelae
A
Sequelae are conditions resulting from disease or trauma
14
Q
what are complications?
A
Complication is a new problem resulting from the presence of a disease
(sinusitis from pneumonia)
15
Q
_____ describes the disappearance of a disease and return of health
A
resolution
16
Q
Alterations/mutations result in abnormal protein production (e.g., cystic fibrosis) is what Etiologic Classification of Disease?
A
Inherited (familial)
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
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
19
Q
disorders that appear in utero or appear shortly after birth?
A
Congenital disease
20
Q
Gradual breakdown of tissue and loss of function (e.g., osteoarthritis) is what Etiologic Classification of Disease?
A
Degenerative
21
Q
Loss of growth control (e.g., lung cancer) is what Etiologic Classification of Disease?
A
Neoplastic
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
23
Q
poison ivy is what type of disorder?
A
Immunologic disease
24
Q
Microorganisms, parasites, toxins, tissue destruction (e.g., influenza) are what Etiologic Classification of Disease?
A
Infectious
25
Trauma or toxicity (e.g., burn) are what Etiologic Classification of Disease?
Physical agent-induced
26
Deficiency and excess of nutrients (e.g., vitamin D deficiency, hypervitaminosis A) are what Etiologic Classification of Disease?
Nutritional
27
Caused by the health care system (e.g., errors, therapy, complication, misdiagnosis) is what Etiologic Classification of Disease?
Iatrogenic
28
Originating in the mind (e.g., somatoform disorders) is what Etiologic Classification of Disease?
Psychogenic
29
when Cause is unknown (e.g., idiopathic scoliosis) what is the Etiologic Classification of Disease?
Idiopathic
30
misdiagnosis is an example of what classification of disease?
Iatrogenic
31
Cell-cell communication occurs via secreted molecules (____) which interact with complementary cell-associated molecules (____)
ligands
receptors
32
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?
murmur
33
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?
Cell surface receptors
34
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?
Intracellular receptors
35
type of receptor on cell membrane and are associated with water soluble hormones
Cell surface receptors
36
type of receptor that is associated with lipid soluble molecules
Intracellular receptors
37
examples of lipid soluble molecules
cortisol. estrogen, testosterone
38
Four types of cell-cell communication
1. autocrine
2. synaptic
3. paracrine
4. endocrine
39
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?
autocrine
40
Rapid onset, short duration, very specific effect is what type of cell-cell communication?
autocrine
41
```
Nervous system (e.g., neurotransmitters in synapse)
is what type of cell-cell communication?
```
Synaptic
42
Rapid onset, short duration, very specific effect
| is what type of cell-cell communication?
Synaptic
43
Chemicals secreted into local area, then rapidly destroyed so only local cells affected (e.g., histamine, eicosanoids)
is what type of cell-cell communication?
Paracrine
44
Slight delay in action, intermediate duration, several actions
is what type of cell-cell communication?
Paracrine
45
Mediators which travel via bloodstream, target cells widely distributed (e.g., protein and steroid hormones) is what type of cell-cell communication?
Endocrine
46
Delayed action, long duration, multiple significant actions is what type of cell-cell communication?
Endocrine
47
when hormone travels through bloodstream and is distributed everywhere is what type of cell communication?
Endocrine
48
Cell growth and division is strictly regulated to address needs of ________, ____, and ____..
tissue growth, development and maintenance
49
Somatic cell division where each daughter cell receives an identical and complete set of 46 chromosomes
Mitosis
50
Gamete (egg and sperm) cell division in which the number of chromosomes is reduced in half (diploid to haploid, 23 in humans)
Meiosis
51
Growth factors are hormones (autocrine, paracrine, endocrine) secreted by cells which affect _________.
the rate of division and path of differentiation of themselves or other cells
52
___ helps cells adapt to stress
Adaptation
53
____ occurs when cells are unable to adapt to stress
injury
54
2 types of cell injury
Reversible injury
| Irreversible injury
55
___ is the end stage of irreversible cellular injury
death
56
2 types of cell death
necrosis and apoptosis
57
what changes start immediately upon injury?
biochemical
58
what changes occur after biochemical derangements?
morphologic
59
The response of the cell to injury depends on:
1. Length of time of exposure to the injurious agent
2. Dose of injurious agent
3. Type of cell and its ability to adapt
60
_____ are less able to adapt to hypoxia than cardiac muscle cells
neurons
61
small dose causes what kind of changes?
minimal
62
Injurious agents interfere with membrane-bound calcium ATPase, allowing ______ to enter cytosol and accumulate in mitochondria and endoplasmic reticulum
calcium
63
Increased intracellular calcium activates (4 enzymes)
1. Phospholipases
2. Proteases
3. ATPases
4. Endonucleases
64
enzyme that destroys membrane phospholipids
Phospholipases
65
enzyme that destroys cell proteins, e.g., cytoskeleton
proteases
66
enzyme that results in ATP depletion
ATPases
67
enzyme that degrades nuclear DNA
Endonucleases
68
Increased intracellular calcium activates enzymes which result in?
Results in biochemical changes, water influx, organelle and cell swelling and loss of function
69
Decrease/loss of ATP within cell due to decrease in oxidative phosphorylation by mitochondria, leading to: (3 things)
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
does lactic acid denature proteins?
yes
71
does lactic acid affect acid base balance?
yes
72
___ changes causes morphological changes
biochemical
73
Morphologic features
| of cell injury (5)
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
morphological changes in cell injury reflect _____ damage.
membrane
75
while examining a ct scan you notice a calcium deposit in the pts coronary artery, this is an indicator of what?
necrotic cell death
76
Critical biochemical events
| 2
1. Inability to reverse mitochondrial dysfunction
| 2. Profound disturbances in plasma membrane function
77
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 ______.
plasma membrane function
78
All cells die either by _______.
necrosis or apoptosis
79
_____ is the type of cell death resulting from irreversible cell injury
Necrosis
80
this type of cell death indicates a pathologic process
necrosis
81
this type of cell death Involves injury to many cells within an area of tissue
necrosis
82
Necrotic cells/tissues initiate an ________, which may further injure surrounding cells and tissues
inflammatory response
83
in necrosis, Release of_____ dissolves affected tissue, may injure surrounding cells and tissues
lysosomal enzymes
84
type of necrosis that results from denaturation of proteins (e.g., ischemic death)
Coagulative necrosis
85
type of necrosis that results from autodigestion resulting in cells dissolving (e.g., bacterial tissue infections and abscess formation)
Liquefactive necrosis
86
type of necrosis that occurs with chronic and granulomatous inflammation, looks “cheesy” (e.g., tuberculosis)
Caseous necrosis
87
heart attack has what type of necrosis in cardiac muscle?
Coagulative necrosis
88
type of necrosis that occurs when fat cells become nectotic, both liquefactive and coagulative necrosis occur (e.g., acute pancreatis)
Fat necrosis
89
bacterial infections/ rapidly growing tumors/ abbesses are associated with what type of necrosis
Liquefactive necrosis
90
granulomas/ tuberculosis are associated with what type of necrosis?
Caseous necrosis
91
type of necrosis associated with adipose tissue
fat necrosis
92
IM injections (corticosteroid shots) have to be in muscle not subcutaneous because it can cause what type of necrosis?
fat necrosis
93
programmed cell death
Apoptosis
94
calcium deposits occurs in areas of _______.
necrotic cell death
95
______ is a distinctive pattern of cell death occurring in specific physiologic and pathologic circumstances
.
apoptosis
96
Physiologic examples of apoptosis (2)
1. Programmed cell death that occurs during embryogenesis and development
2. Hormonal dependent changes in adult tissues
97
Pathologic examples of apoptosis
Certain neurodegenerative diseases, gradual ischemic damage, autoimmune disorders, cancer
98
```
Morphologic characteristics
of apoptosis (3)
```
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
is apoptosis associated with inflammation?
NO
100
are lysosomal enzymes released in apoptosis?
NO
101
when T lymphocytes are killed in thymus gland, the thymus is not inflamed because it undergoes what kind of cell death?
apoptosis
102
large number of cells are involved with what type of cell death?
necrosis
103
single cells or small groups of cells are involved with what type of cell death?
apoptosis
104
dead cells by apoptosis are removed by ______.
macrophages
105
you identify an area of tissue death on right chest with an abscess and inflammation, what process is most likely responsible for the presentation?
necrosis
106
what is atrophy?
Shrinkage in cell size by loss of cell substance
107
If prolonged, atrophy may progress to cell death by _______.
apoptosis
108
This term also used to describe reduction in organ size, usually resulting from disease
atrophy
109
type of atrophy with Normal changes in cells and organs, generally related to developmental or hormonal changes
Physiologic atrophy
110
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?
physiologic
111
type of atrophy with Changes in cells and organs related to some pathology
Pathologic atrophy
112
Loss of innervation (e.g., carpal tunnel syndrome) is what type of atrophy?
Pathologic atrophy
113
Diminished blood supply (e.g., vascular dementia) is what type of atrophy?
Pathologic atrophy
114
Inadequate nutrition (e.g., muscle wasting) is what type of atrophy?
Pathologic atrophy
115
Loss of endocrine stimulation (e.g., pituitary pathology) is what type of atrophy?
Pathologic atrophy
116
hypothenar eminence will be atrophied in what syndrome?
carpel tunnel syndrome
117
what is hypertrophy?
An increase in the size of cells with resulting increase in organ size
118
in hypertrophy, Size is related to _______.
increased cellular components ( e.g., myofilaments)
119
hypertrophy is Physiologic, or pathologic, or both
both
120
______ related to increased functional demand or specific hormonal stimulation
Physiologic hypertrophy
121
does Physiologic hypertrophy enhance function
yes
122
hypertrophy type Physiologically related to increased functional demand or specific hormonal stimulation, causing pathology
Pathologic hypertrophy
123
hypertrophy type that results in reduced function
Pathologic hypertrophy
124
Acromegaly is an example of ______ hypertrophy, caused by growth hormone excess
Pathologic hypertrophy
125
what is an increase in the number of cells in an organ or tissue, possibly resulting in increased volume
hyperplasia
126
Requires DNA synthesis, only occurs in cells capable of proliferating
hyperplasia
127
Stimulated by growth factors, some cytokines and hormones
hyperplasia
128
is hyperplasia physiologic, pathologic, or both
both
129
what is physiologic hyperplasia
- hormonal
i. e. menstrual cycle
- compensatory
i. e. wound healing
130
what is pathologic hyperplasia
* may predispose to neoplasm due to increased DNA synthesis
| i. e. proliferation of cells of prostate gland causing benign prostatic hyperplasia
131
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
metaplasia
132
What is usually caused by chronic irritation and inflammation and may predispose to neoplasia
metaplasia
133
example of metaplasia
Squamous to columnar epithelium change due to acid reflux in distal esophagus – Barrett’s metaplasia
134
Is metaplasia ever normal?
NO - implied that some sort of stress is occurring
135
Deranged cell growth within a tissue, with cells of varied shape, size, appearance, associated with genetic mutations
dysplasia
136
Loses the morphological characteristics of mature, differentiated cells
dysplasia
137
_______ cells may become _______ with continued exposure to offending agent
Metaplastic cells may become dysplastic with continued exposure to offending agent
138
- Related to chronic irritation, inflammation, other pathologic stimuli (e.g., human papilloma virus infection)
- Considered premalignant
dysplasia
139
stages of wound healing
- Inflammatory
- proliferative
- remodeling
140
- immediate to 2-5 days
- Hemostasis (vasoconstriction, platelet aggregation, thrombus formation)
- Inflammation (vasodilation, diapedesis and phagocytosis)
inflammatory phase
141
- 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)
proliferative phase
142
- 3 weeks to 1-2 years
- Reorganization of fibrotic tissue (scar), vasculature
- Tissue tensile strength increases up to ~80% its original strength
remodeling phase
143
Wound edges are approximated (brought together) by sutures or other mechanisms to enhance healing rate and outcome
Healing by first intention (primary union)
144
Wound edges are not approximated, defect fills in over time
Healing by second intention (secondary union)
145
results in a large tissue defect that must be filled by gradual expansion of granulation tissue
healing by second intention
146
- Granulation tissue must grow in from margins
- More intense inflammation, much longer to heal
- Increased likelihood for significant scarring and wound contracture
healing by second intention
147
should you let wounds "air out"?
NO - don't want them to dry out bc then will have to remake new capillaries and epithelial cells
148
Repair of damaged tissue requires replacement of parenchymal cells AND stromal proteins
fibrosis
149
- Fibroblast migration (on plasma protein matrix) and proliferation
- Collagen matrix deposition
- Growth of new blood vessels (angiogenesis)
- Remodeling
components of fibrosis
150
what is the first type of tissue to be produced?
granulation tissue
151
- 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”)
granulation tissue
152
Result of site-specific changes in balance of collagen / matrix synthesis versus degradation by tissue metalloproteinases
tissue remodeling
153
produced by many tissue cells, and they are rapidly inactivated by tissue inhibitors of metalloproteinase produced by many of the same tissues
metalloproteinases
154
what are some modifiers of wound healing?
```
Nutrition
Metabolic status
Circulatory status
Glucocorticoids
Infection
Foreign bodies i
Size, location, type of wound
Early stress on wound
```
155
Tensile strength of wound increases slowly to ___% by __-__ months (its new maximum strength)
Tensile strength of wound increases slowly to 80% by 3-12 months (its new maximum strength)
156
Increased ____ strength related to net collagen ____ and collagen _____ _______
Increased tensile strength related to net collagen deposition and collagen cross linking
157
wound repair pathology
Dehiscence
Hypertrophic Scarring
Contracture
158
opening of a previously closed wound and associated with poor wound closure
dehiscence
159
- 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
dehiscence
160
- 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)
dehiscence
161
- Genetic predisposition, especially with darker skin
- Excessive granulation tissue, blocks re-epithelialization
- Often hyperpigmented
hypertrophic scarring (keloid)
162
- Increased collagen and matrix deposition occurs as wound edges approach each other, followed by collagen crosslinking and “contraction”
- great with healing by second intention
wound contracture
