Pathology 2 Flashcards
(209 cards)
1
Q
What are the forms of repair?
A
Regeneration and scarring
2
Q
What’s regeneration?
A
Repair with the growth of fully functional tissue to replace injured or dead tissue
3
Q
What is required for total pure regeneration?
A
An intact connective tissue scaffold or only superficial injury (so it’s rare)
4
Q
What’s a superficial injury?
A
Only affects epidermal or epithelial layer
5
Q
Scarring replaces injured/dead tissue with ______.
A
Fibrous tissue lacking the specialized function of the tissue it replaces
6
Q
What’s the most common scenario of wound repair?
A
A regeneration/scarring combo
7
Q
Removal of one kidney causes _______. Is this regeneration?
A
Hyperplasia and hypertrophy of the remaining kidney, which doubles in size. Nope, not regeneration.
8
Q
Removal of one lobe of the liver causes ______. Is this regeneration?
A
Hyperplasia and hypertrophy of the remaining lobe, which generate the same volume of fully functional liver tissue as pre-removal. Yep, regeneration.
9
Q
What’s an ulcer?
A
A local defect in the surface of an organ or tissue produced by shedding of inflamed necrotic tissue
10
Q
What’s an erosion?
A
Superficial sloughing of mucosa (or epidermis)
11
Q
T or F: Ulcers are too deep to heal by regeneration.
A
T
12
Q
What’s an adhesion?
A
An abnormal connection between any two things in the body
13
Q
Early on, adhesions are composed primarily of _____. What is this called?
A
Fibrin, fibrinous
14
Q
Later on, adhesions are referred to as _____.
A
Fibrous
15
Q
What’s a fistula?
A
An abnormal opening between two places in the body
16
Q
T or F: Fibrous adhesions are an inevitable side-effect of surgery.
A
T
17
Q
What’s a common complication of fibrous adhesions?
A
Intestinal obstruction
18
Q
_________ cells have self-renewal capacity.
A
Stem
19
Q
Stem cells undergo ____ replication.
A
Asymmetric: in every division, one daughter cell retains self-renewing capacity and the other enters a differentiation pathway to a mature cell.
20
Q
What are pluripotent stem cells?
A
They can give rise to any tissue
21
Q
T or F: Adult stem cells can give rise to any tissue.
A
F: Limited number of tissues
22
Q
What is the replicative capacity of labile cells?
A
They continuously lose cells and replace them by proliferation of mature cells and stem cells
23
Q
What are examples of labile tissues?
A
Skin and linings of the mouth GI tract Bladder Vagina Cervix Uterus Fallopian tubes Exocrine gland ducts Bone marrow
24
Q
What is the replicative capacity of stable cells?
A
They’re composed of cells capable of proliferation, but they’re not normally called on to proliferate
25
What are examples of stable tissues?
```
Liver
Kidney
Pancreas
Smooth muscle tissues
Blood vessel linings
Fibroblasts
```
26
What is the replicative capacity of permanent cells?
They don't proliferate except under extraordinary circumstances
27
What are examples of permanent tissues?
Parenchymal cells of the brain and heart (neurons and cardiac myocytes)
28
Which tissues are particularly vulnerable to radiation injury?
Continuously proliferating labile tissues
29
Erythema
Redness
30
Pruritis
Itching
31
Desquamation
Sloughing
32
Side effects of radiation
- Skin: erythema, pruritis, desquamation, loss of hair
- Chest/Abdomen: vomiting, nausea, diarrhea
- Bone marrow: Leukopenia
33
The process of healing is orchestrated by _____.
Growth factors
34
What does EGF stimulate?
Fibroblast migration and proliferation
35
What does FGF stimulate?
Fibroblast migration and proliferation
Monocyte chemotaxis
Angiogenesis
36
What does PDGF stimulate?
Fibroblast migration and proliferation
Monocyte chemotaxis
(more prevalent early in the process)
37
What does TGF-beta stimulate?
Fibroblast migration and proliferation
Monocyte chemotaxis
Collagen synthesis
38
T or F: TGF-beta is more prevalent early in the repair process.
F: more prevalent later in the process
39
What growth factors mediate monocyte chemotaxis?
PDGF, FGF, TGF-beta
40
What growth factors mediate fibroblast migration and proliferation?
PDGF, EGF, FGF, TGF-beta
41
What growth factors mediate angiogenesis?
FGF and VEGF
42
What growth factors mediate collagen synthesis?
PDGF and TGF-beta
43
What comprises the extracellular matrix?
Basement membrane and interstitium
44
Where is the basement membrane of the ECM?
Right underneath the epithelium and around blood vessels
45
What's the interstitium of the ECM?
Supporting tissue between epithelium and vessels and between cells in connective tissue
46
What does the interstitium of the ECM contain?
Fibrillar collagen, fibrillin, elastin, hyaluronic acid, and proteoglycans
47
Which types of collagen are fibrillar?
I, II, III, and V
48
Review time! What's the general structure of collagen?
3 polypeptide chains braided into a ropelike triple helix
49
What strengthens fibrillar collagen?
Lateral cross links
50
What are characteristics of the classical form of Ehlers-Danlos syndrome?
- A disease that causes defective type V collagen, leading to hypermobile joints and hyperextensible skin
- Autosomal dominant
51
What are characteristics of the vascular type of Ehlers-Danlos syndrome?
- It causes defective type III collagen, which is prevalent in blood vessels and bowel wall
- Autosomal dominant
52
What are characteristics of the kyphoscoliotic type of Ehlers-Danlos syndrome?
- It's due to deficiency of lysyl hydroxyls enzyme, which impairs the cross linking of type I and III collagen
- Results in crooked spines
- Autosomal recessive
53
Fibrillin is secreted by ______ and is a major component of _____.
Fibroblasts, microfibrils
54
Microfibrils serve as scaffolding for the deposition of ________, an integral component of elastin.
Tropoelastin
55
What are the characteristics of Marfan syndrome? :(
- Caused by defects in the fibrillin gene
- Long body, long limbs, fingers, and toes
- Aorta prone to rupture
56
Loss of microfibrils leads to _____.
Excessive TGF-Beta
57
What is being evaluated as treatment for Marfans?
ARBs (angiotensin receptor blockers) that inhibit the activity of TGF-Beta, which is in excess in Marfan syndrome
58
What enzymes catalyze the formation of the covalent bonds cross-linking fibrillar collagen? What cofactor is needed?
Prolyl hydroxylase and lysyl hydroxylase; Vitamin C
59
What happens in vitamin C deficiency?
It weakens blood vessels, resulting in bleeding and poor wound healing
60
What pattern of inheritance do genetic defects in structural proteins tend to have?
Autosomal dominant
61
What pattern of inheritance do genetic defects in enzymes tend to have?
Autosomal recessive
62
What's granulation tissue?
Healing tissue with residual chronic inflammatory cells, cellular debris, fibroblasts, neovascularization, and new collagen
63
What does granulation tissue look like?
Red or pink, soft, and granular
64
What are the number 1 and 2 features that are most characteristic of granulation tissue?
1. Angiogenesis
| 2. Proliferating activated fibroblasts
65
What makes granulation tissue soft?
The new blood vessels of early granulation are leaky and the fluid that leaks out of them makes granulation tissue soft
66
What makes granulation tissue hard?
Replacement of granulation tissue by scar
67
What is organization?
The process replacing injured, necrotic, and inflamed tissue by healing and scar tissue
68
Who's the key player in the process of organization?
Fibroblast
69
What's the order of cell appearance in skin wound inflammation and healing?
1. Neutrophils
2. Macrophages
3. Fibroblasts
4. Lymphocytes
70
What's the order of cell appearance in MI inflammation and healing?
1. Neutrophils
2. Lymphocytes
3. Macrophages
4. Fibroblasts
71
What do macrophages do in skin wounds?
Come early, peak fast, and leave fast
72
What do macrophages do in MI?
Come late, peak slowly, and persist for weeks
73
What's angiogenesis?
The formation of new blood vessels in healing tissue, tumors, and atherosclerosis
74
What mediates angiogenesis?
VEGF (which also increases vascular permeability, endothelial migration, and proliferation)
75
How does angiogenesis work in skin wounds?
Starts early, peaks soon, and dissipates fast
76
How does angiogenesis work in MI?
Begins simultaneously with fibroblast infiltration on day 4, and persists for weeks
77
What are the phases of skin wound healing?
Inflammation
Proliferation
Maturation
78
When does healing by first intention occur?
When wounds are clean, uninfected, and have their edges approximated by sutures
79
When does healing by second intention occur?
In larger wounds with commonly irregular edges
80
In healing by first intention, on what day do all the playas come in?
1: Neutrophils
2: Epithelial cells
3: Macrophages
4: Fibroblasts
5: Granulation, angiogenesis
7-14: Collagen
81
What happens in healing by second intention?
- A larger blood clot fills the space of the wound
- More intense inflammation and more granulation tissue
- Wound contraction by myofibroblasts
- Scar formation
- Tissue remodeling
- Thinning of epidermal layer
82
The third phase of healing is a matter of ______.
Tissue remodeling, which alters the cellular content and extracellular matrix
83
What is the "high point" of healing?
The proliferative phase (middle phase)
84
What are the most characteristic features of the proliferative phase?
1. Angiogenesis
| 2. Fibroblast proliferation
85
What is the most important growth factor driving angiogenesis?
VEGF
86
What do VEGF growth factors do?
Stimulate migration and proliferation of endothelial cells at the site of injured blood vessels, which sprout new blood vessels
87
When is neovascularization harmful?
In some retinal diseases such as wet diabetic retinopathy, macular degeneration, and retinopathy of prematurity
88
How do you treat retinal diseases where neovascularization is harmful?
By injecting antibody to VEGF into the eye
89
What is the most important growth factor driving fibroblast migration, proliferation, and collagen synthesis?
TGF-beta
90
Remodeling of ECM requires ________.
Breaking down collagen and other matrix components
91
What enzymes assist in the break down of collagen and other ECM components? (5)
```
Matrix metalloproteinases (MMP-1, 2, etc)
Cathepsin G
Plasmin
Neutrophil elastase
Serine proteinases
```
92
Matrix metalloproteinases depend on ____ for their action.
zinc
93
How are MMPs controlled?
By TIMPS (tissue inhibitors of metalloproteinases) and by tight control of their synthesis and secretion
94
How does location of a wound affect its healing?
Relative blood supply determines how well a wound heals
95
What can impair wound healing?(11)
1. Infection
2. Age
3. Diabetes
4. Anemia
5. Corticosteroids
6. Mechanical stress
7. Poor perfusion
8. Foreign material
9. Obesity
10. Chemo/radiation
11. Fibroblast aberrancy
96
What is the most important cause of impaired wound healing?
Infection
97
How can corticosteroids delay wound healing?
By inhibiting protein and collagen synthesis
98
How can diabetes mellitus impair wound healing?
Primarily because of microangiopathy (small blood vessel disease) associated with it, but it also pours excess sugar into the wound (nutrients for infecting organisms)
99
How can anemia delay wound healing?
It decreases oxygen delivered to the site of repair
100
Why was grandma right about not picking your scabs?
It can disrupt the underlying partial epidermal layer and granulation tissue, setting back the healing process
101
What's dehiscence?
Rupture of a surgical wound or anastomosis
102
What's a hernia?
Protrusion of a body part somewhere it doesn't belong
103
Keloid
Hypertrophic scar
104
Contracture
Abnormal excess wound contraction resulting in deformity and impaired movement
105
Where is contracture most common and what disease is associated with it?
Palms (Dupuytren's contracture)
Soles (Lederhosen disease)
Penis (Peyronie disease)
106
What's fibrosis?
Excessive interstitial collagen deposition usually due to chronic inflammation, recurring injury, persistent toxin, radiation, or autoimmune attack
107
What causes the WORST fibrosis? And why?
Autoimmune diseases because the inciting agent is continually present and can't be limited or eliminated
108
What's scleroderma?
It shows how bad fibrosis can be! Progressive fibrosis of the fingers until they're fixed into a claw hand, sometimes with gangrene of the fingertips. The face undergoes fibrosis until its frozen into an "iron mask". It kills peristalsis to move food into the stomach. It also leads to renal failure. Basically your life is the worst.
109
Who made the link of disease to malfunction at the cellular level?
Virchow
110
What are common causes of cell injury? (7)
1. Oxygen deprivation
2. Physical agents/trauma
3. Chemical agents and drugs
4. Infectious agents
5. Immunologic reactions
6. Genetic derangements
7. Nutritional imbalances
111
T or F: All cells have potential for exhibiting both reversible and irreversible cell injury.
T
112
If an injurious stimulus is such that a cell can recover, you'll see ______.
Reduction in biochemical and physiological function
113
T or F: You'll see gross pathologic changes due to cell injury first.
Nope, you'll see those last
114
Atrophy
Decrease in the size and function of a cell or organ
115
Common causes of atrophy (6)
1. Disuse
2. Loss of innervation
3. Diminished blood supply
4. Inadequate nutrition
5. Loss of endocrine stimulation
6. Aging
116
What are gyri vs. sulci?
Gyri: brain substance
Sulci: spaces between the substance of the brain
117
If you have brain atrophy, what happens to the sulci?
They get bigger
118
Hypertrophy
Increase in size of a cell caused by an augmented functional demand or specific hormonal stimulation
119
Growth in the size of uterine muscle fibers during pregnancy is an example of _______.
Physiologic hypertrophy
120
Increased thickness of the left ventricular wall of the heart in systemic hypertension is an example of ______.
Pathologic hypertrophy
121
Hyperplasia
Increase in the number of cells in an organ or tissue
122
Increased number of lactational units in the breast during pregnancy is an example of ______.
Physiologic hyperplasia
123
What's an example of pathologic hyperplasia?
Benign prostatic hyperplasia
124
Malignancy of epithelial tissue is known as ______.
Carcinoma
125
Polyploidy
The state of a cell nucleus containing three or more haploid chromosomal sets
126
T or F: Polyploidy may occur naturally or as cellular adaptation.
T
127
T or F: Polyploidy is an indicator of unrestricted cell growth.
It's an indicator but it doesn't always indicate unrestricted cell growth
128
Metaplasia
Conversion of one differentiated cell type to another differentiated cell type
129
T or F: Metaplasia is irreversible.
F
130
What are the types of metaplasia?
Epithelial metaplasia and mesenchymal metaplasia
131
Epithelial metaplasia commonly occurs as a precursor to ______.
Dysplasia/neoplasia
132
T or F: Mesenchymal metaplasia is commonly preneoplastic.
F: rarely if ever
133
What effects can smoking have on respiratory epithelium?
Can change pseudoolumnar ciliated epithelium to squamous epithelium
134
What effects can HPV have on cervical epithelium?
Can change columnar to squamous
135
Dysplasia
Alteration of size, shape, and organization of the cellular components of a tissue
136
What are the characteristics of dysplasia?
- abnormal size and shape of cells
- enlargement, irregularity, and hyperchromasia of the nuclei
- disorderly arrangement of cells within the epithelium
- generally a preneoplastic condition
137
T or F: Dysplasia is almost always preneoplastic.
T
138
Which pigments are brown?
- Iron compounds
- Lipofuschin
- Melanin
139
What entities are responsible physiologically for iron stores?
Ferritin and hemosiderin
140
What is the principal storage form of iron?
Ferritin
141
What does hemosiderin consist of?
Intracellular granules in iron-storing cells
142
What is hemochromatosis?
A hereditary disorder in which too much iron is absorbed or retained
143
What is hemosiderosis?
Iron overload due to systemic or local causes
144
Hemosiderin is visible by _____.
Routine microscopy
145
Hemochromatosis is an (exogenous/endogenous) disease of iron storage, and hemosiderosis is (exogenous/endogenous).
Hemochromatosis: endogenous
Hemosiderosis: exogenous
146
What stain can be applied to brown iron pigment to make it blue?
Prussian blue stain
147
What's lipofuschin?
- "Wear and tear pigment"
- A brown pigment of aging
- A polymer of oxidized lipids which are present in long-lived cells
148
What's melanin?
- Brown pigment normally present in the basal layer of skin, retina, and some other ectodermal derived tissues
- Absorbs harmful UV light
149
Black pigments encountered in pathology most often include ______.
Carbon
150
What is anthracosis?
Black pigment grossly and microscopically in the lungs, pulmonary lymph nodes, and in distant tissues
-Permanent but harmless as long as surrounding tissues don't react to the carbon
151
What happens when silica is inhaled at the same time as carbon?
Bad things happen
152
What benefit does proper calcification provide?
Maintains our skeletal framework
153
What is dystrophic calcification?
- Generally localized process, related to some tissue injury
| - Plasma calcium levels are normal
154
What is metastatic calcification?
- Generalized process, may be calcification of many tissues
- Calcium levels may be elevated
- May be disarrangement of the balance between calcium and phosphate
155
Which is more common: dystrophic or metastatic calcification?
Dystrophic
156
Calcium salts using _________ and _______ stain are purple.
Hematoxylin and eosin
157
When does dystrophic calcification have a positive clinical use?
In mammograms
158
Why might water and electrolytes leak into cells?
Due to vacuole formation or to hydropic swelling
159
T or F: Hydropic swelling is an early indicator of cell damage.
T
160
Which lipids may accumulate in cells under abnormal conditions?
Triglycerides and cholesterol
161
What is xanthelasma?
Soft, yellow, orange-like plaques on the eyelids or on the medial canthus; they represent abnormal lipid deposition
162
How are triglycerides seen grossly?
As yellow, greasy deposits in diseased organs whose cells are engorged with triglyceride droplets and vacuoles (Steatosis)
163
Where is steatosis most common?
Liver (most common!), but also in heart, skeletal muscle, and kidney cortex
164
What is kwashiorkor?
- A disease related to a low protein/high carb diet
| - Results from the lack of protein synthesis and retention of lipid components
165
Abnormal deposition of cholesterol can lead to _______.
Can lead to severe disease or may only be a histologic curiosity
166
________ may increase intracellularly in conditions such as diabetes or hypoxia.
Glycogen
167
Where might you see a Laffora body?
In some severe CNS diseases
168
Where might you see corpora amylaceae?
Typically extracellular; may be seen in the meninges, ventricles, and in the ependyma
-generally of no significance
169
What is Mallory's alcoholic hyalin?
Condensed cytoskeletal protein seen in the cytoplasm of patients who have been exposed to alcohol in extreme amounts over long periods of time
170
Homeothermic
Capable of maintaining body temperature within very narrow limits
171
What temperature reflects the temperature of the core of the body most accurately?
The esophagus at the cardia
172
Normal body temperature can vary due to ___________.
Exogenous or endogenous factors
173
What are examples of exogenous factors that can change the normal core temperature?
```
Climatological environment
Peripheral insulation
Diet
Physical activity
Drugs
```
174
What are examples of endogenous factors that can change the normal core temperature?
```
Rhythms (i.e. circadian rhythm)
Gender
Age and body size
Subcutaneous insulation
Water content
Physiological state
```
175
Most energy is lost as ____.
Heat
176
Total energy expenditure =
Internal heat produced + external work performed + energy stored
177
Radiation
Heat transmitted via electromagnetic waves
178
Conduction
Heat transfer within a solid or between two or more solids in close contact
179
Convection
Heat transfer in a fluid or between a fluid and a solid
180
Evaporation
Heat transfer by means of a change in state, from a liquid to a gas.
181
What factor affects evaporation?
Humidity -- dry air increases evaporation, humid air decreases evaporation
182
What is the zone of thermal neutrality?
The range of ambient temperature in which the body maintains its heat balance without increasing heat production or loss above their minimum level
183
T or F: Higher the ratio SA/V, higher the heat loss.
T duhh
184
What serves as the primary overall integrator of reflexes and the brain's inner thermostat?
Hypothalamus
185
Where are warm fibers located?
In Ruffini's corpsucles
186
Where are cold fibers located?
In the end-bulb of Krause
187
What effect does epinephrine have on metabolic activity?
It increases metabolic activity
188
(Vasodilation/Vasoconstriction) leads to reduced heat loss.
Vasoconstriction
189
Neonatal ______ may occur if brown fat is lacking.
Hypothermia
190
How does thyroid hormone affect metabolic rate and heat production?
TH acts on the sodium/potassium pump and increases O2 consumption. This increases metabolic rate and heat production.
191
(Hot/Cold) temperatures activate thyroid hormone.
Cold
192
What is the relationship between hyperthyroidism and temperature control?
Metabolic rate is increased so heat production increases
193
What is the relationship between hypothyroidism and temperature control?
Metabolic rate decreases and there is decreased heat production (extreme sensitivity to cold)
194
What must happen for thyroid hormones to be maximally active?
The sympathetic nervous system must be simultaneously activated by cold temperatures
195
Sweating is accomplished through _______.
Specialized eccrine sweat glands found in the dermis and epidermis
196
Where don't we have eccrine sweat glands?
Margins of the limbs, sex organs, and ear drums
197
Sweat glands consist of __________.
A deep coiled portion and a duct that opens on the skin
198
The duct of the sweat gland aids in ________.
Resorption of electrolytes (mainly Na and Cl) in the sweat so that the fluid discharged onto the skin has a reduced electrolyte concentration
199
Why do we shiver?
It results from somatic activation of skeletal muscles which asynchronously contract.
200
How can you suppress shivering?
It's normally involuntary, but it can be suppressed by higher cortical input (a learned process)
201
What are differences in body temperature in men and women?
1. Core body temperature cools more slowly in women
2. Women can't create as much metabolic heat through exercise or shivering
3. The rate of cooling of the extremities is faster among women
202
What does the body do during heat exhaustion?
- Vasodilation
| - Excess sweating --> decreases ECF volume --> decreased blood volume --> decreased arterial pressure --> fainting
203
What does the body do in heat stroke?
The body temperature increases to a point of tissue damage
204
What is malignant hyperthermia?
A usually hereditary condition where there is a massive increase in metabolic rate
205
What are the differences between fever and hyperthermia?
1. Fever is regulated, hyperthermia is an impairment
2. Fever is independent of ambient temperature, and hyperthermia is dependent on ambient temperature
3. Fever has increased thermopreferendum, and hyperthermia has decreased thermopreferendum
206
What are some microbial stimuli that can induce fever?
Viruses, bacteria, mycobacteria, and fungi
207
What are some non-microbial pathogenic stimuli that can induce fever?
Antigens, inflammatory agents, plant lectins, or host-derived stimuli
208
What are the benefits of fever?
- enhanced neutrophil migration and T-cell proliferation
- enhanced phagocytosis
- increased IFN production/activity
- increased radical production
- reduced growth rate and viability of iron-dependent microorganisms
- increased survival rate
209
What are some hazardous effects of high or prolonged fever?
- dehydration
- delirium
- cardiopulmonary strain
- negative nutrient balance
- teratological consequences
