Exam 1: Cell Injury, Death (highlights) Flashcards
1
Q
Define atrophy
A
Decrease in cell size
2
Q
Define protooncogenes
A
Differentiation genes
3
Q
Define hypertrophy
A
Increase in cell size
Enlargement in existing cells, increase in organelle number
4
Q
Define etiology
A
Cause of disease
5
Q
When does cell injury occur?
A
When limits of adaptation dare surpassed or when adaptive responses are not available
6
Q
Symptoms are ___, signs are ____
A
Patient feels; doc observes
7
Q
Define edema
A
Accumulation of fluid in body tissues and cavities
8
Q
In reversible injury, limitations to survival include
A
the nature and duration of the injury and concurrent exposure to other cell stressors
9
Q
Irreversible injury
A
When stimulus surpasses limits of survival
10
Q
Will inflammation occur postmortem (autolysis)?
A
No
11
Q
What is normal HR?
A
60-100 BPM
12
Q
What is normal blood sugar?
A
80-100 mg/dL
13
Q
Define necrosis
A
Cell disorganization
“Structural changes that result from cell death”
14
Q
Define apoptosis
A
Programmed cell death
15
Q
Atrophic cells have _____ but are not dead
A
Diminished function
E.g. muscle atrophy
16
Q
Define idiopathic
A
Unknown cause
17
Q
Define hypoxic
A
Tissue and organ atrophy associated with diminished blood or O2 supply
18
Q
What is the most common reason for hypoxia?
A
Tissue or organ loose O2 supply
19
Q
How does pressure influence pathological atrophy?
A
Compress adjacent structures
20
Q
How does denervation contribute to pathological atrophy
A
Interruption of nerve supply
21
Q
How does endocrine deficiency contribute to pathological atrophy
A
Pituitary insufficiency or another hormone inadequacy
22
Q
Hypertrophy increases the size of structures that consists of
A
Non-dividing (permanent) cells
23
Q
Example of hypertrophy with hypertension
A
Increase in size of heart
24
Q
Example of idiopathic atrophy?
A
Alzheimer’s disease
25
What is an enlargement due to proliferation of cell (increase in number) usually concurrently with hypertrophy
Hyperplasia
E.g. prostate cancer
26
What promotes cancer development?
Hyperplasia
Note: if stimulus is removed, hyperplasia disappears
27
Define metaplasia
Substitution of one type of “mature” cell with another “mature” cell type that may be better suited to cope with altered environment.
28
Barrett’s Esophagus
Columnar cell metaplasia of lower esophagus (gastroesophageal reflux)
29
Marrow hyperplasia and extra-medullary hematopoiesis (severe anemia) are examples of
Metaplasia
30
Define dysplasia
Atypical metaplasia, bad growth
31
What kind of growth is pre-cancerous
Dysplasia
E.g. uterine cervical cancer causes cervical dysplasia from HPV virus
32
In what broad category of disorders would you see increased mitosis?
Dysplasia
33
Commons places of dysplasia
Uterine cervix, ducts of mammary gland, skin, oral, respiratory mucosa
34
Define ischemia
Hypoxic injury due to decreased blood flow
“Ischemic hypoxia”
35
If blood was being shunted away from a tissue to a different tissue (e.g. “steal syndromes”), this would cause what kind of injury in the original tissue?
Ischemia hypoxia
36
Define hypoxemia
Decreased blood oxygen levels
37
What happens in hypoxic injury?
- Decreased synthesis and depletion of ATP (happens early on)
- Oxidative phosphorylation is compromised
- When ATP disrupted = work stops, increased membrane permeability and swelling due to increased Na2+ and water
38
What does a pathologically high amount of calcium activate?
- Phospholipases
- Proteases
- ATPases
- Endonucleases
39
Mitochondrial injury leads to
Irreversible damage and cell death
40
What is a “superficial” common sign early on in most forms of cell injury?
Loss of regulated membrane permeability
Which leads to ATP depletion, activation of phopholipases, direct membrane change
41
Function of antioxidants
To remove/degrade free radicals by spontaneous decay and/or enzyme action
42
A high number of enzymes is indicative of
Higher amount of damage, severe injury, death
43
Necrosis is a response from
exogenous stimuli
44
“Intrinsic” (autolysis)
Self-digestion by enzymes derived from lysosomes within injured cell
45
“Extrinsic” (heterolysis)
Enzymes derived from inflammatory leukocytes act on cell components
E.g. neutrophils, macrophages
46
Nuclear changes that look like shrinkage and increased basophilic staining
Pyknosis (condensation)
47
Nuclear changes that look like fragmentation and breakdown of nuclei
Karyorrhexis
48
Nuclear changes that look like dissolution of nucleus
Karyolysis
49
What type of necrosis is characterized by desaturation of cytoplasmic proteins
Coagulation
50
Clinical example of coagulation
Myocardial infarc
51
Tissue that ends up looking like “fried egg whites” is linked to what type of necrosis
Coagulation
52
Tissue that is lysed by enzymes is characteristically this type of necrosis
Liquefaction necrosis
53
A stroke is an example of what kind of necrosis?
Liquefaction necrosis
54
They of necrosis that has the characteristic of being pyogenic (pus forming)
Liquefaction necrosis
55
Pyogenic
pus forming
56
Type of necrosis that has the characteristic of being “cheesy” in nature
Casseous necrosis
57
What kind of necrosis is commonly caused by TB and leprosy infections?
Casseous necrosis
58
What kind of necrosis is associated with hydrolysis of lipid deposits present in adipose tissue?
Fat necrosis
59
Liver and acute pancreatitis is associated with what kind of necrosis?
Fat necrosis
60
The type of necrosis that is characterized by forming fibrotic deposits (scars)
Gummatous necrosis
61
The type of necrosis that is formed during tertiary stages of syphilis
Gummatous necrosis
62
Coagulation necrosis modified by bacterial activity
Gangrene
63
Mummification
Dry gangrene
64
Moist necrosis combined with bacterial infection and more liquefaction
Wet (moist) gangrene
65
Deep, blood-deprived wounds that get contaminated with spore forming anaerobic bacteria is characteristic of
Gas (infectious) gangrene
66
Organisms that release phospholipases and other lyric enzymes that destroy cells and other tissue elements and produce “gas bubbles” at the sites of infection
Gas (infectious) gangrene
67
Define apoptosis
Programmed cell death
68
What happens with pathological increased blood, urea, creation levels?
Kidney problems
69
Lipid “residual bodies” of certain cells
Lipofuscin
70
Lipofuscin is common when?
During normal aging AND in response to chronic degenerative disease
71
Induction
Expansion
72
Intracellular accumulations also known as
Storage Disorders
73
4 Causes of storage disorders
1. Cell metabolism
2. Abnormal endogenous substances
3. Congenital enzyme abnormalities
4. Abnormal exogenous substances
74
Define fatty metamorphosis
Steatosis, fatty change
75
Accumulation of lipids in parenchymal cells
Fatty metamorphosis
76
What storage disorder is common in the liver resulting from alcohol abuse, diabetes and obesity
Fatty metamorphosis
77
Gross changes in a fatty liver
Enlargement, softening, yellow color, blunted margins
78
Accumulation of lipid products is
Pathogenic mechanism of fatty change in the liver
79
Chronic hypoxia (anemia) leads to _____ in muscle
Tigered effect (Alternating yellow and red bands of tissue)
80
Tigered effect
Alternating yellow (fat) and red (muscle) bands of tissue
81
Tigered effect also known as
Thrush breast
82
Tigered effect / thrush breast is associated with what organ?
Heart
83
Clusters of lipid-containing macrophages in the dermis and tendons
Xanthoma
84
Xanthoma associated with
Hyperlipidemia
85
Increased lipids in the dermis and tendons...
Xanthoma
86
“Foam cells” associated with
Lysosomal storage diseases
87
Clinical sign: macular cherry red spot
Tay Sachs disease
88
Clinical sign: cherry red spot in fovea
Niemann-Pick disease
89
Accumulation of ganglioside
Tay Sachs disease
90
Deficiency in sphingomyelinase
Niemann-Pick disease
91
Deficiency in glucocerebrosidase which leads to accumulation of glucocerebrosides
Gaucher’s disease
92
Synthesis of excessive quantities of immunoglobulins (Ig) by plasma cells give rise to large proteinaceous deposits known as
Russell bodies
93
Russell bodies
large proteinaceous deposits
Note: caused by synthesis of excessive quantities of immunoglobulins (Ig)
94
Mallory bodies
Alcoholic hyaline
95
Lewy bodies
Parkinson’s
96
Neurofibrillary tangles
Alzheimer’s and Huntington’s
97
“mad cow disease” Or CDJ
Prion diseases
98
Stress proteins include
Chaperonins and Upiquitin
99
A stress protein that participates in activities of normal cells that include protein folding, disaggregation and intracellular transport
Chaperonins
100
A stress protein that has a role in remolding denatured proteins
Ubiquitin
101
Amyloidosis
Group of diseases in which amyloid is deposited in organs and tissues
102
Where are amyloid materials derived from?
Peptide fragments of larger proteins
103
Excess/abnormal amyloid proteins disease
Alzheimer’s disease
104
Rheumatoid arthritis, Crohn’s disease and TB and leprosy are examples of
Amyloidosis
105
T/F amyloidosis is curable
False.
Note: Conservative therapies such as dietary choices, supplements and antidote-inflammatory agents are employed.
106
Glycogen storage diseases reflect
“Inborn errors” in glucose or glycogen metabolism
107
Deficiency of G6P
Von Gierke’s disease (type I glycogen storage disorder)
108
Defect in a1-glucosidase (a lysosomal enzyme) is the cause of
Pompe’s disease (type II glycogen storage disorder)
Note: Striated muscle including the heart is affected most, fatal by 1-2 yrs old.
109
Protects against UV light
Melanin
110
Congenital lack of melanin
Albinism
111
Patchy areas of skin
Vitiligo
112
Increased ACTH contributes to
Hyperpigmentation of the skin
113
Ferric ion will block what?
Normal breakdown of melanin
This explains the darker pigmentation of skin in hemochromatosis
114
Increased homogentisic acid in urine gives it a black color
Alkaptonuria
115
Tissue discoloration secondary to accumulated homogentisic acid
Ochronosis
116
Soluble deposits of iron-apoferritin complexes
Ferritin
117
The relatively benign iron storage disorder as iron accumulate in macrophages
Hemosiderosis
118
The iron storage is order associated with organ (perenchymal) damage
Hemochromatosis
119
T/F. Small amounts of ferritin is normally in plasma
True. These levels are indicator fo adequacy of body stores
120
“Bronze diabetes”
Hemochromatosis
121
“perenchymal”
Organ
122
Triad of hemochromatosis
Cirrhosis
Pancreatic fibrosis
Bronzed skin
123
The triad (Cirrhosis, Pancreatic fibrosis, Bronzed skin) is indicative of
Hemochromatosis “bronze diabetes”
124
Aging or wear-and-tear pigment
Lipofuscin
125
brown-colored undigestible lipid derivatives
Lipofuscin
126
“Plumbism”
Lead
127
Most common exogenous pigment
Carbon
128
Excess deposits that affect liver, basal ganglia and eyes
Copper
129
What is Wilson’s disease?
Copper accumulation
130
Fetus calcification is known as
dystrophic calcification or phleboliths
131
Anything that increases calcium is
Hypercalcemia
E.g. increased secretion of parathyroid hormone
132
Ectopic bone formation includes
Myositis ossificans
133
Von Gierke’s disease (deposits in liver and kidney) and Pompe’s disease (accumulations in myocardium) are composed of
Glycogen
134
Mallory bodies (inclusions in injured hepatocytes) and amyloidosis (deposits of complex insoluble materials that appear under a number of circumstances) are composed of
Proteins and protein complexes
135
Tay Sachs disease is composed of
Ganglioside
136
Neumann-Pick disease is composed of
Sphingomyelin
137
Xanthoma is composed of
Cholesterol and other lipids
138
Thrush breast is composed of
Intraparenchymal cell triglycerides
139
Alkaptonuria is composed of
Homogentisic acid
140
The “wear and tear” or brown atrophy seeing in aging and chronic injury is composed of
Lipofuscin
141
Hemochromatosis “bronze diabetes” is composed of
Iron
142
Plumbism is composed of
Lead
143
Wilson’s disease is composed of
Copper
144
How many doublings per adult cell according to Hayflick phenomenon?
50
145
Limitations in doublin capacity are known as
Hayflick phenomenon
