4. Altered Cellular and Tissue Biology Flashcards
1
Q
Decrease or shrinkage of cell size
A
atrophy
2
Q
Increase in size of cells
A
hypertrophy
3
Q
Increase in the number of cells (from an increased rate of cellular division)
A
hyperplasia
4
Q
Abnormal changes in size, shape, or organization of mature cells
A
dysplasia
5
Q
Reversible replacement of one mature cell type by another
A
metaplasia
6
Q
What 2 types of cellular adaptation occur in non dividing cells?
A
atrophy and hypertrophy
7
Q
What types of body structures undergo atrophy?
A
skeletal muscles, heart, brain, and secondary sex organs
8
Q
Physiologic vs Pathologic atrophy
A
- Physiologic: normal process that usually occurs in early development (ex. thymus in children) - Pathologic: due to decreased pressure, use, blood, nutrition, hormones, or stimulation (ex. disuse atrophy in skeletal muscle)
9
Q
Explain the ubiquitin-proteasome pathway
A
proteins conjugated to ubiquitin -> degraded by proteasomes (increased activity in atrophy)
10
Q
chronic malnutrition atrophy is often accompanied by what?
A
autophagy -> autophagic vacuoles contain cellular debris and enzymes
11
Q
What types of body structures undergo hypertrophy?
A
striated muscle (skeletal and cardiac) and kidneys
12
Q
Physiologic vs Pathologic cardiac hypertrophy
A
Physiologic: temporary and preserves myocardial structure (ex. endurance training, postnatal development, and pregnancy) Pathologic: includes aging, strenuous exercise, sustained workload or stress
13
Q
What is is called when cardiac hypertrophy is reversed?
A
regression
14
Q
When does renal hypertrophy mainly occur
A
when 1 kidney is removed and the other one has to compensate for the loss
15
Q
Explain compensatory hyperplasia. Where is it significant?
A
adaptive and allows for some organs to regenerate (epidermal and intestinal epithelia, hepatocytes, BM cells, and fibroblasts)
16
Q
Explain hormonal hyperplasia
A
occurs in estrogen-dependent organs in response to hormonal stimulation (uterus and breast)
17
Q
Explain pathologic hyperplasia
A
abnormal proliferation of normal cells (usually in response to excessive hormonal stimulation or GF on those cells)
18
Q
2 most common examples of pathologic hyperplasia
A
- hyperplasia of the endometrium (over secretion of estrogen) - BPH (due to changes in hormonal balance)
19
Q
Dysplasia is also known as what?
A
atypical hyperplasia -> not a true adaptive change
20
Q
Most common tissues to undergo dysplasia
A
epithelial tissue of the cervix (due to HPV) and respiratory tract
21
Q
T/F: Dysplasia means the presence of cancer
A
False; dysplasia does NOT indicate cancer and may not progress to cancer if stimulus is removed early on
22
Q
If metaplasia is not reversed, what can it advance to?
A
Dysplasia and possible cancerous transformations
23
Q
Cellular injuries can be reversible or irreversible -> also know as what?
A
sublethal or lethal
24
Q
Explain the general mechanisms of cellular injury (regardless of cause)
A
- depletion of ATP - mitochondrial damage - O2 and O2-derived free radical membrane damage - protein folding defects - DNA damage - calcium level changes
25
Hypoxia vs Hypoxemia
- Hypoxia: decreased O2 in tissues - Hypoxemia: decreased O2 in bloodstream (most likely to occur first)
26
Most common cause of hypoxia
ischemia (reduced blood supply)
27
What causes ischemia
narrowing of arteries (arteriosclerosis) or complete occlusion by clots (thrombosis)
28
Which is better tolerated - acute or progressive hypoxia? Why?
Progressive -\> allows time for adaptive changes in cells
29
Explain what causes a cell to swell w/ hypoxic injury
decreased mitochondrial O2 -\> decreased ATP -\> Na/K pump failure -\> increased intracellular Na -\> increased intracellular H2O -\> swelling
30
Explain what causes a decrease in protein synthesis w/ cellular hypoxic injury
increase intracellular H20 -\> dilation of ER -\> detachment of ribosomes
31
Explain what causes nuclear chromatin clumping w/ cellular hypoxic injury
decrease in O2 -\> decrease in ATP -\> increase anaerobic glycolysis -\> decrease glycogen -\> increase lactate -\> decrease pH -\> chromatin clumping & DNA damage
32
Explain changes to Na, K, and Ca during cellular hypoxic injury
- increased intracellular Na - increased extracellular K - increased intracellular Ca
33
Where is intracellular Ca released from?
mitochondria and smooth ER
34
Name 4 mechanisms for ischemia-reperfusion injury
- oxidative stress - increased intracellular Ca - inflammation - complement activation
35
Name 3 types of reactive oxygen species (ROS)
- hydroxyl radical (OH-) - superoxide radical (O-) - hydrogen peroxide (H2O2)
36
How does cell structure change after reperfusion injury?
ischemic cell = swollen reperfusion injured cell = necrotic
37
electrically uncharged atom or group of atoms that has an unpaired electron -\> capable of injuring chemical bonds
free radical
38
Effect of free radicals on lipids
lipid peroxidation (destruction of polyunsaturated lipids) -\> increased membrane permeability
39
Effect of free radicals on proteins
fragmentation of polypeptide chains -\> protein misfolding -\> lose ion pumps and transport proteins
40
Effect of free radicals on DNA
causes mutations and decreased protein synthesis
41
List 5 mechanisms to classify chemical injuries by
- direct damage (on-target toxicity) - exaggerated response (ex. OD) - biologic activation to toxic metabolites (includes free radicals) - hypersensitivities and other immune reactions - rare toxicities
42
main systems affected by lead (Pb)
nervous system and blood
43
Lead toxicity is a primary hazard for who?
children and during pregnancy (can cause lower IQ, learning disorders, and ADHD)
44
Blood lead level of intoxication
10 um/dL
45
carbon tetrachloride (CCl4) affects what organ
liver
46
Explain how CO causes hypoxic injury
has a higher affinity for hemoglobin than O2 -\> carboxyhemoglobin
47
Sxs of CO poisoning
dizziness, weakness, N/V, headache, tinnitus, confusion, and chest pain
48
Primary systems affected by ethanol
brain and liver
49
What nutrition deficiencies are associated w/ ethanol?
Mg, B6, thiamine, and phosphorus; folic acid is a problem for chronic drinkers
50
Explain changes seen between acute and chronic alcoholism
- Acute: depresses the CNS (sedation, loss of coordination, delirium) - Chronic: causes structural alterations in tissue that can metabolize ethanol -\> mostly liver
51
What is the spectrum of structural changes to the liver caused by ethanol?
fatty liver (steatosis) -\> fatty w/ inflammation (steatohepatitis) -\> cirrhosis
52
Where is mercury commonly found?
human activity and silver fillings
53
Active substance in marijuana
tetrahydrocannabinol (THC)
54
How does methamphetamine affect the CNS?
CNS stimulant (produces euphoria)
55
How does crack and cocaine affect the CNS?
potent CNS stimulate -\> blocks reuptake of NE, dopamine, and serotonin
56
What is heroin closely related to and what does it do to the CNS?
- closely related to morphine, methadone, and codeine - high affinity for CNS; acts on receptors, enkephalins, and endorphins
57
partial and total deprivation of oxygen
partial: hypoxia total: anoxia
58
O2 fails to reach blood (occurs in entrapment)
suffocation
59
obstruction of internal airways
choking asphyxiation
60
compression/closure of blood vessels or air passages due to external neck pressure
strangulation
61
compression of the neck by body weight due to a noose -\> leaves an inverted V pattern on neck
hanging
62
strangulation that leaves a horizontal pattern on the neck
ligature
63
strangulation that leaves variable external trauma and internal damage (fx of the hyoid bone)
manual
64
prevents delivery of O2 to tissues or blocks utilization of O2
chemical asphyxiants
65
Name 3 types of chemical asphyxiants
CO, cyanide, and hydrogen sulfide
66
alteration of O2 delivery to tissues due to inhalation of fluids (usually water)
drowning
67
little/no water enters the lungs due to vagal-mediated laryngospasms
dry-lung drowning
68
bleeding into skin or underlying tissues -\> takes time to appear
contusion (bruise)
69
collection of blood in soft tissue that appears quickly
hematoma
70
superficial scrape/graze of the skin
abrasion
71
tear or rip in skin
laceration
72
extreme type of laceration where a wide area of skin is pulled away
avulsion
73
wound is longer than it is deep -\> usually has significant external bleeding w/ little internal bleeding
incised wound
74
penetrating sharp-force injury deeper than it is long
stab wound
75
produced by items w/ sharp points but dull edges (ex. stepping on a nail)
puncture wound
76
heavy edged instruments that produce a combo of sharp and blunt force injuries
chopping wound
77
What will affect the appearance of an entrance gunshot wound?
range of the gunshot
78
What is seen w/ contact range entrance gunshot wound?
- searing of the edges - blowback (gaping or jagged) - muzzle imprints
79
What is seen w/ intermediate range entrance gunshot wound?
- tattooing/stippling: fragments of gunpowder abrade but don't enter the skin
80
appearance is the same regardless of range
indeterminate range entrance wound AND exit wound
81
Necrosis vs Apoptosis
- Necrosis: unprogrammed death; cellular swelling -\> lysis; inflammation; many cells affected - Apoptosis: programmed, organized disassembly; membrane bound shrinkage; no inflammation; one cell or small clusters
82
nucleus gets smaller -\> DNA condenses into shrunken particles
pyknosis
83
fading away of nuclear envelope and nuclear material
karyolysis
84
nuclear fragmentation
karyorrhexis
85
Explain coagulative necrosis
ischemia -\> decrease pH -\> protein degeneration -\> albumin becomes firm and opaque
86
Where does coagulative necrosis occur?
kidneys, heart, adrenal glands
87
Explain liquefaction necrosis
autolysis (hydrolytic enzymes) and heterolysis (bacterial infection) -\> tissue becomes soft, liquefies, and segregates -\> forms cysts
88
Where does liquefaction necrosis occur?
neurons and glial cells of the brain
89
Types of bacteria involved in liquefaction necrosis?
- Staph - Strep - E. Coli
90
Explain caseous necrosis?
- mycobacterium is walled off in a granuloma -\> cells disintegrate but not completely digested (combo of coagulative and liquefaction) - will resemble cottage cheese (soft and granular)
91
Type of bacteria involved in caseous necrosis?
TB pulmonary infection (Mycobacterium tuberculosis)
92
Explain fat necrosis
- occurs by lipases -\> break down triglycerides -\> release FAs that combine w/ Ca, Mg, and Na (saponification) -\> white and chalky
93
Where does fat necrosis occur?
breast, pancreas, and other ABD organs
94
Dry vs wet gangrene
- Dry: poor perfusion (coagulative necrosis) - Wet: poor perfusion + pyogenic infection (liquefactive necrosis)
95
Explain gas gangrene
caused by species of Clostridium -\> produces hydrolytic enzymes and toxins -\> destroy connective tissue and membranes -\> gas bubble form in muscle cells -\> death caused by shock
96
List 4 cellular changes characteristic of aging
- atrophy (decrease cell function) - lack of DNA repairs (possible mutations) - DNA, RNA, proteins, and membranes more susceptible to injury - compensatory hypertrophy and hyperplasia
97
List 2 tissue/systemic changes characteristic of aging
- progressive stiffness/rigidity - sarcopenia (loss of muscle mass/strength)
98
List 4 common themes of mechanisms for sarcopenia
- decrease MSK fibers and MSK protein synthesis - disregulation of anabolic hormones - cytokine production + inflammation - decrease nutrition and activity
99
What occurs during algor mortis?
- body temp decreases 1 degree per hour - by 24 hours -\> body temp = environment
100
What is the main event of livor mortis and how it is physically seen?
- blood pools at the lowest point of the body (due to gravity) - purple discoloration where blood pools (line of demarcation) - can see pupils dilate and become nonreactive to light due to decreased retinal pressure (decrease muscle tension)
101
What is the timeframe for rigor mortis?
starts within 6 hours after death and lasts for approximately 36 hours (then body becomes flaccid)
102
What is the cause of rigor mortis?
acid builds up in muscles -\> delete ATP -\> myosin doesn't work for relaxation -\> rigid muscles (small muscles first)
103
What is postmortem autolysis (putrefaction)?
breakdown of tissues that occurs between 24-48 hours (all cells start necrosing)
104
What speeds up/slows down the process of postmortem autolysis?
- warm environment speeds it up - cold slows it down
