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Pathophysiology > Altered Cellular and Tissue Biology > Flashcards

Altered Cellular and Tissue Biology Flashcards

1
Q

Describe adaptation

A

A reversible, structural, or functional response both to normal or physiologic conditions and to adverse or pathologic conditions. Adaptive changes can occur in cell size, number, phenotype, metabolic activity, or functions of cells.

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2
Q

5 types of adaptation

A

– atrophy

– hypertrophy

– hyperplasia

– dysplasia

– metaplasia

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3
Q

Describe physiological adaptation

A

cellular changes in response to normal stimulation

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4
Q

Describe pathological adaptation

A

cellular changes in response to potentially damaging stimuli

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5
Q

Describe atrophy

A
  • reduction in cell size
  • entire organ can shrink
  • less endoplasmic reticulum (tissue and protein synthesis) + fewer mitochondria
  • muscle cells affected
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6
Q

Causes of atrophy

A
  • disuse
  • denervation
  • impaired nutrition
  • decreased hormonal stimulation
  • decreased blood flow (ischemia)
  • aging
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7
Q

Describe hypertrophy

A
  • increase in cell size
  • increased accumulation of proteins (endoplasmic reticulum, mitochondria, plasma membrane)
  • due to mechanical force/stretch, hormonal stimulation, or growth factor stimulation
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8
Q

Example of physiologic hypertrophy

A
  • uterus during pregnancy growing/stretching due to hormonal/trophic stimulation
  • growing muscles from working out due to mechanical/stretch stressors
  • bladder increasing due to restricted flow from enlarged prostate
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9
Q

Example of adaptive and compensatory pathologic hypertrophy

A
  • adaptive: cardiac myeopathy - causes ventricles to enlarge due to chronic hypertension or disease
  • compensatory: If a diseased kidney is removed, the remaining one will enlarge to meet workload demand
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10
Q

Define hyperplasia

A
  • increase in cell number (proliferation)
  • increased rate of cell division
  • often happens alongside hypertrophy
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11
Q

Example of compensatory physiologic hyperplasia

A
  • if part of the liver is removed, cells will regenerate to compensate (if 70% was removed, it would be regenerated in 2 weeks)
  • wound healing
  • calluses
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12
Q

Example of hormonal physiologic hyperplasia

A
  • in estrogen-dependent organs
  • breast growth during puberty and pregnancy
  • uterus during pregnancy
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13
Q

Example of pathologic hyperplasia

A
  • abnormal proliferation of normal cells
  • endometrial hyperplasia
  • prostate gland hyperplasia
  • HPV/warts
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14
Q

Describe metaplasia

A
  • reversible replacement of one mature cell type by another
  • from chronic irritation/inflammation
  • cell type changes to be more likely to survive
  • risk for cancer increases every time cells are irritated/changed
  • stem cells! differentiation
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15
Q

Describe dysplasia

A
  • also called atypical hyperplasia
  • not a true adaptive change
  • abnormal changes in size, shape, and organization of mature cells
  • deranged/disordered growth due to persistent, severe irritation/injury/inflammation
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16
Q

Causes of cellular injury

A
  • physical agents
  • radiation injury
  • chemical injury
  • biologic agents (infection)
  • nutritional imbalances
  • free radical injury
  • hypoxic cell injury
  • impaired calcium homeostasis
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17
Q

Causes of cellular injury by physical agents

A
  • mechanical/blunt force (ex: tear, shearing, crushing)
  • contusion, laceration, gun shot, fractures, sharp force
  • extreme temperature (hypothermic/hyperthermic)
  • electrical
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18
Q

Causes of cellular injury by radiation

A
  • ionizing: removes electrons & can cause DNA/RNA damage, ROS, oxidative stress, and cell death
  • non-ionizing: visible light, microwaves, radio waves
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19
Q

Causes of cellular injury by chemicals

A
  • liver most often affected (where drugs are metabolized)
  • direct damage/on-target toxicity: when chemicals and drugs combine directly with critical molecular substances (ex: cyanide)
  • exaggerated response at target (overdose)
  • biologic activation to toxic metabolites (including free radicals)
  • hypersensitivity reactions
  • rare toxicities
  • ex: chemotherapeutic drugs, drug abuse/addiction, social drugs (alcohol), air pollutants, insecticides, herbicides, carbon monoxide, lead, mercury (xenobiotics)
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20
Q

Causes of cellular injury by biologic agents

A

ex: anthrax
- invasion and destruction

  • toxin production
  • hypersensitivity reactions
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21
Q

Causes of cellular injury by nutritional imbalances

A
  • obesity
  • malnutrition
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22
Q

Define a free radical

A
  • electrically uncharged atom or group of atoms with an unpaired electron
  • unstable: become stabilized by donating or accepting an electron
  • highly reactive: can react with most molecules in their proximity
  • cause chain reactions and difficult to control
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23
Q

Describe hypoxia

A
  • lack of sufficient oxygen
  • most common cause of cellular injury
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24
Q

Ischemia definition

A
  • reduced blood supply to tissue
  • tissue can adapt, undergo reversible injury, or die
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25
Q

Cellular responses to hypoxic cell injury

A

insufficient ATP production

  • lack of ATP = increased anaerobic metabolism (ATP from glycogen), when glycogen is depleted, anaerobic metabolism stops
  • ATP reduction = sodium-potassium pump and sodium-calcium exchange failure → intracellular accumulation of sodium and calcium, potassium leaves cell → sodium and water enter cell freely → cellular swelling and dilation of endoplasmic reticulum → ribosomes detach from rough ER → reduced protein synthesis
  • vacuolation (formation of vacuoles): within cytoplasm, swelling of lysosomes and mitochondria → damage to outer membrane
  • accumulation of calcium: activates multiple enzyme systems that damage the membrane and cytoskeleton, degrade DNA and chromatic, deplete ATP, and lead to cell death
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26
Q

What is ischemia-reperfusion injury?

A
  • occurs with restoration of oxygen
  • results from generation of highly reactive oxygen intermediates (free radicals/oxidative stress)
  • radicals can cause membrane damage and mitochondrial calcium overload
27
Q

Mechanisms of ischemia-reperfusion injury

A
  • oxidative stress
  • increased intracellular calcium
  • inflammation
  • complement activation
28
Q

Impaired calcium homeostasis

A
  • can activate enzymes that shouldn’t be activated and damage/degrade DNA and proteins
  • make the plasma membrane more permeable → activate apoptosis
29
Q

Define intracellular accumulations in cellular injury

A

intracellular build up of substances that can’t be immediately used or eliminated and the resultant metabolic disturbances

(1) normal cellular substances: water, proteins, lipids, carbohydrates

(2) abnormal substances:
- endogenous: products of abnormal metabolism or synthesis
- exogenous: infectious agents or minerals

cells attempt to digest accumulated (stored) substances → excessive amounts of metabolites accumulate in cells → expelled into extracellular matrix → macrophages consume → more and more macrophages migrate to tissue to consume metabolites → tissue begins to swell
ex: enlargement of liver (hepatomegaly) or spleen (splenomegaly)

30
Q

Types of intracellular accumulations

A

(1) normal substances in large amounts
- water (cellular swelling)
- lipids and carbohydrates (fatty change, ex: liver - especially with alcohol abuse)
- melanin (freckles)
- proteins (fx disruption)
- glycogen (diabetes mellitus)
- calcium (calcification)
- bilirubin (jaundice)

(2) abnormal endogenous products
- tay sachs: too much fatty substances build up in brain (rare & inherited)

(3) exogenous
- environmental
- pigments
- tattoos

31
Q

Define dystrophic calcification

A
  • pathologic calcification
  • occurs in dying and dead tissues
  • macroscopic calcium salt deposits in tissue
  • tissue deprived of oxygen supply, dies, becomes calcified
  • calcium salts appear as gritty, clumped granules that can become hard as stone
  • when several layers clump together they look like grains of sand and are called psammoma bodies
  • occurs with cardiovascular disease, chronic tb of lungs and lymph nodes, advanced atherosclerosis, heart valve injury, center of tumors
32
Q

Define metastatic calcification

A
  • pathologic calcification
  • macroscopic calcium salt deposits in normal tissue as a result of hypercalcemia
  • can occur with hyperparathyroidism, toxic levels of vitamin D, hyperthyroidism, Addison disease
33
Q

Systemic manifestations of cellular injury

A

(1) fever
- release of endogenous pyrogens from bacteria or macrophages
- acute inflammatory response

(2) increased heart rate
- increased metabolism from fever

(3) lab values
- leukocytosis
- LDH
- CK
- AST/SGOT
- ALT/SGPT
- ALP
- amylase

34
Q

Importance of lab values in cellular injury

A

lab values are for substances that end -ase which are enzymes → extracellular values of enzymes can be indicative of cell injury)

35
Q

Define apoptosis

A
  • programmed and controlled cell death
  • occurs in a single cell
  • cell is replaced
  • response to physiologic need for cell death as well as pathologic response
  • cells that die by apoptosis release chemical factors that quickly recruit phagocytes to engulf remains of dead cell and reduce changes of inflammation
36
Q

Define necrosis

A
  • process of cellular self-digestion (autodigestion/autolysis) → disorganized and unregulated
  • from non-specific trauma or injury (exogenous/pathologic)
  • affects a group of cells
  • interferes with cell replacement and tissue regeneration
  • rapid loss of membrane structure, organelle swelling, mitochondrial dysfunction
  • karyolysis: nuclear dissolution and lysis of chromatic
  • pyknosis: nucleus shrinks and becomes small, dense mass of genetic material
37
Q

Types of necrosis

A

(1) coagulative

(2) liquefactive

(3) caseous

(4) fat

(5) gangrenous

38
Q

Coagulation necrosis

A
  • kidneys, heart, adrenal glands
  • from hypoxia, ischemia, chemical injury
  • protein denaturation
  • causes albumin to become firm and opaque
39
Q

Liquefaction necrosis

A
  • ischemic injury to neurons and glial cells in brain
  • cells are digested by their own hydrolytic enzymes → pus (tissue becomes soft, liquefies, and segregates)
  • often from bacterial infection
40
Q

Caseous necrosis

A
  • often from pulmonary TB infection
  • combination of coagulative and liquefactive necrosis
  • dead cells disintegrate but debris is not entirely digested by hydrolases → tissue resembles clumped cheese (soft and granular) → granulomatous inflammatory wall encloses area
41
Q

Fat necrosis

A
  • breast, pancreas, other abdominal structures
  • cellular dissolution from lipases
  • lipases break down triglycerides → release free fatty acids (FFAs) → FFAs combine with calcium, magnesium, and sodium ions → create soap (saponification)
  • necrotic tissue appears opaque and chalk-white
42
Q

Gangrenous necrosis

A
  • death of large area of tissue from severe hypoxic injury → bacterial invasion
  • dry, wet, or gas
43
Q

Dry gangrene

A
  • result of coagulative necrosis
  • skin becomes very dry and shrinks (causes wrinkles)
  • color changes to dark brown/black
44
Q

Wet gangrene

A
  • develops when neutrophils invade site and cause liquefactive necrosis
  • usually in internal organs
  • site becomes cold, swollen, pulseless
  • foul odor
  • severe systemic symptoms → death
45
Q

Gas gangrene

A
  • caused by infection of injured tissue by Clostridium
  • anaerobic bacteria produce hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas (crepitus) to form in muscle cells
  • if enzymes lyse membranes of RBCs → death by shock
46
Q

Define cellular aging

A
  • time-dependent loss of structure and function (gradual “wear” and “tear”)
  • increasing molecular disorder (entropy) that affect cellular renewal and repair
  • atrophy, decreased function, loss of cells
  • susceptible to injurious stimuli and mutations
47
Q

Define tissue and systemic aging

A
  • progressive stiffness and rigidity
  • decreased movement of intracellular and extracellular substances
  • decreased immune response
  • decreased hormone production, efficacy, and response
  • muscular and tissue atrophy
  • decrease in height
  • decreased bone mass
48
Q

Effects of frailty

A
  • vulnerable to falls, functional decline, disability, disease, and death
  • affects mobility, balance, muscle strength, motor activity, bone density, cognition, nutrition, endurance, falls, and fractures
49
Q

Replicative senescence

A

process that causes normal cells to stop dividing after a certain number of cell divisions (telomeres too short)

50
Q

Examples of accumulated damage that can lead to cellular aging

A
  • DNA
  • free radicals
  • glycation
51
Q

Define sarcopenia

A

loss of muscle mass and strength

skin is affected by atrophy and wrinkling of epidermis and alterations in underlying dermis, fat, and muscle

52
Q

Define disuse atrophy

A

cell size reduced to be more efficient (O2 + energy)

53
Q

Define denervation in atrophy

A

nerve to muscle connection is damaged/cut leading to altered function or loss of function

54
Q

Physiologic example of atrophy

A

muscles in uterus after pregnancy

55
Q

Pathologic example of atrophy

A
  • ischemia: blood flow reduction causes muscles to atrophy
  • denervation: neurotransmission to muscles stopped
56
Q

Pathologic example of metaplasia

A

ciliated columnar cells in bronchioles adapt to stratified squamous in response to cigarette smoke (can be reversed if smoking stopped)

57
Q

Pathologic example of dysplasia

A
  • cervix: stratified squamous cells exposed to HPV go through dysplastic growth toward cancerous state
  • bronchioles: in pre-term infants, exposure to ventilation can lead to bronchopulmonary dysplasia
58
Q

Define oxidative stress

A

excess reactive oxygen species (ROS) overwhelm endogenous antioxidant systems

59
Q

Describe free radical injury

A

(1) lipid peroxidation: electron stolen from lipids of cell membrane leading to membrane damage and increased permeability

(2) protein alterations: fragmentation of polypeptide chains leading to proteins misfolding

(3) DNA fragmentation: decreased protein synthesis; mutations; cancer

(4) mitochondrial damage: damaged ATP production (stroke, ALS, heart disease)

60
Q

Causes of free radical injury

A
  • chemical/radiation injury
  • inflammation
  • O2 and other gases
  • aging
  • infections
  • ischemia-reperfusion injury
61
Q

Describe antioxidants

A
  • vitamin A, C, E
  • donate electrons
  • remove free radicals
62
Q

Causes of hypoxia

A
  • reduced amount of oxygen in air
  • loss of hemoglobin
  • decreased efficacy of hemoglobin
  • decreased production of RBCs
  • respiratory and cardiovascular diseases
  • poisoning of oxidative enzymes
63
Q

Causes of ischemic injury

A
  • gradual narrowing of arteries (arteriosclerosis)
  • complete blockage of arteries by blood clots (thrombosis)
64
Q

Mechanisms of intracellular accumulations

A

(1) abnormal metabolism: normal, endogenous substance is produced in excess or at an increased rate

(2) abnormal substance accumulates because of defects in protein folding, transport, or abnormal degradation

(3) endogenous substance is not effectively catabolized (lack of enzymes)

(4) accumulation of harmful exogenous materials through inhalation, ingestion, or infection
ex: heavy metals, mineral dusts, microorganisms

Pathophysiology (6 decks)

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