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General Pathology -- Roecker > Gen Pathology Exam 1 Section 1: Cell Injury, Cell Death, and Adaptations > Flashcards

Gen Pathology Exam 1 Section 1: Cell Injury, Cell Death, and Adaptations Flashcards

1
Q

Pathology

A

study of disease, “suffering”
pathos- meaning “experience” or “suffering”
-logia meaning the “study of”

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2
Q

Homeostasis

A

tendency toward a relatively stable equilibrium optimal homeostasis is interchangable with optimal health

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3
Q

Disease

A

structural and/or functional change in the body that is harmful to the organism; a deviation from optimal health

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4
Q

What are the two observable clinical features?

A

sign and symptoms

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5
Q

What is a sign?

A

objective and observable indication of disease; obtained via physical examination
Ex: increased body temp (fever)

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6
Q

What is a symptom?

A

subjective evidence of disease or physical disturbance; patients experience; obtained via oral report from patient history
Ex: pain, blurry vision, and numbness

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7
Q

Cellular Adaptation

A

cell’s attempt to preserve viability while overcoming stressful stimulus

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8
Q

What are 2 factors that influence cell’s ability to overcome a harmful stimulus?

A
  1. the cell type

2. the nature of the cellular stress

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9
Q

When will cell injury occur?

A

when cell is NO longer able to adapt to cellular stressors

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10
Q

etiology

A

the cause, set of causes, or manner of cause of given pathology

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11
Q

What is a “risk factor”?

A

used to label causation agent

Ex: smoking is a risk factor for lung cancer

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12
Q

What two things lay at the core of most disease processes?

A
  1. Genetic susceptibilities (“nature”) Ex: Huntington Disease
  2. Environmental triggers (“nurture”) Ex: environmental role
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13
Q

Huntington Disease

A

neurodegenerative disease; causes severe dementia during middle adult hood and develops via specific genetic mutation

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14
Q

Mesothelioma

A

a cancer of pulmonary pleura; usually in people with history of exposure to asbestos (env. role)

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15
Q

Pathogenesis

A

series of events involved in cellular and molecular changes involved with specific disease process

describes biological mechanisms that describe the structural and functional abnormalities of a disease process

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16
Q

Physiological Adaptations

A

responses expected to occur with normal physiological changes
Ex: hormonal enlargement of uterus and breast during pregnancy
Ex: skeletal muscle hypertrophy following weight training

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17
Q

Pathological Adaptations

A

responses to excessive cellular stress and indicate a loss of optimal structure and function; allow cells to avoid/delay injury
Ex: Cardiac Ventricular hypertrophy
Ex: heavy alcohol consumption

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18
Q

What are non harmful stimuli?

A

changes in cell’s environment assisting it in maintaining homeostasis

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19
Q

What are harmful stimuli?

A

changes in cell’s environment that are sources of cellular stress

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20
Q

Are cellular adaptations reversible?

A

yes

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21
Q

What are the 4 main adaptations to stress?

A
  1. Hypertrophy
  2. Hyperplasia
  3. Atrophy
  4. Metaplasia
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22
Q

Hypertrophy

A

An increase in size of cell, and if severe may increase size of organ or enlarge area of organ.
Achieved due to increase in synthesis of intracellular proteins and organelles
Ex: ventricular hypertrophy

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23
Q

Hyperplasia

A

an increase in the number of cells, due to cellular division; typically results in enlargement of tissue
Ex: Benign Prostatic hyperplasia
Ex: Wart (verruca)

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24
Q

Atrophy

A

shrinkage of cell size, due to loss of cell’s structural proteins; overall size of tissue may decrease
Function is diminished, but it remains viable ( IS NOT DEAD)
Causes: immobilization, denervation, ischemia, malnutrition, aging

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25
Q

What two things does atrophy involve?

A
  1. reduced protein synthesis

2. increase rate protein breakdown

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26
Q

Metaplasia

A

one cell type replaced by another cell type; one adult cell transitioning into a different adult cell type
Ex: Chronic smokers–ciliated columnar epithelia replaced by stratified squamous cells; leads to chronic bronchitis
Ex: Gastroesophageal reflux disease; leads to esophageal cancer

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27
Q

What are the 8 causes of cell injury and death?

A
  1. Ischemia
  2. Hypoxia
  3. Toxic Exposures
  4. Infections
  5. Immunological Reaction
  6. Nutritional Imbalances
  7. Trauma
  8. Aging
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28
Q

Ischemia

A

insufficient blood supply to a tissue

Ex: myocardial infarction (heart attack), cerebral infarction (stroke), ischemia bowel disease, gangrene

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29
Q

What does ischemia most commonly develop from?

A

atherosclerotic plaque formation, blood clots, reduced cardiac output (heart failure), compression of major arteries

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30
Q

Hypoxia

A

organ is NOT receiving adequate oxygen within blood supplying the organ
Ex: pneumonia, carbon monoxide poisoning, a disease inhibiting diaphragm (botulism, Guillain-Barre syndrome) or injury to phrenic nerve

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31
Q

Toxic Exposures

A

depends on how harmful (noxious) it is and concentration and duration of exposure

Examples of toxic poisonous substances:
air pollution, insecticides, asbestos, CO, smoke, alcohol

Examples of innocuous substances:

  1. diabetes (hyperglycemia) causes peripheral vascular disease
  2. water intoxication
  3. retinopathy of prematurity
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32
Q

Infections

A

all forms of infectious microbes (bacteria, viruses, protoxoans, fungi) may injure cells

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33
Q

Immunological Reaction

A

over-activation of normal immune mechanisms may injure cells via autoimmunity or allergies

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34
Q

Nutritional Imbalances

A

deficiencies or excesses of dietary nutrients may inhibit homeostasis and result in pathology

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35
Q

Trauma

A

from mechanical (physical) trauma, thermal trauma, electrical injury, or injury from high-energy radiation (ionizing or irradiation)

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36
Q

Aging- Cellular Senescence

A

reduced capacity for cells to react to stress and maintain homeostasis

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37
Q

Reversible Cellular injury

A

may regain original form and function if stimulus removed

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38
Q

Two Types of Reversible Cellular Injury

A
  1. Cellular Swelling

2. Fatty Change (Steatosis)

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39
Q

Cellular Swelling

A

occurs because not enough ATP to “power” ATP-dependent pumps (Na-K Pump, Calcium Pump)
Results in accumulation of ions w.in cell and therefore accumulation of water in cell

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40
Q

“hydropic change” or “vacuolar degeneration”

A

names for microscopic findings of cellular swelling

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41
Q

Fatty Change (Steatosis)

A

accumulation of lipid (fat) vacuoles w/in a cell’s cytoplasm; found commonly in cells normally involved with lipid metabolism
Ex: in liver

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42
Q

What will persistent or excessive cellular injury eventually cause?

A

it will cause a transition of injured cell from reversible injury to irreversible injury (DEATH)

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43
Q

What 3 things is Cellular Death Associated with?

A
  1. significant mitochondrial damage or dysfunction
  2. a damaged or dysfunctional plasma membrane
  3. genetic or nuclear damage
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44
Q

What are the 2 Primary Pathways for cellular death (irreversible cellular injury)?

A
  1. Apoptosis

2. Necrosis

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45
Q

Apoptosis

A

regulated cell death, controlled cellular breakdown; maintains outer plasma membrane and forms apoptotic bodies that fall away and are removed via phagocytes
(could be physiological or pathological)

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46
Q

Necrosis

A

destroys cell membrane and initiates prominent inflammatory response–> brings phagocytes to area to eliminate dead cellular debris and initiate healing
(always a pathological process)

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47
Q

What are the type types of morphological changes of necrosis?

A
  1. cytoplasmic changes

2. nuclear changes

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48
Q

What 2 types of cytoplasmic changes can occur in necrosis?

A
  1. eosinophilia

2. myelin figures

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49
Q

Eosinophilia

A

necrtotic cells manifest with an increase ink or red appearance with stranded hematoxylin and eosin (H&E) stain

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50
Q

myelin figures

A

necrotic cells contain membrane damage and myelin figures which = “rolled-up” or “scroll-like” area of lipid bilayer that is within a cell

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51
Q

What 3 types of Nuclear Changes can occur in necrosis?

A
  1. Pyknosis
  2. Karyorrhexis
  3. Karyolysis
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52
Q

Pyknosis

A

nuclear shrinking and increase basophilia (blue-staining/darker appearance) due to nuclear DNA condensing

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53
Q

Karyorrhexis

A

after pyknosis, cell fragment/fall apart in the process

54
Q

Karyolysis

A

after karyorrhexis; nucleus continues to degrade and basophilia fades. After 1-2 days, nucleus disappears

55
Q

What are the 5 distinct patterns of necrosis?

A
  1. Coagulative Necrosis (subcategory is Gangrenous Necrosis)
  2. Liquefactive Necrosis
  3. Caseous Necrosis
  4. Fat Necrosis
  5. Fibrinoid Necrosis
56
Q

Coagulative Necrosis

A

most likely to manifest in solid organs that experience severe ischemia; maintains firm texture for a few days to weeks after tissue dies; once WBCs accumulate it will phagocytize necrotic tissue and cavity is left or scar tissue

57
Q

Examples of Coagulative Necrosis

A

Sites of:

  1. myocardial infarction (heart attack)
  2. ischemia to a kidney or adrenal glands
58
Q

Gangrenous Necrosis

A

it is coagulative necrosis in an extremity, occurs in hands and feet; mostly in foot/leg

59
Q

Examples of Gangrenous Necrosis

A

peripheral vascular disease
frostbite
major trauma that obstructs blood supply

60
Q

What are the 3 types of Gangrenous Necrosis?

A
  1. Dry Gangrene = uncomplicated gangrene
  2. Wet Gangrene = when infected w/ opportunistic bacteria–it liquefies
  3. Gas Gangrene = when bacteria infects and gas byproduct and is trapped w/in tissues Ex: Clostridium perfringens
61
Q

Liquefactive necrosis

A

tissues liquify due to WBC’s releasing enzymes that breakdown necrotic tissue; if survive, cavity left behind; usually ass. with bacterial infection, but could be do to deep fungal infections too

62
Q

Examples of liquefactive necrosis

A

hypoxia to cells of CNS, therefore cerebral infarctions (strokes) lead to this

63
Q

Caseous Necrosis

A

tuberculosis infections; produce “cheese-like” pattern; relates to crumbly (friable) cheeses– blue cheese

64
Q

Microscopically, what is caseous necrosis called?

A

“caseous granuloma”

Granulomas = pattern of chronic inflammation that consists of collections of macrophages

65
Q

Fat necrosis

A

(= enzyme necrosis); areas of fat destruction that result in saponification

66
Q

What does Fat necrosis most likely result form?

A

a ruptured pancreas–the enyzmes cause tissue necrosis–> usually due to acute pancreatitis from chronic alcoholism

67
Q

Examples of Fat necrosis

A

direct trauma via vehicle accident or trauma to breast tissue
(also ruptured pancreas due to chronic alcoholism)

68
Q

Fibrinoid necrosis

A

requires microscope to visualize; typically occurs in vessel walls of patients with autoimmune disorder causing vasculitis
(manifests as eosinophilic appearance when biopsy taken)

69
Q

Vasculitis

A

general term for inflammation within vessel walls

70
Q

The two primary pathways for Apoptosis

A
  1. Mitochondrial Pathway

2. Death Receptor Pathway

71
Q

Mitochondrial Pathway of apoptosis

A

intrinsic apoptosis, increase in mitochondrial membrane permeability to cytochrome C and that leaks into cytosol, and increase levels of caspase 9

72
Q

What stimulates Mitochondrial Pathway of apoptosis?

A

genetic damage, accumulation of misfolded proteins, or decease in GF

73
Q

Death Receptor Pathway for apoptosis

A

extrinsic, surface of cell may bind with signaling molecule (like tumor necrosis factor–TNF or Fas ligand) and activate caspase 8

74
Q

What stimulates Death Receptor Pathway of apoptosis?

A

autoreactive (self-reactive) WBC’s that cause autoimmunity or virally-infected cells

75
Q

What do both, Mitochondrial and Death Receptor apoptosis pathways form?

A

apoptotic bodies–> therefore membrane is NOT sig. disrupted

76
Q

Autophagy

A

= “self-eating”; a survival mechanism for cell to avoid death @ time it’s experiencing nutrient deprivation
- sequesters own organelles within autophagic vacuole; then cell’s lysomomes release enzymes that break down the vacuole and use as a source of nutrients

*at a point cell will STOP eating itself and initiate apoptosis

77
Q

5 Mechanisms of Cellular Injury

A
  1. Hypoxia and Ischemia
  2. Ishcemia-Reperfusion Injury
  3. Oxidative Stress
  4. Chemical (Toxis) Injury
  5. Genetic Damage
78
Q

Hypoxia and Ischemia (mechanisms of cellular injury)

A

inhibit cells ability to perform ATP production, via oxidative phosphorylation within mitochondria; ATP needed for protein synthesis and pumps; deprived ATP leads to membrane destruction and trigger necrosis

79
Q

What cells are resistant to Hypoxia and ishcmeia?

A

cells that can switch to glycolysis (but that will increase lactic acid production and may decrease pH and cause injury

80
Q

What cells are high susceptible to Hypoxia and Ischemia?

A

cardiac myocytes or CNS neurons b/c have inability to perform glycolysis; therefor myocardial infarction and cerebral infarction quickly develop during state of ischemia or hypoxia

81
Q

Ischemia-Reperfusion Injury (mechanism of cellular injury)

A

reperfusion of blood to ischemic tissue may cause this injury; will deliver large amounts of WBC’s that initiate inflammatory rxn and produce large amounts of reactive oxidative species (ROS) and further injuries ischemic tissue

82
Q

Oxidative Stress (mechanism of cellular injury)

A

an increase in ROS; injuries variety of cellular componets like;

  • proteins, lipids (lipid bilayer), or nuclear DNA
  • -> may cause apoptosis or necrosis
83
Q

What does oxidative stress occur in?

A

normal redox rxns, exposure to harmful chemicals; hypoxia; ionizing radiation, excessive inflam. rxns, or ischemia-reperfusion injury

84
Q

Chemical (toxic) injury– 2 Main Mechanisms (mechanism of cellular injury)

A
  1. Direct-Injury

2. Latent-Injury

85
Q

Direct-injury mechanism of chemical injury

A

chemical becomes bound to cell and directly kills cell and interferes with fxn –> “cytotoxicity”

occurs–> with anti-cancer chemotherapy medications; exposure to naturally-occurring toxins like Cholera toxin (deadly diarrhea disease)

86
Q

Latent-injury mechanism of chemical injury

A

substance ingested and does NOT cause direct-injury, BUT is converted into a harmful substance via activity of normal metabolism; occurs in SER of liver via cytochrome P-450 system

87
Q

Example of Latent-injury

A

consume toxic levels of Tylenol (acetaminophen) which puts oxidative stress on hepatocytes (liver cells) and damages membranes–> creating acute liver necrosis and liver failure

88
Q

Genetic Damage (mechanism of cellular injury)

A

damage to cell’s DNA will produce mutations that increase risk of cancer formation (carcinogenesis), BUT may also trigger apoptosis via mitochondria pathway

89
Q

Sources of Genetic Damgae

A

ionizing radiation, viral infections, or various chemical like chemotherapeutic medicaitons

90
Q

Intracellular Accumulations definition and causes

A

when abnormal or excessive substances accumulate in a cell due to:

  1. abnormal metabolism
  2. defective protein folding or cellular transportation
  3. lack of an enzyme
  4. ingestion of an indigestible substance
    - some accumulations indicate cell injury or pathology; while others are relatively normal
91
Q

8 Intracellular Accumulations

A
  1. Fatty change (steatosis)
  2. cholesterol
  3. Glycogen
  4. Lipofusion
  5. Melanin
  6. Hemosiderin
  7. Carbon
  8. Tattoo pigment
92
Q

Fatty Change (steatosis) (intracellulaar accumulations)

A

when fat accumulates in cell it is direct evidence of cellular injury; most likely to occur in liver; but also occurs in skeletal muscle, heart, or kidneys

93
Q

Causes of Fatty Change

A

toxic exposure, obesity, protein malnutrition, diabetes mellitus, or ischemia/hypoxia

94
Q

Cholesterols (intracellulaar accumulations)

A

needed for cell membranes; BUT hypercholesterolemia may overload phagocytes and can injury inner lining or arterial walls, specifically endothelial cells and increase onset of atherosclerotic plagues

95
Q

Reasons for abnormally high cholesterol:

A
  • high intake of fats (trans or sat.)

- or decrease cholesterol catabolism

96
Q

Glycogen (intracellulaar accumulations)

A

stores glucose in liver and skeletal muscle tissues; glycogen storage disease is conditions that produce elevated intracellular glycogen (abnormal)

97
Q

Lipofusion (intracellulaar accumulations)

A

normal age-related finding in elderly or cells at end of their life; composed on lipids and proteins; “wear and tear” pigment

98
Q

Melanin (intracellulaar accumulations)

A

normal pigment to skin and produced by melaocytes;; brownish-black pigment; protect vs UV radiation; excessive = freckles (ephelis); UVB stimulates melanocytes to produce melanin

99
Q

Hemosiderin (intracellulaar accumulations)

A

major iron-storage complex within blood and tissues (macrophages in bone marrow, spleen, liver); accumulates at risky levels–> means site has had some bleeding (hemmorrhage) –> such as a bruise OR cells contain excess iron (hemosiderosis)

100
Q

Hemosiderosis

A

= formation of iron overloading and ass. with repetitive blood transfusions

(when iron in excess, viewed with “Prussian Blue” stain)

101
Q

Carbon (intracellulaar accumulations)

A

(coal dust); MOST COMMON exogenous pigment in humans; more likely in inds. living in high populated areas, coal miners, and smokers
- anthracosis

102
Q

anthracosis

A

blackening of the lungs

103
Q

Tattoo Pigments (intracellulaar accumulations)

A

composed of metal salts (iron oxide)

pigment phagotosized by macrophages within dermis and retained for life

104
Q

What are the two main forms of Fatty Liver Disease?

A
  1. Alcoholic Liver Disease

2. Non-alcoholic Fatty Liver Disease

105
Q

Alcoholic Liver Disease

A

alcohol = most common cause of hepatic injury like

  1. hepatic steatosis (fatty liver disease)
  2. hepatitis (inflammation of liver)
  3. cirrhosis (scarring of liver)
106
Q

Excessive alcohol intake is _____all chronic liver disease in US and nearly half of all _____ cases.

A

60%

cirrhosis

107
Q

____ percent of heavy drinkers develop _____. Of these ____ develop ______. Of these ____ develop ____.

A

90-100%; hepatic steatosis
25%; hepatitis
15%; cirrhosis

108
Q

About ____ years of heavy drinking is required to develop cirrhosis

A

20 years

109
Q

______ of heavy drinking required to develop hepatitis

A

few weeks

110
Q

___ and ___ are reversible if stop drinking, and ____ is NOT reversible.

A

hepatic steatosis and hepatitis; cirrhosis

111
Q

Ascitis

A

(ass. with advanced liver disease)
occurs when peritoreal cavity of abdomen accumulates excessive fluid (edema); liver = main source of protein production and when injured it cannot do that –> so decrease proteins in blood results in fluid from blood leaving circulation and accumulate in body tissues

112
Q

Caput Medusae

A

(ass. with advanced liver disease)
when superficial epigastric veins become engorged
advanced liver disease cirrhosis prevents blood from flowing through liver, therefore shunts venous blood from liver to epigastric veins and it occurs as dilated and tortuous superficial abdominal veins

113
Q

Mallory bodies

A

(ass. with advanced liver disease)

intracellular inclusion that are accumulated in liver cells of patients who have alcoholic liver disease

114
Q

Nonalcoholic Fatty Liver Disease

A

degree of inflammation (hepatitis) is less severe; most commonly asymptomatic and need liver biopsy
Stimulated by:
- obesity, Type II diabetes, dyslipidemia (high LDL’s and low HDL’s), and chronic hypertension

115
Q

Hepatocellular carcinoma

A

= MOST COMMON form of primary liver cancer

116
Q

Primary liver cancer vs Secondary Liver cancer

A 
Primary = liver cells give rise to liver cancer
Secondary = liver cells are site for cancer metastasis
117
Q

Viral Infections and Liver Cancer

A

areas with high rates of hepatitis viral infections have higher rates of liver cancer (Africa and Asia when compared to US)

  • Africa and Asia–> liver cancer 20-40 years due to HBV (mom to baby)
  • US —> HCV
118
Q

Do males or females have increased risk of liver cancer?

A

males are 3x more likely than females to develop hepatocellular carcinoma

119
Q

Aflatoxin and liver cancer

A

Aflatoxin = carcinogen produced by certain molds (Aspergillus species); most likely to grow in improperly stored grains, like peanuts
is a “risk factor” for liver cancer

120
Q

Pathological Calcification

A

calcium always in blood

  • some pathological situations may cause Ca+ to be deposited intracellular or in ECM
  • “white granules or clumps” or “gritty deposits”
  • asymptomatic or could be lethal
121
Q

Degree of dysfunction of pathological calcification depends on what 2 things

A
  1. severity of calcification

2. organ or organs involved with calcification

122
Q

Two Primary Categories of Pathological Calcificaiton

A
  1. Dystrophic Calcification

2. Metastatic Calcification

123
Q

Dystrophic Calcification

A

occurs at areas of tissue injury or in response to tissue death; very common and ass. with age related pathologies (like atherosclerosis)
Ex: aortic calcification or Tuberculosis (causes caseous necrosis–> cavities in lungs–> calcification on x-ray)

124
Q

Metastatic Calcificaiton

A

occurs in presence of hypercalcemia = elevated blood calcium levels; and deposits Ca salts into normal tissues
- likely to occur throughout body!!

125
Q

What does Metastatic Calcification commonly originate from?

A
  1. Destruction of bone
  2. renal failure
  3. increase PTH
  4. hyervitaminosis D (Vit. D toxicity)
126
Q

Telomeres

A

short sequences of DNA at ends of chromosomes, protect material during cellular division
- once shorted to point, triggers “replication senescence”

127
Q

Telomerase

A

enzyme; adds nucleotides to ends

  • germ cells = contain high levels
  • stem cells = contain low levels
  • somatic cells = is absent
128
Q

Progeria

A

like Blood Syndrome or Werner Syndrome–> born with rare genetic disorders that accelerate aging

129
Q

Cellular senescence

A

Hayflick limit = cell’s pre-programmed # of cellular divisions; once reach this limit, cell can NO longer divide

130
Q

Defective Protein Homeostasis

A

increase age; decrease synthesis of proteins and increase possibility proteins misfold–> which triggers apoptosis
- disrupts cell’s ability to fxn or survive

131
Q

Inflammation of age

A

due to cellular stress on older cells–> may trigger persistent low-level inflammation
- plays role in development of atherosclerosis and Type II diabetes

132
Q

Blue Zone Project

A

factors ass. with living a long healthy life

General Pathology -- Roecker (7 decks)

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