Exam 1 - Altered Cellular Tissue Biology Flashcards

1
Q

Pathologic change:

A

Change due to a disease process (not normal and shows signs of illness)

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2
Q

Physiologic change:

A

Normal change

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3
Q

Decrease or shrinkage in cell size

A

Atrophy

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4
Q

Causes of pathologic atrophy

A

Decrease in:

  • workload
  • use
  • pressure
  • blood supply
  • nutrition
  • hormone stimulation
  • nervous stimulation
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5
Q

Brain deterioration due to multiple sclerosis or Parkinson’s disease is an example of:

A

Pathologic atrophy

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6
Q

Cellular process that occurs with early development:

A

Physiologic atrophy

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7
Q

Skeletal muscle atrophy

A

Disuse atrophy

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8
Q

Disuse atrophy a type of?

A

Pathologic atrophy

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9
Q

Example of disuse atrophy

A

Patient is bed ridden and muscles shrink

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10
Q

Increase in cell size which consequently increases the size of the affected organ

A

Hypertrophy

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11
Q

Results from a chronic hemodynamic overload

A

Pathologic hypertrophy

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12
Q

Example of pathologic hypertrophy

A

Patient with hypertension, experiences hypertrophy of organs and vasculature. Venous congestion from hypertension causes hypertrophy of the heart and renal organs.

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13
Q

Result caused by increased demand, stimulation by hormones, and growth factors

A

Physiologic hypertrophy

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14
Q

What causes physiologic hypertrophy?

A
  • increased demand

- stimulation by hormones and growth factors

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15
Q

Examples of physiologic hypertrophy

A
  • Increase in muscle cell size in response to heavy work

- pregnancy (hormone induced uterine enlargement)

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16
Q

Increased number of cells in an organ or tissue due to increased rate of cellular division

A

Hyperplasia

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17
Q

Adaptave mechanism that enables certain organs to regenerate

A

Compensatory hyperplasia

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18
Q

Example of conpensatory hyperplasia

A

Removal of part of the liver, the remaining liver cells compensate for the loss and the liver regrows itself

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19
Q

Occurs chiefly in estrogen-dependent organs, such as the uterus and breast

A

Hormonal hyperplasia

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20
Q

Example of hormonal hyperplasia

A

After ovulation, estrogen stimulates the endometrium to grow and thicken
In pregnancy occurs, hormonal hyperplasia (along with hypertrophy) enable the uterus to enlarge

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21
Q

Abnormal proliferation of normal cells

A

Pathologic hyperplasia

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22
Q

What causes pathologic hyperplasia?

A

Excessive hormonal stimulation or effects of growth factors

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23
Q

Example of pathologic hyperplasia

A

Pathologic endometrial hyperplasia

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24
Q

Why does hyperplasia occur? (Both in general, and microscopically)

A
  • In response to an injury that is severe or prolonged.
  • Main mechanism is production of growth factors which stimulate the remaining cells to make new cellular components and then divide
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25
Q

What is pathologic endometrial hyperplasia caused by?

A
  • An imbalance between estrogen and progesterone levels with relative increases of estrogen.
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26
Q

What happens when someone has pathologic endometrial hyperplasia?

A

Excessive menstrual bleeding which can lead to malignant cells.
Can be reversed if imbalance is corrected.

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27
Q

Abnormal changes in the size, shape, and organization of mature cells

A

Dysplasia

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28
Q

Is dysplasia a normal or abnormal adaptation?

A

It is not an adaptave process

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29
Q

What is dysplasia related to?

A

Hyperplasia

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30
Q

Another name for dysplasia?

A

Atypical hyperplasia

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31
Q

Where does dysplasia typically occur?

A

Epithelium

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32
Q

Is dysplasia reversible?

A

Changes can be reversible if the dysplasia does not effect the epithelium all the way to the basement layer

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33
Q

Reversible replacement of one mature cell type by another

A

Metaplasia

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34
Q

Example of metaplasia:

A

A patient has GERD and epithelium of espohagus is damaged. The squamous epithelium may be replaced by glandular epithelium which can better tolerate the acidic environment

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35
Q

What is a free-radical?

A

A type of unstable molecule that is made during normal cellular metabolism

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36
Q

Why are free-radicals dangerous?

A

They can build up in cells and cause damage to other molecules such as, DNA, lipids, and proteins.

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37
Q

What is active cell injury?

A

A variety of changes of stress that a cell suffers due to environment changes (both internal and external changes)

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38
Q

What factors can cause active cell injury?

A
  • physical
  • chemical
  • infectious
  • biological
  • nutritional
  • immunologic
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39
Q

What is apoptosis? What type of tissue does this take place in?

A

“Dropping off” is a distinct type of cellular death
An active process of cellular self-destruction called programmed cell death.
Occurs in both normal and pathologic tissue

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40
Q

What is infiltration?

A

The diffusion or accumulation of foreign substances in amounts excess than normal.

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41
Q

Foreign material collected inside cells is called?

A

Infiltrate

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42
Q

What is ATP depletion? What happens when this takes place?

A

Loss of ATP in the mitocholdrial cells

Results in cellular swelling, decreased protein synthesis, and loss of integrity of the plasma membrane

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43
Q

What are oxygen-derived free radicals? (What happens macroscopically and microscopically?)

A

Lack of cellular oxygen progressing in injury (ischemia). Activated oxygen-specific free radicals causing destruction of cell membranes and cellular structure

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44
Q

What is membrane permeability?

A

Rate of passive diffusion of molecules through the cellular membrane

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45
Q

What does membrane permeability depend on?

A

The electrical charge and polarity of the molecule.

Also, having pores or openings that permit liquids or gasses to pass through the membrane

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46
Q

Cytoplasmic or cellular swelling caused by a shift of extracellular water into the cell

A

Oncosis

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47
Q

What is oncosis?

A

Cytoplasmic or cellular swelling caused by a shift of extra cellular water into the cell

48
Q

What is vacuolation?

A

Formation of vacuoles (small cavities) in the cytoplasm, allowing for cellular swelling

49
Q

What is autophagy?

A

Self-destruction process (recycling factor) and survival mechanism.
Cytoplasmic components and organelles of cells are degraded. Salvaging of key metabolites occurs to promote metabolic and nutritional balance.

50
Q

What is autolysis?

A

Cellular self-digestion (autodigestion).

Destruction of cells or tissues by their own enzymes

51
Q

What occurs before necrosis?

A

Autolysis is a precursor to necrosis

52
Q

Lack of sufficient oxygen

A

Hypoxia

53
Q

Most common cause of cellular injury

A

Hypoxia

54
Q

What causes hypoxia?

A
  • decreased oxygen in air
  • loss of hemoglobin
  • decreased production of red blood cells
  • respiratory/cardiovascular diseases
  • poison
55
Q

Reduced blood supply

A

Ischemia

56
Q

What often causes ischemia?

A

Gradual narrowing of arteries and complete blockage of an artery by a blood clot

57
Q

Most common cause of hypoxia

A

Ischemia

58
Q

Total lack of oxygen

A

Anoxia

59
Q

What causes anoxia?

A

A sudden obstruction (like an embolus)

60
Q

What is a myocardial infarction a direct result of?

A

An acute obstruction in a coronary artery which leads to anoxia

61
Q

What is the sodium/potassium pump?

A

A specific protein inside the cell maintains cellular balance of potassium and sodium.
This pump keeps the internal concentration of potassium high and the internal concentration of sodium low

62
Q

How does an increase or decrease of ATP affect the sodium/potassium pump?

A

The pump is fueled by ATP. A reduction of ATP causes balance or pump fail and leads to intracellular sodium accumulation

63
Q

How do toxic substances create injury?

A
  • We are constantly exposed to toxins. Absorption of chemicals occurs in GI tract after oral injestion.
  • Cellular plasma membrane is ultimately damaged by the toxin.
    • Membrane damage leads to increased cellular permeability which allows contents to flow in and out of the cell.
64
Q

What is direct toxicity?

A

Toxic substance combines with a cellular molecule which creates the avenue for cellular injury

65
Q

What is indirect toxicity?

A

Toxic substances react with other substances inside cell and create toxic metabolites and free radicals

66
Q

How can someone be exposed to carbon monoxide (CO) toxicity?

A
  • By breathing air polluted by gasoline engines, defective furnaces, or appliances
  • work in hazardous occupations such as coal mining, welding, firefighting
  • smoke cigarettes or other products
67
Q

What happens inside the body with higher CO levels?

A
  • CO causes limited oxygen to be carried to body systems and organs.
  • CO has high affinity to hemoglobin attachment (greater than oxygen). So high levels in the blood cause oxygen/hemoglobin attachment to diminish radically.
  • This causes hypoxia in tissues and organs.
68
Q

Lab value used to check for CO toxicity

A

Carboxyhemoglobin (COHb)

69
Q

Clinical manifestations of CO poisoning:

A
  • headache
  • dizziness
  • weakness
  • nausea
  • vomiting
  • chest pain
  • altered mental status
  • bright red, rosy cheeks
70
Q

How does ethanol toxicity occur?

A

Drinking too much alcohol

71
Q

Legal definition of drunk driving:

A

Blood alcohol of 80mg/dL

72
Q

What causes effects of alcohol to vary?

A
  • age
  • gender
  • percent body fat
73
Q

Most common type of degenerative change

A

Oncosis

74
Q

What causes oncosis?

A

Shift of extracellular water inside the cells

75
Q

Most common reason oncosis occurs

A

Failure in ATP production which causes a failure in the sodium/potassium pump

76
Q

What causes carbohydrate (CHO) excess?

A

Result of inherited disorders with insufficient or ineffective forms of enzymes
The excess in CHO settles inside the cell in the liposomes.
CHO also accumulates throughout the body

77
Q

What can carbohydrate (CHO) excess cause?

A
  • corneal clouding
  • joint stiffness
  • intellectual disability (if severe)
78
Q

What causes lipid excess?

A

Result of inherited disorders with insufficient or ineffective forms of enzymes
Excess lipids settle inside liposimes
Lipids also accumulate in heart, muscle, and kidney cells.

79
Q

Predominate area for lipid accumulation?

A

Liver

80
Q

What can lipid accumulation in the liver cause?

A

A fatty liver and stenosis of liver cells, leaving the cells unable to filter and perform effectively

81
Q

What causes glycogen excess?

A

Seen in many genetic disorders.

82
Q

What does glycogen excess cause?

A

Causes glucose and glycogen metabolism issues.

Excessive vacuolation inside the cell.

83
Q

Most common cause of glycogen excess?

A

Diabetes mellitus

84
Q

What happens with protein excess?

Where does it primarily accumulate?

A

Since proteins provide cellular structure, an excess amount of protein pushes against cellular organells, distrupting function and intracellular communication.
Accumulates primarily in immune system and filtration cells of the kidney

85
Q

What can occur due to excess protein?

A

Renal failure

86
Q

Systemic manifestations of cellular injury

A
  • fever
  • increased heart rate
  • increase in leukocytes
  • pain
  • presence of cellular enzymes in extracellular fluid (seen in lab values)
87
Q

What happens with coagulative necrosis?

A

Coagulation (clotting) occurs because of protein breakdown

Which causes protein and albumin to change to a firm opaque state (like a cooked egg white)

88
Q

What does tissue affected by coagulative necrosis look like?

A

Firm and slightly swollen

89
Q

Causes of liquefactive necrosis

A
  • ischemic injury to neurons and glial cells

- bacterial infections

90
Q

What happens to tissue affected by liquefactive necrosis?

A

Tissue becomes soft, liquifies, and is walled off from healthy tissue, forming cysts

91
Q

What causes caseous necrosis?

A

A tuberculosis infection

92
Q

What is caseous necrosis?

A

A combination of coagulative and liquefactive necrosis

Dead cells disintegrate, but cellular debris is not digested completely.

93
Q

What does tissue affected by caseous necrosis look like?

A

Soft and grandular, resembling clumps of cheese

Inflammatory wall encloses and walls off this debris and area

94
Q

Where does fat necrosis occur

A

Breast
Pancreas
Abdominal structures

95
Q

What causes cellular dissolution in fat necrosis?

A

Lipases (powerful enzymes)

96
Q

What does tissue affected by fat necrosis look like?

A

Opaque and chalky white

97
Q

Death of tissue as a result of severe hypoxic injury

A

Gangrenous necrosis

98
Q

Where does gangrenous necrosis commonly take place?

A

Major arteries, especially in the lower leg

99
Q

What leads to the necrotic process with gangrenous necrosis?

A

A subsequent bacterial invasion in the area

100
Q

What causes gas gangrene?

A

Infection of injured tissue by Clostridium

Clostridium destroy connective and cellular membranes and cause bubbles of gas to form in muscle cells

101
Q

Where does gas gangrene take place?

A

Bubbles are in muscle cells

102
Q

Why can gas gangrene be fatal?

A

Enzymes lyse the membranes of red blood cells, destrying their oxygen carrying capacity

103
Q

Clinical manifestations of dry gangrenous necrosis

A

Skin very dry, shrinks, and wrinkles

104
Q

Clinical manifestations of wet gangrenous necrosis

A

Site is cold, swollen, and black. Foul odor present

105
Q

Death of the entire person

A

Stomatic death

106
Q

When do manifestations of postmortem change appear?

A

Within minutes of death

107
Q

Most notable manifestations of stomatic death

A
  • complete cessation of respiration and circulation

- surface of skin becomes pale and yellowish

108
Q

Reduction of body temp after death

A

Algor mortis

109
Q

When does algor mortis take place?

A

Temp begins reducing immediately and rapidly for the first 24 hours.
After 24 hours, body temp equals environment temp

110
Q

Muscle stiffening after death

A

Rigor mortis

111
Q

Why does rigor mortis happen?

A

Accumulation of acidic components in muscles because of CHO and lipid breakdown

112
Q

Which muscles are affected by rigor mortis first?

A

Smaller muscles then larger muscles

113
Q

When do effects of rigor mortis take place?

A

Entire body effected 12-14 hours after death

12-14 hours after that, body becomes flaccid again

114
Q

Blood settling in lowest tissues after death

A

Livor mortis

115
Q

What does livor mortis look like?

A

Lowest tissues develop a purple discoloration

116
Q

State of decay with foul smelling odor

A

Putrefaction

117
Q

When does putrefaction become obvious after death?

A

24-48 hours after death