Cellular Pathology Flashcards

1
Q

Pathology

A

study of disease
- external stimuli produce changes in the cells environment
- cell is challenged to maintain homeostasis
- to survive cells adapt

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2
Q

if cells are unable to adapt what happens?

A

cell death

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3
Q

cellular adaptions include?

A
  • hyperplasia
  • hypertrophy
  • atrophy
  • metaplasia
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4
Q

cellular adaption: hyperplasia

A

increase in the number of cells

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5
Q

physiologic hyperplasia

A

due to a normal stressor or initiator
- menstrual cycle

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6
Q

pathologic hyperplasia

A

due to abnormal stressor or initiator
- endometriosis

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7
Q

hypertrophy

A

increase in the size of the cell

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8
Q

physiologic hypertrophy

A

skeletal muscle hypertrophy with exercise

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9
Q

pathologic hypertrophy

A

left ventricle hypertrophy due to high BP

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10
Q

atrophy

A

decrease in the size of a cell that has at one time been of normal size

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11
Q

physiologic atrophy

A

decrease uterus size after pregnancy

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12
Q

pathologic atrophy

A

loss of stimulus to an organ or muscle; peripheral nerve damage

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13
Q

metaplasia

A

conversion of one cell type to another
- epithelium is normal in appearance but in an abnormal location

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14
Q

physiologic metaplasia

A

cervical ectopy; cellular replacement in presence of estrogen

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15
Q

pathologic metaplasia

A

conversion of columnar epithelial cells to squamous epithelial cells in airways of individuals who smoke

  • can lead to cancer
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16
Q

cell injury

A

occurs when the cells cannot adapt to their new environment

causes:
- physical and chemical agents
- trauma
- infection

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17
Q

hypoxia

A

decreased oxygen

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18
Q

ischemia

A

decreased blood flow

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19
Q

what is vulnerable to cell injury?

A
  • DNA
  • cell membranes
  • protein generation
  • ATP production
20
Q

two types of cellular injury

A
  • reversible cellular injury
    ~ ex. low back pain and
    patient learning better
    posture
  • irreversible cellular injury
21
Q

apoptosis

A

programmed cell death in response to damage to DNA or normal growth and development

22
Q

apoptosis initiation

A

caspases is a catalyst of apoptosis

23
Q

apoptosis execution

A

caspases causes cell death

24
Q

does apoptosis cause an inflammatory response?

A

no, there is NO inflammatory response

25
Q

necrosis

A

uncontrolled cell death
- causes an inflammatory response

26
Q

liquefactive necrosis

A

transformation of tissue into a liquid viscous mass
- most often in high fat and low protein organs (brain) or high enzymatic content (pancreas)
- bacteria, virus, parasite

27
Q

fat necrosis

A

inflammatory process which results in death of fat cells
- most common in breast tissue

28
Q

avascular necrosis a.k.a osteonecrosis

A

death of bone tissue due to a lack of blood supply
- can lead to tiny breaks in bone

29
Q

what causes avascular necrosis?

A
  • joint or bone trauma
  • fatty deposits in blood vessels
  • sickle cells anemia
30
Q

cellular accumulations

A

accumulation of substances in the cells as a result of damage to the cell (external factor) or genetic abnormality (internal factor)

substances:
- calcium
- protein
- iron
- fat
- cholesterol
- glycogen
- pigments

31
Q

cellular accumulations of calcium

A

patients who have hypercalcemia have deposits of the calcium with normal or abnormal tissue

PT implications: should impingement

32
Q

cellular accumulations: protein

A

neurofibrillary tangles seen in alzheimer disease

33
Q

cellular accumulations: iron & its types

A

two types:
- hemosiderosis
- hemochromatosis

34
Q

hemosiderosis

A

accumulation of iron in organs
- liver and pancreas

35
Q

hemochromatosis

A

accumulation of iron in parenchymal cells
- CHF, diabetes, cirrhosis

36
Q

most common cell of hemochromatosis?

A

parenchymal cells

37
Q

fat accumulation

A

organs most commonly affected are the liver, kidney, heart and skeletal muscle

38
Q

cholesterol accumulation

A

blood vessels

39
Q

glycogen accumulation

A

liver and skeletal muscles
- typically due to a genetic disorder

40
Q

pigment accumulation

A

exogenous (tattoo)
endogenous (jaundice)

41
Q

cellular aging

A

the process of becoming older
- a process that is genetically determines and environmentally modulated

42
Q

telomeres

A

protect the end of chromosomes with each cell division they shorten
- eventually DNA is interpreted as nonfunctional

43
Q

what happens to telomeres as we age?

A

as we grow older, telomeres at the end of our chromosomes shrink

  • new research suggests major depression is also linked to shorter telomeres as a sign of ‘accelerated aging’
44
Q

werner syndrome

A
  • autosome recessive
  • rare, inherited disroder marked by rapid aging that begins in early adolescence or young adulthood and an increased risk of cancer

sign and symptoms:
- shorter than average height
- thinning and graying hair
- skin changes
- thin arms and legs
- voice changes
- unusual facial features

45
Q

physical therapy implication: muscular atrophy

A
  • therapeutic exercises
  • strength training
  • aquatic therapy
  • standing programs
  • respiratory management
  • feeding
  • skeletal and scoliosis management
  • assistive devices
46
Q

avascular necrosis PT treatment

A
  • decrease load with assistive device
  • maintain joint mobility
  • strengthen muscles
  • E-stim and US stimulating bone growth