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Pathology > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

what is hypertrophy?

A

increase in the size of cells
NO new cells
physiologic or pathologic

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2
Q

what is hyperplasia?

A 
increase in the number of cells
cells MUST be able to replicate
can occur alongside hypertrophy
physiologic or pathologic
response remains CONTROLLED (i.e. not cancer)
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3
Q

Examples of physiologic & pathologic hyperplasia

A

physiologic:
–hormonal- increase in breast size at puberty
–compensatory- residual tissue growth after removal (i.e. liver regrowth)
pathologic:
–papilloma virus causing warts
–abnormal menstrual bleeding because of hormone imbalance

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4
Q

what is atrophy?

A

cell shrinkage

cells DONT DIE

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5
Q

causes of atrophy

A 
1- decreased workload
2- loss of innervation
3- decreased blood supply
4- inadequate nutrition
5- loss of endocrine stimulation
6- aging
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6
Q

mechanisms of atrophy

A

1- protein synthesis dec. because dec. metabolic activity
2- ubiquitin-proteasome pathway
3- increased autophagy

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7
Q

what is autophagy?

A

process in which a starved cell eats its own components to survive

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8
Q

what is metaplasia?

A
  • reversible cell change
  • switch one adult cell type with another adult cell type
  • influences that induce metaplastic change may predispose a malignant transformation of epithelium
  • EX: smokers respiratory epithelium goes from ciliated columnar to stratified squamous
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9
Q

what are the two types of cell death?

A

necrosis and apoptosis

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10
Q

what is necrosis and its characteristics?

A

-severe damage to membranes causing enzymes to leak out of lysosomes, enter the cytoplasm and digest the cell
-host response occurs (inflammation)
ALWAYS pathologic

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11
Q

what is apoptosis and its characteristics?

A
  • programmed cell death
  • occurs when a cell is deprived of growth factors or DNA/proteins are severely messed up
  • nuclear dissolution without complete loss of membrane integrity
  • pathologic or physiologic
  • NO host response
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12
Q

injurious stimuli to cells include…

A 
1-oxygen deprivation
2-chemical agents
3-infectious agents
4-immunologic rxns
5-genetic factors
6-nutritional imbalances
7-phsical agents
8-aging
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13
Q

what occurs first: morphologic changes of a cell, cellular function or cell death?

A

cellular function may be lost long before cell death occurs and the morphologic changes of cell injury/death lag far behind both

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14
Q

what two phenomena consistently characterize irreversible cell injury?

A

1-inability to correct mitochondrial dysfxn

2-profound disturbances in membrane fxn

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15
Q

what are the morphologic correlates of reversible cell injury and what are they caused by?

A

cellular swelling caused by failure of energy-dependent ion pumps in the plasma membrane=no ionic or fluid homeostasis
fatty change occurs in hypoxic, toxic or metabolic injury

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16
Q

what parts

of a cell show changes with necrosis?

A

cytoplasm- increased pink staining

nucleus- DNA breaks down, either karyolysis, pyknosis or karyorrhexis

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17
Q

fates of necrotic cells

A

may be digested, persist for some time or be calcified

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18
Q

what is coagulative necrosis?

A
  • underlying tissue architecture is preserved for several days
  • structural proteins and enzymes are denatured
  • characteristic of infarcts except in brain
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19
Q

what is liquefactive necrosis

A
  • seen in bacterial or fungal infections
  • hypoxic death of cells within the CNS evokes this
  • dead cells are completely digested and eventually removed
  • creates ‘pus’
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20
Q

what is gangrenous necrosis

A
  • refers to the condition of a limb (typically lower leg) that has lost its blood supply and has undergone coagulative necrosis
  • Wet gangrene- gangrenous necrosis with a bacterial infection too
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21
Q

what is caseous necrosis

A
  • found with TB infections
  • has distinct histological appearance
  • often enclosed by a distinctive inflammatory border: granuloma
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22
Q

what is fat necrosis

A
  • focal areas of fat destruction
  • typically from the release of pancreatic lipases
  • occurs with acute pancreatitis
  • has distinct histological appearance
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23
Q

what is fibrinoid necrosis

A
  • special
  • visible by light microscopy
  • complexes of antigens and antibodies are deposited in the walls of arteries
  • fibrinoid: a bright pink amorphous appearance caused by the immune complexes and fibrin
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24
Q

what allows detection of tissue-specific necrosis using blood or serum samples?

A

leakage of intracellular proteins through the damaged cell membrane and ultimately into the circulation

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25
Q

The cellular response to injurious stimuli depends on what three things?

A

type of injury, its duration and its severity

26
Q

What characteristics of an cell determines how it responds to injurious stimulus?

A

type, status, adaptability and genetic makeup

27
Q

What essential cellular components are disrupted with cellular injury?

A

1-mitochondria and their ability to generate ATP and ROS under pathologic conditions
2- disturbance in calcium homeostasis
3-damage to cellular membranes
4- damage to DNA and misfolding of proteins

28
Q

what are the major causes of ATP depletion in a cell?

A
  • reduced supply of oxygen and nutrients
  • mitochondrial damage
  • actions of some toxins (i.e. cyanide)
29
Q

which cell would survive longer if ATP was depleted: brain or liver. Why?

A

liver because it has greater glycolytic capacity than a brain cell.

30
Q

what two cations accumulate inside an injured cell and lead to more injury?

A

Na+ and Ca++

31
Q

Where in a cell are ROS normally produced and why?

A

in the mitochondria during redox reactions used for energy production

32
Q

What cells use ROS as a weapon? What is it called when they produce the ROS?

A

phagocytic leukocytes, mainly neutrophils and macrophages. a respiratory burst

33
Q

What other reactive free radical is produced in leukocytes besides ROS?

A

nitric oxide

34
Q

under what circumstances are free radical production increased?

A

1-absorption of radiant energy (UV or Xrays)
2- enzymatic metabolism of exogenous chemicals
3-inflammation

35
Q

What methods do cells have of removing free radicals?

A

1- superoxide dismutases (superoxide)
2-glutathione peroxidases (hydrogen peroxide)
3-catalase (hydrogen peroxide)
4- antioxidants

36
Q

what three reactions do ROS use to cause cell injury?

A

1-lipid peroxidation of membranes
2- cross-linking and other changes in proteins
3- DNA damage

37
Q

What biochemical mechanisms contribute to membrane damage, thus increased membrane permeability?

A 
1- decreased phospholipid synthesis
2- increased phospholipid breakdown
3-ROS
4- cytoskeletal abnormalities
5-lipid breakdown products
38
Q

what three sites of membrane damage during cell injury are the most important?

A

mitochondrial membrane
plasma membrane
lysosomal membrane

39
Q

Is ischemia or hypoxia worse for a tissue?

A

ischemia because without the blood flow, glycolysis can’t continue due to lack of substrates whereas with hypoxia, it can continue anaerobically.

40
Q

what is the most important biochemical abnormality in hypoxic cells that leads to cell injury?

A

reduced intracellular generation of ATP as a consequence of reduced supply of oxygen.

41
Q

Irreversible cell damage mainly ends in which process, necrosis or apoptosis?

A

necrosis

42
Q

Why does the restoration of blood flow to ischemic but viable tissues result in the death of cells that are not otherwise irreversibly injured?

A
  • increased generation of ROS by parenchymal and endothelial cells and from infiltrating leukocytes
  • inflammation that’s induced by ischemic injury may increase with reperfusion
43
Q

What two general ways do chemicals damage cells?

A

1- directly by combining with a critical molecular component or cellular organelle
2-must first be converted in the body, typically liver, into reactive toxic metabolites which then act on target cells.

44
Q

which type of cell death does NOT result in inflammation? why?

A

apoptosis because the cell dies in such a way that it is rapidly cleared by phagocytes before its contents are leaked.

45
Q

What are some examples of physiologic apoptosis?

A

1- programmed destruction of cells during embryogenesis
2-involution of hormone-dependent tissues upon hormone deprivation (menstrual cycle and lactation)
3-cell loss in proliferating ce3ll populations (to maintain constant number)
4-elimination of cells that have served their useful purpose (neutrophils after acute inflammation)
5-elimination of potentially harmful self-reactive lymphocytes (prevent autoimmune response)
6-cell death induced by cytotoxic T lymphocytes (protect against viruses and tumors)

46
Q

what are some examples of pathologic apoptosis?

A

1-DNA damage (chemo causes cell damage thus triggering apoptosis in cancer cells)
2-accumulation of misfolded proteins –> ER stress
3- cell injury in certain infections (triggered by virus or host)
4-pathologic atrophy in parenchymal organs after duct obstruction

47
Q

What enzymes are activated to start the process of apoptosis?

A

caspases

48
Q

What two pathways occur after caspases activation? Which one is most common?

A

1- mitochondrial (intrinsic) pathway (MC)

2- the death receptor (extrinsic) pathway

49
Q

What causes the mitochondrial pathway of apoptosis to occur? What caspase is ultimately activated?

A

1- decrease in GF
2- accumulation in DNA damage or misfolded proteins
3- caspase 9

50
Q

What causes the death receptor pathway of apoptosis to occur?

A
  • antigens stimulate cell surface receptors
  • eliminates self-reactive lymphocytes (stop autoimmune) or virus infected cells
  • Caspase 8
51
Q

When a cell undergoes autophagy too long, it signals cell death by what process?

A

apoptosis

52
Q

What are the 4 main pathways of abnormal intracellular accumulations?

A

1-inadequate removal
2-accumulation of an abnormal endogenous substance as a result of genetic or acquired defects
3-failure to degrade a metabolite (storage diseases)
4-deposition and accumulation of an abnormal exogenous substance that the cell cant degrade or export. (ex: silica)

53
Q

What are the two most common causes of fatty change in the liver?

A

alcohol abuse and diabetes associated with obesity

54
Q

In what cells of the liver, kidney, skeletal muscle and heart does fat accumulate?

A

triglycerides accumulate in parenchymal cells

55
Q

What is the most common exogenous pigment? Where is it found and what does it do?

A

Carbon, it is inhaled and phagocytosed by alveolar macrophages and transported through lymphatic channels to the regional tracheobronchial lymph nodes. It aggregates and blackens the draining lymph nodes and pulmonary parenchyma

56
Q

What causes freckles?

A

melanin, an endogenous brown-black pigment that’s synthesized by melanocytes in the epidermis. it acts as a screen against UV rays. freckles are caused by an accumulation of melanin in basal keratinocytes and macrophages.

57
Q

What is Hemosiderin and where is it found?

A

Hemosiderin is a hemoglobin-derived granular pigment that accumulates in tissues when there is a local or systemic excess of iron. Prussian blue staining is used to identify. typically pathologic, though small amounts in bone marrow, spleen and liver is normal. excessive accumulation is called hemosiderosis.

58
Q

What is dystrophic calcification?

A

the deposition of calcium salts and other minerals in dead or dying tissues. it occurs in the absence of derangements in calcium metabolism. occurs in areas of necrosis. Typically found with atherosclerosis and aortic valve stenosis

59
Q

what is metastatic calcification?

A

the deposition of calcium salts in normal tissues. almost always secondary to some derangement in calcium metabolism (hypercalcemia)

60
Q

Which type of calcification is found when calcium metabolism is normal?

A

dystrophic calcification

61
Q

what are the major causes of hypercalcemia?

A

1- increased secretion of PTH
2-destruction of bone (paget’s disease)
3-vitamin D related disorders (sarcoidosis)
4- renal failure

62
Q

What mechanisms are thought to be responsible for cellular aging?

A

1-DNA damage
2-decreased cellular replication–replicative senescence (Werner syndrome, progeria)
3-defective protein homeostasis

Pathology (2 decks)

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