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OSOT 513 > Core concepts of patho-physiology > Flashcards

Core concepts of patho-physiology Flashcards

1
Q

Cell function is controlled in a coordinated fashion….describe how autocrine, paracrine and endocrine cells function

A

Autocrine- cell stimulates self (ex: mucous cells in airways will respond to the environment and will alter their secretions accordingly)
Paracrine- cell simulates other cell close by: eg: if a whole group of mucous cells act at the same time they will communicate and work as a unite
Endocrine- cells stimulate distant cells

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2
Q

what is in charge of higher control?

A

CNS, ANS, PNS

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3
Q

what is homeostasis?

A

static/balance

cells perform normal functions

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4
Q

what happens when a cell is injured?

A

they are driven away from homeostatic state

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5
Q

when does a cell become injured? (as a broad contexts)

A

when there is a disturbance in the balance between external and internal forces

cells will either adapt to the new situation or die

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6
Q

what does the outcome of cell response to injury depend on?

A
  • injury type, duration and severity

- cell type, state and adaptability

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7
Q

what are the two types of cell death?

A

Necrosis: premature death of cells and living tissues: unprogrammed cell death; always detrimental,

Apoptosis: cell sends out signals and macrophages come and eat it; programmed cell death; usual beneficial

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8
Q

what are some ways cells respond to the disease process?

A
  • cells adapt to changes in their environment (cells stay alive)
  • inability to adapt may result in non-functioning or dead cells
  • tissue response to injury is healing
  • abnormal cell growth
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9
Q

what factors play a role in ho the cell responds to disease processes?

A
  • genetic and immune factors

- adverse environmental factors causing the disease

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10
Q

What are some ways that cells adapt?

A
  • modifying metabolic function (eg: if decreased calcium in blood, calcium will be mobilized from bones)
  • alter their structure
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11
Q

What are the 3 types of structural change in cell adaptation?

A
  • increased cellular activity (due to increased # of cells via mitosis, increased size of cells, or both)
  • decreased cellular activity (due to decreased number, size or both of cells)
  • change in morphology of cell from one type to another
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12
Q

What is a pathological stimuli?

A

environmental changes that exceed the acceptable and normal range of adaptation

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13
Q

What is a physiological stimuli?

A

stimuli that cause change that is within the normal range of adaptation

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14
Q

what are examples of external and internal pathological stimuli?

A

external: Oxygen deprivation, physical agents, chemical agents, infectious agents
internal: immunology, genetics, metabolic

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15
Q

Name 4 Pathological External Forces to Cell Injury

A
  1. Lack of Oxygen
  2. physical agents (trauma, freezing, burn, radiation etc.)
  3. chemical agents (drugs, poisons, heavy metals)
  4. Infectious agents (bacteria, virus, parasite)
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16
Q

What is wound healing by first intention?

A

healing that occurs after a surgical incision/clean cut
- acute inflam response> scab formation> PMN enter and scavenge debris> formulation of granulation tissue> replacement from fibrous scar

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17
Q

what is healing by second intent

A

healing that occurs after something like grating

> takes longer to heal, will cause a bigger blood clot

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18
Q

Name 3 Pathological Internal Factors to Cell Injury

A
  1. Immunologic
  2. Genetic
  3. Metabolic
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19
Q

4 Types of Cell Adaptation That Can Either be Physiologic or Pathologic

A
  1. Hyperplasia= increase number of cells (only affects cells that divide)
  2. Hypertrophy= increase cell size causes, which also increase in organ size
  3. Atrophy= decrease in cell size
  4. Metaplasia= change of epithelium type to another.
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20
Q

different cells have differing ability to regenerate…how do epithelial cells vs liver cells vs neurons regenerate as compared to one another

A

epithelial: continually dividing

liver cells: able to divide if required

neurons: no ability to divide

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21
Q

What is wound healing by first intention?

A

healing that occurs after a surgical incision/clean cut
- acute inflam response> scab formation> PMN enter and scavange debris> formulation of granulation tissue> replacement from fibrous scar

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22
Q

name two types of cell injury due to a lack of oxygen

A

myocardia infarct, stroke

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23
Q

List 7 Causes Of Cell Injury

A
  1. Hypoxia (decrease oxygen, thus decrease in ATP)
  2. Ischemia (decrease in blood flow, also involves hypoxia)
  3. Environment factors
  4. Metabolic abnormalities
  5. Immune dysfunction
  6. aging
  7. Nutritional imbalance
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24
Q

What are some cellular systems/structures that are most vulnerable?

A
  • DNA
  • Cell membrane
  • protein generation
  • ATP production
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25
Q

What are some hallmark factors to irreversible cell damage?

A

Loss of mitochondria, damage to plasma or lysosomal membrane

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26
Q

describe how skin wounds heal

A

by filling in the defect with granulation tissue and then replaing the granulation tissue with stronger fibrous tissue- with time the wound contracts and closes due to the contraction of myofibroblasts

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27
Q

name two examples of cell injury due to infectious agents

A

ebola virus, toxin released by bacteria

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28
Q

name two examples of cell injury due to physical agents

A

burn, frost bite

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29
Q

name two examples of cell injury due to chemical agents

A

overuse of alcohol, water contamination by arsenic

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30
Q

What is hyperplasia

A

an increase in tissue size due to an increase in the number of cells

ex: enlarged female breast during pregnancy

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31
Q

Describe wound healing of the skin

A

they heal by fitting in the defect with granulation tissue and then replacing it with stronger fibrous tissue. with time the wound contracts due to contraction of the myofibroblasts

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32
Q

what is coagulative vs liquefactive necrosis?

A

coagulative: most common type, protein denaturation > enzyme breakdown; like you throw an egg in boiling water

liquefactive necrosis: dissolution of tissue; necrotic area is soft and filled w fluid; enzymatic breakdown > protein denaturation

33
Q

What are the 4 different types of Necrosis

A

1) coagulative necrosis= the inactivation of hydrolytic enzymes. Results in solid organs. Most common form
2) liquefactive necrosis= necrotic area is soft and filled with fluid, tissue dissolution
3) caseus necrosis= a form of coagulation with limited liquefaction. Loos like cheese
4) fat necrosis= cells death of fat due to action of enzymes followed by the formation of complexes with calcium

34
Q

True or false, a decrease in the size of the uterus after pregnancy is an example of physiological atrophy

A

true- another example would be brain aging

35
Q

An enlarged thyroid gland as a result of endogenous overproduction of the thyroid stimulating hormone (TSH) is an example of pathological hypertrophy.

A

true- enlarged cardiac muscle cells in response to hypertension is another example

36
Q

An increase in the size of breast cells in response to lactation / pregnancy is an example of which cell adaptation?

A

physiologic hyperplasia

This is correct! An increase in the number of breast cells during pregnancy would be physiological hyperplasia

37
Q

what are two examples of metaplasia?

A

cigarette smoking, barrett’s esophagus

38
Q

what are the 5 clinical signs of acute inflammation?

A

heat, redness, edema, pain, loss of function

39
Q

What is cell atrophy? what is an example?

A

decreased cellular activity as a result of cell size, number or both

ex: osteopenia in rheumatoid arthritis

40
Q

What is metaplasia?

A

Change in cell form from one cell type into another

change in epithelium cells from smoknig

41
Q

what is the function of acute inflammation?

A
  • affected area is filled by transient material called an ‘inflammatory exudate’ (brings protiens, fluids and cells)
  • infective agents in the area of the exudate are destroyed
  • damaged tissue is broken down and debris removed
  • restoration of function, maybe.
42
Q

why is apoptosis necessary when DNA sustains damage?

A

so mutations won’t be propagated. Goes through initiation and execution phases to complete the apoptosis

43
Q

what is complete resolution of acute inflammation?

A

Regeneration of native cells and restoration of normal function with non residual deficit. → ideal outcome

44
Q

Can Metaplasia be reversible?

A

yes

45
Q

Name 3 Functions of Inflammation

A
  1. contain and isolate injury
  2. destroy microorganisms/toxins
  3. prepare tissue for healing and repair
46
Q

describe necrosis vs apoptosis

cues: internal vs external factors, amount of visible evidence left

A

necrosis: unprogrammed cell death mediated mostly by factors external to the cell and likely to leave visible evidence
apoptosis: programmed cell death mediated by factors internal to the cell and unlikely to leave physical evidence

47
Q

what is coagulative vs liquefactice necrosis?

A

coagulative: most common type, protein denaturation > enzyme breakdown; like you throw an egg in boiling water

liquefactive necroisis: disollution of tissue; nectrotic area is soft and filled w fluid; enzymatic breakdown > protein denaturation

48
Q

What are the two types of inflammation

A
  1. acute= most common early tissue response to tissue damage

2. chronic= occurs when body is unable to effectively deal with the injury or the injurious stimulus continues

49
Q

what are the acute inflammation stages

A
  1. vasolidation= mediators cause increase pressure to slow blood flow
  2. mediators increase vascular permeability to increase protein levels
  3. movement of WBC from blood vessels into soft tissue at site of injury, also facilitated by mediators
50
Q

What are some outcomes of acute inflammation?

A
  • resolution
  • abscess
  • ulcer
  • fistula
  • chronic inflammation
  • scar formation
51
Q

what is caseous necrosis vs fat necrosis?

A

Caseous necrosis: necrotic tissue w the appearance of cheese (seen in TB)- from chronic inflam

Fat necrosis: white chalky areas form- enzymes turn fat into necrotic tissue- usually caused by adipose trauma or release of enzymes from adjacent organ

52
Q

what is inflammation?

A

a non-specific coordinated response by vascularized living tissue to injury (tissue response to injury)

53
Q

what are 3 functions of inflammation?

A

contain and isolate the injury

destroy microorganisms/toxins

prepare tissue for healing and repair

54
Q

what are the two components of the body required to mount an inflammatory response?

A

specialized cells

chemical mediators (cytokines, chemokines)

55
Q

what is acute vs chronic inflammation?

A

acute: most common in early tissue response to tissue damage

chronic
- occurs when the body is unable to manage the injury or when the injury stimulus is continuous; ex: bronchiectasis

56
Q

what does chronic inflammation

consist of

A

active inflammation and tissue destruction and repair happening simultaneously

57
Q

what are the 2 components of cell repair?

A
  1. healing= regeneration of cells combined with scarring and fibrosis
  2. regeneration= complete replacement of damaged cells with scar formation
58
Q

Healing by first intention vs second intention

A

First intention= the wound has clean edges and minimal tissue disruptions
- ex. surgical incision

Second intention= wound has unclean edges, with extensive tissue disruption and tissue necrosis. results in a larger scar
- ex. ulcer

59
Q

what are the mediators of inflammation

A

histamine= increase vessel permeability, produced by mast cells

bradykinin= increase vessel permeability, cause pain, derived by plasma proteins

60
Q

What are arachidonic acid derivatives?

A

formations from the phospholipids in the cell wall that metabolize to form various substances that affect inflammation.
- ex: leukotriene, thromboxane

61
Q

what single event in the tissue explains heat and redness in acute inflammation?

A

vasodilation

62
Q

In situations where inflammation does not completely resolve, with return to normal tissue, there are three possible states that might develop. List these three states:

A

abscess formation

healing by fibrosis and scar formation

progression to chronic inflammation

63
Q

what is the function of acute inflammation?

A
  • affected area is filled by transient material called an ‘inflammatory exudate’ (brings protiens, fluids and cells)
  • infective agents in the area of the exudate are destroyed
  • damaged tissue is broken down and debris removed
  • restoration of function, maybe.
64
Q

what are the events in acute inflammation?

A
  • Change in size of caliber of blood vessels: Transient vasoconstriction; Vasodilation → generates heat and redness
  • Increased vascular permeability: Edema formation → fluid (not cells) ; WBCs enter site of injury
  • Kill/clean up organisms, mop of debris, WBC’s are main constituents of puss
65
Q

what is complete resolution of acute inflammation?

A

Regeneration of native cells and restoration of normal function with non residual deficit. → ideal outcome

66
Q

Cellular components to inflammation: neutrophil and eosinophils

A

Neutrophils= first cells to enter the injury site. Kill bacteria and engulf material (phagocytosis), produce chemicals to attract other cells

Eosinophils= kill bacteria, involved during allergic reactions. Present in chronic inflammation

67
Q

what mediates the inflammatory response? (4)

A
  • Histamine: Increase vessel permeability, Released by mast cells, Reduces leukocyte adhesion
  • Bradykinin (produced by enzymatic proteins), Increased vessel permeability, Causes pain, Derived from a plasma protein
  • Complement system: Group of plasma proteins that help kill bacteria. They are activated by either the: Classicall pathway: Alternate pathway
  • Arachidonic acid (AA) and AA derivatives
    derived from phospholipids on cell membrane
    Metabolized from many substances
68
Q

what are mediators of fever?

A

interleukin 1 (IL1), and tumor necrosis factor alpha (TNFa) are cytokines secreted by leukocytes

These act on the hypothalamus stimulating the production of prostaglandins that turn up the body’s heat → fever

Fevers increase blood flow which is meant to assist in delivering inflammatory cells to the site of injury or inflammation; we get fevers bc ^ BF to help deliver inflammatory cells

Fever can kill you if this goes too far.

69
Q

what are the cellular components of inflammation?

A
  • Neutrophil (PMN)- primary one for acute inflammation, Very mobile, First cells to enter site of injury, Able to kill bacteria and engulf material (phagocytosis), Produce chemicals to attract other cells, Short lived
  • Eosinophils- really good at killing parasites,Very mobile, Kill bacteria, Involved in allergic reactions, parasite infections, Longer lived, present in chronic inflammation
  • basophils/mast cells, Release histamine, Basophils are in blood, Mast cells are in tissue
  • Macrophages- act as front line cops and janitors → clean up cells, Major phagocytes → enter site 3-4 days after injury, Present in chronic inflammation
  • lymphocytes/plasma cells, Immune function in chronic inflammation
70
Q

what is an inflammatory exudate?

A

protein rich fluid containing WBCs that forms due to inflammation

71
Q

What is transudate?

A

protein poor fluid containing few cells that forms due to a disturbance in forces across vessel walls

72
Q

what is purulent exudate (pus)?

A

an inflammatory exudate containing many neutrophils usually due to a bacterial infection

73
Q

what is serous inflammation?

A

Inflammation characterized by exudate of clear fluid with few cells

74
Q

what is Fibrinous inflammation?

A

Inflammation characterized by exudate rich in fibrin

eg/ diphtheria, whooping cough

75
Q

Purulent inflammation?

A

inflammation characterized by exudate rich in PMN

76
Q

what is ulcerative inflammation?

A

Inflammation characterized by loss of epithelial lining due to the inflammation (ulceration)

77
Q

Pseudomembranous inflammation?

A

Inflammation characterized by ulceration and a fibrinopurulent exudate and makes a pseudomembrane over the ulcer

78
Q

what is Chronic inflammation?

A
  • Inflammation of prolonged illness or injury duration where active inflammation, tissue destruction, and attempts at healing may all occur at the same time
  • Chronic inflammatory cell exudate
  • Proliferation of fibroblasts
79
Q

what is Granulomatous inflammation?

A

A specialized form of chronic inflammation characterized by the formation of granulomas
eg/ tuberculosis

OSOT 513 (8 decks)

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