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
2
Q
what is in charge of higher control?
A
CNS, ANS, PNS
3
Q
what is homeostasis?
A
static/balance
cells perform normal functions
4
Q
what happens when a cell is injured?
A
they are driven away from homeostatic state
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
6
Q
what does the outcome of cell response to injury depend on?
A
- injury type, duration and severity
- cell type, state and adaptability
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
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
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
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
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
12
Q
What is a pathological stimuli?
A
environmental changes that exceed the acceptable and normal range of adaptation
13
Q
What is a physiological stimuli?
A
stimuli that cause change that is within the normal range of adaptation
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
15
Q
Name 4 Pathological External Forces to Cell Injury
A
- Lack of Oxygen
- physical agents (trauma, freezing, burn, radiation etc.)
- chemical agents (drugs, poisons, heavy metals)
- Infectious agents (bacteria, virus, parasite)
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
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
18
Q
Name 3 Pathological Internal Factors to Cell Injury
A
- Immunologic
- Genetic
- Metabolic
19
Q
4 Types of Cell Adaptation That Can Either be Physiologic or Pathologic
A
- Hyperplasia= increase number of cells (only affects cells that divide)
- Hypertrophy= increase cell size causes, which also increase in organ size
- Atrophy= decrease in cell size
- Metaplasia= change of epithelium type to another.
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
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
22
Q
name two types of cell injury due to a lack of oxygen
A
myocardia infarct, stroke
23
Q
List 7 Causes Of Cell Injury
A
- Hypoxia (decrease oxygen, thus decrease in ATP)
- Ischemia (decrease in blood flow, also involves hypoxia)
- Environment factors
- Metabolic abnormalities
- Immune dysfunction
- aging
- Nutritional imbalance
24
Q
What are some cellular systems/structures that are most vulnerable?
A
- DNA
- Cell membrane
- protein generation
- ATP production
25
What are some hallmark factors to irreversible cell damage?
Loss of mitochondria, damage to plasma or lysosomal membrane
26
describe how skin wounds heal
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
27
name two examples of cell injury due to infectious agents
ebola virus, toxin released by bacteria
28
name two examples of cell injury due to physical agents
burn, frost bite
29
name two examples of cell injury due to chemical agents
overuse of alcohol, water contamination by arsenic
30
What is hyperplasia
an increase in tissue size due to an increase in the number of cells
ex: enlarged female breast during pregnancy
31
Describe wound healing of the skin
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
32
what is coagulative vs liquefactive necrosis?
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
What are the 4 different types of Necrosis
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
True or false, a decrease in the size of the uterus after pregnancy is an example of physiological atrophy
true- another example would be brain aging
35
An enlarged thyroid gland as a result of endogenous overproduction of the thyroid stimulating hormone (TSH) is an example of pathological hypertrophy.
true- enlarged cardiac muscle cells in response to hypertension is another example
36
An increase in the size of breast cells in response to lactation / pregnancy is an example of which cell adaptation?
physiologic hyperplasia
This is correct! An increase in the number of breast cells during pregnancy would be physiological hyperplasia
37
what are two examples of metaplasia?
cigarette smoking, barrett's esophagus
38
what are the 5 clinical signs of acute inflammation?
heat, redness, edema, pain, loss of function
39
What is cell atrophy? what is an example?
decreased cellular activity as a result of cell size, number or both
ex: osteopenia in rheumatoid arthritis
40
What is metaplasia?
Change in cell form from one cell type into another
change in epithelium cells from smoknig
41
what is the function of acute inflammation?
- 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
why is apoptosis necessary when DNA sustains damage?
so mutations won't be propagated. Goes through initiation and execution phases to complete the apoptosis
43
what is complete resolution of acute inflammation?
Regeneration of native cells and restoration of normal function with non residual deficit. → ideal outcome
44
Can Metaplasia be reversible?
yes
45
Name 3 Functions of Inflammation
1. contain and isolate injury
2. destroy microorganisms/toxins
3. prepare tissue for healing and repair
46
describe necrosis vs apoptosis
| cues: internal vs external factors, amount of visible evidence left
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
what is coagulative vs liquefactice necrosis?
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
What are the two types of inflammation
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
what are the acute inflammation stages
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
What are some outcomes of acute inflammation?
- resolution
- abscess
- ulcer
- fistula
- chronic inflammation
- scar formation
51
what is caseous necrosis vs fat necrosis?
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
what is inflammation?
a non-specific coordinated response by vascularized living tissue to injury (tissue response to injury)
53
what are 3 functions of inflammation?
contain and isolate the injury
destroy microorganisms/toxins
prepare tissue for healing and repair
54
what are the two components of the body required to mount an inflammatory response?
specialized cells
chemical mediators (cytokines, chemokines)
55
what is acute vs chronic inflammation?
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
what does chronic inflammation
| consist of
active inflammation and tissue destruction and repair happening simultaneously
57
what are the 2 components of cell repair?
1. healing= regeneration of cells combined with scarring and fibrosis
2. regeneration= complete replacement of damaged cells with scar formation
58
Healing by first intention vs second intention
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
what are the mediators of inflammation
histamine= increase vessel permeability, produced by mast cells
bradykinin= increase vessel permeability, cause pain, derived by plasma proteins
60
What are arachidonic acid derivatives?
formations from the phospholipids in the cell wall that metabolize to form various substances that affect inflammation.
- ex: leukotriene, thromboxane
61
what single event in the tissue explains heat and redness in acute inflammation?
vasodilation
62
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:
abscess formation
healing by fibrosis and scar formation
progression to chronic inflammation
63
what is the function of acute inflammation?
- 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
what are the events in acute inflammation?
- 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
what is complete resolution of acute inflammation?
Regeneration of native cells and restoration of normal function with non residual deficit. → ideal outcome
66
Cellular components to inflammation: neutrophil and eosinophils
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
what mediates the inflammatory response? (4)
- 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
what are mediators of fever?
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
what are the cellular components of inflammation?
- 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
what is an inflammatory exudate?
protein rich fluid containing WBCs that forms due to inflammation
71
What is transudate?
protein poor fluid containing few cells that forms due to a disturbance in forces across vessel walls
72
what is purulent exudate (pus)?
an inflammatory exudate containing many neutrophils usually due to a bacterial infection
73
what is serous inflammation?
Inflammation characterized by exudate of clear fluid with few cells
74
what is Fibrinous inflammation?
Inflammation characterized by exudate rich in fibrin
| eg/ diphtheria, whooping cough
75
Purulent inflammation?
inflammation characterized by exudate rich in PMN
76
what is ulcerative inflammation?
Inflammation characterized by loss of epithelial lining due to the inflammation (ulceration)
77
Pseudomembranous inflammation?
Inflammation characterized by ulceration and a fibrinopurulent exudate and makes a pseudomembrane over the ulcer
78
what is Chronic inflammation?
- 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
what is Granulomatous inflammation?
A specialized form of chronic inflammation characterized by the formation of granulomas
eg/ tuberculosis
