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Bio300 exam 1 > cell and tissue alterations and repair > Flashcards

cell and tissue alterations and repair Flashcards

1
Q

atrophy

A

decreae in cell size

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2
Q

hypertrophy

A

increase in cell size

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3
Q

hyperplasia

A

increase in cell number

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4
Q

metaplasia

A

transform one NORMAL cell type to a different NORMAL cell type within the same tissue type

happens due to environmental stess

ex: smoke in lungs, acid-reflux into esophagus

can be reversed if cell enviornment normalizes

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5
Q

dysplasia

A

concerning finding indicating cell stress caused non-normal cell change

needs treatment

may be precursor to malignant cells

most ineffective

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6
Q

characteristics of cell injury

A

ATP depletion: injured cell produces less ATP

Increased production of oxygen free radicals

increase membrane permeability

increased cytosolic calcium

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7
Q

ATP depletion (cell injury)

A

injured cell produces less ATP

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8
Q

increased production of oxygen free radicals (cell injury)

A

these are damaing molecules to cells

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9
Q

increased membrane permeability (cell injury)

A

because of membrane injury and decreased availibility of ATP to power cell membrane pumps

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10
Q

increased cytosolic calcium

A

membran damage to both cell organelles and outer plasma membrane allows calcium to leak into cytosol

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11
Q

causes of cell injury

A

physical agents: trauma

chemical damage: toxic

infectious, immunologic, inflammatory processes

genetic and nutritional factors

hypoxia and ischemia

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12
Q

hypoxia vs ischemia

A

hypoxia: decreased oxygen in the tissues

ischemia: decreased blood flow (perfusion) to tissues

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13
Q

(important)
mecahnism of cell injury

A
  1. injury from impaired calcium homeostasis
  2. hypoxic-ischemic cell injury
  3. free radical injury
  4. injury from abnormal intracellular accumulations
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14
Q
  1. injury from impaired calcium homeostasis
A

cellular injury—increased membrane permeability—influx of calcium into cytosol

this increase in calcium may trigger irreversible cell injury

increase in calcium ions—activate cellular enzymes (released from lysosomes)—autodestruction of cell by enzymes

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15
Q
  1. injury impaired calium homeostasis

dystrophic calcification

A

calium deposits in damaged or necrosis tissue.

ex:
causes wear and tear on heart valves and damages them

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16
Q
  1. injury impaired calium homeostasis

metastatic calcification

A

calcium salts deposited in normal tissue

associated with HYPERCALCEMIA due to:

-severe renal disease (impaired calcium elimination)

-cancer with extensive bone metastases (with calcium release from bone)

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17
Q
  1. hypoxic-ischemic cell injury
A

caused by decreased level of oxygen (hypoxia) or blood flow (ischemia) to tissue

if blood flow is disrupted then oxygen supply is also disrupted.

this is because RBCs carry oxygen so no blood flow no oxygen

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18
Q
  1. hypoxic-ischemic cell injury

what happens due to decreased oxygen

A

1.↓ oxygen
2.↓ ATP production
3. failure of membrane ion pumps and ↑membrane 4. permeability (things that shouldnt get in can)
5. Na+, Cl-, Ca++ diffuse into cell and K+ diffuses out
6. Ca++ accumulates into mitochondria
7. H2O follows Na+ into cell
8. causes edema
9. if not fixed= Autodestruction of cell by activated enzymes

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19
Q
  1. free radical injury

related terms:
-oxidative stress
-reactive oxygen species (ROS)
-reperfusion injury
-hyperoxic

A

oxygen has 2 unpaired electrons
try to stabilize by binding to things within the cell

they harm cells but binding to:
-lipid peroxidation (cuase damage to lipid based plasma membranes)
-cellular proteins
-DNA

Antioxidant molecules bind to free radicals, stablizing the unpaired electrons to prevent damage
this is why its important to have antioxidants in your diet

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20
Q

free radicals:

A

molecules with an unpaired electron in the outer orbit

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21
Q

treatment for free radical injuries

A

Antioxidant molecules bind to free radicals, stablizing the unpaired electrons to prevent damage

this is why its important to have antioxidants in your diet

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22
Q
  1. Free Radical injury

reperfusion injury

A

if a cell that is hypoxic-ischemic cell injuried already, gets blood flow restored too much then it can cause further injury due to the free radicals binding to the lipids, cell proteins, and DNA.

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23
Q
  1. injury from abnormal intracellular accumlations

-cellular storage disorders

A

things that arnt suppose to be inside are and they cause problems

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24
Q

necrosis vs apoptosis

A

necrosis: proceeds injury

apoptosis: cells destroy themselves

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25
Q

clinical manifestation of cell injury and necrosis

A

widespread cell injury and necrotic cell death produce systemic menifestations of cell inflammation

26
Q

primary intention vs secondary intention

A

primary: surgical incision

secondary: too big for sutures and needs to be filled

27
Q

connective tissue repair

A

inflammatiory phase:
immune system cleans it up (bacteria)

proliferative phase (granulation tissue):
fill in hole with tissue

remodeling phase:
wound gets smaller with time. includes wound contraction

28
Q

requirements for tissue healing

A

-nutrition with adequate protein

-adequate blood flow and oxygenation

-competent inflammatory and immune responses

-good wound care

29
Q

innate immunity

A

nonspecific
happens same way in response to any molecule “non self”
inflammation is key to innate immuity

30
Q

adaptive immunity

A

specific
different and specialized response to each different molecule “non self”

31
Q

primary components of the immune response

A

WBCs

tissue-based immune cells

32
Q

innate immune response

A

barrier: skin mucous membranes
NK cells
inflammation: 2 phases
vascular and cellular
-acute inflammation is a normal, protective process
-chronic inflammation reflects something wrong

33
Q

4 WBCs in innate immunity

A

neutrophil (main one and first responder)

monocytes

eosinophils

basophils

34
Q

WBC of adaptive immune response

A

lymphocytes

35
Q

phases of acute inlammation

A

vascular phase:
first starts with constriction of arterioles and slow down blood, then vasodilation ↑cell pressure causing fluid move out

cellular phase:
getting neutrophil to bacteria, endothelial cells swell and seperate which allows neutrophils to squeeze out of vessel and find the bacteria to perform phagocytosis

36
Q

5 cardinal signs of inflammation

A

redness = vasodilation

swelling = vasodilation

heat = metabolic reaction

pain

loss of function

37
Q

localized inflammation can lead to what at the end

A

exudate:
serous/transudative
purulent (pus)
hemorrhagic
fibrinous
abscess
ulceration
granuloma

38
Q

systemic manifestations of inflammation

A

triggered by the release of cell signaling molecules (cytokines) from immune cells

systemic:
fever
lethargy
lymphadenopathy (enlarged lymph nodes) (cancer if lymph nodes are fixed and nontender)

39
Q

clinical indicators of systemic inflammatory respons include what 3 components of the “acute phase response”

A
  1. rises in acute phase reactant proteins (↑C-reaxctive protein (CRP)
  2. WBC response (↑# of WBCs)

3 systemic inflammatory response (widespread inflammatory response “septic shock”)

40
Q

blood test to assess for inflammation

A

these are nonspecific so they will tell you if you have inflammation but not where or what is causing it.

C-reactive protien (CRP) ↑

Erthrocyte sedimentation rate (ESR) ↑

41
Q

C-reactive protein (CRP)

A

is one of the acute phase response proteins of inflammation.

CRP levels measure the quantity of this protein in the blood

↑ levels of CRP indicates inflammation

42
Q

Erythrocyte sedimentation rate (ESR)

A

↑ ESR indicates inflammation

numeric measure of RATE not quantity

ESR measure the rate of aggregation and fall of RBCs to the bottom of a tube

the increase in the protein causes it to fall to the bottom faster

ex: one paper takes forever bc it floats but a stack of papers fall faster

43
Q

acute vs chronic inflammation

A

acute: normal protective response to foreign invaders

chronic:persistent state of unresolved inflammation which causes damage
not normal or protective

2 common patterns of chronic inflammation:
1. nonspecific chronic inflammation
2. granulomatous lesions (tuberculosis)

44
Q

adaptive immune response

A

speicific
2 types:

humoral immunity: (mediated by B-lymphocytes)
production of immunoglobulins (antibodies) from B lymphocytes

Cell-mediated immunity: (mediated by T-lymphocytes)
production of T-cytotoxic lymphocytes (which destroy cells that have been damaged (viral infection)

45
Q

Antigen

A

a particle (protein) that can elicit a immune response if it is non-self

46
Q

antibodies

A

complex protein produced throuhg the humoral pathway.

they bind only to specific antigens for which the antibodies have been produced to recognize

epitope: area of the antigen where antibodies bind

binding to an antigen causes inflammation

47
Q

IgG

A

protect newborn and can cross placenta

48
Q

IgA

A

in breast milk

49
Q

IgM

A

prominent in early immune responses

50
Q

IgD

A

found on B lymphocytes

needed for maturation of B cells

51
Q

IgE

A

allergic reactions

52
Q

cell mediated immunity of adaptive immune response

A

t helper cells create cytotoxic t cells and they get the pathogen that is presented at the cell surface and destroys it

53
Q

Humoral immunity

A

produce antibiodies that bind to the anitgen and neutralize it

54
Q

5 types of WBCs

A

leukocyte count = WBC count (all WBCS)

1.basophils
2.eosinophils
3.lymphocytes
4.monocytes
5.neutrophils (2 types) (main WBC)
1.segs (main neutrophil)
2.bands

55
Q

difference between a segmented neutrophil and a bands

A

segs: more mature (nucleus is in segments)

bands: not mature (nucleus looks like a band)

56
Q

“blast” cells

A

really immature precurser blood cells

57
Q

agranulocytes

A

dont have granules

lymphocytes: (mature in bone marrow)
t cells
b cells

monocytes:
migrate out of blood vessels and become tissue macrophages
*if you see increased monocytes = chronic inflammation

58
Q

Granulocytes

A

contain inflammatory mediators

neutrophils: acute inflammation
Segs: mature
Bands: immature

Eosinophils: role in allergies and defend against parasites

basophils: cells that migrate nto tissue and become mast cells

59
Q

leukocytosis

A

increased number of WBCs or leukocytes

60
Q

leukopenia

A

decreased white blood cell count

long lasting inflammation can cause a depletion in wbcs

Bio300 exam 1 (8 decks)

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