Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hypertrophy

A

increase in cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hyperplasia

A

increase in cell number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

dysplasia

A

concerning finding indicating cell stress caused non-normal cell change

needs treatment

may be precursor to malignant cells

most ineffective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ATP depletion (cell injury)

A

injured cell produces less ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

increased production of oxygen free radicals (cell injury)

A

these are damaing molecules to cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

increased membrane permeability (cell injury)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

increased cytosolic calcium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

causes of cell injury

A

physical agents: trauma

chemical damage: toxic

infectious, immunologic, inflammatory processes

genetic and nutritional factors

hypoxia and ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hypoxia vs ischemia

A

hypoxia: decreased oxygen in the tissues

ischemia: decreased blood flow (perfusion) to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

free radicals:

A

molecules with an unpaired electron in the outer orbit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  1. injury from abnormal intracellular accumlations

-cellular storage disorders

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

necrosis vs apoptosis

A

necrosis: proceeds injury

apoptosis: cells destroy themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
clinical manifestation of cell injury and necrosis
widespread cell injury and necrotic cell death produce systemic menifestations of cell inflammation
26
primary intention vs secondary intention
primary: surgical incision secondary: too big for sutures and needs to be filled
27
connective tissue repair
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
requirements for tissue healing
-nutrition with adequate protein -adequate blood flow and oxygenation -competent inflammatory and immune responses -good wound care
29
innate immunity
nonspecific happens same way in response to any molecule “non self” inflammation is key to innate immuity
30
adaptive immunity
specific different and specialized response to each different molecule “non self”
31
primary components of the immune response
WBCs tissue-based immune cells
32
innate immune response
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
4 WBCs in innate immunity
neutrophil (main one and first responder) monocytes eosinophils basophils
34
WBC of adaptive immune response
lymphocytes
35
phases of acute inlammation
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
5 cardinal signs of inflammation
redness = vasodilation swelling = vasodilation heat = metabolic reaction pain loss of function
37
localized inflammation can lead to what at the end
exudate: serous/transudative purulent (pus) hemorrhagic fibrinous abscess ulceration granuloma
38
systemic manifestations of inflammation
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
clinical indicators of systemic inflammatory respons include what 3 components of the “acute phase response”
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
blood test to assess for inflammation
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
C-reactive protein (CRP)
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
Erythrocyte sedimentation rate (ESR)
↑ 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
acute vs chronic inflammation
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
adaptive immune response
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
Antigen
a particle (protein) that can elicit a immune response if it is non-self
46
antibodies
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
IgG
protect newborn and can cross placenta
48
IgA
in breast milk
49
IgM
prominent in early immune responses
50
IgD
found on B lymphocytes needed for maturation of B cells
51
IgE
allergic reactions
52
cell mediated immunity of adaptive immune response
t helper cells create cytotoxic t cells and they get the pathogen that is presented at the cell surface and destroys it
53
Humoral immunity
produce antibiodies that bind to the anitgen and neutralize it
54
5 types of WBCs
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
difference between a segmented neutrophil and a bands
segs: more mature (nucleus is in segments) bands: not mature (nucleus looks like a band)
56
“blast” cells
really immature precurser blood cells
57
agranulocytes
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
Granulocytes
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
leukocytosis
increased number of WBCs or leukocytes
60
leukopenia
decreased white blood cell count long lasting inflammation can cause a depletion in wbcs

Bio300 exam 1 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions