Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Goljan Pathology - High Yield Facts > Cell injury > Flashcards

Cell injury Flashcards

1
Q

PO2

A

driving force for diffusion of O2 into tissue

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

SaO2

A

percent heme groups occuied by O2

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

Cyanosis

A

decreased O2 saturation

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

O2 content

A

1.34 x Hb x SaO2 + PaO2

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

Oxygen

A

eceton acceptor in oxidative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hypoxia

A

inadequate O2 leads to ATP depletion

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

Ischemia

A

decreased arterial (or venous) blood flow

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

Respiratory acidosis

A

retention of CO2 always decreases PaO2

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

Ventilation defect

A

impaired delivery of O2 to alveoli; intrapulmonary shunting of blood (e.g., RDS)

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

Perfusion defect

A

absent blood flow to alveoli; increased alveolar dead space e.g., pulmonary embolus)

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

Diffusion defect

A

O2 cannot cross alveolar-capillary interface; interstitial lung disease (e.g., sarcoidosis)

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

Methemoglobin

A

decreased SaO2; heme Fe +3; oxidizing agents (sulfur/nitro drugs); Rx with IV methylene blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical methemogloinemia

A

cyanosis not corrected by O2; chocolate colored blood`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Carbon monoxide

A

decreased SaO2; left-shift O2 binding curve; inhibits cytochrome oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes carbon monoxide poisoning

A

car exhaust, space heaters, smoke inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

S/S carbon monoxide poisoning

A

headache; cherry red color skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cyanide

A

inhibits cytochrome oxidase; systemic asphyxiant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Carbon monoxide + cyanide poisoning

A

house fires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

left-shifted O2

A

decreased 2,3 BPG, carbon monoxide, alkalosis, HbF, methemoglobin, hyothermia

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

right-shifted O2

A

increased 2,3 BPG, high altitude, acidosis, fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

high altitude

A

respriratory alkalosis enhances glycolysis; increased systhesis 2,3 BPG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Mitochondrial poisons

A

damages membrane and drains off protons; alcohol salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Uncoupling agents in mitochondria

A

drain off protons; dinitrophenol, thermogenin (brown fat)

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

Complication mitochondrial poisons/uncoupling agents

A

hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Decreased ATP
impaired Na+/K+ ATPase pump (cellular swelling); reversible
26
Anaerobic glycolysis
ATP synthesis in hypoxia; lactate decreases intracellular pH, denatures proteins
27
Irreversible injury hypoxia
membrane/mitochondrial damage
28
Mitochondrial damage
release cytochrome c activates apoptosis
29
Irreversible injury hypoxia
increases cytosolic Ca2+ activates phospholipase, proteases, endonuclease
30
Free radicals
unpaired electron in outer orbit; damage cell membranes and DNA
31
Free radicals
superoxide, hydroxyl, peroxide, drugs (acetaminophen)
32
Superoxide dismutase
neutralizes superoxide
33
Glutathione
neutralizes peroxide, drug FRs
34
Catalase
neutralizes peroxide
35
Lipofuscin
indigestible lipid of lipid peroxidation; brown pigment increased in atrophy and FR damage
36
Reperfusion injury in heart
superoxide FRs + calcium
37
Mitochondrial injury
cytochrome c in cytosol initiates apoptosis
38
SER hyperplasia
alcohol, barbiturates, phenytoin
39
Complications SER hyperplasia
increases drug metabolism (e.g., oral contraceptives); decreased vitamin D
40
Chediak-Higashi
membrane protein defect in transferring lysosomal enzymes to phagocytic vacuoles
41
Chediak-Higashi
AR; giant lysosomes
42
I cell disease
absent enzyme marker in Golgi apparatus (mannose-6-phosphate); empty lysosomes
43
Rigor mortis
stiff muscles after death due to ATP depletion
44
Fatty change in liver
MCC alcohol (increase in NADH); DHAP -->G3P --> TG
45
Fatty change in liver
increase VLDL pushes nucleus to side
46
Causes fatty change
increase synthesis of TG/FAs, decrease beta-oxidation FAs/ synthesis apoproteins/ release VLDL
47
Fatty change in kwashiorkor
decrease synthesis of apoproteins
48
Ferritin
primary iron storage protien; soluble in blood; serum level reflects marrow storage iron
49
Hemosiderin
insoluble ferritin degradation product visible with Prussian blue stain
50
Atrophy
reduction in cell/tissue mass by either loss or cell shrinkage
51
Brain atrophy
ischemia; Alzhemier's
52
Exocrine gland atrophy in CF
duct obstruction by thick secretions
53
Labile cells
stem cells (skin, marrow, GI tract)
54
Stable cells
in Go phase (smooth muscle, hepatocytes); can enter cell cycle (growth factors, hormones)
55
Permanent cells
cannot replicate; cardiac/striated muscle; neurons
56
Hypertrophy
increase in cell size (structural components, DNA)
57
LVH
increased preload (valve regurgitation), increased afterload (HTN, aortic stenosis)
58
RVH
pulmonary hypertension
59
Bladder smooth muscle hypertrophy
prostate hyperplasia constricts urthra
60
Removal of kidney
hypertrophy of remaining kidney
61
Hyperplasia
increase in number of cells
62
Endometrial hyperplasia
unopposed estrogen (obesity, taking estrogen)
63
RBC hyperplasia
increased EPO (blood loss, ectopic secretion, high altitude)
64
Prostate hyperplasia
increased dihydrotestosterone
65
Gynecomastia
hyperplasia male breast tissue; normal in newborn, adolescent, elderly
66
Metaplasia
one adult cell type replaces another cell type
67
Squamous metaplasia in bronchus
smoking
68
Intestinal metaplasia in stomach
Paneth cells, goblet cells; H. pylori chronic atrophic gastritis
69
Squamous metaplasia bladder
Schistosoma hematobium infection
70
Barrett's esophagus
glandular metaplasia of distal esophagus; due to GERD
71
Dysplasia
atypical hyperplasia or metaplasia are precursors for cancer
72
Squamous dyplasia in cervix
HPV
73
Squamous dysplasia in bronchus
smoking
74
Necrosis
death of groups of cells
75
Coagulation necrosis
preservation of structural outline (due to increase lactic acid)
76
Infarction
pale (e.g., heart, kidney); hemorrhagic (e.g., lung, small bowel); dry gangrene
77
Liquefactive necrosis
brain infarct, bacterial infections; wet gangrene
78
Caseous necrosis
variant coagulation necrosis; granulomas due to TB/systemic fungi
79
Granulomas
acticated macrophages (epitheliod cells); multinucleated giant cells; CD4 T cells
80
Epitheliod cells
gamma-interferon releaed by CD4 T cells activates macrophages
81
Multinucleated giant cells
fusion of epitheliod cells
82
Granulomas
type 4 HSR
83
Enzymatic fat necrosis
associated with pancreatitis; soap formation (Ca2+ & fatty acids)
84
Fibrinoid necrosis
necrosis of immune reactions (immune vasculitis/endocarditis)
85
Postmortem necrosis
autolysis; no inflammatory reaction
86
Dystrophic calcification
calcification of damged tissue; normal serum calcium
87
Dystrophic calcification
pancreatitis; atheroscelerotic plaque
88
Metastatic calcification
calcification of normal tissue; increased seum calcium or phosphorus
89
Nephrocalcinosis
metastatic calcification of collecting tubule basement membranes
90
S/S nephrocalcinosis
polyuria due to nephrogenic diabetes insipidus; renal failure
91
Apoptosis
gene regulated individual cell death
92
Signals activating apoptosis
mullerian inhibitory factor, tumor necrosis factor, hormone withdrawal
93
Signal modulators of apoptosis
P53 suppressor gene, BCL-2 genes
94
BCL-2 genes
anti-apoptosis gene; prevents cytochrome c from leaving mitochondria
95
Caspases
responsible for enzymatic cell death in apoptosis; proteases and endonucleases
96
Marker of apoptosis
esoinophilic cytoplasm, pyknotic (ink dot) nucleus
97
Apoptosis
loss Mullerian epithlium in male fetus; thymus involution; killing cancer cells

Goljan Pathology - High Yield Facts (20 decks)

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