問題一覧
1
Oxygen is restored to cells creating a ROS leading to cell membrane damage.
Reperfusion Injury
2
How do you know hypoxia is occurring?
Lactate, Troponin, Transaminases
3
Ischemia causes increase in extra cellular calcium. Na Ca pump fails. Water and Ca moves into the cell and swells and damages nucleic acids, proteins, cell membrane. Ca activates enzymes lead to cell death.
Calcium Influx Injury
4
Mitochondria can’t make ATP. Electrolyte pump fails and cell swells. ER can’t work to make proteins. Looses membrane potential and structure fails.
Mitochondrial Injury
5
Activated as part of stress response leading to lysozymes breaking down Cellular components in order to salvage primarily ATP.
Autophagy
6
Not a true cellular adaptation. Disordered cell growth with a changes in cell size, shape, and organization associated with chronic irritation, inflammation, pre-cancerous and cancerous growths.
Dysplasia
7
Cellular adaptation that may be reversible in which one cell type is replaced by another.
Metaplasia
8
Pseudostratified columnar epithelium replaced with squamous epithelium.
Metaplasia
9
Squamous epithelium replaced with Columnar epithelium (Barrett’s Esophagus).
Metaplasia
10
Achondroplasia
Dysplasia
11
Cervical Cancer
Dysplasia
12
Cellular adaption by increasing number of cells leads to increased tissue and organ size.
Hyperplasia
13
Endometrium during menses
Hyperplasia
14
Bone marrow in anemia
Hyperplasia
15
Benign prostatic hypertrophy
Hyperplasia
16
Cellular adaptation increasing cell size leading to increased protein synthesis and tissue and organ size.
Hypertrophy
17
Weightlifting and Pregnancy
Hypertrophy
18
Cardiac muscle response to hypertension
Hypertrophy
19
Cellular adaption decreasing cell size and metabolic demand leads to increased cellular efficiency.
Atrophy
20
Thymus in infant
Atrophy
21
Tonsils in adolescents
Atrophy
22
Skin and brain in aging
Atrophy
23
Disuse of muscle (leg in cast)
Atrophy
24
Denervation
Atrophy
25
hydroxyl radicals, superoxide, hydrogen peroxide, nitric oxide
reactive oxygen species
26
must give up or gain electron binding to lipids (cell membrane)
free radical
27
causes inflammation implicated in many diseases (CV disease, DMII, aging, cancer, autoimmune) as a result of damage to cell membrane, DNA, and mitochondria.
reactive oxygen species
28
Can damage cell membrane directly or creating ROS that does the damage, leads to calcium influx injury.
Chemical agents
29
Drugs, metals, ethanol, carbon monoxide
Chemical agents
30
Tylenol, Vancomycin, Cephalosporins, Quinolones.
Therapeutic Medications
31
Arsenic and Cyanide
Non-Therapeutic Medications
32
Occurs naturally, treats leukemia, replaces phosphate in ATP to damage mitochondria
Arsenic
33
Slow accumulation over time deadly
Arsenic
34
Blocks intercellular use of oxygen
Cyanide
35
Single exposure deadly
Cyanide
36
Disrupts calcium homeostasis and substitutes for other substances (iron, Vit D, Mag, Zinc) in metabolism
Lead
37
Found in paint dust soil, builds up over time causing neurological, musculoskeletal, endocrine, reproductive, and dental problems.
Lead
38
Metabolized to Acetaldehyde
Ethanol
39
Replaces nutrients causing deficiencies in magnesium, Vit B6, phosphorus, folic acid and alters protein synthesis.
Ethanol
40
Hepatotoxicity and Cirrhosis caused by.
Acetaldehyde
41
Wernicke Encephalopathy and Peripheral Neuropathy
Ethanol
42
colorless, odorless, created from burning wood, gas, propane, charcoal.
Carbon Monoxide
43
Has a stronger affinity for hemoglobin than oxygen causing ischemia and cell injury
Carbon Monoxide
44
Slows metabolism and ATPase pump for therapeutic effect
Hypothermia
45
Non-Therapeutic Hypothermia
Generates ROS
46
Dose related effects with a “safe” threshold
Deterministic
47
Effect is not dose related, there is no “safe” threshold
Stochastic
48
Physiologic programmed cell death requiring ATP with no negative effects
Apoptosis
49
Pathophysiologic cell destruction, breaking down cell membrane leak into extracellular space resulting in inflammation.
Necrosis
50
Cell destruction for survival activated in stress response leading to lysosomes to catabolize cellular components.
Autophagy
51
Cell recycling to salvage cellular components, primarily ATP. Implicated in cancer and dementia.
Autophagy
52
Thymus, Lymph Nodes, and Mucosal associated with Lymph Tissue
Lymphatic System
53
Nonspecific Response
Innate Immunity
54
Specific Response
Adaptive Immunity
55
Non-specific response to foreign substance in phases, no memory
Inflammation
56
First line of defense with layers of protection (skin, low PH stomach urine, ciliary action).
Innate Immunity Barriers
57
Second line of defense. Respond immediately that includes stages of protection (vascular, plasma protein, and cell mediator responses).
Innate Immunity: Inflammatory Response
58
Vasodilation increases vascular permeability cause WBC to migrate causes redness, swelling, heat, and pain.
Vascular Response
59
Complement, Clotting,and Kinin Cascades.
Stages of Plasma Protein Response
60
Found in connective tissue close to blood vessels and lungs and GI tract.
Mast Cells
61
Release Histamine I and Histamine S. Chemotaxic factors - neutrophils and eosinophils.
Mast Cells
62
Synthesize leukotrines, prostaglandins, platelet-activating factors.
Mast Cells
63
Proteins that produce factors that destroy pathogens activating innate and adaptive responses.
Complements
64
Antigen-Ab complex, complements activated, mast cell degranulation, histamine release, leukocyte chemotaxis, opsonization, cell lysis.
Complememt Cascade
65
Prevents spread, traps antigen, stops bleeding, creates fibrin mesh
Purpose of a clot
66
Short acting, rapidly degrade, primary protein is bradykinin
Kinin Cascade
67
Local effects: vasodilation (common), vascular permeability, smooth muscle contraction, nerve cell stimulation, leukocyte chemotaxis (common).
Kinin Cascade
68
Post injury facilitates blood clotting and passage of cells (RBC, PLT, WBC) and fluid to site.
Cell Mediated Response
69
Recognize patterns and cell damage, and activates complement cascade.
Cellular Receptors
70
Send messages and coordinate the inflammatory response.
Cellular Products
71
In early inflammation, engulf bacteria dead cells and debris.
Neutrophils
72
initiate cellular inflammatory response, long term clean up and healing.
Monocyte
73
Engulf parasites and regulate mast cell response, associated with allergic reactions.
Eosinophils
74
Associated with allergic response, important for Ab response in B-Cells.
Basophils
75
Not a true leukocyte, engulf viruses and some cancer cells.
Natural Killer Cells
76
complement brings leukocyte to inflammation site to recognize, engulf, fuse, and destroy antigen.
Leukocyte Role in Phagocytosis
77
Phagocytes use oxygen to generate ROS, what turns off this destructive mechanism?
Serum Inhibitors
78
Messenger cells that create chemical communication network and mediate ramping up or slowing down immune system.
Cytokines
79
IL, TNF-a, Interferons, Chemokines
4 Cytokine Classes
80
Produced by Macrophages and Leukocytes, alter adhesion molecule expression, stimulate leukocyte production in bone marrow and bring them to inflammation site to enhance and suppress inflammation.
Interleukins
81
Pro-Inflammatory
IL-1 and IL-6
82
Anti-Inflammatory
IL-10
83
Pro-Inflammatory
TNF-a
84
Enhances endothelial cell molecules, starts chemokine production, leads to fever, septic shock, and cachexia.
TNF-a
85
produced my cells infected by viruses. functions to attach to cells not affected by virus to stimulate proteins that prevent viral replication enhancing acquired immunity.
Interferons
86
Produced by macrophages, fibroblasts, endothelial cells in response to PRO-inflammatory cytokines. induces leukocyte chemotaxis and involved in cancer growth.
Chemokines
87
IL-1 act on hypothalamus causing fever, leukocytosis (left shift), synthesize plasma proteins (acute phase reactants, C reactive protein, fibrinogen, ferritin).
Signs of Acute Inflammation
88
Too many cytokines released too quickly at once (PRO-inflammatory ILs). Fever is hallmark symptom. COVID and CAR-T cells.
Cytokine Storm
89
Damages cells and weakens immune system seen in: periodontitis, DMII, obesity, CV disease, Alzheimer’s, insulin resistance, frailty.
Chronic Inflammation
90
Always ready to respond, general response, short duration.
Innate Immunity
91
Must be induced, specific response, generates long term protection and memory.
Acquired Immunity
92
Antigen that induces an immune response.
Immunogenic
93
Presents the antigen to the lymphocytes.
Antigen Presenting Cell
94
too small to be Immunogenic so binds with larger proteins.
Haptens
95
Cellular immunity, stimulate cytokine response to activate leukocyte response or kill target directly. Do not produce Abs. Slow to respond. When impaired likely to have opportunistic infections.
T-Cells
96
Humoral Immunity, work outside cells binding to and neutralizing antigens, secretes Abs, responds quickly, when impaired cause systemic responses and more susceptible to encapsulated organisms.
B-Cells
97
Presenting and packaging known antigen.
Marcophage
98
Presenting and packaging naive antigen
Dendritic cells
99
Occurs in Thymus, has two chains
T-cell
100
On cell surface working as markers for T-cells
Memory T-cells (CD2)
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問題一覧
1
Oxygen is restored to cells creating a ROS leading to cell membrane damage.
Reperfusion Injury
2
How do you know hypoxia is occurring?
Lactate, Troponin, Transaminases
3
Ischemia causes increase in extra cellular calcium. Na Ca pump fails. Water and Ca moves into the cell and swells and damages nucleic acids, proteins, cell membrane. Ca activates enzymes lead to cell death.
Calcium Influx Injury
4
Mitochondria can’t make ATP. Electrolyte pump fails and cell swells. ER can’t work to make proteins. Looses membrane potential and structure fails.
Mitochondrial Injury
5
Activated as part of stress response leading to lysozymes breaking down Cellular components in order to salvage primarily ATP.
Autophagy
6
Not a true cellular adaptation. Disordered cell growth with a changes in cell size, shape, and organization associated with chronic irritation, inflammation, pre-cancerous and cancerous growths.
Dysplasia
7
Cellular adaptation that may be reversible in which one cell type is replaced by another.
Metaplasia
8
Pseudostratified columnar epithelium replaced with squamous epithelium.
Metaplasia
9
Squamous epithelium replaced with Columnar epithelium (Barrett’s Esophagus).
Metaplasia
10
Achondroplasia
Dysplasia
11
Cervical Cancer
Dysplasia
12
Cellular adaption by increasing number of cells leads to increased tissue and organ size.
Hyperplasia
13
Endometrium during menses
Hyperplasia
14
Bone marrow in anemia
Hyperplasia
15
Benign prostatic hypertrophy
Hyperplasia
16
Cellular adaptation increasing cell size leading to increased protein synthesis and tissue and organ size.
Hypertrophy
17
Weightlifting and Pregnancy
Hypertrophy
18
Cardiac muscle response to hypertension
Hypertrophy
19
Cellular adaption decreasing cell size and metabolic demand leads to increased cellular efficiency.
Atrophy
20
Thymus in infant
Atrophy
21
Tonsils in adolescents
Atrophy
22
Skin and brain in aging
Atrophy
23
Disuse of muscle (leg in cast)
Atrophy
24
Denervation
Atrophy
25
hydroxyl radicals, superoxide, hydrogen peroxide, nitric oxide
reactive oxygen species
26
must give up or gain electron binding to lipids (cell membrane)
free radical
27
causes inflammation implicated in many diseases (CV disease, DMII, aging, cancer, autoimmune) as a result of damage to cell membrane, DNA, and mitochondria.
reactive oxygen species
28
Can damage cell membrane directly or creating ROS that does the damage, leads to calcium influx injury.
Chemical agents
29
Drugs, metals, ethanol, carbon monoxide
Chemical agents
30
Tylenol, Vancomycin, Cephalosporins, Quinolones.
Therapeutic Medications
31
Arsenic and Cyanide
Non-Therapeutic Medications
32
Occurs naturally, treats leukemia, replaces phosphate in ATP to damage mitochondria
Arsenic
33
Slow accumulation over time deadly
Arsenic
34
Blocks intercellular use of oxygen
Cyanide
35
Single exposure deadly
Cyanide
36
Disrupts calcium homeostasis and substitutes for other substances (iron, Vit D, Mag, Zinc) in metabolism
Lead
37
Found in paint dust soil, builds up over time causing neurological, musculoskeletal, endocrine, reproductive, and dental problems.
Lead
38
Metabolized to Acetaldehyde
Ethanol
39
Replaces nutrients causing deficiencies in magnesium, Vit B6, phosphorus, folic acid and alters protein synthesis.
Ethanol
40
Hepatotoxicity and Cirrhosis caused by.
Acetaldehyde
41
Wernicke Encephalopathy and Peripheral Neuropathy
Ethanol
42
colorless, odorless, created from burning wood, gas, propane, charcoal.
Carbon Monoxide
43
Has a stronger affinity for hemoglobin than oxygen causing ischemia and cell injury
Carbon Monoxide
44
Slows metabolism and ATPase pump for therapeutic effect
Hypothermia
45
Non-Therapeutic Hypothermia
Generates ROS
46
Dose related effects with a “safe” threshold
Deterministic
47
Effect is not dose related, there is no “safe” threshold
Stochastic
48
Physiologic programmed cell death requiring ATP with no negative effects
Apoptosis
49
Pathophysiologic cell destruction, breaking down cell membrane leak into extracellular space resulting in inflammation.
Necrosis
50
Cell destruction for survival activated in stress response leading to lysosomes to catabolize cellular components.
Autophagy
51
Cell recycling to salvage cellular components, primarily ATP. Implicated in cancer and dementia.
Autophagy
52
Thymus, Lymph Nodes, and Mucosal associated with Lymph Tissue
Lymphatic System
53
Nonspecific Response
Innate Immunity
54
Specific Response
Adaptive Immunity
55
Non-specific response to foreign substance in phases, no memory
Inflammation
56
First line of defense with layers of protection (skin, low PH stomach urine, ciliary action).
Innate Immunity Barriers
57
Second line of defense. Respond immediately that includes stages of protection (vascular, plasma protein, and cell mediator responses).
Innate Immunity: Inflammatory Response
58
Vasodilation increases vascular permeability cause WBC to migrate causes redness, swelling, heat, and pain.
Vascular Response
59
Complement, Clotting,and Kinin Cascades.
Stages of Plasma Protein Response
60
Found in connective tissue close to blood vessels and lungs and GI tract.
Mast Cells
61
Release Histamine I and Histamine S. Chemotaxic factors - neutrophils and eosinophils.
Mast Cells
62
Synthesize leukotrines, prostaglandins, platelet-activating factors.
Mast Cells
63
Proteins that produce factors that destroy pathogens activating innate and adaptive responses.
Complements
64
Antigen-Ab complex, complements activated, mast cell degranulation, histamine release, leukocyte chemotaxis, opsonization, cell lysis.
Complememt Cascade
65
Prevents spread, traps antigen, stops bleeding, creates fibrin mesh
Purpose of a clot
66
Short acting, rapidly degrade, primary protein is bradykinin
Kinin Cascade
67
Local effects: vasodilation (common), vascular permeability, smooth muscle contraction, nerve cell stimulation, leukocyte chemotaxis (common).
Kinin Cascade
68
Post injury facilitates blood clotting and passage of cells (RBC, PLT, WBC) and fluid to site.
Cell Mediated Response
69
Recognize patterns and cell damage, and activates complement cascade.
Cellular Receptors
70
Send messages and coordinate the inflammatory response.
Cellular Products
71
In early inflammation, engulf bacteria dead cells and debris.
Neutrophils
72
initiate cellular inflammatory response, long term clean up and healing.
Monocyte
73
Engulf parasites and regulate mast cell response, associated with allergic reactions.
Eosinophils
74
Associated with allergic response, important for Ab response in B-Cells.
Basophils
75
Not a true leukocyte, engulf viruses and some cancer cells.
Natural Killer Cells
76
complement brings leukocyte to inflammation site to recognize, engulf, fuse, and destroy antigen.
Leukocyte Role in Phagocytosis
77
Phagocytes use oxygen to generate ROS, what turns off this destructive mechanism?
Serum Inhibitors
78
Messenger cells that create chemical communication network and mediate ramping up or slowing down immune system.
Cytokines
79
IL, TNF-a, Interferons, Chemokines
4 Cytokine Classes
80
Produced by Macrophages and Leukocytes, alter adhesion molecule expression, stimulate leukocyte production in bone marrow and bring them to inflammation site to enhance and suppress inflammation.
Interleukins
81
Pro-Inflammatory
IL-1 and IL-6
82
Anti-Inflammatory
IL-10
83
Pro-Inflammatory
TNF-a
84
Enhances endothelial cell molecules, starts chemokine production, leads to fever, septic shock, and cachexia.
TNF-a
85
produced my cells infected by viruses. functions to attach to cells not affected by virus to stimulate proteins that prevent viral replication enhancing acquired immunity.
Interferons
86
Produced by macrophages, fibroblasts, endothelial cells in response to PRO-inflammatory cytokines. induces leukocyte chemotaxis and involved in cancer growth.
Chemokines
87
IL-1 act on hypothalamus causing fever, leukocytosis (left shift), synthesize plasma proteins (acute phase reactants, C reactive protein, fibrinogen, ferritin).
Signs of Acute Inflammation
88
Too many cytokines released too quickly at once (PRO-inflammatory ILs). Fever is hallmark symptom. COVID and CAR-T cells.
Cytokine Storm
89
Damages cells and weakens immune system seen in: periodontitis, DMII, obesity, CV disease, Alzheimer’s, insulin resistance, frailty.
Chronic Inflammation
90
Always ready to respond, general response, short duration.
Innate Immunity
91
Must be induced, specific response, generates long term protection and memory.
Acquired Immunity
92
Antigen that induces an immune response.
Immunogenic
93
Presents the antigen to the lymphocytes.
Antigen Presenting Cell
94
too small to be Immunogenic so binds with larger proteins.
Haptens
95
Cellular immunity, stimulate cytokine response to activate leukocyte response or kill target directly. Do not produce Abs. Slow to respond. When impaired likely to have opportunistic infections.
T-Cells
96
Humoral Immunity, work outside cells binding to and neutralizing antigens, secretes Abs, responds quickly, when impaired cause systemic responses and more susceptible to encapsulated organisms.
B-Cells
97
Presenting and packaging known antigen.
Marcophage
98
Presenting and packaging naive antigen
Dendritic cells
99
Occurs in Thymus, has two chains
T-cell
100
On cell surface working as markers for T-cells
Memory T-cells (CD2)