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Pathophysiology

Pathophysiology
100問 • 2年前
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  • 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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    58問 • 10ヶ月前
    Two Clean Queens

    Child Psych ODD/CD/SUD

    Child Psych ODD/CD/SUD

    Two Clean Queens · 49問 · 10ヶ月前

    Child Psych ODD/CD/SUD

    Child Psych ODD/CD/SUD

    49問 • 10ヶ月前
    Two Clean Queens

    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)