Gen Path - Class 1

Front 1

What is the function of a lysosome?

Back 1

Cleans up waste

Front 2

What is the function of a primary lysosome?

Back 2

House lytic enzymes – fuse with other cytoplasmic vesicles to form secondary

Front 3

What are the three types of secondary lysosomes?

Back 3

(1)Heterophagosomes, (2)Autophagosomes, (3)Lipofuscin

Front 4

What is the function of heterophagosomes?

Back 4

These are large vesicles that result from the fusion of phagosomes that contain ENDOCYTOSED material with lysosomes containing lytic enzymes. Thus, the digestion of material from OUTSIDE the cell takes place within heterophagosomes.

Front 5

What is the function of autophagosomes?

Back 5

Digest cells own organelles

Front 6

What is the function of lipofuscin?

Back 6

aka residual bodies. Remnants of digested materials from autophagosomes or heterophagosomes. Show up as age spots.

Front 7

What is homeostatsis?

Back 7

A state of balance between opposing pressures operating in and around a cell or tissue. A state of equilibrium.

Front 8

Describe the "steady state" in cells.

Back 8

Equilibrium between cells and their environment achieved and maintained.

Front 9

What happens to the cell if the demand exceeds the capacity of the cell to adapt to disequilibrium?

Back 9

The cell can become damaged and cannot return to original steady state, leading to cell injury and/or death

Front 10

What are the two types of cell injury?

Back 10

(1)Reversible, (2)Irreversible

Front 11

Describe reversible cell injury.

Back 11

Reversible injury, cell recovery, and return to normal function

Front 12

Define reversible cell injury.

Back 12

Adverse conditions that cause a cellular response that remains within the range of homeostasis. Injury stops--original steady state

Front 13

*How long does reversible cell injury typically last?

Back 13

Typically mild or short-lived

Front 14

What are three causes of reversible cell injury?

Back 14

(1)Brief hypoxia, (2)brief anoxia, (3)low concentration of toxins

Front 15

What kind of changes can reversible cell injury lead to?

Back 15

Hydropic changes

Front 16

How can the hydropic changes be reversed?

Back 16

Hydropic change is Reversible if toxin is removed or energy source is restored (oxygen). Cell can revert back to steady state homeostasis

Front 17

What can anoxia or any energy deprivation cause?

Back 17

AA decreased function in Na+/K+ pump. Can’t maintain concentration gradient -- Na+ flows into cell (Cl- follows) --` increased [NaCl]INSIDE cell

Front 18

What is the result if water can easily flow into the cell?

Back 18

Swelling

Front 19

What are three functional changes that can occur with reversible cell injury?

Back 19

(1)Reduced energy production, (2)Decreased protein synthesis, (3)Increased autophagy

Front 20

Why is cell energy production reduced?

Back 20

Swollen mitochondria generate less ATP

Front 21

How does protein synthesis decrease?

Back 21

pH of cell becomes acidic (due to anaerobic glycolysis producing lactic acid) which slows metabolism and degranulation of theRER

Front 22

How does autophagy increase?

Back 22

Damaged proteins are phagocytised and lysosome enzymes are released. A large amount of this occurring could damage other cellular components

Front 23

Describe the two types of irreversible cell injury.

Back 23

(1)Apoptosis and programmed cell removal, (2)Cell death and necrosis

Front 24

What are three causes of irreversible cell injury?

Back 24

(1)heavy doses of toxins, (2)anoxia, (3)prolonged hypoxia

Front 25

What three changes in the nucleus can irreversible cell injury cause?

Back 25

(1)Pyknosis, (2)Karyorrhexis, (3)Karyolysis

Front 26

What is pyknosis?

Back 26

condensation of chromatin

Front 27

What is karyorrhexis?

Back 27

fragmentation of nucleus -- ‘nuclear dust’

Front 28

What is karyolysis?

Back 28

lysis of chromatin

Front 29

How can irreversible cell injury affect the cell membrane?

Back 29

Causes loss of cell integrity and rupture of the cell membrane

Front 30

Where do dead cells release their contents?

Back 30

Dead cells release their contents into extracellular fluid. Shown in laboratory blood tests – something is really wrong!

Front 31

What are six causes of cell injury?

Back 31

(1)Hypoxia and anoxia, (2)Re-oxygenation, (3)Toxic injury, (4)Microbial Pathogens, (5)Mediators of Inflammation and Immune Reactions, (6)Genetic and Metabolic Disturbances

Front 32

*What is the most common cause of cell injury?

Back 32

Hypoxia and Anoxia

Front 33

What are three ways hypoxia and anoxia can occur?

Back 33

(1) Obstruction of airways, (2)decreased oxygen transportation (pneumonia, severe anemia), (3)cyanide poisoning

Front 34

What is re-oxygenation?

Back 34

Short lived reversible cell injury due to hypoxia may be repaired by re-oxygenation

Front 35

What is the risk of re-oxygenation?

Back 35

Oxygen toxicity. (Oxygen radicals formed ionized iron or production of hydrogen peroxide.Too much oxygen too fast may form oxygen radicals.)

Front 36

How can re-oxygenation occur?

Back 36

Postperfusion myocardial injury

Front 37

What are three ways a cell can experience toxic injury?

Back 37

(1)Ingestion of heavy metals, (2)Carbon tetrachloride, (3)Drugs and alcohol

Front 38

Is ingestion of heavy metals a direct or indirect toxin?

Back 38

Direct toxin

Front 39

What is an example of a heavy metal that could be ingested?

Back 39

Mecury

Front 40

What is carbon tetrachloride

Back 40

commercial metal cleaning product

Front 41

Is carbon tetrachloride a direct or indirect toxin?

Back 41

Indirect toxin

Front 42

What happens when carbon tetrachloride is ingested?

Back 42

When ingested is metabolized into a toxic free radical

Front 43

How can drugs and alcohol contribute to cell toxicity?

Back 43

Drug overdose

Front 44

What are two ways that microbial pathogens can injure the cell?

Back 44

(1)Bacteria produce toxins, (2)Viruses

Front 45

How can bacteria producing toxins injure the cell?

Back 45

Food poisoning

Front 46

What two ways can viruses injure the cell?

Back 46

(1)Direct cytopathic effect - invade cells and kill from within, (2)Indirect cytopathic effect - integrate into cellular genome and causes the immune system to attack it’s own cell

Front 47

What are three examples of mediators of inflammation and immune reactions?

Back 47

(1)Cytokines, (2)interferons, (3)complement proteins

Front 48

How do mediators of inflammation and immune reactions injure the cell?

Back 48

Eliminate infectious diseases but also kill own body’s cells

Front 49

How do genetic and metabolic disturbances?

Back 49

Many genetic diseases cause disturbances to metabolism and accumulation of toxic metabolites

Front 50

What is an example of genetic and metabolic disturbances that injure the cell?

Back 50

Diabetes Mellitus – pathological changes to small blood vessels -- ischemia

Front 51

What are the five types of cell adaptations?

Back 51

(1)Atrophy, (2)Hypertrophy, (3)Hyperplasia, (4)Metaplasia, (5)Dysplasia

Front 52

What is atrophy?

Back 52

Decrease in size of a cell, tissue, organ or entire body. Can be a reduced size of a cell, reduced number of cells or both.

Front 53

What happens to cells during aging?

Back 53

Aging and damaged organelles are eaten by autophagosomes and digested

Front 54

What happens to undigested cell residues?

Back 54

Undigested residues form lipid-rich brown pigment called lipofuscin

Front 55

What happens to undigested cell proteins?

Back 55

Undigested proteins are taken up by ubiquitin (scavenger protein) and marked for destruction.

Front 56

What is physiologic atrophy?

Back 56

occurs with age and includes entire body

Front 57

What is pathologic atrophy?

Back 57

occurs as a result of inadequate nutrition or stimulation

Front 58

What are three examples of pathologic atrophy?

Back 58

(1)Ischemia, (2)nerve damage, (3)malnutrition

Front 59

What is hypertrophy?

Back 59

Increase size of tissue or organs due to enlargement of individual cells. Hypertrophy alone in cardiac and skeletal muscle – cells can not divide.

Front 60

What is hyperplasia?

Back 60

Increase in size of tissue or organs due to an increased number of cells. Increased proliferation or formation of cells.

Front 61

What are two examples of hyperplasia?

Back 61

(1)Chronic stimulation – callus, (2)Hormones - uterus

Front 62

What is metaplasia?

Back 62

Change of one cell type into another, but it is not normal in that area. Pre-pre-cancer.

Front 63

What is an example of metaplasia?

Back 63

Smokers – columnar cells of the bronchial mucosa -- stratified squamous epithelium

Front 64

Is metaplasia reversible or irreversible?

Back 64

Reversible

Front 65

What can happen if the stimulus causing metaplasia remains?

Back 65

If stimulus remains the metaplasia may progress to dysplasia

Front 66

What is dysplasia?

Back 66

Pre-cancer. Disorderly arrangement of cells and nuclear change. Can progress to neoplasia (Cancer).

Front 67

What are three causes of intercellular accumulations?

Back 67

(1)A result of an overload of metabolites or exogenous material, (2)Metabolic disturbances that prevent secretion of metabolic by products and normal secretions, (3)Very complex mechanisms

Front 68

What are the three types of intercellular accumulations?

Back 68

(1)Anthracosis, (2)Hemosiderosis, (3)Lipid accumulation

Front 69

What is anthracosis?

Back 69

Exogenous material accumulation. Early stages of black lung. Seen in lungs of coal miners and cigarette smokers

Front 70

What is hemosiderosis?

Back 70

Accumulation of brown pigment – hemosiderin. Derived from hemolyzed red blood cells.

Front 71

What is an example of hemosiderosis?

Back 71

Hereditary hemochromatosis – genetic disorder of liver. Over-absorption of iron from food

Front 72

What is lipid accumulation?

Back 72

Fatty livers due to chronic alcohol abuse or diabetes mellitus

Front 73

What are the two reasons that cells die?

Back 73

(1)Necrosis, (2)Apoptosis

Front 74

What are the four types of necrosis?

Back 74

(1)Coagulative, (2)Liquefactive, (3)Caseous, (4)Enzymatic fat Necrosis

Front 75

Which type of necrosis is the most common?

Back 75

Coagulative

Front 76

What is the cause of coagulative necrosis?

Back 76

Anoxia. Rapid inactivation of hydrolytic enzymes -- prevents lysis

Front 77

What is the outcome of coagulative necrosis?

Back 77

Cell membrane is preserved, organelles and nucleus coagulate

Front 78

What type of tissues does coagulative necrosis affect?

Back 78

Solid internal organs: heart, liver, kidneys

Front 79

What the cause of liquefactive necrosis?

Back 79

Cell is completely digested by hydrolytic enzymes – ex brain infarct

Front 80

What is the outcome of liquefactive necrosis?

Back 80

Dissolution of tissues -- soft and liquify

Front 81

What tissues does liquefactive necrosis affect?

Back 81

Brain, skin, joints

Front 82

What type of necrosis is a special form of coagulative necrosis?

Back 82

Caseous Necrosis

Front 83

What is the cause of caseous necrosis?

Back 83

TB patients -- center part of tuberculous granuloma becomes necrotic and cells fall apart. Cheesy. Also found with fungal infections (histoplasmosis)

Front 84

What organ does caseous necrosis affect?

Back 84

Lungs

Front 85

What type of necrosis is a special form of liquefactive necrosis?

Back 85

Enzymatic Fat Necrosis

Front 86

What is the cause of enzymatic fat necrosis?

Back 86

Lipolytic enzymes and limited to fat tissues usually around the pancreas

Front 87

What is the outcome of enzymatic fat necrosis?

Back 87

Rupture of pancreas. Enzymes release into adjacent fat tissue degrade fat into glycerol and free fatty acids. Forms calcium soaps.

Front 88

What are two types of necrosis complications?

Back 88

(1)Gangrene, (2)Calcification

Front 89

Where is gangrene often seen?

Back 89

Often seen in necrotic tissue especially on extremities

Front 90

What are the two types of gangrene?

Back 90

(1)Wet gangrene, (2)Dry gangrene

Front 91

How is wet gangrene caused?

Back 91

Bacterial infection -- inflammation and secondary liquefaction

Front 92

How is dry gangrene causes?

Back 92

Dried out necrotic tissue, dark black, mummified

Front 93

What is calcification?

Back 93

Necrotic tissue attracts calcium salts. Arteries with atherosclerosis, damaged heart valves, tumours.

Front 94

What is dystrophic calcification?

Back 94

Calcification of necrotic tissue

Front 95

What is apoptosis?

Back 95

Active form of PROGRAMMED cell death by ‘suicide genes’

Front 96

Does apoptosis affect single cells or groups of cells?

Back 96

Single cells. Cell divides into apoptotic bodies -- taken up by macrophages

Front 97

What are two types of apoptosis?

Back 97

(1)Physiologic apoptosis, (2)Pathologic apoptosis

Front 98

What is an example of physiologic apoptosis?

Back 98

Fetal development

Front 99

What is an example of pathologic apoptosis?

Back 99

Liver cells infected with hepatitis

Front 100

Is the cause of necrosis exogenous or endogenous injury?

Back 100

Exogenous

Front 101

Is the cause of apoptosis exogenous or endogenous injury?

Back 101

Exogenous or endogenous

Front 102

What is the mechanism of necrosis?

Back 102

Vital processes are inhibited

Front 103

What is the mechanism of apoptosis?

Back 103

Active programmed process

Front 104

What cells are affected by necrosis?

Back 104

Multiple, organs

Front 105

What cells are affected by apoptosis?

Back 105

Single

Front 106

What type of cell changes are seen with necrosis?

Back 106

Swollen, ruptured, cell membrane ruptured

Front 107

What type of cell changes are seen with apoptosis?

Back 107

Rounded up, fragmented, cell membrane in tact

Front 108

What is the outcome of necrosis?

Back 108

Cell membrane ruptures, tissue death, bacterial infections

Front 109

What is the outcome of apoptosis?

Back 109

Phagocytosis by macrophages