Bio 570 Test _Lecture 3_1/29

Front 1

Describe normal pathway of ethanol.

Back 1

Most of alcohol in the blood is metabolized in the liver through onen major and two accessory pathways. Normally ethanol hangs around and is eventually converted into acetaldehyde via ADH (a catalyst enzyme).

Front 2

Describe normal pathway of ethanol.

Back 2

Acetaldehyde is then progressively broken down intoCO2 and H20.

Front 3

Describe pathway developed by alcoholics.

Back 3

Activation of two secondary pathways called 1)MEOS (microsomal ethanol oxidizing system)/
2) Catalase
is important in accelleration of ethanol metabolism =(tolerance).

Front 4

Describe pathway developed by alcoholics.

Back 4

Ethanol induced cellular injury results from the activation of the multiple pathways which lead to acetaldehyde formation and accumulation.

Front 5

Describe harmful effects of acetaldehyde accumulation.

Back 5

Very reactive so is mediator of widespread tissue damage. Causes: increased cell permeability, depositon in fat, enlargement of liver, interuption of protein transport, increace in intracellular water, depression of fatty acid ocidation, acute liver cell necrosis.

Front 6

What are the most serious consequences of alcohol abuse?

Back 6

1) Liver disorders
2) Nutritional Disorders

Front 7

Cell Death-eventually leads to cellular dissolution, or necrosis. Define Necrosis.

Back 7

Necrosis is the process process of cellular self -digestion or autodigestion (autolysis) after cell death.

Front 8

Name and describe two ways Cell death occurs.

Back 8

1)Necrosis--(irreversible injury) changes produced by enzymatic digestion of dead cellular elements (autolysis)
2)Apoptosis-"programed cell death"-vital process that helps eliminate unwanted cells--specific pathway that is active, once active, body programmed to kill cells

Front 9

Name four major types of necrosis.

Back 9

1)Coagulative Necrosis
2)Liquefactive Necrosis
3)Caseous Necrosis
4)FatNecrosis
5)Gangrenous Necrosis
6)Gas Gangrene Necrosis

Front 10

Describe Coagulative Necrosis

Back 10

Coagulative N=Caused by protein denaturation/loss of structure
where-kidneys, heart, adrenal glands;
Why=results from hypoxia caused by severe ischemia or chemical injury.
EX=MI, ingestion of mercuric chloride.

Front 11

Describe Liquefactive necrosis. Cause/example

Back 11

Liquefactive=lisosomes(organelle with low PH),release hydrolases, hydrolases digest cells
Why=ischemic injury (blockage in heart/brain, bacterial. (can b periph)
How=brain cells rich in digestive hydrolytic enzymes, cells digested by their own hydrolases so tissue liquefies.
EX=staph, strep, e.coli

Front 12

Describe Caseous Necrosis. Cause/EX

Back 12

Caseous=not common caused by infx (not kidney).
COMBINATION of coagulative and liquifactive.
How=activate hydrolases, denature proteins.
ex=infarcted heart/infarcted brain

Front 13

Describe Fat Necrosis. Cause/EX

Back 13

Fat N=Cellular dissolution caused by enzymes called lipases, break down triglycerides, =free fatty acids=combine with ca, mg, na, =soaps (soponification). Occurs in breast, pancreas

Front 14

Describe Gangrenous Necrosis.

Back 14

Gangrenou=death of tissue resulting from severe hypoxic injury subsequent bac inv
WHy=arteriosclerosis, blockage of major arteries.
Types=Dry=coagulative necrosis, Wet=neutrophils invade=liquefactive (internal organs)

Front 15

Describe Gas Gangrene. Cause/EX

Back 15

Gas Gangrene=
Cause=infection of injury of tissue by clostridium. an anaerobic bacteria produces hydrolytic enzymes and toxins causing bubbles of gas in muscle cells.

Front 16

What is the difference between necrosis and apoptosis?

Back 16

Cells die naturally by apoptosis, or programmed cell death -due to reach maturity or function is not needed. In Necrosis an outside influence injures the cell. the cell swells, teh membrane splits, and chemicals leak out.

Front 17

Cellular injury leads to acute inflammation, which may result either in resolution and healing or in progression into chronic inflammation.

Back 17

Chronic inflammation, in turn, may result in healingn or in progression into the development of a granuloma. the final step is usually healing and reconstruction of teh damaged tissue.

Front 18

Describe the steps of the inflammatory process.

Back 18

1)Cell Injury 2)Acute inflammation 3) healing
or 4) chronic inflammation-healing or 5) chronic inflammation-granuloma formation

Front 19

Describe the mechanisms of cellular injury that initiate the Acute inflammatory response.

Back 19

Begins after nonlethal cell injury.
How=trauma, oxygen or nutrient deprivation, genetic or immune defects, chemical agents, microorganisms, temp extremes, or ionizing radiation.

Front 20

Describe the process of the acute inflammatory response.

Back 20

immediate vascular effects, first arterioles near the site dilate increasing blood flow to the inflammed site,increases exudaton of plasma and blood cells into the tissues=edema and swelling, blood moves slower and thickens-clot, leukocytes migrate to area to clean, neutrophils ingest bacteria etc leave via pus or lymph, cells, platelets and proteins accumulate, cascades help in clotting, macrophages clean

Front 21

List in order steps of the Acute inflammatory response.
(Chart)
Steps are interdependent so induction of one can result in induciton of other two.

Back 21

-Cellular injury
-Mast cell degranulation
-Activaton of three plasma
systems
-Complement system
-Clotting System
-Kinin System
-Release of Subcellular
components
Finally result is development of microscopic changes....

Front 22

List in order steps of the Acute inflammatory response.
(Chart)
Steps are interdependent so induction of one can result in induciton of other two.

Back 22

Microscopic changes=
-vasodilation (redness, heat)
-Vascular permeability (edema)
-Cellular infiltration (pus)
-Thrombosis (clots)
-Stimulation of nerve endings (pain)

Front 23

List the three plasma systems activated in the acute inflammatory response.

Back 23

1) Complement system
2)Kinin System
3) CLotting system.

Front 24

Describe the Compliment System.

Back 24

-involves series of 10 proteins,
-activated by antigen-antibody complexes,
-mediates inflammatory process,
-can be activated by endotoxins (bacteria), don’t have to have this system being activated

Front 25

Describe the Clotting System

Back 25

-formation of meshwork
-traps exudates, chemicals, microorganisms, foreign bodies
-prevents spread of whatever the injurious agent is
-forms clot, stops bleeding
activated by intrinsic or extrinsic pathways

Front 26

Describe the Kinin System

Back 26

Kinin-bradykinin-
-bradykinin (dilates BV via bradykinin which helps induce the pain response)
-causes contraction of smoothe muscle
-increases vascular permeability of cells

Front 27

what controls the plasma systems

Back 27

C1esterase inhibitor protein
ie. no c1esterase inhibitor=hereditary angioneurotic edema=cont dilate blood vessels increased perm around nerves, system unchecked.

Front 28

Name 6 Leukocytes inflammatory cells.

Back 28

Granulocytes-can degranulate and release stuff
Agranulocytes-cannot *
1)Neutrophils
2)Monocytes*
3)Lymphocytes*
4)Eusinophis
5)Basophils
6)Mast cells

Front 29

function of Neutrophils

Back 29

first phagocytic leukocytes
ingest bacteria, dead cells and debris.
neutrophils-most common (55-70% of leukocytes). Drawn to injured sites via neutrophil chemotaxis.

Front 30

Function of Monocytes

Back 30

Monocytes * 5-8% of leukocytes, in blood they are called monocytes. Once they enter the tissue, they are called macrophages. They engulf, endocytosis. Cell permeability changes of the inflame response allows monocytes to move into tissues and become macrophages leave blood invade tissue (macrophage and monocyte )

Front 31

Function of Lymphocytes

Back 31

Lymphocytes* B cells (lead to antibody formation) and T cells most of their function is about immunity (HIV)

Front 32

Function of Eosinophils

Back 32

Help to control infl response, act dir against parasites
Eosinophils 2-5% of leukocytes, parasitic defense. (does not phagocitize, or engulf it!!!!)
Will help eliminate the parasite-saddles up next to parasite and pukes on it
Puke is acidi and it digests the parasite

Front 33

Function of Basophils

Back 33

similar to mast cells-activate response via 1)degranulation=release granular contents into matrix and 2)synthesis of mediators
Basophils -<1% of leukocytes, mediator release (histamine) (not very common in this response)

Front 34

Describe Mast Cells

Back 34

cellular bags of granules
• Mast Cells-(theses are granulated) REM they degranulate during the acute inflammatory response
-immune system cells
- release mediators like histamine-may draw cells to the site, may cause vasodilation; etc. Releases histamine , releases neutrophil chemotaxis factor (calls neutrophils to the site.
-it itself is a mediator

Front 35

Describe the chronic inflammatory response

Back 35

Inflammaton becomes chronic b/c of persistance of infection, an antigen, or a foreign body in the wound. Char by persistence of acute infl processes.

Front 36

List elements of persistance of infection, antigen, or foreign body

Back 36

-Persistent acute inflammation
-Neutrophil degranulation and death
-Lymphocyte activation\-Fibroblast activation
a) Pus formation
b) TIssue scaring
c)cell infiltration-wound healing

Front 37

INSERT CIR here

Back 37

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