Cell Injury and Inflammation Flashcards

1
Q

Causes of Cell Injury

A
  • ischemia (lack of blood flow or oxygen to an area)
  • infectious agents (bacteria and virus kill cells)
  • immune reactions (immune system becomes too excited and causes hypersensitivities or autoimmune)
  • genetic factors
  • mechanical factors
  • nutritional factors
  • physical factors
  • chemical factors
    -psychosocial factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Factors Influencing healing

A
  • physiological variables (age, growth factors, vascular sufficiency)
  • general health of the individual, immunocompetency, psychological/emotional well being
  • the presence of comorbidities (DM, decreased oxygen perfusion, hematologic disorders, cancer, incontinence, Alzheimers, neurologic impairment, immobility
  • tobacco, alchohol, caffeine
  • nutrition
  • infections
  • type of tissue
  • medical treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Secondary Injury

A

complications after intial injury; usually the result of hypoxic-ischemia (brain cant get oxygen) injury caused by cerebral edema (swelling of brain) or intracranial hematomas (bleeding in brain)

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

Phases of healing

A
  1. hemostasis and degeneration
  2. inflammation
  3. proliferation and migration
  4. remodeling and maturation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adaptation

A

the extent to which the cell is able to alter mechanisms and regain homeostasis in the altered environment

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

What does “reversible injury” depend on?

A
  1. mechanism of injury
  2. length of time the injury is present w/o intervention
  3. severity of the injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mild injury

A
  • leads to sublethal alterations-may be reversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Moderate or severe injury

A
  • Leads to lethal alterations - likely irreversible - lead to cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the pathway of Ischemia, one of the causes of cell injury

A

blood flow is insufficient (partial = hypoxia, total = anoxia) causing lack of ATP to be made which causes a build up of ions and fluid intracellularly, causing the cell to swell

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

Causes of Ischemia (what is it?) (know the condition names)

A
  • obstruction of the respiratory tree (suffocation)
  • inadequate transportation of O2 across the respiratory tract (pneumonia)
  • arterial lumen obstruction and narrowing (atherosclerosis)
  • intravascular clot (thrombus)
  • inadequate transport of O2 in the blood (anemia)
  • the inability of cell to use O2 (CO poisoning)

partial (hypoxia) or total (anoxia) reduction in O2 supply = loss of aerobic metabolism = reduction ATP synthesis = accumulation of ions and fluid = cells swell - comprised function

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

Infectious agents

A
  • bacteria, viruses and others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

immune reactions

A

overzealous in its activity, leading to hypersensitivities ranging from a mild allergy to life-threatening anaphylactic reactions or autoimmune disorders

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

Chemical factors

A

two catagories:
1. substances that can injure cells directly (heavy metals)
2. substances that require metabolic transformation into the toxic agent (carbon tetrachloride)

Production of reactive oxygen species (ROS)
- formation of free radicals

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

Free radicals

A
  • natural by-product of using O2
  • it is when a normal oxygen atom lose one of four paired electrons, becomes a chain rxn
  • excessive amounts = oxidative stress = cell injury or death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Oxidation

A

when a molecule loses an electron

oxidation as a by product of metabolism damages cell membranes, leading to intrinsic cellular damage, a part of the normal aging process

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

Other causes for free radical formation

A
  • exposure of toxic chemicals
    -exposure to high level of oxygen
  • irradiation
  • UV
  • fluorescent light
  • pollutants
  • tobacco smoke
  • pesticides
  • drug overdose
  • heat stress
    -reperfusion injury
  • prolonged exercise

*intense or prolonged strenuous exercise leads to oxidative stress and may be harmful

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

Antioxidants

A
  • they neutralize the extra free radicals and stop chain reaction
  • endogenous antioxidants; enzymatic (scavengers) and nonenzymatic defense mechanisms
  • exogenous antioxidants; 200 have been identified in food or plant substances (found outside the body)
  • *moderate PA and exercise strengthen the antioxidant defense system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Genetic Factors

A
  1. alterations in the structure of number of chromsoomes that induce multiple abnormalities (down syndrome; 3rd chromosomes in the 21st pair)
  2. single mutations of genes cause changes in the amount or functions of proteins (sickle cell anemia, low-density lipoprotein receptor deficiency and a-antitrypsin deficiency)
  3. multiple gene mutations that interact with environmental factors to cause multifactorial disorders (hypertension and type 2 diabetes)

I would just remember structure/number alteration, single gene mutation, genes interacting with environment

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

Mechanical Factors

A

physical stress theory says changes in physical stress should cause a predictable adaptive response in tissue

  • tissue response to physical stress includes decreased stress tolerance (atrophy), maintenance, increased stress tolerance (hypertrophy), injury and death
  • soft tissues are influenced by the history of recent physical stresses so that the accumulation of individual stresses can cause injury
  • trauma (bone fracture or ligaments rupture)
  • other causes; repeated episodes of moderate-magnitude force, slow degradation of tissues tolerance, low loads sustained over long time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Nutritional Factors

A

imbalances in essential nutrients

  • excessive nutrient intake, (leads to obesity)
  • dietary deficiency (abnormal level or vitamins, kwashiorkor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Physical factors

A
  • blunt or penertrating trauma (brain contusions, internal organ damage, blood loss, delayed death of infections or organ failure)
  • extremes of physical agents (temp; burn or frostbite), radiation and electricity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Psychosocial factors

A

feat, tension or anxiety may influence individual threshold values for tissue adaptation and injury

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

Cellular aging

A

Aging changes can significantly influence homeostasis and the recovery process (Mitochondrial DNA is big target for age changes)

  • LIPOFUSCIN (natural waste product) pigmant is most well described age-association change in postmitotic cells (found in high concentrations in OLDER cells, so often used as a marker of cellular agin)
24
Q

Theories of Cellular Again

A
  • with aging, cells experience decreased capacity to respond to stress = progressive decline in homeostatic balance = pathology

*Pathologic changes associated with aging vary from person to person but usually consist of reduced functional reserve caused by atrophy of tissues or organs

  • aerobic training can help improve function of mitochondria, cardiac and skeletal muscle cells
25
Q

Acute Reversible Cell Injury (Mechanism)

A
  • impairment of ion homeostasis in cell (increased NA and Ca)
  • causes influx of interstitial fluid and cell swells
  • reduced metabolism occurs causing more cellular damage
  • cell forms plasma blebs that seal off and detach from cell surface
  • ribosomes detach from rough ER causing reduced protein synthesis and cycle of damage continues

simple: blebs (swellings) form and ribosomes detach from ER in response to acute reversible injury to a cell, continuing cycle of damage

nucleus remains undamaged in cell, normal cell fxn can return after removal of the stressor or injurious stimulus

26
Q

Cellular adaptations in chronic cell injury (reversible)

A

Cells adapt when injury occurs, common adaptation - atrophy, hypertrophy, hyperplasia metaplasia and dysplasia

(focus on atrophy); Bone loss, muscle wasting and brain cell loss are examples of tissue/organ atrophy associated with aging

(then if stressor is removed it can return to normal cell)

27
Q

Reversible cell injury - intracellular accumulations or storage

A

fatty liver

  • when liver is injured, accumulation of lipids occurs, because protein synthesis reduction (blebs and info above) means there are no protien vesicles to take lipids out of the cells
28
Q

Irreversible cell Injury

A

CELL DEATH

occurs via apoptosis (programmed cell death) or neurosis (end point of pathological process, degradation)

29
Q

Apoptosis
Cell Size
Nucleus
Plasma membrane
Cellular contents
Adjacent inflammation
Physiological or pathologic role

A

Cell Size: reduced/shrinks

Nucleus; fragmentation

Plasma membrane; intact

Cellular contents; intact

Adjacent inflammation; no

Physiological or pathologic role; often physiological

30
Q

Necrosis:
Cell Size
Nucleus
Plasma membrane
Cellular contents
Adjacent inflammation
Physiological or pathologic role

A

Cell Size; enlarged (swelling)

Nucleus; pyknosis, karyorrhexis, karyolsis

Plasma membrane; disrupted

Cellular contents; enzymatic digestion

Adjacent inflammation; frequent

Physiological or pathologic role; invariably pathologic

31
Q

What can trigger inflammation

A
  • infections, tissue necrosis, foreign bodies and immune reactions
32
Q

Clinical manifestations of acute inflammation

A

Erythema (redness) - vasodilation and increased blood flow

Heat - vasodilation and increased blood flow

Edema - fluid and cells leaking from local blood vessels

Pain - for direct trauma, chemicals like bradykinins, histamines, serotonin. For internal pressure, welling of nerve endings

33
Q

Inflammation fxn

A
  • process initiated after cell injury
  • removal of injurious agent, cellular debris and initiation of the healing process

normally protective but can potentially damage adjacent tissue

34
Q

Characteristics of acute inflammation

A
  • Vasodilation (increased blood flow, redness and heat)
  • Increased capillary permeability (permits passage of plasma proteins and WBCs to site of injury and causes loss of fluid, ultimately causing increased blood viscosity)
  • CLOTTING of the fluid in the interstitial spaces because of increased fibrinogen and other proteins to wall off the invader
  • migration of WBCs from the microcirculation (accumulation at injury site causing swelling)
35
Q

Factors affecting bloodblow

A
  • Histamine and bradykinins: Increase blood flow by dilating blood vessels.
  • Serotonin: Decreases blood flow by constricting blood vessels.
  • Anaphylatoxins: Increase blood flow by dilating blood vessels.
  • Leukotrienes: Can either constrict or dilate blood vessels, depending on the context.
  • Prostaglandins: Typically increase blood flow by dilating blood vessels.

BAPH dialtes
S constricts
L varies

36
Q

Acute inflammation cellular infiltrate

A

platelets
neutrophils
monocyte/macrophages
fibrocytes/fibroblasts
endothelial cells

37
Q

Chronic inflammation cellular infiltrate

A

monocytes/macrophages
lymphocytes**
plasma cells
fibrocytes/fibroblasts
endothelial cells

38
Q

difference between acute vs chronic inflammation cellular infiltrate

A

lymphocytes in chronic

39
Q

Edema Vs Effusion

A

edema - fluid and cells leaking from local blood vessels into the extravascular spaces

effusion - (leakage into body cavity or joints) general term for escape of fluid, can be transudate (fluid with low protein content) or an exudate (fluid with high protein content)

40
Q

Hemorrhagic; sanguineous Exudate

A

bright red or bloody, RBC

bloody, sang

41
Q

Serosanguineous Exudate

A

blood-tinged yellow or pink, RBCs

sang - blood, but not straight up blood

42
Q

Serous Exudate

A

thin clean yellow or straw colored, albumin and immunoglobins

S for Straw (yellow)

43
Q

Purulent Exudate

A
  • viscous, cloudy pus, cellular debris from necrotic cells and dying neutrophils

P for Pus (cloudy bc cellular debris)

44
Q

Catarrhal Exudate

A

thin clear mucus

C for Clear

45
Q

Leukocyte Accumulation (characteristic of acute inflammation response)

A
  • WBS (leukocytes, neutrophils, mono/macrophages)
  • remove or eliminate injurious stimulus by releasing enzymes and toxic substances that kill, inactive, and degrade microbial agents, foreign antigens or necrotic tissue
  • neutrophils rapidly die out within 24 hrs
  • monocytic/macrophage cells are responsible for cleaning cellular debris

MARGINATION, ADHESION, DIAPEDESIS, CHEMOTAXIS

46
Q

How do the WBCs get to injury cite?

A

chemotaxis (chemical signals)

47
Q

Chemical Mediators of inflammation

A

multifunctional, responsible for vascular and leukocyte responses in an acute inflammatory response

cell-derived and plasma derived

cell derived; histamine, platelets, arachnoid acid derivatives, cytokines

48
Q

Histamine

A
  • in mast cells, basophils, platelets (stored in granules = fast response)
  • causes endothelial contraction, forming gaps and increasing blood vessel permeability, allowing blood cells to exit the interstitial spaces (vascular leak)
  • ## can also be a vasodilator and bronchoconstrictor
49
Q

Name the three inflammatory mediators derived from phospholipids

A
  • PFA
  • prostaglandins
  • leukotrienes
50
Q

Platelet-activation factor (PFA) and Arachidonic acid derivatives

A
  • involved in pain response of inflammation
  • PFA can increase strength of other inflammatory mediators
  • arachidonic acid derivatives are in the pathway that produces prostaglandins (cause pain) and leukotrienes (cause inflammation)

-

51
Q

What do aspirin and corticosteroids do to stop pain and inflammation

A

inhibit pathways in the phospholipid mediators (arachnoid/prosoglandins) to stop pain and inflammation

52
Q

Cytokines

A
  • polypeptide substances produced by leukocytes
  • Systemic hormonal inflammatory effects
  • autocrine affect (hormones impact themselves)
  • paracrine affect (other cells)

ex; IL-I causes fever and TNF indice IL-I

so if you see those in the vlood, patient probably has fever and pain

53
Q

What are examples of phagocytes and what do they do

A

neutrophils, monocytes and macrophages

inactive and remove inflammatory stimulus to begin healing

54
Q

Factors affecting blood flow

A

Histamine
Serotonin
Bradykinins
Anaphylatoxins
Leukotrienes/prostaglandins

55
Q

Diagnosing inflammatory process

A
  • leukocyte counts
  • increased WBCs is an indication of active inflammatory reaction (typically to an infection or tissue injury)
  • decreased WBC is indicator of severe infections (sepsis)