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Pathophysiology Midterm 1 > Class 2 > Flashcards

Class 2 Flashcards

1
Q

Causes of Cellular injury

A 
Hypoxia
Free Radicals
Chemical Injury
Intentional & Unintentional injuries
Cellular swelling
Excess lipids & carbohydrates
Calcium excess & hardening
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2
Q

Hypoxia

A

Lack of oxygen (most common cause of cellular injury)

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3
Q

4 cellular disruptions

A
  1. ATP depletion
  2. Oxygen & oxygen-derived free radicals
  3. Intracellular calcium & loss of calcium steady state
  4. Defects in membrane permeability.
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4
Q

Apoptosis

A

active process of cell death (programmed)

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5
Q

Ischemia

A

reduced blood supply to tissues caused by arterioscelrosis & thrombosis

  • a decrease in ATP levels causes Na+ & K+ pump & Na+ & Ca2+ exchange to fail which accumulates ions intracellularly,.
  • If O2 is not restored, lysosomes swell and irreversible damage occurs
  • Acute: clot suddenly obstructs vessel
  • Chronic: body compensates for collateral circulation around blockage
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6
Q

Myocardial Infarction

A

Cell death & obstruction in coronary artery (heart attack)

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7
Q

Reperfusion Injury

A

Generation of reactive O2 intermediates & cause further membrane damage & mitochondrial calcium overload

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8
Q

Complement

A

Destroy pathogens directly & activate other components of inflammatory response

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9
Q

Dehiscence

A

Wound pulls apart at suture site & is associated with infection (worse with obesity)

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10
Q

Evisceration

A

Sutures open and abdominal organs protrude.

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11
Q

Keloid

A

Excess scar tissue formation

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12
Q

Contracture

A

Excessive contraction that shrinks the wound further than needed, (common in burns)

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13
Q

Stenosis

A

Narrowing of blood vessel or organs

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14
Q

Primary Intention

A

Damage is not extensive & heal is under minimal loss Ex: suture surgical wound

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15
Q

Secondary Intention

A

Extensive damage & takes longer to heal and contract Ex: Open wound

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16
Q

Debridement

A

Cleaning of the wound

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17
Q

Gangrene

A

Death of tissue caused by severe hypoxic injury (lack of O2) most commonly via arteriosclerosis

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18
Q

Atrophy

A

Shrinking in cellular size
Physiologic: early development
Pathologic: decreased workload, blood supply, nutrition (Autophagic vacuoles due to malnutrition)

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19
Q

Proteosomes

A

Protein catabolic complex & ubiquitin-proteosome pathway –> both involved in protein catabolism
Proteins –> ubiquitin

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20
Q

Hypertrophy

A

Increased size of cells & therefore the affected organ

  • Kidneys & heart are prone to it
  • Increases accumulation of protein
  • Triggered via mechanical or hormones
  • Only occurs in non-dividing cells
  • Can be physiologic or pathologic
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21
Q

Hyperplasia

A

Increased number of cells due to increased rate of cellular division

  • Compensatory (regeneration)
  • Hormonal (estrogen)
  • Pathologic (abnormal proliferation, menses)
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22
Q

Dysplasia

A

Abnormal changes in size, shape & organization of cells

-Involved in breast cancer development

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23
Q

Metaplasia

A

Reversible replacement of one mature cell type by another less differentiated type

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24
Q

5 signs of inflammation

A

Redness (due to increased RBC at site)
Warmth (due to RBC)
Loss of Function (decreased tissue strength)
Swelling (Increased movement of fluid outside vessels)
Pain (prostaglandins activate nerve receptors)

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25
Q

Cellular injury

A

Cell no longer is able to maintain homeostasis, possible recovery if stressor is removed in time

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26
Q

5 types of Necrosis (Cell Death)

A

Liquifaction –> ischemic damage to nerve cells
Coagulative (clotting) –> hypoxia cause by severe ischemia kidneys/heart
Fat Necrosis –> caused by lipases (opaque/chalky) livers, breast & abdominal
Caseous Necrosis –> due to tuberculosis pulmonary infection (clumped cheese)
Gangrenous Necrosis –> associated with diabetes mellitus, lack of bl. flow. (Gas, wet or dry)
– Dry is due to coagulative necrosis
– Wet is due to liquifactive necrosis
Gas Gangrene –> caused by the Clostridium species, results in bubbles of gas to form in muscle cells

27
Q

Anoxia

A

total lack of O2 caused by sudden obstruction

28
Q

Free Radicals & Reaction O2 Species

A

Electrically uncharged atom having an unpaired election (unstable)

  • Can cause damage to DNA (fragmenting) decreasing protein synthesis
  • Damage vital proteins that affect ion pumps & transport mechanisms
  • Destroy membranes & cell wall
  • Lipid peroxidation (destruction of polyunsaturated lipids)
  • Damaging mitochondria causing liberation of Ca2+ into cytosol
29
Q

Chemical Injury Types

A 
Carbon tetrachloride
Lead
Carbon Monoxide (higher affinity to hemoglobin than O2)
Ethanol (Alcohol(
Mercury
Street drugs
30
Q

Physical Injury Types

A

Blunt Force –> mechanical energy application resulting in tearing, shearing or crushing
Contusions (bruises)
Abrasions (scrape)

31
Q

Phenylketonuria (PKU)

A

newborn disease caused by genetic defect of not having certain enzymes required for protein degeneration resulting in nervous damage.

32
Q

ATP Depletion (Cellular Injury Disruption)

A

Lack of ATP = Na-K pump stops working = accumulation of Na+ inside the cell (swelling)
Decrease of protein synthesis = ER dilation = ribosome detachment
Fats, pigments & glycogen inflitrates

33
Q

Free Radicals Activation (Cellular Injury Disruption)

A

Damage cell membrane & structures within cell

34
Q

Calcium Homeostasis Disruption (Cellular Injury)

A

Lack of Ca decreases activation of enzyme in cell therefore no breakdown & Ca accumulates in mitochondria
Free Ca2+ results in the activation of
- Protein kinases (phosphorlyation of protein)
- Phospholipases (Membrane damage)
- Proteases (Cytoskeletal damage)
- Endonuclease (Nucleus chromatin damage)

35
Q

Defects in Membrane Permeability

A

Imbalance of electrolytes and can lead to shrinking or swelling of cell and therefore necrosis

36
Q

Systemic Manifestations of Cellular Injury

A 
Fatigue
Malaise
Fever
Loss of appetite
Elevated plasma enzymes
Inflammatory Response
37
Q

Inflammatory Response

A

Second line of defense, innate immunity

Activated by cellular injury or death

38
Q

Inflammation Goals

A

Limit & control injury process
Prevent & limit infection & further damage
Initiate adaptive immune response
Initiate health

39
Q

Inflammatory Vascular Response

A
  1. Brief vasoconstriction (dunno why?)
  2. Vasodilation (slower blood velocity & increased bl. flow)
  3. Increased vascular permeability (allow leakage out of vessel causing swelling, allows increased movement of RBC)
  4. White blood cell adherence to inner walls
40
Q

Inflammatory Response Order

A
  1. Neutrophils
  2. Monocytes
  3. Macrophages
  4. Mast cells
  5. Platelets
  6. Lymphocytes
41
Q

Neutrophils

A

Arrive 1st & battle with injurious agent

Present in exudate (die off within 6-12 hrs)

42
Q

Monocytes

A

Immature macrophages that travels to inflammation site to mature.

43
Q

Macrophages

A

Surround bacteria and replace neutrophils for a longterm dense phagocytozing the bacteria

44
Q

Mast Cells

A

Release histamine to increase permeability to encourage leakage of white blood cells

45
Q

Platelets

A

Cause clotting of wound and injury

46
Q

Lymphocytes

A

Debride & repair

47
Q

Histamine/Leukotrienes

A

Cause vasoconstriction
Increased vascular permeability
Released by mast cells

48
Q

Prostaglandins

A

Sets of pain
Increased permeability
Sets off inflammatory response

49
Q

Bradykinin

A

Dilation of blood vessels
Induces pain
Smooth muscle contraction
Increased vascular permeability

50
Q

Complement system proteins

A

Destroy pathogens directly or activate other components of inflammatory response

51
Q

Fever

A

Systemic Inflammatory Mechanism

Caused by pyrogens (act directly on hypothalamus & therefore temperature) & interleukin-1

52
Q

Leukocytosis

A

Increased number of circulating WBC’s
Causes fatigue, loss of appetite, lymphadenitis (swollen lymphnodes)
Elevated erythrocyte sedimentation rate

53
Q

Chronic Inflammation

A 
Arthritis**
Inflammation last longer than 2 weeks due to failed acute inflammation (microbes didn't undergo phagocytosis b/c of good cell wall because of high lipid/wax content in microbe, toxins, chemicals)
Granuloma (isolated infected area) --> dense infiltration of lymphocytes & macrophages (can differentiate into epithelioid cells & fuse together)
Limits prostaglandin (increases inflammatory response)
54
Q

Causes of Inflammatory Injury

A

Macrophages & Lymphocytes arrive first rather than neutrophils
Histamine, antibodies, lymphokines, complement & proteases can further delay healing
Fibroblast infiltration & keloid formation (scar tissue) leads to loss of function

55
Q

Manifestations of Chronic Inflammation

A
  • Hyperplasia of spleen or lymphnodes
  • Leukocytosis & increased antibody production
  • Elevates erythrocyte sedimentation rate
  • Low grade fever
  • Anemia
  • Pain
  • Activity Intolerance
  • Depression
  • Fatigue
  • Insomnia
  • Anorexia
56
Q

Resolution

A

Returning injured tissue to original structure & function

Tissues must be able to undergo regeneration (extensive injury but no infection)

57
Q

Repair

A

Replace old tissue with scar tissue (keloid) which is consistent of collagen to restore tensile strength but no full function

58
Q

Healing Process

A

Debride (clean) -> Seal (epithelialization)-> Fill in -> Shrink (contraction)

59
Q

Factors Affecting Tissue Repair

A

Age (metabolism)
Temperature (cool skin slows rate of cell division)
Moisture (dry, cells can’t divide or migrate well)
Nutrition (proteins & vitamin C for collagen & carbs for nrg)
Blood supply **
Tension on tissue (obesity)
Drugs & stress hormones
Chronic diseases

60
Q

Phases of Healing

A
  1. Inflammation (debride)
  2. Proliferation/New Tissue Formation (Reconstructive phase)
  3. Remodelling & Maturation Phase
61
Q

Reconstructive Phase

A

Begins 3-4 days after injury, and goes for 2 weeks
Seal & fill**
Fibroblast proliferation (secreting collagen)
Epithelialization (Epithelial cells divide to seal top of wound)
Contraction (Pulling of muscles to decrease wound size)
Cellular differentiation

62
Q

Remodelling Phase

A

Takes up to 2 years depending on damage extent
Continuation of cellular differentiation
Scar tissue formation
Scar remodelling

63
Q

Complications of Wound Healing

A

Hemorrhage (provides accumulated bl for bacteria to grow)
Fibrous adhesion (overactive fibroblasts cause surface cells to stick together and bind organs)
Infection
Excess scar formation –> Keloids
Strictures & Contractures (too much collagen or scar tissue, cell malfunction)
Dehiscence

Pathophysiology Midterm 1 (8 decks)

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