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MOD > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

3 Lines of Defense

A
  1. Skin and Mucous Membranes (tears, saliva, gut flora, stomach acid)
  2. Inflammatory Response (nonspecific and acute)
  3. Immune Response
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2
Q

What are the 7 etiologies that can cause inflammation?

A

Microorganisms, Hypoxia/Ischemia, Nutritional Deficiencies, Trauma/Surgery, Radiation, Caustic Chemicals, and Extreme Heat/Cold

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3
Q

2 Main Components of the Vascular Response

A

Increased Blood Flow to injury site
Increased blood vessel permeability at in the injury site

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4
Q

3 Major Components of Acute Inflammation

A

Vascular Response, Cellular Response, and Inflammatory Mediators

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5
Q

What are the 2 major anatomical changes that occur during the vascular response?

A

Increased blood vessel dilation
Increased blood vessel permeability

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6
Q

What are the steps of the vascular response?

A
  1. Transient vasoconstriction
  2. Local blood vessels dilate (vasodilation) to increase blood flow to area and enhance the transport of blood and cells.
  3. Endothelial cells lining the vessels contract to open up gaps in the intracellular junctions, which is increased permeability.
  4. Increased vessel permeability allows for plasma and cells to travel to the injured tissue.

This results in dilution of the pathogen via exudation of fluid, stagnated blood flow in the vessel at that location, slowing the spread of the offending agent, and clotting elements can move into the injury site.

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7
Q

What are the 3 types of capillaries?

A

Continuous, Fenestrated, and Sinusoids (discontinuous)

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8
Q

Where do I find fenestrated capillaries?

A

Endocrine organs, small intestine, and the choroid plexus.

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9
Q

Where do I find continuous capillaries?

A

CNS (blood-brain barriers) and lungs.

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10
Q

Where do I find sinusoidal capillaries?

A

Bone marrow, spleen, and liver.

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11
Q

What are the 3 major patterns of vascular response?

A

Immediate Transient: post minor injury
Immediate Sustained: post major injury (most common)
Delayed Hemodynamic: 4-24 hrs post injury.

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12
Q

What is the cellular response and its 4 steps?

A

Movement of phagocytic WBCs into area of injury.

  1. Margination/Adhesion
  2. Migration/Diapedesis
  3. Chemotaxis
  4. Phagocytosis
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13
Q

What are the steps of margination/adhesion?

A
  1. An injury causes cytokine release.
  2. Cytokines (IL-1 and TNF-alpha) increased expression of adhesion molecules, specifically selectin.
  3. Leukocytes have slowed migration and begin marginating/pavementing along the periphery of vessels.
  4. Adhesion to the vessel walls.
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14
Q

What is migration/diapedesis?

A

It is when WBCs extend their pseudopods and pass through the capillary wall via ameboid movement.

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15
Q

What is chemotaxis and the components of it?

A

Chemotaxis is when leukocytes travel throughout the tissue to the site of injury.
It is signaled by cytokines and complements (C3a and C5a)

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16
Q

What is phagocytosis and opsonization?

A

Phagocytosis is the engulfment of cells.
Opsonization is the recognition and attachment of a cell, done usually by C3b.

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17
Q

What is a Neutrophil?

A

AKA a polymorphonuclear neutrophil (PMNs) or segmented neutrophil (segs)
It is the primary phagocyte to arrive early to the injury site and arrives in ~90 minutes with a duration of 10 hrs.
Presence of bands or left-shift means there is a lot of inflammation.

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18
Q

What is leukocytosis?

A

The increased production/presence of WBCs. Usually neutrophils.

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19
Q

Eosinophils

A

For allergic and primarily parasitic infections.

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20
Q

Basophils

A

For inflammation and allergic reactions
Can release histamine
Bonds with IgE

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21
Q

Mast Cells

A

Similar to basophils but reside in portals of entry and act as sentinel position cells. Also commonly seen in allergic and parasitic infections with IgE.

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22
Q

Monocyte

A

Largest WBC
Arrives ~24 hrs post injury, majority cell type after 48 hrs.

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23
Q

Platelets/Thrombocytes

A

Helps mediate vascular response
Involved in hemostasis and thrombosis
Releases inflammatory mediators

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24
Q

Endothelial cells

A

Involved in vascular response
Synthesizes and releases inflammatory mediators

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25
Q

What are the general effects of an inflammatory mediator?

A

Affects vasodilation, chemotaxis, platelet aggregation, endothelial cell stickiness, pain, and vascular permeability.

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26
Q

What are the inflammatory mediators?

A

Plasma proteins, Histamine, Cytokines, Platelet Activating Factor, Prostaglandins, and Leukotrienes

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27
Q

What are the 3 Plasma Proteins?

A

Kinins, Complements, and the clotting system

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28
Q

What are Kinins?

A

A plasma protein that causes vasodilation, increased vascular permeability, smooth muscle contraction and is involved in the pain response. Most common is bradykinin. They are broken down by Kininases and ACEs.

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29
Q

What is the clotting system?

A

Plasma proteins involved in clotting. Generally, fibrinopeptides are formed along with a thrombus.
Thrombin is the key protease enzyme.
Functions include expression of endothelial adhesion molecules and production of prostaglandins, PAF, and chemokines.

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30
Q

What is the complement system?

A

Inactive plasma proteins that become activated in a cascade to degrade subsequent complements.
Functions include vasodilation and increased vascular permeability, smooth muscle contraction, leukocyte activation, adhesion, and chemotaxis, augmentation of phagocytosis, and mast cell degranulation.
Most common are C3a and C5a.

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31
Q

Histamine

A

An inflammatory mediator released by mast cells, basophils, and platelets.
Plays a major role in vascular response via H1 receptor, causing vasodilation and increased vascular permeability.
It is one of the first mediators of inflammation.

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32
Q

Cytokines

A

Signal inflammatory mediators made up of 5 categories: chemokines, lymphokines, interleukins, interferons, and tumor necrosis factors.

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33
Q

IL-1 and TNF-alpha

A

early and major mediators of the inflammatory response.
They are responsible for inducing fever, adhesion of leukocytes to the endothelium, chemotaxis, general acute-phase response, and in the pain response.

34
Q

Arachidonic Acid

A

The precursor to both leukotrienes and prostaglandins. It is formed from cell membrane phospholipids.
Inhibited by corticosteroids, which prevent its formation.

35
Q

Cyclooxygenase Pathway

A

Forms prostaglandins and thromboxane.
Inhibited by NSAIDs like aspirin.
Inhibited by corticosteroids as well since they prevent arachidonic acid formation.

36
Q

Prostaglandins

A

Involved in vascular permeability, vasodilation, and the pain response. Synthesis is inhibited by NSAIDs.

37
Q

PGE1 and PGE2

A

Prostaglandins known for inducing inflammation and potentiating effects of other inflammatory mediators, especially histamine.

38
Q

Thromboxane A2

A

Promotes platelet aggregation and vasoconstriction

39
Q

Leukotrienes

A

Functionally similar to histamine
Functions include increased vascular permeability, adhesion of endothelial cells, chemotaxis, and further histamine release.
Competitively Inhibited by leukotriene receptor antagonists and non-competitively inhibited by 5-LOX inhibitors.

40
Q

What condition is treated with leukotriene receptor antagonists?

A

Asthma

41
Q

What is SRS-A and its significance?

A

Slow-Reacting Substance of Anaphylaxis: a group of leukotrienes that can cause a slow and sustained bronchoconstriction.
It is of importance in asthmatic bronchitis and anaphylaxis.

42
Q

Platelet Activating Factor (PAF)

A

Derived from cell membrane phospholipids
Induces platelet aggregation, stimulates platelets to release vasoactive mediators and to synthesize thromboxanes.
Increases vascular permeability, activates neutrophils, and is a chemoattractant for eosinophils.

43
Q

Nitric Oxide

A

Smooth Muscle Relaxation
Antagonism of platelet functions: adhesion, aggregation, and degranulation.
Reduction of leukocyte recruitment.
Assists in microbicidal action by phagocytes.

44
Q

What is involved in the pain response?

A

Bradykinin, IL-1, TNF-alpha, and prostaglandins

45
Q

What are the 5 cardinal signs of inflammation?

A

Erythema (Redness, Rubor)
Heat (Calor)
Swelling (Edema, Tumor)
Pain (Dolor)
Loss of Function

46
Q

What is the specific phenomenon that is responsible for erythema?

A

Vasodilation leading to Increased blood flow which is red, causing redness to appear.

47
Q

What is the specific phenomenon that is responsible for heat?

A

Vasodilation leading to increased blood flow. Blood is very warm so that area becomes warm.

48
Q

What is the specific phenomenon that is responsible for swelling?

A

Increased vascular permeability means fluid leaks out of the vessels and into the ECF and tissues.

49
Q

What is the specific phenomenon that is responsible for pain?

A

Compression of the tissues as a result of swelling. Direct elicitation of pain due to inflammatory mediators.

50
Q

What is the specific phenomenon that is responsible for loss of function?

A

Compression of tissues/muscles reduces mobility. Pain causes a mental block in moving.

51
Q

What are the local manifestations of inflammation?

A

Any of the cardinal signs or exudates

52
Q

What is an exudate?

A

Fluid that is secreted from a site of injury due to the vascular response.

53
Q

Exudates

A

Serous, Sanguinous, Fibrinous, Purulent/Suppurative, Hemorrhagic, and Membranous/Pseudomembranous

54
Q

Abscess

A

A localized area of inflammation that contains purulent exudate. It is often walled off from healthy tissue by fibroblasts.

55
Q

Ulceration

A

Necrotic, eroded areas of epithelium with subepithelial inflammation. Most often caused by traumatic injury or vascular compromise.

56
Q

Acute-Phase Response

A

It begins hours to days after the initial insult and changes the concentrations of plasma proteins.
It involves fever, leukocytosis, lethargy, skeletal muscle catabolism and increased ESR.

57
Q

What causes Fever (Pyrexia)?

A

IL-1, IL-6, and TNF-alpha as a result of resetting of the thermoregulatory set point in the hypothalamus.

58
Q

What causes leukocytosis?

A

IL-1 and other cytokines.

59
Q

What causes lethargy?

A

IL-1 and TNF-alpha mediation on the CNS.

60
Q

What is the purpose of skeletal muscle catabolism?

A

Provides amino acids for use in the immune response, tissue repair, and regeneration.

61
Q

What is ESR and what affects it?

A

ESR is a lab test that measures, over an hour, how long it takes for RBCs to settle at the bottom of a test tube.

Elevated ESR is caused by elevated acute-phase proteins (fibrinogen and CRP), along with anemic patients (aside from sickle cell anemia).

62
Q

What is CRP and what affects it?

A

CRP is a lab test measuring the level of C-reactive protein (an acute-phase protein) in the blood. C-reactive proteins bind to the surface of microorganisms to assist in their destruction, regulate the immune response, and clear out necrotic cells.

Elevated CRP is associated with inflammation, obesity, HTN, DM, smoking, aging, depression, sleep disturbances, and increased CV risk.

Used to measure the activity level of inflammation or an autoimmune disease.

63
Q

Why do we use CRP and ESR? How are they different?

A

Both measure the level of inflammation, but they are affected by different things.

CRP is also more susceptible to acute changes, making it a more real-time indicator while ESR is used as a long-term indicator since it changes more slowly.

64
Q

When do I usually see neutropenia?

A

Viral infections

65
Q

When do I usually see Eosinophilia?

A

Parasitic infections and Allergic reactions

66
Q

When do I usually see Neutrophilia?

A

Bacterial infections

67
Q

What is the difference between Lymphangitis and Lymphadenitis?

A

Lymphangitis is an inflammatory reaction or infection in a lymph vessel, commonly caused by streptococcus pyogenes and appears as a red, tender streak that extends proximally.

Lymphadenitis is an inflammatory reaction or infection in a lymph node draining an infected area, commonly caused by infectious or necrotic material in that area.
It appears as bumps in the skin where lymph nodes are located and is often swollen, tender, mobile, rubbery, or erythematous or fluctuant. Lymphadenitis may require an I/D.

68
Q

What is similar about lymphangitis and lymphadenitis?

A

Treatment is identical, including antimicrobials, anti-inflammatories, cold compresses, and analgesics. Both conditions can occur at the same time.

69
Q

What is the definition of shock?

A

A life-threatening condition caused by a lack of adequate circulation and oxygenation of the body. It is highly fatal.

Untreated, it will lead to multiple organ system failure quickly and then death.

70
Q

What are the 5 types of shock?

A

Cardiogenic, Hypovolemic, Distributive (includes Anaphylactic, Neurogenic, and Septic)

71
Q

What is cardiogenic shock and what causes it?

A

Cardiogenic shock is due to the inability of the heart to pump the required amount of blood to all the organs.

Caused by cardiac arrhythmias, damaged heart muscle and/or valves, cardiac tamponade, and heart muscle rupture.

72
Q

Common symptoms of shock

A

Tachypnea
Tachycardia
Dehydration
CP and/or arryhthmia
Oliguria
Pale, cool, clammy skin
hypotension
AMS

73
Q

What is Hypovolemic shock, the two types, and common causes of each?

A

Hypovolemic shock is due to decreased intravascular volume, which leads to impaired perfusion of vital organs.

It is caused by either hemorrhagic shock or non-hemorrhagic shock.

Hemorrhagic (blood loss): trauma or GI bleeding.
Non-hemorrhagic (fluid loss): Diarrhea or hyperemesis

74
Q

What is distributive shock?

A

Shock due to severe vasodilation causing periphera vascular resistance. Includes anaphylactic, neurogenic, and septic shocks.

75
Q

What is Anaphylactic Shock and what causes it?

A

Severe, rapid allergic or hypersensitivity reaction with potential to be fatal. Involves skin (90%), Respiratory (70%), GI and CV (45%).

Caused by allergens.

76
Q

What is Neurogenic Shock?

A

Damage to the ANS causes a sudden loss of sympathetic stimulation to the blood vessels, leading to massive vasodilation and resulting in severe hypotension.

77
Q

What is Septic Shock?

A

Systemic vasodilation secondary to an infection and/or dysregulation of the inflammatory response.
It is an exaggerated, unregulated, and self-sustaining inflammatory response to an infection.

It results in excessive vasodilation, tissue ischemia, direct cell injury, and an altered rate of apoptosis.

78
Q

What is SIRS?

A

Systemic inflammatory response syndrome, which is largely mediated by IL-1 and TNF-alpha.

79
Q

How does septic shock affect the CV system?

A

Circulatory: Severe hypotension and hypoperfusion.
Excessive vasoactive mediators causes decreased vascular resistance.
Third spacing of fluid causes increased vascular permeability.

80
Q

How does Septic Shock affect the GI, kidneys, and liver?

A

GI: increased permeability allows bacteria and bacterial endotoxins to enter systemic circulation.

Liver: impaired elimination of bacteria and toxins from the GI due to cellular injury.

Kidney: impaired filtration of waste and toxins from blood due to cellular injury and hypoperfusion.

81
Q

How does Septic Shock affect the Lungs and CNS?

A

Nervous: Encephalopathy due to cell signaling changes and dysfunction of the blood-brain barrier.

Lungs: pulmonary edema and hypoxemia.

MOD (16 decks)

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