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MOD S1 > Lecture 2 E1-Acute Inflammation/ Cardinal Manifestations > Flashcards

Lecture 2 E1-Acute Inflammation/ Cardinal Manifestations Flashcards

1
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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2
Q

what is the first line of defense

A

skin and mucus membrane
- tears, saliva, gut flora, gastric acid
- help rid our body of bacteria before it gets into the system

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3
Q

what is the second line of defense

A

inflammatory response
- non specific and rapid
- acute inflammation expected (this is normal but patients may think it is an infection if they see a bit of red swelling)
- can happen without a pathogen

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4
Q

what is the third line of defense

A

the immune response

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5
Q

what is etiology of acute inflammation and what are some types of etiologies

A

any damage or alteration to normal tissue ( cause of disease)

-microorganisms
- hypoxia/ischemia
-nutritional deficiencies(iron, B12)
- trauma/surgery
-radiation (sunburn, treatment)
- caustic chemicals
- extreme heat/cold (burns, frostbite)

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6
Q

2 Main Components of the Vascular Response in acute inflammation

A

Increased Blood Flow to injury site

Increased blood vessel permeability at in the injury site

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7
Q

what is the point of the cellular response of acute inflammation

A

removal of offending agent and damaged tissue

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8
Q

3 Major Components of Acute Inflammation

A

Vascular Response,
Cellular Response, and
Inflammatory Mediators

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9
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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10
Q

what does increased vessel permeability allow?

A

allowing WBC, other cells, and nutrients to get into our tissues easily

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11
Q

What are the steps of the vascular response?

A
  1. Transient vasoconstriction for possibility of blood loss ( initial step- doesn’t last long)
  2. Local blood vessels dilate (vasodilation) to increase blood flow to area and enhance the transport of blood and cells. (within seconds-minutes)
  3. Endothelial cells lining the vessels contract to open up gaps in the intracellular junctions, which is increased permeability. (allowing WBC and plasma to enter injured site)
  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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12
Q

What are the 3 types of capillaries?

A

Continuous, Fenestrated, and Sinusoids (discontinuous)

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13
Q

Where do I find fenestrated capillaries?

A

Endocrine organs, small intestine, and the choroid plexus.

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14
Q

what is the most common type of cappilary

A

continuous capillaries

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15
Q

Where do I find continuous capillaries?

A

CNS (blood-brain barriers) and lungs.

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16
Q

Where do I find sinusoidal capillaries?

A

Bone marrow, spleen, and liver.

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17
Q

What are the 3 major patterns of vascular response?

A

Immediate Transient: post minor injury
- hitting in face makes you turn red due to vasodilation then goes away
Immediate Sustained: post major injury (most common)
- response lingers
Delayed Hemodynamic: 4-24 hrs post injury.
-exposure to chemicals, sunburn

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18
Q

What is the cellular response?

A

Movement of phagocytic WBCs into area of injury.
- granulocytes (neutrophils)
- monocytes

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19
Q

what are the 4 steps of the cellular response

A
  1. Margination/Adhesion
  2. Migration/Diapedesis
  3. Chemotaxis
  4. Phagocytosis
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20
Q

What are the steps of margination/adhesion (step 1)?

A
  1. An injury causes cytokine (chemical mediators) release (influence cells on vessels to release selectins) .
  2. Cytokines (IL-1 and TNF-alpha) cause an 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(allows advancement to step 2).
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21
Q

what is selectin and what does it do

A

surface protein and adhesion molecule,
allows WBC to stick to vessel walls to stop them from moving
- think of velcro strips on the floor and rolling tennis ball on them

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22
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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23
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)

  • cytokines move to move the concentrated area of the leukocytes to where injury is “leaves a trail to the injury”
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24
Q

What is phagocytosis and opsonization?

A

Phagocytosis is the engulfment of cells.

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25
Q

what is opsonization

A

the recognition and attachment of a cell, done usually by C3b.

  • tagging ( coat with antibodies) harmful cells so WBC can recognize it is harmful and engulf then kill it
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26
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 (first responder) and arrives in ~90 minutes with a duration of 10 hrs.
- patrol the body when there is no injury present then bump up speed when there is one

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27
Q

how are neutrophils maintained

A

need to be constantly replaced to maintain their numbers

  • causes increase in circulating WBC -leukocytosis
  • due to the increased demand, immature forms may be released and these forms are called “bands/left shift/bandinia”
    immature forms released if there is intense infection requiring more neutrophils
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28
Q

What is leukocytosis?

A

The increased production/presence of WBCs in serum. Usually neutrophils.
can be caused by inflammation or infection (or medications, bone marrow disease)- intereferes with margination (steroids inhibit)

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29
Q

Eosinophils

A

For allergic and primarily parasitic infections.

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30
Q

Basophils

A

For inflammation and allergic reactions
Can release histamine
Bonds with IgE

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31
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.
-first responders that degranulate cells

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32
Q

Monocyte (8)

A
  • Largest WBC
  • Arrives ~24 hrs post injury,
  • way longer life span than PMNs
    -majority cell type after 48 hrs(now is the main cell in injury site).
  • NOT a granulocyte
  • engulf larger and greater quantities of foreign material than neutrophils
  • more efficient, and give an ADAPTIVE immune response when recognized specific pathogens
  • called a macrophage when it is inside tissue
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33
Q

Platelets/Thrombocytes

A

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

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34
Q

erythrocytes

A

red blood cells, transport oxygen to tissues

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35
Q

Endothelial cells

A

-Involved in vascular response
-Synthesizes and releases inflammatory mediators
- help get WBC to target with selectins

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36
Q

What are the general effects of an inflammatory mediator?(6)

A

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

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37
Q

What are the inflammatory mediators?

A

Plasma proteins (3), Histamine, Cytokines, Platelet Activating Factor, Prostaglandins, and Leukotrienes

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38
Q

What are the 3 Plasma Proteins?

A

Kinins, Complements, and the clotting system

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39
Q

What are Kinins?

A

A plasma protein that causes
-vasodilation,
- increased vascular permeability,
- smooth muscle contraction ( nonvascular- kicks out or restricts pathogens)
-involved in the pain response.

Most common is bradykinin (most important in inflammatory response).
They are broken down by Kininases and ACEs.(angiotensin converting enzyme)

float around in blood stream

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40
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 (selectin) and production of prostaglandins, PAF, and chemokines (inflammatory mediators).

since inflammation is not specific, clots can form in CASE needed

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41
Q

What is the complement system?

A

-present in inactivated forms in plasma
(activated to become proteolytic enzymes)
(degrade other complement proteins in a cascade)

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42
Q

major function of the complement system (5)

A
  • vasodilation and increased vascular permeability
  • smooth muscle contraction
  • leukocyte activation, adhesion, chemotaxis
  • augmentation of phagocytosis
  • mast cell degranulation (release what is in granules
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43
Q

what effector molecules are present during complement system

A

C3a and C5a (help with immune repsosne)

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44
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.

stuffy nose- blood vessels open

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45
Q

Cytokines

A

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

46
Q

IL-1, IL-6, and TNF-alpha main roles

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.
can cause a lot of symptoms and excess inflammation

47
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.

cells get damaged and arachidonic acid shows up and breaks down to protstaglandins and leukotrienes.

48
Q

Arachidonic pathway and why steroids work better than aspirin

A

both anti inflammatories but steroids are higher up on the chart meaning that they stop many of the processes below from even starting (stop arachidonic acid from being formed) whereas aspirin has to deal with all of those already happening

49
Q

Cyclooxygenase Pathway

A

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

50
Q

Prostaglandins

A

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

51
Q

What do NSAIDs and aspirins inhibit

A

enzyme in cyclooxygenase pathway for prostaglandin synthesis

52
Q

PGE1 and PGE2

A

Prostaglandins known for inducing inflammation and potentiating effects of other inflammatory mediators, especially histamine.
- keeps production going otherwise inflammation may stop before we need it to

53
Q

Thromboxane A2

A

Promotes platelet aggregation and vasoconstriction

54
Q

Leukotrienes

A
  • Functionally similar to histamine ( but take awhile to to made and released unlike 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.
55
Q

What condition is treated with leukotriene receptor antagonists?

A

Asthma

56
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.

  • steroids should help with anaphylaxis but if you don’t check hours after the anaphylaxis, wheezing could start
57
Q

what do 5-lipoxygenase inhibitors do

A

block enzyme in lipoxygenase pathway to convert arachidonic acid to leukotrienes

58
Q

Platelet Activating Factor (PAF)

A

Derived from cell membrane phospholipids

Activates platelets
- Induces platelet aggregation,
- stimulates platelets to release vasoactive mediators and to synthesize thromboxanes.

Increases vascular permeability,
activates neutrophils, and
is a chemoattractant for eosinophils.

59
Q

Nitric Oxide (NO)

A

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

(“NO” inflammation)
- discourage new WBC to area
-help kill pathogens inside phagocytes

60
Q

What is involved in the pain response?

A

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

61
Q

What are the 5 cardinal signs of inflammation and what are there causes?

A

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

62
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.

63
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.

64
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.

65
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.

66
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.

67
Q

What are the local manifestations of inflammation?

A

Any of the cardinal signs or exudates

68
Q

What is an exudate?

A

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

69
Q

List possible exudates

A

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

70
Q

what is serous exudate

A

watery, lower in protein; derived from plasma entering inflammatory site
not very specific

71
Q

what is fibrinous exudate

A

large amounts of fibrinogen- thick sticky meshwork (adhesions)
(see in large abdominal surgeries)

72
Q

what is purulent/suppurative exudate

A

pus (degraded WBC, proteins, tissue debris) infection

73
Q

what is hemmorrhagic exudate

A

severe tissue injury causing damage to blood vessels or significant leakage of RBC from capillaries (hematoma)

74
Q

what is membranous/ pseudomembranous exudate

A

form on mucous membranes; necrotic cells in fibropurulent base
adherent, sticks to bottom often

75
Q

what is sanguineous exudate

A

thin, red or pink, watery; plasma with a few RBC mixed in
not very specific

76
Q

Abscess

A

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

77
Q

Ulceration

A

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

78
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.

79
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.

80
Q

What causes leukocytosis?

A

IL-1 and other cytokines.

81
Q

What causes lethargy?

A

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

82
Q

What is the purpose of skeletal muscle catabolism?

A

Provides amino acids for use in the immune response, tissue repair, and regeneration.
- uses proteins/ amino acids for energy elsewhere so its not just because they’re constantly laying

83
Q

what are acute phase proteins

A

acute phase reaction causes liver to dramatically increase production of proteins like fibrinogen and C reactive protein (CRP) that play a role in the immune response

84
Q

What is ESR and what affects it?

A

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

proteins cause RBC to clump together more quickly than normal

Elevated ESR is caused by elevated acute-phase proteins (fibrinogen and CRP), along with falsely positive in anemic patients (because there aren’t as many RBC as there should be so its easier to clump)

elevated sed rate= increased inflammation

changes slower in response to inflammation than CRP

85
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 (helps get rid of dead cells) , obesity, HTN, DM, smoking, aging, depression, sleep disturbances, and increased CV risk.

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

86
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.

87
Q

When do I usually see neutropenia?

A

Viral infections

88
Q

When do I usually see Eosinophilia?

A

Parasitic infections and Allergic reactions

89
Q

When do I usually see Neutrophilia?

A

Bacterial infections

90
Q

when do I usually see neutropenia and/or lymphocytosis

A

viral infection

91
Q

when do you usually see left shift

A

infection

92
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 (if fluctuant- can feel fluid moving).

93
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.

94
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.

95
Q

What are the 5 types of shock?

A

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

96
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.

heart cant pump well, has enough blood but not getting circulated

97
Q

Major symptoms of shock

A
  • extreme hypotension
  • oliguria (decreased urine output)
  • pale, cool, clammy skin (in fight/flight- shunting blood to organs like heart/brain)
  • altered mental status ( early-agitation, irritability, anxiety…. late- confusion, delirium, coma)
  • metabolic acidosis- breakdown in tissues and will see acid from this
98
Q

other possible shock symtpoms

A

tachypnea
tachycardia
dehydration
chest pain/irregular HR
varies with the cause!

99
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

100
Q

What is distributive shock?

A

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

enough blood but vessels all opened up, low pressure, low circulation

101
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.

102
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.

lose fight/flight, now only have parasympathetic rest digest

103
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. (pro-inflammatory mediators exceed boundaries of local injury)

It results in excessive vasodilation, tissue ischemia(death- due to no circulation), direct cell injury, and an altered rate of apoptosis.

multiple major organ systems suffer negative impact

104
Q

What is SIRS?

A

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

105
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.

106
Q

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

A

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

107
Q

how does septic shock affect the liver

A

impaired elimination of bacteria and toxins from the GI due to cellular injury.
- hypoperfusion
-direct cellular injury

108
Q

how does septic shock affect the kidneys

A

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

109
Q

How does Septic Shock affect the CNS?

A

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

110
Q

how does septic shock affect the lungs

A

pulmonary edema and hypoxemia.

MOD S1 (18 decks)

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