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Mechanisms of Disease I > Chapter 3 Lecture (Dr. Dobson) TEST 1 > Flashcards

Chapter 3 Lecture (Dr. Dobson) TEST 1 Flashcards

1
Q

Necrosis

A

Cell Size:
- ENLARGED (Swelling)

Nucleus:
- PYKNOSIS —-> Karyorrhexis ——> Karyolysis

Plasma Membrane:
- Disrupted

Cellular Contents:
- Enzymatic Digestion; May leak out of Cell

Adjacent Inflammation:
- FREQUENT!!!!

Physiologic or pathologic Role:
- Invariably PATHOLOGIC (Culmination of Irreversible Injury)

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2
Q

Apoptosis

A

Cell Size:
- Reduced (Shrinkage)

Nucleus:
- Fragmentation into Nucleosome Size Fragments

Plasma Membrane:
- Intact; Altered structure, especially orientation of Lipids

Cellular Contents:
- Intact; may be released in Apoptotic Bodies

Adjacent Inflammation:
- NO!!!!!!!!

Physiologic or pathologic Role:
- Often physiologic, means of eliminating UNWANTED CELLS; may be Cell Pathologic after some forms of Cell Injury, ESPECIALLY DNA DAMAGE!!!!!

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3
Q

Acute Inflammation

A

1) Acute respiratory distress syndrome
- Neutrophils

2) Asthma
- Eosinophils; IgE antibodies

3) Glomerulonephritis
- Antibodies and complement; neutrophils, monocytes

4) Septic shock
- Cytokines

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4
Q

Chronic Inflammation

A

1) Arthritis
- Lymphocytes, macrophages; antibodies?

2) Asthma
- Eosinophils; IgE antibodies

3) ATHEROSCLEROSIS!!!!!
- Macrophages; lymphocytes

4) Pulmonary Fibrosis
- Macrophages; fibroblasts

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5
Q

Acute Inflammation Description

A

Onset:
- FAST, Minutes or Hours

Cellular Infiltrate:
- Mainly Neutrophils

Tissue Injury, Fibrosis:
- Usually mild and Self Limited

Local and Systemic Signs:
- Prominent

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6
Q

Chronic Inflammation Description

A

Onset:
- Slow: Days

Cellular Infiltrate:
- Monocytes/ Macrophages and Lymphocytes

Tissue Injury, Fibrosis:
- Often severe and Progressive

Local and Systemic Signs:
- Less

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7
Q

The initial, rapid response to infections and tissue damage is called ACUTE INFLAMMATION

A

Initial step in mounting an Acute Inflammatory response is RECOGNIZING THE OFFENDING AGENTS(s):
• Receptors in plasma membrane, endosomes, and cytosol (toll-like receptor)

  • Cytosolic sensors of cell damage (uric acid, ATP, DNA, K+) activate an INFLAMMASOME
  • Other cellular receptors such as Fc receptors that recognize opsonized microbes
  • Circulating proteins i.e. complement, Mannose-Binding Lectin, Collectin
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8
Q

At the same time as phagocytes and other sentinel cells in the tissues recognize the presence of the foreign or abnormal substance, they react by liberating CYTOKINES, LIPID MESSENGERS, AND OTHER MEDIATORS OF ACUTE INFLAMMATION

A

This acute inflammatory has THREE MAJOR COMPONENTS:

(1) Dilation of small vessels leading to an increase in blood flow (erythema or Rubor, and heat or Calor).
- Initially in arterioles and then capillaries

(2) INCREASED PERMEABILITY in microvasculature leading to loss of protein-rich fluid (swelling or tumor).
- Loss of intravascular fluid (hemoconcentration) combined with vessel dilation —> STASIS

  • Stasis allows neutrophils to MARGINATE peripherally in the vessels
    (3) Leukocyte recruitment to sites of inflammation
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9
Q

Steps of Elimination

A

1) Recognition by Macrophages, other Sentinel Cells in tissue
2) VASODILATION, Increased Vascular Permeability
3) ELIMINATION of Microbes, Dead Tissue

***The Mediator of Inflammation are the substances that INITIATE and REGULATE Inflammatory Reactions

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10
Q

Recognition of microbes or dead cells (Step 1) induces several responses in leukocytes that are collectively called LEUKOCYTE ACTIVATION

A

*** Leukocyte Activation —-> PHAGOCYTOSIS and INTRACELLULAR KILLING!!!!!

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11
Q

Process of Phagocytosis

A

1) RECOGNITION AND ATTACHMENT
- Microbes bind to Phagocyte Receptors

2) ENGULFMENT
- Phagocyte Membrane zips up around Microbe

3) FUSION OF PHAGOSOME WITH LYSOSOME
- Phagolysosome

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12
Q

Killing of microbes is accomplished by reactive oxygen species (ROS, also called REACTIVE OXYGEN INTERMEDIATES) and reactive nitrogen species, mainly derived from Nitric Oxide (NO), and these as well as lysosomal enzymes destroy phagocytosed debris

A

ROS:

  • NADPH Oxidase
  • Myeloperoxidase

NO:
- iNOS

Lysosomal Enzymes:
- Secondary Granules

* ALL THESE “KILLERS” CAN LEAD TO COLLATERAL DAMAGE INVOLVING NORMAL TISSUE***

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13
Q

Histamine

A

Source:
- Mast cells, basophils, platelets

Action:
- VASODILATION, Increased vascular permeability, endothelial activation

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14
Q

Prostaglandins

A

Source:
- Mast cells, leukocytes

Action:
- VASODILATION, PAIN, FEVER

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15
Q

Leukotrienes

A

Source:
- Mast cells, leukocytes

Action:
- Increased Vascular Permeability, CHEMOTAXIS, leukocyte adhesion, and activation

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16
Q

Cytokines (TNF, IL-1, IL-6)

A

Source:
- Macrophages, endothelial cells, cells

Action:
- LOCAL: endothelial activation (expression of adhesion mast molecules).

  • SYSTEMIC: fever, metabolic abnormalities,
    hypotension (shock)
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17
Q

Chemokines

A

Source:
- Leukocytes, activated macrophages

Action:
- Chemotaxis, leukocyte activation

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18
Q

Platelet- Activating Factor

A

Source:
- Leukocytes, mast cells

Action:
- VASODILATION, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

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19
Q

Complement

A

Source:
- Plasma (produced in liver)

Action:
- Leukocyte CHEMOTAXIS and activation, direct target killing (MEMBRANE ATTACK COMPLEX), vasodilation (mast cell stimulation)

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20
Q

Kinins

A

Source:
- Plasma (produced in liver)

Action:
- Increased Vascular Permeability, smooth muscle contraction, vasodilation, PAIN!!!!

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21
Q

Vasodilation

A
  • Prostaglandins PGI2 (Prostacyclin), PGE1, PGE2, PGD2
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22
Q

Vasoconstriction

A
  • Thromboxane A2

- Leukotrienes C4, D4, E4

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23
Q

Increased Vascular Permeability

A
  • Leukotrienes C4, D4, E4
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24
Q

Chemotaxis, Leukocyte Adhesion

A
  • Leukotrienes B4

- HETE

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25
Q

Lipoxin A4 and B4

A
  • INHIBITION of Inflammation!!!
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26
Q

TNF

A

Source:
- Macrophages, mast cells, T lymphocytes

Action:
- Stimulates expression of endothelial adhesion molecules and secretion of other cytokines; systemic effects

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27
Q

IL-1

A

Source:
- Macrophages, endothelial cells, some epithelial cells

Action:
- Similar to TNF; greater role in fever

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28
Q

IL-6

A

Source:
- Macrophages, other cells

Action:
- Systemic effects (acute phase response)

29
Q

CHEMOKINES

A

Source:
- Macrophages, endothelial cells, T lymphocytes, mast cells,
other cell types

Action:
- RECRUITMENT of leukocytes to sites of inflammation; migration of cells in normal tissues

30
Q

IL-17

A

Source:
- T lymphocytes

Action:
- Recruitment of neutrophils and monocytes

31
Q

IL-12

A

Source:
- Dendritic cells, macrophages

Action:
- Increased production of IFN-γ

32
Q

IFN- Gamma

A

Source:
- T lymphocytes, NK cells

Action:
- Activation of macrophages (increased ability to kill microbes and tumor cells)

33
Q

Complement System

A

A) The complement system is a collection of SOLUBLE PROTEINS and membrane receptors that function mainly in host defense against microbes and in pathologic inflammatory reactions.

B) These proteins are Inactive until C3 is Activated by cleavage/proteolysis:

  1. Classic pathway
  2. Alternative pathway
  3. Lectin pathway

C) All three pathways of complement activation lead to the formation of an active enzyme called the C3 CONVERTASE, which splits C3 into two functionally distinct fragments, C3a and C3b**

34
Q

Actions of the Principal Mediators of Inflammation

A

▪ Vasoactive amines, mainly HISTAMINE: vasodilation and increased vascular permeability

▪ ARACHIDONIC ACID metabolites (prostaglandins and leukotrienes): several forms exist and are involved in vascular reactions, leukocyte chemotaxis, and other reactions of inflammation; antagonized by lipoxins

▪ CYTOKINES: proteins produced by many cell types; usually act at short range; mediate multiple effects, mainly in leukocyte recruitment and migration; principal ones in acute inflammation are TNF, IL-1, and chemokine

▪ COMPLEMENT PROTEINS: Activation of the complement system by microbes or antibodies leads to the generation of multiple breakdown products, which are responsible for leukocyte chemotaxis, opsonization, and phagocytosis of microbes and other particles, and cell killing

▪ KININS: produced by proteolytic cleavage of precursors; mediate vascular reaction, pain
- BRADYKININ increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and PAIN when injected into the skin.

35
Q

Morphologic Patterns of Acute Inflammation

A
  • The morphologic hallmarks of acute inflammatory reactions are dilation of small blood vessels and accumulation of leukocytes and fluid in the extravascular tissue.

FOUR SPECIAL PATTERNS:

  1. Serous inflammation
  2. Fibrinous inflammation
  3. Purulent (suppurative) inflammation/abscess
  4. Ulcer
36
Q

SEROUS INFLAMMATION

A
  • Serous inflammation is marked by the exudation of cell-poor fluid into spaces created by cell injury or into body cavities lined by the peritoneum, pleura, or pericardium —> EFFUSION
37
Q

FIBRINOUS EXUDATE

A
  • A fibrinous exudate develops when the vascular leaks are large or there is a local procoagulant stimulus.
  • A fibrinous exudate is characteristic of inflammation in the lining of body cavities, such as the Meninges, PERICARDIUM (Fig. 3-14 A), and pleura.
38
Q

PURULENT INFLAMMATION

A
  • Purulent inflammation is characterized by the production of pus, an exudate consisting of NEUTROPHILS, the liquefied debris of necrotic cells, and edema fluid.
  • The MOST FREQUENT CAUSE of purulent (also called SUPPURATIVE) inflammation is INFECTION WITH BACTERIA that cause liquefactive tissue necrosis, such as staphylococci; these pathogens are referred to as PYOGENIC (pus-producing) bacteria.
39
Q

ULCER

A

-An ulcer is a local defect, or EXCAVATION, of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflamed necrotic tissue

40
Q

Chronic Inflammation

A
  • Chronic inflammation is a response of prolonged duration (weeks or months) in which inflammation, tissue injury and attempts at repair coexist, in varying combinations.
41
Q

Causes of Chronic Inflammation

A

• PERSISTENT INFECTION i.e. mycobacteria, virus, fungi, parasites

• HYPERSENSITIVITY DISEASE i.e. autoimmune disease, RA or IBD,
bronchial asthma

• PROLONGED EXPOSURE TO POTENTIALLY TOXIC AGENTS
- Analogous to Step One in ACUTE INFLAMMATION

42
Q

Chronic Inflammation is Characterized by what type of Cells?

A

1) Macrophages
2) Lymphocytes
3) Plasma Cells

43
Q

Dominant Cells in Most CHRONIC INFLAMMATORY Reactions are MACROPHAGES

A
  • The dominant cells in most chronic inflammatory reactions are MACROPHAGES, which contribute to the reaction by secreting cytokines and growth factors that act on various cells, by destroying foreign invaders and tissues, and by activating other cells, notably T lymphocytes.
  • MACROPHAGES are tissue cells derived from Hematopoietic Stem Cells in the bone marrow and from progenitors in the embryonic yolk sac and fetal liver during early development.
    1) Circulating (in blood) = MONOCYTES
    2) Liver macrophages = KUPFFER cells
    3) In Spleen and Lymph Node they are called SINUS HISTIOCYTES
    4) In CNS they are referred to as MICROGLIAL Cells
    5) Macrophages in the lung = Macrophages
44
Q

Classic M1 Macrophages

A
  • Activated by Microbes and IFN-Gamma!!!

1) Microbicidal Actions: Phagocytosis and Killing of many Bacteria and Fungi
- ROS
- NO

2) Inflammation
- IL-12
- IL-1
- IL-23
- Chemokines

45
Q

Alternative M2 Macrophages

A
  • Activated by IL-13, Il-4

1) Tissue Repair, Fibrosis
- TGF- Beta

2) Anti-Inflammatory Effects
- IL-10
- TGF-Beta

46
Q

Types of CD4+ Cells and Cytokines

A
  • TH1 and TH2 are distinguishes by Cytokines but also by Cytokine Receptors and Adhesion Molecules they express
  • Other CD4+ Cells Produce various Mixtures of Cytokines, not readily classified

1) TH1:
- IFN-Gamma
* ** Intracellular Microbes

2) TH2:
- IL-4
- IL-5
- IL-13
* ** HELMINITHIC Parasites

3) TH17:
- IL-17A
- IL-17F
- IL-22
* ** Extracellular Bacteria, Fungi

** Activated B lymphocytes and Antibody-producing plasma cells are often present at sites of chronic inflammation!!!!!!!

47
Q

Eosinophils

A
  • BILOBED Nucleus
  • 2 to 4% of WBC
  • Recruited to sites of Inflammation
  • FUCNITON: Involved in Allergy, Parasitic Infections
  • CONTAINS: Eosinophilic Granules
  • GRANULES CONTAIN: Major Basic Protein
  • Terminally differentiated
48
Q

Granulomatous Inflammation

A

** GRANULOMATOUS Inflammation is a form of chronic inflammation characterized by collections of activated Macrophages, often with T lymphocytes, and sometimes associated with Central Necrosis!!!!!!!!!!!!!!!!!!

  • Granulomas are encountered in certain specific pathologic states; recognition of the granulomatous pattern is important because of the limited number of conditions (some life-threatening) that cause it
  • —> NEED TO CULTURE FOR TB!!!!!!!!!!!!!!!!
49
Q

Tuberculosis

A
  • TUBERCULOSIS is the prototype of a granulomatous disease caused by infection and should ALWAYS be excluded as the cause when GRANULOMAS are identified.

1) CASEOUS Necrosis
2) MULTINUCLETATED Giant Cells

50
Q

Chronic Inflammation Key Concepts

A

▪ Chronic inflammation is a prolonged host response to persistent stimuli.

▪ It is caused by microbes that resist elimination, immune responses against self and environmental antigens, and some toxic substances (e.g. silica); underlies many medically important diseases.

▪ It is characterized by coexisting inflammation, tissue injury, attempted repair by scarring, and immune response.

▪ The cellular infiltrate consists of macrophages, lymphocytes, plasma cells, and other leukocytes.

▪ It is mediated by cytokines produced by Macrophages and Lymphocytes (notably T lymphocytes); bidirectional interactions between these cells tend to amplify and prolong the inflammatory reaction.

▪ Granulomatous inflammation is a pattern of chronic inflammation induced by T cell and macrophage activation in response to an agent that is resistant to eradication.

51
Q

Summary of Acute and Chronic Inflammation

A
  • Inflammation (acute and chronic) are associated with cytokine-induced systemic reactions that are collectively called the ACUTE-PHASE RESPONSE/ REACTION.
  • The cytokines TNF, IL-1, and IL-6 are important mediators of the Acute-Phase Reaction; other cytokines, notably type I Interferons, also contribute to the reaction (IFN-α, IFN-β, and more).
52
Q

Systemic Effects of Inflammation

A

1) FEVER
2) Acute- Phase Reactants
3) LEUKOCYTOSIS

53
Q

Fever

A
  • Prominent manifestation especially when associated with infection LPS (exogenous pyrogens) ———–> IL-1 and TNF (endogenous pyrogens) that increased cyclooxyrgenase —————> AA converted to PGE2

Normal: 98.6F or 37C

54
Q

Acute Phase Reactants

A
  • “Plasma Proteins, mostly synthesized in the liver, whose plasma concentrations MAY INCREASE SEVERAL HUNDRED-FOLD as part of the response to
    inflammatory stimuli”

Three clinically important acute-phase reactants:

  1. C-reactive protein (CRP)
  2. Fibrinogen
  3. Serum amyloid associated protein (SAA)
  4. HEPCIDIN
55
Q

C Reactive Protein

A
  • Elevated Levels —-> INCREASED Risk for MI
56
Q

Fibrinogen

A
  • Rouleaux Formation (ESR)

“Protein gets in-between RBC and stacks them like Pennies”

57
Q

Serum Amyloid Associated Protein (SAA)

A
  • Secondary AMYLOID
58
Q

Hepcidin (Iron Regulating Peptide)

A
  • ANEMIA of Chronic Disease !!!!!!!!
59
Q

Leukocytosis

A

WBC Normal Values:
- WBC Count: 5, 000 to 10,000

  • Neutrophil: 50 to 70%
  • Segmenter: 50 to 65%; Stab: 0 to 5%
  • Eosinophil: 0 to 3%
  • Basophil: 0 to 1%
  • Lymphocytes: 20 to 40%
  • Monocytes: 2 to 6%
60
Q

Leukocytosis Infections

A
  • A common feature of inflammatory reactions, especially those induced by bacterial infections.
  • * WBC count can elevate up to 20K*****
  • When extremely elevated (40K-100K) looks like LEUKEMIA = leukemia reaction

BACTERIAL INFECTIONS = Neutrophils (Neutrophilia)

VIRAL INFECTIONS = Lymphocytes (Lymphocytosis)

ALLERGIES and PARASITES = Eosinophils (Eosinophilia)

Decreased White Cells = Leukopenia

61
Q

Left Shift

A
  • Mote things coming from the Stem Cells earlier than the point where they properly mature
62
Q

Sepsis

A
  • In severe bacterial infections (SEPSIS), the large amounts of bacteria and their products in the blood stimulate the production of enormous quantities of several cytokines, notably TNF and IL-1.
  • High blood levels of CYTOKINES cause various widespread clinical manifestations such as:
    1) Disseminated intravascular coagulation
    2) Hypotensive shock
    3) Metabolic disturbances including insulin resistance and hyperglycemia.
  • This clinical triad is known as SEPTIC SHOCK
63
Q

Tissue Repair

A
  • CRITICAL to the survival of an organism is the ability to repair the damage caused by toxic insults and inflammation.

** Tissue REPAIR is dependent on ability of injured cells to proliferate, and their interaction with the Extracellular Matrix (ECM)****

** Permanent Tissues (tissues that are not capable of dividing) cannot proliferate so no regeneration. Therefore injury results in scar (e.g. BRAIN and HEART)

64
Q

Cell Proliferation

A

LABILE TISSUE:
- Hematopoietic Surface:
A) Epithelia skin, oral cavity, vagina/cervix, eye

B) GI tract, uterus, fallopian tubes

C) salivary glands, pancreas, biliary tract bladder

65
Q

Tissue Repair Parts

A
  • MACROPHAGES play a central role in repair by clearing offending agents and dead tissue, providing growth factors for the proliferation of various cells, and secreting cytokines that stimulate fibroblast proliferation and connective tissue synthesis and deposition
  • ANGIOGENESIS is the process of new blood vessel development from existing vessels. Requires growth factors, Notch signaling, ECM proteins, and enzymes. The laying down of connective tissue occurs in two steps:
    (1) Migration and proliferation of fibroblasts into the site of injury

(2) Deposition of ECM proteins produced by these cells.

66
Q

Transforming Growth Factor Beta

A
  • TRANSFORMING GROWTH FACTOR-β (TGF-β) is the MOST IMPORTANT CYTOKINE for the Synthesis and Deposition of Connective Tissue Proteins.
  • It is produced by most of the cells in granulation tissue, including alternatively activated macrophages.
  • The levels of TGF-β in tissues are primarily regulated not by the transcription of the gene but by the Posttranscriptional activation of latent TGF-β, the rate of secretion of the active molecule, and factors in the ECM, notably integrins, that enhance or diminish TGF-β activity.
  • TGF-β stimulates fibroblast migration and proliferation, increased synthesis of collagen and fibronectin, and decreased degradation of ECM due to inhibition of metalloproteinases.
  • TGF-β is involved not only in scar formation after injury but also in the development of fibrosis in lung, liver, and kidneys that follows chronic inflammation.
  • TGF-β is also an ANTI-INFLAMMATORY CYTOKINE that serves to limit and terminate inflammatory responses. It does this by INHIBITING lymphocyte proliferation and the activity of other leukocytes.
67
Q

Why do all injuries or Insults NOT HEAL PERFECTLY?

A
  • Infection (clinically one of the most important causes of delay in healing)
  • Diabetes
  • Nutritional status
  • Glucocorticoids (steroids)
  • Mechanical factors
  • Poor perfusion
  • Foreign bodies
  • The type and extent of tissue injury affects the subsequent repair. Complete restoration can occur only in tissues composed of stable and labile cells.
  • The location of the injury and the character of the tissue in which the injury occurs are also important.
68
Q

First and Second Intention Healing

A
  • MACROPHAGES are key cellular constituents of tissue repair, clearing extracellular debris, fibrin, and other foreign material, and promoting ANGIOGENESIS and ECM DEPOSITION.
  • COLLAGEN FIBERS are now evident at the incision margins. By day 5, NEOVASCULARIZATION reaches its peak. Migration of fibroblasts to the site of injury is driven by chemokines, TNF, PDGF, TGF-β, and FGF. Their subsequent proliferation is triggered by multiple growth factors, including PDGF, EGF, TGF-β, and FGF, and the cytokines IL-1 and TNF.
  • At first a provisional matrix containing Fibrin, Plasma Fibronectin, and Type III Collagen is formed, but in about 2 weeks this is REPLACED by a Matrix composed primarily of Type I Collagen!!!!!
  • Ultimately, the original granulation tissue scaffold is converted into a pale, avascular SCAR, composed of spindle-shaped fibroblasts, dense collagen, fragments of elastic tissue, and other ECM components.
  • The dermal appendages that have been destroyed in the line of the incision are PERMANENTLY LOST.
  • The Epidermis recovers its normal thickness and architecture. By the END of the First Month, the SCAR is made up of ACELLULAR Connective Tissue devoid of inflammatory infiltrate, covered by intact epidermis.
69
Q

Too Much Fibrosis

A
  • Eye
  • Lung
  • GI
  • Heart
  • Skin
  • Liver

Mechanisms of Disease I (7 decks)

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