1
Q
Define inflammation
A
Protective
- Fight foreign antigens
- Phagocytosis of pathogens and debris from dead & damaged cells for tissue repair
2
Q
Tissue response to injury (diagram)
A
3
Q
Acute inflammation
A
- Non-specific functions
- Generate an acute inflammatory exudate, a transient material that carries proteins, fluid & cells (mostly PMNs) from local blood vessels into the damaged area to mediate local defenses
- Exudate can destroy infective agent
- Damage tissue can be broken down & liquified and removed by phagocytic cells
- 4 cardinal signs of celsus
- Rubor- redness
- Calor - heat
- Dolor - pain
- Tumor - swelling
- these leads to loss of function
4
Q
The elements and players in acute inflammation
A
- Exudate: an extravascular fluid that has a high protein concentration and contains cellular debris
- Transudate: fluid with low protein concentration (mostly albumin), with little or no cellular material and a low specific gravity
5
Q
Acute inflammatory exudate
A
- Purulent (PMNs), Fibrinous (Fibrin), or Serous (Fluid)
- Fluid containing salts and a high concentration of proteins including Ig
- Fibrin, a high color molecular weight filamentous insoluble protein
- Many neutrophilic polymorphonuclear leukocytes (PMNs)
- A few macrophages and lymphocytes
6
Q
Acute inflammatory exudate; the fluid components
A
- small vessels dilate, initially with increased blood flow, but then the flow slows
- Endothelial cells contract compromising integrity of tight junctions
- Fluid, salts and soluble proteins, including fibrinogen are released
- Hageman factor (Factor XII)
- Activated in the exudate when it contacts extravascular collagen
- Stimulates conversion of fibrinogen to fibrin causing increased vascular permeability and attracts PMNs (chemotaxis)
- Activates the kinin system (bradykinin) producing vascular dilation, causes pain, and activates complement
- Bradykinin facilitates plasminogen activator generation of plasmin which lyses fibrin. But plasmin also activates complement, Hageman factor and, in lysing fibrin, increases vascular permeability
7
Q
The complement system
A
- A cascade of 9 plasma proteins with numerous intermediary peptides. In acute inflammation the main products are
- C3a = increases permeability, liberates histamine.
- C5a = increases permeability, liberate histamine and induces endothelial cell adhesion molecules
- C345 complex = chemoattractive to PMNs
- C3b = opsonizes bacteria to facilitate phagocytosis
8
Q
Acute inflammatory mediator (Histamine)
A
- main pre-formed mediator
- Released from mast cells, basophils and platelets
- Produces transient dilation of arterioles
- Primary cause of early phase of increased vascular permeability
9
Q
Acute inflammatory mediator (Mast Cells)
A
10
Q
Dendritic cell
A
- Dendritic cells are APC aka acessory cells. Their main fxn is to recognize and process antigenic material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune system.
- Dendritic cells are present in those tissues that are in contact with the external environment
- Skin & conjunctiva
- Not the central cornea - langerhan cells
- Inner lining of the nose, lungs, stomach and intestines.
- They can also be found in an immature state in the blood. Once activated, they migrate to the lymph nodes wehre they interact with T cells & B cells to initiate and shape the adaptive response.
11
Q
List the mediators released by mast cells
A
12
Q
Acute inflammatory mediator - Cytokines
A
- Small group of proteins (~5-20 kDa) that are important in intercellular signaling.
- Cytokines include
- chemokines
- Interferons (IFNs)
- Interleukins (IL)
- Lymphokines
- Tumor necrosis factors (TNF)
- Cytokines are produced by..
- macrophages
- T and B lymphocytes
- mast cells
- vascular endothelial cells
- fibroblasts
- certain stromal cells
- Cytokines modulate the balance betwen humoral (B-cell) and T cell based immune response
- They regulate the maturation, growth, and responsiveness of particular cell populations
- IFN are produced when a cell is infected by a virus, inhibiting protein synthesis in surrounding cells so virus will not take over protein machinery of that cell.
- Acutely IL-1, IL-8 and TNFa
- induce prostacyclin synthesis
- pyrogenic, anorexic, stimulate acute phase protein synthesis in the liver
- Induce platelet activating factor (PAF) and nitric oxide (NO) synthesis
- Induce cell adhesion molecules (selectins & integrin binding ligands - chemokines) on endothelium
- Attract PMNs (IL-8)
13
Q
Describe IL-1, IL-8 and TNF-a (cytokines)
A
- IL-1
- Locally
- vasodilation
- chemotactic for monocytes and neutrophils
- Systemically:
- Initiates hypothalamic fever response
- Promotes pain.
- Uncontrolled IL-1 may also play an important role in atherogenesis (Formation of fatty plaque in the arteries)
- Locally
- TNF-a
- In systemic inflammation it contributes to the acute phase reaction.
- Produced by activated macrophages (mainly), CD4+ lymphocytes, NK cells, neutrophils, mast cells, eosinophils, & neurons
- Local increase concentration of TNF cause cardinal signs of inflammation = heat, swelling, redness, pain, and loss of function
- In high concentrations of TNF induce shock
- IL-8 (aka neutrophil chemotactic factor)
- Produced by macrophages and other cell types such as epithelial cells, airway smooth muscle cells and endothelial cells.
- Endothelial cells store IL-8 in their storage vesicles, the weibel-palade bodies
- It draws granulocytes to the area, prompts them to degranulate and promotes phagocytosis
- IL-8 can be secreted by any cells with toll-like receptors that are involved in the innate immune response. Usually, it is the macrophages that see an antigen first, and thus are the first cells to release IL-8 to recruit other cells
14
Q
Weibel-Palade Bodies in vascular endothelium
A
15
Q
Acute inflammatory mediators - prostaglandins and leukotrienes
A
- Derived from arachidonic acid, released from cell membranes by phospholipase A2
- Cyclo-oxygenase pathway (COX)
- Produces thromboxane A2 = aggregates platelets
- Prostacyclin = inhibits platelet aggregation
- Prostaglandins = which increase vascular permeability and enhance uveo-scleral outflow (in eye)
- Lipoxygenase pathway
- Produces leukotrienes = vasoconstriction & increased permeability of venules
- LTB4 = stimulates leukocyte adhesion to endothelium
16
Q
C-Reactive protein
A
- Indicator of systemic inflammation
- CRP is an annular, pentameric protein made by the liver and found in plasma, whose levels rise in response to systemic inflammation. It is an acute-phase protein that increases following IL-6 secretion by macrophages and T cells. Its physiological role is to bind to lysophosphatidylcholine expressed on the surface of dead or dying cells (and some types of bacteria) in order to activate the complement system via the C1Q complex.
- C-reactive protein is measured in milligrams per liter of blood (mg/L) Normal CRP levels are below 3.0 mg/dL
- Any systemic inflammatory disease (e.g. rheumatoid arthritis, seronegative spondyloarthropathies, giant cell arteritis and even some cancers) can elevate CRP levels
- It is important to remember, however, that CRP is an extremely nonspecific test and can be elevated in any systemic inflammatory condition
17
Q
Erythrocyte sedimentation rate
A
- General indicator of systemic inflammation
- Measures the degree to which red blood cells settle out of anti-coagulated blood in 1 hr in mm. As inflammatory activity increases, more fibrinogen is present in the blood, causing RBCs to clump more readily and fall faster
- Normal ESR for men = (age in years)/2
- Normal ESR for women = (age in years + 10)/2
- Today, it is still reported mm/hr even though the test is done under 30 seconds
- Values increase with age but values above 30 are usually of concern
18
Q
Acute Inflammatory Mediators - Platelet-activating Factor (PAF)
A
- Synthesized and released by mast cells and basophils where it can be stimulated by IgE mechanisms
- Also made and released by platelets, PMNs, monocytes and endothelial cells
- Causes vasoconstriction, increased permeability
- Promotes platelet aggregation
19
Q
Acute inflammatory mediators - Nitric oxide (NO)
A
- Nitric oxide is a free radical (dot on N)
- locally synthesized by endothelium and macrophages via NO synthase activity
- potent vasodilation but short duration
- increases vascular permeability
- serves as a reactive oxygen intermediary
- Drugs like nitroglycerin, used to dilate coronary arteries in acute angina attacks are precursors
- Research using NO to prevent death of ganglion cells in glaucoma.
20
Q
First glaucoma drug with an NO donor
A
- VYZULTA = latanoprostene bunod is rapidly metabolized in the eye to latanoprost acid, an F2 alpha prostaglandin analog and to butanediol mononitrate; latanoprost acid is thought to lower intraocular pressure by increasing outflow of aqueous humor through both the TM and uveoscleral routes. The butanediol mononitrate (butylated nitric oxide donor - bunod) is though to help preserve the optic nerve through vascular vasodilation
21
Q
Classical complement pathway
A
- The classical pathway of complement activation is a mediator of the specific antibody response. It is triggered by antigen-bound antibody molecules. it is the binding of a specific part of the antibody molecule to the C1 component that initiates this pathway
22
Q
The alternative complement pathway
A
The alternative complement pathway constitutes the humoral component of natural defenses against infection which can operate without antibody participation.
23
Q
Events of inflammation mediated by complement products
A
24
Q
Complement membrane attack complex
A
- A way to kill off infected or other unwanted cells
- Rolling the complement pathway all the way down to C9 results in a complex forming in cell membranes that create permeable pores
- If enough of these pores are formed the cell swells and bursts
25
Cell adhesion molecules (CAMS)
* stimulated by cytokines (e.g. IL-1, TNF-a)
* They stimulate endothelial cell activatio to allow PMN adhesion
* PMN activation (respiratory burst)
* Neutrophil chemikinesis/chemotaxis
26
Chemotaxis
* Margination (WBC stick to damage vessels)
* Pavementing (WBC stick to capillaries)
* Emigration
* Migration
* The other term used to describe white cell emigration from the vessels is diapedesis
27
Neutrophils - granulocytes
* This granulocyte has very tiny light staining granules (the granules are very difficult to see). The nucleus is frequently multi-lobed with lobes connected by thin strands of nuclear material. These cells are capable of phagocytizing foreign cells, toxins, and viruses
* When taking a differential WBC count of normal blood, this type of cell would be most numerous. Normally, neutrophils account for 50-70% of all leukocytes. If the count exceeds this amount, the cause is usually due to an acute infection such as appendicitis, smallpox or rheumatic fever. If the count is considerably less, it may be due to a viral infection such as influenza, hepatitis, or rubella
28
Basophil
* Basophilic granules in this cell are large, stain deep blue to purple, and are often aso numerous they mask the nucleus. These granules contain histamines (cause vasodilation) and heparin (anticoagulant)
* In differential WBC count we rarely see these as they represent less than 1% of all leukocytes. If the count showed an abnormally high number of these cells, hemolytic anemia or chicken pox may be the cause
29
Eosinophil
* A granulocyte has large granules that are pink (or red) in a stained preparation. The nucleus is bi-lobed. The granules contain digestive enzymes that are particularly effective against parasitic worms in their larval form. These cells also phagocytize antigen - antibody complexes
* These cells account for less than 5% of the WBC's. increases beyond this amt may be due to parasitic diseases, bronchial asthma or hay fever. Eosinopenia may occur when the body is severely stressed.
30
Monocyte - Agranulocytes
* This cell is the largest of leukocytes and is agranular. The nucleus is most often "U" or kidney bean shaped; the cytoplasm is abundant and light blue (more blue than this micrograph illustrates).
* These cells leave the blood stream (diapedesis) to become macrophages. As a monocyte or macrophage, these cells are phagocytic and defend the body against viruses and bacteria
* These cells account for 3-9% of all leukocytes. In people with malaria, endocarditis, typhoid fever, and rocky mountain spotted fever, monocytes increase in number
31
Lymphocyte
* An agranular cell with very large nucleus for the size of the cell. This cell is much smaller than the three granulocytes. The T lymphocytes act against virus infected cells and tumor cells. The B-lymphocytes produce antibodies as plasma cells
* This is the 2nd most numerous leukocyte, accounting for 25-35% of cells counted in a differential WBC count. when the number of these cells exceeds the normal amt, one would supsect infectious mononucleosis or a chronic infection.
* Pt with AIDS keep a careful watch on their T-cell level, an indicator of the AIDS virus activity
32
Derivative Cells
* The plasma cell - derived from B lymphocytes. They produce antibodies
* Histiocyte - form of macrophage derived from monocytes
33
Function of a Neutrophil
* Increase in number in acute inflammation
* short life span once activated
* Motile across vessel walls in directional fashion (diapedesis followed by chemotaxis)
* Contain granules rich in proteases
* Generate free radicals to kill engulfed bacteria
* makes arachidonic acid which makes Prostaglandins
* Actively phagocytic
34
Define Respiratory burst in PMNs
* **Respiratory burst (oxidative burst)** - is the rapid release of reactive oxygen species, chemotaxis brings them to the inflammatory site. This can cause rapid depletion of glycogen reserves in the cell.
* (Ex. Superoxide dismutase and hydrogen peroxide in inflammatory cells, including PMNs)
* **NADPH oxidase -** in vasculature, produces superoxide, which spontaenously recombines with other molecules to produce reactive **free radicals**. The superoxide reacts with NO, resulting in the formation of peroxynitirite, reducing the bioactive NO needed to dilate terminal arterioles
* **NADPH oxidase** - reduce **O2 to oxygen free radical and then H2O2**. Neutrophils and monocytes use **myeloperoxidase** to further **combine H2O2 with Cl-** to produce **hypochlorite** = this destroys bacteria
* Without **NADPH oxidase** = No reactive oxygen = **CHRONIC GRANULOMATOUS INFLAMMATION**
35
Extracellular traps
* DNA (nuclear or mitochondrial) and histones are forced out from inflammatory cells (PMN, mast cells) by process of cell membrane destruction.
* **Etosis -** PMN cell death
* Complexes that can trap & destroy bacteria
* **Elastase**
* **Cathepsin G**
* **Proteinases or defensins**
* **Bacterial permeability increasing protein (BPI**
* **Myeloperoxidase (MPO).**
* Some bacteria can escape by releasing DNAses that cleave ET backbone
36
Necrosis, apoptosis, netosis (etosis)
37
T/F Histones can be antimicrobial agents?
* **True**
* Highly alkaline proteins found in cell nuclei
* Package DNA into **nucelosomes**
* Chief protein components of chromatin, acting as pools around which DNA winds & play role in **gene regulation**
* When released through **etosis** (PMN cell death), some have antimicrobial properties as part of ETs
38
Phagocytosis
39
Clinical parameters in acute inflammation
Even in localized inflammation can stimulate cytokine-induced systemic reactions (except in the eye, which suppresses these)
In the acute phase, we expect
- fever (caused by exogenous pyrogenes - such as bacterial lipopolysaccharides and endogenous pyrogenes such as IL-1 and TNF)
- leukocytes
- sometimes increased pulse & BP, shivering, chills & CNS effects like anorexia, somnolence and malaise
40
Define Chronic Inflammation
* When a damaging stimulus persists for **weeks/months and/or complete healing cannot occur** - chronic inflammation ensues
* This **activates the immune system** and the nature of cellular response gradually changes to lymphocytes and plasma cells, macrophages, formation of granulation tissue and some scarring if the antigen or bug can ultimately be defeated
* In chronic inflammation the process of both tissue destruction and attempts at healing occur simultaneously
41
Chronic inflammation arises most often in which settings?
* Persistent infections (ex. abcess)
* Hypersensitivity Diseases (e.g. autoimmune)
* Prolonged exposure to endogenous or exogenous toxins (ex. asbestos, silica/excessive deposition of pro-inflammatory lipids in athersclerosis)
* Some of these chronic inflammatory diseases can lead to malignancy (e.g viral hepatitis, mesothelioma or lung cancer from asbestos)
42
PMNs depart & different cells participate - **Mononuclear cells**
* Mononuclear cells
* **Monocytes** - become macrophages
* **Macrophages**"activate" lymphocytes:
* Lymphocytes - T cells & B cell subsets
* Plasma cells (converted B-cells)
43
In chronic inflammation, _______ are the main effectors in chronic inflammation. They secrete:
Macrophages
* Some of the mediators of acute inflammation, especially PAF and arachidonic acid
* Highly reactive oxygen metabolites
* Proteases and hydrolytic enzymes to prepare for phagocytosis of necrotic tissue
* Cytokines that stimulate fibroblast proliferation and collagen synthesis for repair
* Growth factor to stimulate blood vessel and fibroblast growth
44
If there is a chronic allergic component or if the microbe represents a parasitic infestation, _____ will play a role.
**Eosinophils**
elevation in bloodstream as measured in a complete blood count (CBC) with "differential", in which not just the total white count is provided but the percentages and types of cells are counted
45
Granulomatous Inflammation
If it becomes clear that the agent persists and chronic inflammation cannot defeat it, the system scales back and seeks only to contain it.
46
Non-granulomatous (Chronic) vs. Granulomatous inflammation
* **Non-granulomatous reactions** (chronic inflammation as we have discussed it) are agressive inflammation due to antigen of high virulence that the immune system believes it can eventually clear
* These usually produce all of the cardinal signs of inflammation: **RUBOR, CALOR, DOLOR, and TUMOR**
* As we discussed, the principle cells responders, after the first responders have left the scene (poly's, eosinophils) are macophages, lymphocytes and antibody - producing plasma cells
* **Granulomatous reactions** are a sub-set of chronic inflammation that also manifest lymphocytes and plasma cells
* But, in addition, modified, non-phagocytic macrophages called **epitheloid cells** are present. These macrophages can merge together to form giant cells that are phagocytic
* They are less apt to produce **calor, rubor and dolor** in the way that non granulomatous inflammation does
47
Name 3 types of multinucleated giant cells
48
Describe **Th-1** and **Th-2** cells
* Th-1 & Th-2 cells are sub-classes of T helper cells. The cytokines of each group tend to inhibit the cells of the other group
* **Th-1**
* prouce IFN-y and IL-2
* usually dominate responses against intracellular pathogens such as bacteria & viruses
* Granulomas produced in TB are therefore Th-1 dominated
* **Th-2**
* produce IL-4, IL-5, IL-6, IL-10, and IL-13
* dominate responses against extracellular pathogens
* Granulomas produced in response to foreign materials are therefore Th-2 dominated
49
On a cellular and clinical level, granulomatous diseases are characterized by the formation of \_\_\_\_\_\_
**Granulomas**
* **Granuloma formation** immune strategy to deal with pathogens that learned to evade the immune system.
* These include pathogens being able to resist dying after phagocytosis or masquerading themselves to remain just below the radar for producing an all-out immunological assualt
* **Epithelioid macrophages**, along with **giant cells**, coaelesce to form granulomas to wall off these organisms or antigens to prevent further growth or spread (tolerate pathogen)
50
TB & C3 fraction
* Tubercle bacilli can produce & secrete a protein that can pass for the **C4-b** fraction of the complement cascade that plays such a central role in inflammation
* Activating the complement pathway triggers the cascade and, in the process, the **C2a** fraction is produced
* The **C4-b mimic**, produced by the bug, passes for C4-b and can combine with the C2a fragment produced by the host
* That complex forms a C3 convertase enzyme that then deposits C3 onto the surface of the bacillus
* TB bug is covers itself with C3 to promotes itself to be eaten by the phagocytosis. The TB bug remains inside the vesicle out of reach from the immune system. The wall of the TB is able to resist the enzymes & low pH of the phagocyte
* TB can become quiescent (less sx) or replicate & destroy host cell spreading to macrophages, while destroying host tissue along the way. (ex. lung & lacrimal gland)
* Or it can be activated by the pt taking steroids that inhibit the macrophages, lead to re-release of TB bugs)
* but the system does know bug/antigen is there and so it builds a wall of epithelioid cells and giant cells around the bug or antigen. THIS WALL IS **GRANULOMA**
51
Sign & sx of granulomatous depends on...?
where and how many of these focal, yellow, granulomas are produced and the amount of destruction of normal tissue that their presence creates
52
Granulomatous Diseases
* Infectious
* TB, syphilis, leprosy, histoplasmosis cryptococcosis, coccidioidomycosis, blastomycosis
* cat scratch disease, lyme disease
* Non-infectious
* Sarcoidosis
* Crohn's disease
* Berylliosis
* churg-Strauss syndrome
* Pulmonary rheumatoid nodules
* Aspiration of food & other particulate material into the lung
* We will look at one example from each category TB & SARCOID
53
How does the granulomas relate to the key diagnostic findings in sarcoid?
* Elevated ACE levels
* Elevated serum calcium levels
* Hilar adenopathy
* Positive Gallium scan
54
Describe Elevated ACE (Angiotensin converting enzyme levels)
* ACE is produced by the normal pulmonary endothelium and catalyzes conversion of angiotensin I to angiotensin II - a very potent vasoconstrictor that elevates BP. This process has been targeted by the development of drugs called ACE inhibitors that are commonly used to decrease vasoconstriction as means of treating systemic HTN
* ACE Levels increase in sarcoidosis because the cells of granulomatous tissue also produce ACE. Increasing ACE does not increase BP in sarcoid since there is not an unlimited source of substrate (angiotensinogen)
* Serum ACE activity, expressed in units/L, in normal subjects, is 10-70
55
What occurs in elevated serum calcium levels?
* Granulomas develop in bone, producing radiolucent defects that can lead to fractures
* In the process, as bone is destroyed, calcium is released into the blood, explaining why pt with sarcoid often have elevated serum calcium levels
56
Gallium scan
Injection of citrated gallium67 partitions out with medium to large accumulations of granulomatous tissue
Destruction of normal lacrimal gland tissue by granulomas accounts for sx of dry eye in sarcoid
57
Granulomas in the iris
* Koeppe nodules - Pupillary margin in both non-granulomatous granulomatous uveitis
* Bussarca nodules - pathogonomic for granulomatous uveitis
58
What does this image show?
Granuloma of lid margin and conjunctiva
59
Describe TB signs and sx
* signs and sx of granulmoatous disease are almost entirely the result of where and how many of these focal, yellow, granulomas are produced and the amount of destruction of normal tissue that their presence creates
60
Ghon Complex
The initial focus of infection is small **subpleural granuloma** accompanied by **granulomatous hilar lymph node infection.**
Together, these make up the Ghon complex
61
Cavitary TB of lungs
In secondary TB
62
Miliary TB
When resistance to infection is particularly poor, a miliary pattern of spread can occur in which there are a myriad of small millet seed (1-3mm) sized granulmoas, either in lung or in other organs
28% of those with miliary TB will have choroidal involvement
63
Granulomas in choroid in TB will look like what?
Headlight in fog
64
Granulomatous disease - Signs & sx of Sarcoidosis
* **Signs & Sx of Sarcoidosis**
* Tender reddish bumps or patches on the skin
* Red & teary eyes or blurred vision
* Swollen and painful joints
* Enlarged and tender lymph glands in neck, armpits, and groin
* Enlarged lymph glands in chest & around lungs
* Hoarse voice
* Pain in the hands, feet, or other bony areas due to formation of cysts (an abnormal sac-like growth) in bones
* Kidney stone formation
* Enlarged liver
* Development of abnormal or missed heart beats (arrhythmias), inflammation of covering of the heart (pericarditis), or heart failure
* Nervous system effects, including hearing loss, meningitis, seizures, or psychiatric disorders (for ex. dementia, depression
* Because these bugs and antigens are effective a staying just barely above the radar, most granulomatous diseases usually run a long, slow course of exacerbations and seeming remission
* Untreated, some can go away on their own (sarcoid) and some eventually lead to death (TB), especially when coupled with immunocompromise, as with AIDS
* They are rarely raging inflammatory processes. Indeed if you look at the list of signs and sx of the most common presentation of sarcoid (left), you will notice that **FEVER** is not even on the list.
65
Autoimmune Granulomatous conditions
66
Pyogenic Granuloma
Granulomas that are not granulomas
67
Granulation Tissue
* When wounds are too large to suture closed, the wound is often left to "**GRANULATE IN**" through a process called healing be secondary intention.
* In doing so, a base is created for subsequent epithelialization
* The type of itssue that fills the void is called granulation tissue. years ago this was also referred to as "proud flesh"
68
Granulation tissue
New thin-walled, leaky blood vessels in a minimal collagen matrix, with lots of hyaluronate to hold water and build tissue volume (as it does in the vitreous), together with non-granulomatous inflammatory cells. No epithelioid or giant cells
69
What happens if a break in conjunctival epithelium occurs that is too large to self-repair?
Proliferation of new primitive CT (granulation tissue) will fill and extrude from the opening in the conjunctival epithelium
70
T/F pyogenic granulomas are not granulomas
T. They are granulation tissue, composed of new, thin walled and friable blood vessels. There is no epithelial covering
Thus, if pyogenic granulomas are manipulated, it is usually very easy to get them to bleed
Indeed, pt with pyogenic granulomas often report blood-stained tears
71
Granulomatous inflammation
* Granulomatous diseases are sub-set of chronic inflammation caused by pathogens/antigens with low virulence that can remain barely above the radar system that would normally trigger an aggressive inflammatory response
* They are antigens that are hard for the immune system to effectively clear using its usual set of weapons
* The general pattern of signs and symptoms differ in granulomatous vs granulomatous disease, with granulomatous diseases producing less of the classic signs of inflammatory (rubor, calor, dolor, tumor). But they also tend to be more chronic, because the immune system cannot effectively eliminate them
72
Hordeolum vs Chalazion
To understand difference between non-granulomatous and granulomatous inflammation
73
\_\_\_\_\_ is the most common granulomatous disease seen in optomteric practice
Chalazion
Pathophys
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