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Block 2 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Why would acetylcholinesterase inhibitors be used to treat glaucoma (in addition to pilocarpine)?

A
  • Increased acetylcholine in the synapse would stimulate muscarinic receptors
  • Ciliary muscles are contracted by muscarinic stimulation –> aqueous humor drainage from the eye
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2
Q

Appearance of lymphocytes under light microscope

A
  • Light microscope - almost entirely nucleus with just a small bit of cytoplasm
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3
Q

appearance of lymphocyte in EM

A
  • EM - large nucleus with patches of euchromatin
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4
Q

Why do you not see nodules in primary lymph tissues (bone marrow, thymus)?

A
  • Because no activation occurs in primary tissues
  • You only see follicles when activation is occurring
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5
Q

Bone marrow organization

A
  • Diffuse organization
  • No follicles
  • Not encapsulated
    • No trabeculae
  • Organized as chords and sinusoids (sinusoidal capillaries)
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6
Q

What is the purpose of sinusoidal capillary? Where is it located?

A
  • bone marrow
  • B-cells and T-cells born in the bone marrow can leave bone marrow and get into blood circulation via sinusoidal capillaries
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7
Q

How does bone marrow appear histologically?

A
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8
Q

What are the main supporting structures of lymph tissue?

A
  • Reticular fibers
  • **Except the thymus, which has keratin fibers
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9
Q

Reticular Fibers

A
  • Type 3 collagen
  • Very thin compared to type 1 collagen
  • Supporting structure of most lymph tissues (except thymus, which uses keratin)
  • Special silver stain
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10
Q

Summary features of thymus histologically

A
  • Diffuse organization
  • No nodules/follicles (b/c primary lymph organ)
    • But does have lobules defined by trabeculae
  • Fully encapsulated
    • See trabeculae
  • Has cortex and medulla
  • Hassel’s corpuscles is defining feature
  • **No afferent vessels to thymus, but there are efferent vessels
  • **Uses keratin instead of reticular fibers
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11
Q

Histology of thymus

A
  • Cortex stains bluer than medulla
  • No nodules but there are lobules
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12
Q

Other cells in the thymus aside from lymphocytes

A
  • Macrophages
  • Dendritic cells
  • Epithelioreticular cells
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13
Q

epithelioreticular cells

A
  • Supporting cells of the thymus
  • Synthesize keratin for supporting structure
  • Involved in T-cell education
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14
Q

Histology of epithelioreticular cells

A
  • They are found in the thymus
  • Recognize then by a nucleus that’s larger and euchromatic (lighter) than surrounding lymphocytes
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15
Q

Thymic venule purpose

A
  • T-cells that finish differentiation into the thymus go into the general circulation (to travel to secondary lymphoid organs) via venules
  • Process is called intravasation
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16
Q

Hassal’s corpuscles

A
  • Distinguishing feature of the thymus
  • Found in the medulla of the thymus, especially in the older thymus
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17
Q

Young thymus vs adult thymus

A
  • Older thymus has more adipose tissue
  • T-cells leave thymus to populate other organs and the thymus shrinks as a person ages - this is called thymic involution
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18
Q

Summary of MALT histology features

A
  • Nodules/follicles present (b/c secondary lymphoid organ where activation occurs)
  • Not encapsulated
    • No trabeculae
  • Located in lamina propria. Exists as a specialized type of connective tissue.
  • Can be either diffuse (in the gut) or nodular (in the esophagus)
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19
Q

Primary vs. secondary nodules/follicles

A
  • Primary follicles do not have a lighter region inside of them. The lighter region is the germinal center, so primary follicles lack a germinal center.
  • Secondary follicles have a germinal center.
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20
Q

Histology of primary follicle

A
  • No germinal center
  • Follicles only found in secondary lymphoid organs
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21
Q

Histology of secondary follicle

A
  • Has a germinal center
  • Follicles only found in secondary lymphoid organs
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22
Q

How to distinguish a B-cell from a plasma cell?

A
  • B-cell has nucleus that is very large
  • Plasma cells have eccentric nucleus, lots of endoplasmic reticulum, and a perinuclear hof (due to lots of golgi)
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23
Q

Plasma cell histology

A
  • Eccentric nucleus
  • Perinuclear Hof (due to lots of golgi)
  • Can see tons of ER under electron microscope
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24
Q

Intraepithelial lymphocytes

A
  • Specialized T-cells that can recognize free antigen without antigen presentation
  • They are found between epithelial cells in MALT
  • Considered part of innate immunity
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25
Q

Peyer’s patches and appendix

A
  • Both types of MALT
  • These are both GALT - gut associated lymphatic tissue
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26
Q

Tonsils

A
  • Recognize secondary follicles
  • Half-encapsulated
    • Non-encapsulated side is the lumenal side
  • **Crypt = distinguishing feature of tonsils
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27
Q

Histology of tonsilar crypts

A
  • Crypts are distinguishing feature of tonsils
  • These are extensions of stratified squamous epithelium
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28
Q

Lymph Node purpose

A
  • To filter (monitor) lymph fluids
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29
Q

How does lymph fluid get moved around the body if there is no pump in the lymph system?

A
  • There are lots of one-way valves
  • Every time your skeletal muscle contracts, it moves lymph fluid
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30
Q

Organization of lymph node

A
  • Secondary nodules/follicles
  • Fully encapsulated
    • Trebaculae exist
  • Cortex, deep cortex, medulla, lymphatic sinus
  • Unique to lymph node: high endothelial venule
  • **Lymph nodes have both afferent and efferent vessels. (Contrast with thymus which has only efferent.) Lymph nodes are the only organs with afferent vessels.
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31
Q

High endothelial venule purpose

A
  • Extravasation
  • Most of the lymphocytes coming to the lymph node arrive via the blood instead of afferent lymphatics
  • Lymphocytes move from the capillaries into lymph tissue via these high endothelial venules
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32
Q

Histology of high endothelial venules

A
  • Low magnification recognize with unique appearance shown on left image
  • Bottom right image shows a typical venule, which is flatter. Top right image shows a high endothelial venule, whose cells appear more cuboidal.
  • Locate high endothelial venules in the deep cortex region
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33
Q

Medullary sinus

A
  • The sinus of the lymph node
  • Lymph fluid drains into medullary sinus and then from here gets drained into efferent lymphatic vessels to leave the lymph node
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34
Q

Distribution of cells in the lymph node

A
  • Outer layer: Cortex
    • Primary and secondary follicles seen here
    • B-cell area
  • Next layer: Deep cortex
    • Find high endothelial venules here
    • T-cell region
  • Inner layer: Medulla
    • Plasma cells (and B-cells) live here
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35
Q

Histology of lymph node at low magnification

A
  • Recognize high endothelial venules
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36
Q

Purpose of the spleen

A
  • Filter (monitor) blood
  • Destroys old red blood cells (in red pulp)
  • Has immune function (in white pulp)
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37
Q

Summary features of the spleen

A
  • Has nodules/follicles
  • Fully encapsulated
    • Trabeculae present
  • Contains white pulp, red pulp, venus sinus
  • Unique features: central artery, PALS
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38
Q

Splenic circulation

A
  • Blood enters via splenic artery
  • Blood gets taken deeper into spleen via trabecular arteries
  • When artery leaves trabecula it goes into white pulp area and is called a central artery
  • The central artery is surrounded by lymphocytes and we call this the peri-arterial lymphatic system (PALS)
    • PALS is a layer of lymphocytes covering the central artery and it’s the main component of the white pulp
  • Blood from central arteries gets dumped into marginal zone (also white pulp) and then percolates into the venus sinus to return to blood circulation
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39
Q

White pulp

A
  • Found in the spleen
  • PALS and marginal zone are in white pulp area
  • White pulp surrounds central artery
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40
Q

3 different sinuses and their functions

A
  • Capillary sinusoid - in bone marrow - lymphocytes leave bone marrow and enter blood circulation
  • Lymphatic sinus - located in medulla of lymph node - collects lymphatic fluid that is carried away by efferent vessels
  • Venus sinus - located in spleen - carries blood from spleen back to general circulation
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41
Q

Histology of spleen

A
  • White pulp stains blue
    • Central artery should be in the middle of the white pulp
    • Recognize follicles with germinal centers
  • Red pulp stains lighter than white pulp
    • Organized as cords and sinuses
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42
Q

Splenic venus sinus

A
  • Located in red pulp
  • Collects blood from spleen and delivers it back to general circulation
  • Endothelial cells are unique b/c of ribbon-like appearance. This allows blood to come into venus sinus.
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43
Q

Where does T-cell development take place?

A
  • Thymus
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44
Q

What cells are present in the thymus?

A
  • Thymocytes
  • Dendritic cells
  • Epithelial cells
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45
Q

Cause of DiGeorge’s Syndrome

A
  • Thymus does not develop
  • Results in immunodeficiency
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46
Q

What is a double negative T-cell?

A
  • The cell expresses neither CD4 or CD8 on its surface
  • This is the earliest stage of T-cell development
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47
Q

Which loci do RAG enzymes act on first in the T-cells?

A
  • Beta, gamma, and delta
  • NOT alpha
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48
Q

Why does beta rearrangement usually occur instead of gamma or delta?

A
  • There are 2 clusters of genes on the beta locus
  • If rearrangement fails at the first locus, rearrangement can still occur at the second cluster
  • Gamma and delta regions do not have 2 clusters
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49
Q

What is triggered by successful beta chain rearrangement (TCR)?

A
  • A surrogate alpha chain pails with the beta chain –> pre-TCR
  • Further beta rearrangement is stopped
  • Proliferative burst for successful beta-chain thymocytes –> T cells express BOTH CD4 and CD8
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50
Q

What is a double positive T-cell?

A
  • Expresses both CD4 and CD8 on its cell surface
  • Occurs after successful beta chain rearrangement –> proliferative burst
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51
Q

Why does alpha rearrangement usually occur before gamma or delta?

A
  • There are so many different V-alpha regions compared to the gamma and delta gene segments
  • Unproductive rearrangement at one V-alpha region –> cell can try again with another alpha region. That’s not true of gamma and delta segments
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52
Q

What happens after successful alpha chain rearrangement?

A
  • Unlike with beta-chain rearrangement, the RAG enzymes maintain the ability to rearrange alpha chain again
  • This allows continued alpha-chain rearrangement through positive selection –> allows T-cell a better chance at recognizing self MHC molecules
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53
Q

What is positive selection? When does it occur?

A
  • Occurs after successful beta chain and alpha chain rearrangement
  • This is the process of selecting T-cells that recognize self-MHC for further development
  • Cortical epithelial cells play a role
  • After positive selection the thymocytes become either CD4 or CD8 T-cells
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54
Q

What cells in the thymus are responsible for educating T-cells during positive selection?

A
  • Cortical epithelial cells
  • Display both MHC1 and MHC2 molecules on their surface
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55
Q

When do thymocytes begin expressing EITHER CD4 or CD8?

A
  • After positive selection
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56
Q

When is TCR alpha rearrangement turned off?

A
  • After positive selection
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57
Q

What is negative selection? When does it occur?

A
  • The process of deleting T-cells that recognize self peptides
  • Occurs after positive selection
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58
Q

What is the major mechanism in T-cell development of preventing autoimmune disorders?

A
  • Negative selection
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59
Q

What is the major mechanism in T-cell development that results in MHC restriction?

A
  • Positive selection
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60
Q

What cells assist in negative selection?

A
  • Dendritic cells
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61
Q

AIRE

A
  • A transcription factor that occupies the promotor of MANY genes in the thymus
  • Drives really low levels of protein expression found in different tissues in the body
  • Major role in negative selection during T-cell development
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62
Q

APECED - autoimmune polyendocrinopathy-candiasis ectodermal dystrophy

A
  • Autoimmune disorder resulting from mutations in AIRE transcription factor
  • T-cells cannot undergo proper negative selection
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63
Q

Function of T-regulatory cells

A
  • These are generated during T-cell development
  • They prevent T-cells of the same clone from recognizing/attacking self peptides once they’re all released into the body
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64
Q

What are the 2 mechanisms of central tolerance in T-cell development?

A
  1. Negative selection
  2. Production of T-regulatory cells
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65
Q

Bare lymphocyte syndrome revisited

A
  • Dysfunction in TAP
  • Do not express MHC1 on cell surface
  • This means there are no MHC1 markers on thymic epithelial cells –> body cannot generate CD8 T-cells (b/c they are educated using thymic epithelial cells)
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66
Q

Bone Marrow transplant implications of T-cell development

A
  • Donor and recipient MHC markers must match
  • Donor bone marrow is transplanted
  • Dendritic cells in recipient come from donor bone marrow. They display donor MHC molecules.
  • T-cells in recipient come from donor bone marrow. But they are educated on thymic epithelial cells FROM THE RECIPIENT.
  • T-cells must be educated to recognize MHC markers that will allow them to recognize donor MHC markers on dendritic cells.
  • If MHC markers don’t match, recipient cannot raise an immune response.
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67
Q

T-cell activation overview

A
68
Q

What causes naive T-cells to leave the thymus and enter general circulation?

A
  • Sphingosine-1-phosphate concentration gradient
  • (S1P is higher in the blood)
69
Q

High endothelial venules

A
  • Specialized endothelial cells in the lymph node through which T-cells enter lymph node
70
Q

T-cell rolling

A
  • T-cell is in blood circulation
  • When it gets to endothelial cells in lymph node, L-selectin on the T-cell interacts with residues on the endothelial cells. This causes it to slow down and is called “rolling.
71
Q

Diapadesis of T-cell (from blood into lymph node)

A
  • T-cell rolling causes T-cell to slow down
  • Binding of LFA-1 on T-cell to ICAM-1 on endothelial cell causes it to stop and then the T-cell can get through endothelial cells (diapadesis)
72
Q

Two signals must occur for T-cell to be activated

A
  1. Recognition of MHC-peptide
  2. CD28 on T-cell must bind B7 on dendritic cell
73
Q

How is B7 expression induced on dendritic cells?

A
  • Dendritic toll-like receptors recognize pathogen –> B7 expression on cell surface
74
Q

What is special about dendritic cells?

A
  • They express B7 on their cell surface (one of the few cells that does this)
  • They are central to T-cell activation
  • They can activate T-cells through both MCH1 and MHC2 pathways due to cross linking
75
Q

What is cross presentation?

A
  • The process that allows dendritic cells to express peptide in both MHC1 and MHC2 molecules
  • Dendritic cells can engulf a virus, which would NORMALLY lead to MHC2 presentation. But special interferon signaling allows dendritic cells to present viral peptides on MHC1 molecules without the dendritic cells themselves being infected first.
76
Q

Naive T-cells receive both signals to become activated. What’s next?

A
  • Formation of the immunological synapse.
  • ITAMS on CD3 and TCR-zeta become phosphorylated –> signaling cascade
  • NFAT, NF-kappaB, AP1 are all transcription factors that become activated
  • These result in IL-2 transcription
  • IL-2 binds to T-cell (autocrine mechanism) and result in clonal expansion
77
Q

Deficiency in gamma portion of IL-2 receptor

A
  • Causes a form of X-linked SCID
  • Results because gamma portion of IL-2 receptor is also used in IL-7 receptor, which is the cause of SCID
78
Q

Mechanisms of T-cell negative regulation

A
  1. T-cell anergy
  2. T-cell apoptosis
  3. CTL4
  4. T-regulatory cells
79
Q

T-cell anergy - what is it? what is its purpose?

A
  • If TCR recognizes peptide-MHC but does NOT receive costimulatory signal (CD28 binding B7), the T-cell goes into a period of prolonged HYPOresponsiveness
  • This is a safeguard against hyperactiation of T-cells
  • T-cell only proliferates when B7 is present, which is only present on dendritic cells that have recognized a pathogen
80
Q

What happens if T-cell does not receive costimulatory signal (CD28 binding B7)?

A
  1. T-cell anergy
  2. T-cell apoptosis (Fas and Fas ligand)
81
Q

What is the mechanism of T-cell apoptosis when the costimulatory signal is absent?

A
  • Fas receptor is always present on T-cell surface
  • When T-cell recognizes MHC-peptide but does NOT bind B7, Fas ligand expression is turned on in that T-cell
  • Fas ligand binds Fas receptor –> apoptosis (autocrine signaling)
82
Q

CTL4

A
  • Important in negative regulation of T-cells
  • When T-cells proliferate in response to CD28 binding B7, there needs to be a way to turn them off. This is it.
  • CD28 binds B7 –> clonal expansion AND simultaneous expression of CTL4 receptor
  • CTL4 receptor has a higher affinity for B7 than CD28 does. So it results in contraction of B-cell population after some time.
83
Q

T regulatory cells

A
  • Important in negative regulation of T-cells
  • Generated in the thymus during T-cell development
  • Express FoxP3 transcription factor
  • Recognize MHC2-peptide on antigen presenting cells and suppress the activation of CD4 cells
84
Q

Autoimmune lymphoproliferative syndrome (ALPS)

A
  • Results from mutations/defects in Fas or Fas ligand –> T-cell populations cannot contract properly –> enlarged lymph nodes
85
Q

Immunodysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX)

A
  • Results from mutations in FoxP3
  • Lack T-regulatory cells
86
Q

CD4 T-cells

A
  • Th1
  • Th2
  • Tfh
  • Th17
87
Q

CD8 T-cells

A
  • Cytotoxic T-cells
88
Q

What is the function of Th1 cells?

A
  • Activate macrophages for more effective killing
89
Q

Which effector T-cells act at the site of infection?

A
  • Cytotoxic T-cells
  • Th1
  • Th17
90
Q

Which effector T-cells remain in the lymph node?

A
  • Th2
  • Tfh
91
Q

How do Th1 cells activate macrophages?

A
  • CD40 ligand on Th1 binds CD40 receptor on macrophage
  • Th1 secretes IFN-gamma, which binds to macrophage
  • Both signals together activate macrophage
92
Q

What happens if mycobacteria still survive even after macrophage activation?

A
  • granuloma formation
93
Q

What is the role of Th2 and Tfh?

A
  • Help B-cells differentiate into plasma cells
    • B-cells need a signal from BCR AND help from one of these T-cells to become a plasma cell
94
Q

How do Tfh and Th2 activate B-cells?

A
  • Effector T-cells recognize peptide-MHC2 complex on B-cells
  • Effector T-cells have CD40 ligand, which binds CD40 receptor on B-cells
  • Effector T-cells release cytokine (IL-4 for Th4; IL-21 for Tfh), which bind to the B-cell.
  • Both signals - CD40 ligand and IL binding - cause B-cell clonal expansion and differentiation into plasma cells
95
Q

What is the function of Th17?

A
  • Recruit neutrophils to site of infection
96
Q

What is the functon of cytotoxic T-cells?

A
  • To kill virally infected cells
  • This is triggered by viral peptide recognition on MHC1 molecules
  • These are CD8 T-cells
97
Q

How do cytotoxic T-cells kill their targets?

A
  1. perforin and granzymes
  2. Fas ligand on T-cell is induced; Binds Fas receptor on target cell
  3. Secretes IFN-gamma –> inhibits viral replication in cells in the vicinity, activates macrophages
98
Q

Cytokine that triggers Th1 differentiation

A
  • IL-12
99
Q

Cytokine that triggers Th2 differentiation

A
  • IL-4
100
Q

Cytokine that triggers Tfh differentiation

A
  • IL-6 and IL-21
101
Q

Cytokine that triggers Th17 differentiation

A
  • IL-6
  • TGF-beta
102
Q

Effector cytokine of Th1

A

IFN-gamma

103
Q

Effector cytokine of Th2

A

IL-4

104
Q

Effector cytokine of Tfh

A

IL-21

105
Q

Effector cytokine of Th17

A

IL-17

106
Q

What is the purpose of the primary immune response?

A
  1. Clear the infection
  2. Strengthens immune system temporarily against re-infection
  3. Produce memory cells to provide long-term protection against the same pathogen
107
Q

Overview of B-cell Activation

A
108
Q

Two signals needed by a B-cell in order to activate

A
  1. BCR signal - recognition of free antigen
  2. Helper T-cell signals
  • CD40L on helper T-cell binds CD40 on B-cell
  • Cytokine (IL-4) from helper T-cell binds B-cell receptor
109
Q

What is linked T-cell help?

A
  • Mechanism by which T-cells help B-cells produce antibodies against non-protein antigens
  • T-cells can only recognize peptide fragments, but B-cells can recognize things like carbohydrates
  • B-cell recognizes carbohydrate antigen that is linked to the protein, chews it up, displays PROTEIN in MHC2 molecule
  • T-cell recognizes protein component but still helps B-cell proliferate and generate Abs for the carbohydrate component
110
Q

Where does B-cell activation occur?

A
  • Area between B-cell center (outer cortex) and T-cell area (inner cortex)
111
Q

Where do B-cells go AFTER activation?

A
  • Dark zone of the germinal center
112
Q

What is Activated Induced Cytidine Deaminase (AID)?

A
  • This enzyme gets expressed when B-cells are activated
  • It is the master regulator of somatic hypermutation and class-switching
113
Q

Follicular dendritic cells

A
  • Display the original antigen that the BCR recognized
  • These are in the light zone
  • The B-cell undergoes somatic hypermutation and then “samples” the original antigen from the surface of the FDC’s.
  • Purpose is to ensure that somatic hypermutation does not result in B-cells that no longer recognize the original antigen and prevent B-cells that might actually recognize self
114
Q

After B-cells undergo somatic hypermutation and Class switching, what happens?

A
  • They can return to dark zone to proliferate more
  • They can exit germinal center as memory cells
  • They can exit the germinal center as plasma cells
115
Q

What are the primary antibodies used/generated for vaccines?

A
  • IgG (blood, skin, tissues)
  • IgA (mucosal surfaces)
  • IgM (blood, but less useful b/c IgM doesn’t undergo any maturation)
116
Q

Antibodies that neutralize pathogens

A

IgG

IgA

117
Q

Antibodies that do opsonization primarily

A

IgG

118
Q

Antibodies that result in complement activation

A

IgM

IgA

119
Q

Antibody that binds virus-infected host cells and promotes lysis by NK cells

A

IgG

120
Q

Subunit vaccines

A
  • Generate antibodies against particular surface components on a virus
  • Ex: Hep B virus vaccine
121
Q

Vaccines against bacterial toxins

A
  • Generate antibodies that neutralize the bacterial toxins
  • Made by purifying the toxin and treating with formalin so it is inactive –> toxoid
  • Ex: diptheria, tetanus
122
Q

Vaccines against polysaccharides

A
  • Directed against outer capsule of bacteria
  • Generate antibodies that promote complement fixation
  • a unique type of inactivated subunit vaccine composed of long chains of sugar molecules that make up the surface capsule of certain bacteria. Pure polysaccharide vaccines are available for three diseases: pneumococcal disease, meningococcal disease, and Salmonella Typhi.
123
Q

Conjugate vaccines

A
  • bacterial polysaccharide is conjugated to a carrier protein
  • Elicits linked T-cell help against polysaccharide antigens
  • ex: H.influenzae
124
Q

Live vs. inactivated vaccines

A
  • Inactivated = treated so they can no longer replicate
  • Live vaccines = treated so they are very poor at replication
125
Q

Passive immunity

A

ex: IVIG infusions
ex: used for antivenoms

126
Q

Sabin vs. Salk vaccines

A
  • Sabin = live, attenuated
    • Can replicate clunkily
    • Non-pathogenic
    • Humoral AND cell-mediated immunity (i.e. B-cells can work on it via humoral but cytotoxic T-cells work on it via cell-mediated)
  • Salk = inactive
    • Dead
    • Cannot replicate
    • Results in humoral response only (once the cell is infected, the B-cell cannot get to it)

https://www.youtube.com/watch?v=Ovype5DUI04

127
Q

Protein vs. polysaccharide vaccines

128
Q

What are the Thelper cells in germinal centers

A

Tfh

129
Q

How are memory T-cells produced?

A
130
Q

Central memory T-cells vs. Effector memory T-cells

A
  • Central memory T-cells express L-selectin and CCR7. L-selectin is an adhesive molecule; CCR7 is a chemokyne. These allow central T-cells to stay in lymphoid organs.
  • Effector memory T-cells do not express either of these molecules on their cell surface –> they can leave lymphoid organs
131
Q

what are the main cells of the acute inflammatory response?

A

neutrophils

132
Q

what are the main cells of the chronic inflammatory response?

A

lymphocytes

133
Q

Transudate vs. Exudate

A
  • Transudate = low protein content
  • Exudate = high protein content
134
Q

Common causes of transudates

A
  • Heart failure
  • Renal disease
  • Associated with high proportion of non-cellular fluid
135
Q

Common cause of exudates

A
  • Inflammation
136
Q

Types of exudates

A
  • non-cellular
  • cellular
  • mixed
137
Q

Example of non-cellular exudate

A
  • fibrinous exudate
138
Q

Types of cellular exudate

A
  • Purulent
  • Suppurative
  • Cellulitis/phlegmonous
139
Q

Key characteristic of purulent exudate

A
  • No tissue destruction
140
Q

Key characteristic of suppurative exudate

A
  • Tissue destruction by liquefactive necrosis
141
Q

Key characteristic of cellulitis

A
  • Movement of inflammatory fluid
  • Requires clinical diagnosis, cannot diagnose on the slides
142
Q

Septic shock

A
  • Systemic response to acute inflammation
143
Q

The triad that you see with septic shock

A
  • Disseminated intravascular coagulation
  • Hypoglycemia
  • Hypotension/heart failure
144
Q

Disseminated intravascular coagulation

A
  • Sign of acute inflammation
  • Cytokines induce expression of a protein called tissue factor, which is involved in coagulation. This results in blood clots (thrombi) in your vessels and death of the tissue.
  • If you use up all of this tissue factor protein during coagulation response, you don’t have enough leftover to clot effectively when you are actually bleeding. So a cut leads to bleeding excessively.
  • Paradoxical coagulation and bleeding is called “disseminated intravascular coagulation”
145
Q

Granulomatous Inflammation

A
  • A subtype of chronic inflammation
  • Main cells: macrophages
146
Q

Hallmark of granulomatous inflammation

A
  • macrophage mobs = granuloma
  • Giant cells = multinucleated fusion of macrophages
  • Lymphocytes surrounding the granuloma
147
Q

Types of granulomatous inflammation

A
  • Immune
    • ex: TB
  • Foreign body
    • ex: sutures
148
Q

Outcomes of Inflammation

A
  • Resolution
    • Injurious agent is removed
  • Healing by connective tissue replacement
    • Scarring
  • Chronic inflammation
149
Q

What must be true for complete resolution of inflammation to occur?

A
  • Injury must not cause permanent damage
  • Tissue must have regenerative capacity
150
Q

What must be true for scar formation to occur?

A
  • Tissue is not capable of regeneration
  • There is significant tissue destruction
  • There is abundant fibrinous exudate
151
Q

What are the hallmarks of scarring?

A
  • Removal of dead tissue by macrophages
  • Dead tissue replaced by granulation tissue
    • See proliferating fibroblasts
    • See blood vessels
152
Q

What process is going on if you see granulation tissue?

A
  • Healing
  • When there’s healing, we call it organization. Because the tissue will eventually organize into a scar.
  • Fibroblasts secrete collagen that will undergo restructuring to form a scar.
  • We call this granulation tissue “organizing exudate”
153
Q

what happens with too much granulation tissue?

A

–exuberant granulation tissue

154
Q

well-differentiated vs. poorly-differentiated

A
  • Well-differentiated means the tumor resembles normal cells/tissue
  • Poorly-differentiated means it’s hard to tell what tissue the tumor arose from
155
Q

Characteristic of benign tumors

A
  • Well-differentiated
  • circumscribed (clear borders)
156
Q

Characteristic of malignant tumors

A
  • METASTASIS
  • invasive
157
Q

Dysplasia

A
  • disordered growth
  • pre-cancerous
158
Q

Hallmarks of dysplasia

A
  • pleomorphism
  • nuclear abnormalities
    • High N-C ratio
    • Mitotic figures
159
Q

Desmoplasia

A
  • Stroma surrounds a malignant neoplasm
  • **Characteristic of malignancy
160
Q

What is the purpose of desmoplastic stroma?

A
  • Host response: wall off the bad tissue
  • Cancer: Recruit blood vessels to help it grow
161
Q

Barrett’s esophagus

A
  • Example of metaplasia (cells change from one type of epithelium to another in response to damage)
  • Example of the adeno-carcinoma sequence
    • Metaplasia turns to dysplasia turns to cancer
162
Q

Adenoma

A
  • Benign tumor of gland-forming epithelium
163
Q

carcinoma

A
  • Malignant tumor of the epithelium
164
Q

sarcoma

A

malignant tumor of non-epithelium (mesenchyme)

165
Q

adenocarcinoma

A
  • malignant tumor of gland-forming epithelium
166
Q

squamous cell carcinoma

A
  • malignant tumor of squamous epithelium (as opposed to gland-forming epithelium)
167
Q

polyp

A

tissue growing into any hollow organ.

Block 2 (5 decks)

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