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MS1 - Pathology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

list 4 ways cells can adapt to stress what describe what they are

A
  1. hypertrophy - increase in cell SIZE
  2. hyperplasia - increase in cell NUMBER
  3. atrophy - decrease in cell SIZE
  4. metaplasia - change in cell PHENOTYPE
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2
Q

list 2 biochemical pathways that can cause hypertrophy

A
  1. phosphoinositide 3-kinase/Akt pathway

2. signaling downstream of G protein couples receptors

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3
Q

list 2 ways hypertrophy can manifest

A
  1. increase entire CELL size

2. increase the size of ORGANELLES (can be induced by drugs and can lead to increased tolerance to them)

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4
Q

what is hyperplasia?

can it occur along side with hypertrophy?

A

an increase in the NUMBER of cells

sure can

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5
Q

list 2 types pf physiologic hyperplasia? when would each be used?

A
  1. hormonal - increases functional capacity of tissue when needed (puberty, pregnancy)
  2. compensatory - increases tissue mass after damage or resection (liver transplant)
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6
Q

what is pathologic hyperplasia usually caused by? give 2 examples of this condition.

A

caused by an excessive amount of hormones or growth factors

endometrial hyperplasia, benign prostatic hyperplasia

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7
Q

list 6 common causes of atrophy

A
  1. decreased workload
  2. loss of innervation
  3. diminished blood supply
  4. inadequate nutrition
  5. loss of endocrine stimulation
  6. prolonged tissue pressure
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8
Q

list 2 mechanisms for atrophy

A
  1. decreased protein synthesis

2. increased protein degradation (uniquitin-proteosome pathway)

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9
Q

what are lipofuscin granules (brown atrophy)

A

cellular debris in autophagic vacuoles that resist digestion in lysosomes. they persist as membrane-bound residual bodies

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10
Q

define metaplasia

A

a reversible change in which one differentiated cell type is replaced by a different cell type

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11
Q

list 3 examples of metaplasia

A
  1. conversion of pseudostratified ciliated columnar epithelium in the respiratory tract with squamous epithelium in chronic smokers (loss of mucociliary elevator)
  2. barrett esophagus: conversion of esophageal squamous epithelium with intestine-like columnar cells due to refluxed gastric acid
  3. myositis ossificans: bone formation in muscle
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12
Q

list 4 cellular morphologic alterations (due to injury) that are reversible (in sequence?)

A
  1. swelling of the cell and its organelles
  2. blebbing of the plasma membrane
  3. detachment of ribosomes from the ER
  4. clumping of nuclear chromatin
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13
Q

what are some signs that a tissue is experiencing cellular swelling?

A
  1. pallor, increased turgor and increase in weight of the organ (it can be difficult to detect at the cellular level under light microscopy)
  2. however, small, clear cytoplasmic vacuoles (pinched off ER) can sometime be seen
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14
Q

what are the causes of necrosis and apoptosis? how do they work?

A

necrosis: sever membrane damage (lysozyme enzymes leak out and digest the cell)
apoptosis: cell’s DNA or proteins are damaged beyond repair (nuclear dissolution and fragmentation of the cell without loss of membrane integrity)

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15
Q

list the order of irreversible cell changes over the duration of an injury

A

1st. biochemical alterations (leads to cell death)
2nd. ultrastructural changes of cell (blebbing, mito. changes, dilation of ER, nuclear alterations)
3rd. light microscopy changes
4th. gross morphological changes

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16
Q

necrotic tissue can display increased eosinophilia in a H & E stain. why?

A

because the necrotic cells lose most of their cytoplasmic RNA (which binds hematoxylin [blue]) but has increased denatured cytoplasmic proteins (which binds eosin [red])

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17
Q

define karyolysis, pyknosis and karyorrhexis and hoe they appear under microscopy.

A

karyolysis: loss of DNA due to degradation by endonucleases (the basophilic [blue] nucleus slowly fades away)
pyknosis: condensation/shrinkage of the nucleus (the basophilia of the nucleus increases as it shrinks in the cell)
karyorrhexis: the nucleus undergoes fragmentation (nucleus breaks apart then completely disappears around 1 to 2 days)

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18
Q

list 6 patterns of tissue necrosis

A
  1. coagulative
  2. liquefactive
  3. gangrenous
  4. caseous
  5. fat
  6. fibrinoid
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19
Q

list 3 characteristics of coagulative necrosis. what is a common cause of this?

A
  1. the tissue will mostly maintain its architecture (you can identify which tissue is damaged under microscopy)
  2. the tissue will be very firm
  3. it will consist mostly of anucleate, eosinophilic [red] cells

most commonly caused by ischemia

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20
Q

list 2 characteristics of liquefactive necrosis. what are some common causes? where does it most commonly occur?

A
  1. its characterized by the digestion of dead cells
  2. it’s typically creamy and yellow (mixture of dead leukocytes and purulent matter)

commonly caused by bacterial infections and sometimes fungal

most common in CNS cells

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21
Q

what other types of necrosis are commonly seen along with gangrenous necrosis. what tissues does gangrenous necrosis typically affect.

A
  1. coagulative necrosis due to the loss of blood supply
  2. liquefactive necrosis due to bacterial infection in affected tissues (wet gangrene)

it typically involves multiple tissues at the same time

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22
Q

what does a caseous necrotic lesion look like micro and macroscopically

what condition is it cormally associated with?

A

microscopically: amorphous granular debris ( fragments and lysed cells) enclosed in a distinctive inflammatory border (higher concentration of WBCs around an area with few nuclei visible)
macroscopically: white, cheeselike and crumbly

normally associated with the foci of a TB infection

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23
Q

what is fat necrosis?

what is a cause of it?

what does it look like microscopically? macroscopically?

A

focal area of fat destruction

release of activated pancreatic lipase into the pancreatic substance and/or paritoneal cavity

microscopically: shadowy outlines of nectoric fat cells with basophilic [blue] calcium deposits. almost looks like brown fat mixed in with white fat
macroscopically: white, chalky, rice-like granules

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24
Q

what is the cause of fibrinoid necrosis?

what do they look like microscopically?

A

the deposition of immune complexes and fibrin in blood vessles

microscopically: they appear as an amorphous, (acellular?) band around a blood vessel

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25
Q

what % of ATP depletion can a cell handle before some of its critical functions are affected?

A

5 to 10%

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26
Q

depletion of ATP in the cell can cause a loss in the activity of the Na efflux pump. how would this effect the cell (in excessive amounts)?

A

it would cause in increase of intracellular sodium, which would cause an influx of Ca and an efflux of K resulting in cellular (and ER) swelling, loss of microvilli and membrane blebbing

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27
Q

depletion of ATP in the cell can cause an increase on anaerobic glycolysis. how would this effect the cell (in excessive amounts)?

A

it would cause a decrease in glycogen, increase in lactic acid (and therefore a decrease in pH) and ultimately result in clumping of nuclear chromatin

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28
Q

depletion of ATP in the cell can cause ribosomes in a cell to detach from the ER. how would this effect the cell (in excessive amounts)?

A

it would cause a decrease in protein synthesis which would lead to lipid deposition

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29
Q

list 3 things that can damage a mitochondria

A
  1. increased cytosolic Ca
  2. reactive oxygen species
  3. oxygen deprivation
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30
Q

what is the consequence of the formation of a mitochondrial high-conductance pore

what does it span?

A

loss of mito. membrane potential which leads to a failure in oxidative phosphorylation, then depletion of ATP, then necrosis

spans both the membranes and connects the matrix to the cytosol

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31
Q

where would you find cytochrome C and caspaces in mitochondria? how do they relate to apoptosis?

A

they are found in between the two membrane layers. they can initiate apoptosis via increasing the permeability outer membrane

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32
Q

where is Ca typically found in the cell? what is the result of it leaving these areas?

A

sequestered in the ER and mitochondria

an increase in cytosolic Ca can activate numerous enzymes (proteases, endonucleases, ATPases) this inducing apoptosis via direct activation of mito. caspases

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33
Q

list 3 pathologic reactions caused by free radicles

A
  1. lipid peroxidation (unsaturated double bonds of lipids attacked)
  2. oxidative modification of proteins
  3. lesions in DNA
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34
Q

differentiate hypoxia and ischemia

A

hypoxia is reduced oxygen availability whereas ischemia is a decrease in oxygen AND nutrients due to reduced blood flow

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35
Q

which type of injury is more sever, ischemia or hypoxia?

A

ischemia because it prevents both aerobic energy production (due to reduced oxygen availability) AND anaerobic energy production (due to reduced glycotic substances getting to the tissue)

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36
Q

list the sequence of events of ischemic cell injury (4 steps)

A
  1. oxygen tension within the cell decreases (therefore depletion of energy and everything associated with that)
  2. influx of Ca
  3. progressive loss of glycogen
  4. decreased protein synthesis
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37
Q

what is one approach for reducing the damage of ischemic cell injury? what tissue is this method most useful with?

A

induce transient hypothermia (core body temp down to 92 degrees) thus producing a reduced metabolic demand on the stressed cells, decreased swelling, suppressed the formation of free radicles and inhibition the host inflammatory response

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38
Q

what is a ischemia-reperfusion injury?

what is the proposed mechanism for this?

A

the loss of cells in addition to those that were irreversibly damaged from ischemia due to reperfusion of blood to the area.

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39
Q

list 4 proposed mechanism for ischemia-reperfusion injury

A
  1. overproduction of free radicles (more ROS & RNS made and decreased activity of antioxidants)
  2. influx of Ca into cells
  3. production of inflammatory cytokines to tissue
  4. activation of the complement system in tissue
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40
Q

for the following cell death types, tell whether they cause acute inflammation:

  1. necrosis
  2. apoptosis
A
  1. necrosis - yup

2. apoptosis - nope

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41
Q

name 4 ways cells are lost due to pathologic apoptosis

A
  1. excessive DNA damage
  2. accumulation of misfolded proteins
    3 viral (all intracellular pathogens?) infection
  3. atrophy of parenchymal cells (functional cells of an organ) after duct obstruction [ex. pancreas, parotid gland, kidney]
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42
Q

differentiate the morphology of a apoptotic cell vs. a necrotic cell

A

Apoptotic: cell (and organelles) shrinks, chromatin condenses (nucleus may also break apart), blebbing off of non-leaking, dense apoptic bodies.

necrotic: initial swelling, loss of plasma (and organelle) membrane integrity, contents leak out to neighboring cells

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43
Q

what are the two groups of caspases? what is the general function of these groups? which specific caspases fall into these groups?

A
  1. initiators (caspase-8 &9) - caspaces become catalytically active
  2. executioners (caspase-3 & 6) - caspases trigger the degradation of critical cellular components
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44
Q

what are the two mechanisms of apoptosis and what are they associated with? what caspases do they activate?

A
  1. intrinsic (increased permeability of mitochondria) - activation of caspase-9
  2. extrinsic (death receptor-initiated)
    - activation of caspase-8 & 10
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45
Q

where is phosphatidylserine usually found? how does it relate to apoptosis?

A

it’s normally found in the inner leaflet of the plasma membrane. it’s flipped to the outer leaflet in apoptic cells which allows macrophages to recognize and therefore phagocytize it

46
Q

what is the sequence of events of autophagy? when does this occure?

A

1st. cytoplasm is sequestered in an autophagic vacuole.
2nd. the vacuole fuses with a lysosome to form an autophagosome

occurs when the cell is starving

47
Q

list 4 situations leading to intracellular accumulation

A
  1. [removal problem] normal endogenous substance is produced at normal (or increased) rate but metabolism is not fast enough to eliminate it
  2. [production problem] abnormal endogenous substance (misfolded protein) accumulated because on an inability to transport and/or degrade these substances
  3. [inherited metabolic problem] normal endogenous substance accumulated because of a defect in enzymes needed for metabolism of the substance
  4. [EXOgenous problem] abnormal exogenous substance accumulated because cell can neither degrade nor transport the substance
48
Q

what is steatosis? what organs does this usually occur in (4)?

A

abnormal accumulation of triglycerides within parenchymal cells

liver, heart, muscle and kidney

49
Q

list 3 substances that appear yellow under microscope (H & E stain?)

A
  1. necrotic tissue (liquefactive?)
  2. granulomas
  3. fat
50
Q

what is a xanthoma?

A

intracellular accumulations of cholesterol within macrophages (high cholesterol levels). appear as yellow bumps around the eyes (also in tendons)

51
Q

what is cholesterolosis?

A

focal accumulation of cholesterol filled macrophages in the lamina propria of the gallbladder. the gall bladder will look like a strawberry due to its reddish appearance and the yellow (cholesterol) spots

52
Q

what is niemann-pick (type C) disease?

A

a lysosomal storage disease caused by a mutation in a cholesterol transport enzyme. causes accumulation of cholesterol in multiple tissues

53
Q

how does intracellular accumulation of protein appear under microscopy?

A

rounded, eosinophilic [red] droplets/vacuoles/aggregations in the cytoplasm

54
Q

how would a hyaline change appear under microscopy?

A

homogeneous, glassy and pink

55
Q

what is lipofuscin? where does it look like? where is it usually found? what does it indicate?

A

an endogenous insoluble pigment (AKA wear-and-tear pigment).

its a collection of fine yellow-brown granules in the cytoplasm.

its often found perinuclear and is most prominent in the liver and heart

it’s indicative of free radical injury and lipid peroxidation, although it is not harmful itself.

56
Q

what is the only endogenous brown-black pigment?

A

melanin

57
Q

what is hemosiderin? what is its function? in which cell type would you normally find this?

A

a golden yellow/brown pigment.

it serves as one of the major storage forms of iron.

it’s normally found in mononuclear phagocytes (monocytes and macrophages) of the bone marrow, spleen and liver

58
Q

in what substance do you find the highest concentration of bilirubin?

A

in the bile (its a major pigment of the bile)

P.S. it does NOT contain iron

59
Q

what are the two types of pathologic calcification? where would these normally deposit? how do these relate to calcium metabolism?

A
  1. dystrophic calcification - calcification of dying/necrotic tissue (coagulative, caseous or liquefactive). no apparent problem with Ca metabolism
  2. metastatic calcification - calcium deposits in normal/healthy tissue. likely a problem with Ca metabolism
60
Q

what is extravasation?

A

the movement (leaking out) of WBCs from capillaries to the inflamed tissue (towards a chemotactic stimuli)

61
Q

what type of WBC predominated in the early stages of inflammation (the early first 6-24 hours)?

what about the late stages (24-48 hours)?

what is the exception to this?

A

early: neutrophills (with acute inflammation think neurotphils)
late: monocytes (they become the dominant population of WBC in chronic inflammation)
exception: Pseudomonas bacteria continually recruits neutrophills for several days

62
Q

what is the sequence of events of the immune system to an infection (3)?

A
  1. edema (of capillaries?)
  2. neutrophil recruitment
  3. monocyte/macrophage recruitment
63
Q

what are the 3 steps (in order) of phagocytosis?

A
  1. recognition and attachment of particle to be ingested
  2. engulfment (with pseudopods) and formation of a phagocytic vacuole
  3. killing / digestion of ingested material (phagosome fuses with lysosome)
64
Q

what is chediak-higashi syndrome? what does it cause (5)?

A

it’s an autosomal recessive condition where there is a defect in the fusion of cellular vesicles (ex. fusion of phagosomes and lysosomes)

  • increased suceptibility to infection (can’t effictively kill bacteria)
  • albinism (melanocytes can’t release melanin)
  • nervous system problems (trouble releasing neurotransmitters)
  • platelet problems
  • leukocyte abdormalities (NK cells can’t degranulate)
65
Q

what is chronic granulomatous disease?

A

a genetic defect where phagocytes can’t make ROS used to kill bacteria. the result is macrophages forming granulomas around the bacteria (because initial neutrophil defense in inadequate)

66
Q

how would a problem with the bone marrow affect the immune system?

A

it would result in a reduced amount of leukocytes

67
Q

what are the two sources of inflammation mediators?

A
  1. cells (in intracellular granules)

2. plasma proteins (produced mainly in liver, inactive precursors)

68
Q

list 2 major vasoactive amines. what cells make them?

A
  1. histamine (mast cells granules, basophils, platelets)
  2. serotonin (platelets, some neuroendocrine cells in GI)

(these are some of the first mediators released in the inflammatory response)

69
Q

list 2 functions of histamine

A
  1. dilation of arterioles
  2. increased permeability of venules (considered the principle mediator of the immediate transient phase of increased vascular permiability)
70
Q

what vasoactive mediator is stimulated when platelets aggregate?

A

serotonin

71
Q

what class of molecules is arachidonic acid used as a precursor for? list 3 specifics.

A

eicosinoids

  1. prostiglandins
  2. leukotrienes
  3. lipoxins
72
Q

list 2 enzyme classes that make eicosinoids. which class makes which?

A
  1. cyclooxygenases (prostiglandins)

2. lipoxygenases (leukotrienes, lipoxins)

73
Q

of the following cyclooxygenase enzymes, list which is constituativelt active and which is inducible.

  1. COX-1
  2. COX-2
A
  1. COX-1 = constitutive

2. COX-2 = inducible

74
Q

list the 5 most important prostiglandins in inflammation. what do they do?

A
  1. PGE2 - hyperalgesic (increased pain sensitivity)
  2. PGD2 - vasodialation, increased permeability of post-capillary venules, chemoattractant for neutrophils
  3. PGF2(alpha) - smooth muscle contraction of uterus, bronchi and arterioles
  4. PGI2 [prostacyclin] - vasodialator, inhibits platelet aggragation, amplifies other mediators
  5. TxA2 [thromboxane]
75
Q

list 3 lipoxygenases and what they do.

A
  1. 5-lipoxygenase = converts AA to 5-hydroxyeicosatatraenoic acid
  2. LTB4 = neutrophil attractant/activator, increases adhesion WBC adhesion to venule walls, generation of ROS
  3. LTC4/LTD4/LTE3 = intense vasoconstriction, bronchospasm and increased vascular permiability
76
Q

list 2 roles of lipoxins

A
  1. inhibits leukocyte recruitment
  2. inhibits neutrophil chemotaxis and adhesion to endothelium

basically they’re anti-inflammatory (they may be negative regulators to leukotrienes)

77
Q

what does platelet-actiating factor (PAF) do when active? what about at very low concentrations?

A

vasoconstriction and broncoconstriction

at low [ ] causes vasodilation and increased venule permeability

78
Q

what enzyme do phagocytes use to create ROSs (specifically superoxide)?

A

NADPH oxidase

79
Q

list 2 functions of NO

A
  1. promotes vasodialation (relaxes vascular smooth muscle)

2. inhibits the cellular component of the inflammatory response

80
Q

name 2 major cytokines secreted by activated macrophages that mediate inflammation

A
  1. TNF (tumor necrosis factor)

2. IL-1

81
Q

what are the systemic effects (5) of TNF and IL-1?

A

systemic:

  • fever
  • leukocytosis (WBC count above average)
  • increased acute-phase proteins
  • decreased appetite
  • increased sleepiness
82
Q

what are the local effects of TNF and IL-1 on the vascular epithelium (3)? the leukocytes (2)? fibroblasts (2)?

A

Vascular epithelium:

  • increased expression of leukocyte adhesion molecules
  • further production of IL-1 and chemokines
  • increased procoagulative activity (and decreased anticoagulative)

leukocytes:

  • activation
  • production of cytokines

fibroblasts:

  • proliferation (for healing wounds)
  • increased collagen synthesis
83
Q

what is cachexia? hoe does it relate to TNF and IL-1?

A

AKA “wasting syndrome”. its characterized by loss of body mass that can not be corrected nutritionally.

one of the effects of TNF and IL-1 is regulation of energy balance by promoting lipid and protein mobilization and suppressing appetite. in cases where these are expressed for a long sustained time, then cachexia can occur

84
Q

what are the 2 primary functions of chemokines?

A
  1. they act mainly as chemoattractants for specific types of leukocytes
  2. they also control the normal migration of cells through various tissues
85
Q

what are the 4 major groups of chemokines? what are they grouped according to?

A
  1. C-X-C chemokines (alpha)
  2. C-C (beta)
  3. C (gamma)
  4. CX3C

they are grouped according to the conserved cysteine (C) residue in the protien

86
Q

what cells do the following chemokines work on?

  1. C-X-C
  2. C-C
  3. C
  4. CX3C
A
  1. C-X-C: activates and chemotaxis of neutrophils
  2. C-C : chemotaxix of monocytes, eosinophils and basophils but NOT neutrophils
  3. C: specific to lymphocytes
  4. CX3C - oddball, don’t worry about this one
87
Q

what types of granules would you find in a neutrophil?

A
  1. specific (secondary)

2. azurophil (primary)

88
Q

list the 3 plasma protein systems that mediate inflammation

A
  1. complement
  2. kinin
  3. clotting systems
89
Q

what is the most critical step in complement activation?

A

proteolysis of C3

90
Q

what are the anaphylatoxins? what do they do (3)?

A

they are the small cleavage products of complement proteins (C3a, C5a and somewhat C4a)

  • they stimulate the release of histamine from mast cells
  • increase vascular permeability and vasodialation
  • work as chemoattractants
91
Q

list 2 function of C5a

A
  1. most powerful chemotactis for neutrophils, monocytes, enosinophils and basophils
  2. activates the lipoxygenase pathway of AA metabolism in neutrophils and monocytes
92
Q

that are the 3 stages/function of complement?

A
  1. phagocytosis/opsinization - C3b binds bactrerial cell walls and act as receptors for opsinization via phagocytes
  2. cell lysis/MAC - pokes holes in the cell wall leading to bacterial destruction
  3. anaphlatoxins - C3a and C5a recruit WBCs
93
Q

what is the intrinsic clotting pathway activated by?

A

hageman factor (factor XII) - its normally circulating in the plasma in its inactive form

94
Q

starting with the hageman factor, what is the cascade that leads to activation of bradykinin?

A
  • hageman factor (factor XII) gets activated
  • factor XII converts prekallikrein into its active proteolytic form (killikrein)
  • killikrein cleaves kininogen to produce bradykinin
95
Q

what does bradykinin do? what degrades it?

A
  • increases vascular permeability
  • contraction of smooth muscle
  • pain when injected into skin
  • dilation of blood vessels

its very short lived and is inactivated by kininase

96
Q

list 2 molecules that get cleaved by kallikrein and what they form

A
  1. kininogen to make bradykinin
  2. plasminogen to make plasmin (which is part of the fibrinolytic system, it cleaves fibrin to prevent clots for becoming problematic.)
97
Q

what is the purpose of the fibrinolytic system? whare are its 2 main proteins?

A

its function is the cleave fibrin (to soluabilize it) thus prevent the forming fibrin clot form becoming pronlematic.

  1. plasminogen (cleaves fibrin)
  2. kallikrein (cleaves plasminogen and kininogen [kinin cascade])
98
Q

what 2 functions does factor XII have?

A
  1. activates the clotting cascade leading to the formation of thrombin (which cleaves fibrinogen to fibrin)
  2. cleaves prekallikrein to kallikrein (which cleaves kininogen to bradykinin [kinin cascade] and plasminogen to plasmin [fibrinolytic system] and cleaves C5 to C5a [complement])
99
Q

what does thrombin do?

A

it part of the clotting cascade. it cleaves fibrinogen to fibrin

100
Q

what does kallikrien do (3)?

A
  1. cleaves kininogen to bradykinin [kinin cascade]
  2. plasminogen to plasmin [fibrinolytic system]
  3. cleaves C5 to C5a [complement]
101
Q

what does plasmin do (2)?

A
  1. is cleaves fibrin (to make it more soluble) thus forming fibrin split products
  2. it cleaves C3 to C3a [complement cascade]
102
Q

list 4 systems activated by the hageman factor and briefly what they do

A
  1. kinin system - makes vasoactive products
  2. clotting system - formation of thrombin (and clots)
  3. fibrinolytic system - makes plasmin (degraded fibrin to make fibrinopeptides)
  4. complement system - a bunch of stuff
103
Q

list 3 morphological hallmarks of acute inflammation

A
  1. dilation of small blood vessels
  2. slowing of blood flow
  3. accumulation of leukocytes and fluids at site
104
Q

what is serous inflammation? what cell types cause it? give an example of it.

A

inflammation marked by the outpouring of a thin fluid (serous)

it comes from mesothelial cells (peritoneal, pleural, pericardial cavities)

skin blister

105
Q

what kind of fluids can effuse out in serous inflammation?

A
  1. serous (clear)
  2. blood
  3. kylus (milky white)
106
Q

what characteristic are needed for firbous inflammation to occur?

where would you normally find this type of inflammation?

A

the vasculature must have large leakages allowing big proteins to leak out and there must be a procoagulative stimuli nearby (like cancer)

most commonly found lining the body cavities (meninges, pericardium and pleura).

107
Q

what does fibrous inflammation look like histologically

A

an eosinophilic meshwork of threads OR an amorphous (no cells) coagulum

108
Q

what happens if fibrinous inflammation is not cleared up?

A

if the fibrin is not removed it will stimulate the ingrowth of fibroblasts and blood vessels resulting in scarring.

the fibrinous exudate gets converted to scar tissue (organization)

109
Q

what is the result of scar tissue formation via fibrinous inflammation in the pericardial sac

A

it forms opaque fibrous thickenings of the pericardium and epicardium.

ultimately the pericardial space gets obliterated.

110
Q

large amounts of neutrophils, liquifactive necrosis and edema fluid is characteristic of what type of inflammation?

what causes this?

A

suppurative inflammation - (lots of yellow purulent matter)

pyogenic bacteria do

111
Q

what causes ulcers?

A

the sloughing (shedding) of inflamed necrotic tissue

MS1 - Pathology (2 decks)

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