Pathology of Inflammation Flashcards

1
Q

serous inflammation

A
  • serous exudate: fluid (result of increased vascular permeability) that is watery and not infectious - this can be mucous, drippy nose, etc.
  • viral infections usually
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2
Q

fibrinous inflammation

A
  • fibrinous exudate: this is often bacterial (ex: strep throat)
  • because the holes in the vasculature are large enough for fibrin, this is often more severe inflammation. this fibrin can accumulate, causing issues like fibrinous pericarditis
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3
Q

purulent inflammation

A
  • this is essentially pus that is caused by pus-forming bacteria (strep, staph)
  • also has dead neutrophils (killed by bacteria) and tissue debris
  • can form in respiratory tract
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4
Q

ulcerative inflammation

A
  • localized lesion with pus/inflammation on the skin or an internal mucous surface
  • this results in localized necrosis of tissue - think about how this would happen!
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5
Q

abscess

A
  • localized purulent inflammation
  • an older abscess becomes surrounded by a capsule with granulation tissue
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6
Q

granulation tissue

A
  • connective tissue that results from tissue damage, or can form the capsule around an abscess
  • contains macrophages, myofibroblasts (specialized fibroblasts), fibroblasts (replicate and form CT matrix), and angioblasts (create blood vessels to area)
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7
Q

empyema

A
  • an accumulation of pus in a preformed cavity
  • think of as an abscess in a preformed cavity like the thoracic cavity, gallbladder, etc.?
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8
Q

granuloma

A
  • mass of chronic immune cells
  • composed of epithelioid cells (modified macrophages), lymphocytes, and multi-nucleated giant cells (form when macrophages fuse together)
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9
Q

are granulomas and granulation tissue related?

A
  • no, these have distinct functions
  • a granuloma is a mass of chronic immune cells, which can cause inflammation due to chronic action of these cels
  • granulation tissue is a response to tissue healing that results in a scar if all goes properly and a keloid if it contains type III collagen
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10
Q

how are granulomas and phagocytosis related?

A
  • defects in phagocytosis can result in chronic granulomatous disease
  • this is because a granuloma is a mass of chronic immune cells, and if these immune cells are not properly phagocytosing the pathogen that they want to get rid of, they will just stick around? and cause inflammation by releasing cytokines, etc.
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11
Q

chronic granulomatous disease

A
  • usually x-linked recessive, but can be autosomal recessive
  • caused by mutations in proteins of NADPH oxidase system
  • basically, phagocytic cells cannot make free radicals, so consequently they do not make hydrogen peroxide. this is necessary for them to actually break down the things that they engulf
  • catalase will destroy the little hydrogen peroxide that is made, so there really will be no hydrogen peroxide or free radical activity
  • macrophages will fuse together to form multinucleated giant cells
  • this manifests as severe infections in lungs, skin, visceral organs, and bones because phagocytic cells cannot properly dispose of the pathogen
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12
Q

sarcoidosis

A
  • idiopathic (unknown cause) inflammatory disease
  • characterized by discrete granulomas in multiple organ systems
  • this usually does not result from microorganisms
  • usually involves the lung
  • individuals like fire fighters exposed to particulates may be at increased risk - maybe particulates are the cause of the inflammation/granulomas?
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13
Q

describe the pathophysiology of sepsis

A
  • start after an infectious episode: LPS (endotoxin) released from Gram neg bacteria or exotoxin released from Gram pos bacteria
  • damage to endothelium, which increases TF and PAI-1 - these are procoagulants, causing microvascular occlusions
  • cytokines and free radicals are produced from endothelium, neutrophils, and monocytes (all happening in the bloodstream = bad)
  • free radicals also cause vascular occlusion
  • monocytes produce their three inflammatory cytokines, which will act on the liver, which will produce complement, which will be involved in chemotaxis, further contributing to vascular instability
  • overall, microvascular occlusion and vascular instability lead to coagulopathy (coagulation throughout circulatory system), fever, vasodilation, and capillary leaking
  • these lead to sepsis and multiple organ failure by creating septic shock!!
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14
Q

define shock

A
  • hemodynamic disturbance characterized by systemic hypoperfusion
  • this = inadequate oxygen supply to vital organs
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15
Q

describe ways that systemic hypoperfusion (shock) can occur

A
  • cardiogenic shock: reduced cardiac output
  • hypovolemic shock: massive blood loss
  • distributive shock: massive dilation of blood vessels (this is typically seen in septic shock)
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16
Q

what happens to the heart in septic shock?

A
  • initially, cardiac output will increase to try to raise blood pressure
  • as it progresses, reduced return of blood to the heart = reduced preload = reduced cardiac output = hypotension = septic shock = multiple organ failure
17
Q

septic shock in the respiratory system

A
  • tachypnea: rapid breathing
  • dyspnea: difficulty breathing
  • ARDS: respiratory distress
18
Q

septic shock in CNS

A
  • agitation
  • apathy
  • coma
19
Q

septic shock in cardiovascular system

A
  • tachycardia: rapid heart rate
  • hypotension
  • hypoxemia
20
Q

septic shock in renal system

A
  • oliguria: low urine output
  • azotemia: too much nitrogen and other waste products in the blood
21
Q

septic shock in liver and GI system

A
  • ileus: intestines not moving food through properly
  • mucosal hemorrhage
  • abnormal liver function
  • jaundice
22
Q

septic shock in hematopoetic system

A
  • disseminated intravascular coagulation: coagulation within the blood vessels in an attempt to fix all the broken spots
  • bleeding from vessel puncture sites