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Step1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Apoptosis

A

Programmed cell death
ATP required
Intrinsic and extrinsic pathways: activation of cytosolic caspases that mediate cellular breakdown

No significant inflammation (unlike necrosis)
Characterized by sequentially eosinophilic cytoplasm, cell shrinkage, nuclear shrinkage (pyknosis), membrane blabbing, nuclear fragmentation (karyorrhexis), and formation of apoptotic bodies, which are then phagocytosed

DNA laddering is a sensitive indicator of apoptosis with endonucleases cleavage yielding 180 bp fragments

Radiation therapy causes apoptosis of tumors and surrounding tissue via free radical formation and dsDNA breakage

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2
Q

Intrinsic pathway

A

Involved in tissue remodeling in embroygenesis

Occurs when a regulating factor is withdrawn from a proliferating cell population (IL2 and leukocytes) or after exposure to injurious stimuli (radiation, hypoxia)

Changes in proportions of anti- and pro-apoptotic factors lead to increased mitochondrial permeability and cytochrome release.

BAX and BAK are pro apoptotic proteins while Bcl-2 is anti-apoptotic

Bcl-2 prevents cytochrome c release by binding to inhibiting Apaf1, which normally induces the activation of caspases. Thus Bcl-2 over expression leads to decreased caspase activation and tumor genesis

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3
Q

Extrinsic pathway

A

2 pathways:

  1. Ligand receptor interactions (Fas ligand binding to Fas)

After Fas cross links w/ FasL, multiple Fas molecules coalesce, forming a binding site for Fas associated protein with death domain (FADD), which intern binds inactive caspases and activate them

Necessary in thymic medullary negative selection. Mutations in Fas increase the numbers of circulating self-reacting lymphocytes due to failure of negative selection

  1. Immune cell (Tc release of perforin and granzyme B)
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4
Q

Necrosis

A

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury

Characterized by intracellular component leak and inflammation

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5
Q

Coagulative necrosis

A

Occurs in tissues supplied by end arteries (liver, kidney)

Proteins denature first followed by enzymatic degradation

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6
Q

Liquefactive necrosis

A

Occurs in CNS due to high fat content (brain, brain bacterial abscess)

Enzymatic degradation occurs first due to release of lysosomal enzymes

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7
Q

Caseous necrosis

A

Occurs in TB and systemic fungi infections

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8
Q

Fatty necrosis

A

Occurs either enzymatic (pancreatitis) or nonenzymatic (breast trauma), results in calcium deposits that appear dark blue on staining

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9
Q

Fibrinoid necrosis

A

Occurs in vasculides (HSP, Churg-Strauss), stains amorphous and pink on H&E stain

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10
Q

Gangrenous

A

Dry (ischemic coagulative) and wet (infection), common in limbs and GI tract

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11
Q

Reversible cell injury

A

Reverse w/ O2

Causes:
ATP depletion

Cellular/mitochondrial swelling due to decreased activity of Na/K pump w ATP depletion

Ribosomal detachment due to decreased protein synthesis

Nuclear chromatin clumping

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12
Q

Irreversible cell injury

A

Causes:
Nuclear pyknosis, karyorrhexis, karyolysis

Plasma membrane damage

Lysosomal rupture

Mitochondrial permeability

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13
Q

Susceptible ares of ischemia

A

Brain: ACA/MCA/PCA boundary areas (watershed)

Heart: subendocardium

Kidney: straight segment of proximal tubule

Liver: area around central vein

Colon: splenic flexure, rectum (watershed)

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14
Q

Watershed areas

A

Regions that receive dual blood supply from most distal branches of 2 large arteries, which protect these areas from single-vessel focal blockage but make them vulnerable to ischemia during systemic hypoprofusion

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15
Q

Red infarct

A

Occur in tissues w/ multiple blood supplies such as liver, lungs, and intestine

Often 2ndary to repression injury, which is due to damage by free radicals

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16
Q

Pale infarct

A

Occur in solid tissue with a single blood supple, such as heart, kidney, and spleen

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17
Q

Atrophy

A

Reduction in size and/or number of cells

Causes:
Decreased endogenous hormones (post menopausal ovaries)
Increased exogenous hormones (steroids)
Decreased innervation (motor neuron damage)
Decreased blood flow/nutrients
Decreased metabolic demand (prolonged hospitalization)
Occlusion of secretory ducts (CF)

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18
Q

Inflammation

A

Characterized by redness, pain, heat, swelling, and loss of function

Vascular component: increased vascular permeability, vasodilation, endothelial injury

Cellular component: neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release

19
Q

Acute inflammation

A

Mediated by neutrophil, eosinophil, and antibody

Rapid onset, lasting minutes to days

Outcomes include complete resolution, abscess formation, or progression to chronic inflammation

20
Q

Chronic inflammation

A

Mediated by mononuclear cell and fibroblasts

Persistant destruction and repair

Associated w/ blood vessel proliferation and fibrosis

Outcomes include scarring and amyloidosis

21
Q

Chromatolysis

A

Following axonal injury in neurons

Round cellular swelling
Displacement of nucleus to the periphery
Dispersion of Nissl bodies (RER) throughout cytoplasm

Changes reflect increase protein synthesis in effort to repair the damaged axon

22
Q

Dystrophic calcification

A

Calcium deposition in tissues 2ndary to necrosis

Tends to be localized

Seen in TB (lungs and pericardium), liquefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi

Is not directly associated w/ hypercalcemia

23
Q

Metastatic calcification

A

Widespread deposition of calcium in normal tissue 2ndary to hypercalcemia (primary hyperparathyroidism) or high calcium-phosphate product (chronic renal failure)

Calcium deposits predominantly in interstitial tissue of kidney, lungs, and gastric mucosa (these tissue lose acid quickly and high pH favors calcium deposition)

24
Q

Leukocyte extravasation

A

Primary occurs at post capillary venues

  1. Margination and rolling: mediated by selectin and Sialyl-Lewis (carbohydrate involved in cell-cell recognition)
  2. Tight binding: mediated by ICAM-1 and LEA-1 (integrin)
  3. Diapedesis: leukocyte travels between endothelial cells and exits blood vessel, mediated by PECAM-1
  4. Migration: leukocyte travels through interstitial to site of injury or infection guided by chemotactic agents such as IL8 and LTB4o
25
Q

Free radical injury

A

Free radicals damage cells via membrane lipid per oxidation, protein modification, and DNA breakage

Initiated via radiation exposure, metabolism of drugs (phase I), redox reaction, leukocyte oxidative burst

Free radicals can be removed by enzymes (catalase, glutathione peroxidase), spontaneous decay, or antioxidants (vitamin A, C, E)

Pathologies of free radical injury: 
Retinopathy of prematurity
Bronchopulmonary dysplasia
Acetaminophen overdose
Iron overload
Reperfusion injury
26
Q

Inhalation injury

A

Most common pulmonary complications after exposure to fire

Inhalation of products of combustion leads to chemical tracheobronchitis, edema, and pneumonia

27
Q

Hypertrophic scars

A

Increased collagen synthesis

Parallel collagen alignment

Scarring confined to borders of original wound

Infrequently recur following resection

28
Q

Keloid scars

A

Highly elevated collagen synthesis

Disorganized collagen alignment

Scarring extends beyond borders of original wound

Frequently recur following resection

More common in AA

29
Q

PDGF (platelet derived)

A

Secreted by activated platelets and macrophages

Induces vascular remodeling and smooth muscle cell migration

Stimulates fibroblast growth for collagen synthesis

30
Q

FGF (fibroblast)

A

Stimulates all aspects angiogenesis

31
Q

EGF (epidermal)

A

Stimulates cell growth via tyrosine kinases

32
Q

TGFbeta

A

Angiogenesis, fibrosis, cell cycle arrest

33
Q

Metalloproteinases

A

Tissue remodeling

34
Q

Inflammatory phase of wound healing

A

Immediate

Mediated by platelets, neutrophils, and macrophages

Clot formation, increased vessel permeability and neutrophil migration into tissue

Macrophages clear debris 2 days later

35
Q

Proliferative phase of wound healing

A

2-3 days after wound

Mediated by fibroblasts, myofibroblasts, endothelial cells, macrophages

Deposition of granulation tissue and collage, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction

36
Q

Remodeling phase of wound healing

A

1 week after wound

Mediated by fibroblasts

Type III collagen replaced by type 1 collagen
Increases tensile strength of tissue (70-80% tensile strength returns at 3 months, little after)

37
Q

Granulomatous diseases

A

Th1 cells secrete IFNgamma, activating macrophages

TNFalpha from macrophages induce and maintain granuloma formation

Anti-TNF drugs can, as a side effect, cause sequestering granulomas to breakdown, leading to disseminated disease

Always test for latent TB before starting anti-TNF therapy

Examples: Churg-Strauss, TB, sarcoidosis, Wegner, fungal infections

38
Q

Exudate

A

Thick, cellular, protein rich, specific gravity > 1.020

2ndary to lymphatic obstruction, inflammation/infection, malignancy

39
Q

Transudate

A

Thin, hypocellular, protein poor, specific gravity < 1.020

2ndary to increased hydrostatic pressure (CHF), decreased oncotic pressure (cirrhosis), or sodium retention

40
Q

Erythrocyte sedimentation rate

A

Products of inflammation coat RBC and cause aggregation, causing RBCs to fall at faster rate

Increased ESR: anemias, infection, inflammation, cancer, autoimmune disorders

Decreased ESR: sickle cell (altered shape), polycythemia (RBCS “dilute” aggregation), CHF

41
Q

Iron poisoning

A

Leading cause of fatality from toxicologic agents in children

Causes cell death 2ndary to per oxidation of membrane lipids

Acute: nausea, vomiting, gastric bleeding, lethargy
Chronic: metabolic acidosis, scarring leading to GI obstruction

Treatment: chelation (deferasirox) and dialysis

42
Q

Amyloidosis

A

Abnormal aggregation of proteins into beta-pleated sheet structures leading to cellular damage and apoptosis

Stain w/ congo-red to show deposits

AL (primary): due to deposition of light chains, associated with plasma cell disorders, affecting multiple organs (nephrotic syndrome, restrictive cardiomyopathy, arrhythmia, neuropathy)

AA (secondary): due to fibrils composed of serum Amyloid A, seen w/ chronic conditions (RA, IBD, protracted infection)

Dialysis related: due to fibrils composed of beta2-microglobulin in patients w/ ESRD, present w/ carpal tunnel syndrome

Heritable: neurologic/cardiac amyloidosis due to transthyretin gene mutation

Age-related: deposition of transthyretin in myocardium and other sites

Organ specific: Amyloid deposition localized to one organ, ie Alzheimer disease due to amyloid-beta protein cleaved from amyloid precursor protein

43
Q

Lipofuscin

A

Yellow-brown “wear and tear” pigments shown w/ H&E stain associated w/ normal aging

Formed by oxidation and polymerization of autophagocytosed organellar membranes

Deposits in elderly heart, liver, kidney, eye

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