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Emma II > Pathology E1 > Flashcards

Pathology E1 Flashcards

1
Q

Reversible changes

A

hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia

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2
Q

hypertrophy

A

inc in cell size, no new cells
(tissues with cells NOT capable of rep)

due to inc func demand/gfac/hormonal stim (activated growth factors, ion channels, oxygen supply, etc).

can co-exist w/ hyperplasia

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3
Q

Pathologic hypertrophy exp.

A

increased workload
hypertension
cardiocyte hypertrophy

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4
Q

Physiologic hypertrophy exp.

A

increased workload
pumping iron
skeletal muscle cell hypertrophy

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5
Q

Hyperplasia

A

inc in cell # –> inc in tissue/organ mass
(tissue with cells CAPABLE of rep)

exp. proliferation from stem cells, physiologic/pathologic hyperplasia

often co-exists w/ hypertrophy

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6
Q

Pathologic hyperplasia exp.

A

benign prostatic hyperplasia

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7
Q

Physiological hyperplasia

A

rapid growth via cell division in endometrial glands/stroma during proliferative phase of menstruation

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8
Q

hyperplasia + hypertrophy exp.

A

uterus during pregnancy

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9
Q

Atrophy

A

reduced cell size/organelles (long-term –> also dec in cell #)
dec workload/metabolic activity/protein synthesis
inc pro degrad
inc autophagy

via ischemia, denervation, aging, hormone withdrawal (mammary gland during menopause)

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10
Q

Metaplasia

A

Replacing cell types
Often adaptive response to stress
Via reprogramming stem cells

exp. respiratory epithelium in smoker (columnar to squamous), barrett’s esophagus during acid reflux (SSNKE –> intestinal columnar)

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11
Q

Dysplasia

A

Disordered growth/maturation
Response to persistence of injurious influence

*usu regresses upon removal of stimulus

Shares cytological features w/ cancer
exp. cervical dysplasia (SSKNE –> disordered)

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12
Q

General mechanisms of cell injury

A
  • ATP prod/depletion
  • Irrv. mitochondria damage (leakage of apoptotic proteins)
  • Entry of Ca (inc mito perm, activ of cell enzymes)
  • Oxygen/free radicals
  • Defects in memb permeability
  • Protein misfolding/DNA damage
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13
Q

Hypoxia vs ischemia

A

hypoxia–> dec oxygen (Low pO2 in blood), anaerobic E prod can continue

ischemia–> dec oxygen AND substrates (Mechanical obstruction of blood flow), aerobic/anaerobic compromised

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14
Q

Progression of ischemic cell injury

A

onset
reversible
irreversible
reperfusion injury (inc ROS formation, inflammation, Ca2+ mobilization)

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15
Q

Reversible cell injury (volume)

A

temporary loss of volume and E regulation

  • Altered membrane permeability (Na+, Ca2+, water influx; K+, Mg2+ efflux). Cell swells
  • inc wet weight of tissue, dec dry weight
  • Small molecule leakage and intracellular acidification
  • TEMPORARY loss of selective permeability
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16
Q

Reversible cell injury (Energy)

A

Drop in oxygen…
-ATP depletion, inc anaerobic metabolism (dec glycogen stores, inc lactic acid and Pi –> dec intracellular pH –> dec enzyme act)

-Ribosome detachment from RER
Dec protein synthesis

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17
Q

Reversible cell injury (Morphology)

A

Light microscopy

  • Cell swelling –> hydropic change (vacuolar degeneration) –> lighter staining
  • Some chromatin clumping

EM
-inc h2o, dilation of ER, dec glycogen stores, condensed mito, PM blebbing, blunting microvilli, myelin figures

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18
Q

Irreversible cell injury

A
  • perm loss of selective permeability
  • lg molecule leakage (troponin)
  • inc anaerobic metabolism (inc glycolysis, inc lactate, dec pH)
  • MPTP (high conductance), leakage
  • membrane abnormalities –> cytochrome C leakage
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19
Q

Serum signs for irreversible cell injury

A

troponin
myoglobin
CK-MB isoenzyme
lactase dehydrogenase

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20
Q

Irrev cell injury (morphology)

A

Light

  • Pyknosis: Nucleus shrinks
  • Karyolysis: Nuclear degen, “halo.” (basophilia fades)
  • Karyorrhexis: Nuclear fragments.

EM
matrix granules
flocculent densities
swelling/rupture

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21
Q

Ischemia/reperfusion injury

A

cell death after reestab blood flow

  • oxidative stress
  • more Ca flow (myocyte hypercontracture)
  • wbc accumulation (Ab deposit, complement activation, etc)
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22
Q

MPTP

A

Uncoupling of oxidative phosphorylation by mitochondrial permeability transition with release of cyt. C to cytosol. (inc [Ca2+]in will cause mitochondrial damage)

*irreversible injury

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23
Q

cytochrome C

A

pro-apoptotic

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24
Q

Calcium homeostasis

A

[extracellular Ca] > [intracellular Ca]

  • Intracellular Ca sequestered in mitochondria or ER
  • maintained by Ca2+/Mg2+ ATPase

Injury –> inc cytoplasmic Ca –> inc damaging enzymes (phospholipases, proteases, endonucleases, ATPase) and opening of MPTP

Injury –> inc cytoplasmic Ca (preferentially taken up by mito) –> depleted ATP prod

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25
Q

Generation of ROS

A

Formed from UV/X-rays, enzymatic action (CCl4), O2 reaction with free transition metals, nitric oxide

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26
Q

Defenses against ROS

A

-Metal binding proteins (transferrins, ferritin, lactoferrin)
-Antioxidants (Vit A, C, E)
-Enzymes (SOD, glutathione peroxidase, catalase)
Fenton Reaction

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27
Q

damage by ROS

A
  • Lipid peroxidation (attacks double bonds –> propagation and membrane damage) *vit E halts
  • Oxidative protein modification (inc proteasomal degradation, disulfide linkage)
  • genetic lesions (ss/dsDNA breaks)
  • Ca influx
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28
Q

Func of SOD, glutathione peroxidase, catalase to remove ROS

A

SOD (O2 rad –> H2O2)
Glutathione peroxidase (OH rad –> H2O)
Catalase (in peroxisomes)

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29
Q

Glutathione peroxidase ratio

A

Indic cell’s ability to detoxify ROS

Oxidative stress …
[oxidized glutathione]>[reduced glutathione]

(GSSG>GSH)

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30
Q

CCl4 –> free radical mediated cell injury

A

CCl4 + e –> CCl3- + Cl-

CCl3- –> highly reactive free radical –> lipid per oxidation, membrane damage, FA change and necrosis in liver

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31
Q

Autophagy

A

cell “self-eating”

  • controlled (ATG) and selective
  • adaptive mech during stress/damage/development/diffrentiation
  • failure –> accumulation of cell damage/aging
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32
Q

Autophagy process

A 
Initiation
Form phagopore (isolation membrane) 
Form autophagosome (double membrane)
Fusion w/ lysosome
Form autophagolysosome
Degrade/reuse contents
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33
Q

Fenton reaction

A

OH radicals formed from H2O2 by converting Fe3+ to Fe2+.

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34
Q

Necrosis

A
  • “accidental cell death”
  • caused by irreversible cell injury
  • morphologic changes following cell death, resulting from denaturation/enzymatic digestion of lethally injured cell
  • ALWAYS pathologic
  • clear INFLAMM. RESPONSE
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35
Q

Coagulative Necrosis

A

Most common (exp. ischemia –> infarct)

  • enzyme digestion/protein denaturation
  • tissue architecture intact but eosinophilic/anucleate (“ghost-town”)
    • phagocytes remove the debris
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36
Q

Caseous necrosis

A
  • “cheese-like” necrotic region
  • pink granuloma w/I distinct inflamm border

Comm w/ TB (granuloma with eosinophilic center, surr by macrophages (epithelioid cells), multinucleated giant cells and lymphocytes

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37
Q

Liquefactive Necrosis

A

Whole cell digestion to viscious pus (removed by phagocytes)
- some focal bacteria/occas fungal infec

CNS –> hypoxic death (infarcts of the brain) –> liquefactive necrosis

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38
Q

Fat necrosis

A

focal fat destruction comm due to release of pancreatic lipases into substance of pancreas/peritoneal cavity (acute pancreatitis)

TAGs–> FFAs saponify with Ca –> chalky spots

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39
Q

Fibrinoid necrosis

A

Result of immune-complex (Ag-Ab) deposition in small blood vessels combining with fibrin to cause necrotic vasculitis

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40
Q

Lipid accumulation

A

Usu involves liver

small droplets –> coalesce to vacuoles –> push nuclei to periphery

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41
Q

atherosclerosis

A

CHL/CHL esters in cytoplasm of smc and macrophages in tunica intimacy of aorta and large arteries

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42
Q

Niemann-pick disease (C)

A

lysosomal storage disease w/ defective enzyme involved in CHL trafficking. CHL accumulation in multiple organs

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43
Q

In disorders with high blood levels of CHL, _______ store CHL. When these cells accumulate in subcutaneous tissue, they form _______.

A

In disorders with high blood levels of CHL, macrophages store CHL. When these cells accumulate in subcutaneous tissue, they form xanthomas.

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44
Q

Hyaline Change

A

Histologic term, not a specific marker
Accumulation of homogenous, glassy, eosinophillic substance in cells

Intracellular: Russell bodies, alcoholic hyaline
Extracellular: hyalinized walls of arterioles

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45
Q

Alcoholic Hyaline

A

Accumulation of keratin intermediate filaments in fatty liver (mallory bodies)

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46
Q

Abnormality in either glucose or glycogen metabolism

A

excessive intracellular deposit of glycogen (exp. DM - accumulation in renal tubular cells, hepatocytes, heart muscle cells and beta cells)

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47
Q

Lipofuscin

A

Insoluble byproduct of lipid peroxidation; sign of oxidative stress
Composed of lipid-containing residues of lysosomal digestion
- ‘wear-and-tear’ pigment, seen in everyone, accumulates with age
- yellow-brown

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48
Q

Hemosiderin

A

Hb-derived (Fe containing); systemic buildup causes hemosiderosis (not assoc w tissue/organ damage)

(inherited hemochromatosis–> if accumulated in heart, pancreas or liver can cause fibrosis, heart failure and diabetes.)

-golden yellow/brown, granular/crystalline

xs iron –> ferritin (Fe + apoferritin) forms hemosiderin granules

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49
Q

Dystrophic Calcification

A

Normal Ca2+ metabolism and serum Ca2+

  • pathologic calcification
  • found in nonviable/dying tissues
  • exp. atheroma, damaged heart valves, TB lymph nodes etc.
  • can cause organ dysfunction

Ca deposition as fine, white granules (basophilic, amorphous) found in necrotic tissue, valvular dysfunction and atheromas.

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50
Q

Metastatic Calcification

A

Abnormal Ca2+ metabolism, high serum Ca2+ (hypercalcemia)

Comm hypercalcemia causes: hyperparathyroidism, bone destruction, vitamin D deficiency, or renal failure.

Normally found: GI mucosa, kidneys, lungs, vasculature

Sim morphology to dystrophic calcification

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51
Q

Ionizing radiation

A

XR, gamma rays, particulate radiation

enough E to completely eject e- from atom that absorbs radiation “ionization”

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52
Q

Non-ionizing radiation

A

UV (when absorbed can result in excitation of molec/dimer formation)

cannot eject e- on affected atoms but can raise them to higher orbital states

exp. pyrimidine dimers on DNA

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53
Q

O2 Effect

A

Increased response to radiation in presence of oxygen (“normoxic” envio) (formation of perhydroxy radicals)

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54
Q

Damaged prostate/bone –> elevated enzymes in blood?

A

acid phosphatase (AcP)

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55
Q

Damaged cardiac muscle –> elevated enzymes in blood?

A 
creatine kinase (CK), MB isoform
aspartate transaminase (AST)
lactate dehydrogenase (LDH)
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56
Q

Damaged liver –> elevated enzymes in blood?

A 
aspartate transaminase (AST)
alanine transaminase (ALT)
  • AST –> substance abuse, EtOH
    ALT–> liver disease (hepatitis, viral damage)
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57
Q

Damaged striated muscle –> elevated enzymes in blood?

A

creatine kinase (CK), MM isoform

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58
Q

Damaged pancreas –> elevated enzymes in blood?

A

lipase

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59
Q

Damaged pancreas/ovary/salivary glands –> elevated enzymes in blood?

A

amylase

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60
Q

Damaged liver/bone/intestine/kidney/placenta –> elevated enzymes in blood?

A

alkaline phosphatase (ALP)

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61
Q

General morphology of necrosis

A
  • inc eosinophilia, blebbing, swelling, nuclear changes (pyknosis, karyorrhexis, karyolysis)
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62
Q

Necrosis mechanism of cell death

A
  • cell death via swelling, dec ATP, inc membrane perm, release of macromolecules autolysis, INFLAMMATION
  • 2 concurrent processes: enzymatic digestion and denaturation of proteins
  • involves number of cells
  • irrev loss of homeostasis
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63
Q

Morphology of coagulative necrosis

A
  • cell swelling
  • organelle swelling
  • chromatin clumping
  • membrane damage
  • nuclear changes (enucleate cells)
  • inflammation
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64
Q

Apoptosis

A

cell deletion by fragmentation into membrane-bound particles that are phagocytosed by other cells

E dependent

NO immune response triggered

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65
Q

Causes of apoptosis

A 
embryogenesis
hormone dependent involution
in proliferating populations
in tumors
in immune/inflammatory responses
in atrophy 
in viral diseases
in response to injurious stimuli
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66
Q

Morphology of apoptosis

A 
cell SHRINKAGE
chromatin condensation
cytoplasmic blebs and apoptotic bodies
phagocytosis of apoptotic cells and bodies
little/no inflammation
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67
Q

Features of apoptosis

A 
Extrinsic/intrinsic activation
Suppressors/promoters
Caspase activation/proteolytic cascade
Endonucleases, DNA ladder
Fragmentation (apoptotic bodies)
Phagocyte recognition (phosphatidyl serine --> eat me)
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68
Q

Exp of intracellular accumulation due to metabolic rate being too low for adequate removal

A 
fatty liver (steatosis)
CHL and CEs
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69
Q

Intracellular accumulation due to buildup bc of too slow metabolic rate/ or if cannot be degraded normally

A

Russel Bodies in plasma cells
Alpha 1 antitrypsin deficiency Alzheimer disease
Amyloidosis

caused by defects in synthesis, folding, transport, secretion

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70
Q

Lysosomal storage diseases

A

accumulation of endogenous materials

exp. Gaucher’s Disease (defect in glucocerebrosidase causing buildup of glucosylceramide)

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71
Q

Intracellular accumulation of exogenous substances

A

Exp. carbon buildup in lung

72
Q

Endogenous pigment accumulation

A

Exp. Hemosiderin (one of major storage forms of iron)

73
Q

Electromagnetic spectrum and its ability to prod bio effects

A

UV/XR/gamma rays, etc

Shorter wavelength

  • higher frequency
  • greater photon E
  • greater ability to prod bio effects
74
Q

Critical difference between non-ionizing and ionizing radiation

A

Dif size of individual packet of E and NOT total E involved

Non-ionizing: size packet enough to raise e- to higher level
Ionizing: size packet lg enough to eject one or more e- from absorbing molec

75
Q

Critical target of radiation

A

damages to DNA

76
Q

Indirect action of ionizing radiation

A

radiation interacts with other atoms or molecules (esp. WATER) to prod free radicals –> damage critical targets

^dominant effect of XR/gamma-rays

77
Q

Direct action of ionizing radiation

A

radiation itself hits DNA molecule and produces damage to DNA molecules

^dominant effect of particulate radiation (neutrons/alpha particles)

78
Q

Effects of radiation on cells

A
  1. Damage repaired completely
  2. Damage exceeds repair capability –> dies via necrosis or apoptosis
  3. Irreparable damage –> reproductive death of cell
  4. Damage –> gene mut –> cancer
  5. Damage –> gene mut (heritable)
79
Q

The oxygen effect

A

Hypoxic cells –> more resistant to radiation than normoxic cells

After radiation, most cells tumor are hypoxic.

Reoxygenation –> mix of aerated/hypoxic cells present in tumor

Tx: More effective cell killing w/ mult doses (FRACTIONATION)

80
Q

2 factors that dictate which cells are most affected by radiation

A
  1. Cell cycle (M phase most sensitive, then G2, G1) (S phase, most resistant)
  2. Cell type
    resistant: mature cells, more differentiated
    sensitive: stem cells, younger, higher metabolic activity, higher prolif/growth rate
    fetus>child>adult
81
Q

Early effects of ionizing radiation

A

NO specific morphological changes. Change same as those due to ischemia/toxins/cell injury

  • occur in hrs-weeks
  • dep on cell cycle
  • cell death via necrosis/apoptosis
  • acute inflammatory response
  • early vascular injury, not very specific
  • presence of hyaline deposits –> thought to initiate delayed phase of radiation injury
82
Q

Delayed effects of ionizing radiation

A

Mostly due to vascular consequences

  • degenerative/reparative, involve any organ/tissue
  • DAMAGE TO MICROVASCULATURE
  • collagen hyalinization + tunica media thickening
  • narrowing/obliteration of vascular lumen
  • chronic ischemia –> parenchymal degeneration

-FIBROSIS (occurs later, comm in cancer therapy)

83
Q

Nonneoplastic complications of radiation

A 
cataracts, myocardial fibrosis, constructive pericarditis,
esophogeal structure
pulmonary fibrosis
stricture of small intestine
nephritis
transverse myelitis
congenital malformations
sterility
radiodermatitis
84
Q

Effects of UV light

A

UV=non-ionizing, a human carcinogen

SKIN (premature aging, cancers)
EYES (cataract risk)
REDUCED IMMUNE RESPONSE

85
Q

Mitochondrial (intrinsic) pathway of apoptosis

A

Initiated by cell injury –> BCL2 –> caspase activation

86
Q

Death receptor (extrinsic) pathway of apoptosis

A

Initiated by receptor-ligand interactions (FAS, TNF) –> caspase activation

87
Q

Consequences of mitochondrial dysfunction cumulating in cell death by necrosis

A

dec O2 supply, toxins, radiation –> mito damage/dysfunction –> dec ATP gen, inc prod ROS –> multiple cell abnormalities –> necrosis

88
Q

Consequences of mitochondrial dysfunction cumulating in cell death by apoptosis

A

dec survival signals, DNA, protein damage –> inc pro-apoptotic proteins –> leakage of mitochondrial proteins –> apoptosis

89
Q

ACUTE vs CHRONIC INFLAMMATION immune response

A

ACUTE - innate

CHRONIC - adaptive (cellular and/or humoral)

90
Q

Acute inflammation etiology

A

Physical injury, ischemia, Gram negative or positive bacteria

91
Q

Chronic inflammation etiology

A

Fungi, mycobacteria, parasites

Autoimmune diseases

92
Q

Acute inflammation characteristic features

A
  • Tissue necrosis
  • Vascular changes
  • Fluid and cell exudation:
    neutrophils followed by
    macrophages

(early/resolves)

93
Q

Chronic inflammation characteristic features

A

local expression of an ongoing immune response
- Cellular infiltration: Lymphocytes, macrophages, plasma
cells
-special form = the GRANULOMA
- Can be simultaneous with tissue necrosis, acute inflammation, and repair and regeneration

(late/persistent)

94
Q

Causes of chronic inflammation

A

PERSISTENT INFECTIOUS PATHOGENS (viruses, bacteria, fungi, parasites)

Immune responses (to foreign antigens (HS rxns), to self-antigens (AI diseases))

Rxns to non-degradable foreign bodies
-exogenous
-endogenous
(^mostly innate response)

95
Q

Intracellular Vesicular pathogens and immune response

A

Bacteria fungi, protozoa

Activates CD4+ Th1 cells and macrophages.

96
Q

Intracellular cytoplasmic pathogens and immune response

A

Viruses, bacteria, protozoa

Activates CD8 T cells. NK cells, NKT cells
gamma-delta cells.

97
Q

Extracellular Interstitial space/blood.lymph pathogens and immune response

A

Viruses, bacteria, spirochetes, protozoa, fungi, worms

Activates CD4+ Th2 cells, B-cells (release IgG via plasma cells), phagocytes and the complement system. Note parasites will also attract eosinophils.

98
Q

Extracellular Epithelial surfaces pathogens and immune response

A

Bacteria, worms

Activates CD4+ Th2, Th17 cells, B-cells (release IgA via plasma cells)

99
Q

Chronic inflammation w/ INTRACELLULAR VESICULAR pathogens - THE CD4 Th1 CELL RESPONSE

A

Macrophages use PRRs to sense invading pathogens –> MHC II and costimulatory molec expression, IL12 stim TH1 –> present antigen to T cells, which further activate macrophages by secreting IFN-gamma

(M1-type macrophage - PROINFLAMMATORY)
Inc phagocytosis, degradative lysosomal enzymes
Enhanced killing –> Reactive N and O species/bacteriostatic peptides
Prod of proinflammatory cytokines, derivatives of arachidonic acid, growth factors

(CD4 TH1 activated macrophages)
Pathology 
Lymphocytes
Macrophages (multinucleated giant cells)
Granuloma formation
Fibrosis (scarring)
Pathogens:
TB
Leprosy (tuberculoid)
Deep fungal diseases
Leishmaniasis (cutaneous)
100
Q

Chronic inflammation w/ intracellular vesicular pathogens - THE IMPAIRED CD4 Th1 CELL RESPONSE

A

Impaired macrophage bacteriolytic function
(treg, no IL12, so no T cell stim)

(M2 macrophage - ANTIINFLAMMATORY)
No reactive N and O species,         
Prod of IL-10
Profibrotic, angiogenic growth factors: aid in wound healing 
^non-killing, more healing

No costimulation T regulatory cells
Pathology:
Macrophages containing microorganisms
No granuloma formation

Pathogens Lepromatous leprosy
Visceral leishmaniasis

101
Q

Chronic inflammation w/ intracellular cytoplasmic pathogens - the CD8 response

A

Cd8 T cell –> target cell death…

  • -> perforin, granzymes, Fas L
  • -> IFN-gamma, TNF-alpha, TNF-beta

Pathology:
Cell/tissue necrosis
Lymphocytes
Macrophages

Exp.
Viral diseases (vaccinia, influenza, rabies, hepatitis)
Listeriosis

102
Q

Chronic inflammation w/ extracellular (interstitial/blood/lymph) pathogens - THE CD4 Th2 CELL RESPONSE

A

Activates CD4+ Th2 cells (–> IL-4, IL-5, IL-13), B-cells (release IgG via plasma cells), phagocytes and the complement system. *Note parasites will also attract eosinophils via IL-5

  • Activation of B cells secreting Ab to eliminate extracellular pathogens and neutralize toxins
Pathology:
Lymphocytes, plasma cells
Neutrophils, EOSINOPHILS
Macrophages (M2)
Fibrosis (scarring)
Exp.
Pyogenic cocci (exp. chronic appendicitis. pyelonephritis) 
Spirochetes
Toxins
Parasites
syphilis
103
Q

Chronic inflammation w/ EXTRACELLULAR pathogens (EPITHELIAL surfaces) - THE CD4 Th17 CELL RESPONSE

A

NEUTROPHIL recruitment and activation (via IL-17, prod by TH17), killing of pathogens

Pathology: 
Neutrophils
Lymphocytes
Macrophages 
Granuloma formation

Pathogens:
Klebsiella
Helicobacter
Fungi (candida)

AUTOIMMUNE DISEASES

104
Q

Chronic inflammation is char predominantly by…

A

macrophages, lymphocytes, plasma cells

105
Q

Acute inflammation is char predominantly by…

A

edema (exudate) and neutrophils (–> macrophages)

106
Q

Granulomatous

A

Special type of chronic inflammation

neutrophils can’t digest offending agent, macrophages get stuffed with indigestible substance and form a nodule-granuloma to wall off the offender

107
Q

The accumulation of macrophages loaded with mycobacteria typically seen in lepromatous leprosy are a likely consequence of:

A

A defective Th1 response

108
Q

In chronic inflammation, neutrophils are recruited by a subset of CD4 T cells producing…

A

IL-17 (TH17 cells)

*neutrophils are also attracted by bacterial products C5a and LTB4

109
Q 
Cell mediated (type IV, CD4 T)                
Delayed HS rxn
Classical, tuberculin type
A 
Typical antigens:
Microbial extracts (i.e. tuberculin)

Clinical picture:
Erythema, induration

Histopathology:
Cellular infiltrate (lymphocytes, macrophages)
110
Q

Cell mediated (type IV, CD4, CD8 T)
Delayed HS rxn
Allergic contact dermatitis

A

Typical antigens:
Urushiol (poison ivy, oak)
Nickel, chromate, leather

Clinical picture:
Blistering, erythema, induration

Histopathology:
Epidermal vesiculation Cellular infiltrate (lymphocytes, macrophages, eos)

111
Q

Diseases variously based on Th1, Th2 (Ab), Th17 or cytotoxic (CD8) responses, or a combo directed against self antigens…

A

Lupus erythematosus
Rheumatoid arthritis (*)
Scleroderma
Dermatomyositis

Thyroiditis (Hashimoto’s,
Graves disease)
Type-1 diabetes mellitus (*)
Addison’s disease

Autoimmune gastritis with pernicious anemia
Crohn’s disease and ulcerative colitis (*)
Primary biliary cirrhosis

Multiple sclerosis(*)
Myasthenia gravis

Atherosclerosis

Pemphigus Pemphigoid
Vitiligo Alopecia areata
Psoriasis(*) Lichen planus

  • TH17 cell driven conditions
112
Q

The usual chronic inflammatory reaction to non-degradable substances is in the form of foreign body __________ composed of __________ (histiocytes) and ______________________

A

The usual reaction to non-degradable substances is in the form of foreign body granulomas composed of macrophages (histiocytes) and multinucleated giant cells

*substances are largely non-immunogenic, so do not elicit adaptive immune responses, so lymphocytes/plasma cells are typically rare or absent

113
Q

Exp. of non-degradable substances causing chronic inflammation

A
  • Exogenous
    Mineral: silica (sand, glass), beryllium, zirconium
    Plant (thorn), animal (insect parts)
    Medical: suture material, synthetic grafts, implants
-    Endogenous
Calcium, urate crystals, atheroma
Storage material
Keratin, hair
Dead tissue
114
Q

GRANULOMATOUS INFLAMMATION

A
  • circumscribed collections of inflammatory cells that aggregate around a central “nidus”
  • can be composed of macrophages, giant cells, lymphocytes, eosinophils and neutrophils
115
Q

Classification of granulomatous diseases

A

Immune (hypersensitivity)-type granulomas

  1. Caused by microorganisms: i.e. mycobacteria, fungi, spirochetes, parasites
  2. Unknown cause: i.e. sarcoidosis, Crohn’s disease

Non-immune (foreign body)-type granulomas

  1. Exogenous materials: i.e. suture material
  2. Endogenous materials: i.e. crystals, keratin, dead tissue
116
Q

SCHISTOSOMIASIS (BILHARZIA)

A

Exp. of a chronic (granulomatous) inflammation

second most important human parasitic disease in the world after malaria

Granuloma mediated by CD4 T cells, Rich in eiosiniphils bc of PARASITES

117
Q

CHRONIC INFLAMMATION

A

LONG-LASTING INFLAMMATION IN WHICH AFFECTED TISSUES ARE INFILTRATED MAINLY BY MACROPHAGES, LYMPHOCYES AND PLASMA CELLS

Most cases, EXPRESSION OF AN ADAPTIVE IMMUNE RESPONSE

CAN FOLLOW OR BE ADMIXED WITH ACUTE INFLAMMATION, TISSUE REPAIR AND REGENERATION

118
Q

APC –> IL-12 –> TH1 –> IFN-gamma

role in chronic inflammation?

A

killing of intracellular pathogens via activating macrophages

119
Q

APC –> IL-4 –> TH2 –> IL-4, IL-5, IL-13

role in chronic inflammation?

A

Killing of extracellular pathogens by stimulating antibody production by B cells

120
Q

Neutrophils

A

first on the scene, 4-24 hours and undergo apoptosis in 24-48 hours

Look like messy smiley face, multi-lobed, pink cytoplasmic granules

phagocytose foreign material and kill bacteria

121
Q

Monocytes

A

“the clean up crew” arrive after 24 hours (usually day 3), can proliferate, in the tissue –> “macrophages”

122
Q

Lymphocytes

A

arrive typically late and are associated with chronic inflammation (*viruses)

huge dark nucleus, little cytoplasm

123
Q

Plasma cells

A

late, produce antibodies

124
Q

Eosinophils

A
  • early responders
  • associated with allergic reaction, parasites, drug (Amiodarone), asthma, etc

pink granules

125
Q

Manifestations of acute inflammation

A

Purulent (suppurative) - accumulation of pus (dead neutrophils)

Fibrinous (fibrin-rich exudate(proteinRICH). Fibrinogen leaves vessel –> fibrin forms in x-cell space

Serous- fluid accumulation via transudate (protein POOR, few cells)

126
Q

Acute inflammation sequence

A

Initiation of inflammation
Increased vascular permeability
Leukocyte extravasation

127
Q

Acute inflammation initiation

A

Signal comes from TLR of epithelial and dendritic cells that recognizebacteria and dead cells

Cells secrete cytokines (TNF, IL-1)

128
Q

Vascular changes of acute inflammation

A 
brief vasoconstriction
arteriolar vasodilation (slows blood down, *main vascular change of acute, manifests as erythema/warmth)
129
Q

Histamine

A

Key mediator of inflammation

  • in mast cells/basophils and platelets
  • premade in intracellular granules
pruritus
stim vasodilation of arterioles
vascular permeability
endothelial activation (H1 receptor)
hypotension, flushing, headache, tachycardia
bronchoconstriction

anaphylaxis/angioedema in sever rxns

130
Q

Timing of vascular mediators in acute inflammation

A

Immediate response (15-30 min)
Histamine *
Bradykinin ** PAIN
leukotrienes

Sustained response (4-24 hrs +): 
Histamine *
Bradykinin ** PAIN
leukotrienes
TNF and IL-1 (cytokines with local and systemic effects)
  • –> most imp mediator of inflamma
131
Q

Increased vascular permeability

A

Fluid –> extravascular tissues

rbc more concentrated –> inc blood viscosity and a reduction of flow

132
Q

Transudate vs. exudate

A

transudate - fluid that passed through the blood vascular wall as a result of hydrodynamic forces.
Low content of cells and protein

Exudate - fluid that escaped from the blood vasculature, usually as a result of inflammation.
High protein and cell content

133
Q

Expression of selectins regulated by the cytokines

A

TNF and IL-1

134
Q

Selectins and their localization

A

L-selectin on leukocytes
E selectin on endothelium
P selectin on platelets
(p-selectin and von Willebrand factor released from Weibel-Palade bodies granules of endothelial cells due to histamine and thrombin)

rel mediated by TNF, IL-1

135
Q

TNF-1 and IL-1 –> induce expression of ligands for integrins such as…

A

VCAM-1 (vascular cell adhesion molecule) the ligand for beta1 integrin (VLA-4)

ICAM-1 (intercellular adhesion molecule) , the ligand for beta2 integrin LFA-1

Mac-1 mediates arrest (the brakes)

136
Q

Chemokine bind to ____________

A

endothelial cell proteoglycans

137
Q

Transmigration

A
  1. Margination –> neutrophils accumulation along endothelial surface
  2. rolling and selectins (E/P/L)
  3. adhesion and integrins (VCAM, ICAM, MAC –> ligands on endothelial surface, for integrins on leukocyte)
  4. Transmigration: binding to PECAM-1 (platelet ENDOTHELIAL CELL adhesion molecule)
    * piercing basement membrane (collagenase) –> eneters extravascular tissue
138
Q

Leukocytes normally express integrins in _______ state. VLA-4 and LFA -1 integrins turn into __________ during inflammation.

A

Leukocytes normally express integrins in low affinity state. VLA-4 and LFA -1 integrins turn into high affinity state during inflammation.

139
Q

Chemotaxis

A
  • Exogenous (bacterial products)
  • Endogenous
    Chemokines (IL-8)
    Complements (C5a)
    arachidonic acid metabolite, leukotriene B4 (LTB4)
140
Q

Neutrophils and phagocytosis

A

Neutrophils will phagocytize opsonized (IgG/C3b-bound) bacteria –> phagolysosome

mechanisms of killing…
Myeloperoxidase – reactive oxygen sp.
NADPH oxidase enzyme – free radicals

141
Q

Vasoactive Mediators (reg/resolution of acute inflammation)

A

Substances that initiate and regulate inflammatory reactions

  • Vasoactive amines (histamine & serotonin)
  • Lipid products (prostaglandins and leukotrienes)
  • Cytokines/chemokines (TNF,IL-1,IL-8)
  • Products of complement activation
142
Q

Platelets - vasoactive mediator

A

Histamine, serotonin, & Thromboxane A2.

143
Q

Cytokines vs chemokine

A

cytokines –> proteins prod by leukocytes, macrophages, etc, mediate/regulate immune and inflammatory rxns
Exp. TNF, IL-1, IL-6, IL17

chemokines (type of cytokine) –> small proteins acting as chemoattractants for specific leukocytes
Exp. IL-8

144
Q

TNF

A

Expression of endothelial adhesion molecule, Secretion of other cytokines
Systemic effect

Prod via Macrophage, Mast cell, T lymphocyte

145
Q

IL-1

A

Similar to TNF
FEVER

Prod via macrophages

146
Q

IL-6

A

Systemic effect (acute phase response)

Prod via macrophages

147
Q

Chemokines (IL-8)

A

Recruitment of leukocytes,
Migration of cells in normal tissue

Prod via macrophages, T-lymphocytes

148
Q

IL-17

A

Recruitment of neutrophils and monocytes

Prod by T lymphocyte

149
Q

Bradykinin

A

vascular permeability, contraction of smooth muscle, vasodilation and PAIN

(Kallikrein –activator of FXII, chemotaxis, C5 to C5a)

150
Q

Vasodilation mediator

A

Histamine

Prostaglandins

151
Q

Increased vascular permeability mediator

A

HISTAMINE

152
Q

Chemotaxis, leukocyte activation

A

TNF/IL-1

chemokines

153
Q

FEVER

A

IL-1

also TNF and prostaglandins

154
Q

Pain

A

prostaglandins, brandykinin

155
Q

Systemic effects in setting of acute inflammation

A

Fever (via IL1, TNF)
Leukocytosis (IL1, TNF-alpha)
Acute phase reactants (IL6 –> hepatocytes, inc synth of serum proteins)
Sepsis, septic shock, worse

156
Q

Outcomes of acute inflammation

A

ulcer - shedding of inflamed necrotic tissue
fistula - abnormal patent connection between two organs
abscess - accumulation of pus walled off with fibrosis

157
Q

Lab tests to assess inflammation

A 
WBC  (leukocytosis)
CRP, best
ESR (erythrocyte sedimentation rate), worst
Lactate dehydrogenase (tissue damage)
ALT/AST (cellular damage) 
Albumin
158
Q

Acute Phase Reactants

A

IL-6 acts on liver to make these

CRP
Serum amyloid protein
Slbumin
ESR

159
Q

Acute inflammation initiation

A

Signal comes from TLR of epithelial and dendritic cells that recognize bacteria and dead cells

Cells secrete cytokines –> TNF and IL-1

160
Q

Vascular changes of acute inflammation

A

brief vasoconstriction

arteriolar vasodilation

161
Q

APC –> TGF-beta –> T-reg cell –> IL-10, TGF-beta

role in chronic inflammation?

A

Down-regulation of Th1, Th2, Th17 cells

162
Q

APC –> IL-23, IL-1, IL-6, TGF-beta –> Th17 cell –> IL-17, CSFs, IL-22, TNF-alpha

role in chronic inflammation?

A

Killing of extracellular pathogens through recruitment of neutrophils

163
Q

wbc left shift

A

IL-1 and TNF mediated leukocytosis

inc in # of immature leukocytes in blood, like neutrophil band cells

164
Q

Elevated ESR

A

(Erythrocyte sedimentation rate) if elevated –> inflammatory fx promote RBC rouleaux formation (fibrinogen)

never use this

165
Q

Elevated CRP

A

Indic inflammation, can monitor disease state, best marker of inflammation

166
Q

Decreased albumin

A

catabolized during inflammation

167
Q

Plasma cells usually seen in

A

Chronic inflammation (usually admixed with lymphocytes)

Infection with Syphilis (perivascular plasma cells)

Neoplastic processes (proliferation of clonal plasma cells; multiple myeloma)

*note very blue cytoplasm (where Ig is sitting)

168
Q

Granuloma formation (usually without necrosis)may be seen in

A 
Fungal infections
Infections with parasites
Foreign body reactions
Sarcoidosis
Crohn’s disease
Some bacterial infections
169
Q

Pressures driving fluid out of capillaries, into tissues

A
  1. Plasma hydrostatic pressure
  2. Tissue osmotic pressure

vasodilation –> inc blood flow –> inc hydrostatic pressure –> fluid from capillaries into tissue –> TRANSUDATE

170
Q

Pressures driving fluid into capillaries

A
  1. Tissue hydrostatic pressure

2. Plasma osmotic pressure

171
Q

Labile cells

A

continuously divide, usually undergo hyperplasia

exp. epithelia (skin, respiratory urinary, genital mucosa), hemopoietic cells

172
Q

Stable cells

A

Normally exhibit slow turnover, but can replicate rapidly in response to gfacs to completely regenerate original tissues

exp. Glandular organs (liver, kidney, pancreas, endocrine glands)
Mesenchymal tissues (bone, cartilage, vessels)
Glia
173
Q

Permanent cells

A

Do not divide. No or limited mitotic activity in post natal life

exp. Skeletal, Cardiac Muscle
Smooth muscle
Neurons

174
Q

myocardial necrosis –>

brain necrosis –>

A

myocardial necrosis –> coagulative necrosis

brain necrosis –> liquefactive necrosis

175
Q

t-PA (tissue plasminogen activator)

A

thrombolytic med, restores blood flow to blocked coronary arteries

Can cause paradoxical injury (reperfusion injury)

176
Q

Cardiac muscle enzymes elevated in blood

A 
Creatine Kinase (CK), MB isoform
Aspartate transaminase (AST)
Lactate dehydrogenase (LDH)

Emma II (24 decks)

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