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STEP 1 (5) > Pathology-Inflammation > Flashcards

Pathology-Inflammation Flashcards

1
Q

Basics of apoptosis

A

Programmed cell death (ATP required) based on the extrinsic or intrinsic pathways, both of which activates cytosolic caspases

No significant inflammation (unlike necrosis)

Marked by cell shrinkage, nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, nuclear fragmentation (karyorrhexis), and formation of apoptotic bodies

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2
Q

What is DNA laddering?

A

A sensitive index of apoptosis- during karyoorhexis, endonucleases cleave internucleosomal regions, yielding fragments in multiples of 180 bps.

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3
Q

Describe the intrinsic apoptotic pathway

A

Involved in tissue remodeling in embryogenesis.

Occurs when a regulating factor is withdrawn from a proliferating cell population (e.g. decreased IL-2 after a completed immunologic reaction causing apoptosis) Also occurs after exposure to injurious stimuli (e.g. radiation, toxins, and hypoxia)

Changes in cell regulators increase mitochondrial permeability and allow leakage of cytochrome C. BAX and BAK are proapopotic and Bcl2 is anti-apoptotic

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4
Q

How does Bcl-2 prevent apoptosis?

A

Prevents cytochrome c by binding to and inhibiting Apaf-1 which normally induces the activation of caspases.

NOTE: If Bcl2 is overexpressed (as in follicular lymphoma) then you see tumor formation

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5
Q

Describe the extrinsic apoptotic pathway

A

2 pathways: Ligand receptor interations (FasL binding to Fas (CD95)) and immune cell (cytotoxic T cell release of perforin and granzyme B).

Note that Fas-FasL interaction is needed in thymic medullary negative selection and defective interaction is a part of autoimmune disorders. As Fas crosslinks FasL, multiple Fas molecules coalesce, forming a binding site for a death domain-containing contianing adaptor protein, FADD. FADD binds inactive caspases, activating them

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6
Q

Overview of Necrosis

A

Enzymatic degradation and protein denaturation of cell due to exogenous injury causing intracellular components to leak and cause an inflammatory rxn (unlike apoptosis)

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7
Q

Coagulative necrosis

A

Seen in ischemia/infarcts in most tissues except brain

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8
Q

Liquefactive necrosis

A

Seen in bacterial abscesses, and brain infarcts due to increased fat content in which neutrophils release lyosomal enzymes that digest the tissue (enzymatic degradation first, then proteins denature)

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9
Q

Caseous necrosis

A

Seen in TB, systemic fungi (e.g. Histo capsulatum) and Nocardia

Macrophages wall off the infecting microrgansism and form granular debris surrounded by lymphocytes and macrophages

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10
Q

Fat necrosis

A

Seen in acute pancreatitis (saponification) and nonenzymatic breast trauma in which damaged cells release lipase, which breask down fatty acids in cell membranes

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11
Q

Gangrenous necrosis

A

Dry due to ischemia (coagulative) and wet due to superinfection (liquefactive)

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12
Q

What are some REVERSIBLE findings of cell injury?

A

ATP depletion

Cellular/mitochondrial swelling (decreased NaKATPase)

Nuclear chromatin clumping

Decreased glycogen

Fatty change

RIbosomal/polysomal detachment (decreased protein synthesis)

Membrane blebbing

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13
Q

What are some IRREVERSIBLE findings of cell injury?

A

Nuclear pyknosis, karorrhexis, and karyloysis

Plasma membrane damage (degradation of membrane phospholipids)

Lysosomal rupture

Mitochondrial permeability/vacuolization

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14
Q

What are the most susceptible regions of the brain to infarct?

A

ACA/MCA/PCA boundary areas (watershed)

These regions receive dual blood supply but are susceptible to iscehmia from systemic hypoperfusion (pyramidal and Hippocampal cells susceptible)

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15
Q

What are the most susceptible regions of the HEART to infarct?

A

Subendocardium (LV)

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16
Q

What are the most susceptible regions of the KIDNEY to infarct?

A

Straight segment of the proximal tubule (medulla)

thcik ascending limb (medulla)

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17
Q

What are the most susceptible regions of the LIVER to infarct?

A

Area around central vein (zone III)

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18
Q

What are the most susceptible regions of the COLON to infarct?

A

splenic flexure and rectum

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19
Q

What is the difference between red and pale infarcts?

A

Red: hemorrhagic occurring in venous occlusion and tissues with multiple blood supplies, such as liver, lung, and intestine (reperfusion injury)

Pale: Anemic infarcts occurs in solid organs with a single blood supple such as heart, kidney, and spleen

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20
Q

Atrophy is the reduction in size and/or no. of cells. What are some causes?

A

Reduction i endogenous hromones (e.g. post-meopausal ovaries)

Increased exogenous hormones (e.g. steroid use)

Decrease innervation (e.g. motor neuron damage)

Decreased blood flow/nutrients

Occlusion of secretory duts

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21
Q

What are the main clinical findings of inflammation?

A

Rubor (redness), pain, calor, (heat), tumor (swelling), and loss of function

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22
Q

What is Chromatolysis?

A

Process involving the neuronal cell body following axonal injury with increased protein synthesis in an effort to repair the damaged axon and marked by:

Round cellular swelling

Dispalcement of the nucleus to the periphery

Dispersion of Nissl Substance

23
Q

What is dystrophic calcification?

A

Calcium deposition in ABNORMAL TISSUES secondary to injury or necrosis

Tends to localized (e.g. calcific aortic stenosis)

Seen in TB (lungs and pericardium), liquefactvie necrosis of chronic abscesses, fat necrosis, inarcts, thrombi, schistosomiasis, Monckeberg ateriolosclerosis, congenital CMV and toxo, and psammoma bodies

Is NOT directly associated with serum calcium levels (pts are usually normo-calcemic)

24
Q

What is metastatic calcification?

A

Widespread (ie. diffuse, metastatic) deposition of calcium in NORMAL tissues secondary to hypercalcemi (e.g. primary hyperPTHism, sarcoidosis, hypervitaminosis D) or high calcium-phosphate product levels (e.g. chronic renal failure with secondary hyperPTHism, long-term dialysis, warfarin)

Ca2+ deposits predominantly in interstitial tissues of kidney, lung, and gsatric mucosa (these tissues lose acid quickly and increased pH favors deposition)

Pts are not usually normo-calcemic

25
Q

Where does leukocyte extravasation mainly occur?

A

postcapillary venules (high yield)

26
Q

Describe the 1st step of leukocyte extravasation

A

Margination and rolling (defective in leukocyte adhesion deficiency type II- low Sialyl Lewis)

Vasculature mediators: E and P selectin and GlyCAM-1, CD34

Cell mediators: Sialyl LewisX (both selectins) and L-selectin for GlyCAM-1

27
Q

Describe the 2nd step of leukocyte extravasation

A

Tight-binding (defective in leukocyte adhesion deficiency type I-decreased CD18 integrin subunit)

Vasculature mediators- ICAM-1 (CD54) (to CD11/18 integrins (LFA-1, Mac-1) on cells); VCAM-1 (CD106) (to VLA-4 integrin on cells)

28
Q

Describe the 3rd step of leukocyte extravasation

A

Diapedesis- WBC trvales between endothelial cells and exits the blood vessel

Vasculature mediator: PECAM-1 (CD31) to PECAM1 (CD31) on cells (same on both)

29
Q

Describe the 4th step of leukocyte extravasation

A

Migration-WBC travels through interstitium to site of injury/infection guided by chemotactic signals such as C5a, IL-8, LTB4, kallkrein, etc.

30
Q

How do free radicals hurt cells?

A

Via membrane lipid peroxidation, protein modification, and DNA breakage

31
Q

How does inhalation injury occur (e.g. from smoke, heat, particulates, or irritants)?

A

Chemical tracheobronchitis, edema, pneumonia, and possibly ARDS

32
Q

How much strength is regained via scar formation?

A

70-80% of tensile strength regained at 3 months and little additional strength is regained after

33
Q

What is the role of PDGF?

A

Secreted by activated platelets and macrophages and induces vascular remodeling and smooth muscle cell migration

Stimulates fibroblast growth for collagen synthesis

34
Q

What is the role of FGF?

A

Stimulates angiogenesis

35
Q

What is the role of EGF?

A

Stimulates cell growth via tyrosine kinases (e.g. EGFR, as expressed by ERBB2)

36
Q

What is the role of TGF-B?

A

Angiogenesis, fibrosis, and cell cycle arrest

37
Q

What is the role of Metalloproteinases?

A

Tissue remodeling

38
Q

What are the initial mediators of wound healing?

A

Inflammation up to 3 days after wound formation mediated by neutrophils, platelets, and macrophages and marked by clot formation, increased vessel permeability and neutrophil migration into tissue and macrophages clearing debris after

39
Q

What are the later mediators of wound healing?

A
  1. Proliferative (day 3- weeks after wound)- Fibroblasts, myofibroblasts, endothelial cells, keratinocytes, and macrophages cause deposition of granulation tissue and collagen, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction
  2. Remodeling (1 week-6+ months)- Fibroblasts replace type III collagen with type I collagen to increase tensile strength
40
Q

What are the major granulomatous diseases?

A

Bartonella henselae (cat scratch fever)

Beryllosis

Eosinophilic granulomatosis with polyangiitis (Churg Strauss)

Crohn Disease (non caseating)

Foreign Bodies

Francisella tularensis

Fungal infections (caseous necrosis)

Wegener

Listeria monocytogenes)

M. leprae, M. tuberculosis

tertiary syphillis

Sarcoidosis (noncaseating)

Schistosomiasis

41
Q

How do granulomas form?

A

Th1 cells secrete IFN-y, activating macrophages.

TNF-a from macrophages induces and maintains granuloma formation (always chek for latent TB before starting anti-TNF drugs)

42
Q

Describe ‘exudate’

A

Cellular, protein rich, with a SP > 1.020

and typically due to lymphatic obstruction, inflammation/infection, and malignancy

43
Q

Describe ‘transudate’

A

Hypocellular, protein-poor, with an SP < 1.012

and typically due to incrased hydrostatic pressure, decreased oncotic pressure (e.g. cirrhosis, nephrotic syndrome), or Na+ retention

44
Q

What is an ESR?

A

Test when products of inflammation (e.g. fibrinogen) coat RBCs and cause aggregation with denser RBC aggregates falling at a faster rate within a tube.

45
Q

What are some common causes of elevated ESR?

A

Anemia, infection, inflammation (temporal arteritis), cancer (MM), pregnancy, and autoimmune disorders

46
Q

What are some common causes of decreased ESR?

A

Sickle cell anemia, polycythemia

HF

Microcytosis

Hypofirinogenemia

47
Q

What causes AL amyloidosis?

A

Due to deposition of protein form Ig LIGHT CHAINS that can occur as plasma cell disorder or associated with multiple myeloma.

Oftn affects multiple organs, including renal (nephrotic syndrome), cardiac (restrictive cardiomyopathy), hematologic (easy bruising, splenomegaly), GI (hepatomegaly), and neurologic (neuropathy)

48
Q

What causes AA (secondary) amyloidosis?

A

Seen with chronic inflammatory conditions such as rheumatoid arthritis, IBD, spondyloarthropathy, protracted infection.

Often multisystem like AL

49
Q

What causes Dialysis-related amyloidosis?

A

Fibrils composed of B2-microglobulin in pts with ERSD and/or long term dialysis (may present as carpal tunnel syndrome)

50
Q

What causes age-related amyloidosis?

A

Due to deposition of normal transthyretin in myocardium and other sites (slower progression relative to AL cardiomyopathy)

51
Q

Describe the amyloid seen in Alzheimer disease?

A

Due to deposition of B-amyloid protein cleaved from APP (chrom 21)

52
Q

What is another disease commonly associated with amyloidosis?

A

Islet amyloid polypeptide (IAPP) seen in DM type II

53
Q

What is lipofuscin?

A

A wear and tear yellow-brown pigment associated with normal aging and formed by oxidation and polymerization of autophagocytosed organellar membranes.

STEP 1 (5) (11 decks)

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