Usmle: Pathology - Inflammation

Front 1

Apoptosis

Back 1

-Programmed cell death caused by the activation of capsases
-No inflammation
-Intrinsic Pathway; Involved in tissue remodeling. Bcl-2 is anti-apoptotic, BAX/BAK are pro-apoptotic
-Extrinsic Pathway; (1) Fas ligand/Fas receptor (2) Cytotoxic T-cell release perforin and granzyme B
-Apoptotic bodies are phagocytosed

Front 2

Necrosis

Back 2

-Cell death that is always pathologic and accompanied by inflammation

Front 3

Types of necrosis

Back 3

-Coagulative; infarction (except in the brain), wedge shaped. First protein denaturation then enzymatic degradation.
-Liquefactive; brain and bacterial infection. Damage due to lysosomal enzymes
-Caseous; looks like cottage cheese, common in TB
-Fatty; Pancreatitis, saponification
-Fibroid; in vessels, malignant hypertension, stains pink
-Gangrenous; Dry (ischemic coagulative) Wet (superimposed with infection). Common in limbs

Front 4

Cell Injury; Reversible

Back 4

-Cellular swelling; membrane blebs (decreased ATP -> decreased Na/K pump)
-ER swelling (ribosome dissociation -> decreased protein synthesis)
-Decreased oxygen -> fermentation -> lactic acid -> clumping of proteins/chromatin
-Fatty change

Front 5

Cell Injury; Irreversible

Back 5

-Nuclear breakdown (pyknosis, karyorrhexis, and karyolysis)
-Membrane damage (plasma/mitochondiral)
-Lysosomal rupture

Front 6

Red vs. Pale Infarcts

Back 6

-Red; hemmorrhagic, occurs in loose tissue with multiple blood supplies (liver, lungs)
-Pale; occurs in solid tissues with single blood supply (heart, kidney, spleen)

Front 7

Shock; Distributive (septic, neurogenic and anaphylactic)

Back 7

-High output failure
-Decreased pulmonary capillary wedge pressure
-Vasodilation (warm,dry skin)
-Failure to increase BP with IV fluids

Front 8

Shock; Hypovolemic/cardiogenic

Back 8

-Low output failure
-Decreased pulmonary capillary wedge pressure in cardiogenic, increase in hypovolemic
-Vasoconstriction (cold,clammy skin)
-Able to increase BP with IV fluids

Front 9

Causes of Atrophy

Back 9

-Decreased endogenous hormones (post-menopausal ovaries)
-Increased exogenous hormones (steroid use)
-Decreased innervation
-Decreased blood flow
-Decreased metabolic demand (prolonged hospitalization)

Front 10

Inflammation components

Back 10

Vascular: increased vascular permeability, vasodilation, endothelial injury
Cellular: Neutrophils leave circulation to injured tissue -> phagocytosis, degrandulaiton and inflammatory mediator release

Front 11

Acute inflammation

Back 11

-Neutrophil mediated
-Rapid onset
-Outcomes; complete resolution, abscess formation, and progression to chronic inflammation (viral infection)

Front 12

Chronic inflammation

Back 12

-Macrophage mediated
-Characterized by destruction and repair
-Blood vessel formation and fibrosis
-Gramuloma formation; nodular collections of epitheloid macrophages (histiocytes) and giant cells

Front 13

Pathologic Calcifications

Back 13

Dystrophic; when the deposition occurs locally in dying tissues (heart valves) and seen in TB, fat necrosis and infarcts/thrombi
Metastatic; the deposition of calcium salts in otherwise normal tissues (kidney, lungs and gastric mucosa); almost always a result of hypercalcemia secondary to some disturbance in calcium metabolism

Front 14

Leukocyte extravasation

Back 14

1. Margination and rolling (E and P selectins on vessel)
2. Tight-binding (ICAM-1/VCAM-1 on vessel)
3. Diapedesis (PECAM-1 on vessel)
4. Migration (chemotactic agents - C5a, IL-8, LTB4 and bacterial products)

Front 15

Pathologic scars

Back 15

-Hypertrophic; increased collagen synthesis, confined to the boarders of the original wound and infrequently recurs following resection
-Keloid; larger increase in collagen synthesis, extends beyond original wound, frequently recurs following resection

Front 16

Phases of wound healing

Back 16

-Inflammatory; clots forms PMNs enter tissue, macrophages clean up
-Proliferative; deposition of granulation tissue (fibrin, myofibrin and capillaries)
-Remodeling; Type III collagen replaced by Type I -> increases tensile strength of tissue

Front 17

Exudate

Back 17

-Cellular, protein rich, specific gravity > 1.02
-Due to; lymphatic obstruction, inflammation/infection or malignancy

Front 18

Transudate

Back 18

-Hypocellular, protein poor, specific gravity <1.012
-Due to; increased hydrostatic pressure, decreased oncotic pressure (cirrhosis) and Na+ retention

Front 19

Erythrocyte sedimentation rate

Back 19

-Products of inflammation (fibrinogen) coat RBCs and cause aggregation -> RBCs fall at a faster rate within the test tube

Front 20

Lipofuscin

Back 20

-Yellow-brown wear and tear pigment associated with normal aging.

Front 21

Healing via secondary intention

Back 21

-The healing of a more extensive wound such as an infarct, laceration or mechanical trauma where there is more extensive cell loss and parenchymal cells alone cannot restore normal architecture

Front 22

Fibrinoid Necrosis

Back 22

Front 23

Coagulative Necrosis - Gross

Back 23

Front 24

Coagulative Necrosis

Back 24

Front 25

Cellular swelling and fatty change

Back 25

Front 26

Acute Inflamation

Back 26

Front 27

Non-necrotizing Granuloma

Back 27

Front 28

Necrotizing Granuloma

Back 28

Front 29

Iron Deposits

Back 29