Pathology Terms

Anatomical - study of gross and microscopic changes in cells and tissues of the body caused by disease

Clinical - measurement and identification of substances, cells and microorganisms in body fluids

• Anatomical Pathology
• analysis of biopsy and surgical specimens
• EG: diagnosis of malignancy

• Anatomical Pathology
• analysis of exfoliated and aspirated cells
• EG: Pap smear

• Anatomical Pathology
• Diagnosis of blood disorders
• EG: lymphomas

• Anatomical Pathology
• Analysis of tissues removed after death
• EG: study for cause of death

• Urinalysis (urine)
• Hematology (blood cell indices)
• Chemistry (electrolytes, enzymes)
• microbiology (bacterial culture)
• transfusion medicine (blood typing)

• glycogen, basement membranes, carbohydrate-rich molecules
• "Pass on the carbs"

Basement Membranes, fungi

"Silver lining"

Acid-Fast Bacilli (TB)

"Jerry's got TB"

Hemosiderin (iron)

Collagen

Amyloid

Fat

A deficiency of blood flow to an organ or tissue

Tissue Necrosis caused by impairment of arterial or venous blood supply

• No O2 --> No ATP. Therefore, NA isn't pumped out and seeps in, bringing water with it. Hydropic Change
• Less glucose, so anaerobic glycolysis increases, pH decreases. Ribosomes diss, cristae misalign
• Ca levels rise
• Membrane Blebbing

ROS are usually reduced numerous times such that you get no superoxide formation. However, if you don't have the electrons necessary to do so, you may get an accumulation of superoxide (free radical - O2-*)

Endogenous sources: macrophages create, NO, neutrophils

Exogenous Sources: radiation, drugs/toxins, pollutants

• If you have an ischemia, the has been damaged and hasn't been doing it's normal functions; therefore it doesn't have the e- necessary to reduce the ROS. (you get incomplete O2 reduction)
• If you unblock the ROS, you get a buildup of ROS that the cell can't handle, and you cause more cell injury

• Grossly: 18-24 hours
• LM: 4-12 hours

after injury

Necrosis is typically more eosinophilic (less nuclei)

Nuclear shrinkage

Nuclear Fragmentation

Nuclear Dissolution

• Still see structure, but no nuclei
• Caused by Ischemia
• Eosinophilia is a typical feature

• Seen in two distinct conditions:
• 1) Ischemia in the brain (stroke)
•     autolysis is dominant
• 2) Abscess formation just about anywhere in the body
•     PMNs everywhere

• Dry - a form of coagulative
• Wet - bacterial infection on top of necrosis
• Gas - results from puncture wound infection

• Cheeeeeese
• Can only use this to describe it grossly.

otherwise, we're looking at a granuloma

• Two Types:
• 1) Enzymatic: in pancreas after acute inflammation. leakage of pancreatic ducts causes digestive enzymes to attack local fat cells. You see "ghost cells" that are more basophilic.
• 2) non-Enzymatic: "trauma fat necrosis"

• Vessel damage dueto malignant hypertension, autoimmune disease. 
• The site is very eosinophilic

• ATP-dependent planned cell death.
• Intrinsic: Cytochrome C leakage
• Extrinsic: Death-receptor mediated.

Affects single cells

• 'eating yourself'
• Can lead to apoptosis

• Fatty Change
• Intracellular accumulation 
• Acute: microvesicular, drugs/toxins, fatty acids, response to drugs/toxins. life-threatening
• Chronic: macrovesicular, alcohol, triglycerides, response to alcohol. reversible

• Normal in cell, upregulated in response to injury
• Intracellular protein accumulation
• Heat Shock Proteins + Intermediate Filaments
• Attempts to re-fold or stabilize damaged proteins to avoid intermediate aggregation
• Hyaline

Homogenous, glassy, pink material

• Intracellular Pigment Accumulation, heme derived
• Storage form of Iron
• Hemosiderosis: short term harmless accumulatoin
• Hemochromatosis: long term w/ harm to cell. 
•    Primary: Hereditory, increase in intenstinal    iron absorption due to mutation
•    Secondary: multiple causes, esp blood         transfusions

Localized macrophages containing hemosiderin in the lungs. Indicate heart failure

Regeneration Nodule + Fibrosis

See it as hemochromatosis

• Intracellular Pigment Accumulation: Heme-derived
• Transported bound to albumin, brought to liver for conjugation to form water-soluble form
• Yellow color
• Jaundice if deposits in skin

Intracellular Pigment Accumulation - Exogenous

• Interstitial Accumulation
• An aggregation of misfolded amyloid proteins. Two beta pleated sheets
• Amyloid Light Chain: plasma cell Ig-secreting neoplasms
• Amyloid Assosciated: derived from precurser to serum amyloid A protein. Released as part of acute inflammation
• Congo red stain

• Interstitial Accumulation
• Metastatic: High serum Ca, normal Tissue. Diffuse all over the place
• Dystrophic: Normal serum Ca, abnormal Tissue. Locallized

• 1) Swelling
• 2) Redness
• 3) Heat
• 4) Pain
• 5) Loss of function

Redness + Heat = Erythema

Redness + Heat (cardinal signs of acute inflammation)

• 1) Transient vasoconstriction of arterioles: "knee jerk reaction" - may not occur. Thromboxane
• 2) Vasodilation of arterioles: hydrostatic pressure >> colloid pressure, so net flow will not become out of vessel. This leads to...
• 3) Hyperemia: increased amount of blood in tissue (Edema is increased ISF)
• 4) Change in capillary permeability: mediated by histamine and seratonin. Leads to more outflow and edema
• 5) Formation of Exudate

Increased amount of blood in tissue

Increased Instersitial fluid

Mediate the initial response for increase capillary permeability in the hemodynamic events of acute inflammation. Increase in capillary permeability leads to edema and increased hydrostatic pressure

• Edema is water and electrolytes
• Exudate (>1.5 g/dL)
• Transudate (< 1.5 g/dL)

• 1) Fibrinous: increase in fibrin. Ex: fibrinous pericarditis
• 2) Serous: fluid-filled. Ex: inflammation following a burn
• 3) Serosanguineous/Sanguineous: bloody
• 4) Purulent: Pus. basically a fibrinous exudate + many inflammatory cells

• Viscosity increases because of increase in cell concentration (hemoconcentration)
• blood flow slows down (stasis) and becomes so packed that you can actually see it in slides (vascular congestion)

The increase in blood cell concentration due to fluid loss in acute inflammation

Slowing of blood flow in acute inflammation. Due to hemoconcentration

Due to hemoconcentration, blood vessels become so packed that you can see them packed full of cells in histological slides

• Lympathic drainage increases to drain the edema
• Lymphangitis: lymphatics become inflammed
• Lymphandenitis: Lymph nodes become inflammed

inflammation of lymphatics in acute inflammation

Inflammation of lymph nodes in acute inflammation

• My Poor Disease Can't Proliferate
• Margination: because of increased viscosity, WBCs get pushed to periphery
• Pavementation: light binding to epithelial cells (selectin - light, intergrins - loose)
• Diapedesis: change in cell morphology that let's it migrate through epithelial cells to inflammation
• Chemotaxis: gradients/chemicals direct cell where to do
• Phagocytosis

• Part of cell recruitment in acute inflammation
• WBCs get pushed to periphery due to increase in viscosity

• Part of cell recruitment in acute inflammation
• Binding of cell to epithelial cells (selectins-light. Integrins - tight)

• Part of cell recruitment in acute inflammatoin
• Change in cell morphology to allow it to pass through epithelial cells

• Part of cell recruitment in acute inflammation
• Gradients/chemicals tell cells where to go once out of blood stream

• PMNs are most important
• Macrophages start to appear after 24/48 hours, and take over as the dominant cell type at around day 5, as chronic starts
• Eosinophils
• Mast cells - mediate inflammatory response (histamine and heparin)
• Lymphocytes

• Looking for increased leukocyte concentration in the blood
• Leukocytosis: increased leukocytes in blood (more lymphoctes and neutrophils)

• Increased leukocytes in blood
• Lymphocytosis: increased lymphocytes
• Neutrophilia: increased neutrophils

• Decreased leukocytes in blood
• Lymphopenia: decreased lymphocytes in blood
• Neutropenia: Decreased neutrophils in blood

A vesicle > 5mm in diamter. filled w/ exudate, probably serous

slough produced by chemical or thermal burns, or gangrene

• Localized inflammation and ulcer of the skin, usually in hairy area
• A carbuncle is a shit ton of furuncles, will see erythema and swelling

• Erysipelas: A spreading infection of the dermis which produces a raised, red, painful lesion of skin
• Cellulitis: A spreaking inflammation of the subcutaneous connective tissues

• IFN-Gamma from T Cells, IL-4 from others
• TFN is most important mediator of chronic: without it, granuloma doesn't form

Most important mediator of chronic inflammation. Without it, granulomas do not form

Macrophage activation by T cells

PMNs, Exudate

Mononuclear cells (giant cells in granuloma), fibrosis

• Langhan (horseshoe)
• Asteroid Body
• Schaumann Body

• Granuloma made around indigestible material
• epithelioid cells in center, mononuclear cells make ring. 
• Will sometimes see thick fibrous ring as well
• Giant cells

Causes eosinophelia, which normally happens in the course of Acute on Chronic inflammation

• No nuclei in center
• Tuberculosis

• Nuclei in center.
• Saroidosis

• usually infection before first one clears.
• eosinophilia (eotaxin)

Looking for macrophages, angiogenesis, fibroblasts

Resolution is restoration to pre-injury state

• Regeneration is replacement of lost cells by cells of the same type
• May result in loss of function

• Repair is replacement of cells to connective tissue (fibrosis)
• May result in loss of function

• the conversion of dead tissue or inert material into granulation tissue.
• happens in fibrinous exudates, thrombi, infarcts, wounds

• Light pink and softly granular grossly
• Contains macrophages, fibroblasts, new vessel formation, mast cells
• Presence of granulation tissue means healing is taking place

• occurs with "clean cuts"
• minimal myofibroblast activity

• Happens when wound edges can't be matched
• Lots of myofibroblast activity