Pathology Exam 1: Basic Mechanisms

Front 1

a "pre-programmed" response of tissue to injury; involves the microcirculation plus cellular and acellular components of the blood

Back 1

inflammation

Front 2

List the cellular components of inflammation (6)

Back 2

PMNs, monocytes, lymphocytes, eosinophils, basophils, platelets

Front 3

short-lived, "end-stage" phagocytic cell

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Polymorphonuclear leukocytes

Front 4

large phagocytc cell capable of reproduction; tissue monocytes are termed histiocytes or macrophages

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Monocytes

Front 5

source of antibody producing plasma cells; humoral immunity

helpers, killers, suppressors; cell-mediated immunity

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B & T Lymphocytes

Front 6

List the acellular components of inflammation as explained in the lecture

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histamine, prostaglandins, platelet-activating factor, cytokines, nitric oxide, complement system, kinins, clotting pathway, thrombolytic pathway

Front 7

a vasoactive polypeptide which causes increased short-term vascular permeability; released from mast cells, basophils, and platelets

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histamine

Front 8

vascular constriction, dilation, permeability; leukocyte adhesion; pain

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prostaglandins, leukotrines

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synthesized by mast cells, basophils, platelets, neutrophils, monocytes, endothelium; causes vasoconstriction, increased vascular permeability and platelet aggregation

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platelet-activating factor

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products released by activated lymphocytes and monocytes, some of which are capable of attracting other leukocytes; improving phagocytic activity; cause fever and anorexia; stimulate fibroblasts

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cytokines (lymphokines)

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made by endothelium and macrophages; causes vascular dilation and increased vascular permeability; can mediate cell and bacterial killing

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nitric oxide

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a circulating protine system of proenzymes which, when activated (usually by antigen-antibody complexes - esp IgM), form several fragments, which augment the inflammatory process

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complement system

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a series of small polypeptides derived from serum which, after enzymatic conversion, produce prolonged vascular permeability; causes pain; activates complement

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kinins

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results in coagulation of blood by formation of fibrin from fibrinogen

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clotting pathway

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feed back mechanism to prevent excessive clotting

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thrombolytic pathway

Front 16

List the cardinal signs of inflammation (5)

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rubor, tumor, calor, dolor, loss of function

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rubor

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redness

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tumor

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swelling

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calor

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heat

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dolor

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pain

Front 21

List the general characteristics of acute inflammation

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-relatively short duration; nonspecific response to tissue damage
-cell type, leukocytes, predominantly neutrophils

Front 22

Explain the sequence of events in an acute inflammatory process

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1. transient vasoconstriction of arterioles
2. vasodilation resulting in increased blood flow
3. increased permeability of the microvasculature (histamine & kinin) w/ slowing of the ciruclation, outpouring of protein-rich fluid (fibrinogen/fibrin & immunoglobulin) into extravascular tissues, stasis (dilated small vessels packed with red cells)
4. leukocytic margination (neutrophils first, then smaller numbers of monocytes along the vascular endothelium, emigration
5. phagocytosis, lysosomal activity

Front 23

List four outcomes of acute inflammation

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-resolution/restitution - restoration to normal structure and function
-healing by scarring - deposition of vascular granulation tissue; gradual progression to dense collagenous scar tissue with low vascularity
-abscess formation (e.g. clostridum)
-progression to chronic inflammation

Front 24

Define chronic inflammation

Back 24

longer duration injury-dependent response linked w/ the immune system

Front 25

List mechanisms that may lead to chronic inflammation

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may follow acute inflammation, repeated bouts of acute inflammation, or may be due to specific agents that classically cause a chronic inflammatory response (such as tubercle bacilli, virus); indicates activation of the immune system

Front 26

List the cell types characteristic of chronic inflammation

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macrophages, lymphocytes, plasma cells

Front 27

List the tissue reactions characteristic of chronic inflammation

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proliferation of blood vessels and connective tissue, scar

Front 28

Specific type of chronic inflammation.

Back 28

granulomatous inflammation

Front 29

List the cell types composing in a granuloma

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-ephitheloid cells - abundant pale-pink, plump cytoplasm
-lympocytes
-Langhans' or foreign body-type giant cells may be present (represent fusion of macrophages)

Front 30

List at least four diseases that are characterized by granulomatous inflammation

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tuberculosis, leprosy, deep fungal infections, sarcoidosis, etc.

Front 31

small collections of modified macrophages ("ephitheloid cells"), usually surrounded by a rim of lymphocytes

Back 31

granuloma

Front 32

List 2 factors that appear to be involved in the formation of granulomas

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1. presence of indigestible organisms or particles
2. presence of cell-mediated immunity to the inciting agent (delayed hypersensitivity)

Front 33

outpouring of a thin fluid, derived from the blood serum or the secretions of serous mesothelial cells (e.g. skin blister resulting from a bum)

Back 33

serous inflammation / transudate

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exudate of large amounts of plasma proteins, including fibrinogen; histologically fibrin is identified by its tangled, threadlike eosinophilic meshwork

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fibrinous inflammation / exudate

Front 35

production of large amounts of pus;

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suppurative or purulent inflammation / exudate

Front 36

refers to excessive elaboration of mucin encountered in inflammatory states affecting any mucus-secreting mucosa (e.g. common cold)

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catarrhal inflammation

Front 37

characterized by a bloody exudate

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hemorrhagic inflammation

Front 38

formation of a membrane, usually made up of precipitated fibrin, necrotic epithelium, and inflammatory white cells; encountered only on mucosal surfaces, most commonly in the pharynx, larynx, respiratory passages, and intestinal tract; (e.g. diphtheria exotoxin causes necrosis of surface epithelial cells and their desquamation; clostridium toxin affects the intestinal mucosa and is related to patients receiving broad-spectrum antibiotics)

Back 38

pseudomembranous inflammation

Front 39

a focal accumulation of neutrophils and liquefactive necrosis

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pus

Front 40

a localized collection of pus

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abscess

Front 41

a local defect of the surface of an organ or tissue, which is produced by the sloughing of inflammatory necrotic tissue

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ulcer

Front 42

List systemic effects of inflammation

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fever, chills, leukocytosis, altered sleep patterns, decreased appetite, etc

Front 43

labile cells; define, give examples

Back 43

continue to proliferate throughout life; e.g. surface epithelia and blood cells

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stable cells; define, give examples

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retain the capacity to proliferate, however they do not normally replicate; e.g. parenchymal cells of the glandular organs of the body, such as the liver, kidney, pancreas; cells derived from mesenchyme, such as fibroblasts, smooth muscle cells, osteoblasts, chondroblasts; vascular endothelial cells

Front 45

permanent cells; define, give examples

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cannot reproduce themselves; e.g. nerve cells, skeletal and cardiac muscle cells

Front 46

a process associated with repair; the ability to completely replicated permanently injured parenchymal cells

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regeneration

Front 47

a process associated with repair;

Back 47

scar formation

Front 48

Describe the formation of granulation tissue

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characterized by proliferation of new small blood vessels and fibroblasts; new granulation tissue is often edematous b/c the new blood vessels have leaky interendothelial junctions

Front 49

Describe healing by "primary union" and give an example of an injury that would heal by primary union

Back 49

healing of a clean wound, such as a surgical incision, with little scar tissue

Front 50

Describe healing by "secondary union" and give an example of an injury that would heal by secondary union

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healing of a large tissue defect with much scar tissue; "healing from the bottom up" - waiting for granulation and all other tissue to reform

Front 51

Explain the formation of "exuberant granulations" and keloids as a result of wound healing

Back 51

Keloids?

Front 52

Restoration of the site of acute inflammation to normal

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Resolution; give example

Front 53

Healing by scarring, accompanied by some loss of function

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Organization; give example

Front 54

Explain the factors influencing wound healing (systemic)

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age, nutritional status, general health status, (corticosteroids, steroids)

Front 55

Explain the factors influencing wound healing (local)

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infection, adequacy of blood supply, presence of foreign bodies, specific tissue injured

Front 56

List general cases of cell injury

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hypoxia, chemical agents and drugs; physical agents; microbiological agents; immunologic reactions; genetic defects; nutritional imbalances; aging

Front 57

List the major biological systems affected by cell injury

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aerobic respiration; integrity of cell membrane (e.g. swelling); synthesis of enzymatic and structural protein; integrity of genetic apparatus

Front 58

List factors influencing the outcome of cell injury

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duration and severity of injury; type, state, and adaptability of the cell; nutritional, hormonal status and metabolic needs of the cell

Front 59

List the main ultrastructural changes of cell injury

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cell membranes (ER, ribosomes); mitochondria; cytoskeleton, DNA

Front 60

List and describe the light microscopic patterns of cell injury

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cellular swelling (cloudy selling, hydropic degeneration); fatty change; necrosis

Front 61

cell death

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necrosis

Front 62

type of necrosis; loss of nucleus but w/ preservation of the cell outlines and tissue architecture; conversion of the cell to an acidophilic, opaque "tombstone"; results from ischemia or chemical injury

Back 62

coagulation necrosis / ischemic necrosis

Front 63

type of necrosis; results from action of hydrolytic enzymes; commonly encountered in focal bacterial lesions, where enzymes of bacterial and leukocytic origin contribute to the digestion of deal cells; also characteristic of ischemic destruction of brain tissue (e.g. pancreas/pancreatitis)

Back 63

liquefaction (colliquative) necrosis

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type of necrosis; encountered when lipases escape from fat; lipases catalyze the decomposition of triglycerides to produce free fatty acids; the fatty acids combine with serum calcium to create calcium soap; histologically - amorphous granular basophilic deposits, opaque, chalky-white clouds, volcano

Back 64

enzymatic fat necrosis

Front 65

type of necrosis; combination of coagulative and liquefactive necrosis encountered principally in the center of tuberculous infections; grossly - soft, friable, whitish-gray debris; histologically - amorphous granular debris enclosed within a granulomatous inflammatory wall

Back 65

caseous necrosis
(e.g. granulomatous inflammation w/ central necrosis)

Front 66

type of necrosis; usually applied to a limb which has lost its blood supply and has been attacked by bacterial agents; tissues have undergone ischemic cell death and coagulative necrosis, followed by liquefactive necrosis (e.g. appendicitis)

Back 66

gangrenous necrosis

Front 67

Describe and state the clinical significance of intracellular accumulations of lipid

Back 67

small or large vacuoles in cytoplasm of cells associated with a variety of mechanisms; e.g. fatty exchange in hepatocytes may be due to alcohol abuse, protein malnutrition, diabetes mellitus, obesity, and hepatotoxins

Front 68

Describe and state the clinical significance of intracellular accumulations of protein

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may accumulate in association with heavy proteinuria leading to pinocytic reabsorption of protein in cells of the proximal convoluted tubules of the kidney; or excessive synthesis of proteins, such as immunoglobulins, which deposit in the cytoplasm of plasma cells as Russell bodies

Front 69

Describe and state the clinical significance of intracellular accumulations of glycogen

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seen in patients with an abnormality in either glucose or glycogen metabolism, such as diabetes mellitus or glycogen storage diseases

Front 70

Describe and state the clinical significance of intracellular accumulations of carbon (anthracotic pigment)

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inhaled air pollutant becomes phagocytized by alveolar macrophages and deposited in regional lymph nodes; severe exposure may result in coal worker's pneumoconiosis

Front 71

Describe and state the clinical significance of intracellular accumulations of lipofuscin

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a brownish-yellow granular cytoplasmic pigment, accumulates in a variety of tissues, heart, liver, and brain, as a function of age; "wear and tear" pigment

Front 72

Describe and state the clinical significance of intracellular accumulations of melanin

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brown-black pigment responsible for skin and hair pigmentation

Front 73

Describe and state the clinical significance of intracellular accumulations of hemosiderin

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hemoglobin-derived, golden-yellow to brown granular or crystalline pigment in which form iron is stored in cells; seen in association with hemorrhage, chronic congestion, or iron overload; can be seen with Prussian Blue stain for iron

Front 74

"pre-programmed cell death"

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apoptosis

Front 75

"shrinkage in size of a cell, tissue or organ due to loss of cell substance"

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atrophy

Front 76

"a form of physiologic organ atrophy involving apoptosis of cells"

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involution

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"increase in size of the cells of a tissue or organ"

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hypertrophy

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"increase in the number of cells of a tissue or organ"

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hyperplasia

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"one adult cell type is replaced by another adult cell"

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metaplasia

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"failure of full development"

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hypoplasia

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"almost complete failure of development"

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aplasia

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"complete absence of an organ or tissue"

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agenesis

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"abnormal growth; sometimes used to indicate premalignant change"

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dysplasia

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"lack of differentiation"

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anaplasia

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"normal growth"

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euplasia

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"degenerative changes"

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retroplasia

Front 87

"regenerative changes; stimulated cells can be benign or malignant"

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proplasia