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General Pathology
| Question | Answer |
|---|---|
| Things to include in a description | -size -color -consistency -shape -surface -margins -distribution -location |
| Things to include in a morphologic diagnosis | -severity -duration -distribution -modifier -anatomic site -lesion |
| Etiology | MINI VAN DITTI -metabolic -inflammatory -neoplastic -infectious -vascular -anomalies of development -nutritional -degenerative -idiopathic -traumatic -toxic -iatrogenic |
| Main difference between cell injury and cell death | -cell injury is reversible -cell death is not reversible |
| Things that injure cell membranes | -trauma -free radicals -weaponized pores |
| Free radicals damage cell membranes by ____ | Lipid peroxidation |
| Sources of free radicals | -radiation injury -toxicity -inflammation (neutrophils) -normal cell function |
| Weaponized pores are formed mainly by ____ and ____ | -complement system (MAC) -bacterial toxins |
| Things that can cause DNA injury | -free radicals (thymine dimers) -viruses (insertion) -toxins (aflatoxin binds to DNA) -radiation (thymine dimers) |
| Things that interfere with cellular energy supply | -toxins (aflatoxin inhibits FA oxidation) -hypoxia |
| Things that damage cellular proteins | -toxins (ricin inhibits ribosomes) -heat denatures proteins (cells need HSP) |
| Ways that a cell is injured | -cell membrane injury -DNA injury -interference with energy supply -inhibition of protein synthesis/damage to proteins |
| Characteristics of HSP's | -produced in response to stress -act intracellularly to bind, chaperone, and refold proteins -also degrade proteins |
| Medical relevance of HSP's | -autoimmune diseases often target HSP -linnked to tumor resistance to anti-cancer drugs -increased HSP expression related to survival of anoxia |
| Cells that are highly susceptible to cell injury | Neurons |
| 4 things that accumulate in a cell | -fat -protein -glycogen -H2O |
| 4 mechanisms of fatty change | -excessive entry of fatty acids -defective oxidation of fatty acids (toxins) -decreased apoprotein synthesis -defective secretion of lipoproteins (alcohol) |
| Feline hepatic hepatic lipidosis syndrome | fat cat stops eating > mobilization of fat > lipid processing in liver overwhelmed > protein reduced by anorexia > fatty change > icterus and anorexia |
| Fatty change occurs most commonly in ___ and ___ livers | -fat cat -fat pregnant cow |
| Horses at high risk for hepatic lipidosis | -Morgans -miniatures |
| Common causes of liver injury (resulting in fatty change) | -aflatoxin -alcohol |
| Gross morphology of fatty change | -organ is enlarged -tan/yellow -may float if severe enough -friable |
| Histological morphology of fatty change | -clear, round, discrete cytoplasmic vacuoles |
| Differences between fatty change and fatty infiltration | -most common in RV and pancreas -fat accumulates INTRACELLULARLY in non-adipose cells |
| Hisological morphology of protein accumulation | -eosinophilic cytoplasmic droplets -relatively rare |
| Causes of glycogen accumulation in liver | -canine steroid hepatopathy -diabetes mellitus -storage diseases -neonates |
| Canine steroid hepatopathy pathogenesis | -excess endogenous/exogenous glucocorticoids -leads to induction of glycogen synthetase -leads to XS glycogen production -accumulates in hepatocyte -leads to dysfunction and increased liver enzymes (ALP) |
| Gross morphology of glycogen accumulation | -liver is enlarged -orange/brown -friable |
| Microscopic morphology of glycogen accumulation | -midzonal hepatocytes are swollen with clear cytoplasm -midzonal = between portal triads |
| How does diabetes mellitus lead to glycogen accumulation? | -hyperglycemia leads to XS hepatic glycogen accumulation -fatty change is often present |
| Hydropic degeneration | -rapidly reversible -follows ischemia -usually only seen in epithelium -cells enlarged (identical to glycogen) -may reverse OR progress (rupture and death) |
| Types of cell death | -necrosis -ischemia -hypoxia -infarct |
| Define necrosis | -death of cells PRIOR to death of organism |
| Define ischemia | -lack of blood flow (worse than hypoxia alone) |
| Define infarct | -focal area of ischemic necrosis |
| Mechanisms of reperfusion injury | -restored blood flow to ischemic tissue increases damage via: -provides oxygen >> free radicals! -neutrophil infiltration damages viable tissue |
| Gross changes associated with cell death | -softening -color change (lighter or darker) -possible peripheral rxn -ulceration (full thickness necrosis) |
| Softening in the brain | -malacia |
| Nuclear changes associated with cell death | -pyknosis -karyorrhexis -karyolysis |
| Pyknosis | -nucleus is shrunken and densely basophilic |
| Karyorrhexis | -fragmented nucleus |
| Karyolysis | -faded or absent nucleus |
| Cells do not show signs of death UNLESS... | -animal continues to live for several hours |
| 2 types of host reaction to necrosis | -local and systemic -local: hyperemia and leukocyte infiltrate -systemic: SIRS |
| Cause of local inflammation following cell death | -immune system reacts to mitochondria release |
| SIRS | -systemic inflammatory response syndrome -causes damage to endothelial cells throughout the body -occurs if significant amt of cell contents enter circulation |
| Morphologic classifications of necrosis | -coagulative -liquafactive -caseous -fat -fibrinoid |
| Common causes of coagulative necrosis | -ischemia -toxins |
| Coagulative necrosis | -identifying characteristic: tissue architecture is preserved -examples: infarct (focal) and toxins (diffuse) |
| Common causes of liquefactive necrosis | -bacterial infection -neutrophilic infiltrate |
| Liquefactive necrosis | -tissue becomes liquefied -examples: abscess or malacia of nervous system |
| Common causes of caseous necrosis | -specific bacterial infections -ESPECIALLY Mycobacterium spp. |
| Caseous necrosis | -loss of architecture -tissue is solid and friable -frequently present at center of granuloma -EX: tuberculosis and caseous lymphadenitis |
| Pathogenesis of enzymatic fat necrosis | -pancreatitis causes release of enzymes(lipase) -digestion of abdominal fat into FFA -FFA precipitate calcium to form soap |
| Types of fat necrosis | -enzymatic -nutritional/toxic |
| Gross appearance of fat necrosis | -chalky white spots in abdominal fat -firm, but not hard |
| Microscopic appearance of fat necrosis | -normally clear adipocytes become red (dead) then blue (mineralized) -inflammatory rxn may/may not be present |
| Pathogenesis of nutritional/toxic fat necrosis in fish-eating carnivores | -diet high in rancid fish leads to -XS oxidized fats, which leads to -antioxidant deficiency -causes free radical injury of adipose tissue -often vitamin E/selenium responsive |
| Microscopic and gross appearance of fat necrosis in fish-eating carnivores | -gross: yellow/orange fat -microscopic: similar to enzymatic, but with yellow pigment |
| Pathogenesis of nutritional/toxic fat necrosis in ruminants | -unknown! -predisposing factors: grazing fescue, breed (Channel Island breeds), and age |
| Gross and microscopic morphology of fat necrosis in ruminants | -gross: very firm, opaque abdominal fat that may obstruct intestines -microscopic: similar to enzymatic, but less inflammatory |
| Fibrinoid necrosis | -occurs ONLY in blood vessels -vessel wall is necrotic and hypereosinophilic -causes: infectious agents, toxins, or hypertension |
| Types of gangrene | -dry gangrene -wet gangrene -gas gangrene |
| Dry gangrene | -coagulative necrosis, typically ischemic -EX: ergotism or frostbite |
| Wet gangrene | -liquefactive necrosis -typically involves bacteria -EX: dog bite |
| Gas gangrene | -necrosis with gas bubbles -formed by certain bacteria -EX: blackleg |
| Examples of physiologic apoptosis | -embryogenesis -immune tolerance (lymphocyte maturation) -regression of temporary tissues -tissue homeostasis |
| Examples of pathologic apoptosis | -virus induced -viral inhibition -autoimmunity -neoplasia |
| Define pathologic apoptosis | -excessive or deficient apoptosis results in disease |
| Example of virus-induced apoptosis | -CD4 lymphocyte depletion by immunodeficiency viruses |
| Example of viral inhibition of apoptosis | -poxviruses -epstein-barr virus (mono) |
| How does pathologic apoptosis cause autoimmune disease? | -mutations that decrease apoptosis result in autoreactive cells |
| Steps of apoptosis | 1.signaling 2.control 3.execution 4.removal |
| 4 ways cells signal for apoptosis | 1. p53 response to DNA damage 2. TNF and Fas-Fas membrane binding 3. Perforin/granzyme pathway (caspase activation) 4. Lack of growth factors or hormones |
| 2 control molecules in apoptosis | -p53 is a proapoptotic molecule that responds to DNA damage -Bcl2 is an anti-apoptotic molecule |
| Control step (apoptosis) | -determines whether or not cell will commit to or abort apoptotic pathway -depends on signaling molecules |
| The execution step in apoptosis is mediated by _____. | -caspases |
| Mechanism of cell execution | -activation of endonucleases (chop) -protein cross-linking causes shrinkage -activation of proteases eliminates architecture |
| How are cells removed after apoptosis? | -phagocytosis -surface membrane phospholipid flips and is exposed on surface of cell -phagocytes recognize signal and eat cell |
| Morphology of apoptotic cells | -shrink (small, more dense) -chromatin condenses along nuclear membrane -apoptotic bodies are formed by cytoplasmic blebs -phagocytosis forms tingible body macrophages |
| Autolysis | -disintegration of cells and tissues after death of the organism |
| Differences between necrosis and autolysis | -autolysis lacks host response -autolysis is diffuse |
| Rapidly autolyzing tissues | -gall bladder -intestinal mucosa -pancreas |
| Post-mortem interval | -the time between death and necropsy |
| Factors contributing to autolysis | -tissue type -temperature -bacteria -insulation |
| Common postmortem lesions | -gas accumulation -gastric rupture -organ impression -postmortem discoloration -algor mortis -livor mortis -rigor mortis -euthanasia artifact |
| How do you differentiate between antemortem and postmortem bloat? | -bloat line (result of congestion) |
| 2 types of postmortem gas accumulation | -bloat -emphysema |
| 3 types of postmortem discoloration | 1. bile imbibition (yellow/green) 2. hemoglobin imbibition (red/brown) 3. pseudomelanosis (dark green/black) >> due to bacteria forming iron sulfide |
| Algor mortis | -cooling of the body -depends on environment and insulation |
| Livor mortis | -pooling of blood on the down side -purple discoloration |
| Rigor mortis | -contraction/stiffening of muscles after death -due to depletion of ATP and glycogen -starts at 2 to 4 hrs -lasts for 24 to 48 hrs |
| Euthanasia artifact | -crystalline precipitation of euthanasia solution -grossly: yellow/white pinpoint plaques on endocardium, epicardium, lungs -microscopically: crystalline ghosts in myocardium -red/brown staining of tissue |
| Effects of formalin fixation | -kills: stops autolysis and putrefaction -penetrates: 1 cm -hardens: cross-links proteins |
| Factors affecting histopathology | -friction -compression -electric current -prior sectioning of surgical margins |
| 7 disturbances of circulation | 1. Edema 2. Hyperemia 3. Congestion 4. Hemorrhage 5. Shock 6. Thrombosis 7. Disseminated Intravascular Coagulation |
| Define edema | -accumulation of excess watery fluid into the interstitial space or body cavities |
| Subcutaneous edema | -dependent edema (in lower areas due to gravity) -EX: intermandibular edema ("bottle jaw") -pitting edema: indicates slightly longer duration |
| Morphology of pulmonary edema | -gross: tracheal froth and interlobular edema -microscopic: fluid within alveoli |
| Seroma | -focal pocket of fluid accumulation -usually due to trauma -different from cyst (NOT lined by epi) |
| Anasarca | -generalized edema |
| 2 types of edema (based on mechanism) | -inflammatory edema: increased vascular permeability -noninflammatory edema: result of circulatory disturbance |
| 3 factors affecting development of noninflammatory edema | 1. increased hydrostatic pressure 2. decreased (IV) oncotic pressure 3. decreased lymphatic drainage |
| Conditions leading to increased hydrostatic pressure (and edema) | -decreased cardiac output (congestive heart failure) -impaired venous return (vein obstructed by thrombus or direct pressure) |
| Conditions that lead to decreased oncotic pressure (and edema) | -XS loss of protein (PLN, PLE, or parasites) -decreased protein synthesis (liver dz or malnutrition) -NOT ANEMIA |
| Conditions that lead to lymphatic obstruction (and edema) | -trauma -neoplasia -parasites -direct pressure |
| Hyperemia and congestion both refer to ..... | -regional increase in blood volume within vessels -look identical microscopically |
| Define hyperemia | -active dilation of arterioles to increase blood flow to an area or tissue by release of vasoactive chemicals (histamine) or by neurogenic means (blushing) |
| 2 types of hyperemia | -physiologic hyperemia: post-exercise, GI tract, cheeks -grossly bright red (high O2) -pathologic hyperemia: acute inflammation |
| Congestion | -PASSIVE dilation of vessels due to decreased CO and "back up" of blood in veins -usually veins and capillary beds affected -grossly appears dark red (low O2) -mechanism similar to edema (increased hydrostatic P) |
| Pulmonary congestion | -occurs because of LEFT heart failure -capillary congestion pushes RBC's into the alveoli (diapedesis) -RBC's are digested by alveolar macrophages -hemosiderin filled macrophages = heart failure cells |
| Hepatic congestion | -occurs with RIGHT heart failure -2 types: acute and chronic |
| Acute hepatic congestion | -high protein fluid exudes through capsule of liver -fibrinogen >> fibrin -grossly: liver is enlarged and may have fibrin on surface |
| Chronic hepatic congestion | -blood accumulates in centrilobular sinusoids -reticular pattern grossly ("nutmeg liver") -liver will be HEAVIER than normal |
| Hypostatic congestion | -gravity pulls blood to the "down" side of the body -affects the lungs during anesthesia -also affects organ appearance post-mortem |
| Splenic congestion is usually caused by.... | -barbiturates -due to relaxation of smooth muscle trabeculae and capsule |
| 5 examples of congestion | 1. pulmonary congestion 2. hepatic congestion 3. hypostatic congestion 4. torsion of viscus 5. barbiturates |
| Define hemorrhage | -escape of blood from the CV system of a living organism |
| 3 destinations for hemorrhage | -outside world -into a body cavity -into tissue |
| Epistaxis | -blood from the nose |
| Hematemesis | -vomiting up blood (digested or not digested) |
| Hemoptysis | -coughing up blood |
| Hematochezia | -fresh blood in the feces |
| Cardiac tamponade | -cardiac dysfunction due to blood (or fluid) in the pericardium compressing the heart |
| Hematoma | -3D extravascular clot |
| Splenic hematoma | -BENIGN -occur at sites of lymphoid nodular hyperplasia -can rupture (hemoabdomen) -impossible to differentiate grossly from neoplasia |
| Descriptive terms for hemorrhages | -petechial: pinpoint to 2 mm -ecchymotic: larger, 3mm to 3cm -paintbrush: linear streaks |
| 3 factors that determine the effect of hemorrhage | 1. Location (worst = brain, spinal cord, and pericardial sac) 2. Rate 3. Quantity (>30% leads to shock) |
| Define shock | -severe systemic hypoperfusion |
| Four categories of shock | 1. cardiogenic 2. hypovolemic 3. anaphylactic 4. septic |
| Cardiogenic shock | -failure of the heart to pump blood |
| Hypovolemic shock | -loss of blood or plasma volume |
| Anaphylactic shock | -vasodilation caused by IgE-mediated hypersensitivity reaction |
| Septic shock | -systemic bacterial or fungal infection |
| Pathogenesis of septic/endotoxic shock | -infectious agent accesses blood -releases endotoxins (LPS) when lysed -LPS activates endothelial cells, monocytes, complement -activated cells release CK's -circulating CK's wreak havoc in body (shock, ARDS, SIRS, DIC) |
| Circulating cytokines due to endotoxin result in... | 1. vasodilation, reduced CO > hypotension > shock 2. acute respiratory distress syndrome 3. systemic inflammatory response syndrome 4. activation of coagulation cascade >> DIC |
| Septic shock is often the cause of death in which 2 diseases? | -parvoviral enteritis -equine colic |
| Define thrombosis | -coagulation of blood within the intact cardiovascular system |
| Thrombus | -an intravascular PATHOLOGIC mass of coagulated blood |
| Characteristics of normal clotting | -forms only when needed -only as large as needed -localized to area of damage -dissolves when no longer needed |
| 4 steps of blood coagulation | 1. brief vasoconstriction 2. platelet rxn (requires Von Willebrand factor) 3. coagulation cascade >> fibrin 4. anticoagulation mechanisms |
| Anticoagulation factors | -antithrombin III -thrombomodulin -protein C -plasminogen activators |
| Virchow's triad | -three factors predisposing to thrombosis -endothelial injury, alterations to blood flow, and increased blood coagulability |
| Examples of endothelial injury | -trauma -parasites -atherosclerosis (fatty) -arteriosclerosis (fibrosis or mineralization) -inflammation (CK's) |
| Mechanism by which alteration to blood flow predisposes to blood flow | -decreased flow allows platelets to contact endothelium -clotting factors and inhibitors cannot interact with each other normally -activation of endothelial cells >> thrombus |
| Things that lead to turbulence | -cardiac dysfunction (hypertrophic cardiomyopathy) -chronic IV catheter -aneurysm |
| Define aneurysm | -focal pathologic dilated segment of a blood vessel |
| Alterations of blood flow that predispose to thrombosis | -turbulence -stasis |
| Things that increase blood coagulability | -corticosteroids reduce fibrinolysis -PLN/PLE reduce antithrombin III -pancreatitis activates coag cascade -dehydration -steroid hormones |
| Embolus | -an intravascular mass carried by the bloodstream to a site distant from its origin (most are derived from thrombi) |
| ______ emboli may follow severe trauma with bone fractures. | fat |
| _______ emboli occur frequently in vessels around the spinal cord. | -fibrocartilaginous |
| Types of embolus | -fat -fibrocartilagenous -tumor -gas |
| Microscopic morphology of thrombi | -lines of zahn (alternating layers of fibrin, platelets, and RBC's) -lines of zahn NOT present in postmorten clots |
| Gross morphology of thrombi | -chicken fat clot: serum and RBC's have separated (horses) -chicken fat clots asc. with illness in other species |
| 4 different fates of thrombi | 1. dissolution 2. propagation 3. embolization 4. organization 5. recanalization (allow blood flow through or around thrombus) |
| Define infarct | -regional area of ischemic necrosis caused by blood flow obstruction |
| Infarct-resistant organ | -have dual blood supply -liver: portal and hepatic flow -lung: pulmonary and bronchial aa. |
| Pulmonary thrombi | -obstruction of pulmonary aa. >> hypoxia -lungs radiographically and grossly normal -no infarction, but animal will be tachypnic with low pO2 |
| Pathogenesis of saddle thromboemboli | -cardiac dysfunction -left atrial dilation -turbulence -formation of LA thrombi -dislodges from heart -lodges at iliac bifurcation -cold, nonfunctional hind limbs :( |
| Saddle thromboemboli are often seen in _____ but less often seen in _____. | -cats with heart dz -dogs with arteriosclerosis of cd aorta -in dogs it is a saddle THROMBUS |
| DIC | -pathologic activation of the coagulation system leading to hypercoagulation and secondary hemorrhage throughout the body |
| Progression of DIC | -abnormal coagulation profile -formation of microthrombi consumes clotting factors/platelets -consumptive coagulopathy (spontaneous bleeding) -petechiae and ecchymoses -multiple organ failure -death |
| Causes of DIC | -heat stroke -pancreatitis -massive tissue injury -sepsis -venomous snake bite |
Created by:
caldrid3