PATHOLOGY EXAM 2 Flashcards
1
Q
IF INJURY/DEFECT OCCURS AT EMBRYO STAGE
A
DEATH/ABORTION
DEFECT CARRIED TO TERM
2
Q
DEFINE EDEMA
A
ABNORMAL ACCUMULATION OF EXCESS INTRACELLULAR FLUID IN INTERSTITIAL SPACE OR BODY CAVITIES
CAPACITY FOR LYMPHATIC RETURN IS EXCEEDED
3
Q
GRANULOMATOUS EXUDATE
A
GRANULOMAS, MASS LESIONS, ENLARGED ORGANS
MACROPHAGES, LYMPHOCYTES
CHRONIC
BLASTOMYCOSIS, RHODOCOCCUS, HISTOPLASMA, JOHNES DZ
4
Q
EDEMA CAN BE
A
TRANSUDATE OR EXUDATE
EXCESS FLUID IN INTERSTITIAL TISSUE OR CAVITIES
5
Q
TRIFECTA THAT MAKES A THROMBUS
A
ENDOTHELIAL INJURY
ABNORMAL BLOOD FLOW
HYPERCOAGUBILITY
6
Q
IF INJURY/DEFECT OCCURS AT ZYGOTE STAGE
A
DEATH AND RESORPTION
7
Q
HYPOVOLEMIC SHOCK
A
DECREASED CIRCULATING BLOOD VOLUME (DUE TO HEMORRHAGIC DIARRHEA, VOMITING, LOSS OF FLUIDS)
8
Q
BLOOD MALDISTRIBUTION
A
DECREASED PERIPHERAL RESISTANCE
BLOOD POOLS IN PERIPHERAL TISSUES
9
Q
HISTOLOGICAL HALLMARKS OF INFLAMMATION
A
NEUTROPHILS, EDEMA, FIBRIN, MUCOUS
10
Q
CAUSES OF BLOOD MALDISTRIBUTION
A
- ANAPHYLAXIS TYPE 1 HYPERSENSITIVITY
- NEUROGENIC NEURO INJURY CAUSES LOSS OF TONE
- SEPTIC ENDOTOXIC SHOCK FROM G.BACCILI INDUCES DAMAGE TO ENDOTHELIUM- TRIGGERS COMPLEMENT, VASODILATION, DIC
11
Q
M2 MACROPHAGES
A
ANTIINFLAMMATORY
WOUND REPAIR AND FIBROSIS
12
Q
DIAPEDESIS
A
DUE TO DEFECT IN VASCULAR WALL, INCREASED PERMEABILITY
INFLAMMATION
RBCS ABLE TO ESCAPE
13
Q
PULMONARY CONGESTION
A
LEFT CHF
14
Q
CHRONIC INFLAMMATION EQUALS THREE THINGS
A
NEOPLASIA
ABSCESS
GRANULOMA
15
Q
DEFINE EXUDATE
A
OPAQUE, PROTEIN RICH, HIGH CELLULARITY, HIGH SPECIFIC GRAVITY, INFLAMMATORY
16
Q
WHAT DOES THROMBIN DO?
A
CONVERTS FIBRINOGEN TO FIBRIN
17
Q
CARDIOGENIC SHOCK
A
FAILURE OF HEART TO MAINTAIN NORMAL OUTPUT
BLOOD PUMPING NOT SUFFICIENT
18
Q
HEMOTHORAX
A
BLOOD IN THORACIC
19
Q
COMPONENTS OF A THROMBUS
A
- FIBRIN
- RBCS
- PLATELETS
20
Q
SHOCK
A
STATE OF CARDIOVASCULAR COLLAPSE
DUE TO
- ACUTE REDUCTION OF EFFECTIVE CIRCULATING BLOOD FLOW (HYPOVOLEMIA)
- INADEQUATE PERFUSION OF CELLS AND TISSUES
21
Q
PATHOGENESIS OF ARTHOGRYPOSIS
A
- LIMBS DO NOT MOVE DURING DEVELOPMENT
- MUSCLES DO NOT GROW CORRECTLY
- CONN TISSUE MATURES
- LIMB FIXED IN CONTRACTED/FLEXED POSITION
22
Q
PULMONARY EDEMA
A
NONINFLAMMATORY= LEFT CHF
INFLAMMATORY- DAMAGE TO PULMONARY ENDOTHELIUM, PNEUMONIA, ACUTE RESP DISTRESS SYNDROME, CHRONIC, HEART FAILURE, THICKENED ALVEOLAR WALLS, HEMOSIDERIN
23
Q
CAUSES OF EDEMA
A
- INCREASED HYDROSTATIC BLOOD PRESSURE
- DECREASED ONCOTIC PRESSURE
- INFLAMMATION
- LYMPHATIC OBSTRUCTION
24
Q
INTENSE INFLAMMATION RESPONSE
A
ATTEMPT TO ISOLATE INFLAMMATION RESPONSE
FORMATION OF A WALL- ABSCESS
25
ANATOMICAL MALFORMATION
FAILURE TO DEVELOP, FAILURE TO CLOSE/FUSE, FAILURE TO CANNALIZE/SEPARATE, CYSTS
26
HYPEREMIA
LOCAL INCREASE IN BLOOD VOLUME AND FLOW IN ARTERIES
27
HEMOSTASIS
MECHANISMS TO SEAL AN INJURED VESSEL TO PREVENT BLOOD LOSS
28
SUPPURATIVE/ PURULENT EXUDATE
YELLOW/GREEN/OPAQUE
NEUTROPHILS
PYOMETRA
29
PATHOGENESIS DEPENDS ON TISSUE AND TIMING IN UTERO. IN WHAT STAGE WILL DEFECT BE CARRIED TO TERM?
EMBRYO
30
EFFUSION
EXTRAVASCULAR FLUID ACCUMULATING IN AN ANATOMICAL SPACE
1. EXUDATE
2. TRANSUDATE
31
WHAT CELLS REGENERATE THE BEST?
LABILE CELLS- SKIN AND GIT
32
ASCITES
HYDROPERITONEUM
FLUID IN ABDOMINAL CAVITY
33
BIOCHEMICAL DEFECTS
GENETIC MUTATION, LACK OF SPECIFIC ENZYMES, LYSOSOMAL STORAGE DISEASES
ANIMAL LOOKS NORMAL AT BIRTH DO NOT SEE SIGNS OF DEFECT UNTIL LATER IN LIFE
34
FIBROSIS
PRODUCTION OF FIBROUS CONNECTIVE TISSUE
FIBRINOUS= ACUTE
FIBROUS= CHRONIC
OCCURS WHEN PARENCHYMAL STRUCTURE IS DESTROYED
35
DISORDERS OF GROWTH
1. NEOPLASIA
2. CELLULAR ADAPTATION
3. DEVELOPMENTAL ANOMALIES
A. BIOCHEMICAL DEFECT.
B. ANATOMICAL MALFORMATION
36
FIBRINOUS EXUDATE
RUBBERY/WHITE
NEUTROPHILS
INJURY TO ENDOTHELIUM
37
IDEAL CONDITIONS OF INFLAMMATION
RETURN TO NORMAL
ELIMINATION OF SOURCE OF INJURY
RESOLUTION OF INFLAMMATION RESPONSE
RESTORATION OF NORMAL TISSUE ARCHITECTURE
38
ANASARCA
GENERALIZED WITHIN SUBQ TISSUE
39
GRANULOMATOUS INFLAMMATION
FORM OF CHRONIC INFLAMMATION
| DOMINATED BY MACROPHAGES SURROUNDED BY LYMPHOCYTES AND FIBROSIS
40
HEMOPERICARDIUM
BLOOD WITHIN PERICARDIAL SAC
CARDIAC TAMPENADE HEART CANT PUMP
41
DEFINE TRANSUDATE
NON INFLAMMATORY
TRANSPARENT
PROTEIN POOR
LOW SPECIFIC GRAVITY
42
WHAT WOULD HAPPEN IF AN ANIMAL WAS BORN WITH ABNORMAL B2 INTEGRINS ?
BACTERIAL INFECTION GALORE
| NEUTROPHILIA
43
PHYSIOLOGICAL HYPEREMIA
DIGESTION
EXERCISE
NEUROVASCULAR
44
CAUSE OF HEMORRHAGE
TRAUMA, SEPIS, CHEMICAL AGENTS, NEOPLASIA, COAGULATION ABNORMALITIES
45
PATHOLOGICAL HYPEREMIA
INFLAMMATION
| REDNESS, RUBOR (CARDINAL SIGN)
46
GROSS APPEARANCE OF EDEMA
WET, GELATINOUS, HEAVY, WILL OOZE AT CUT SURFACE
47
ACUTE INFLAMMATION EQUALS THREE THINGS
NEUTROPHILS
EDEMA
FIBRIN
48
EMBOLISM
PIECES OF THROMBUS BREAK OFF AND MOVE DOWNSTREAM BECOMING LODGED IN SMALLER VESSELS
49
EPISTAXIS
NOSE BLEED
50
CARDINAL SIGNS OF INFLAMMATION
RUBOR,CALOR,TUMOR,DOLOR,FUNCTION LAESO
REDNESS, HEAT, SWELLING, PAIN, LOSS OF FUNCTION
51
ACUTE INFLAMMATION
OCCURS SIMULTANEOUSLY WITH ACTIVATION OF INNATE IMMUNE SYSTEM
52
INFARCTION
LOCALIZED AREA OF ISCHEMIC NECROSIS WHEN VEINS OR ARTERIES ARE OCCLUDED
VENOUS-INTENSIVE HEMORRHAGIC, BLOOD BACKS UP
ARTERIAL- INITIALLY HEMORRHAGIC, BECOME PALE OVER TIME DUE TO LACK OF BLOOD FLOW
53
WOUND HEALING STEPS
1. HEMOSTASIS- PLATELETS AGGREGATE AT SITE OF INJURY REDUCES BLOOD LOSS, BINDS EDGES OF WOUNDS, INITIATES ANGIOGENESIS
2. INFLAMMATION- CARDINAL SIGNS SEEN E=DEGRADATION OF DEBRIS BY LEUKOCYTES
3. PROLIFERATION- REGENERATION, GRANULATION TISSUE FORMS “PROUD FLESH” EPITHELIZATION, ANGIOGENESIS, FIBROSIS
4. MATURATION- REMODELING OF GRANULATION TISSUE, MATURATION OF FIBROSIS, *WOUND CONTRACTION, REESTABLISHMENT OF CELL INTERACTION
54
UNDER NORMAL CONDITIONS HEMOSTASIS IS ....
ANTITHROMBOTIC AND PROFIBROLYTIC
DURING INJURY IT IS ANTIFIBROLYTIC AND PROTHROMBOTIC
55
HEMOTHROSIS
BLOOD WITHIN JOINT CAPSULE
56
STEPS OF ACUTE INFLAMMATION
1. VASODILATION- LEADS TO HYPEREMIA AND TRANSUDATE
2. INCREASED VASCULAR PERMEABILITY
3. EMIGRATION OF LEUKOCYTES
57
BOTTLE JAW
SUBMANDIBULAR EDEMA
58
LEUKOCYTE ACTIVATION CASCADE
1. MARGINATION- MOVE TOWARDS PERIPHERY OF LUMEN
2. ROLLING- WEAK BINDING OF SELECTINS
3. ADEHESION B2 INTEGRINS OF LEUKOCYTES BIND TO ICAM OF ENDOTHELIAL CELL
4. EMIGRATION- TRANSENDOTHELIAL MIGRATION
5. CHEMOTAXIS- MIGRATION WITHIN EXUDATE
6. ACTIVATION- PHAGOCYTOSIS/DEGRANULATION
59
WHAT IS PRIMARY INTENTION?
WOUNDS WITH OPPOSED EDGES
60
ROLES OF INFLAMMATION
1. DILUTE, ISOLATE, ELIMINATE CAUSE
| 2. REPAIR DAMAGED TISSUE
61
HEMORRHAGIC EXUDATE
BLOOD CLOTS AND INFLAMMATION
VASCULAR DAMAGE
BLACKLEG, HOOKWORM, ENTERITIS
62
SUFFUSIVE HEMORRHAGE
CONTINUOUS, COALESCING
63
IF INJURY/DEFECT OCCURS DURING EMBRYO PHASE
```
ABORTION
MUMMIFICATION
STILLBIRTH
WEAK NEONATE
PERSISTENT VIREMIA/IMMUNOTOLERANCE
```
64
TRANSUDATE
FLUID THT IS ULTRAFILTRATE OF PLASMA
LOW FILTRATE, LOW SPECIFIC GRAVITY, TRANSLUCENT, LOW CELLULARITY
INCREASED HYDOSTATIC PRESSURE, DECREASE COLLOID OSMOTIC PRESSURE
65
DISSEMINATION INTRAVASCULAR COAGULATION
1. INCREASED COAGULATION+FORMATION OF LOTS OF FIBRIN LOTS
2. DROP IN PLATELETS + PROTHROMBIN BECAUSE THEYRE BEING USED TO FORM CLOTS IN FIRST PHASE =HEMORRHAGE- BLEEDING CANT STOP
3. FIBRINOLYSIS IS ACTIVATED AS RESPONSE TO FIRST PHASE- HEMORRHAGE BECOMES MOST SEVERE
66
PUS
INFLAMMATORY EXUDATE RICH IN LEUKOCYTES/NEUTROPHILS AND CELL DEBRIS
PURLENT, SUPPURATIVE EXUDATE
67
HYDROTHORAX
FLUID IN THORACIC CAVITY
68
CATARRHAL EXUDATE = MUCOID, MUCOPURULENT
CONTAINS PUS AND MUCOUS
ACUTE
GAMMAHERPES VIRUS, RHINITIS
69
GENETIC DEFECTS CAN BE WHAT 4 THINGS
1. INHERITED GENES
2. SPONTANEOUS SOMATIC MUTATIONS
3. CHROMOSOMAL DEFECTS
4. BREED DISPOSITION
70
HEMORRHAGE
ESCAPE OF BLOOD FROM THE VESSELS
71
EFFECTS OF THROMBUS
1. BENEFICIAL- ASSISTS TO CONTROL HEMORRHAGE
2. NEGLIGIBLE- PRESENT IN BLOOD VESSELS BUT NOT REQUIRED DUE TO COLLATERAL CIRCULATION
3. HARMFUL- MAJOR BLOOD SUPPLY OF VITAL ORGANS- INSUFFICIENT OR NO COLLATERAL SITUATION
72
HEPATIC CONGESTION
NUTMEG LIVER
| RIGHT SIDED HF
73
AN ANATOMICAL DEFECT CAN BE WHAT 4 THINGS
1. IN UTERO INF
2. TERATOGENS
3. NUTRITIONAL DEFICIENCIES
4. GENETIC DEFECT
74
THROMBOSIS
INAPPROPRIATE ACTIVATION OF HEMOLYTIC PROCESS
75
PYOGRANULOMA
CENTER OF NEUTROPHILS
76
HEMOSTASIS FAILUE DUE TO
HEPATIC DISEASE, THROMBOCYTOPENIA, BACTERIAL INF, TOXINS, NUTRITIONAL DEFICIENCY
77
INFLAMMATION IS A REACTION OF _______ TISSUE TO INJURY
VASCULARIZED, LIVING
78
HEMOPTYSIS
COUGHING BLOOD
79
STEPS OF HEMOSTASIS
1. VASOCONSTRICTION
2. PLATELET AGGREGATION
3. COAGULATION CASCADE
80
RESULTS OF ACUTE INFLAMMATION
RESOLUTION, HEALING BY REPAIR, CHRONIC INFLAMMATION, ABSCESS FORMATION
81
RHEXUS
TEAR IN VASCULAR WALL
| BLOOD CONSTITUENTS AND RBCS ESCAPE
82
ORGANIZING HEMATOMA AKA BRUISE COLORS
HEMOGLOBIN RED/BLUE
HEMOSIDERIN YELLOW/BROWN
BILIRUBIN BLUE/GREEN
83
COMPLEX GRANULOMA
CENTER OF CASEOUS NECROSIS
84
DURING WOUND HEALING INFLAMMATION MATRIX METALLOPROTEINS DO WHAT?
DEGRADE ECM
85
SEROUS EXUDATE
CELL POOR FLUID
VESICLE FORMATION
ACUTE
PHOTOSENSITIZATION, HEARTWATER DISEASE
86
M1 MACROPHAGES
PHAGOCYTOSIS OF BACTERIA AND FUNGI
| INFLAMMATION
87
FAILURE TO ELIMINATE INSULT
SCAR FORMATION
| PERSISTENCE OF INFLAMMATION CELLS
88
VERMINOUS THROMBUS
CLOT IN CRANIAL MESENTERIC ARTERY DUE TO STRONGYLUS VULVARGIS
89
CHRONIC INFLAMMATION
PREDOMINATED BY MACROPHAGES, PLASMA CELLS, LYMPHOCYTES
PROLIFERATION OF FIBROBLASTS, SMALL BLOOD VESSEL, PARENCHYMAL CELL
MAY RESULT IN TISSUE DESTRUCTION
90
POST MORTEM CLOTTING
| TWO TYPES
1. RED OR CURRENT JELLY CLOT
RAPID CLOTTING, BLOOD COMPONENTS EVENLY DISTRIBUTED
2. CHICKEN FAT COT
PROLONGED COAGULATION, COMPONENTS SEPARATED
91
SADDLE THROMBUS
CLOT AT BIFURCATION OF ABDOMINAL AORTA
92
WHAT IS SECONDARY INTENTION?
GAPING WOUNDS, SEPTIC WOUNDS, FOREIGN BODIES, DELAYED WOUND HEALING
93
EXUDATE
INCREASE IN PROTEINS, OPAQUE, INCREASED CELLULAR DEBRIS
MAIN CAUSE IS INFLAMMATION, INCREASE IN ENDOTHELIUM
94
EXUDATION
ESCAPE OF FLUID, PROTEINS, BLOOD CELLS FROM VASCULAR SYSTEM INTO INTERSTITIUM OR BODY CAVITIES
IMPLIES ALTERATION OF NORMAL PERMEABILITY OF LOCAL BLOOD VESSELS
