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SG 3 PATHOLOGY > PATHOLOGY EXAM 2 > Flashcards

PATHOLOGY EXAM 2 Flashcards

1
Q

IF INJURY/DEFECT OCCURS AT EMBRYO STAGE

A

DEATH/ABORTION

DEFECT CARRIED TO TERM

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2
Q

DEFINE EDEMA

A

ABNORMAL ACCUMULATION OF EXCESS INTRACELLULAR FLUID IN INTERSTITIAL SPACE OR BODY CAVITIES

CAPACITY FOR LYMPHATIC RETURN IS EXCEEDED

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3
Q

GRANULOMATOUS EXUDATE

A

GRANULOMAS, MASS LESIONS, ENLARGED ORGANS
MACROPHAGES, LYMPHOCYTES
CHRONIC
BLASTOMYCOSIS, RHODOCOCCUS, HISTOPLASMA, JOHNES DZ

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4
Q

EDEMA CAN BE

A

TRANSUDATE OR EXUDATE

EXCESS FLUID IN INTERSTITIAL TISSUE OR CAVITIES

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5
Q

TRIFECTA THAT MAKES A THROMBUS

A

ENDOTHELIAL INJURY
ABNORMAL BLOOD FLOW
HYPERCOAGUBILITY

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6
Q

IF INJURY/DEFECT OCCURS AT ZYGOTE STAGE

A

DEATH AND RESORPTION

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7
Q

HYPOVOLEMIC SHOCK

A

DECREASED CIRCULATING BLOOD VOLUME (DUE TO HEMORRHAGIC DIARRHEA, VOMITING, LOSS OF FLUIDS)

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8
Q

BLOOD MALDISTRIBUTION

A

DECREASED PERIPHERAL RESISTANCE

BLOOD POOLS IN PERIPHERAL TISSUES

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9
Q

HISTOLOGICAL HALLMARKS OF INFLAMMATION

A

NEUTROPHILS, EDEMA, FIBRIN, MUCOUS

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10
Q

CAUSES OF BLOOD MALDISTRIBUTION

A
  1. ANAPHYLAXIS TYPE 1 HYPERSENSITIVITY
  2. NEUROGENIC NEURO INJURY CAUSES LOSS OF TONE
  3. SEPTIC ENDOTOXIC SHOCK FROM G.BACCILI INDUCES DAMAGE TO ENDOTHELIUM- TRIGGERS COMPLEMENT, VASODILATION, DIC
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11
Q

M2 MACROPHAGES

A

ANTIINFLAMMATORY

WOUND REPAIR AND FIBROSIS

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12
Q

DIAPEDESIS

A

DUE TO DEFECT IN VASCULAR WALL, INCREASED PERMEABILITY
INFLAMMATION
RBCS ABLE TO ESCAPE

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13
Q

PULMONARY CONGESTION

A

LEFT CHF

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14
Q

CHRONIC INFLAMMATION EQUALS THREE THINGS

A

NEOPLASIA
ABSCESS
GRANULOMA

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15
Q

DEFINE EXUDATE

A

OPAQUE, PROTEIN RICH, HIGH CELLULARITY, HIGH SPECIFIC GRAVITY, INFLAMMATORY

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16
Q

WHAT DOES THROMBIN DO?

A

CONVERTS FIBRINOGEN TO FIBRIN

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17
Q

CARDIOGENIC SHOCK

A

FAILURE OF HEART TO MAINTAIN NORMAL OUTPUT

BLOOD PUMPING NOT SUFFICIENT

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18
Q

HEMOTHORAX

A

BLOOD IN THORACIC

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19
Q

COMPONENTS OF A THROMBUS

A
  1. FIBRIN
  2. RBCS
  3. PLATELETS
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20
Q

SHOCK

A

STATE OF CARDIOVASCULAR COLLAPSE

DUE TO

  1. ACUTE REDUCTION OF EFFECTIVE CIRCULATING BLOOD FLOW (HYPOVOLEMIA)
  2. INADEQUATE PERFUSION OF CELLS AND TISSUES
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21
Q

PATHOGENESIS OF ARTHOGRYPOSIS

A
  1. LIMBS DO NOT MOVE DURING DEVELOPMENT
  2. MUSCLES DO NOT GROW CORRECTLY
  3. CONN TISSUE MATURES
  4. LIMB FIXED IN CONTRACTED/FLEXED POSITION
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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

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23
Q

CAUSES OF EDEMA

A
  1. INCREASED HYDROSTATIC BLOOD PRESSURE
  2. DECREASED ONCOTIC PRESSURE
  3. INFLAMMATION
  4. LYMPHATIC OBSTRUCTION
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24
Q

INTENSE INFLAMMATION RESPONSE

A

ATTEMPT TO ISOLATE INFLAMMATION RESPONSE

FORMATION OF A WALL- ABSCESS

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25
Q

ANATOMICAL MALFORMATION

A

FAILURE TO DEVELOP, FAILURE TO CLOSE/FUSE, FAILURE TO CANNALIZE/SEPARATE, CYSTS

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26
Q

HYPEREMIA

A

LOCAL INCREASE IN BLOOD VOLUME AND FLOW IN ARTERIES

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27
Q

HEMOSTASIS

A

MECHANISMS TO SEAL AN INJURED VESSEL TO PREVENT BLOOD LOSS

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28
Q

SUPPURATIVE/ PURULENT EXUDATE

A

YELLOW/GREEN/OPAQUE
NEUTROPHILS
PYOMETRA

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29
Q

PATHOGENESIS DEPENDS ON TISSUE AND TIMING IN UTERO. IN WHAT STAGE WILL DEFECT BE CARRIED TO TERM?

A

EMBRYO

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30
Q

EFFUSION

A

EXTRAVASCULAR FLUID ACCUMULATING IN AN ANATOMICAL SPACE

  1. EXUDATE
  2. TRANSUDATE
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31
Q

WHAT CELLS REGENERATE THE BEST?

A

LABILE CELLS- SKIN AND GIT

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32
Q

ASCITES

A

HYDROPERITONEUM

FLUID IN ABDOMINAL CAVITY

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33
Q

BIOCHEMICAL DEFECTS

A

GENETIC MUTATION, LACK OF SPECIFIC ENZYMES, LYSOSOMAL STORAGE DISEASES

ANIMAL LOOKS NORMAL AT BIRTH DO NOT SEE SIGNS OF DEFECT UNTIL LATER IN LIFE

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34
Q

FIBROSIS

A

PRODUCTION OF FIBROUS CONNECTIVE TISSUE
FIBRINOUS= ACUTE
FIBROUS= CHRONIC
OCCURS WHEN PARENCHYMAL STRUCTURE IS DESTROYED

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35
Q

DISORDERS OF GROWTH

A
  1. NEOPLASIA
  2. CELLULAR ADAPTATION
  3. DEVELOPMENTAL ANOMALIES
    A. BIOCHEMICAL DEFECT.
    B. ANATOMICAL MALFORMATION
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36
Q

FIBRINOUS EXUDATE

A

RUBBERY/WHITE
NEUTROPHILS
INJURY TO ENDOTHELIUM

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37
Q

IDEAL CONDITIONS OF INFLAMMATION

A

RETURN TO NORMAL
ELIMINATION OF SOURCE OF INJURY
RESOLUTION OF INFLAMMATION RESPONSE
RESTORATION OF NORMAL TISSUE ARCHITECTURE

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38
Q

ANASARCA

A

GENERALIZED WITHIN SUBQ TISSUE

39
Q

GRANULOMATOUS INFLAMMATION

A

FORM OF CHRONIC INFLAMMATION

DOMINATED BY MACROPHAGES SURROUNDED BY LYMPHOCYTES AND FIBROSIS

40
Q

HEMOPERICARDIUM

A

BLOOD WITHIN PERICARDIAL SAC

CARDIAC TAMPENADE HEART CANT PUMP

41
Q

DEFINE TRANSUDATE

A

NON INFLAMMATORY
TRANSPARENT
PROTEIN POOR
LOW SPECIFIC GRAVITY

42
Q

WHAT WOULD HAPPEN IF AN ANIMAL WAS BORN WITH ABNORMAL B2 INTEGRINS ?

A

BACTERIAL INFECTION GALORE

NEUTROPHILIA

43
Q

PHYSIOLOGICAL HYPEREMIA

A

DIGESTION
EXERCISE
NEUROVASCULAR

44
Q

CAUSE OF HEMORRHAGE

A

TRAUMA, SEPIS, CHEMICAL AGENTS, NEOPLASIA, COAGULATION ABNORMALITIES

45
Q

PATHOLOGICAL HYPEREMIA

A

INFLAMMATION

REDNESS, RUBOR (CARDINAL SIGN)

46
Q

GROSS APPEARANCE OF EDEMA

A

WET, GELATINOUS, HEAVY, WILL OOZE AT CUT SURFACE

47
Q

ACUTE INFLAMMATION EQUALS THREE THINGS

A

NEUTROPHILS
EDEMA
FIBRIN

48
Q

EMBOLISM

A

PIECES OF THROMBUS BREAK OFF AND MOVE DOWNSTREAM BECOMING LODGED IN SMALLER VESSELS

49
Q

EPISTAXIS

A

NOSE BLEED

50
Q

CARDINAL SIGNS OF INFLAMMATION

A

RUBOR,CALOR,TUMOR,DOLOR,FUNCTION LAESO

REDNESS, HEAT, SWELLING, PAIN, LOSS OF FUNCTION

51
Q

ACUTE INFLAMMATION

A

OCCURS SIMULTANEOUSLY WITH ACTIVATION OF INNATE IMMUNE SYSTEM

52
Q

INFARCTION

A

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
Q

WOUND HEALING STEPS

A
  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
Q

UNDER NORMAL CONDITIONS HEMOSTASIS IS ….

A

ANTITHROMBOTIC AND PROFIBROLYTIC

DURING INJURY IT IS ANTIFIBROLYTIC AND PROTHROMBOTIC

55
Q

HEMOTHROSIS

A

BLOOD WITHIN JOINT CAPSULE

56
Q

STEPS OF ACUTE INFLAMMATION

A
  1. VASODILATION- LEADS TO HYPEREMIA AND TRANSUDATE
  2. INCREASED VASCULAR PERMEABILITY
  3. EMIGRATION OF LEUKOCYTES
57
Q

BOTTLE JAW

A

SUBMANDIBULAR EDEMA

58
Q

LEUKOCYTE ACTIVATION CASCADE

A
  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
Q

WHAT IS PRIMARY INTENTION?

A

WOUNDS WITH OPPOSED EDGES

60
Q

ROLES OF INFLAMMATION

A
  1. DILUTE, ISOLATE, ELIMINATE CAUSE

2. REPAIR DAMAGED TISSUE

61
Q

HEMORRHAGIC EXUDATE

A

BLOOD CLOTS AND INFLAMMATION
VASCULAR DAMAGE
BLACKLEG, HOOKWORM, ENTERITIS

62
Q

SUFFUSIVE HEMORRHAGE

A

CONTINUOUS, COALESCING

63
Q

IF INJURY/DEFECT OCCURS DURING EMBRYO PHASE

A 
ABORTION 
MUMMIFICATION 
STILLBIRTH
WEAK NEONATE 
PERSISTENT VIREMIA/IMMUNOTOLERANCE
64
Q

TRANSUDATE

A

FLUID THT IS ULTRAFILTRATE OF PLASMA

LOW FILTRATE, LOW SPECIFIC GRAVITY, TRANSLUCENT, LOW CELLULARITY

INCREASED HYDOSTATIC PRESSURE, DECREASE COLLOID OSMOTIC PRESSURE

65
Q

DISSEMINATION INTRAVASCULAR COAGULATION

A
  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
Q

PUS

A

INFLAMMATORY EXUDATE RICH IN LEUKOCYTES/NEUTROPHILS AND CELL DEBRIS

PURLENT, SUPPURATIVE EXUDATE

67
Q

HYDROTHORAX

A

FLUID IN THORACIC CAVITY

68
Q

CATARRHAL EXUDATE = MUCOID, MUCOPURULENT

A

CONTAINS PUS AND MUCOUS
ACUTE
GAMMAHERPES VIRUS, RHINITIS

69
Q

GENETIC DEFECTS CAN BE WHAT 4 THINGS

A
  1. INHERITED GENES
  2. SPONTANEOUS SOMATIC MUTATIONS
  3. CHROMOSOMAL DEFECTS
  4. BREED DISPOSITION
70
Q

HEMORRHAGE

A

ESCAPE OF BLOOD FROM THE VESSELS

71
Q

EFFECTS OF THROMBUS

A
  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
Q

HEPATIC CONGESTION

A

NUTMEG LIVER

RIGHT SIDED HF

73
Q

AN ANATOMICAL DEFECT CAN BE WHAT 4 THINGS

A
  1. IN UTERO INF
  2. TERATOGENS
  3. NUTRITIONAL DEFICIENCIES
  4. GENETIC DEFECT
74
Q

THROMBOSIS

A

INAPPROPRIATE ACTIVATION OF HEMOLYTIC PROCESS

75
Q

PYOGRANULOMA

A

CENTER OF NEUTROPHILS

76
Q

HEMOSTASIS FAILUE DUE TO

A

HEPATIC DISEASE, THROMBOCYTOPENIA, BACTERIAL INF, TOXINS, NUTRITIONAL DEFICIENCY

77
Q

INFLAMMATION IS A REACTION OF _______ TISSUE TO INJURY

A

VASCULARIZED, LIVING

78
Q

HEMOPTYSIS

A

COUGHING BLOOD

79
Q

STEPS OF HEMOSTASIS

A
  1. VASOCONSTRICTION
  2. PLATELET AGGREGATION
  3. COAGULATION CASCADE
80
Q

RESULTS OF ACUTE INFLAMMATION

A

RESOLUTION, HEALING BY REPAIR, CHRONIC INFLAMMATION, ABSCESS FORMATION

81
Q

RHEXUS

A

TEAR IN VASCULAR WALL

BLOOD CONSTITUENTS AND RBCS ESCAPE

82
Q

ORGANIZING HEMATOMA AKA BRUISE COLORS

A

HEMOGLOBIN RED/BLUE
HEMOSIDERIN YELLOW/BROWN
BILIRUBIN BLUE/GREEN

83
Q

COMPLEX GRANULOMA

A

CENTER OF CASEOUS NECROSIS

84
Q

DURING WOUND HEALING INFLAMMATION MATRIX METALLOPROTEINS DO WHAT?

A

DEGRADE ECM

85
Q

SEROUS EXUDATE

A

CELL POOR FLUID
VESICLE FORMATION
ACUTE
PHOTOSENSITIZATION, HEARTWATER DISEASE

86
Q

M1 MACROPHAGES

A

PHAGOCYTOSIS OF BACTERIA AND FUNGI

INFLAMMATION

87
Q

FAILURE TO ELIMINATE INSULT

A

SCAR FORMATION

PERSISTENCE OF INFLAMMATION CELLS

88
Q

VERMINOUS THROMBUS

A

CLOT IN CRANIAL MESENTERIC ARTERY DUE TO STRONGYLUS VULVARGIS

89
Q

CHRONIC INFLAMMATION

A

PREDOMINATED BY MACROPHAGES, PLASMA CELLS, LYMPHOCYTES
PROLIFERATION OF FIBROBLASTS, SMALL BLOOD VESSEL, PARENCHYMAL CELL
MAY RESULT IN TISSUE DESTRUCTION

90
Q

POST MORTEM CLOTTING

TWO TYPES

A
  1. RED OR CURRENT JELLY CLOT
    RAPID CLOTTING, BLOOD COMPONENTS EVENLY DISTRIBUTED
  2. CHICKEN FAT COT
    PROLONGED COAGULATION, COMPONENTS SEPARATED
91
Q

SADDLE THROMBUS

A

CLOT AT BIFURCATION OF ABDOMINAL AORTA

92
Q

WHAT IS SECONDARY INTENTION?

A

GAPING WOUNDS, SEPTIC WOUNDS, FOREIGN BODIES, DELAYED WOUND HEALING

93
Q

EXUDATE

A

INCREASE IN PROTEINS, OPAQUE, INCREASED CELLULAR DEBRIS

MAIN CAUSE IS INFLAMMATION, INCREASE IN ENDOTHELIUM

94
Q

EXUDATION

A

ESCAPE OF FLUID, PROTEINS, BLOOD CELLS FROM VASCULAR SYSTEM INTO INTERSTITIUM OR BODY CAVITIES

IMPLIES ALTERATION OF NORMAL PERMEABILITY OF LOCAL BLOOD VESSELS

SG 3 PATHOLOGY (6 decks)

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