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PATHOLOGY EXAM 1 Flashcards

1
Q

MICROFILAMENTS ARE THE THINNEST T/F

A

TRUE

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2
Q

MICROTUBULES ARE STRUCTURAL IN THE MATRIX AND ARE STATIC T/F

A

FALSE- MICROTUBULES CONSTANTLY STRETCH AND ELONGATE

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3
Q

NAME THE TWO MICROTUBULES- IN WHICH DIRECTION DO THEY TRAVEL

A

KINESINS- MOVE NEG TO POS - TO+

DYENINS- MOVE POS TO NEG + TO -

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4
Q

NAME THE FIVE PATHOLOGICAL PROCESSES

A
  1. DEGENERATION AND NECROSIS
  2. INFLAMMATION AND REPAIR
  3. CIRCULATORY DISORDERS
  4. DISORDERS OF GROWTH
  5. DEPOSITS AND PIGMENTATIONS
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5
Q

DEFINE DISEASE

A

ANY DEVIATION FROM NORMAL STRUCTURE OR FUNCTION

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6
Q

DEFINE PATHOGENESIS

A

SEQUENCE OF EVENTS LEADING TO FULL EXPRESSION OF DISEASE

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7
Q

DEFINE ETIOLOGY

A

CAUSAL AGENT

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8
Q

MORPHOLOGICAL DIAGNOSIS MDX

A

PATHOLOGICAL PROCESS, LOCATION, DISTRIBUTION, DURATION, SEVERITY

CHRONIC, PURULENT, GENERALIZED DERMATITIS

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9
Q

ETIOLOGICAL DIAGNOSIS EDX

A

PATHOLOGICAL PROCESS, LOCATION, CAUSE

CHRONIC, PURULENT, GENERALIZED BACTERIAL DERMATITIS

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10
Q

RED CAPPED TUBE IS FOR

A

CULTURE

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11
Q

PURPLE CAPPED TUBE IS FOR

A

FLUID ANALYSIS AND CYTOLOGY

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12
Q

FOR TOXICOLOGY COLLECT WHAT THREE SAMPLES

A

URINE
STOMACH CONTENTS
FAT

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13
Q

WHICH BSL IS REQUIRED TO PERFORM A ROUTINE NECROPSY ON A DOMESTIC ANIMAL?

A

BSL2

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14
Q

WHICH BODY CAVITY DO YOU OPEN FIRST DURING A POSTMORTEM ?

A

ABDOMEN

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15
Q

COLLECT ____ SAMPLES FIRST, THEN ______ SAMPLES

A

MICROBIOLOGICAL, HISTOLOGICAL

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16
Q

DEFINE AUTOLYSIS

A

SELF DIGESTION/ DEGRADATION OF CELLS+ TISSUES BY HYDROLYTIC ENZYMES NORMALLY PRESENT IN TISSUES

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17
Q

PUTREFACTION

A

PROCESS BY WHICH POSTMORTEM BACTERIA BREAK DOWN TISSUES (COLOR, TEXTURE CHANGE, GAS, ODOR)

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18
Q

RATE OF DECOMPOSITION DEPENDS ON

A

CAUSE OF DEATH
ENVT AND BODY TEMP
MICROBIAL FLORA

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19
Q

TISSUES WHERE ENZYMES DEGRADE FASTER

A

GI, PANCREAS, GALL BLADDER, ENDOCRINE GLANDS, KIDNEY, LIVER

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20
Q

THE PRESENCE OF ______ IS MOST LIKELY TO TO BE MICROSCOPICALLY OBSCURED BY DECOMPOSITION.

A

CELL INJURY (NECROSIS)

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21
Q

RIGOR MORTIS

A

OCCURS 1-2 HOURS AFTER DEATH
PERSISTS 1-2 DAYS
CONTRACTION OF MM AFTER DEATH DUE TO DEPLETION OF ATP

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22
Q

POST MORTEM BLOOD CLOTS

A

SHINY, ELASTIC
PERFECT CAST OF LUMEN
ELASTIC
UNATTACHED

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23
Q

ANTE MORTEM CLOTS

A

ATTACHED TO VESSEL WALLS
DRY AND DULL
LAMINATED
FRIABLE

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24
Q

HEMOGLOBIN IMBIBITION

A

RED STAINING OF INTIMA OF HEART AND VESSELS DUE TO HB RELEASE FROM RBCS

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25
ALGOR MORTIS
COOLING OF BODY POSTMORTEM DEPENDS ON BODY TEMP OF THE ANIMAL AT TIME OF DEATH BRAIN TEMP DECREASES AFTER 18HOURS
26
BILE IMBIBITION
BILE PENETRATES WALL AND STAINS NEARBY TISSUES - GALL BLADDER, LIVER, INTESTINES, DIAPHRAGM
27
LIVER MORTIS
VARIATION IN COLOR OF TISSUES DUE TO MOVEMENT OF BLOOD AFTER DEATH AKA HYPOSTATIC CONGESTION
28
BLOAT
HERBIVORES AND RUMINANTS BLOAT FASTER | ASSOCIATED CHANGES- RECTAL/VAGINAL PROLAPSE, FROTH IN THE TRACHEA, RUPTURED VISCERA
29
HOW TO TELL BLOAT FROM RUMINAL TYMPANY
RUMINAL TYMPANY HAS A CHARACTERISTIC BLOAT LINE IN THE ESOPHAGUS
30
PSEUDOMELANOSIS
GREEN TO BLACK DISCOLORATION OF TISSUE POSTMORTEM DUE TO DECOMP OF BLOOD BY BACTERIA FORMING H2S COMMON SEEN- KIDNEY, LIVER, SPLEEN
31
CELL ADAPTION IS AN IRREVERSIBLE CHANGE T/F
FALSE IT IS REVERSIBLE
32
WHAT ARE THE 5 TYPES OF CELL ADAPTATION?
1. ATROPHY 2. HYPERPLASIA 3. HYPOTROPHY 4. METAPLASIA 5. DYSPLASIA
33
HYPERPLASIA
=MORE CELLS! MORE LIKELY TO AFFECT LABILE CELLS- EPIDERMIS, INTESTINAL EPITHELIUM, BONE MARROW
34
HORMONAL HYPERPLASIA
MAMMARY GLAND DURING PREGNANCY
35
COMPENSATORY HYPERPLASIA
HEPATECTOMY
36
PATHOLOGICAL HYPERPLASIA
EXCESSIVE HORMONES OR GROWTH FACTOR , REPEATED IRRITATION, VIRAL INFECTION
37
HYPERTROPHY
=BIGGER CELLS! INCREASE IN SIZE AND FUNCTION MORE ORGANELLES AND STRUCTURAL PROTEINS MORE COMMON IN STABLE CELLS- BONE, CARTILAGE,MM, HEART, NEURONS
38
PHYSIOLOGICAL HYPERTROPHY
WEIGHTLIFTER
39
ATROPHY
=SMALLER CELLS AFTER NORMAL GROWTH IS REACHED DECREASE IN NUMBER OF CELLS, METABOLIC ACTIVITY, PROTEIN SYNTHESIS CAUSE: DECREASED WORKLOAD, DENERVATION, DECREASED O2 BLOOD SUPPLY, INADEQUATE NUTRITION, LOSS OF ENDOCRINE, AGING
40
HYPOPLASIA
INCOMPLETE OR UNDER DEVELOPMENT
41
APLASIA
LACK OF DEVELOPMENT
42
HYPOTROPHY
PROGRESSIVE LOSS OF VITALITY
43
METAPLASIA
=CHANGE IN TYPE OF CELL RESPONSE TO CHRONIC IRRITATION. MAY RESULT IN DECREASED FUNCTION, INCREASED PROPENSITY FOR NEOPLASIA *EPITHELIAL CELLS IRRITATION IN LUNGS, VIT A DEFICIENCY, ESTROGEN TOXICITY, MAMMARY TUMORS, REFLUX IN ESOPHAGUS
44
DYSPLASIA
``` =UNORGANIZED CELLS CHANGE IN SHAPE, SIZE, ORGANIZATION ABNORMAL DEVELOPMENT *EPITHELIUM ASSOCIATED WITH NEOPLASTIC/ MALIGNANT TRANSFORMATION ```
45
REVERSIBLE CELL INJURY
CHANGES FUNCTION OF THE CELL 1. CELLULAR SWELLING- DEPLETION OF ATP 2. LIPIDOSIS
46
IRREVERSIBLE CELL CHANGES ***IN ORDER OF APPEARANCE ***
1. BIOCHEMICAL ALTERATIONS 2. ULTRASTRUCTURAL CHANGES 3. LIGHT MICROSCOPY CHANGES 4. GROSS MORPHOLOGICAL CHANGES NECROSIS- ALWAYS PATHOLOGICAL APOPTOSIS- NORMAL FUNCTION
47
HIGHLY VULNERABLE TO HYPOXIA AND CELL SWELLING
``` CARDIOMYCTES PROXIMAL RENAL TUBULE EPITHELIUM HEPATOCYTES ENDOTHELIUM CNS ```
48
ULTRASTRUCTURAL CHANGES
1. PLASMA MEMBRANE ALTERATIONS 2. MITOCHONDRIAL CHANGES 3. DILATION OF ER 4. NUCLEAR ALTERATIONS
49
CAUSE OF ACUTE CELL SWELLING
LOSS OF IONIC FLUID HOMEOSTASIS DUE TO CHANGE IN OXYGEN SUPPLY
50
LOSS OF IONIC FLUID HOMEOSTASIS CAUSED BY
1. FAILURE OF ENERGY PRODUCTION 2. CELL MEMBRANE DAMAGE 3. INJURY TO ENZYMES REGULATING ION CHANNELS OF MEMBRANE
51
CHANGE IS OXYGEN SUPPLY DUE TO
1. PHYSCIAL/MECHANICAL INJURY 2. HYPOXIA 3. BACTERIA/VIRUSES 4. TOXIC AGENTS 5. FREE RADICALS 6. IMMUNE MEDIATED INJURY
52
GROSS APPEARANCE OF ACUTE CELL SWELLING
SLIGHTLY SWOLLEN ORGAN WITH ROUNDED EDGES | PALLOR
53
HISTIOLOGIC APPEARANCE OF ACUTE CELL SWELLING
CELLS ARE ENLARGED WITH PALE CYTOPLASM
54
HYDROTROPIC AND FATTY CHANGE = CELL SWELLING DUE TO _____
UPTAKE OF H2O OR LIPIDS THEN DISINTEGRATION INTO ORGANELLES
55
HYPERTROPHIC CHANGE
CELL ENLARGEMENT DUE TO INCREASE IN NUMBER OF ORGANELLES
56
ACUTE CELL SWELLING PROGNOSIS DEPENDS ON___
TYPE OF CELL | NUMBER OF CELLS EFFECTED
57
LIPIDOSIS
ACCUMULATION OF TRIGLYCERIDES AND OTHER LIPID METABOLITES WITHIN PARENCHYMAL CELLS FORMATION OF INTRACYTOPLASMIC VACUOLES HEART MM, SKELETAL MM, KIDNEY LIVER- CLINICAL MANIFESTATION= CHANGE IN FUNCTION; ELEVATED LIVER ENZYMES+ICTERUS
58
ETIOLOGY OF LIPIDOSIS
1. HYPOXIA 2. TOXICITY 3. METABOLIC DISORDERS (ABNORMALITY IN SYNTHESIS/UTILIZATION/MOBILIZATION OF FAT
59
CAUSES OF HEPATIC LIPIDOSIS PHYSIOLOGICAL NUTRITIONAL ENDOCRINE
PHYSIOLOGICAL- HEAVY EARLY LACTATION-KETOSIS IN RUMINANT, PREGNANCY TOXEMIA NUTRITIONAL- OBESITY, STARVATION, PROTEIN CALORIE MALNUTRITION ENDOCRINE DISEASES- DIABETES MELLITUS, FELINE FATTY LIVER SYNDROME, FAT COW SYNDROME, NIEMANN PICK DISEASE
60
GROSS APPEARANCE OF HEPATITIS LIPIDOSIS
LIVER- DIFFUSE YELLOW, EDGES ARE ROUNDED, BULGE UPON SECTIONING, TISSUE IS SOFT, FRIABLE, CUTS EASILY, GREASY, MAY FLOAT IN FIXATIVE OR WATER
61
HISTOLOGICAL APPEARANCE OF HEPATIC LIPIDOSIS
WELL DILINEATED, LIPID FILLED VACUOLES IN CYTOPLASM
62
IRREVERSIBLE CELL INJURY | TWO THINGS :)
1. APOPTOSIS= PHYSIOLOGICAL NO INFLAMMATION | 2. NECROSIS= PATHOLOGICAL INFLAMMATION
63
IRREVERSIBLE INJURY HISTOLOGICALLY
SEVERE SWELLING OF MITOS, EXTENSIVE DAMAGE TO PLASMA MEMBRANES, SWELLING OF LYSOSOMES
64
# DEFINE NECROSIS TWO MAIN PROCESSES
CELL DEATH AFTER IRREVERSIBLE INJURY (HYPOXIA, ISCHEMIA, DIRECT CELL MEMBRANE DAMAGE) 1. DENATURATION OF PROTEINS 2. ENZYMATIC DIGESTION OF CELLS
65
ULTRASTRUCTURAL CHANGES DURING NECROSIS
1. KARYOLYSIS- NUCLEAR FADING 2. PYKNOSIS- NUCLEAR SHRINKAGE 3. KARYORRHEXIS- NUCLEAR FRAGMENTATION
66
COAGULATIVE NECROSIS
ARCHITECTURE OF DEAD TISSUE PRESERVED | COMMON CAUSE= ISCHEMIA
67
GANGRENOUS NECROSIS
USUALLY SEEN IN DISTAL EXTREMITIES LIKELY DUE TO ISCHEMIA DRY GANGRENE- NO BACTERIAL SUPERINFECTION WET GANGRENE- TISSUE LOOKS WET, LIQUEFACTIVE= BACTERIAL SUPERINFECTION
68
CASEOUS NECROSIS
CHEESELIKE NECROTIC DEBRIS = DEAD WBCS CHRONIC ETIOLOGY- MYCOBACTERIUM OR FUNGAL INFECTION DYSTROPHIC CALCIFICATION- COMMONLY OCCURS IN CENTER OF LESION. LOSS OF ARCHITECTURE
69
LIQUEFACTIVE NECROSIS
CANNOT RECOGNIZE CELL ARCHITECTURE TISSUES OF HIGH LIPID CONTENT IE BRAIN! BACTERIAL OR FUNGAL INFECTION
70
ABSCESSES
LOCALIZED COLLECTION OF PUS SURROUNDED BY FIBROUS CONNECTIVE TISSUE 1. SEPTIC- FROM INF ACCUMULATION 2. STERILE- NON LIVING IRRITANTS
71
FAT NECROSIS | THREE TYPES
1. ENZYMATIC NECROSIS - PANCREATIC ENZYMES ESCAPED THE PANCREAS —> LEADS TO SAPONIFICATION 2. TRAUMATIC NECROSIS- DYSTOCIA, STILLBIRTH, RECUMBANCY 3. NECROSIS OF ABDOMINAL FAT
72
FIBRINOID NECROSIS
ONLY SEEN HISTOLOGICALLY IN THE BLOOD VESSELS ACCUMULATION OF IMMUNE COMPLEXES
73
APOPTOSIS
PROGRAMMED CELL DEATH NO INFLAMMATION INTRINSIC PATHWAY= CYTOCHROME C EXTRINSIC PATHWAY= CASPASE 8
74
MECHANISMS OF CELL INJURY (THERE ARE 6)
1. DECREASE IN ATP 2. MITOCHONDRIAL DAMAGE 3. INFLUX OF CA 4. INCREASE IN REACTIVE OXYGEN SPECIES 5. MEMBRANE DAMAGE 6. DAMAGE TO PROTEINS AND DNA
75
WHAT CAUSES HYPOXIA ?
``` INADEQUATE OXYGENATION OF BLOOD REDUCED OXYGEN TRANSPORT REDUCED BLOOD SUPPLY BLOCKAGE OF CELL RESP ENZYMES VIRUSES, BACT, PROTOZOA, FUNGI ```
76
INTRINSIC PATHWAY OF APOPTOSIS ACTIVATION
CYTOCHROME C
77
EXTRINSIC PATHWAY OF APOPTOSIS
CASPASE 8

SG 3 PATHOLOGY (6 decks)

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