Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SG 3 PATHOLOGY > PATHOLOGY EXAM 1 > Flashcards

PATHOLOGY EXAM 1 Flashcards

1
Q

MICROFILAMENTS ARE THE THINNEST T/F

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

FALSE- MICROTUBULES CONSTANTLY STRETCH AND ELONGATE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DEFINE DISEASE

A

ANY DEVIATION FROM NORMAL STRUCTURE OR FUNCTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DEFINE PATHOGENESIS

A

SEQUENCE OF EVENTS LEADING TO FULL EXPRESSION OF DISEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DEFINE ETIOLOGY

A

CAUSAL AGENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MORPHOLOGICAL DIAGNOSIS MDX

A

PATHOLOGICAL PROCESS, LOCATION, DISTRIBUTION, DURATION, SEVERITY

CHRONIC, PURULENT, GENERALIZED DERMATITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ETIOLOGICAL DIAGNOSIS EDX

A

PATHOLOGICAL PROCESS, LOCATION, CAUSE

CHRONIC, PURULENT, GENERALIZED BACTERIAL DERMATITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

RED CAPPED TUBE IS FOR

A

CULTURE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PURPLE CAPPED TUBE IS FOR

A

FLUID ANALYSIS AND CYTOLOGY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

FOR TOXICOLOGY COLLECT WHAT THREE SAMPLES

A

URINE
STOMACH CONTENTS
FAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

BSL2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

WHICH BODY CAVITY DO YOU OPEN FIRST DURING A POSTMORTEM ?

A

ABDOMEN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

COLLECT ____ SAMPLES FIRST, THEN ______ SAMPLES

A

MICROBIOLOGICAL, HISTOLOGICAL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

DEFINE AUTOLYSIS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

PUTREFACTION

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

RATE OF DECOMPOSITION DEPENDS ON

A

CAUSE OF DEATH
ENVT AND BODY TEMP
MICROBIAL FLORA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TISSUES WHERE ENZYMES DEGRADE FASTER

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

CELL INJURY (NECROSIS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

POST MORTEM BLOOD CLOTS

A

SHINY, ELASTIC
PERFECT CAST OF LUMEN
ELASTIC
UNATTACHED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ANTE MORTEM CLOTS

A

ATTACHED TO VESSEL WALLS
DRY AND DULL
LAMINATED
FRIABLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HEMOGLOBIN IMBIBITION

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ALGOR MORTIS

A

COOLING OF BODY POSTMORTEM
DEPENDS ON BODY TEMP OF THE ANIMAL AT TIME OF DEATH
BRAIN TEMP DECREASES AFTER 18HOURS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

BILE IMBIBITION

A

BILE PENETRATES WALL AND STAINS NEARBY TISSUES - GALL BLADDER, LIVER, INTESTINES, DIAPHRAGM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

LIVER MORTIS

A

VARIATION IN COLOR OF TISSUES DUE TO MOVEMENT OF BLOOD AFTER DEATH

AKA HYPOSTATIC CONGESTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

BLOAT

A

HERBIVORES AND RUMINANTS BLOAT FASTER

ASSOCIATED CHANGES- RECTAL/VAGINAL PROLAPSE, FROTH IN THE TRACHEA, RUPTURED VISCERA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

HOW TO TELL BLOAT FROM RUMINAL TYMPANY

A

RUMINAL TYMPANY HAS A CHARACTERISTIC BLOAT LINE IN THE ESOPHAGUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

PSEUDOMELANOSIS

A

GREEN TO BLACK DISCOLORATION OF TISSUE POSTMORTEM
DUE TO DECOMP OF BLOOD BY BACTERIA FORMING H2S

COMMON SEEN- KIDNEY, LIVER, SPLEEN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

CELL ADAPTION IS AN IRREVERSIBLE CHANGE T/F

A

FALSE IT IS REVERSIBLE

32
Q

WHAT ARE THE 5 TYPES OF CELL ADAPTATION?

A
  1. ATROPHY
  2. HYPERPLASIA
  3. HYPOTROPHY
  4. METAPLASIA
  5. DYSPLASIA
33
Q

HYPERPLASIA

A

=MORE CELLS!

MORE LIKELY TO AFFECT LABILE CELLS- EPIDERMIS, INTESTINAL EPITHELIUM, BONE MARROW

34
Q

HORMONAL HYPERPLASIA

A

MAMMARY GLAND DURING PREGNANCY

35
Q

COMPENSATORY HYPERPLASIA

A

HEPATECTOMY

36
Q

PATHOLOGICAL HYPERPLASIA

A

EXCESSIVE HORMONES OR GROWTH FACTOR , REPEATED IRRITATION, VIRAL INFECTION

37
Q

HYPERTROPHY

A

=BIGGER CELLS!
INCREASE IN SIZE AND FUNCTION
MORE ORGANELLES AND STRUCTURAL PROTEINS
MORE COMMON IN STABLE CELLS- BONE, CARTILAGE,MM, HEART, NEURONS

38
Q

PHYSIOLOGICAL HYPERTROPHY

A

WEIGHTLIFTER

39
Q

ATROPHY

A

=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
Q

HYPOPLASIA

A

INCOMPLETE OR UNDER DEVELOPMENT

41
Q

APLASIA

A

LACK OF DEVELOPMENT

42
Q

HYPOTROPHY

A

PROGRESSIVE LOSS OF VITALITY

43
Q

METAPLASIA

A

=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
Q

DYSPLASIA

A 
=UNORGANIZED CELLS 
CHANGE IN SHAPE, SIZE, ORGANIZATION 
ABNORMAL DEVELOPMENT 
*EPITHELIUM 
ASSOCIATED WITH NEOPLASTIC/ MALIGNANT TRANSFORMATION
45
Q

REVERSIBLE CELL INJURY

A

CHANGES FUNCTION OF THE CELL

  1. CELLULAR SWELLING- DEPLETION OF ATP
  2. LIPIDOSIS
46
Q

IRREVERSIBLE CELL CHANGES **IN ORDER OF APPEARANCE **

A
  1. BIOCHEMICAL ALTERATIONS
  2. ULTRASTRUCTURAL CHANGES
  3. LIGHT MICROSCOPY CHANGES
  4. GROSS MORPHOLOGICAL CHANGES

NECROSIS- ALWAYS PATHOLOGICAL
APOPTOSIS- NORMAL FUNCTION

47
Q

HIGHLY VULNERABLE TO HYPOXIA AND CELL SWELLING

A 
CARDIOMYCTES 
PROXIMAL RENAL TUBULE EPITHELIUM 
HEPATOCYTES 
ENDOTHELIUM 
CNS
48
Q

ULTRASTRUCTURAL CHANGES

A
  1. PLASMA MEMBRANE ALTERATIONS
  2. MITOCHONDRIAL CHANGES
  3. DILATION OF ER
  4. NUCLEAR ALTERATIONS
49
Q

CAUSE OF ACUTE CELL SWELLING

A

LOSS OF IONIC FLUID HOMEOSTASIS DUE TO CHANGE IN OXYGEN SUPPLY

50
Q

LOSS OF IONIC FLUID HOMEOSTASIS CAUSED BY

A
  1. FAILURE OF ENERGY PRODUCTION
  2. CELL MEMBRANE DAMAGE
  3. INJURY TO ENZYMES REGULATING ION CHANNELS OF MEMBRANE
51
Q

CHANGE IS OXYGEN SUPPLY DUE TO

A
  1. PHYSCIAL/MECHANICAL INJURY
  2. HYPOXIA
  3. BACTERIA/VIRUSES
  4. TOXIC AGENTS
  5. FREE RADICALS
  6. IMMUNE MEDIATED INJURY
52
Q

GROSS APPEARANCE OF ACUTE CELL SWELLING

A

SLIGHTLY SWOLLEN ORGAN WITH ROUNDED EDGES

PALLOR

53
Q

HISTIOLOGIC APPEARANCE OF ACUTE CELL SWELLING

A

CELLS ARE ENLARGED WITH PALE CYTOPLASM

54
Q

HYDROTROPIC AND FATTY CHANGE = CELL SWELLING DUE TO _____

A

UPTAKE OF H2O OR LIPIDS THEN DISINTEGRATION INTO ORGANELLES

55
Q

HYPERTROPHIC CHANGE

A

CELL ENLARGEMENT DUE TO INCREASE IN NUMBER OF ORGANELLES

56
Q

ACUTE CELL SWELLING PROGNOSIS DEPENDS ON___

A

TYPE OF CELL

NUMBER OF CELLS EFFECTED

57
Q

LIPIDOSIS

A

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
Q

ETIOLOGY OF LIPIDOSIS

A
  1. HYPOXIA
  2. TOXICITY
  3. METABOLIC DISORDERS (ABNORMALITY IN SYNTHESIS/UTILIZATION/MOBILIZATION OF FAT
59
Q

CAUSES OF HEPATIC LIPIDOSIS
PHYSIOLOGICAL
NUTRITIONAL
ENDOCRINE

A

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
Q

GROSS APPEARANCE OF HEPATITIS LIPIDOSIS

A

LIVER- DIFFUSE YELLOW, EDGES ARE ROUNDED, BULGE UPON SECTIONING, TISSUE IS SOFT, FRIABLE, CUTS EASILY, GREASY, MAY FLOAT IN FIXATIVE OR WATER

61
Q

HISTOLOGICAL APPEARANCE OF HEPATIC LIPIDOSIS

A

WELL DILINEATED, LIPID FILLED VACUOLES IN CYTOPLASM

62
Q

IRREVERSIBLE CELL INJURY

TWO THINGS :)

A
  1. APOPTOSIS= PHYSIOLOGICAL NO INFLAMMATION

2. NECROSIS= PATHOLOGICAL INFLAMMATION

63
Q

IRREVERSIBLE INJURY HISTOLOGICALLY

A

SEVERE SWELLING OF MITOS, EXTENSIVE DAMAGE TO PLASMA MEMBRANES, SWELLING OF LYSOSOMES

64
Q

DEFINE NECROSIS

TWO MAIN PROCESSES

A

CELL DEATH AFTER IRREVERSIBLE INJURY (HYPOXIA, ISCHEMIA, DIRECT CELL MEMBRANE DAMAGE)

  1. DENATURATION OF PROTEINS
  2. ENZYMATIC DIGESTION OF CELLS
65
Q

ULTRASTRUCTURAL CHANGES DURING NECROSIS

A
  1. KARYOLYSIS- NUCLEAR FADING
  2. PYKNOSIS- NUCLEAR SHRINKAGE
  3. KARYORRHEXIS- NUCLEAR FRAGMENTATION
66
Q

COAGULATIVE NECROSIS

A

ARCHITECTURE OF DEAD TISSUE PRESERVED

COMMON CAUSE= ISCHEMIA

67
Q

GANGRENOUS NECROSIS

A

USUALLY SEEN IN DISTAL EXTREMITIES
LIKELY DUE TO ISCHEMIA

DRY GANGRENE- NO BACTERIAL SUPERINFECTION
WET GANGRENE- TISSUE LOOKS WET, LIQUEFACTIVE= BACTERIAL SUPERINFECTION

68
Q

CASEOUS NECROSIS

A

CHEESELIKE
NECROTIC DEBRIS = DEAD WBCS
CHRONIC
ETIOLOGY- MYCOBACTERIUM OR FUNGAL INFECTION
DYSTROPHIC CALCIFICATION- COMMONLY OCCURS IN CENTER OF LESION.
LOSS OF ARCHITECTURE

69
Q

LIQUEFACTIVE NECROSIS

A

CANNOT RECOGNIZE CELL ARCHITECTURE
TISSUES OF HIGH LIPID CONTENT IE BRAIN!
BACTERIAL OR FUNGAL INFECTION

70
Q

ABSCESSES

A

LOCALIZED COLLECTION OF PUS SURROUNDED BY FIBROUS CONNECTIVE TISSUE

  1. SEPTIC- FROM INF ACCUMULATION
  2. STERILE- NON LIVING IRRITANTS
71
Q

FAT NECROSIS

THREE TYPES

A
  1. ENZYMATIC NECROSIS - PANCREATIC ENZYMES ESCAPED THE PANCREAS —> LEADS TO SAPONIFICATION
  2. TRAUMATIC NECROSIS- DYSTOCIA, STILLBIRTH, RECUMBANCY
  3. NECROSIS OF ABDOMINAL FAT
72
Q

FIBRINOID NECROSIS

A

ONLY SEEN HISTOLOGICALLY
IN THE BLOOD VESSELS
ACCUMULATION OF IMMUNE COMPLEXES

73
Q

APOPTOSIS

A

PROGRAMMED CELL DEATH
NO INFLAMMATION
INTRINSIC PATHWAY= CYTOCHROME C
EXTRINSIC PATHWAY= CASPASE 8

74
Q

MECHANISMS OF CELL INJURY (THERE ARE 6)

A
  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
Q

WHAT CAUSES HYPOXIA ?

A 
INADEQUATE OXYGENATION OF BLOOD 
REDUCED OXYGEN TRANSPORT 
REDUCED BLOOD SUPPLY 
BLOCKAGE OF CELL RESP ENZYMES 
VIRUSES, BACT, PROTOZOA, FUNGI
76
Q

INTRINSIC PATHWAY OF APOPTOSIS ACTIVATION

A

CYTOCHROME C

77
Q

EXTRINSIC PATHWAY OF APOPTOSIS

A

CASPASE 8

SG 3 PATHOLOGY (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions