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MTAP 2 > Histopath Midterm > Flashcards

Histopath Midterm Flashcards

1
Q

“Study of Diseases”

A

Pathology

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2
Q

What class of cells?:

frequently dividing; undergo cell division to replace lost cells

A

Labile cell

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3
Q

What class of cells?:

Epithelial cells of the skin

A

Labile cell

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4
Q

What class of cells?:

not typically dividing; undergo cell division only to replace injured cells

A

Stable cell

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5
Q

What class of cells?:

Parenchymal cells of liver and kidney

A

Stable cell

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6
Q

What class of cells?:

do not undergo replication ff. maturation

A

Permanent cell

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7
Q

What class of cells?:

Neurons/Nerve cells

A

Permanent cell

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8
Q

DECREASE in tissue or organ size

A

Atrophy

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9
Q

Give one example of physiologic atrophy

A
  • Atrophy of thymus at puberty
  • Decrease in uterus size after childbirth
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10
Q

Type of atrophy that occurs if blood supply to an organ becomes reduced or below critical level

A

Vascular atrophy

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11
Q

Type of atrophy that may develop secondary to pressure atrophy

A

Vascular atrophy

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12
Q

Persistent pressure on the organ or tissue may directly injure the cell

A

Pressure atrophy

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13
Q

Due to lack of nutritional supply to sustain normal growth

A

Starvation/Hunger atrophy

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14
Q

Due to lack of hormones needed to maintain normal size and structure

A

Endocrine atrophy

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15
Q

Inactivity or diminished activity/function

A

Atrophy of disuse

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16
Q

Too much workload can cause general wasting of tissues

A

Exhaustion atrophy

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17
Q

INCREASE in tissue or organ size due to an increase in SIZE of cells making up the organ

*NO NEW CELLS ARE PRODUCED

A

Hypertrophy

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18
Q

Increase in the size of skeletal muscle due to frequent exercise

A

Physiologic hypertrophy

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19
Q

Increase in the size of heart muscle (myocardium) due to hypertension

A

Pathologic hyperthropy

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20
Q

Increase in size of organ as a response to deficiency

Usually occurs when one of the paired organs is removed

A

Compensatory hypertrophy

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21
Q

INCREASE in tissue size or organ size due to an increase in the NUMBER of cells making up the organ

*NEW CELLS ARE FORMED

A

Hyperplasia

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22
Q

-Increase in breast and uterus size due to pregnancy
- Increase in breast size during puberty due to glandular stimulation

A

Physiologic hyperplasia

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23
Q
  • Diffuse crowding of epithelial cells in Graves disease
  • Increase in the number of lymph nodules in TB of cervical lymph nodes
A

Pathologic hyperplasia

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24
Q

Develops usually together with compensatory hypertrophy

A

Compensatory hyperplasia

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25
Q

Involves transformation of adult cell type into another adult cell type

A

Metaplasia

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26
Q

Metaplasia is (reversible/irreversible) process

A

Reversible

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27
Q

aka atypical metaplasia/pre-neoplastic lesion

A

Dysplasia

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28
Q

Change in cell size, shape, and orientation

A

Dysplasia

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29
Q

Dysplasia is (reversible /irreversible) process

A

Reversible

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30
Q

aka De-differentiation

A

Anaplasia

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31
Q

Anaplasia is (reversible/irreversible) process

A

Irreversible

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32
Q

Transformation of adult cells to embryonic/fetal cells

A

Anaplasia

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33
Q

T/F: Neoplasia is NOT a cellular adaptation mechanism

A

True

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34
Q

Hypoxic injury can be IRREVERSIBLE after:
___ = for neurons
___ = for myocardial cells and hepatocytes
___ = for skeletal muscles

A

3-5 minutes
1-2 hours
Many hours

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35
Q

Reversible injury: Gross changes

A
  • Organ pallor
  • Increased weight
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36
Q

Reversible injury: Microscopic changes

A
  • Cellular swelling (first manifestation)
  • Fatty degeneration
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37
Q

Irreversible injuries are due to:

A
  • Enzymatic digestion of cells
  • Protein denaturation
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38
Q

Cytoplasmic changes in
Irreversible injury

A
  1. Larger cells “cloudy swelling”
  2. Increased eosinophilia
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39
Q

Nuclear changes in irreversible
injury

A
  1. Pyknosis – condensation of nucleus
  2. Karyolysis – fragmentation/segmentation of nucleus
  3. Karyorrhexis – dissolution of nucleus
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40
Q

Physiologic cell death; Programmed cell death.

A

Apoptosis

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41
Q

Death of single cell in a cluster of cells

A

Apoptosis

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42
Q

Cell shrinkage = intact membrane = no leakage of cellular components = NO INFLAMMATION

A

Apoptosis

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43
Q

Chief morphologic features in apoptosis

A
  • Chromatin condensation
  • Chromatin fragmentation
  • Cell shrinkage
  • Cytoplasmic bleb formation
  • Phagocytosis of apoptotic cells
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44
Q

Pathologic cell death
Accidental cell death

A

Necrosis

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45
Q

Cell swelling = membrane is not intact = there is leakage of cellular components = THERE IS INFLAMMATION

A

Necrosis

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46
Q

Type of necrosis?

  • due to sudden cut-off of blood supply
  • cell death is due to ISCHEMIA.
A

Coagulative necrosis

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47
Q

Type of necrosis?

Action of hydrolytic enzymes (lysozyme) is blocked.

A

Coagulative necrosis

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48
Q

Type of necrosis?

Appearance:
- Microscopically, cell outlines are preserved but appears GHOSTLY (nothing inside)
- On gross, affected organs somewhat firm, appearing like a boiled material.

A

Coagulative necrosis

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49
Q

Type of necrosis?

i.e. Myocardial infarction

A

Coagulative necrosis

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50
Q

Type of necrosis?

Softening of organs is due to action of hydrolytic enzymes (lysozyme); there is complete digestion of cells.

A

Liquefactive necrosis

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51
Q

Type of necrosis?

Appearance:
- On gross, affected organ appears liquefied, creamy yellow due to increased pus

A

Liquefactive necrosis

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52
Q

Type of necrosis?

i.e. Brain infarction, Suppurative bacterial infection

A

Liquefactive necrosis

53
Q

Type of necrosis?

Combination of coagulative and liquefactive necrosis

A

Caseous necrosis

54
Q

Type of necrosis?

Appearance
- On gross, tissue/organ appears greasy resembling “cheese”
- Microscopically it appears as amorphous granular debris surrounded by granulomatous inflammation

A

Caseous necrosis

55
Q

Type of necrosis?

Usually seen in TB

A

Caseous necrosis

56
Q

Type of necrosis?

  • Seen in immune reactions of the blood vessel.
  • Vessel wall appears thick due to deposition of fibrin in vessel wall.
A

Fibrinoid necrosis

57
Q

Type of necrosis?

  • Gross appearance CANNOT be noted
  • Changes are too smal
A

Fibrinoid necrosis

58
Q
A
59
Q

Type of necrosis?

  • Destruction of fat cells due to release of pancreatic lipases
  • Death of fat tissues (adipose) due to loss of blood supply
A

Fat necrosis

60
Q

Type of necrosis?

Appearance:
- On gross, necrotic material appears “chalky white”.
- On microscopy, infiltrates of foamy macrophage adjacent to adipose tissues

A

Fat necrosis

61
Q

Type of necrosis?

  • Seen in pancreatitis
  • Affected organ is usually breast
A

Fat necrosis

62
Q

Not a specific pattern of necrosis

A

Gangrenous necrosis

63
Q

Type of necrosis secondary to ischemia

A

Gangrenous necrosis

64
Q

_ _ _ _ _ _ _ _ = refers to tissue death due to interruption of blood supply, usually in lower extremities (limb)

A

Gangrene

65
Q

Skin appears dry, black, and is observed in various stages of decomposition

A

Gangrenous necrosis

66
Q

Due to venous occlusion i.e. embolism of foot

A

Wet gangrene

67
Q

Due to arterial occlusion i.e. bacterial infection

A

Dru gangrene

68
Q

Ultimate goal of inflammation

A
  1. To remove the initial cause of injury
  2. To remove consequences of injury
69
Q

5 Cardinal Signs

A

Dolor – pain
Rubor – redness due to increase rate of blood flow
Calor – heat
Tumor – swelling
Function laesa – destruction of functioning units of the cell

70
Q
  • Rapid response to an injurious agent
  • May progress to chronic inflammation if it fails to subside in the course of several weeks.
A

Acute inflammation

71
Q
A
71
Q

Hallmark signs (2) of acute inflammation

A
  1. exudation – escape of fluid, CHON, and blood cells from vascular system)
  2. edema – excess of fluid in interstitial tissues and serous cavities
72
Q

Cellular infiltrate in acute inflammation

A

Neutrophils

73
Q

Inflammation of prolonged duration

A

Chronic inflammation

74
Q

Cellular infiltrate of chronic inflammation

A

Mononuclear cells (macrophage, lymphocytes, plasma cells)

75
Q

Type of healing?

  • No destruction of normal tissues
  • Cause of injury is neutralized.
  • Vessels returned to their normal permeability state.
  • Excess fluid is reabsorbed.
  • Clearance of mediators and inflammatory cells.
A

Simple resolution

76
Q

Type of healing?

Replacement of lost or necrotic tissues with a new tissue SIMILAR to those that were destroyed

A

Regeneration

77
Q

Type of healing in which severely damaged or non-regenerable tissues are repaired by the laying down of connective tissue aka SCAR

A

Replacement

78
Q

Death of entire body

A

Somatic death

79
Q

Can be observed immediately after death
o CNS/nervous failure
o Respiratory failure
o Cardiac failure

A

Primary changes in somatic death

80
Q

Can be observed few hours after death

A

Secondary changes in somatic death

81
Q

Cooling of the body

A

Algor mortis

82
Q

Rate of cooling of the body (deg F per hour)

A

7 degrees Farenheit per hour

83
Q

Can be used to establish time of death

A

Algor mortis/cooling of the body

84
Q

Algor mortis/cooling of the body is ____ in cold weather, lean malnourished individuals

A

faster

85
Q

Algor mortis/cooling of the body is ____ in infectious diseases.

A

delayed

86
Q

Stiffening of the body

A

Rigor mortis

87
Q

Rigor mortis/stiffening of the body:
- starts __ hrs ff. death
- completes __ at hrs
- remains for __ hrs
- persists for __ days

A
  • starts 2-3 hrs ff: death
  • completes at 6-8 hrs
  • remains for 12-36 hrs
  • persist for 3-4 days.
88
Q

Rigor mortis/stiffening of the body is ____ by warm environment and in infants

A

hastened

89
Q

Rigor mortis/stiffening of the body is ____ by cold temperature and obese individuals

A

delayed

90
Q

Purplish discoloration of the skin

A

Livor mortis

91
Q

Sinking of fluid blood into capillaries of the dependent body parts

A

Livor mortis

92
Q

Can determine if body position has changed at the scene of death

A

Livor mortis

93
Q
  • Occur slowly or immediately after death.
  • Settling and separation of RBCs from the fluid phase
A

Post-mortem clotting

94
Q

Self-destruction due to the release of hydrolytic enzymes

A

Autolysis

95
Q

Rotting and decomposition by bacterial action.

A

Putrefaction

96
Q

Drying and wrinkling of cornea and anterior chamber

A

Dessication

97
Q

Autopsy aka ____

A

Necropsy

98
Q

Type as to manner of incision?

Cadaver is opened from both shoulders down from xiphoid area and incised down to pubis

A

Y-shaped incision

99
Q

Y-shaped incision is usually done in ___ cadavers

A

adult

100
Q

Type as to manner of incision?

Cadaver is opened from the midline of the body from the suprasternal notch down to the pubis.

A

Straight-cut incision

101
Q

Autopsy Technique?

  • Organs are removed one by one and studied individually.
  • i.e. Cranial cavity  Thoracic cavity  Cervical region  Abdominal cavity
  • Advantage: Quick and suitable for beginners
  • Disadvantage: Causes loss of continuity
A

Rudolph Virchow’s Method

101
Q

Straight-cut incision is usually done in ___ cadavers

A

children and infant

102
Q

Autopsy technique?

  • Involves “in-situ” dissection in part, combined with en block removal.
  • Advantages: In infected bodies (HIV, Hepa B), considered good in children
  • Disadvantage: Difficult to perform
A

Carl Rokitansky’s Method

103
Q

Autopsy technique?

  • Involves “en-bloc” removal of organs
  • i.e. Cervico-thoracic, abdominal, pelvic organs are removed in 3 blocks, neuronal system is removed as another block
  • Advantage: Excellent preservation, handling of organs easier
  • Disadvantage: Inter-relationships is difficulty to study, if disease is extending to all blocks
A

Anton Ghon’s Method

104
Q

Autopsy technique?

  • Organs are removed “en masses”
  • All organs are removed “en masse” and disseacted as organ block
  • Advantages: Organs inter-relationships are preserved, body can be handled over quickly
  • Disadvantages: Organs difficult to handle
A

M. Lettule’s Method

105
Q
  • Process of tumor formation
  • Abnormal proliferation of cells
  • New cells are produced BUT functionless
A

Neoplasia

106
Q

Parts of tumor (2)

A
  1. Parenchyma – neoplastic cells
  2. Stroma – CT framework holding the neoplastic cells; provides blood supply.
107
Q

Benign/Malignant Tumor?

Slowly growing mass

A

Benign tumor

108
Q

Benign/Malignant Tumor?

Irregular surface, non-capsulated, attached to deep structures

A

Malignant

109
Q

Benign/Malignant Tumor?

Invasive to other organs

A

Malignant

110
Q

Benign/Malignant Tumor?

No spread and metastasis

A

Benign

111
Q

Benign/Malignant Tumor?

Poorly, moderately, or well differentiated

A

Malignant

112
Q

Benign/Malignant Tumor?

No reccurence after surgery

A

Benign

113
Q

Benign/Malignant Tumor?

Bleeding from cut surfaces is common

A

Malignant

114
Q

Bening tumors are named by adding suffix __

A

-oma

115
Q

Malignant tumors are named by adding suffix __ or __

A

-sarcoma or -carcinoma

116
Q

Benign/Malignant Tumor?

Remarkable pressure effect on neighboring tissue

A

Malignant

117
Q

Purpose of grading tumors

A

To determine the % of differentiated and undifferentiated cells

118
Q

Normal/Abnormal

Differentiated cells: ___
Undifferentiated cells: ___

A

Differentiated cells = normal
Undifferentiated cells = abnormal

119
Q

Classification used to grade tumors

A

Broder’s classification

120
Q

Broder’s Classification
Grade I-IV

A

table

121
Q

Value of tumor grading

A
  1. Guide for treatment
  2. Prognostic guide
122
Q
  • Based on the size of primary lesions, extent of spread to regional lymph nodes and presence or absence of metastases
  • To determine spread of cancer
A

Staging of tumors

123
Q

Classification used in staging of tumors

A

TNM classification

124
Q

T/N/M?

Size of tumor

A

T

125
Q

T/N/M?

Number of nodes involved

A

N

126
Q

T/N/M?

Presence/absence of metastasis

A

M

127
Q
A

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