Histopath Midterm Flashcards

(129 cards)

1
Q

“Study of Diseases”

A

Pathology

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

What class of cells?:

frequently dividing; undergo cell division to replace lost cells

A

Labile cell

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

What class of cells?:

Epithelial cells of the skin

A

Labile cell

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

What class of cells?:

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

A

Stable cell

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

What class of cells?:

Parenchymal cells of liver and kidney

A

Stable cell

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

What class of cells?:

do not undergo replication ff. maturation

A

Permanent cell

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

What class of cells?:

Neurons/Nerve cells

A

Permanent cell

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

DECREASE in tissue or organ size

A

Atrophy

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

Give one example of physiologic atrophy

A
  • Atrophy of thymus at puberty
  • Decrease in uterus size after childbirth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Vascular atrophy

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

Type of atrophy that may develop secondary to pressure atrophy

A

Vascular atrophy

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

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

A

Pressure atrophy

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

Due to lack of nutritional supply to sustain normal growth

A

Starvation/Hunger atrophy

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

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

A

Endocrine atrophy

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

Inactivity or diminished activity/function

A

Atrophy of disuse

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

Too much workload can cause general wasting of tissues

A

Exhaustion atrophy

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

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

Increase in the size of skeletal muscle due to frequent exercise

A

Physiologic hypertrophy

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

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

A

Pathologic hyperthropy

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

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

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

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

A

Physiologic hyperplasia

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

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

Develops usually together with compensatory hypertrophy

A

Compensatory hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Involves transformation of adult cell type into another adult cell type
Metaplasia
26
Metaplasia is (reversible/irreversible) process
Reversible
27
aka atypical metaplasia/pre-neoplastic lesion
Dysplasia
28
Change in cell size, shape, and orientation
Dysplasia
29
Dysplasia is (reversible /irreversible) process
Reversible
30
aka De-differentiation
Anaplasia
31
Anaplasia is (reversible/irreversible) process
Irreversible
32
Transformation of adult cells to embryonic/fetal cells
Anaplasia
33
T/F: Neoplasia is NOT a cellular adaptation mechanism
True
34
Hypoxic injury can be IRREVERSIBLE after: ___ = for neurons ___ = for myocardial cells and hepatocytes ___ = for skeletal muscles
3-5 minutes 1-2 hours Many hours
35
Reversible injury: Gross changes
- Organ pallor - Increased weight
36
Reversible injury: Microscopic changes
- Cellular swelling (first manifestation) - Fatty degeneration
37
Irreversible injuries are due to:
- Enzymatic digestion of cells - Protein denaturation
38
Cytoplasmic changes in Irreversible injury
1. Larger cells “cloudy swelling” 2. Increased eosinophilia
39
Nuclear changes in irreversible injury
1. Pyknosis – condensation of nucleus 2. Karyolysis – fragmentation/segmentation of nucleus 3. Karyorrhexis – dissolution of nucleus
40
Physiologic cell death; Programmed cell death.
Apoptosis
41
Death of single cell in a cluster of cells
Apoptosis
42
Cell shrinkage = intact membrane = no leakage of cellular components = NO INFLAMMATION
Apoptosis
43
Chief morphologic features in apoptosis
- Chromatin condensation - Chromatin fragmentation - Cell shrinkage - Cytoplasmic bleb formation - Phagocytosis of apoptotic cells
44
Pathologic cell death Accidental cell death
Necrosis
45
Cell swelling = membrane is not intact = there is leakage of cellular components = THERE IS INFLAMMATION
Necrosis
46
Type of necrosis? - due to sudden cut-off of blood supply - cell death is due to ISCHEMIA.
Coagulative necrosis
47
Type of necrosis? Action of hydrolytic enzymes (lysozyme) is blocked.
Coagulative necrosis
48
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.
Coagulative necrosis
49
Type of necrosis? i.e. Myocardial infarction
Coagulative necrosis
50
Type of necrosis? Softening of organs is due to action of hydrolytic enzymes (lysozyme); there is complete digestion of cells.
Liquefactive necrosis
51
Type of necrosis? Appearance: - On gross, affected organ appears liquefied, creamy yellow due to increased pus
Liquefactive necrosis
52
Type of necrosis? i.e. Brain infarction, Suppurative bacterial infection
Liquefactive necrosis
53
Type of necrosis? Combination of coagulative and liquefactive necrosis
Caseous necrosis
54
Type of necrosis? Appearance - On gross, tissue/organ appears greasy resembling “cheese” - Microscopically it appears as amorphous granular debris surrounded by granulomatous inflammation
Caseous necrosis
55
Type of necrosis? Usually seen in TB
Caseous necrosis
56
Type of necrosis? - Seen in immune reactions of the blood vessel. - Vessel wall appears thick due to deposition of fibrin in vessel wall.
Fibrinoid necrosis
57
Type of necrosis? - Gross appearance CANNOT be noted - Changes are too smal
Fibrinoid necrosis
58
59
Type of necrosis? - Destruction of fat cells due to release of pancreatic lipases - Death of fat tissues (adipose) due to loss of blood supply
Fat necrosis
60
Type of necrosis? Appearance: - On gross, necrotic material appears “chalky white”. - On microscopy, infiltrates of foamy macrophage adjacent to adipose tissues
Fat necrosis
61
Type of necrosis? - Seen in pancreatitis - Affected organ is usually breast
Fat necrosis
62
Not a specific pattern of necrosis
Gangrenous necrosis
63
Type of necrosis secondary to ischemia
Gangrenous necrosis
64
_ _ _ _ _ _ _ _ = refers to tissue death due to interruption of blood supply, usually in lower extremities (limb)
Gangrene
65
Skin appears dry, black, and is observed in various stages of decomposition
Gangrenous necrosis
66
Due to venous occlusion i.e. embolism of foot
Wet gangrene
67
Due to arterial occlusion i.e. bacterial infection
Dru gangrene
68
Ultimate goal of inflammation
1. To remove the initial cause of injury 2. To remove consequences of injury
69
5 Cardinal Signs
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
- Rapid response to an injurious agent - May progress to chronic inflammation if it fails to subside in the course of several weeks.
Acute inflammation
71
71
Hallmark signs (2) of acute inflammation
1. exudation – escape of fluid, CHON, and blood cells from vascular system) 2. edema – excess of fluid in interstitial tissues and serous cavities
72
Cellular infiltrate in acute inflammation
Neutrophils
73
Inflammation of prolonged duration
Chronic inflammation
74
Cellular infiltrate of chronic inflammation
Mononuclear cells (macrophage, lymphocytes, plasma cells)
75
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.
Simple resolution
76
Type of healing? Replacement of lost or necrotic tissues with a new tissue SIMILAR to those that were destroyed
Regeneration
77
Type of healing in which severely damaged or non-regenerable tissues are repaired by the laying down of connective tissue aka SCAR
Replacement
78
Death of entire body
Somatic death
79
Can be observed immediately after death o CNS/nervous failure o Respiratory failure o Cardiac failure
Primary changes in somatic death
80
Can be observed few hours after death
Secondary changes in somatic death
81
Cooling of the body
Algor mortis
82
Rate of cooling of the body (deg F per hour)
7 degrees Farenheit per hour
83
Can be used to establish time of death
Algor mortis/cooling of the body
84
Algor mortis/cooling of the body is ____ in cold weather, lean malnourished individuals
faster
85
Algor mortis/cooling of the body is ____ in infectious diseases.
delayed
86
Stiffening of the body
Rigor mortis
87
Rigor mortis/stiffening of the body: - starts __ hrs ff. death - completes __ at hrs - remains for __ hrs - persists for __ days
- starts 2-3 hrs ff: death - completes at 6-8 hrs - remains for 12-36 hrs - persist for 3-4 days.
88
Rigor mortis/stiffening of the body is ____ by warm environment and in infants
hastened
89
Rigor mortis/stiffening of the body is ____ by cold temperature and obese individuals
delayed
90
Purplish discoloration of the skin
Livor mortis
91
Sinking of fluid blood into capillaries of the dependent body parts
Livor mortis
92
Can determine if body position has changed at the scene of death
Livor mortis
93
- Occur slowly or immediately after death. - Settling and separation of RBCs from the fluid phase
Post-mortem clotting
94
Self-destruction due to the release of hydrolytic enzymes
Autolysis
95
Rotting and decomposition by bacterial action.
Putrefaction
96
Drying and wrinkling of cornea and anterior chamber
Dessication
97
Autopsy aka ____
Necropsy
98
Type as to manner of incision? Cadaver is opened from both shoulders down from xiphoid area and incised down to pubis
Y-shaped incision
99
Y-shaped incision is usually done in ___ cadavers
adult
100
Type as to manner of incision? Cadaver is opened from the midline of the body from the suprasternal notch down to the pubis.
Straight-cut incision
101
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
Rudolph Virchow’s Method
101
Straight-cut incision is usually done in ___ cadavers
children and infant
102
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
Carl Rokitansky’s Method
103
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
Anton Ghon’s Method
104
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
M. Lettule’s Method
105
- Process of tumor formation - Abnormal proliferation of cells - New cells are produced BUT functionless
Neoplasia
106
Parts of tumor (2)
1. Parenchyma – neoplastic cells 2. Stroma – CT framework holding the neoplastic cells; provides blood supply.
107
Benign/Malignant Tumor? Slowly growing mass
Benign tumor
108
Benign/Malignant Tumor? Irregular surface, non-capsulated, attached to deep structures
Malignant
109
Benign/Malignant Tumor? Invasive to other organs
Malignant
110
Benign/Malignant Tumor? No spread and metastasis
Benign
111
Benign/Malignant Tumor? Poorly, moderately, or well differentiated
Malignant
112
Benign/Malignant Tumor? No reccurence after surgery
Benign
113
Benign/Malignant Tumor? Bleeding from cut surfaces is common
Malignant
114
Bening tumors are named by adding suffix __
-oma
115
Malignant tumors are named by adding suffix __ or __
-sarcoma or -carcinoma
116
Benign/Malignant Tumor? Remarkable pressure effect on neighboring tissue
Malignant
117
Purpose of grading tumors
To determine the % of differentiated and undifferentiated cells
118
Normal/Abnormal Differentiated cells: ___ Undifferentiated cells: ___
Differentiated cells = normal Undifferentiated cells = abnormal
119
Classification used to grade tumors
Broder's classification
120
Broder's Classification Grade I-IV
*table*
121
Value of tumor grading
1. Guide for treatment 2. Prognostic guide
122
- 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
Staging of tumors
123
Classification used in staging of tumors
TNM classification
124
T/N/M? Size of tumor
T
125
T/N/M? Number of nodes involved
N
126
T/N/M? Presence/absence of metastasis
M
127