Histopath Midterm Flashcards
“Study of Diseases”
Pathology
What class of cells?:
frequently dividing; undergo cell division to replace lost cells
Labile cell
What class of cells?:
Epithelial cells of the skin
Labile cell
What class of cells?:
not typically dividing; undergo cell division only to replace injured cells
Stable cell
What class of cells?:
Parenchymal cells of liver and kidney
Stable cell
What class of cells?:
do not undergo replication ff. maturation
Permanent cell
What class of cells?:
Neurons/Nerve cells
Permanent cell
DECREASE in tissue or organ size
Atrophy
Give one example of physiologic atrophy
- Atrophy of thymus at puberty
- Decrease in uterus size after childbirth
Type of atrophy that occurs if blood supply to an organ becomes reduced or below critical level
Vascular atrophy
Type of atrophy that may develop secondary to pressure atrophy
Vascular atrophy
Persistent pressure on the organ or tissue may directly injure the cell
Pressure atrophy
Due to lack of nutritional supply to sustain normal growth
Starvation/Hunger atrophy
Due to lack of hormones needed to maintain normal size and structure
Endocrine atrophy
Inactivity or diminished activity/function
Atrophy of disuse
Too much workload can cause general wasting of tissues
Exhaustion atrophy
INCREASE in tissue or organ size due to an increase in SIZE of cells making up the organ
*NO NEW CELLS ARE PRODUCED
Hypertrophy
Increase in the size of skeletal muscle due to frequent exercise
Physiologic hypertrophy
Increase in the size of heart muscle (myocardium) due to hypertension
Pathologic hyperthropy
Increase in size of organ as a response to deficiency
Usually occurs when one of the paired organs is removed
Compensatory hypertrophy
INCREASE in tissue size or organ size due to an increase in the NUMBER of cells making up the organ
*NEW CELLS ARE FORMED
Hyperplasia
-Increase in breast and uterus size due to pregnancy
- Increase in breast size during puberty due to glandular stimulation
Physiologic hyperplasia
- Diffuse crowding of epithelial cells in Graves disease
- Increase in the number of lymph nodules in TB of cervical lymph nodes
Pathologic hyperplasia
Develops usually together with compensatory hypertrophy
Compensatory hyperplasia
Involves transformation of adult cell type into another adult cell type
Metaplasia
Metaplasia is (reversible/irreversible) process
Reversible
aka atypical metaplasia/pre-neoplastic lesion
Dysplasia
Change in cell size, shape, and orientation
Dysplasia
Dysplasia is (reversible /irreversible) process
Reversible
aka De-differentiation
Anaplasia
Anaplasia is (reversible/irreversible) process
Irreversible
Transformation of adult cells to embryonic/fetal cells
Anaplasia
T/F: Neoplasia is NOT a cellular adaptation mechanism
True
Hypoxic injury can be IRREVERSIBLE after:
___ = for neurons
___ = for myocardial cells and hepatocytes
___ = for skeletal muscles
3-5 minutes
1-2 hours
Many hours
Reversible injury: Gross changes
- Organ pallor
- Increased weight
Reversible injury: Microscopic changes
- Cellular swelling (first manifestation)
- Fatty degeneration
Irreversible injuries are due to:
- Enzymatic digestion of cells
- Protein denaturation
Cytoplasmic changes in
Irreversible injury
- Larger cells “cloudy swelling”
- Increased eosinophilia
Nuclear changes in irreversible
injury
- Pyknosis – condensation of nucleus
- Karyolysis – fragmentation/segmentation of nucleus
- Karyorrhexis – dissolution of nucleus
Physiologic cell death; Programmed cell death.
Apoptosis
Death of single cell in a cluster of cells
Apoptosis
Cell shrinkage = intact membrane = no leakage of cellular components = NO INFLAMMATION
Apoptosis
Chief morphologic features in apoptosis
- Chromatin condensation
- Chromatin fragmentation
- Cell shrinkage
- Cytoplasmic bleb formation
- Phagocytosis of apoptotic cells
Pathologic cell death
Accidental cell death
Necrosis
Cell swelling = membrane is not intact = there is leakage of cellular components = THERE IS INFLAMMATION
Necrosis
Type of necrosis?
- due to sudden cut-off of blood supply
- cell death is due to ISCHEMIA.
Coagulative necrosis
Type of necrosis?
Action of hydrolytic enzymes (lysozyme) is blocked.
Coagulative necrosis
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
Type of necrosis?
i.e. Myocardial infarction
Coagulative necrosis
Type of necrosis?
Softening of organs is due to action of hydrolytic enzymes (lysozyme); there is complete digestion of cells.
Liquefactive necrosis
Type of necrosis?
Appearance:
- On gross, affected organ appears liquefied, creamy yellow due to increased pus
Liquefactive necrosis
Type of necrosis?
i.e. Brain infarction, Suppurative bacterial infection
Liquefactive necrosis
Type of necrosis?
Combination of coagulative and liquefactive necrosis
Caseous necrosis
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
Type of necrosis?
Usually seen in TB
Caseous necrosis
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
Type of necrosis?
- Gross appearance CANNOT be noted
- Changes are too smal
Fibrinoid necrosis
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
Type of necrosis?
Appearance:
- On gross, necrotic material appears “chalky white”.
- On microscopy, infiltrates of foamy macrophage adjacent to adipose tissues
Fat necrosis
Type of necrosis?
- Seen in pancreatitis
- Affected organ is usually breast
Fat necrosis
Not a specific pattern of necrosis
Gangrenous necrosis
Type of necrosis secondary to ischemia
Gangrenous necrosis
_ _ _ _ _ _ _ _ = refers to tissue death due to interruption of blood supply, usually in lower extremities (limb)
Gangrene
Skin appears dry, black, and is observed in various stages of decomposition
Gangrenous necrosis
Due to venous occlusion i.e. embolism of foot
Wet gangrene
Due to arterial occlusion i.e. bacterial infection
Dru gangrene
Ultimate goal of inflammation
- To remove the initial cause of injury
- To remove consequences of injury
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
- Rapid response to an injurious agent
- May progress to chronic inflammation if it fails to subside in the course of several weeks.
Acute inflammation
Hallmark signs (2) of acute inflammation
- exudation – escape of fluid, CHON, and blood cells from vascular system)
- edema – excess of fluid in interstitial tissues and serous cavities
Cellular infiltrate in acute inflammation
Neutrophils
Inflammation of prolonged duration
Chronic inflammation
Cellular infiltrate of chronic inflammation
Mononuclear cells (macrophage, lymphocytes, plasma cells)
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
Type of healing?
Replacement of lost or necrotic tissues with a new tissue SIMILAR to those that were destroyed
Regeneration
Type of healing in which severely damaged or non-regenerable tissues are repaired by the laying down of connective tissue aka SCAR
Replacement
Death of entire body
Somatic death
Can be observed immediately after death
o CNS/nervous failure
o Respiratory failure
o Cardiac failure
Primary changes in somatic death
Can be observed few hours after death
Secondary changes in somatic death
Cooling of the body
Algor mortis
Rate of cooling of the body (deg F per hour)
7 degrees Farenheit per hour
Can be used to establish time of death
Algor mortis/cooling of the body
Algor mortis/cooling of the body is ____ in cold weather, lean malnourished individuals
faster
Algor mortis/cooling of the body is ____ in infectious diseases.
delayed
Stiffening of the body
Rigor mortis
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.
Rigor mortis/stiffening of the body is ____ by warm environment and in infants
hastened
Rigor mortis/stiffening of the body is ____ by cold temperature and obese individuals
delayed
Purplish discoloration of the skin
Livor mortis
Sinking of fluid blood into capillaries of the dependent body parts
Livor mortis
Can determine if body position has changed at the scene of death
Livor mortis
- Occur slowly or immediately after death.
- Settling and separation of RBCs from the fluid phase
Post-mortem clotting
Self-destruction due to the release of hydrolytic enzymes
Autolysis
Rotting and decomposition by bacterial action.
Putrefaction
Drying and wrinkling of cornea and anterior chamber
Dessication
Autopsy aka ____
Necropsy
Type as to manner of incision?
Cadaver is opened from both shoulders down from xiphoid area and incised down to pubis
Y-shaped incision
Y-shaped incision is usually done in ___ cadavers
adult
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
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
Straight-cut incision is usually done in ___ cadavers
children and infant
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
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
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
- Process of tumor formation
- Abnormal proliferation of cells
- New cells are produced BUT functionless
Neoplasia
Parts of tumor (2)
- Parenchyma – neoplastic cells
- Stroma – CT framework holding the neoplastic cells; provides blood supply.
Benign/Malignant Tumor?
Slowly growing mass
Benign tumor
Benign/Malignant Tumor?
Irregular surface, non-capsulated, attached to deep structures
Malignant
Benign/Malignant Tumor?
Invasive to other organs
Malignant
Benign/Malignant Tumor?
No spread and metastasis
Benign
Benign/Malignant Tumor?
Poorly, moderately, or well differentiated
Malignant
Benign/Malignant Tumor?
No reccurence after surgery
Benign
Benign/Malignant Tumor?
Bleeding from cut surfaces is common
Malignant
Bening tumors are named by adding suffix __
-oma
Malignant tumors are named by adding suffix __ or __
-sarcoma or -carcinoma
Benign/Malignant Tumor?
Remarkable pressure effect on neighboring tissue
Malignant
Purpose of grading tumors
To determine the % of differentiated and undifferentiated cells
Normal/Abnormal
Differentiated cells: ___
Undifferentiated cells: ___
Differentiated cells = normal
Undifferentiated cells = abnormal
Classification used to grade tumors
Broder’s classification
Broder’s Classification
Grade I-IV
table
Value of tumor grading
- Guide for treatment
- Prognostic guide
- 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
Classification used in staging of tumors
TNM classification
T/N/M?
Size of tumor
T
T/N/M?
Number of nodes involved
N
T/N/M?
Presence/absence of metastasis
M
