HISTOPATH HANDOUT Flashcards
Frequently dividing cells, to replace lost cells of the body
Labile cells
Not typically diving; do not frequently undergo cell division– only to replace injured cells
Stable cell
Do not undergo replication following maturation
Permanent cell
Incomplete or defective development of tissue/organ
Aplasia
The affected organ shows no resemblance to its normal mature structure; happens in “PAIRED” organs
Ex. Kidney, Gonads
Aplasia
Complete non-appearance of organ.
Agenesia
Failure or tissue/organ to reach normal mature adult size
Hypoplasia
Failure of organ to form an opening
Atresia
Acquired decrease in tissue / organ size
Atrophy
Develops as consequence of maturation
Physiologic atrophy
Ex. Atrophy of thymus at puberty; decrease in uterus size after child birth
Physiologic atrophy
Occurs if blood supply to an organ becomes reduced or below critical level
Vascular atrophy
Persistent pressure on the organ or tissue may directly injure the cell or may secondarily promote diminution of blood supply
Pressure atrophy
Due to lack of hormones needed to maintain normal size and structure
Endocrine atrophy
Due to lack of nutritional supply to sustain normal growth
Hunger/starvation atrophy
Inactivity or diminished activity/function
Atrophy of disuse
Too much workload can cause general wasting of tissues
Exhaustion atrophy
Increase in tissue / organ size due to an increase in size of cells
Hypertrophy
Cellular adaptation that don’t produce new cells
Hypertrophy
Ex. Hypertrophy of skeletal muscle because of frequent exercise
Physiologic hypertropy
Ex. Hypertrophy of myocardium due to hypertension
Pathologic hypertrophy
Response to a deficiency; occurs when one of the organ paired organs is removed
Compensatory hypertrophy
Increased in tissue or organ size due to an increase in the number of cells making up the organ
Hyperplasia
Involves transformation of adult cell type into another adult cell type
Metaplasia
Cells involved are epithelial cells
Epithelial metaplasia
Cells involved are connective tissue
Mesenchymal metaplasia
Atypical metaplasia; change in cell size, shape and orientation
Dysplasia
Involves transformation of adult cells to embryonic or fetal cells
Anaplasia
The affected cell may recover
Reversible injury
Inability of cells to recover
Irreversible injury
Hypoxic injury can be irreversible after?
________ for neurons
1-2 hours for _________
________ for skeletal muscle
3-5 minutes
For myocardial cells and hepatocytes
May hours
Gross changes of reversible changes
Organ pallor
Increased weight
Microscopic changes of irreversible changes
Cellular swelling
Fatty denaturation
Irreversible changes are due to
enzymatic digestion of cells
Protein denaturation
Cytoplasmic changes in irreversible injury
- Larger cells “cloudy swelling”
- Increased eosinophilia
Cytoplasmic changes of irreversible injury that causes condensation of nucleus
Pyknosis
Cytoplasmic changes of irreversible injury that causes fragmentation /segmentation of nucleus
Karyolysis
Cytoplasmic changes of irreversible injury that causes dissolution of nucleus
Karyorrhexis
Programmed cell death
Apoptosis
Accidental cell death
Necrosis
There is leakage of cellular components that causes inflammation
Necrosis
Death of single cell in cluster of cells
Apoptosis
Cell death is due to ischemia
Coagulative necrosis
Microscopically cell outlines are preserved
Coagulative necrosis
On gross, affected organs somewhat firm, appearing like a boiled material
Coagulative necrosis
Ex. Myocardial infarction
Coagulative necrosis
Complete digestion of cells ; on gross, affected organ appears liquefied, creamy yellow
Liquefactive necrosis
Ex. Brain infarction and suppurative bacterial infarction
Liquefactive necrosis
On gross, tissue/organ appears greasy resembling cheese
Caseous necrosis
Microscopically it appears as amorphous granular debri surrounded by granulomatous inflammation
Caseous necrosis
Necrosis usually seen in TB
Caseous necrosis
Seen in immune reaction of the blood vessel; deposition of fibrin in vessel wall
Fibrinoid necrosi
Destruction of fat cells due to release of pancreatic lipases
Death of fat tissues due to loss of blood supply
On gross, necrotic material appears Chalky white
On microscopy, infiltrates of foamy macrophage adjacent to adipose tissues
Fat necrosis
Seen in pancreatitis
Affected organ is usually breast
Fat necrosis
Necrosis secondary to ischemia
Gangrenous necrosis
due to venous occlusion
Wet gangrene
Due to arterial occlusion
Dry gangrene
Tissue reacting to injury
Inflammation
What are the ultimate goal of inflammation?
- To remove the initial cause of injury
- To remove consequences of injury
PAIN
Dolor
Redness due to increase rate of blood flow
RUBOR
HEAT
CALOR
TUMOR
Swelling
Destruction of functioning units of the cell
Function laesa
Rapid response to an injurious agent
Acute inflammation
Hallmark signs of acute inflammation?
Exudation and edema
Cellular infiltrate of acute inflammation
Neutrophils
Inflammation of prolonged duration
Chronic inflammation
Cellular infiltrate of chronic inflammation
Mononuclear cells (macrophage, lymphocytes, and plasma cells)
Resolution of inflammation
Healing
Replacement of loss or necrotic tissues with a new tissue that is similar to those that were destroyed
Regeneration
Changes can be observed immediately after death
Primary changes
Changes that can be observed immediately after death
Primary changes
Changes that can be noted FEW HOURS after death
Secondary changes
Death of the entire body
Somatic death
Cooling of the body
Algor mortis
Algor mortis happens @ a rate of ?
7 F/hr
Stiffening of the body
Rigor mortis
Rigor mortis starts ______ ff death, completes at ______ and stiffness remains for _______ , persist for ________
2-3 hrs
6-8 hrs
12-36 hrs
3-4 days
Purplish discoloration of skin
Livor mortis
Sinking of fluid blood into capillaries of the dependent body parts
Livor mortis
Importance: can determine if body position has changed at the scene of death
Livor mortis
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
Faster in: cold weather, lean malnourished individuals Delayed in infectious diseases followed by increase in temperature
Algor mortis
Hasten stiffness; warm environment and in infants
Delay: cold temperature and obese individuals
Rigor mortis
Examination of death body
Autopsy
Autopsy is also known as
Necrosy
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
Adult cadavers
Autopsy carried by government agencies
Medico legal autopsy
cadaver is opened from the midline of the body from the suprasternal notch down to the pubis.
Straight cut
Straight cut incision is usually done in
Children and infants
Autopsy techniques in which organs are removed one by one
Rudolf Virchow
Involves “in situ dissection”
Carl Rokitansky
Involves en-bloc removal of organs
Anton GHON
Organs are removed “em-masses”
Maurice Letulle
Process of tumor formation; abnormal proliferation ofcells:; new cells are produced are “FUNCTIONLESS”
Neoplasia
Parts of tumors:
- Parenchyma
- Stroma
Parenchyma
Neoplastic cells
Stroma
Connective tissue framework
Purpose: to determine the percentage of the differentiated and undifferentiated cell
Grading of tumors
Purpose: to determine the percentage of the Differentiated cells and undifferentiated cell
Grading of tumors
Purpose: to determine the percentage of the Differentiated cells and undifferentiated cell
Grading of tumors
Staging of tumors are based on the:
- size of primary lesions
- extent of spread to regional lymph nodes
- presence or absence of metastases
T
size of tumor
N
Number of lymph nodes involved
M
Presence of metastasis
Example of wet gangrene
Embolism of foot
Example pf dry gangrene
Bacterial infection
Example of dry gangrene
Bacterial infection
Example of dry gangrene
Bacterial infection
Stimulus: cigarette smoking
Original tissue: ?
Metaplastic tissue:?
Cilliated columnar epithelium of bronchi
Original tissue: transitional epithelium of bladder
Stimulus: ?
Trauma of bladder
Original tissue:?
Stimulus: gastric acidity
Metaplastic tissue:?
Esophageal squamous epithelium
Columnar epithelium
Example: renal hypertrophy
Compensatory hypertrophy
