Histopathology Flashcards
Cell that frequently divide to replace lost cells
Labile cells
not typically dividing to replace injured cells
Do not frequently go cell division
Only undergo replication to replace injured cells
Stable cells
Stable cells examples
Parenchymal cells of liver and kidneys
Cell class that do not undergo replication following maturation
Permanent Cell
Permanent cell example
neurons (nerve cell)
incomplete or defective development of tissue/organ. Shows no resemblance to the normal mature structure. Usually happens in paired organs (kidneys, gonads)
Aplasia
complete non-appearance of organ.
Agenesia
failure of tissue/organ to reach normal mature adult size
Hypoplasia
Failure of organ to form an opening
Example:
Imperforate anus (without opening)
Microtia - absence of ear canal
Atresia
Cellular adaptation mechanisms
Atrohpy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Anaplasia
acquired decrease in tissue or organ size
Atrophy
Atrophy that occurs as consequence of maturation
example:
Atrophy of thymus at puberty
Decrease in uterus size after childbirth
Physiologic
Pathologic atrophy:
occurs if blood supply becomes reduced or below the critical level (may develop as a result of pressure atrophy)
Vascular atrophy
Pathologic atrophy:
persistent pressure on the organ or tissue may directly injure the cell or may secondarily promote diminution of blood supply
Pressure atrophy
Pathology atrophy:
due to lack of hormones needed to maintain normal size and structure
Endocrine atrophy
Pathologic atrophy:
due to lack of nutritional supply to sustain normal growth
Hunger/Starvation atrophy
Pathologic atrophy:
too much workload can cause general wasting of tissues
Exhaustion atrophy
Pathologic atrophy:
Inactivity/diminished activity/functions
Atrophy of disuse
Increase in tissue/organ size due to an increase in size of cells making up the organ
Hypertrophy
hypertrophy of skeletal muscles due to frequent exercise
Physiologic hypertrophy
Hypertrophy of the myocardium (hypertension)
Aortic valve disease
Pathologic hypertrophy
Type of hypertrophy that may develop as response to a deficiency (usually in paired organs– when one is removed)
Compensatory
Example of compensatory hyperthrophy
Renal hypertrophy
Increase in tissue or organ size due to an increase in the number of the cells making up the organ (new cells are formed)
Hyperplasia
Hyperplasia:
Happens in response to the need increase in uterus, breast during pregnancy.
Increase in breast size during puberty (glandular stimulation)
Physiologic Hyperplasia
Type of hyperplasia:
Erythroid bone marrow hyperplasia in people in high altitude
Physiologic hyperplasia
Type of hyperplasia:
Grave’s disease - diffuse crowding of epithelial cells
Hyperplasia of endometrium due to excessive estrogen
TB of cervical lymph nodes - there is increase in the number of lymph nodules
Pathologic
Occur frequently together with hypertrophy and can be triggered by the same mechanism
Compensatory
Involves transformation of adult cell type into another adult type (reversible process)
Metaplasia
Mesenchymal metaplasia involves:
Connective tissues
Original tissue:
Ciliated columnar epithelium of bronchi
Stimulus: Cigarette smoking
Metaplastic tissue:
Squamous epithelium
Original tissue:
Transitional epithelium of bladder
Stimulus:
Trauma of bladder
Squamous epithelium
Original tissue: Columnar glandular epithelium
Stimulus: Vitamin A deficiency
Metaplastic tissue:
Squamous epithelial cells
Original tissue: Esophageal squamous
Stimulus: Gastric acidity (too much drinking coffee)
Metaplastic tissue:
Columnar epithelium
Dysplasia is also known as
atypical metaplasia
Pre-neoplastic lesion
Change in cell size, shape, and orientation (reversible).
May lead to cancer but not necessarily
Dysplasia (atypical metaplasia)
dedifferentiation (irreversible) transformation of adult cells into embryonic/fetal cells
anaplasia
Causes of cell injury
Anoxia - lack of oxygen supply
Infectious agents
Mechanical agents/Trauma
Chemical Agents - carcinogens (chloroform, benzene)
No.1 cause of cell injury
Oxygen deprivation
Hypoxic cell injury for neuron is irreversible after (minutes)
3-5 minutes
Hypoxic cell injury in myocardial cells and hepatocytes is irreversible after (time)
1-2 hours
Skeletal muscle hypoxic injury is irreversible after (time)
many hours
Appearance of affected organs in gross change
Organ pallor (pale), Increased weight
Earliest change of tissue is seen
Microscopically
First manifestation of cellular change
cellular swelling
Irreversible changes
Enzymatic digestion of cells
Protein denaturation
Cytoplasmic changes
Nuclear changes
Cytoplasmic changes includes
Increased eosinophilia (pink/orange)
Large cells “cloudy swelling”
Irreversible nuclear changes
Pyknosis
Karyolysis
Karyorrhexis
condensation of nucleus
pyknosis
fragmentation/segmentation of nucleus
Karyorrhexis
Physiologic cell death
Programmed cell death
Death of single cell in a cluster of cells
Apoptosis
Cell shrinkage - integrity of membrane remains intact
Cellular components do not leak out = no inflammation
Chief morphologic features:
Chromatin condensation
Chromatin fragmentation
Cell shrinkage
Cytoplasmic bleb formation
Phagocytosis of apoptotic cells
Apoptosis
Pathologic cell death
Accidental cell death
Cell swelling
Leakage of cellular components = Inflammation
Change in organ can be seen in gross
Necrosis
Type of Necrosis:
due to to sudden cut off of blood supply
Coagulative
Type of Necrosis:
Due to ischemia
Appears ghostly (cell outline is maintained)
Usually happens in solid organs (liver, kidneys, heart)
Microscopically cell outlines are preserved
On gross, affected organs somewhat firm, appearing like a boiled material
Actions of hydrolytic enzyme is blocked (normal cell death releases lysozyme - hydrolytic enzyme for cell self destruction)
I.e. Myocardial Infarct
Coagulative
Type of Necrosis:
On gross, affected organ appears liquefied, creamy yellow (increased pus)
Liquefactive
Type of Necrosis:
Softening of organs is due to actions of hydrolytic enzymes
Complete digestion of cells
i.e. brain infarct and supporative bacterial infections
Liquefactive
Type of Necrosis:
On gross, tissue organ appears greasy resembling “cheese”
Caseous
Type of Necrosis:
Combination of coagulative and liquefactive
Usually seen in TB
Microscopically it appears as amorphous granular debri surrounded by granulomatous inflammation
Caseous (cheeselike)
Type of Necrosis:
Seen in immune reactions of the blood vessel
Deposition of fibrin in vessel wall
Cannot be seen in gross examination
Can only be microscopically
Fibrinoid
Type of Necrosis:
Destruction of fat cells due to release of pancreatic lipases
Fat
Type of Necrosis:
Death of fat tissues due to loss of blood supply
On gross, appears chalky white
Microscope, infiltrates of foamy macrophage adjacent to adipose tissues
Seen in pancreatitis
Affected organ is usually breasts
Fat
Type of Necrosis:
necrosis secondary to a ischemia
Not a specific pattern of necrosis
Gangrenous
Type of Necrosis:
Refers to a limb that loss its blood supply in the lower extremities
Skin - dry, black, and is observed in various stages of decomposition
Gangrenous
due to venous occlusion, example of this is SUPPURATIVE BACTERIAL INFECTION
wet gangrene
due to arterial occlusion and example of this is FOOT EMBOLISM
Dry gangrene
Tissue reaction to injury
Inflammation
Goal of Inflammation:
1)To remove the initial cause of the injury
2)To remove the consequences of injury
Cardinal signs of inflammation
Dolor
Rubor
Calor
Tumor
Functio laesa
Cardinal sign of inflammation: pain
dolor
Cardinal sign of inflammation: redness due to increase blood flow
Rubor
Cardinal signs of inflammation: heat
Calor
Cardinal signs of inflammation: swelling
Tumor
Cardinal Signs of Inflammation: destruction of functioning units of the cell
Functio laesa
Type of inflammation:
rapid response to an injurious agent
acute inflammation
Hallmark sign of acute inflammation
Exudation: escape of fluid proteins, blood cells from the vascular system)
Edema: excess to fluid in interstitial tissues and cavities
escape of fluid proteins, blood cells from the vascular system)
Exudation
excess to fluid in interstitial tissues and cavities
Edema
Cellular infiltrate of acute inflammation
neutrophils
Prolonged duration of inflammation
Chronic inflammation
Cellular infiltrate of Chronic inflammation
Mononuclear cells (monocytes, macrophage, lymphocytes, plasma cells)
Resolution of inflammation
Healing
Healing stage:
No destruction of normal tissues
Offending agent is neutralized
Vessels return to their normal permeability state
Excess fluids is reabsorbed
Clearance of mediators and inflammatory cells
Simple resolution