HPCT WEEK 1 Flashcards
Covers a body surface or lines a body cavity
Forms most glands
Functions are:
Protection
Absorption, secretion, and ion
Filtration
Forms slippery surfaces
Epithelial Tissue
Most diverse and abundant tissue
Main classes are:
____ tissue proper
Blood-Fluid ____ tissue (blood)
Cartilage and Bone tissue - Supporting ____ tissues
Connective tissues
Components of connective tissue
Cells
Matrix (Protein fibers, Ground substances)
Common embryonic origin
Mesenchyme
Cells found in connective tissue proper
Fibroblasts, Macrophages, Lymphocytes, Adipocytes, Mast cells, Stem cells
Fibers:
Collagen - Very strong and abundant, long and, straight
Elastic - Branching fibers with a wavy appearance when relaxed
Reticular - Form a network of fibers that form a supportive frameworks in soft organs (i.e Spleen and Liver)
Ground susbtances:
Along with fibers, fills the extracellular space
The origin of a disease
Refers to why a disease arises
Etiology
Refers to the steps in the development of disease.
It describes how etiologic factors trigger cellular and molecular changes
Describes how a disease develops
Pathogenesis
Refers to the structural alterations in cells or tissue
Either Gross morphologic changes (Anatomic/Macroscopic)
or
Microscopic Changes
Morphologic changes
Referring to the clinical features (acute or malignant), course and prognosis of the disease
Functional derangements and Clinical Significance
Indication of a disease perceived BY THE PATIENT
Symptoms
Objective findings noticed BY THE DOCTOR on examination of the patient
Signs
Start of the disease
Onset
PREDICTION of the outcome of the disease
Prognosis
Outcome of the disease
Fate
New disease conditions that may occur during or after the usual course of the original disease
Complications
Undergoes replication all throughout life
Labile cells
Does not undergo replication unless injury
Stable cells
Does not undergo divisions following maturation
Permanent cells
Incomplete or defective development of tissue/organs
Affected organs shows no resemblance to normal mature form
Aplasia
Complete NON-APPEARANCE of organ
Agenesia
Failure of organ to form an opening
Atresia
Failure of organ to reach normal mature adult size
Hypoplasia
A state that lies intermediate between normal cell and injured cell
Cellular adaptation
Acquired decrease in tissue/organ size
Atrophy
The decrease in size happens as a consequence of maturation
Physiologic atrophy
Occurs if blood supply to an organ or tissue may directly injure the cell or may secondarily promote diminution of blood supply
Vascular Atrophy
Persistent PRESSURE on the organ or tissue may directly injure the cell or may secondarily promote diminution of blood suppliy
Pressure Atrophy
Due to lack of nutritional supply to sustain normal growth
Hunger atrophy
Due to lack of HORMONES needed to maintain normal size and structure
Endocrine Atrophy
Cardinal sign:pain
Dolor
Cardinal sign:Redness
Rubor
Cardinal sign:heat
Calor
Cardinal sign:swelling
Tumor
Cardinal sign: Destruction of functioning units of the cell
Function laesa
Watery, low protein fluid (Inflammation)
Serous inflammation
Fibrinogen is present in exudate (Inflammation)
Fibrinous inflammation
Pus / Purulent exudates (Inflammation)
Purulent / Suppurative inflammation
Blood and elements of exudates are present (Inflammation)
Hemorrhagic inflammation
Mucus is the main component (Inflammation)
Catarrhal Inflammation
Form of chronic inflammation characterized by collection of activated macrophages, T Lymphocytes, and sometimes associated with central necrosis
Granulomatous Inflammation
Pertains to the process of ensuring and maintaining personal as well as environmental health and safety in the laboratory
Risk management
Used to define the maximum allowable airborne concentration of a chemical
Permissible Exposure limits, Threshold Limit values, Occupational exposure Limits
Every Chemical should be labeled with
Chemical name and all ingredients (if mixture)
Manufacturer’s name and address or name of the person making the reagent
Date Purchased or made
Expiration date
Hazard warnings and safety procedures
Chemicals that cause reversible inflammatory effects
Irritants
Chemicals that cause destruction or irreversible alterations when exposed to living tissue
Corrosive chemicals
Cause allergic reactions in some exposed workers, not just in hypersensitive individuals
Sensitizers
Substances that can induce tumors, not only in experimental animals but also in humans
Carcinogens
Chemicals capable of causing death by ingestion, skin contact or inhalation at certain specified concentrations
Toxic materials
Intracellular changes associated with reversible injury (Plasma membrane)
Blebbing, Blunting, or distortion of microvilli, and loosening of intracellular attachments
Intracellular changes associated with reversible injury (Mitochondrial changes)
Swelling and the appearance of phospholipid-rich amorphous densities
Intracellular changes associated with reversible injury
Dilation of the endoplasmic reticulum with detachment of ribosomes and dissociation of polysomes
Intracellular changes associated with reversible injury (Nuclear alteration)
With clumping of chromatin (Pyknosis)
Intracellular changes associated with reversible injury (Myelin figure)
Phospholipid masses, derived from damage cellular membranes
Cell injury results from
Functional and biochemical abnormalities
Phospholipases increase will cause
membrane damage
Proteases increase will cause
break down of both membrane and cytoskeletal proteins
Endonucleases are responsible for
DNA and chromatin fragmentation
Mitochondrial damage
Decrease ATP, Increase ROS (reactive oxygen species)
Entry of Calcium
Increase mitochondrial permeability and will cause activation of multiple cellular enzymes
Membrane damage (Plasma membrane)
Loss of cellular components (cellular swelling)
Membrane damage (Lysosomal membrane)
Enzymatic digestion of cellular components (Necrotic to the cells)
Protein misfolding, DNA damage
Activation of pro-apoptotic proteins (apoptosis)
Cell size: Enlarge (Swelling)
Nucleus: Pyknosis > Karyorrhexis > Karyolysis
Plasma membrane: Disrupted
Cellular contents: Enzymatic digestion; may leak out of the cell
Adjacent inflammation: Frequent
Physiologic or pathologic role: Invariably pathologic
Necrosis
Cell size: Reduce (Shrinkage)
Nucleus: Fragmentation into nucleosome size fragments
Plasma membrane: Intact; altered structure
Cellular contents: Intact
Adjacent inflammation: No
Physiologic or pathologic role: Often physiologic. Means of eliminating unwanted cells, may be pathologic after some forms of cell injury, especially DNA and protein damage
Apoptosis
Types of cell death that is associated with loss of membrane integrity and leakage of cellular content
Necrosis
Individual organ removal
Virchow
Organ dissection in-situ
Rokitansky
En-masse dissection and organ separation
Letulle
Separate block dissection and organ separation
Ghon
Organ remove one by one from the cranial cavity down to the abdominal organs
For high-risk autopsies where permission is LIMITED TO ONE ORGAN
Good for DEMONSTRATING PATHOLOGICAL CHANGES in individual organs but the relationship between various organs may be hard to interpret
Virchow
En masse removal then subsequently dissected into organ blocks
Best technique for PRESERVING THE VASCULAR SUPPLY and relationships between organs, and for routine inspection because it is fast and the body can be made available to the undertaker
Letulle
Thoracic and cervical organs, abdominal organs, and the urogenital system are removed in functionally related blocks preserving ANATOMICAL RELATIONSHIPS
Simple to execute and appears as a compromise between Virchow and Letulle techniques
Gohn
In situ dissection (In local) combined with en bloc removal
Rokitansky
Computation for time of death
37c - Current body temp / 0.78 (C)
98.6F - Current body temp / 1.4 (F)
Rigor mortis occurs in ___ after death
2-3 hours
Starts in small muscle group (Head and Neck)
Fixed in 6-8 hours completed in 8-12 hours. Post mortem staining
Livor mortis
Takes out even more surrounding tissue.
Takes out some of the abnormality but not all
Incision biopsy
Removes the entire area in question
Excision biopsy
Simplest, least invasive test and uses the smallest needle to simply remove cells from the are of abnormality.
Not always adequate to obtain a diagnosis
FNAB
Considered as the primary technique for obtaining diagnostic full-thickness skin specimens
Use of circular blade that is rotated down through the epidermis and dermis, and into the subcutaneous fat, yielding a 3-4mm cylindrical core of tissue sample
Punch Biopsy
Removes not only cells, but also a small amount of the surrounding tissue
Provides additional information to assist in the examination of lesion
Core needle biopsy
Yield pleural fluid, directly aspirated from lungs
Thoracentesis / Chest tube thoracostomy
Samples are acquired though this procedure is received by hematology section or histopathology section
Similar to CSF collection
Bone marrow biopsy
Represent responses of cells to normal stimulation by hormones or endogenous chemical mediators.
Physiological Adaptation
Responses to stress that allow cells to modulate their structure and function
Pathologic adaptations
An increase in the size of cells resulting in increase in the size of the organ
No new cells are made
Occurs in tissues incapable of cell division
Hypertrophy
Enzyme substrate that colors viable myocardium magenta. Failure to stain is due to enzyme loss after cell death
Triphenyltetrazolium chloride
Takes place if the tissue contains cell populations capable of replication. It may occur concurrently with hypertrophy and often in response to the same stimuli
New cells are produced
Hyperplasia
Residual tissue grows after removal or loss of part of an organ
Compensatory hyperplasia
Shrinkage in the size of the cell by the loss of the cell substance
Decreased cell and organ size as a result of decreased nutrient supply or disuse
Associated with decreased synthesis and increased proteolytic breakdown of cellular organelles
Atrophy
Decreased workload
Loss of innervation
Inadequate Nutrition
Loss of endocrine stimulation
Aging
Causes of Atrophy
A reversible change in which one adult cell type is replaced by another adult cell type
Response to chronic irritation that makes cells better able to withstand the stress
Usually induced by altered differentiation pathway of tissue stem cells
May result in reduced functions or increased propensity for malignant transformation
Metaplasia
Occurs in epithelium exposed to mechanical trauma or chronic irritation of prolonged inflammation
Prolonged Vitamin A deficiency
Most commonly leading to replacement of columnar cells by stratified squamous epithelium
Epithelial Metaplasia
Occurring in connective tissues whereby fibroblasts are transformed into more highly differentiated forms such as osteoblasts, fat cells or tissue macrophages
Mesenchymal metaplasia
Cells may accumulate abnormal amounts of various substances. It may be harmless or associated with varying degrees of injury
The substance may be located at:
Cytoplasm
Within organelles (Lysosomes)
In the nucleus,
May be synthesized by the affected cells or may be produced elsewhere
Intracellular accumulations
Mechanism / Pathways of abnormal intracellular Accumulations
- Abnormal metabolism - Inadequate removal of a normal substance secondary to defects
- Defect in protein folding, transport - Accumulation of an abnormal endogenous substance
- Failure to degrade a metabolite
- Deposition and accumulation of an abnormal exogenous substance
Refers to any abnormal accumulation of triglycerides within parenchymal cells
Mostly seen in the liver
AKA steatosis
Fatty Change
Causes of steatosis
Toxins, protein malnutrition, diabetes mellitus, obesity, anoxia
Common causes of fatty change in the liver
Alcohol abuse and diabetes
Alter mitochondrial and the Smooth Endoplasmic Reticulum function
Inhibits fatty acid oxidation
Hepatotoxins (Alcohol)
Decrease the synthesis of apoproteins
CCI4 and Protein Malnutrition
Inhibits fatty acid oxidation
Anoxia
Increases fatty acid mobilization
Starvation
Immunoglobulins that may occur in the Rough Endoplasmic Reticulum of some plasma cells
Found in the peripheral areas of tumors
Eosinophilic Russel bodies
Is an eosinophilic cytoplasmic inclusion in liver cells that is highly characteristic of alcoholic liver disease
Damaged intermediate filaments within the hepatocytes
Mallory Body, or Alcoholic Hyalin
Are aggregates of hyperphosphorylated tau protein that are most commonly known as primary marker of Alzheimer’s disease
Found in the brain in alzheimer disease aggregated protein inclusion
Neurofibrillary tangle
____ Accumulates in renal tubular epithelium, cardiac myocytes, and B cells of the islet of langerhans
Glycogen
Most common exogenous pigment
A ubiquitous air pollutant. When inhaled, it is phagocytosed by alveolar macrophages and transported through lymphatic channels to the regional tracheobronchial lymph nodes
Aggregates of the pigment blacken the draining lymph nodes and pulmonary parenchyma
Carbon
Heavy accumulations may induce emphysema or a fibroblastic reaction that can result in a serious lung disease called coal worker’s pneumoconiosis
Exogenous carbon
An endogenous, brown-black pigment that is synthesized by melanocytes located in the epidermis and acts as a screen against harmful ultraviolet radiation
Melanocytes are the only source
Melanin
A hemoglobin-derived granular pigment that is golden yellow to brown and accumulates in tissues when there is a local or systemic excess of iron
Identified by its staining reaction (blue color) with the prussian blue dye
Hemosiderin
Hemosiderin types
1. Accumulation is primarily within tissue macrophages and is NOT ASSOCIATED WITH TISSUE DAMAGE
Hemosiderosis
Hemosiderin types
2. Extensive accumulation within parenchymal cells, WHICH LEADS TO TISSUE DAMAGE, SCARRING, and ORGAN DYSFUNCTION
Hereditary Hemochromatosis
An insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues particularly the heart, liver, and brain as a function of age or atrophy
Represents complexes of lipid and protein that derive from the free radical-catalyzed peroxidation of polyunsaturated lipids of subcellular membranes
Not injurious to the cell but is a marker of a past free radical injury
Brown pigment when present in large amounts imparts an appearance to the tissue that is called brown atrophy
Lipofuscin or wear-and-tear pigment
Abnormal deposition of calcium salts, together with smaller amount of iron, magnesium, and other minerals.
Pathologic Calcification
When the deposition occurs in dead or dying tissues, it occurs in the absence of calcium metabolic derangements in calcium metabolism
(Normal serum level of calcium)
Dystrophic
Deposition of calcium salts in normal tissues
Always reflects some derangement in calcium metabolism
Increase calcium in serum (Hypercalcemia)
Metastatic
Encountered in areas of necrosis of any type
Virtually inevitable in the atheroma of advance atherosclerosis
Dystrophic calcification
Initiation in ______ sites occurs in membrane bound
Extracellular sites
Initiation of ______ calcification occurs in the mitochondria of dead or dying cells that have lost their ability to regulate intracellular calcium
Intracellular calcification
Definition: Deposits of calcium salts in dead and degenerated tissue
Calcium metabolism: Normal
Serum Calcium level: Normal
Reversibility: Irreversible
Causes: aging or damaged heart valves
Dystrophic
Definition: Deposits calcium salts in normal tissues
Calcium metabolism: Deranged
Serum Calcium level: Hypercalcemia
Reversibility: Reversible upon correction of metabolic disorders
Causes: Hypercalcemia
Metastatic
A protective response involving
host cells
blood vessels
proteins and other mediators
Inflammation
It’s main goal is to eliminate the initial cause of cell injury, its protective mission by
diluting
Destroying
Neutralizing
Inflammation
Exogenous cases of inflammation
Physical agents -
a. Mechanic agents such as fractures, foreign, sand
b. Thermal agents: burns, Freezing
Chemical agents - Toxic gases, acids, bases
Biological agents - Bacteria, viruses, parasites
Endogenous cases of inflammation
Circulation disorders - Thrombosis, infarction, hemorrhage
Enzyme activation - acute pancreatitis
Metabolic products deposals - uric acid, urea
Changes in inflammation
Tissue damage
Cellular-vascular response
Metabolic changes
Tissue repairs
Onset: Fast
Cellular infiltrate: PMN (Mainly neutrophils)
Tissue injury, fibrosis - Mild and self-limited
Local and systemic signs - Prominent
Acute
Onset: Slow
Cellular Infiltrate: monocytes/macrophages and lymphocytes
Tissue injury, fibrosis: Often sever and progressive
Local and systemic signs: Less prominent, may be subtle
Chronic
An immediate and early response to an injurious agent
Short duration
Acute inflammation
Acute inflammation is characterized by
exudation of fluids and plasma proteins
Emigration of neutrophilic leukocytes to the site of injury
Cardinal signs of acute inflammation:
Due to dilation of small blood vessels within damage tissue (Cellulitis)
Rubor (Redness)
Cardinal signs of acute inflammation:
Results from increased blood flow (hyperemia ) due to regional vascular dilation
Calor (Heat)
Cardinal signs of acute inflammation:
Due to accumulation of fluid in the extravascular space
Tumor (Swelling)
Cardinal signs of acute inflammation:
Results from the stretching and destruction of tissues due to inflammatory edema
Dolor (Pain)
Cardinal signs of acute inflammation:
Inflamed area is inhibited by pain
Sever swelling may physically immobilize the tissue
Function laesa (Loss of function)
Chemicals of acute inflammation
Bradykinins
Prostaglandins
Serotonin
High protein content, High RBC, Pus present
Exudates
Low pus cells, Low protein content
Transudates
A peripheral position of white cells along the endothelial cells
Margination
Rows of leukocytes tumble slowly along the endothelium
Rolling
Endothelium can be lined by white cells. The binding of leukocytes with endothelial cells is facilitated by cell adhesion molecules
- Selectins, immunoglobulins, integrins
Pavementing
The process of movement of leukocytes by extending pseudopodia through the vascular wall
Diapedesis
Unidirectional attraction of leukocytes from vascular channels towards the site of inflammation within the tissue space guided by chemical gradients
Chemotaxis
The important chemotactic factors of neutrophils are:
C5a - Complement system, bacteria, and mitochondrial products of arachidonic acid metabolism
Leukotriene B4
Cytokine (IL-8)
Process of engulfment and internalization by specialized cells of particulate material
Phagocytosis
Leukocyte molecule: Sialyl-Lewis X
modified proteins
Major role: Rolling
P-selectin
Leukocyte molecule: Sialyl-Lewis X
modified proteins
Major role: Rolling and adhesion
E-selectin
Leukocyte molecule: L-selectin
Major role: Rolling Neutrophils, monocytes)
GlyCam-1, CD34
Leukocyte molecule:C11/CD18, Integrins (LFA-1, Mac-1)
Major role: Firm adhesion, transmigration
ICAM-1 (immunoglobulin Family)
Leukocyte molecule: VLA-4 Integrin
Major role: Adhesion
VCAM-1 (Immunoglobulin family)
Leukocyte molecule: CD31 (homotypic interaction)
Major role: Transmigration of leukocytes through endothelium
CD31
What is the defect of the ff:
Bone marrow suppression: Tumors (including leukemias, radiation, and chemotherapy)
Production of leukocytes
What is the defect of the ff:
Diabetes, malignancy, sepsis, chronic dialysis
Adhesion and Chemotaxis
What is the defect of the ff:
Anemia, sepsis, diabetes, malnutrition
Phagocytosis and microbicidal activity
What is the defect of the ff:
Leukocyte adhesion deficiency 1
Defective leukocyte adhesion because of oil mutations in Beta chain of CD11/CD18 integrins
What is the defect of the ff:
Leukocyte adhesion deficiency 2
Defective leukocyte adhesion because of mutations in fucosyl transferase required for synthesis of sialylated oligosaccharide (receptor for selectins)
What is the defect of the ff:
Chronic granulomatous disease
Decreased oxidative burst
What is the defect of the ff:
X-Linked
Phagocyte oxidase (membrane component)
What is the defect of the ff:
Autosomal recessive
Phagocyte oxidase (cytoplasmic component)
What is the defect of the ff:
Myeloperoxidase deficiency
Decreased microbial killing because of defective MPO-H202 system
What is the defect of the ff:
Chediak-lligashi syndrome
Decreased leukocyte functions because of mutations affective protein, involved in lysosomal membrane traffic
Steps of the inflammatory response (5Rs)
- Recognition of the injurious agent
- Recruitment of leukocytes
- Removal of the agent
- Regulation of the response
- Resolution (Repair)
Characterized by the outpouring of a watery, relatively protein-poor fluid that, depending on the site of injury
Fluid in a serous cavity is called an effusion
Serous inflammation
Resulting in greater vascular permeability allows large molecules to pass the endothelial barrier
A fibrinous exudate is characteristic of inflammation in the lining of body cavities such as the meninges, pericardium, and pleura
Fibrinous inflammation
Manifested by the presence of large amount of purulent exudate
Consisting of neutrophils, necrotic cells, and edema fluid (Staphylococci)
Suppurative inflammation