Pathological Procedures Flashcards
Define neoplasia?
A form of abnormal growth that is independent of normal growth regulating factors. It is always pathological
Outline clinical symptoms associated with a diagnosis of neoplasia?
Feel a mass
See enlargement of an area
Fatigue
Fever/ chils
Night sweats
Loss of appetite
Loss of weight
Pain
Headaches
Nausea
Vomiting
Macroscopic and microscopic appearances of uterine fibroid?
Macro - well-defined, Pale nodule, +/- bossalated, infarction, Haemorrhage. Can be serosa, subserosal or intramural
Micro - well-defined, spindle cells with cigar shaped nuclei, +/- atypia
There are 2 mechanisms for cell death what are they?
Apoptosis
Necrosis
How do apoptosis and Necrosis differ?
Apoptosis - programmed, no inflammatory response, no extra damage to tissues, controlled, pyknosis, karyohexis and karyolysis, active
Necrosis - incidental, responds to stimuli, inflammatory response, damage to surrounding tissues, uncontrolled, swelling and discolouration, passive
Define metaplasia?
The reversible change of one form of mature epithelium into another mature epithelium in response to an external stimuli
Give 2 examples of metaplasia with appropriate clinical settings
Cervix - hormone changes, in adolescence cause cervix to enlarge and transformation zone to move into the vagina where the pH is more acidic. Delicate columnar epithelium of the canal changes into squamous epithelium of the vagina.
Oesophagus - continual acid reflux damages the cuboidal epithelium of the Oesophagus to change into mucus secreting stomach or duodenal epithelium for protection
Describe the histological features of acute inflammation, including cell types and potential outcomes?
Neutrophil infiltrate, oedema in surrounding tissues, fibrin deposits to wall off stimulus.
Abscess formation, progression to chronic inflammation, recovery and removal of inflammatory components and debris
Describe the histological features of chronic inflammation, including cell types and potential outcomes?
Lymphocytes, histiocytes infiltrate, increase fibrin deposits, collagen laid down, cells that can regenerate do so or scar formation begins
Define hamatoma
Pool of mostly clotted blood in an organ, tissue, or body cavity
Define neoplasm
New growth of tissue that is not normal
Define carcinoma
Tumour that begins in epithelial cells
Define sarcoma
Tumour that begins in bone or soft tissue
Describe with examples the main routes of malignant tumour spread?
Adjuvent spread - to adjacent tissues, uterine to colon
Lymphatic - to nearest lymph node then through the lyphatics to be deposited at a new organ MM to lymph nodes
Transcoelimic - across body cavities ovarian to liver
Blood - through he vessel wall to a new organ colon to liver as it is filtered
Give 3 examples of tumour markers and their tumours of origin?
PSA - hyperplasia or malignancy of the prostate
CA 125 - ovarian cancer
CEA - increased risk of colon cancer
What are the advantages and disadvantages of using tumour markers clinically?
Aid diagnosis
Non-invasive tests
Direct the patient pathway
Not specific for tumours
What is the microscopic appearance of granuloma to us inflammation?
Multineucleate giant cells
Epitheloid histiocytes
Lymphocytes
Necrosis
Name 4 conditions where granuloma to us inflammation can occur?
Foreign body reaction
Infective diseases - tuberculosis
Sarcoidosis
Crohn’s disease
Describe the 3 pathological processes involved in the development of a thrombus, with examples?
Hypercoaguability - something that triggers coagulation of the body at an inappropriate time or increases the level above normal - surgery, trauma, malignancy, pregnancy, infection, IBD, Autoimmune conditions
Circulatory status - natural or acquired areas that allow blood flow to remain static - immobility, venous obstruction, varicose veins, fibrillation, dysfunction, congenital abnornalities
Vascular damage - damage to the vessel wall - cellulitis, atherosclerosis, venopuncture, fractures, long travel, disruption or break in the endothelial wall.
What is an embolism?
An obstruction of a blood vessel by an embolus
What is the pathological effect of an embolism
The tissues distal to the embolism are deprived of blood and oxygen. If severe or prolonged this will lead to tissue death
Name 6 types of emboli?
Thrombus,
Foreign body,
Air,
Metastatic tumour
Atherosclerosis /fat
Infection
Describe with examples, autosomal dominant disorder
A disorder or disease that is spread via genetic information and only requires one copy of the gene
Polycystic kidney disease
Huntington’s disease
Describe with examples, X-linked recessive disorder
Disease or disorder that is spread by the X chromosome and requires both X chromosomes to carry the gene in females and only the X chromosome in males. It’s more likely to affect males than females.
Red-green colourblindness
Haemophilia A
Define apoptosis
The process of programmed cell death
What are the morphological features seen in cells undergoing apoptosis?
Karyohexis
Karyolysis
Pyknosis
Blebbing of cytoplam
Give an example of a normal process in which apoptosis occurs
Webbing between fingers and toes during embryonic development
What is acute inflammation?
A rapid response to acute tissue injury or infection. It delivers neutrophil and immune cells to the damaged area
What are the classic signs of acute inflammation?
Heat
Pain
Redness
Swelling
What is the acute inflammatory process?
Damage - vasodilation - increased permeability - oedema - neutrofil activation and migration - phagocytosis - complement cascade activation - immunoglobulins - Fibrinogen leaved - fibrin formed - sealing stimulant and helping with scar formation
What is the aim of acute inflammation?
To isolate and contain the site of injury or infection,
Destroy toxins and microbes
Prepare the site for repair
What is the Macroscopic appearance of acute inflammation?
Red
Swollen
Exudate
+/- Necrosis
What is the microscopic appearance of acute inflammation?
Neutrophil line the vessels
Fiberous tissue has clear spaces (oedema)
Congestion
What are the complications that arise from acute inflammation?
Pus formation - abscess formation - increase in liminal pressure - immune response further damaging wall = rupture and associated comolications
What types of acute inflammation are there?
Suppurative
Fiberous
Serous
What is suppurative inflammation?
Purulent
Exudate rich in neutrophil
Often due to bacterial infections
If closed off = abscess
What is fibrinous inflammation?
Exudate rich in plasma proteins
Common to cavity membranes (Pleural, pericardium)
Can lead to adhesions between organs
What is serous inflammation?
Fluid in the response has little protein and cells (transudate)
Eg skin in response to burn
What is serous inflammation?
Fluid in the response has little protein and cells (transudate)
Eg skin in response to burn
What is the outcome of acute inflammation?
Resolution - normal architecture and function eg after Sun burn
Healing - scar formation when tissue cannot regenerate. Structural integrity with impairment of function eg modified bone after a fracture
Abscess formation - progresses to chronic inflammation eg appendicitis, lobular pneumonia
What happens when control of inflammatory processes fails?
Autoimmune disorders
How long does an acute inflammatory response last before it becomes chronic?
After 3 days
What types of tissue repair are there?
Regeneration
Replacement
What happens to a tissue if it regenerates?
Original cells type and function returned
In prepare what happens to the tissue if it undergoes replacement?
New cell/tissue type usually with some or total loss of function
When it comes to repair what types of tissues are there?
Labile
Stable
Permanent
What are labile tissues?
Tissues that constantly divide and regenerate during repair processes
Skin, mucosa and haemopoietic tissues
What are stable tissues?
Tissues that divide until fully mature then stop. Can regenerate after injury
Connective tissue, liver and pancreas
What are permanent tissues, in regards to repair?
Tissues with limited ability to replicate
Usually replaced after injury
Neurons, skeletal and cardiac muscle
Repair can be delayed due to what factors?
Stimuli remaining
Foreign body remaining
Poor nutrition
Poor circulation
Pre-exsisting diabetes
Medication (steroids)
What is primary intention?
A rapid process with a low rate of infection and only a small amount of scarring
What type of wound undergoes primary intention?
The edges of the wound are close together and fit easily together
Surgery
What happens during first intension?
Wound fills with blood
Clot forms containing fibrin
Fibrin binds the wound together
Clot dries
Infection prevented
Vasodialtion
Increase permeability
Vessel permeability increases
Oedema in surrounding tissues
Migration and activation of neutrophils
Phagocytosis of damaged tissue
Fibrin contains any infectious agents
Neutrophil die forming pus and exudate
Fibroblasts from surrounding tissue migrate to clot
Fibroblasts produce collagen and extracellular matrix components
I labile tissues capillaries revasculise the area
Fibrin clot breaks down and removed
Delicate connective tissue (granulation tissue) is laid down forming a scar
What is granulation tissue?
Delicate connective tissue that forms in wounds during repair
What is the function of granulation tissue?
The form a scar when a tissue is unable to regenerate after injury
What is the Macroscopic appearance of a scar?
Start off as a shiney red patch but become more white as the capillaries are compressed and the granulation tissue increases
What is secondary intention?
Repair process when the edges of a wound are far apart or do not fit easily together
4th degree burns
Skin tears
What process occurs in secondary intention?
Blood fills wound
Clots but fibrin is not enough to seal the wound
This slows down the repair process and the wound is still open to infection
Vasodilation
Increase permeability
Vessel permeability increases
Oedema in surrounding tissues
Migration and activation of neutrophils
Phagocytosis of damaged tissue
Fibrin contains any infectious agents
Neutrophil die forming pus and exudate
Fibroblasts from surrounding tissue migrate to clot
Fibroblasts produce collagen and extracellular matrix components
I labile tissues capillaries revasculise the area
Fibrin clot breaks down and removed
Delicate connective tissue (granulation tissue) is laid down forming a scar
What process occurs in secondary intention?
Blood fills wound
Clots but fibrin is not enough to seal the wound
This slows down the repair process and the wound is still open to infection
Vasodilation
Increase permeability
Vessel permeability increases
Oedema in surrounding tissues
Migration and activation of neutrophils
Phagocytosis of damaged tissue
Fibrin contains any infectious agents
Neutrophil die forming pus and exudate
Fibroblasts from surrounding tissue migrate to clot
Fibroblasts produce collagen and extracellular matrix components
I labile tissues capillaries revasculise the area
Fibrin clot breaks down and removed
Delicate connective tissue (granulation tissue) is laid down forming a scar
As it is harder to form a scar the wound contracts, pulling the sides together causing debilitating scars (puckering)
What are the differences between primary and secondary intension?
Secondary intention has…
Increased inflammatory response
More debris for phagocytes to remove
More risk of infection
More granulation tissue
What is angiogenesis?
Formation of new capillaries
What happens during granulation tissue formation?
Angiogenesis
Space between capillaries is filled by lymphocytes, macrophages, proliferation Fibroblasts and loose oedematous extracellular matrix
Thin walled vessels leak increasing inflammatory infiktration
Overtime vessels regress and collagen is laid down
Inflammatory cells die or return to circulation
Fibroblasts become activated, increase in size, form collagen
Collagen becomes organised forming and early scar
Fibroblasts regress
Overtime cellularity if the scar decreases
Give an example of specialist repair and why?
Bone after a fracture
Scar tissue would not be able to weight bear
How do bones undergo repair?
Following injury embryonic development is reactivated
Fracture
Bleeding
Haematoma forms
Acute inflammatory process occurs
Granulation tissue is formed (soft tissue callus)
Callus holds bone together
Stem cells from carribium layer of peristeum are activated
Cells divide forming chrondocytes and osteoblasts
Chondrocytes form cartilage nous matrix
Osteoblasts form osteoid
Granulation tissue gives way
Osteoblasts surround osteoid
Osteoid becomes mineralised to form a boney callus
Initial bone is haphazard (woven)
Over months oxsteoclasts remodel it and Osteoblasts build to form lamellar bone with trabecukated architecture
What causes cells to adapt?
An ever changing environmemt
Give an example of physiological adaptation to cells?
Thyroid gland in pregnancy
Increase TSH acts on thyroid epithelium
This is within normal range
Give examples of environmental (pathological) adaptations?
Toxins
Poisons
Infectious organisms
What are the possible outcomes for environmental (pathological) adaptations?
Malfunction
Cell death
What happens to cells when a stimuli is removed?
They revert to the normal form or undergo adaptive change
Give examples of adaptive change?
Hyperplasia
Atrophy
What happens if an adaptive change is sucessful?
The cell survives
What happens if an adaptive change is unsucessful?
The cell dies
Usually takes several morphological changes for this to occur
What can influence if a cell survives an adaptive change?
Magnitude of stimuli
Type of stimuli
Duration of stimulus
Vunerability of cell (Neurons are more vulnerable to hypoxia than Fibroblasts)
Immunosupression
Immunodeficiency
Poor nutrition
How can adaptive changes be seem Macroscopically?
Cloudy
Swelling
Hydropic degeneration
Fatty change
Are adaptive changes reversible?
Yes, generally, once stimulus is removed
What is autophagy?
Removal of damaged organelles
Synthesis of new proteins
What is steatosis and where can it occur?
Fatty change
Subleathal metabolic dearragement
Usually in high energy demanding cells
Liver due to chronic alcohol abuse
Myocardium or skeletal muscle due to lack of use
What is Necrosis?
A form of cell injury that results in the premature death by autolysis
What causes Necrosis to occur?
Stimuli that remain unchecked
Irreversible cell damage
What are the types of Necrosis?
Colliquative
Coagulative
Caseous
Fibrinoid
What is colliquative necrosis?
Dead tissue is semi-liquid
Eg ischeamia
What is Coagulative necrosis?
Dead tissue is firm
Eg abscess
What is Caseous necrosis?
Soft, cream cheese consistency
Eg tuberculosis
What is fibrinoid Necrosis?
Occurs in the walls of blood vessels?
What is the microscopic appearance of Necrosis?
Pale staining
Cytoplasmic vaculation
No definition to the cytoplasm
Nuclear condensation
What happens in a cell if it undergoes reversible cell damage?
Mitochondria fail to produce ATP
Ion pumps in membranes fail
Loss of ion fluid homestasis
Free radicles accumulate
If this fails to correct then the damage becomes irreversible
What happens in a cell if it undergoes lethal injury?
Damage to organelles
Lysosomes release autodigestion enzynes
Autolysis
Cell membranes loose specialist structures (microvilli)
Cell function is lost
What is apoptosis?
Programmed cell death. A highly organised process to alter the cell and cause cell death. Affects individual cells only
Give an example of pathological apoptosis?
Cancer
Failure of apoptosis is a key factor in cancer formation
Give an example of embryonic apoptosis
Webbing between toes and fingers
Give an example of regressive apoptosis?
Menstrual cycle and endometrium
List examples of causes of apoptosis?
Radiation
Certain viruses (HPV)
membrane damage
Mitochondrial damage
DNA damage
Immune mediated attack
What is process of apoptosis?
Cells loose specialist structures
Loose attachment to other cells
Cells become rounded
Pyknosis
Karohexis
Karolysis
Blebbing of cytoplasm
Apoptotic bopsies form expressing membrane surface factors encourage phagocytosis
What is the aim of apoptosis?
Part of embryonic development
Part of everyday cell turnover
Eliminate damaged and disease cells
What triggers apoptosis?
Intrinsic and extrinsic pathways
What is the microscopic appearance of apoptosis?
Nuclear enlargment
Pyknosis - chromatic condensation
Karohexis
Karolysis
Naked cytoplasm
Vacuoles in cytoplasm