Pathology Flashcards
(97 cards)
1
Q
Explain that all cells must be able to adapt to stress in order to maintain energy production, perform their functions and replicate
A
Cells within a multicellular organism require:
- nutrients/food
- H2O
- O2
- Removal of waste products
Homeostasis: maintenance of body components within appropriate limits
2
Q
Describe the types of environmental stresses that can induce cell and tissue injury
A
Environmental stresses that can induce cell and tissue injury include:
- Trauma injury
- Temperature change
- Drugs/chemicals
- Excess nutrients
- Irradiation
- Excess functional demand
- Infectious agents
3
Q
Describe the cellular responses to stress
A
Cells can undergo adaptation -> response to increased functional demand or reversible cell injury
- Hypertrophy
- Hyperplasia
- Atrophy
- Metaplasia
- Dysplasia
Cells can undergo apoptosis or necrosis -> response to irreversible cell injury
4
Q
Describe how reversible injury may cause adaptive responses at the cellular and organism level
A
1) Increased functional demand - cells respond by increasing cell size resulting in hypertrophy
2) Decreased functional demand - cells respond by decreasing cell size resulting in atrophy
3) Increased endocrine stimulation - cells respond by increasing cell proliferation resulting in hyperplasia
4) Decreased endocrine stimulation - cells respond by decreasing cell proliferation resulting in atrophy
5) Persistent tissue injury = cells adapt by cell and tissue growth resulting in hypertrophy and hyperplasia
6) Lack of nutrients/poor blood supply/ ageing/extensive tissue injury - cells cannot adapt and reduce in cell size and number leading to atrophy
5
Q
Describe the different forms of adaptation
A
Atrophy - decrease in cell size
Hypertrophy - increase in the size of a cell
Hyperplasia - increase in the number of a cell type
Metaplasia - Replacement of one differentiated cell type with another cell type
Dysplasia - Alteration in size, shape, and organization of cellular components of a tissue
Anaplasia - anaplasia is the loss of differentiation (only describes cancers)
6
Q
Describes the mechanisms of cell death - apoptosis and necrosis
A
Necrosis - cell death with substantial alterations in the structure of dying cell. Results in an inflammatory response. Caused by external sources.
- Coagulative necrosis - outline of all cell preserved and tissue is firm
- Liquefactive necrosis - dead tissue turns to liquid (e.g. pus)
- Caseous necrosis - found in tuberculosis
Apoptosis - internal self-destruct mechanism. Apoptotic blobs form which do NOT provoke inflammation
7
Q
Describe the mechanisms of ageing
A
Internal mechanisms:
- Telomere shortening
- “clock genes”
External mechanisms:
- damage to cell structure
- Damage to DNA
8
Q
Define “tumour” (neoplasm)
A
- Abnormal mass of tissue
- Growth of the abnormal tissue exceeds and is uncoordinated with adjacent normal tissue
- Growth persists even after stimuli that evoked the change is stopped
- Can be benign or malignant (cancer)
9
Q
Define “neoplasia”
A
- The presence or formation of new, abnormal growth of tissue. Unregulated cell division leading to new growth of tissue.
10
Q
Define “benign neoplasm”
A
Benign neoplasms lack the ability to invade the neighbouring tissue or metastasize. Considered non-cancerous
11
Q
Define “malignant neoplasm (Cancer)”
A
Malignant neoplasms grow rapidly and invade adjacent tissue and have the capacity to spread to other parts of the body (metastasize)
12
Q
Define “pleomorphism”
A
Enlarged deep blue stained nucleus. High nucleus to cytoplasm ratio. Pleomorphism is characteristic of malignant tumours
13
Q
Define “hamartoma”
A
A tumour-like growth, composed of disorganized but mature cells/tissues indigenous to the site. Completely benign
14
Q
Define “dysplasia”
A
Disordered growth of cells but non-invasive (benign). Common in epithelia. Pre-malignant growth
15
Q
Define “metastasis”
A
Spread of cancer from one tissue to another without direct contact or connection. Usually via blood, lymph or another vessel
16
Q
List different types of tumours according to their tissue of origin and behaviour
A
Benign tumour ends in -oma.
Malignant tumour ends in -sarcoma or -carcinoma (except leukaemia and lymphoma)
Sarcoma - malignant tumour develop from mesodermal tissue:
- connective tissue: fat -> liposarcoma, cartilage -> chondrosarcoma
- Blood vessels -> angiosarcoma
- Haematolymphoid -> leukaemia/lymphoma
- Muscle -> leiomyosarcoma
Carcinoma - malignant develop from epithelial tissue
- Squamous tissue -> squamous cell carcinoma
- Secretory -> adenocarcinoma
17
Q
List general features of benign versus malignant neoplasms
A
Benign tumours:
- looks very similar to normal tissue
- Does NOT invade surrounding tissue
- Recognized by abnormal growth
Malignant tumours
- Nucleus looks BLUE and enlarged
- Necrosis present
- Cells are crowded and overlapping
- Tissue morphology is abnormal
- Poorly defined borders (spread to adjacent tissue)
18
Q
Compare benign and malignant neoplasms in terms of evidence of rate of growth, differentiation and relation to adjacent tissues
A
Benign:
- normal number and structure for mitoses, normal nuclei, normal nucleoli, no necrosis/haemorrhage
- ordered cell orientation, near normal morphological resemblance, near normal functional resemblance
- no desmoplasia, readily recognized demarcation, never observed distant spread
Malignant:
- may have 3+ poles during mitoses, increased number, abnormal structure during mitoses,
- nucleus looks blue, pleomorphic enlarged (nuclear to cytoplasm ratio), hyperchromatic, irregular
- prominent, multiple nucleoli
- necrosis/haemorrhage present
- multiple nuclei overlapping -> loss of polarity, crowded nuclei
- variable to none morphological resemblance (anaplasia), looks like a whole different tissue
- variable to no functional resemblance
- desmoplasia present -> fibres around tumour are reacting to tumour
- Poorly defined demarcation due to invasion
- Frequent distant spread - metastasis
19
Q
Outline the main routes of metastasis, giving an example of each:
A
- Lymphatic spread: through lymphatic ducts and lymph nodes
- Haematogenous spread: through blood vessels into circulation
- Transcoelomic spread: metastatic cells spread across a body cavity.
20
Q
Outline the metastatic cascade
A
1) primary tumour forms
2) cells penetrate basement membrane
3) cells travel through ECM
4) penetration into blood vessel
5) platelets adhere to cell mass (forms bolus)
6) cell mass adheres to blood vessel wall
7) cells penetrate blood vessel wall
8) New metastatic tumour forms in new site
21
Q
Explain the ways in which tumours affect the host clinically
A
Mechanical effects:
- Disfigurement
- Obstruction in tubes and ducts
- Loss of organ function
- Ulceration (breakage in epithelial surface)
Functional effects:
- can cause overactive endocrine organs resulting in excess hormone
Cancer cachexia
- weight loss, weakness, anorexia
- due to increased metabolic rate and systemic inflammation
Paraneoplastic syndrome:
- syndrome that can’t be explained why they happen, but are common with people with tumours
- cancer hormones cause abnormal tissue formation
22
Q
Outline main features of the epidemiology of cancer in Australia with reference to incidence and mortality
A
- 123, 930 new cases of cancer (incidence)
- 45, 780 deaths from cancer (mortality)
- Overall: lung is most deadly
- Newest cases: breast (females) and prostate (male)
23
Q
Outline factors implicated in the aetiology (causes) of cancer, with reference to:
A
- Age
- Hereditary: very rarely is there clear inherited risk of cancer, some increased risk in blood relatives
- Environmental: smoking, alcohol, obesity, diet, radiation, chemical carcinogens, oncogenic virus
- Acquired predisposing condition: immunodeficiency, chronic inflammation
24
Q
Explain how a tumour arises from clonal expansion of a single precursor cell that has undergone genetic damage, outlining that non-lethal cumulative genetic damage may result from inherited (germline) or acquired (somatic) mutations
A
Carcinogenesis:
- A single precursor cell can have non-lethal genetic mutations: inherited mutations (germline mutations), acquired mutations (somatic mutations) such as environmental factors or spontaneous mutations
- Mutation can accumulate
- the single precursor cell undergoes clonal expansion to form a tumour
25
List the mechanisms by which nuclear damage may give rise to a malignant phenotype
HALLMARKS OF CANCER:
- self-sufficiency in growth signals
- insensitive to growth-inhibitors
- Evasion of apoptosis
- Limitless replicative potential
- sustained angiogenesis
- Ability to invade and metastasize
NEW HALLMARKS:
- evasion of immune system
- Reprogramming of energy metabolism
- genomic instability
- tumour promoting inflammation
Proto-oncogenes - naturally occurring genes which, if mutated, can cause cancerous characteristics.
- Six categories of proto-oncogenes:
1) growth factors
2) growth factors receptors
3) non-receptor signal transducing proteins with tyrosine kinase activity
4) signal transducing G-proteins
5) nuclear regulatory factors (transcription factors)
6) cyclins and cyclin-dependent kinases
26
Outline examples of screening programs that can lead to early detection of cancer
Screening programs:
- Breast self-examination and mammography
- Pap smears
- Faecal occult blood testing
- Digital prostate examination
- Self-examination for moles
- Blood tests for proteins released by tumour cells
27
Explain the components of the diagnosis of neoplasia, with particular reference to histopathological assessment and adjuncts to histopathological assessment
Diagnosis of neoplasm:
1) clinical assessment: history, physical examination, investigative tests
2) histopathological assessment: type of tumour, grading, staging
Adjuncts to histopathological assessment:
- immunochemistry -> staining tissue section with specific antibodies
- flow cytometry -> detecting expressed antigens
- Molecular and cytogenetic tests -> looking for specific genetic mutations
28
Explain the relevance of acute inflammation to medicine and dentistry
Acute inflammation is important because it plays a role in initiating healing, host defence's and adaptive immune response. In procedures which deal with invasion of tissue it is best to understand what complications can arise because a clinically simple procedure can be complicated by inflammation
29
Define the term 'inflammation' and describe the roles of the inflammatory response and the cardinal signs of inflammation
Inflammation - the reaction of vascularized living tissues to local injury or infection, characterized by movement of fluid and leukocytes from the blood into the affected tissue.
Roles of inflammatory response:
- initiation of healing process
- Deliverer leukocytes to site of injury
- kill microbes
- remove dead cells
Cardinal signs of inflammation
- Heat - increased blood flow (hyperaemia)
- Redness - increased blood flow (hyperaemia)
- Swelling - fluid movement from blood into tissue (exudation)
- Pain - increased sensitivity of pain receptors
30
Describe the position of inflammation within the wider context of host protective responses against micro-organisms
Inflammation is an innate immune response which is triggered by moderate to mild injury of the tissues. Bacteria, fungi or viruses infect and invade the barriers and innate immune response is activated within 6 hours. Whereas adaptive immune response occurs in around 5 days time. Innate immunity is directed by natural killer cells, plasma proteins (complement) and neutrophils. Acute inflammation is the first step to all damage to tissue.
31
Explain the distinctions between acute and chronic inflammatory processes
Acute inflammation - rapid and relatively short-lived stereotypic response, characterized by movement of polymorphonuclear leukocytes (mostly neutrophils and some eosinophils) and fluid into the affected tissue.
Chronic inflammation - persistent inflammation lasting between months and years leading to scarring of tissue. Failure to eliminate the causation of acute inflammation or autoimmunity can cause chronic inflammation. Characterized by simultaneous tissue damage and repair.
32
Describe the roles of lymphocytes
Leukocytes - white blood cells
Lymphocytes:
- leukocytes of the lymph responsible for adaptive immunity
- B cells and T cells
- 20-30% of all leukocytes
- Single large, round nucleus
- 7 um diameter
33
Describe the roles of monocytes/macrophages
- form multinucleate phagocytic cells for removing infected cells and cell debris
- 3-8% of all leukocytes
- Largest leukocytes of 18um diameter
- Semilunar-shaped nucleus
- Differentiate into macrophages when they leave blood vessels
34
Describe the roles of neutrophils
- Granular polymorphonuclear leukocyte
- Faint granules (often tri-lobed nucleus)
- phagocytize bacteria
- Most abundant (40-75% of leukocytes)
- 12-15 um diameter
35
Describe the roles of eosinophils
- Granular polymorphonuclear leukocyte
- Usually bi-lobed nucleus with darker granules than neutrophils
- 12-17um in diameter
- 2-4% of leukocytes
- Function in allergy and parasitic infections by releasing prostaglandins and cytokines to recruit other immune cells
36
Describe the roles of basophils
- Release histamine, causing vasodilation and inflammation in allergic reactions
- < 1% of the leukocytes
- Allergic reactions and
- Filled with granules, overlying nucleus
37
Describe the mechanisms underlying the cardinal signs of inflammation: heat
Increased vasodilation and blood flow to the site of infection results in increased temperature because of concentration of blood at the site of tissue injury.
38
Describe the mechanisms underlying the cardinal signs of inflammation: redness
Increased vasodilation and blood flow to the site of infection results in increased redness of the tissue because of concentration of blood at the site of tissue injury.
39
Describe the mechanisms underlying the cardinal signs of inflammation: swelling
Swelling is caused by the accumulation of fluid in the tissue by oedema. Increased permeability of tissues allows for fluid movement between compartments and for easier migration of immune cells to site of infection. Accumulation of salts and migrating cells pulls water into tissue
40
Describe the mechanisms underlying the cardinal signs of inflammation: pain
Pain is due to the release of bradykinin, histamines, that stimulate nerve endings
41
Describe the 5th cardinal sign
Loss of function - caused by tissue damage to affected organ
42
Explain the stereotypic nature of acute inflammation
- Injury or infection occurs
- exudation and neutrophil infiltration occurs
- Resolution follows
- Rarely, pus and chronic inflammation occur then healing
43
Describe the components of the acute inflammatory response
1. microcirculation: post-capillary venules become very permeable during acute inflammation
2. cells recruited: endothelial cells, neutrophils (early), and macrophages (later)
3. soluble factors: vasoactive mediators, chemokines, complement/coagulation cascades
44
Describe soft tissue injury, the recommended treatments, and the process through which long-term complications are reduced
Soft tissue injury is an acute inflammation response. No granuloma formation
Rest - immobilize and support injury
Ice - cool the affected area for 20 minutes every 2 hours for the first 48 hours
Compression - compression covering injured parts
Elevation - raise the injured area above the level of the heart
Referral - refer to qualified professional for definitive diagnosis and continuing care.
45
Explain the role of 'exudation' in the inflammatory process
Exudate:
1) How: endothelial of blood vessel become highly permeable and increased blood flow to injury --> upregulation of adhesion molecules allows neutrophil migration from blood vessels (sticks to walls)
2) Why: cells, proteins, and fluids can move to injured tissue.
- Fluid dilutes toxins and increase flow of lymphatics
- Proteins for complement system, fibrin components and antibodies
- Neutrophils for destruction of microbes
46
Describe what is meant by the following statement: "Inflammation: friend or foe?"
Inflammation creates a toxic environment to destroy pathogens but can also harm host cells. Acute inflammation can lead to chronic inflammation or systemic inflammation. The destruction of infected tissue can result in loss of function of the affected organ.
47
Outline the place of pathology in clinical medicine
Pathology: medical specialty concerned with detection of disease and injury by the examination of body organs, tissue and teeth.
- Enables diagnosis and management of diseases
- Provides scientific basis of medicine and dentistry
- In 70% of diagnoses and medical decisions
48
Outline anatomical pathology
Study of organs and tissues to determine the causes and effects of particular diseases
49
Outline chemical pathology
Study of biochemical basis of diseases and the monitoring of metabolic processes via "biomarkers"
50
Outline haematology
Clinical and laboratory aspects of primary disorders of blood
51
Outline genetics
Chromosomal abnormalities, co-dominant mutations, recessive mutations, polymorphisms, SNP associations
52
Outline microbiology
Diagnosing bacterial, viral, fungal and parasitic infection
53
Outline the factors that determine the response to injury
The response to injury depends upon:
- Nature and duration of the stimulus -> type of stimulus, how invasive is the inflammatory stimulus
- Degree of destruction caused by the injurious agent -> how much injury is caused
- Type of tissue injured -> potential of tissue to regenerate
- difficulty of eliminating micro-organisms
54
Define 'resolution'
Acute restoration of the original structure (quick return to normal tissue)
55
Define 'organization'
Formation of granulation tissue leading to acute healing by fibrosis (replacement tissue)
56
Define 'suppuration'
Formation of pus (liquid produced by infected tissue consisting of dead WBC, debris and serum
57
Define 'granuloma'
- Nodular (sphere/ball) chronic inflammatory lesion
- containing predominantly macrophages, lymphocytes and fibroblasts
- Formed in response to a persistent irritant: e.g. micro-organism or foreign body at injury site
58
Define 'granulation tissue'
- only in damaged tissue. Wraps the abscess;
- Newly formed tissue consisting of macrophages, blood vessels and fibroblasts
- Involved in healing damaged tissues through fibrosis
59
Define 'regeneration'
Replacement of injured tissue by parenchymal cells of the same type of tissue
60
Define 'repair'
Replacement of injured tissue by fibrous tissue (or different than the original tissue
61
Define 'healing'
Regeneration and repair or combination of the two
62
Define 'Chronic inflammation'
Inflammation of prolonged duration in which active inflammation, tissue destruction and tissue repair are proceeding simultaneously.
63
List the types of chronic inflammation
- Suppurative
| - Granulomatous
64
List the characteristics of all chronic inflammatory lesions
- Persistent
- Cellular infiltration
- Destruction of normal tissue
- Formation of fibrous connective tissue
65
Define 'abscess'
A collection of pus that has built up within the tissue of the body. Redness, pain, warmth and swelling occur in areas where abscesses occur.
66
Define 'ulcer'
A break in a bodily membrane that impedes the organ of which that membrane is a part of from continuing its normal functions
67
Define 'pyogenic granuloma'
Vascular lesion that occurs on mucosa and skin
68
Describe the possible forms of progression of acute inflammation with reference to: resolution
Acute restoration of original structure:
- Removal of fluid
- Rapid restitution of original tissue architecture and function
69
Describe possible forms of progression of acute inflammation with reference to: organization
acute healing with fibrous tissues formation of granulation tissue
70
Describe possible forms of progression of acute inflammation with reference to: healing
longer term process with fibrosis (collagen) and/or cell regeneration
71
Describe possible forms of progression of acute inflammation with reference to: suppuration
Formation of pus:
- increased permeability of endothelial cell layer -> movement of plasma fluid, proteins and neutrophils
- accumulated spots of dead and dying microorganisms and dead cells and tissue
- Granulation tissue surrounds the abscess
72
Outline the characteristics of granulation tissue
- Granulation tissue ONLY exists in tissue where damage has occurred
- Consists of macrophages, newly formed micro-vessels and fibroblasts:
1) migration from the outside injury site to inside the damaged tissue
2) macrophages removes debris and fibrin
3) vessels grow to supply oxygen and nutrients to fibroblasts (from injury periphery to centre)
4) Fibroblasts secrete the fibrous tissue
- Granulation tissue will "wrap" the damaged tissue
- Involved in granulomatous chronic inflammation
73
Define 'labile cells'
Normally proliferate to replace cells that are continuously being lost
- e.g. gut epithelium, bone marrow stem cells
74
Define 'stable cells'
Do not normally proliferate but capable of doing so when required:
- e.g. fibroblasts, endothelial cells or hepatocytes
75
Define 'permanent cells'
Rarely proliferate
| - e.g. CNS neurons, cardiac myocytes
76
List the characteristics that are common to all chronic inflammatory lesions
Characteristics of all chronic inflammatory lesions:
- Persistent
- cellular infiltration
- Destruction of normal tissue
- Formation of fibrous connective tissue
77
Outline the characteristics of chronic suppurative inflammation, with reference to osteomyelitis as an example
Chronic suppurative inflammation characteristics:
- prolonged form of acute suppurative inflammation (looks the same histologically)
- Lots of pus containing neutrophils and macrophages
- Ongoing recruitment of neutrophils: no neutrophils in chronic granulomatous inflammation
- Example: osteomyelitis:
1) very difficult to get antibiotics to bone tissue
2) massive neutrophil infiltration
3) Local damage to the bone and destruction of vessels
4) results in dead bone
78
Summarize the characteristics of an abscess and an ulcer
Abscess - a collection of pus that has built up within the tissue of the body.
- Redness, pain, warmth, and swelling occur in areas where abscesses occur.
Ulcer - a discontinuity in a bodily membrane that impedes the organ of which that membrane is a part of from continuing its normal functions.
79
Define granuloma and describe chronic granulomatous inflammation
No neutrophils in chronic granulomatous inflammation. Just types of macrophages and lymphocytes
Granuloma = collection of histocytes (e.g. macrophages, epithelioid cells, and multinucleated giant cells) in an tight, ball formation. May also include lymphocytes, fibroblasts, and fibrosis (collagen). May contain necrotic nuclei. Granuloma effectively "walls off" the offending agent from surrounding tissue.
80
Outline causes and histological characteristic + example of 'immune type' of chronic granulomatous inflammation
Immune type:
- Micro-organisms that survive inside "resting" normal tissue cells.
- Cytokines (interferon-gamma) activates macrophages to kill pathogens.
- Other cytokines regulate the actions of cells within the lesions
- E.g. tuberculosis
- Histological characteristic:
1) central caseous necrosis (central melting)
2) epithelioid cell cells and Langhans-type giant cells (both types of macrophages)
3) Fibrosis around periphery
81
Outline causes and histological characteristic & example of 'unknown origin' type of chronic granulomatous inflammation
- Tissue replacing functional tissue which is not characteristic of resident tissue/organ.
- E.g. Sarcoidosis
- Histological characteristic:
1) No central necrosis
2) epithelioid cells and langhans giant cells (both are types of macrophages)
3) Lymphocytes and peripheral fibrosis
4) Fibrosis around periphery
82
Outline causes and histological characteristic & example of 'foreign body granuloma' type of chronic granulomatous inflammation
- Foreign body introduced into tissues
- Nearly the same as chronic granulomatous inflammation of unknown origin, except that fibrosis is less
- e.g. Old types of sutures.
- Histological characteristic (similar to unknown origin):
1) foreign body giant cells
2) few lymphocytes
3) no central necrosis
4) diffuse fibrosis
5) may see the foreign body (cotton fibres)
83
Outline the characteristics of mixed-type chronic inflammation with reference to rheumatoid arthritis as an example
Mixed-type chronic inflammation:
- Involves both neutrophils and macrophages/lymphocytes over protracted periods
- Initiating agent is typically not known
- e.g. Rheumatoid Arthritis:
1) neutrophils in synovial fluid
2) lymphocytes and macrophages in pannus
84
Define "regeneration"
Growth of cells and tissues to restore a lost structure
- Requires an intact tissue as a scaffold
- possible by cells with a high mitotic capability or presence of stem cells
85
Define 'healing'
Tissue response to a wound
- Inflammatory processes in internal organs
- Cell necrosis in organs are incapable of regeneration (e.g. myocardium).
- Healing is a combination of regeneration and scar formation (fibrous tissue) in variable proportions:
1) e.g. superficial wounds - fully healed by regeneration
2) e.g. deep wound, damage in the dermis leads to a collagenous scar.
- Healing takes a relatively long time
86
Define 'healing by first intention'
Small injury where margins of the wound can attach to each other; no infection
87
Define 'healing by second intention'
Injury is larger and wound margins can't attach to each other
- Granulation tissue forms
- Scar forms
- Infection
88
Define 'granulation tissue (soft callus)
New connective tissue found in tissue repair after injury
- Proliferation of many cells: Macrophages, epithelial cells, endothelial cells, fibroblasts
- Collagen and elastin
- Highly vascular
89
Define 'fibrosis (hard callus)'
The thickening and scarring of connective tissues via fibroblasts
90
Define 'angiogenesis'
Formation of new blood vessels
91
Define 'inflammation'
Reaction of vascularized living tissue to local injury or infection, characterized by the movement of fluid and leukocytes from the blood into the affected tissue
92
Outline the control mechanisms of cell proliferation and tissue growth
- Quiescent stable cells are recruited (cells outside cell cycle)
- Quiescent cells enter cell cycle to contribute to tissue growth
93
Outline the basic cell cycle and the concept of stem cells
- Stem cells are pluripotent cells that can differentiate into multiple cell types
- Able to regenerate new tissue that matches the original tissue
94
Outline the regenerative capacity of different types of cells (labile cells, stable cells, and permanent cells) and give examples of tissue renewal (turnover) in blood cells, small intestinal epithelial cells and skin cells
Labile cells - normally proliferate to replace cells that are continually being lost: e.g. gut epithelium, bone marrow stem cells
Stable cells - do not normally proliferate but capable of doing so when required: e.g. fibroblasts, endothelial cells or hepatocytes
Permanent cells - rarely proliferate: e.g. CNS neurons, cardiac myocytes
Tissue renewal - entire tissue is replaced:
- Blood turnover -> 10^8 - 10^9 cells per hour
- Small intestine turnover -> every 3-5 days
- Skin turnover -> every 3-4 weeks
95
Four stages and time scale of healing?
1. Haemostasis (seconds to minutes)
- Stop the bleeding
- Vasoconstriction
- Blood clot (i.e. platelet plug)
2. Inflammation (minutes to hours)
- Ward off bacterial
- Neutrophils kill bacteria
- Monocytes turn to macrophages (produce growth factors for fibroblasts)
- Lymphocytes modulate inflammation
3. Proliferation (3 days for weeks)
- Granulation tissue forms
- Scar forms
- Angiogenesis occurs (necessary to provide nutrients to wound site)
- Fibroblasts proliferate and produce collagen
- Epithelialization occurs (growth of new epithelial tissue)
4. Remodelling (weeks to months)
- Fibroblasts transform to myofibroblasts (stimulated by TGF-beta)
- Myofibroblasts contract edges of wound
- Metalloproteinases: collagen synthesize and degradation control
- Strength of wound increases
96
List the differences between healing by first intention and healing by second intention
First intention:
- small distance between margins
- No infection
- Margins are sutured
Second intention:
- Far distance between margins
- Infection
- Margins are devitalized, bruised, or necrotic
97
Summarize the principal steps of healing by first intention, the processes that occur in each step and the timescale of each step, with reference to the rate of healing and the tensile strength of a healing wound
First intention - margins can be attached
1. platelets and fibrin form blood clot
2. neutrophils infiltrate to check for infection
3. macrophages clean up debris
4. Fibroblasts repair connective tissue
5. New blood vessels sprout
6. collagen forms scar over months to years
