Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 1 > Pathology > Flashcards

Pathology Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the mechanisms of ageing

A

Internal mechanisms:

  • Telomere shortening
  • “clock genes”

External mechanisms:

  • damage to cell structure
  • Damage to DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define “neoplasia”

A
  • The presence or formation of new, abnormal growth of tissue. Unregulated cell division leading to new growth of tissue.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define “benign neoplasm”

A

Benign neoplasms lack the ability to invade the neighbouring tissue or metastasize. Considered non-cancerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define “pleomorphism”

A

Enlarged deep blue stained nucleus. High nucleus to cytoplasm ratio. Pleomorphism is characteristic of malignant tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define “hamartoma”

A

A tumour-like growth, composed of disorganized but mature cells/tissues indigenous to the site. Completely benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Define “dysplasia”

A

Disordered growth of cells but non-invasive (benign). Common in epithelia. Pre-malignant growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

List the mechanisms by which nuclear damage may give rise to a malignant phenotype

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline examples of screening programs that can lead to early detection of cancer

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Explain the components of the diagnosis of neoplasia, with particular reference to histopathological assessment and adjuncts to histopathological assessment

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Explain the relevance of acute inflammation to medicine and dentistry

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define the term ‘inflammation’ and describe the roles of the inflammatory response and the cardinal signs of inflammation

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the position of inflammation within the wider context of host protective responses against micro-organisms

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Explain the distinctions between acute and chronic inflammatory processes

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the roles of lymphocytes

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the roles of monocytes/macrophages

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the roles of neutrophils

A
  • Granular polymorphonuclear leukocyte
  • Faint granules (often tri-lobed nucleus)
  • phagocytize bacteria
  • Most abundant (40-75% of leukocytes)
  • 12-15 um diameter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe the roles of eosinophils

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the roles of basophils

A
  • Release histamine, causing vasodilation and inflammation in allergic reactions
  • < 1% of the leukocytes
  • Allergic reactions and
  • Filled with granules, overlying nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the mechanisms underlying the cardinal signs of inflammation: heat

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the mechanisms underlying the cardinal signs of inflammation: redness

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the mechanisms underlying the cardinal signs of inflammation: swelling

A

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
Q

Describe the mechanisms underlying the cardinal signs of inflammation: pain

A

Pain is due to the release of bradykinin, histamines, that stimulate nerve endings

41
Q

Describe the 5th cardinal sign

A

Loss of function - caused by tissue damage to affected organ

42
Q

Explain the stereotypic nature of acute inflammation

A
  • Injury or infection occurs
  • exudation and neutrophil infiltration occurs
  • Resolution follows
  • Rarely, pus and chronic inflammation occur then healing
43
Q

Describe the components of the acute inflammatory response

A
  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
Q

Describe soft tissue injury, the recommended treatments, and the process through which long-term complications are reduced

A

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
Q

Explain the role of ‘exudation’ in the inflammatory process

A

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
Q

Describe what is meant by the following statement: “Inflammation: friend or foe?”

A

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
Q

Outline the place of pathology in clinical medicine

A

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
Q

Outline anatomical pathology

A

Study of organs and tissues to determine the causes and effects of particular diseases

49
Q

Outline chemical pathology

A

Study of biochemical basis of diseases and the monitoring of metabolic processes via “biomarkers”

50
Q

Outline haematology

A

Clinical and laboratory aspects of primary disorders of blood

51
Q

Outline genetics

A

Chromosomal abnormalities, co-dominant mutations, recessive mutations, polymorphisms, SNP associations

52
Q

Outline microbiology

A

Diagnosing bacterial, viral, fungal and parasitic infection

53
Q

Outline the factors that determine the response to injury

A

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
Q

Define ‘resolution’

A

Acute restoration of the original structure (quick return to normal tissue)

55
Q

Define ‘organization’

A

Formation of granulation tissue leading to acute healing by fibrosis (replacement tissue)

56
Q

Define ‘suppuration’

A

Formation of pus (liquid produced by infected tissue consisting of dead WBC, debris and serum

57
Q

Define ‘granuloma’

A
  • 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
Q

Define ‘granulation tissue’

A
  • 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
Q

Define ‘regeneration’

A

Replacement of injured tissue by parenchymal cells of the same type of tissue

60
Q

Define ‘repair’

A

Replacement of injured tissue by fibrous tissue (or different than the original tissue

61
Q

Define ‘healing’

A

Regeneration and repair or combination of the two

62
Q

Define ‘Chronic inflammation’

A

Inflammation of prolonged duration in which active inflammation, tissue destruction and tissue repair are proceeding simultaneously.

63
Q

List the types of chronic inflammation

A
  • Suppurative

- Granulomatous

64
Q

List the characteristics of all chronic inflammatory lesions

A
  • Persistent
  • Cellular infiltration
  • Destruction of normal tissue
  • Formation of fibrous connective tissue
65
Q

Define ‘abscess’

A

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
Q

Define ‘ulcer’

A

A break in a bodily membrane that impedes the organ of which that membrane is a part of from continuing its normal functions

67
Q

Define ‘pyogenic granuloma’

A

Vascular lesion that occurs on mucosa and skin

68
Q

Describe the possible forms of progression of acute inflammation with reference to: resolution

A

Acute restoration of original structure:

  • Removal of fluid
  • Rapid restitution of original tissue architecture and function
69
Q

Describe possible forms of progression of acute inflammation with reference to: organization

A

acute healing with fibrous tissues formation of granulation tissue

70
Q

Describe possible forms of progression of acute inflammation with reference to: healing

A

longer term process with fibrosis (collagen) and/or cell regeneration

71
Q

Describe possible forms of progression of acute inflammation with reference to: suppuration

A

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
Q

Outline the characteristics of granulation tissue

A
  • 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
Q

Define ‘labile cells’

A

Normally proliferate to replace cells that are continuously being lost
- e.g. gut epithelium, bone marrow stem cells

74
Q

Define ‘stable cells’

A

Do not normally proliferate but capable of doing so when required:
- e.g. fibroblasts, endothelial cells or hepatocytes

75
Q

Define ‘permanent cells’

A

Rarely proliferate

- e.g. CNS neurons, cardiac myocytes

76
Q

List the characteristics that are common to all chronic inflammatory lesions

A

Characteristics of all chronic inflammatory lesions:

  • Persistent
  • cellular infiltration
  • Destruction of normal tissue
  • Formation of fibrous connective tissue
77
Q

Outline the characteristics of chronic suppurative inflammation, with reference to osteomyelitis as an example

A

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
Q

Summarize the characteristics of an abscess and an ulcer

A

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
Q

Define granuloma and describe chronic granulomatous inflammation

A

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
Q

Outline causes and histological characteristic + example of ‘immune type’ of chronic granulomatous inflammation

A

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
Q

Outline causes and histological characteristic & example of ‘unknown origin’ type of chronic granulomatous inflammation

A
  • 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
Q

Outline causes and histological characteristic & example of ‘foreign body granuloma’ type of chronic granulomatous inflammation

A
  • 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
Q

Outline the characteristics of mixed-type chronic inflammation with reference to rheumatoid arthritis as an example

A

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
Q

Define “regeneration”

A

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
Q

Define ‘healing’

A

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
Q

Define ‘healing by first intention’

A

Small injury where margins of the wound can attach to each other; no infection

87
Q

Define ‘healing by second intention’

A

Injury is larger and wound margins can’t attach to each other

  • Granulation tissue forms
  • Scar forms
  • Infection
88
Q

Define ‘granulation tissue (soft callus)

A

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
Q

Define ‘fibrosis (hard callus)’

A

The thickening and scarring of connective tissues via fibroblasts

90
Q

Define ‘angiogenesis’

A

Formation of new blood vessels

91
Q

Define ‘inflammation’

A

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
Q

Outline the control mechanisms of cell proliferation and tissue growth

A
  • Quiescent stable cells are recruited (cells outside cell cycle)
  • Quiescent cells enter cell cycle to contribute to tissue growth
93
Q

Outline the basic cell cycle and the concept of stem cells

A
  • Stem cells are pluripotent cells that can differentiate into multiple cell types
  • Able to regenerate new tissue that matches the original tissue
94
Q

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

A

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
Q

Four stages and time scale of healing?

A
  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
Q

List the differences between healing by first intention and healing by second intention

A

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
Q

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

A

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

Block 1 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions