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medicine 1 (just learning outcomes) > FoM_PoD > Flashcards

FoM_PoD Flashcards

1
Q

what is a tumour

A 
A tumour (or neoplasm) is an abnormal growing mass of tissue 
Its growth is uncoordinated with that of surrounding normal tissue
Its growth continues after the removal of any stimulus which may have caused the tumour
It is an irreversible change
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2
Q

what are the different types of tumours

A

benign

malignant (= cancer)

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3
Q

what is cancer

A

A fundamental property of cancer (or malignant tumour) is its ability to invade into adjacent tissue and to metastasise (spread) and grow at other sites within the body

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4
Q

what are the most common types of cancer in the uk

A 
prostate
breast
lung
colon
melanoma
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5
Q

what is the classification of tumours

A

Important for understanding tumour behaviour

Important for determining outcome (prognosis) and selecting therapy

Based on tissue of origin
-Epithelium
-Connective tissue (mesenchyme)
-Blood cells
-Lymphoid tissue
-Melanocytes
-Neural tissue
-Germ cells (ovary/testis)
Benign v malignant
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6
Q

what is the nomenclature of epithelial tumours

A

glandular:

  • benign - adenoma
  • malignant - adeno-carcinoma

squamous:

  • benign - squamous papilloma
  • malignant - squamous carcinoma
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7
Q

what is the nomenclature of connective tissue tumours

A

bone:

  • benign - osteoma
  • malignant - osteo-sarcoma

fat:

  • benign - lipoma
  • malignant - lipo-sarcoma

fibrous tissue:

  • benign - fibroma
  • malignant - fibro-sarcoma
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8
Q

what is the nomenclature of tumours of blood cells

A

white blood cells:

- malignant - leukaemia

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9
Q

what is the nomenclature of tumours of lymphoid tissue

A

lymphoid tissue:

- malignant - lymphoma

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10
Q

what is the nomenclature of tumours of melanocytes

A

melanocyte:

  • benign - naevus
  • malignant - melanoma
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11
Q

what is the nomenclature of tumours of neutral tissue

A

central nervous system:
- astrocytoma

peripheral nervous system:
- schwannoma

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12
Q

what is the nomenclature of germ cell tumours

A 
Teratomas
Tumour composed of various tissues
Develop in ovary/testis
Ovarian teratomas usually benign
Testicular teratomas usually malignant
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13
Q

what are the features of benign tumours

A
  • Non-invasive growth pattern
  • Usually encapsulated
  • No evidence of invasion
  • No metastases
  • Cells similar to normal
  • Benign tumours are “well-differentiated”
  • Function similar to normal tissue
  • Rarely cause death
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14
Q

what are the features of malignant tumours

A
  • Invasive growth pattern
  • No capsule or capsule breached by tumour cells
  • Cells abnormal
  • Cancers often “poorly differentiated”
  • Loss of normal function
  • Often evidence of spread of cancer
  • Frequently cause death
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15
Q

what are the properties of cancer cells

A

Loss of tumour suppressor genes

  • Adenomatous polyposis (APC)
  • Retinoblastoma (Rb)
  • BRCA1

Gain of function of oncogenes

  • B-raf
  • Cyclin D1
  • ErbB2
  • c-Myc
  • K-ras, N-ras

Altered cellular function

Abnormal morphology

Cells capable of independent growth

But no single feature is unique to cancer cells

Tumour biomarkers

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16
Q

give examples of tumour biomarkers

A

Onco-fetal proteins
Oncogenes
Growth factors and receptors
Immune checkpoint inhibitors

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17
Q

what is the clinical use of tumour biomarkers

A

Screening
Diagnosis
Prognostic
-Identifying patients with a specific outcome
Predictive
-Identifying patients who will respond to a particular therapy

Alpha-fetoprotein
-Teratoma of testis
-Hepatocellular carcinoma
Carcino-embryonic antigen (CEA)
-Colorectal cancer
Oestrogen receptor
-Breast cancer
Prostate specific antigen
-Prostate cancer
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18
Q

what is tumour growth

A

Tumour growth is balance between cell growth and cell death

  • Angiogenesis
  • Apoptosis
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19
Q

what is tumour angiogenesis

A

New blood vessel formation by tumours
Required to sustain tumour growth
But provides route for release of tumour cells into circulation
More blood vessels in a tumour equals poorer prognosis

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20
Q

what is apoptosis

A

Mechanism of programmed single cell death
Active cell process
Regulates tumour growth
Involved in response to chemotherapy and radiotherapy

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21
Q

spread of cancer

A

Fundamental property of cancer
Invasion and metastasis
Major clinical problem of cancer is formation of metastatic (secondary) tumours
Prognosis depends on extent of cancer spread

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22
Q

process of tumour spread

A

normal -> tumour -> metastasis

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23
Q

modes of spread of cancer

A

Local spread
Lymphatic spread
Blood spread
Trans-coelomic spread

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24
Q

tumour invasion

A

malignant tumour -> invasion into connective tissue -> invasion into lymph/blood vessels

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25
Q

Tumour Metastasis Via Lymphatics

A

Adherence of tumour cells
to lymph vessels
-> Invasion from
lymphatics -> Invasion into lymph node -> Formation of metastasis in lymph node -> Clinical evidence of metastasis

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26
Q

tumour trans-coelomic spread

A

Special form of local spread
Spread of tumour cells across body cavities e.g. pleural or peritoneal cavities
Tumours of lung, stomach, colon and ovary show trans-coelomic spread

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27
Q

tumour metastasis

A

Tumour metastasis is major clinical problem
Sites of metastasis not related to tissue blood flow
Depends on both tumour and tissue related factors
Metastatic niche

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28
Q

uncommon sites of metastasis

A

spleen
kidney
skeletal muscle
heart

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29
Q

common sites of metastasis

A 
tumour:
breast 
prostate
colorectal
ovary

tissue:
bone
liver
omentum/peritoneum

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30
Q

what are the local effects of benign tumours

A

pressure

obstruction

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31
Q

what are the local effects of malignant tumours

A 
Pressure
Obstruction
Tissue destruction
-Ulceration/infection
Bleeding
-Anaemia
-Haemorrhage
Pain
-Pressure on nerves
-Perineural infiltration
-Bone pain from pathological fractures
Effects of treatment
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32
Q

what are the systemic effects of malignant tumours

A

Weight loss-cancer cachexia
Secretion of hormones
“Normal” - (produced by tumours of endocrine organ - but abnormal control of hormone production/secretion)
“Abnormal”/inappropriate - (produced by tumour from an organ that does not normally produce hormone)
Paraneoplastic syndromes - (Cannot be explained by local or metastatic effects of tumours e.g. neuropathy, myopathy)
Effects of treatment

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33
Q

early detection of cancer

A 
Important to detect cancer at early stage 
Reduce/prevent morbidity/mortality
Detection at pre-invasive stage
-Identification of dysplasia/intraepithelial neoplasia
Requires effective test
-Sensitive/specific
-Acceptable
Cervical cancer screening
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34
Q

dysplasia

A 
Pre-malignant change 
Earliest change in the process of malignancy that can be visualised
Identified in epithelium
No invasion
But can progress to cancer
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35
Q

what are the features if dysplasia

A 
Disorganisation of cells
-Increased nuclear size
-Increased mitotic activity
-Abnormal mitoses
Grading of dysplasia
-High grade
-Low grade
No invasion
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36
Q

cervical cancer screening

A

Established NHS program
Aims to reduce incidence of squamous carcinoma of cervix
Detection of oncogenic human papilloma virus from squamous epithelium of cervix

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37
Q

what is cell division

A

mechanism of cellular replication
nuclear division plus cytokinesis
generates two genetically identical daughter cells

Cell Cycle = ordered series of events between mitotic divisions

consists of the interphase and the mitotic phase

38
Q

what does the interphase involve

A

during which the cell grows and accumulates nutrients needed for mitosis; the cell is synthesizing RNA, producing protein and growing in size

G1, a growth phase,

S phase, during which the DNA is replicated,

and G2, a further growth phase

39
Q

what does the mitotic phase involve

A

mitosis - phase during which the cell splits itself into two distinct cells

cytokinesis - new cell is completely divided

40
Q

how is the cell controlled

A

The molecular events that regulate the cycle are ordered and directional- it is impossible to reverse the cycle

Cycle phases must be in correct sequence

DNA synthesis and mitosis must occur sequentially

Quality control
-each daughter cell must receive a full chromosome complement
-detection and repair of genetic damage
mutations in DNA sequences must not pass on

Division is coordinated and tightly controlled

Regulation of the cell cycle allows detection and repair of genetic damage as well as the prevention of uncontrolled cell division
genome replicated only once; daughter cells missing all or part of crucial genes die
Errors in mitosis can either kill a cell or cause mutations
possession of extra copies of certain genes also deleterious
ensures genetic fidelity
25 x 106 cell divisions sec-1 in humans

> 1013 cells in the body

Monitor and regulate progress

Prevent progression at specific points

G1/S restriction point

control is achieved by checkpoints in the cycle: G1/S transition is a rate-limiting step in the cell cycle and is also known as Restriction point; Cells that progress through this point are committed to enter S phase
prior to restriction point progress through G1 depends on external stimuli after restriction point progression becomes autonomous
progress can be arrested if certain molecular events are incomplete; The cell cannot proceed to the next phase until checkpoint requirements have been met.
Several checkpoints are designed to ensure that damaged or incomplete DNA is not passed on to daughter cells. Two main checkpoints exist: the G1/S checkpoint and the G2/M checkpoint.
Inadequate nutrient supply - G1 arrest
External stimulus lacking - G1 arrest

Abnormal cell size - G1 or G2 arrest

DNA not replicated - S arrest
DNA damage detected - G1 or G2 arrest
Chromosome misalignment - M-phase arrest
External factors
Hormones, growth factors, cytokines

Intrinsic factors
critical checkpoints - Restriction point (R) in G1

41
Q

cell cycle checkpoint activators

A

System of cyclically active and inactive enzyme switches

Catalytic sub-unit cyclin-dependent kinases (CDKs) (determines a cell’s progress through the cell cycle) activated by a regulatory sub-unit cyclins

The active enzyme complex = CDK/cyclin complex

42
Q

cell cycle checkpoint activators

A

System of cyclically active and inactive enzyme switches

Catalytic sub-unit cyclin-dependent kinases (CDKs) (determines a cell’s progress through the cell cycle) activated by a regulatory sub-unit cyclins

The active enzyme complex = CDK/cyclin complex

43
Q

cyclins and cyclin-dependent kinases

A

Different CDK/cyclin complexes operate at sequential stages of the cycle

Active CDK/cyclin complexes phosphorylate target proteins

Phosphorylation results in activation/inactivation of target proteins

Substrates regulate events in the next cycle phase

When activated by a bound cyclin, CDKs perform a common biochemical reaction - phosphorylation that activates or inactivates target proteins to orchestrate coordinated entry into the next phase of the cell cycle.
Different cyclin-CDK combinations determine the downstream proteins targeted.
A pro-mitotic extracellular signal, induces G1 cyclin-CDK complexes- become active and prepare the cell for S phase, promoting the expression of transcription factors that in turn promote the expression of S cyclins and of enzymes required for DNA replication.

44
Q

cell cycle inhibitors

A

CDK inhibitors (CKIs)
-Inhibitor molecules binding to cyclin/CDK complexes
INK4A gene family e.g. p16
CIP/KIP gene family e.g. p21 p27

Two families of genes, the cip/kip family and the INK4a prevent cell cycle progression
The INK4a family includes p16INK4a, which binds to CDK4 and arrests the cell cycle in G1 phase, and p14 which prevents p53 degradation
The cip/kip family includes the genes p21, p27 and p57. They halt cell cycle in G1 phase, by binding to, and inactivating, cyclin-CDK complexes. p21 is activated by p53

45
Q

retinoblastoma gene

A

key role in regulating the cell cycle

Encodes a 110 kDa phosphoprotein (pRb) expressed in almost every human cell

Hypophosphorylated pRb is active
cells remain in G1 phase

Active cyclin D/CDK complexes phosphorylate pRb as the cell cycle progresses

Phosphorylated/inactive pRb loses affinity for E2F transcription factor
E2F is a powerful signal for cell cycle activation

In the hypophosphorylated state, pRb is active and carries out its role as tumor suppressor by inhibiting cell cycle progression.

pRb inhibits the cell cycle

Rb gene mutations favour cell proliferation

Mutations in other genes controlling pRb phosphorylation mimic the effect of pRb loss

  • Mutational activation of cyclin D or CDK4
  • Mutational inactivation of CDKIs also drive proliferation
46
Q

carcinogenesis

A

failure of cell cycle control

Balance between proliferation and apoptosis disrupted

Mutations in genes regulating cell division, apoptosis, and DNA repair cause a cell to lose control of proliferation

Uncontrolled proliferation of cells forms tumours

Two frequently disrupted regulatory pathways -

            1. The cyclin D-pRb-E2F pathway
            2. p53 pathway

Environmental agents

  • Chemicals
  • Radiation
  • Oncogenic viruses

Inherited factors

47
Q

p53

A

maintains the integrity of the genome
Cells with mutated p53 do not G1 arrest or repair damaged DNA
Genetically damaged cells proliferate and form malignant neoplasms

48
Q

cancer relating to the cell cycle

A

Virtually all cancers are dysregulated at G1-S
mutated cell cycle regulating genes:
cyclin D CDK4 p16 Rb

Cells with mutated p53 proliferate and form malignant neoplasms

49
Q

what is the two-hit hypothesis of oncogenes

A

hypothesis in which both alleles, remember that alleles are the copies for a certain gene. you have two copies of any given gene as you have one copy on the chromosome you got from your mum and another on the chromosome you got from your dad. in the two-hit hypothesis, both alleles must be mutated before the effect is manifested because if only one of the alleles is damaged, you have a “back up” second copy that can still produce the protective protein so you need two hits for each if the alleles that you have

50
Q

tumour suppressor genes

A

anti-oncogenes

Genes that protect a cell from forming cancers

Generally follow the “two-hit hypothesis”

  • Tumour suppressor alleles are usually recessive
  • Loss of both normal allelic copies gives rise to cancer

Mutation causes ‘loss of function’

Normal regulatory genes

-Normal growth-inhibiting genes
Genes negatively regulating mitosis – Rb, INK4A family
Genes regulating apoptosis – p53

-Genes regulating DNA repair

Mutation causes loss of function

51
Q

inherited cancer syndromes

A

account for 5-10% of all cancers

genetic predisposition to develop cancer

early onset of multiple tumours

52
Q

proto-oncogenes

A

Normal genes coding for normal growth regulating proteins

Growth factors

Growth factor receptors

Signal transduction

53
Q

oncogenes

A

cancer causing genes

Derived from proto-oncogenes with ‘gain of function’

Activated by –

Alteration of proto-oncogene structure
point mutation
chromosome rearrangements + translocations

Dysregulation of proto-oncogene expression
gene amplification
over-expression

oncogene activation:

Chromosomal rearrangements: translocations

  • Overexpression
    Burkitt lymphoma - c-myc moves close to IgH gene
    Mantle cell lymphoma cyclin D1 gene-IgH

-Recombination to form chimeric proteins
Chronic myeloid leukaemia

54
Q

chemical carcinogenesis

A

Purine and pyrimidine bases in DNA are critically damaged by oxidizing and alkylating agents

Chemical carcinogens react with DNA forming covalently bound products (DNA adducts)

Adduct formation can lead to activation of oncogenes and loss of anti-oncogenes

55
Q

radiation carcinogenesis

A

Purine and pyrimidine bases in DNA are critical targets for radiation damage

High-energy radiation is carcinogenic if received in sufficient doses

  • ultraviolet radiation (UV-B present in sunlight)
  • X-rays
  • Gamma radiation
56
Q

viral carcinogenesis

A

ONCOVIRUSES

  • virus genome inserts near a host proto-oncogene
    viral promoter causes proto-oncogene over-expression
  • virus directly inserts an oncogene into host DNA causing cell division

Viruses known to cause cancer in humans

  • HPV (genital, throat and anal cancers)
  • Hepatitis B (liver cancer)
  • EBV (lymphoma)
57
Q

multistep carcinogenesis

A

All sporadic cancers harbour multiple genetic aberrations

Mutations accumulate with time

Activation of several oncogenes and loss of two or more anti-oncogenes occurs in most cancers

58
Q

what is acute inflammation

A

fundamental response maintaining integrity of organism

  • dynamic homeostatic mechanism
  • higher organisms

series of protective changes occurring in living tissue as a response to injury

59
Q

what are the cardinal signs of inflammation

A 
rubor 	- redness
calor 	- heat
tumor 	- swelling
dolor 	- pain
loss of function
all of these explained by the sequence of Pathological events taking place
60
Q

what are the causes of acute inflammation

A

micro-organisms - bacteria, fungi, viruses, parasites
-pathogenic organisms cause infection

mechanical - trauma - injury to tissue
-all injuries even sterile (eg surgery)

chemical - upset stable environment

  • acid or alkali - upset pH
  • bile and urine - irritation when in inappropriate place eg peritoneum

physical - extreme conditions

  • heat - sunburn
  • cold - frostbite
  • ionising radiation

dead tissue
-cell necrosis irritates adjacent tissue

hypersensitivity
-several classes of reaction

61
Q

what is the process of acute inflammation

A

series of microscopic events
localised to affected tissue
take place in the microcirculation
result in the clinical symptoms and signs of acute inflammation - the cardinal signs

62
Q

what is microcirculation

A

capillary beds, fed by arterioles and drained by venules
extracellular “space” and fluid and molecules within it
lymphatic channels and drainage
Starling forces control flow (fluid flux) across membrane
Q = LpS{(Pc - Pi) - (p - i)}
dynamic balance
hydrostatic and colloid osmotic pressures
compartments and physical constants

63
Q

what are the steps in acute inflammation (pathogenesis)

A

changes in vessel radius - flow
change in the permeability of the vessel wall - exudation
movement of neutrophils from the vessel to the extravascular space

64
Q

Local changes in vessel radius and blood flow

A 
1. transient arteriolar constriction
  few moments, probably protective
2. local arteriolar dilatation
  active hyperaemia
3. relaxation of vessel smooth muscle
  ? autonomic NS or mediator derived
called the “Triple Response” - flush, flare, wheal
Do this yourself and see the effect

increased radius - why increased flow?

Poiseuille’s law
-Q = P x r4/8L
-flow is proportional to radius to the power of four
-(Q fluid flux, P pressure gradient, r radius,  viscosity, L length)
For full details see Cardiovascular System
-increased arteriolar radius causes increased local tissue blood flow
-results in observed redness and heat

65
Q

what are the effects of exudation

A

oedema formed
oedema is accumulation of fluid in the extravascular space
explains swelling of tissue in acute inflammation
swelling causes pain - reduce function

66
Q

what are the phases of neutrophils

A

margination - neutrophils move to endothelial aspect of lumen
pavementing - neutrophils adhere to endothelium
emigration - neutrophils squeeze between endothelial cells - active process - to extravascular tissues
(note meaning of diapedesis)

67
Q

what is the resolution of acute inflammation

A 
inciting agent isolated & destroyed
macrophages move in from blood and phagocytose debris; then leave
epithelial surfaces regenerate
inflammatory exudate filters away
vascular changes return to normal
inflammation resolves
68
Q

what are the benefits of acute inflammation

A 
rapid response to non-specific insult
cardinal signs and loss of function
-transient protection of inflamed area
neutrophils destroy organisms and denature antigen for macrophages
plasma proteins localise process
resolution and return to normal
69
Q

what are the outcomes of acute inflammation

A

resolution
suppuration
organisation
chronic inflammation

70
Q

inflammation at various anatomical locations

A

“structure”-itis
peritoneal cavity -peritonitis
meninges -meningitis
appendix -appendicitis

lungs -pneumonia

pleural cavity -pleurisy

71
Q

what is the role of neutrophils

A 
mobile phagocytes 
recognise foreign antigen 
move towards it - chemotaxis 
adhere to organism
granules possess oxidants (eg H2O2) and enzymes  (eg proteases) 
release granule contents 
phagocytose & destroy foreign antigen

consequence of neutrophil action
neutophils die when granule contents released
produce a “soup” of fluid, bits of cell, organisms, endogenous proteins - pus
might extend into other tissues, progressing the inflammation

72
Q

what are the mediators of acute inflammation

A

molecules on endothelial cell surface membrane
molecules released from cells
molecules in the plasma
molecules inside cells

73
Q

what is the effect of mediators of acute inflammation

A 
vasodilatation
increased permeability
neutrophil adhesion
chemotaxis
itch and pain
74
Q

what are the systemic effects of acute inflammation

A 
pyrexia - raised temperature
-endogenous pyrogens from white cells act centrally
feel unwell
-malaise, anorexia, nausea
-abdominal pain and vomiting in children
neutrophilia - raised white cell count
-bone marrow releases/produces
75
Q

what are the outcomes of acute inflammation

A 
resolution
suppuration
organisation
dissemination
chronic inflammation
76
Q

what are the outcomes of acute inflammation - suppuration

A

pus formation
-dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris

pyogenic membrane surrounds pus

  • capillary sprouts, neutrophils, fibroblasts
  • walls off pus
77
Q

what are the outcomes of acute inflammation - organisation

A
  • granulation tissue characteristic
  • healing and repair
  • leads to fibrosis and formation of a scar
78
Q

what are the outcomes of acute inflammation - dissemination

A
  • spread to bloodsteam - patient “septic”
  • bacteraemia - bacteria in blood
  • septicaemia - growth of bacteria in blood
  • toxaemia - toxic products in blood
79
Q

what is chronic inflammation

A 
inflammation in which the cell population is especially
-lymphocytes
-plasma cells
-macrophages
features tissue or organ damage, (necrosis), loss of function
healing and repair
-granulation tissue
-scarring and fibrosis
may follow from ongoing acute inflammation 
-and commonly does
-“acute on chronic inflammation”
but also arises as primary pathology
tends to be long-term
80
Q

what are the clinical presentations of chronic -inflammation

A

often no specific “sore bit”

malaise and weight loss
-tuberculosis (lung, lymph node, bone, kidney, skin) – systemic effect

loss of function

  • autoimmune thyroiditis (functional gland destruction) – hypothyroidism
  • Crohn’s disease (GI tract ulceration and fibrosis) – pain, diarrhoea, gut obstruction
  • leprosy (cutaneous nerve destruction) – loss of sensation
81
Q

when do we see chronic inflammation

A

arising from acute inflammation

  • follows on from acute
  • large volume of damage
  • inability to remove debris
  • fails to resolve – ongoing acute insult

arising as a primary lesion

  • no preceding acute phase
  • only see chronic changes
82
Q

what is the outcome of chronic inflammation

A

granulation tissue is characteristic of organization

involves new vessel formation – angiogenesis

results in healing and repair

leads to fibrosis and formation of a scar

83
Q

what is angiogenesis

A

new vessels form- capillary buds

Vascular Endothelial Growth Factor (VEGF) released by hypoxic cells stimulates proliferation

enzyme secretion aids process

enable blood supply to enter damaged tissue

generic nature:
angiogenesis and organisation in thrombosis

limits thrombus propagation

reinstatement of flow

angiogenesis in malignant tumours

angiogenesis occurs as tumour grows

potential for therapeutic control

fibrosis and scarring in atherosclerosis

similarities with chronic inflammation

84
Q

general nature of angiogenesis

A

angiogenesis and organisation in thrombosis

limits thrombus propagation

reinstatement of flow

angiogenesis in malignant tumours

angiogenesis occurs as tumour grows

potential for therapeutic control

fibrosis and scarring in atherosclerosis

similarities with chronic inflammation

85
Q

granulation tissue mechanism and function

A

capillaries grow into inflammatory mass

access of plasma proteins

macrophages from blood and tissue

fibroblasts lay down collagen to repair damaged tissue

collagen replaces inflammatory exudate

patches tissue defects

replaces dead or necrotic tissue

contracts and pulls together

86
Q

which cell types are involved in chronic inflammation

A 
macrophage
endothelial cell
fibroblast
pus blood clotting
fibrin
87
Q

what are the special roles in chronic inflammation

A

distinguish from separate roles of polymorph, mast cells, eosinophil and lymphocyte/plasma cell

88
Q

what are the causes of chronic inflammation

A

significance, particularly of fibrosis/scarring

89
Q

common examples of chronic inflammation

A

briefly- burns and contractures; cirrhosis of the liver; tubular ulcer/pyloric stenosis; ureter/hydronephrosis. fracture healing

90
Q

primary chronic inflammation

A

autoimmune disease

  • autoantibodies directed against own cell and tissue components – autoantigens
  • damage or destroy organs, tissues, cells, cell components
  • thyroiditis, rheumatoid disease, pernicious anaemia (chief/parietal cells), systemic lupus erythematosis (nuclear antigen)

lymphocytes, plasma cells, macrophages, fibrosis

material resistant to digestion

  • mycobacteria, Brucella, viruses
  • cell wall resistant to enzymes

exogenous substances

  • sutures, metal and plastic eg joint replacements, mineral crystals, glass,
  • not provoke immune response

endogenous substances

  • necrotic tissue, keratin, hair
  • cannot easily be phagocytosed

granulomatous inflammation common

91
Q

pathogenesis of chronic inflammation

A

cells and their roles

  • lymphocytes
  • plasma cells
  • macrophages
  • fibroblasts

tissue components

  • granulation tissue
  • collagen
92
Q

what is the role of lymphocytes in chronic inflammation

A

cells that are part of immune system

small round cells with lots of subtypes and functions

main types of lymphocyte

  • T-cell
  • B-cell

main functions

  • immune response
  • immune memory

medicine 1 (just learning outcomes) (2 decks)

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