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PHASE 2 > Introduction to clinical sciences (brief) > Flashcards

Introduction to clinical sciences (brief) Flashcards

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1
Q

Acute inflammation

A

Initial and often transient series of tissue reactions to an injury. Lasts hours-days

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2
Q

List 5 causes of acute inflammation

A
  1. Physical agents (trauma, radiation, UV)
  2. Biological agents (bacteria, virus)
  3. Chemicals (acid, alkali)
  4. Autoimmune disease (hypersensitivity)
  5. Tissue necrosis
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3
Q

Clinical features of acute inflammation and reason for them

A
  1. Redness - blood vessel dilatation
  2. Swelling - oedema due to increased vascular permeability
  3. Heat - increased blood flow
  4. Pain - stretching of tissue due to oedema
  5. Loss of function
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4
Q

Cells present in acute inflammation

A

Neutrophil polymorphs

Lymphocytes, fibroblasts, macrophages, mast cells & eosinophils (allergy)

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5
Q

Chemical mediators of vascular dilatation

A

Histamine, prostaglandin E2, nitric oxide, PAF, VIP

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6
Q

Chemical mediators of vascular permeability

A

Immediate: Histamine
Prolonged: Bradykinin, nitric oxide, C5a, PAF, leukotriene B4

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7
Q

Chemical mediators of neutrophil adhesion to endothelium

A

IL-1, IL-8, C5a, leukotriene B4, TNF-a

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8
Q

Chemical mediators of neutrophil chemotaxis

A

Leukotriene B4, IL-8

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9
Q

Outcomes of acute inflammation

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression to chronic inflammation
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10
Q

Constituents of pus

A

Living, dead and dying neutrophils and bacteria, cellular debris, lipid globules

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11
Q

Abscess

A

Walled off collection of pus

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12
Q

Ulcer

A

Break in skin or mucous membrane that fails to heal

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13
Q

Chronic inflammation

A

The subsequent and prolonged tissue reactions to injury (lasts months-years)

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14
Q

Cells that predominate in chronic inflammation

A

Lymphocytes, plasma cells, macrophages

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15
Q

Causes of chronic inflammation

A
  1. Primary chronic inflammation (autoimmune, agents resisting phagocytosis, granulomatous inflammation)
  2. Transplant rejection
  3. Progression from acute
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16
Q

Clinical features of chronic inflammation

A
  1. Chronic ulcer
  2. Chronic abscess
  3. Granulomatous inflammation
  4. Fibrosis
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17
Q

Granuloma

A

Aggregation of epithelioid histiocytes. Form when the body attempts to wall off a foreign agent but fails to eliminate it.

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18
Q

Epithelioid histiocytes

A

Cells with large vesicular nuclei, elongated shape and plentiful eosinophilic cytoplasm. Arranged in clusters

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19
Q

Granulomatous inflammation

A

Form of chronic inflammation characterised by granuloma formation

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20
Q

Gliosis

A

Fibrosis in the brain

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21
Q

Keloid

A

A thick scar that grows massively - more collagen released and excessive fibroblast proliferation

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22
Q

Abrasion

A

Top layer of cells scraped off (underlying tissue fine), scab forms and then is sloughed off

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23
Q

Healing by 1st intention

A
  • Incision sutured, weak fibrin joins the edges
  • Coagulated blood forms scab
  • Capillaries proliferate to bridge gap and fibroblasts secrete collagen
  • Strong collagen join - scar formation
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24
Q

Healing by 2nd intention

A
  • Damage too extensive to join sides together
  • Phagocytosis removes debris
  • Granulation tissue forms, organisation, early fibrous scar
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25
Atheroma
Accumulation of materials in vessel wall (lipids, cholesterol), causing restriction of blood flow
26
Constituents of an atheroma
Cholesterol, platelets, macrophages, foam cells, smooth muscle cells, collagen, elastin
27
Tx for atheroma (preventative)
Low dose aspirin = 75mg (anticoagulant)
28
Atherosclerosis
Disease characterised by atherosclerotic plaques in the intima of large/medium sized arteries, causing narrowing of lumen. Predisposes thrombosis
29
Risk factors of athersclerosis
1. Increasing age 2. High LDL cholesterol diet 3. Hypertension 4. Familial history 5. Male 6. Poorly controlled diabetes 7. Smoking 8. Alcohol
30
Process of atherosclerosis
1. Endothelial damage due to irritants (cigarette toxins, HTN etc.) 2. LDL accumulates in damaged endothelium 3. Monocytes attracted to site of damage, transform into macrophages and phagocytose LDL 4. LDL filled macrophages die and become foam cells (release cytokines to attract more monocytes) 5. Foam cell presence stimulates smooth muscle cells to invade and secrete collagen and elastin - forms fibrous cap
31
Thrombosis
Process by which a solid mass of blood constituents is formed within an intact vascular system during life
32
Thrombus
A solid mass of blood constituents in a vascular system
33
Virchow's triad
Predisposing factors for thrombosis: 1. Change in blood flow 2. Change in blood constituents 3. Change in vessel surface
34
Process of thrombosis
Epithelium damaged - collagen exposed so extrinsic coagulation cascade activated (and subsequently intrinsic). Platelets aggregate and fibrin mesh forms. This can cause a larger plaque to form.
35
Outcomes of thrombus formation
1. Breaks down 2. Changes to scar tissue 3. Recannulisation/ revascularisation 4. Embolus 5. Occludes vessel and causes infarction
36
Embolus
Solid mass in the blood carried through circulation until it gets stuck and blocks a vessel. Most commonly pulmonary embolism from DVT
37
Infarction
Ischaemic death of tissue due to inadequate oxygen supply
38
Ischaemia
Reduction in blood flow to a tissue or part of the body caused by constriction or occlusion of blood vessels supplying it
39
Apoptosis
Programmed cell death
40
Which enzymes causes apoptosis
Caspases
41
Which factors reduce/enhance apoptotic inducing factors
Bcl-2 family reduces | Bax-Bax dimers enhance
42
Factors inhibiting apoptosis
1. Growth factors 2. Extracellular matrix 3. Sex steroids
43
Factors inducing apoptosis
1. Viruses 2. Ionising radiation 3. Growth factor withdrawal 4. Free radicals
44
Necrosis
Traumatic cell death characterised by loss of plasma membrane integrity and bioenergetic failure
45
Some causes of necrosis
Thrombi, emboli, ischaemia and subsequent infarction
46
Disease involving necrosis
Avascular necrosis of the femoral head, scaphoid fracture, caseous necrosis (seen in TB)
47
Hypertrophy
Increase in size of tissue by an increase in the size of constituent cells
48
Pathological example of hypertrophy
Left ventricular hypertrophy
49
Hyperplasia
An increase in size of tissue by increase in number of constituent cells
50
Physiological example of hyperplasia
Endometrial hyperplasia in the uterus during pregnancy
51
Pathological example of hyperplasia
Enlarged prostate
52
Atrophy
Decrease in size of tissue caused by reduction in constituent cell size/number
53
Physiological example of atrophy
Thymus atrophy after puberty
54
Pathological example of atrophy
Alzheimer's disease
55
Metaplasia
A fully differentiated cell changing to another fully differentiated cell type
56
Pathological example of metaplasia
Barrett's oesophagus - squamous epithelium changes to columnar epithelium as a result of excessive stomach acid exposure
57
Dysplasia
Imprecise term for the morphological changes seen in cells in the progression to becoming cancer
58
5 general effects of ageing
1. Deafness - hair cell loss 2. Osteoporosis - lack of oestrogen, vit D, calcium in early life 3. Cataracts - UV damage resulting in cross-linking of proteins in the eye 4. Sarcopenia - loss of skeletal muscle 5. Dermal elastosis - less collagen and elastin in the skin
59
Neoplasm
Lesion resulting from autonomous, abnormal growth of cells which persists after the initiating stimulus has been removed
60
2 classifications of neoplasms
Behavioural | Histological
61
Benign tumour
Non invasive, well defined, close histological resemblance to parent cell
62
Malignant tumour
Invasive, irregular border, hyperchromatic & pleomorphic nucleus, poor resemblance to parent cell
63
Benign tumour of non-secretory, non-glandular epithelial cells
Papilloma
64
Benign tumour of secretory or glandular epithelial cells
Adenoma
65
Malignant tumour of non-secretory, non-glandular epithelial cells
Carcinoma
66
Malignant tumour of secretory or glandular epithelial cells
Adenocarcinoma
67
Benign tumour of connective tissue
Cell origin + oma
68
Malignant tumour of connective tissue
Cell origin + sarcoma
69
Benign tumour morbidity
1. Pressure on adjacent structures 2. Obstruction of flow of fluid 3. Excessive hormone production (thyroid) 4. Tranformation to malignant tumour
70
Adipose tissue tumour
Lipoma/sarcoma
71
Cartilage tumour
Chondroma/sarcoma
72
Striated muscle tumour
Rhabdomyoma/sarcoma
73
Smooth muscle tumour
Lieomyoma/sarcoma
74
Vascular tumour
Angioma/sarcoma
75
Bone tumour
Osteoma/sarcoma
76
Melanocyte tumour
Melanoma
77
Mesothelial cell tumour
Mesothelioma
78
Lymphoid cells tumour
Lymphoma
79
Unknown cell type tumour
Anaplastic
80
Teratoma
Germ cell tumour made up of one or more germ cell layers (endoderm, mesoderm, ectoderm)
81
Blastoma
Neoplasm composed of embryonic cells derived from the blastema of an organ/tissue
82
Tumour angiogenesis
Recruitment of blood vessels into a tumour
83
Carcinogenesis
Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations
84
Oncogenic
Tumour causing
85
Lesion
Localised abnormality
86
Tumour
Any abnormal swelling
87
Metastasis
Malignant tumour spread from site of origin to form secondary tumours at distant sites
88
Process of metastasis
1. Primary tumour vascularised 2. Tumour cells detach 3. Intravasation (enter blood vessels) 4. Evasion of host defences (e.g. natural killer cells) 5. Adhere to endothelium 6. Extravasation 7. Growth and vascularisation of secondary tumour
89
TNM system of tumour grading
Tumour size Number of lymph node metastases Metastases (anatomical extent)
90
Microinvasive carcinoma
Cancer cells invade the basement membrane
91
Enzymes that a tumour uses to invade tissue
Proteases, matrix metalloproteinases, collagenase, cathepsin D, urokinase-type plasminogen activator
92
Pathways for metastasis
Lymphatics, blood vessels
93
Cancers that usually metastasis to bone
1. Breast 2. Thyroid 3. Lung 4. Kidney 5. Prostate
94
Gatekeeper genes
Prevent apoptosis (BRCA1/2)
95
Caretaker genes
Repair DNA p53 RB1

PHASE 2 (6 decks)

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