Brainscape's Knowledge GenomeTM

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


See full index

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

Introduction to clinical sciences (brief) Flashcards

1
Q

Acute inflammation

A

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

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

Cells present in acute inflammation

A

Neutrophil polymorphs

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

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

Chemical mediators of vascular dilatation

A

Histamine, prostaglandin E2, nitric oxide, PAF, VIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Chemical mediators of vascular permeability

A

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

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

Chemical mediators of neutrophil adhesion to endothelium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Chemical mediators of neutrophil chemotaxis

A

Leukotriene B4, IL-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Outcomes of acute inflammation

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression to chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Constituents of pus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Abscess

A

Walled off collection of pus

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

Ulcer

A

Break in skin or mucous membrane that fails to heal

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

Chronic inflammation

A

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

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

Cells that predominate in chronic inflammation

A

Lymphocytes, plasma cells, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of chronic inflammation

A
  1. Primary chronic inflammation (autoimmune, agents resisting phagocytosis, granulomatous inflammation)
  2. Transplant rejection
  3. Progression from acute
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical features of chronic inflammation

A
  1. Chronic ulcer
  2. Chronic abscess
  3. Granulomatous inflammation
  4. Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Granuloma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Epithelioid histiocytes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Granulomatous inflammation

A

Form of chronic inflammation characterised by granuloma formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Gliosis

A

Fibrosis in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Keloid

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Abrasion

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Healing by 2nd intention

A
  • Damage too extensive to join sides together
  • Phagocytosis removes debris
  • Granulation tissue forms, organisation, early fibrous scar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Atheroma

A

Accumulation of materials in vessel wall (lipids, cholesterol), causing restriction of blood flow

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

Constituents of an atheroma

A

Cholesterol, platelets, macrophages, foam cells, smooth muscle cells, collagen, elastin

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

Tx for atheroma (preventative)

A

Low dose aspirin = 75mg (anticoagulant)

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

Atherosclerosis

A

Disease characterised by atherosclerotic plaques in the intima of large/medium sized arteries, causing narrowing of lumen. Predisposes thrombosis

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

Risk factors of athersclerosis

A
  1. Increasing age
  2. High LDL cholesterol diet
  3. Hypertension
  4. Familial history
  5. Male
  6. Poorly controlled diabetes
  7. Smoking
  8. Alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Process of atherosclerosis

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

Thrombosis

A

Process by which a solid mass of blood constituents is formed within an intact vascular system during life

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

Thrombus

A

A solid mass of blood constituents in a vascular system

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

Virchow’s triad

A

Predisposing factors for thrombosis:

  1. Change in blood flow
  2. Change in blood constituents
  3. Change in vessel surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Process of thrombosis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Outcomes of thrombus formation

A
  1. Breaks down
  2. Changes to scar tissue
  3. Recannulisation/ revascularisation
  4. Embolus
  5. Occludes vessel and causes infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Embolus

A

Solid mass in the blood carried through circulation until it gets stuck and blocks a vessel. Most commonly pulmonary embolism from DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Infarction

A

Ischaemic death of tissue due to inadequate oxygen supply

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

Ischaemia

A

Reduction in blood flow to a tissue or part of the body caused by constriction or occlusion of blood vessels supplying it

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

Apoptosis

A

Programmed cell death

40
Q

Which enzymes causes apoptosis

A

Caspases

41
Q

Which factors reduce/enhance apoptotic inducing factors

A

Bcl-2 family reduces

Bax-Bax dimers enhance

42
Q

Factors inhibiting apoptosis

A
  1. Growth factors
  2. Extracellular matrix
  3. Sex steroids
43
Q

Factors inducing apoptosis

A
  1. Viruses
  2. Ionising radiation
  3. Growth factor withdrawal
  4. Free radicals
44
Q

Necrosis

A

Traumatic cell death characterised by loss of plasma membrane integrity and bioenergetic failure

45
Q

Some causes of necrosis

A

Thrombi, emboli, ischaemia and subsequent infarction

46
Q

Disease involving necrosis

A

Avascular necrosis of the femoral head, scaphoid fracture, caseous necrosis (seen in TB)

47
Q

Hypertrophy

A

Increase in size of tissue by an increase in the size of constituent cells

48
Q

Pathological example of hypertrophy

A

Left ventricular hypertrophy

49
Q

Hyperplasia

A

An increase in size of tissue by increase in number of constituent cells

50
Q

Physiological example of hyperplasia

A

Endometrial hyperplasia in the uterus during pregnancy

51
Q

Pathological example of hyperplasia

A

Enlarged prostate

52
Q

Atrophy

A

Decrease in size of tissue caused by reduction in constituent cell size/number

53
Q

Physiological example of atrophy

A

Thymus atrophy after puberty

54
Q

Pathological example of atrophy

A

Alzheimer’s disease

55
Q

Metaplasia

A

A fully differentiated cell changing to another fully differentiated cell type

56
Q

Pathological example of metaplasia

A

Barrett’s oesophagus - squamous epithelium changes to columnar epithelium as a result of excessive stomach acid exposure

57
Q

Dysplasia

A

Imprecise term for the morphological changes seen in cells in the progression to becoming cancer

58
Q

5 general effects of ageing

A
  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
Q

Neoplasm

A

Lesion resulting from autonomous, abnormal growth of cells which persists after the initiating stimulus has been removed

60
Q

2 classifications of neoplasms

A

Behavioural

Histological

61
Q

Benign tumour

A

Non invasive, well defined, close histological resemblance to parent cell

62
Q

Malignant tumour

A

Invasive, irregular border, hyperchromatic & pleomorphic nucleus, poor resemblance to parent cell

63
Q

Benign tumour of non-secretory, non-glandular epithelial cells

A

Papilloma

64
Q

Benign tumour of secretory or glandular epithelial cells

A

Adenoma

65
Q

Malignant tumour of non-secretory, non-glandular epithelial cells

A

Carcinoma

66
Q

Malignant tumour of secretory or glandular epithelial cells

A

Adenocarcinoma

67
Q

Benign tumour of connective tissue

A

Cell origin + oma

68
Q

Malignant tumour of connective tissue

A

Cell origin + sarcoma

69
Q

Benign tumour morbidity

A
  1. Pressure on adjacent structures
  2. Obstruction of flow of fluid
  3. Excessive hormone production (thyroid)
  4. Tranformation to malignant tumour
70
Q

Adipose tissue tumour

A

Lipoma/sarcoma

71
Q

Cartilage tumour

A

Chondroma/sarcoma

72
Q

Striated muscle tumour

A

Rhabdomyoma/sarcoma

73
Q

Smooth muscle tumour

A

Lieomyoma/sarcoma

74
Q

Vascular tumour

A

Angioma/sarcoma

75
Q

Bone tumour

A

Osteoma/sarcoma

76
Q

Melanocyte tumour

A

Melanoma

77
Q

Mesothelial cell tumour

A

Mesothelioma

78
Q

Lymphoid cells tumour

A

Lymphoma

79
Q

Unknown cell type tumour

A

Anaplastic

80
Q

Teratoma

A

Germ cell tumour made up of one or more germ cell layers (endoderm, mesoderm, ectoderm)

81
Q

Blastoma

A

Neoplasm composed of embryonic cells derived from the blastema of an organ/tissue

82
Q

Tumour angiogenesis

A

Recruitment of blood vessels into a tumour

83
Q

Carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

84
Q

Oncogenic

A

Tumour causing

85
Q

Lesion

A

Localised abnormality

86
Q

Tumour

A

Any abnormal swelling

87
Q

Metastasis

A

Malignant tumour spread from site of origin to form secondary tumours at distant sites

88
Q

Process of metastasis

A
  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
Q

TNM system of tumour grading

A

Tumour size
Number of lymph node metastases
Metastases (anatomical extent)

90
Q

Microinvasive carcinoma

A

Cancer cells invade the basement membrane

91
Q

Enzymes that a tumour uses to invade tissue

A

Proteases, matrix metalloproteinases, collagenase, cathepsin D, urokinase-type plasminogen activator

92
Q

Pathways for metastasis

A

Lymphatics, blood vessels

93
Q

Cancers that usually metastasis to bone

A
  1. Breast
  2. Thyroid
  3. Lung
  4. Kidney
  5. Prostate
94
Q

Gatekeeper genes

A

Prevent apoptosis (BRCA1/2)

95
Q

Caretaker genes

A

Repair DNA
p53
RB1

PHASE 2 (6 decks)

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