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Phase 2a > Updated ICS > Flashcards

Updated ICS Flashcards

1
Q

What are the main causes of acute inflammation?

A

Infections
Hypersensitivity reactions
Physical agents (trauma, temp)
Chemicals
Bacterial toxins
Tissue necrosis

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2
Q

How does acute inflammation appear?

5 cardinal signs

A
  • Rubor
  • Calor
  • Tumour
  • Dolor
  • Loss of function
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3
Q

What are the stages of acute inflammation?

A

Vasodilation
Exudation of fluid
Neutrophil action

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4
Q

What happens in the vasodilation stage of acute inflammation?

A

to enhance blood flow in nearby capillaries and tissues and provide blood components for managing the primary injury and initiating repair. (rubor and calor).

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5
Q

What happens during exudative stage of acute inflammation?

A

Mast cells, basophils, and platelets at the injury site release histamine.
Leads to the blood vessels becoming more permeable and the formation of an exudate (protein-rich fluid) within the tissues.

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6
Q

How do neutrophils act in acute inflammation?

A

neutrophils to line up along the endothelium near the injury site, known as margination.
roll along the endothelium, then adhere.
Finally, the neutrophils migrate through the blood vessel walls

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7
Q

What does diapedesis suggest?

A

Severe vascular injury, e.g. tear in the vessel wall

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8
Q

What is the sequelae of acute inflammation?

possible next stages

A
  • Resolution
  • Suppuration + pus (excessive exudate)
  • Repair and organisation (leading to fibrosis)
  • Chronic inflammation if persistent causal agent
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9
Q

What can cause chronic inflammation?

A

Ongoing infection- TB, leprosy
Endogenous material- necrosis
Exogenous materials- asbestos
Autoimmune conditions- rheumatoid arthritis
Primary granulomatous disease- Crohn’s, sarcoidosis
Transplant rejection

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10
Q

How does chronic inflammation appear?

A

Ulcer – open sore
Abscess – closed + pus
Granuloma
Fibrosis

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11
Q

What are the hallmarks of chronic inflammation?

A

Infiltration with mononuclear cells – Macrophages, lymphocytes, and monocyte replace neutrophils
Tissue destruction
Healing

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12
Q

What cells are involved in chronic inflammation?

A
  • Macrophages are present in acute and chronic inflammation. They are important for phagocytosis, antigen presentation, and cytokine synthesis.
  • Lymphocytes
  • Plasma cells are differentiated antibody-producing B lymphocytes.
  • Eosinophils are often found in allergic reactions and parasitic infections
  • Fibroblasts/Myofibroblasts
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13
Q

What is a granuloma?

A

Epithelioid histocytes aggregates surrounded by lymphocytes

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14
Q

What conditions have non-caseating granulomas?

A

Crohn’s
Sarcoidosis

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15
Q

What condition may have a caseating granuloma?

A

TB (Langhans giant cell)

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16
Q

What are the effects of chronic inflammation?

A
  • Impaired function
  • Fibrosis
  • atrophy
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17
Q

What is a thrombus?

A

Solid mass of coagulated blood formed within circulation

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18
Q

What causes exudative fluid?

pathogenesis

high protein count

A

Increased vascular permeability- inflammation

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19
Q

What causes transudative fluid?

patho

low protein count

A

Increased hydrostatic pressure

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20
Q

Examples of causes for an exudative effusion

A

Malignancy
Rheumatoid arthritis
Infectious
Appendicitis

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21
Q

Examples of causes of transudative effusion

A

Hypoalbuminaemia
CHF
Portal vein obstruction
Renal insufficiency

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22
Q

What makes up virchow’s triad?

A
  • Stasis
  • Hypercoagulability
  • Damage to venous wall
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23
Q

What can cause hypercoagulability?

A

Malignancy, autoimmune diseases, sepsis, pregnancy, smoking

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24
Q

What can cause blood stasis?

A

Immobility
varicose veins
shock
congestive heart failure
venous obstruction
hypovolaemia
AF

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25
Q

What can cause damage to a vessel wall?

A

Inflammation
trauma
surgery
central lines
HTN

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26
Q

What can an arterial thrombus lead to?

A

MI
Stroke

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27
Q

What can a venous thrombus lead to?

A

DVT
PE

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28
Q

How is an arterial thrombus treated?

A

anti-platelets, e.g. aspirin

29
Q

How is a venous thrombus treated?

A

anti-coagulants, e.g. warfarin

30
Q

What can happen to a thrombus?

A

Body dissolves and clears it
Organised by macrophages into a scar
Recanalisation: capillaries grow into thrombus and form larger vessels
Emboli: fragments break off into circulation
Death

31
Q

What is an embolus?

A

mass of material in the vascular system able to become lodged in a vessel and block its lumen

32
Q

What can become an emboli?

A

Most emboli are derived from thrombi
atheromatous plaque material
fragments of tumour
amniotic fluid
gas
fat

33
Q

What triggers the external clotting pathway?

A

external trauma which causes blood to escape the circulation

34
Q

What triggers the intrinsic pathway?

A

internal damage to the vessel wall.

35
Q

What are the platelet stages in forming a clot?

A

adhesion, activation and aggregation.

36
Q

What are the risk factors for atherosclerosis?

A

HTN
DM
smoking
Dyslipidaemia (increase in LDL, low HDL)
age
family hx
African-american

37
Q

What is atheroma?

A

condition characterised by focal accumulation of lipid in the intima of arteries causing their lumen to be narrowed, wall weakend and predisposing them to thrombosis

38
Q

What is atherosclerosis?

A

atheroma causing hardening of arteries
formation of focal elevated plaques in the intima of large/medium arteries

39
Q

What makes up an atheroma?

A

vascular smooth muscle cells, collagen, macrophages, lymphocytes and elastin

lipids

40
Q

What do statins do?

A

lower the blood levels of LDL

41
Q

What is apoptosis?

A

individual cell deletion in physiological growth control and disease

42
Q

What do different levels of apoptosis lead to?

A
  • activated or prevented by stimuli
  • reduced apoptosis leads to cell accumulation (neoplasia)
  • increased apoptosis results in excessive cell loss (atrophy)
43
Q

What are the two pathways for apoptosis?

A

Intrinsic
Extrinsic

44
Q

What can trigger the intrinsic pathway of apoptosis?

A
  • Biochemical stress
  • DNA damage (this activates the p53 gene – which halts the cell cycle and initiates DNA repair. If this repair attempt is unsuccessful, apoptosis can be induced)
  • Lack of growth factors
45
Q

What modulates the intrinsic pathway of apoptosis?

A

Bcl-2 inhibits
Bax increases apoptosis

46
Q

What is necrosis?

A

Death of tissues following bioenergetic failure and loss of plasma membrane integrity
Induces inflammation and repair
Causes ischaemia, metabolic trauma

47
Q

What’s gangrene?

A

necrosis with putrefaction

48
Q

What disease has caseous necrosis?

A

TB

49
Q

What is hypertrophy?

A

increase in cell size without division

50
Q

What is hyperplasia?

A

increase in cell number by mitosis

51
Q

What is atrophy?

A

decrease in size of an organ/ cell by reduction in cell size or numbers, often involving apoptosis

52
Q

What is metaplasia?

A

transformation of one type of differentiated cell into another fully differentiated cell type

53
Q

Example of metaplasia

A

Barrett’s oesophagus: replacement of normal squamous epithelium of the oesophagus by columnar glandular epithelium

54
Q

What is hypoplasia?

A

Failure of development of an organ

55
Q

What is dysplasia?

A

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

56
Q

What is ischaemia?

A

An inadequate blood supply to tissue

57
Q

What is infarction?

A

death of tissue due to ischaemia

58
Q

What is a neoplasm?

A

abnormal growth of tissue

tumour

59
Q

What is carcinogenesis?

A

Transformation of normal cells into neoplastic cells through permanent genetic changes

60
Q

Features of benign tumours

A

Doesn’t invade basement membrane (non-invasive)
Exophytic (grows outwards)
Low mitotic activity (slow growth rate)
Remains localised
Necrosis and ulceration rare
Close histological resemblance to parent tissue

61
Q

Features of malignant tumours

A

Invades basement membrane (invasive)
Can spread by metastasis
Endophytic (grows inwards)
High mitotic activity (high growth rate)
Necrosis and ulceration common

62
Q

What is a carcinoma?

A

malignant tumour of epithelium

63
Q

What are the benign epithelial tumours?

A

Papilloma
Adenoma

64
Q

What are the routes of tumour metastasis?

A
  • Haematogenous
  • Lymphatic
  • Transcoelomic (peritoneal, pleural and pericardial cavities)
65
Q

How does TNM staging work for tumours?

A

T- primary tumour
N- lymph node involvement
M- metastases

66
Q

What ages are screened for bowel cancer?

A

starting from the age of 50-60 up to 74 in England

67
Q

Who is screened for breast cancer?

A

women (including some transgender women), some transgender men and some non-binary people aged 50-70 in the UK.

68
Q

Who is cervical screening offered to?

A

women, some transgender men and some non-binary people aged 25-64 in the UK.

69
Q
A

Phase 2a (14 decks)

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