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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
What can cause damage to a vessel wall?
Inflammation trauma surgery central lines HTN
26
What can an arterial thrombus lead to?
MI Stroke
27
What can a venous thrombus lead to?
DVT PE
28
How is an arterial thrombus treated?
anti-platelets, e.g. aspirin
29
How is a venous thrombus treated?
anti-coagulants, e.g. warfarin
30
What can happen to a thrombus?
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
What is an embolus?
mass of material in the vascular system able to become lodged in a vessel and block its lumen
32
What can become an emboli?
Most emboli are derived from thrombi atheromatous plaque material fragments of tumour amniotic fluid gas fat
33
What triggers the external clotting pathway?
external trauma which causes blood to escape the circulation
34
What triggers the intrinsic pathway?
internal damage to the vessel wall.
35
What are the platelet stages in forming a clot?
adhesion, activation and aggregation.
36
What are the risk factors for atherosclerosis?
HTN DM smoking Dyslipidaemia (increase in LDL, low HDL) age family hx African-american
37
What is atheroma?
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
What is atherosclerosis?
atheroma causing hardening of arteries formation of focal elevated plaques in the intima of large/medium arteries
39
What makes up an atheroma?
vascular smooth muscle cells, collagen, macrophages, lymphocytes and elastin ## Footnote lipids
40
What do statins do?
lower the blood levels of LDL
41
What is apoptosis?
individual cell deletion in physiological growth control and disease
42
What do different levels of apoptosis lead to?
- activated or prevented by stimuli - reduced apoptosis leads to cell accumulation (neoplasia) - increased apoptosis results in excessive cell loss (atrophy)
43
What are the two pathways for apoptosis?
Intrinsic Extrinsic
44
What can trigger the intrinsic pathway of apoptosis?
- 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
What modulates the intrinsic pathway of apoptosis?
Bcl-2 inhibits Bax increases apoptosis
46
What is necrosis?
Death of tissues following bioenergetic failure and loss of plasma membrane integrity Induces inflammation and repair Causes ischaemia, metabolic trauma
47
What's gangrene?
necrosis with putrefaction
48
What disease has caseous necrosis?
TB
49
What is hypertrophy?
increase in cell size without division
50
What is hyperplasia?
increase in cell number by mitosis
51
What is atrophy?
decrease in size of an organ/ cell by reduction in cell size or numbers, often involving apoptosis
52
What is metaplasia?
transformation of one type of differentiated cell into another fully differentiated cell type
53
Example of metaplasia
Barrett's oesophagus: replacement of normal squamous epithelium of the oesophagus by columnar glandular epithelium
54
What is hypoplasia?
Failure of development of an organ
55
What is dysplasia?
imprecise term for the morphological changes seen in cells for the progression to becoming cancer
56
What is ischaemia?
An inadequate blood supply to tissue
57
What is infarction?
death of tissue due to ischaemia
58
What is a neoplasm?
abnormal growth of tissue ## Footnote tumour
59
What is carcinogenesis?
Transformation of normal cells into neoplastic cells through permanent genetic changes
60
Features of benign tumours
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
Features of malignant tumours
Invades basement membrane (invasive) Can spread by metastasis Endophytic (grows inwards) High mitotic activity (high growth rate) Necrosis and ulceration common
62
What is a carcinoma?
malignant tumour of epithelium
63
What are the benign epithelial tumours?
Papilloma Adenoma
64
What are the routes of tumour metastasis?
- Haematogenous - Lymphatic - Transcoelomic (peritoneal, pleural and pericardial cavities)
65
How does TNM staging work for tumours?
T- primary tumour N- lymph node involvement M- metastases
66
What ages are screened for bowel cancer?
starting from the age of 50-60 up to 74 in England
67
Who is screened for breast cancer?
women (including some transgender women), some transgender men and some non-binary people aged 50-70 in the UK.
68
Who is cervical screening offered to?
women, some transgender men and some non-binary people aged 25-64 in the UK.
69

Phase 2a (14 decks)

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