Updated ICS Flashcards
What are the main causes of acute inflammation?
Infections
Hypersensitivity reactions
Physical agents (trauma, temp)
Chemicals
Bacterial toxins
Tissue necrosis
How does acute inflammation appear?
5 cardinal signs
- Rubor
- Calor
- Tumour
- Dolor
- Loss of function
What are the stages of acute inflammation?
Vasodilation
Exudation of fluid
Neutrophil action
What happens in the vasodilation stage of acute inflammation?
to enhance blood flow in nearby capillaries and tissues and provide blood components for managing the primary injury and initiating repair. (rubor and calor).
What happens during exudative stage of acute inflammation?
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.
How do neutrophils act in acute inflammation?
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
What does diapedesis suggest?
Severe vascular injury, e.g. tear in the vessel wall
What is the sequelae of acute inflammation?
possible next stages
- Resolution
- Suppuration + pus (excessive exudate)
- Repair and organisation (leading to fibrosis)
- Chronic inflammation if persistent causal agent
What can cause chronic inflammation?
Ongoing infection- TB, leprosy
Endogenous material- necrosis
Exogenous materials- asbestos
Autoimmune conditions- rheumatoid arthritis
Primary granulomatous disease- Crohn’s, sarcoidosis
Transplant rejection
How does chronic inflammation appear?
Ulcer – open sore
Abscess – closed + pus
Granuloma
Fibrosis
What are the hallmarks of chronic inflammation?
Infiltration with mononuclear cells – Macrophages, lymphocytes, and monocyte replace neutrophils
Tissue destruction
Healing
What cells are involved in chronic inflammation?
- 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
What is a granuloma?
Epithelioid histocytes aggregates surrounded by lymphocytes
What conditions have non-caseating granulomas?
Crohn’s
Sarcoidosis
What condition may have a caseating granuloma?
TB (Langhans giant cell)
What are the effects of chronic inflammation?
- Impaired function
- Fibrosis
- atrophy
What is a thrombus?
Solid mass of coagulated blood formed within circulation
What causes exudative fluid?
pathogenesis
high protein count
Increased vascular permeability- inflammation
What causes transudative fluid?
patho
low protein count
Increased hydrostatic pressure
Examples of causes for an exudative effusion
Malignancy
Rheumatoid arthritis
Infectious
Appendicitis
Examples of causes of transudative effusion
Hypoalbuminaemia
CHF
Portal vein obstruction
Renal insufficiency
What makes up virchow’s triad?
- Stasis
- Hypercoagulability
- Damage to venous wall
What can cause hypercoagulability?
Malignancy, autoimmune diseases, sepsis, pregnancy, smoking
What can cause blood stasis?
Immobility
varicose veins
shock
congestive heart failure
venous obstruction
hypovolaemia
AF
What can cause damage to a vessel wall?
Inflammation
trauma
surgery
central lines
HTN
What can an arterial thrombus lead to?
MI
Stroke
What can a venous thrombus lead to?
DVT
PE
How is an arterial thrombus treated?
anti-platelets, e.g. aspirin
How is a venous thrombus treated?
anti-coagulants, e.g. warfarin
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
What is an embolus?
mass of material in the vascular system able to become lodged in a vessel and block its lumen
What can become an emboli?
Most emboli are derived from thrombi
atheromatous plaque material
fragments of tumour
amniotic fluid
gas
fat
What triggers the external clotting pathway?
external trauma which causes blood to escape the circulation
What triggers the intrinsic pathway?
internal damage to the vessel wall.
What are the platelet stages in forming a clot?
adhesion, activation and aggregation.
What are the risk factors for atherosclerosis?
HTN
DM
smoking
Dyslipidaemia (increase in LDL, low HDL)
age
family hx
African-american
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
What is atherosclerosis?
atheroma causing hardening of arteries
formation of focal elevated plaques in the intima of large/medium arteries
What makes up an atheroma?
vascular smooth muscle cells, collagen, macrophages, lymphocytes and elastin
lipids
What do statins do?
lower the blood levels of LDL
What is apoptosis?
individual cell deletion in physiological growth control and disease
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)
What are the two pathways for apoptosis?
Intrinsic
Extrinsic
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
What modulates the intrinsic pathway of apoptosis?
Bcl-2 inhibits
Bax increases apoptosis
What is necrosis?
Death of tissues following bioenergetic failure and loss of plasma membrane integrity
Induces inflammation and repair
Causes ischaemia, metabolic trauma
What’s gangrene?
necrosis with putrefaction
What disease has caseous necrosis?
TB
What is hypertrophy?
increase in cell size without division
What is hyperplasia?
increase in cell number by mitosis
What is atrophy?
decrease in size of an organ/ cell by reduction in cell size or numbers, often involving apoptosis
What is metaplasia?
transformation of one type of differentiated cell into another fully differentiated cell type
Example of metaplasia
Barrett’s oesophagus: replacement of normal squamous epithelium of the oesophagus by columnar glandular epithelium
What is hypoplasia?
Failure of development of an organ
What is dysplasia?
imprecise term for the morphological changes seen in cells for the progression to becoming cancer
What is ischaemia?
An inadequate blood supply to tissue
What is infarction?
death of tissue due to ischaemia
What is a neoplasm?
abnormal growth of tissue
tumour
What is carcinogenesis?
Transformation of normal cells into neoplastic cells through permanent genetic changes
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
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
What is a carcinoma?
malignant tumour of epithelium
What are the benign epithelial tumours?
Papilloma
Adenoma
What are the routes of tumour metastasis?
- Haematogenous
- Lymphatic
- Transcoelomic (peritoneal, pleural and pericardial cavities)
How does TNM staging work for tumours?
T- primary tumour
N- lymph node involvement
M- metastases
What ages are screened for bowel cancer?
starting from the age of 50-60 up to 74 in England
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.
Who is cervical screening offered to?
women, some transgender men and some non-binary people aged 25-64 in the UK.
