Brainscape's Knowledge GenomeTM

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


See full index

1. Essential Medical Science > Inflammation > Flashcards

Inflammation Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What is Inflammation?

A

A protective response to injury, Essential to survival

Aims to rid the body of the initial cause of the injury and the consequences of such injury. Acute or chronic

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

What is Acute Inflammation?

A

The initial tissue reaction to injury, Lasts minutes, hours or days. Characteristic cell is the neutrophil polymorph

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

What are Physical Characteristics of Acute Inflammation?

A

Redness (rubor), Heat (calor), Swelling (tumor), Pain (dolor), Loss of function (functio laesa)

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

What are Causes of Acute Inflammation?

A

Physical agents (thermal injury – burns, frostbite), Infections, Hypersensitivity reactions, Chemicals, Tissue necrosis

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

What is Serous inflammation?

A

Thin fluid from plasma or mesothelial cell secretions. Accumulation results in effusion eg pleural effusion.

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

What are the Major Components of Acute Inflammation? (3)

A

1) Changes in vessel calibre
2) Increased vascular permeability and fluid exudate formation
3) Cellular exudate formation
Vessels undergo changes which are designed to maximize the movement of plasma proteins and cells into the site of infection or injury.

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

What is Exudate?

A

Extravascular fluid with high protein concentration, containing cellular debris. Implies inflammation

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

What is Transudate?

A

Low protein, little or no cellular component

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

What is Oedema?

A

Excess fluid in interstitial tissue/ serous cavities – exudate or transudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Pus?

A

inflammatory exudate rich in neutrophils, dead cell debris and microbes
Abscess –localised collections of pus. Pyogenic (pus producing bacteria ) eg streptococcus. Can eventually become walled off and replaced by connective tissue

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

What Changes in Vessel Calibre occur in Acute Inflammation?

A 
Vasodilation (initial transient vasoconstriction): 
Early change (15mins to several hours), Increases blood flow (<10x), Heat and redness, Mediated by histamine and NO on vascular smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is calor? What causes it?

A

Hot = calor = vascular dilatation,

Caused by hyperaemia and systemic increase in temperature due to cytokines

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

What is rubor? What causes it?

A

Red = rubor caused by vascular dilatation

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

What is tumor? What causes it?

A

Swollen = tumor caused by inflammatory exudate into surrounding tissues, localised oedema

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

What causes Formation of the Fluid Exudate in Acute Inflammation?

A

Increased permeability of microvasculature results in escape of protein rich fluid into tissue
Causes: - chemical mediators e.g. histamine, NO, leukotriene, direct vascular injury e.g. trauma, endothelial injury – bacteria and toxins

Different tissues have different susceptibility to chemical mediators e.g. cns insensitive to histamine but skin, conjunctiva and bronchial mucosa are – e.g. hayfever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the effect of Acute Inflammation on hydrostatic pressure ?

A

Normally high hydrostatic pressure inside vessel due to plasma proteins forces fluid out but returns at venous end when hydrostatic pressure is low.
In acute inflammation, hydrostatic pressure is increased and plasma proteins escape into extravascular space increasing colloid osmotic pressure. More fluid leaves vessels - exudation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the effect of high Fluid Exudate in Acute Inflammation?

A

Dilution of toxins, Entry of antibodies, Transport of drugs, Fibrin formation, Delivery of nutrients and oxygen, Stimulation of the immune response, High turnover

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

How does cellular Exudate form in Acute Inflammation?

A

Loss of fluid into tissues and increased calibre of vessels – slower blood flow and increased viscosity of blood – stasis
Neutrophils line up along vascular endothelium, stick to endothelium and migrate through wall into tissues. (margination of neutrophils then pavementing of neutrophils (adhesion on vascular endothelium) they then pass through endothelial cells and the basal lamina into the adventitia)

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

What are neutrophils?

A

Produced in bone marrow, Commonest white cell in blood, Increase in acute inflammation, Motile, amoeboid, can move into tissues, Directional chemotaxis, Short lifespan (hours in tissues)

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

What are Chemical Mediators of Acute Inflammation involved in?

A

Vasodilatation, Migration of neutrophils, Chemotaxis

Increased vascular permeability

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

What are cell derived Mediators of Acute Inflammation?

A

Histamine (released by mast cells, increases vascular dilation and permeability), Prostaglandins (PG2=PH2=TXA2-vasoconstriction and platelet aggregation/PGI2 opposite of TXA2/ PGD2,PGE2 and PGF2-vasodilation and potentiate oedema) , Lysosomal components, Leukotrines (vasoactive properties- vasoconstriction and inc permeability some i.e LB4 act as chemotaxis), Cytokines

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

What are Plasma derived mediators of Acute Inflammation?

A

Complement system, Kinin system, Coagulation system

Fibrinolytic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is used for Laboratory assessment of inflammation?

A

Full blood count, Erythrocyte sedimentation rate

Acute phase proteins eg C-reactive protein

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

What happens to an inflamed capillary bed?

A

Expansion of capillary bed, deposition of fibrin and other plasma proteins, neutrophil emigration (rolling and adhesion (via selection) adhesion continues then results in transmigration (integrins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What can acute inflammation result in? (4)

A

Usual result=resolution
Excessive exudate=supuration=discharge of pus and repair and organisation
Excessive necrosis=repair and organisation=fibrosis
Persistant causal agent= Chronic inflammation which causes fibrosis.

26
Q

What is Fibrinous inflammation?

A

Fibrinous inflammation – increased vascular permeability can result in large molecules such as fibrinogen entering tissues and forming fibrin. Characteristic of inflammaiton of linings of body cavities e.g. pericardium, pleura. Can be removed by firbrinolyis and removal of debris by macrophages. If not can lead to scarring (organisation) obliteration of pericardium -

Fibrin impedes movement of microorganisms , trapping the and facilitating phagocytosis, acts as a scaffold for granulation tissue formation

27
Q

What can be harmful side effects of acute inflammation?

A

Digestion of normal tissues e.g. abscess cavities
Swelling e.g. acute epiglottitis
Inappropriate inflammatory response e.g. hayfever

28
Q

General effects of acute inflammation?

A

Pyrexia, Lymph node enlargement, Nausea, malaise, anorexia, Leukocytosis, Polymorhs and macrophages produce substances which act on hypothalamus

29
Q

What is an abscess?

A

An abscess is a collection of pus; it is a complication of acute inflammation

30
Q

What are the 5 signs of acute inflammation

A

Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio laesa (loss of function)

31
Q

What are the three stages of acute inflammation?

A

Vascular changes: Initial vasoconstriction followed by dilation and increased vascular permeability
Extravasation of white blood cells: Organised sequential process Margination – adhesion – transmigration - chemotaxis
Phagocytosis: Recognition – engulfment – killing

32
Q

What is the mechanism of exudate formation?

A

Exudation is aided by endothelial cell contraction and vasodilation, which typically is most pronounced in venules. Chemical mediators producing endothelial contraction include: histamine, leukotrienes, bradykinin, platelet activating factor, and the C3a and C5a components from complement activation. Mediators of this process over a longer term include tumor necrosis factor and interleukin-1. Chemical mediators that promote vasodilation include: histamine, prostaglandins, and nitric oxide.

33
Q

How does Polymorph infiltration occur?

A

Margination to EC then rolling , adhesion the diapedesis(slips through EC’s) then chemotaxis then phagocytosis and killing.

34
Q

How does phagocytosis and killing occur?

A

Opsonisation of particles by IgG or C3, Engulfment

Killing: Reacive oxygen species/Myeloperoxidase (makes HOCl)‏

35
Q

What is dolor? What causes it?

A

Dolor (pain) Caused by to cytokines (bradykinin, serotonin, prostaglandins) and physical pressure

36
Q

What is Functio laesa? What causes it?

A

Functio laesa (loss of function) Caused by to pain and swelling

37
Q

What is Suppuration?

A

Suppuration is the formation of pus: Living & dead neutrophils, Cell/ tissue debris, Bacteria
Usually suppuration is due to a bacterium (pyogenic bacteria). Pus is yellow-green in colour.
Suppuration forms an ABSCESS - a collection of pus in the body – eg. in an organ, soft tissue, skin
Abscesses are not accessible to antibiotics

38
Q

How do you manage a abscess

A

Aim : To remove all of the infected material, To encourage healing
“Incision and drainage”: May pack with antiseptic soaked gauze to help “granulate”
Send a sample to the microbiology lab (why?): Swab/ Pus/ Tissue
Surgical excision: Eg appendicectomy
Antibiotic “cover” appropriate to the organisms

39
Q

Pathology of healing of abscess?

A

Organising abscess, Granulation tissue contains capillaries, oedema, white cells and fibroblasts
Angiogenesis occurs in healing (VEGF)‏
Fibroblasts proliferate in granulation tissue and secrete ECM and collagen (FGF)‏ Fibroblast contraction shrinks the wound. Scars become less cellular and more fibrous with age – maximum strength after 3+ months

40
Q

What are the advantages and disadvantages of scar formation?

A

Advantages: Prevents infection + Protects against mechanical trauma
Disadvantages: Stops regeneration

41
Q

Acute Inflammation- What type of immunity is it? How long does it take? What are its features?

A

Innate immunity. Hours-days. Blood vessel dilatation and increased permeability. Fluid exudation, rich in proteins e.g. Ig, fibrinogen, C’. Neutrophil recruitment, mast cells, macrophages.

42
Q

Acute Inflammation- Outcomes (3)

A

Resolution - phagocytosis of insulting agent, fibrinolysis, phagocytosis of debris.
Repair - organisation (replacement by granulation tissue) fibrous scar.
Chronic inflammation – organisation + macrophages/lymphocytes/plasma cells.

43
Q

Chronic Inflammation- What type of immunity is it? How long does it take? What are its features?

A

Innate & adaptive immunity. Weeks-months-years.
Angiogenesis. Fibrosis.
Macrophages, lymphocytes, plasma cells.

44
Q

What are symptoms of Chronic Inflammation?

A

Amyloidosis. Cachexia. Anaemia of chronic disease.

45
Q

What is Chronic Inflammation?

A

Inflammation of prolonged duration, Concomitant tissue destruction and repair. Mononuclear inflammatory cells.
Fibrosis.

46
Q

Causes of Chronic Inflammation

A

Progression from acute e.g. helicobacter pylori.
Recurrent episodes of acute e.g. chronic cholecystitis.
Persistent infection by certain microorganisms (difficult to remove).e.g. TB, leprosy
Prolonged exposure to potentially toxic agents (endogenous e.g. bone, exogenous e.g. asbestos fibres (can =interstitial fibrosis, sutures). Can result in cirrhosis
Autoimmunity e.g. Hashimoto’s thyroiditis, RA
Unknown e.g. Crohn’s disease, ulcerative colitis, sarcoidosis.

47
Q

What cells are involved in Chronic Inflammation?

A

Connective tissue cells ( mast cells, fibroblasts and Macrophages) BV cells (lymphocytes, plasma cells, PMNs, platelets, monocytes, Clotting factors, eosinophils, basophils) Connective tissue matrix ( elastic fibres, collagen fibres and proteoglycans)

48
Q

What occurs in granulation?

A

New blood vessels (angiogenesis), Collagen deposition by fibroblasts=scar

49
Q

What is a Granuloma?

A

Granuloma= collection of activated epithelioid macrophages (pink cytoplasm, indistinct cell membranes, oval nucleus)
Arises when macrophages try to phagocytose something they can’t degrade

50
Q

What is Granulomatous inflammation?

A

Granuloma= collection of activated epithelioid macrophages (pink cytoplasm, indistinct cell membranes, oval nucleus)
Surrounded by mononuclear leucocytes, Caseating or non-caseating, May also contain multinucleate giant cells

51
Q

What causes Granulomatous inflammation?

A

Bacterial (TB, leprosy, syphilis, cat-scratch), Parasitic (schistosomiasis), Fungal (histoplasma, cryptococcus), Inorganic metals or dust (silicosis, berylliosis), Foreign body (suture, vascular graft), Unknown (sarcoidosis, ulcerative colitis) I.e. limited number of associated conditions, therefore informs further tests

52
Q

What is acute liver failure?

A 
•Sudden overwhelming insult
•Drugs (e.g. paracetamol OD), Viruses (Hep A, B, D, E), Acute onset AIH 
•Liver cannot regenerate
•Require super-urgent liver transplant. 
All hepatocytes die at once
53
Q

What is chronic liver failure?

A

•Many causes – drugs, infections and viruses (e.g. Hep C), autoimmune disease, alcohol, obesity
•Repeated damage and repair through inflammation, regeneration of residual hepatocytes and repair through scar tissue (fibrosis)
Persistent ongoing damage and injury
Inflammatory response
Heal through fibrosis and regeneration = Cirrhosis

54
Q

What is Chronic Inflammation

A

•The cause of the injury doesn’t go away
•Continuing attempts to overcome the injury
–Infection, toxin, autoimmunity, metabolic
•Inflammatory cell infiltrate – different patterns in different circumstances
–Lymphocytes, eosinophils, plasma cells, macrophages, granulomas
•Fibroblasts, blood vessels, scar tissue, fibrosis

55
Q

Repair and Regeneration in liver injury

A

•Regeneration:
•Damaged tissue replaced by cells of the same time
•Tissue retains some or all of its initial structure and function
Cellular repair mechanisms
–Regeneration of labile and stable cells
–Liver cells usually live 6 months
–Can regenerate very quickly when they need to e.g. partial hepatectomy
Repair:
•Original tissue replaced by scar tissue
•Scar tissue – result of wound healing
–More or less permanent fibrous tissue at sites of previous tissue damage
With time increasing damage leads to more scarring and less regenerative potential.

56
Q

What is cirrhosis?

A

•Cirrhosis – end stage of chronic liver disease – when cause of liver injury persists alongside the body’s attempts to repair it
•Eventually there may be insufficient regeneration, and liver failure results.
•Liver transplantation is the only cure for end stage liver disease
Insufficient ability to regenerate following an insult = liver failure.

57
Q

Microscopic view of cirrhosis?

A

Microscopically: Regenerative nodules of hepatocytes

Surrounded by sheets of fibrous tissue

58
Q

What two processes need to be involved in true cirrhosis?

A

Nodule formation and fibrosis

59
Q

What are some causes of cirrhosis?

A

•Alcohol
•Viruses (Hepatitis B and C)
•Autoimmune
•Metabolic (Iron and Copper storage, Obesity)
•Bile duct obstruction (PBC, PSC)
ALL cause continuing inflammation which continues to damage the liver during repair and regeneration.
Liver cells still present, but portal vein blood bypasses the sinusoids
so the liver cells cannot perform their functions.
Pressure inside the liver increases = portal hypertension.

Cirrhosis = end stage of chronic liver disease, unless the cause can be removed

60
Q

What are consequences of cirrhosis? (4)

A

•Portal hypertension – stiff scarred liver, increased blood flow from portal vein
–Results in bleeding oesophageal varices
•Oedema – synthetic failure – inadequate liver cell function–low albumin and hormonal changes
•Risk of infection – change in immune system
•Carcinogenesis – late effect of chronic inflammation and cell replication

61
Q

What is ascites?

A

Consequence of liver failure
– transudate of fluid into peritoneal cavity
– low albumin, high portal pressure, change in hormonal regulation of fluid balance

1. Essential Medical Science (8 decks)

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