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Semester 2 Pathological Processes > L4: Acute Inflammation > Flashcards

L4: Acute Inflammation Flashcards

1
Q

What is inflammation?

A

Response of living tissue to injury
Protective mechanism–> can cause local and systemic complications (sometimes worse than initial thing)
Controlled–> Chemical mediators

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2
Q

What are the characteristic of acute inflammation?

A 
Immediate
Short Duration 
Innate
Sterotyped --> same
Limits danger
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3
Q

What are the different stages of inflammation?

A

Vascular phase–> Changes in blood flow, accmulation of exudate
Cellular phase–> Delivery of neutrophils

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4
Q

What can cause inflammation?

A

Trauma
Hypersensitivity
Microorganism
Other illnesses

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5
Q

What are the cardinal signs of inflammation?

A
  1. Rubor–> Redness
  2. Tumor–> Swelling
  3. Calor–> Heat
  4. Dolor–> Pain
  5. Loss of function (functio laesa)
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6
Q

During the vascular phase what changes in blood flow occur?

A

Transient vasoconstriction (seconds)
Vasodilation (minutes)–> heat and redness
Increased permeability –> fluid and cells can escape

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7
Q

What controls the movement of fluid?

A

Starling Law

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8
Q

What does Starling Law state?

A

Movement of fluid is controlled by the balance of hydrostatic pressure and oncotic pressure

Different to Frank-Starling law of the heart

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9
Q

What is the difference between hydrostatic and oncotic pressure?

A

Hydrostatic pressure–> pressure exerted on vessel wall by a fluid–> pushes fluid away
Oncotic pressure–> pressure exerted by proteins, in the interstitial fluid–> pulls fluid towards

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10
Q

What happens to the capillaries during inflammation?

A

Vasodilation–> increased hydrostatic pressure in capillary
Increased vessel permeability–> plasma proteins move into the interstitium–> increased oncotic pressure in interstitium
Fluid movement–> out of vessel into interstitium–> Odema (swelling/tumor)

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11
Q

What happens to the blood when the fluid moves out? What effect does this have on the flow of blood?

A

Increases viscosity of blood

Reduces the flow through the vessel–> stasis

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12
Q

What are the different types of interstitial fluid? Compare and contrast then?

A

Exudate–> increased vascular permeability

  • -> protein rich fluid (delivers protein to area of injury)
  • -> occurs in inflammation

Transudate–> Not related to inflammation

  • -> vascular permeability unchanged
  • -> fluid movement due to ↑hydrostatic pressure, ↓capillary oncotic pressure
  • -> interstitial fluid–> protein free
  • -> occurs in–> HF, Hepatic failure, renal failure
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13
Q

How does the vessel wall become permeable?

A
  • Retraction of endothelial cells –> NO, histmaine, leukotrienes
  • Direct injury–> burns, toxins, trauma
  • Leukocyte dependent injury–> enzymes, toxic O2 species released by inflammatory cells
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14
Q

How is the vascular phase of inflammation effective?

A

Increased interstitial fluid–> dilutes the toxins
Increased exudate–> delivers proteins
e.g. fibrin–> forms a mesh to limit the spread of toxins–> physical barrier
e.g. immunoglobulins–> adaptive immune response–> targeted destruction of pathogens

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15
Q

Where does the fluid drain to?

A

Lymph nodes

  • -> delivery of antigens to lymphocytes
  • -> adaptive immune response activated
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16
Q

What is the main function of the cellular phase?

A

Immune cells to site of inflammation

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17
Q

What is the main WBC involved in acute inflammation?

A

Neutrophil
Larger than RBC (just)
Trilobed nucleus
Granulocyte

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18
Q

How do neutrophils escape the circulation?

A 
↑ Viscosity of blood, movement slows
Margination--> adhesion to capillary 
Rolling--> rolls along surface
Adhesion-->attached more tightly to capillary 
Emigration (diapedesis)--> escaping
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19
Q

What adheres the neutrophil to the surface?

A

Selectins

Integrins

20
Q

What are selectins?

A

Expressed on activated endothelial cells
Activated by chemical mediators
Weak bonds–> responsible for rolling

21
Q

What are integrins?

A

Neutrophil surface
Change from low affinity to high affinity state
Responsible for adhesion

22
Q

What makes neutrophils move through the interstitium?

A

Chemotaxis
Move towards highest concentration of chemoattractant
Chemoattractant: bacterial peptides, Inflammatory mediators
Neutrophil cytoskeleton rearranges to allow movement

23
Q

What is the role of neutrophils? How do they do it?

A

To engulf pathogens –> Phagocytosis

  • -> phagosome fused with lysosome
  • -> produces secondary phagolysosome
  • -> release inflammatory mediators–> propagate inflammatory response
24
Q

How do the neutrophils know what to phagocytose?

A

Opsonisation– recognition system

  • -> proteins bind to surface of pathogen enhancing attachment of phagocytes
  • -> Toxin covered in opsonins–> C3b and Fc
  • -> receptor for C3b and Fc on neutrophil surface
25
Q

What are the mechanisms used by neutrophils to kill bacteria?

A

Oxygen dependent and oxygen independent pathways

26
Q

What are the features of the oxygen dependent pathway?

A 
Reactive oxygen intermediates (ROS, RNS and free radicals)
ROS
--> Superoxide anion 
--> OH• 
--> H2O2
RNS
--> NO
--> NO2
27
Q

What are the features of the oxygen independent pathway?

A

Enzymatic destruction

  • Lysozymes
  • Hydrolytic enzymes
  • Defensins
28
Q

What is the draw back to the neutrophil response?

A

Activated neutrophils can cause damage to host tissue

29
Q

What are the two outcomes of the cellular phase of acute inflammation?

A

Removal of pathogens and necrotic tissue

Release of inflammatory mediators

30
Q

What are inflammatory mediators?

A

Modulates the inflammatory response in some way

Chemical messengers–> control and coordinate, varying chemical structures, overlapping functions

31
Q

Where do the chemical mediator originate from?

A

Activated inflammatory cells
Platelets
Endothelial cells
Toxins

32
Q

What controls the chemical mediators?

A

Inhibitors–> stop inflammation from going on endlessly

Short half lives –> seconds to minutes–> effects last minutes to hours

33
Q

Where do the endogenous mediators come from?

A

Supplied by plasma, leukocytes, and local tissues

34
Q

How are the mediators classified?

A
  • Vasoactive amines –> histamine and serotonin
  • Vasoactive peptides–> bradykinin (↑ vascular permeability)
  • Complement components–> C3a and C5a–> forms membrane attack complex (tube)–> punches holes in bacteria causing them to die
  • Clotting and fibrinolytic cascade–> generate inflammatory mediators
  • Phospholipid derived mediators –> prostaglandins, thromboxanes and leukotrienes
  • Cytokines and chemokines –> IL, TNF, interferons
  • Exogenous mediators of inflammation–> in tissue= inflammation, in blood= septic shock
35
Q

What are the main roles of the inflammatory mediators?

A

Vasodilatation–> histamine, serotonin, prostagladins, NO
Increased vascular permeability –> histamines, serotonin, prostaglandins
Chemotaxis–> Leukotrienes B4, C5a and C3a, chemokines, and bacterial peptides, TNF-α
Phagocytosis–> C3b complement plasma precursor
Pain –> bradykinin, substance P

Vasoconstriction–> histamine, bradykinins, leukotrienes, C3a and C5a??? look up in workbook

36
Q

What are the local complications of acute inflammation?

A

Damage to normal tissues
Swelling–> compression of tubes e.g. airways, bile duct
Exudate–> compression of organs e.g. cardiac temponade
Loss of fluid–> dehydration e.g. burns
Pain and loss of function–> muscle atrophy, psycho-social consequences

37
Q

What are the systemic complications?

A

Inflammatory mediators in the blood stream
Fever–> pyrogens (inflammatory mediators)–> acts on hypothalamus to alter temperature
Exogenous sources - NSAIDs- block COX activity - ↓ prostaglandins reduce fever

Leucocytosis–> ↑WBC –> measured in blood

Acute Phase response–> causes discomfort/ unwell (malaise), reduced appetite, altered sleep, tachycardia–> induced rest!!
–> changes in levels of plasma proteins (liver changes pattern of protein synthesis)–> ↑CRP–> marker of inflammation

Septic shock–> huge release of chemical mediators, widespread vasodilatation, increase vascular permeability–> hypotension and tachycardia–> multiorgan failure–> often fatal

38
Q

What happens after acute inflammation?

A

1- Complete resolution
2- Repair with connective tissue
3- Progression to chronic inflammation

39
Q

What is meant by complete resolution?

A

Mediators–> short half lives- diluted/inactivated/degraded
Vessel calibre and permeability –> normal
Neutrophils undergo apoptosis and get phagocytosed
Exudate –> lymphatics
Regeneration of tissue architecture if preserved

40
Q

Why would it need repairing with connective tissue? Problem with this?

A

Extensive damage –> tissue destruction

Leads to fibrosis

41
Q

What happens if the acute inflammation is unable to kill the pathogen?

A

Chronic inflammation

Prolonged inflammation with repair

42
Q

What is appendicitis? Why does it happen?

A

Inflammation of the appendix
Blocked lumen–> faecolith (hard faeces)
Accumulation of bacteria and exudate–> ↑ pressure–> perforation

43
Q

What is pneumonia? What causes it? Signs and symptoms? Risk factors?

A

Common respiratory tract infection
Caused by–> Streptococcus pneumoniae, haemophilus influenza
S and S–> SoB, cough, sputum, fever (accumulation of exudate–>builds up–> prevents gaseous exchange)
Risk factors–> smoking–> destroy mucocillary escalator
Pre-existing lung conditions–> COPD, Astham, Malignancy

44
Q

What is meningitis? What are the signs and symptoms?

A

Inflammation of the meninges
Mainly caused by; Neisseria meningitides, E.Coli, Group B Streptococcus
Headache, neck stiffness, photophobia (sensitive to light), atered mental state –> rapidly fatal

45
Q

What is an abscess?

A

Accumulation of dead and dying neutrophils
With associated liquefactive necrosis
Can cause compression of the surrounding structures–> pain and blockage of ducts

46
Q

What happens if you get inflammation of serous caivities?

A

Exudate pours into the serous cavities
Pleural space–> pleural effusion
Peritoneal space–> ascities (distension of abdomen)
Pericardial space–> pericardial effusion

47
Q

Can you get disorders of acute inflammation?

A

Yes but rare
Hereditary angio-oedema
Alpha-1 antitrypsin deficinecy
Chronic granulomatous disease

Semester 2 Pathological Processes (16 decks)

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