Brainscape's Knowledge GenomeTM

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


See full index

J Term 2 mix > MOD2 > Flashcards

MOD2 Flashcards

1
Q

5 causes for acute inflammation

A
  1. physical agents
  2. chemicals
  3. microbial infections
  4. hypersensitivity reactions
  5. anything causing tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

3 Key features + some characteristics

A
  1. Vascular and cellular Rxns: accumulation of fluid exudate and neutrophils
  2. Controlled by a variety of chemical mediators
  3. Meant to be protective but it can lead to complications and systemic effects

-short-acting, innate, stereotyped

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

Clinical features - 5 cardinal signs

A

Rubor, tumor, calor, functio laeso, dolor

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

Steps of the vascular phase

A
  1. transient vasoconstriction
  2. vasodilation (tumor and calor) increasing blood flow
  3. increased permeability due to a balance of hydrostatic (forcing things out due to relative pressure) and oncotic pressures (Net flow of protein-rich fluid going into the spaces - leads to an edema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is starling’s law

A

Movement of fluid across a vessel wall governed by the balance between hydrostatic and osmotic pressure between intra and extravascular space

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

Name the mechanisms of vascular leakage

A
  1. endothelial cell contraction - causing a gap mediated by histamine, C5a and NO
  2. endothelial cell injury: direct (trauma, chemicals, toxins) and indirect (ROS, proteolytic enzymes)
  3. structural reorganization: being transported from one side to the other. Mediated by interleukin 1 and TNF
  4. Transcytosis: VEGF induces angiogenesis, increasing the channels in endothelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does vascular stasis occur and what does it help?

A

Losing fluid leads to increased concentration of RBCs, resulting in decreased velocity and stasis

Aids neutrophil margination

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

What is transudate and where/why would you see it

A

Lower protein content:
In heart failure, you would have a back up of blood in the venule end - increasing hydrostatic pressure and causing more plasma to leak out - edema

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

Name the types of exudate and what is exudate

A

High protein content

  • purulent (full of pus) would see in meningitis and TB
  • Hemorrhagic
  • serous (blister-like, fluid strips overlying epithelium, pain and profuse exudate, few inflamm. cells make it clear unless there’s a bacterial infection
  • fibrinous: fibrin leaking out gives a bread and butter appearance. e.g; surface of the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Primary leukocyte in acute inflammation? How many hours is it active for

A

Neutrophils, 6-24 hours

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

What aids rolling of neutrophils

A

Selectins are expressed by endothelial cells and bind to carbohydrate ligands called Slex on neutrophils
Aided by IG-1 and TNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What aids adhesion?

A

Integrins - expressed by neutrophils bind to integrin ligand on the endothelium, aided by C5a, leukotriene B4, IL-1 TNF

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

What aids diapedesis and what is it?

A

Neutrophils emigrating through the endothelium
Chemotaxins (e.g; C5a, leukotriene B4, endogenous cytokines, exogenous bacterial products, clotted blood)
Stimulate neutrophils to migrate through the inter-endothelial cell junction
Receptor ligand binding through selectins and integrins

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

What is chemotaxis

A

movement along concentration gradients of chemoattractions and chemotaxins

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

3 steps in how Neutrophils escape from the vessels (not diapedesis)

A
  1. relaxation of inter endothelial cell junction
  2. digestion of BM
  3. movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is opsonization? Name 3 common opsonins and 4 receptors they can bind to

A

Marking an antibody for ingestion of phagocytes (e.g; neutrophils and macrophages)
C3b, plasma proteins, IgG
Toll-like receptors, G-protein coupled receptors, opsonin receptors, cytokine receptors

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

Explain the two killing mechanisms of the phagolysosome

A
  1. Oxygen-dependent: free radicals released into the phagosome, superoxide converted to hydrogen peroxide through myeloperoxidase from neutrophil granules
  2. Oxygen Independent: uses enzymes; lysozyme, protease, nuclease and phospholipase to perforate holes in the microbial membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where do endogenous chemical mediators come from

A

plasma proteins, leukocytes and local tissues

19
Q

Where do exogenous chemical mediators come from

A

gram (-) bacteria

20
Q

Name the 2 vasoactive amines and what produces them

A

Histamine - increases permeability and vasodilation, platelets, basophils and MAST cells

Serotonin: immediate-early response to injurious stimuli - causes dilation, permeability and pain. Platelets

21
Q

Name a vasoactive peptide, what it does and where it comes from

A

Bradykinin; from the plasma precursors kininogen (in the kinin system)
Pain permeability and dilation

22
Q

Where do prostaglandins come from and what do they do?

Name 2 ‘Other’ chemical mediators

A

From arachidonic acid metabolites from membrane phospholipids, vasodilation, fever pain and itching

NO, leukotrienes

23
Q

What does the coagulation/fibrinolytic cascade form and activate?

A

Form thrombin and fibrin, and activates the kinin and complement systems

24
Q

What is a byproduct of the kinin system

A

Gram (-) bacteria

25
Q

What composes and activates the complement system? What does it do?

A

Normally inactive enzymatic proteins C3b and C5a made in the liver and present in the blood are activated by: antibody-antigen complexes in infection, proteolytic enzymes from necrotic cells, gram (-) bacteria, by-products of kinin and fibrinolytic systems

Generates: C3b - opsonin, C5a attracts neutrophils and C5-9 Membrane attack complex that causes lysis through cell membrane perforation

26
Q

List 5 examples of anti-inflammatories

A 
Aspirin/NSAIDs
antihistamine
corticosteroids
TNF alpha antagonists - infliximab
leukotriene antagonists
27
Q

What 3 things are TND alpha antagonists used for

A

Crohns, rheumatoid, psoriatic athritis

28
Q

2 Hallmarks of acute inflammation

A
  1. exudate

2. infiltrate of inflammatory cells

29
Q

What are 3 benefits of exudation?

A
  1. delivers plasma proteins, immunoglobulins, inflammatory mediators to the area of injury
  2. Diluting toxins and reducing their impact
  3. Edema elicits lymphatic drainage: delivering antigens to the immune system and microorganisms to phagocytes
30
Q

What is a consequence of edema eliciting lymphatic drainage?

A

Lymphadenopathy can occur if there’s too much fluid draining into the lymph system

31
Q

6 Local consequences of Acute inflammation

A
  1. swelling; in air spaces and in brain
  2. Inappropriate inflammation; hypersensitivity reaction
  3. exudation of fluid - can enter the pericardial space
  4. prolonged pain and loss of function
  5. digestion of host tissues by harmful enzymes released by neutrophils
  6. The cardinal signs
32
Q

A systemic consequence is pyrexia - how does it occur?

A

Pyrogenic cytokines (TNF and IL-2) are released from macrophages and neutrophils, they act on the anterior hypothalamus increasing the synthesis of prostaglandins - which increase Body temperature

33
Q

How does the body undergo leucocytosis following acute inflammation

A

Macrophages and endothelial cells secrete colony-stimulating factors so the BM produces more leukocytes
-IL-1 and TNFa accelerate the release from the BM

34
Q

What kind of leukocyte would you primarily see in…

a) bacterial infection
b) viral

A

a) neutrophils

b) lymphocytes

35
Q

What does the test C reactive protein do

A

Made and released from the liver during acute inflammation and can be measured to suggest if an infection is present

36
Q

In the acute phase response in the liver, what are 3 constitutional symptoms, some acute-phase proteins and why you have lower protein synthesis

A

Constitutional symptoms: malaise, anorexia and nausea

Acute-phase proteins: CRP, fibrinogen, alpha1antitrypsinm, haptoglobin, serum amyloid A protein

Dropped albumin level in the blood as the body is trying to fight off infection

37
Q

Explain the normal sequelae of acute inflammation

A

Resolution; mediators and neutrophils have short half-lives and degrade quickly.

  • Stimulus is removed
  • Exudate drains into lymphatics
  • Fibrin is broken down by a thrombolytic process
  • replacement of injured cells
38
Q

Name 3 abnormal results of acute inflammation

A
  1. Suppuration - excess exudate, can form pus and abscesses
  2. Chronic inflammation - granulation tissue, fibrous scar and angiogenesis
  3. Death
39
Q

What walls off abscesses

A

Pyogenic membrane

40
Q

What dangerous locations can exudate accumulate?

A

Ascites: an abnormal buildup of fluid in the abdomen

Pleural and Cardiac cavity - fibrous exudate can cause the lung to stick to the pleural wall and the patient may have a sharp pain on breathing and cardiac impairment

41
Q

What is hereditary angioedema and 2 consequences

A

Autosomal dominant, deficiency of C1 esterase inhibitor that inhibits bradykinin, family history of sudden death
Can have a:
1. Non-itchy cutaneous angioedema - deep skin buildup of fluid
2. Intestinal edema - abdominal pain as intestine can swell up

42
Q

What is alpha 1 antitrypsin deficiency and 2 consequences

A

Autosomal recessive
Low levels of A1AT means you don’t have a protease inhibitor - therefore inflammation goes unchecked
Can have a…
1. Emphysema: Type of COPD as breathing tubules are narrowed and air sacs damaged
2. Cirrhosis: liver doesn’t function properly due to excessive ECM and collagen break down
SO when someone is aged 40-50 with liver cirrhosis and has minimal alcohol consumption consider this disease

43
Q

What is chronic granulomatous disease? What are the consequences?

A

Defect in neutrophil function, the neutrophil is unable to generate superoxide and can’t kill the bacteria.

  • Chronic infections from the first year of life
  • Abscesses: caused by a bacterial infection
  • Granulomas: a mass of granulation tissue typically produced in response to infection, inflammation or presence of the foreign substance

J Term 2 mix (8 decks)

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