Pathology-Alaa > Inflammation > Flashcards

Inflammation Flashcards

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1
Q

what is inflammation? what is its purpose?

A

response to injury of vascularised living tissue. to deliver defensive materials to the injury site

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2
Q

what leads to edema during inflammation

A

-arteriolar dilatation leads to increase in hydrostatic p. - increased permeability of vessel walls leads to loss of protein into interstitium

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3
Q

why is there ‘leucocytosis’ in acute inflammation?

A

macrophages and injured tissues produce ‘colony stimulating factors’ that stimulate the bone marrow to produce more neutrophils.

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4
Q

What is the role of histimine in inflammation?

A

-vasodiolater -causes pain -venular leakage (increased permeability, causes blood endothlaila cells to contract and pull apart forming gap where PP cam pass)

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5
Q

how does the neutrophils do their job of phagocytosing?

A

contact, Recognition, Internalisation

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6
Q

What r the chemical mediators of inflammation?

A

*Proteases (pp made by liver)

*Cytokines / chemokines

*Prostaglandins / Leukotrienes

*vasoactive amines ex: hist & seratonin 

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7
Q

Give 4 complications of gall stones (cholelithiasis) &; explain why they occur?

A

Kk

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8
Q

normally, the endothelium of the capillaries & venues act as a semi-permeable membrane. what does this mean?

A

it allows some escape of water and some electrolytes, but keeps the PP in!

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9
Q

Describe the changes in blood flow and blood vessels during inflamm.

A
  • vasoconstriction (few secs)
  • vasodilation of arterioles causing increase in Bf in capillaries and high P. 😱
  • venules become more permeable (leaky), allows exudate to go in the tissues (Leaves blood)
  • circulating blood becomes more viscous>> slows circulation (swelling)
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10
Q

What is pyrexia?

A

fever

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11
Q

What do ca 2+ In the cell target?

A

Atpase Phospholipase Protease Endonuclease

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12
Q

what causes the sense of ‘heat’ and erythema at the area of inflammation?

A

vasodilation of the vessels, therefore increasing BF

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13
Q

mechanism of resolution in acute inflammation

A

– Mediators r short lived & r degraded

– Exudate drains to lymphatics

– Fibrin is degraded by plasmin and other proteases

– Neutrophils apoptose, break up & phagocytosed

– Damaged tissue might be able to regenerate.

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14
Q

What is anaphalyxis?

A

a serious, life-threatening allergic reaction

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15
Q

what is the link btw gallstones and hepatic abscess?

A

m

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16
Q

Another important mediator is derived from arachidonic acid. Name it

A

Prostaglandin

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17
Q

how does the lymphatic system play a role during inflammation?

A

during lymphatic drainage, lymphs delivers micro-organims to phagocytes and antigens to immune system

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18
Q

Systemic Effects of Acute Inflammation (4)

A
  1. Fever
  2. Leukocytosis
  3. Acute phase response 
  4. Shock
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19
Q

what is the acute phase response? how is it triggered

A

Decreased appetite, raised pulse rate, altered sleep patterns

• Acute phase repsonse is changes in patterns of protein synthesis. ( occurs w/ in hours of injury)

-triggered via cytokines released during inflammation

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20
Q

What r the roles of selectin and integrins when neutrophils bind to them

A

selectins>> produces ROLLING of neutrophils integrins>> makes them STOP and adhere

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21
Q

why is exudation of fluid important?

A

Delivers pp to injury, Immunoglobulins, mediators, Fibrinogen Dilutes toxins Increases lymphatic drainage 

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22
Q

In acute inflammation, what changes occur in the tissues?

A
  • change in blood flow
  • exudation of fluid into tissue
  • infiltration of inflammatory cells
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23
Q

how do neutrophils escape from blood vessels? how long does this take?

A

they don’t use the gaps that exudate was released from, via Pcam, they transmigrate the endothelium and then produce collagenases that digest (dig) the basement membrane and they enter the tissue.

3-9 mins

DIAPEDISIS

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24
Q

what is exudate? transudate? edema?

A

ex= extracellular fluid that has HIGH protein content Trans= extracellular fluid that has LOW protein content EDEMA= excess of fluid in the interstitiam, can be exudate or transaudate.

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25
what is Ascites?
gastroenterological term for **accumulation of fluid in the peritoneal cavity** that exceeds 25 mL
26
what is an abscess? what type of necrosis has occurred there?
collection of pus that has built up within the tissue of the body. bc its on a solid tissue, may cause high p\> pain! \*\*liquefactive in its centre
27
what causes lobar pneumonia? what is the lung filled with
Streptococcus Pneumoniae Exudate
28
\*\* NEUTROHPILIA IS SEEN DURING BACTERIAL INFECTION!
reminder ;p
29
What is the difference between lobar pneumonia and bronchopneumonia?
**Lobar pneumonia** affects all or part of a lobe with other areas generally normal. **Bronchopneumonia** is especially seen in young and old patients. It has a patchy distribution and generally *_involves more than one lobe and often both lungs._*
30
What r the clinical feautures of inflammation and what caused them?
Rubor-redness \>vasoldilation and increased bf Dolor-pain Calor-heat \> increased bf Tumor -swelling \> exudate Loss of function
31
How do neutrophils move to site of inflammation?
**Chemotaxis** via chemotaxins released from the injured site ex: c5a, LTB4, (which neutrophils have receptors for)
32
U cant get acute inflammation in catilage why
Bc theres no blood supply
33
is immigration of neutrophils a passive or active process?
active, it requires energy
34
Often, the body's acquired immune response is triggered without the innate response being triggered first, that is, without a preceding acute inflammatory reaction. Give examples in which this happens
Virus infection is a good example. Most viruses don't trigger a neutrophil reaction: it starts with lymphocytes. Tuberculosis is another. Sarcoidosis and many other longstanding inflammations often start directly with chronic inflammation.
35
what is histimine? where is it stored? what stimulates is release? how long does it take for its response?
* its a vasoactive amine which r the first mediatprs to appear in acute inflammation * mast cells, basophils and platelets, * C3b, c5A, interlukin * 1...............1/2 hr
36
What is chemotaxis? Explain the process and chemicals involved
Directed movement towards a "chemotaxin" (released from injured area)
37
What do we call a reaction in which the dominant cell type is the macrophage, usually forming groups?
Granuloma
38
during inflammation, what causes the increase in hydrostatic P. in vessels?
arteriolar dilatation
39
in an abscess, what causes the exudate to be 'creamy white'?
rich w/ neutrophils
40
do neutrophils have multiple nuclei?
41
What is an example of a bacterial chemotaxin?
Endotoxin found on the outer surface of gram - bacteria.
42
roles of specific mediators involved in Vasodilation, chemotaxis, phagocytosis, pain
) -Pain\> bradykinin & prostaglandin & histimine
43
How do neutrophils escape from vessels?
Viscous blood pushes them towards the periphery, the marginate across the periphery of the blood vessels and roll, then via their recepters, they bind to "integrins and selectins" on the endothelial surfaces of bv and STOP, they produce collegenases that digest the basment membrane and enter in.
44
what is hyperaemia? how is it initiated?
an excess of blood in the vessels supplying an organ or other part of the body. arterioror f dilation
45
What is the primary leucocyte involved in inflamamtion?
Neutrohpils (also called polymorphs)
46
what is PUS?
Puss are dead neutrophils and is a mixture of bacteria.
47
what is chronic granulomatous disease?
genetic condition, where phagocytes can't generate the free radical 'superoxide.' As a result, bacteria is phagocytosed but not killed! (no oxygen burst) \>\> leads to chronic infections There is a deficiency in the nadph oxidase enzyme.
48
Explain starlings law in fluid loss from bv
hydrostatic p. in vessel increases= fluid wants to flow out of it. oncotic p. in vessels increases= fluid wants to come in. (fluid dayman yabb ykoon bl area ily feeha more solutes)
49
explain process of margination
due to inflammation, blood is viscous and flows slowly (stasis). this causes neutrophils to line up at the edge of blood vessels and stick along the endothelium
50
how can fever sometimes be useful?
bacteria cannot survive in temp high (40-41)
51
what r the local complications of acute inflammation?
-damage to normal tissue -loss of fluid (exudate) CT -obstruction of tubes -pain & loss of function
52
What may happen after the development of acute inflammation?
1) Complete resolution. 2) chronic inflammation = abscess. 3) Chronic inflammation and fibrous repair, probably with tissue regeneration. 4) Death.
53
FRESH BLOOD IS NOT CHEMOTACTIC,
BUT CLOTTED BLOOD IS
54
Prostaglandins are synthesised from arachidonic acid via a certain pathway. What do we call this pathway?l
It's the cyclo-oxygenase pathway.
55
what leads to 'swelling' in inflammation?
when circulation slows down during the changes that occurred.
56
what is a seroma?
a tissue space filled with clear, sterile fluid that occurs as a post-operative complication
57
What does High ALT in blood indicate? And when do we measure it
Means there is hepatocellular injury, Screening for liver function
58
a patient comes in with a high fever, why do we give him aspirin? what is fever? explain the underlying cause of the fever and mechanism of aspirin
when inflammation is present, macrophages r present in large numbers, they produce cytokines (TNF, IL-1) that can increase the synthesis of Prostaglandin E2 in hypothalamus and cause changes in thermostat. \*\*\*ASPIRIN= inhibts cyclo-oxygenease (enzymes that produces prostaglandins
59
why is formation of fibrin crucial in blood clotting?
causes a meshwork, this is important, bc its a good way to LOCALIZe inflammation, & manages to ideally stop it from spreading
60
describe the clinical course of lobar pneumonia? can it be treated?
Worsening fever, prostration, hypoxaemia over a few days. Dry cough and breathlessness. • If treated can revolve completely if not....dead.
61
does plasma viscosity increase or decrease as a systemic effect on acute inflammation?
it increases in the acute phase reaction
62
Acute phase proteins
– C-reactive protein (CRP) (Clinically useful) – a1 antitrypsin – Haptoglobin – Fibrinogen – Serum amyloid A protein
63
Causes of acute inflammation
- microbial infections - hypersensitvity reactions - tissue necrosis - physical & chemicals agents - Trauma - Foreign bodies (sutures, dirt)
64
What do neutrophils make leukotrienes from?
Arachiodinic acid
65
what r opsonins? explain their use, give example
A substance that coats foreign materials and makes them easier to phagocytose ## Footnote *phagocytosis is faciliated by opsonins on the bacteria (neutrophils r attracted to the bacteria with jam) Ex: C3b, Fc, IgG*
66
What feauture occurs when chemotaxins bind to the surface recepters om neutrohpils?
Calcium and sodium rushes into the cell, it swells amd reorganizes the ctyoskeleton, assuming a triangular shape that points towards the site of inflammation
67
in acute inflammation, is the rate of bf consistently increased?
no, it slows down as fluid leaves the capillaries.
68
explain the killing mechanisms of phagocytes organisms
**O2 dependent** (using oxygen derived free radicals) -respiratory burst via ***nadph oxidase*** – Produces *superoxide* and hydrogen peroxide. **O2 independent** (using ***enzymes***) – proteases, phopholipases, nucleases, lysosomes
69
clinical examples of inflammation(4)
-lobar pneumonia -acute appendicitis -bacterial meningitis -ascending cholangitis
70
what happens in STASIS?
RBC clump in the middle bf SLOWS as cells r moving slower
71
What causes inflammation to be a LIMITED process?
the fact that the chemical mediators r SHORT LIVED
72
fluid loss in inflammation is exudate or transudate?
exudate (has high protein content)
73
A patient died from a shock due to prior inflammation elsewhere in the body. what could be a reason for this?
if inflammatory mediators SPREAD throughout the body in the bs, inflammation can occur elsewhere, causing vasodilation & increased permeability and a MASSIVE drop in BP.
74
what are the effects of prostaglandins and where do they arise from? how can we block them?
-produced during inflammation via the membrane phospholipids, -makes the skin sensitive to pain & fever -can be blocked via ASPIRIN and NSAIDS (these inhibit the cyclo-oxygenease that produces prostaglan. from arachnoid acid
75
what r the main forces that drive fluid IN and OUT of the vessels
-the hydrostatic p inside vessel (fluid goes out of it) -the osmotic p inside vessels (fluid goes in)
76
Explain how aspirin helps releive pain
block prostaglandin synthesis and thus suppress the inflammatory response.
77
types of exudate seen in inflammation (4)
-pus/abscess -haemmorrhagic exudate -serous exudate -fibrinous exudate
78
what happens after margination? explain the processes (with ligands and stuff involved)
viscous blood further pushes the neutrophils in the periphery causing them to ROLL via selectins and they STOP and stick firmly by binding their Integrins to (ICAM) on the endothelial lining of the vessel
79
What r some examples of inherited disorders of the acute inflammatory process? (3)
* Hereditary angio-oedema * Alpha-1 antitrypsin deficiency * Chronic granulomatous disease
80
Extremely rare autosomal dominant inherited deficiency of C1-esterase inhibitor ...name it
inherited angioedema
81
Chemotaxis
Chemotaxis is the directional movement towards (or away from) a chemical attractant
82
Define chemotaxis and Diapedisis
**Chemotaxis** is the directional movement towards a chemical attractant **Diapedesis** is the passage of blood cells through intact blood vessel walls
83
how is bradykinin produced?
The enzyme Kallikrein cleaves kininogen and bradykinin is produced!
84
treatment of abscess?
incision and drainage is an effective treatment for an abscess
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