Brainscape's Knowledge GenomeTM

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


See full index

Pathology lectures > 11th lecture chronic inflammation > Flashcards

11th lecture chronic inflammation Flashcards

granulamatous inflammation (note the book only deals with tuberculosis)

1
Q

define chronic inflammation?

A

a response of prolonged duration (weeks or months) in which inflammation, tissue injury and attempts at repair coexist.

inflammation + tissue injury + repair

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

causes of chronic inflammation?

A
  • persistent infection (tuberculosis)
  • hypersensitivity diseases-autoimmune diseases
  • prolonged exposure to potentially toxic agents, either exogenous and endogenous
  • Foregin bodies

some inflammation can go straight to chronic inflammation with no acute phase. HCV (hepatitis C virus) infection is already chronic.

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

what are the cellular players in chronic inflammation?

A 
macrophages
lymphocytes,
plasma cells
eosinophils
mast cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Morphological features of chonic inflammation?

A
  • infiltration with mononuclear cells
  • tissue destruction
  • attempts at healing.

No exudative phase (no vascular changes present)

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

what is the primary cell during chronic inflammation?

A

macrophages are the primary cells in chronic inflammation while neutrophils were the primary cell type in acute inflammation.
lineage of the monocytes!
2 forms of activation, classic and alternative pahtways.

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

what are the 2 forms of macrophages activation.

A

CLASSIC:
mediated by Th1 lymphocytes which will secrete INF-gamma turning monocytes into M1 macrophage;
using ROS, NO, lysosomal enzymes they kill the bacteria and fungi.
ALTERNATIVE:
mediated by Th2 lymphocytes secreting IL-13 and IL-4 making monocytes into M2 macrophages which will cause:
anti-inflammatory effects wound repair, fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
what is the role of 
Lymphocytes, 
eosinophils, 
mast cells,
leukocytes
A

LYMPHOCYTES: mediators of adapative immunity, provides defense against infectious pathogens, if present in chronic inflammation, and if activated the inflammation tends to persist and become severe
EOSINOPHILS: in immune reactions mediated by IgE and in parasitic infections (eosinophilic infections can occur in the GI tract without the parasite being present)
MAST CELLS: in both acute and chronic inflammatory reactions
LEUKOCYTES: acute and chronic

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

examples of acute and chronic inflammation?

A

chronic bronchitis due to smoking. At the same time there will be an acute inflammation due to bacterial infection.

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

what determines the morphology of the macrophages?

A

morphology depends on the ingested material:
foamy cytoplasm: (eat lipids)
haemosiderin-laden: (eat hemocyderine)
epitheloid cells: (modified macrophages)
giant cells: (fusion of epithelial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q 
explain the following:
circatrisatio-cicatrix formation?
EXAMPLES:
- pleuritis chronica adhaesiva
- pericarditis chronica adhesiva
- cicatrix myocardii
- cirrhosis hepatis
A

mostly caused by classical pathway activate macrophages, causing fibrosis.
fibrinous pleuritis, pericarditis (adhesion of pleural/pericardial layers)

  • pleuritis chronica adhaesiva (thickening and adhesion of pleura layers)
  • pericarditis chronica adhesiva (same thing as above)
  • cicatrix myocardii (after myocardial infraction we will have scar tissue called this)
  • cirrhosis hepatis (chronic inflammation of the liver resulting in scar tissue of liver)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe chronic H. pylori infection? (name the statistics associated with it).

A
  • majority will get simple gastritis (high gastrin but normal acid secretion) Normal outcome
  • 10 % will develop duodenal ulcer but are protected from gastric cancer.
  • 1% of patients will have atrophy of gastric mucosa and increased risk of gastric cancer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the link between chronic H-pylori infection and malignancy/malignant tumors?

A

long standing chronic inflammation can result in MALT lymphoma on the background of chronic inflammation. This can develop in salivary glands and stomach, and thyroid gland.

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

what is the process of HCV infection?

A

-HCV infection
-chronic hepatitis
-cirrhosis
-HCC & ESLD
(HCC = Hepatocellular carcinoma)
(ESLD = End-stage liver disease)

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

define granulomatous inflammation? what are the characteristics?

A

a form of chronic inflammation characterized by the presence of granuloma.
CHARACTERISTICS: the presence of granuloma; which is made up of:
- epitheloid cells (modified macrophages) compulsory component
- Giant cells (fusion of epitheloid cells)
- lymphocytes
- fibroblasts

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

how do we classify granulomas?

A

2 different classifications: morphological pattern or immunological background.
IMMUNOLOGICAL granulomas: (2 kinds)
- Immunological granulomas (T lymphocytes are essential secreting IL-2, IL-12, thus macrophages will become epitheloid cells.
- NON-immunological granulomas (no lymphocytes) Example: foreign-body granulomas (keratin, lipogranuloma, surgical suture)

MORPHOLOGICAL patterns:

  • necrotising: (central necrosis)
  • non-necrotising:

IMMUNOLOGICAL GRANUMOLMAS can be sub-classified.

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

what are the sub-classifications of immunological granulomas?

A

infective: clearly there is an infective agent

non-infective: etiology is insidious (we don’t know what infective agent is behind the infection.

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

different types of giant cells?

A
  • Langhans (horse-shoe shaped) in tuberculosis
  • Foreign-body type (random arranged nuclei)
  • Touton: (nuclei are arranged in rings) such as xanthogranulomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the most common infectious disease in the world?

A

tuberculosis

Caused by : mycobact, tuberculosis

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

what type of special staining used to identify tuberculosis pathogen?

A

Zieh-Neelsen
auramin
PCR

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

what are the phases of tuberculosis?

A

PRIMARY phase: 1st meeting with the bacteria. Characterized by the Ranke-ghon complex; the granuloma (tuberculoma) inflammation of the lymphatic vessels called lympagentitis and inflammation of the lymph node (lymphadenitis)
POST PRIMARY phase: some bacteria remain viable from the primary phase and because of immune suppression the bacteria that remains can be reactivated. (reinfection can occur)

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

what does a tuberculosis granuloma look like?

A

the necrotic area is surrounded by a layer of epithelioid cell and then a layer of lymphocyte and langhan type multinucleated giant cells.

lymphocytes make interferon and interleukine to allow the macrophages to change into epithelioid cells.

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

what are the sings and symptoms of tuberculosis?

A 
fever
night sweats
loss of appetite
fatigue 
weight loss.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Granulomatous inflammation syphilis caused by?

A

treponema pallidum
(spiral cocci)

Can be acquired to congenital.

24
Q

what characterizes the 3 phases of aquired from of syphilis?

A

primary: ulcer durum, bubo indolens = enlarged painless lymph node near the site of infection.
secondary: bacteria is spreading via hematogenic way bacteremia= bacteria in blood. exanthaemas= rashes over the entire body.
tertiary: appearance of granulomas called gumma (in syphilis)

25
Q

what are the results of tertiary AQUIRED form of syphilis.

NOTE: tertiary is one of the 3 forms.

A

in secondary the bacteria spreads via the circulation. The bacteria will cause the epithelial cells to proliferate and he patient will develop endarteritis obliterans.
This will cause Cardiovasc: aneurysma (because the vasa vasorum will be obstructed in the AORTA forming an aneurysm)
Neurological disorders: tabes dorsalis (because of the involvement of the spinal cord leading to paralysis problem as the dorsal root is most affected)
CNS problems result in paralysis progressiva

26
Q

what characterizes the severe form of the CONGENITAL syphilis?

A
  • pemphigus syphiliticus: blisters of the skin of the newborn baby
  • hepato-splenomegaly: The liver and spleen is filled with bacteria
  • pneumonia alba: color of the lung in newborn is almost white (indicating inflammation)
  • Dubois-abscess: small abscesses (collection of pus) in the thymus, especially in the hassall corpuscule.
27
Q

what characterizes the mild form of the CONGENITAL syphilis?

A
  • Hutchison’s triad:
    1. hutchinson’s teeth: blunted incisor teeth,
    2. inflammation of the cornea (interstitial keratitis
    3. Deafness from auditory nerve disease.
28
Q

Rheumatic fever (granulomatous inflammation) description?

A

non-infective immuno-granuloma

CAUSE: post streptococcal disease, involving the heart, joints, brain.

29
Q 
what kindof granulomas are:
tuberculosis:
syphilis: 
Rheumatic fever:
Sarcoidosis:
foreign body granulomas:
A

tuberculosis: immuno-granuloma infective
syphilis: immuno-granuloma infective
Rheumatic fever: immuno-granuloma non-infective
Sarcoidosis: immuno-granuloma non-infective
foreign body granulomas: non-immune granulomas with no lymphocytes, epitheloid cells, or giant cells.

30
Q

During rheumatic fever the heart is affected how?

A

in the post-sterptococcal disease the antibodies that are produced against them will recognize different structures of the endocardium, myocardium and pericardium.

This is called MOLECULAR MIMICRY.
pancarditis = inflammation of the entire heart (all 3 layers)

31
Q

In rheumatic fever the inflammation of the endocardium is characterized by?

A

Deposition of fibrinoid material in the endocardium. Fibrinoid necrosis. and fibrin rich deposition in the valves surfaces.
these small depositions are called VEGETATIONS.
NON-infective vegetation’s.

32
Q

In rheumatic fever the inflammation of the myocardium is characterized by?

A

myocarditis (rheumatoid granulomas are called aschoff bodies) made of epitheloid cells with caterpillar like nuclei called Aschoff giant cells + lympoplasmatic infiltrate.

33
Q

what are the giant cells in the rheumatic fever called?

A

aschoff bodies. (they are rarely present)

34
Q

Describe Sarcoidosis? what type of granuloma is it?

A

Sarcoidosis: immuno-granuloma non-infective. (unknown ethology of the infection). (since we don’t know the cause we treat the symptoms)
can affect: eye, lymph node, lungs, heart, joints, skin. Most severely affected organ is the lung.

35
Q

what do we have in sarcoidosis (what happens to the tissue and inside the body)?

A

non-caseating (without necrosis) non-infective granulomas. Scarring granuloma with alot of firboblasts.
Giant cells with:
-Asteroid body: star shaped inclusion in the cytoplasm.
-schaumann’s body: large concentric laminated calcified structures.

36
Q

what is the result of sarcoidosis for the lung.

A

the lung contains lots of:
-granulomas
-fibrosis
-scar tissue.
pulmonary hypertension then cor pulmonale.
if the disease appears intravascular the pulmonary pressure is much higher.

37
Q

Describe foreign body granulomas?

A

foreign body granulomas: non-immune granulomas with no lymphocytes, epitheloid cells, or giant cells.

no lymphocytes and thus no IL secreted thus they cannot transform macrophages into epitheloid cells.
hagment factor (coagulation protein 12) causes the organization of foreign body granulomas.
38
Q

what is the central factor for organizing the foreign body granulomas?

A

Hagment factor

people deficient in hagment factor do not form foreign body granulomas.

39
Q

what are hagment factors caused by?

A

surgical sutures, splinters.

40
Q

what is keratin-pearl granuloma characteristic of? what about lipogranuloma?

A

malignant tumors that produce keratin such as squamous cell carcinoma. Keratin production experiencing tumor invasion and thus keratin is released into the surroundings. Giant cells surround keratin deposits.
Lipogranuloma is present in breast and abdomen and giant cells surround lipid droplets

41
Q

what are some of the harmful consequences of inflammation?

A

a. inflammatory reaction against harmless lesions
b. hypersensitive, autoimmune diseases
c. too intense reaction: endotoxin shock
d. autoinflammatory disorders (diabetes, atherosclerosis)

42
Q

what is the result of failure of inflammation?

A

a. congenital defects: neutrophil defect,

b. acquired lesions: leukocyte malfunction, splenectomy.

43
Q

what is the difference between regeneration and healing?

A

regeneration: proliferation of residual (uninjured cells).
Healing: deposition of connective tissue to form a scar.

44
Q

what are some of the different types of cells during regeneration?

A

Labile cells: “continuous replicators” that are stoped from replicating via contact inhibition. (skin, mucous, oviducts, urothelium)
Stable cells: “discontinuous replicators” only proliferate when needed: liver, fibroblasts, osteoblasts.
Permanent cells: “non-replicators” CNS, heart cells (limited ability to divide).

45
Q

where are the stem cells located in the liver?

A

in the herring canals near the portal vein. If they divide they form oval cells that proliferate along the canals of herring forming a bile duct structures and then differentiate into small hepatocytes which proliferate and replace the lost tissue upon maturation.
The liver lobule will then become enlarged.

46
Q

definition of healing?

A

a process in which the body is trying to achieve the original anatomical integrity of the injured part and to restore full function.

47
Q

in the context of wound healing define: primary and secondary intention?
(Primary and secondary healing)

A

Primary intention: the edges of the wound are cleaned and a ligature holds them together. healing occurs quickly with small amount of scar tissue. Scar tissue layer down in 1 month.
Secondary intention: edges are separated with lots of lost tissue. possible contamination. Slow healing. lots of scar tissue, wound contracture.

48
Q

what is the process of scar formation/healing?

A

haemostasis
inflammation
proliferation
maturation and remodeling

49
Q

what processes occur during haemostasis phase of healing? 3-5 days

A
  1. vasoconstriction
  2. blood clot formation
  3. platelets aggregation
  4. platelets degranulation
  5. vasodilatation
50
Q

what processes occur during inflammatory phase of healing? 3-5 days

A

Chemotaxis

  • leukocytes
  • Neutrophils
  • Macrophages
51
Q

what processes occur during proliferating phase of healing? 3rd week

A
  1. angiogenesis (proliferation of vessels)
  2. fibroblasts migration
  3. formation of granulation tissue (if needed)
  4. re-epithelialization
52
Q

what processes occur during remodeling phase of healing? weeks to years.

A
  1. disappearance of fibroblasts
  2. collagen type 3 replaced with collagen type 1 which is stronger
  3. remodeling of scar tissues, the tensile strength of scar tissue gradually increases.
53
Q

how long does it take for the tensile strength of the wound to get close to that of the initial strength?

A

30 days to reach about half the strength.

54
Q

what factors affect wound healing?

A

local and systemic factors: (see other cards)

55
Q

what are the local factors affecting wound healing?

A

wound sepsis
blood supply
wound tension (langer lines for surgeons)
foreign bodies
previous irradiation
poor technique (surgery see langer lines)

56
Q

what are the systemic factors affecting wound healing?

A
  • nutritional deficiencies
  • systemic diseases (haemophilia, diabetes, immunosupression)
  • therapeutic agents (chemotherapy)
  • Age
57
Q

what are some complications of wound healing?

A
  • infection
  • dehiscence: surgical incision reopens
  • incisional hernia
  • hypertrophic scaring
  • keloid scarring: tough heaped-up scar due to excessive collagen production.
  • contractures: shortening and hardening of muscle leading to joint immobility.
  • Exuberant granulations: “proud flesh” excessive granulation formation.

Pathology lectures (24 decks)

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