Brainscape's Knowledge GenomeTM

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


See full index

PATHOANA > Pathology if inflammation.causes, manifestation, types > Flashcards

Pathology if inflammation.causes, manifestation, types Flashcards

1
Q

definition of inflammation

A

complec local mesenchymal and vascular reaction of living tissue on different types of damage

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

systemic manifesarions of local inflammation

A

nausea, ^temp, headache, fatigue, enlarged LN, leukocytosis

long lasting chriniz–>AA amyloidosis

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

SIRS-systemic inflammatory response syndrome

A

pathogenesis of sepsis

leads to MODS

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

physiological role of inflammation

A
  1. eliminate cause of inflammation and minimize tissue dmaage
  2. stop spreading of the cause of inflammation (surrond it)
  3. activate processes of regeneration and repair(healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pathological role of inflammation

A

excessive or long lastin reaction leading to tissue damage

role in pathogenesis of many diseases

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

factors determining inflammatory responese

A
  1. features of pathogen
  2. response of host organism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

feature of pathogenbi

A
  1. type and mechanism of tissue
  2. virulence
  3. infectious dose
  4. portal of entrance
  5. products of pathigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

response of host organism

A
  1. systemic disaese (dm, Chronic renal insufficency-CHRI, cirrhosis, alcholism, BM failure)
  2. tumors
  3. function status of IS-psecific and nonspeficific
  4. type and localization of damaged tissye
  5. local host factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

components of inflamamtion

A

1 cellualr
2. humoral

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

cellular compinent of inflammation

A
  • neutrophils
    -eosinophils
  • monocytes/macrophagesa dn tissue macrophages (histiocytes)
  • lymphocytes and plasma cells
  • mast cells
    -thromocytes
    -endothelial cells
    -fibroblast/fibrocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

humoral component of inflammaiton

A
  1. cell derived:
    • histamine, serotonin: vasoactive
    • prostagladnins, leujotrines: arachionic acid
    • free oxy radical, nitric oxide, cytokines, neuropeptides
  2. plasma derived
    • liver
      1.components of complement
      2. factor X11 (hageman factor) : vessle dia
      3. processes of hemostasos, including blood coagualtion and fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

macroscopical features of inflammaiton

A

typical for acute inflammaiton
1: Calor=Heat (^temp)
- VASODILATION AND HYPEREMIA=HIGHER BLOOD PERFUSION
- hitg metabolic rate=heat

2: Rubor=redness
- dilated vv full of blood

3: tumor=swelling
- leaking water form vv–>acc in interstitium–>inflammatory edema
- exsudate

4: dolor=pain
- inflammatory mediator stimulate nerve fibers–>pain

5: functio leasa=loss of fucntion
- tissue damaged–>not normal funciton

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

microscopical feature of inflammation types

A

alteration, exsudation, proliferation

1/2 are increased/advanced

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

signs (Features) of inflammaiton-histologically

A
  1. VASCUALR CHNAGES (sec to minutes)
  2. infiltrattion of tissue with the inflammatory cells=inflammatory infiltarte/7celluzation (hours-days)
  3. biochemical, metabolic and morphological changes in involved tissye, even in severe distant organs-liver, spleen, ln
  4. act of IS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is altera5ion and what is ti caused by

A

to alter=damage
- represented by development of dystrophies and necrosis

caused by presence of microorganism, their toxins and immunopathological mechnaism: unfectionys inflammations

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

where can it be seen

A
  • microscopic-monocellular necrosis in vrial hepatitis
  • macroscopic: casefication in granulomas of TB
17
Q

examples of alteration

A
  • Viral encephalitits
  • viral heptatitis
  • deiphteric myocarditic: by corynebacterium diptheria
18
Q

what is exsudation

A

leakage of fluid, proteins, blood cells from vv to interstitium, on mucosal surfaces or into cavities (pleural, peritoneal, pericardial cavitiies)

19
Q

exsudate leakage is produced after fullfillment of which processes

A
  1. Vasodilation
    - lead to redness and increased temp
  2. increaseed vascular permeability
    - bc of mediaters or direct damage to vv wall
    - opening of gapes btw endothelial cells
  3. exsudation + leukocyte emigration
  4. vascular stasits
20
Q

what is transudate

A
  • when filtrattion of fluid is higher that reabsoprtion into vv.
  • permeability of vv is NOT CHNGES: only fluid escapes

hypostattic tissue edema due to heart failure

21
Q

what is proliferation and what does it include

A

Proliferation is the development of granulation tissue which is vascularized pink tissue with granular apperanc

includes:
- multiplication of inflamamotry cells in inflammed tissue
- prolif of vv/endothelial cells(angiogenesis)
- prolif of interstitial cells-fibroblasts
- formaiton and remodeltation of new tissue

22
Q

what is non-specific grnaulation tisuse and what is it compised of

A

-typically seen in chronic inflammaiton and healing
-responsible for healing and repair
- composed of
1. new forming vv: proliferation of ENDOTHELIAL CELLS
2. FIBROBLASTS
- make collagen and EM

23
Q

what will nonspecific granuation tissue turn into

A

collagenous, hypocellualr, hypovascular tissue; aka SCAR

by healing, scarificaiton and fibrotization

24
Q

what is specific granulation tissue

A
  • not a tissye visible in process of healing
  • NOT PROLIFERATING VV, NO VV
  • composed of:
    • histiocytes whcih get cahnged into epitheloid cells: epitheloid hitstiocytes
      -
25
Q

type of inflammation axx to time

A

peracute: days-week
acute: 1-3e
subacute: 3-6w
chronic: m-y

26
Q

tyoe of inflammaiton acc to cells

A

acute: polymorphonuclears-nucleus and macrophages

chronic: lymphocytes, plasma, macro, fibrobalst

27
Q

if we have allergic /parasitic etiology we can se

A

macro and eosinophils

28
Q

if we have viral etiology

A

lymohocytes

29
Q

what are liable cells

A

cells able to regenerate,

30
Q

what is stabile cells or permanent cells

A

no ability to proliferate (musclem nervoys tissue)
- striated, cardiac muscle and most smooth muscle(not uterus)
- damage fixed only by repair–>non-specific grnaulation tissye–>fibrous scar

31
Q

what is exacerbation

A

where acute inflammation may be reactivated, chronic–>acute

PATHOANA (13 decks)

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