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PATHOANA > local circulatory disorders > Flashcards

local circulatory disorders Flashcards

1
Q

thrombosis

A

intravital/intravascualar blood caugualtion

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2
Q

why does thormbosis happen

A

disbalance btw coagulative and thrombotic factors

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3
Q

types of thrombus

A

parietal: attached to eall os vv, but vv is still permable

obturative: whole vv and blood stopped

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4
Q

red thrombus

A
  • mainly eryhtocytes
  • venous sys, when BF is slow bc of sedimentaiton +fibrin
    -deep vein thrombosis
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5
Q

white thrombus

A
  • thromocytes
    -pale color, yellow white
  • rapid blood steraem–>ARTERIAL BF and cardiac cavities
  • active coagulaiton
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6
Q

mixed thrombus

A
  1. bead thrombus: rapid, arterial wall
    - white head and red are behind
  2. layered: aneurysms, quit blood flow /blood stasis
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7
Q

hyaline thombus

A

-microscopically visible thrombi form thrombocytes and fibrin (shock, DIC)
- cappilaries
-thromobo and fibrin
- sever disturbance of capp BF
-stagnation

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8
Q

virchow triad

A
  1. Hypercoaguability
  2. stasis
  3. vessle wall injury
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9
Q

disturbance of blood floq

A
  1. slow blood flow-stenosis and strictures of vv, stagnation of blood by global circulatory disorders
    -venous sytsem
  2. tuburlent BF-by intraluminal blockage of BF=endothelial damage
    -arterial and cardiac chmaber
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10
Q
  1. alteration of vv wall
A
  1. internal injury of endothelium-atherscleoris
  2. alteration of vv form ext enviroment
  3. inflamamiton, tumorus infiltarte, trauma
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11
Q
  1. chnages in blood composition
A
  1. thickening of blood (polycythemia)
    - less fluid more proteins or cells
    -dehydration
  2. disbalance btw hemocoagualtive and thromobolytic factros=thrombofil conditions
    - inbron: rare, aquired: more comon
    INBORN:
    - APC-act protein c-resistnace (f.leiden): point mutation of prothrombin 2, lack of antithrombin 3, protien c and protien s.
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12
Q

4p rule

A

pulmo, pancreas, prostate, placenta

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13
Q

lysis of thrombus-small pariental thrombi in circulating blood

A

-fibrinolysis act to dissolve or lyse thombus
-most common and most favorable

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14
Q

organiszation of thrombus

A
  • organization in fibrotic tissue-small thrombi in tissues wiht abundant collateral
  • parielta –>resorbed by macrophages–>non specific grnaukltion tissue–<fibrotic tissue and sacr

recanalization of thrombus-large, obturative¨
- non specific granulation tissue will penetrate thrombus–>vv fuse and dilate–>penetrattin by multiple vv and reneaval partially of blood flow
- dont chnage into scar

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15
Q

purified thrombus

A
  • internal dissolution of large thrombi with limited adherence to vv wall (intracardial thrombi)
  • dissolved or chnaged into fluid material with proteins and greu color-pus
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16
Q

embolsim

A

plugging of vv lumen by insoluble material

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17
Q

thrmobit embolization

A
  1. sudden, massice–>acute right heart failure
  2. succesive->chronic right heart failure
    - smaller and plug vv subsequently
    -silent
    -intermittent cough, expectoration of blood formlung or small fine pain in chest

both lead to detah but succesive takes time

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18
Q

fat embolization

A

-release of fat droplets form subcutaneous adipose tissue by trauma of from boone marrow by bone fractures

19
Q

air embolization

A
  • spreafing of air into veins by operations or traumas
    -during TG operaiton

caissons disease/diver disease:
- perosn is exposed to rapid decrease in pressure typically in divers ascending to quickly
-brain embolism

20
Q

subcellular embolization

A

-plugging of vv by cellular debris form atherosclerotic plates, tumors
- material from necrotic dead tissue, infarction, malignant tumor or atherosclarotic plaques

21
Q

porogenous metastasis

A

spreading of pathologic proces in hollowed organs by implatation, intramural spreading or direct contact of walls
-sprading thorugh body cavities

22
Q

phlebitis

A
  • happens in veins
  1. thrombophlebitis: inflammation of superficial veins
    - venus varices
  2. phlebothrombosis: deep venous
23
Q

steal syndorme

A

-outflow of blood to better permeable vv according pressure difference in vv
like arteriovenous aneursm-pathological connection btw arterial and venous vv
- peripheral artery will lack of blood

24
Q

manifestation of local circualtory disorders

A
  1. hyperemia
  2. ischemia
  3. bleeding
25
Q

hyperemia

A

-increased BF thorugh tissue

  1. arterial-dilatttion of arterial sphincter and opening of reverse vessles
    - physiological
    - tissue gets mire blood by dialtion of arterioles
    - muscles in physical act or HIT after food intake
  2. peristaltic hypermia
    - reflec and by local mediators induced hyperemia of tissue caused by tissue injury (inflammaton)
    -increased permeability of vv–>spreading of fluid and plasma proteins to interstitium, later spreading of blood cells
    -apthological: stasis in capp netowk
  3. venous hyperemia
    -obturation (thromotic, compressice) of veins draining the tissue
    - blocage of venous outflow
    - when v blood cant get outside circulatory bed–>acc and become hypermeia
    -hemorrhagic infarction
26
Q

ischemia

A

-regressive tissue change caused by insufficient by blood supply
-atrophy, dyrstrohy and necrosis

27
Q

factors influencing ischmie

A
  1. type of tissue(oxy need)
    - soft tissue, skin, CT and bone=RESISTANT OT ISCHEMIA
  2. functional act of tissue
  3. anatomy of vascualr netowk
    -heart and brain->NO ANASTOMOSIS
28
Q

infarction

A

most severe form of ischemia
1,arterial induced tissue ischemia causing necrosis
- lack of arterial blood

  1. plugging of vv by thrmobus of embolus
  2. distinct stenosis of artery+increased tissue need for blood and ocy
  3. serous hypotension of systemic circulation (shock inafrction- watershed areas-brain, LI, cardiac muscle)
29
Q

white infarction

A
  • coagulative necrosis with mninmal reflux of blood form surronding vital tissue (anemic infarction)
    -arterial induced
30
Q

red infaction

A

-spleen, lungs

31
Q

bleeding

A

-spreding of blood fomr vv into tissues /body cavities

32
Q

bleeding per rhexim

A

-local disruption of vv continutiy(ruptur/trauma to vv)
-rupture of aneurysm of atherosclerotic plate
-acute local inhur of vv integrity
- focal blleding, extensive or lethal
-easly stopped bc local

33
Q

bleeding per diabrosim

A

-diffuse injudry of vv wall infiltartive process(tumor, inflamamiton)
- like inflamamiton or tumor

34
Q
A
35
Q

bleeding per diapedeism

A

-spreasifin of blood cells outside the vessle without disruption of vv wall continuity(seroious hyperemia, shock, toxemia)

36
Q

petechiae bleeding

A

small, spotty, local
-very small dots on organs or tissues

37
Q

purpura

A

-numeroys and more extensive spotty bleeding

-larger but not fused together
-if fused.>ecchymoses–>suffisiones

38
Q

site of bledding

A

epistaxis: form nose,

hematemesis: vomiting fresh blood

hemoptoe: expectoraiton of food

hemoptysiss: expectoration of sputum which contian blood

gastro/enterorrhagia/melaena:

heamturia: blood in urine

39
Q

uterine bleeding

A
  1. hypermenorrhea: voluminor mentrual bleeding, time is normal
  2. mennorhagia: extended time, amount is normal
  3. emtorrhagia: uterine bleedding wihtout connection wiht menstrual cycle
40
Q

accoridng to presence-where oyu find blood

A

hemothroax-pleural caity

hemopericardium-pericardium

hemoperitoneum-abdominal cavity

hemarhos-bleeding into joints

apolexia- destructuive arterial bleeding-kidney and brian

hemeocephalus-brian chambers

41
Q

bleeding conditions

A
  1. thrombocytopenia
  2. coagukaopathies
  3. vasculopathoes
42
Q

thrombocytopenia-decreased nr of thromobocytes

A

-infection, drug, tumors
- not massice bleeding
-HYPERSPLENISM

IDIOPATHIC THROMBOCYTOPENIA PURUPURA(ITP)
-antibodies again thrmobocytes, unknow

IMMUNO-THROMBOCYTOPENIA
- generalized infla (SLE), lymphomas, HIV, durg injury, heparin induced

43
Q

coagulotpathies

A

INBORN-hemophilias
- A: deficiency of 8: C
- B: 9
-defiecnit of von willebranf factor

ACQUIRED:
-disorder of formaiton of coaguaktion facotrs in liver
-lack of vit K: malabsroption syndorme, ATB tehrapy

DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)-masisve act of coagualtion cascade with formaiton of microthrombi–>consumption of coagulative factors–>hemorrhagic diathesis+injury of microcirculation–>injury of organs (kidney, lung)

44
Q

vascullopathies (purpuras)

A

-disturbance of vv wall structure causing bleeding

INBIRN: herediatry telangiectasias
AQUIRED: lack of vit c (moller -barlowova disease) (SCURVY)
- INADEQUATE COLLAGEN SYNTHESIS
- ADULT-SCRUVY
- CHILDREN-GROWTH RETADETION

SENILE PURPURA.IMMUNE REACITON
-eldrelry
- insufficnet coll prod or not good quality
- wrinkles, vv are very fine, easy bleeding bc of alteraiotn to ewall

HENOCH -SCHONLEIN PURPURA
-immune reaction 3 type-very sevre
-deposition of antigen-antibody complexes in subendothelial space–>act of comlement
- in children after viral infectio of upper resp tract-meningococcal infection

PATHOANA (13 decks)

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