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PATHOANA 1 > local circulatory disorders > Flashcards

local circulatory disorders Flashcards

(44 cards)

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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

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A

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

19
Q

air embolization

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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

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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

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A

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

22
Q

phlebitis

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

steal syndorme

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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

Study These Flashcards
A
  1. hyperemia
  2. ischemia
  3. bleeding
25
hyperemia
-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
ischemia
-regressive tissue change caused by insufficient by blood supply -atrophy, dyrstrohy and necrosis
27
factors influencing ischmie
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
infarction
most severe form of ischemia 1,arterial induced tissue ischemia causing necrosis - lack of arterial blood 2. plugging of vv by thrmobus of embolus 3. distinct stenosis of artery+increased tissue need for blood and ocy 4. serous hypotension of systemic circulation (shock inafrction- watershed areas-brain, LI, cardiac muscle)
29
white infarction
- coagulative necrosis with mninmal reflux of blood form surronding vital tissue (anemic infarction) -arterial induced
30
red infaction
-spleen, lungs
31
bleeding
-spreding of blood fomr vv into tissues /body cavities
32
bleeding per rhexim
-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
bleeding per diabrosim
-diffuse injudry of vv wall infiltartive process(tumor, inflamamiton) - like inflamamiton or tumor
34
35
bleeding per diapedeism
-spreasifin of blood cells outside the vessle without disruption of vv wall continuity(seroious hyperemia, shock, toxemia)
36
petechiae bleeding
small, spotty, local -very small dots on organs or tissues
37
purpura
-numeroys and more extensive spotty bleeding -larger but not fused together -if fused.>ecchymoses-->suffisiones
38
site of bledding
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
uterine bleeding
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
accoridng to presence-where oyu find blood
hemothroax-pleural caity hemopericardium-pericardium hemoperitoneum-abdominal cavity hemarhos-bleeding into joints apolexia- destructuive arterial bleeding-kidney and brian hemeocephalus-brian chambers
41
bleeding conditions
1. thrombocytopenia 2. coagukaopathies 3. vasculopathoes
42
thrombocytopenia-decreased nr of thromobocytes
-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
coagulotpathies
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
vascullopathies (purpuras)
-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 1 (13 decks)

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