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PATHOANA > Global circulatory disroder: causes and manifestations > Flashcards

Global circulatory disroder: causes and manifestations Flashcards

1
Q

disorders affecting endocardium

A
  1. thrombosis
  2. endocarditis
    - blood clot including bacteria effect in cardiac lining
  3. disorders of heart valves
    -stenosis and insufficiency
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2
Q

disorders affecting myocardium

A
  1. chronic ischemic heart disease(atherosclerosis)
  2. heart infarction-most sevre of ischmia
  3. myocarditis-rheumatoid myocarditis
  4. cardiomyopathies
    -unkowwn
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3
Q

disorders affecting pericardium

A
  1. Inflammatory exsudate
    - acc of pluid in pericardium
    -ventricle cant dilate during diastole–>decreased CO
    -after inflammaion–>exsudate in reabsorbed–>ahesions in pericardium–>cardiac failure
  2. Tamponade
    - fluid in pericardium–very voluminous–>compress cardiac muscle
    - bleeding from aorta rupture
    - compression of myocardial muscle–>no movemnet–>diastolic cardiac failure
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4
Q

disorders of heart beat

A
  1. disturbanves of peripheral blood ions
    -K(POTASSIUM INHIBITION) and Ca(RIGOR MORTIS)
  2. diseases of myocardium
    - conductive system
    - blockage of spread impulses
  3. disease of conductive system of heatt
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5
Q

congenital malformaiton of heart: without shunt

A

-25%
-less ocmmon
-no micture of blood form small and large
balcgae of this blood leakage
- pulmonary stenosis, aortal stenosis, contarction of aorta

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6
Q

ccoarction/contraction of aort

A

-distal form ducts arteriosus (post ductal-adult or proximal (preductal/infantile

ADULT
- hypertension in upper extremetises
-weak pulse and decreased BP in lower
-claudication and coldness

INFANTILE:
-right ventricular hypertorphy, left is samlles
-cyanosis in lower hald
, upper is unaffected

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7
Q

aortic stenosis and atresi

A

-bicuspid valve

-valcular, subvalvular and supravalvular steanosis
-pressure hypertrophy of left, dialtion of aortic root

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8
Q

pulmonary stenosis

A

-no cyanosis
- fusion of cusps of pulmonary valve–>obstruction
-dilation of pulmonary trunk
-atresia: no communication btw right heart and lungd–<blood form right go thorugh intramitral septal defect, … PDA

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9
Q

congenital disorders-with shunt

A

-75%
- more commen
-from systemic(left) to pulmoanry(right)

Left-right shunt -55%
- bc systemic BP is higer
- septal defects
-ductus arteriosus perisstent

right-left shunt-20%¨
- increase pulmonary pressure
- with reduced pulmonary perfusion: tetralogy of fallot
- increased p.perfusion: transporition of large veessles

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10
Q

VSD-ventricular septal defect

A

increased pulmonary flow
^volume of left=hypertrophy
pressure hypertrophy of right

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11
Q

ASD-atrial septal defect

A

-pulmonary hypertension–>late cyanotic heart disease and rihgt heart failure
- fossa ovalisa/ostium secundum

right volume hypertrophy
-volume atrophy of left

coarctioon of aorta, VSD, pulmonary or aortic stenosis

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12
Q

tetralogy of fallot

A
  • reduced pulmonary perfusion

-gretaer pulmonary stenosis, VSD mild–>^resistance of outflow form rihgt

  • right pressure hyperthrophy
    -smalle tricuspid
    -smaller left side
    -enlarged aortic orifice
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13
Q

transposition of large vv

A

^pulmonary perfusion

  • ^pulmonary flow and ^volume of left
    -no cyanosis
    -^pressure hypertorphy of right
    -volume hypertrophy of left
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14
Q

disorders affecting small/pulmonary circulaiton (BP)

A
  1. pulmonary hypertension
    ACUTE:
    -sudden increase of pulmonary BP by massive embolism of lung
    - lead to acute load on cardiac act and acute cardiac failyre(heart to weak to comrpess blood fomr high pressue)
    CHRONIC:
    a. vasoconstriciton of pulmonary arteries by hypoxia
    - by constriciton of pulmanry arteries
    -hypertension of lungs
    -chronic bronchitis and sleep apnea
    b. vasculitis, collagenosis, chronic interstitial pneumonias
    - inflamamition of CT btw alveoli aka interstitium
    - no place form blood–>leave lung
    -destruction of pulmonary vv
    c. succesive or repeated lung embolism
    d. primary pulmonary hypertension- unkown and rare
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15
Q

disroders affecting the large/systemic circualtion- chronic systtemic hypertensions

A

-more than 140/90

  1. essential hyoertenion
    - most common in miidle and elderly
    -unkown
    - brain center is affected
    - risk factors: body consittution, familair predisposiotion, diet, stress
  2. seconadry hypertension
    a. reno-aprenchymatous hypertension-destruction of kidney parnechyme
    -acc of salt and watter–>chronic hypertension

b. reno-vascualr hypertension-stenosis/blocakge of renal artery
-act of RAA systemt

c. endocrine hypertension-pheochromocytoma, cushings syndrome, conns syndrome, androgenital syndrome,acromegaly

d. hypertension in preganncy-preclampsy/eclampsy

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16
Q

disroders affecting the large/systemic circualtion- acute systemic hypertension

A
  1. pheochromocytoma
  2. ## hypertension crisis
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17
Q

disroders affecting the large/systemic circualtion- chrincic systemic HYPOTENSION

A
  • unkown and rare
  • young female wiht reduced BP
  • utretaed yntil symptomatic
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18
Q

disroders affecting the large/systemic circualtion-acute systemic hypotension

A

collapse and shock

-collapse bening

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19
Q

collapse

A

-acute systemic hypotenison
-imbalance btw effective BV and volume of vv
- not sufficicnet blood volume to filll the vv
- maybe acc or sudden dialtion, but no blood is lost

  1. acute failure of sympatico adrenergic system–<acc of blood in venous system of legs
    2.increased sti of paarsymoptetic
    -irritation of peripherl brnaches of vagal nerve-plexus solaris, testes, ear, pressure on bulb of eye
  2. emotions, stress, fear , pain
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20
Q

shock

A

-acute systemic hypotension
- alteration of vital fucntion of body beacuse of sudden reduction of CO or effectivve circulaiton BV
-

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21
Q

classificaiton of shock

A
  1. cardiogenic shock
    - alteration of ehart as pump–>dcearse BP
    -myocardial infarction
  2. hypovolemic shock
    -bleeding, bruning, dehydratin
  3. distributive shock
    - losos of fluid form vv into tissues
    -subtypes:
    a. septic shock-generalized inflamamiton of blood
    - dialtion of all peripheral blood system and injury of vv wall causes fluid lead

b. anaphyalctic shock
- acute allergic situation–>hsitmine–>acute dialtion–>acute systemic hypotension–<shock aka lethal

c. neurogenic shock
- lesion of spinal cord
- symp ferdig–>acute dilation of vv

d. vasogenic shock
- sibstances ot dialte
- work more

22
Q

compensatory reactions of shock

A
  1. centralization of blood: sti of symp and prod of catecholamines->cont of peripheral arterioles and venules
    - ORGNAS OF CENTRALIZAITION: BRAIN-HEART AND SUPRARENAL GLANDS
  2. prod of ADH
  3. hypoperfusion of the kidney
23
Q

stages of shock

A
  1. non progressive stage(revrsible)
    - BP is mainatin
    a. initial ohase(reversinle)
    b . compensatory pahse
  2. progressive stage-mer apthomechanisms of blind cycle
    c. progressive phase
    - decrease of BP
    - failure of compensatur mechnism
    - irrvesibe
    d. terminal phse

-multiorgan failure

24
Q

morphology of lunsg

A

-dont suffer from ischemia
-oxy still present, no ischemia
-affect mostly vv and alveolar lining
-distruvances of small capillary bed by formaiton of thrombi, edema of the interstitium becuse of fluid leakage outside capillary, bleeding, and protiens will accumulate in alveoli
-lagre, hevy, red in color, hemorrhagic edematous fluid
-edema with erythrocytes

later injury of oneumocytes –>collapse of alveoli

25
Q

morphology of kindey in shock

A
  • severly hypoperfused
  • acute tubular necrosis
  • pale cortex, red medulla
    -interstitial edeam
    -hyaline thrombi
    -coarse casts in tubulus
26
Q

morphology of GIT in shock

A
  • ischmic insjury of pancreas–>pnacreatitis

-pancreatitis and duodenitis
-stress ulcers
-hemorrhagic infarcciton of intesitne
-mucosal necrosis–>bleeding, thobosis in micor

27
Q

morphology of heart i hsock

A

-subendocardial bleeding
-necrosis of myocytes
.-microinfarctions
-loss of glycogen
-acc of lipids

28
Q

morphology of liver in shoc

A

-centrolubular necross(around central vein)
-blood leaks into lobules form periphery to center-so cneter has low oxy
-shock of center of lobues is most affcetd by sichmia
- vasculisation and steatosis of hepatocytes

29
Q

morpholgy of shock in brain

A

-lesions are rare
-microscopic hemorrhages
-watershed necrosis

30
Q

disroder of blood volume and composition: polyglobuly

A
  • increased volume of blood -volume overload of heart
  • heart work more–>ecxausted
  • thick blood–>vanskelig of leak

^BV AND BP

31
Q

disroder of blood volume and composition: anemia

A

-reduced production of eryhtrocytes, increased destruction of erythrocytes, pathologic distrubution fo erythrocytes
- tissue are suffering form ischemia so blood has to work more for pumping–>exhausted

32
Q

disroder of blood volume and composition: hydraemia

A

increased amount of fluid in blood-întake of fluid per os/by infusions

33
Q

disroder of blood volume and composition: hypohydraemia(dehydration)

A

^viscosity of blood–>reduction of BF

  • burning, git infection or starving
34
Q

disroder of blood volume and composition: hyperproteeinemia

A

-multiple myeloma-^viscosity of blood, neuropathy

35
Q

disroder of blood volume and composition: hypoproteinemia

A

-loss of proteins/reduced synthetizaition–>decreased oncotic pressure of blood (edemas)

-

36
Q

heart failure with increased CO

A

anemia, hypohydraemia, AV shunts(blood can regurgiatet)

37
Q

failure of right heart

A

pulmonary circulaiton

38
Q

failure of left

A

systemic

39
Q

forward failure

A

-tissyes are getting altered bc they dont get enough blood
- lack of blood

40
Q

backward failure

A

-blood is stying in herat
-stassi of blood before the heart

41
Q

acute pulmonary hypertension or ischemia

A

dialtion-acute overload of heart without time to adaption.

only dilate, larger with thin walls

42
Q

chronic pulmnary hypertension

A

hyperthrophy of rigth

43
Q

cocentric hypertrophy

A

-chronic pressure overload of heart
- cardiomyocytes hyperthrophy
. LEFT HAS THICKER WALL

44
Q

eccentric hypertrophy

A

-chronic volume overload of heart
-anemia, hydrahydration, regurgation

  • wall gets thicke rand VOLUME of chmaber is bigger

hyperthrophy with fdilation

45
Q

cyanosis

A

-deoxygenated hemoglbbulin >50g/l
-increased BV
-decreased saturation of blood

  • cyanosis by acc of deoxygented hemoglobulin
  • blood stay invv..>looses oxy–>when venous blood decreases stauration beneath 80%—>deoxy blood increase –>cyanosis

-

46
Q

cyanotic induration of organs(chronic failure)

A
  • chronic stasis of blood-backward failure
  • parenchymatous organs
  1. venous congestion with chronic ischemia–>cyanosis–<regressive chnages
    - veins full of blood
    - oxy absorbed–>deoxy blood–>cyanosis
  2. chronic edema–>intersttial fibrosis–>hardening of organs
    - larger and heavier, pruple, harder to touch
    - NUTMEG LIVER AND SPLEEN
47
Q

Chronic venostasis of lungs (brown induration)

A
  • ventilaed
    -edema–>fibrotizaiton–>induration
  • some small hemorrhages–>when absorbed–>remain hemosiderin in tissue–>brown color
48
Q

forward failure of left

A

-systemic lack blood
TIREDNESS , FATIGUE, EXHAUSTION, weakness
- disturbances of brian fucniton

49
Q

backward failure of left

A
  • stasis before left chmaber
    -blood in lungs
    DYSPNOE(edema in lungs), ORTHOPNOE
50
Q

forwrd failure of heart

A

=forward failure of left hear

51
Q

backward failure of right heart

A

-stasis of blood in WHOLE BODY
- congestion of veins-neck veins and varices of leg veins
-congestion of GIT: loss of appetitte, tympanities
- congestion i kidney(proteinuria), liver (hepatomegaly, nut meg liver) and spkeen–>cyanosis
- edema +increase of weight-firstly in legs then body (anasarc)
- pleural exsudate: acc where there is spce

52
Q

sign common for failure of right and left

A

Nykturia-night urination

act of sympaticus
-^HR
, arryhtmias
tachypneoa
codl and wet skin

PATHOANA (13 decks)

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