Global circulatory disroder: causes and manifestations Flashcards
disorders affecting endocardium
- thrombosis
- endocarditis
- blood clot including bacteria effect in cardiac lining - disorders of heart valves
-stenosis and insufficiency
disorders affecting myocardium
- chronic ischemic heart disease(atherosclerosis)
- heart infarction-most sevre of ischmia
- myocarditis-rheumatoid myocarditis
- cardiomyopathies
-unkowwn
disorders affecting pericardium
- Inflammatory exsudate
- acc of pluid in pericardium
-ventricle cant dilate during diastole–>decreased CO
-after inflammaion–>exsudate in reabsorbed–>ahesions in pericardium–>cardiac failure - Tamponade
- fluid in pericardium–very voluminous–>compress cardiac muscle
- bleeding from aorta rupture
- compression of myocardial muscle–>no movemnet–>diastolic cardiac failure
disorders of heart beat
- disturbanves of peripheral blood ions
-K(POTASSIUM INHIBITION) and Ca(RIGOR MORTIS) - diseases of myocardium
- conductive system
- blockage of spread impulses - disease of conductive system of heatt
congenital malformaiton of heart: without shunt
-25%
-less ocmmon
-no micture of blood form small and large
balcgae of this blood leakage
- pulmonary stenosis, aortal stenosis, contarction of aorta
ccoarction/contraction of aort
-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
aortic stenosis and atresi
-bicuspid valve
-valcular, subvalvular and supravalvular steanosis
-pressure hypertrophy of left, dialtion of aortic root
pulmonary stenosis
-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
congenital disorders-with shunt
-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
VSD-ventricular septal defect
increased pulmonary flow
^volume of left=hypertrophy
pressure hypertrophy of right
ASD-atrial septal defect
-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
tetralogy of fallot
- reduced pulmonary perfusion
-gretaer pulmonary stenosis, VSD mild–>^resistance of outflow form rihgt
- right pressure hyperthrophy
-smalle tricuspid
-smaller left side
-enlarged aortic orifice
transposition of large vv
^pulmonary perfusion
- ^pulmonary flow and ^volume of left
-no cyanosis
-^pressure hypertorphy of right
-volume hypertrophy of left
disorders affecting small/pulmonary circulaiton (BP)
- 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
disroders affecting the large/systemic circualtion- chronic systtemic hypertensions
-more than 140/90
- essential hyoertenion
- most common in miidle and elderly
-unkown
- brain center is affected
- risk factors: body consittution, familair predisposiotion, diet, stress - 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
disroders affecting the large/systemic circualtion- acute systemic hypertension
- pheochromocytoma
- ## hypertension crisis
disroders affecting the large/systemic circualtion- chrincic systemic HYPOTENSION
- unkown and rare
- young female wiht reduced BP
- utretaed yntil symptomatic
disroders affecting the large/systemic circualtion-acute systemic hypotension
collapse and shock
-collapse bening
collapse
-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
- 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 - emotions, stress, fear , pain
shock
-acute systemic hypotension
- alteration of vital fucntion of body beacuse of sudden reduction of CO or effectivve circulaiton BV
-
classificaiton of shock
- cardiogenic shock
- alteration of ehart as pump–>dcearse BP
-myocardial infarction - hypovolemic shock
-bleeding, bruning, dehydratin - 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
compensatory reactions of shock
- centralization of blood: sti of symp and prod of catecholamines->cont of peripheral arterioles and venules
- ORGNAS OF CENTRALIZAITION: BRAIN-HEART AND SUPRARENAL GLANDS - prod of ADH
- hypoperfusion of the kidney
stages of shock
- non progressive stage(revrsible)
- BP is mainatin
a. initial ohase(reversinle)
b . compensatory pahse - progressive stage-mer apthomechanisms of blind cycle
c. progressive phase
- decrease of BP
- failure of compensatur mechnism
- irrvesibe
d. terminal phse
-multiorgan failure
morphology of lunsg
-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
morphology of kindey in shock
- severly hypoperfused
- acute tubular necrosis
- pale cortex, red medulla
-interstitial edeam
-hyaline thrombi
-coarse casts in tubulus
morphology of GIT in shock
- ischmic insjury of pancreas–>pnacreatitis
-pancreatitis and duodenitis
-stress ulcers
-hemorrhagic infarcciton of intesitne
-mucosal necrosis–>bleeding, thobosis in micor
morphology of heart i hsock
-subendocardial bleeding
-necrosis of myocytes
.-microinfarctions
-loss of glycogen
-acc of lipids
morphology of liver in shoc
-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
morpholgy of shock in brain
-lesions are rare
-microscopic hemorrhages
-watershed necrosis
disroder of blood volume and composition: polyglobuly
- increased volume of blood -volume overload of heart
- heart work more–>ecxausted
- thick blood–>vanskelig of leak
^BV AND BP
disroder of blood volume and composition: anemia
-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
disroder of blood volume and composition: hydraemia
increased amount of fluid in blood-întake of fluid per os/by infusions
disroder of blood volume and composition: hypohydraemia(dehydration)
^viscosity of blood–>reduction of BF
- burning, git infection or starving
disroder of blood volume and composition: hyperproteeinemia
-multiple myeloma-^viscosity of blood, neuropathy
disroder of blood volume and composition: hypoproteinemia
-loss of proteins/reduced synthetizaition–>decreased oncotic pressure of blood (edemas)
-
heart failure with increased CO
anemia, hypohydraemia, AV shunts(blood can regurgiatet)
failure of right heart
pulmonary circulaiton
failure of left
systemic
forward failure
-tissyes are getting altered bc they dont get enough blood
- lack of blood
backward failure
-blood is stying in herat
-stassi of blood before the heart
acute pulmonary hypertension or ischemia
dialtion-acute overload of heart without time to adaption.
only dilate, larger with thin walls
chronic pulmnary hypertension
hyperthrophy of rigth
cocentric hypertrophy
-chronic pressure overload of heart
- cardiomyocytes hyperthrophy
. LEFT HAS THICKER WALL
eccentric hypertrophy
-chronic volume overload of heart
-anemia, hydrahydration, regurgation
- wall gets thicke rand VOLUME of chmaber is bigger
hyperthrophy with fdilation
cyanosis
-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
-
cyanotic induration of organs(chronic failure)
- chronic stasis of blood-backward failure
- parenchymatous organs
- venous congestion with chronic ischemia–>cyanosis–<regressive chnages
- veins full of blood
- oxy absorbed–>deoxy blood–>cyanosis - chronic edema–>intersttial fibrosis–>hardening of organs
- larger and heavier, pruple, harder to touch
- NUTMEG LIVER AND SPLEEN
Chronic venostasis of lungs (brown induration)
- ventilaed
-edema–>fibrotizaiton–>induration - some small hemorrhages–>when absorbed–>remain hemosiderin in tissue–>brown color
forward failure of left
-systemic lack blood
TIREDNESS , FATIGUE, EXHAUSTION, weakness
- disturbances of brian fucniton
backward failure of left
- stasis before left chmaber
-blood in lungs
DYSPNOE(edema in lungs), ORTHOPNOE
forwrd failure of heart
=forward failure of left hear
backward failure of right heart
-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
sign common for failure of right and left
Nykturia-night urination
act of sympaticus
-^HR
, arryhtmias
tachypneoa
codl and wet skin
