Hemodynamics cumulative Flashcards
Differentiate thrombus from clot (in general )
Clot:-Platelets not involved.
- Occurs outside vessel (test tube, hematoma) or inside (Postmortem)
- Red
- Gelatinous
- Not attached to the vessel wall
- No lines of Zah
Features of arterial thrombus (gross and histological)
- pale infarct
- Microscopy - lines of Zahn • Alternate pale and dark lines • Light – platelets and fibrin • Dark - RBCs
FAtes of thrombus
- progression
- formation of an embolus
- resolution/ dissolution
- organization and recanalization
Sites of thrombosis – arterial
Heart (mural) • Aorta (on atherosclerotic plaque) • Aneurysm (mural) • In other arteries (occlusive) • Coronaries • Carotids, cerebral • Femoral • Mesenteric
Formation of venous thrombosis
Takes the shape of vessels in which it forms • Redder than arterial thrombus • Superficial veins of legs (varicosities)- rarely embolize • Deep veins of legs (90%) • Deep calf veins- (at or above the knee) femoral, popliteal, iliac
clinical signs and symptoms of venous thrombosis
- • Asymptomatic in 50%- due to collaterals
- but deep veins have a large risk to embolise as compared to superficial veins (emobolism tends to go to pulmonary circulation)
• Trousseau’s Syndrome
unexplained thrombophlebitis (thrombus associated edema ) Underlying cause could be pancreatic tumor or any coagulatin acitivation tumor- release of procoagulant)
affect of an arterial thrombus
• Acute - Infarct • Slow - atrophy, fibrosis • Heart - systemic emboli
Effect of a venous thrombus
• Edema, congestion • Rarely- the pressure of edema leads to secondary block of the artery leading to infarction • Embolization to lungs
define embolism
Occlusion of a part of vascular tree by a mass (solid, liquid, gas) that is carried by the blood to a site distant from its point of origin to the site where it becomes impacted
what is the most common site of an embolism and what is most clinically significant emobolis
Statistically the commonest origin is from the deep leg veins and reaches the lungs but most of these are clinically silent -The commonest clinically significant thromboemboli arise from the heart (80%) Embolize to the lower extremities (75%), and brain (10%
Pulmonary Thromboembolism
The commonest origin is from the deep leg veins and reaches the lungs but most of these are clinically silent
- The commonest origin is from the deep leg veins and reaches the lungs but most of these are clinically silen
Pulmonary thromboembolism
• Massive • Sudden obstruction of 60% of pulmonary vasculature; sudden death, no time to develop infarction • Major • Multiple medium sized vessels occluded – dyspnea, pain • Infarction only in 10% because of collateral circulation by bronchial arteries • Minor • Small vessels obstructed, get lysed, remain asymptomatic
(Recurrent pulmonary emboli – pulmonary hypertension
MAJOR is the only time you see an infarction
most likely site of origin in pulmonary thromboembolis
- in the deep veins of legs
Most likely site of systemic thromboembolism
- mural thrombus
- paradoxycal thrombus (carried from the venous side to the arterial side -atherosclerotic plaque
effect of a thrmboemobolism
Effect : embolize to the lower extremities (75%) and brain (10%) • they block an end artery leading to infarction
etiology Fat embolus
Trauma to bone, subcutaneous tissue, burns • Fat globules enter the circulation by rupture of the marrow vascular sinusoids or rupture of venules
pathogensis of fat embolism
• Mechanical blockage - Globules enlarge in circulation, platelets adhere • Biochemical injury – Free fatty acids are released from adipose tissue in the circulation and are toxic to endothelial cells – DIC, clogged pulmonary and systemic capillaries
Clinical features of Fat embolism
fat embolism syndrome (fat embolism syndrome characterized by pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, and a diffuse petechial rash )
- s appear 1 to 3 days after injury as the sudden onset of tachypnea, dyspnea, tachycardia, irritability, and restlessness, which can progress rapidly to delirium or coma
fat embolism syndrome features
fat embolism syndrome characterized by pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, and a diffuse petechial rash
lab investigations of FAt embolism
Sudan 4 black stains. osmium acid and oil red
- fat glbules in sputum and urine,
- No tested treatment, just keep them hemodynamically stable and maintain oxygenation
Fatal in about 10% of cases
Prognosis of fat embolism
No tested treatment, just keep them hemodynamically stable and maintain oxygenation
Fatal in about 10% of cases
FAt embolism staining technique requirements
frozen section of tissues since routine processing through alcohol will dissolve the fat
Air embolism etiopathogensis
• Air may be introduced into the venous circulation through neck wounds, thoracocentesis, Cut in internal jugular vein, and hemodialysis • Child birth, abortion • 150 ml of air causes death • Air bubbles tend to coalesce and physically obstruct the flow of blood in the right ventricle, lungs, and the brain
difference between fat embolism and bone marrow embolism
fat embolism mostly due to long bone trauma -yellow marrow trauma
Bone marrow embolism –due to CPR /red marrow trauma
Rising to quickly to 10 m height under water –> leads to ?
Nitrogen embolism
The bends, Caisson’s disease aka ?
nitrogen embolism
nitrogen embolism pathoethiology
• Deep sea diving without using Caisson’s chamber (exposed to high pressure) • Scuba diving (deeper than 10 meters) • O2, N2 dissolve in high amounts in blood and tissues due to high pressure • Sudden resurfacing releases N2, O2 • O2 reabsorbed, N2 bubbles out – ruptures tissues and in vessels it forms emboli • Platelets adhere to N2 – form secondary thrombi and aggravate the ischemia • Brain (death), muscles, joints (bends), lungs – edema, hemorrhage (chokes
clinical features of nitrogen embolism
Brain (death), muscles, joints (bends), lungs – edema, hemorrhage (chokes)
caissons disease
chronic form of presistant gas emboli in bones
Necrosis in femur, tibia, humeru
Treatmen of nitrogen embolism
Pressure chamber – slow decompression
bone marrow embolism
• Seen in small pulmonary vessels after vigorous cardiac resuscitation • Incidental finding at autopsy • Not a cause of death
amniotic fluid embolism etiolgy
- Pregannt young females who recently gave birth
pathogensis of amniotic fluid embolism
The underlying cause is the entry of amniotic fluid (and its contents) into the maternal circulation via tears in the placental membranes and/or uterine vein rupture. Histologic analysis shows squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tracts in the maternal pulmonary microcirculation
what is found in the amniotic fluid embolism
Histologic analysis shows squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tracts in the maternal pulmonary microcirculation
clinical features of amnitoic fluid
-arise after labour (immediate or after few hours) - characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma.
prognosis of amniotic fluid embolism
usually fatal, survivors have permanent neurological damage
lab finding of amniotic fluid embolism
↓platelets & clotting factors ↑ PT/PTT - DIC -Diffuse alveolar damage -pulmonary edema
Atherosclerotic emboli pathogensis
Involves small dislodged fragments of atherosclerosis from main renal artery in to smaller intrarenal branches producing small infarcts
clinical symptoms of atherosclerotic emboli
no clinical symptoms
-Rarely- infarction- eg gut- bleeding, braintransient ischemia, blind spots e
what is a infarction in a gross image called ? what is histopathological name ?
- gross–> infarction
- histo—>necrosis
causes of infarction ?
Thrombosis (99)% of the time
- • Hemorrhage in atherosclerotic plaque • Torsion of blood vessels • Venous or arterial or both • Hypoperfusion • Secondary to MI • Severe hemorrhage • Septic shock • Vasculitis • Rupture • thrombosis
White infarct pathogenesis
- pale looking
- arterial block
- organ doesnt get the blood looks pale (no bleeding)
- happens in solid organs that then undergo coagulative necrosis
Red infarct pathogenesis
Large amount of bleeding into the organ • Soft organs with tissue spaces - lungs • Tissues with dual blood supply (lungs and small intestine)bleeding from anastamosing vessels • Venous infarcts (congestion followed by infarction) • When flow is reestablished after arterial occlusion and necrosis also known as re perfusion injury
repurfusion injury
a blocked or infarcted area suddenly receives blood –> leads to more injury
repurfusion injury
a blocked or infarcted area suddenly receives blood –> leads to more injury due to sudden increase of oxygen
what leads to the brwon ring formation around the infarcted organ
hemosidderin accumulation from break down of RBC
where do the infarction in organs most likely occur
occlusion of the vessel occurs at the apex or that periphery of the organ forming the base
Factors that influence the development of infarctio
• Nature of the vascular supply • Rate of development of occlusion • Sudden is dangerous and leads to infarction, slow occlusion leads to ischemia, fibrosis • Tissue vulnerability to hypoxia • Brain versus skeletal muscle, bone • Oxygen carrying capacity of blood • Anemia
what adaptation leads to less infarct
dual blood supply /anastomosis /collateral circulation
what type of organs undergo rapid infarct
-with single venous supply (Testis or ovaries ???
VEnous thrombosis –>
leads to congestion
Cerebral infarction 12 hrs in
• Starts as coagulation necrosis • Softening, color changes • May have hemorrhage due to reperfusion
cerebral infarction 48 hrs in
Edema of the infarcted region, acts like a intracerebral mass causing raised intracranial pressure • Microglia engulf necrotic material, Gitter cells
Myocardial infarction
Coronary atherosclerosis with superimposed thrombosis • Left anterior descending is the commonest involved • Coagulation necrosis • Initially blotchy, later pale scar tissue • Cardiac enzymes raised in serum • Presents with severe chest pain (angina)
Edema due to ( causes) ?
Heart failure
- reduced oncotic pressure (liver)
- nutrition deficiency
- kidney dysfunction
- Na retention
- lympathic obstruction
- membrane permeability
pathway of fluid from tissue spacce to heart
Lymphatics–> thoric duct –> L subclavian vein–> superior vena cava –> heart
anascara and ascites definition
anascara –> genralized severe accumulation of fluid (all over the body
Ascites –> fluid accumulation only in the peritonieum
Chest pain, dyspnea, increased tropnin level and inverted T –> points to what –> leading to what ?
MI (congestive heart failure leading to edema due to increased hydrostatic pressure
increased hydrostatic pressure due to
Impaired venous return • Congestive heart failure • Venous obstruction or compression • Thrombosis • External pressure (e.g. tumor) • Hypervolemia • Sodium retention (renal failure) • Usually generalized--imp
ascites, edema, jaundice –> due to
liver failure /albumin loss
Reduced plasma oncotic pressure due to
• Reduced albumin synthesis – malnutrition, liver disease • Increased albumin loss – renal disease • Reduced albumin absorption – protein losing enteropathy • Usually generalized
lymphatic blockage features
- localized !!
- normal levels of protein/albumin
- Filarial nematode could be a cause
Altered membrane permeability
- Inflammation
- Acute
- chronic
- Angiogenesis
- Burns
Renal disease
- Damages basement membrane
- Excess albumin loss – hypoalbuminemia (Nephrotic Syndrome)
- Decreased plasma oncotic pressure - edema
- Glomerulonephritis
- inflammatory damage with clogging of glomerular capillaries – reduced GFR
- Secondary hyperaldosteronism – sodium and water retention
Glomerulonephriti
- inflammatory damage with clogging of glomerular capillaries – reduced GFR
- Secondary hyperaldosteronism – sodium and water retention
transudate features
Due to increased hydrostatic expression
- no proteins
- no fibrin/inflammatory cells
Exudate
high in protein !
inflammatory
myxedema
non pitting edema
- due to hypothyroidism
- puffy features, enlarged tongue
pitting edema
systemic disease involving lung, heart, kidneys
Pulmonary edema features
severly congested alveolar cappilaries lead to blood and fluid spilling into the alveolis–> pink staining on H&E stains.
Frothy sputum
cyanosis due to lack of gas exchange
what does papilledema indicate
increased intracranial pressure
cerebral vasogenic edema ?
- BBB dysfunction
- due to infections, trauma or neoplasms
Cerebral cytotoxic edema ?
- Intracellular edema – due to cell injury
* Hypoxic-ischemic insult
cerebral edema treatment
mannitol and steroids
tentorial herniation
uncal herniation displacement of the
temporal lobe
• presses on cranial nerve III and parasympathetic fibers –
impaired ocular movements, pupillary dilation
• Duret hemorrhages in midbrain and pons
Tonsillar herniation
Tonsillar herniation through the foramen magnum • Brain stem compression – respiratory centers in medulla oblongata • Death due to cardio-respiratory arrest
Hyperemia
Arteriolar dilation !
active increase in the volume of blood in tissues
(red:oxygenated blood)
• Caused by arteriolar dilation
• Physiological - blushing, skeletal muscle during exercise
• Pathological - inflammation
congestion
passive/ venous blockage/always pathological/deoxygenated blood
Lung morphology in acute pulmonary congestion
Alveolar septal EDEMa
- alveolar cappilaries engorged
- mainly due to Left ventricular failure
Lung morphology in chronic pulmonary CONGESTION
brown induration
- Thickened FIBROTIC septae
- heart failure cells (hemosidrein laden macrophages present
Heart failure cells
hemosiderin laden macrophages)
liver morphology in acute congestion
Central vein gets engorged
- surrounding lobe/tissue die (central hepatocytes)
Happens in budd chiari syndrome or right heart failure
budd chiari syndrome
acute passive venous congestion
Nutmeg liver
Chronic Congestion
-Central region of hepatic lobule is reddish brown accentuated
against the surrounding zones of uncongested tan liver
which zone of the liver gets effected the most in chronic congestion
Zone 3
longstanding chronic congestion of liver twill lead to –>
cirrhosis ?
petechiae
pin point hemorrhage in skin or
conjunctiva; represents rupture of capillary or arteriole
melena ?
blood in stool
consequences of severe hemorrhage ?
f severe – hypovolemic shock
consequences of recurrent hemorrhage
• If recurrent – iron deficiency anemi
Leukocytosis buzz word
DIC >\??
causes of DIC
- Idiopathic
- Diffuse endothelial injury
- Gram negative sepsis (endotoxic)
- Viral, ricketssiae
- Immunologic injury (type II, III, SLE)
- Release of thromboplastic agents in circulation – activation of coagulation
- Amniotic fluid embolism
- snake bite
- Promyelocytic leukemia
- Extensive tissue necrosis, burns
- Mucin, proteolytic enzymes from carcinoma
IL-1 and TNFa increases when ? and what does it increase (in relation to coagulation ?
released when endotoxins are present in the blood –> acitvate monocytes
- Increase tissue factor (
Lab test for DIC
FDP and D-dimers
Management of DIC
HeParin replace platelets
Factor V mutation
Recurrent thrombotic episodes at such a young age strongly suggest an inherited coagulopathy. The factor V (Leiden) mutation affects 2% to 15% of the population, and more than half of all individuals with a history of recurrent deep venous thrombosis have such a defect. Inherited deficiencies of the anticoagulant proteins antithrombin III and protein C can cause hypercoagulable states, but these are much less common than factor V mutation
