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Hemodynamics-AF > Hemodynamics cumulative > Flashcards

Hemodynamics cumulative Flashcards

1
Q

Differentiate thrombus from clot (in general )

A

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
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2
Q

Features of arterial thrombus (gross and histological)

A
  • pale infarct

- Microscopy - lines of Zahn • Alternate pale and dark lines • Light – platelets and fibrin • Dark - RBCs

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3
Q

FAtes of thrombus

A
  • progression
  • formation of an embolus
  • resolution/ dissolution
  • organization and recanalization
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4
Q

Sites of thrombosis – arterial

A

Heart (mural) • Aorta (on atherosclerotic plaque) • Aneurysm (mural) • In other arteries (occlusive) • Coronaries • Carotids, cerebral • Femoral • Mesenteric

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5
Q

Formation of venous thrombosis

A

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

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6
Q

clinical signs and symptoms of venous thrombosis

A
  • • 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)
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7
Q

• Trousseau’s Syndrome

A 
unexplained thrombophlebitis (thrombus associated edema )
Underlying cause could be pancreatic tumor or any coagulatin acitivation tumor- release of procoagulant)
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8
Q

affect of an arterial thrombus

A

• Acute - Infarct • Slow - atrophy, fibrosis • Heart - systemic emboli

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9
Q

Effect of a venous thrombus

A

• Edema, congestion • Rarely- the pressure of edema leads to secondary block of the artery leading to infarction • Embolization to lungs

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10
Q

define embolism

A

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

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11
Q

what is the most common site of an embolism and what is most clinically significant emobolis

A

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%

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12
Q

Pulmonary Thromboembolism

A

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

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13
Q

Pulmonary thromboembolism

A

• 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

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14
Q

most likely site of origin in pulmonary thromboembolis

A
  • in the deep veins of legs
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15
Q

Most likely site of systemic thromboembolism

A
  • mural thrombus

- paradoxycal thrombus (carried from the venous side to the arterial side -atherosclerotic plaque

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16
Q

effect of a thrmboemobolism

A

Effect : embolize to the lower extremities (75%) and brain (10%) • they block an end artery leading to infarction

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17
Q

etiology Fat embolus

A

Trauma to bone, subcutaneous tissue, burns • Fat globules enter the circulation by rupture of the marrow vascular sinusoids or rupture of venules

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18
Q

pathogensis of fat embolism

A

• 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

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19
Q

Clinical features of Fat embolism

A

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

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20
Q

fat embolism syndrome features

A

fat embolism syndrome characterized by pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, and a diffuse petechial rash

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21
Q

lab investigations of FAt embolism

A

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

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22
Q

Prognosis of fat embolism

A

No tested treatment, just keep them hemodynamically stable and maintain oxygenation
Fatal in about 10% of cases

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23
Q

FAt embolism staining technique requirements

A

frozen section of tissues since routine processing through alcohol will dissolve the fat

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24
Q

Air embolism etiopathogensis

A

• 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

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25
Q

difference between fat embolism and bone marrow embolism

A

fat embolism mostly due to long bone trauma -yellow marrow trauma

Bone marrow embolism –due to CPR /red marrow trauma

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26
Q

Rising to quickly to 10 m height under water –> leads to ?

A

Nitrogen embolism

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27
Q

The bends, Caisson’s disease aka ?

A

nitrogen embolism

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28
Q

nitrogen embolism pathoethiology

A

• 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

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29
Q

clinical features of nitrogen embolism

A

Brain (death), muscles, joints (bends), lungs – edema, hemorrhage (chokes)

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30
Q

caissons disease

A

chronic form of presistant gas emboli in bones

Necrosis in femur, tibia, humeru

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31
Q

Treatmen of nitrogen embolism

A

Pressure chamber – slow decompression

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32
Q

bone marrow embolism

A

• Seen in small pulmonary vessels after vigorous cardiac resuscitation • Incidental finding at autopsy • Not a cause of death

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33
Q

amniotic fluid embolism etiolgy

A
  • Pregannt young females who recently gave birth
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34
Q

pathogensis of amniotic fluid embolism

A

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

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35
Q

what is found in the amniotic fluid embolism

A

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

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36
Q

clinical features of amnitoic fluid

A 
-arise 
after labour (immediate or after few hours)
- characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma.
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37
Q

prognosis of amniotic fluid embolism

A

usually fatal, survivors have permanent neurological damage

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38
Q

lab finding of amniotic fluid embolism

A 
↓platelets & clotting factors
↑ PT/PTT
- DIC 
-Diffuse alveolar damage
-pulmonary edema
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39
Q

Atherosclerotic emboli pathogensis

A

Involves small dislodged fragments of atherosclerosis from main renal artery in to smaller intrarenal branches producing small infarcts

40
Q

clinical symptoms of atherosclerotic emboli

A

no clinical symptoms

-Rarely- infarction- eg gut- bleeding, braintransient ischemia, blind spots e

41
Q

what is a infarction in a gross image called ? what is histopathological name ?

A
  • gross–> infarction

- histo—>necrosis

42
Q

causes of infarction ?

A

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

43
Q

White infarct pathogenesis

A
  • pale looking
  • arterial block
  • organ doesnt get the blood looks pale (no bleeding)
  • happens in solid organs that then undergo coagulative necrosis
44
Q

Red infarct pathogenesis

A

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

45
Q

repurfusion injury

A

a blocked or infarcted area suddenly receives blood –> leads to more injury

46
Q

repurfusion injury

A

a blocked or infarcted area suddenly receives blood –> leads to more injury due to sudden increase of oxygen

47
Q

what leads to the brwon ring formation around the infarcted organ

A

hemosidderin accumulation from break down of RBC

48
Q

where do the infarction in organs most likely occur

A

occlusion of the vessel occurs at the apex or that periphery of the organ forming the base

49
Q

Factors that influence the development of infarctio

A

• 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

50
Q

what adaptation leads to less infarct

A

dual blood supply /anastomosis /collateral circulation

51
Q

what type of organs undergo rapid infarct

A

-with single venous supply (Testis or ovaries ???

52
Q

VEnous thrombosis –>

A

leads to congestion

53
Q

Cerebral infarction 12 hrs in

A

• Starts as coagulation necrosis • Softening, color changes • May have hemorrhage due to reperfusion

54
Q

cerebral infarction 48 hrs in

A

Edema of the infarcted region, acts like a intracerebral mass causing raised intracranial pressure • Microglia engulf necrotic material, Gitter cells

55
Q

Myocardial infarction

A

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)

56
Q

Edema due to ( causes) ?

A

Heart failure

  • reduced oncotic pressure (liver)
  • nutrition deficiency
  • kidney dysfunction
  • Na retention
  • lympathic obstruction
  • membrane permeability
57
Q

pathway of fluid from tissue spacce to heart

A

Lymphatics–> thoric duct –> L subclavian vein–> superior vena cava –> heart

58
Q

anascara and ascites definition

A

anascara –> genralized severe accumulation of fluid (all over the body

Ascites –> fluid accumulation only in the peritonieum

59
Q

Chest pain, dyspnea, increased tropnin level and inverted T –> points to what –> leading to what ?

A

MI (congestive heart failure leading to edema due to increased hydrostatic pressure

60
Q

increased hydrostatic pressure due to

A 
Impaired venous return
• Congestive heart failure
• Venous obstruction or
compression
• Thrombosis
• External pressure (e.g.
tumor)
• Hypervolemia
• Sodium retention (renal
failure)
• Usually generalized--imp
61
Q

ascites, edema, jaundice –> due to

A

liver failure /albumin loss

62
Q

Reduced plasma oncotic pressure due to

A 
• Reduced albumin
synthesis –
malnutrition, liver
disease
• Increased albumin
loss – renal disease
• Reduced albumin
absorption – protein
losing enteropathy
• Usually generalized
63
Q

lymphatic blockage features

A
  • localized !!
  • normal levels of protein/albumin
  • Filarial nematode could be a cause
64
Q

Altered membrane permeability

A
  • Inflammation
  • Acute
  • chronic
  • Angiogenesis
  • Burns
65
Q

Renal disease

A
  • 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
66
Q

Glomerulonephriti

A
  • inflammatory damage with clogging of glomerular capillaries – reduced GFR
  • Secondary hyperaldosteronism – sodium and water retention
67
Q

transudate features

A

Due to increased hydrostatic expression

  • no proteins
  • no fibrin/inflammatory cells
68
Q

Exudate

A

high in protein !

inflammatory

69
Q

myxedema

A

non pitting edema

  • due to hypothyroidism
  • puffy features, enlarged tongue
70
Q

pitting edema

A

systemic disease involving lung, heart, kidneys

71
Q

Pulmonary edema features

A

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

72
Q

what does papilledema indicate

A

increased intracranial pressure

73
Q

cerebral vasogenic edema ?

A
  • BBB dysfunction

- due to infections, trauma or neoplasms

74
Q

Cerebral cytotoxic edema ?

A
  • Intracellular edema – due to cell injury

* Hypoxic-ischemic insult

75
Q

cerebral edema treatment

A

mannitol and steroids

76
Q

tentorial herniation

A

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

77
Q

Tonsillar herniation

A 
Tonsillar herniation through the
foramen magnum
• Brain stem compression – respiratory centers in medulla
oblongata
• Death due to cardio-respiratory arrest
78
Q

Hyperemia

A

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

79
Q

congestion

A

passive/ venous blockage/always pathological/deoxygenated blood

80
Q

Lung morphology in acute pulmonary congestion

A

Alveolar septal EDEMa

  • alveolar cappilaries engorged
  • mainly due to Left ventricular failure
81
Q

Lung morphology in chronic pulmonary CONGESTION

A

brown induration

  • Thickened FIBROTIC septae
  • heart failure cells (hemosidrein laden macrophages present
82
Q

Heart failure cells

A

hemosiderin laden macrophages)

83
Q

liver morphology in acute congestion

A

Central vein gets engorged
- surrounding lobe/tissue die (central hepatocytes)
Happens in budd chiari syndrome or right heart failure

84
Q

budd chiari syndrome

A

acute passive venous congestion

85
Q

Nutmeg liver

A

Chronic Congestion
-Central region of hepatic lobule is reddish brown accentuated
against the surrounding zones of uncongested tan liver

86
Q

which zone of the liver gets effected the most in chronic congestion

A

Zone 3

87
Q

longstanding chronic congestion of liver twill lead to –>

A

cirrhosis ?

88
Q

petechiae

A

pin point hemorrhage in skin or

conjunctiva; represents rupture of capillary or arteriole

89
Q

melena ?

A

blood in stool

90
Q

consequences of severe hemorrhage ?

A

f severe – hypovolemic shock

91
Q

consequences of recurrent hemorrhage

A

• If recurrent – iron deficiency anemi

92
Q

Leukocytosis buzz word

A

DIC >\??

93
Q

causes of DIC

A
  • 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
94
Q

IL-1 and TNFa increases when ? and what does it increase (in relation to coagulation ?

A

released when endotoxins are present in the blood –> acitvate monocytes

  • Increase tissue factor (
95
Q

Lab test for DIC

A

FDP and D-dimers

96
Q

Management of DIC

A

HeParin replace platelets

97
Q

Factor V mutation

A

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

Hemodynamics-AF (1 decks)

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