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Pathology > Lec5-6 Hemodynamics > Flashcards

Lec5-6 Hemodynamics Flashcards

1
Q

Distribution of water in body– percent of body mass? Intracellular vs interstitial vs intravascular?

A

Body is 60% water by mass:
40% intracellular [in cell]
15% intercellular or interstitial [between cells]
5% intravascular [in blood vessels]

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2
Q

Normal plasma osmolality? Major osmole? Osmolarity intracellular vs intercellular vs intravascular?

A

280 mosm/L
major osmole is sodium
electrolytes, glucose, proteins, urea also contribute
Intravascular, interstitial, intracellular spaces always have equal osmolarity

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3
Q

Osmosis– definition? 2 requirements for osmosis to occur?

A

Fluid moves from one chamber to equalize osmotic gradient
2 requirements:
1. driving force [difference in osmolarity]
2. semipermeable membrane

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4
Q

Water and molecule movement and distributions – what can move where (between intracellular, intercellular, intravascular?

A
  • water moves freely between intravascular, interstitial, intracellular so always equal osmolarity
  • small solutes move through clefts in blood vessel endothelium between intravascular and interstitial [together = extracellular] so always same concentration of small solutes
  • small solutes can’t pass through cell membrane so have conc. gradient between intra and extracellular
  • large molec [proteins] and cells do not move freely, trapped inside cell or inside intravascular space so get concentration gradients
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5
Q

Effect of half normal vs normal saline fluid on hypotensive patient

A

Half normal: decreases osmolarity of intravascular space, so water moves to intracellular/intrerstitial space to equalize osmotic pressure, all 3 spaces expand a little

Normal: osmolarity of intravascular stays the same, water and electrolytes move to interstitial to equalize concentration gradient, extracellular spaces expand [by more than for half normal]

Normal saline = better treatment for increasing intravascular volume

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6
Q

Starling’s Equation

A

Jv = Kf * [(Pc + Πi) – (Πc + Pi)]

  • Jv = fluid movement in ml/min
  • Kf = hydraulic conductance, easyness of getting out of tube
  • Filtration [movement out] = (Pc + Πi)
    • Pc = outward hydrostatic P by blood in capillary
    • Πi = outward oncotic P by proteins in interstitium
  • Absorption [movement in] = (Πc + Pi)
    • Πc = inward oncotic P by proteins in capillary
    • Pi = inward hydrostatic P by interstitium
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7
Q

How does fluid end up in wrong place? [4 Mech]

A

When filtration > absoprtion

  1. low Πc: hypoalbuminemia, lose protein in urine
    - – nephrotic syndrome, hepatic cirrhosis, malnutrtion [kwashiokor]
  2. high Pc: heart failure
    - – right sided = peripheral edema
    - – left sided = pulmonary edema
  3. high Kf: sepsis and inflammation
    - – capillary leak syndrome in meningitis
  4. lymphatic impairment [from surgery, mechanical]
    - – increased interstitial fluid
    - – increased Πi
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8
Q

Cause/effect of low capillary oncotic pressure

A

caused by hypoalbuminemia = losing protein in urine

get more filtration than absorption, fluid leaves intravascular = edema

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9
Q

Cause/effect of high capillary hydrostatic pressure

A

caused by heart failure

    • right sided heart failure –> peripheral edema
    • left sided heart failure –> pulmonary edema
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10
Q

Cause/effect highly permeable blood vessels

A
    • High Kf [hydraulic conductance] due to sepsis and inflammation
    • ex. capillary leak syndrome in meningitis
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11
Q

Cause/effect impaired lymphatics

A
    • due to surgery or mechanical reason
    • extra filtrate in interstitial space can’t get returned to circulatory system
    • get increased interstitial fluid
    • get increased Πi
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12
Q

Definition of Edema

A
  • Too much interstitial [intercellular] fluid
  • Can be localized or generalized
  • different from hydropic change/cell swelling which is intracellular edema
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13
Q

Definition of Anasarca

A

generalized edema

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14
Q

Definition of Effusion

A

type of edema - excess fluid in body cavity

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15
Q

Definition of Hydrothorax

A
  • Pleural Effusion

- Excess free fluid in pleural cavity

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16
Q

Causes of Transudate

A
  • high intravascular hydrostatic P [high Pc]
  • – cardiac/vascular problem, deep vein thrombus, congestive heart failure
  • low intravascular osmotic P [low Πc]
  • – low plasma protein, nephrotic syndrome, chronic liver disease, protein malnutrition
  • Lymphatic obstruction [high Πi]
  • – inflammation, post-surgical, tumor
  • Excess body fluid due to Na retention in setting of renal dysfunction
    • increase Na intake –> retention water
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17
Q

What is Dependent pitting edema? Exudate or transudate? 3 main Causes?

A
  • swelling occurs underneath skin usually in arms/legs/ankles, can be depressed
  • transudate edema
  • due to congestive heart failure, pulmonary edema, renal disfunction
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18
Q

What is Hemostasis? Functional components?

A 
Arrest of hemorrhage in response to vascular injury
Functional components:
- blood coagulation
- platelet aggregation
- endothelial cell interaction
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19
Q

What is Hemorrhage

A

bleeding, escape of blood from vessels

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20
Q

What is a Hematoma

A

localized collection of blood [usually clotted] within tissue or space

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21
Q

What is Thrombosis

A

Active process of transformation flowing liquid blood to semisolid in heart/vessel of living organism

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22
Q

What is a Thrombus

A

coagulated blood containing platelets, fibrin, entrapped cellular elements

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23
Q

Blood coagulation pathway steps

A
  1. vessel severed/injured
  2. plasma in vessel contacts tissue factor [TF]
  3. TF binds factor VII and activates it
  4. active VIIa-TF complex activates factor X
  5. Xa converts prothrombin –> thrombin and fibrinogen to fibrin
  6. VIIa-TF activates IX to amplify thrombin generation through intrinsic pathway

Fibrinolysis controls size of thrombus

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24
Q

What is Tissue Factor

A

extrinsic to blood, plays key role in initiating coagulation

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25
Q

Are coagulation factors present in blood in absence of injury?

A

Yes – in inactivated form

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26
Q

Inhibitors of platelet aggregation?

A
  • Prostacylin [PGI2] and Nitric Oxide [NO] released by epithelial cells
  • Antithrombin III: binds heparin like molec on epithelial cell surface –> inactivates thrombin, factors Xa/IXa
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27
Q

Role of platelets in thrombosis

A
  • form initial hemostatic plug

- release Ca, ADP, Thromboxane A etc that attract more circulating platelets to site of injury

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28
Q

Virchow’s triad

A

Causes of thrombosis

  1. endothelial injury
  2. alteration in flow
  3. hypercoagulable blood
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29
Q

Cause of endothelial injury?

A

Most important for arterial thrombus

  • ruptured atherosclerotic plaque
  • inflamed cardiac valve [endocarditis]
  • inflamed vessel [vasculitis]
  • MI
  • hypertension, turbulent flow, bacterial products
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30
Q

Most likely cause arterial thrombus

A

injured endothelium

31
Q

Most likely cause venous thrombus

A

altered flow - obstruction

32
Q

Cause of altered flow?

A
  • anuerysms
  • atherosclerotic plaques
  • atrial fibrillation
  • dilated cardiac ventricles
  • obstruction = particularly important in venous thrombus
33
Q

Cause of hypercoagulable blood?

A

primary: inherited coagulation factor or inhibitor abnormality
- factor V leiden – alternate form favor V that can’t be inactivated by activated protein C
- prothrombin gene mutation
- Protein C or S deficiency
- Antithrombin III deficiency
- Homocysteinuria

secondary

  • oral contraceptives
  • pregnancy
  • cancer
  • polycythemia
  • antiphospholipid antibody syndrome
34
Q

Thrombin-Thrombomodulin rxn

A
  • Thrombin binds thrombomodulin on epithelial cell surface and activates protein C
  • active protein C with protein S cause proteolysis of Va and VIIa
35
Q

Lines of zahn

A
  • alternating layers of paler fibrin/platelets and red blood cells
  • indicated thrombus that formed in flowing blood
  • allows you to differentiate from clot
36
Q

Clot

A
  • Blood solidified OUTSIDE vascular system or has solidified in blood vessels POSTMORTEM
37
Q

Thrombus vs clot

A
  • Clot not attached to wall of vessel
  • “Chicken fat” appearance of plasma in clot
  • “Currant jelly” appearance of RBCs in clot
  • No lines of zahn in clot
38
Q

5 Possible outcomes thrombus

A
  • propagation
  • lysis
  • organization and recanalization
  • become infected
  • embolize
39
Q

embolus

A

sold, gas, or liquid other than liquid blood that travels through vessels and lodges somewhere

40
Q

5 types of emboli

A
  • thromboemboli
  • atheroemboli
  • fat
  • air
  • tumor
41
Q

Thromboemboli

A
  • Most common = pulmonary thromboembolus
  • most common source = deep leg veins
  • possible manifestations
  • – asymptomatic
  • – sudden death [saddle embolus]
  • – pulmonary hemorrhage/infarction
  • – chronic pulmonary hypertension
42
Q

Arterial Embolus

A
  • Embolus ends up in the systemic circulation

- Cause occlusion blood vessels in systemic organs [brain, heart, etc] or lower extremities

43
Q

Paradoxical Embolus

A
  • thrombus forms in vein and travels through patent foramen ovale into artery and enters systemic circulation
  • normally if no patent foramen ovale would have traveled to lungs first and get pulmonary embolism
44
Q

Atheroemboli

A

Debri from ruptured atherosclerotic plaque embolized from aorta to brain, kidney, toes, etc

45
Q

Air Embolism

A

Caused by

  • delivery through ruptured vein
  • chest trauma
  • cardiac surgery
  • decompression sickness
46
Q

Fat Embolism

A
  • after fracture or orthopedic surgery –> fat from marrow released into circulation
  • lipid obstructs vessels, releases fatty acids causes endothelial injury
  • pulmonary fat emboli cause edema, diffuse respiratory dysfunction
  • can also embolize to brain/kidneys/heart
47
Q

Infarction

A

Area of irreversible tissue necrosis due to ischemia

48
Q

Ischemia

A

imbalance of oxygens supply and demand due to loss of blood flow from obstructed arterial flow or reduced venous drainage

49
Q

White infarct

A
  • due to arterial occlusion
  • single blood supply
  • not reperfused
  • wedge shaped area of infarction
  • solid tissue
  • kidney, heart, spleen
50
Q

Red infarct

A
  • due to venous occlusion
  • dual blood supply
  • reperfused
  • loose tissue
  • brain, lungs, liver, GI tract, testicular torsion
51
Q

Disseminated Intravascular Coagulation

A
  • excessive secondary activation of coagulation leads to thrombus formation in microvasculature
  • causes micro-infarction of multiple organs
  • uses up/depletes clotting factors and platelets
  • leads to hemorrhage, bleeding diathesis [ high susceptibility to bleeding]
  • uncontrolled hemorrhage may lead to shock
52
Q

Causes of DIC [disseminated intravascular coagulation]

A
  • Release of TF - tumors, tissue injury, obstetrical complication
  • Endothelial injury
  • Bacterial Sepsis - IMPORTANT FOR QUIZ
  • Burns
53
Q

DIC [disseminated intravascular coagulation] pathology in tissues

A
  • many venules/capillaries/arterioles have fibrin-platelet thrombi
  • ischemic changes in many organs –> multi-organ failure
    schistocytes in blood
54
Q

Schistocytes

A
  • fragmented RBCs
  • sign of microangiopathic hemolytic anemia
  • sign of DIC [disseminated intravascular coagulation]
55
Q

Diagnosis DIC

A

Laboratory
- decreased platelets + fibrinogen
- prolonged lab tests of coagulation [takes long time for blood to clot in test tube]
- fibrin-split products in blood [product of plasmin degradation of fibrin thrombus]
Morphology
- schistocytes on peripheral blood smear
- fibrin-platelet thrombi histologically

56
Q

Treatment DIC

A
  • Treat underlying disease

- Heparin

57
Q

Shock – 3 causes?

A

circulatory collapse = global hypotension with widespread hypoperfusion of tissues

3 Causes

  • cardiogenic [MI, arrhythmia]
  • hypovolemic [hemorrhage]
  • septic [microbial infection]
58
Q

Effect of hypoperfusion

A
  • lactic acidosis [low pH]
  • hypotension
  • tissue ischemia and necrosis
  • multi-organ system failure
59
Q

Septic shock

A
  • secondary to infection [ usually gram + or -]
  • bacterial products / inflammatory mediators –> vasodilation and increased vascular permeability
  • often leads to DIC
60
Q

Compensated shock

A
  • normal BP, no urine output
  • tachycardia
  • peripheral vasoconstriction in hypovolemic/cardiogenic shock
  • recovery possible
61
Q

Decompensated shock

A
  • low BP
  • widespread tissue hypoperfusion/hypoxia –> lactic acidosis
  • renal insufficiency
62
Q

Irreversible shock

A
  • low BP, lactic acidosis, organs die

- leads to death

63
Q

Pathology of shock

A
  • necrosis of areas farthest from arterial supply
  • – centrilobular necrosis liver
  • – mucosal necrosis intestines
  • – subendocardial necrosis of heart
  • necrosis of vulnerable cells
  • – diffuse hypoxic neuronal injury of brain
  • – epithelial necrosis of kidney
64
Q

Does ADP inhibit or promote thrombus formation?

A

Promotes – ADP is released from platelets when they are activated and cause activation of other platelets for aggregation to form thrombus

65
Q

Thromboxane A2

A

Produced by activated platelets, promotes activation of more platelets and thrombus formation

66
Q

What is the effect of high hydrostatic pressure?

A

get heart failure

    • left –> leads to pulmonary edema
    • right –> leads to passive congestion in liver, periphery/limbs [generalized edema]
67
Q

What is the cause of low oncotic pressure

A
  • not taking in enough [malnutrition]
  • peeing too much [nephrotic sundrome]
  • protein losing enteropathy
  • inflammation from infection, tumor, sarcoidosis
68
Q

What is protein losing enteropathy

A
  • condition of GI tract that results in net loss of protein from body
  • causes: crohn’s, celiac, amyloidosis,
69
Q

What is in transudate? Cell content, Protein, specific gravity, endothelial intact or not intact, etiology?

A
  • no cells
  • not much protein
  • specific gravity < 1.012
  • intact endothelium, ultrafiltrate
  • due to F. S. equation mechanisms
70
Q

What is in exudate? Cell content, Protein, specific gravity, endothelial intact or not intact, etiology?

A
  • lots of cells mostly neutrophils
  • lots of protein
  • specific gravity > 1.020
  • endothelium not intact, increased vascular permeability
  • due to infection
71
Q

Is transudate associated with increased vascular permeability?

A

NO!!!

72
Q

What are 5 inherited diseases that lead to hypercoagulation?

A
  • factor V leiden – alternate form factor V that can’t be inactivated by activated protein C
  • prothrombin gene mutation
  • Protein C or S deficiency
  • Antithrombin III deficiency
  • Homocysteinuria
73
Q

What is factor V leiden?

A

alternate form of factor V that can’t be inactivated by activated protein C

74
Q

What is the antigen in goodpastures?

A

Collagen IV in glomerular basement membrane

Pathology (15 decks)

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