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ACEM pathology > 14 fluid and haemodynamic > Flashcards

14 fluid and haemodynamic Flashcards

1
Q

Causes of edema

A

Increased Hydrostatic Pressure
Reduced Oncotic Pressure
Lymphatic Obstruction
Sodium/Water Retention

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2
Q

Edema (def)

A

Increased fluid in the interstitial tissue spaces.
In different body cavities:
a. hydrothorax
b. hydropericardium
c. hydroperituneum (ascites)
d. anscara: severe, generalized oedma with subcutaenous tissue swelling

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3
Q

Transudate

A

Protein-poor, specific gravity less than 1.012. (Fluid leakage)

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4
Q

Exudate

A

In inflammatoy edema. Protein rich, specific gravity greater than 1.020. (Fluid and protein leakage)

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5
Q

INCREASED HYDROSTATIC PRESSURE

A 
Impaired venous return
Congestive heart failure  
Constrictive pericarditis  
Ascites (liver cirrhosis)  
Venous obstruction or compression
Thrombosis    
External pressure (e.g., mass)
Lower extremity inactivity with prolonged dependency
Arteriolar dilation
Heat  
Neurohumoral dysregulation
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6
Q

REDUCED PLASMA ONCOTIC
PRESSURE (HYPOPROTEINEMIA)

A

Protein-losing glomerulopathies (nephrotic syndrome)
Liver cirrhosis (ascites)
Malnutrition
Protein-losing gastroenteropathy

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7
Q

LYMPHATIC OBSTRUCTION
(LYMPHEDEMA)

A

Inflammatory
Neoplastic
Postsurgical
Postirradiation

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8
Q

Na+ RETENTION

A

Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium
Renal hypoperfusion –> Increased renin-angiotensin-aldosterone secretion

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9
Q

Congestive heart failure edema

A

INCREASED VENOUS PRESSURE DUE TO FAILURE

DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTION (secondary aldosteronism)

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10
Q

Nephrotic vc nephrotic syndroms

A

Both leads to hypoalbuminemia.

NephrOtic: proteins move into urine

NephrItic: small pores in podocytes leads to loss of RBC and proteins, cause hematuria.

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11
Q

Peu d’orange

A

In breast carcinoma infiltration and obstruction of superficial lymphatics can cause edema ov overlying skin.

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12
Q

Subcutaneous dependent edema

A

Gravity dependent. Typical for cardiac failure, particularly RV.

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13
Q

Edema due to renal sysfunction or nephrotic syndrome

A

More severe than cardiac edema, and affects all parts of the body equally.

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14
Q

Pulmonary edema

A

Seen most frequently in left ventricular failure, but also in renal failure, ARDS, pulmonary infections and hypersensitivity reactions.
Weigh 2-3 times normal, on section: frothy, blood-tingled fluid (air, edema fluid and extravasated red cells)

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15
Q

Edema of the brain

A

May be localized to places of focal injury (infarct, abcsess, neoplasm) or generalized (encephalitis, hypertensive crisis, obstruction of venous outflow).
Generalized: swollen, narrowed sulci, distended gyri.
May cause herniation throug foramen magnum.

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16
Q

Hyperemia and congestion

A

Local increased volume of blood in a particular tissue.

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17
Q

Hyperemia

A

Active process resulting form augmented blood flow due to arteriolar dilation. Eg: infl, excercise

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18
Q

Congestion

A

Passice process resulting form impaired venous return out of a tissue. May be systemic (heart failure), or local (isloated venous obstruction). Leads to cyanosis. Commonly occure together with edema.
Chronic passive congestion: hypoxia, death of tissue, fibrosis. If capillary rupture –> hemociderin-laden macroph.

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19
Q

Morphology acute pulmonary congestion

A

Alveolar capillaries engorged with blood, septal edema and/or focal minute intra-alveolar hemorrhage.

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20
Q

Morphology chronic pulmonary congestion

A

Septa become thickened and fibroticHemociderin-laden macrophages (heart failure cells) in alveolar spaces

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21
Q

Morphology acute hepatic congestion

A

Central vein and sinusoids are distended with blood, mey be central hepatocyte degeneration. Periportal hepatocytes have less hypoxia, only fatty change is seen.

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22
Q

Morphology chronic passive congestion of the liver

A

Nutmeg liver: central regions of hepatic lobules are red-brown, surrounding zones are uncongested tan, sometimes fatty.
Micro: centrilobular necrosis, , hemorrhage, hemociderin-laden macroph.

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23
Q

Brain herniation due to edema

A
  1. Subfalcine herniation
  2. Transtenrorial herniation
  3. Tonsillar herniation
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24
Q

Hemorrhage

A

Extravasation of blood from vessles into the extravascular space

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25
Q

Hematoma

A

Accumulation of blood. Insignificant; bruise. Significant; massive retriperitoenal hematoma resulting form ruptupe of a dissecting aortic aneurysm

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26
Q

Petechiae

A 
Minute (1-2 mm) hemorrhages into the skin, mucous membr, serosal surf. 
Associated with:
1. local increase IV pressure, 
2. thrombocytopenia, 
3. defective platelet function or 
4. clotting factor deficiencies
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27
Q

Purpura

A 
3-5 mm hem
Associated with:
(same as peteciae pluss:)
1. vasculitis
2. trauma
3. increased vascular fragility
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28
Q

Ecchymoses

A 
1-2 cm, subcutaneous (brusies)
Colour changes in hematoma due to phagocytises and degradation of RBC:
1. hemoglobin: red-blue
2. bilirubin: blue-green
3. hemosiderin: golden-brown
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29
Q

Large accumulations of blood in body cavities

A
  1. hemothorax
  2. hemopericardium
  3. hemoperitoneum
  4. hemarthrosis
30
Q

Normal hemostasis(def)

A

Consequence of thightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing tha rapid formation of a localized hemostatic plug at the site of vascular injury.
Pathologic form: thrombosis.
Involve three components: vascular wall, platelets, coagulation cascade.

31
Q

Steps of normal hemostasis

A

A. Vasoconstriciton: after vascular injury, local neurohumoral factors (endothelin) induce transient vasoconstr.
B. Primary haemostasis: platelet adhere (via Gplb receptor) to exposed ECM by binding to vWF and are activated, undergoing shape change and granule release.

Released ADP and TXA2 lead to further platelet aggregation (binding fibrinogen to platelet GpIIb-IIIa rec), to form primary hemostatic plug.

C. Local activation of coagulation cascade (involving tissue factor and platelet phospholipid) results in polymerization, “cementing” the platelets to definitive secondary hemostatic plug.
D. Counter-regulatory mechanism, such as release of t-PA and thrombomodulin, limit hemostatic process to the site of injury.

32
Q

PLATELET ADHESION

A

Primarily to the subendothelial ECM

Regulated by vWF, which bridges platelet surface receptors to ECM collagen

33
Q

Platelet secretion

A

Both granules. Agonist binds to surface receptors and initiate an IC phosphorulation cascade which leads to degranulation. Dense bodies are spesially important; ADP for platelet aggregation, calcium for coagulation cascade.

34
Q

Platelet aggregation

A

ADP
TxA2 (Thromboxane A2)
THROMBIN from coagulation cascade also
FIBRIN further strengthens and hardens and contracts the platelet plug

35
Q

Platelet events

A
  1. ADHERENCE to ECM
  2. SECRETION of ADP and TxA2
  3. EXPOSE phospholipid complexes
  4. Express TISSUE FACTOR
  5. PRIMARY -> SECONDARY PLUG
  6. STRENGTHENED by FIBRIN
36
Q

Cofactors in coagulation cascade

A

Ca++
Phospholipid (from platelet membranes)
Vit-K dep.
Prot. S, C, Z

37
Q

Vit K dependent factors in coagulation cascade

A

II
VII
IX
X

38
Q

Virchow’s triad

A

Three primary influences on thrombus formation

1) endothelial injury
2) stasis or turbulence of flow
3) blood hypercoagulability

39
Q

Primary (genetic) hypercoagulable states

A 
Common
a. mutaion in factor V gene (Leiden)
b. mut in prothrombin gene
c. mut in methyltetrahydrofolate gene
Rare
d. antithrobin III deficiency
e. protein C def
f. protein S def
Very rare
g. fibrinolysis defects
40
Q

Secondary (acquired) hypercoagulable states

A 
High risk for throbosis
1. prolonged imobilisation
2. MI
3. atrial fibrillation
4. tissue damage
5. cancer
6. prosthetic cardiac valve
7. DIC
8. heparin-induced thrombocytopenia
9. antiphospholipid ab syndrome (lupus anticoagulant sy)
Lower risk:
a. cardiomyopathy
b. nephrotic sy
c. hyperestrogenic states (pregnancy)
d. oral contraceprive use
e. sickle cell anemia
f. smoking
41
Q

Properties of endothelium related to thrombus formation

A
  1. ANTI-Platelet PROPERTIES
    a. Protection from the subendothelial ECM
    b. Degrades ADP (inhib. Aggregation)
  2. ANTI-Coagulant PROPERTIES
    a. Membrane HEPARIN-like molecules
    b. Makes THROMBOMODULIN –> Protein-C
    c. TISSUE FACTOR PATHWAY INHIBITOR
  3. FIBRINOLYTIC PROPERTIES (TPA)
42
Q

Arterial thrombi characteristics

A
  1. Arterial and cardiac thrombi typically begins at sites of endothelial injury or turbulence
  2. arterial thrombi grow retrograde
43
Q

Venous thrombi characteristics

A
  1. Venous thrombi occur at sites of stasis

2. extend in the direction of the blood flow

44
Q

Lines of Zahn:

A

laminations, pale platelet and fibrin layers alternating with darker erythrocyte rich layers. Antemortem.

45
Q

Mural thrombi:

A

in heart chambers or in the aortic lumen. Abnormal myocardial contraction or endomyocardial injury promotes cardial mural thrombi. Ulcerated atherosclerotic plaques and aneurysmal dilation promote aortic thrombosis.

46
Q

Arteral thrombi:

A

frequently occlusive, produced by platelet and coagulation ativation. Meshwork of platelets, fibrin, erythrocytes, and degenerating leukocytes. White “flux” thrombus in arteries. Mixed “coral” thrombus with changing layers in big arteries, heart and aneurisms. Hyaline thrombus in capillaries.

47
Q

Venous thrombosis:

A

(phlebothrombosis): occlusive, can create a long cast of the lumen. It is largely the result of activation of the coagulation cascade, and platelets play a secondary role. Contain more erythrocytes; red or stasis thrombi. Strands of grey fibrin.

48
Q

Postmortem clots:

A

gelatinous with a dark red dependent portion where red cells have setteled by gravity, and a yellow supernatant. They are not attached to the vessel wall.

49
Q

Vegetations

A

thrombi on heart valves. Bacterial or fungal blood born infecions can cause valve damage, leading to thrombothic masses (infective endocarditis). Nonbacterial thrombotic endocarditis; sterile hypercoagulative states. Sterile verrucous endocarditis (Libman-Sacks endocarditis) can occure in the setting of SLE (uncommon).

50
Q

What is the fate of thrombus

A
  1. Propagation: thrombi accumulate platelets and fibrin, eventually causing vessel obstruction
    2 Embolization: Thrombi dislodge or fragment and are transported elsewhere in the vasculature
  2. Dissolution: Thrombi are removed by fibrinolytic activity
  3. Organization and recanalization;: Thrombi induce inflammation and fibrosis. These can eventually recanalize, or they can be incorporated into a thickened vessel wall.
51
Q

Trousseau’s syndrome

A

Trousseau’s syndrome is migratory thromboplebitis

Increased risk of thromboembolic phenomena seen in disseminated cancers due to tumour-assosiated procoagulant release.

52
Q

Paradoxial emboli

A

A small fraction of systemic emboli arise in the veins, but end up in the arterial circulations, through interatrial or interventricular defects.

53
Q

Saddle embolus

A

Emboli in the pulmonary artery branchin point.

54
Q

Types of emboli

A 
99% dislodged from thrombi.
Fat droplets, 
bubbles of nitrogen,
 atherosclerotic debris (cholesterol emboli), 
tumor fragments, 
bits of bone marrow, 
foreign bodies such as bullets
55
Q

Pulmonary emboli

A

60-80% are clinically silent
When 60% or more of pulm circ is obstructed: Cor pulmonale (RV failure), CV collapse or sudden death.
In medium size a: Lead to hemorrhage, but normally not infarct (left-sided heart failure leads to massive infarct)
In small arterioles: infarct
Many emboli over time: pulm hypertension, RV failure

56
Q

Systemic emboli

A

80% cardiac/20% aortic aneurysm
Embolization lodging site is proportional to the degree of flow (cardiac output) that area or organ gets, i.e., brain, kidneys, legs

Limbs – 75% Brain – 10%

57
Q

Other emboli; fat, air, amniotic

A

FAT (long bone fx’s ): Occurs in 90% of those with severe trauma, only 10% develop fat embolism syndrome

Pathogenesis: Mechanical obstruction
Platelet aggregation
Local endothelial injury

Fat embolism syndrome: typically begins 1-3 days after injury (fatal in 10%) and is characterized by:
Tachycardia
Tachypnoea Irritability
Diffuse petechial rash in 20-50% (not due to thrombocytopenia)
Thrombocytopenia

AIR (SCUBA bends)

AMNIOTIC FLUID, very prolonged or difficult delivery, high mortality
1 in 50 000 deliveries Mortality >80%

Pathogenesis:
Tear in placental membrane results in leakage
of amniotic fluid into systemic circulation
Clinically:
Shock, seizures, coma
Pulmonary oedema
DIC

Diagnosed by finding fetal epithelial cells in the maternal pulmonary vasculature

58
Q

Infarct def

A

area of necrosis secondary to decreased blood flow

All infarcts wedge shaped with irregular margins. All have some degree of haemorrhage but in white infarcts, few extravasated red cells are rapidly lysed to form haemosiderin, therefore they become more pale with time.
Ischaemic coagulative necrosis is the dominant histological change with liquefactive necrosis occurring in CNS. Some parenchymal regeneration may occur but most infarcts are replaced by scar

59
Q

Anemic infartct

A

White/pale infarct.

Caused by arterial occlusions in the heart, spleen, kidney

60
Q

Hemorrhagic infarct

A

Red infarcts; red cells goes in to necrotic tissue.
In lungs and GIT form arterial occlusion. Tissues are loose and have double blood supplies.
Can also be venous occlusion

61
Q

Types of shock

A
  1. CARDIOGENIC: (Acute, Chronic Heart Failure)
  2. HYPOVOLEMIC: (Hemorrhage or Leakage)
  3. SEPTIC: (“ENDOTOXIC” shock, #1 killer in ICU)
  4. NEUROGENIC: (loss of vascular tone)
  5. ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased vascular permeability)
62
Q

Septic shock events

A 
SYSTEMIC VASODILATION (hypotension) -->
↓ MYOCARDIAL CONTRACTILITY -->
DIFFUSE ENDOTHELIAL ACTIVATION -->
LEUKOCYTE ADHESION -->
ALVEOLAR DAMAGE -->  (ARDS)
DIC
VITAL ORGAN FAILURE --> CNS

Caused by gram-negative bacilli that produce endotoxins Endotoxins are bacterial wall lipopolysaccharides (LPS).

LPS binds and activates leucocytes and endothelial cells causing release of mediators. At low doses, TNF, IL1, IL6 and IL8 predominate (note that they peak in this order, preceded by the peak of endotoxin)

At high doses NO and PAF become significant and endothelial injury may result. LPS also directly activates complement.

63
Q

Clinical stages of shock

A 
1. NON-PROGRESSIVE
a COMPENSATORY MECHANISMS
b CATECHOLAMINES
c VITAL ORGANS PERFUSED
2. PROGRESSIVE
a HYPOPERFUSION
b EARLY “VITAL” ORGAN FAILURE
c OLIGURIA
d ACIDOSIS
3. IRREVERSIBLE
a HEMODYNAMIC CORRECTIONS of no use
64
Q

Clinical progression of symproms in shock

A 
Hypotension -->
Tachycardia -->
Tachypnea -->
Warm skin --> Cool skin --> Cyanosis
Renal insufficiency -->
Obtundance
Death
65
Q

Describe the intrinsic clotting cascade?

A

Slow pathway – takes 1-6 minutes to cause clotting Trigger – exposure to collagen fibres (or any electronegative surface), or trauma to blood

Activation of factor XII is catalysed by Kallikrein and HMW kininogen

Activated factor XII activates factor XI.
Activated factor XI activates factor IX.
Activated factor IX forms a complex with factor VIII, which activates factor X (prothrombin activator)

Calcium and phospholipids from platelets are also required.

66
Q

Describe the extrinsic clotting system?

A

Rapid pathway – takes 15 seconds to cause clotting Trigger – release of tissue thromboplastin – a protein and phospholipid mixture that activates factor VII. Tissue thromboplastin and activated factor VII activate factor IX and X.

Calcium, phopholipids and factor V also required.

67
Q

What are the anticoagulant factors produced by endothelium?

A

Prostacyclin and NO which are vasodilators and antiaggregators. Tissue plasminogen activator (and TPA inhibitors) – activates plasminogen Thrombomodulin – binds thrombin, complex activates protein C
Protein S

68
Q

What are the procoagulant factors produced by endothelium?

A

Von Willebrand Factor – essential for binding of platelets to extracellular matrix. Tissue thromboplastin – activates extrinsic clotting cascade.

69
Q

Describe thromboxane A2 and prostacyclin?

A

Thromboxane A2 has an aggregating effect that is counteracted by prostacyclin that has an antiaggregating effect.

70
Q

What is antithrombin III?

A

Circulating protease inhibitor that binds to serine proteases in clotting cascade and blocks their action. Affects thrombin, factors IX, X, XI and XII. Other proteases include alpha1 antiprotease, alpha2 macroglobulin, alpha2 antiplasmin.

71
Q

What is heparin?

A

Mixture of sulfated polysaccharides which facilitates binding of antithrombin III.

72
Q

Describe the fibrinolytic system?

A

Thrombomodulin is a thrombin binding protein produced by endothelial cells (except cerebral microcirculation). Thrombomodulin-thrombin complex activates protein C.

Activated protein C inactivates factor VIII and V and inactivates inhibition of TPA.
Plasmin formed from plasminogen by action of thrombin, TPA and kallikrein Plasminogen is also activated by binding to endothelium. Plasmin lyses fibrin.

ACEM pathology (4 decks)

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