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MOD Exam I > Robbins Ch 4: Hemodynamic Disorders, Thromboembolic Disease and Shock > Flashcards

Robbins Ch 4: Hemodynamic Disorders, Thromboembolic Disease and Shock Flashcards

1
Q

Elevated 1 or diminished 2 can disrupt the balance fluid movement across vessels leading to edema.

A
  1. hydrostatic pressure

2. colloid osmotic pressure

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2
Q

Accumulation of fluid within tissue is known as _

A

edema

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3
Q

Accumulation of fluid within body cavity is known as_

A

effusion

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4
Q

As a cause of edema, increase in hydrostatic pressure are mainly caused by disorders that impair _

A

Venous return

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5
Q

How does one with cirrhosis or nephrotic syndrome cause edema?

A

Both leads to diminished albumin which is the major protein in plasma responsible for oncotic pressure.

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6
Q

Dependent edema is commonly associated with edema in _

A

Lower extremity (gravity associated)

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7
Q

Periorbital edema is commonly associated with what disease?

A

severe renal disease. Renal dysfunction often appears initially in parts of the body containing loose connective tissue such as the eyelids.

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8
Q

Morphologically, what changes are seen in gyri and sulci in brain edema?

A

Narrowed sulci and distended gyri.

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9
Q

Peritoneal effusions results most commonly from 1 and are prone to 2.

A
  1. portal hypertension

2. seeding by bacteria, leading to serious and sometimes fatal infections.

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10
Q

Hyperemia and congestion both stem from increased _

A

Blood volume within tissues.

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11
Q

Hyperemia is _1_process in which arteriolar dilation leads to increased blood flow. Give an example of hyperemia.

A
  1. Active process

Example: site of inflammation or skeletal muscle during exercise

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12
Q

Congestion is a _ process resulting from reduced outflow of blood from a tissue.

A

passive

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13
Q

In long-standing chronic passive congestion, the associated 1 may result in 2 injury and scarring

A
  1. chronic hypoxia

2. Ischemic

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14
Q

In chronic congestion, why is clusters of hemosiderin-laden macrophages seen?

A

Capillary rupture which produce small hemorrhagic foci and subsequent catabolism of extravasated red cells leads to this appearance.

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15
Q

What is the morphology of acute pulmonary congestion?

A

Congested tissue usually appear dusky reddish-blue color. In acute pulmonary congestion, engorged alveolar capillaries, alveolar septal edema, and focal intraalveolar hemorrhage is seen.

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16
Q

What is the morphology of chronic pulmonary congestion?

A

The septa are thickened and fibrotic, and the alveoli often contain numerous hemosiderin-laden macrophages called heart failure cells.

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17
Q

What is the morphology of acute hepatic congestion?

A

Central vein and sinusoids are distended. The centrilobular areas may be necrotic while the periportal hepatocytes may only develop fatty changes.

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18
Q

What is the morphology of chronic passive hepatic congestion?

A

Contrilobular regions are grossly red-brown and slightly depressed (cuz of cell death) and are accenutated against the surrounding zones of uncongested tan liver (nutmeg liver). microscopically there is centrolobular hemorrhage, hemosiderin-laden macrophages and variable degrees of hepatocyte dropout and necrosis.

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19
Q

Arteriolar vasoconstriction occurs immediately and markedly reduces blood flow to injured areas mediated by _.

A

reflex neurogenic mechanisms and augmented by the local secretion of factors such as endothelin which is a potent endothelium-derived vasoconstrictor.

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20
Q

Primary hemostatsis is _

A

formation of the platelet plug

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21
Q

Explain what happens in primary hemostasis.

A

Disruption of endothelium exposes subendothelial vWF and collagen which promote platelet adherence and activation. Activation of platelet results in dramatic shape change (from round to disk), and release of secretory granules which recruits more platelets.

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22
Q

What is tissue factor and what role does it play in the secondary hemostasis?

A

Tissue factor is a membrane-bound procoagulant glycoprotein that is normally expressed by subendothelial cells. During injury tissue factor become exposed and binds and activates factor VII which sets in motion a cascade of reaction.

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23
Q

Explain what happens in secondary hemostasis.

A

Tissue factor binds and activates VII which sets in motion a cascade of reactions that culminates in thrombin generation. Thrombin cleaves fibrinogen to fibrin to create a fibrin meshwork. Thrombin is alos a potent activator of platelet leading to more platelet aggreation

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24
Q

Which cytoplasmic granules of platelets contain the P-selectin adhesion molecule?

A

alpah-granules

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25
Q

what are the contents of the dense granules of platelets?

A

ADP, ATP, ionized Calcium, serotonin and Epi.

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26
Q

What are the contents of alpha granules of platelets?

A

P-selectin, fibrinogen, caogulation factor V, vWF, fibronectin, platelet factor 4, PDGF, TGFbeta.

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27
Q

vWF interacts with what surface receptor on platelet?

A

GpIb

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28
Q

what acts as the bridge between the exposed collagen on endothelium and the platelet surface molecule GpIb?

A

vWF

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29
Q

Bernard soulier syndrome is a bleeding disorder due to genetic defect of what molecule?

A

GpIb

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30
Q

Once bound, platelet rapidly change shape. this change is accompanied by alterations in glycoproteins 1 that increases its affinity for 2 and by the translocation of negatively charged 3 to platelet surface.

A
  1. IIb/IIIa
  2. fibrinogen
  3. phospholipids (mainly phosphatidylserine. These serve as the nucleation sites for the assembly of coagulation factor complexes.
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31
Q

protease-activating receptor (PAR) is switched on by a proteolytic cleavage carried out by _

A

thrombin.

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32
Q

Recruitment of platelet occurs platelet activation and _ release.

A

ADP

Thromboxane A2.

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33
Q

During platelet aggregation, what forms a bridge between adjacent platelets, leading to their aggregation?

A

Fibrinogen

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34
Q

Glanzmann thrombasthenia is a bleeding disorder due to inherited deficiency of _

A

GpIIb/IIIa

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35
Q

In the coagulating cascade, Ca binds to 1 residues which are present on factors 2 ,3 , 4 and 5.

A
  1. gamma-carboxylated glutamic acid
  2. II
  3. VII
  4. IX
  5. X
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36
Q

What cofactor is required for the enzymatic reactions that produce y-carboxylated glutamic acid in the coagulating cascade?

A

Vitamin K

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37
Q

which factors are part of the intrinsic pathway in the coagulating cascade?

A

II, V, VIII, IX, X, XI, XII and fibrinogen

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38
Q

Which factors are part of the extrinsic pathway in the coagulating cascade?

A

II, V, VII, and X.

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39
Q

Prothrombin time (PT) is an assay that assesses the function of proteins in the _ pathway.

A

extrinsic pathway

40
Q

the partial thromboplastin time (PTT) assay screens the function of proteins in the _ pathway

A

intrinsic pathway

41
Q

PT assay requires what addition components to be added to the plasma?

A

Tissue factors, phospholipids, and Ca

42
Q

PTT assay, clotting of plasma can be initiated by addition of 1 that activate factor 2 together with phospholipids and Ca clotting time can be recorded

A
  1. negative-charged particles like glass beads

2. Factor XII (Hageman factor)

43
Q

Deficiency of which factor is incompatible with life?

A

Factor II aka prothrombin

44
Q

patients with deficiency of which factor do not bleed and are prone to thrombosis?

A

Factor XII

45
Q

XI deficiency is associated with _

A

mild bleeding.

46
Q

which factors complex is most important activator of factor IX?

A

factors VIIa/tissue factor complex

47
Q

What factor complex is the most important activator of factor X?

A

Factor IXa/VIIIa

48
Q

What are the roles of thrombin?

A
  1. Conversion of fibrinogen into cross-linked fibrin and activating factor XIII.
  2. Platelet activation - potent inducer of platelet activation and aggregation through it’s ability to activate PARs
  3. Pro-inflammatory effects by activating PARs which are present on inflammatory cells (leukocytes).
  4. Anticoagulant effects, when it encounters normal endothelium it switches from procoagulant to an anticoagulant.
49
Q

How is Thrombin able to amplify the coagulation process?

A

By activating factor XI, V and VIII. Also stabilizes the secondary hemostatic plug by activating factor XIII.

50
Q

What enzyme breaks down fibrin and interferes with its polymerization?

A

Plasmin

51
Q

How does plasminogen get converted to plasmin?

A
  1. Factor XII-dependent pathway OR

2. plasminogen activator like t-TA.

52
Q

_ acts as a counterregulatory factors such that it binds and rapidly inhibits free plasmin

A

alpha2-plasmin inhibitor

53
Q

Active protein C is able to inactivate what factors?

A

Factors Va and VIIIa

54
Q

Thrombomodulin inhibits thrombin, and activates _

A

Protein C

55
Q

What do normal endothelium release that which inhibit platelet activation and aggregation?

A

Prostacyclin, Nitric oxide, and adenosine diphosphatase.

56
Q

Explain antithrombotic properties of endothelium.

A
  1. Platelet inhibitory effects: releases PGI, NO, ADPase,
  2. Anticoagulant effects: shields coagulation factors from tissue factor and expression factors that oppose coagulation like thrombomodulin, endothelial protein C receptor, heparin-like molecules and tissue factor pathway inhibit. Protein C inhibits factor Va and VIIIa. Heparin-like molecules activate antithrombin III which then inhibit thrombin and factors IXa, Xa, XIa, and XIIa.
  3. Fibrinolytic effects: normal endothelium synthesizes t-PA.
57
Q

Tissue factor pathway inhibit (TFPI) requires protein S as a cofactor and is able to bind and inhibit what factor complex?

A

Tissue factor - VIIa complex.

58
Q

Defects of primary hemastasis (platelet or vWF disease) often presents with

A

small bleeds in skin or mucosal membranes and usually forms petechiease, minute 1- to 2-mm hemorrhages, or purpura which are slightly bigger.

59
Q

A defect of the secondary hemostatsis is due to defect of 1 and often presents with bleeds into 2.

A
  1. Coagulation factor defects

2. soft tissues like muscle or joints.

60
Q

How would hemorrhages due to a generalized defect involving small vessels present?

A

Palpable purpura and ecchymose.

61
Q

Blood loss less than what percent usually has little impact in healthy adults?

A

20%

62
Q

what is the Virshow triad?

A

The triad of events that lead to a thrombosis. It includes: 1. endothelial injury, 2. stasis or turbulent blood flow, and 3: hypercoaugulabiliy.

63
Q

Of the factors in Virchow’s triad what is the most important factor leading to thrombosis?

A

Endothelial injury cuz it can impact the other two–it can alter local blood flow and affect coagulability.

64
Q

Due to inflammation and other noxious stimuli, endothelium can present with procaogulant changes and antiribinolytic effects. What are some procoagulant changes that it can present?

A
  • down regulate expresion of thrombomodulin which can result in sustained activation of thrombin and can in turn stimulate platelets and augment inflammation through PARS.
  • Downregulate expression of anticoagulant like Protein C and tissue factor protien inhibitor.
  • activated endothelial cells secrete plasminogen activator inhibitors (PAI) which inhibit fibrinolysis and downregulate tPA.
65
Q

In about 2-15% of caucasian carry a single nucleotide mutation in factor V leading to disease called factor V Leiden. What are the clinical significances of this disease and where exactly is the mutation?

A
  • pt presents with recurrent DVT.

- Mutation: Glutamine to arginine substitution in amino acid residue 506 leading to resistance to activated protein C.

66
Q

What are some factors that can lead to hypercoagulability?

A
  1. Factor V Leiden - resistance to protein C due to glutamine to arg substititon
  2. Single nucleotide change in the 3’ untranslated region of prothrombine gene leading to elevated prothrombin levels
  3. elevated levels of homocysteine leading to thioester linkages formed between homocystein metabolites anda variety of protein including fibrinogen. can be due to inherited deficiency of cysthione beta-synthetase.
  4. deficiencies of anticoagulants such as antithrombin III, protein C, or protein S.
67
Q

What are some inherited causes of thrombophilia?

A
  • Cardiac failure, truama
  • use of oral contraceptive use
  • hyperestrogenic state of pregnancy –> increased sysnthesis of coagulation factors and reduced anticoagulatn
  • cancer
68
Q

In heparin-induced thrombocytopenia, administration of 1 induces the appearance of antibodies that recognize complexes of heparin and platelet factor 2 on surface of platelets, and also heparin-like molecules and platelet factor_3_-like proteins on endothelial cells. Leads to pro-thrombotic state

A
  1. unfractionated heparin
  2. IV
  3. IV
69
Q

What clinical presentations are associated with antiphospholid antibody syndrome?

A
  • recurrent thromboses
  • repeated miscarriages
  • cardiac valve vegetation
  • thrombocytopenia
  • PE
  • pulmonary hypertension
  • stroke
  • bowel infarction or renovascular hypertension
  • renal microangiopathy
70
Q

Arterial or cardiac thrombi usually begin at sites of 1 2_, whereas venous thrombi occur at sites of _

A
  1. turbulence or endothelial injury

2. sites of stasis.

71
Q

In what direction does arterial thrombi flow? Venous thrombi?

A

Arterial flows retrograde

Venous flows direction of blood flow.

72
Q

What are lines of Zahn and where is it seen?

A

Lines of Zahn are plate platelet and fibrin deposits alternating with darker red cell rich layers.
Seen on thrombi

73
Q

Superficial venous thrombi typically occur in _ veins in the setting of varicosities. Do these usually embolize?

A

Saphenous Vein.

No

74
Q

What is Trousseau syndrome?

A

Migratory thrombophlebitis as seen in disseminated cancers.

75
Q

DIC is complication of a large number of condition associated with systemic activation of _

A

thrombin

76
Q

Where do pulmonary emboli usually originate?

A

deep venous thromboses

77
Q

what is paradoxical embolism?

A

when a venous embolus passes through an IA or IV defect and gains access to systemic arterial circulation

78
Q

Cor pulmonale occurs when an emboli obstruct _ % of more of the pulmonary circulation.

A

60%

79
Q

Where do systemic emboli usually arise?

A

Mural thrombi (2/3 associated with LV wall infarcts and 1/4 with LA dilation and fibrillation)

80
Q

About 75% of systemic emobli rest in 1 and about 10% in 2.

A
  1. lower extremities

2. brain

81
Q

A patient with pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia is associated with what kind of emboli? what kind of symptom usually ensues 1 to 3 days later?

A

Fat emboli as seen in fat embolism syndrome. 1-3 days later they present with sudden onset of tachypnea, dyspnea, and tachycardia; irritability and restlessness and can progress to delirium or coma.

82
Q

Rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is responsible for the painful condition called _

A

the bends

83
Q

Decompression sickness results from _

A

sudden decreases in atmospheric pressure as seen in scuba and deep sea divers.

84
Q

Gas bubbles in the vasculature of lungs that cause edema and hemorrhage and focal atelectasis or emphysema leads to this respiratory distress.

A

Chokes

85
Q

The more chronic form of decompression sickness is called _

A

caisson disease

86
Q

In _ disease, perssitence of gas emboli in skeletal system leads to multiple foci of ischemic necrosis, commonly in sites like femoral heads, tibia, and humeri.

A

Casisson disease

87
Q

Red infarcts are usually seen in what tissues?

A
  1. Venous occlusions like testicular torsion
  2. In loose, spongy tissues like lung
  3. Tissues with dual circulations like lung and small intestine
  4. in tissues previously congested by sluggish venous outflow
  5. when flow is reestablished to a site of previously arterial occlusion and necrosis.
88
Q

White infarcts usually occur in _

A

with arterial occlusion in solid organs with end-arterial circulation like heart, spleen, and kidney. White infarct with time become paler and more sharply defined.

89
Q

The dominant histologic chraceristic of infarction show characteristic of what kind of necrosis?

A

ischemic coagulative necrosis.

90
Q

A septic infarction can be morphologically identified via presence of

A

abscess.

91
Q

_ is a state in which diminished CO or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia.

A

Shock

92
Q

Cardiogenic shock is associated with _ 1
Hypovolemic shock is associated with _2
Shock associated with systemic inflammation is triggered by _3

A
  1. low CO due to myocardial pump failure
  2. low CO due to low blood volume as seen in massive hemorrhage or fluid loss from burn
  3. microbial infection, burns, trauma, or pancreatitis.
93
Q

Septic shocks are commonly triggered by what class of bacteria?

A

Gram-positive followed by gram-negative and fungi

94
Q

In pathogenesis of Septic shock, explain the chain of events of the inflammatory response.

A
  1. Microbial wall constituents engage receptors on cells of the innate immune system and trigger proinflammatory response. TLRs recognize microbe-drived substances containing PAMPs, G-protein coupled receptors detect bacterial peptides, and NOD1 and NOD2 is also involved.
  2. Activated immune cells produce TNF, IL, IFNy, IL12, IL18 and other mediates like HMGB1. ROS, lipid mediators like PG and PAF are also activated.
  3. Complement cascade is activated via proteolytic activity of plasmin resulting in anaphylotoxins (C3a, C5a), chemotactic fragments (C5a), opsonins (C3b).
  4. Coagulation pathway is activated directly through factor XII and indirectly through altered endothelial function.
  5. Widespread activation of thrombin further augment inflammation by triggering PARs on inflammatory cells.
  6. Activated endothelium also upregulate production of NO and other vasoactive inflammatory mediates which contribute to vascular smooth muscle relaxation and systemic hypotension
95
Q

In pathogenesis of septic shock, explain the metabolic abnormalities.

A
  1. insulin resistance and hyperglycemia
  2. TNF, IL1, stress-induced hormones like glucagon, GH, and glucocorticoids, and catecholamines all drive gluconeogenesis
  3. Pro-inflammatory cytokines suppress insulin release while promoting insulin resistance in liver and other tissues impairing the surface expression of LGUT4.
  4. Hyperglycemia decreases neutrophil function, thereby decreasing bactericidal activity and increasing adhesion molecule expression on endothelial cells.
  5. Cellular hypoxia and diminished oxidative phosphorylation leads to increased lactate production and lactic acidosis.
96
Q

What is Waterhouse-Friderichsen syndrome?

A

Commonly seen with septic shock. It is a condition of adrenal gland failure due to bleeding into the gland depressing the synthetic capacity of intact adrenal glands or frank adrenal necrosis due to DIC.

MOD Exam I (4 decks)

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