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MOD Exam 1 > Chapter 4: Hemodynamic Disorders, Thromboembolic Disease, and Shock > Flashcards

Chapter 4: Hemodynamic Disorders, Thromboembolic Disease, and Shock Flashcards

1
Q

Reduced plasma osmotic pressure is caused by what?

A
  • Liver disease; protein malnutrition = decreased synthesis of albumin
  • Nephrotic syndrome (kidney) = increased loss of albumin
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2
Q

Increased hydrostatic pressure is caused by what?

A

Most often due to impaired venous return, may be localized (i.e., DVT) or systemic (i.e., CHF)

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3
Q

CHF may lead to renal hypoperfusion, which results in the activation of?

Affect on hydrostatic pressure and plasma colloid osmotic pressure?

A
  • Activation of the RAAS system (reabsorbs sodium and water follows)
  • Causes increased hydrostatic pressure due to intravascular volume expansion
  • Decreased vascular colloid osmotic pressure due to dilution
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4
Q

What can cause edema via lymphatic obstruction?

Surgical removal and/or radiation of what can lead to severe edema of the UE?

A
  • Trauma, fibrosis, invasive tumors, and microbes
  • Decreased ability of lymph system to take up the fluid results in lymphedema
  • -* Surgical removal and/or radiation of the breast and associated axillary LN’s in breast cancer pt’s.
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5
Q

What effect does the parasitic filariases have on the lymphatics?

Results in?

A
  • Obstructive fibrosis of the lymph channels and nodes
  • Edema of the external genitalia and lower limbs that can be very extreme and called elephantiasis
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6
Q

How do you describe Transudative effusion?

A

Protein poor, serous, straw-colored; non-inflammatory

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7
Q

Characteristics of exudative effusion?

A

Protein rich, opaque (cloudy), increased WBCs; inflammatory

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8
Q

Subcutaneous edema is important because it may signify what?

A

Cardiac or renal disease

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9
Q

Edema resulting from renal dysfunction initially appears where?

What is a characteristic sign of severe renal disease?

A
  • Parts of the body containing loose CT, such as the eyelids.
  • Periorbital edema is a characteristic finding of severe renal disease
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10
Q

Pulmonary edema is most commonly secondary to?

A

CHF (left ventricular failure)

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11
Q

Ascites is often seen in context of _________ disease?

A

Severe liver disease

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12
Q

Increased blood volume in tissue, either locally or systemically is called what?

Result of what?

A
  • Hyperemia
  • Active process w/ arteriolar dilation = increased arterial blood delivery to a given location (i.e., sites of inflammation or in skeletal muscle during exercise)
  • Often physiologic
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13
Q

Congestion is the result of what?

Causes what?

Chronic cases lead to what?

A
  • Passive process that = decreased blood outflow; systemic (i.e., cardiac failure) or localized obstruction
  • Increases hydrostatic pressure, which may lead to edema
  • Chronic cases may lead to hypoxia and ischemia
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14
Q

In chronic pulmonary congestion, which is often caused by CHF, the septa are thick and fibrotic, and the alveoli contain what telltale (diagnostic) sign?

A

Hemosiderin-laden macrophages, called heart failure cells

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15
Q

Morphologically, what appearance do congested tissues take on?

A
  • Dusky, reddish-blue color (cyanosis) due to red cell stasis and deoxygenated hemoglobin
  • “Blue and bloated’‘
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16
Q

What is the morphology seen with chronic passive hepatic congestion?

A
  • Nutmeg liver = centrilobular regions are grossly red-brown and slightly depressed
  • Microscopically there is centrilobular hemorrhage and hemosiderin-laden macrophages
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17
Q

What is the 1st thing that happens in Hemostasis at the site of vascular injury?

What mediates this process?

A
  • Arteriolar vasoconstriction (AKA vasospasm)
  • Neurogenic reflexes mechanisms and augmented by factors such as endothelin released from the endothelium
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18
Q

Where do platelets come from?

A

Megakaryocytes from bone marrow

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19
Q

What is the 2nd event at the site of injury during hemostasis?

Mediated by?

A
  • Exposure of subendothelial von Willebrand factor (vWF) and collagen promote platelet adherance and activation
  • Platelets shape change to flate plate w/ spiky protrusions to increase S.A.
  • Platelets also release granules which recruit more platelets to the area to form a primary hemostatic plug
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20
Q

What do alpha-granules of platelets contain?

Which adhesion molecule on their membranes?

A

Fibrinogen

Factor V

vWF

Wound healing: fibronectin, platelet factor 4, PDGF

On their membranes: P-selectin

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21
Q

What do delta-granules of platelets contain?

A

Ca2+

ADP

ATP

Serotonin

Epinephrine

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22
Q

Platelet adhesion occurs via what interaction?

A

vWF binds to platelet surface receptor GpIb

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23
Q

As the platelet becomes activated and takes on a new shape, resembling a spiky sea urchin, what alterations to the platelet occur?

A
  • Glycoprotein IIb/IIIa increases its affinity for fibrinogen
  • Translocation of negatively charged phospholipids (particularly phosphatidylserine) to the platelet surface
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24
Q

Activated platelets produce what potent inducer of platelet aggregation?

What inhibits this?

A
  • Thromboxane A2 (TxA2)
  • Cyclooxygenase required for synthesis (inhibted by aspirin)
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25
Q

Platelets aggregate and link through what interaction?

A

Fibrinogen - GpIIb/IIIa

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26
Q

During secondary hemostasis what occurs to consolidate the initial platelet plug?

What are the mediators?

A
  • Tissue factor is exposed at the site of injury, which can then bind and activate factor VII
  • Results in the generation of thrombin, which cleaves circulating fibrinogen into insoluble fibrin, creating a fibrin meshwork and also recruits and activates more platelets
  • Ultimately this process stabilizes the clot
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27
Q

What additional role does thrombin serve on endothelium?

A

Acts on normal endothelium to limit clot size

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28
Q

Which counterregulatory molecules limit the clotting to the site of injury?

A
  • tPA
  • Thrombomodulin
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29
Q

Thrombin is a potent inducer of platelet activation and aggregation through its ability to activate platelets through what kind of receptor?

What is the name of the receptor?

A
  • GPCR
  • Protease-activated receptor (PAR)
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30
Q

Assembly of reaction complexes for the clotting cascade depends on ____?

Where does this molecule bind and on what factors?

A
  • Dependent on Ca2+, which binds γ-carboxylated glutamic acid residues present on:
  • Factors X, IX, VII, and II (prothrombin)
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31
Q

Glanzmann thrombasthenia is a inherited genetic deficiency of?

Defect of?

A

GpIIb-IIIa

Defect of primary hemostasis, platelets are impaired

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32
Q

Enzymatic reactions that produce γ-carboxylated glutamic acid residues use what as a cofactor?

Are antagonized by what drug?

A
  • Vitamin K as a cofactor
  • Antagonized by coumadin
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33
Q

What is the the most potent activator of factor IX and of factor X?

A
  • Factor (7a) VIIa/TF complex activates Factor IX
  • Factor (9a) IXa/Factor (8a) VIIIa complex activates Factor X
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34
Q

Thrombin feeds back and amplifies the coagulation cascade by activating what which factors?

A

XI, VIII, and V

(eleven, eight, five)

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35
Q

What does PT measure; which factors?

What must you add?

A
  • Extrinsic pathway; factors VII, X, V, II, fibrinogen
  • Add TF, phospholipids and Ca2+

(10, 7, 5, 2, fibrinogen)

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36
Q

What does PTT measure; what factors?

What must you add?

A
  • Intrinsic pathway; factors XII, XI, IX, VII, X, V, II, fibrinogen
  • Add negatively charged surface, phospholipids, Ca2+

(12, 11, 10, 9, 7, 5, 2, fibrinogen)

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37
Q

The mild bleeding tendency seen in patients with factor XI deficiency is likely explained by what?

A

Thrombin’s ability to activate factor V, VIII, and XI, a feedback mechanism that amplifies the coagulation cascade

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38
Q

Fibrinolysis is largely accomplished through the enzymatic activity of?

Breaks down what?

What is one of the breakdown products?

A
  • Plasmin which breaks down fibrin and interferes w/ its polymerization
  • Breakdown product = D-dimers
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39
Q

The generation of plasmin from plasminogen is accomplished how?

What is the most important plasminogen activator; when is it most active?

A
  • By factor XII-dependent pathway
  • t-PA is most important activator; synthesized by endothelium and is most active when bound to fibrin
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40
Q

Once activated plasmin is tightly controlled by?

A

α2-plasmin inhibitor

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41
Q

Which factors are released by the intact endothelium that inhibit platelet activation and aggregation?

A
  • PGI2
  • NO
  • Adenosine diphosphatase
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42
Q

What do heparin-like molecules on surface of endothelium activate?

What does this do?

A
  • antithrombin III
  • Inactivates thrombin, factors IX, X, XI, XII

*clinical utility of heparin is based on ability to stimulate antithrombin III activity

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43
Q

What induces the release of t-PA and why is this important?

A

Thrombin induces release of t-PA by endothelial cells, promoting fibrinolysis

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44
Q

Defects of of primary hemostasis (platelet defects or vW disease) may be acquired, what are some of the causes?

A
  • Aspirin use inhibiting cyclooxygenase –> decrease TxA2 –> decreased platelet aggregation
  • Renal failure —> uremia –> decreased platelet function
  • Thrombocytopenia (low platelet count): if very low intracerebral hemorrhage can occur and be fatal
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45
Q

What does protein C do?

What does it require the help of?

A
  • Inactivates factors V and VIII
  • Vitamin K-dependent protease that requires a cofactor, protein S
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46
Q

Defects of primary Hemostasis is associated with what?

Classic finding?

A
  • Mucocutaneous bleeding (i.e., epistaxis, GI bleeding, or menorrhagia)
  • Petechia (1-2mm) and purpura (4-10mm)
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47
Q

What is Bernard-Soulier syndrome?

A
  • GpIb deficiency
  • Defect of primay hemostasis
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48
Q

Defects in secondary hemostasis are due to defects in?

How do they present?

A
  • Coagulation factor deficiency(ies) either heriditary or acquired
  • Often present with bleeding into joints (hemarthrosis) or soft tissue
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49
Q

Hemophilia A and B are caued by deficiencies in what factors?

A
  • Hemophilia A = Factor VIII deficiency
  • Hemophilia B = Factor IX deficiency
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50
Q

What makes up the Virchow triad in thrombosis?

A

1) Endothelial injury: procoagulant changes or anti-fibrinolytic effects
2) Abnormal blood flow: stasis or turbulence
3) Hypercoagulability (AKA thrombophilia)

51
Q

What occurs in Disseminated Intravascular Coagulation (DIC)?

Characteristics of DIC?

A
  • Activation of the coagulation and fibrinolysis systems —> simultaneous production of thrombin and plasmin
  • Widespread microthrombi
  • Consumption of coagulation factors and platelets (AKA consumptive coagulopathy)
52
Q

What do the lab studies show in DIC (PT, PTT, fibrinogen, D-dimer, platelet count)?

A
  • Elevated PT and PTT
  • Low fibrinogen
  • Increased D-dimer
  • Low platelets (thrombocytopenia)
53
Q

Where are most coagulation factors made?

What occurs to PT and PTT with dysfunction of this organ?

A
  • Liver
  • Decreased function = decreased synthesis = elevation of PT and PTT
54
Q

Vitamin K is essential for production of what important components of the coagulation system?

A

Factors X, IX, VII, II (prothrombin), Protein C and S

(10, 9, 7, 2, Prot. C & S)

55
Q

Vitamin K deficiency is seen in?

A
  • Patients receiving warfarin/Coumadin
  • Malnourished or prolonged parental nutrition
  • Prolonged antibiotics (Vit K is synthesized by gut microflora)
  • Newborn infants
56
Q

What is the definition of a Massive Transfusion?

What does it cause?

A
  • Replacement of 1.5 x blood volume in 24 h
  • Increased PT and PTT, decreased fibrinogen and platelets
57
Q

When does endothelial dysfunction result in a prothrombotic environment?

A
  • Chronic inflammation
  • HTN
  • Hyperlipidemia and homocystinemia
  • Circulating toxins (from cigarette smoke)
58
Q

In endothelial injury the expression of which anticoagulants are downregulated?

What are the antifibrinolytic effects?

A

Procoagulant effects:

  • Decreased thrombomodulin (by cytokines)
  • Decreased protein C
  • Decreased TF inhibitor

Antifibrinolytic effects:

  • Decreased t-PA (by secreted PAIs)
59
Q

Arterial thrombi arise at sites of?

Venous thrombi at sites of?

A
  • Turbulence in arteries and heart (arterial and cardiac thrombosis)
  • Stasis in vein (venous thrombi)
60
Q

Altered blood flow contributes to thrombosis in several clinical settings, what are some examples?

A
  • Ulcerated atherosclerotic plaques
  • Aneurysms
  • Infarcted myocardial tissue
  • Prolonged immobilization (bed rest)
61
Q

What is the defect in Factor V Leiden; resistant to?

Most common among what population?

A
  • Arg –> Glu substitution, increased risk for venous thrombosis
  • Resistant to protein C (important counterregulatory pathway lost)
  • Most common among Caucasians (2-15% have at least one mutated gene)
  • 60% of patients with recurring DVT has this mutation
62
Q

What is the 2nd most common inherited cause of hypercoagulability?

What gene?

Increased risk for?

A
  • Single nucleotide change in (G20210A) in 3’-untranslated region of prothrombin gene
  • Leads to elevated prothrombin and almost 3-fold increase in risk of venous thrombosis
63
Q

Marked elevation of Homocysteine may be caused by an inherited deficiency of what enzyme?

Contributes to what problems?

A
  • Cystathione β-synthetase
  • Arterial and venous thrombosis, as well as development of atherosclerosis
64
Q

What are some examples of secondary (acquired) hypercoagulability (list 9)?

A
  • Immobilization (bed rest/long flights)
  • MI or atrial fib
  • Cancer
  • Hyperestrogenic state
  • Oral contraceptives
  • Tissue injury (surgery, fracture, burn)
  • Smoking
  • Heparin-induced thrombocytopein (HIT) syndrome
  • Antiphospholipid antibody syndrome
65
Q

Heparin-induced thrombocytopenia (HIT) syndrome occurs following the administration of?

Induces the appearance of?

A
  • Unfractionated heparin
  • May induce the appearance of Abs that recognize complexes of heparin and platelet factor 4 on surface of platelets and endothelial cells
  • Effect of the Ab binding produce a pro-thrombic state, even in the face of heparin administration and low platelet counts
66
Q

What must be considered when a patient younger than 50 presents with thrombosis even when acquired risk factors are present?

A

Inheritable causes of hypercoagulability (factor V Leiden or prothrombin mutations)

67
Q

Antiphospholipid Antibody syndrome has clinical manifestations, including recurrent?

What Ab?

Abs suspected of binding to?

Can give a false positive?

A
  • Recurrent thromboses, repeated miscarriages, cardiac valve vegetations, and thrombocytopenia
  • Anticardiolipid antibody
  • Suspected Ab targets include β2-glycoprotein I, which associates w/ surfaces of endothelial cells and trophoblasts, and thrombin
  • Can give a false positive syphilis test
68
Q

Depending on the vascular bed involved what are some of the clinical manifestations of Antiphospholipid Antibody Syndrome?

A
  • Pulmonary embolism
  • Pumonary HTN - from recurrent subclinical PE’s
  • Stroke
  • MI
  • Bowel infarction
  • Renal failure
69
Q

Antiphospholipid Antibody syndrome can be secondary and primary, what designates these forms?

A

Secondary = individuals w/ well-defined auto-immune disease, such as systemic lupus erythematous

Primary = pt’s exhibit only manifestations of a hypercoagulable state

70
Q

What is Migratory Thrombophlebitis (aka Trousseau’s syndrome)?

A
  • Seen with malignant cancers (pancreatic, lung) where they reduce prothrombotic mucin
  • Tumor associated inflammation and coagulation factors (TF and factor VIII), as well as procoagulants (i.e., Mucin) all increase risk of thromboembolism in disseminated cancer
71
Q

Thrombi are often laminated with what morphological characteristic?

Indicates and helps distinguish how?

A
  • Lines of Zahn: alternating red and tan regions (containing RBCs and platelets/fibrin, respectively)
  • Indicating that the thrombus formed in flowing blood, helps distinguish antemorten clots from bland non-laminated clots occuring postmortem
72
Q

Common sites of arterial thrombi include?

A
  • Coronary, cerebral, and femoral arteries
  • Sites of turbulence or endothelial injury
73
Q

Venous thrombi are typically richer in _____ and form ______?

A

Venous thrombi are typically richer in RBCs and form casts

74
Q

Common sites of venous thrombi include?

A

Veins of leg (superficial and deep), UE’s

75
Q

Thrombi occuring in the heart or within the aorta are termed?

Occur in the setting of?

A
  • Mural thrombi
  • Occur in setting of MI or aortic aneurysm
76
Q

In enusing days to weeks following a thrombus, the thrombi will undergo dissolution which is the result of?

How does the age of the thrombi effect this and any therapeutic ?

A
  • Dissolution by fibrinolysis
  • Older thrombi are more resistant to lysis
  • Therapeutic administration of t-PA is generally effective only when given during first few hours of a thrombic event
77
Q

Thrombi on heart valves are called?

A

Vegetations

78
Q

What occurs in organization (which cell types come in) and recanalization of a thrombus?

A

Organization: thrombus replaced by fibroblasts, smooth muscle, and endothelial cells

Recanalization: new capillaries and small vessels grow through the structure

79
Q

DIC is not a single disease, but rather, a complication arising from different causes such as?

A
  • Sepsis
  • Childbirth complications
  • Massive trauma
  • Malignancy
80
Q

What type of cells may be found in DIC?

A

Intravascular hemolysis –> Schistocytes

81
Q

Most common factor to be clinically significantly inhibited is?

May occur in multiple clinical scenarios, such as?

A
  • Factor VIII (Hemophilia A)
  • B-cell lymphoma/plasma cell neoplasms or Amyloidosis
82
Q

A mixing study is used to determine what?

What will not correct if there is inhibitor present?

A
  • Whether abnormal clotting times are due to a decreased amount of factor or presence of an inhibitor (i.e., an antibody)
  • PTT will remain prolonged if inhibitor present
83
Q

Thrombi are focally attached to the underlying vascular surface where the site of injury occured, which direction do arterial and venous thrombi extend?

Both toward?

A
  • Artierial thrombi grow retrograde
  • Venous thrombi extend in direction of blood flow
  • BOTH sources of thrombi extend towards the heart
84
Q

Weakening of the vessel wall that can occur from trapped leukocytes and platelets releasing lysosomal enzymes within the center of a thrombus that later becomes infected may result in _________ if unchecked?

A

Mycotic aneurysm

85
Q

>95% of Pulmonary Embolisms arise from?

A

Deep venous thrombi (DVT) of the legs

86
Q

In PEs what can become occluded?

How does risk of PEs change with recurrence?

A
  • Main pulmonary artery, straddle pulmonary artery bifurcation (saddle embolus), or pass out into the smaller, branching arteries
  • Patient who has had one PE is at high risk for more
87
Q

Superficial venous thrombi typically occur where?

Cause what?

A
  • Saphenous veins
  • Local congestion, swelling, pain, and tenderness, but rarely embolize
  • Associated edema and impaired venous drainage predispose overlying skin to development of infections and ulcers (varicose ulcers)
88
Q

Deep venous thrombi typically occur in which veins?

Why are they more serious?

Symptoms?

A
  • Popliteal, femoral, and Iliac Vs.
  • Can embolize to the lung
  • 50% are asymptomatic; some cause edema and pain
89
Q

Sudden death or right heart failure from PE may occur when?

A

60% of the pulmonary arterial circulation is obstructed

90
Q

Most systemic emboli (80%) arise from?

A

Intracardiac mural emboli (LV wall and LA dilation/fibrillation

91
Q

Vast majority of arterial emboli (systemic thromboembolism) travel to and come to rest where?

Other places include?

A
  • Majority to lower extremities (75%)
  • Brain (10%)
  • Others: intestines, kidneys, spleen, UE’s
92
Q

What are the other sites of systemic thromboembolism?

A
  • Aortic aneurysms
  • Atherosclerotic plaques
  • Cardiac valves (“vegetations”)
  • Paradoxical emboli
93
Q

Fat and marrow embolisms are usually caused by?

Where does it translocate?

Very common incidental finding after?

A
  • Bone fracture (long bones), the trauma of which pushes marrow/fat globules into venous sinuses and then travesl to the lungs
  • Vigorous CPR
94
Q

What is a paradoxical embolism?

A

Venous embolus passed through defect in heart and gains access to systemic arterial circulation

95
Q

What is fat embolism syndrome?

Characterized by?

What is the onset like?

A
  • Symptomatic fat and marrow emolisms (minority of patients)
  • Pulmonary insufficiency, neurological sx’s, anemia, and thrombocytopenia
  • Typically 1-3 days after injury there is sudden onset of tachypnea, dyspnea, and tachycardia; irritability and restlessness can progress to delirium or coma
96
Q

What causes the biochemical injury seen in Fat Embolism Syndrome?

A
  • Release of free fatty acids from fat globules causes local toxic injury to endothelium
  • Platelet activation
  • Granulocyte recruitment
97
Q

Air embolisms must be what size to produce a clinical effect?

How can they be introduced?

A
  • Greater than 100cc
  • Surgically (vascular, neurosurgical, or laparoscopic)
98
Q

What is Caisson disease?

Most common sites?

A
  • Persistence of gas emboli in skeletal system leads to multiple foci of ischemic necrosis
  • Femoral head, tibia, and humerus
99
Q

What is an Amniotic Fluid Embolism?

85% of survivors have?

A
  • 5th most common cause of maternal mortality
  • Amniotic fluid and/or fetal tissue enter maternal circulation via tear in placental membranes or rupture of uterine veins
  • 85% of survivors have permanent neuro deficits
100
Q

What is seen at the onset of Amniotic Fluid Embolism and is followed by?

If survived, commonly seen?

A
  • Onset: severe dyspnea, cyanosis, and shock
  • Followed by: neurologic impairment (headaches, seizure, coma)
  • If survived, then pulmonary edem and frequently DIC
101
Q

Histologically what kind of cells will be seen in pulmonary arterioles as a result of an Amniotic Fluid Embolism?

A

Fetal squamous cells

102
Q

Much of the morbidity/mortality for Amniotic Fluid Embolism is caused by the biochemical activation of?

A

Coagulation factors and innate immune system

103
Q

What is infarction?

Due to what?

A
  • Ischemic nerosis via occlusion of arterial supply or venous drainage
  • Arterial thrombosis or thromboembolism
  • Less common causes include: torsion, vessel trauma, compression due to tumor or edema, and herniation
104
Q

What is characteristic of a red (hemorrhagic) infarct, where are they most often found?

A
  • Tissue with a dual blood supply (lung, small intestine)
  • Venous occlusion (torsion)
  • Previously congested tissue
  • Reperfused necrotic tissue after arterial occlusion
105
Q

What is characteristic of a white (anemic) infarct, where are they most often found?

A
  • Arterial occlusions in solid organs with end-arterial circulation
  • Spleen, kidney, or heart
106
Q

What is the morphology of an infarct both macro- and microscopically?

A
  • Wedge-shaped, involving the geographic distribution of the occluded vessel
  • Ischemic coagulative necrosis; except brain = liquefactive
  • Most infarct ultimately replaced by scar
107
Q

What is the most common cause of death in US ICUs?

Mortality rate?

Causative organism?

A
  • Septic Shock
  • >20% mortality
  • Gram positive bacteria
108
Q

When does a septic infarct occur?

What can it be converted to?

A
  • Infected cardiac valve vegetations embolize or when microbes seed necrotic tissue
  • Infarct converted to an abscess w/ a correspondingly greater inflammatory response
109
Q

What causes shock?

A

Diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia

110
Q

What causes cardiogenic, hypovolvemic, and shock associated with systemic inflammation?

A

Cardiogenic = decreased cardiac output; MI, tamponade, arrhythmias

Hypovolemic = low cardiac output due to low blood volume; such as massive hemorrhage or fluid loss from severe burns

Sytemic inflammatory effects = microbial infections, burns, trauma, or pancreatitis; massive outporuing of inflammatory mediators (innate and adaptive) causing vasodilation, vascular leakage, and venous pooling

111
Q

What are the main characteristics of septic shock (i.e., pathogenesis)?

A
  • Microbial products (PAMPs) induce innate immune cells to release cytokines (i.e., TNF, IL-1, IFN-y, HMGB1); upregulation of endothelial adhesion molecules; activation of complement cascade; microbial components can directly activate coagulation through factor XII
  • Vasodilation –> Decreased BP
  • Increased permeability –> leakage and edema, impeding perfusion
  • Systemic increase of thrombin –> DIC in ~50% (procoagulant state)
112
Q

Hyperinflammatory state initiated by sepsis also activates counter-regulatory immunosuppressive mechanisms, what is one proposed mechanism for the immune suppression?

A

Shift from TH1 (pro-inflammatory) to TH2 (anti-inflammatory) cytokines

113
Q

What metabolic disturbances can septic shock cause?

Inflammatory cytokines impair what?

A
  • Insulin resistance and hyperglycemia
  • Cytokines suppress GLUT-4
  • Adrenal insufficiency and defecit of glucocorticoids
114
Q

Cellular hypoxia and decreased ox-phos in septic shock leads to what?

A

Increased lactate production and lactic acidosis

115
Q

How does septic shock affect organs?

The damage is occuring due to?

A
  • Accumulated damage secondary to hypoxia
  • Decreased perfusion secondary to decreased BP, vascular leakage, edema, stasis and thrombi
  • Kidneys, liver, lungs (ARDS), and heart most affected
116
Q

What is the treatment for septic shock?

A
  • Treat underlying infection - antibiotics
  • IV fluids, pressors, and oxygen
117
Q

In the initial nonprogressive stage of shock what is occuring and the net effect/goal of these mechanisms?

A
  • Compensatory mechanisms and perfusion of vital organs maintained by:
  • Baroreceptor reflex
  • Sympathetic discharge –> Catecholamines
  • Renal conservation of volume (RAAS) and release of ADH
  • Net effect: tachycardia, peripheral vasoconstriction, and renal conservation of fluid
118
Q

What characterizes the progressive phase of shock?

A
  • Tissue hypoperfusion and widespread hypoxia
  • Aerobic —> anaerobic metabolism (lactic acidosis)
  • Arterioles dilate and blood begins to pool in microcirculation (stasis)
119
Q

In cardiogenic/hypovolemic shock, how does the patient present?

Septic shock?

A
  • Hypovolemic/cardiogenic shock: hypotension, tachypnea; skin is cool, clammy, and cyanotic
  • Septic shock: skin initially warm and flushed due to peripheral vasodilation
120
Q

What are the group of secreted bacterial proteins that can cause a syndrome similar to septic shock, called toxic shock syndrome?

Describe them.

A
  • Superantigens
  • Polyclonal T-lymphocyte activators that induce release of high levels of cytokines
  • Result in variety of clinical manifestations, ranging from diffuse rash to vasodilation, hypotension, shock, and death
121
Q

Lungs are seldom affected in pure hypovolemic shock because are somewhat resistant to hypoxic injury, however what can happen to lungs if shock is caused by sepsis or trauma?

A

Diffuse alveolar damage, so-called shock lung

122
Q

What induces conformational change to express the GpIIb-IIIa complex to be exposed?

A

ADP

123
Q

What is the cause of nutmeg liver?

What is the cause of chronic hepatic congestion?

A

Chronic hepatic congestion/central vein congestion

can lead to portal HTN

Severe heart failure

MOD Exam 1 (6 decks)

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