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
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)
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
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.
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
6
Q
How do you describe Transudative effusion?
A
Protein poor, serous, straw-colored; non-inflammatory
7
Q
Characteristics of exudative effusion?
A
Protein rich, opaque (cloudy), increased WBCs; inflammatory
8
Q
Subcutaneous edema is important because it may signify what?
A
Cardiac or renal disease
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
10
Q
Pulmonary edema is most commonly secondary to?
A
CHF (left ventricular failure)
11
Q
Ascites is often seen in context of _________ disease?
A
Severe liver disease
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
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
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
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’‘
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
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
18
Q
Where do platelets come from?
A
Megakaryocytes from bone marrow
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
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
21
Q
What do delta-granules of platelets contain?
A
Ca2+
ADP
ATP
Serotonin
Epinephrine
22
Q
Platelet adhesion occurs via what interaction?
A
vWF binds to platelet surface receptor GpIb
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
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)
25
Platelets aggregate and link through what interaction?
Fibrinogen - GpIIb/IIIa
26
During secondary hemostasis what occurs to consolidate the initial platelet plug?
What are the mediators?
- **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
27
What additional role does thrombin serve on endothelium?
Acts on normal endothelium to limit clot size
28
Which counterregulatory molecules limit the clotting to the site of injury?
- tPA
- Thrombomodulin
29
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?
- GPCR
- Protease-activated receptor (PAR)
30
Assembly of reaction complexes for the clotting cascade depends on \_\_\_\_?
Where does this molecule bind and on what factors?
- Dependent on Ca2+, which binds γ-carboxylated glutamic acid residues present on:
- Factors X, IX, VII, and II (prothrombin)
31
Glanzmann thrombasthenia is a inherited genetic deficiency of?
Defect of?
GpIIb-IIIa
Defect of **primary hemostasis**, platelets are impaired
32
Enzymatic reactions that produce γ-carboxylated glutamic acid residues use what as a cofactor?
Are antagonized by what drug?
- Vitamin K as a cofactor
- Antagonized by coumadin
33
What is the the most potent activator of factor IX and of factor X?
- Factor VIIa/TF complex activates Factor IX
- Factor IXa/Factor VIIIa complex activates Factor X
34
Thrombin feeds back and amplifies the coagulation cascade by activating what which factors?
XI, VIII, and V
35
What does PT measure; which factors?
What must you add?
- Extrinsic pathway; factors VII, X, V, II, fibrinogen
- Add TF, phospholipids and Ca2+
36
What does PTT measure; what factors?
What must you add?
- Intrinsic pathway; factors XII, XI, IX, VII, X, V, II, fibrinogen
- Add negatively charged surface, phospholipids, Ca2+
37
The mild bleeding tendency seen in patients with factor XI deficiency is likely explained by what?
**Thrombin's** ability to activate **factor V, VIII, and XI**, a feedback mechanism that **amplifies** the coagulation **cascade**
38
Fibrinolysis is largely accomplished through the enzymatic activity of?
Breaks down what?
What is one of the breakdown products?
- **Plasmin** which breaks down **fibrin** and interferes w/ its polymerization
- Breakdown product = **D-dimers**
39
The generation of plasmin from plasminogen is accomplished how?
What is the most important plasminogen activator; when is it most active?
- By factor XII-dependent pathway
- **t-PA** is **most important** activator; synthesized by endothelium and is most active when bound to fibrin
40
Once activated plasmin is tightly controlled by?
α2-plasmin inhibitor
41
Which factors are released by the intact endothelium that inhibit platelet activation and aggregation?
- PGI2
- NO
- Adenosine diphosphatase
42
What do heparin-like molecules on surface of endothelium activate?
What does this do?
- antithrombin III
- Inactivates thrombin, factors IX, X, XI, XII
\***clinical utility of heparin** is based on ability to stimulate **antithrombin III activity**
43
What induces the release of t-PA and why is this important?
**Thrombin** induces release of t-PA by endothelial cells, promoting **fibrinolysis**
44
Defects of of primary hemostasis (platelet defects or vW disease) may be acquired, what are some of the causes?
- **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
45
What does protein C do?
What does it require the help of?
- Inactivates factors V and VIII
- Vitamin K-dependent protease that requires a cofactor, **protein S**
46
Defects of primary Hemostasis is associated with what?
Classic finding?
- **Mucocutaneous** bleeding (i.e., epistaxis, GI bleeding, or menorrhagia)
- **Petechia** (1-2mm) and **purpura** (4-10mm)
47
What is Bernard-Soulier syndrome?
- GpIb deficiency
- Defect of **primay hemostasis**
48
Defects in secondary hemostasis are due to defects in?
How do they present?
- Coagulation factor deficiency(ies) either heriditary or acquired
- Often present with bleeding into **joints** (hemarthrosis) or **soft tissue**
49
Hemophilia A and B are caued by deficiencies in what factors?
- Hemophilia A = Factor **VIII** deficiency
- Hemophilia B = Factor **IX** deficiency
50
What makes up the Virchow triad in thrombosis?
1) **Endothelial injury**: procoagulant changes or anti-fibrinolytic effects
2) **Abnormal blood flow**: stasis or turbulence
3) **Hypercoagulability (AKA thrombophilia)**
51
What occurs in Disseminated Intravascular Coagulation (DIC)?
Characteristics of DIC?
- 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
What do the lab studies show in DIC (PT, PTT, fibrinogen, D-dimer, platelet count)?
- Elevated PT and PTT
- Low fibrinogen
- Increased D-dimer
- Low platelets (thrombocytopenia)
53
Where are most coagulation factors made?
What occurs to PT and PTT with dysfunction of this organ?
- Liver
- Decreased function = decreased synthesis = elevation of PT and PTT
54
Vitamin K is essential for production of what important components of the coagulation system?
Factors X, IX, VII, II (prothrombin), Protein C and S
55
Vitamin K deficiency is seen in?
- Patients receiving warfarin/Coumadin
- Malnourished or prolonged parental nutrition
- Prolonged antibiotics (Vit K is synthesized by gut microflora)
- Newborn infants
56
What is the definition of a Massive Transfusion?
What does it cause?
- Replacement of **1.5 x blood volume in 24 h**
- Increased PT and PTT, decreased fibrinogen and platelets
57
When does endothelial dysfunction result in a prothrombotic environment?
- Chronic inflammation
- HTN
- Hyperlipidemia and homocystinemia
- Circulating toxins (from cigarette smoke)
58
In endothelial injury the expression of which anticoagulants are downregulated?
What are the antifibrinolytic effects?
**Procoagulant effects:**
- Decreased **thrombomodulin** (by cytokines)
- Decreased **protein C**
- Decreased **TF inhibitor**
**Antifibrinolytic effects:**
- Decreased **t-PA** (by secreted **PAIs**)
59
Arterial thrombi arise at sites of?
Venous thrombi at sites of?
- **Turbulence** in arteries and heart (arterial and cardiac thrombosis)
- **Stasis** in vein (venous thrombi)
60
Altered blood flow contributes to thrombosis in several clinical settings, what are some examples?
- Ulcerated atherosclerotic plaques
- Aneurysms
- Infarcted myocardial tissue
- Prolonged immobilization (bed rest)
61
What is the defect in Factor V Leiden; resistant to?
Most common among what population?
- 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
What is the 2nd most common inherited cause of hypercoagulability?
What gene?
Increased risk for?
- 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
Marked elevation of Homocysteine may be caused by an inherited deficiency of what enzyme?
Contributes to what problems?
- Cystathione β-synthetase
- Arterial and venous thrombosis, as well as development of atherosclerosis
64
What are some examples of secondary (acquired) hypercoagulability (list 9)?
- 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
Heparin-induced thrombocytopenia (HIT) syndrome occurs following the administration of?
Induces the appearance of?
- 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
What must be considered when a patient younger than 50 presents with thrombosis even when acquired risk factors are present?
Inheritable causes of hypercoagulability (factor V Leiden or prothrombin mutations)
67
Antiphospholipid Antibody syndrome has clinical manifestations, including recurrent?
What Ab?
Abs suspected of binding to?
Can give a false positive?
- 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
Depending on the vascular bed involved what are some of the clinical manifestations of Antiphospholipid Antibody Syndrome?
- Pulmonary embolism
- Pumonary HTN - from recurrent subclinical PE's
- Stroke
- MI
- Bowel infarction
- Renal failure
69
Antiphospholipid Antibody syndrome can be secondary and primary, what designates these forms?
**Secondary** = individuals w/ well-defined auto-immune disease, such as **systemic lupus erythematous**
**Primary** = pt's exhibit only manifestations of a hypercoagulable state
70
What is Migratory Thrombophlebitis (aka Trousseau's syndrome)?
- 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
Thrombi are often laminated with what morphological characteristic?
Indicates and helps distinguish how?
- **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
Common sites of arterial thrombi include?
- Coronary, cerebral, and femoral arteries
- Sites of turbulence or endothelial injury
73
Venous thrombi are typically richer in _____ and form \_\_\_\_\_\_?
Venous thrombi are typically richer in **RBCs** and form **casts**
74
Common sites of venous thrombi include?
**Veins of leg** (superficial and deep), UE's
75
Thrombi occuring in the heart or within the aorta are termed?
Occur in the setting of?
- Mural thrombi
- Occur in setting of MI or aortic aneurysm
76
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 ?
- 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
Thrombi on heart valves are called?
Vegetations
78
What occurs in organization (which cell types come in) and recanalization of a thrombus?
**Organization:** thrombus replaced by **fibroblasts, smooth muscle,** and **endothelial cells**
**Recanalization:** new capillaries and small vessels grow through the structure
79
DIC is not a single disease, but rather, a complication arising from different causes such as?
- Sepsis
- Childbirth complications
- Massive trauma
- Malignancy
80
What type of cells may be found in DIC?
Intravascular hemolysis --\> Schistocytes
81
Most common factor to be clinically significantly inhibited is?
May occur in multiple clinical scenarios, such as?
- Factor VIII (Hemophilia A)
- B-cell lymphoma/plasma cell neoplasms or Amyloidosis
82
A mixing study is used to determine what?
What will not correct if there is inhibitor present?
- 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
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?
- Artierial thrombi grow **retrograde**
- Venous thrombi extend in direction of **blood flow**
- **BOTH** sources of thrombi **extend towards the heart**
84
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?
Mycotic aneurysm
85
\>95% of Pulmonary Embolisms arise from?
Deep venous thrombi (DVT) of the legs
86
In PEs what can become occluded?
How does risk of PEs change with recurrence?
- 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
Superficial venous thrombi typically occur where?
Cause what?
- 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
Deep venous thrombi typically occur in which veins?
Why are they more serious?
Symptoms?
- Popliteal, femoral, and Iliac Vs.
- Can embolize to the lung
- 50% are asymptomatic; some cause edema and pain
89
Sudden death or right heart failure from PE may occur when?
60% of the pulmonary arterial circulation is obstructed
90
Most systemic emboli (80%) arise from?
Intracardiac mural emboli (LV wall and LA dilation/fibrillation
91
Vast majority of arterial emboli (systemic thromboembolism) travel to and come to rest where?
Other places include?
- Majority to lower extremities (75%)
- Brain (10%)
- Others: intestines, kidneys, spleen, UE's
92
What are the other sites of systemic thromboembolism?
- Aortic aneurysms
- Atherosclerotic plaques
- Cardiac valves ("vegetations")
- Paradoxical emboli
93
Fat and marrow embolisms are usually caused by?
Where does it translocate?
Very common incidental finding after?
- Bone fracture (long bones), the trauma of which pushes marrow/fat globules into venous sinuses and then travesl to the lungs
- Vigorous CPR
94
What is a paradoxical embolism?
Venous embolus passed through defect in heart and gains access to systemic arterial circulation
95
What is fat embolism syndrome?
Characterized by?
What is the onset like?
- 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
What causes the biochemical injury seen in Fat Embolism Syndrome?
- Release of free fatty acids from fat globules causes local toxic injury to endothelium
- Platelet activation
- Granulocyte recruitment
97
Air embolisms must be what size to produce a clinical effect?
How can they be introduced?
- Greater than 100cc
- Surgically (vascular, neurosurgical, or laparoscopic)
98
What is Caisson disease?
Most common sites?
- Persistence of gas emboli in skeletal system leads to multiple foci of ischemic necrosis
- Femoral head, tibia, and humerus
99
What is an Amniotic Fluid Embolism?
85% of survivors have?
- 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
What is seen at the onset of Amniotic Fluid Embolism and is followed by?
If survived, commonly seen?
- Onset: severe dyspnea, cyanosis, and shock
- Followed by: neurologic impairment (headaches, seizure, coma)
- If survived, then pulmonary edem and **frequently DIC**
101
Histologically what kind of cells will be seen in pulmonary arterioles as a result of an Amniotic Fluid Embolism?
Fetal squamous cells
102
Much of the morbidity/mortality for Amniotic Fluid Embolism is caused by the biochemical activation of?
Coagulation factors and innate immune system
103
What is infarction?
Due to what?
- 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
What is characteristic of a red (hemorrhagic) infarct, where are they most often found?
- Tissue with a **dual** blood supply (lung, small intestine)
- Venous occlusion (torsion)
- Previously congested tissue
- Reperfused necrotic tissue after arterial occlusion
105
What is characteristic of a white (anemic) infarct, where are they most often found?
- Arterial occlusions in solid organs with **end-arterial circulation**
- Spleen, kidney, or heart
106
What is the morphology of an infarct both macro- and microscopically?
- Wedge-shaped, involving the geographic distribution of the occluded vessel
- Ischemic **coagulative** necrosis; except brain = liquefactive
- Most infarct ultimately replaced by **scar**
107
What is the most common cause of death in US ICUs?
Mortality rate?
Causative organism?
- Septic Shock
- \>20% mortality
- Gram positive bacteria
108
When does a septic infarct occur?
What can it be converted to?
- Infected cardiac valve vegetations embolize or when microbes seed necrotic tissue
- Infarct converted to an **abscess** w/ a correspondingly greater inflammatory response
109
What causes shock?
Diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia
110
What causes cardiogenic, hypovolvemic, and shock associated with systemic inflammation?
**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
What are the main characteristics of septic shock (i.e., pathogenesis)?
- 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
Hyperinflammatory state initiated by sepsis also activates counter-regulatory immunosuppressive mechanisms, what is one proposed mechanism for the immune suppression?
Shift from TH1 (pro-inflammatory) to TH2 (anti-inflammatory) cytokines
113
What metabolic disturbances can septic shock cause?
Inflammatory cytokines impair what?
- Insulin resistance and hyperglycemia
- Cytokines suppress GLUT-4
- Adrenal insufficiency and defecit of glucocorticoids
114
Cellular hypoxia and decreased ox-phos in septic shock leads to what?
Increased lactate production and lactic acidosis
115
How does septic shock affect organs?
The damage is occuring due to?
- 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
What is the treatment for septic shock?
- Treat underlying infection - **antibiotics**
- IV fluids, pressors, and oxygen
117
In the initial nonprogressive stage of shock what is occuring and the net effect/goal of these mechanisms?
- 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
What characterizes the progressive phase of shock?
- Tissue hypoperfusion and widespread hypoxia
- Aerobic ---\> anaerobic metabolism (lactic acidosis)
- Arterioles dilate and blood begins to pool in microcirculation (stasis)
119
In cardiogenic/hypovolemic shock, how does the patient present?
Septic shock?
- **Hypovolemic/cardiogenic shock:** hypotension, tachypnea; skin is cool, clammy, and cyanotic
- **Septic shock:** skin initially warm and flushed due to peripheral vasodilation
120
What are the group of secreted bacterial proteins that can cause a syndrome similar to septic shock, called toxic shock syndrome?
Describe them.
- 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
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**?
Diffuse alveolar damage, so-called **shock lung**
122
What induces conformational change to express the GpIIb-IIIa complex to be exposed?
ADP
