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244 Cards in this Set
- Front
- Back
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are hypotension and shock synomynouse
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No, because shock can present with near normal BP do to a hypertensive patient in shock
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third spacing
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blood accumulating from internal bleeding within the GI tract of another body cavity
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hypovolemic shock
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decrease in intravascular blood volume
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cardiogenic shock
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heart failure resulting in decrease perfusion of peripheral tissue
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vasodilatory (distributive) shock
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blood being sequestered in the peripheral circulatory system and decrease amount returning to the heart
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obstructive shock
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obstruction of blood into or out of the heart
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compensated shock
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brief decline in the CO triggers a compensatory mechanism that restores BP to near normal levels
tachycardia (<100 bpm) pallor (cutaneous vasoconstriction) |
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decompensated shock
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occurs when compensatory mechanisms fail to maintain normal BP
supine pressure can still be normal organ hypoperfusion: chest pain, confusion, decreased urine output, increased ANS activity (tachycardia > 100 bpm) |
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refractory shock
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supine BP falls to levels below necessary to maintain tissue viability
anaerobic metabolism takes over leading to increased blood lactate levels impaired myocardial contractility from cytokine release |
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why doesn't chronic blood loss lead to hypovolemic shock
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compensatory mechanisms increase plasma volume and CO as number of RBCs decrease
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class 1 hemorrhagic shock
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sudden reduction of 10-15% of blood volume, causes no change in BP due to compensatory mechanisms
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primary insult in sudden decrease in intravascular volume
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prevents filling of the venous capacitance bed and decrease venous return to the heart - decreased preload
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class 2 hemorrhagic shock
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sudden reduction of 15-30% of blood volume, compensatory mechanisms are unable to maintain homeostasis resulting in orthostatic hypotention, but supine BP remains normal
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compensatory mechanisms for hypovolemic shock
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increased sympathetic tone: increased HR, contractility, preload, and afterload
activation of the RAAS vasopressin alteration in transcapillary fluid exchange |
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what does administration of supplemental O2 to patients in hemorrhagic shock do
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may decrease CNS sympathetic discharge and worsen their symptoms
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activation of RAAS in hypovolemic shock
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B1 receptor in the kidneys release renin
ATN II increases SVR aldosterone stimulates resorption of NaCl increases preload |
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how does increased sympathetic discharge increased transcapillary fluid exchange
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constricts the precapillary resistance vessels which decreases hydrostatic pressure allowing more resorption at the venule end
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class 3 hemorrhagic shock
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reduction of blood volume by 30-40%
supine hypotension tachycardia >120 bpm urine output fall to 5-15 mL/hr |
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class 4 hemorrhagic shock
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reduction in blood volume by >40%
MODS develops and refractory shock ensues |
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what produces myocardial depressant factor
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ischemic pancreas during cardiovascular shock
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what overrides a1 adrenergic receptors and causes relaxation of precapillary sphincters
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tissue hypoperfusion leading to local accumulation of tissue metabolites
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when could bradycardia occur during hypovolemic shock
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paradoxically occurs in extreme cases of massive blood loss in which the heart pumps extra hard activating mechanoreceptors that increase vagal tone
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what parts of the kidney are susceptible to hypoperfusion
criteria |
third portion of the proximal tubule
thick ascending limb both are located in the medulla and have high ATP demand |
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loss of what cells leads to shock lung
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type II alveolar cells remove excess fluid from alveolus, damage to these results in pulmonary edema
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distribution of 1 L of intravenous fluids:
isotonic NaCl and 5% dextrose |
isotonic NaCl - 3/4 goes to the interstitium and 1/4 to the intravascular compartment, none to intracellular compartment
5% dextrose - 2/3 goes intracellular compartment and the rest mostly goes to interstitium |
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fluid that can result in metabolic acidosis
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Isotonic Saline because conatins 154 mEq/L of Cl
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fluid that can result in metabolic alkalosis
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Ringer's lactate because contains 29 mEq/L of bicarb
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primary source of infection in septic shock
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lung
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hyperactive immune response
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mediated by Th1 cells characterized by uncontrolled inflammation and septic shock (TNF-a, IL-1,2,6 and HMGB1)
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hypoactive immune response
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mediated by Th2 cells characterized by more prolonged illness and superinfections (IL-4,10,13)
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what type of patients develop septic shock
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patients must be immunodeficient
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cytokine with delayed response produced by activated macrophages stimulated by other cytokines, geared more toward maintaining inflammation
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High mobility group box 1 (HMGB1)
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strong attractant for neutrophils
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C5a
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causes immune suppression by triggering apoptosis of B and T cells, produced by Th2 cells
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IL-10
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what stimulates VSM cells to produce iNOS during severe sepsis and shock
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LPS
TNF-a IL-1 and 6 |
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responsible for the systemic vasodilation that develops in severe sepsis and septic shock
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NO
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mechanism of NO during septic shock
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1. NO induces cGMP release which activates myosin phosphatase to dephosphorylate myosin leading to VSM relaxation
2. NO also open Katp channels leading to hyperpolarization and inability for calcium to mediate vasoconstriction 3. myocardial depression |
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inflammatory cytokines increase production of CRH and ACTH increasing serum cortisol concentration, why are adrenergic receptors still unresponsive to vasopressors
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because increased production of NO and down-regulation of adrenergic receptors
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what activates production of bradykinin
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endotoxin activates Hageman factor (XII) to increase production of bradykinin
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what stimulates the extrinsic clotting pathway by stimulating production of tissue factor (III)
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endotoxin
TNF-a |
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what is the function of tissue factor
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1. initiates extrinsic clotting pathway
2. binds protease activated receptors (PARs) on macrophages which leads to TNF-a production and release |
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role of TNF-a in coagulation
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1. enhances intravascular clotting by: decreasing AT III, activated protein C, and tissue factor pathway inhibitor
2. decreases fibrinolysis by: increasing plasminogen activator inhibitor-1 and increasing thrombin activatable fibrinolysis inhibitor |
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role of plasminogen activator inhibitor-1 (PAI-1)
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inhibits ability to form plasmin from plasminogen
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role of thrombin activatable fibrinolysis inhibitor (TAFI)
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inhibits the ability of formed plasmin to degrade fibrin
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actions of activated protein C (detrecogin-a)
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1. prevents tissue factor from binding PAR - decreases TNF-a release
2. inhibits cofactors V and VIII 3. blocks PAI-1 and TAFI - enabling fibrinolysis 4. inhibits B and T cell apoptosis |
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initiating event of cardiovascular manifestations of sepsis
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widespread vascular dilation lowering SVR
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agents that contribute to lowered SVR
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NO (major player)
prostaglandins B-endorphins |
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drugs that are used to close Katp channels
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sulfonylurea drugs
vasopressin |
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what mediates AV shunting and microthrombi formation
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AV shunting - No mediated
microthrombi - platelet and neutrophil aggregates |
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what disrupts tight junctions causing epithelial cells to lose polarity and leak plasma
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superoxide radicals released by neutrophils
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what type of organism is more likely to induce ARDS
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gram-negative
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useful to distinguish ARDS from cardiogenic pulmonary edema
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BNP levels:
<100 effectively rules out cardiogenic edema >500 highly suggestive of cardiogenic edema |
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characteristics of DIC
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increased FSPs
decreased fibrinogen thrombocytopenia (<20,000) increased PT and PTT |
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what two cells become insulin resistent leading to hyperglycemia during sepsis
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hepatocytes
adipocytes |
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hemodynamic findings of septic shock (vasodilatory shock)
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increased CO
decreased SVR increased LVEDV and P low/normal EF normal/high PAWP normal RVEDV and P normal JVP |
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mechanism of cell-bound CD14
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LPS binds to LBP which shuttles the molecule to cell-bound CD14. LPS is then passed to MD-2 which interacts with TLR-4, which activates MAP kinase and NF-kB
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mechanism of soluble CD14
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forms complexes with LPS or peptidoglycan of gram-positive.
CD14-LPS complex attach directly to vascular endothelial cells to stimulate cytokine CD14-peptidoglycan complex attaches to TLR-2 on inflammatory cells |
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mechanism of NOD-1 and 2
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recognize fragments of gram-positive peptidoglycans, are found intracellularly
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why is cardiac output increased during septic shock
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tachycardia + decreased afterload + increased preload
EF is actually decreased from normal ~55% |
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what form of shock has
decreased A-V oxygen difference why |
septic shock
AV shunting, microthrombi, and mitochondrial shutdown all decrease oxygen uptake by the cells |
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does urine output increased with fluid in decreased renal function during MODS
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No, there is parenchymal renal failure from renal vasoconstriction/hypoperfusion
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complement pathway associated with acquired immunity
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classical pathway
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what antibody is more efficient activator of the classical pathway
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IgM
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what activates C1q
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antibodies (IgG and IgM)
CRP |
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C1q deficiency
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autoimmune diseases because plays an important role in the opsonization of RNA complexes from apoptotic cell fragments via CRP activation
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what does CRP attach to
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chromatin and RNA complexes from apoptotic cell fragments
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C1 esterase
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cleaves both C4 and C2 resulting in C3 convertase (C4bC2a)
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what type of microorganism is most susceptible to MAC complex
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gram-negative due to outer lipid membrane
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anaphylatoxins
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C3a, C4a, and C5a
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neutrophil chemotaxin
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C5a
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eculizumab
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anti-C5a antibody
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what two things leave C4 and C2
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C1 esterase
MBL with bound mannose |
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associated with recurrent childhood infections in children between 6 months and 2 years of age
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MBL deficiency
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most important complement pathway for natural immunity
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alternative pathway
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activators of the alternative pathway
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complex polysaccharides
LPS teichoic acid |
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what actives C3b to form C3 convertase in the alternative pathway
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Factor D
activates C3b that combined with factor B |
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proteins important for opsonization
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C3b/C3bi
IgG |
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decay acceleration factor (CD55)
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prevents lysis of host cells by promoting the decay of cell bound C3 convertase
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protectin (CD59)
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prevents host cell lysis by inhibiting the addition of C9 to C5b78
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which microorganism contains both RCA proteins to prevent complement-mediated destruction
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HIV
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increases the affinity for C3b inactivating factors H and I
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sialic acid
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bind to C5b67 and prevent complex formation of MAC assembly
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Clusterin
S-protein |
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3 bacteria that contain sialic acid in the capsules
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Group B strep
Neisseria meningitidis K1 E. coli |
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how does EBV and HIV gain entry to B and T cells respectively
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EBV - CR2 on B cells
HIV - CR3 on T cells |
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attach to apoptotic cell fragments and orchestrate their destruction by activating the classical pathway
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C1q
C4 CRP |
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associated with autoimmune complex diseases with excessive classical pathway activation. decreased CH50, C3, and C4
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inherited early classical pathway deficiencies (C1q, C2, or C4)
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associated with recurrent Neisseria infections
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late complement deficiency components (C5-9)
properdin deficiency C3 deficiency |
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enhances the stability of the amplification C3 convertase on microbial surfaces
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properdin
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disease associated with C1 esterase inhibitor deficiency
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angioedema
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main cause of angioedema
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the inability of C1 esterase inhibitor to decrease production of bradykinin
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what leads to a decrease in C1 esterase inhibitor
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patients with already low function or levels can have an attack precipitated by tissue trauma that increases the production of plasmin - plasmin degrades C1-INH
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what can precipitate an angioedema attack
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local tissue trauma activates plasmin
ACE inhibitor - decrease bradykinin breakdown |
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angioedema treatment
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ecallantide - kallikrein antagonist
danazol - increase C1-INH production Tranexamic acid - inhibits conversion of plasminogen to plasmin |
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deficient CD55 and CD59 due inability to incorporate GPI anchor protein on RBCs leads to what
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paraxysmal nocturnal hemoglobinuria
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antibody that blocks MAC formation by binding C5
what is required if taking this drug |
Eculizumab
vaccination for Neisseria infections |
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what does free plasma hemoglobin from RBC lysis consume
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nitric oxide leading to:
erectile dysfunction and thrombotic episodes |
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lab values in a patients with PNH
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increased serum LDH
decreased serum NO increased serum Hb increased reticulocytes |
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autoantibody that binds to and stabilizes C3bBb (C3 convertase)
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C3 nephritic factor
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associated with partial lipodystrophy
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C3 nephritic factor
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associated with decreased CH50, C3, and C4
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immune complex diseases
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associated with decreased CH50 and C4, but normal C3
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hereditary angioedema (C1 esterase deficiency)
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associated with decreased CH50 and C3, but normal C4
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gram-negative sepsis
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associated with decreased CH50, but normal C3 and C4
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late complement deficiency
C5-9 |
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what would the levels of CH50, C3, and C4 be in a patient with PNH
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all normal because not enough complement consumed to affect blood levels
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what is needed to phagocytize encapsulated bacteria
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IgG and C3b
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different levels of CH50, C3, and C4 in uncontrolled activation of alternative and classical pathway
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classical - decreased CH50, C3, and C4
alternative - decreased CH50 and C3, with normal C4 |
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oxygen content (CaO2)
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total amount of O2 transported in 100 mL of blood
sum of the amount dissolved plus amount carried by hemoglobin |
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oxygen tension
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partial pressure of O2 in arterial blood = PaO2
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normal CaO2, PaO2, dissolved O2, %Hb saturation, and P50 at normal atmospheric pressure
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PaO2 = 100 mmHg
CaO2 = ~20 mL dissolved O2 = 0.3 mL %Hb saturation = 97.4% P50 = 27 mmHg |
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what percent of O2 transported by Hb dissociates to reach a PvO2 of 40 mmHg
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about 25% - leaving %Hb saturation to about 74.7%
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why does breathing in 100% oxygen not raise CaO2 dramatically like PaO2 does (>600 mmHg)
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because Hb is nearly 100% saturated already and cannot dissolve much more
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about how much O2 per dL does tissue utilize
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5 mL of O2 per dL (100 mL)
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what does PvO2 drop to during strenuous aerobic exercise and why
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drops to about 15 mmHg because the cells are using more oxygen
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what is the rate limiting step during stenuous exercise to supply enough oxygen to the tissues
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cardiac output in someone that cannot increase their CO by 6 times normal - everyone can release enough O2 from Hb
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CaO2, PaO2, and %Hb saturation, and P50 in a person with chronic anemia who's Hb has dropped by 50% to 7.5 g/dL
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CaO2 = ~10 mL of O2/dL
PaO2 = 100 mmHg %Hb saturation = 97.4% P50 = right-shift due to increased production of 2,3-DPG |
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compensatory mechanisms found in chronic anemia
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increased cardiac output
increased RBC production of 2,3-DPG |
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causes for increased cardiac output seen during compensatory mechanism in chronic anemia
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increased HR - SNS activity
decreased afterload - decreased viscosity and SVR increased preload - increased RAAS activity |
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manifestations seen in chronic anemia
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dyspnea
systolic murmur - turbulence across the aortic and pulmonic valves chronic respiratory alkalosis pallor cerebral hypoxia generalized weakness |
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patients presents with a decrease of CaO2 by 50% to ~10 mL/dL and decreased P50
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carbon monoxide poisoning
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hypoxic hypoxia
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CaO2 is low because PaO2 is low
develops from acute or chronic lung disease |
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anemic hypoxia
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PaO2 is normal but the CaO2 is low because of reduced O2 carrying capacity
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differentiate %SaO2 and %HbO2 in chronic anemia vs. carbon monoxide poisoning
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Chronic anemia - both are normal
CO poisoning - normal %SaO2, but decreased %HbO2 |
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%SaO2
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detects the percent of oxygenated Hb compared to the total amount of Hb that is still available for oxygenation
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%HbO2
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detects the percent of oxygenated-Hb compared to the total amount of all types of Hb
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ischemic hypoxia
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PaO2 and CaO2 are normal but tissue oxygenation is inadequate because of decreased blood flow to tissue
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differentiate the venous O2 content (CvO2) in distributive shock vs. cardiogenic shock
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distributive - AV shunting causes the CvO2 to be increased
cardiogenic - CvO2 reduced because of the decreased blood flow and more time for O2 to be extracted from blood |
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histotoxic hypoxia
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cyanide poisoning
PaO2 and CaO2 are normal but tissue is unable to utilize O2 |
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in what situation is CvO2 higher than normal
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distributive shock
cyanide poisoning |
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only situation with decreased PaO2
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lung disease
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two situations with decreased %HbO2
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CO poisoning
lung disease |
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normal value for AV oxygenation difference in Vol%
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25 Vol% (5mL/20mL)
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differentiate oxygenation failure and ventilation failure
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oxygenation - decreased PaO2 < 50 mmHg due to decreased PO2
ventilation - decreased PaO2 < 50 mmHg and increased PaCO2 > 50 mmHg |
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respiratory failure characterized by increased PaCO2
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alveolar hypoventilation
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Alveolar gas equation
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PAO2 = [0.21 x (760-47)] - PaCO2 / R
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characteristics of alveolar hypoventilation
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decreased PaO2
increased PaCO2 normal (A-a)O2 gradient PaO2 + PaCO2 = 110-140 |
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exists when thickening of the alveolar-capillary membrane prevents O2 equilibration between RBC and alveoli
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diffusion abnormality
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characteristics of diffusion abnormality
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decreased PaO2
normal/low PaCO2 increased (A-a)O2 gradient that is increased greatly during strenuous exercise 100% O2 decreases O2 gradient and raises PaO2 > 600 |
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occurs whenever deoxygenated blood mixes with oxygenated blood
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shunt
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what accounts for the normal (~10) A-a O2 gradient
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normal anatomic shunts in the bronchial and thesebian circulations
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what is the most severe cause of physiologic shunting
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alveolar flooding due to cardiogenic and non-cardiogenic pulmonary edema
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characteristics of physiologic shunt
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decreased PaO2
normal/low PaCO2 increased (A-a)O2 gradient 100% supplemental O2 will actually increase the O2 gradient while failing to increase PaO2 to 600 mmHg |
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how to calculate %shunt if patient is breathing 100% FiO2
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1. (A-a)O2 gradient divided by 20
2. 5% shunt for every 100 below PaO2 of 600 mmHg |
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why are patients able to maintain a normal to low PaCO2 with respiratory failure due to V/Q mismatch
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1. hypoxemia stimulates respiratory centers to increase the RR
2. hypoxic vasoconstriction redirects blood flow to better ventilated respiratory units |
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V/Q = 0
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physiologic shunt
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V/Q = infinity
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dead space - maybe due to pulmonary embolism
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why will the administration of supplemental oxygen to patients with chronic hypoxemia cause acute respiratory acidosis
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1. causes respiratory centers to stop hyperventilating and blow off excess CO2
2. decrease the hypoxic vasoconstriction |
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what happens when medullary vasomotor centers begin to fail from cerebral dysfunction due to hypotension
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lose their capacity to regulate ANS activity and maintain sympathetic tone
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what happens to the autonomic response from acute to chronic hypoxemia
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severe hypoxemia results in loss of CNS ability to increase SNS activity resulting in bradycardia, systemic vasodilation, cyanosis
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two main categories of pulmonary edema
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permeability (ARDS)
hemodynamic (CHF) |
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cell responsible for the build of Na transport back to the interstitium is plasma enters the alveolus
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type 1 pneumocytes
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channels located on the apical and basilar sides of pneumocytes that help transport water back into the interstitium from the alveolus
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apical - ENaC channels transport Na and K
basilar - Na/K ATPase keeps the gradient for the apical ENaC channels |
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where does water flow to get into the interstitium from the alveolus
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passively through aquaporin channels in type 1 pneumocytes and paracellular junctions
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4 ways to upregulate Na transport by alveolar cells - mechanism
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1. B2 agonists - ENaC and Na/K
2. glucocorticoids - Na/K 3. EGF and TGF 4. oxygen-derived free radicals - ENaC |
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why does pulmonary edema develop at high altitudes
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decreased superoxide formation which helps upregulate Na rebsorption into the alveolar cells
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capillary fibltration coefficient
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describes the ease which water crosses vascular endothelium - as K increases so does filtration
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osmotic reflection coefficient
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describes the protein permeability of the vascular endothelium - as o decreases so does the permeability
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normal oscmotic coefficient for pulmonary capillaries
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0.7 - lower than most other capillary beds
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two edema safety factors
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seiving effect
lymphatics |
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seiving effect
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increase in capillary hydrostatic pressure causes water to flow out of the capillaries leaving increased protein concentration within the capillary - as a result the increased water in the interstitium also decreases protein concentration - these along with increased hydrostatic pressure of the interestitium minimize degree of fluid filtration
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hemodynamic pulmonary edema
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occurs when the pulmonary capillary hydrostatic pressure rises to a level that overwhelms physiologic compensatory mechanisms and safety factors
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equation for critical capillary pressure to develop edema
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5.7 X plasma albumin concentration
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clinical presentation of hymodynamic pulmonary edema
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dyspnea
bilateral end-inspiratory crackles dullness to percussion increased VTF S3 at apex enlarged cardiac silhouette PAWP > 18 |
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permeability pulmonary edema
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caused by injury to the pulmonary microvascular endothelium that creates gaps between damaged endothelial cells
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what happens to the filtration and reflection coefficients in permeability edema
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K - increases
o - decreases |
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3 phases of ARDS
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1. exudative phase
2. proliferative phase 3. fibrotic phase |
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characterized by neutrophil accumulation, protein-rich edema fluid inside the alveoli and hyaline membrane formation from fibin and dead alveolar cells
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exudative phase of ARDS
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characterized by fibroblast proliferation
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proliferative phase of ARS
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when does fibrotic phase of ARDS occur
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instead of alveolar macrophages clearing away the hyaline membrane, they release procoagulants and fibrogenic cytokines that trigger uncontrolled fibroblast proliferation
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differentiate aucte lung injury and ARDS
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ALI - PaO2/FiO2 < 300
ARDS - PaO2/FiO2 < 200 |
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what correlates with the risk of death in ARDS
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increased amounts of dead-space ventilation
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clinical presentation of ARDS
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severe dyspnea
diffuse inspiratory crackles and wheezes bilteral dullness increased VTF normal cardiac exam PAWP < 15 |
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why does widespread MODS frequently develop in mechanically ventilated ARDS patients
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increase in soluble Fas-ligand which binds CD95 to initiate cell apoptosis
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why does oxygen-induced pulmonary toxicity occur
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increased free radical formation
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differentitae hyemodynamic from permeability pulmonary edema
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permeability - acute onet, normal cardiac exam, central distribtuion of alveolar infilatrates, PAWP < 18, BNP < 100
hemodynamic - slower onset, S3, enlarged heart, peripheral distribution of alveolar infilatrates, PAWP > 18, BNP > 500 |
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cells most responsible for alveolar epithelial destruction in ARDS
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neutrophils - produce oxygen-free radical and proteases
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4. Identify which parameter of the Starling equation for fluid movement is primarily responsible for the development of cardiogenic pulmonary edema and adult respiratory distress syndrome
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Cardiogenic pulmonary edema – increased capillary hydrostatic pressure is the mainly responsible
ARDS – inflammation resulting in increased superoxide production from neutrophils destroys the permeability of the endothelial walls resulting in increased K and decreased o |
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what does pulmonary edema due to the mechanism of respiration
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increases workload during breathing - decreased lung compliance
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differentiate the mechanisms responsible for hypoxemia in patients with cardiogenic and non-cardiogenic pulmonary edema
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Hypoxemia results from ventilation-perfusion mismatch
Shunt is seen in both cardiogenic and non-cardiogenic pulmonary edema Dead-space ventilation is only seen in non-cardiogenic due to fibrosis obliterating some of the capillaries in the interstitial space |
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patholophysiological effects of smoking
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1. injures epithelial cells and causes fragments to activate TLR an initiate inflammatory response
2. chemokines and cytokines released stimulate Th1 and CD8 cells 3. Th1 cells amplify the inflammatory response by releasing additional cytokines and chemokines that attract macrophages and neurtrophils 4. oxidezes anti-proteases 5. stimulates ceramide production - accelerates apoptosis 6. impairs bronchociliary movement, causes hypertrophy and hyperplasia of mucus glands and triggers smooth muscle contractioni |
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what should you suspect in a patient with emphysema developing during their 3rd/4th decade of life
|
a-antitrypsin deficiency
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cells responsible for tissue destruction from cigarette smoke
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CD8 - release proteolytic enzymes
macrophages - release metalloproteinases and oxygen-derived free radicals that inactivate a-antitrypsin |
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cell responsible for tissue destruction from inherited a-antitrypsin deficiency
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neutrophils - release serine proteases (elastase)
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why does airway compression not occur during passive exhalation
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because the intrapleural pressure remains subatmospheric (negative)
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why does dynamic compression occur
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when intrapleural pressure exceeds intra-airway pressure when people increase their intrapleural pressure in order to exhale forcefully
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equi-pressure point
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location in the airway when intrapleural pressure exactly matches intra-airway pressure
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why does EPP move closer to alveoli in patients with emphysema
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decreased elastic forces and surface tension means that higher intrapleural pressures are needed, also there is still less driving force than normal and therefore less intra-airway pressure
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what happens to a patients lung compliance with emphysema at normal FRC values
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increased compliance - >200mL change in volume for every 1 cm change in H20 pressure
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why does V/Q ratio greatly increase in the apices of patients with emphysema
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because enzyme tissue destruction leads to destruction of blood vessels and therefore decreased blood flow - much more decrease in blood flow than ventilation
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clinical presentation of emphysema
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long history of dyspnea of exertion
mild hypoxemia increased AP diameter decreased diaphragmatic excurtion early inspiratory crackles cachexia |
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advantages of pursing lips in emphysema
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increases tidal volume
moves EPP closer to mouth decreases PaCO2 by 5% increases oxygen saturation by 3% |
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why does EPP move closer to the mouth with pursed lips
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increases intra-airway pressure and therefore EPP is moved into cartilagenous part of the conducting system and no dynamic compression occurs
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why should you be careful with B2 agonists in patients with emphysema
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increase metabolic rate and energy expenditure - cachexic already
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what increases the resistance at the level of conducting airways in patients with chronic obstructive bronchitis
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mucus plugging
inflammation peribronchiolar fibrosis |
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cause of the majority of airway narrowing in COB
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peribronchiolar fibrosis
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why does CO2 retention occur in COB and not emphysema
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because there are no high V/Q areas of the lung to compensate in chronic bronchitis, unlike emphysema
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clinical presentation of chronic bronchitis
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productive cough
dyspnea hyperinflation early-to-mid inspiratory crackles expiratory wheezes pulmonary HTN |
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CO diffusion capacity seen in emphysema, COB, and asthma
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emphysema - decreased
COB and asthma - normal |
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define asthma
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reactive airway disease that is characterized by reversible airflow obstruction - expiratory airflow increases > 15% with bronchodilators
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neurotransmitteres involved in mediating contraction of airway smooth muscle
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increased Ca due to IP3 and DAG
-ACh via M3 receptors -substance P -histamine, leukotrienes, PGD2 and PGF2 |
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neurotransmitterse involved in mediating relaxation of airway smooth muscle
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increased intracellular cAMP to decrease Ca
-VIP -PGE2 -NO -epinephrine |
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two neurotransmitters released from the nonadrenergic, noncholinergic neurons
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substance P - excitatory
VIP - inhibitory |
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prostaglandin involved in relaxation of bronchiol smooth muscle
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PGE2
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what contributes most to airway narrowing in asthma
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airway inflammation mediated by Th2 and Th17 cells
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Th2 cells are chemotactic for what other cells
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basophila
eosinophils neutrophils |
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interleukin important for the development and survival of eosinphils
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IL-5
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interleukin important for expression of mucus production and differentiation of cells into mucus-producing goblet cells
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IL-13
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interluekins associated with allergic asthma
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IL-4 - causes B cells to produce IgE
IL-5 - proliferation and maturation of eosinophils |
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predominant airway inflammatory cell in asthma
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eosinphils
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released from eosinphils, stops respiratory cilia and blocks M2 receptors
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major basic protein
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differentiate the early and late phases of allergic asthma and treatment options
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1. early response from preformed mediators - treat with B2 agonists or cromolyn
2. late phase from newly formed mediators via Th2 response attracting eosinophils and neutrophils - treat with corticosteroids or cromolyn |
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disintguish regulation of mast cell secretion via concentration of cAMP
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increased cAMP (B-agonists and PGE2) inhibit mast cell mediator release
decreased cAMP (ACh) enhances mast cell mediator release |
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how do viruses trigger non-allergic asthma
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increase airway sensitivity to substance P
increase ACh release from vagal nerve endings via M2 receptor dysfunction trigger NK and Th1 cells to release IFN-y (triggers TNF-a and IL-1B release from macrophage) |
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two causes for nocturnal asthma
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gastroesophageal reflux
airway cooling *both stimulate vagal afferent nerve release of ACh |
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up to 20% of asthmatics have aspirin hypersentivity
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**
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Samter's triad
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nasap polys
asthma hypersensitivity to aspirin and other NSAIDS |
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why do NSAIDS cause bronchospasm in some patients
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already have imbalance between PGE2 and leukotrienes, when NSAIDS block PGE2 synthesis there is uncontrolled leukotriene production
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why does B-agonists initially worsen hypoxemia in asthma
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because production vasodilation in poorly ventilated lung segments
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best pulmonary function test to differentiate asthma from ephysema
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CO diffusion test
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what can be used to measure amount of eosinophil inflammation
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exhaled NO
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asthmatic breath sounds
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expiratory to inspiratory ratio exceeds 3:1
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differentiate the T cell mediated inflammation in emphysema and asthma
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emphysema - Th1
asthma - Th2 and Th17 |
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describe mechanism for glucocorticoid resistance in patients with predominant emphysema
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histone deacetylase 2 activity is reduced in macrophages of cigarette smokers - glucocorticoids normally reduce neurtophil and macrophage mediated inflammation by using HDAC2 - because HDAC2 activity is markedly reduced in emphysema, corticostoids are ineffective at reducing disease progression
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which cell mediates most of the inflammation of pulmonary fibrosis
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Th2 helper T cell
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results from repetitive epithelial cell injury and fibroblast activation that leads to abnormal wound healing
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idiopathic pulmonary fibrosis
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three drugs associated with pulmonary fibrosis
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bleomycin
amiodarone nitrofurantoin |
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what is the critical step in abnormal wound healing of pulmonary fibrosis
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loss of integrity of the basement membrane
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what role does angiotensin II have in abnormal wound healing of pulmonary fibrosis
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subnormal re-epithelialization because ATN II induces apoptosis of epithelial cells limiting the re-epithelialization of the alveoli
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describe the role of TGF-B and caveolin-1 in pulmonary fibrosis
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TGF-B is a growth factor release from injured epithelial cells and decreases the expression of caveolin-1 by fibroblasts.
Caveolin-1 is an inhibitor of pulmonary fibrosis because it decreases the production of EM by fibroblasts |
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what two things appear to cause an unregulated synthesis of collagen and EM
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decreased caveolin-1
increased TGF-B |
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why is airway resistance low in pulmonary fibrosis and what does this do to pulmonary mechanics
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decreased because the retractive forces exerted by the fibrotic lung are abnormally high and keep the airway open
FEV1/FVC and FEF 25-75 ratios are greater than normal |
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three things that leads to hypoxemia in pulmonary fibrosis
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1. V/Q mismatch from increased dead-space
2. diffusion abnormality from fibrosis and decreased surface area 3. neovascularizations leading to intrapulmonary shunts |
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what causes hypoxemia to get worse during physical exertion in a patient with pulmonary fibrosis
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increased CO decreases the time alloted for diffusion in a lung with alveolar-capillary membrane thickening
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clinical findings in a patient with pulmonary fibrosis
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rapid and shallow breathing
cyanosis clubbing velcro crackles during late inspiration early pulmonary HTN ground glass infiltrates on CXR |
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why does the LVEDP underestimate the amount of volume actually in the LV
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because the dilated RV pushed the IV septum to the left decreasing the LV cavity and therefore the smaller volume still shows a near normal pressure
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differentiate elevated CVP and systemic hypotension DDx:
major pulmonary embolism syndrome, cardiac tamponade, RV infarction |
MPE - normal to low PAWP
Tamponade - normal to high PAWP RV infarction - low PAWP **all have low CO, high SVR, and low PvO2 |
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develops when small-to-medium sized emboli occlude the pulmonary artery proximal to the anastomoses with the bronchial circulation
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dyspnea without infarction syndrome
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when would a larger embolus lead to pulmonary infarction
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when bronchial circulation is unable to compensate
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PaO2, %HbO2, CaO2, and CvO2 in:
Anemia, CO poisoning, CN poisoning, lung disease |
Anemia - normal PaO2 and %HbO2 with decreased CaO2 and CvO2
CO poisoning - normal PaO2 with decreased %HbO2, CaO2, and CvO2 CN poisoning - normal PaO2, %HbO2, and CaO2 with increased CvO2 Lung disease - decreased everything - only thing with decreased PaO2 |
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hereditary form of idiopathic pulmonary arterial hypertension
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1. decreased bone morphogenic protein receptor-type 2 - prevents normal apoptosis in precapillary pulmonary arterioles
2. over-expression of serotonin transporter 5-HT |
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is cyanosis more likely to develop in severe polycythemia or severe anemia
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polycythemia
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when does cyanosis develop
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when 5 grams or more of reduced Hb is present in systemic capillary blood
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central cyanosis
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arterial oxygen desaturation or abnormal hemoglobin doesn't release oxygen - mucous membranes and the skin are affected
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peripheral cyanosis
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slow transit of blood or excessive oxygen utilization by the tissues - skin affected while sparing the mucous membranes
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what should you think whenever a young woman has an unexplained episode of syncope during exertion
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idiopathic pulmonary hypertension
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