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104 Cards in this Set
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- Back
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What are the lab results of TTP?
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↓ platelet count & prolonged bleeding time; normal PT + PTT; peripheral blood smear show thrombocytopenia & schistocytes, and reticulocytosis
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Pt w/fever, thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal failure
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Thrombotic thrombocytopenic purpura (TTP) - widespread formation of platelet thrombi w/scant fibrin (hyaline thrombi) -> no activation of coagulation system
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Hemolytic uremic syndrome (HUS)
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Occurs in children w/infection -> GI w/bloody diarrhea (disenterry) -> ate a raw hamburger or petting zoo-> E. coli O157:H7 -> oliguria, hematuria, microangiopathic hemolytic anemia, prominent neurological changes -> generalized endothelial damage -> thrombocytopenia (low platelet count)
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What are the 2 pathways of coagulation?
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1. Extrinsic pathway, 2. intrinsic pathway
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What is the extrinsic coagulation pathway?
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mediated by tissues - Factor VII (liver)= mediator -> factor VIIa
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; If u have liver problems u have ↓ factor VII + ↓ clotting -> bleeds a lot;
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As a surgeon u make sure u do a CBC(complete blood count) + look at efficiency of extrinsic pathway -> if u don’t make factor VII -> cant do surgery. Most likely cause = alcohol; (utilize Prothrombin time(PT))
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What does prothrombin time(PT) tell u?
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Tells u how efficient extrinsic pathway is; If ↑ PT time -> problem in extrinsic pathway(ie Factor VII)
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What is the intrinsic coagulation pathway?
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Factor XII -> XIIa; utilize Partial thromboplasmin time (PTT)
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What does partial thromboplasmin(PTT) time tell u?
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Tells u how efficient intrinsic pathway is; if ↑ PTT time -> problem in intrinsic pathway (ie factor XII)
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ED -> pt is bleeding from every orifice -> eye, ears, mouth, etc -> platelet count is 20k -> give platelet transfusion -> want to bring platelet count up -> and if it doesn't stop -> pt has an antibody that is form against the platelet. What disease is it?
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ITP (immune thrombocytopeinc purpura) -> do emergent splenectomy
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What is the cause of Immune thrombocytopenic purpura(ITP)?
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Auto-antibodies against Gp Iib-IIIa + Gp-Ib-IX (made in the spleen) -> ALSO platelets are being degraded in the spleen -> leads to bleeding
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What is the difference between acute ITP vs chronic ITP?
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Acute ITP = children + viral infectinon; chronic ITP = female + childbearing years + first manifestation of systemic lupus erythematosus (SLE) + petechiae, ecchymoses, menorrhagia, and nosebleeds
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What are the lab results of ITP?
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↓ platelet count + prolonged bleeding time; Normal PT + PTT; Peripheral blood smear = thrombocytopenia + enlarged immature platelets (aka megathrombocytes); Bone marrow biopsy = ↑ megakaratocytes that are immature
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What is the MOA of blood clots in an atheromatous blood vessel?
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Blood vessel is 50% occluded b/c of atherosclerosis -> no symptoms -> now there is a fissure /cracks thru atheroma -> body tries to stop bleeding -> platelets aggregate -> MI
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How do u prevent a thrombus?
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To prevent this give glycoprotein-II - B - IIIA inhibitor -> thus preventing platelets from adhering; Physician will now prescribe a baby aspirin -> salicylate = inhibitor of thromboxane -> will primarily inhibit thromboxane formation -> inhibits platelet aggregation
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Be careful w/cuts b/c might take longer to clot the blood
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What is the bleeding time test?
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Cut yourself -> normal = 2-> 7 mins -if its longer then u have a ↓ platelets or deficiency in how they work
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What are the 3 ways to block lymph?
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1. Tumor-> spac occupying lesion -> blocks lymph node, 2. Surgical -> radical masectomy -> swollen right arm and hand -> due to blockage of lymph, 3. Parasitic infestation -> filariasis -> elephantiasis -> cause = blocked lymph
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Pt w/pneumonia -> difficulty breathing -> what type of fluid is leaking out?
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antigens in lung has ↑ size of pores -> proteins leak out -> draws fliud w/it -> specific gravity > 1.02 aka 1.1 (exudate)
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Types of hypersensitivity (ACID)
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Type I = Allergy
Type II = Cellular Type III = Inflammatory Type IV = Delayed |
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Type II = Cellular
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Type III = Inflammatory
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Type IV = delayed
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Transudate vs exudate
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Transudate = edema + low protein (<1.020); exudate = edema + high protein (>1.020)
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What are the types of exudates(>1.020)?
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1. Purulent(pus), 2. fibrinous, 3. eosinophilic, 4. hemorrhagic
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Define: hyperemia
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An excessive amount of BLOOD in a tissue or organ secondary to vasodilation(active)
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Define: congestion
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Excessive amount of blood in tissue/organ due to diminished venous outflow (passive)
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What is the procedure of clotting after u get a cut?
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Cut urself -> bleeding -> bleeding stops by itself -> platelets adhere
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Very firsts step of platelet adhesion?
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platelets adhere to area of injury
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How does von willibran factor(vwF) work?
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Von willibran factor (sub endothelial layer) doesn’t come in contact w/blood -> until u get a cut -> now blood(velcro) + von willibran factor (half of Velcro) -> now platelet adheres to the blood vessel
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How do Gp-I-B and vWF combine?
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Glycoprotein-I-B (platelet Velcro) + von willibran factor(epithelium velcro) -> platelet adhesion occurs(activated-glycoprotein-II-B/3A) -> need to aggregate platelets ontop of one another -> forms clot/thrombus
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What are the 4 possible outcomes of a pt who is bleeding?
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Pt comes in -> 4 possible outcomes
1. Platelets (150 - 350k) - if not enough platelets -> bleeding tendency -> pt w/ rash on legs -> microscopic hemorrhages (petechiae) ->. Bruise on elbow (dime -> quarter size (purpura) ->ecchymosis (larger); very first thing to do is a CDC (check platelet concentration) -> if 25k platelets = thrombocytopenia -> causes bleeding, 2. CBC = 250k -> dysfunctional platelets (not adhering/aggregating) -> measure glycoprotein-I-B -> deficient-> but cant adhere now = bernard sulliares syndrome , 3. Measure glycoprotein-II-B-3A -> cant aggregate -> glandsmins thrombocinia, 4. Has to have deficiency of von willibrands factors(cant do platelet adhesion) |
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1. Platelets (150 - 350k) - if not enough platelets -> bleeding tendency -> pt w/ rash on legs -> microscopic hemorrhages (petechiae) ->. Bruise on elbow (dime -> quarter size (purpura) ->ecchymosis (larger); very first thing to do is a CDC (check platelet concentration) -> if 25k platelets = thrombocytopenia -> causes bleeding, 2. CBC = 250k -> dysfunctional platelets (not adhering/aggregating) -> measure glycoprotein-I-B -> deficient-> but cant adhere now = bernard sulliares syndrome , 3. Measure glycoprotein-II-B-3A -> cant aggregate -> glandsmins thrombocinia, 4. Has to have deficiency of von willibrands factors(cant do platelet adhesion)
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What is the function of TXA2?
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TXA2 (Thromboxane) -> local affect -> vasoconstrictor -> stimulant for platelet aggregation -> platelets release serotonin + ADP
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What are the potent mediators of platelet aggregation?
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ADP or thromboxanes
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Define: edema?
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Presence of excess fluid in the intercellular space
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What are the causes of edema?
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1. ↑ hydrostatic pressure (congestive heart failure, portal hypertension, renal retention of salt & water, venous thrombosis), 2. hypoalbuminemia + ↓ colloid osmotic pressure (liver disease, nephrotic syndrome, protein deficiency-> kwashiorkor), 3. lymphatic obstruction (lymphedema, tumor, surgical removal of lymph node drainage, parasitic infestation (filariasis->elephantiasis)), 4. ↑ endothelial permeability (inflammation, type I hypersensitivity, drugs-bleomycin, heroin))
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Define: anasarca
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Severe generalized edema(hypoalbulenimia = most common cause = causes systemic edema)
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Define: effusion
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Fluid w/in the body cavities
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What is the result of ↓ osmotic pressure in the blood?
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Osmotic pressure in blood vessels -> edema; If diminished plasma concentration -> cant reabsorb fluid back into vascular compartment -> more fluid in interstitial space
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What is the MOA of osmotic pressure in the blood?
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If lots of albumin in blood vessel it will suck more fluid back into the interstitum -> returned fluid via lymphatic's -> progressive chronic fluid (lymphedema)
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What are the causes of hypoalbuminemia -> ↓ osmotic pressure
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1. Liver disease -> cant make as much albumin, 2. Nephritic syndrome -> kidneys filter proteins into the urine!! -> ↓ albumin in blood, 3. Kwashiorkor -> not eating protein -> ↓ albumin made
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What is the MOA of ↑ hydrostatic pressure?
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↑ blood flow in and the ↓ outflow -> outflow cant keep up thus u accumulate fluid(edema)
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What is the most common cause of ↑ hydrostatic pressure?
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Most common = ↑ in venous pressure -> flow thru capillary = diminished -> edema
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What are the 4 ways to get edema via ↑ hydrostatic pressure?
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1. Left sided congested heart failure -> left is unable to pump out all the blood received from the right -> thus the volume is stuck in the lungs(difficulty breathing), 2. Portal hypertension = pt w/cirrhosis of liver -> scar tissue increases -> blood flow thru vascular supply diminished -> blood backs up in portal vein -> fluid in peritoneum (Splanchinc viscera) aka ascites, 3. Kidneys retaining salt b/c of aldosterone release or kidneys retaining water b/c of ADH release by posterior pituitary-> High blood pressure -> ↑ plasma volume -> edema, 4. Clot blocks the out flow of blood(venous thrombosis) -> edema
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DVT (leg) -> clot in the lung -> edema
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What is the disease of deficiency of Glycoprotein-Ib?
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Bernard-soulier syndrome
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What is the disease of deficiency of Glycoprotien-Iib-IIIa
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Glanzmann thrombasthenia
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What is the disease of deficiency of von willebrand factor?
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Von willebrand disease
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Define: infarction
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Localized area of necrosis secondary to ischemia
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Anemic infarcts
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Pale/white color(occurs in solid organs w/single blood supply- spleen, kidney, heart)
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Hemorrhagic infarcts - color?
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Red - is red b/c there is dual blood supply; also occurs w/venous occlusion (ie testicular torsion)
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Coagulation necrosis
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Organs
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Liquefactive necrosis
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Brain necrosis
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Shock
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Inadequate tissue perfusion
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Most common cause of shock
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Dehydration
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Anaphylactic shock
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Too low BP due to severe vasidilation (histamine)
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Septic shock
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Infection in blood
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Multiple system organ failure
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Days duration of shock (4 organ failures = 100% lethal)
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How do u get waterhouse-friderichsen syndrome?
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Neisseria meningitidis septicemia -> bilateral hemorrhagic infarction -> acute adrenal insufficiency(aka adrenal glands fill themselves w/blood)
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What are the 3 stages of shock
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1. Stage -I - Compensation -> ↑ sympathetic tone, 2. stage II - decompression - ↓ in tissue perfusion, 3. stage III - irreversible organ failure -> death
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Major causes of shock
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1. Cardiogenic shock(heart pump failure), 2. hypovolemic shock(reduced blood volume), 3. septic shock (bacterial infection), 4. neurogenic shock (generalized vasodilation), 5. anaphylactic shock (type I hypersensitivity)
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Cardiac tampanode
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Heart cant fill properly
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Which way does the wedge point in an infarction?
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Wedge is pointing towards the apex
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Where are the clotting factors made?
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Liver - clotting factors are proenzymes that must be converted to the active form(Ca2+)
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EDTA
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Chelate Ca2+ -> prevents clotting
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What are the contact factors that activate the intrinsic coagulation pathway?
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1. Subendothelial collagen, 2. high molecular weight kinogen(HMWK), 3. kallikrein
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What are the contact factors that activate the EXTRINSIC coagulation pathway?
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Tissue factor
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First step in formation of clot
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Platelet adhesion -> they piggy back on each other after this
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Hemophilia A
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Deficiency in factor VIII (aka classic hemophilia)
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Hemophilia B
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Deficiency in factor IX(aka christmas disease)
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Child w/weird gait. Knee problems -> blue knee -> measure PT and PTT
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Extrinsic pathway = PT = normal; intrinsic pathway = PITT = prolonged; bleeding time = normal b/c there is no problems in platelets
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Major problems in hemophilia in children? treatment?
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Heme-arthrosis = Knee problems -> running causes bleeding -> accumulation of blood in knee joint -> restricts movement; if blood in joints -> give factor VIII
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Tissue plasminogen activator
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Plasminoginlysis(blows up clots)
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How do u measure weather a pt has a thrombus?
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DVT -> thrombus (on venous side) -> emboluls(circulating clot) -> pulmonary embolus (in the lungs); Lab test = angiogram or D-dimer(assess fibrin breakdown products)
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Vitamin K deficiency
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↓ factors II, VII, IX, X -> induced hemophilia
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Von wiliebrand disease
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Inherited bleeding disorder characterized by either a deficiency or qualitive defect in von willebrand factor -> cut -> platelets will not adhere
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Bernard suliuers disease
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Glycoprotein I-B deficiency -> doesn’t allow adhesion to vWF
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Platelet adhesion =
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glycoprotien I-B + vWF
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Von williebrands disease
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Petechia, ecchimosis, bleeding time ↑ (tells u platelets are not working - either not enough (thrombocytopenia or defect in quality of platelets)
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Wristoseton test
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Tells u if there are vWF
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Weibel palade bodies
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vWF
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Disseminated intravascular coagulation
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Always secondary to another disorder - acute, subacute, or chronic thrombohemorrhagic disorder characterized by the excessive activation of coagulation, which leads to the formation of thrombi in the microvasculature of the body; aka pathologic activation of intrinsic/extrinsic clotting pathway of coagulation; mainly in pregnant women
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LPS from E.coli -> stimulates TNF -> activates clotting
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DIC- 85% lethal
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PT and PTT in DIC
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Prolonged b/c they are all being used
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Elevated D-dimer
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↑ in micro thrombi throughout the body
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Pt who is bleeding from everywhere
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DIC - Treat underlying disorder (if septic shock -> treat it) = ↑ prothrombin time (PT)
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MOA of atrial fibrillation
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Atrial fibrillation - no blood flow form atria -> ventricles -> only way to get blood is passively -> valves close fibrillation doesn’t allow blood to flow efficiently -> pt has high risk to developing clot in left atria -> clots to brain -> stroke
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Define: thrombosis
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Pathologic formation of an intravascular fibrin-plaetelet thrombus
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What is vichow's triad
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Factors that give u thrombus - 1. endothelial injury, 2. alteration in laminar blood flow, 3. hypercoaguability of blood,
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What's the difference between thrombus vs blood clot
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Thrombus = intravascular + lines of zahn + presence of platelets, blood clot = extravascular + no lines of zahn + no platelets
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Mural thrombi
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Formation of clot formed right on the left ventricle -> leads to stroke or GI infarct
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What is the most common type of embolism
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thromboemboli
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Fat embolus MOA
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Fat emboli-> from long bone fracture -> caused by automobile accident -> difficulty breathing -> but more severe b/c fat emboli causes severe CNS problems -> coma seizure
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Saddle embolus MOA
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DVT in femoral vein -> detaches -> pulmonary artery occlusion -> chest pain-> difficulty breathing -> if embolus is large enough(saddle embolus) -> death
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Gas embolus MOA
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Decompression sickness (the bends -> caisson disease)
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What is the MOA of infarction of pulmonary embolism
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Lung had dual blood supply thus its hard to infarct -> can get infarct when there is pre-existing heart disease -> ↓ CO -> ↓ broncial circulation -> occulude pulmonary circulation -> now inadequate blood supply -> infarct (hemorrhagic infarct)
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What is the MOA for sudden death of pulmonary embolism?
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Saddle embolus -> dies very rapidly -> pt in hospitla due to orthopedic problem -> walk to bathroom -> falls and dies -> nurse sees normal electrocardiogram -> but when palpate for pulse (electrical M dissociation) -> embolus was so big there was no blood to the left ventricle -> but cant generate pressure b/c blood is not moving -> instantaneous death!!
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What is the MOA for chronic pulmonary hypertension?
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Hypercoagulability -> PE in the lungs -> turns fibrotic -> chronic pulmonary hypertension -> blood is trying to go thru narrow blood vessels -> hypertension -> right ventricle has to pump blood from pulmonary artery thru the lungs -> right heart has to work much harder to pump blood thru lungs
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Define: paradoxical emboli
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Venous embolus that gains access to the systemic circulation by going thru a septal defect; Venous thrombosis in veins -> embolus in IVC -> goes thru patent foramen ovale -> happens when u sneeze/cough -> pressures that rise interthoracici cavity allows it to move right -> left
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Protein C
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Important inhibitor of two procoagulants, factor V and factor VIII
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Which organs have only a single blood supply?
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1. Brain, 2. kidney, 3. heart, 4. spleen
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Breast cancer removal -> what problem can it cause?
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Leads to lymphedema (arm or breast)
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