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Fiser Absite Practice Questions 2015

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295 views536 pages

Fiser Absite Practice Questions 2015

absi review

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Ugo
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© © All Rights Reserved
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The ABSITE REVIEW: Practice Questions 2 Edition Steven M. Fiser MD ‘The ABSITE Review: Practice Questions 2" Edition Steven M. Fiser MD Hancock Surgical Consultants, LLC Richmond, Virginia ‘This book is not intended for clinical use. Extreme care has been taken to ensure the accuracy of the information contained in this book and to devise the safest and most conservative way of practicing general surgery. However, the authors and publishers are not responsible for errors or omissions in the book itself or from any consequences from application of the information in the book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication Application of this information remains the professional responsibilty of the practitioner. The specific circumstances surrounding any individual patient requires individual diagnosis and treatment. Extreme care has been taken to ensure that the drug dosages herein are accurate, however iliness such as renal failure and other disease states can affect dose. The reader should check the package insert for any drug being prescribed to see the current recommended indications, warnings, and precautions. ‘Some drugs and devices in this text have FDA clearance only for certain indications. Itis the responsibilty of the health care provider to ascertain the FDA status of any drug or device before use ‘The American Board of Surgery inc. does not sponsor nor endorses this book. Allrights reserved. This book is protected by copyright. No part may be reproduced in any means, including photocopying, without the express written consent of the copyright owner The author has never had access to the ABSITE exams used by the American Board of ‘Surgery Inc, other than to take the exam. This book is meant to educate general surgery residents, not reconstruct the ABSITE t © 2015 Hancock Surgical Consultants, LLC re not with The and vever id d isthe any ner, Contents: Cell biology Hematology Blood products Immune System and Wound Healing Transplantation Infection Antibiotics Pharmacology Anesthesia Patient Safety, Outcomes, Ethical-Legal Fluids and Electrolytes Nutrition Oncology Trauma Critical Care Burns Head and Neck Adrenal Gland Thyroid Parathyroid Pituitary Gland Breast Thoracic Cardiac Vascular Gastrointestinal Hormones Esophagus Stomach Liver Biliary System Pancreas Spleen Small Bowel Colon and Rectum Rectum and Anus Hernias and Abdominal Wall Urology Gynecology Neurosurgery Orthopaedics Pediatric Surgery Skin and Soft Tissue Statistics 20 24 36 46 61 70 88 100 140 116 160 182 191 202 208 220 228 230 254 267 273 307 310 325 342 362 395 403 423 459 470 478 489 497 519 531 Cell Biology 1 3. 4 5 6 DNA polymerase is involved in a, Transcription b. Transtation c. Duplication 6. Protein carboxylation Answer c. DNA polymerase is responsible for duptication of DNA. DNA polymerase chain reaction uses oligonucleatides to amplify specific DNA sequences (a tool used in research). RNA polymerase is involved in: ‘a. Transcription b. Translation Duplication d. Protein carboxylation ‘Answer c. RNA polymerase is responsible for transcription, the process by which DNA is copied into mRNA. Proteins are synthesized from: a DNA b. rRNA cc tRNA ¢. mRNA Answer d. Ribosomes translate mRNA into specific proteins (amino acid sequences} : ‘Anti-viral protease inhibitors used in patients with HIV work by a. _ Preventing protein precursor cleavage b. Activating lysosomes: : ©. Degrading nbosomes | d. Inhibiting RNA polymerase : Answer a. Protease inhibitors prevent viral replication by selectively binding viral proteases and preventing protein precursor cleavage, which is necessary for the production of infectious viral partick Steroid hormones a, Bind a receptor on the plasma membrane and activate a plasma membrane enzyme b. Bind a cytopiasmic mRNA c, Bind a receptor in the nucleus and affect transcription of RNA 4. Donotenter the cell receptor, enter the nucleus, and affect transcription of Answer b. Steroid hormones bind a receptor in the cell cytoplasm, enter the nucleus as a steroid-receptor complex, and then affect transcription of MRNA for protein synthesis, Thyroid hormone affects transcription after binding a receptor that resides in the nucleus. Steroid and thyroid hormones require 1-2 hours before having effects, Cells divide during what phase of the cell cyci a GI b 6S c G2 aM Answer d. Cells divide during the M phase (mitosis) Cell cycle - 4 phases G1 - Most variable part, determines cell cycle length Growth factors affect cell during G1 (synthesis) - cell is preparing for division Protein synthesis, DNA replication (DNA polymerase) G2 (G2 checkpoint) ~ stops cell from proceeding into mitosis if there is DNA damage to allow repair (maintains DNA stability) M (mitosis) - cell divides Omeprazole acts by binding: ‘a. He Histamine receptor b HIKATPase c Acetylcholine receptor d.— Gastrin receptor Answer b. Omeprazole blocks the proton pump (H / K ATPase) in parietal cells, 8 Tyrosine kinase: ‘a. Phosphorylates tyrosine residues b. — Decarboxylates tyrosine residues c. Carboxylates tyrosine residues 4d. De-phosphorylates tyrosine residues Answer a. Tyrosine kinase phosphorylates tyrosine residues. imatinib (Gleevec) is @ receptor tyrosine kinase inhibitor used in patients with malignant GIST (gastro-intestinal stromal tumors) 9. What receptor does erythromycin bind to increase gastrointestinal motility? a. Somatostatin receptor b, Acetylcholine and dopaminergic receptors ©. GABA receptor dd. Motilin receptor Answer d. Erythromycin binds the motiin receptor and can be used to increase motility viral the 10. What portion of the lipopolysaccharide complex accounts for its toxicity? a. Lipid A b. Lipid B ©. Lipid C 4. Lipid D of Answer a. Lipid A is the toxic portion of the lipopolysaccharide complex found with gram negative sepsis. Lipid A is the most potent stimulant for TNF- alpha release, 11. Of the following, which is the most critical component in the neovascularization of e ‘tumor metastases? for a HER receptor b. VEGF receptor ¢. Neu receptor d. FGF receptor Answer b. One of the most critical elements in the neovascularization of metastases is the VEGF (vascular endothelial growth factor) receptor. Many new chemotherapeutic strategies target the VEGF receptor (a tyrosine kinase) or VEGF itset. 12. All of the following are true except Desmosomes anchor cells to each other Hemidesmosomes anchor cells to platelets Gap junctions allow communication between cells Tight junctions are water impermeable eoge Answer b. Hemidesmosomes anchor cells to extra-cellular matrix. Desmosomes and hemidesmosomes — anchor cells (cell-cell and cell~extracellular matrix molecules, respectively) Tight junctions - occluding junctions that occur between cells; form a water impermeable barrier (eg skin epithelium, bladder epithelium) Gap junctions ~ formed between cells to allow communication 13, _Allof the following are true except a. Keratin is found in hair and nails, b. —Desmin is found in muscle cc. _Vimentin is found in skin d. The above are intermediate filaments Answer c. Vimentin is found in fibroblasts. Intermediate filaments: Keratin (hair and nails) Desmin (muscle tissue) imentin (fibroblasts) 14. Protein kinase A is activated by aa) b. Diacylglycerot cc. cAMP d ADP Answer c. Protein kinase A is activated by CAMP (2 second messenger) Adenylate cyclase forms cAMP from ATP. 15. Protein kinase C is activated by: a Ca b ATP c, cAMP ¢ ADP. Answer a. Protein kinase C is activated by Ca or diacylglycerol (both second messengers). Diacylglyceroi (DAG) and inositol triphosphate (IP) and formed from PIP, by phospholipase C. Ga is released from the mitochondria 16. All of the following are true except 2. Cholesterol increases plasma membrane fluidity b. __Intra-cellular calcium level is very low compared to extra-cellular level cc. — G proteins are GTPases d, The Golgi apparatus is the major site of ATP production Answer d. Mitochondria are the major site of ATP production, nd Hematology Which of the following is the correct order of responses following vascular injury. Vasoconstriction, thrombin generation, platelet adhesion Platelet adhesion, vasoconstriction, thrombin generation Thrombin generation, vasoconstriction, platelet adhesion Platelet adhesion, thrombin generation, vasoconstriction Vasoconstriction, platelet adhesion, thrombin generation enoge Answer e. vasoconstriction, platelet adhesion, thrombin generation Thromboxane: a. Decreases platelet aggregation by increasing release of calcium in platelets b. Decreases platelet aggregation by decreasing release of calcium in platelets ©. Increases platelet aggregation by increasing release of calcium in piatelets d. Increases platelet aggregation by decreasing release of calcium in platelets Answer c. Thromboxane causes platelet aggregation by increasing Ca“ in Platelets. This results in exposure of the Gp Iibillia receptor and platelet binding Prostacyclin a. Decreases platelet aggregation and causes vasodilatation b. Decreases platelet aggregation and causes vasoconstriction c. Increases platelet aggregation and causes vasodilatation d. Increases platelet aggregation and causes vasoconstriction Answer a. Prostacyclin decreases platelet aggregation and causes vasodilatation (mediated through increased cAMP in platelets). All of the following are true except: Prostacyclin is synthesized in endothelium Thromboxane is released from platelets, ASA inhibits cyclooxygenase ‘Thromboxane is regenerated in platelets within 24 hours after ASA Tx Bleeding risk is best assessed with history and physical exam paoce Answer d. Thromboxane is not regenerated in platelets as cyclooxygenase is irreversibly inhibited and platelets do not have nuclear material to re-synthesize cyclooxygenase, Endothelium does contain DNA and can re-synthesize cyclooxygenase Which of the following is required in formation of the pro-thrombin complex Magnesium) Potassium Selenium Cobalamin Calcium eeocm Answer e. Calcium is required in formation of the prothrombin complex. The pro-thrombin complex (Xase complex) uses X, V, calcium, platelet factor 3, and pro-thrombin (Factor I!) Which of the following coagulation factors is not synthesized in the liver: a. Factor V b. Factor VI Factor Vil dé. Factor Vili €. Factor IX 24 25. 26. 27 28. 29 Answer d. Factor Vill is synthesized in vasoular endothelium, WF (von Willebrand Factor) is also synthesized in vascular endothelium and is important in hemostasis (links Gplb receptor on platelets to collagen) Which of the following deficiencies results in a normal PT (INR) and prolonged PTT: a. Factor Vil b. Factor V Factor X d. Factor Il Factor Vill Answer e. Factor Vill (8) ‘Which of the following deficiencies results in a prolonged PT (INR) and normal PTT a. Factor VI b. Factor Vil ¢, Factor Vil d. Factor IX e. Factor X Answer b. Factor Vil (7) Which of the following factors has the shortest halt-life Factor Vi Factor Vil Factor Vill Factor IX Factor X Answer b. Factor Vil (7) All of the following are Vit K dependent factors except: a. Factor il b. Factor V c. Factor Vil d. Factor IX e. Factor X Answer b. Factor V All of the following platelet problems are true except a Bernard-Soulier disease involves a Gplb receptor defect b. Glanzmann thrombasthenia involves a Gpllbillia receptor defect c. —_Uremia involves down-regulation of WWF d. Vit K deficiency leads to decreased platelet production ‘Answer d. Vit K deficiency leads to decreased Vit K dependent factor production (li, Vil, IX and X; also protein C and protein S) Al of the following apply to von Willebrand disease except Type Ill disease does not respond to DDAVP (desmopressi Type | and Ill disease have reduced quantity of circulating WWF Type Ill is the MC type itis the MC congenital bleeding disorder The defect is in platelet adhesion paece Answer c. Type lis the most common type of von Willebrand disease All of the following are true for hemophilia A (Factor Vill deficiency) except a. Factor Vill levels should be raised to 100% pre-op before major surgery b. 1" line therapy for hemarthrosis is aspiration of the joint tant ©. Factor Vili levels should be maintained at 80-10% for 14 days post-op after major surgery d. Hemophilia A and hemophilia B have the same bleeding risk which is dependent on factor levels Answer b. 1" line therapy for hemarthrosis is recombinant factor Vill and ice. Range of motion exercises are started well after the bleeding is controlled for hemarthrosis. t line Tx (and often definitive Tx) for any bleeding issues (eg joint, intra- cerebral, contained GI bleed [eg duodenal hematomal) associated with hemophilia A is Factor Vill replacement (for Hemophilia B — Factor IX). Allof the following are true of hemophilia A and B except: a. Patients with severe, life-threatening bleeds and high factor Vill or IX antibody titers should be treated with Factor Vil concentrate b. DDAVP is not effective for Hemophilia B Both have prolonged PT. Both are sex linked recessive Answer ¢. Both hemophilia A and B have prolonged PTT. DDAVP can be used for mild cases of Hemophilia A (stimulates release of Factor Vill / VWF) All the following are true of antiphospholipid antibody syndrome (APAS) except a. Classically has an elevated PTT (from lupus anticoagulant antibodies) that is not corrected with FFP (hypercoaguable with elevated PTT) Is associated with elevated anti-cardiolipin antibodies Patients are prone to spontaneous abortions Cardiolipin is a cell membrane phospholipid 's associated with elevated anti-lupus anticoagulant antibodies pees Answer d, Cardiolipin is a mitochondrial membrane phospholipid All of the following are true of hypercoaguable states except a, Antithrombin Ill deficiency is associated with heparin resistance b. The mutation for Factor V Leiden is on protein C c. The MC acquired hypercoaguiabilty disorder is smoking d. _ Hyperhomocysteinemia treatment is with folate and cyanocobalamin Answer b. Resistance to activated protein C (Factor V Leiden) is caused by a mutation on Factor V. itis the MC congenital hypercoagulability disorder. The primary mechanism of uremia induced coagulopathy is: a. Preventing conversion of fibrinogen to fibrin b. Down regulation of the Gplb receptor Inhibition of von Willebrand factor (VWF) release d. Down regulation of the Gp libilia receptor e, Inhibition of Antithrombin Ill Answer c. Uremia causes inhibition of vWF release and is the key dysfunctional element in uremic coagulopathy A.50 yo man on chronic hemodialysis is scheduled to undergo open inguinal hemia Fepair. Which of the following is the best therapy to help prevent intra-op bleeding a. Hemodialysis b. Platelets c. DDAVP d. Factor Vil concentrate Answer a. For non-acute situations, hemodialysis the day prior to surgery is the best preventative therapy for avoiding uremia and intra-op bleeding. 36. 36. A 60 yo man on chronic hemodialysis presents with a clotted AV fistula graft and encephalopathy (BUN 125). You emergently place a temporary dialysis line which continues to bleed around the site. The best initial treatment for this patient is: a. Hemodialysis, b. Platelets c. DDAVP d. Factor Vil concentrate Answer c. The best acute treatment for bleeding associated with uremia is DDAVP (which causes release of WWF [and Factor Vill] from endothelium). If that fails, platelets should be given Prior to aortic valve replacement, you are unable to get the patient's activated clotting time (ACT) and PTT to an appropriate range that is safe for cardio-pulmonary bypass despite several rounds of heparin (ACT and PTT are normal). ‘The patient was on heparin prior to surgery. The most appropriate next step is: ‘Abandon surgery DDAVP Anti-thrombin It Factor Vill concentrate Cryoprecipitate ‘Answer c. Pre-operative heparin therapy can decrease anti-thrombin Ill levels and cause relative anti-thrombin Ill deficiency resulting in heparin resistance. ‘Txis recombinant anti-thrombin Ill, If not available, FFP should be given (has highest concentration of AT-iI}) Ant-thrombin Ill deficiency can also present as fresh red thrombus foliowing heparin administration for vascular procedures (eg fresh thrombus in an aortic graft after finishing the proximal anastomosis and moving the cross clamp) After placing a left ventricular assist device (LVAD), diffuse bleeding occurs. Fibrinogen level is 20. The most appropriate next step is a FFP b. DDAVP c. — Cryoprecipitate d. Factor Vii concentrate fe. Recombinant WWF:VIIl Answer c. Cryoprecipitate has the highest concentration of fibrinogen Normal fibrinogen levels should be > 100. Cryoprecipitate contains high concentrations of Factor Vill, vWF, and fibrinogen ‘The best treatment for thrombolytic overdose (eg urokinase, tissue plasminogen activator (tPAl) is ‘a. Aminocaproic acid (Amicar) b. FFP. c. Packed red blood cells d. Cryoprecipitate Answer a. Thrombolytics work by converting plasminogen into plasmin. Plasmin then degrades fibrin, Aminocaproic acid (Amicar) works by binding plasminogen and preventing the conversion of plasminogen to plasmin Fibrinogen levels < 100 are associated with increased risk and severity of bleeding. Tx with aminocaproic acid is indicated ng Is ce. as gen 10 38. 40. at 42, 43, Prostatectomy or TURP can release urokinase, causing fibrinolysis and bleeding issues (eg persistent hematuria); Tx — aminocaproic acid (Amicar) Which of the following would indicate disseminated intravascular coagulation (DIC), as ‘opposed to simple fibrinolysis: Elevated D-dimer b. Elevated fibrin split products Decreased fibrinogen d. Decreased platelet count Answer d. Fibrinolysis is not associated with a decreased platelet count. DIC results in an elevated PT and PTT, decreased platelets, and decreased fibrinogen, ‘4.50 yo man is admitted for sigmoid diverticulitis (on CT scan). Despite fluid resuscitation and antibiotics he has the following lab values: BP 90/60, HR 105, WBC. 20, PTT 100, platelets 36, INR 2.3, fibrinogen 40, elevated D-dimer, and elevated fibrinogen split products. The most essential step to improve this patient condition is a. Rule out pulmonary embolism b, Colonoscopy c. FFP, cryoprecipitate, and platelets d, Sigmoidectomy Answer d. This patient has DIC based on lab values. Although blood products should be given pre-op, they will likely be soon consumed by the DIC process. ‘The most important issue here is to remove the DIC source (ie sigmoidectomy for diverticulitis) All of the following are true of deep venous thrombosis (DVT) except The MC source of pulmonary embolism (PE) is lio-femoral DVT The left leg develops DVT 2x more commonly than the right IVC filters should be placed above the renal veins ‘An infected indwelling catheter with tip thrombosis requires removal ‘An upper extremity DVT (eg arm swelling) related to an indwelling catheter is treated with catheter removal and heparin eaece ‘Answer c. IVC filters should be placed below the renal veins. If placed above renal veins, an embolus that clogs the filter can result in renal failure. HD catheters with infected thrombosis can't be salvaged (require removal). All of the following are true of DVT risk except a. The risk is elevated in pregnant patients compared to non-pregnant patients, b. The risk is elevated in patients undergoing surgery for malignancy compared to those without malignancy ©. The risk is elevated in patients undergoing open gastric bypass compared to those undergoing laparoscopic gastric bypass d. The risk is elevated in patients with Leiden Factor @, The best therapy for prevention of post-thrombotic syndrome is early thrombolytics Answer c. DVT risk is the same for patients undergoing open gastric bypass ‘compared to laparoscopic gastric bypass. The pneumoperitoneum created intre- op (increasing risk of DVT) for patient undergoing laparoscopy is equally Weighted by decreased ambulation post-op (increasing risk of DVT) in patients undergoing open surgery. Most adult surgery in-patients should receive DVT prophylaxis. ‘A 25 yo woman develops severe left leg pain and swelling to the level of her buttock. Her leg is massively swollen on exam with a blue appearance. Duplex U/S shows an 44, 48. 46 iliofemoral DVT. She still has motor and sensation in the extremity. The most appropriate next step is: Open thrombectomy Heparin only Catheter directed thrombolytics INC filter Answer c. This patient has phlegmasia cerulea dolens. This can result in leg gangrene so therapy is indicated. Catheter directed thrombolytics are superior to just heparin therapy alone for this condition, Your patient has a recurrent pulmonary embolism despite appropriate anticoagulation and you decide to place an IVC filter. Pre-procedure U/S shows a lio-caval DVT, the majority of which goes down the left common iliac vein. The most appropriate next step is ‘2. Access the left femoral vein b. Access the right femoral vein ¢. Access the right internal jugular vein 4. Access the left internal jugular vein Answer c. Patients with iliocaval DVT who require IVC filters should have them placed using the intemal jugular vein as access (the right internal jugular vein is easier than the left for IVC filter placement). You start Coumiadin on a patient with @ pulmonary embolus. Three days later, he starts sloughing off skin across his arms and legs. All of the following are true of this patients most likely condition except a. Thisis prevented by starting heparin before Coumadin b. Patients with protein C deficiency are more susceptible c. The skin sloughing is caused by skin necrosis d. This patient most likely has hemophilia A Answer d. Warfarin induced skin necrosis occurs when Coumadin is started without being on heparin 1%. It results from a relative hypercoaguable state because of the shorter half-life of protein C and S compared to factors Il, Vil, IX and X (Vit K dependent factors), Protein C and S decrease after Coumadin before the other factors decrease, resulting in a hypercoaguable state. Patients with protein C deficiency are at increased risk for warfarin induced skin necrosis. It is prevented by starting heparin before giving Coumadin. Al of the following are true except a. — Low molecular weight heparin (LMVVH) binds Anti-thrombin Ill (AT-Ill) and neutralizes Factors lla and X LMWH is not reversed with protamine Fondaparinux is a direct thrombin inhibitor Argatroban works independently of AT-IIh Dabigatran (Pradaxa, a direct thrombin inhibitor) requires dose adjustment for renal insufficiency Answer a. LMWH (eg Lovenox) binds AT-III and inhibits Factor Xa only. Unfractionated heparin binds AT-IIl and inhibits Factors lla and Xa A 50 yo woman receiving heparin suffers a small stroke. Her platelet count is 88 (baseline platelet count at admission was 225). Her PTT is 85. Which of the following is most accurate for diagnosing HIT in this patient: a. IgG to heparin b. Current platelet count of 88 c PTT 85 4d, Admission platelet count of 225, Answer a. Antibodies to heparin (most commonly IgG to heparin-PF4 complex) is the most accurate way of diagnosing HITT. 48, Which of the following is the best choice for continued anticoagulation in the above patient a. Continued IV heparin with steroids b. Subcutaneous heparin leg ¢. Low molecular weight heparin (Lovenox) d. Argatroban ‘Answer d. Direct thrombin inhibitors (eg Argatroban, Bivalirudin [Angiomax]) are on the treatment of choice for suspected HITT. re Argatroban is preferred for patients with renal insufficienoy (has hepatic metabolism) and bivalirudin is preferred for patients with liver problems (has renal metabolism) 49, A 80 yo manis diagnosed with stage Il colon CA. He had a drug-eluting coronary artery stent placed 1 month ago and is on clopidogrel (Plavix). The most appropriate next step is vem a Surgery while on Plavix b. Hold the Plavix only and operate after 5-7 days ©. Hold the Plavix, start a short-acting Iib/ilia inhibitor, and operate in 5-7 days d. Hold the Plavix and only start the Hlb/iiia inhibitor if stent thrombosis occurs s ‘Answer c. Holding Plavix, starting a short-acting IIbiliia inhibitor, and operating in 8-7 days is appropriate. Abruptly stopping Plavix within the first year of drug- eluting stent placement is associated with stent thrombosis and acute myocardial infarction. BLEEDING RISK = History and Physical Exam - best way to predict bleeding risk od = Normal circumcision - does not ruie out bleeding disorders; can stil have clotting factors from mother (eg hemophilia A - factor Vill crosses placenta) x = Abnormal bleeding with tooth extraction or tonsillectomy - picks up 99% of patients with a bleeding disorder = MCC of surgical bleeding - incomplete hemostasis = Warfarin, Plavix, and ASA - hold for 5-7 days prior to major surgery skin NORMAL COAGULATION / ANTI-COAGULATION = Initial response to vascular injury (in order) ~ vasoconstriction, platelet adhesion, and thrombin generation d = Coagulation Factors *¢ _Allare synthesized in the liver except Factor Vill (synthesized in endothelium) © WWF (cofactor for Vill) - also synthesized in endothelium * Exposed collagen, prekallikrein, kininogen and Factor XII initiate the intrinsic pathway nt * Tissue factor and Factor VI initiate in the extrinsic pathway * Vit dependent cofactors - Il, Vil, IX and X; also protein C and protein S ‘Warfarin inhibits these factors * Factor Vil - has shortest half-life = Prothrombin complex (Xase complex) * Includes Factor X, Factor V, calcium, platelet factor 3, and prothrombin * Prothrombin complex forms on platelets; catalyzes formation of thrombin 9 = Thrombin (Key to coagulation cascade) * Converts fibrinogen to fibrin (and fibrinogen degradation products) * Activates factors V and Vill * Activates platelets © Generated on platelet surtace (prothrombin complex above) * _ Fibrin + platelets = platelet plug (hemostasis) = VWF - links Gplb on piatelets to collagen

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