0 ratings0% found this document useful (0 votes) 295 views536 pagesFiser Absite Practice Questions 2015
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content,
claim it here.
Available Formats
Download as PDF or read online on Scribd
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, LLCre 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
531Cell 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
aMAnswer 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 exceptDesmosomes 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 IX24
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 jointtant
©. 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 indicatedng
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 an44,
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