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% Document Info
\author{happyfeet2020}
\pdfinfo{
  /Title (hemostasis.pdf)
  /Creator (Cheatography)
  /Author (happyfeet2020)
  /Subject (Hemostasis Cheat Sheet)
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\fancyhead[L]{
\noindent
\begin{multicols}{3}
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    \vspace{-7pt}
    {\parbox{\dimexpr\textwidth-2\fboxsep\relax}{\noindent
        \hspace*{-6pt}\includegraphics[width=5.8cm]{/web/www.cheatography.com/public/images/cheatography_logo.pdf}}
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\columnbreak
\begin{tabulary}{11cm}{L}
    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{Hemostasis Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{happyfeet2020} via \textcolor{DarkBackground}{\uline{cheatography.com/144934/cs/31239/}}}
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\noindent
\begin{multicols}{3}
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  \mymulticolumn{2}{p{5.377cm}}{\bf\textcolor{white}{Cheatographer}}  \\
  \vspace{-2pt}happyfeet2020 \\
  \uline{cheatography.com/happyfeet2020} \\
  \end{tabulary}
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Published 19th March, 2022.\\
   Updated 19th March, 2022.\\
   Page {\thepage} of \pageref{LastPage}.
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  \vspace{-5pt}
  %\includegraphics[width=48px,height=48px]{dave.jpeg}
  Measure your website readability!\\
  www.readability-score.com
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\begin{multicols*}{4}

\begin{tabularx}{3.833cm}{x{1.54485 cm} x{1.88815 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Stages of Hemostasis}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{1. Vessel Spasm}} & Response to inflammation. Initiated by endothelial injury. Reflex vessel restriction by the smooth muscle layer reducing blood flow. Only last 1 minute. Thromboxane A2 released from platelets contribute to vasoconstriction. This happens locally at the site of the injury \tn 
% Row Count 13 (+ 13)
% Row 1
\SetRowColor{white}
{\bf{2. Formation of Platelet Plug}} & Platelets are attracted to damaged vessel wall by the release of von willebrand factor. Once they encounter vWF they activate and change from disk shaped to star shaped then flat sphere like shaped. Then they adhere to collagen and aggregation occurs. Aggregation is mediated by the release of granules- ADP and TXA2 (more of these = more aggregation). Glycoprotein IIb and IIIa receptors bind fibrinogen and link platelets together. This leads to the platelet plus formation. \tn 
% Row Count 35 (+ 22)
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\begin{tabularx}{3.833cm}{x{1.54485 cm} x{1.88815 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Stages of Hemostasis (cont)}}  \tn
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{\bf{3. Blood Coagulation}} & Results in conversion of inactive soluble fibrinogen to insoluble fibrin. {\emph{Vitamin K}} is necessary for synthesis of factors {\bf{VII, IX, X, prothrombin, protein C}}. {\emph{Calcium}}  is required by activated factor {\bf{X}} to convert prothrombin to thrombin.  Involves intrinsic, extrinsic and common pathway. Regulated by natural anticoagulants (Antithrombin II, Protein C-inactivates factor V and VIII, plasmin- breaks down fibrin). \tn 
% Row Count 20 (+ 20)
% Row 3
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{\bf{4. Clot Retraction}} & Serum is squeezed out of the clot and the edges of the vessels are joined. Failure of clot retraction is indicative of low platelet count. \tn 
% Row Count 27 (+ 7)
% Row 4
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{\bf{5. Clot Dissolution}} & Needed for permanent tissue repair. Process known as fibrinolysis (getting rid of clot). Plasmin digests fibrin, factors V, VIII, XII, prothrombin. Plasminogen is activated to plasmin by enzymes (one is factor XII or Hageman factor). \tn 
% Row Count 38 (+ 11)
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\mymulticolumn{2}{x{3.833cm}}{These 5 stages are the holy grail of wound healing. \newline vWF is produced by endothelial cells, platelets and connective tissue. disorder?}  \tn 
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\begin{tabularx}{3.833cm}{x{1.0299 cm} x{2.4031 cm} }
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\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Hemostasis}}  \tn
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{\bf{Definition}}: & The process which causes the bleeding to stop. Maintains blood fluidity and prevents blood from leaving the vascular compartments \tn 
% Row Count 5 (+ 5)
% Row 1
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{\bf{Main Factors}}: & 1. Cell membrane 2. Platelets 3. Coagulation cascade \tn 
% Row Count 7 (+ 2)
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\SetRowColor{LightBackground}
\mymulticolumn{2}{x{3.833cm}}{{\emph{Abnormal function of hemostasis}}: thrombosis (inappropriate clotting) or bleeding/hemorrhaging *insufficient clotting)}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{3.833cm}{X}
\SetRowColor{DarkBackground}
\mymulticolumn{1}{x{3.833cm}}{\bf\textcolor{white}{Coagulation Cascade}}  \tn
\SetRowColor{LightBackground}
\mymulticolumn{1}{p{3.833cm}}{\vspace{1px}\centerline{\includegraphics[width=5.1cm]{/web/www.cheatography.com/public/uploads/happyfeet2020_1647633540_tumblr_oy2uacyw5h1uh8gw2o1_1280.jpg}}} \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}-}
\end{tabularx}
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\begin{tabularx}{3.833cm}{x{1.64784 cm} x{1.78516 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Blood Testing for Coagulability}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{PT- Prothrombin time}} & Tests {\emph{extrinsic }} and {\emph{common}} pathway.  Looking at time to clot. Used to monitor {\emph{warfarin}}.  Normal is 11-13 seconds. PT is increased with warfarin \tn 
% Row Count 8 (+ 8)
% Row 1
\SetRowColor{white}
{\bf{ PTT- Partial thromboplastic time}} & Tests {\emph{intrinsic}} pathway. Used to monitor {\emph{heparin}}. Normal range is 30-50 seconds. \tn 
% Row Count 13 (+ 5)
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\begin{tabularx}{3.833cm}{p{0.3433 cm} p{0.3433 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Hypercoagulability  (increased platelet function)}}  \tn
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\mymulticolumn{2}{x{3.833cm}}{} \tn 
% Row Count 0 (+ 0)
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\SetRowColor{LightBackground}
\mymulticolumn{2}{x{3.833cm}}{Hypercoagulability results in platelet adhesion and formation of clots which leads to disruption of blood flow.}  \tn 
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\begin{tabularx}{3.833cm}{x{1.47619 cm} x{1.95681 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Increased Clotting Activity}}  \tn
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{\bf{Primary:}} & {\emph{Genetics}}. Mutations in factor V and prothrombin genes. Results in inability of factor Va to be deactivated by protein C. Examples: Factor V Leiden disorder where clotting persists and predisposes to DVT. Other disorders are inherited deficiencies of antithrombin III, protein C/S. \tn 
% Row Count 13 (+ 13)
% Row 1
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{\bf{Secondary:}} & {\emph{Acquired}}. Stasis due to bed rest (slows normal blood flow and allows accumulation of clotting factors)cancer, birth control, smoking and obesity, MI. \tn 
% Row Count 20 (+ 7)
% Row 2
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{\bf{Antiphospholipid Syndrome}}: & AKA Hughes syndrome. Autoimmune hypercoagulable state caused by antiphospholipid antibodies. Provokes blood clots in arteries in veins.  Can be primary or secondary (due to lupus). \tn 
% Row Count 29 (+ 9)
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\begin{tabularx}{3.833cm}{x{1.51052 cm} x{1.92248 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Bleeding Disorders}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{Platelet Disorders:}} & normal range: 150,000- 400,000/ml. Signs of disorders include: \tn 
% Row Count 3 (+ 3)
% Row 1
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 & Petechia, purpura, ecchmyosis, bleeding from mucous membrane \tn 
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{\emph{Thrombocytopenia:}} & Low circulating platelets. Due to decreased production by bone marrow (aplastic anemia, leukemia, HIV) or increased pooling of platelets in the spleen, or decreased platelet survival  or nutritional deficiencies (B12, iron, folic acid), \tn 
% Row Count 17 (+ 11)
% Row 3
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 & Types: idiopathic, thrombotic or hemolytic uremia syndromes or heparin induced. \tn 
% Row Count 21 (+ 4)
% Row 4
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{\emph{Decreased platelet function:}} & Caused by asprin, uremia (increased urea in blood coats the platelets causing glycoproteins not to function) or genetic disorders \tn 
% Row Count 27 (+ 6)
% Row 5
\SetRowColor{white}
 & Genetic disorders: Bernard Soulier- GpIIb disorder so vWf has nowhere to bind, Von Willebrand Disease-no vWF to bind platelets. Leads to decreased platelet adhesion *Vasopressin can stimulate release of vWF for tx. Glanzmann thrombocytopenia- GpIIb-IIIa so platelets cant bind together \tn 
% Row Count 40 (+ 13)
\end{tabularx}
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\vfill
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\begin{tabularx}{3.833cm}{x{1.51052 cm} x{1.92248 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Bleeding Disorders (cont)}}  \tn
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\SetRowColor{LightBackground}
{\emph{Coagulation Cascade Disorders}}: & Deficiencies or impairments of one or more  coagulation factors due to defective synthesis, inherited disease or increased consumption. Prevents fibrinogen from converting to fibrin. Will see bleeding in deep tissues like hematomas. Elevated PTT and PT. \tn 
% Row Count 12 (+ 12)
% Row 7
\SetRowColor{white}
 & Hemophilia A- Factor VIII deficiency: X-linked recessive disorder, affects mostly males. Soft tissue bleeding of GI, hip, knee, elbow and ankle joints. Can lead to joint fibrosis and contractures. Tx is factor VIII replacement therapy. Only affects intrinsic pathway. \tn 
% Row Count 25 (+ 13)
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\begin{tabularx}{3.833cm}{x{1.64784 cm} x{1.78516 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Anticoagulants}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\emph{Warfarin (Coumadin)}}: & Vitamin K antagonist. Blocks epoxidase reductase, leads to depletion of reduced vit K (which is essential for synthese of factors II, VII,IX,X, protein c/s) \tn 
% Row Count 8 (+ 8)
% Row 1
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 & Uses: Prevention of thrombosis in predisposed patients. AE- bleeding \tn 
% Row Count 12 (+ 4)
% Row 2
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{\emph{Heparin(IV)/ LMW Heparin (lovenox)}}: & Induces a conformational change in antithrombin III making it more accessible to proteases -\textgreater{} increase inactivation of thrombin \tn 
% Row Count 19 (+ 7)
% Row 3
\SetRowColor{white}
 & Uses: Prophylaxis and tx of thromboembolic diseases, unfractionated (IV heparin) used with antiplatelet agents for tx of acute coronary syndromes. Lovenox is an efficient catalyzation of factor Xa inactivation. \tn 
% Row Count 30 (+ 11)
\end{tabularx}
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\vfill
\columnbreak
\begin{tabularx}{3.833cm}{x{1.64784 cm} x{1.78516 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Anticoagulants (cont)}}  \tn
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 & AE: bleeding and heparin induced thrombocytopenia \tn 
% Row Count 3 (+ 3)
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\begin{tabularx}{3.833cm}{x{1.7165 cm} x{1.7165 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Novel Oral Anticoagulants}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{Apixaban (Eliquis), Rivaroxaban (Xarelto)}}: & Direct inhibitor of free and clot-bound factor Xa which prevents the conversion of prothrombin to thrombin. Prevents clot formation. \tn 
% Row Count 7 (+ 7)
% Row 1
\SetRowColor{white}
 & {\emph{Uses:}} A- reduces stroke and systemic embolism, prophylaxis of DVT/PE after hip or knee surgery. R- same but prophylaxis of venous thromboembolic events for hip/knee surgery pts. \tn 
% Row Count 16 (+ 9)
% Row 2
\SetRowColor{LightBackground}
 & {\emph{AE:}} easy bruising, bleeding, back or muscle pain, hypotension. \tn 
% Row Count 20 (+ 4)
% Row 3
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{\bf{Dabigatran (Pradaxa)}}: & Direct thrombin inhibitor which prevents conversion of fibrinogen to fibrin. \tn 
% Row Count 24 (+ 4)
% Row 4
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 & {\emph{Uses}}: Prevents thromboembolism in pts with AF, DVT, PE \tn 
% Row Count 27 (+ 3)
% Row 5
\SetRowColor{white}
{\bf{Betrixaban (Bevyxxa):}} & \seqsplit{Cofactor-independent} direct inhibitor of factor Xa. \tn 
% Row Count 30 (+ 3)
\end{tabularx}
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\vfill
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\begin{tabularx}{3.833cm}{x{1.7165 cm} x{1.7165 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Novel Oral Anticoagulants (cont)}}  \tn
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 & {\emph{Uses}}: prophylaxis of VTE in moderate to severe restricted mobility patients. \tn 
% Row Count 4 (+ 4)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{3.833cm}}{{\emph{Rivaroxaban interacts with Aspirin}}. \newline {\emph{All drugs will have bleeding as a side effect!}}}  \tn 
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\begin{tabularx}{3.833cm}{x{0.89258 cm} x{2.54042 cm} }
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\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Inhibition of Anticoagulation}}  \tn
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{\bf{Protamine}}: & Antagonist of heparin. \tn 
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 & {\emph{Uses}}: IV administration if there is life threatening hemorrhage/heparin excess \tn 
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\begin{tabularx}{3.833cm}{x{1.7165 cm} x{1.7165 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Thrombolytic Agents}}  \tn
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\SetRowColor{LightBackground}
{\bf{Streptokinase}}: & Forms a stable complex with plasminogen which then cleaves other plasminogen molecules into plasmin \tn 
% Row Count 5 (+ 5)
% Row 1
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 & {\emph{Uses}}: PE, STEMI, arterial thrombosis, DVT. {\emph{AE}}:systemic fibrinolysis, hemorrhage \tn 
% Row Count 10 (+ 5)
% Row 2
\SetRowColor{LightBackground}
{\bf{Recombinant Tissue Plasminogen Activator}}: & Binds to newly formed thrombi and makes it a potent activator of plasminogen. Cleaves plasminogen into plasmin which then cleaves fibrin into fibrin degradation products \tn 
% Row Count 19 (+ 9)
% Row 3
\SetRowColor{white}
 & {\emph{Uses}}: PE,STEMI, Acute ischemia stroke. {\emph{AE}}: bleeding \tn 
% Row Count 22 (+ 3)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
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\begin{tabularx}{3.833cm}{x{1.30454 cm} x{2.12846 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Antiplatelet Agents}}  \tn
% Row 0
\SetRowColor{LightBackground}
{\bf{Aspirin (ASA)}} & Non selective COX inhibitor. Irreversible inhibition of COX-1= inhibits platelet aggregation for 10 days.  Stops conversion of arachidonic acid to thromboxane A2 (potent platelet aggregation inducer). \tn 
% Row Count 9 (+ 9)
% Row 1
\SetRowColor{white}
 & {\emph{Uses}}: Pain/inflammation/fever, reduces risk of MI/unstable angina, prevents strokes due to blood clots \tn 
% Row Count 14 (+ 5)
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 & {\emph{AE}}: hemorrhagic stroke, GI bleeding \tn 
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\mymulticolumn{2}{x{3.833cm}}{{\bf{PDE Inhibitors}}} \tn 
% Row Count 17 (+ 1)
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Cilostazol (Pletal) & Antiplatelet and vasodilator. Inhibitors phosphodiesterase II -\textgreater{} suppresses cAMP degradation -\textgreater{} increases cAMP in platelets and blood vessels -\textgreater{} inhibition of platelet aggregation and vasodilation \tn 
% Row Count 26 (+ 9)
% Row 5
\SetRowColor{white}
 & {\emph{Uses}}: Intermittent claudication symptoms (by widening the vessels in teh legs which helps with blood flow). \tn 
% Row Count 31 (+ 5)
\end{tabularx}
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\vfill
\columnbreak
\begin{tabularx}{3.833cm}{x{1.30454 cm} x{2.12846 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Antiplatelet Agents (cont)}}  \tn
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 & {\emph{AE, DI}}: heart failure, tachycardia, interacts with NSAIDs and aspirin. \tn 
% Row Count 3 (+ 3)
% Row 7
\SetRowColor{white}
Pentoxifylline (Trental) & Inhibits erythrocyte phosphodiesterase -\textgreater{} increases cAMP activity, decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity \tn 
% Row Count 11 (+ 8)
% Row 8
\SetRowColor{LightBackground}
 & {\emph{Uses}}: Intermittent claudication, chronic occlusive arterial disease \tn 
% Row Count 14 (+ 3)
% Row 9
\SetRowColor{white}
 & {\emph{AE}}: muscle aches, headaches, GI discomfort \tn 
% Row Count 16 (+ 2)
% Row 10
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{3.833cm}}{{\bf{ADP Receptor Pathway Inhibitor}}} \tn 
% Row Count 17 (+ 1)
% Row 11
\SetRowColor{white}
Clopidogrel (Plavix) & Irreversibly binds to P2Y12 which prevents the binding of ADP receptors on platelets which prevents GPIIb-IIIa activation -\textgreater{} inhibits platelets aggregation \tn 
% Row Count 24 (+ 7)
% Row 12
\SetRowColor{LightBackground}
 & {\emph{Uses}}: reduces risk of MI/stroke, better than aspirin in decreasing CV outcomes \tn 
% Row Count 28 (+ 4)
% Row 13
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 & {\emph{AE, DI}}: upper RTI, joint, chest pain, depression, bleeding. DI- Ibuprofen \tn 
% Row Count 32 (+ 4)
\end{tabularx}
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\begin{tabularx}{3.833cm}{x{1.30454 cm} x{2.12846 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{3.833cm}}{\bf\textcolor{white}{Antiplatelet Agents (cont)}}  \tn
% Row 14
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{3.833cm}}{{\bf{GPIIb-IIIa Antagonist}}} \tn 
% Row Count 1 (+ 1)
% Row 15
\SetRowColor{white}
Abicixmab (Reopro) & Binds to intact platelet GPIIb/IIIa receptor and blocks access of large molecules to receptor through steric hinderance or conformational change. Prevents cell adhesion \tn 
% Row Count 8 (+ 7)
% Row 16
\SetRowColor{LightBackground}
 & {\emph{Uses}}: prevents cardiac ischemic complications in vascular surgeries or pts w/ unstable angina, intended for use with aspirin and heparin \tn 
% Row Count 14 (+ 6)
% Row 17
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 & {\emph{AE}}: N\&V, hypotension, vision changes, back pain \tn 
% Row Count 17 (+ 3)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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% That's all folks
\end{multicols*}

\end{document}