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56 Cards in this Set
- Front
- Back
what are the 4 phases of hemostasis |
1. Vascular Phase: vasoconstiction to decrease bleeding. vWF and PGI2 is released
2. Platelet Phase: platelets adhere and form a plug. Plateslets are activated and release- ADP, Ca, 5HT 3. Coagulation- form a clot. Extrinsic path required endo damage (TF, 7) intrinsic has it all in the cyto (12, 11, 9, 8) Fibrinolysis: plasmin breaks up the fibrin that holds the clot together. |
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are defects in the vascular phase of coagulation usually acquired or inherited
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Acquired
trauma, sepsis, steroids, aging **congenital vascular disorders are rare |
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are defects in the platelet phase of coagulation usually acquired or inherited
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Acquired (like vascular defects), common
ASA ITP- idiopathic thrombocytopenia |
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are defects in the coagulation phase of coagulation usually acquired or inherited
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either, this is really the one time we see CONGENITAL is in the coagulation
Congenital: deficit in clotting factor function or production (hemophilia or vWF) Acquired- drugs like heparin, coumadin, AB or liver disease |
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are defects in the fibrinolysis phase of coagulation usually acquired or inherited
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acquired
**DIC |
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if you pt has a bleeding disorder what q's do you want to ask in the history
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C: how much, petechia, purpura,
O: recent or life long, length of episode L: mucosal, GI. GU, intracranial, hemarthrosis D: E: liver disease, EtOH. meds, uremia, infection, malignancy, ASA, anticoagulants R: A: previous episode, previous transfusion- any reactions, why need the transfusion, S: Fx |
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if your pt has a bleeding disorder what should we look for on PE
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Gen: rarely leads to dx but often gives an idea of extent of bleeding
Vitals: asses blood loww(HR, BP) Gen: mental status change BLood loss: examine site, it is oozing or gushing SKin: ecchymosis, petechia, prupura Mucoas: bleeding? LN: can be indicative of AIDS, lymphoma, infectinon when supraclavicular or inguinal nodes are palpated HSM: Liver- infiltrative process. Spleen- hypersplenism, myeloproliforative disorder, lymphoma Joints: hemarthrosis Pelvic and rectal exam |
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why is a LN exam important in your pt w/bleeding
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Supraclavicular or inguinal nodes can suggest infection, lymphoma or AIDS
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if your pt is bleeding bc of lymphoma whay might you expect on PE
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splenomegaly
Supraclavicular or inguinal nodes |
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what are two exams that can be done to better asses bleeding
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DRE
pelvic |
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if your pt has a bleeding disorder what are the first 2 q's you ask yourself
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1. How much blood have they lost, how are they tolerating it.
2. Do they have a disorder in platelets, coagulation or mixed. Usually more bleeding in a congenital coagulation disorder seen in a man |
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in a primary platelet disorder what is ...
1. congenital or acquired 2. who 3. whats the bleed like 4. what ppt it? 5. whats PE |
Primary Platelet
1. acquired 2. seen in kids and women 3. mild bleed 4. seen after trauma, procedure or spontaneous 5. see petechiea, purpura, mucosal bleed |
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on PE your pt has petechia, purpura, and mucosal bleed
is this platelet or coagulation who gets this adn what ppt it? |
its a primary platelet thing
seen in women and kids, its a more mild bleed. its an acquired problem Seen after procededure or trauma |
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in a primary coagulation disorder what is ...
1. congenital or acquired 2. who 3. whats the bleed like 4. what ppt it? 5. whats PE |
1. congenital
2. males 3. moderate to profuse hemorrhage 4. post traumatic or spontanoues (like the platelet) 5. Deep MM, joint, UT, intracranial hemorrhage |
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a man comes in with a congenital bleeding disorder. is it likely platelet or coagulation proble,. whats PE like
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coagulation
**lots of blood. deep mm, joint, UT, and intracranial bleed contrast w/primary platelt disorders which are more common in women and kids and are characterized by mild hemorrhage and petechia, purpura and mucosal bleeding. these are acquired |
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in mixed platelet and coagulative disorders what is....
1. who gets it 2. congenital or acquired 3. how bad is the bleed 4. when does it happen 5. what is PE like |
1. who gets it. lots of ppl
2. ACQUIRED 3. bleed varies in severity 4. caused by trauma, sepsis, OB hemorrhage, transfusion, insect bite, 5. see signs of multi organ failure, purpura, bleeding |
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is the following caused by platelet, coaguation or mix dosorder
1. acquired 2. congential 3. seen in men 4. seen in women 5. LOTS of blood 6. see multi organ failure 7. seen as a result of OB hemorrhage 8. seen after trauma 9. mucosal bleed 10. seen after transfusion 11. mild bleed 12. intracranial hemorrhage 13. deep mm/joint bleed 14. UT bleed |
1. acquired: platelet and mixed
2. congentia: coagulationl 3. seen in men: coagulation 4. seen in women: platelet 5. LOTS of blood: coagulation 6. see multi organ failure: mix 7. seen as a result of OB hemorrhage: mix 8. seen after trauma: all 3!! 9. mucosal bleed: platelet 10. seen after transfusion: mix 11. mild bleed: platelet 12. intracranial hemorrhage: coagulation 13. deep mm/joint : coagulation 14. UT bleed: coagulation |
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summarize primary platelet disorders
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1. seen in kids and women, mild bleeding, its acquired. Bleeding occurs in mucosa, see petechia,
Splenomegaly indicates sequestration of platelets or other blood products HALLMARK is petechia that occurs spontaneously, after trauma/procedure |
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summarize primary coagulation disorders
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seen more in men bc of x linked inheritance
*can also be acquired with anticoagulatn tx bleeding is usually significant, deep and delayed by like 6-12 hours **intracranial bleed, hemarthralgia, ecchymosis can have signs of liver failure (jaundice), telangiectasia, HSM, Lymphadenopathy can suggest lymphoma, leukemia, or infectious disease, AIDS |
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what is teh most common acquired mixed platelet coagulation mixed disorder
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DIC
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summarize platelet/coagulation mixed disorders
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1. no sex/age predlication
2. DIC is most common initiating factors include- trauma, sepsis, OB hemorrhage, transfusion reaction, snake bites. Multi-organ faliure, unusual bleeding tendencies, **if an initial presentation is not platelet or coagulation its considered mixed until proven otherwise |
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your pt comes in with abnormal bleeding, what tests do you run
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Pt
PTT bleed time platelets |
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what 4 thigns cause thrombocytopenia
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1. decreased BM productino of platelets
2. increased platelet destruction 3. dilutional- seen after massive transfusion, hemorrhage 4. Combination- increased destriction and decreased production seen in liver disease |
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thrombotic thrombocytopenic purpura
how does it present? |
microangiopathic hemolytic anemia, thrombocytopenia, purpura, fever, renal failure, neurological sx
seen in young women peripheral smear shows schistocytes medical emergency |
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your 27 yo female presents with microangiopathic hemolytic anemia, thombocytopenia, purpura, and schistocytes. whats the deal
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TTP
**can also have fever, renal failure, and neuro sx. medical emergency |
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whats ITP
how is it dx |
dx of EXCLUSION
IgG AB to platelets is made and platelets are destroyed Kids: preceded by virus, self limited in kids Adults: chronic form, more common in women. insiduous onset and unpredictable course |
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how is ITP diff in kids and adults
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Kids: self limited, follows virus. its when you have IgG against platelets
Adults: chronic form, insidious onset, unpredictable course **more common in women |
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does hemophilia A paint a representative picture of a coagulation disorder
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yep
male, congenital, deep bleeds into mm and joints, UT, intracranial bleeds Hemophilia has factor 8 deficit so PTT is long. they dont get GI or nose bleeds often |
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whats vWF
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coagulation disorder
AD- decrease in vWF see lots of mucosal and cutaneous bleeds, menorrhagia nad GI bleeds are common simliar to hemophilia A but also has a platelet defecit increased bleed time, normal platelet count, increased PTT |
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is hemophilia a coagulation disorder or platelet
what is the only lab that is increased? |
coagulation
only the PTT is increased, its a factor 8 dificit its in males and is sex linked recessive deeo mm/joint bleeds. UT and intracranial bleeds (yep, sounds like a coagulation disorder, men, congenital, deep bleeds) bleed can be delayed after injury. Nose bleed and GI bleed is RARE |
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what are all of the primary coagulation disorders
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1. hemophilia
2. vWF 3. acquired coagulation defects |
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how are vWF and Hemophilia A distinguised via labs
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Hemophilia A: PTT is long
vWF- PTT and bleed time is long, platelets are normal |
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what is the promary coagulation disroder that is characterized by cutaneous and mucosal bleeds
what about the coagulation that is more deep bleeds in mm and joints, intracranial bleeds and UT |
vWF
Hemophilia A |
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what does liver do to bleeding
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cant make clotting factors so will be a coagulation disorder
**seen in EtOH, CA, hepatitis, meds, toxins |
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what clotting factors are part of
1. extrinsic path 2. intrinsic path 3. 3. made by liver 4. not made by liver 5. vit K dependent |
1. extrinsic path- TF, 7
2. intrinsic path- 12 11 9 8 3. common path: 2 5 10 3. made by liver: all except vWF 4. not made by liver: vWF 5. vit K dependent: 2 7 9 10 |
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whats the abnormal lab in vit K deficit
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long PT and PTT
K is 2 7 9 10 |
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talk about DIC
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its a mixed disorder
caused by infarct, trauma, OB, Ca, transfusion, platelets and coagulation factors are sonsumed |
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does hemophilia A paint a representative picture of a coagulation disorder
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yep
male, congenital, deep bleeds into mm and joints, UT, intracranial bleeds Hemophilia has factor 8 deficit so PTT is long. they dont get GI or nose bleeds often |
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whats vWF
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coagulation disorder
AD- decrease in vWF see lots of mucosal and cutaneous bleeds, menorrhagia nad GI bleeds are common simliar to hemophilia A but also has a platelet defecit increased bleed time, normal platelet count, increased PTT |
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is hemophilia a coagulation disorder or platelet
what is the only lab that is increased? |
coagulation
only the PTT is increased, its a factor 8 dificit its in males and is sex linked recessive deeo mm/joint bleeds. UT and intracranial bleeds (yep, sounds like a coagulation disorder, men, congenital, deep bleeds) bleed can be delayed after injury. Nose bleed and GI bleed is RARE |
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what are all of the primary coagulation disorders
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1. hemophilia
2. vWF 3. acquired coagulation defects |
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how are vWF and Hemophilia A distinguised via labs
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Hemophilia A: PTT is long
vWF- PTT and bleed time is long, platelets are normal |
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what is the promary coagulation disroder that is characterized by cutaneous and mucosal bleeds
what about the coagulation that is more deep bleeds in mm and joints, intracranial bleeds and UT |
vWF
Hemophilia A |
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what does liver do to bleeding
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cant make clotting factors so will be a coagulation disorder
**seen in EtOH, CA, hepatitis, meds, toxins |
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what clotting factors are part of
1. extrinsic path 2. intrinsic path 3. 3. made by liver 4. not made by liver 5. vit K dependent |
1. extrinsic path- TF, 7
2. intrinsic path- 12 11 9 8 3. common path: 2 5 10 3. made by liver: all except vWF 4. not made by liver: vWF 5. vit K dependent: 2 7 9 10 |
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whats the abnormal lab in vit K deficit
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long PT and PTT
K is 2 7 9 10 |
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talk about DIC
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its a mixed disorder
caused by infarct, trauma, OB, Ca, transfusion, platelets and coagulation factors are sonsumed |
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what are hte lab findings in DIC
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long PT, PTT and Thrombin time (TT)
**its when platelets and coagulation facotors get eaten up adn you bleed schistocytes are seen |
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what is in FFP (fresh frozen plasma)
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coagulation factors,
good for pts w/DIC |
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what are hte 3 main goals of tx for a pt w/bleeding
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1. stop the blood
2. treat the cause of bleeding 3. replace lost blood parts |
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what are some benefits of blood COMPONENT tx
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1. you only give the pt what they need (DIC needs FFP bc it has coagulation factors)
2. decrease risk of transfusion reaction 3. economical 4. decreased transmission of disease 5. banked blood looses its clotting factors and platelets fast |
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whats PRBC
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packed red blood cells
**replenish lost blood cell mass |
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FFP
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used to replace clotting factors (2 5 7 9 10 11)
used to reverse cumadin tx massive transfusions tx TTP and DIC |
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your pt lost TONS of blood adn you need to transfule like a zillion units, what else do you want to add
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FFP- make sure they get their clotting factors
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ut oh, we gave that guy a bit too much coumadin, now he wont stop bleed. what can we do
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FFP- it has coagulation factors
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who gets platelet transfusions
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thrombocytopenia <50,000 or abnormal bleeding
**increases the platelet count by like 10,000 |