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Summer 3 > Bleeding disorders > Flashcards

Bleeding disorders Flashcards

1
Q

What are visible signs of bleeding

A

Petechiae: <2mm, subQ bleeding, do NOT blanch (occur periorbital 2/2 vomiting)
Purpura: 2-10 mm, palpable or not
Ecchymosis: >1cm, extensive areas of bruising

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2
Q

What labs do you get when you suspect bleeding

A

CBC w/ PLT count
peripheral smear
PT/INR, aPTT
Bleeding time

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3
Q

What is a platelet count

A 
# of PLT (thrombocytes) only, not quality 
Normal: 150-450 
<40= prolonged bleeding from vascular injury can occur 
<20= spontaneous bleeding can occur
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4
Q

What is bleeding time

A

Measure of time for hemostasis (clot formation)
Screen microvascular and platelet function
Prolonged in platelet disorders and severe thrombocytopenia

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5
Q

How does hemostasis occur after an injury (overview of steps)

A
  1. Vasoconstriction
  2. Platelet plug formation
  3. Coagulation cascade
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6
Q

What happens during vasoconstriction

A

Vascular spasm; occurs immediately after injury
Smooth muscle on damaged vessels constricts and reduces amount of blood flow to the area, limiting blood loss
Collagen is exposed and promoted platelets to adhere

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7
Q

What happens during platelet plug formation

A

Platelets clump together (adhesion) on damaged endothelium and form a plug, then degranulate (thromboregulation)
Plug formation is activated by vWF
Platelets adhere to exposed collagen and release ADP and thromboxin A2= increased vasoconstriction

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8
Q

What happens during the coagulation cascade

A

Secondary hemostasis: clotting factors are activated after platelet plug forms
Causes formation of fibrin
Comprised of: Intrinsic pathway, Extrinsic pathway, and Common pathway

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9
Q

What helps regulate clotting in the coagulation cascade to ensure too much clotting doesn’t happen

A

Protein C, S, and ATIII

A deficiency in these makes you more likely to clot!

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10
Q

What happens in the intrinsic pathway

A

After damaged surface, factor XIIa, XIa, IXa, VIIIa go to Xa

Xa activates thrombin, fibrin, XIIIa, and clot is formed

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11
Q

What happens in the extrinsic pathway

A

After trauma, factor VII* and VIIa form tissue factor
Those along with factor X go to Xa
Xa activates thrombin, fibrin, XIIIa, and clot is formed

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12
Q

What is PT

A 
Prothrombin time; 
Prolonged with abnormalities in the extrinsic* (or common) pathway 
Used to monitor warfarin therapy 
Assess liver function and damage 
DIC
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13
Q

What is PTT or aPTT

A

Activates partial thromboplastin time
Prolonged with abnormalities in the intrinsic* (or common) pathway
Used to monitor UFH therapy (NOT LMWH)
Hemophilia, vW disease, liver damage, VK deficiency
DIC

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14
Q

What is INR

A

More accurate reflection of PT since PT is not standardized
Standardized ratio of PT:control
Results independent of reagents or methods used
Goal level is dependent on underlying need for anticoagulation (this is why we use it to monitor warfarin)

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15
Q

What are clotting disorders (cant clot well)

A

Associated with excessive or repetitive bleeding at unusual sites with normal activity
Can be congenital or acquired

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16
Q

What are Hemophilia A&B

A

A: factor VIII deficiency (MC)
B: IX deficiency (christmas dz)
-both are congenital bleeding disorders

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17
Q

Both hemophilia A&B are

A

X linked, recessive d/o that affect males mainly, or females born to affected dad and carrier mom
Severity correlates to factor levels (<1% factor level= extremely severe)

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18
Q

How do Hemophilia A&B present

A

Most ASx in first few months of life
First episode of Sx bleeding w/in first 2 years of life
Sever pain in weight bearing joints (hemophilic arthropathy)
Repeat episodes of bleeding

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19
Q

Where is bleeding MC in hemophilia A&B

A 
Joints (hemarhtrosis; severe if spontaneous) 
muscles 
skin
GI
GU
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20
Q

Labs for Hemophilia A will show

A

Platelets and PT: normal!

aPTT: prolonged (indicative of intrinsic pathway, factor VIII)

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21
Q

How do you manage hemophilia A

A

Factor VIII concentrate infusions
Desmopressin (increases release of vWF to help clot)
-Pt ed: avoid trauma, high risk activity, ASA, and go to genetic counseling

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22
Q

What are dysfunctional platelets

A

Congenital (abn vary) or Acquired (MC; drugs, alcoholism, myeloproliferative)

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23
Q

Lab studies for dysfunctional platelets will show

A

normal count
normal morphology
prolonged bleeding time
-nothing is wrong with the amount or the shape, but they just don’t work!

24
Q

How do you manage platelet dysfunction

A

dc offending agent
hemodialysis in uremic cases
platelet transfusion if serious bleeding

25
Q

What is splenic sequestration

A

Splenomegaly/hypersplenism: Thrombocytopenia

Post-splenectomy: reactive thrombocytosis

26
Q

What causes increased destruction of platelets

A

ITP: autoimmune destruction of platelets

27
Q

What causes increased consumption of platelets

A

TTP
HUS
DIC

28
Q

What is ITP

A

Antibody mediated destruction of platelets causes reduced PLT lifespan
Primary: 2/2 AI mechanisms leading to PLT destruction and underproduction NOT triggered by an associated condition
Secondary: associated with another condition (hepatitis, SLE, HIV, CLL)

29
Q

Explain acute vs chronic ITP

A

Acute: self limited, MC in kids, IgG associated, preceded by viral URI
Chronic: MC in females, peak at 20-50, insidious onset, associated w/ other AI dz or HIV

30
Q

What are clinical features of ITP

A 
ASx! or 
Petechiae, purpura, hemorrhagic bullae on skin 
Epistaxis, oral bleeding, menorrhagia 
SAH, ICH
*NO splenomegaly*
31
Q

Lab studies for ITP may show

A

Thrombocytopenia (<20)
Coag studies are normal
Bone marrow may show increased megakaryocytes
Diagnosis of exclusion

32
Q

How do you manage ITP

A

Avoid PLT antagonists (NSAIDs, ASA)
Acute: resolves spontaneously
Chronic: high dose prednisone or DXM. IVIG. Refractory? splenectomy or Danazol
Emergency: stop bleeding and give platelet transfusion

33
Q

Why is platelet transfusion not a long term Tx in ITP

A

Because the body’s natural response to any platelet it to destroy it. So if you put more in, they will help acutely, but eventually the body will attack!
You need to get to the root of the problem! the spleen

34
Q

What is heparin induced thrombocytopenia (HIT)

A

Life threatening complication of exposure to heparin
Results from auto-AB against endogenous platelet 4 in complex with heparin
Removal of IgG coated platelets by macrophages
Associate with arterial and venous thrombosis (hypercoagulable)

35
Q

How do you manage HIT

A

D/C HEPARIN!! switch to a different anticoag

36
Q

What is TTP

A

Rare, often fatal, MC idiopathic disorder affecting 20-50 y/o females > males

37
Q

How does TTP present

A

Abrupt onset (acute, chronic, or relapsing)
Fever, fatigue, abdominal pain (pancreatitis)
*HA, AMS, FND that wax and wane
skin pallor, petechiae, purpura, jaundice

38
Q

What happens in TTP

A

Microangiopathic hemolytic anemia + Thrombocytopenia
Endothelial layer of small vessels is damaged= fibrin deposition and plt aggregation
As RBC travel thru damaged vessels they’re fragmented= intravascular hemolysis

39
Q

What is hemolytic uremic syndrome

A

Looks identical to TTP (microangiopthic hemolytic anemia + thrombocytopenia)
Rapid RBC destruction causes renal insufficiency, also due to obstruction of small renal arteries
MC in infants and kids after an E. Coli infection

40
Q

You can tell it’s HUS and not TTP because

A

HUS lacks neurologic findings (TTP has HA, AMS, FND)
Also, HUS has more associated renal problems (TTP does not)
TTP has fever, HUS does not

41
Q

How does HUS present

A

abdominal pain and bloody diarrhea x 5-10 days

Anemia, thrombocytopenia, fatigue (like TTP)

42
Q

Labs for TTP and HUS will show

A

Microangiopathic hemolytic anemia: Reticulocytosis, increased LDH and indirect bili, Negative Coomb’s test
Thrombocytopenia
Schistocytes (helmet cells) on peripheral smear
Normal coag tests
Renal insufficiency

43
Q

How can you tell it’s TTP and not DIC

A

DIC will have all abnormal coagulation tests! TTP has normal ones

44
Q

How do you manage TTP-HUS

A

Adults: Corticosteroids! also Plasmapheresis, and if refractory try Rituximab
Kids: IVF, electrolyte repletion
(high risk mortality in adults)

45
Q

What is DIC (disseminated intravascular coagulation)

A

Potentially life threatening condition where proteins that control blood clotting become overactive
Typically associated with a severe underlying systemic illness

46
Q

What are the steps in DIC

A

1: Extensive thrombosis
2: clotting factors and platelets are used up= bleeding and hemorrhage
Essentially widespread platelet consumption

47
Q

What is the MOA of DIC

A

Widespread activation of coagulation cascade
increased fibrin clots that entrap platelets
Microthrombi cause RBC destruction and small vessel occlusion
Massive consumption of platelets, fibrin, and coag factors
uncontrolled bleeding

48
Q

Clinical conditions associated with DIC are

A 
Sepsis 
Trauma 
Cancer 
Obstetric complications 
Vascular d/o (giant hemangioma) 
Reaction to toxins (snake venom) 
Immune d/o (allergic rxn, hemolytic transfusion, transplant rejection)
49
Q

How does DIC present clinically

A

Bleeding > Clotting
Multiple organ systems
Origin of hemorrhage usually microvascular (petechiae, GI, lung, obstetrics)
Hallmark: Bleeding from IV site or surgical wound!

50
Q

Labs for DIC will show

A

Decreased platelets and fibrinogen
Increased PT and PTT
Increased fibrinolysis= increased fibrin degradation products
Increased D-dimer (sensitive to fibrin degradation products)
Microangiopathic hemolytic anemia
Schistocytes on peripheral smear

51
Q

How do you manage DIC

A

Quick recognition, Aggressive Tx
Transfusion: Cryoprecipitate (fibrin replacement), FFP (coag factors), Plt, RBC
-If triggered by a specific condition, treat the condition and it may resolve

52
Q

What is vW disease

A

Autosomal dominant congenital coagulopathy
Reduced levels of factor VIII antigen or ristocetin factor
6 major types, type 1 MC
All types have vWF deficiency
Acquired may be 2/2 bone marrow malignancy, valproic acid, or SLE

53
Q

vWF serves two main functions

A

Facilitates platelet adhesion by linking plt membrane to vascular subendothelium
Plasma carrier for factor VIII
SO: low vWF= bleeding

54
Q

How does vW disease present

A

Bleeding
Spontaneous hemarthrosis and soft tissue bleed (not as common as in hemophilia)
Bleeding worse with ASA
Bleeding decreases with estrogen and pregnancy (hypercoagulable states)

55
Q

Labs for vW disease may show

A 
Prolonged bleeding time (bleeding time is normal in hemophilia) 
Low vWF (confirmation test) 
INR normal
56
Q

How do you manage vW disease

A 
Desmopressin for type 1 (increases vWF release!) 
Factor VIII infusion 
Humate P (derived from human plasma, has factor VIII and vWF)

Summer 3 (12 decks)

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