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ABC > Conditions > Flashcards

Conditions Flashcards

1
Q

Primary hemostasis: clinical features (+most common?)

A

Mucosal and skin bleeding, eg:

  • epistaxis (most common)
  • hemoptysis, GI bleeding, hematuria, menorrhagia
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2
Q

Primary hemostasis: severe, can’t miss complication?

A

Intracranial bleeding

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3
Q

Idiopathic thrombocytopenic purpura (ITP): definition? epi?

A

Splenic autoantibodies (IgG) against platelet antigens causing thrombocytopenia

Most common cause of thrombocytopenia in adults and children

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4
Q

ITP: presentation and course in children

A

Acute form, presents weeks after viral infection or immunization

Self-limited, resolves within weeks

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5
Q

ITP: presentation and course in adults

A

Chronic form, usually in women of childbearing age

Can be primary or secondary (e.g. to SLE)

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6
Q

ITP: first line Tx

A

Corticosteroids - good response in children, adults often relapse

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7
Q

ITP: refractory Tx

A

IVIG - splenic macrophages consume IVIG complexes instead of antibody:platelet complexes

Splenectomy

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8
Q

Thrombotic thrombocytopenic purpura (TTP): definition

A

Formation of pathologic microthrombi causes:

  • consumption of platelets –> thrombocytopenia
  • shearing of RBC’s –> microangiopathic hemolytic anemia
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9
Q

TTP: pathophysiology

A

ADAMTS13 normally cleaves vWF multimers into monomers for degradation

In TTP, decreased ADAMTS13 due to acquired autoantibody prevents vWF degradation –> abnormal platelet adhesion –> microthrombi

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10
Q

Microangiopathic hemolytic anemia: feature of which conditions?

A

1) Physical “chopper”: prosthetic heart valves, cardiac assist devices, disease heart valves (aortic stenosis)
2) Thrombosis “chopper”: TTP, HUS, DIC

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11
Q

Hemolytic uremic syndrome (HUS): presentation

A

Classic triad:

1) Microangiopathic hemolytic anemia
2) Uremia (microthrombi in kidneys –> acute renal failure)
3) Thrombocytopenia

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12
Q

HUS: causes

A

Shiga-toxin producing E. coli (STEC):

- E. coli O157:H7 (exposure to undercooked beef) toxin damages endothelial cells –> platelet microthrombi

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13
Q

TTP: presentation

A

Fatigue, weakness
Derm: petechiae, purpura (due to MAHA)
GI: bleeding, nausea, vomiting
CNS abnormalities

Minimal renal failure/injury despite renal involvement
[contrast with HUS]

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14
Q

MAHA: RBC on histology?

A

Schistocytes - RBC’s are getting sheared by microthrombi

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15
Q

TTP: Tx

A

Plasmaphoresis

Corticosteroids

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16
Q

HUS: Tx

A

Supportive care for symptoms

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17
Q

Bernard-Soulier syndrome: pathophysiology

A

Genetic GPIb deficiency causes impaired platelet adhesion

18
Q

Bernard-Soulier syndrome: blood smear findings

A

Mild thrombocytopenia
Enlarged platelets

**
Mild thrombocytopenia: lack of GPIb - platelets don’t tend to live as long and tend to be destroyed

Enlarged platelets: more immature

19
Q

Glanzmann thrombasthenia: pathophysiology

A

Genetic GpIIb/IIIa deficiency causes impaired platelet aggregation

20
Q

Hemophilia A: presentation

A

Deep tissue, joint, postsurgical bleeding

21
Q

Hemophilia A: pathophysiology

A

Factor VIII deficiency

22
Q

Hemophilia A: FH

A

X-linked recessive OR de novo with no FH

23
Q

Hemophilia A: labs

A

Increased PTT
Normal PT
Low Factor VIII

Normal platelet count

24
Q

Hemophilia A: Tx

A

Recombinant Factor VIII

25
Q

Hemophilia B: pathophysiology

A

Factor IX deficiency

26
Q

Coagulation factor inhibitor: pathophysiology

A

Acquired antibody against a coagulation factor, most commonly VIII (8)

27
Q

How to differentiate: hemophilia A vs coagulation factor inhibitor?

A

Presentation and labs similar

Need to do a MIXING TEST (patient’s plasma + normal plasma)

  • if PTT corrects (due to normal factor in normal plasma) –> hemophilia A
  • if PTT remains abnormal –> inhibitor present
28
Q

von Willebrand’s Disease: pathophysiology

A

vWF deficiency –> impaired platelet adhesion

29
Q

von Willebrand’s Disease: presentation

A

Mild mucosal and skin bleeding

Do not usually see deep tissue, joint, or postsurgical bleeding

30
Q

von Willebrand’s Disease: labs

A
  • Increased PTT b/c vWF helps to stabilize Factor VIII
  • Abnormal ristocetin test (Normal: ristocetin causes vWF to bind to platelet GpIb –> aggregation. Abnormal: impaired aggregation)
31
Q

von Willebrand’s Disease: treatment

A

Desmopressin (ADH analog)

Induces endothelial cells to release more vWF from Weibel-Palade bodies

32
Q

Vitamin K deficiency: causes

A

1) Newborns - don’t yet have gut flora that normally produces Vit K (thus given Vit K injection at birth to prevent hemorrhagic disease of newborn)
2) Long-term antibiotic use - disrupts gut flora
3) Malabsorption - can lead to deficiency of fat-soluble vitamins (incl Vit K)

33
Q

Heparin-induced thrombocytopenia: pathophysiology

A

IgG antibody against Heparin-Platelet Factor 4 complexes –> consumed by spleen –> thrombocytopenia

Fragments of destroyed platelets can activate other platelets and cause thrombosis

34
Q

Heparin-induced thrombocytopenia: presentation

A
  • New onset thrombocytopenia 5-10 days after initiation of heparin
  • Venous/arterial thrombosis (presenting finding in 25% pts - but note not all thrombosis in pts on heparin represent HIT since these pts have higher baseline risk of thrombosis anyways)
  • Necrotic skin lesions at heparin injection sites
35
Q

Disseminated intravascular coagulation (DIC): definition

A

Pathologic activation of coagulation cascade involving:

  • widespread microthrombi
  • bleeding due to consumption of platelets, esp from IV sites and mucosal surfaces
36
Q

DIC: name 5 associated causes

A

Secondary to:

  • pregnancy: tissue factor in amniotic fluid enters maternal bloodstream
  • sepsis (E. coli, N. meningitidis): endotoxins induce endothelial cells to produce tissue factor
  • adenocarcinoma (mucin activates coagulation)
  • APML - Auer rods composed of granules can enter bloodstream and activate coagulation
  • rattlesnake bite venom
37
Q

DIC: best screening test

A

Elevated D-dimer

- D-dimer = fragments of cross-linked fibrinogen

38
Q

DIC: presentation

A

Bleeding (64%): petechiae, ecchymosis + directly from IV sites, mucosal surfaces

Acute renal failure (25%)

Hepatic, respiratory dysfunction

Shock

39
Q

Disorders of fibrinolysis: pathophysiology (+name 2 causes)

A

Plasmin overactivity –> excessive cleavage of serum fibrinogen, e.g. due to:

  • radical prostatectomy: release of urokinase activates plasmin
  • liver cirrhosis: decreased a2-antiplasmin production
40
Q

Disorders of fibrinolysis: presentation

A

Similar to DIC

41
Q

Disorders of fibrinolysis vs DIC

A

Disorders of fibrinolysis:

  • normal D-dimer b/c fibrin cross-links were never formed
  • normal platelet count
  • increased PT/PTT

DIC:

  • increased D-dimer
  • decreased platelet count due to consumption
  • increased PT/PTT
42
Q

Disorders of fibrinolysis: Tx

A

Aminocaproic acid - blocks activation of plasminogen

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