Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

ABC > Conditions > Flashcards

Conditions Flashcards

(42 cards)

Start Studying
1
Q

Primary hemostasis: clinical features (+most common?)

A

Mucosal and skin bleeding, eg:

  • epistaxis (most common)
  • hemoptysis, GI bleeding, hematuria, menorrhagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Primary hemostasis: severe, can’t miss complication?

A

Intracranial bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ITP: presentation and course in children

A

Acute form, presents weeks after viral infection or immunization

Self-limited, resolves within weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ITP: first line Tx

A

Corticosteroids - good response in children, adults often relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ITP: refractory Tx

A

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

Splenectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Thrombotic thrombocytopenic purpura (TTP): definition

A

Formation of pathologic microthrombi causes:

  • consumption of platelets –> thrombocytopenia
  • shearing of RBC’s –> microangiopathic hemolytic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hemolytic uremic syndrome (HUS): presentation

A

Classic triad:

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MAHA: RBC on histology?

A

Schistocytes - RBC’s are getting sheared by microthrombi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

TTP: Tx

A

Plasmaphoresis

Corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HUS: Tx

A

Supportive care for symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bernard-Soulier syndrome: pathophysiology

Study These Flashcards
A

Genetic GPIb deficiency causes impaired platelet adhesion

18
Q

Bernard-Soulier syndrome: blood smear findings

Study These Flashcards
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

Study These Flashcards
A

Genetic GpIIb/IIIa deficiency causes impaired platelet aggregation

20
Q

Hemophilia A: presentation

Study These Flashcards
A

Deep tissue, joint, postsurgical bleeding

21
Q

Hemophilia A: pathophysiology

Study These Flashcards
A

Factor VIII deficiency

22
Q

Hemophilia A: FH

Study These Flashcards
A

X-linked recessive OR de novo with no FH

23
Q

Hemophilia A: labs

Study These Flashcards
A

Increased PTT
Normal PT
Low Factor VIII

Normal platelet count

24
Q

Hemophilia A: Tx

Study These Flashcards
A

Recombinant Factor VIII

25
Hemophilia B: pathophysiology
Factor IX deficiency
26
Coagulation factor inhibitor: pathophysiology
Acquired antibody against a coagulation factor, most commonly VIII (8)
27
How to differentiate: hemophilia A vs coagulation factor inhibitor?
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
von Willebrand's Disease: pathophysiology
vWF deficiency --> impaired platelet adhesion
29
von Willebrand's Disease: presentation
Mild mucosal and skin bleeding Do not usually see deep tissue, joint, or postsurgical bleeding
30
von Willebrand's Disease: labs
- 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
von Willebrand's Disease: treatment
Desmopressin (ADH analog) Induces endothelial cells to release more vWF from Weibel-Palade bodies
32
Vitamin K deficiency: causes
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
Heparin-induced thrombocytopenia: pathophysiology
IgG antibody against Heparin-Platelet Factor 4 complexes --> consumed by spleen --> thrombocytopenia Fragments of destroyed platelets can activate other platelets and cause thrombosis
34
Heparin-induced thrombocytopenia: presentation
- 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
Disseminated intravascular coagulation (DIC): definition
Pathologic activation of coagulation cascade involving: - widespread microthrombi - bleeding due to consumption of platelets, esp from IV sites and mucosal surfaces
36
DIC: name 5 associated causes
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
DIC: best screening test
Elevated D-dimer | - D-dimer = fragments of cross-linked fibrinogen
38
DIC: presentation
Bleeding (64%): petechiae, ecchymosis + directly from IV sites, mucosal surfaces Acute renal failure (25%) Hepatic, respiratory dysfunction Shock
39
Disorders of fibrinolysis: pathophysiology (+name 2 causes)
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
Disorders of fibrinolysis: presentation
Similar to DIC
41
Disorders of fibrinolysis vs DIC
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
Disorders of fibrinolysis: Tx
Aminocaproic acid - blocks activation of plasminogen

ABC (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions