Glanzmann's thrombasthenia
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Glanzmann's thrombasthenia
Cardio Exam 2
Cardio Exam 2
Renin-angiotensin-aldosterone system
Arterial disease
Hypertension
Renal artery stenosis
Cushing syndrome
Pheochromocytoma
Hypertriglyceridemia
Familial hypercholesterolemia
Shock
Abetalipoproteinemia
Orthostatic hypotension
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Dyslipidemias: Pathology review
ACE inhibitors, ARBs and direct renin inhibitors
Calcium channel blockers
Thiazide and thiazide-like diuretics
Adrenergic antagonists: Beta blockers
Lipid-lowering medications: Statins
Miscellaneous lipid-lowering medications
Lipid-lowering medications: Fibrates
Anatomy of the heart
Baroreceptors
Chemoreceptors
Peripheral artery disease
Atrial flutter
Premature atrial contraction
Wolff-Parkinson-White syndrome
Atrial fibrillation
Atrioventricular nodal reentrant tachycardia (AVNRT)
Ventricular tachycardia
Premature ventricular contraction
Ventricular fibrillation
Brugada syndrome
Long QT syndrome and Torsade de pointes
Atrioventricular block
Bundle branch block
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Class I antiarrhythmics: Sodium channel blockers
Class III antiarrhythmics: Potassium channel blockers
Class II antiarrhythmics: Beta blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Coagulation (secondary hemostasis)
Platelet plug formation (primary hemostasis)
Clot retraction and fibrinolysis
Antiplatelet medications
Anticoagulants: Direct factor inhibitors
Anticoagulants: Warfarin
Anticoagulants: Heparin
Thrombolytics
Loop diuretics
Role of Vitamin K in coagulation
Hemophilia
Bernard-Soulier syndrome
Glanzmann's thrombasthenia
Hemolytic-uremic syndrome
Thrombotic thrombocytopenic purpura
Von Willebrand disease
Heparin-induced thrombocytopenia
Disseminated intravascular coagulation
Antithrombin III deficiency
Protein C deficiency
Antiphospholipid syndrome
Factor V Leiden
Protein S deficiency
Mixed platelet and coagulation disorders: Pathology review
Coagulation disorders: Pathology review
Platelet disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Hyperlipidemia
Tricuspid valve disease
Mitral valve disease
Pulmonary valve disease
Aortic valve disease
Positive inotropic medications
Assessments
Flashcards
0 / 10 complete
USMLE® Step 1 questions
0 / 2 complete
High Yield Notes
3 pages
Flashcards
Glanzmann's thrombasthenia
0 of 10 complete
Questions
USMLE® Step 1 style questions USMLE
0 of 2 complete
A 9-year-old boy is brought to the emergency department by his parents due to prolonged bleeding following a tooth extraction earlier in the day. Past medical history is noncontributory. Temperature is 37.5°C (99.5°F), pulse is 88/min, respirations are 14/min, and blood pressure is 112/62 mmHg. Physical exam shows gingival bleeding and petechiae. Laboratory testing is obtained, and the results are shown below.
*Reference Range: 2-7 minutes
Which of the following conditions is the patient at greatest risk of developing?
| Laboratory value | Result |
| Hematologic | |
| Hemoglobin | 12 g/dL |
| Hematocrit | 40% |
| Platelet count | 95,000/mm3 |
| Leukocyte count | 9,000/mm3 |
| Coagulation studies | |
| Prothrombin time (PT) | 12 seconds |
| Activated partial thromboplastin time (aPTT) | 29 seconds |
| Bleeding time* | 15 minutes |
Which of the following conditions is the patient at greatest risk of developing?
External References
First Aid
2024
2023
2022
2021
Glanzmann thrombasthenia p. 417, 432
Summary
Glanzmann's thrombasthenia is a rare autosomal recessive bleeding disorder caused by defects in platelet aggregation. In Glanzmann's thrombasthenia, platelets are deficient in the fibrinogen receptor GpIIb/IIIa necessary for proper platelet aggregation. This leads to easy bruising, mucosa bleeding, and prolonged bleeding from even minor cuts. It can also cause internal bleeding, which can be life-threatening.