[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Red cells and bleeding disorders](https://durgical.com/en/general-pathology/areas/red-cells/) › Platelet function disorders

# Platelet function disorders

- Lesion

Platelets can be present in normal numbers but fail to stick, clump or release their signals. Inherited and drug or kidney causes exist.

Updated Nov 12, 2026

## Key points

- Bernard–Soulier: autosomal recessive GPIb/IX deficiency, giant platelets and mild thrombocytopenia; no agglutination with ristocetin.
- Glanzmann: autosomal recessive GPIIb/IIIa deficiency; no aggregation with ADP, collagen, epinephrine or thrombin; normal ristocetin response.
- Storage-pool disorders: absent dense or α granules, weak secondary aggregation.
- Aspirin irreversibly acetylates cyclooxygenase for the platelet's lifespan.
- Uraemia: bleeding corrected by dialysis; desmopressin helps temporarily.

## What it is

Qualitative platelet disorders cause mucocutaneous bleeding with normal or near-normal counts. Inherited forms teach the steps of the platelet plug: defective adhesion (Bernard–Soulier syndrome, lack of GPIb/IX, the vWF receptor), defective aggregation (Glanzmann thrombasthenia, lack of GPIIb/IIIa, the fibrinogen receptor) and defective secretion (storage-pool disorders). Acquired forms are much more common: aspirin and other NSAIDs inhibit cyclooxygenase and thromboxane A2, and uraemia impairs adhesion, secretion and aggregation.

## Step by step

- Adhesion: GPIb/IX binds vWF on exposed subendothelium (lost in Bernard–Soulier and in vWD).
- Activation: platelets release ADP and synthesize thromboxane A2 (blocked by aspirin; weak in storage-pool disease).
- Aggregation: activated GPIIb/IIIa binds fibrinogen bridges between platelets (lost in Glanzmann).
- Any broken step leaves a weak primary plug and mucocutaneous bleeding.

## Platelet function disorders

| Disorder | Defect | Step lost | Key test findings |
| --- | --- | --- | --- |
| [Bernard–Soulier syndrome](https://durgical.com/en/conditions/inherited-platelet-function-disorders/) | GPIb/IX deficiency | Adhesion to vWF | Giant platelets, low count, no response to ristocetin |
| [Glanzmann thrombasthenia](https://durgical.com/en/conditions/inherited-platelet-function-disorders/) | GPIIb/IIIa deficiency | Aggregation | Normal count and size, no aggregation with ADP or collagen, ristocetin normal |
| Storage-pool disorders | Few dense or α granules | Secretion and amplification | Weak second wave of aggregation |
| Aspirin and NSAIDs | Cyclooxygenase inhibition | Thromboxane A2 synthesis | Impaired aggregation with arachidonic acid |
| [Uraemia](https://durgical.com/en/conditions/chronic-kidney-disease/) | Toxins affecting several steps | Adhesion, secretion, aggregation | Normal count; improves with dialysis |

## Clinical notes

- Easy bruising, nosebleeds, heavy menses and bleeding after dental work despite a normal platelet count.
- Wiskott–Aldrich syndrome combines small platelets, eczema and immunodeficiency.

## Memory aid

Bernard–Soulier cannot stick (Ib), Glanzmann cannot clump (IIb/IIIa), aspirin cannot signal (no thromboxane).

## Test yourself

Think of the answer, then tap the question to see it.

## Which glycoprotein is missing in Glanzmann thrombasthenia?

GPIIb/IIIa, the fibrinogen receptor needed for aggregation.

## Which platelet disorder shows giant platelets and no agglutination with ristocetin?

Bernard–Soulier syndrome (GPIb/IX deficiency).

## How does aspirin impair platelet function?

It irreversibly inhibits cyclooxygenase, blocking thromboxane A2 synthesis for the life of the platelet.

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## Elsewhere in DurgiPedia

- [Primary hemostasis and platelets](https://durgical.com/en/physiology/primary-hemostasis-and-platelets/)
- [Thromboxane A₂ (TXA₂)](https://durgical.com/en/biochemistry/molecules/thromboxane-a/)
- [Prostaglandin and thromboxane synthesis](https://durgical.com/en/biochemistry/pathways/prostaglandin-and-thromboxane-synthesis/)

## Connections

## Related 3

- [Bleeding disorders: overview](https://durgical.com/en/general-pathology/bleeding-disorders-overview/)
- [Von Willebrand disease](https://durgical.com/en/general-pathology/von-willebrand-disease/)
- [Arachidonic acid metabolites in inflammation, and the drugs that block them](https://durgical.com/en/general-pathology/arachidonic-acid-metabolites-in-inflammation-and-the-drugs-that-block-them/)

## Related conditions 4

- [Inherited platelet function disorders (Glanzmann thrombasthenia, Bernard–Soulier syndrome)](https://durgical.com/en/conditions/inherited-platelet-function-disorders/)
- [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/)
- [Wiskott–Aldrich syndrome](https://durgical.com/en/conditions/wiskott-aldrich-syndrome/)
- [Von Willebrand disease](https://durgical.com/en/conditions/von-willebrand-disease/)

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Glanzmann thrombasthenia: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/glanzmann-thrombasthenia/) (MedlinePlus, US National Library of Medicine, 2026); [Bernard-Soulier syndrome: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/bernard-soulier-syndrome/) (MedlinePlus, US National Library of Medicine, 2026).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/general-pathology/platelet-function-disorders/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/platelet-function-disorders/