Every test in the lecture in one place: what it measures, its pathway, its reference value, what an abnormal result suggests, and the patterns that tie results together. Every value comes from the lecture deck; the slide is cited on each row.
| Test | What it measures | Phase / pathway | Reference (varies by lab) | Abnormal means | Slide |
|---|---|---|---|---|---|
| ★Platelet count | How many platelets there are (complete blood count) | Primary hemostasis | Adults 140,000–400,000 per microliter; children 150,000–450,000 | Low = thrombocytopenia (deck: below 100,000); high = thrombocytosis (deck: above 350,000). Below 50,000 bruises easily; below 20,000 spontaneous bleeding and petechiae; below 10,000 risk of intracranial bleeding. | 13, 26 |
| Mean platelet volume | Uniformity of platelet size | Primary hemostasis | 7.4–10.4 femtoliters | Used in the differential diagnosis of thrombocytopenia. | 13 |
| Peripheral blood smear | Platelet morphology | Primary hemostasis | — | Gray platelets (macrothrombocytopenia), neutrophil inclusions, clumps (spurious low count), schistocytes (thrombotic thrombocytopenic purpura). | 11, 14, 15, 34 |
| ★von Willebrand studies | von Willebrand factor antigen and activity, plus factor VIII level | Primary hemostasis | — | Abnormal = von Willebrand disease, the most common inherited bleeding disorder. | 11 |
| Platelet function testing | Whether platelets aggregate and work: light transmission aggregometry, lumiaggregometry, platelet function analyzer, flow cytometry | Primary hemostasis | — | Abnormal with normal clotting times and bleeding = platelet dysfunction: von Willebrand types 2 and 3, uremia, drugs. | 11, 29, 34 |
| Bleeding time | Minutes for a standardized skin puncture to stop bleeding (bedside) | Primary hemostasis | 3–10 minutes (varies by method) | Only useful if platelet count is above 100,000 per microliter; thrombocytopenia itself lengthens it. | 16, 17 |
| PT (prothrombin time) | Time for a clot to form after tissue factor is added to plasma; prothrombin is liver-made and vitamin K dependent | Secondary: extrinsic + common | 11–13 seconds (varies by laboratory) | Prolonged: factor VII or common pathway deficiency, liver disease, vitamin K deficiency, warfarin. | 19 |
| ★INR (international normalized ratio) | The PT expressed so it is comparable between laboratories | Secondary: extrinsic + common | 0.8–1.2; on anticoagulation typical goal 2.0–3.0 | On warfarin: low = clot risk, high = bleeding risk. Off warfarin: bleeding disorder, clotting disorder, liver disease or vitamin K deficiency. | 20 |
| ★aPTT (activated partial thromboplastin time) | Time for a clot to form after a phospholipid activator is added to plasma | Secondary: intrinsic + common | 21–35 seconds; above 70 seconds signifies spontaneous bleeding | Prolonged: factor VIII, IX, XI deficiency; von Willebrand disease; heparin; dabigatran; inhibitor; lupus anticoagulant; factor XII. | 18 |
| Thrombin time | Screening test of secondary hemostasis (the deck gives no definition) | Secondary | (no value given) | Raised by heparin and dabigatran, in disseminated intravascular coagulation and with low or abnormal fibrinogen; normal in a simple factor deficiency. | 12, 24, 29 |
| Fibrinogen | The substrate thrombin turns into fibrin; Clauss assay preferred over PT-derived | Secondary | 2.0–4.0 grams per liter | Low = bleed (below 0.5 g/L: hemorrhage after traumatic surgery). High = clot (above 7.0 g/L: coronary and cerebrovascular risk); raised in tissue damage or inflammation. | 12, 21 |
| Mixing study | Patient plasma mixed with normal plasma, then the prolonged test repeated | Secondary | — | Corrects = factor deficiency. Does not correct = inhibitor. | 12 |
| Factor assays | Level of one specific factor | Secondary | — | Confirm a deficiency; inherited or acquired; acquired can raise or lower factors. | 12, 21 |
| ★D-dimer | Degradation product of cross-linked fibrin (plasmin acting on it) | Fibrinolysis | Below 250 micrograms per liter | Raised = both thrombin and plasmin were generated; NONSPECIFIC (acute thrombosis, disseminated intravascular coagulation, pregnancy, many illnesses). A normal result helps exclude thrombosis. | 22, 23 |
| Fibrin monomers | Thrombin activity on fibrinogen | Fibrinolysis / intravascular coagulation | — | Positive = thrombin activity, consistent with intravascular coagulation; negative does NOT exclude it; also positive in severe liver disease and inflammation. | 22 |
| Condition | PT (prothrombin time) | aPTT (activated partial thromboplastin time) | Thrombin time | Fibrinogen | D-dimer | Platelets | Platelet function | What to think | Slide |
|---|---|---|---|---|---|---|---|---|---|
| ★Acute DIC (disseminated intravascular coagulation) | ↑ Up | ↑ Up | ↑ Up | ↓ Down | ↑ Up | ↓ Down | Abnormal | Consumption: long clotting times, low fibrinogen and platelets, raised D-dimer and fibrin degradation products; protein C, antithrombin and protein S fall. | 24, 29, 30 |
| Acute thrombosis | Normal | Normal | — | Normal | ↑ Up | Normal | — | Only the D-dimer rises (nonspecific). | 24 |
| Vitamin K antagonist, liver disease, factor VII deficiency | ↑ Up | Normal | — | Normal | Normal | Normal | — | Isolated long PT: extrinsic pathway and vitamin K dependent factors (an oral factor Xa inhibitor is also listed). Early liver failure: platelet function normal. | 24, 29, 32 |
| Heparin or dabigatran | Normal | ↑ Up | ↑ Up | Normal | Normal | Normal | — | Long aPTT and thrombin time; with heparin the reptilase time stays normal and the mixing study does not correct. | 24, 29 |
| Hemophilia A or B | Normal | ↑ Up | Normal | — | — | Normal | Normal | Mixing study corrects. Low factor VIII with normal von Willebrand studies = hemophilia. | 29, 27 |
| von Willebrand disease | Normal | ↑ Up | — | — | — | Normal | Abnormal | aPTT rises through low factor VIII; platelet function is abnormal. | 29 |
| Inhibitor (factor VIII, IX, XI, XII) or lupus anticoagulant | Normal | ↑ Up | Normal | Normal | Normal | Normal | — | Mixing study does not correct. Lupus anticoagulant or factor XII deficiency: no bleeding history. | 24, 29 |
| Low fibrinogen | ↑ Up | ↑ Up | ↑ Up | ↓ Down | — | — | — | Both clotting times and the thrombin time rise; mixing corrects. | 29 |
| ★Uremia, aspirin or nonsteroidal anti-inflammatory drugs | Normal | Normal | — | — | — | Normal | Abnormal | Platelet dysfunction: normal clotting times and count, abnormal platelet function analysis. | 29 |
| Immune thrombocytopenia, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, heparin-induced thrombocytopenia | Normal | Normal | — | — | — | ↓ Down | Normal | A low platelet count with normal clotting times. | 29 |
| Liver failure, late or severe | ↑ Up | ↑ Up | — | — | — | ↓ Down | Abnormal | Both clotting times rise and platelets fall. | 29 |
Isolated prolonged aPTT (slide 27)
| Step | Do | Result and next | Slide |
|---|---|---|---|
| 1 | Isolated prolonged aPTT | Rule out heparin effect first. | 27 |
| 2 | Measure fibrinogen activity | High (above 100 mg/dL): mix. Low (below 100 mg/dL): fibrinogen antigen → low = hypofibrinogenemia, normal = dysfibrinogenemia. | 27 |
| 3 | 1:1 mixing study | Corrects = factor deficiency; fails to correct = inhibitor. | 27 |
| 4 | If it corrects | Factor VIII assay. Low without an inhibitory curve → von Willebrand antigen and activity: abnormal = von Willebrand disease, normal = hemophilia. Normal factor VIII → assays for factors IX, XI, XII. | 27 |
| 5 | If it fails to correct | Phospholipid dependence (dilute Russell viper venom time): yes = lupus anticoagulant; no = specific factor inhibitor (inhibitor screen, Bethesda assay). | 27 |
Suspected inherited bleeding disorder (slide 28)
| Screens | Think | Clinical clue | Next tests | Slide |
|---|---|---|---|---|
| Screens normal | Platelet disorders and mild von Willebrand disease | Skin bruising, petechiae, mucous membrane bleeding | Platelet function analyzer closure time or bleeding time, count and morphology, aggregation, von Willebrand studies | 28 |
| Screens normal | Deficiency of inhibitors of the fibrinolytic system | Severe bleeding: hemarthroses, hematoma after trauma or surgery | Euglobulin clot lysis time; alpha-2 antiplasmin; plasminogen activator inhibitor 1 | 28 |
| Screens normal | Factor XIII deficiency | Umbilical stump bleeding; lifelong severe bleeding of any tissue | Clot stability test; factor XIII assay | 28 |
| PT only prolonged | Factor VII deficiency | Clotting factor deficiency: large palpable ecchymoses, deep bleeding into joints and muscles with hematoma | Selective factor assays | 28 |
| aPTT only prolonged | Factor VIII (hemophilia A), IX (hemophilia B) or XI; severe von Willebrand disease | As above | Selective factor assays | 28 |
| PT and aPTT prolonged | Normal thrombin time: factor X, V or II. Prolonged thrombin time: hypofibrinogenemia or dysfibrinogenemia | As above | Fibrinogen activity and antigen assays | 28 |
| Platelet count | Bleeding risk | Slide |
|---|---|---|
| Below 50,000 per microliter | May bleed excessively with mild or moderate trauma and with surgery involving mucous membranes; bruises easily | 26 |
| Below 20,000 | Spontaneous bleeding; petechiae | 26 |
| Below 10,000 | Risk of spontaneous intracranial bleeding and serious hemorrhage | 26 |
| Kind | Finding | Slide |
|---|---|---|
| Quantitative | Thrombocytopenia and extreme thrombocythemia (above 1,000 × 109 per liter) can both cause bleeding. Confirm a low count in a citrated or heparinized tube to exclude pseudothrombocytopenia induced by ethylenediaminetetraacetic acid (clumping). | 34 |
| Morphology | Macrothrombocytopenia (gray platelet syndrome); neutrophil inclusions (May-Hegglin anomaly, a myosin heavy chain 9 disorder); platelet clumps; schistocytes in thrombotic thrombocytopenic purpura. | 14, 15, 34 |
| Qualitative | Normal PT and aPTT with bleeding suggests platelet dysfunction; abnormal platelet function testing points to von Willebrand types 2 and 3, uremia or drugs. | 34 |
| Causes of a low count | Impaired production; increased destruction (immune mechanisms, microangiopathy such as thrombotic thrombocytopenic purpura and hemolytic uremic syndrome, consumptive coagulopathy such as DIC); dilution (massive transfusion); sequestration (hypersplenism). | 25, 36 |