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Abnormal bleeding Flashcards

1
Q

What are the two main types of bleeding encountered in dentistry?

A

Post-operative bleeding – occurs after procedures such as extractions, surgeries, biopsies, trauma, or periodontal therapy 🛠️🦷
Spontaneous bleeding – occurs without dental intervention, often due to local or systemic pathology ⚠️

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2
Q

Give 4 examples of dental procedures that may result in post-operative bleeding 🧾🔪

A

Tooth extractions 🦷
Oral surgery or trauma 🛠️
Periodontal therapy (scaling/root planing) 🧼
Vital pulp exposure during caries management 🧪

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3
Q

Name 3 local causes and 3 systemic causes of spontaneous oral bleeding 🔍🧠

A

Local:

Gingivitis 🪥
Trauma 🩹
Ulcers/infections 🦠
Systemic:

Liver disease 🧬
Coagulopathies (e.g., hemophilia) 🩸
Thrombocytopenia 🧪

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4
Q

List 6 physiological or clinical consequences of significant blood loss 🏥

A

Patient distress 😰
Inflammation and infection from blood in tissues 🦠
Nausea and vomiting if swallowed 🤢
Aspiration/airway obstruction 😮‍💨
Hypovolemic shock 💔
Reduced oxygen-carrying capacity 🫁

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5
Q

What is the effect of blood loss on platelet count and protein levels? 📉🧫

A

Decreased platelet count, impairing clot formation 🩸
Loss of plasma proteins, affecting osmotic balance and clotting factor availability ⚖️

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6
Q

What are the 4 key pillars of managing bleeding in dental practice? 🦷🛠️🧠

A

History-taking and preparation 📋
Atraumatic surgical technique ✂️
Local haemostatic measures 🧽
Clear post-op instructions and follow-up 📞

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7
Q

List at least 3 local haemostatic methods used in dentistry 🛑

A

Direct pressure with gauze 🩹
Suturing 🧵
Haemostatic agents (Surgicel, Gelfoam, oxidised cellulose) 🧽
Tranexamic acid mouthwash 🧪

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8
Q

What are the essential post-operative instructions to prevent bleeding? 📝🚫

A

Avoid rinsing, hot food, alcohol, and smoking 🚬🥵
Rest and elevate the head 🛏️
Apply pressure if bleeding restarts ⏱️
Provide emergency contact info ☎️

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9
Q

What are the three components of Virchow’s Triad? 🔺

A

Vessel wall injury 💥
Altered blood flow 🌊
Changes in coagulation factors 🧬

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10
Q

What are the 4 steps of haemostasis? ⛔🧪

A

Vascular spasm 💢
Platelet plug formation 🧷
Coagulation 🩸
Fibrous tissue repair 🧶

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11
Q

Describe the three steps in platelet plug formation 🧲🧪

A

Adhesion to collagen 🧬
Activation (release of ADP and thromboxane A2) 💥
Aggregation of more platelets to form plug 🧲

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12
Q

How does aspirin affect platelet function? 💊🧠

A

It irreversibly inhibits cyclooxygenase (COX), preventing thromboxane A2 synthesis, which is necessary for platelet aggregation ❌🩸

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13
Q

How long does aspirin’s effect last and why? 🕒

A

~10 days, because platelets have no nucleus and cannot regenerate COX enzymes 🧬❌

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14
Q

What is the mechanism of clopidogrel? 🧬💥

A

Clopidogrel blocks the P2Y12 receptor on platelets, inhibiting ADP-induced platelet aggregation 🚫🩸

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15
Q

Should aspirin or clopidogrel be stopped prior to a dental procedure? Why or why not? 🤔🦷

A

No – stopping increases thrombotic risk 🧠💥 and bleeding can usually be managed with local measures 🩹

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16
Q

What does warfarin inhibit in the liver? 🍷🧠

A

It inhibits vitamin K epoxide reductase, blocking synthesis of clotting factors II, VII, IX, X 🔒🧬

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17
Q

What is INR and what should it be before dental extraction? 🔢🩺

A

INR = International Normalised Ratio 🌍🧪
Should be <4.0 for extractions ✅
Check INR within 72 hrs if stable, 24 hrs if unstable ⏱️📋

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18
Q

. Name 4 commonly used NOACs 🚫🩸

A

Apixaban
Rivaroxaban
Edoxaban
Dabigatran

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19
Q

How do we manage bleeding in dentistry?

A

Be prepared ✅
Manage patient expectations 🧍‍♂️
Check bleeding/clotting history 📋
Use careful surgical technique ✂️
Apply local measures: pressure, sutures, etc 🩹
Be patient
Provide good post-op care and follow-up 👩‍⚕️

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20
Q

What happens during vascular spasm?

A

Smooth muscle in the vessel wall contracts
Reduces blood flow to the injury
More effective in arteries due to higher pressure

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21
Q

What enhances Factor X and prothrombin activation during platelet plug formation?

A

Tissue damage
Collagen exposure
Platelet activation
Enhanced adhesion & aggregation

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22
Q
A
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23
Q

How long does it take for a tooth socket to clot in a patient on aspirin?

A

It may take longer
But it will clot eventually
Use pressure, gauze, and patience

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24
Q

How does warfarin work?

A

Inhibits vitamin K action in the liver
Reduces production of factors II, VII, IX, X
Full effect: 7 days
Stopping takes days
Interacts with metronidazole, fluconazole, etc, St Johns WORT , cranberry juice , carbamazepine ,miconazole

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25
What is the safe INR level for dental extractions?
<4.0 is generally safe Stable INR (e.g. 3.4, 3.5, 3.6): check within 72 hours Unstable INR: check within 24 hours
26
What’s the extraction protocol based on INR values?
INR 2–3: extract one side only INR 3–4: extract one quadrant at a time Avoid IDB unless necessary Always suture and give post-op advice
27
Why are NOACs becoming more common than warfarin?
Predictable effect No INR monitoring Fewer food/drug interactions Once/twice daily dosing
28
What are some disadvantages of NOACs?
No reversal agent (in most cases) Half-life up to 17 hours Risk of bleeding if not timed carefully
29
Management of patients on NOACs for dental surgery?
Do not stop medication routinely Use local measures Consider omitting morning dose if taken twice daily Liaise with medical team for complex cases
30
What lab tests assess bleeding risk?
INR – warfarin effect Platelet count – normal: 150–450 x 10⁹/L APTT – intrinsic pathway/heparin Bleeding time – platelet function PT – extrinsic pathway
31
What are signs a patient may have a coagulopathy?
asy bruising Prolonged bleeding History of heavy periods or joint bleeds Family history Liver disease or medications (e.g. warfarin)
32
: How do you manage a patient with coagulopathy pre-op?
Get haematology advice Check clotting status (INR, APTT, platelets) Plan atraumatic procedure Use local haemostasis Suture, Curacel, Tranexamic acid
33
What is tranexamic acid and how does it work?
Antifibrinolytic Inhibits plasminogen activation Prevents breakdown of fibrin clot Used as a mouthwash post-extraction to stabilise clot
34
: What is Virchow’s Triad?
Virchow’s Triad describes the three main contributors to thrombosis: Vessel wall damage Abnormal blood flow Altered coagulation (hypercoagulability)
35
How can each point of Virchow’s Triad be affected by disease?
Vessel damage – Trauma, surgery, inflammation Abnormal blood flow – Stasis (immobility, atrial fibrillation), turbulence (atherosclerosis) Hypercoagulability – Genetic disorders (e.g. Factor V Leiden), cancer, pregnancy, dehydration, medications
36
ow can local measures in a dental socket affect each point of Virchow’s Triad to promote clotting?
Vessel damage – Pressure & trauma help initiate vascular spasm & platelet plug Abnormal flow – Gauze pressure reduces blood flow = encourages clot formation Altered coagulation – Local agents (e.g. oxidised cellulose, tranexamic acid) enhance clot stability
37
What are the differences between antiplatelets, warfarin, and NOACs?
Antiplatelets (e.g. aspirin, clopidogrel): Inhibit platelet aggregation Warfarin: Vitamin K antagonist – reduces synthesis of clotting factors II, VII, IX, X NOACs (e.g. Rivaroxaban, Apixaban): Directly inhibit specific clotting factors (Xa or thrombin)
38
A patient is on warfarin with INR 2.5. What does this mean?
Their blood takes 2.5 times longer than normal to clot. This is within the safe range (2.0–4.0) for most dental procedures.
39
A patient not on medication has INR 0.5. Should they see their doctor?
Yes — this is abnormally low, meaning blood is clotting too quickly. Could suggest a lab error or hypercoagulable state. Needs medical assessment.
40
A patient on Rivaroxaban has INR 1.0. Should they see their doctor?
No — INR is not a reliable marker for NOACs like Rivaroxaban. Instead, assess bleeding risk based on last dose timing, renal function, and liaise with their GP if needed.
41
Patient returns 3 hours post-extraction with socket bleeding. What is the most likely cause?
Local clot dislodgement — due to trauma, rinsing, or inadequate pressure after extraction.
42
How would you manage this patient? LOCAL CLOT DISLODGEMENT
Calm the patient Clean the socket gently Apply gauze with firm pressure for 10–15 minutes If bleeding persists: Suture Use oxidised cellulose or haemostatic agents Consider tranexamic acid mouthwash Give post-op advice and review instructions
43
A patient with thrombocytopaenia has a platelet count of 150 x 10⁹/L. Can they proceed with extraction?
Yes — this is within the normal range (150–450 x 10⁹/L). Proceed with care and use local haemostatic measures
44
What is the relationship between platelet activation and the clotting cascade?
Platelets form the initial plug Their granules release substances (e.g. thromboxane A2, ADP) These activate clotting factors → leads to fibrin mesh that stabilises the clot Platelets + clotting cascade = complete haemostasis
45
What are the advantages of NOACs over warfarin?
No routine monitoring (INR) Rapid onset/offset Fewer food & drug interactions Fixed dosing Lower risk of intracranial bleeding
46
What are the disadvantages of NOACs?
Shorter half-life → missed doses = risk No routine lab monitoring = harder to assess effect Limited reversal agents (but improving) Expensive Caution needed in renal impairment
47
What information is in the Orange Book (anticoagulant therapy booklet)?
INR values Dosing information Warfarin strength (mg) Indication for therapy Doctor or anticoag clinic details
48
How can you tell if a patient has a “stable INR”?
INR remains within target range (e.g. 2.0–3.0) No major fluctuations over time INR checked regularly (e.g. every 4–12 weeks) No recent dose changes
49
How does oxidised cellulose promote blood clotting?
Forms a physical matrix for clotting Swells and becomes gel-like in the socket Promotes platelet adhesion and activation Aids in fibrin formation
50
How does tranexamic acid mouthwash promote clotting?
Inhibits plasminogen activation → reduces fibrinolysis Prevents clot breakdown Stabilises the clot within the socket Used post-op (10 mL, 2–4 times/day)
51
What dental procedures are commonly associated with bleeding?
Tooth extraction, surgery, biopsies, trauma, periodontal therapy, and exposure of vital pulp.
52
What are some causes of spontaneous bleeding?
Local causes and systemic conditions such as bleeding disorders or anticoagulant medication use.
53
What are clinical effects of blood loss in dental patients?
Patient distress, infection/burning in tissues, vomiting (from blood in the stomach), airway obstruction, hypovolemic shock, reduced oxygen-carrying capacity, protein loss, and reduced clotting ability due to decreased platelets.
54
What are key principles of bleeding management?
Be prepared, manage patient expectations, take bleeding/clotting history, use careful surgical technique, apply local measures (pressure, sutures), and ensure proper post-op care and follow-up.
55
What is the significance of the liver in coagulation?
The liver produces clotting factors; liver dysfunction can impair coagulation.
56
57
What are the four stages of haemostasis?
Vascular spasm, platelet plug formation, blood coagulation, and fibrous tissue repair.
58
What is the role of vascular spasm?
Smooth muscle contraction in vessels to reduce blood loss, especially in arteries with high flow.
59
What initiates platelet plug formation?
Tissue damage and exposure of subendothelial collagen.
60
What are the stages of platelet plug formation?
Platelet adhesion → platelet release (thromboxane A2) → platelet aggregation.
61
What enhances platelet adhesion and aggregation?
Tissue damage, collagen exposure, and platelet activation lead to activation of Factor X and prothrombin.
62
How does aspirin affect bleeding?
Irreversibly inhibits COX enzyme in platelets, preventing thromboxane A2 production → reduced aggregation.
63
How does clopidogrel affect bleeding?
Irreversibly binds to P2Y12 receptor → inhibits ADP-mediated aggregation.
64
How does ibuprofen differ from aspirin and clopidogrel?
Reversibly binds to platelets; effects are temporary and mainly anti-inflammatory.
65
Who is likely to be on aspirin or clopidogrel?
Patients with vascular disease, IHD, thromboembolic disease, stroke, or peripheral vascular disease.
66
Should aspirin or clopidogrel be stopped before dental procedures?
No; stopping increases risk of thrombotic events. Use local measures instead.
67
How does antiplatelet therapy affect socket bleeding time?
Bleeding may take longer to stop, but it will eventually stop with proper measures.
68
What triggers the intrinsic pathway?
Exposure of collagen (endothelial damage).
69
What triggers the extrinsic pathway?
Tissue damage and release of tissue factor.
70
What is the role of Factor X?
Common pathway activator; essential for thrombin generation and fibrin clot formation.
71
What does INR measure?
Warfarin effect via prothrombin time.
72
What does APTT assess?
Heparin effect via intrinsic pathway.
73
: What is a normal platelet count?
200–400 × 10⁹/L.
74
When is bleeding time used?
To assess platelet function (less commonly used now).
75
Who commonly takes warfarin?
Patients with AF, valve replacements, thromboembolic disease, and some cardiac conditions.
76
How does warfarin work?
Inhibits vitamin K recycling → prevents liver from activating clotting factors II, VII, IX, X.
77
What antibiotics increase warfarin’s effect?
Metronidazole, fluconazole, miconazole, etc.
78
What is a safe INR level for dental extractions?
<4.0
79
What should be done before extraction if INR is unstable?
: Check INR within 24 hours.
80
When should extractions be scheduled in warfarin patients?
Early in the week and early in the day.
81
What are the advantages of DOACs?
Predictable effect, no INR monitoring, no food interaction, single point of action.
82
What questions screen for coagulopathies?
Do you bruise/bleed easily? On blood thinners? Any liver disease?
83
How do you manage a dental patient with coagulopathy?
Consult haematologist, check clotting tests pre-op, manage expectations, use local haemostatic measures (pressure, gauze, sutures, Curacel).
84
What local measures can be used to stop dental bleeding?
Direct pressure, sutures, gauze packing, haemostatic agents (e.g., Curacel), proper post-op instructions.

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