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XLA/blood stuff Flashcards

1
Q

Signs and symptoms of anaemia

A

Palor, fatigue, nausea, hypo-tension when standing up, dizziness, palpitations, glottitis, angular stomatitis, heart murmurs,

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2
Q

Tests to determine what type of anemia

A

MCV, FBC, APTT, PT, Hb, WBC

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3
Q

Microcytic anaemia and how to treat

A

Due to less iron (malabsorption, diet, extra demand, blood loss) or thalassaemia (hereditary). Treat with ferrous sulphate. Iron only affects the blood cells

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4
Q

Macrocyctic anaemia causes and symptoms.

A

B12 or B9 deficiency - diet or malabsorption e.g. lack of intrinsic factor for absorbtion of B12 at terminal ilium. Affects WBC, platelets, nerves.

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5
Q

Treatment for macrocytic anaemia

A

Treat with B12 injections or parenteral hydroxocobalamin and oral folate.

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6
Q

Pernicious anaemia

A

Autoimmune disorder where body produces Ig that attack the intrinsic factor so not enough B12 absorbed. Treat by giving B12 injections.

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7
Q

Haemolytic anaemia

A

Hereditary e.g. sickle cell where RBC/Hb defect or abnormal metabolism or acquired e.g. immune problem or infection.

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8
Q

Normal haemostasis

A

Vasoconstriction, platelet adhesion and aggregation and fibrin formation via coagulation cascade forming a plug/clot and then repair.

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9
Q

Thrombocytopenia definition

A

reduced platelet count

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10
Q

Thrombocytosis definition

A

Increased platelet count

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11
Q

Haemostatic problems

A

Primary = involves platelets and VWF and vessel walls and leads to excessive bleeding and bruising.
Secondary involves coagulation cascade and shows as bleeding in joints but no bruising.

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12
Q

Types of inherited bleeding disorders

A

Haemophilia A and B, VWF disorder, Ehlers-Danos syndrome.

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13
Q

Haemophilia A and B

A

A = factor 8, B = factor 9 deficiency. Sex X-linked inherited. Secondary homeostatic problem e.g. bleeding in joints but normal bruising.
Causes a prolonged APTT

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14
Q

Treatment of haemophilia A or B

A

Give missing factor or DDAVP if mild haemophilia A.

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15
Q

VWF disease

A

Reduced clotting factor and platelet problems = excessive bleeding and bruising. Also protects against factor 8 break down normally so give DDAVP bc less VWF = less factor 8. Prolongs APTT

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16
Q

Types of thrombosis

A

Blood coagulation in vessels. Arterial or venous.

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17
Q

Arterial thrombosis

A

High pressure system, lots of platelets so treat with anti-platelet drugs. No inherited risk factors but acquired risk factors e.g. diet, smoking, obesity.

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18
Q

Venous thrombosis

A

Low pressure, lots of fibrin so treat with anti-coagulants. Inherited and acquired risk factors e.g. cancer, obesity, age.

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19
Q

Causes of thrombocytopenia

acquired

A

. Enlarged spleen storing more of the platelets.
. Increased breakdown of platelets e.g. ITP or DIC.
. Failure of platelet production e.g. if have leukemia or B12/9 deficiency.

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20
Q

ITP

acquired

A

Inherited thrombocytopenia. Autoimmune condition that destroys platelets. Treat using immunoglobulins or remove spleen or steroids.

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21
Q

DIC

acquired

A

Dissemination Intravascular coagulation. Break down of haemostatic balance, thrombosis and bleeding at the same time.

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22
Q

Acquired anti-platelet function abnormalities

A

Due to anti-platelet drugs, kidney or liver failure.

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23
Q

How does vitamin K deficiency affect bleeding

A

Less clotting factors so prolonged prothrombin time.

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24
Q

Drugs that can cause bleeding disorders

A

Anti-platelets
Anticoagulants
Steroids
Drugs that affect liver, kidneys and bone marrow.

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25
Q

Effects of heparin and how to monitor

A

Inhibits coagulation cascade. Increases anti-thrombin activity so indirect thrombin inhibitor. Monitor with APTT.

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26
Q

Effects of Warfirin and how to monitor

A

Inhibits vitamin K dependent clotting factors by blocking vitamin K epoxin reductase which is needed to activate vitamin K. Monitor with PT/INR.

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27
Q

Direct oral anticoagulants and pro/cons

A

Inhibit factor 2a and 10a.
Limited interaction with other drugs and substances, don’t need monitoring, faster action, fixed dose.
But no specific antidotes and removed by kidneys.

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28
Q

How to measure coagulation after you’ve drawn blood

A

Add citrate to chelate the Ca2+ and clotting factor and stop clotting. In lab, add Ca2+ and factor needed to initiate intrinsic or extrinsic pathway and measure time.

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29
Q

Intrinsic pathway activated by and measured by ..?

A

Phospholipids released from cell membranes after trauma and factor 9 activate it. Measured by APTT.

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30
Q

Extrinsic pathway measured by and activated by ..?

A

Activated by tissue factor and measured using PT (prothrombin time)

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31
Q

Clotting factors involved in intrinsic pathway

A

8, 9, 10, 2

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32
Q

Clotting factors involved in extrinsic pathway

A

7, 9, 10, 2

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33
Q

INR

A

International normalised ration is patient’s PT compared to average PT. But 2 doesn’t mean 2x as slow because these are specific lab conditions and don’t take into account intrinsic pathway or platelets.

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34
Q

Final common pathway

A

After intrinsic/extrinsic pathway and converts fibrinogen -> fibrin.

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35
Q

Acquired bleeding disorders

A

Due to drugs, cancer, liver or kidney failure,

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36
Q

How do liver problems affect bleeding

A

Liver makes all the vitamin k dependent coagulation factors and some other coagulation factors so without them coagulation cascade won’t happen = bleeding problems and prolonged PT time.

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37
Q

How are the kidneys involved in bleeding

A

They regulate platelet function and calcium homeostasis so disease = more bleeding and coagulation problems.

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38
Q

How does cancer affect bleeding

A

Can lead to myelosuppression so bone marrow is suppressed and less platelets made.

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39
Q

Examples of blood thinners

A

Warfarin, heparin, aspirin, clopidogrel, NOACs.

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40
Q

How do NOACs act

A

Inhibit factors 2 or 10 which are involved in the final common pathway for coagulation cascade.

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41
Q

How does Asparin act

A

Binds to COX on platelets and stops them functioning. Lasts the life-cycle of the platelet. Blocking COX = blocks production of thromboxane A2 from platelets, needed for platelet aggregation.

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42
Q

What is arachidonic acid metabolized into

A
  1. Leukotrienes to attract WBC.
  2. Prostoglandins cause pain and regulate gastric acidity.
  3. Thromboxane A2, released from platelets and causes platelet aggregation. Needs COX.
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43
Q

How does Warfarin act

A

Blocks vitamin K epoxide reductase so Vit K epoxide not converted back to Vit K so not enough Vit K to make the active forms to activate the Vit K dependent coagulation factors.

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44
Q

How does Heparin act

A

Activates antithrombin 3 which blocks factors 2 and 10 needed in final common pathway to make fibrin.

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45
Q

How does clopidogrel act

A

Inhibits the P2Y12 receptor on platelets needed for platelet aggregation and forming fibrin meshwork.

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46
Q

How can the effects of warfarin be reversed

A

Give an excess of vitamin K

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47
Q

How can the effects of heparin be reversed

A

Give protamine sulphate (salmon semen)

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48
Q

How to manage patients on blood thinners.

A

Check INR for warfarin (<4 is okay), or give factors 8/9/DDAVP or stop using medication on day of surgery for the others.

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49
Q

Types of bleeding after surgery/XLA

A

Primary at the time.
Reactionary is up till 48h after due to clot falling out etc.
Secondary is a week later bc of infection.

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50
Q

Ways to stop bleeding after XLA

A

Check haemostasis before sending patient off. Compress site by biting on gauze or applying pressure. Compress socket. Use haemostatic packs to absorb the blood. Pack using sponges and suture stops pack falling out and compresses blood vessels.

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51
Q

What to use for ongoing bleeding after XLA

A

tranexamic acid or reverse the anticoagulant e.g. vitamin K or protamine sulphate.

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52
Q

What information needs to be included on a prescription

A

Name, age, address, DoB, name of medication, amount, frequency, form, route, duration. Signature of dentist and stamp of practice and date.

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53
Q

What is the haematocrit

A

Solid constituents of the blood. Should make up less than half for good viscosity.

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54
Q

Haematopoiesis

A

Blood cells made in the bone marrow. Stem cells can differentiate into themselves or into mature cells. Controlled by hormones.

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55
Q

RBC function and structure

A

Convert glucose to pyruvate and send it to the liver. Hb binds to O2 and transports it around the body. Biconcave circular disc shape makes them flexible so they can move through narrow capillaries.

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56
Q

Polycythaemia

A

Making too many RBC. Means that the blood is more viscous so harder to pump around the body so can increase the risk of heart attack and stroke. Can be useful e.g. if have bad lungs than extra RBC made to increase 02 carrying capacity.

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57
Q

Plasma proteins

A

Albumin to keep fluid in the vessels.
Carrier proteins for hormones, nutrients.
Ig and platelets - inactive form normally.

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58
Q

What antigens need to be matched up before a blood transfusion?

A

ABO and Rhesus D+/-

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59
Q

ABO antigen

A

ABO sugars on RBCs need the genes for them. The body makes Ab for the other blood types after exposure to food and bacteria e.g. don’t need to be infected. Blood groups don’t go through the placenta so baby is safe.

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60
Q

Rhesus antigen

A

D + or -

Blood group passes through the placenta so mothers are given anti D to stop their body’s Ab attacking the baby.

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61
Q

What can a myeloblast differentiate into

A

Basophils, eosinophils, neutrophils, macrophages.

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62
Q

Neutrophil functions

A

Cytotoxins cause inflammation and symptoms. Phagocytosis.

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63
Q

Lymphocyte functions

A

B-cells make plasma cells and Ig.

T-cells can be helper cells to make the Ig or cytotoxic cells to stop cellular invasion.

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64
Q

Types of leukaemia

A

Acute or chronic. Caused by the proliferation of abnormal WBC (not enough space for normal cells)

65
Q

Acute leukaemia and treatment

A

The proliferation of undifferentiated cells. AML in adults (acute myeloid leukaemia) or ALL in children (acute lymphoid leukaemia). Treat by chemotherapy or bone marrow transplant. Can kill v quickly.

66
Q

Chronic leukaemia

A

The proliferation of mature/differentiated cells. Less severe and doesn’t need treatment.

67
Q

Myeloma

A

Malignancy and proliferation of plasma cells = extra Ig. Can dissolve bones and cause anaemia and renal failure. Treat by oral chemotherapy.

68
Q

Analgesia vs anesthesia

A

Analgesia is taking away pain sensation whereas anaesthesia is taking away all sensation

69
Q

What are the contents of an LA cartilage

A

LA, vasoconstrictor, reducing agent to stop oxidation of the vasoconstrictor, vehicle e.g. isotonic solution, fungicide

70
Q

Chemical contents of LA

A

Base
Aromatic ring - dissolves and lets molecules pass through fatty myelin
Amino group - dissolves and lets molecules pass through the interstitial fluid (soluble)
Intermediate group - amide or ester

71
Q

How does the LA reach the nerves

A

Aromatic and amino groups dissolve and let the molecules pass through myelin membrane and interstitial fluid.
LA is soluble in water so when it dissolves, it is a solution of uncharged free base and + charged molecules.
Uncharged molecules can pass through the myelin lipid membrane but the charged molecules are what act on the nerve. Amount of uncharged molecules depends on the pKa of the molecules and the pH of the tissues e.g. if there’s an infection the pH will be lower so need more LA to get enough uncharged molecules.

72
Q

How does the LA cause numbing effects

A

Indirect - uncharged molecules cause swelling of the membrane so closes the sodium ion channels.
Direct - Charged molecules bind to receptors that block the sodium ion channels = no action potential

73
Q

Advantages of vasoconstrictors

A

Faster effects, longer lasting bc molecules not carried away as fast, less bleeding, stronger effects.

74
Q

Disadvantages of adrenaline and alternatives

A

Limit to how much you can give because has effects on heart and glucose and blood pressure. Can use felypressin instead (+ Prilocaine LA) but not for pregnant women. Noradrenaline causes blood pressure problems.

75
Q

How is the LA removed from the body/broken down

A

Esters are broken down by esterase in plasma and then by liver whereas amides are just broken down in liver so esterases have a shorter half-life e.g. articaine.

76
Q

Ideal characteristics of LA

A

Has an effect on the nerves but doesn’t damage them
Non-toxic systemic effects
Fast acting and lasts a suitable length of time
Reliable effects
Stable and long shelf-life

77
Q

Different types of LA

A 
Lidocaine
Articaine
Prilocaine
Benzocaine
Mevipocaine
Buvipocaine
78
Q

Mepivacaine

A

Doesn’t contain a vasoconstrictor so is good for unwell patients. A good surface anaesthetic.

79
Q

Buvipocaine

A

Long lasting so used for post-op pain

80
Q

Benzocaine

A

Topical anaesthetic

81
Q

Articaine

A

Better at penetrating bone so less need for blocks e.g. for haemophiliacs. But don’t use for blocks (only infiltrations) bc can cause pain, tingling and burning)

82
Q

Prilocaine

A

Contains felypressin vasoconstrictor instead of adrenaline so good for people w heart problems.

83
Q

How to calculate dose of lidocaine

A

2% lidocaine, 1:80,000 adrenaline.
4.4mg x kg = total mg allowed.
Total mg/44mg = total cartilages. (20mg is the amount in an ml, 2.2ml in cartilage)
OR 1/10th of a cartilage per kg.

84
Q

Equipment needed to give LA injection

A

Cartilage, needle (longer needle = thicker gauge), aspirating system.

85
Q

Aspirating methods

A

Self-aspirating = negative pressure behind the needle means that fluid is drawn up on its own.
Positive aspirating = draw back the handle to actively draw fluid.

86
Q

Intra-ligamentary injections

A

Inject into PDL around tooth using a fine needle that can inject into a high-pressure system. Need less LA and has local effects on that tooth only so good for children or haemophiliacs. But can damage the PDL/pulp because constricts the blood flow in this area.

87
Q

Amide vs ester as an intermediate group in the LA

A

Amides are more stable, can be autoclaved and less allergic.

88
Q

Complications when/after extracting teeth

A 
Failure to extract tooth/fracture
Infection
Pain/swelling
Bleeding
Dry socket
Trismus
Oro-antral communication
Tooth or root in sinus
Fractured tuberosity
89
Q

Failure to extract the tooth/fracture causes, management

A

Age, RCT of the tooth can make the tooth brittle. Large restorations, caries, or TSL means not much crown to hold onto, ankylosis or abnormal anatomy.
Check radiographs, refer to a specialist or do trans-alveolar approach (raise mucoperiosteal flap and remove bone, section and remove the tooth and then suture). Use different instruments e.g. luxators and elevators.

90
Q

Infection after XLA management and symptoms

A

Due to history/current infections. Can be painful or abscess or cause trismus. Give antibiotics or drain the abscess.

91
Q

Pain and swelling after XLA management

A

Give non-steroid anti-inflammatory drugs (NSAIDs) or analgesics.

92
Q

Bleeding after XLA management and causes

A

Patients with bleeding problems. Compress socket and apply firm pressure and check haemostasis. Suture socket to compress the vessels or place a haemostatic pack/sponge. Reverse anti-coagulants e.g. give vitamin K or protamine sulphate, or tranexamic acid.

93
Q

Dry socket after XLA causes and management

A

Localised infection in the socket due to clot falling out and more frequent in smokers. Irrigate and pack with alveogyl.

94
Q

Trismus after XLA causes

A

Due to swelling, haematoma, cancer, abscess, pain.

95
Q

Oro-antral communication after XLA symptoms and management

A

Symptoms = Some of the sinus wall come away with the tooth, can’t get an oro-seal, void in the socket after XLA, fluid in nose or air in the mouth (bubbles).
Manage by repairing the communication (or respiratory epithelium will line it) and giving antibiotics and decongestants e.g. nasal drops.

96
Q

Fractured tuberosity after XLA signs and management

A

Mobility of adjacent teeth or palatal mucosa. Manage by suturing it back.
Avoid by manually supporting alveolus/tooth during extraction.

97
Q

Tooth or root in sinus after XLA management

A

Surgically extract and give antibiotics.

98
Q

Precautions when anaesthetising radiated patients

A

Vasoconstriction in that area due to radiation so don’t use a vasoconstrictor in the LA e.g. mepivacaine, so that the area can heal.

99
Q

Precautions when anaesthetising patients with bleeding and heart problems.

A

Don’t do deep injections/blocks on patients with bleeding problems e.g. use articaine instead.
Don’t use adrenaline on patients with heart conditions or blood pressure problems e.g. hypertension - use prilocaine instead (felypressin instead of adrenaline)

100
Q

Topical LA examples

A 
Benzocaine 20% lidocaine
Xylonor gel 5% for children
EMLA cream (pre-IV)
101
Q

Max doses for lidocaine, prilocaine and articaine

A 
Lidocaine = 4.4mg/kg
Articaine = 7mg/kg (children =5mg/kg)
Prilocaine = 6mg/kg
102
Q

Less painful palatal anaesthetic for children

A

Intrapapillary injection first on either side of the tooth (syringe parallel to the occlusal plane and needle perpendicular to the gum) and then when palate blanches, do a palatal infiltration.

103
Q

Reasons for LA failure to numb

A 
Acute infection
Injected in the wrong place
Abnormal nerve anatomy
Not enough LA
The mental status of the patient e.g. might be scared and feel like they're in pain.
104
Q

How to use the BNF

A

Index and section on interactions at the back. Sections are organised by drug class w a preamble at the start of the sections. If a serious adverse reaction to drugs marked w black triangle then these need to be reported.

105
Q

LA for children management

A 
Communicate, easy fun language
Tell show demonstrate
Interact
Positive enforcement
Inject v slowly and keep talking to them. Tight mucosa.
106
Q

What is pericoronitis and its symptoms

A

Inflammation of the soft tissue covering an erupting tooth e.g. the operculum, normally wisdom teeth (happens if upper throat infection or feeling run down). Will cause localised inflammation and swelling (could spread and lead to trismus or airway problems), pain, pus and debris can get stuck under the flap and bad breath.

107
Q

Extra and intra-oral and special tests to diagnose pericorontitis

A

Lymph nodes and swelling (swollen lymph nodes could mean infection spread). Intra-oral, check if there is any other thing that can be causing the pain/check the inflammation is localised. Test vitality and sensibility of the tooth.

108
Q

Management of pericoronitis

A

Remove or reduce the opposing tooth.
Irrigate under the flap and w saline and use chlorhexidine. Advise the patient to keep the area clean, use Corsodyl and OHI. Can give antibiotics if worried about infection or spreading (e.g. Metronidazole or penicillin)

109
Q

What can lead to poor healing of the tooth socket after XLA

A 
Smoker
Steroids
Not following POIG
Current infection at the site
Systemic illness e.g. uncontrolled diabetes, immune problems.
Previous radiotherapy
110
Q

What pathology/diagnoses are there for poor tooth socket healing

A
  • Dry socket/localised osteitis
  • Infected socket
  • Delayed healing
  • Osteomyelitis
  • MRONJ/BRONJ
  • Osteoradionecrosis
111
Q

Dry socket symptoms and management

A

Localised osteitis due to the clot falling out. Pain not managed by analgesias, foul tastes and smell, localised inflammation. Manage by irrigating w saline solution under the flap and packing w alveogyl.

112
Q

Infected socket symptoms and management

A

Infection of the socket, similar symptoms to a dry socket (pain, foul tastes and smell, local inflammed tissues) + signs of infection e.g. pus, swollen lymph nodes. Irrigate and pack w alveogyl + prescribe antibiotics e.g. metronidazole.

113
Q

Delayed healing management

A

Manage by debridement of the area (curettage) +/- dressing.

114
Q

Osteomyelitis symptoms and management

A

Infection of the cancellous bone. V painful, altered sensation, pus, sinus and can cause fractured jaws. Give antibiotic and debride area. If fractured refer to OMFS

115
Q

Osteoradionecrosis

A

Due to the previous radiotherapy. Area of bone necroses removed (debridement) and repair bone.

116
Q

MRONJ/BRONJ

A

Medically/bisphosphonate-related osteonecrosis of the jaw. An area that doesn’t heal after 8 weeks and was not previously radiated. Debride the area and repair the bone.
The area can get infected

117
Q

How to manage patients who have had previous radiotherapy

A

Preventative work
Operative anticipatory work before radiotherapy
Antibiotics.

118
Q

Bisphosphinate therapy

A

For Osteoporosis or to inhibit Oc activity (antagonist) e.g. in Pagent’s disease, hypercalcaemia of tumours. Increases risk of osteonecrosis.

119
Q

Resolution vs regeneration vs repair and what it depends on

A

Resolution = tissue goes back to normal
Regeneration = normal tissue remade
Repair = via scar tissue
Depends on the type of tissue (e.g. labile, stable or permanent cells), size and type of injury.

120
Q

cells involved in mature vs immature granulation tissue

A

Fibroblasts
Neutrophils
Epithelial cells
Phagocytes
More fibroblasts and collagen in mature granulation tissue.
Fewer fibroblasts and more neutrophils in immature. Less organised.

121
Q

Phases of wound healing and key cells involved at each stage (not bone)

A

Haemostasis - platelets,
Inflammation - neutrophils, phagocytes,
Proliferation - epithelial cells, fibroblasts, keratinocytes
Remodelling

122
Q

Haemostasis’ role in wound healing

A

Platelets and coagulation cascade make a clot (fibrin, trapped leucocytes and erythrocytes). Release of cytokines and GF

123
Q

Inflammation’s role in wound healing

A

Brings macrophages and neutrophils (stimulated by C’, leukotrienes, cytokines, prostaglandins). They do phagocytosis stimulate the release of more cytokines and GF (VEGF, FGF which stimulate endothelial cells)

124
Q

Proliferation stage of wound healing (not-bone)

A

The proliferation of fibroblasts, endothelial cells, keratinocytes,
GF and cytokines.

125
Q

Remodelling stage of wound healing (not-bone)

A

The organisation of granulation tissue and epithelial lining.

126
Q

Primary vs secondary intention in wound healing

A 
Primary = bringing together the damaged walls and mechanically holding them together e.g. using stitches = quicker healing, less or no scar.
Secondary = closure of the site by contraction and natural process. Slower and more scarring.
127
Q

Bone socket healing stages and timeline

A

Haemostasis
Proliferation
Remodelling
1h = clot formation
1 week = granulation tissue, acute inflammation and some epithelial proliferation.
2-3 weeks = complete granulation tissue, chronic inflammation areas, lamellar bone laid down at base and sides of the socket, more epithelial proliferation.
2 months = lamellar bone fills socket and being remodelled into the woven bone. Complete epithelial proliferation to form a lining. Chronic inflammation sites.
3 months = woven bone -> cancellous or compact bone and some resorption from Oc. KSSE lining.

128
Q

Factors influencing bone socket healing

A 
Previous radiation
Blood flow
Nutrition (vitamin C affects collagen)
Medication
Systemic illness e.g. uncontrolled diabetes
Steroids
Smoking
129
Q

Signals that control healing process

A

Cytokines, fibronectin, VEGF, FGF, EGF, PDGF, TGF beta, KGF

130
Q

Factors that control epithelial cell growth

A

Basal cells stimulate stem cells. Lack of contact and GF from platelets (KGF, EGF, PDGF).

131
Q

Factors that control angiogenesis

A

Macrophages (release VEGF, FEF) and broken endothelial cells. Blood vessel grows from the stump/remains of an old one.

132
Q

Factors that control fibroblast activation, proliferation, migration and secretion

A

Activated by TGF to become myofibroblasts.
FGF, TGF, PDGF
Fibronectins aid migration
Secretion of ECM, collagen,

133
Q

Summary of pathway to healed wound from coagulation

A
  1. Coagulation -> C’ and platelet aggregation -> release of cytokines.
  2. Cytokines -> TGF, PDGF, KGF, EGF and macrophages/neutrophils (which release VEGF, FGF)
  3. Wound healing
    - Fibroblasts = collagen and ECM = granulation tissue (FGF, TGF, PDGF)
    - myofibroblasts and endothelial cells = blood vessels (EGF, VEGF, PDGF)
    - keratinocytes = re-epithelialisation (KGF, EGF)
134
Q

Types of wounds

A

Chronic Wound
Scar
Non-scarring

135
Q

Problems with scars

A 
Contraction (muscle and ligament shrinkage)
Keloids
Aesthetics
Hypertrophic
Loss of function and growth
Neuroma
136
Q

Chronic wounds

A

Stay in the inflammatory stage e.g. don’t heal. Increased protease and less GF. Can lead to infection and necrosis.

137
Q

Foetal/scarless wounds

A

E.g. oral mucosa. Younger phenotype (telomerase), an increase of some growth factors (KGF, TGF 3, EGF) and less PDGF, TGF 1,2. Less inflammation and neutrophils, increased keratinocytes and contraction ability.

138
Q

Aids to wound healing

A

Dressing
Increased oxygen and pressure environment
Negative pressure
Leeches/maggots
Creating a foetal environment e.g. less TGF1,2 and more TGF3.
More GF and ECM.

139
Q

Keloids

A

Scarring problem - extra collagen bundles and collagen 3, abnormal cross-linking and turnover and cytokine levels = growths. Treat by using anti-inflammatories, corticosteroids or dressings.

140
Q

Types of oro-facial pain

A 
Pulpitis
Periapical pathology
TMJ
Trigeminal neuralgia
Burning mouth syndrome
Due to inflammation, neuropathic or vascular
141
Q

Peripheral and central ways of reducing oral pain/pain management methods

A 
Remove cause
Anaesthesia
Physical methods e.g. physiotherapy, acupuncture
Psychological methods e.g. CBT
Medication

Peripheral methods = remove the cause, LA, anti-inflammatories.
Central = GA, CBT, anti-convulsants, anti-depressents, relaxants, NSAIDs

142
Q

How is prostoglandin made

A

Phospholipids -> arachidonic acid (can be stopped by steroids).
Arachidonic acid -> prostaglandins via COX-1 or COX-2 enzymes (cyclooxygenase).
COX-1/2 are found and act in different muscles and make different prostaglandins that have diff actions.

143
Q

What do prostoglandins do

A

COX1 pathway = reduce gastric acid/protect the GI tract. Platelet function (thrombosis), water permeability so controls temperature homeostasis and renal/uterine regulation. Causes pain.
COX2 pathway = pain and inflammation and swelling.

144
Q

What can arachidonic acid also be made into (not prostaglandins)

A

Leukotrienes and then cytokines used for cell infiltration, stimulate the release of GF, inflammation, airway constriction.

145
Q

COX 1 inhibitors effects and side effects

A

Anti-inflammatories but cause GI ulcers, irritation and bleeding, increased bleeding and bleeding time, asthma problems, increased risk of MI. Affect COX1 and COX2. E.g. ibuprofen and aspirin

146
Q

How can the side effects of COX-1 inhibitors/NSAIDs be reduced

A

Proton-pump inhibitors given which reduce gastric acidity so stop GI bleeding/ulcer side effects.

147
Q

Contraindications for NSAIDs

A

Pregnant (can cause haemorrhage, changes in labour pulmonary hypertension in the fetus), breastfeeding (ep aspirin), asthmatics, children, old people taking aspirin, if already on NSAIDs, people w bleeding problems e.g. on Warfarin.

148
Q

COX-2 inhibitors effects

A

Anti-inflammatories and don’t cause GI side effects but increased risk of MI.

149
Q

Where are COX enzymes usually found

A

COX1 = kidneys, platelets, stomach

150
Q

Paracetamol effects and dosage

A

Anti-inflammatory w less side effects.

500-1mg QDS (max = 4mg in an 24h)

151
Q

Overdosing on paracetamol effects and antidote

A

Acetyl cysteine = antidote

Overdose causes nausea, vomiting and liver failure.

152
Q

Opioids used in dentistry and action

A

Affect the CNS via endorphins. Codeine, co-codamol and dihydrocodeine used. Not v good for normal dental pain.

153
Q

Specific analgesia examples

A

Trigeminal neuralgia - neuropathic drugs
Chronic pain - anticonvulsants, antidepressants or relaxants
Temporal artiritis - steroids.

154
Q

What to prescribe for a healthy patient after a normal XLA

A

Paracetamol: 500ug-1mg QDS orally and 2x200mg of ibuprofen TDS. 3 days worth.

155
Q

Co-codamol and dose

A

Paracetamol and codeine - different strengths.

1-2 tablets QDS (max 8/day)

156
Q

Ibuprofin dose

A

2 x 200mg TDS (2.4g max dose)

157
Q

Children’s analgesia dosages

A 
<1 = 1/8 of adult dose
1-5 = 1/4 of adult dose
6-12 = 1/2 of adult dose
12+ = adult dose
158
Q

What is a sequestrum

A

A dead bone left in the socket - leads to infection and forms a draining sinus

BODC (4 decks)

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