OMFS Flashcards

1
Q

IE manifestations/features x8+ how to mx

A

“FROM JANE:”
Fever,
Roth spots-eye,
Osler nodes-palms, Murmur,
Janeway lesions-sole/palms petechiae,
Anemia,
Nail bed SPLINTER hemorrhage, and
Emboli-> [neuro] seizure/dyspnea=SOB [respi].

mx: referral; they would do blood culture before empirical IV Abx-> switch to targetted Abx therapy with Blood culture results

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2
Q

LA with epiNEphrine - dosage and duration of action

A

Lidocaine [90-200mins] + Mepivacaine[120-240mins] 4.4mg/kg

bupivacaine [180mins-600mins] 1.3mg/kg

articaine is 7mg/kg [60-240mins]

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3
Q

Tachyphylaxis is the appearance of progressive

A

decrease in response to a given dose after repetitive administration

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4
Q

LN swollen in neck- 6 things to note

A

1) pain - benign/inflammatory causes, if non tender - suspect malignancy/mycobacterial cause
2) consistency -soft [benign/infl]; hard [breast cancer metastasis]/ rubbery is Hodgkin lymphoma

3) fixation -mobile [benign/infl]; fixed [malig/TB]
4) location- anterior to SCM [benign/infl]; dorsal to Sternocleidomastoid muscle [M/TB]

5) progression [acute -benign/inf]; slow progression [m/tb]

6) size ->1cm -infection

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5
Q

painful Generalized lymphadenopathy (enlargement of ≥ 2 noncontiguous lymph node groups)

A

Viral infections
CMV
HIV
Mumps, measles, rubella
VZV

Bacterial infections
Syphilis

Parasitic infections
Malaria
Toxoplasmosis

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6
Q

painless Generalized lymphadenopathy (enlargement of ≥ 2 noncontiguous lymph node groups)

A

Malignancy
Malignant lymphoma (NHL, Hodgkin lymphoma)
Leukemia

Autoimmune
Circulating immune complexes (due to medication or allergies)
Sjogren syndrome

Others
Hyperthyroidism
Tuberculosis
Amyloidosis
Sarcoidosis

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7
Q

Painful localised lymphadenopathy

A

Oral/genital herpes
Chancroid
Kawasaki disease (usually unilateral cervical lymphadenopathy)
Mononucleosis (bilateral cervical lymphadenopathy)
Rubella (especially postauricular nodes), mumps

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8
Q

Painless localised lymphadenopathy 3x

A

Tuberculosis
Metastases
Residual lymph nodes after overcoming an infection

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9
Q

What is Ludwig angina?Characteristics/symptoms?

A

Ludwig’s Angina is a rapidly progressing cellulitis affecting the sublingual, submandibular, and submental spaces on bilaterally/ may be a “bull neck” appearance.

This condition is characterized by significant neck swelling, possibly extending to the clavicles, and can raise + protrude- the tongue[WOODY tongue], posing a risk to the airway.

Symptoms include fever, malaise, neck pain, limited neck movement, difficulty swallowing (dysphagia), voice changes (dysphonia), slurred speech (dysarthria), drooling, and sore throat,

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10
Q

L. angina possibly spread from sub mand. space to–>

Mx: 7x

A

Submd space can
extend to the lateral pharyngeal space->retropharyngeal space and potentially to the mediastinum, leading to serious complications.

1 Hospital Admission for severe infections for IV antibiotics, airway mx, and possible incision and drainage.
2. Empirical Antibiotics: Initiate with amoxicillin-clavulanate [Clavulanic acid inactivates some beta-lactamase enzymes that are produced by bacteria, therefore preventing enzymatic destruction of amoxicillin] and metronidazole [Aerobic+Anaerobic]; Analgesia -NSAID/OPOID-tramadol
3.Extraction if non-restorable or consider pulpectomy +Periodontal Debridement
4 OHI: Use CHX mouth rinses to reduce bacterial load.
5 Hydration and Nutrition: Ensure hydration and maintain nutritional intake with a soft or liquid diet if needed.
6 Continued targetted ABX after results out.
7 f/up+ monitor

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11
Q

complications of L. Angina

A

Complications may include respiratory obstruction due to lateral pharyngeal space involvement, leading to rapid breathing (tachypnea), shortness of breath (dyspnea), fast heart rate (tachycardia), noisy breathing (stridor), and restlessness.
Patients may experience systemic symptoms like fever, chills, a high white blood cell count (leukocytosis), and elevated sedimentation rate.

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12
Q

LA MOA
Benefits

A

LA-> temporarily block nerve conduction reversibly and thereby provide pain relief during procedures; without loss of consciousness and central control of vital functions such as respiration.

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13
Q

cellulitis mechanism of spread

A

Strep milleri->synthesise hyaluronidase; allows infective organisms to spread through CT

generates metabolic by-products=>
favourable envrionment for anaerobic growth
o Lowered pH too!

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14
Q

abcess how is it formed

A

Anaerobic bacteria predominate synthesise
collagenase->liquefactive necrosis of tissues.

Invading WBC lyse-> microabscesses
formation

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15
Q

microorganisms related to dry socket

A

Actinomyces viscous; Streptococcus mutans
=retard alveolar post-extraction healing

  • Treponema Denticola->Fibrinolytic activity
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16
Q

Mx and meds used for Dry socket

A

Local measures:
oPlacement-medicaments/dressing externally
(i.e.Alvoygyl/BIPP Bismuth iodoform paraffin paste)
alvogyl-eugenol (analgesic, anti-inflammatory), butamben (anesthetic), and iodoform (antiseptic)
o Surgical/intervention
o Socket packing
o Review every few days

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17
Q

Cavernous Sinus Thrombophlebitis -what, symptoms

A

An infection and inflammation+ clot formation in the cavernous sinus.
Orodental infections are responsible for approximately 10% of the cases.

Clinical Presentation
Eye Symptoms:
Edematous Periorbital Enlargement: Involving the eyelids and conjunctiva.
Proptosis, Chemosis, and Ptosis
Pupil dilation, excessive tearing (lacrimation), sensitivity to light (photophobia), and potential loss of vision.

Nasal Area Symptoms:
Canine Space Involvement: Presents with swelling along the lateral border of the nose, potentially extending to the medial aspect of the eye and periorbital area.
Induration and Swelling: Noted on the adjacent forehead and nose, suggesting spread or severe localized inflammation.
Pain: Occurs over the eye and along the distribution of the ophthalmic and maxillary branches of the trigeminal nerve, =involvement of these sensory pathways due to the spreading infection.

Advanced Toxemia and Meningeal Involvement:
Meningitis: Inflammation of the meninges, characterized by symptoms such as stiffening of the neck, irregular breathing patterns, tachycardia (fast heart rate), and tachypnea (rapid breathing).
Neurological Deterioration: =experience deepening stupor and possibly delirium.
Severe Complications: progression of the infection might lead to the formation of brain abscesses.

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18
Q

diagnosis of candidiasis

A

clinical signs,with positive microscopic findings/culture, +ve response to anti-fungal therapy, necessary to confirm diagnosis
potassium hydroxide KOH TEST- smear preparation
* dx aid:-tissue culture of smears,cytology,
o Sabourand’s medium
oPeriodic acid schiff-see hyphae/Pseudohyphae

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19
Q

oral cancer diagnosis methods and TOOLs

A

1 gold standard -visual examination and palpation .
2. VELscope =direct fluorescence visualization device to detect high-grade oral PML and delineate the margin of the lesion.
2 1% Toluidine Blue (ORASCAN) stains nuclei acid [DNA]=Adjunct tools=> chemiluminescent light sources that use toluidine blue improves the brightness and sharpness of the lesion’s margin and assist in the identification of mucosal lesions that were not considered under the conventional visual examination.

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20
Q

orascan purpose x2

A

Purpose:
Used as a diagnostic tool in oral cancer screening.
Helps to establish the borders for biopsy procedures.

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21
Q

TNM classification

A

Clinical assessment of the anatomical extent of disease
Tumour
T 1 < 2 cm
T 2 < 2 – 4 cm
T 3 > 4 cm
T 4 Infiltrating deep structures

Nodes
N 1 Mobile palpable nodes < 3 cm on same side
N 2 Contra or bilateral mobile nodes 3 – 6 cm
N 3 Fixed node(s) > 6 cm

Metastases M 1 Distant metastases present

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22
Q

VZV + salicylate=>

A

reyes syndrome in children; rare but when viral infection alters the metabolism of salicylates and leads to accumulation of metabolites in the liver, which causes hepatic mitochondrial injury that prevents hepatic ATP production+ hepatic failure.

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23
Q

HSV-1 infection - mx of pain

A

Rest: Emphasized to support recovery.
Antipyretic: Used to manage fever.
Topical/systemic corticosteroids-oracort E
Topical Analgesics:
Benzydamine (NSAID): Available as a gel or mouthwash for pain relief.
Lignocaine/benzocaine Gel: Effective for pain relief, but use with caution in young children.

Salicylate: Not recommended due to potential risks, such as Reye’s syndrome.

Topical Antiseptic:
Chlorhexidine (CHX): Available in swab form or as a 0.2% mouthwash.
Difflam C Mouthwash: Used for its antiseptic properties.

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24
Q

HSV - OHI and dietary mx

A

Oral Hygiene
Soft-bristled Toothbrush: Should be discarded after illness to prevent reinfection.
Cotton Buds/Swabs with CHX: For gentle cleaning.
Moist Warm Cloth: For cleaning without causing irritation.
Toothpaste: May cause stinging pain and should be used cautiously.

Nutrition and Hydration
Soft, Bland Diet: Foods like pudding, yogurt, and porridge recommended.
Cool Foods/Drinks: Such as ice chips or shavings to soothe the throat.
Avoid Irritants: Such as alcohol, tobacco, citrus fruits, tomatoes, and carbonated drinks to prevent aggravation of symptoms.

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25
Q

hsv - medication mx

A

Targeted Therapy
Acyclovir: Used particularly for severe cases or immunocompromised patients if started within 72 hours of infection onset.
Dosage: 200mg 5x/day for 5 days for adults and >2yrs old.
Benefits: Decreases the duration of fever, pain, lesions, and viral shedding.
Limitations: Does not change the frequency or severity of recurrent herpes simplex infections (RHSI).

Additional Care Considerations
Fever and Pain Management: Aim to reduce both fever and pain effectively.
Prevent Secondary Infections: Critical to prevent complications.
Adequate Fluid Intake: Essential to prevent dehydration.
Isolation and Infection Control: Important to prevent spread during the contagious period.

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26
Q

progression of Progression of Symptoms
HSV
Progression of Symptoms
HSV
incubation:
Prodromal period
resolves by

A

Progression of Symptoms
Incubation: 5-7 days.
Prodrome: 1-2 days, with symptoms like fever, malaise, headache, nausea.
Active Infection: Characterized by vesiculation and ulceration, with fever typically decreasing by the third day and symptoms reducing by the sixth day.
Resolution: Symptoms generally resolve after 10-14 days.

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27
Q

Absolute CI of adrenaline in LA

A
  1. <6/12 MI
  2. <6 CVAccident
  3. <6/12 CABG
  4. uncontrolled HTN > 200mg/115mmHg
  5. unstAble Angina pectoris
  6. uncontrolled thyrotoxicosis
  7. Congestive heart failure
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28
Q

relative contraindications of ADRENALINE in LA- use only _ catridge , aspirate and avoid hemostat with epinephrine

A
  1. dm on hypoglycemics
  2. HTN -controlled
  3. cardiac arrythmia
  4. NON selective beta blockers [PROp/timolol] and digoxin for arrythmias
  5. hepatic or renal failure- metabolism of amide LA and excretion is affected
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29
Q

PT prothrombin time, duration, which pathway,+ which factors

A

PT 10-13 sec extrinsic pathway + common pathway [1,2,5,7, 10] I, II, VII and X

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30
Q

WBC
platelets; normal and what level what procedure can be done?

A

wbc 4500-10,000/mL
platelets 150k-450k/uL;

> 80k major surg
50k minor surg
30k-50k routine procedure
<30k defer all tx
transfused 1hr before procedure and regularly to maintain at least >30k-40k range until healing occurs

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31
Q

APartial thromboplastin time,duration, which pathway+ factor- used to monitor what?

A

25-35 sec
intrinsic + common pathway
xii
xi [hemophilia c-autosom dom.]
ix [hemophilia b- X-linked]
viii [hemophilia a- X-linked]

also monitor for heparin

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32
Q

TT-,duration, which pathway- measures ability to form initial … from…

A

9-13sec
common pathway
ability to form initial clot from fibrinogen

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33
Q

bleeding time

check the function of …

A

7-9mins - duration to arrest bleeding

platelets and blood vessels and primary hemostasis

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34
Q

INR- measures what/which pathway? pt on .. therapy stable range

A

0.8-1.2 normal
measure extrinsic pathway
RATIO OF pt PT to standard PT

for monitoring patients on warfarin therapy 2.0-3.0

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35
Q

hemophilia level of factor of VIII [%]

A

mild >5% -rarely bleed spontaneously
moderate 1-5%
severe <1% -bleed spontaneously into muscle and joints at young age

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36
Q

mx of hemophilia A

A

factor viii [ ]
prothrombin complex [ ]
cryoprecipitate if ddvap unavailable
desmopressin [ddvap]- mild hemophilia A

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37
Q

warfarin - MOA, used for

A

-block vit k epoxide reductase in liver
also (-) vit k dependent clotting factors like ii-thrombin, vii, ix, x ; C+S -> dec clotting ability

  • use to tx/prevent
    ->DVT, Pulm embolism
    -> atrial fib
    -> post MI, cardiac valve replacement
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38
Q

reversal of warfarin

A

stop the warfarin [long half life]

oral/parenteral vit k - few doses
emergency - FFP, prothrobim complex [ ]

39
Q

warfarin interaction - INCREASE RISK OF BLEEDING

A

nsaids/cox-2 -or , aspirin, tramadol
azole antifungal - fluconazole/miconazole

antibiotics - macrolides- erythr/azi/clarithromycin, tetracycline, metronidazole [ amoxy/ clindamycin is safe]

“sickfaces.com group”: Sulfonamides, Isoniazid-tb, Cimetidine, Ketoconazole, Fluconazole, Alcohol (binge drinking), Ciprofloxacin, Erythromycin, Sodium valproate, Chloramphenicol, Omeprazole, Metronidazole, and Grapefruit juice are P450 inhibitors.

40
Q

DRUGS THAT INHIBIT WARFARIN

A

immunosuppressant like azathioprine, cyclosporine

carbamezepine, rifampin, phenytoin

Induction of CYP450 Enzymes: All these drugs enhance the activity of liver enzymes that metabolize warfarin.
Increased Metabolism: Leads to a faster breakdown of warfarin.
Reduced anticoagulant effect, requiring dose adjustments of warfarin.

41
Q

mx pt on warfarin

A

-PT/INR required (w/in 24hrs)
<2.5 -routine procedures + local measure
2.3-3 - omfs
>3 defer, refer to physician

if cessation of warfarin 2-3 days before- resume on evening
<3 - tx
>3 defer until INR controlled

Requires periprocedural bridging anticoagulation- in hosp setting
- cessation of warfarin
start iv/sc heparin
- inr 24 hr
stop heparin 6-8 hrs be4 procedure

42
Q

dabigatran -what, indicated for?; adv

A

direct THROMBIN inbitor [oral]

AFib ; post-surg thromboprophylaxis of knee/hip replacement

rapid onsent ; short halft life, less interaction with food/drug; no monitoring needed

43
Q

dabigatran mx; reversal agent

A

if major surgery, discuss to discont
1-2 days pre op
1 day post op

emergency , PROthr complex [ ] / aFviii / hemodialysis
reversal agent is monoclonal Ab - idaru/cizumab

44
Q

dagibatran interaction/avoid NAC

A

NSAID,
azole antifungal
carbamezepine,

45
Q

rivaroxa ban/ apixaban/ edoxaban reversal agent

A

andexanet alfa, pcc in severe bleed

46
Q

rivaroxa ban
onset [….] hr
half life [….]hr

A

orally active agent act on f Xa ->preventing the formation of thrombin
rapid onset 2-4 hr
short half life 5-9 hrs

47
Q

antiplatelet -aspirin moa

A

irreversible inactivation of cox1 enzyme-> suppress PG and THROMBOXANE TXA2-> (-) platelet aggregation for 7-10 days

48
Q

clopidogrel and ticlopidine MOA

A

irreversibly block ADP receptor
(-) activation of glycoprotein IIb/IIIa pathway–>platelet aggregation for 7-10 days

49
Q

mx of antiplatelet

A

no need to stop - if stop need stop 7-10 days pre op and recommence 3 days post op

local measure and tranexamic m/w
>3 teeth, multiple visits - refer omfs, kiv stop clopidogrel /ticlopidine

50
Q

spongiostan /gelfoam

A

absorbable [4-6wks] gelatin sponge - pig skin
act as mechanical matrix for clotting + provide structural support

51
Q

surgicel

A

oxidised regenerated cellulose
for mechanical activation of clotting cascade, denatures blood proteins; bacteriostatic, resorable in 4-8 wks

52
Q

tranexamic acid

A

antifibrinolytic ; binds to plasminogen, inactivates it and prevent conversion to plasmin and the degradation of fibrin clots

500mg tablet disolved in 10-20ml of water then rinse 10ml 4x/day for 2 days

53
Q

achieve hemostasis/local measure

A

careful wound debridement - curretage - granulation tissue

wound compression, pressure with gauze
tranexamic acid soaked gauze
absorable - spongiostan /surgicel
NON absorbable hemostatic agent is bone wax
suturing

54
Q

DM WHAT

A

INC in blood glucose lvl dt absolute or relative def of insulin leading to CHD, CVA, ESRD, infections-> death

55
Q

dm diagnosis + key % and mmol/L

Red blood cells live for an average of …days, so …. gives an indication of …. It’s different to a blood glucose test, which measures how much sugar is in the blood….

A

120days
how much sugar there has been in your blood over the past few months….intra-day

hbA1c[glycated haemoglobin]-2-3months- ideal
normal <5.7% =6.5mmol/L
5.7- 6.4%=6.5-7.5mmol/L [prediabetes]
>6.4% DM=7.6mmol/L
poor control is 8-10%
uncontrolled is >10% //>13.9mmol/L

hyperglycemic >13.9mmol/L-use ketones DKA-polyuria, polydipsia, polyphagia; reduced alertness, ketonemia, ketouria

56
Q

DM how affect repair/healing 5*

A

Blood Vessels: microvascular and macrovascular changes->Thickened basement membrane and impaired blood flow reduce leukocyte migration, nutrient delivery, oxygen perfusion, and waste elimination.
Host Response: impaired immune system-Neutrophil dysfunction, poor chemotaxis-migrate to site of infection affected, and poor phagocytosis.
AGEs: Decreased collagen and bone matrix production, increased degradation, impaired fibroblast/keratinocyte function-> abnormal cross-linking of collagen fibers, reducing the flexibility and functionality of matrix-> poor wound healing.
Macrophage Activation: Increased cytokine secretion, prolonged to inflammation.
Neuropathy: Reduced sensation peripheral areas, delayed recognition of injuries, worsened infections at time of tx.

57
Q

simvastatin, lovastatin, and atorvastatin contraindicated with… and why; and extra interaction with…?

A

Macrolides (erythromycin +clarithromycin)
Azole antifungals
Cyclosporine

Statins metabolized by CYP3A4 (simvastatin, lovastatin, and atorvastatin) must not be combined with CYP3A4 inhibitors=> increases statin concentrations + risk of rhabdomyolysis!->amaged muscle tissue releases its proteins and electrolytes into the blood->damage the heart and kidneys -> permanent disability / death.

also interact with warfarin

58
Q

cancer chemotherapy [chemo] causes …that typically resolves following…. and recovery of damaged tissue, while RT cause… and induce …. damage resulting in ….. risk for patient.

the most common acute oral complications to cancer therapies is .. 6xM.O.S.T. x.P—-> lead to , 8x [D.T. D.M. Q.P.]

A

acute toxicity that typically resolves following discontinuation of therapy and recovery of damaged tissues, while radiation therapy can cause acute oral toxicities AND can induce permanent tissue damage, resulting in lifelong risk for the patient.

The most common oral complications related to cancer therapies are Mucositis, opportunistic infection (viral or fungal), salivary gland dysfunction-viscous; taste disturbance; hyposalivation/Xeros., , and
pain.

These complications, in turn, may lead to dehydration, dysgeusia (change in taste), dysphagia (difficulty swallowing), and malnutrition, poor
QOL ; period dis-CAL and mobility + dental caries [cervical]

59
Q

what other complications associated with chemo and BMT/HSCT

CHEMO assoc with chronic presentation of … related atrophy dt …. and …..[oral] + …. [facial symptom]

chronic complications …

RT also affect in chronic …. and …

A

chemo and BMT/HSCT increased risk of bleeding and immunoSup.

Chemo assoc with anemia related atrophy dt myelosupp. and neutropenic ulcers too and atypical facial pain -dt vinca alkaloids

Chronic oral complications- secondary malignancy

RT- ORN, trismus

60
Q

asthmatic pt mx

A

prophylatic inhaler puff - beta 2 agonist= sympathomimetic=bronchodilation -salbutamol

if inhaled CCs >1.5mg daily of beclomethasone then consider supplemental steroids

61
Q

High doses of chemotherapy in pediatric patients can cause abnormal … development such as altered… development,…growth or …development, esp in c’ren younger than…

A

dental development, such as
altered tooth development, craniofacial growth or skeletal development, especially in those children younger than 9 years of age.

62
Q

some cases, such as acute leukemia, where induction chemotherapy may begin ……of diagnosis, there may be ……to institute elective dental therapy.

A

within days …
no time

63
Q

Communication from the oncology team about cancer details…5x.

Communication from the dental provider might include data regarding ….5x with the goal of treatment planning and treating or stabilizing oral disease that could potentially cause complications during cancer treatment

A

(type, stage, etc.), treatment approach, blood counts, and comorbid conditions.

active caries, periodontal or endodontic disease, teeth requiring extraction, or other urgent dental care

64
Q

Normal saline solution may be prepared by

A

1 teaspoon of table salt to 4 cups of water
The solution can be administered either at room temperature or refrigerated, depending on patient preference.
The patient is generally instructed to rinse and swish approximately 1 tablespoon of the solution and spit it out; this may be repeated as often as necessary to maintain oral comfort. Saline solution can enhance oral lubrication, directly, as well as by stimulating salivary glands to increase salivary flow.

sodium bicarbonate (baking soda) may be added (1 to 2 tablespoons per 4 cups of water), if viscous saliva is present.

65
Q

ORNJ occurs rarely in people receiving less than …of radiation and generally occurs months or years following radiotherapy.

A

60 (Gy)

66
Q

Cancer metastases to the bone and hypercalcemia of malignancy are typically managed …. a rare but serious adverse effect of these therapies is….

A

with antiresorptive agents (i.e., IV bisphosphonates, denosumab);

medication-related osteonecrosis of the jaw (MRONJ).

67
Q

American Association of Oral and Maxillofacial Surgeons (AAOMS), MRONJ definition includes :

A

(1) current or previous treatment with antiresorptive therapy alone or in combination with immune modulators or antiangiogenic agents;
(2) exposed bone or bone that can be probed through an intraoral or extraoral fistula in the maxillofacial region that has persisted for more than 8 weeks; and
(3) no history of radiation therapy to the jaws or metastatic disease to the jaws.

68
Q

Osteonecrosis is… of bone due to …. involving exposed mandibular or maxillary bone, which usually manifests with …., although it may be asymptomatic. ONJ typically occurs following tooth extractions or other dentoalveolar surgeries, but in some cases, it can occur ….

A

necrosis .. dt obstruction of blood supply

pain and purulent discharge

spontaneously

69
Q

how MRONJ happens?

A

suppression of bone turnover and remodeling by the antiresorptive agents impairs the body’s ability to repair microfractures in the maxilla and mandible

70
Q

differential diagnosis of MRONJ includes

A

alveolar osteitis, OM, sinusitis, gingivitis/periodontitis, or periapical pathosis.

71
Q

RISK FACTOR OF MRONJ old dse op

A

O - Older than 65 years
L - Long-term or high-dose antiresorptive/antiangiogenic agents (more than 2 years) IV/oral
D - Diabetes

D-Dentures
S - Smoking
E-Exo/surgery

O - Oncology patients (multiple myeloma, breast, lung cancer)
P-Periodontitis

72
Q

eg of antiresorptive agents are

A

bisphosphonates and RANKL (receptor activator for nuclear factor-kappa B ligand) inhibitors.

2 parenteral bisphosphonates, pamidronate (Aredia®)22 and zoledronic acid (Zometa®/Reclast]), and ibandronate (Boniva) (e.g., hypercalcemia of malignancy).

orally – including alendronate (Fosamax),
risedronate (Actonel)

Denosumab is a monoclonal antibody against RANKL, a ligand required for osteoclastic precursors to differentiate into mature osteoclasts

73
Q

monoclonal antibodies against VEGF (e.g., bevacizumab),
tyrosine kinase inhibitors (e.g., sorafenib, sunitinib),
mammalian target of rapamycin (mTOR) pathway inhibitors (e.g., everolimus), and immunomodulatory agents (e.g., thalidomide, lenalidomide)

A

antiangiogenic agents

74
Q

bilateral lesions intraoral/multifocal- white or yellow lesions

A

linea alba,
lichen planus
leukoedema-disappear with stretching
white sponge nevus-hereditary no tx
pv
fordyce’s granules
OHL
thrush

75
Q

single white /red lesion

A

traumatic keratosis
material alba- can be wiped off
chemical trauma
lichenoid contact reaction
Carcinoma
papiloma
leukoplakia

76
Q

nystatin interact with..to form …

A

CHX..
complex which is ineffective

77
Q

EBV diagnosis via

A

ISH- in situ hybridization and histopathological examination

78
Q

why leukoplakia has high rate of recurrence and MT?

A
  1. field of cancerisation - epith elsewhere in the area has premalignant disease and myb subclinical - chromosomal abnormalities in clinically normal mucosa
  2. continuous exposure of carcinogens- tobacco smoke, spirits-alcohol, 3UV , 4SPICES- areca nuts, 5sepsis
79
Q

chronic T cell mediated disorder of Strat Sq Epi ; mast cell degranulation, Matrix metalloproteinases (MMPs) activation seen in

A

OLplanus

80
Q

mx olplanus

A

not symp, not erosive - monitor / flup

symp + erosive= topical CCS and kiv Antifungal if suspect fungal oppor. infection

not response, CI in CCS, then topical tacrolimus / cyclosporine [ both TOPICAL CALCINEURIN -ors to (-) T cell activation] then lastly topical retinoids and PUVA -PHOTOdynamic therapy

81
Q

methyldopa is used for.. and assoc with … reaction

A

HTN

OLICHENOID drug reaction

82
Q

In contrast to BPs, RANK-L
inhibitors do not…and their effects on ….diminished within ….

A

bind to bone,

bone remodeling are mostly

six months of
treatment cessation

83
Q

drug holiday for MRONJ/ eg denosumab prevention; when? by aaomfs 2022

A

evidence to support or
refute drug holiday remains inconclusive.

3months following the last dose of DMB when the level of osteoclast inhibition is waning. It can then be
reinstituted 6-8 weeks postsurgery.

84
Q

normal Hb level for males is 14 to 18 g/dl; that for females is 12 to 16 g/dl.

ANEMIA is?

A

WHO criteria for anemia
Men: Hb < 13 g/dL
Women: Hb < 12 g/dL
Pregnant women: Hb < 11 g/dL

if<10g/DL

85
Q

“CUSHINGOID” is the acronym for side effects of corticosteroids:

A

Cataracts, Ulcers, Striae/Skin thinning, Hypertension/Hirsutism/Hyperglycemia,

Infections, Necrosis (of the femoral head), Glucose elevation, Osteoporosis/Obesity, Immunosuppression, Depression/Diabetes.

Moon facies, buffalo hump

86
Q

ddx for desquamative gingivitis

A

Oral Lichen Planus
* Mucous Membrane Pemphigoid (MMP)

* Pemphigus Vulgaris (PV)
* SLE)
* DLE)

87
Q

BENIGN white oral plaque/ lesion assoc with chronic smoking? // TOBACCO

PML and
CANCER-related to smoking

A

benign: TOM’s
1. tobacco pouch keratosis (not true leukoplakia)- dt Smokeless tobacco -regress if not biopsy if >1month post cessation
2. oral melanotic macule [2* to smoking]
3. smoker’s Melanosis-Anterior Lab ging.
4.Nicotinic stomatitis- greyish white hard palate with red spots dt inflm minor salivary glands and thermal injury in PIPE smokers

PML: SPLERO
1. Sublingual keratosis
2. PALATAL Red-W LESIONS IN REVERSE SMOKERS// ulcerations
3. Leukoplakia-cannot be rubbed off and cannot be characterized clinically or pathologically as any other condition.
4. Erythroplakia-Red, velvety patches; cannot be characterized as any other condition.
5. Rigidity-Oral Submucous Fibrosis: A chronic, progressive condition characterized by mucosal rigidity due to fibrosis of the submucosal tissues-> LMO. It is strongly associated with areca nut chewing (often found in some tobacco
products) and carries a high risk of malignant transformation
6 Oral sq cell Ca-> Ca

88
Q

OLP etiological factors

A

a. Drug history (Current/past)
-Hypertension, DM (Diabetes Mellitus), Liver disease, HBV (Hepatitis B Virus), HCV
c. DLE (Discoid Lupus Erythematosus) / SLE (Systemic Lupus Erythematosus)
d. GVHD (Graft-Versus-Host Disease)
e. Psychological state (Stress)

89
Q

signs and symptoms suggestive of a malignant tumor in the oral cavity include:
U CAN B HEARD TWICE SD

A

U - Ulcers (Non-healing>2/52)
C - Color (White/red patches, speckled lesions, nodular white lesions=verrucous leukoplakia)
A - Appearance (Exophytic: fungating, papillary, verrucous; Endophytic: rolled borders, invasive, ulcerated)
N - Nodules (Indurated, fixed to tissues)
B - Bleeding (Unexplained)
H - Hoarseness (Chronic sore throat)
E - Enlarged lymph nodes (LN involvement, B symptoms)
A - Altered sensation (Paraesthesia; painless initially)
R - Radiographic appearance (Moth-eaten/root resorption)
D - Dysphagia (Difficulty swallowing/chewing, reduced tongue mobility-smf)
T - Teeth + taste (Loose, non-healing extraction sockets; dysguesia)
W - Well/ill-defined borders (Regular or ill-defined, uni- or bilateral)
I - Inflammation (Swelling, poor denture fit)
C - Clinical progression (Rapid changes)
E - Etiology (Medical history, syphilis, HIV, familial history; social history: alcohol, tobacco;>50y male)
S- lat/ventral -tongue, FOM, soft palate,gums,lining of the mouth/lower lip
D- dysplasia

A:Asymmetry
* B: Border irregularities
* C: Colour variegation
* D: Diameter>6mm
* E:Elevation(surface)
for Malg melanoma

90
Q

prevention of oral cancer 7x

A

1 Avoid alcohol, spirit
2 avoid tobacco; smoke
3. use UV protection, sun
4. HPV vaccination, sex
5. maintain good oral hygiene,- prevent sepsis-candidiasis
6. manage nutrition - avoid areca nuts [spices]
7. mx -immune status.

91
Q

HbA1c, or glucose meter [mmol/l] which more important.

A

both are important- to avoid hypoglycemia that is not evident in HbA1c 7% reading]

92
Q

mx of hypoglycemia

A

ABC ,Check the blood sugar level with a glucose meter (finger prick). If it is too low (below 4.0mmol/l), take a sweet drink like a fruit juice or sweets (not sugar-free) to raise the glucose level quickly.

Check the blood glucose level again after 10 to 15 minutes. If it is still low, take something sweet again. It is important to seek medical attention promptly if the symptoms persist.

93
Q

Symptoms of hypoglycaemia

A

generally, early warning signs of hypoglycaemia include:
1Feeling shaky, weak, dizzy, irritable and hungry
2Having a fast heartbeat
3Headache
4Mood swings
5A staggering gait
6 trouble seeing clearly,
7feel confused,
8have a seizure or
8 LOC

94
Q

why La ineffective in infected tissue?

A

LAs Weak bases prepared as hydrochlorides for stability and solubility.

pKa of most LAs: 7.5-9.5.
At physiological pH (7.4), charged forms predominate. Charged forms cannot easily penetrate cell membranes.
Non-ionized forms penetrate membranes.
LAs => ionized forms which block Na chnls in the nerve cells.

Tissue pH and Anesthetic pKa
Inflammation->inf mediators->Lower pH: Acidic environment reduces the non-ionized form of the drug.
Less Effective: Fewer non-ionized molecules to penetrate the nerve.
Inflammation causes vasodilation, dilute La and reduce efficacy.
Necrosis: No extracellular fluid to buffer, LA remains ineffective.
Tachyphylaxis: Repeated administration results in decreased response

Considerations: Use regional block over local infiltration, deposit a larger volume of LA.

.