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Pediatric Dentistry Boards > Special needs patients part 2 > Flashcards

Special needs patients part 2 Flashcards

1
Q

Short acting bronchodilators: what are their names? what is their method of action?

A

Albuterol: beta2 agonist, bronchodilator-relaxes smooth muscle

Ipatroprium (Atroven): anticholinergic, used w/b2 agonists, relaxes smooth muscle by blocking acetylcholine receptors in smooth muscle

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2
Q

Long term control medications: what kinds of medicines are they? what are their effects? What are their methods of ingesting and examples? risks?

A
  1. Corticosteroids : anti inflammatory and immunosuppressive
  2. Inhaled: fluticason (flovent) and budesamide (pulmicort) or systemic : prednisolone
  3. Risks: Low risk in general, suppressed adrenal fxn, decreased bone density, increased risk for cataracts, growth retardation
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3
Q

Other classes of medications for asthma treatment

A
  1. Long acting Beta2 agonists: 12 hr activity
    - used when inhaled corticosteroids cannot control asthma alone. Combined with inhaled corticosteroids ex: advair, symbicort
  2. Leukotriene receptor antagonist: blocks chain rxn that causes inflammation, tablet form (ex singulair accolate)
  3. Anti IgE (xolair) used for severe persistent asthma. Injections 1-2 times/month
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4
Q

Oral findings in asthma patients?

Dentofacial findings?

A

Decreased salivary flow,
increased caries, dental erosion, calculus, gingivits
- Evidence of steroid use
- High palate, increased anterior face heigh, increased overjet, and greater incidence of posterior xbite

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5
Q

Dental treatment can trigger asthma…why?

A

Dental tx can result in 15% decreased lung fxn

  • Prolonged supine position
  • position of dental instruments
  • tooth dust
  • sealant materials
  • aerosols
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6
Q

Caution with sedation for asthma? what’s okay ?

A

Nitrous oxide OK for mild-moderate, severe asthma it will irritate their airway.
- Caustion with narcotics and barbituates for asthma. Antihistamines like vistaril are possible.

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7
Q

Congenital heart disease: incidence? percent of congenital anomalies?

A
  • 1/8000 live birts

- approx 30% of congenital anomalies (pretty common)

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8
Q

Heart Murmors: prevalence? normal/abnormal?

A

Related to increased blood flow velocity across a NORMAL valve

  • common, present in 80% of all children
  • Vast majority (90%) are normal
  • systolic murmurs may be innocent
  • diastolic murmurs and continuous murmurs are abnormal
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9
Q

Cardiac Defects:

- Increased Pulmonary blood flow– examples of this? clinical presentation? what occurs over time?

A

L to R shunts: ASD, VSD, PDA, and AV

  • increase in pulmonary blood flow at the expense of systemic circulation
  • enlarged heart
  • Appears as CHF over time
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10
Q

Cardiac Defects:
Decreased pulmonary blood flow :
examples of? Clinical presentation? Risks?

A

R to L shunt: tetralogy of fallot, tricuspid atresia, ASD or VSD + obstructive defect + overarching aorta

  • Pt appears cyanotic due to hypoxemia
  • Highest risk of endocarditis
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11
Q

Tetralogy of Fallot : whats the tetra?

A
  1. Pulmonary stenosis
  2. Right ventricular hypertrophy (right ventricle is trying to beat against the narrow pulmonary artery)
  3. Overarching aorta
  4. VSD
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12
Q

Cardiac defects:

Obstructive defects: types? clinical appearance? what occurs over time?

A
  • Anatomic narrowing impededs flow : physical defect ie Coarction of the aorta, aortic stenosis, pulmonic stenosis
  • Appear as congestive heart failure over time
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13
Q

Cardiac Defects:

Primary pump failure

A
  • Dilated cardiomyopathy: abnormality of myocardium which limites ability of heart to contract. Etio: disease/meds
  • Hypertrophic cardiomyopathy: dysrhymias, can result in syncope, sudden death Etio: the heart gets thicker/stronger and eventually impedes/blocks the aorta, most often effects the ventricular septum
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14
Q

Cardiac Defects:

- Congestive Heart failure: etiology? manage how/meds?

A

Heart unable to pump adequate amount of blood to systemic circulation at normal pressure to meet metabolic demands.
- Managed medically, surgically, or combo
–Remove accumulated fluid,
–Improve cardiac fxn
–Improve tissue oxygenation
–Reduce demands on heart
Meds: digoxin (increases contractility of heart) and diuretics (decreases fluids)

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15
Q

Cardiac Defects: long QT syndrome

- What is it? Prevalence? What happens? tx?

A
  • Delayed repolarization of the heart following heartbeat
  • May lead to palpitations, v-fib, sudden death
  • Dx difficult: 2.5% of normal patients have a prolonged Q-T wave use LQTS scoring system to categorize
  • Tx: meds, severe cases, placement of implantable cardioverter-defibrillator (ICD)
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16
Q

Prevalence of hypertension in children?

A

2% of children 4-15yrs

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17
Q

Benefits of bioprosthetic valvue? vs a mechanical valve?

A

Bioprosthetic valve: porcine, human, bovine–benefits good hemodynamics and no need for anticoagulants
- Mechanical valves: limited life span (10yrs), doesn’t grow w/the patient, readily available, replacements available, need anticoagulants and limited to the left side of the heart

18
Q

Oral findings for children with cardiac defects?

A
  • Increased caries
  • poorer oral health than siblings, increase in untreated caries in cases of severe CHD
  • gingival bleeding related to plaque (fear of inciting bleeding by tooth brushing?)
19
Q

Infective Endocarditis : incidence in population/children? What is it? symptom?

A

5 cases per 100,000 person years (very low incidence in general population and less freq in children)

  • Microbial infection : affects valves, muscle, defects
  • Symptoms: may appear as other infection (fatigue, fever, rash) 7-14 day typical incubation period
20
Q

Risks of transient bacteremia: most to least?

A

Dental procedures (done infrequently) : extractions 10-100%; perio sx (40-80%); Sc/rp (10-80%), teeth cleaning (40%) and RD placement (10-30%)

Routine daily procedure (done frequently):
-Toothbrushing/flossing (20-70%); Toothpicks (20-40%); Chewing food (10-50%)

21
Q

Cardiac patients who will receive SBE? Other patients at high risk?

A
  1. Prosthetic heart valve
  2. Previous infective endocarditis
  3. Congenital heart disease : (unrepaired cyanotic CHD, including palliative shunts/conduits; completely repaired congenital heart defect w/prosthetic material or device needed 6 months after procedure; repaired CHD w/residual defects)
  4. Cardiac transplant receipients who develop cadiac valvulopathy
  5. Also patients with compromised immunity (HIV, SCID, neutropenia, cancer tx, stem cell/organ transplant)
  6. Pts w/shunts and central lines (at time of placement, VA, VC, VV shunts at greatest risk)
  7. Pts w/prosthetic joints for high risk procedures w/in 2 years of implant sugery or w/hx of joint infection)
22
Q

Hemostasis Process:

  1. Primary : what is this step called? what occurs first? what are the factors involved? blood vessel reaction?
  2. Secondary: same ?s as above, and describe in/extrinsic pathway activation/production
A
  1. Primary: platelet aggregation
    - Injury causes platelets to aggregate
    - Release of vWF and collagen fibers from endothelium
    - Platelets adhere to subendothelial matrix-vWF-collagen
    - Vasoconstriction occurs
  2. Secondary: coagulation cascade
    - Extrinsic pathway activated when injuy exposes blood to Tissue factor
    - Intrinsic pathway produces factor X
    - Common pathway generates thrombin
23
Q

Using the cell based model of coaguation–describe the 1. initiation and 2. amplification phases of the pathway

A
  1. Initiation:
    - Tissue factor binds to FVII (this activates the extrinsic pathway via factors 9 and 10, eventually leading to thrombin production)
  2. Amplification: mainly occurs in platelets
    - Thrombin then activates platelets, factors 5, 8 and 9 to release vWF. Overall the amplification phase ends with 5a and 8a being bound to activated platelets
24
Q

3/3 Propagation phase of the cell based model of coagulation:

A
  1. Propagation: results in prothrombin production
    - activated factors 8 and 9 form a complex on the platelet membrane which leads to activating factor 10
    - 10a binds with 5a&raquo_space;prothrombinase
    - prothrombinase complex converts prothrombin to thrombin
25
Q

How does fibrinolysis occur?

A
  • Plasmin dissolves fibrin clot-

- Plasmin is regulated by anti-plasmin and plasminogen activator inhibitors

26
Q

Anticoagulant medications: name them, what do they do?

A

Aspirin
NSAIDS
- Warfarin (coumadin) : inhibits production of vitamin K dependent factors (2, 7, 9 and 10)
- Pradaxa: direct thrombin (production) inhibitor

27
Q 
Screening- what are these testing for?
PT?
PTT?
Platelet count?
PFA-100 ?
Bleeding time?
What is better at detecting vWF disease?
A
  • PT: tests for factors 1, 2, 5, 7, 10, thrombin and fibrinogen (extrinsic pathway)
  • PTT: Tests for factors 8, 9, 10, 11, 5, 1, and 2, thrombin and fibrinogen (intrinsic pathway)
  • Platelet count: platelet phase
  • PFA-100 : platelet function
  • Bleeding time: platelet phase vascular –inaccurate in young children
  • -PFA-100 is better than bleeding time for vWF
28
Q

Low, intermediate and high risk dental procedures?

A
  1. Low: supragingival restorations or prophylaxis, infiltration anesthesia
  2. Intermediate: subgingival restorations, single EXT, endo, nerve blocks
  3. High: multiple EXTs, perio sx, gingival curettage
29
Q

Clinical manifestations of a PRIMARY process defect: What is the primary process? Examples of the syndromes? and clinical manifestations

A 
Primary process: platelet aggregation
- Defects in platelet #/fxn
- Von Willebrand Disease
Clinical Manifestations: 
- longer bleeding time, 
- bleeding from superficial and deep cuts, - -
- petechiae, small/multiple ecchymoses, 
- spontaneous bleeding : epistaxis, CNS, pulmonary
30
Q

Clinical manifestations of a SECONDARY process defect: What is the secondary process? Examples of the syndromes? and clinical manifestations

A

Secondary process: coagulation cascade
- Defect in coagulation pathway
- hemophilia A and B
Clinical manifestations:
– no significant bleeding after superficial cuts, instead, significant bleeding after DEEP cuts, –
– no petechiae-instead LARGE widespread ecchymoses,
– hematoma, hemarthrosis (bleeding/bruise in joints),
– spontaneous bleeding–musculoskeletal and CNS

31
Q

von Willebrand disease: a defect of which process (1/2ndardy?), what does vWF do? Prevalence? inheritance? when is it detected/how?

A

Primary process is affected

  • vWF plasma protein in endothelium
  • 1% of population is affected, most common inherited coagulation disorder
  • Defecienct or defective vWF
  • Often detected after prolonged bleeding episode
  • low levels of vWF, low levels of factor 8, may have a longer PTT
  • Prolonged bleeding time, abnormal platelet function test
32
Q

Where is vWF made? What does it do?

A
  • Produced in endothelial cells of vessels
  • Functions as a bridge between platelets and injury site in vessel, helps in platelet plug formation
  • Protects factor 8 from quick degredation
33
Q

Management of vWF disease: what are patients likely to respond to it? What is its method of action? how long does it take and how is it administered

A
  1. Desmopressin (DDAVP)
    - a synthetic peptide for mild hemophilia A or vWD
    - Causes rapid release of factor 8 and vWF
    - 30-45 min to take effect
    - IV or subq; also stimate a nasal spray
  2. Amicar
34
Q

Amicar: what is it? how does it work? how long does it take? hows it administered? dosage?

A

e-aminocaproic acid it is effective in stablizing clots

  • Anti-fibrinolytic inhibits activation of plasminogen to plasmin
  • 2 hours to peak effect
  • give IV or PO : 50 mg/kg q6h until healed (usually 7 days)
  • may be given alone or w/desmopressin
35
Q

Thrombocytopenia: a defect of which process? due to which causes and why? lab results?

A
  1. Primary process defect
    - An insufficient # of platelets
    - May be due to LOW production of platelets : aplastic anemia, cancer in bone marrow
    - May be due to INCREASE BREAKDOWN of platelets: idiopathic thrombocytopenic purpura (ITP) and drug-induced immune thrombocytopenia
    Labs show low platelets on CBC
    - PT/PTT normal
    - Clinical manifestations: bruising, epistaxis, gingival beleding, petechiae (like other primary process defects)
36
Q

Hemophilia: which process is defective? What are inheritance patterns? break down % of each type of hemophilia, which are relatively more common, what about severity?

A

X linked recessive inheritance
1/3 of cases are new mutations
- Hemophilia A (Factor 8): 85%
- Hemophilia B (Factor 9): 15%

–Of those w/hemophilia A it is mostly like (70%) that they will have a SEVERE form
–Of those w/Hemophilia B 50% will have a severe form and 30% moderate
Severe is less than 1% of factor activity; moderate 1-5%

37
Q

Bleeding w/hemophilia: what occurs in the pathways? Clinically how is this manifested: to the body? the mouth?

A
  • normal platelet plug form (primary)
  • secondary cascade does not do well therefore delayed and malformation of fibrin clot
  • bleeding is not faster, but is prolonged
  • Have deep bleeding into joints or muscles
  • increased bleeding from open wounds
  • bleeding will appear to stop, then restart.
  • exfoliating primary teeth can pose a problem (sharp edges, etc)
38
Q

What are two important complication of hemophilia treatment?

A
  1. Antibodies that block activity of clotting factors occurs in 15% of severe hemophilia A patients and 2.5% of hemophilia Bs
    - -occurs after a number of factor exposures
    - -Tx: high dose of clotting factor, bypassing agents, efforts to induce immune tolerance
  2. Arthropathy: can occur w/o injury, chronic/acute pain, joint degenerates, can exhibit ROM,
  3. bleeding in to CNS/airway
  4. HIV/hepatitis infections (blood transfusions)
39
Q

Treatment for Hemophilia: medical mgmt? and what about playing sports?

A

General prophylaxis: use clotting factors 2-3x week

  • prevent bleeds
  • goals, decrease join disease/hospitalizations/time lost from school or work
  • *they can participate in sports! decreases obesity and does not increase risk of joint hemorrhage, puts less stress on joints
40
Q

Mgmt of hemorrhage? what are the goals? The amount/dose needed?

A

Need to have factor level to achieve and maintain clot

  • goal 30-40% of normal
  • 1 unit factor 8/kg = a 2% increase in factor 8 level
  • 1 unit of factor9/kg = 1% increase in factor 9
41
Q

Thrombotic disorders: acquired examples and inherited (w/incidence?)

A
  1. Acquired thrombotic disorders: short duration, pregnancy, surgery, immobilization
  2. Inherited:
    a) related to impaired function of protein C - anticoagulation system
    b) Factor V Leiden: incidence 5% in north america, predominant in whites, results in increase in prothrombin
42
Q

Management of thrombotic disorders: acute and long term?

A

Acute: heparin for several days, followed by warfarin for 3-6 months
Long term: Anti-coagulant therapy

Pediatric Dentistry Boards (23 decks)

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