Special needs patients part 2 Flashcards
Short acting bronchodilators: what are their names? what is their method of action?
Albuterol: beta2 agonist, bronchodilator-relaxes smooth muscle
Ipatroprium (Atroven): anticholinergic, used w/b2 agonists, relaxes smooth muscle by blocking acetylcholine receptors in smooth muscle
Long term control medications: what kinds of medicines are they? what are their effects? What are their methods of ingesting and examples? risks?
- Corticosteroids : anti inflammatory and immunosuppressive
- Inhaled: fluticason (flovent) and budesamide (pulmicort) or systemic : prednisolone
- Risks: Low risk in general, suppressed adrenal fxn, decreased bone density, increased risk for cataracts, growth retardation
Other classes of medications for asthma treatment
- Long acting Beta2 agonists: 12 hr activity
- used when inhaled corticosteroids cannot control asthma alone. Combined with inhaled corticosteroids ex: advair, symbicort - Leukotriene receptor antagonist: blocks chain rxn that causes inflammation, tablet form (ex singulair accolate)
- Anti IgE (xolair) used for severe persistent asthma. Injections 1-2 times/month
Oral findings in asthma patients?
Dentofacial findings?
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
Dental treatment can trigger asthma…why?
Dental tx can result in 15% decreased lung fxn
- Prolonged supine position
- position of dental instruments
- tooth dust
- sealant materials
- aerosols
Caution with sedation for asthma? what’s okay ?
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.
Congenital heart disease: incidence? percent of congenital anomalies?
- 1/8000 live birts
- approx 30% of congenital anomalies (pretty common)
Heart Murmors: prevalence? normal/abnormal?
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
Cardiac Defects:
- Increased Pulmonary blood flow– examples of this? clinical presentation? what occurs over time?
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
Cardiac Defects:
Decreased pulmonary blood flow :
examples of? Clinical presentation? Risks?
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
Tetralogy of Fallot : whats the tetra?
- Pulmonary stenosis
- Right ventricular hypertrophy (right ventricle is trying to beat against the narrow pulmonary artery)
- Overarching aorta
- VSD
Cardiac defects:
Obstructive defects: types? clinical appearance? what occurs over time?
- Anatomic narrowing impededs flow : physical defect ie Coarction of the aorta, aortic stenosis, pulmonic stenosis
- Appear as congestive heart failure over time
Cardiac Defects:
Primary pump failure
- 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
Cardiac Defects:
- Congestive Heart failure: etiology? manage how/meds?
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)
Cardiac Defects: long QT syndrome
- What is it? Prevalence? What happens? tx?
- 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)
Prevalence of hypertension in children?
2% of children 4-15yrs
Benefits of bioprosthetic valvue? vs a mechanical valve?
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
Oral findings for children with cardiac defects?
- 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?)
Infective Endocarditis : incidence in population/children? What is it? symptom?
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
Risks of transient bacteremia: most to least?
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%)
Cardiac patients who will receive SBE? Other patients at high risk?
- Prosthetic heart valve
- Previous infective endocarditis
- 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)
- Cardiac transplant receipients who develop cadiac valvulopathy
- Also patients with compromised immunity (HIV, SCID, neutropenia, cancer tx, stem cell/organ transplant)
- Pts w/shunts and central lines (at time of placement, VA, VC, VV shunts at greatest risk)
- Pts w/prosthetic joints for high risk procedures w/in 2 years of implant sugery or w/hx of joint infection)
Hemostasis Process:
- Primary : what is this step called? what occurs first? what are the factors involved? blood vessel reaction?
- Secondary: same ?s as above, and describe in/extrinsic pathway activation/production
- 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 - Secondary: coagulation cascade
- Extrinsic pathway activated when injuy exposes blood to Tissue factor
- Intrinsic pathway produces factor X
- Common pathway generates thrombin
Using the cell based model of coaguation–describe the 1. initiation and 2. amplification phases of the pathway
- Initiation:
- Tissue factor binds to FVII (this activates the extrinsic pathway via factors 9 and 10, eventually leading to thrombin production) - 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
3/3 Propagation phase of the cell based model of coagulation:
- 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»_space;prothrombinase
- prothrombinase complex converts prothrombin to thrombin
How does fibrinolysis occur?
- Plasmin dissolves fibrin clot-
- Plasmin is regulated by anti-plasmin and plasminogen activator inhibitors
Anticoagulant medications: name them, what do they do?
Aspirin
NSAIDS
- Warfarin (coumadin) : inhibits production of vitamin K dependent factors (2, 7, 9 and 10)
- Pradaxa: direct thrombin (production) inhibitor
Screening- what are these testing for? PT? PTT? Platelet count? PFA-100 ? Bleeding time? What is better at detecting vWF disease?
- 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
Low, intermediate and high risk dental procedures?
- Low: supragingival restorations or prophylaxis, infiltration anesthesia
- Intermediate: subgingival restorations, single EXT, endo, nerve blocks
- High: multiple EXTs, perio sx, gingival curettage
Clinical manifestations of a PRIMARY process defect: What is the primary process? Examples of the syndromes? and clinical manifestations
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
Clinical manifestations of a SECONDARY process defect: What is the secondary process? Examples of the syndromes? and clinical manifestations
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
von Willebrand disease: a defect of which process (1/2ndardy?), what does vWF do? Prevalence? inheritance? when is it detected/how?
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
Where is vWF made? What does it do?
- 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
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
- 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 - Amicar
Amicar: what is it? how does it work? how long does it take? hows it administered? dosage?
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
Thrombocytopenia: a defect of which process? due to which causes and why? lab results?
- 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)
Hemophilia: which process is defective? What are inheritance patterns? break down % of each type of hemophilia, which are relatively more common, what about severity?
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%
Bleeding w/hemophilia: what occurs in the pathways? Clinically how is this manifested: to the body? the mouth?
- 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)
What are two important complication of hemophilia treatment?
- 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 - Arthropathy: can occur w/o injury, chronic/acute pain, joint degenerates, can exhibit ROM,
- bleeding in to CNS/airway
- HIV/hepatitis infections (blood transfusions)
Treatment for Hemophilia: medical mgmt? and what about playing sports?
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
Mgmt of hemorrhage? what are the goals? The amount/dose needed?
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
Thrombotic disorders: acquired examples and inherited (w/incidence?)
- Acquired thrombotic disorders: short duration, pregnancy, surgery, immobilization
- 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
Management of thrombotic disorders: acute and long term?
Acute: heparin for several days, followed by warfarin for 3-6 months
Long term: Anti-coagulant therapy
