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USMLE Pediatrics > 1 > Flashcards

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USMLE® Step 1 flashcards
1
Q

What is allergic rhinitis?

A

Watery, itchy eyes; nasal pruritus/congestion postnasal drip with cough; wheezing; headache; Allergic salute (rhinorrhea and nasal pruritus), nasal crease; vigorous grinding of eyes. Established by 6 years of age. Perennial symptoms are more common than seasonal.

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2
Q

What are the physical signs of allergic rhinitis?

A

Allergic shiners, conjunctival injection, chemosis (edema), stringy discharge, cobblestoning of tarsal conjunctiva. Transverse nasal crease (from allergic salute). Pale nasal mucosa thin and clear secretions polyps.

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3
Q

What are the laboratory findings in allergic rhinitis?

A

Eosinophilia and eosinophils in nasal and bronchial secretions; increased serum IgE. IgE–specific allergens on radioallergosorbent testing. Skin test.

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4
Q

What is the treatment of allergic rhinitis?

A

Intranasal corticosteroids. Less GI absorption with fluticasone, mometasone, budesonide. Second gen antihistamine (cetirizine, fexofenadine, loratadine) nonsedating. Diphenhydramine sedating. Remove allergen.

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5
Q

What is the secondary treatment of allergic rhinitis?

A

Cromolyn and nedocromil are least effective, but safe. Immunotherapy consists of gradual increase in dose of an allergen. Immunotherapy should not be used for atopic dermatitis, food allergy, latex allergy, urticaria, or children

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6
Q

What are the causes of eosinophilia?

A

Neoplasms, asthma/allergy, Addison disease, collagen vascular disorders, parasites.

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7
Q

What is allergic conjunctivitis?

A

Seasonal is most common. Caused by ragweed, grass pollens. Itchy eyes, chemosis, watery discharge. Association with atopic dermatitis, asthma, and rhinitis.

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8
Q

What is the treatment for allergic conjunctivitis?

A

Combined topical antihistamine and vasoconstrictive agent. Patanol, methylprednisolone.

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9
Q

What are the signs of insect venom allergy?

A

IgE reaction to stings from Hymenoptera. Urticaria, angioedema, pruritus, anaphylaxis; fever, malaise, emesis, nausea. Delayed/late response: serum sickness, nephrotic syndrome, vasculitis, neuritis, encephalitis. Skin testing.

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10
Q

What is the treatment for insect venom allergy?

A

Systemic antihistamine; remove stingers by scraping. If anaphylaxis: epinephrine injector pen. Venom immune therapy.

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11
Q

What are the most common food allergies?

A

Egg, milk, peanuts, nuts, fish, soy, wheat. Any food may cause a food allergy. Most infants and young children outgrow milk and egg allergy (in 3 years); nut or seafood allergies are retained for life. IgE, often cell–mediated.

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12
Q

What is the presentation of food allergy?

A

Urticaria, angioedema. flushing, atopic dermatitis. Oral pruritus, nausea, vomiting, diarrhea, abdominal pain, gastroenteritis. Predominantly cell–mediated; therefore, allergy tests not useful.

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13
Q

What are the physical signs of food allergy?

A

Nasal congestion, rhinorrhea, sneezing, laryngeal edema, dyspnea, wheezing, asthma. Food elimination and challenge test is diagnostic.

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14
Q

What are urticaria and angioedema?

A

IgE–mediated activation of mast cells in skin. Systemic allergens: food, drugs, venoms. Allergen may penetrate skin, causing urticaria. Radiocontrast, EBV, hepatitis B, opiates, NSAIDs.

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15
Q

What are the physical causes of urticarias?

A

Physical urticarias are caused by temperature, pressure, stroking, vibration, light. Other angioedemas are hereditary angioedema and C1 esterase–inhibitor deficiency.

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16
Q

How is urticaria and angioedema diagnosed?

A

Skin tests, RAST.

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17
Q

What is the treatment for urticaria and angioedema?

A

Responds to avoidance of trigger and oral antihistamine. Severe symptoms are treated with epinephrine, short–burst corticosteroids. H1 plus H2 antagonists. IVIg or plasmapheresis.

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18
Q

What is anaphylaxis?

A

Cutaneous, respiratory, cardiovascular, gastrointestinal symptoms after exposure to latex, antibiotics, IVIg, radiocontrast agents, foods (peanut), insect stings, oral medications.

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19
Q

What is the treatment for anaphylaxis?

A

Epinephrine, diphenhydramine; O2 airway management. Epinephrine IV for severe hypotension; IV fluid expansion; H1 antagonist; corticosteroids; nebulized, short–acting beta–2 agonist for wheezing; H2 antagonist for oral allergens.

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20
Q

What is atopic dermatitis (eczema)?

A

Familial with strong maternal influence; allergic rhinitis and/or asthma. Increased eosinophils and IgE. Half start by 1 year of age; most by 1 and 5 years of age. Cutaneous hyperreactivity and pruritus

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21
Q

What are the clinical signs of eczema?

A

Erythematous papules, serous exudate, excoriation. Infants have rash on face, scalp, extensor surfaces of extremities. Older children have long–standing disease with flexural rash and lichenification.

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22
Q

What is the treatment for eczema?

A

Topical corticosteroids. Sedating antihistamines at night; for pruritus. Glucocorticoids are rarely needed for generalized eczema.

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23
Q

What is contact dermatitis?

A

Caused by irritants or allergy. Delayed hypersensitivity reaction (type IV). Caused by jewelry (especially nickel), shoes, clothing, and plants (poison ivy).

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24
Q

6–year–old boy with end–expiratory wheezing, nasal flaring, tachypnea, intercostal retractions. Family history of asthma and atopic dermatitis. What is the diagnosis?

A

Asthma

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25
Q

What is asthma?

A

Chronic inflammation of airways with obstruction. Onset

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26
Q

What are the clinical signs of asthma?

A

Diffuse wheezing, expiratory then inspiratory. Prolonged expiratory phase. Rhonchi, excessive mucus. Increased work of breathing.

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27
Q

How is asthma diagnosed?

A

Lung function: FEV1/FVC

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28
Q

What are the chest x–ray signs of asthma?

A

Flattening of the diaphragms because of hyperinflation. Peribronchial thickening.

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29
Q

What are the quick–relief asthma medications?

A

Short–acting beta–agonists: albuterol, levalbuterol, terbutaline, metaproterenol. Last 4–6 h. Used for rescue. Anticholinergics: ipratropium bromide are much less potent than beta agonists and are added in hospital. Prednisone 3–10 d; methylprednisolone.

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30
Q

What are the long–term controller medications for asthma?

A

Cromolyn, nedocromil only for mild; 4 x/day. Inhaled corticosteroids are best. Budesonide, fluticasone, mometasone (second gen) greater potency. Nebulized budesonide; 1–2x/day. Long–acting beta: salmeterol, formoterol.

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31
Q

What are the indications for long–acting beta agonists?

A

Salmeterol and formoterol are add–on medications used q12hours (not BID) and are not for rescue or monotherapy. Must use with inhaled corticosteroid.

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32
Q

What are the leukotriene–modifying agents?

A

Inhibitors of synthesis (zileuton >12 years old). Receptor antagonists: montelukast, zafirlukast. Not as effective as inhaled corticosteroids.

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33
Q

What is the role of theophylline in the treatment of asthma?

A

Rarely used. Oral theophylline is sometimes used for steroid–dependent asthma for some steroid–sparing effects. Monitor levels (narrow therapeutic window).

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34
Q

What is the treatment of asthma exacerbations?

A

O2. Inhaled albuterol q20min for one hour: add ipratropium q6h if no response. Corticosteroids PO or IV. Discharge if SaO2 >92% after 4 hours in room air. Home treatment with albuterol q3–4 hour MDI and 3–7–day oral steroid.

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35
Q

Which patients should be hospitalized for asthma exacerbations?

A

Moderate–severe flare–ups without improvement within 1–2 hours with peak expiratory flow F

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36
Q

What is the treatment of asthma that does not respond to routine therapy?

A

Intravenous beta agonist. Intravenous theophylline, Heliox (70:30 He:O2). Intravenous MgSO4, which is a smooth–muscle relaxant.

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37
Q

What is the significance of a normal absolute neutrophil count in the evaluation of suspected immune deficiency?

A

Eliminates congenital or acquired neutropenia and both forms of leukocyte adhesion deficiency (counts are elevated in these disorders).

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38
Q

Which immunodeficiency syndrome is associated with a low platelet count?

A

Wiskott–Aldrich syndrome

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39
Q

What immunodeficiency syndrome is associated with Howell–Jolly bodies?

A

Asplenia

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40
Q

What screening tests are indicated for suspected B–cell defect?

A

Quantitative immunoglobulins. Normal IgA excludes Ab deficiencies. Antibody titers to tetanus, diphtheria (assesses formation of IgG antibodies to protein Ag). Ab titers to S. pneumoniae and H. influenza.

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41
Q

What screening tests are indicated for suspected T–cell defects?

A

Absolute lymphocyte count. Candida albicans intradermal skin test is best test.

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42
Q

What screening tests evaluate for phagocytic defects?

A

Absolute neutrophil count. Respiratory burst assay.

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43
Q

What is the initial screening for recurrent infections?

A

CBC, manual differential, platelet count, smear.

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44
Q

What conclusion about a patient?s immune system can be drawn if the absolute lymphocyte count is normal?

A

T–cell defect is unlikely.

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45
Q

What is the best test for screening for complement deficiency?

A

CH5O (total hemolytic complement). Measures the status of entire complement system. C3 and C4 can be easily measured.

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46
Q

What tests will evaluate antibody deficiency?

A

Immunoglobulin levels. Antibody titers to protein Ags (diphtheria, tetanus). Antibody titers to polysaccharide antigens (pneumococcal vaccine). IgG subclasses B–cell enumeration.

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47
Q

What tests will evaluate cell–mediated immunity?

A

Lymphocyte count, HIV. Delayed hypersensitivity skin tests: Candida, mumps, tetanus toxoid. CD3, CD4, CD8 counts. T–cell proliferation response to mitogens. Chest x–ray for thymic hypoplasia. Fluorescent in situ hybridization for DiGeorge.

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48
Q

What tests will evaluate splenic dysfunction?

A

Howell Jolly bodies, Hb electrophoresis, Tc–99 spleen scan.

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49
Q

What tests will evaluate phagocytic function?

A

WBC neutrophil count and morphology, neutrophil respiratory burst assay test for chronic granulomatous disease. Chemotactic assay, phagocytic assay for chronic granulomatous disease, Chediak–Higashi.

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50
Q

What tests will evaluate the complement system?

A

CH50 and individual complement assays.

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51
Q

What types of infections are associated with defects of antibodies, phagocytes, and complement?

A

Encapsulated bacteria, enteroviral infections (Coxsackie A and B, echovirus, enterovirus).

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52
Q

What disorders are associated with T cell defects?

A

Opportunistic infections, failure to thrive, bronchiectasis, CNS enteroviral infection.

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53
Q

What types of infections are associated with neutrophil killing defects?

A

Recurrent staphylococcal abscesses and Gram–negative infections

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54
Q

What tests will diagnose agammaglobulinemia?

A

Enumeration of B cells with flow cytometry using antibodies to B–cell specific CD antigens. X–linked B cells are absent in Bruton agammaglobulinemia. In common variable, IgA deficiency, B cells are present.

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55
Q

What tests will diagnose T–cell deficiency?

A

Enumeration of T cells for CD2, CD3, CD4, CD8. Performed on any infant who is lymphopenic for severe combined immunodeficiency. T–cell function is measured by mitogen stimulation; measurement of cytokine production.

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56
Q

What tests will diagnose phagocytic cell defects?

A

Neutrophil respiratory burst test with rhodamine dye.

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57
Q

What tests will diagnose natural killer cell defects?

A

Flow cytometry for natural killer–specific CD antigens (CD16, CD56).

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58
Q

What types of infections are associated with phagocyte deficiency?

A

Multiple infections with catalase positive organisms, such as staph aureus. Complement deficiency results in susceptibility to infection with Neisseria.

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59
Q

What is Bruton agammaglobulinemia?

A

X–linked boys. Develops 6–9 mth. Pyogenic infections (S pneumoniae, H influenza, M pneumoniae), HBV, enteroviruses. Lymphoid hypoplasia. Decrease in immunoglobins. Flow cytometry shows absence of B cells.

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60
Q

What is the treatment for Bruton agammaglobulinemia?

A

Monthly intravenous immune globulin and antibiotics for infections.

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61
Q

What is common variable immune deficiency?

A

Hypogammaglobulinemia with normal B cells. Failure of differentiation of B cells into Ig–providing cells, genetic defect. S pneumoniae, H influenza, M pneumoniae, HBV. Normal lymphoid tissue. Increased lymphomas.

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62
Q

What is selective IgA deficiency?

A

Absence of serum and secretory IgA. Most common B–cell defect. Males and females.

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63
Q

What is the presentation of selective IgA deficiency?

A

Respiratory, gastrointestinal, urogenital, and skin infections; autoimmune disease and increased malignancies. Serum antibodies to IgA; therefore, fatal anaphylactic reactions if given blood with IgA.

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64
Q

What is transient hypogammaglobulinemia of infancy?

A

Physiologic nadir of IgG at 3–4 mths, then increases to normal. Extension of physiologic hypogammaglobulinemia for more than 6 mths is abnormal. Most synthesize Ig normally by 11 mths. Increased otitis media, which responds to antibiotics.

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65
Q

What is IgG subclass deficiency?

A

One or more of the 4 subclasses of Ig6 are decreased despite a normal total IgG.

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66
Q

What is the prognosis for defects of cellular immunity (T cell defects)?

A

T cell defects are more severe; no survival beyond infancy or early childhood without treatment.

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67
Q

What are the characteristics of DiGeorge syndrome?

A

Decreased T cells. Widely spaced eyes, low–set ears, fish mouth.

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68
Q

What is the treatment for DiGeorge syndrome?

A

Transplantation of thymic tissue of MHC–compatible sibling or half–matched parenteral bone marrow.

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69
Q

What is DiGeorge syndrome?

A

Dysmorphogenesis of 3, 4 pharyngeal pouches; thymic, parathyroid hypoplasia; hypocalcemic seizures. Tetany, anomalies of great vessels. Esophageal atresia, Bifid uvula, short philtrum, hypertelorism.

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70
Q

What are the immunologic abnormalities of DiGeorge syndrome?

A

Decreased IgA, increased IgE. Low lymphocytes, decreased CD3 T cells; absent respiratory burst.

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71
Q

What are the complications of DiGeorge syndrome?

A

Opportunistic infections by fungi, viruses, P jiroveci. Graft–versus–host disease; special care with blood transfusions.

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72
Q

What is severe combined immunodeficiency?

A

Absence of all adaptive immune function and natural killer function. In first few months of life there is diarrhea, pneumonia, otitis media, sepsis, skin infections, wasting. Candida, P jiroveci, varicella, measles, parainfluenza, CMV, EBV.

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73
Q

What are the immunologic defects of severe combined immunodeficiency?

A

No immunoglobulin or natural killer function. GVHD from maternal T cells crossing placenta. Lymphopenia. No thymus, absent lymphoid tissue.

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74
Q

What are the types of severe combined immunodeficiency?

A

X–linked is most common. Autosomal recessive is less common. Adenine deaminase (ADA) deficiency SCID has the lowest antibody and lymphocyte count.

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75
Q

What is the treatment for severe combined immunodeficiency?

A

Bone narrow transplant or death by 1 year of age.

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76
Q

What is the difference between combined immunodeficiency and severe combined immunodeficiency?

A

Combined immunodeficiency has low but not absent T–cell function.

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77
Q

What is Wiskott–Aldrich syndrome?

A

X–linked recessive, atopic dermatitis. Thrombocytopenia with normal megakaryocytes but small defective platelets (petechiae). Susceptibility to infection, adenopathy. Splenomegaly, lymphadenopathy; bleeding circumcision.

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78
Q

What is the presentation of Wiskott–Aldrich syndrome?

A

Atopic dermatitis and recurrent infection; primarily encapsulated bacterial pneumonia, meningitis, sepsis; later, P carinii, herpes. Impaired humoral response. Patients have decreased IgM, increased IgA and IgE, and slightly low IgG. T cells decreased.

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79
Q

What are the complications of Wiskott–Aldrich syndrome?

A

Malignancy, infections, bleeding. Death occurs in teens unless bone marrow transplant.

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80
Q

What is ataxia–telangiectasia?

A

Decreased response to B, T cell mitogens. Decreased CD3, CD4 cells. Humoral and cellular deficiency. IgA deficiency. Hypoplastic thymus, helper T defects. Sinopulmonary disease, viral.

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81
Q

What are the physical abnormalities of ataxia–telangiectasia?

A

Mask facies, tics, drooling, irregular eye movements. Ataxia, wheelchair by 10 yrs. Oculocutaneous telangiectasias.

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82
Q

What is chronic granulomatous disease?

A

X–linked. Neutrophils and monocytes can ingest but not kill catalase–positive microorganisms. Recurrent lymphadenitis, pneumonia, skin infections. Hepatic abscesses, osteomyelitis. Infections with catalase–positive organisms: S aureus.

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83
Q

How is chronic granulomatous disease diagnosed?

A

Flow cytometry test using dihydrorhodamine 123 fluorescence (DHR test).

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84
Q

What is the treatment for chronic granulomatous disease?

A

Bone marrow transplant and daily TMP–SMZ.

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85
Q

What is leukocyte adhesion deficiency?

A

Rare recessive. Impairment in neutrophil function. Infants have recurrent bacterial infections of skin, mouth, respiratory tract, genital mucosa; chronic ulcers; S. aureus, enteric gram–negatives, fungal. No inflammation or pus.

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86
Q

How is leukocyte adhesion deficiency diagnosed?

A

Flow cytometry. Treatment is bone marrow transplant.

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87
Q

What is Chediak–Higashi syndrome?

A

Rare autosomal recessive syndrome of recurrent infection, bleeding diathesis: oculocutaneous albinism, peripheral neuropathy, lymphomas; defective neutrophil degranulation. Infection of mucous membranes, skin, and respiratory tract.

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88
Q

What is Coloboma of iris?

A

Often autosomal dominant. Defect of lid, iris, lens, retina, or choroid. Always inferior: keyhole appearance of iris; in lid, manifests as cleft.

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89
Q

What are the causes of leukocoria?

A

Retinoblastoma, cataract, retinopathy of prematurity, retinal detachment, larval granulomatosis.

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90
Q

What are the causes of congenital cataracts?

A

Prematurity (disappear in weeks). Autosomal dominant. TORCH (esp rubella); also, measles, polio, influenza, varicella, vaccinia. Galactosemia. Trisomies, deletions and duplications, XO. Drugs, steroids, toxins, and trauma.

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91
Q

What is ectopia lentis?

A

Instability or displacement of lens; usually caused by trauma. Also caused by uveitis, glaucoma, cataract, aniridia, tumor. Marfan syndrome, homocystinuria, Ehlers–Danlos.

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92
Q

What are the causes of ophthalmia neonatorum?

A

Chemical conjunctivitis: first day. Gonorrhea: first week. Chlamydia: second week.

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93
Q

What is dacryostenosis?

A

Congenital nasolacrimal duct obstruction characterized by excessive tears, mucoid material from the lacrimal sac, erythema.

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94
Q

What is the treatment of dacryostenosis?

A

Nasolacrimal massage three times a day and warm water cleansing. Usually resolves by less than 1 year of age.

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95
Q

What is strabismus?

A

Misalignment of the eyes from abnormal innervation of muscles.

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96
Q

How is strabismus diagnosed?

A

Hirschberg corneal light reflex: light reflex should be symmetric and slightly nasal to center of each pupil.

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97
Q

What is pseudostrabismus?

A

Transient pseudostrabismus in infants. Up to 4 months of age is common

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98
Q

What is ophthalmia neonatorum?

A

Redness, chemosis, edema, purulent discharge. Chemical conjunctivitis is most common 24 h from silver nitrate. N gonorrhea: 2–5–days. Serosanguineous discharge, then purulent. C. trachomatis: 5–14–day incubation.

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99
Q

How is ophthalmia neonatorum diagnosed?

A

Gram stain, culture, tarsal scraping for Giemsa stain (intracytoplasmic inclusions), and PCR

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100
Q

What is the treatment for gonococcal conjunctivitis?

A

N. gonorrhea: ceftriaxone x 1 dose IM and saline irrigation.

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101
Q

What is the treatment of Chlamydia conjunctivitis?

A

Erythromycin PO for 2 weeks and saline irrigation.

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102
Q

What are the signs of bacterial conjunctivitis?

A

Conjunctival hyperemia, edema, mucopurulent exudate (crusting of lids together), eye discomfort. Unilateral or bilateral. S. pneumonia, H. influenza, S. aureus, other streptococci.

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103
Q

What is the treatment of bacterial conjunctivitis?

A

Topical ciprofloxacin.

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104
Q

What are the signs of viral conjunctivitis?

A

Watery discharge, bilaterally. Occurs with upper respiratory infection with adenovirus, enterovirus. Epidemic keratoconjunctivitis is caused by adenovirus type 8.

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105
Q

What are the causes keratitis?

A

Corneal infection by H. simplex, adenovirus, S. pneumoniae, S. aureus, pseudomonas, chemicals.

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106
Q

What are the causes of dacryocystitis?

A

S. aureus, H. influenza, S. pneumoniae. Dacryoadenitis is caused by S. Aureus, streptococci, cytomegalovirus, measles, Epstein–Barr virus, trauma.

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107
Q

What are the causes of retinopathy of prematurity?

A

Prematurity, hyperoxia.

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108
Q

What are the complications of retinopathy of prematurity?

A

There can be mild to severe vasoproliferative scarring and blinding retinal detachment.

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109
Q

What is retinoblastoma?

A

Most common primary malignant intraocular tumor; autosomal recessive. Average age is 15 months. Rarely discovered at birth. Initial signs are leukocoria (white mass), strabismus. CT scan.

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110
Q

What are the symptoms of corneal abrasions?

A

Pain, tearing, photophobia, decreased vision.

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111
Q

How are corneal abrasions diagnosed?

A

Anesthetize eye, then fluorescein and blue–filtered light (Wood’s lamp)

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112
Q

What is the treatment of corneal abrasions?

A

Pain relief and topical antibiotics.

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113
Q

What is periorbital cellulitis?

A

Inflammation of lids and periorbital tissue. Caused by trauma, infected skin wound, respiratory infection, bacteremia (H influenza type b, S pneumoniae, S aureus). Sinusitis progresses to orbital cellulitis.

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114
Q

What is the treatment of periorbital cellulitis?

A

Oral or IV antibiotics (cover for S. aureus and gram positive resistant strains)

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115
Q

9 year–old boy with swelling around eye after an insect bite. Edema, erythema, proptosis. Decreased eye movements. What is the diagnosis?

A

Orbital cellulitis

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116
Q

What is orbital cellulitis?

A

Infection of orbital tissue. Ophthalmoplegia, chemosis, inflammation, fever, leukocytosis. Nontypeable H. influenza, S. aureus, beta hemolytic strep, S. pneumoniae, anaerobes. CT scan.

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117
Q

What is the treatment of orbital cellulitis?

A

Intravenous antibiotics for S. aureus.

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118
Q

Which bacteria cause otitis externa?

A

Normal flora of external canal includes P aeruginosa (most common cause), S. aureus (second most common cause), coagulase–negative Staphylococcus, diphtheroids, Micrococcus spp., and viridans streptococci.

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119
Q

What is malignant otitis media?

A

Malignant external otitis is invasive to temporal bone and skull base with facial paralysis, vertigo, cranial nerve abnormalities.

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120
Q

What is the treatment of otitis externa?

A

Topical neomycin, colistin or polymyxin, or topical ciprofloxacin and corticosteroid.

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121
Q

What is the age of onset of otitis media?

A

Most in first 2 years. Boys more than girls.

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122
Q

What are the causes of otitis media?

A

Bacterial in 75%; S. pneumonia (40%), nontypeable H. influenza (25%), Moraxella catarrhalis (15%), other 5%: Group A strep, S aureus, gram negatives (neonates and hospitalized infants), rhinovirus, RSV.

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123
Q

What are the symptoms of otitis media?

A

Ear pain, fever, otorrhea, irritability. Fullness/bulging, retraction, intense erythema, opacity (effusion), decreased mobility. High beta lactam resistance (50% S pneumoniae, 40% of nontypeable H flu, all M catarrhalis).

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124
Q

What is the treatment of otitis media?

A

Amoxicillin (high dose) for 10 d. Alternate is azithromycin. Amoxicillin–clavulanic acid is effective against beta–lactamase. IM ceftriaxone for severe infection. Cefdinir is palatable. Myringotomy or tympanocentesis.

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125
Q

What is otitis media with effusion?

A

Tympanic membrane fullness or retraction with no erythema. Routine antibiotic prophylaxis is not recommended. Tympanostomy tubes.

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126
Q

What is a local complication of otitis media?

A

Acute mastoiditis. CT scan of temporal bone.

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127
Q

What is the treatment of refractory acute mastoiditis?

A

Myringotomy, IV antibiotics (S. pneumoniae, Nontypeable H. influenzae, P. aeruginosa); mastoidectomy.

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128
Q

What is acquired cholesteatoma?

A

Cyst–like growth within middle ear caused by long–standing chronic otitis media. Progressively expands and can be life–threatening.

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129
Q

How is acquired cholesteatoma diagnosed?

A

White opacity of eardrum, malodorous ear discharge. CT scan . Treatment is surgery.

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130
Q

What are the signs of labyrinthitis?

A

Vertigo, tinnitus, nausea and vomiting, nystagmus, hearing loss.

131
Q

What is choanal atresia?

A

Unilateral or bilateral bony (most) or membranous septum between nose and pharynx. Cyanosis while trying to breathe through nose, then become pink with crying. Mouth breathing is adequate.

132
Q

How is choanal atresia diagnosed?

A

Inability to pass catheter 3–4 cm into nasopharynx. Fiberoptic rhinoscopy. CT scan.

133
Q

What is the treatment for choanal atresia?

A

Establish oral airway. Transnasal repair with stent.

134
Q

What are the signs of a nasal foreign body?

A

Unilateral purulent, malodorous bloody discharge. Nasal speculum or otoscope; lateral skull film if radiopaque.

135
Q

What are the causes of epistaxis?

A

Digital trauma (nose picking). Dry air (especially winter); located on anterior septum (Kiesselbach plexus), allergy, inflammation from viral infections, nasal steroid sprays, severe GERD, congenital vascular anomalies, clotting disorders, hypertension.

136
Q

What is the treatment of epistaxis?

A

Local oxymetazoline or phenylephrine, nasal packing; cautery.

137
Q

What are nasal polyps?

A

Benign pedunculated tumors from chronically inflamed nasal mucosa. Most common cause is cystic fibrosis. Hyponasal speech and mouth breathing; rhinorrhea glistening, gray, grape–like masses; obstruction.

138
Q

What is the treatment of nasal polyps?

A

Intranasal steroids, systemic steroids; surgical removal.

139
Q

What is sinusitis?

A

Acute sinusitis is most commonly caused by viruses; self–limited; 2% are complicated by bacterial sinusitis.

140
Q

What are the causes of acute sinusitis?

A

S. pneumonia, nontypeable H. influenzae, M. catarrhalis; S. aureus in chronic cases. Predisposed with URI, allergy, cigarette smoke exposure.

141
Q

What are the causes of chronic sinusitis?

A

Immune deficiency, cystic fibrosis, ciliary dysfunction, abnormality of phagocytic function, gastroesophageal reflux disease, cleft palate, nasal polyps, nasal foreign body.

142
Q

What are the clinical features of sinusitis?

A

Nasal congestion, discharge, fever, cough, bad breath, decreased smell; headache, face pain, sinus tenderness, erythema; swelling of nasal mucosa, discharge.

143
Q

How is sinusitis diagnosed?

A

Persistent URI symptoms for at least 10 days. Severe respiratory symptoms with purulent discharge and temperature of at least 38.9 C for at least 3 consecutive days. CT shows mucosal thickening, opacification, air–fluid levels.

144
Q

What is the treatment for sinusitis?

A

High dose amoxicillin. Alternative: cefuroxime, cefpodoxime, azithromycin. If treatment failure or resistance (antibiotic in previous 3 mths, daycare,

145
Q

What are the causes of acute pharyngitis?

A

Viruses, group A beta–hemolytic strep (GABHS), GABHS is uncommon less than 2–3 years of age; increased incidence in childhood.

146
Q

What are the symptoms of streptococcal pharyngitis?

A

Rapid onset of severe sore throat and fever; headache and gastrointestinal symptoms.

147
Q

What are the signs of streptococcal pharyngitis?

A

Red pharynx, tonsillar enlargement with yellow, blood–tinged exudate, petechiae, strawberry tongue, increased and tender anterior cervical nodes.

148
Q

What is scarlet fever?

A

Caused by GABHS that produce streptococcal pyrogenic exotoxins. Findings of pharyngitis plus circumoral pallor, diffuse red, finely papular erythematous rash with a sandpaper texture. Pastia’s lines.

149
Q

How is strep pharyngitis diagnosed?

A

Rapid strep test; if positive, throat culture is not necessary. Confirm a negative rapid test with a culture.

150
Q

What is the treatment of strep pharyngitis?

A

Penicillin treatment hastens recovery by 12–24 hours and prevents acute rheumatic fever.

151
Q

What are the causes of cervical lymphadenitis?

A

Viral, bacterial, pharyngitis, cat scratch disease, tuberculosis, atypical mycobacteria, mumps, thyroglossal duct cyst, branchial cleft cyst, cystic hygroma, allergy.

152
Q

What are the complications of cervical lymphadenitis?

A

Retropharyngeal and lateral pharyngeal abscess characterized by extension of localized infection of oropharynx.

153
Q

What are the signs of cervical lymphadenitis?

A

Fever, irritability, decreased oral intake, drooling, neck stiffness, torticollis, refusal to move neck, muffled voice, stridor. Incision and drainage, C and S. Most infections are polymicrobial (GABHS, anaerobes, S. aureus)

154
Q

What is the treatment of cervical lymphadenitis?

A

Third–generation cephalosporin plus ampicillin/sulbactam or clindamycin. Surgical drainage.

155
Q

What is a peritonsillar abscess?

A

Bacterial invasion through capsule of tonsil. Usually an adolescent with recurrent history of acute pharyngotonsillitis. Sore throat, fever, dysphagia, trismus, drooling.

156
Q

What are the clinical signs of peritonsillar abscess?

A

Asymmetric tonsillar bulge with displacement of uvula away from the affected side (hot potato voice). GABHS and mixed oropharyngeal anaerobes.

157
Q

What is the treatment of peritonsillar abscess?

A

Antibiotics and needle aspiration. Incision and drainage. Tonsillectomy if recurrence or complications (rupture with aspiration).

158
Q

What are the indications for tonsillectomy for strep pharyngitis?

A

7 strep pharyngitis documented infections within the past year. 5/year for 2 years. 3/year for 3 years. Unilateral enlarged tonsil (neoplasm most likely but rare).

159
Q

What are the indications of adenoidectomy?

A

Chronic nasal or sinus infection failing medical treatment. Recurrent or chronic otitis media in children with tympanostomy tubes and persistent otorrhea. Nasal obstruction with chronic mouth–breathing and loud snoring.

160
Q

What are the indications for tonsillectomy and adenoidectomy?

A

Upper airway obstruction caused by hypertrophy resulting in sleep–disordered breathing and complications.

161
Q

9–year–old snores and is apneic each night for 20 seconds and wakes from sleep. Poor growth and poor school performance. Mouth breathing, a hyponasal voice, 4+ tonsils without exudates. What is the diagnosis?

A

Obstructive sleep apnea.

162
Q

What is obstructive sleep apnea?

A

Prolonged, partial, upper airway obstruction. Cause heart failure, RVH, developmental delay, poor growth, death. The most common cause is adenotonsillar hypertrophy. Occurs in all ages, peak 2–5 years.

163
Q

What are the signs of obstructive sleep apnea?

A

Mouth breathing and snoring, restlessness, frequent awakenings, daytime somnolence, poor school performance. Hyponasal speech, enlarged nostrils.

164
Q

What are the laboratory abnormalities associated with obstructive sleep apnea?

A

Polycythemia, chronic respiratory acidosis with metabolic compensation, right ventricular hypertrophy.

165
Q

How is obstructive sleep apnea diagnosed?

A

Lateral soft tissue x–ray (enlarged adenoids). Polysomnography.

166
Q

What is the treatment of obstructive sleep apnea?

A

Weight loss, adenotonsillectomy, continuous positive airway pressure (CPAP), oxygen, topical nasal steroids, short–term nasal decongestants.

167
Q

What are the signs of congestive heart failure in infants?

A

Feeding difficulties, easily become fatigued, sweating while feeding, rapid respirations.

168
Q

What are the symptoms of congestive heart failure in older children?

A

Shortness of breath, dyspnea on exertion.

169
Q

What are the physical signs of congestive heart failure?

A

Tachycardia, tachypnea, poor weight gain, growth. Hepatosplenomegaly suggests right–sided heart failure. Crackles indicate pulmonary edema, LVH. Cyanosis and clubbing from hypoxia. Murmurs.

170
Q

A 4–year–old with a soft musical 2/6 murmur best heard at the left lower sternal border. What is the diagnosis?

A

Innocent murmur.

171
Q

What are innocent murmurs?

A

Innocent murmurs are caused by flow through normal heart, vessels, and valves. 30% of children 3–7 y have an innocent murmur caused by fever, infection, anxiety. Never greater than grade 2/6. Soft, vibratory, and musical at the left lower midsternum.

172
Q

What is the differential diagnosis of innocent murmurs?

A

Pulmonary flow (higher pitched; heard in the second left parasternal space with patient lying down). Venous hum (heard in the neck or anterior chest); disappears with compression of the jugular vein.

173
Q

What are the causes of congenital heart disease?

A

Usually the cause is unknown. Associated with teratogens, such as alcohol and rubella. Trisomies; Marfan, Noonan, DiGeorge syndromes.

174
Q

Which genetic syndromes are associated with ventricular septal defects?

A

Down syndrome, Edward syndrome, Patau syndrome, Apert syndrome.

175
Q

What is the Eisenmenger syndrome?

A

Occurs when an untreated left–to–right shunt becomes bidirectional or right–to–left. Characterized by cyanosis. High pulmonary blood flow causes medial hypertrophy of pulmonary vessels, irreversible, increased pulmonary vascular resistance.

176
Q

2–month–old with poor weight gain, and tachypnea. Harsh, pansystolic 3/6 murmur at the left lower sternal border, and hepatomegaly. What is the diagnosis?

A

Ventricular septal defect.

177
Q

What factor determines the amount of shunting in ventricular septal defect?

A

Shunt determined by ratio of pulmonary vascular resistance to systemic vascular resistance. As PVR falls in first few weeks of life, shunt increases. When PVR is greater than SVR, Eisenmenger syndrome develops.

178
Q

What are the clinical findings in ventricular septal defect?

A

Asymptomatic if the defect is small with normal pulmonary artery pressure; large defects cause dyspnea, feeding difficulties, poor growth, heart failure. Harsh holosystolic murmur over lower left sternal border, thrill; loud pulmonic S2.

179
Q

What is the treatment of ventricular septal defect?

A

A small muscular VSD is more likely to close in 1–2 years than a membranous defect. Medical treatment for heart failure is indicated to control failure and prevent pulmonary vascular disease.

180
Q

What are the complications of ventricular septal defect?

A

Large defects lead to heart failure, failure to thrive, endocarditis; pulmonary hypertension.

181
Q

What are the signs of atrial septal defect (ASD)?

A

Few symptoms early in life because of left–to–right shunt. Older children with large defects have exercise intolerance. Loud S1, wide fixed splitting of S2. Systolic ejection murmur along left upper sternal border caused by increased pulmonary flow.

182
Q

What are the chest x–ray findings in atrial septal defect?

A

Enlargement of right ventricle and right atria; pulmonary congestion, edema.

183
Q

What is the treatment of atrial septal defect?

A

Most defects in term infants close spontaneously; symptoms often do not appear until the third decade. Surgery or transcatheter device closure if symptomatic or 2:1 shunt.

184
Q

What is endocardial cushion defect?

A

Contiguous ASD and VSD; atrioventricular valves are abnormal. Left–to–right shunt at both atrial and ventricles; some right–to–left shunting with desaturation (intermittent cyanosis). Increased volume load on ventricles.

185
Q

What are the complications of endocardial cushion defect?

A

Heart failure, infections, minimal cyanosis, hepatomegaly, and failure to thrive.

186
Q

What are the signs of Eisenmenger physiology?

A

Increase in heart size with precordial lift. Loud Sp; widely fixed split S2. Pulmonary systolic ejection murmur, low–pitched diastolic rumble at left sternal border; mitral insufficiency (apical harsh holosystolic murmur to left axilla).

187
Q

What are the chest x–ray signs of endocardial cushion defect?

A

Significant cardiomegaly, increased pulmonary artery blood flow and edema. Trisomy 21 is associated with endocardial cushion defects.

188
Q

What are the ECG findings in endocardial cushion defect?

A

Biventricular hypertrophy, right atrial enlargement, superior QRS axis.

189
Q

What is patent ductus arteriosus?

A

Ductus arteriosus fails to close; blood flows from aorta to pulmonary artery. More common in girls by a 2:1 ratio. Associated with maternal rubella infection and premature infants.

190
Q

What is the clinical presentation of patent ductus arteriosus?

A

Heart failure, wide pulse pressure, bounding arterial pulses, and a machinery (to–and–fro) murmur.

191
Q

What are the diagnostic findings in patent ductus arteriosus?

A

Chest x–ray shows enlarged pulmonary artery, pulmonary congestion, edema and a large heart.

192
Q

What are the ECG findings in patent ductus arteriosus?

A

Left ventricular hypertrophy, then biventricular hypertrophy.

193
Q

What is the treatment for patent ductus arteriosus?

A

May close spontaneously. If a PDA persists beyond the first week of life, it is unlikely to close spontaneously. Indomethacin induces closure of PDA. Surgical closure.

194
Q

What is the presentation of pulmonic stenosis?

A

Right ventricular hypertrophy. Arterial saturation is normal. Neonate with severe pulmonary stenosis has right–to–left shunt via foramen ovale.

195
Q

Which congenital syndromes are associated with pulmonic stenosis?

A

Pulmonic stenosis is a common defect in Noonan syndrome. Pulmonic stenosis is common in Alagille syndrome (arteriohepatic dysplasia).

196
Q

What are the signs of pulmonic stenosis?

A

Ejection click after S1 in left upper sternal border; low–to–medium–pitched SEM. Worsening causes decreased sound of P2; with increasing severity, murmur becomes harsher and the peak is delayed further into systole.

197
Q

What are the ECG findings in pulmonic stenosis?

A

Right ventricular hypertrophy; tall, spiked P–waves; right atrial enlargement.

198
Q

What are the chest x–ray findings in pulmonic stenosis?

A

Dilatation of pulmonary artery; normal–to–increased right ventricle size and decreased pulmonary vascularity.

199
Q

What are the complications of pulmonary stenosis?

A

Heart failure, endocarditis, secondary subvalvular muscular and fibrous hypertrophy.

200
Q

What is the treatment of pulmonic stenosis?

A

Balloon valvuloplasty; surgery.

201
Q

What is aortic stenosis?

A

Most aortic stenoses are caused by a bicuspid aortc; usually asymptomatic. Supravalvular stenosis is sporadic, familial, or with Williams syndrome (mental retardation, elfin facies, heart disease, idiopathic hypercalcemia).

202
Q

What is the clinical presentation of critical aortic stenosis?

A

Severe aortic stenosis will present early in infancy with left ventricular failure. If significant decrease in cardiac output, the intensity of murmur at right upper sternal border may be minimal.

203
Q

What are the signs of mild to moderate aortic stenosis?

A

Usually asymptomatic with normal growth. Often discovered on physical examination. Older children will rarely: syncope, fatigue, angina, dizziness; decreased pulses, increased heart, LV apical thrust. Click at apex of left sternal border.

204
Q

What are the signs of severe aortic stenosis?

A

Decreased S1 and S2. HF. Mild cases have normal life, usually no progression. Moderate to severe stenosis causes increasing gradient, resulting in right ventricular failure (hepatomegaly, edema, exercise intolerance).

205
Q

What are the characteristics of the aortic stenosis murmur?

A

Systolic ejection murmur in the upper–right second intercostal space; louder (harsher) and longer the murmur indicate a greater degree of obstruction; radiates to neck and left midsternal border.

206
Q

What are the ECG findings in aortic stenosis?

A

Left ventricular hypertrophy and strain.

207
Q

What are the chest x–ray findings in aortic stenosis?

A

Prominent ascending aorta; valve calcification in older children; increased heart size. Echocardiogram is the best test.

208
Q

What is the treatment for aortic stenosis?

A

Balloon valvuloplasty, surgery, valve replacement.

209
Q

What is coarctation of the aorta?

A

Narrowing between transverse arch to iliac bifurcation; 90% just below origin of left subclavian artery at origin of ductus arteriosus (juxtaductal coarctation)

210
Q

What is discrete juxtaductal coarctation (adult type)?

A

Ascending aortic blood flows through narrowed segment to reach descending aorta. LV hypertrophy, HTN. Mild obstruction later. Increased BP in vessels proximal to coarctation and decreased BP, pulses below.

211
Q

What are the physical signs of coarctation of the aorta?

A

Femoral pulses absent; bounding in arms, carotids; delayed femoral pulse. Normally, leg systolic is 10 mmHg higher than arms. In coarctation, leg systolic is decreased. Pressure greater in R arm than L suggests coarctation of L subclavian.

212
Q

What are the characteristics of the murmur in coarctation of aorta?

A

Short systolic murmur along left sternal border at third–to–fourth intercostal space. The murmur radiates to the neck. Collateral circulation and rib notching.

213
Q

What is tubular hypoplasia aortic coarctation (preductal, infantile type)?

A

Severe narrowing of neck vessels extending to ductus. Right ventricular blood flows across the PDA to supply descending aorta; perfusion of the lower part of the body is dependent upon right ventricular output.

214
Q

What are the signs of tubular hypoplasia aortic coarctation?

A

Differential cyanosis (upper body pink, lower is cyanotic). Lower body hypoperfusion, acidosis, heart failure; systolic murmur along left sternal border, loud S2.

215
Q

Which genetic syndrome has a high association with coarctation of the aorta?

A

Coarctation of the aorta has a high association with Turner syndrome (70% with bicuspid aortic valve).

216
Q

In an asymptomatic child with hypertension, what disorder should be suspected?

A

Coarctation of aorta.

217
Q

What is post–coarctectomy syndrome?

A

Postoperative mesenteric arteritis associated with acute hypertension and abdominal pain, nausea, vomiting, intestinal hemorrhage, bowel necrosis, or small bowel obstruction.

218
Q

What is the treatment of post–coarctectomy syndrome?

A

Nitroprusside, esmolol, or captopril; intestinal decompression.

219
Q

What are the common cyanotic heart disease?

A

Tetralogy of Fallot. Transposition of the great vessels. Truncus arteriosus. Total anomalous pulmonary venous return. Tricuspid atresia. Pulmonic stenosis.

220
Q

What are the chest x–ray findings in coarctation of the aorta?

A

Severe coarctation causes an increased heart size and pulmonary congestion. Adult type is associated with increased size of subclavian artery. Notching of inferior border of ribs. Poststenotic dilatation of ascending aorta.

221
Q

What are the ECG findings in aortic coarctation?

A

Left ventricular hypertrophy in older children; in neonates, right ventricular hypertrophy or biventricular hypertrophy.

222
Q

What is the treatment for aortic coarctation?

A

Neonate PGE1 infusion to maintain patent ductus and adequate lower extremity blood flow; surgery after stabilization.

223
Q

5–month–old with restlessness, cyanosis, gasping. Symptoms resolve in the knee–chest position. Underweight, with a harsh holosystolic murmur and a single second heart sound. What is the diagnosis?

A

Tetralogy of Fallot.

224
Q

What are the components of tetralogy of Fallot?

A

Pulmonary stenosis and infundibular stenosis (obstruction to right ventricular outflow), VSD, overriding aorta (overrides the VSD), right ventricular hypertrophy.

225
Q

What is the pathophysiology of tetralogy of Fallot?

A

Blood shunted right–to–left across VSD with cyanosis. Severe obstruction causes ductal dependent cyanosis. Older children are dusky blue with dyspnea on exertion, clubbing. Squats increase systemic vascular resistance and decrease LR shunt.

226
Q

What are paroxysmal hypercyanotic attacks (Tet spells)?

A

Acute onset of hyperpnea and restlessness, increased cyanosis, gasping, syncope.

227
Q

What is the treatment for tetralogy of Fallot spells?

A

Place in lateral knee–chest position, oxygen, morphine, beta–blockers.

228
Q

What are cardiac signs of tetralogy of Fallot?

A

Substernal right ventricular impulse, systolic thrill along third–to–fourth intercostal space on left sternal border, loud and harsh systolic ejection murmur (upper sternal border); single S2 or a soft pulmonic component.

229
Q

What are the chest x–ray signs of tetralogy of Fallot?

A

Hypertrophied right ventricle causes the apex to be uplifted above the diaphragm causing a boot–shaped heart (coeur en sabot) plus dark lung fields because of decreased pulmonary blood flow.

230
Q

What are the ECG signs of tetralogy of Fallot?

A

Right axis deviation plus right ventricular hypertrophy.

231
Q

What complications can occur with tetralogy of Fallot before correction?

A

Cerebral thromboses, brain abscess, bacterial endocarditis, heart failure.

232
Q

What is the treatment for tetralogy of Fallot?

A

PGE1 infusion to prevent ductal closure; palliative systemic to pulmonary shunt. Corrective surgery electively at 4–12 months of age.

233
Q

What is the pathophysiology of tricuspid atresia?

A

Absence of outlet from the right atrium to the right ventricle. The entire venous return enters the left atrium via a foramen ovale or ASD; left ventricular blood enters ventricle via a VSD and is augmented by patent ductus arteriosus.

234
Q

What is the clinical presentation of tricuspid atresia?

A

Present at birth with severe cyanosis. Increased left ventricular impulse, holosystolic murmur along left sternal border, single S2.

235
Q

What are the chest x–ray signs of tricuspid atresia?

A

Decreased pulmonary circulation.

236
Q

What are the ECG signs of tricuspid atresia?

A

Left axis deviation plus left ventricular hypertrophy, echocardiogram is diagnostic.

237
Q

What is the treatment for tricuspid atresia?

A

Prostaglandin E1 to maintain patent ductus arteriosus until aortopulmonary shunt can be performed. Atrial balloon septostomy, then surgical correction.

238
Q

What is Ebstein anomaly?

A

Downward displacement of tricuspid into RV. RA dilated; tricuspid regurgitant. RV output is decreased because of RV outflow obstruction by tricuspid. Increased RA volume shunts blood through foramen ovale or ASD. Cyanosis. Lithium.

239
Q

What is the clinical presentation of Ebstein anomaly?

A

May not present until adolescence or adulthood. If severe the newborn has cyanosis, huge heart. Holosystolic murmur of tricuspid insufficiency over left chest, gallop rhythm.

240
Q

How is Ebstein anomaly diagnosed?

A

Chest x–ray shows massive heart size (right atrium enlarged); decreased pulmonary blood flow may be visible if tricuspid obstruction is severe.

241
Q

What are the ECG signs of Ebstein anomaly?

A

Tall and broad P waves, right bundle branch block, and prolonged PR interval

242
Q

What is the treatment of Ebstein anomaly?

A

Prostaglandin E1, systemic–to–pulmonary shunt, then surgery.

243
Q

What arrhythmias are associated with Ebstein anomaly?

A

Wolff–Parkinson–White syndrome and episodes of supraventricular tachycardia.

244
Q

Newborn with severe cyanosis, chest x–ray showing decreased pulmonary blood flow plus left axis deviation and left ventricular hypertrophy. What is most likely diagnosis?

A

Tricuspid atresia.

245
Q

What is transposition of the great arteries?

A

Aorta arises from RV; pulmonary artery arises from LV; dextroposition of aorta anterior and right of pulmonary artery. 2 parallel circuits; foramen ovale and PDA are needed to provide some mixture of desaturated/ oxygenated blood.

246
Q

What is the clinical presentation of transposition of the great arteries?

A

With intact septum (simple TGA), as PDA starts to close, there is development of severe cyanosis and tachypnea; S2 is single and loud; murmurs absent.

247
Q

How is transposition of the great arteries diagnosed?

A

Chest x–ray shows cardiomegaly, narrow mediastinum, and normal–to–increased pulmonary blood flow. Egg on a string appearance is caused by a narrow heart base plus absence of main segment of the pulmonary artery

248
Q

What is the treatment for transposition of the great arteries?

A

Prostaglandin keeps the ductus arteriosus patent. Balloon atrial septostomy. Arterial switch surgery in first 2 weeks.

249
Q

What is truncus arteriosus?

A

Single arterial trunk from the heart supplies all circulations. Truncus overlies a ventricular septal defect and receives blood from both ventricles.

250
Q

What is the clinical presentation of truncus arteriosus?

A

Pulmonary blood flow is increased, which causes in heart failure with minimal cyanosis. If uncorrected, Eisenmenger physiology occurs. Initially, systolic ejection murmur with a loud thrill, single S2, and minimal cyanosis.

251
Q

What is the most common cyanotic lesion in the immediate newborn period?

A

Transposition of the great arteries. More common in infants of diabetic mothers.

252
Q

What are the chest x–ray findings in transposition of the great arteries?

A

Heart enlargement with increased pulmonary blood flow.

253
Q

What is total anomalous pulmonary venous return?

A

Complete anomalous drainage of pulmonary veins into systemic venous; total mixing of blood within heart causes cyanosis. RA blood enters RV and pulmonary artery or goes to LA via foramen ovale or ASD.

254
Q

What is pulmonary insufficiency?

A

Isolated pulmonary insufficiency is rare; usually occurs with other lesions or severe pulmonary hypertension. Decrescendo diastolic murmur at upper and mid sternal border. Generally well tolerated without treatment.

255
Q

What is mitral insufficiency?

A

Usually with AV septal defects, cardiomyopathy, dilated annulus, abnormal chordae tendineae, and deformed leaflets. Left atrial and LV hypertrophy with dilatation; increased pulmonary venous pressure causes pulmonary hypertension.

256
Q

What are the signs of mitral insufficiency?

A

High–pitched, holosystolic murmur at apex respiratory infections, fatigue, and pulmonary edema/congestive heart failure.

257
Q

What are the ECG findings in mitral insufficiency?

A

Bifid P waves, left ventricular hypertrophy.

258
Q

What are the chest x–ray findings in mitral insufficiency?

A

Increased left atrial size, prominent left ventricle. Treatment is mitral valvuloplasty.

259
Q

What is mitral valve prolapse?

A

Abnormal valve cusps are usually not detected until adolescence or adulthood; girls>boys. Chest pain, palpitations, premature ventricular contractions. Apical late systolic murmur, preceded by a click. Endocarditis prophylaxis if mitral insufficiency.

260
Q

What is the pathophysiology of tricuspid insufficiency?

A

Usually associated with Ebstein anomaly. Often with right ventricular dysfunction, volume overload, or myocardial disease. Causes perinatal asphyxia in neonate.

261
Q

What valve disorder is associated with Marfan syndrome?

A

Mitral valve prolapse is a common finding in Marfan syndrome.

262
Q

7–year–old boy with fevers for 3 weeks, chills; history of bicuspid aortic valves and recent dental procedure. What is the diagnosis?

A

Infective endocarditis.

263
Q

What are the two most common causes of infective endocarditis?

A

Streptococcus viridans (alpha hemolytic) and Staphylococcus aureus. S. viridans occurs after dental procedures. Fungal endocarditis is associated with open heart surgery.

264
Q

What conditions predispose to infective endocarditis?

A

Coagulase–negative Staphylococcus is associated with intravenous catheters. Preexisting congenital and rheumatic heart disease is a risk factor for endocarditis. Most cases occur after surgical or dental.

265
Q

What is the most common cause of endocarditis in patients with underlying heart disease?

A

Strep viridans is more common in patients with underlying heart disease or after dental procedures. Staphylococcal endocarditis is more common in those without underlying heart disease.

266
Q

What is the clinical presentation of infective endocarditis?

A

Prolonged fevers, weight loss, fatigue, myalgia, arthralgia, headache, nausea, vomiting, new heart murmur. Splenomegaly, petechiae, embolic stroke, CNS abscess/hemorrhage, mycotic aneurysm (all events more with Staph). Roth spots are retinal exudates.

267
Q

What skin findings are associated with infective endocarditis?

A

Vasculitis from Ag–Ab complexes. Osler nodes: tender, pea–sized, nodules on pads of fingers and toes. Janeway lesions are painless, small, erythematous lesions on palms and soles. Splinter hemorrhages are linear lesions beneath nails.

268
Q

What are the major Duke criteria for infective endocarditis?

A

Two positive blood cultures. Evidence on echocardiogram of intracardiac or valve lesion, prosthetic regurgitant flow, abscess, partial dehiscence of prosthetic valve, or new valvular regurgitant flow.

269
Q

What are the minor Duke criteria for the diagnosis of infective endocarditis (2 major or 1 major + 3 minor or 5 minor)?

A

Predisposing conditions, fever, emboli, vascular signs, immune complex disease (glomerulonephritis, arthritis, positive rheumatoid factor, Osler node, Roth spots), positive blood culture, echocardiographic signs not meeting major.

270
Q

What are the complications of infective endocarditis?

A

Most common is heart failure from aortic or mitral lesions. Systemic or pulmonary emboli, myocardial abscess, myocarditis, valve obstruction, heart block, meningitis, osteomyelitis, arthritis, renal abscess, immune complex–glomerulonephritis.

271
Q

What is the treatment for streptococcus viridans endocarditis?

A

Penicillin G for 4 weeks, or penicillin (or ceftriaxone) plus gentamicin for 2 weeks.

272
Q

What is the treatment for enterococcal (group D) endocarditis?

A

Ampicillin plus gentamicin for 4–6 weeks. If penicillin allergic: vancomycin plus gentamicin for 4–6 weeks.

273
Q

What is the treatment for staphylococcus aureus endocarditis?

A

Nafcillin or oxacillin plus 5 days of gentamicin for 4–6 weeks. With prosthetic valve, use vancomycin plus gentamicin for 4–6 weeks.

274
Q

What is the treatment for methicillin–resistant S. aureus endocarditis?

A

Vancomycin (may add trimethoprim/sulfamethoxazole) for 4–6 weeks.

275
Q

What is the treatment of Staphylococcus epidermidis endocarditis?

A

Vancomycin for 6 weeks.

276
Q

What is the treatment for HACEK organism endocarditis?

A

Ceftriaxone (or other 3rd generation cephalosporin) for 4 weeks (6 weeks in prosthetic valves).

277
Q

What are the HACEK organisms of infective endocarditis?

A

Haemophilus spp, Actinobacillus, Actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae; slow–growing gram negative organisms of normal flora.

278
Q

What procedures require endocarditis prophylaxis?

A

Tonsillectomy, adenoidectomy, respiratory surgery; rigid bronchoscopy; prostatic surgery, cystoscopy, urethral dilatation, esophageal sclerosis/dilation, ERCP, biliary surgery, intestinal mucosa, dental procedures with bleeding.

279
Q

Which cardiac conditions require endocarditis prophylaxis?

A

Artificial heart valves. History of infective endocarditis. Unrepaired cyanotic congenital heart disease. Completely repaired congenital heart defect with prosthetic. A cardiac transplant which develops a problem in a heart valve.

280
Q

What antibiotic are recommended for endocarditis prophylaxis?

A

Oral amoxicillin, or IV ampicillin, cefazolin, or ceftriaxone. If allergic to penicillins: oral cephalexin, clindamycin, azithromycin, or clarithromycin.

281
Q

What conditions do not require endocarditis prophylaxis?

A

Isolated secundum ASD. Repaired ASD, VSD, PDA. Coronary artery bypass graft. Mitral valve prolapse without regurgitation or thickened valves; Kawasaki without valvular dysfunction. Rheumatic fever without valve dysfunction. Pacemakers, defibrillators.

282
Q

8–year–old girl with severe joint pain in elbows and wrists. Fever, sore throat 1 month ago. Swollen, painful joints and a heart murmur. Elevated erythrocyte sedimentation rate and high antistreptolysin titers. What is the diagnosis?

A

Acute rheumatic fever

283
Q

What is the cause of acute rheumatic fever?

A

Caused by group A Streptococcus infection several weeks prior. Antibiotics against Streptococcus prevent acute rheumatic fever. Immune–mediated disease caused by antigens shared between strep components and heart, brain, joint tissue.

284
Q

What are the Jones criteria for acute rheumatic fever?

A

Evidence of Streptococcus infection; 2 major or 1 major and 2 minor criteria. Major: carditis, polyarthritis, erythema marginatum, chorea, subcutaneous nodules. Minor: fever, arthralgia, elevated acute phase reactants (ESR), prolonged PR interval.

285
Q

What is the treatment for acute rheumatic fever?

A

Oral penicillin or erythromycin for 10 days; then long–term prophylaxis. Aspirin in patients with arthritis or carditis without CHF. Carditis or CHF: prednisone, aspirin, digoxin, salt restriction, diuretics. Mitral, aortic, tricuspid disease.

286
Q

What is the prevention of acute rheumatic fever?

A

Continuous antibiotic prophylaxis. If carditis, continue prophylaxis into adulthood. If carditis is not present, discontinue prophylaxis after patient is in twenty. IM benzathine penicillin G q4 weeks. If compliant: penicillin V PO BID or sulfadiazine.

287
Q

What are the causes of dilated cardiomyopathy?

A

Majority are idiopathic (familial). Nonviral infection, (hypothyroidism), metabolic (storage disease), (connective tissue), hereditary muscle or muscular dystrophies, abnormality of coronary arteries, tachyarrhythmias.

288
Q

What is the clinical presentation of dilated cardiomyopathy?

A

Tachycardia, decreased pulse pressure, cool, pale skin, decreased pulses, increased jugular venous pressure, hepatomegaly, edema, rales; cardiomegaly, mitral/tricuspid insufficiency, gallops, FTT, abdominal pain, HF; emboli; arrhythmias.

289
Q

What is the treatment for dilated cardiomyopathy?

A

Antiarrhythmic, implantable cardioverter–defibrillator, anticoagulation, beta blocker (metoprolol, carvedilol); carnitine, transplant.

290
Q

What is hypertrophic cardiomyopathy?

A

Obstructive, left–sided congenital heart disease. Decreased compliance, decreased left ventricular filling, mitral insufficiency. Autosomal dominant. Caused by hypertrophy of the interventricular septum.

291
Q

What is the presentation of hypertrophic cardiomyopathy?

A

Weakness, fatigue, dyspnea on exertion, palpitations, angina, dizziness, syncope; sudden death. Left ventricular lift, SEM at left sternal edge and apex (increased after exercise, during Valsalva, and standing).

292
Q

What are the ECG findings in cardiomyopathy?

A

Left ventricular hypertrophy, ST depression, T–wave inversion; intracardiac conduction defect. Chest x–ray shows cardiomegaly.

293
Q

What is the treatment for hypertrophic cardiomyopathy?

A

No strenuous exercise because of risk of sudden death. Digoxin and aggressive diuresis are contraindicated. Beta blockers (propranolol) and calcium channel blockers (verapamil).

294
Q

What is restrictive cardiomyopathy?

A

Decreased ventricular compliance and inadequate filling. Idiopathic or associated with sarcoidosis, scleroderma, amyloidosis or inborn errors (mucopolysaccharidoses), malignancy, radiation therapy.

295
Q

What is the clinical presentation of restrictive cardiomyopathy?

A

Dyspnea, edema, ascites, hepatomegaly, elevated jugular venous pressure, pulmonary congestion, cardiomegaly.

296
Q

What are the ECG findings in restrictive cardiomyopathy?

A

Prominent P waves; ST depression, T–wave inversion. Chest x–ray shows increase in heart size.

297
Q

What is the treatment of cardiomyopathy?

A

CHF therapy. Calcium channel blocker, antiarrhythmics, implantable cardiac defibrillator. Heart transplant.

298
Q

What disorder should be suspected in a young patient with sudden cardiac death?

A

Suspect hypertrophic cardiopathy in an athlete with sudden death.

299
Q

5 year–old with dyspnea, malaise, and fatigue; recent viral syndrome; holosystolic murmur and hepatomegaly. What is the diagnosis?

A

Myocarditis.

300
Q

What is myocarditis?

A

Inflammation, necrosis of heart. Infection most commonly by Coxsackie B, adenovirus. Diphtheria, bacterial, rickettsial (Rocky Mountain spotted fever), parasitic, fungal. Connective tissue disease, granulomatous disease, toxins, idiopathic.

301
Q

What is the clinical presentation of myocarditis?

A

Left heart failure, arrhythmias, sudden death. Fever, respiratory distress/failure, acidosis, shock, distant heart sounds, weak pulses, mitral insufficiency, gallop; hepatitis, aseptic meningitis, rash. Fever, large heart plus arrhythmia.

302
Q

What are the laboratory abnormalities in myocarditis?

A

Increased erythrocyte sedimentation rate. Increased creatinine phosphokinase isoenzymes (CK–MB). Increased lactate dehydrogenase. Positive serum viral titers or polymerase chain reaction. Cardiomegaly and pulmonary edema.

303
Q

What are the ECG findings in myocarditis?

A

Sinus tachycardia, decreased QRS voltage, and ST/T–wave abnormalities

304
Q

What is the treatment of myocarditis?

A

Treat congestive heart failure. Pericardiocentesis for pericardial tamponade. Heart transplant, intravenous immune globulin.

305
Q

What is endocardial fibroelastosis?

A

Dilated ventricular cavity in infants. White, opaque fibroelastic thickening of endocardium of left ventricle caused by severe congenital heart disease or left obstructive disease; biopsy.

306
Q

What is the clinical presentation of endocardial fibroelastosis?

A

Congestive heart failure; death within 1–6 months. Chest x–ray: cardiomegaly.

307
Q

What are the echocardiogram findings in endocardial fibroelastosis?

A

Bright–appearing endocardial surface and poorly functioning left ventricle.

308
Q

What is the treatment of endocardial fibroelastosis?

A

Treat failure; heart transplant.

309
Q

What is pericarditis?

A

Inflammation leads to accumulation of fluid in the pericardial space (serous, fibrinous, purulent, hemorrhagic).

310
Q

What are the causes of pericarditis?

A

Viruses are most common cause of pericarditis (Coxsackie B, adenovirus, influenza, echovirus). Purulent: bacterial infection with pneumonia. Systemic lupus, uremia, neoplasm: Hodgkin, leukemia, lymphosarcoma.

311
Q

What is the treatment of pericarditis?

A

Pericardial drainage, removal of adhesions, and antibiotics. Acute rheumatic fever and juvenile rheumatoid arthritis: steroids or aspirin.

312
Q

What is pulsus paradoxus?

A

A drop in blood pressure greater than 20 mm Hg during inspiration with pericarditis indicates cardiac tamponade.

313
Q

What is the clinical presentation of pericarditis?

A

Sharp, stabbing precordial pain, radiation to left shoulder and back; worse supine; relief with sitting and leaning forward (referred pain from diaphragmatic irritation). Cough, dyspnea, abdominal pain, vomiting.

314
Q

What are the signs of pericarditis?

A

Friction rub muffled heart sounds, narrow pulse pressure, tachycardia, neck vein distension, and pulsus paradoxus.

315
Q

What are the ECG signs of pericarditis?

A

Low–voltage QRS, mildly elevated ST, generalized T–wave inversion; electrical alternans (QRS with varying amplitudes).

316
Q

What are the chest x–ray signs of pericarditis?

A

Cardiomegaly with water bottle appearance; constrictive pericarditis causes a small heart. Echocardiogram is most sensitive.

317
Q

What is the most common cause of hypertension in children?

A

Renal causes are most common in children.

318
Q

At what age should blood pressure be routinely checked?

A

BP check beginning at 3 y. 4 extremities should be checked if HTN (coarctation). BP increases with age. If mild hypertension, repeat twice over next 6 weeks. If consistently >95% for age, further evaluation is necessary.

319
Q

What is the epidemiology of secondary hypertension?

A

Secondary HTN is most common in infants and younger children. Umbilical artery catheters may cause renal artery thrombosis. Causes in early childhood are renal, coarctation, endocrine, medications. In adolescence: essential.

320
Q

What are the causes of secondary hypertension in children?

A

UTI is most common cause; renal and renovascular hypertension, acute glomerulonephritis, Henoch–Schönlein with nephritis, HUS, acute tubular necrosis, renal trauma, leukemic infiltrates, mass lesions, renal artery stenosis.

321
Q

What are the screening tests for evaluation of hypertension?

A

CBC, urinalysis, urine culture, electrolytes, glucose, BUN, cr, calcium, uric acid; lipids. Echocardiogram for LVH. Renal ultrasound. Peripheral plasma renin activity is a useful screen for renovascular and renal disorders.

322
Q

What is the treatment for essential hypertension?

A

Weight control, aerobic exercise, no–added–salt diet, monitor blood pressure. A diuretic or beta blocker is the first choice in essential hypertension. If not sufficient, calcium channel blocker is added to the diuretic; ACE inhibitor for renovascular.

323
Q

What is the treatment of hypertension caused by neural crest tumors in children?

A

High catecholamine levels are treated with alpha blocker (phentolamine, phenoxybenzamine) and a beta blocker with dual action (labetalol).

USMLE Pediatrics (4 decks)

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