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5430: Ped's and Women's Health > Exam 2: Lectures > Flashcards

Exam 2: Lectures Flashcards

1
Q

-Type of allergic reaction
-Trigger/antigen exposure causes allergy cascade that results in tissue injury from inflammation and hyper-responsiveness
-Genetic, environmental, and immunologic factors are involved

A

Atopic disorders

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2
Q

-Chronic inflammatory changes in the connective tissues
-Exact patho is unknown, but believed to be autoimmune
-Clinical presentation is due to autoantibodies

A

Rheumatic autoimmune disorders

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3
Q

-Inflammation of nasal epithelium d/t release of chemical mediators from antigen-antibody reactions

A

Allergic rhinitis

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4
Q

Clinical findings:
-rhinorrhea
-nasal pruritus
-congestion
-sneezing

A

Allergic rhinitis

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5
Q

Allergic rhinitis management

A

Avoid triggers
Oral or intranasal antihistamines
Intranasal corticosteroids
Leukotriene inhibitors
Immunotherapy (allergy shots) for severe symptoms not responsive to other methods

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6
Q

-Acute and chronic skin eruption that disrupt the protective ability of the skin
-65% of patients will develop symptoms w/in the 1st year of life
-1/3 of patients will develop asthma in addition to this disorder

A

Atopic dermatitis

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7
Q

Clinical findings:
-Pruritus
-Eczematous changes in the skin
-Acute: itching, erythema, papule/vesicle/edema, generalized dryness, serous discharge and crusting
-Chronic: lichenification, excoriation, generalized dryness

A

Atopic dermatitis

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8
Q

Management of atopic dermatitis:

A

Cotton clothing
Hydrate skin (emollients, ointments)
Pharmacologic anti-itch medication
Topical low-potency corticosteroids (high-potency will dry skin further)

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9
Q

Autoimmune disease
Onset in children < 16 y/o with chronic inflammation for at least 1 synovial joint for 6 weeks
Girls > boys

A

Juvenile Rheumatoid Arthritis (JRA)

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10
Q

+Rheumatoid factor and ANA are present in what type of JRA?

A

Polyarticular

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11
Q

Oligoarticular
Polyarticular
Systemic
Enthesitis

A

4 types of JRA

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12
Q

Management of JRA

A

Refer to rheumatology and PT
NSAIDs, oral corticosteroids can help with inflammation

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13
Q

-Chronic systemic autoimmune disorder
-ANA production and multi-organ system involvement

A

Systemic lupus erythematosus (SLE)

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14
Q

Clinical findings:
-Organ involvement dependent
-Butterfly rash to face is common
-Photosensitivity
-Mouth ulcers
-Arthralgia
-low grade fever
-fatigue/malaise
-anorexia/loss of weight
-joint pain/stiffness

A

SLE

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15
Q

+ANA in 97% of children with this disorder

A

SLE

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16
Q

Management of SLE:

A

-Refer to pediatric rheumatology
-Will need pain management

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17
Q

Clinical findings:
-Myofascial pain
-Fatigue
-Trigger points on PE
-Vague and/or variable multi-organ involvement

A

Fibromyalgia syndrome

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18
Q

Diagnostic criteria:
-3 months or longer
-Hx of pain
-11-18 trigger points
-Exclusion of other disease processes

A

Fibromyalgia syndrome

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19
Q

Management of fibromyalgia syndrome:

A

PT
Therapy
NSAIDs

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20
Q

Severe persistent fatigue not relieved by sleep or rest with the presence of 4 of 8 symptoms of criteria for diagnosis

A

Chronic fatigue syndrome (CFS)

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21
Q

Management for CFS

A

Psychologic support
Exercise

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22
Q

Autoimmune inflammatory process triggered as a complication of Group A Strep
Diagnosed based on Jones criteria

A

Acute Rheumatic Fever

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23
Q

Management of acute rheumatic fever

A

Antibiotics to treat Group A Strep
Anti-inflammatory therapy for arthritis
CXR, echo, and EKG for heart monitoring
Refer to cardiology for changes in CXR, echo or EKG

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24
Q

Systematic vasculitis in kids
Dx with clinical findings
Etiology is unknown

A

Henoch-Scholein Purpura (HSP)

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25
Q

Clinical findings:
-Palpable cutaneous purpura concentrated on dependent areas of the body
-Arthritis
-Colicky abdominal pain
-Vomiting
-Hematuria
-gross or occult GIB

A

HSP

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26
Q

Management of HSP

A

-Admit if moderate GIB or renal involvement
-Follow up UA and BP for 3 months after symptom resolution
-Self-limiting for 3-4 weeks normally

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27
Q

MCV < 78 fL

A

Microcytic

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28
Q

MCV 78-98 fL

A

Normocytic

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29
Q

MCV > 98 fL

A

Macrocytic

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30
Q

MCV is the…

A

RBC size

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31
Q

MCH is the…

A

Hemoglobin weight of the RBC

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32
Q

If a reticulocyte count does not improve with treatment of the anemia, what is the concern for in regards to the RBC?

A

RBC production (concern for marrow or splenic issues)

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33
Q

Acute anemia is most common in which age group?

A

Newborns d/t blood loss at birth and shorter RBC lifespan

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34
Q

Common cause of anemia in infancy:

A

Nutritional anemia d/t rapid growth and dietary adjustments are occuring

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35
Q

Common cause of anemia in early childhood:

A

Infections

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36
Q

Common cause of anemia in adolescents:

A

Rapid growth leaving them vulnerable to nutritional anemia
Adolescent females at risk of anemia 2/2 heavy menstruation

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37
Q

How does growth affect RBCs?

A

Increased need for RBC mass

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38
Q

H/H 2 standard deviations below the reference range for a specified age group

A

Anemia

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39
Q

Where does erythropoiesis occur?

A

Spleen and liver
Declines significantly after birth

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40
Q

Where does hematopoiesis occur?

A

Bone marrow

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41
Q

Beta thalassemia is more prevalent in which populations?

A

Black and Mediterranean descent

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42
Q

Alpha thalassemia is more prevalent in which populations?

A

Black and Asian descent

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43
Q

Red cell enzyme defects (G6PD, sickle cell trait) are more prevalent in which populations?

A

Mediterranean, African, and southeast Asian

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44
Q

Besides OLDCARTS, pallor, fatigue, lethargy, dizziness, anorexia, jaundice, urine color, and FTT, what is an important aspect to assess when considering anemia in children?

A

Loss of milestones and growth

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45
Q

Focused assessment for anemia should include:

A

Skin, eyes, mouth, face, chest, hands, and abdomen

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46
Q

Differentials:
-Diamond-Blackfan anemia (congenital pure red cell aplasia)
-Transient erythroblastopenia of childhood
-Aplastic crisis (may be seen with Parvovirus B19)

A

Marrow failure
Generally develops gradually, chronic anemia

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47
Q

Differentials:
-Anemia of chronic disease in renal failure
-Chronic inflammatory diseases
-Hypothyroidism
-Severe protein malnutrition

A

Impaired erythropoietin production

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48
Q

Differentials:
-Nutritional anemia (2/2 iron, folate, or Vit B12 deficiency)
-Congenital dyserythropoietic anemia
-Sideroblastic anemia
-Pure red cell aplasia/maturational arrest

A

Defect in red cell maturation

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49
Q

Iron deficiency anemia and thalassemias are…

A

Microcytic (MCV < 78)

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50
Q

Folic acid and Vitamin B12 deficiencies are…

A

Macrocytic (MCV >98)

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51
Q

Genetic deficiency
Alpha or beta chain affected (alpha chain is not compatible with life)
Leads to premature RBC death

A

Thalassemias

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52
Q

Normal Hgb (11.5-14.5)
Low MCV (< 78)

A

Thalassemia

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53
Q

Normal Hgb
High MCV

A

Aplastic anemia

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54
Q

High Hgb (> 14.5)
Low MCV

A

IDA, HgH disease, sickle beta thalassemia

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55
Q

High Hgb
Normal MCV

A

Liver or chronic disease

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56
Q

High Hgb
High MCV (> 98)

A

Folate or Vitamin B12 deficiency

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57
Q

Do children normally have a severe reaction to COVID-19?

A

No, they’re generally asymptomatic or mild in symptoms with a 1-2 week duration of disease

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58
Q

Clinical findings:
-Persistent fever
-Hypotension
-GI symptoms
-Rash
-Myocarditis
-Labs showing increased inflammation

A

Multisystem inflammatory syndrome in children

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59
Q

If a patient presents with MIS-C what is the next step?

A

Transfer to hospital as this is a serious condition

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60
Q

Can paxlovid be given to children?

A

Yes if they are 12 years or older and have risk factors that put them at increased risk of severe disease development

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61
Q

Vaccine type:
MMR, OPV, varicella, flumist, rotavirus

A

Attenuated, weakened live virus

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62
Q

Vaccine type:
IPV, Hepatitis A

A

Killed, inactivated

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63
Q

Vaccine type:
DTap and TDap

A

Toxid, toxin produced by bacterium

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64
Q

Vaccine type:
HIB, Hep B, influenza, pertussis, pneumococcal, meningococcal, HPV

A

Subunit and conjugate

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65
Q

Diseases: hand-foot-mouth, herpangina, pleurodynia, acute hemorrhagic conjunctivitis, pericarditis, viral meningitis, pancreatitis, orchitis, neonatal sepsis
Transmission: fecal-oral and respiratory droplets
Increased prevalence in the summer and fall

A

Enteroviruses

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66
Q

Clinical findings:
Sudden onset high fever
Fever lasts 1-4 days
Loss of appetite
Sore throat
Vomiting
Diarrhea
Rash on tonsils, uvula, pharynx and soft palate

A

Herpangina

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67
Q

Clinical findings:
-Fever
-Vesicular eruption on buccal mucosa
-Maculopapular rash that moves to a vesicular rash of the hands and feet

A

Hand-foot-mouth

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68
Q

Primary infection in the liver
Highly contagious
Spread through person-to-person contact via fecal-oral, food, and water

A

Hep A virus

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69
Q

Clinical findings:
Preicteric: acute febrile illness
Jaundice phase: appears shortly after onset of symptoms

A

Hep A virus

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70
Q

What diagnostics are used for Hep A?

A

IgM and IgG for Hepatitis A

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71
Q

Management of Hep A:

A

Supportive care
Gamma globulin w/in 2 weeks of exposure (prior to symptoms and diagnosis)

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72
Q

Cause of sever liver disease
Highly contagious
Spread through mucous membranes exposed to blood or sexual secretions
Large decline in the US d/t vaccination rates

A

Hep B virus

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73
Q

You are testing your patient to rule out Hep B. They come back with a Anti-HBs positive. Do they have an active Hep B infection?

A

No, this shows proper immunity

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74
Q

When is the primary infection period for children with HSV-1?

A

Infancy to 4 years old

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75
Q

When obtaining a viral culture of a vesicle to rule out HSV-1 or HSV-2, what is the best section of the vesicle to sample?

A

The fluid if it is open and draining to determine the causative agent

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76
Q

What is the causative agent of mono?

A

EBV (Epstein Barr Virus)

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77
Q

Clinical findings:
-Fever
-Sore throat
-Lymphadenopathy
-Splenomegaly
-Hepatomegaly
-Skin rash
-Periorbital edema
-Abdominal complaints
-Fatigue
-Weakness

A

Mono

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78
Q

You have a patient come into your office with fever, sore throat, and lymphadenopathy. Strep test is negative, rapid monospot is positive. The patient is a 15 y/o F who plays basketball and wants to know when she can return to play. You tell her:

A

At least 4 weeks to prevent possible splenic rupture as mono can increase risk of splenomegaly

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79
Q

HHV-6 and HHV-7
Most show + HHV-6 titers

A

Roseola Infantum

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80
Q

Clinical findings:
-Sudden onset fever 101-103 for 3-6 days
-Lymphadenopathy
-Lethargy
-Vague GI complains
-URI symptoms
-Rash that starts after fever breaks
-Rash: diffuse, nonpruritic, maculopapular begins on trunk and spreads to extremeties, lasts 2-3 days

A

Roseola Infantum

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81
Q

What is the management for Roseola Infantum?

A

Supportive care

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82
Q

Common and highly contagious
85% decrease in infections since vaccine
Spread by droplets, contact, airborne

A

Varicella

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83
Q

Small pruritic, vesicular, red rash

A

Varicella

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84
Q

You have a young patient who comes in with a pruritic, vesicular, red rash all over. Their immunizations are up-to-date, but they are too young to have recieved their varicella vaccine. They attend day care where there has been a recent chicken pox outbreak. You diagnosis the child with chickenpox. The parent asks if they can give the child aspirin to help with the inflammation. What would you advise?

A

The parent should avoid aspirin as this can cause Reyes syndrome in children taking aspirin with varicella

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85
Q

You have an 11 y/o F who presents today with a pruritic, vesicular rash to her T6 dermatome on the L side of her back. She states she had been playing out in the woods and thought it was just poison ivy. When she itches the rash, it burns and hurts. Her IUTD, she has a PMH of chickenpox at 5 months old. She is presently going through puberty placing stress on her body. Although rare, you suspect she has shingles because:

A

Shingles is a reactivation of the latent varicella virus that she contracted at 5 months old, she is under stress that can trigger shingles activation, and the rash is vesicular on a dermatome, not crossing the midline.

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86
Q

Clinical findings:
Sudden onset high fever
Headache
Chills
Coryza
Vertigo
Sore throat
Body aches
Vomiting
Diarrhea
Anorexia
Cough

A

Flu

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87
Q

Can tamiflu be prescribed to children?

A

Yes for children 2 weeks of age or older with symptom onset in < 48 hours

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88
Q

On a newborn screening, the newborn screens positive for HIV. Who should be primarily managing their care?

A

Pediatric HIV specialist

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89
Q

You are meeting a newborn for their first post-hospital wellness visit. When obtaining a history you find that the baby is on Zidovudine daily for the next 6 weeks. You see their newborn screen is positive for HIV and mom shares she is HIV +. You understand the baby is on Zidovudine as:

A

A prophylactic measure as mom’s antibodies will continue to circulate out baby’s system over the next few months

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90
Q

What is the most contagious disease of childhood?

A

Measles

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91
Q

Cough, coryza, conjunctivitis

A

3 C’s of measles

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92
Q

Diagnostic testing for measles:

A

IgG, IgM antibodies
IgG decreases after acute phase of infection

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93
Q

Clinical findings:
-Maculopapular rash that coalesces
-Starts behind ears, travels to forehead
-Rash moves in a cephalocaudal pattern

A

Measles

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94
Q

If the child is exposed to measles and is eligible for vaccination, how long of a period do you have to get them vaccinated?

A

72 hours from exposure

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95
Q

Painful enlargement of the salivary (parotid) glands

A

Mumps

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96
Q

You just diagnosed a patient with mumps. The parent wants to know when the child can return to daycare as the parent will have to be out of work to care for the child. You advise:

A

The child can return to daycare/school after 9 days from the onset of parotid swelling

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97
Q

What are the diagnostic tests for mumps?

A

IgG, IgM antibodies
Elevated amalaise
Lymphocytosis

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98
Q

3 stages of Rubella

A

Prodrome, lymphadenopathy, rash

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99
Q

“slap cheek” rash is characteristic of…

A

Fifth’s disease/erythema infectiosum

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100
Q

How long will B19-specific IgM be present in the body after contracting parvovirus B19?

A

6-8 weeks

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101
Q

If you have a patient that comes in with an unknown tick bite and erythema migrans rash, do you need to preform any other diagnostics?

A

No, erythema migrans is diagnostic for Lyme

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102
Q

What is a key factor in tick-borne illness transmission?

A

Length of time the tick is attached/imbedded

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103
Q

Primary treatment for Lyme disease is:

A

Doxy

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104
Q

If you suspect Lyme disease, but there is in no EM rash present, what would you order?

A
  1. ELISA, if positive then,
  2. Western blot for Lyme
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105
Q

When treating for MRSA, what is a diagnostic needed prior to abx initiation?

A

Wound culture and sensitivity

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106
Q

What age is meningococcal most prevalent in children?

A

11-23 y/o

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107
Q

Does the meningitis vaccine protect against all strains of meningococcal disease?

A

No

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108
Q

You complete a PPD on a child that is 8 y/o. They come back for the reading of the PPD and they are found to have induration of 10mm. Is this a positive test?

A

No this is a negative test

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109
Q

What level of induration is present in a positive PPD for a child older then 4 y/o?

A

> 14mm

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110
Q

What is the level of induration present in a positive PPD for a child younger then 4 y/o?

A

> 10mm

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111
Q

What is fever of unknown origin (FUO) defined as?

A

Fever for most days for 3 or more weeks
No known cause after extensive workup

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112
Q

Fever without focus and fever of unknown origin require what kind of history and physical?

A

Comprehensive and detailed

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113
Q

Diagnostics to consider for fever without focus:

A

CBC, blood cultures, UA, stool culture (or stool sample with diarrhea present)

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114
Q

Diagnostics to consider for fever of unknown origin:

A

CBC with diff
ESR
Blood cultures
CSF studies
UA and culture
LFTs
EBV titer
CMV titer
ASO titer
CXR

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115
Q

UTI, pyelonephritis, URI, localized infection, JRA, and leukemia are the most common cause of what in children less then 6 y/o

A

Fever of unknown origin

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116
Q

What is the leading cause of heart disease in children?

A

Kawasaki’s disease

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117
Q

Clinical findings:
-Conjunctival hyperemia
-Erythematous rash
-Edema of the hands and feet
-Polymorphous erythematous rash
-Unilateral lymphadenopathy

A

Kawasaki’s disease

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118
Q

Characteristics:
Brachycephaly
Flat nasal bridge
Small ears
Cardiac anomalies

A

Trisomy 21

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119
Q

Characteristics:
Mental retardation
FTT
Prominent occiput
Small features

A

Trisomy 18

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120
Q

Survival rate for Trisomy 18:

A

5% survive the 1st year of life

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121
Q

Characteristics:
Mental retardation
Capillary hemangiomas
Cleft lip/palate
Deafness

A

Trisomy 13

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122
Q

Characteristics:
Broad chest
Webbed neck
Lymphedema of hands/feet
Lower hairline
Urinary tract anomalies

A

Turner’s syndrome (XO)

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123
Q

Characteristics:
Usually identified when testes fail to enlarge
Typically tall and lanky
Sterile
Learning disabilities

A

Klinefelter syndrome (XXY)

124
Q

You have a 10 y/o F who comes in for her annual well-care visit. She is c/o pain in her legs. She has grow significantly since her visit last year. Her current Tanner stage is 3, last year she was a stage 2. You know her leg pain is most likely r/t what and will last approximately how long (intermittently)?

A

Her leg pain is r/t growing from growth spurts. Her growth spurt probably started last year when she was Tanner stage 2, will peak around Tanner stage 4 and end when she reaches Tanner stage 5.

125
Q

You have an 11 y/o M who presents today for his annual well-care visit. He is presently healthy, Tanner stage 1. He is wondering why his female peers are getting taller then him and wants to know when he will start growing more. You tell him that at what stage will his growth spurt occur?

A

Tanner Stage 3

126
Q

Unilateral shortening and fibrosis of the sternocleidomastoid muscle d/t:
Intrauterine crowding
Muscle trauma during difficult delivery
Soft tissue compression leading to compartment syndrome
Congenital abnormalities of soft tissue differentiation within the SCM muscle

A

Congenital muscular torticollis

127
Q

Treatment for CMT?

A

Referral to PT for repositioning, ROM, strengthening

128
Q

If your patient has CMT at birth that is not resolved with PT by age 1, what is the next step?

A

Referral to ortho for probable surgical intervention

129
Q

Why are clavicular fractures common in infants?

A

It is the first bone to ossify and can be broken during birth, infancy, and childhood

130
Q

How do most fractures of the upper extremities occur in children?

A

Falling on an outstretched arm/hand (FOOSH)

131
Q

You have an infant with a clavicular fracture at birth due of LGA. The parents have been keeping the child’s arm immobilized by pinning the sleeve of the onsie to the body of the onsie. The child is brought into the practice 2 weeks after birth for follow up. What will you recommend in regards to motion?

A

The child can be unpinned and no longer needs to be in a sling, immobilization was only needed for the first 1-2 weeks.

132
Q

A 14 y/o M hockey player presents to the practice day 2 post-injury. He was elbowed from above and seen in the ED 2 days ago with a confirmed clavicular fracture. The ED placed him in a sling. He is wondering how long he will have to wear his sling for and when he can return to play.

A

He will need to be in the sling for 3-4 weeks with repeat x-rays to show evidence of healing. At the 4 week mark, he can start PT with gentle ROM. It could take up to 6-12 months for full callus formation and will be out for the rest of the present season.

133
Q

Skin tag or fully formed extra digit
Genetic disorder
Treated with a ligation suture for removal

A

Polydactyly

134
Q

Digits (fingers or toes) fused by skin or bone
Autosomal dominant inheritance pattern
Cosmetically fixed by plastics, preferred until older and child can help with post-op

A

Syndactyly

135
Q

Digit locks and catches when flexed/extended
Most commonly seen in the thumb
Tx: Refer to ortho for possible surgery to prevent contractures

A

Congenital trigger finger

136
Q

Abnormal curvature of the spine present at birth

A

Congenital scoliosis

137
Q

One or more vertebra don’t completely form causing a sharp angle to form in the spine that can worsen with growth

A

Hemivertebra

138
Q

Scoliosis treatment involves:

A

Referral to orthopedic surgeon
Bracing if not severe curvature

139
Q

Scoliometer is useful in diagnosing scoliosis to help with what process?

A

Determining who needs x-ray

140
Q

Disproportionate short stature
Autosomal dominant disorder
Avg height: 4 ft

A

Achondroplasia

141
Q

When charting growth for a child with achondroplasia, do you use the WHO and CDC growth charts?

A

No, achondroplasia has it’s own growth chart that has been developed

142
Q

You have a 2 y/o F with achondroplasia who is brought in today by the parent. The parent expresses concerns that the child is not walking independently and her words at not fully comprehensible. The child has 2 older siblings without achondroplasia and the parent is concerned there is something wrong with their daughter. What is your response to this parent?

A

Walking independently may be delayed until 2-3 y/o in children with achondroplasia d/t their hypotonic ligamentous laxity and larger head making if difficult for them to balance. Her language is developing, but may be more difficult to understand d/t tongue thrust. This should resolve in the next few years as she continues to grow.

143
Q

How often do you examine the hips in a child?

A

Every well-child visit from birth to 2 y/o

144
Q

Ortolani, Barlow, and Galezzi are all maneuvers for:

A

Hip displacment

145
Q

You have a newborn who has a subluxation of the L hip s/p birth. The parent is wondering if there is anything that needs to be done. You inform them that the next step is:

A

Watchful waiting, most birth subluxations will spontaneously correct in about 2 weeks

146
Q

The infant you saw 2 weeks ago is back for a follow-up. Their subluxation has not resolved. What is your next step?

A

Referral to ortho for possible Pavlik harness or spica cast

147
Q

You have a child who comes in for their 9 month well-child exam. On exam you find a positive Ortolani. What is the next step?

A

Send to ED for reduction of the hip follow by hip spica casting with referral to ortho

148
Q

You have a 13 y/o M who presents today with his mom after noting that her son has been limping a lot more recently. He is slightly overweight, Tanner Stage 2, and denies c/o pain unless he is running at lacrosse practice. On exam you a limp in gait and slightly uneven legs. You order an x-ray that shows a posteriorly displaced femur with a SH Type 1. You diagnose the child with a SCFE with what next steps?

A

Immediate immobilization and urgent referral to ortho surgery knowing that SCFE have an increased risk of AVN and needs surgical intervention asap to prevent bone collapse

149
Q

Bowlegged

A

Genu varum

150
Q

Knock kneed

A

Genu valgum

151
Q

When is it normal to see a child presenting with genu varum (bowlegging)?

A

Up to 2/3 y/o

152
Q

When is it normal to see a child presenting with genu valgum?

A

4-6 y/o (preschool age)

153
Q

Varus degree > 15
Angle does not decrease by 2nd year of life
Asymmetric
Short stature
Rapidly progressing

A

Red flags for pathologic disease causing genu varum

154
Q

You have a 3 y/o F presenting with genu varum. It is measuring at 18 degrees. The parent has no complaints and says the child is moving well independently. What is the next step?

A

Refer to orthopedics for assessment

155
Q

Older then 6/7 y/o
Tibial-femoral angle > 15 degrees
Increasing severity
Short stature
Asymmetric
Obesity

A

Red flags for pathologic causes of Genu valgum

156
Q

Your patient is coming in for their 7 y/o well-child visit. On exam you noted genum valgum is still present. The child has no complaints and mentions that they love playing soccer. You measure the tibial-femoral angle and find it to be 17. What is the next step in their treatment plan?

A

Bracing at night

157
Q

Abnormal medial rotation resulting in an in-toeing of the feet, primarily noted when walking

A

Medial tibial torsion

158
Q

Abnormal lateral rotation resulting in an out-toeing of the feet, primarily noted when walking

A

Lateral tibial torsion

159
Q

What is the treatment for tibial torsion?

A

Referral to orthopedics to help with alignment, stretching, and possible surgical intervention

160
Q

Does lateral tibial torsion spontaneously resolve or resolve with stretching?

A

No only medial does

161
Q

Complicated, multi-factorial deformity of primarily genetic origin

Components:
-Ankle joint plantar flexed
-Subtalar joint inverted
-Forefoot abducted

A

Club foot

162
Q

When are the joints most flexible for initiating correction of childhood MS deformities

A

Birth-first few days of life

163
Q

C-shaped lateral aspect of the foot
Congenital foot deformity

A

Metatarsus adductus

164
Q

How is metatarsus adductus treated?

A

Stretching of the foot, specifically overstretching laterally to “open” the C-shape 5x with each diaper change for at least 8 months
If does not resolve in 4-8 months: refer to ortho

165
Q

Congenital bone fragility disorder
Clinical findings: frequent fractures, bruising easy, deafness
High prevalence of abuse concern

A

Osteogenesis imperfecta

166
Q

Is there a cure for OI?

A

No, there is no cure and needs an interdisciplinary team approach to care

167
Q

Child lies supine with hips and knees flexed
+: knee on affected side is lower

A

Galezzi’s sign

168
Q

Idiopathic, avascular necrosis (AVN) of femoral head

A

Legg-Calve-Perthes disease

169
Q

Clinical findings:
Acute: sudden onset of groin or knee pain, pain at night w/ weight bearing or stiffness, some restriction of hip ROM
Chronic: recurring mild/aching hip pain referred to knee/thigh/groin, limp, stiffness in AM or after rest

A

Legg-Calve-Perthes disease

170
Q

PE findings:
Antalgic gait w/ leg shortening
+ Trendelenburg
Muscle spasms
Thigh atrophy
Limited hip abduction, internal rotation and extension
Pain with leg rolling
Short stature

A

Legg-Calve-Perthes disease

171
Q

You suspect your patient has Legg-Calve-Perthes disease, what is the next step in your management plan?

A

Immediate referral to orthopedics

172
Q

Salter-Harris Type:
Break the bone through growth plate, no shift of the bone
Often not visible on x-ray
Generally heals well
Treated w/ cast immobilization

A

Type 1

173
Q

Salter-Harris Type:
Break through part of the bone at the growth plate and crack through the bone shaft.
Generally heals well, may need surgical intervention
Most common type of growth plate fracture
Treated w/ cast immobilization

A

Type 2

174
Q

Salter-Harris Type:
Break through the bone at the growth plate, separates bone end from bone shaft and completely disrupts the growth plate.
May result in arrested growth
Treated with surgery

A

Type 3

175
Q

Salter-Harris Type:
Cross through portion of growth plate and break off piece of bone end
More common in older children
Treated with surgery

A

Type 4

176
Q

Salter-Harris Type:
Break through bone shaft, growth plate, and end of bone.
Commonly results in arrested growth of the bone.
Treated with surgery with internal fixation

A

Type 5

177
Q

Salter-Harris Type:
Similar to Type 5, but broken pieces are missing
Open or comminuted fracture
Requires surgery for repair and fixation with possible reconstructive surgeries

A

Type 6

178
Q

Pain in the posterior aspect of the heel
Common in athletes 5-11 y/o
Tenderness on medial and lateral compression of posterior calcaneus

A

Sever’s disease

179
Q

Inflammation of the tibial tuberosity
Common cause of knee pain in pt 10-15 y/o
Caused by repetitive microtrauma

A

Osgood-Schlatter’s disease

180
Q

Stretching of a ligament

A

Sprain

181
Q

Stretching of a muscle or a tendon

A

Strain

182
Q

PRICE

A

Protection, rest, ice, compression, elevate

183
Q

Most ankle sprains occur in which fashion?

A

Inversion of the foot

184
Q

Sprain classification:
Partial tear
Joint stable, minimal pain, swelling and ecchymosis
Slight or no functional loss
Able to bear weight with minimal pain

A

1st degree

185
Q

Sprain classification:
Incomplete tear
Moderate functional loss
Joint stable
Severe swelling > 4cm and ecchymosis

A

2nd degree

186
Q

Sprain classification:
Complete tear
Loss of ligament integrity
Unstable joint
Loss of function and motion
Unable to bear weight

A

3rd degree

187
Q

Ligament grading:
Stretching of fibers w/o significant structural damage

A

Grade 1

188
Q

Ligament grading:
Partial disruption of fibers w/ increased instability

A

Grade 2

189
Q

Ligament grading:
Complete tearing of ligament with significant instability

A

Grade 3

190
Q

Knee ligament tear:
Foot planted
Knee flexed
Changes direction applying rotational force to the knee
2nd most common knee injury

A

ACL tear

191
Q

Knee ligament tear:
Blow to anterior proximal tibia with knee flexed

A

PCL tear

192
Q

Knee ligament tear:
Valgus stress or external rotational force with legs firmly planted
Frequently football and basketball injuries
Often associated with an ACL injury
Most common knee injury

A

MCL tear

193
Q

Knee ligament tear:
Varus stress or rotational force sustained with feet planted and hyperflexed

A

LCL tear

194
Q

Excessive lateral traction applied to neck and shoulder during birth
Paralysis or weakness of muscles innervated by spinal nerves C5-8 and T1

A

Brachial plexus injury

195
Q

Clinical findings:
Unable to abduct arm from shoulder or rotate arm externally
Keeps shoulder in adduction and internal rotation, extension of the elbow and flexion of wrist and fingers
Limp wrist and hand with absent grip reflex

A

Brachial plexus injury

196
Q

What is the treatment for brachial plexus injuries?

A

Splinting for 2 weeks (minimum)
PT
Most cases spontaneously resolve

197
Q

Hallmark symptom: gradual onset of pain in the shoulder

A

Subacromial impingement

198
Q

What sport are humeral fractures commonly seen with?

A

Baseball as an overuse injury from throwing

199
Q

Most commonly dislocated joint in pediatrics
Forceful abduction and external rotation (w/ or w/o fall)

A

Glenohumeral dislocation/subluxation

200
Q

Clinical findings:
Pt holding arm in cradle-type position
Unable to actively more arm
Pain with passive ROM
Tender fullness palpated in anterior axilla

A

Glenohumeral dislocation

201
Q

Treatment of glenohumeral dislocation

A

Reduce and immobilize
Transport to ED for reduction

202
Q

Clinical findings:
Swollen, painful elbow
Obvious deformity
Limited ROM
Palpable depression over triceps
Presence of ecchymosis

A

Supracondylar fracture

203
Q

Clinical findings:
Acute medial elbow pain
Unable to continue to play sport d/t pain
Inflammation involving ulnar nerve with numbness to ring/pinky finger
Local, minor swelling
Tenderness on palpation

A

“Little Leaguer’s Elbow”

204
Q

Swollen elbow
Localized lateral tenderness
s/p FOOSH
Thurston-Holland fragment on x-ray

A

Lateral condyle fracture

205
Q

Subluxation of proximal radial head
Commonly in ages 1-4 y/o
Sudden traction on outstretched arm while pull of radius distally causes slipping of the annular ligament

A

Nursemaid’s elbow

206
Q

Can nursemaid’s elbow be reduced in the office by the PCP?

A

Yes

207
Q

Most common fracture of childhood:

A

Forearm fractures

208
Q

In children prior to adolescents, is back pain a common complaint?

A

No, this should be a red flag in younger children

209
Q

In adolescents is back pain normally muscular, neurologic, or bone related?

A

Muscular

210
Q

Unilateral pain over posterior elements of lower lumbar vertebrae during single-leg hyper-extension causing pain near L4/5

A

Stork test

211
Q

When is the stork test used?

A

Testing for spondylolysis

212
Q

What is the treatment for spondylolysis?

A

Rest, back bracing (specifically anti-lordosis extension), PT
Can return to exercise when pain-free for 2-3 months
Return to play 6 months after diagnosis

213
Q

Refusal to walk or crawl ( <3 y/o)
C/O abdominal pain and tenderness of hamstrings (>3 y/o)
Fever, irritability
Symptoms relieved with prone position

A

Discitis

214
Q

What is the treatment for discitis

A

Abx for 3-4 weeks (generally cephalosporin 4x/day)
NSAID/Tylenol for pain
Bed rest for 3 weeks

215
Q

Concussion Grade:
No LOC
Symptoms resolve in < 15 min
Difficult to recognize appropriately

A

Grade 1

216
Q

Concussion Grade:
No LOC
Symptoms persist > 15 minutes (longer then 1 hr, require medical obeservation)

A

Grade 2

217
Q

Concussion Grade:
LOC

A

Grade 3

218
Q

Racoon eyes
Blood in external ear canal (Battle’s sign)
CSF leakage in ears or nose
Cranial nerve palsies
Possible fx on xray

A

Basilar skull fracture signs

219
Q

Multiple injuries
Varied stages of healing
FTT
Retinal hemorrhage
Burns, bruises, welts, bald spots, human bite marks
Vague complaints: ab pain, sleep disturbances
Clothing inappropriate for season
Behavioral issues

A

Signs of abuse

220
Q

Female Tanner Stage 1

A

Breast: pre-pubertal
Pubic hair: pre-pubertal, no hair or villus hair only

221
Q

Female Tanner Stage 2

A

Breast: breast bud stag
Pubic hair: scant amount of downy, straight hair along the labia

222
Q

Female Tanner Stage 3

A

Breast: further enlargement of the breast and areola
Pubic hair: darker, coarser, curly hair that spreads sparsely across the central region

223
Q

Female Tanner Stage 4

A

Breast: areola and papilla form a secondary mound (“double scoop”)
Pubic hair: adult type hair covering the pubes but not extending to the medial thighs

224
Q

Female Tanner Stage 5

A

Breast: adult breast contour, projection of the papilla only
Pubic hair: adult type hair extends onto the medial thighs

225
Q

Male Tanner Stage 1

A

Genitalia: pre-pubertal
Pubic hair: pre-pubertal, no hair or villus hair only

226
Q

Male Tanner Stage 2

A

Genitalia: thinning and reddening of the scrotum, enlargement of the testes
Pubic hair: scant amount of downy, straight hair along the labia

227
Q

Male Tanner Stage 3

A

Genitalia: penis increase in length, continued enlargement of the testes
Pubic hair: darker, coarser, curly hair that spreads sparsely across the central region

228
Q

Male Tanner Stage 4

A

Genitalia: penis increases in breadth, development of the glans, continued enlargement of the testes
Pubic hair: adult type hair covering the pubs but not extending to the medial thighs

229
Q

Male Tanner Stage 5

A

Genitalia: adult male genitalia
Pubic hair: adult type hair extends onto the medial thighs

230
Q

Is constitutional growth delay a concern?

A

No, they are just “late bloomers” and will catch up

231
Q

When there is a concern for growth hormone deficiency, what is the believed causative agent and organ?

A

Deficiency in growth hormone releasing factor is the believe causative agent
The hypothalamus is the affecting organ

232
Q

Clinical findings:
Short stature
Increased subcutaneous adiposity
Hypoglycemia
Microphallus (boys)
Delayed bone age
Child-like face with a prominent forehead
High-pitched voice
Slow growth velocity

A

Growth hormone deficiency

233
Q

If you have a patient with GH < 10mg/mL after two stimulation tests of <18mg/mL on a combined arginine-GHRH stimulation test, what is the next step?

A

Refer to pediatric endocrinologist for management of GHD

234
Q

What is the most common cause of growth hormone excess?

A

Pituitary adenoma

235
Q

Pre-epiphyseal fusion GHE symptoms

A

Sudden increase in growth velocity resulting i extreme height

236
Q

Post-epiphyseal fusion GHE symptoms

A

Acromegaly, coarse facial features, protruding jaw, large hands/feet, thickened skin

237
Q

Gonadarche onset 9.5 y/o
Pubarche before 8 y/o
Thelarche before 7 y/o
Menarche before 10 y/o

A

Precocious puberty

238
Q

No breast development by 13 y/o
Menarche >5 yrs from thelarche
Menarche > 16 y/o
No testicular enlargement by 14 y/o
> 5 yrs between gonadarche and Tanner St. 5

A

Delayed puberty

239
Q

What is the most common cause of hypothyroidism in adolescents?

A

Hashimoto’s

240
Q

When is congenital hypothyroidism normally detected?

A

Newborn screening

241
Q

If a patient presents with hyperthyroidism, when will it normally appear in children?

A

11-15 y/o

242
Q

What is the most common clinical finding of hyperthyroidism in children?

A

Behavioral disturbances

243
Q

Is surgery recommended to hyperthyroid management in children?

A

No, first line treatment is anti-thyroid medications in children with surgery reserved for adult management

244
Q

When trying to differentiate between T1 and T2 diabetes, what can be drawn to help determine the underlying pathology?

A

GAD antibodies

245
Q

When educating parents on re-hydrating their child to prevent dehydration, what is an important aspect to include?

A

The use of electrolyte containing drinks such as pedialyte as using water only can cause water intoxication if they child has also lost significant electrolytes.

246
Q

Chronic inflammatory disease w/ exacerbation and remissions anywhere in the intestines

A

Crohn’s disease

247
Q

Clinical findings:
Diarrhea
Rectal bleeding
Abdominal pain
Growth failure
Malnutrition
Pubertal delay
Bone demineralization

A

Crohn’s disease

248
Q

Who manages Crohn’s disease primarily for the child?

A

Pediatric GI

249
Q

Recurring bloody diarrhea w/ acute and chronic inflammation limited to the colon and rectum with associated weight loss d/t chronic caloric insufficiency

A

Ulcerative colitis

250
Q

Clinical findings:
Fever
Weight loss w/ anorexia
Delayed growth or puberty
Arthritis/arthralgia of large joints
Diarrhea w/ or w/o frank blood and mucus
Lower ab cramping, LLQ pain, pain w/ stooling, tenderness on palpation
Oral ulcers
Skin lesions

A

UC

251
Q

Do children always have ulcers or erosions noted with UC?

A

No, this is normally a later sign and is the reason many kids are often mis-diagnosed with Crohn’s

252
Q

What dietary changes are appropriate for patient’s with UC?

A

High protein, high carbohydrate, decreased fiber
Avoid lactose (poorly tolerated)
Vitamin and iron supplements (poor absorption)

253
Q

Which organism is the biggest causative agent for acute diarrhea?

A

Rotavirus

254
Q

Clinical findings:
Anorexia
Low-grade fever
Watery, bloodless diarrhea
Vomiting
Abdominal cramping
Dehydration
Weight loss

A

Rotavirus

255
Q

When considering differentials for acute diarrhea, what are diagnostic testing used to help narrow down the differentials?

A

Stool exam (if available sample)
Stool pH
Occult test
Stool ova and parasite, WBC w/ culture
Rotavirus antigen w/ ELISA

256
Q

One or more liquid to semi-liquid stool per day for >14 days

A

Chronic diarrhea

257
Q

Besides the acute diarrhea testing, what testing would be added for chronic diarrhea to help narrow differentials?

A

Sweat chloride test
Lactose intolerance testing
UA w/ C&S

258
Q

What is the most common parasitic infection of the GI tract in the US?

A

Giardia lambia

259
Q

Mountain water source
Municipal water and food sources
Contaminated well water
Fecal-oral route of transmission
Associated: ab cramping, flatulence, watery/greasy stools
+ stool culture

A

Giardia

260
Q

Peri-rectal itching, worse at night

A

Pinworms (enterbius vermicularis)

261
Q

How do you treat pinworms?

A

Mebendazole (Vermox)

262
Q

Clinical findings:
Bloating
Flatulence
Abdominal cramping
Loose, watery diarrhea (15 min- 2 hours after consumption of the product)
Abdominal distention
Pain increased with palpation
Borborygmi

A

Lactose intolerance

263
Q

Clinical findings:
Atopic dermatitis
Urticaria
Angioedema (rare)
Rhinitis
Asthma
Anaphylaxis (rare)
Chronic diarrhea, weight loss, FTT

A

Milk allergy

264
Q

Autoimmune disorder with genetic predisposition affecting small intestine leading to flattening of the small intestinal mucosa

A

Celiac Disease

265
Q

What conditions is there a higher co-morbid prevalence of Celiac with?

A

Down Syndrome, Turner Syndrome, Type 1 Diabetes

266
Q

Is a UA diagnostic for UTI/Pyelo?

A

No, it only helps to raise or lower suspicion. Urine Culture is diagnostic

267
Q

Do you treat asymptomatic bacteriuria?

A

If there is no leukocytes on a UA, there is no treatment

268
Q

What are the antibiotics for UTI treatment?

A

Bactrim, Amoxicillin, cephalosporins, cipro (if PNC and ceph allergy)

269
Q

When do you repeat a urine culture on a patient with a UTI or pyelo?

A

In 48-72 if symptoms persist to check for abx resistance

270
Q

Regurgitation of urine from the bladder into the ureters and potentially up to the kidneys

A

Vesicoureteral reflux (VUR)

271
Q

PMH UTI, abnormal voiding pattern, unexplained febrile illness, chronic constipation, UTI symptoms are all RF for?

A

VUR

272
Q

In patients with VUR, what is the treatment management?

A

Treat underlying comorbid condition
Interval urine cultures
Prophylactic abx
Refer to Nephro

273
Q

Your patient is brought in by mom for noted red urine with voiding. You obtain a sample today and dipstick the urine. It comes back with > +1 hematuria and +1 protein. What is your next step?

A

Refer to nephro

274
Q

When would you consider referring a patient for a renal biopsy?

A

Gross hematuria

275
Q

If your patient has asymptomatic hematuria, when would you re-evaulate?

A

Every 1-2 years

276
Q

Clinical findings:
Edema (periorbital)
Low urine production
GI symptoms
Anorexia
Irritability, fatigue
Muscle wasting, malnutrition, growth failure
HTN
Chronically ill-appearing

A

Nephrotic syndrome

277
Q

Genetic disorder causing excessive excretion of protein in the urine from increased GFR

A

Nephrotic syndrome

278
Q

What diagnostic testing is indicated for nephrotic syndrome?

A

UA, urine protein, CBC, BMP, Lipid panel, C3/C4 complement, ANA, karotyping can be considered

279
Q

What is the management for nephrotic syndrome?

A

Control edema
Refer to nephrology
Hospital if severe symptoms

280
Q

Noninfectious, inflammatory response of the kidneys

A

Nephritis

281
Q

Classic form of glomerulonephritis

A

Poststreptococcal GN

282
Q

Clinical findings:
Strep skin or pharyngeal infection in past 2-3 weeks
Abrupt onset of gross hematuria
Decreased urine output
Lethargy, anorexia, N/V, chills, fever, backache
Transient HTN
Edema, circulatory congestion
Ear malformations
Flank/abdominal pain
CV angle tenderness
Rash/arthralgia

A

Nephritis/GN

283
Q

What is the management for PSGN?

A

Supportive care (normally will spontaneously remit)
Severe oliguria/HTN-> admit
Abx if positive cultures

284
Q

Does IgA nephropathy have a good outcome?

A

No, it has a poor outcome d/t the autoantibodies

285
Q

Dysfunction of the renal tubule transport capability leading to low serum CO2

A

Renal tubular acidosis

286
Q

Clinical findings:
Failure to gain weight
Polyuria/polydipsia
Muscle weakness
Irritability before/satiation after eating
Preference for liquids
Arrested growth curve after the 1st year

A

Renal tubular acidosis

287
Q

How is renal tubular acidosis treated?

A

Oral alkalizing medications to correct acid/base balance

288
Q

What is the most common GI tumor malignancy?

A

Wilms tumor

289
Q

Clinical findings:
Age 2-5 y/o
Palpable mass
Increased abdominal size
Pain with rapid growth
Hemorrhage
Possible L varicocele if spermatic vein obstructed

A

Wilm’s Tumor

290
Q

Can a child with a Wilms tumor play sports before or after treatment?

A

Yes, but they need a kidney protector and should avoid high impact sports

291
Q

Can a male child with hypospadias be circumcsized?

A

It is not recommended, they should instead by referred to pedi urology

292
Q

When should you refer a patient with cryptorchidism (undescended testes)?

A

Prior to 6 months for best outcomes with surgical intervention ideally around 9-15 months

293
Q

Is there specific treatment for a hydrocele?

A

No, it generally resolves spontaneously. If the fluid continues to fluctuate in a communicating hydrocele for > 1 yr, can refer to urology

294
Q

Clinical findings:
Swelling in the inguinal area/scrotum
Premature child, weight-lifter, obesity
Transillumination doesn’t occur
Silk glove sign

A

Inguinal hernia

295
Q

What is the management for an inguinal hernia?

A

Attempt to reduce
Refer to urology for reduction, these do not spontaneously resolve

296
Q

Are testicular masses normally malignant?

A

Yes, they are almost always malignant and require prompt referral to oncology

297
Q

If a patient has a paraphimosis that you cannot reduce, what is the next step?

A

ED immediately as this is a surgical emergency

298
Q

Your patient presents with inflammation of the glans of the penis. They are fussy and a culture collected is positive for bacteria. What is the next step?

A

Antibiotics and warm soaks for comfort

299
Q

What is the most common cause of scrotal trauma?

A

Sports

300
Q

You happen to be rotating in the ED today. You have a 16 y/o M patient come to see you for sudden onset, L sided (unilateral) scrotal pain. He is ill-appearing and anxious. On exam you find ipsilateral scrotal erythema and edema with progressive L sided swelling, redness, and warmth. When examining him, his testis are exquisitely painful and transillumination reveals a solid mass. He has no cremasteric reflex. What is your next step?

A

STAT page urology and obtain a STAT bedside US for concern of testicular torsion that is a medical emergency

301
Q

Clinical finding:
Painful scrotal swelling
+ sexual activity
Dysuria, frequency
Fever, N/V
Scrotal edema/erythema
Epididymis hard, enlarged, and tender
Cremasteric reflex normal
Possible hydrocele, urethral discharge, prostate tenderness

A

Epididymitis

302
Q

What is the common causative agent of epididymitis?

A

Gonorrhea or Trich

303
Q

What is the management for epididymitis?

A

Symptom management
Ceftriaxone and doxycycline (together)
Treat sexual partners

304
Q

“Blue dot” sign is positive in what diagnosis?

A

Torsion of the appendix testis

305
Q

Hey you, yeah you

A

GO CRUSH THIS TEST!

5430: Ped's and Women's Health (6 decks)

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