Truelearn Content Flashcards
Common Etiologies of Secondary Lactase Deficiency
Small intestinal epithelial damage after infection
Symptoms due to malabsorption of CHO
Secondary Lactase Deficiency Clinical Presentation
Symptoms after reintroducing dietary dairy
-abdominal pain
-bloating and flatulence
-watery diarrhea
Secondary lactase deficiency management and prognosis
Temporary dairy restriction
Typically transient and resolves in weeks to months
What is Primary Nocturnal Enuresis
Nighttime urinary incontinence beyond age 5
No hx of prolonged periods of nighttime dryness
Etiologies if Primary Nighttime Enuresis
Delayed maturation of bladder control
Decreased bladder capacity
Increased nocturnal urine output
Risk Factors of Primary Nocturnal Enuresis
Males aged 5-8
Family hx is the greatest risk factor
Evaluation of Primary Nocturnal Enuresis
Urinalysis to rule out UTI, DM, and DI
Voiding diary
Management of Primary Nocturnal Enuresis
Treat any Comorbid conditions
Restrict evening fluids
Enuresis alarm
Pharmacotherapy (desmopressin)
Etiology of Craniopharyngioma
From Remnants of Rathke’s Pouch
Bimodal age: 5-14 and 50-75
Benign and slow growing
Craniopharyngioma Clinical Manifestations
Compress optic chiasm: bitemporal hemianopsia
Compress pituitary stalk: endocrine dysfunction
-dec ADH = diabetes insipidus
-dec LH and FSH = pubertal delay
-dec TSH and GH = growth failure
Craniopharyngioma Brain Imaging
Calcified and/or cystic suprasellar mass
Craniopharyngioma Management
Surgical resection
Radiation treatment
Trisomy 18 etiology
Increased risk with maternal age
Trisomy 18 = “Edward’s”
Trisomy 18 MSK Defecects
FGR and small for gestational age
Microcephaly, micrognathia, low-set ears, prominent occiput
Clenched hands with overlapping fingers
Limited hip abduction
Rocker-bottom feet
Trisomy 18 additional physical findings
Cardiac VSD
hypotonia
Hypoventilation; inc risk of aspiration
Renal defects
Prognosis in Trisomy 18
95% of patients die in 1st year
Causes of Death: heart failure, respiratory failure
HSV Encephalitis Etiology
Primary infection with HSV or reactivation of latent infection
Typically affects Temporal Lobes
HSV Encephalitis Clinical Presentation
Altered mental status
Fever
Headache
Seizure
HSV Encephalitis CSF Findings
Lymphocytosis
Normal glucose
Increased protein
Increased RBC
HSV DNA on PCR
HSV Encephalitis Brain MRI
Temporal lobe hemorrhage/edema
HSV Encephalitis Treatment
IV Acyclovir
12 Months Language Markers
1st words
Point to desired object
Use several gestures with vocalizing
Recognize names of 2 objects
-look when objects are named
15 Months Language Markers
3 to 5 words
Points to 1 body part
mature Jargoning
18 Month language Markers
Use 10 to 25 words
Point to self
Imitate environmental sounds
24 Month Language markers
50+ words
Use 2 word sentences
50% intelligibility
Follow 2 step commands
36 Month Language markers
200+ words
Use 3 word sentences
75% Intelligibility
Use Pronouns correctly
Vit A Deficiency
Night blindness
Dry Conjunctiva/Cornea
Follicular Hyperkeratosis
Growth Retardation
Vit D Deficiency
Craniotabes
Frontal Skull Bossing
Bowlegs
Beading of ribs
Vit E Deficiency
Sensory and motor neuropathy
Ataxia
Hemolytic Anemia
Vit K Deficiency
Bleeding: Gums, Skin, Joints
Etiology of Congenital Dacryostenosis
Incomplete Canalization of Distal Nasolacrimal Duct
Clinical Presentation of Congenital Dacryostenosis
Increased Tearing and discharge
Eyelash Crusting
Clear Conjunctivae on exam
Management of Congenital Dacryostenosis
Observation and lacrimal skin massages
Probe duct if >6 months
Complications of Congenital Dacryostenosis
Dacryocystitis
Dacryostocele
Poor Prognostic Signs in Drowning
Arterial blood pH < 7.1
Delayed initiation of CPR
Prolonged CPR efforts
Submerged > 5 minutes
Complications of Drowning
ARDS
-fluid washes out surfactant
Arrhythmia
Cerebral Edema
Etiology of Diamond-Blackfan Anemia
Congenital defect of erythroid progenitor cells
apoptosis of RBC
Diamond-Blackfan Anemia Clinical Presentation
Craniofacial Abnormalities
Triphalangeal Thumbs
Macrocytic Anemia
Reticulocytopenia
Treatment of Diamond-Blackfan Anemia
Corticosteroids
RBC Transfusions
Complications of Diamond-Blackfan Anemia
Increased risk of malignancy
Etiology of Wiskott-Aldrich Syndrome
XLR defect in WAS protein Gene
-impaired cytoskeleton remodeling in WBC and platelets: Immune dysfunction
Wiskott-Aldrich Syndrome Clinical Presentation
Early in life: infants/toddlers
Eczema
Recurrent infections: Bacterial, viral, fungal
Thrombocytopenia
-Petechiae, hematemesis, hematochezia
Diagnosing Wiskott-Aldrich Syndrome
Microthrombocytopenia
-decreased platelet # and size
Confirm with genetic testing
Treatment for Wiskott-Aldrich Syndrome
Stem Cell Transplant
Causes of Osteomyelitis in Children
Staph Aureus: most common
Neonates: E. Coli and Group B Strep
Puncture wounds: Pseudomonas Aeruginosa
Sickle Cell Patients: Salmonella
Causes of Septic Arthritis in Children
Staph Aureus
Group A Strep: >3 months of age
Group B strep: < 3 months of age
Gram (-) Bacilli: < 3 months of age
Acute Presentation of Mumps
Unvaccinated patient
Acute Parotitis preceded by viral prodrome
Complications of Mumps
Acute Pancreatitis
Aseptic Meningitis
Orchitis and Infertility
Sensorineural Hearing loss
Acute Lymphoblastic Leukemia Clinical
Peak age 2-5 years
Nonspecific: fever, fatigue, wt loss
Anemia: pallor, fatigue
Thrombocytopenia: bruise, petechiae
Neutropenia: recurrent infection
Lymphadenopathy
Hepatosplenomegaly
Bone pain
Mediastinal Mass
-airway compression
-dysphagia
-SVC syndroem
Leptomeningeal spread
-Neuro S/S
Testicular enlargement
Acute Complications of Meningococcal Meningitis
Adrenal Hemorrhage
-primary adrenal insufficiency
Death
DIC
Multiorgan Failure
Shock
SIADH
Delayed Complications of Meningococcal Meningitis
Central DI
Cranial Nerve Defecits
Hearing Dysfunction of deafness
Normal Pressure Hydrocephalus
Seizure Disorders
Celiac Disease Pathophysiology
Immune-mediated inflammation of small intestine
–chronic malabsorption
Inflammation triggered by Gliadin
Celiac Disease Clinical
GI S/S: Abd pain, bloat, diarrhea
Wt loss
Iron Deficiency Anemia
Vit D Deficiency
Dermatitis Herpetiformis
Celiac Disease Diagnosis
Screen: Tissue Transglutaminase IgG
Confirm: duodenal Biopsy
-Crypt Hyperplasia
-villous atrophy
Celiac Disease Management
Gluten-free diet
Oligoarticular Juvenile Idiopathic Arthritis
age 2-4 years
Arthritis in <5 Joints
Polyarticular Juvenile Idiopathic Arthritis
Age 2-5 or 10-14 years
Arthritis in >5 Joints
Systemic Juvenile Idiopathic Arthritis
Arthritis in >1 joint for >6 weeks
Other features of Oligo/Polyarticular Juvenile Idiopathic Arthritis
Females > Males
Uveitis
Other Features of Systemic Juvenile Idiopathic Arthritis
Females = Males
Fever > 2 weeks
Evanescent Rash
Anemia
Hepatosplenomegaly
Leukocytosis
Lymphadenopahy
Inc. Inflammatory Markers
Etiology of Inhibitor Development
seen in 25% of patients with Severe Factor VIII Deficiency
Ab formation against infused Factor VIII
–leads to decreased Factor Function
Clinical Manifestations of Inhibitor Development
Increased Bleeding Frequency
Refractory Hemorrhage
Prolonged pTT with normal PT
Management of Inhibitor Development
Regular screening
Treat acute bleeds with bypass products
-recombinant activated factor VII
Etiology of Measles (Rubeola)
Airborn transmission of Rubeola Virus
Prevented by Live-Attenuated Vaccine
Symptoms 1-3 weeks after inhalation of infectious particles
Measles (Rubeola) Clinical Presentation
Prodromal: Cough, Coryza, Conjunctivitis, Koplik Spots
Fever
Maculopapular Rash
-Cephalocaudal: Starts on face centrifugal spread
-spares palmes and soles
Complications of Measles (Rubeola)
Blindness
Encephalitis
Pneumonia
-most common in infants/immunocompromised
Treatment of Measles
Supportive Care
Vit A for hospitalized patients
