STUDY GUIDE- EXAM 2 Flashcards
1
Q
anemia (3 q’s)
A
2
Q
sickle cell (2 q’s)
A
3
Q
murmurs (4 q’s)
A
4
Q
chest pain (2 q’s)
Chest pain common complaint; rarely serious
A
Most common – musculoskeletal origin
Chronic chest pain – usually psychogenic
Chest pain with cardiac cause usually consistent over time
5
Q
chest pain history?
A
Past medical/family history of sudden death, heart disease, asthma, Marfan syndrome, SCD
Past sports activities
Previous trauma/muscle strains
Characteristics of chest pain
Relation to exercise, syncope, dyspnea
OLDCARTS
6
Q
chest pain physical exam?
A
Cardiac murmur, rubs, clicks
Point tenderness of one or more costochondral joints
Irregular heart rhythm
Shortness of breath, coughing, wheezing
Rales, wheezing, tachypnea
7
Q
chest pain dx?
A
Febrile, pulmonary, cardiac condition – CXR
Exercise-induced asthma – PFT
Rhythm disturbance – Holter monitor/stress test
Signs of CHD, pericarditis, myocarditis – ECG
8
Q
chest pain differential dx?
A
Costochondritis, Tietze syndrome, idiopathic pain, precordial catch syndrome, other musculoskeletal
Esophagitis, foreign body ingestion, exercise-induced bronchospasm
9
Q
Management
chest pain?
A
Reassurance after serious causes ruled out
Refer to pediatric cardiology for
Chest pain that worsens with exercise; angina
Positive findings on examination, ECG, CXR
Concerning personal/family history
10
Q
blood pressure (2 q’s)
A
Systolic/diastolic/both >95th percentile
Take BP on three separate occasions
High-normal/prehypertensive >90th percentile
11
Q
> 95th to 99th percentile
HTN
A
stage I
12
Q
> 99th percentile
A
stage 2 HTN
13
Q
HTN
A
Increasing risk related to obesity
14
Q
Secondary hypertension usually under age 6
A
15
Q
History HTN
A
Assess whether primary or secondary
Neonatal history of prolonged mechanical ventilation, prematurity, SCA
Prior hospitalizations, trauma
Diet, activity, smoke exposure
Sleep history/sleep apnea
Medications
Chronic illnesses, history of UTI
Headache, chest pain, dyspnea, muscle weakness, palpitations
Family history of MI, stroke, HTN, others
16
Q
Physical exam HTN
A
Body habitus, overweight, metabolic syndromes
Dysmorphic features
Edema, pallor, flushing, skin lesions of tuberous sclerosis, SLE, neurofibromatosis
Upper/lower extremity central pulses
Fundi, thyroid, abdominal mass, flank bruit, visual acuity, facial palsy
Elevated BP
17
Q
DX studies HTN
A
Laboratory evaluation for underlying causes
If <10 years with secondary HTN: CBC, ESR, CRP, UA/culture, electrolytes, BUN, creatinine, plasma renin, renal nuclear scans, renal US
If renal vascular disease suspected, refer to pediatric nephrologist
Echocardiogram if cardiac involvement
18
Q
Management of BP HTN
A
BP annually all children 3 years and older
Prehypertension: two follow-up BPs
Hypertension: if overweight: treatment of obesity with lifestyle changes. Refer to nephrologist if HTN persistent
Medication management
19
Q
Complications
HTN?
A
Increased left ventricular mass, other heart changes; renal disease
Lifestyle changes should be taught
20
Q
cholesterol (2 q’s)
A
Clinical findings – does not usually present in children; screen those at risk
History – family history of premature heart disease, males, hypertension, DM, smoking, reduced HDL
Physical examination – tendon xanthomas, arcus corneae, tuberous xanthomas
Diagnostic studies – lipoprotein analysis; universal screening for all 9-11 years old
21
Q
Management
HTN?
A
Lifestyle changes – dietary, exercise; clinical dietician referral
Pharmacotherapy – in children >10 years who continue to have elevated LDL and various risk factors after 6-12 months of lifestyle changes
HMG-CoA reductase inhibitors (statins) for severe hypercholesterolemia >10 yrs. old.
Younger children refer to lipidologist.
Multiple treatment options.
Refer to lipidologist for initiation of pharmacologic therapy.
22
Q
hordelolum/chalazion (1 q)
A
23
Q
27 Chalazion
A
- Chronic, sterile inflammation of eyelid caused by lipogranuloma of meibomian glands
- Deeper in tissue than hordeolum
- Starts as a slightly reddened and swollen area to eyelid that, after a few days, the redness resolves leaving a round, flesh colored, painless mass/nodule that is slow-growing
- Differential dx:
- hordeolum, blepharitis, sebaceous cell cancer
- Management:
- warm compresses
- Refer to ophthalmologist
*
24
Q
25 Hordeolum (Stye)
A
- Infection of the sebaceous gland, eyelid(s) (external), or meibomian glands of eyelid (internal)
- S. aureus or P. aeruginosa
- Tender, edematous, erythematous furuncle at the upper/lower lid margin and may point through the skin
- Differential dx: blepharitis, chalazion, lid cellulitis, granuloma, sebaceous cell cancer
25
Management of Stye?
* Management:
* furuncle may rupture on own
* warm compresses TID-QID x 10-15 min to facilitate rupturing
* cleanse eyelids/lashes with weakened no-tear shampoo
* erythromycin ophthalmic ointment 0.5% TID-QID x 7-14d
* if recurrent, non-resolving, or enlarging hordeolum - refer to ophthalmologist
26
conjunctivitis (3 q's) -look up YouTube videos
this is also called pink eye
27
conjunctivitis "pink eye"
inflammation of the conjunctiva causes redness, swelling, drainage, very common and contagious
28
conjunctivitis what are some prevention measures?
wash hands
avoid sharing cosmetics
avoid touching face
change bedding frequently
29
newborn conjunctivitis?
opthalmia neonatorum- if the baby is exposed to chlamydia or gonorrhea
when babies are born we prophylactically administer erythromycin
30
what are some symptoms of pink eye?
redness, itching, swollen eyelids, crusting of the eyelids that can cause them to be glued shut
31
bacterial conjunctivitis has?
purulent drainage
32
treatment for bacterial conjunctivitis
ophthalmic antibiotic drops
33
How is conjunctivitis contracted?
direct contact with fingers or objects to the eyes
resp secretions or contaminated eye drops
34
What are the symptoms of conjunctivitis?
itchiness
tearing
redness
stringey discharge
swelling
35
There are three types of conjunctivitis?
viral
bacterial
allergic
& assessing discharge is important
36
What are the tests for conjunctivitis?
schemer test
immunologic tests
exam of stained conjunctival strappings
37
viral conjunctivitis may not require treatment
use of cold compresses and artificial tears to reduce discomfort
38
How do you clean Childs eye with conjunctivitis?
clean Childs eye inner canthus outward
remove crust that form with warm moist compresses
39
What is a risk factor for ROP?
Retinopathy of prematurity
excessive O2
40
visual screening (1 q)
* Red reflex (darken room)
* Visual acuity testing (started at 4 yrs old; if glasses/contacts, measure with corrective lenses)
* Color vision testing - not routinely administered
* Peripheral vision testing (checks function of CN II)
* Ocular mobility and alignment - corneal light reflex (evaluate extraocular muscles); cover/uncover test (checks alignment)
* Extraocular muscle functioning - corneal light reflex and cover tests
41
Myopia (Nearsightedness)
Distance blurred
* Objects nearby are in focus; those at a distance are blurred
* Onset is typically in elementary school age patients and progresses throughout adolescence
* Treatment requires glasses or contact lenses
* Daily use of low dose atropine 0.01% eye drops has been shown to slow myopia progression by approx. 50% - side effects include minimal pupil dilation and loss of accommodation without reduction in visual acuity
42
Hyperopia (Farsightedness
* Sees clearly both at a distance and at near because the child can focus on near objects through the process of accommodation if the hyperopia is not excessive
* Large amounts of uncorrected hyperopia can cause estropia (crossed eyes) as accommodation and convergence are closely
linked
* Typically diminishes with age and does not require glasses
43
acute otitis media (4 q)
44
otitis media effusion (2 q's)
∙ Middle ear fluid w/o s/sx AOM
∙ Decreased TM mobility
∙ Decreased sound/hearing
∙ Refer to ENT after 3 months w/o resolution in otherwise healthy child
45
What does the fluid in the ear look like? otitis media effusion?
clear amber colored or opaque
46
True or false otitis media effusion can turn into otitis media?
true
47
antibiotics are not needed for otitis media w/ effusion
because this is not an infection
48
pharyngitis (2 q's)
49
If rapid strep throat test comes back positive for pharyngitis?
start antibiotic therapy amoxicillin 50 mg/kg/day
50
If rapid strep throat culture is - for pharyngitis?
send another culture
51
If the child has no fever and upper resp infection for pharyngitis treat with
symptomatic supportive care
52
What are the sx's of pharyngitis?
Fever
tender cervical nodes
tonsillar exudate
S. progenes
- fam h/o thematic fever
53
Results for pharyngitis come back with Group A streptococcus what med would you order?
clindamycin for 10 days
54
If pharyngitis is bilateral
may need to be in the hospital for observation
55
nasal drainage (3 q's)
allergic rhinitis
sinusitis
foreign body
allergic= watery both sides
sinusitis= green/yellow both sides
foreign body= 1 side purulent- horrible smelling discharge
56
WBC differentials (look up YouTube video on it) 1 q
* Leukocytes
* Protect body from invasion by foreign organisms/distribute antibodies
* WBC < 500/mm3 – risk for fatal infection
* WBC > 30,000/mm3 – indicates massive infection or leukemia
57
* Granulocytes- smalll WBC with granules inside of them
– Neutrophils
– Eosinophils
– Basophils
neutro- fight infection
eosinophils- can contribute to infection (develops allergic reactions)
basophils- allergic & antigen response
58
Neutrophils
* Major function is phagocytosis
* Primary WBC in fighting bacterial infection
* Relative increase in number of circulating immature neutrophils (bands, etc.) = “shift to left”
59
Lymphocytes
* Originate in bone marrow; differentiate in lymphoid tissues – spleen, liver, thymus, lymph nodes, intestines
* T-cell – cell-mediated response
* B-cell – precursors of humoral response
60
Monocytes
* Relatively immature cells; migrate to tissues
61
* Agranulocytes
– Lymphocytes
– Monocytes
Lymphocytes- T cell, B cell
Monocytes- immature cells
62
* Main causes of anemia?
* excessive blood loss
* abnormalities of RBCs
* excessive blood cell destruction (hemolysis) – shortened life span
* deficient red blood cell production (ineffective hematopoiesis)
63
the #1 most preventative factor in iron deficiency anemia, B12 and folate deficiency anemias?
DIET!!
64
* Anemia
* Epidemiology?
– IDA most common
– Alpha-thalassemia – genetic
65
* Workup for anemia?
– Hct/Hgb screening
– CBC; RBC indices and morphology
– Reticulocyte count
– Peripheral smear
66
TIBC?
measures the maximum amount of iron that can be carried
* Transfuse - Hgb < 8
*
67
* Assessment of RBC Disorders
* Physical examination?
– Vital signs; growth
– Pallor, jaundice
– Petechiae
– Retinal hemorrhage
– Excessive bruising; bleeding from mucous membranes
– Lymphadenopathy
– Frontal bossing
– Joint/extremity pain
– Heart murmurs
– Hepatomegaly/splenomegaly
– Congenital anomalies
68
* Microcytic anemia
* Decreased Hgb, Hct and RBC
* Low MCV: Microcytic (small)
* RDW: increased (variation in cell sizes-anisocytosis)
* Hgb color: Hypochromic (Pale)
* Low MCHC
* Ferritin < 30 n=30-400 (men)
* TIBC- high due to low iron stores
* Reticulocyte count: normal
* Occult blood test may or may not be positive: if positive - refer to GI
69
70
* Iron Deficiency Anemia
* Iron deficiency anemia the most common anemia worldwide among: children ages 2-4, women ages 12-49 , and underdeveloped countries
* Usually from underlying cause: malabsorption of iron, and/or inadequate dietary intake
* Medications that inhibit iron absorption are:
histamine receptor 2 antagonist, sulfonamides (Bactrim)
* Most common cause of occult blood loss: GI tract from PUD, colon cancer UC, Crohn’s disease, hemorrhoids, and menorrhagia
* Poor absorption: gastric bypass surgery – (most iron is absorbed in the upper jejunum), celiac sprue, IBD such as Crohns or IBS.
71
* Iron Deficiency Anemia
* Minimum laboratory screening – Hgb
– CBC provides information about RBCs
– Ferritin is an acute phase reactant
72
* Iron Deficiency Anemia
Labs: CBC, ferritin, TIBC, reticulocyte count and PBS:
* Decreased Hgb, Hct and RBC
* Low MCV: Microcytic (small)
* RDW: increased (variation in cell sizes-anisocytosis)
* Hgb color: Hypochromic (Pale)
* Low MCHC
* Ferritin < 30
* TIBC- high due to low iron stores
* Reticulocyte count: normal
* Occult blood test may or may not be positive: f
73
* Beta- thalassemia:
– Heterozygous (thalassemia minor): mild microcytic anemia, asymptomatic, mild hemolysis, slight reticulocytosis, and splenomegaly
Treatment if needed, monitored by a hematologist
– Homozygous (Cooley’s anemia and thalassemia major): hemolytic anemia, transfusion dependant, bone deformities, hepatomegaly, splenomegaly, iron overload that leads to cardiomyopathy, DM, hypogonadism, and growth retardation
Treatment is managed by a hematologist and may include: splenectomy, transfusions of blood and iron chelation, bone marrow transplant, and hydroxyuria
74
* Thalassemia
CBC ,PBS, and hemoglobin electrophoresis reveal:
* Low MCV: Microcytic (small)
* RDW: increased or normal (variation in cell sizes-anisocytosis)
* Hgb color: Hypochromic (Pale)
* Reticulocytosis: increased reticulocytes
75
* Alpha thalassemia
Hgb electrophoresis reveals: no change in the Hgb A and F but Hgb H is absent. Ferritin levels are normal and the decrease in the Hct and Hgb count is mild
76
* Beta thalassemia
Minor- Hgb electrophoresis reveals: elevated Hgb A and sometimes F with an absent Hgb H. Ferritin levels are normal and the decrease in in Hct and Hgb count is mild.
Major- hgb electrophoresis reveals: small to absent amounts of Hgb A and a dominant Hgb F. Severe anemia is present with a low ferritin and significantly low Hct and Hgb.
77
* Sideroblastic Anemia
* Normoblasts fail to use iron for normal Hgb synthesis.
* Results in excess iron deposits within the mitochondria of the normoblast (sideroblasts)
* GI tract continues to absorb iron
* Iron toxicity occurs as the body deposits excess iron
within the organs and causes organ failure (hemochromatosis)
78
* Sideroblastic anemia
* Results from molecular defects in hemoglobin.
* Iron delivery usually normal but cellular uptake and utilization are impaired
ringed sideroblasts that are found within the bone marrow
79
* Sideroblastic Anemia dx?
* Final diagnosis is made by a bone marrow biopsy with a Prussian blue stain – refer
80
* Normocytic, normochromic anemias include
ACD, acquired aplastic anemia, sickle cell anemia, HUS, TTP and DIC
81
Hemolysis, Elevated Liver enzymes, and Low Platelet syndrome (HELLP)
82
* Macrocytic Anemia: Treatment
* Goal of treatment: correct underlying cause while addressing the anemia
* If the cause of B12 deficiency is not pernicious anemia, then oral supplementation :
– Cobalamin 1000 mcg daily until B12 levels return to normal (6-12 weeks)
* Pernicious anemia
– Vitamin B12 1000 mcg daily IM X 7 days then
weekly for 1 month, then monthly for life
* Folic acid deficiency
– Folic acid 1 mg PO daily
83
* Macrocytic Anemia: Follow up and Education
* Follow up for B12 deficiency
* Monthly CBC and vitamin B12 levels once oral therapy is initiated
* If IM therapy - CBC and B12 levels every 2 weeks
* Folic acid deficiency
* CBC and folate level every 2-3 months after oral therapy is initiated
* Potassium: monitor once therapy is initiated
* Increase dietary intake of folic acid
* Increase dietary intake of B12 by increasing fish, meat, liver, asparagus, broccoli, oatmeal, and milk
* Educate on signs and symptoms of macrocytic anemia
* Avoid irritating foods if mouth and tongue are sore
* Support if neurological damage occurs
* Guard against infection and educate on signs and
symptoms of infection
* Polycythemia
* An increase in the erythrocyte volume which increases the viscosity of the blood
* Hct > than 51% in women and 54% in men
* 2 Types
84
* Glucose-6-Phosphate Dehydrogenase Deficiency
* May cause drug-induced hemolytic anemia
* Symptoms associated with infections, exposure to oxidant metabolites of drugs
* History
– Recent infection
– Oxidant drug ingestion – ASA, sulfonamides, antimalarials, antihelmintics, naphthaquinolones, fava beans
* Physical examination
– Pallor, jaundice if chronic hemolysis
– Pallor, jaundice, lethargy, irritability headache, red/dark urine after drug ingestion
85
Hodgkin disease
* Hodgkin disease
– Malignancy of reticuloendothelial and lymphatic systems – involves B cells
– Originates in cervical lymph node
* Clinical findings
– Painless enlargement of lymph nodes
– Chronic cough
– Fever, decreased appetite, weight loss of >10%, drenching night sweats
* Lymphomas
> 75% survival rate at >20 years follow-up
86
Granulocytes
* Developing neutrophil stages: stem cells, myeloblasts, promyelocytes, myelocytes, metamyelocytes, band forms, and, finally, mature segmented neutrophils
* Process takes approximately 6 to 11 days.
* Major function of PMN leukocytes is phagocytosis of harmful particles and cells, particularly bacterial organisms
* Neutrophils are the primary WBC involved in fighting bacterial infections.
* Increase in the number of circulating immature neutrophils is referred to as a “shift to the left”.
* Indicative of an inflammatory process or the body's immunologic response to an acute bacterial infection.
* CBC Interpretation
* The phrase “shift to the right” indicates an increase in the total lymphocyte count
87
Agranulocytes - Leukocytes
Lymphocytes
* Lymphocytes (or immunocytes) comprise 25% to 35% of WBCs. Although not phagocytic, they protect the body against specific antigens.
* An important defense component.
* Primary components of the immune system
* Elevated with viral infections
88
Monocytes
* Elevated in infections and inflammation; primary function is phagocytosis of bacteria and cellular debris
89
* Effects of Iron Deficiency
– Possible cognitive defects
– Increased absorption of lead
– Anorexia with Hgb <8 g/dL
– Developmental delays/social-emotional disturbances
90
Immune thrombocytopenia purpura (1 q)
The body produces antibodies against thrombocytes and platelets
this causes purpura small bleeding spots beneath the skin
this causes low platelets
triggers- virus, cancer, meds
IgG causes this condition
91
Treatment for ITP
glucocorticoids
IVIG
platelet transfusions
92
sizing of lesions
primary and secondary skin lesions
93
atopic (powerpoint presentation)
Chronic autoimmune pruitic
affects creases and flexor surfaces
94
what is the atopic triad?
allergic rhinitis
atopic derm
asthma
increased igE
.can be allergic to egg, milk, peanuts
very signifiant family history
fillagrin gene
hardness of water
what are the protective factors?
early daycare
exposure to pets
exposure to farm animals
keratosis pilaris- chicken skin atopic sigmata
you want to avoid allergens or triggers
95
what is the dx of atopic germ?
3 or more sx's
skin crease
h/o asthma or hay fever
dry skin past year
sx's before age 2
flexural surfaces
96
neonatal derm (2-3 q)
97
acne (2)
98
cafe au lait (2)
99
impetigo (1)
100
cellulitis (1)
101
nasolacrimal duct obstruction
Dacryostenosis
* Prevents tears from flowing
* Dacryocystitis occurs when the involved duct gets inflamed/infected (usually S. aureus)
* Fairly common in newborns; membrane at birth covering duct that does not break down as soon as it should
* 96% of infants affected resolves by 12 months of age
* PE: Tearing, stickiness, mucoid discharge from inner canthus; may become purulent
* Concurrent blepharitis or conjunctivitis may occur
* With dacryocystitis there will be tenderness and swelling to lacrimal duct and tear sac, crusting/sticking of eyelids; may have fever and expression of purulent discharge
* CBC may show elevated WBC; obtain C&S if purulent discharge
102
Dacryostenosis (nasolacrimal duct obstruction)
* Differential dx: conjunctivitis, foreign body, dacryocele (distention of sac d/t blockage)
* Management:
* daily massage of lacrimal sac
* erythromycin ophthalmic ointment 0.5% TID-QID x 5-7 days
* polymixin B/trimethoprim 1 gtt TID-QID x 7-21 days
* saline gtts to nares and suction
* Complication of cellulitis may occur
* Referral to ophthalmologist if no improvement of mucopurulent drainage or recurrent infectio
103
Visual Screening: Ages/Methods
* *ALWAYS get an ocular history and inspect the eye.
104
Visual Screening
* NB - 3 months: red reflex
105
Visual Screening
* 3 - 6 months: red reflex, ability to fix and follow
106
Visual Screening: Ages/Methods
* 6 - 12 months: (and until child can perform visual acuity testing), red reflex, corneal light reflex, fix and follow with each eye, alternate occlusion
107
Visual Screening: Ages/Methods
* 3 years and older - red reflex, visual acuity, corneal light reflex, cover/uncover test, may attempt ophthalmoscopy exam
108
Indications for Ophthalmology Referral
* If RR if abnormal or asymmetric
* Any structural abnormality
* Failure to fix and follow
* Failure to adapt equally to covering each eye
* Asymmetric corneal light reflex
* Visual acuity = to or worse than 20/50 at 3 yrs old
or = to or worse than 20/40 at 5 yrs old
109
otitis externa (1)
110
epistaxis education?
1. sit up learn forward
2. pinch anterior nose
3. hold for 5-15 minutes DO NOT LOOK
4. nasal saline can help
5. humidified air at night
6. Vaseline on tip of nose
7. right nostril use left hand point nasal spray outwards
111
For a nose bleed how do you want to point the spray?
You want to point the spray lateral away from the septum!
112
otitis media clinical findings
113
otitis media complications
114
acute otitis externa swimmers ear complications
115
Transposition of the great arteries
116
Tet of fallot
117
chest pain- angina
