1. WBC COUNT
2. BASIC SCIENCES
2.1. BIOSTATISTICS
2.1.1. STATISTICAL SIGNIFICANCE
2.1.1.1. BASIC TERMS
2.1.1.2. CONFIDENCE INTERVAL
2.1.1.2.1. IT MEASURES HOW RELIABLE AN ESTIMATE IS
2.1.1.2.2. USED TO CALCULATE THE PROBABILITY THAT THE DIFFERENT MEANS BETWEEN 2 GROUPS IS REAL
2.1.1.3. T-TEST
2.1.1.3.1. IT REQUIRES NORMALLY DISTRIBUTED, CONTINUOUS MEASUREMENTS
2.1.1.4. CHI-SQUARED TEST
2.1.1.4.1. SIMILAR TO T-TEST, EXCEPT IT IS USED FOR CATEGORICAL MEASURES
2.1.1.4.2. ANOVA (ANALYSIS OF VARIANCE)
2.1.1.4.3. USED TO CALCULATE WHETHER OR NOT A DIFFERENCE BETWEEN TWO PERCENTAGES/PROPORTIONS (NOT MEANS) IS REAL
2.1.2. STATISTICAL DISTRIBUTIONS
2.1.2.1. CONTINUOUS PROBABILITY DISTRIBUTION, WHICH IS A FUNCTION THAT PREDICTS THE PROBABILITY THAT AN OBSERVATION WILL FALL ON A GIVEN VALUE
2.1.2.2. THERE ARE VARIOUS PATTERNS OF DISTRIBUTION
2.1.2.2.1. NORMAL DISTRIBUTION
2.1.2.2.2. SKEWED DISTRIBUTION
2.1.2.3. STATISTICAL CHARACTERISTICS
2.1.2.3.1. MEAN
2.1.2.3.2. MODE
2.1.2.3.3. MEDIAN
2.1.3. HYPOTHESES AND ERROR TYPES
2.1.4. INCIDENCE AND PREVALENCE
2.1.5. SPECIFICITY, SENSITIVITY, PPV, NPV
2.1.6. ABSOLUTE RISK REDUCTION
2.1.7. NUMBER NEEDED TO TREAT OR HARM
2.1.8. PRECISION AND ACCURACY
2.1.9. VALIDITY
2.1.10. INTERNAL VALIDITY
2.1.11. EVALUATING RISK
2.1.12. ATTRIBUTABLE RISK
2.2. BIOCHEMISTRY
2.2.1. GENETICS
2.2.1.1. CYSTIC FIBROSIS
2.2.1.1.1. AN AUTOSOMAL RECESSIVE DEFECT IN A TRANSMEMBRANE CHLORIDE CHANNEL (USUALLY A DELETION OF Phe508) RESULTS IN THICKENED MUCUS SECRETIONS, SEVERELY AFFECTING FUNCTION OF THE PANCREATIC, PULMONARY, AND REPRODUCTIVE SYSTEMS
2.2.1.1.2. MOST COMMON LETHAL GENETIC DISEASE IN WHITES
2.2.1.1.3. GENE: CFTR (A CHLORIDE CHANNEL) ON CHROMOSOME 7
2.2.1.1.4. DIAGNOSIS
2.2.1.1.5. DEFECTIVE GENE RESULTS IN:
2.3. IMMUNOLOGY
2.3.1. IMMUNE DEFICIENCIES
2.3.1.1. DIGEORGE SYNDROME (THYMIC HYPOPLASIA)
2.3.1.1.1. DIGEORGE SYNDROME RESULTS FROM FAILURE OF DEVELOPMENT OF THE 3RD AND 4TH PHARYNGEAL POUCHES, WHICH GIVE RISE TO THE THYMUS AND PARATHYROID GLANDS
2.3.1.1.2. CATCH-22 IS A MNEMONIC USED TO DESCRIBE THE FEATURES OF DIGEORGE SYNDROME:
2.3.1.1.3. THE MOST COMMON CAUSE OF DEATH IN DIGEORGE SYNDROME IS CONGENITAL HEART DISEASE
2.3.2. IMMUNOSUPPRESSANTS
2.3.2.1. TRANSPLANT REJECTION
2.3.2.1.1. HYPERACUTE REJECTION OCCURS WHEN THERE IS THE PRESENCE OF PREFORMED ANTIBODIES AGAINST THE DONOR’S HLA OR ABO ANTIGENS AT TIME OF TRANSPLANTATION, LEADING TO REJECTION OF THE TRANSPLANT WITHIN MINUTES
2.3.2.1.2. ACUTE REJECTION IS A COMBINATION OF A TYPE IV AND TYPE II HYPERSENSITIVITY REACTION
2.3.2.1.3. CHRONIC REJECTION IS CHARACTERIZED BY EPISODIC BOUTS OF REJECTION OCCURRING MONTHS TO YEARS AFTER TRANSPLANTATION
2.3.2.1.4. GRAFT VS. HOST DISEASE IS A COMMON COMPLICATION OF ALLOGENEIC BONE MARROW TRANSPLANTATION IN WHICH FUNCTIONAL IMMUNE CELLS IN THE DONOR MARROW RECOGNIZE THE RECIPIENT AS FOREIGN AND MOUNT AN IMMUNOLOGIC ATTACK AGAINST THE RECIPIENT
2.4. PATHOLOGY
2.4.1. RESPONSES TO INJURY
2.4.1.1. ACUTE INFLAMMATION IS THE INNATE IMMUNITY’S IMMEDIATE RESPONSE TO ANY INSULT CHARACTERIZED BY MOST PROMINENTLY BY NEUTROPHILS, AS WELL AS EOSINOPHILS AND ANTIBODIES LASTING FOR MINUTES TO DAYS
2.4.1.1.1. EOSINOPHILS ARE THE PREDOMINANT INFLAMMATORY CELLS IN ALLERGIC REACTIONS AND PARASITIC INFESTATIONS
2.4.1.2. THE CARDINAL SIGNS OF INFLAMMATION ARE:
2.4.1.2.1. RUBOR (REDNESS)
2.4.1.2.2. DOLOR (PAIN)
2.4.1.2.3. CALOR (HEAT)
2.4.1.2.4. TUMOR (SWELLING)
2.4.1.2.5. FUNCTION LAESA (LOSS OF FUNCTION)
2.4.1.3. PROSTAGLANDINS (PG) I2, D2, AND E2 CAUSE VASODILATION AND INCREASED VASCULAR PERMEABILITY
2.4.1.4. FLUID EXUDATION: VASCULAR PERMEABILITY INCREASES, FACILITATING EXTRAVASATION OF IMMUNE CELLS AND NUTRIENTS AND THE CARRYING AWAY OF TOXIC METABOLITES OF THE INFLAMMATORY RESPONSE, RESULTING IN NET FLUID EXUDATION
2.4.1.4.1. BEGINS WITH A BRIEF PERIOD OF ARTERIOLAR VASOCONSTRICTION FOLLOWED SHORTLY BY DILATATION OF ARTERIOLES, CAPILLARIES, AND POSTCAPILLARY VENULES
2.4.1.4.2. THE RESULTING INCREASE IN BLOOD FLOW TO THE AFFECTED AREA CLINICALLY MANIFESTS AS REDNESS AND INCREASED WARMTH
2.4.1.4.3. FLUID EXUDATION MAY ALSO BE CAUSED BY ENDOTHELIAL INJURY OR CONTRACTION OF ENDOTHELIAL CELLS IN POSTCAPILLARY VENULES, WITH WIDENING OF INTERENDOTHELIAL GAPS
2.4.1.4.4. INCREASED CAPILLARY PERMEABILITY RESULTS IN LEAKAGE OF PROTEINACEOUS FLUID CAUSING EDEMA
2.4.1.5. NEUTROPHILS ENTER TISSUE VIA THE LEUKOCYTE ACTIVATION PATHWAY AND PARTICIPATE IN PHAGOCYTOSIS, DEGRANULATION, AND INFLAMMATORY MEDIATOR RELEASE
2.4.1.6. FOLLOWING NEUTROPHILS (1-2 DAYS LATER), MACROPHAGES MANAGE THE NEXT STEP OF THE INFLAMMATORY PROCESS, WHICH CAN BE ANY OF THE FOLLOWING:
2.4.1.6.1. RESOLUTION AND HEALING
2.4.1.6.2. CONTINUED ACUTE INFLAMMATION
2.4.1.6.3. ABSCESS FORMATION
2.4.1.6.4. CHRONIC INFLAMMATION
2.4.1.7. CONTINUED ACUTE INFLAMMATION RESULTS WHEN MACROPHAGES RELEASE INTERLEUKIN (IL)-8 LEADING TO RECRUITMENT OF MORE NEUTROPHILS AND MORE PUS FORMATION
2.4.1.8. RESOLUTION AND HEALING IS ACHIEVED WHEN MACROPHAGES PRODUCE ANTI-INFLAMMATORY CYTOKINES SUCH AS TGFΒ AND IL-10
2.4.1.9. ABSCESS FORMATION IS CHARACTERIZED BY FIBRIN-LINED CAVITY FILLED WITH PUS (NEUTROPHILS, MONOCYTE/MACROPHAGES, AND LIQUIFIED CELLULAR DEBRIS)
2.4.1.10. MACROPHAGES MAY PRESENT ANTIGEN TO ACTIVATE LYMPHOCYTES (CD4+ HELPER T CELLS) LEADING TO CHRONIC INFLAMMATION
2.4.1.11. ACUTE-PHASE REACTANTS ARE FACTORS WHOSE SERUM CONCENTRATION SIGNIFICANTLY CHANGES IN RESPONSE TO INFLAMMATION
2.4.1.11.1. IN RESPONSE TO INJURY, MACROPHAGES AND OTHER INFLAMMATORY CELLS SECRETE INTERLEUKINS IL-1, IL-6 AND TNF-α AND IFN-γ AND THE LIVER RESPONDS BY SIGNIFICANTLY INCREASING OR DECREASING THE PRODUCTION OF ACUTE-PHASE REACTANTS
2.4.1.12. THE FOLLOWING ACUTE PHASE REACTANTS ARE ELEVATED IN THE SERUM IN RESPONSE TO INFLAMMATION:
2.4.1.12.1. C-REACTIVE PROTEIN
2.4.1.12.2. FERRITIN
2.4.1.12.3. FIBRINOGEN
2.4.1.12.4. HEPCIDIN
2.4.1.12.5. SERUM AMYLOID A
2.4.1.13. THE FOLLOWING ACUTE-PHASE REACTANTS ARE REDUCED IN THE SERUM IN RESPONSE TO INFLAMMATION:
2.4.1.13.1. ALBUMIN
2.4.1.13.2. TRANSFERRIN
3. FAMILIAL HYPERLIPIDEMIAS
4. HEMATOLOGIC CHANGES THAT OCCUR DURING PREGNANCY INCLUDE AN INCREASE IN:
4.1. PLASMA VOLUME
4.1.1. PREGNANCY LEADS TO A 50% INCREASE IN PLASMA VOLUME, BUT ONLY A 30% INCREASE IN RBC VOLUME, WHICH RESULTS IN DILUTIONAL ANEMIA
4.1.2. CHOLESTEROL SYNTHESIS DIORDERS
4.2. ELEVATED PLASMA AND URINE LEVELS OF LEUCINE, ISOLEUCINE, VALINE, AND ALLOISOLEUCINE, WITH DECREASED PLASMA ALANINE
4.3. RBC VOLUME
5. MITOCHONDRIAL DISORDERS
6. CARBOHYDRATE METABOLISM DISORDERS
7. INTRODUCTION OF SOLID FOODS
8. INBORN ERRORS OF METABOLISM
8.1. HOMOCYSTINEMIA/URIA
8.2. PURINE METABOLISM DISORDERS
8.3. PHENYLKETONURIA
8.4. MAPLE SYRUP URINE DISEASE
8.4.1. INHERITED DISORDER OF BRANCHED-CHAIN AMINO ACID METABOLISM IN WHICH ELEVATED LEVELS OF LEUCINE, ISOLEUCINE, VALINE, AND CORRESPONDING OXOACIDS ACCUMULATE IN THE BODY FLUIDS
8.4.2. DEFINITION
8.4.2.1. DEFICIENCY OF BRANCHED CHAIN KETOACID DEHYDROGENASE
8.4.3. SIGNS/SYMPTOMS
8.4.3.1. POOR FEEDING, VOMITING IN FIRST WEEK OF LIFE, PROCEEDING TO LETHARGY AND COMA
8.4.3.2. ALTERNATING HYPERTONICITY AND FLACCIDITY, CONVULSIONS, HYPOGLYCEMIA
8.4.3.3. NOTE THAT IF MOM HAS BEEN TAKING FENUGREEK TO BOOST MILK PRODUCTION, THIS CAN LEAD TO A SIMILAR SWEET SMELL IN BOTH MOM AND BABY
8.4.3.3.1. ODOR OF MAPLE SYRUP IN URINE, SWEAT, CERUMEN
8.4.4. DIAGNOSIS/SCREENING
8.4.4.1. URINE PRECIPITANT TEST AND NEUROIMAGING IN THE ACUTE STATE CAN SHOW CEREBRAL EDEMA
8.4.4.2. IT IS NORMALLY INCLUDED IN THE NEWBORN SCREENING FOR METABOLIC DISORDERS
8.4.5. TREATMENT
8.4.5.1. PATIENT SHOULD BE ON A LOW BRANCHED-CHAIN AMINO ACID DIET
8.4.5.2. FREQUENT SERUM LEVEL MONITORING
8.4.5.3. IN THE ACUTE STAGE INTRAVENOUS ADMINISTRATION OF AMINO ACIDS OTHER THAN BRANCHED CHAIN AMINO ACIDS
8.4.5.4. EMERGENT HEMODIALYSIS OR PERITONEAL DIALYSIS IF PATIENT IS ACIDOTIC.
8.4.5.5. LIVER TRANSPLANTATION CAN DEFINITIVELY TREAT MAPLE SYRUP URINE DISEASE
8.5. HARTNUP DISEASE
8.6. TYROSINEMIA
8.7. UREA CYCLE DEFICIENCIES
8.8. FATTY ACID OXIDATION DISORDERS
8.9. ORGANIC ACID DISORDERS
8.10. LIPODESES
8.11. MUCOPOLYSACCHARIDOSES
9. CHARACTERISTICALLY, CELIAC DISEASE MANIFESTS DURING INFANCY AND BEFORE SCHOOL AGE
9.1. IN THE CLASSIC FORM OF CHILDHOOD CELIAC DISEASE, SYMPTOMS AND SIGNS OF MALABSORPTION BECOME OBVIOUS WITHIN SOME MONTHS OF STARTING A GLUTEN-CONTAINING DIET
9.1.1. CHILDREN MAY PRESENT WITH FAILURE TO THRIVE, AND PROXIMAL MUSCLE WASTING MAY BE SEEN
9.1.1.1. GASTROINTESTINAL SYMPTOMS OF CELIAC SPRUE INCLUDE:
9.1.1.1.1. FOUL-SMELLING DIARRHEA
9.1.1.1.2. ABDOMINAL PAIN
9.1.1.1.3. WEIGHT LOSS
9.1.1.1.4. BLOATING
9.1.1.1.5. FATIGUE
9.1.1.1.6. STEATORRHEA
9.1.1.2. EXTRAINTESTINAL MANIFESTATIONS OF CELIAC SPRUE INCLUDE:
9.1.1.2.1. ANEMIA
9.1.1.2.2. NEUROLOGIC SYMPTOMS (MOTOR WEAKNESS, PARASTHESIAS)
9.1.1.2.3. DERMATITIS HERPETIFORMIS
9.1.1.2.4. HORMONAL DISORDERS (AMENORRHEA/INFERTILITY IN WOMEN, IMPOTENCE/INFERTILITY IN MEN)
10. STEP 2 CK
10.1. INTERNAL MEDICINE
10.1.1. DERMATOLOGY
10.1.1.1. STEVEN-JOHNSON SYNDROME
10.1.1.1.1. STEVENS-JOHNSON SYNDROME (SJS) IS A SEVERE FORM OF ERYTHEMA MULTIFORME INVOLVING MUCOUS MEMBRANES AND SEVERE PLAQUE FORMATION. IT IS AN IMMUNE-MEDIATED HYPERSENSITIVITY REACTION THAT LEADS TO NECROSIS AND SLOUGHING OF THE EPIDERMIS
10.1.1.1.2. STEVENS-JOHNSON SYNDROME REPRESENTS THE SAME PROCESS AS TOXIC EPIDERMAL NECROLYSIS (TEN)
10.1.1.1.3. THERE ARE 4 ETIOLOGIC CATEGORIES FOR SJS:
10.1.1.1.4. SJS PRESENTS WITH A 2-3 DAY PRODROMAL PERIOD OF FEVER AND FLU-LIKE SYMPTOMS PRIOR TO THE DEVELOPMENT OF MUCOCUTANEOUS LESIONS
10.1.1.1.5. IN A PATIENT’S FIRST DRUG-EXPOSURE RELATED CASE OF SJS, THE DRUG EXPOSURE TYPICALLY OCCURS ONE TO THREE WEEKS BEFORE THE DEVELOPMENT OF SYMPTOMS
10.1.1.1.6. THE TIME COURSE FROM PRODROME UNTIL HOSPITAL DISCHARGE RANGES BETWEEN TWO TO FOUR WEEKS
10.1.1.1.7. BLISTERING AND SWELLING OF THE ORAL CAVITY IS ALSO SEEN IN PATIENTS WITH SJS
10.1.1.1.8. THERE ARE NO SPECIFIC DIAGNOSTIC STUDIES FOR SJS, BUT A HISTORY SUGGESTIVE OF DRUG EXPOSURE/ILLNESS, POSITIVE CLINICAL SYMPTOMS, AND A SKIN BIOPSY CAN HELP CONFIRM CLINICAL SUSPICION
10.1.1.1.9. ON PHYSICAL EXAMINATION A PATIENT WITH SJS WILL TYPICALLY HAVE AN ERYTHEMATOUS RASH WHICH MAY HAVE THE APPEARANCE OF A TARGET
10.1.1.1.10. OTHER SIGNS THAT RAISE CONCERN OF SJS INCLUDE:
10.1.1.1.11. LESIONS TYPICALLY START ON THE FACE AND THORAX BEFORE SPREADING, AND SPARE THE SCALP
10.1.1.1.12. AFTER A FEW DAYS, THE SKIN RASHES PROGRESSES TO VESICLES AND BULLAE, AND THE SKIN BEGINS TO SLOUGH
10.1.1.1.13. MUCOUS MEMBRANES ARE ALMOST ALWAYS INVOLVED IN SJS, INCLUDING THE ORAL MUCOSA (INCLUDING TONGUE), CONJUNCTIVA, URETHRA, AND PULMONARY MUCOSA
10.1.1.1.14. SKIN BIOPSIES ARE FAIRLY SPECIFIC AND TYPICALLY SHOW LYMPHOCYTES WITHIN PERIVASCULAR STRUCTURES AND FULL THICKNESS EPIDERMAL DETACHMENT WITH A NORMAL IMMUNOFLUORESCENCE
10.1.1.1.15. THE MORTALITY RATE OF SJS IS ABOUT 10%
10.1.1.1.16. BECAUSE THE MOST COMMON CAUSE OF SJS IS A REACTION TO MEDICATION, THE MOST IMPORTANT FIRST STEP IN TREATMENT IS TO STOP THE OFFENDING MEDICATION
10.1.2. GASTROENTEROLOGY
10.1.2.1. CELIAC SPRUE
10.1.2.1.1. CELIAC SPRUE (I.E. GLUTEN INTOLERANCE) IS AN IMMUNE-MEDIATED DESTRUCTION OF THE MUCOSA OF THE JEJUNUM
10.1.2.1.2. PATHOGENESIS INVOLVES THE INGESTION AND BIOCHEMICAL BREAKDOWN OF GLUTEN (FOUND IN WHEAT, BARLEY, RYE), AND THE SUBSEQUENT AUTOIMMUNE INFLAMMATORY REACTION TO GLIADIN, AN ALCOHOL-SOLUBLE FRACTION OF GLUTEN
10.1.2.1.3. CELIAC SPRUE HAS A STRONG HEREDITARY COMPONENT--HLA HAPLOTYPES DQ2 AND DQ8 ARE STRONGLY LINKED TO DISEASE
10.1.2.1.4. OTHER THAN DISEASE IN A FIRST-DEGREE RELATIVE, RISK FACTORS FOR CELIAC SPRUE INCLUDE:
10.1.2.1.5. FOR SUSPECTED CELIAC DISEASE, THE BEST INITIAL TEST IS A SERUM LEVEL OF IMMUNOGLOBULIN A ANTI-TISSUE TRANSGLUTAMINASE ANTIBODY (IGA TTG)
10.1.2.1.6. OTHER USEFUL LAB TESTS INCLUDE:
10.1.2.1.7. THE GOLD STANDARD IN DIAGNOSING CELIAC SPRUE IS A DUODENAL BIOPSY, WHICH SHOWS:
10.1.2.1.8. RADIOGRAPHIC STUDIES MAY BE USEFUL IN UNTREATED CELIAC SPRUE
10.1.2.1.9. THE PRIMARY TREATMENT OF CELIAC SPRUE IS THE AVOIDANCE OF GLUTEN-CONTAINING PRODUCTS, SUCH AS WHEAT, BARLEY AND RYE
10.1.2.1.10. CELIAC SPRUE MAY RESULT IN THE FOLLOWING LONG TERM COMPLICATIONS:
10.1.2.1.11. TROPICAL SPRUE
10.1.2.2. HEPATIC ENCEPHALOPATHY
10.1.2.2.1. IT OCCURS WHEN AMMONIA CLEARANCE IS COMPROMISED (DUE TO CHRONIC LIVER DYSFUNCTION) AND CONSEQUENTLY BUILDS UP AND CROSSES INTO THE CNS
10.1.2.2.2. PATIENTS PRESENT WITH
10.1.2.2.3. DIAGNOSIS IS BASED ON SERUM AMMONIA LEVELS, AND EVALUATING LIVER FUNCTION VIA THE FOLLOWING:
10.1.2.2.4. TREATMENT IS AIMED AT AMMONIA REDUCTION, WHICH CAN BE ACHIEVED THROUGH:
10.1.3. PULMONOLOGY
10.1.3.1. CYSTIC FIBROSIS
10.1.3.1.1. CYSTIC FIBROSIS (CF) IS AN AUTOSOMAL RECESSIVE INHERITED DISEASE CAUSED BY A MUTATION IN THE GENE CODING FOR A COMPLEX CHLORIDE CHANNEL
10.1.3.1.2. CF IS CAUSED BY MUTATIONS IN THE GENE THAT CODES FOR THE CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) PROTEIN
10.1.3.1.3. CF IS THE MOST COMMON LIFE-SHORTENING AUTOSOMAL RECESSIVE DISEASE IN CAUCASIANS, AND OCCURS ONCE IN EVERY 2000 TO 3000 LIVE BIRTHS
10.1.3.1.4. SYMPTOMS OF CYSTIC FIBROSIS USUALLY BEGIN TO PRESENT IN EARLY CHILDHOOD AND COMMONLY INCLUDE MECONIUM ILEUS, RESPIRATORY SYMPTOMS, AND FAILURE TO THRIVE
10.1.3.1.5. THE MAJORITY OF CYSTIC FIBROSIS CASES IN THE UNITED STATES ARE NOW DETECTED THROUGH NEWBORN SCREENING
10.1.3.1.6. IN ADULTS AND OLDER CHILDREN, TWO CRITERIA MUST BE MET FOR THE DIAGNOSIS OF CF:
10.1.3.1.7. FINDINGS CONSISTENT WITH CYSTIC FIBROSIS ON PHYSICAL EXAM INCLUDE WHEEZING, INCREASED ANTEROPOSTERIOR DIAMETER OF THE THORAX, DIGITAL CLUBBING, AND POOR WEIGHT GAIN/FAILURE TO THRIVE
10.1.3.1.8. WHILE CHEST X-RAY IS NOT USED FOR DIAGNOSIS, THE CHEST X-RAYS OF CYSTIC FIBROSIS PATIENTS MAY SHOW HYPERINFLATION, BRONCHIECTASIS, CYST FORMATION, AND FLATTENING OF THE DIAPHRAGMS
10.1.3.1.9. THE COMPLICATIONS OF CYSTIC FIBROSIS ARE MANY AND VARIED
10.1.3.1.10. TREATMENT OF CF VARIES BASED ON THE SPECIFIC MUTATION AND SEVERITY OF DISEASE, BUT TYPICALLY INCLUDES:
10.1.3.1.11. CYSTIC FIBROSIS LUNG DISEASE EXACERBATIONS ARE TYPICALLY TREATED WITH AGGRESSIVE CHEST PHYSIOTHERAPY AND ADDITIONAL ANTIBIOTICS
10.2. OBSTETRICS
10.2.1. A HEALTHY PREGNANCY
10.2.1.1. PHYSIOLOGIC CHANGES OF PREGNANCY
10.2.1.1.1. CARDIOVASCULAR CHANGES THAT OCCUR DURING PREGNANCY INCLUDE AN INCREASE IN CARDIAC OUTPUT AND A DECREASE IN BLOOD PRESSURE, BOTH OF WHICH IMPROVE UTEROPLACENTAL PERFUSION
10.2.1.1.2. RESPIRATORY
10.2.1.1.3. RENAL CHANGES THAT OCCUR DURING PREGNANCY INCLUDE AN INCREASE IN RENAL BLOOD FLOW, INCREASED RENAL SIZE, AND URETERAL DILATION
10.2.1.1.4. ENDOCRINE
10.2.1.1.5. HEMATOLOGY
10.2.1.1.6. GASTROINTESTINAL CHANGES THAT OCCUR DURING PREGNANCY INCLUDE DELAYED STOMACH EMPTYING AND A DECREASE IN LOWER ESOPHAGEAL SPHINCTER TONE
10.2.1.1.7. LOW RISK ACTIVITIES THAT CAN CONTINUE DURING PREGNANCY INCLUDE:
10.3. PEDIATRICS
10.3.1. HEALTH SUPERVISION
10.3.1.1. OVERVIEW OF IMMUNIZATIONS
10.3.1.1.1. THERE ARE TWO MAIN TYPES OF VACCINES: LIVE ATTENUATED VACCINES AND INACTIVATED VACCINES
10.3.1.1.2. THE CENTER FOR DISEASE CONTROL (CDC) DISTRIBUTES AN ANNUAL IMMUNIZATION SCHEDULE FOR CHILDREN AND ADOLESCENTS, AS WELL AS A CATCH-UP SCHEDULE
10.3.1.1.3. IN GENERAL, A VACCINE IS CONTRAINDICATED IF AN ANAPHYLACTIC REACTION TO THAT VACCINE IS EXPERIENCED AND SHOULD BE DISCONTINUED
10.3.2. NEONATOLOGY
10.3.2.1. NEWBORN EXAM - SKIN
10.3.2.2. NEWBORN EXAM - CRANIOFACIAL
10.3.2.3. NEWBORN EXAM - NECK, CHEST, ABDOMINAL, GENITAL, EXTREMITIES
10.3.3. NEONATOLOGY (NICU)
10.3.3.1. NEONATAL RESPIRATORY DISTRESS SYNDROME (NRDS)
10.3.4. NORMAL GROWTH AND DEVELOPMENT
10.3.4.1. NEWBORN GROWTH RATE
10.3.4.2. NEWBORN CALORIC REQUIREMENT
10.3.4.3. BREAST FEEDING VS BREAST MILK JAUNDICE
10.3.4.3.1. BREAST FEEDING JAUNDICE ALSO KNOWN AS “NOT ENOUGH MILK JAUNDICE” IS AN ABNORMAL UNCONJUGATED HYPERBILIRUBINEMIA DURING THE FIRST WEEK OF LIFE RESULTING FROM DECREASED ENTERAL INTAKE AND INCREASED ENTEROHEPATIC CIRCULATION OF BILIRUBIN. THERE IS NO ASSOCIATED INCREASE IN BILIRUBIN PRODUCTION
10.3.4.3.2. BREAST MILK JAUNDICE IS NORMAL EXTENSION OF PHYSIOLOGIC JAUNDICE OF THE NEWBORN, UNCONJUGATED HYPERBILIRUBINEMIA IN THE FIRST WEEK OF LIFE. IT BEGINS AFTER THE FIFTH DAY OF LIFE AND CONTINUES FOR SEVERAL WEEKS
10.3.4.3.3. TAKE HOME POINT:
10.3.4.4. FORMULA TYPES
10.3.4.5. GROWTH CHARTS
10.3.4.6. INTRAUTERINE FACTORS FOR GROWTH
10.3.4.7. TEETH
10.3.4.8. APPROACH TO A CHILD WITH MICROCEPHALY
10.3.4.9. FAILURE TO THRIVE
10.3.4.10. DEVELOPMENTAL MILESTONES: 1 MONTH
10.3.4.11. DEVELOPMENTAL MILESTONES: 2 MONTHS
10.3.4.12. DEVELOPMENTAL MILESTONES: 4 MONTHS
10.3.4.13. DEVELOPMENTAL MILESTONES: 6 MONTHS
10.3.4.14. DEVELOPMENTAL MILESTONES: 9 MONTHS
10.3.4.15. DEVELOPMENTAL MILESTONES: 12 MONTHS
10.3.4.16. DEVELOPMENTAL MILESTONES: 2 YEARS
10.3.4.17. DEVELOPMENTAL MILESTONES: 3 YEARS
10.3.4.18. DEVELOPMENTAL MILESTONES: 4 YEARS
10.3.4.19. DEVELOPMENTAL MILESTONES: 5 YEARS
10.3.4.20. PRIMITIVE REFLEXES
10.3.4.21. DEVELOPMENTAL DELAY
10.3.4.22. LEARNING DISABILITIES
10.3.4.23. SLEEP
10.3.4.24. FLUID MANAGEMENT OF THE PEDIATRIC PATIENT
10.3.4.25. BREAST FEEDING
10.3.4.25.1. THE AMERICAN ACADEMY OF PEDIATRICS (AAP) AND WORLD HEALTH ORGANIZATION (WHO) STRONGLY ADVOCATE BREASTFEEDING AS THE PREFERRED FEEDING FOR ALL INFANTS AND SHOULD BE INITIATED SOON AFTER BIRTH
10.3.4.25.2. STAGES OF LACTOGENESIS
10.3.4.25.3. BENEFITS FOR THE INFANT
10.3.4.25.4. BENEFITS FOR THE MOTHER
10.3.4.25.5. COMPLICATIONS
10.3.4.25.6. CONTRAINDICATIONS
10.3.4.25.7. POSSIBLE VITAMIN DEFICIENCIES IN BREAST FED INFANTS REQUIRES THAT THESE INFANTS RECEIVE:
10.3.4.26. APPROACH TO A CHILD WITH MACROCEPHALY
10.3.4.27. DEVELOPMENTAL MILESTONES: 18 MONTHS
10.3.5. PEDIATRIC CARDIOLOGY
10.3.5.1. TRANSPOSITION OF THE GREAT VESSELS
10.3.5.2. ATRIAL SEPTAL DEFECT (ASD)
10.3.5.3. AORTIC COARCTATION
10.3.5.4. PATENT DUCTUS ARTERIOSUS
10.3.5.5. TETRALOGY OF FALLOT
10.3.5.6. VENTRICULAR SEPTAL DEFECT (VSD)
10.3.5.7. HYPOPLASTIC LEFT HEART SYNDROME
10.3.5.8. EBSTEIN'S ANOMALY
10.3.5.9. TRUNCUS ARTERIOSUS
10.3.5.10. TOTAL ANOMALOUS PULMONARY VENOUS RETURN
10.3.5.11. TRICUSPID ATRESIA
10.3.5.12. PULMONARY ATRESIA
10.3.5.13. PEDIATRIC AORTIC STENOSIS
10.3.6. PEDIATRIC DERMATOLOGY
10.3.6.1. STEVENS-JOHNSON SYNDROME/TOXIC EPIDERMAL NECROLYSIS
10.3.7. PEDIATRIC ENDOCRINOLOGY
10.3.7.1. CONGENITAL HYPOTHYROIDISM (CRETINISM)
10.3.7.2. PRECOCIOUS PUBERTY
10.3.7.3. MCCUNE ALBRIGHT SYNDROME
10.3.8. PEDIATRIC GASTROENTEROLOGY
10.3.8.1. ESOPHAGEAL ATRESIA
10.3.8.2. ESOPHAGEAL FOREIGN BODY
10.3.8.3. PEPTIC ULCER
10.3.8.4. PYLORIC STENOSIS
10.3.8.5. DUODENAL ATRESIA
10.3.8.6. INTUSSUSCEPTION
10.3.8.7. MECKEL'S DIVERTICULUM
10.3.8.8. CONSTIPATION
10.3.8.9. HIRSCHSPRUNG'S MEGACOLON
10.3.8.10. IMPERFORATE ANUS
10.3.8.11. GILBERT SYNDROME
10.3.8.12. CRIGLER-NAJJAR SYNDROME
10.3.8.13. ALAGILLE SYNDROME
10.3.8.14. ZELLWEGER SYNDROME
10.3.8.15. REYE SYNDROME
10.3.8.16. A1-ANTITRYPSIN DEFICIENCEY
10.3.8.17. HEPATOBLASTOMA
10.3.8.18. BACTERIAL ENTERITIS/ENTEROPATHOGENS
10.3.8.19. MALROTATION
10.3.8.20. CONSTIPATION
10.3.9. PEDIATRIC HEMATOLOGY & ONCOLOGY
10.3.9.1. PEDIATRIC SICKLE CELL ANEMIA
10.3.9.2. HEMOLYTIC DISEASE OF THE NEWBORN (ERYTHROBLASTOSIS FETALIS)
10.3.9.3. FANCONI ANEMIA
10.3.9.4. ANEMIAS IN THE PEDIATRIC POPULATION
10.3.9.5. INHERITED HEMATOLOGIC DISORDERS
10.3.10. PEDIATRIC INFECTIOUS DISEASE
10.3.10.1. BOTULISM
10.3.10.2. MENINGOCOCCEMIA
10.3.10.3. OCCULT BACTEREMIA IN CHILDREN
10.3.10.4. SEPSIS IN CHILDREN
10.3.10.5. HIV
10.3.10.6. RUBEOLA
10.3.10.7. RUBELLA
10.3.10.8. ERYTHEMA INFECTIOSUM
10.3.10.9. SCARLET FEVER
10.3.10.9.1. DEFINITION
10.3.10.9.2. SIGNS/SYMPTOMS
10.3.10.9.3. DIAGNOSIS/SCREENING
10.3.10.9.4. COMPLICATIONS
10.3.10.9.5. TREATMENT
10.3.10.10. VARICELLA
10.3.10.11. HAND-FOOT-MOUTH DISEASE
10.3.10.12. TORCH INFECTIONS
10.3.10.13. MUMPS
10.3.10.14. ROCKY MOUNTAIN SPOTTED FEVER
10.3.10.15. TOXIC SHOCK SYNDROME
10.3.10.16. COCCIDIODOMYCOSIS
10.3.10.17. HISTOPLASMOSIS
10.3.10.18. SCHISTOSOMIASIS
10.3.10.19. VISCERAL LARVA MIGRANS
10.3.10.20. ANIMAL BITES
10.3.10.21. NEONATAL SEPSIS
10.3.11. PEDIATRIC NEPHROLOGY
10.3.11.1. RENAL TUBULAR ACIDOSIS
10.3.11.2. WILMS TUMOR
10.3.11.3. RENAL DYSPLASIA
10.3.11.4. RENAL HYPOPLASIA
10.3.11.5. FANCONI SYNDROME
10.3.11.6. HORSESHOE KIDNEY
10.3.11.7. FEBRILE PROTEINURIA
10.3.11.8. RENAL VEIN THROMBOSIS IN INFANCY
10.3.11.9. CRYPTORCHIDISM
10.3.12. PEDIATRIC ORTHOPEDICS AND RHEUMATOLOGY
10.3.12.1. OSTEOGENESIS IMPERFECTA
10.3.12.2. DUCHENNE MUSCULAR DYSTOPHY
10.3.12.3. EHLERS-DANLOS SYNDROME
10.3.12.4. KAWASAKI'S DISEASE
10.3.12.5. TORUS FRACTURE
10.3.12.6. GROWTH PLATES
10.3.12.7. OSTEOMYELITIS
10.3.12.8. SEPTIC ARTHRITIS
10.3.12.9. TRANSIENT SYNOVITIS
10.3.12.10. OSGOOD-SCHLATTER DISEASE
10.3.12.11. LEGG-CALVE-PERTHES DISEASE
10.3.12.12. SLIPPED CAPITAL FEMORAL EPIPHYSIS
10.3.12.13. THE LIMPING CHILD
10.3.12.14. TODDLER'S FRACTURE
10.3.12.15. DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)
10.3.12.15.1. PREVIOUSLY KNOWN AS CONGENITAL HIP DYSPLASIA
10.3.12.15.2. DISORDER OF NEWBORNS WITH INSTABILITY IN THEIR HIP JOINTS, WHICH MAY PROGRESS TO A CHRONIC DISLOCATION IF IT IS NOT DIAGNOSED EARLY
10.3.12.15.3. ALTHOUGH THERE IS NO STRONG GENETIC RISK, THE “FOUR FS” ARE SEEN IN PATIENTS WITH DEVELOPMENTAL DYSPLASIA OF THE HIP:
10.3.12.15.4. DIAGNOSIS AND EXAM FINDINGS
10.3.12.15.5. OTHER CLINICAL FINDINGS AND WORKUP OF DDH
10.3.12.15.6. TREATMENT
10.3.12.16. OSTEOID OSTEOMA
10.3.12.17. SALTER-HARRIS FRACTURE CLASSIFICATION
10.3.12.18. GREENSTICK FRACTURE
10.3.12.19. SUBLUXATION OF THE RADIAL HEAD
10.3.12.20. PEDIATRIC OSTEOPETROSIS
10.3.12.21. JUVENILE IDIOPATHIC ARTHRITIS
10.3.12.21.1. JUVENILE IDIOPATHIC ARTHRITIS (JIA) IS THE MOST COMMON RHEUMATIC DISEASE IN CHILDREN THAT REFERS TO A GROUP OF DISORDERS THAT ALL SHARE THE CHARACTERISTIC OF ARTHRITIS
10.3.12.21.2. THE CRITERIA FOR CLASSIFICATION INCLUDE THE FOLLOWING:
10.3.12.21.3. JUVENILE IDIOPATHIC ARTHRITIS OCCURS IN ABOUT 22/100,00 CHILDREN AND AFFECTS GIRLS MORE THAN BOYS
10.3.12.21.4. THE MOST COMMON SUBTYPES IN DESCENDING ORDER ARE: OLIGOARTHRITIS, POLYARTHRITIS, AND SYSTEMIC-ONSET ARTHRITIS
10.3.12.21.5. THE ETIOLOGY OF JIA IS NOT COMPLETELY UNDERSTOOD BUT TWO COMPONENTS ARE CONSIDERED NECESSARY: IMMUNOLOGIC SUSCEPTIBILITY AND AN EXTERNAL TRIGGER
10.3.12.21.6. CLINICAL SYMPTOMS
10.3.12.21.7. A RARE BUT POTENTIALLY FATAL COMPLICATION IS MACROPHAGE-ACTIVATING SYNDROME THAT CAN PRESENT AT ANY TIME IN THE DISEASE COURSE
10.3.12.21.8. JIA IS A CLINICAL DIAGNOSIS OF EXCLUSION WITHOUT ANY DIAGNOSTIC LABORATORY TESTS
10.3.12.21.9. IMAGING
10.3.12.21.10. THE GOAL OF TREATMENT IS TO ACHIEVE REMISSION AND STOP JOINT DAMAGE
10.3.12.22. JUVENILE RHEUMATOID ARTHRITIS (JRA)
10.3.13. PEDIATRIC PULMONARY
10.3.13.1. CROUP
10.3.13.2. INHALED FOREIGN BODY
10.3.13.3. EPIGLOTTITIS
10.3.13.4. BACTERIAL TRACHEITIS (PSEUDOMEMBRANOUS CROUP)
10.3.13.5. PEDIATRIC PNEUMONIA
10.3.13.6. BRONCHIOLITIS
10.3.13.6.1. BRONCHIOLITIS IS INFLAMMATION OF THE BRONCHIOLES THAT RESULTS IN INFLAMMATORY BRONCHIOLAR OBSTRUCTION
10.3.13.6.2. BRONCHIOLITIS MOST COMMONLY OCCURS IN CHILDREN UNDER 2 YEARS OF AGE, WITH TWICE AS MANY GIRLS AFFECTED AS BOYS
10.3.13.6.3. RESPIRATORY SYNCYTIAL VIRUS (RSV) IS THE MOST COMMON CAUSE OF BRONCHIOLITIS, BUT OTHER COMMON RESPIRATORY VIRUSES MAY ALSO CAUSE BRONCHIOLITIS
10.3.13.6.4. SINCE BRONCHIOLITIS IS CAUSED BY INFECTION WITH VARIOUS RESPIRATORY VIRUSES, EPIDEMICS OCCUR DURING THE COLD AND FLU SEASON (NOVEMBER TO APRIL)
10.3.13.6.5. PATIENTS WITH CARDIAC DISEASE, LUNG DISEASE, OR IMMUNODEFICIENCIES, AND THOSE LESS THAN 3 MONTHS OF AGE, ARE AT RISK FOR SEVERE DISEASE REQUIRING HOSPITALIZATION FOR RESPIRATORY SUPPORT
10.3.13.6.6. PATIENTS TYPICALLY PRESENT WITH A GRADUAL ONSET OF UPPER RESPIRATORY SYMPTOMS SUCH AS:
10.3.13.6.7. PATHOPHYSIOLOGY
10.3.13.6.8. WHILE BRONCHIOLITIS IS A CLINICAL DIAGNOSIS, MANY HOSPITALS TEST ALL YOUNG CHILDREN WITH SYMPTOMS OF BRONCHIOLITIS FOR RESPIRATORY SYNCYTIAL VIRUS (RSV)
10.3.13.6.9. WORSENING AIRWAY OBSTRUCTION CAN LEAD TO HYPOXIA AND APNEA
10.3.13.6.10. TREATMENT IS PRIMARILY SUPPORTIVE AND INCLUDES SUCTIONING, BRONCHODILATORS, AND SUPPLEMENTAL OXYGEN
10.3.13.7. OTHER IMPORTANT PEDIATRIC PULMONOLOGY TOPICS
10.3.14. PEDIATRIC SYNDROMES
10.3.14.1. TRISOMY 18
10.3.14.2. TRISOMY 13
10.3.14.3. TURNER SYNDROME
10.3.14.4. INFANTILE SPINAL MUSCULAR ATROPHY
10.3.14.5. TRISOMY 21
10.3.14.6. VACTERL AND CHARGE
11. STEP 1
11.1. ORGAN SYSTEMS
11.1.1. IN UP TO ONE QUARTER OF CHILDREN DIAGNOSED, RICKETS MAY BE A PRESENTING SYMPTOM
11.1.2. CARDIOLOGY
11.1.2.1. LARGE VESSEL VASCULITIS
11.1.2.1.1. GIANT CELL (TEMPORAL) ARTERITIS
11.1.2.1.2. TAKAYASU ARTERITIS
11.1.2.2. PATHOLOGY
11.1.2.3. PHARMACOLOGY
11.1.2.3.1. ANTIHYPERTENSION DRUGS: ANGIOTENSIN AGENTS
11.1.3. ENDOCRINOLOGY
11.1.3.1. HYPOTHALAMIC-PITUITARY AXIS
11.1.3.1.1. ANTERIOR PITUITARY
11.1.3.2. ENDOCRINE PANCREAS
11.1.3.2.1. DIABETES MELLITUS
11.1.3.2.2. TYPE I DIABETES MELLITUS
11.1.3.2.3. TYPE II DIABETES MELLITUS
11.1.3.3. ENDOCRINE PHARMACOLOGY
11.1.3.3.1. DIABETES MELLITUS PHARMACOLOGY
11.1.3.4. OTHER PATHOLOGY
11.1.3.4.1. CARCINOID SYNDROME
11.1.4. GASTROENTEROLOGY
11.1.4.1. PATHOLOGY
11.1.4.1.1. CARCINOID
11.1.5. HEMATOLOGY/ONCOLOGY
11.1.5.1. HEMATOLOGICAL DISORDERS
11.1.5.1.1. OVERVIEW OF ANEMIA
11.1.5.1.2. THROMBOTIC MICROANGIOPATHIES
11.1.5.2. HEMATOLOGIC MALIGNANCIES
11.1.5.2.1. LYMPHOMA: NON-HODGKIN
11.1.5.3. HEMOSTASIS
11.1.5.3.1. THROMBOCYTOPENIA
11.1.5.3.2. ANTIPHOSPHOLIPID SYNDROME
11.1.6. ORTHOPEDICS & RHEUMATOLOGY
11.1.7. PULMONOLOGY
11.1.7.1. PATHOLOGY
11.1.7.1.1. NASOPHARYNGEAL DISORDERS
11.1.7.2. PHYSIOLOGY
11.1.7.2.1. OXYGEN-HEMOGLOBIN DISSOCIATION CURVE
11.1.8. REPRODUCTIVE
11.1.8.1. ANATOMY
11.1.8.1.1. PROSTATE
11.1.8.1.2. LIGAMENTS OF THE UTERUS
11.1.8.1.3. GONADAL DRAINAGE
11.1.8.1.4. UTERINE TUBES
11.1.8.1.5. VAGINA
11.1.8.1.6. TESTES
11.1.8.1.7. EXTERNAL GENITALIA - FEMALE
11.1.8.1.8. UTERUS
11.1.8.1.9. EXTERNAL GENITALIA - MALE
11.1.8.1.10. OVARIES
11.1.8.1.11. CERVIX