USMLE KNOWLEDGE

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USMLE KNOWLEDGE by Mind Map: USMLE KNOWLEDGE

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. INTRODUCTION OF SOLID FOODS

6. INBORN ERRORS OF METABOLISM

6.1. HOMOCYSTINEMIA/URIA

6.2. CARBOHYDRATE METABOLISM DISORDERS

6.3. PURINE METABOLISM DISORDERS

6.4. PHENYLKETONURIA

6.5. MAPLE SYRUP URINE DISEASE

6.5.1. DEFINITION

6.5.1.1. INHERITED DISORDER OF BRANCHED-CHAIN AMINO ACID METABOLISM IN WHICH ELEVATED LEVELS OF LEUCINE, ISOLEUCINE, VALINE, AND CORRESPONDING OXOACIDS ACCUMULATE IN THE BODY FLUIDS

6.5.1.2. DEFICIENCY OF BRANCHED CHAIN KETOACID DEHYDROGENASE

6.5.2. SIGNS/SYMPTOMS

6.5.2.1. POOR FEEDING, VOMITING IN FIRST WEEK OF LIFE, PROCEEDING TO LETHARGY AND COMA

6.5.2.2. ALTERNATING HYPERTONICITY AND FLACCIDITY, CONVULSIONS, HYPOGLYCEMIA

6.5.2.3. ODOR OF MAPLE SYRUP IN URINE, SWEAT, CERUMEN

6.5.2.4. 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

6.5.3. DIAGNOSIS/SCREENING

6.5.3.1. URINE PRECIPITANT TEST AND NEUROIMAGING IN THE ACUTE STATE CAN SHOW CEREBRAL EDEMA

6.5.3.2. IT IS NORMALLY INCLUDED IN THE NEWBORN SCREENING FOR METABOLIC DISORDERS

6.5.4. TREATMENT

6.5.4.1. PATIENT SHOULD BE ON A LOW BRANCHED-CHAIN AMINO ACID DIET

6.5.4.2. FREQUENT SERUM LEVEL MONITORING

6.5.4.3. IN THE ACUTE STAGE INTRAVENOUS ADMINISTRATION OF AMINO ACIDS OTHER THAN BRANCHED CHAIN AMINO ACIDS

6.5.4.4. EMERGENT HEMODIALYSIS OR PERITONEAL DIALYSIS IF PATIENT IS ACIDOTIC.

6.5.4.5. LIVER TRANSPLANTATION CAN DEFINITIVELY TREAT MAPLE SYRUP URINE DISEASE

6.6. HARTNUP DISEASE

6.7. TYROSINEMIA

6.8. UREA CYCLE DEFICIENCIES

6.9. FATTY ACID OXIDATION DISORDERS

6.10. ORGANIC ACID DISORDERS

6.11. LIPODESES

6.12. MUCOPOLYSACCHARIDOSES

6.13. MITOCHONDRIAL DISORDERS

7. CHARACTERISTICALLY, CELIAC DISEASE MANIFESTS DURING INFANCY AND BEFORE SCHOOL AGE

7.1. IN THE CLASSIC FORM OF CHILDHOOD CELIAC DISEASE, SYMPTOMS AND SIGNS OF MALABSORPTION BECOME OBVIOUS WITHIN SOME MONTHS OF STARTING A GLUTEN-CONTAINING DIET

7.1.1. CHILDREN MAY PRESENT WITH FAILURE TO THRIVE, AND PROXIMAL MUSCLE WASTING MAY BE SEEN

7.1.1.1. IN UP TO ONE QUARTER OF CHILDREN DIAGNOSED, RICKETS MAY BE A PRESENTING SYMPTOM

7.1.1.2. GASTROINTESTINAL SYMPTOMS OF CELIAC SPRUE INCLUDE:

7.1.1.2.1. FOUL-SMELLING DIARRHEA

7.1.1.2.2. ABDOMINAL PAIN

7.1.1.2.3. WEIGHT LOSS

7.1.1.2.4. BLOATING

7.1.1.2.5. FATIGUE

7.1.1.2.6. STEATORRHEA

7.1.1.3. EXTRAINTESTINAL MANIFESTATIONS OF CELIAC SPRUE INCLUDE:

7.1.1.3.1. ANEMIA

7.1.1.3.2. NEUROLOGIC SYMPTOMS (MOTOR WEAKNESS, PARASTHESIAS)

7.1.1.3.3. DERMATITIS HERPETIFORMIS

7.1.1.3.4. HORMONAL DISORDERS (AMENORRHEA/INFERTILITY IN WOMEN, IMPOTENCE/INFERTILITY IN MEN)

8. STEP 2 CK

8.1. INTERNAL MEDICINE

8.1.1. DERMATOLOGY

8.1.1.1. STEVEN-JOHNSON SYNDROME

8.1.1.1.1. 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

8.1.1.1.2. STEVENS-JOHNSON SYNDROME REPRESENTS THE SAME PROCESS AS TOXIC EPIDERMAL NECROLYSIS (TEN)

8.1.1.1.3. THERE ARE 4 ETIOLOGIC CATEGORIES FOR SJS:

8.1.1.1.4. SJS PRESENTS WITH A 2-3 DAY PRODROMAL PERIOD OF FEVER AND FLU-LIKE SYMPTOMS PRIOR TO THE DEVELOPMENT OF MUCOCUTANEOUS LESIONS

8.1.1.1.5. 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

8.1.1.1.6. THE TIME COURSE FROM PRODROME UNTIL HOSPITAL DISCHARGE RANGES BETWEEN TWO TO FOUR WEEKS

8.1.1.1.7. BLISTERING AND SWELLING OF THE ORAL CAVITY IS ALSO SEEN IN PATIENTS WITH SJS

8.1.1.1.8. 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

8.1.1.1.9. ON PHYSICAL EXAMINATION A PATIENT WITH SJS WILL TYPICALLY HAVE AN ERYTHEMATOUS RASH WHICH MAY HAVE THE APPEARANCE OF A TARGET

8.1.1.1.10. OTHER SIGNS THAT RAISE CONCERN OF SJS INCLUDE:

8.1.1.1.11. LESIONS TYPICALLY START ON THE FACE AND THORAX BEFORE SPREADING, AND SPARE THE SCALP

8.1.1.1.12. AFTER A FEW DAYS, THE SKIN RASHES PROGRESSES TO VESICLES AND BULLAE, AND THE SKIN BEGINS TO SLOUGH

8.1.1.1.13. MUCOUS MEMBRANES ARE ALMOST ALWAYS INVOLVED IN SJS, INCLUDING THE ORAL MUCOSA (INCLUDING TONGUE), CONJUNCTIVA, URETHRA, AND PULMONARY MUCOSA

8.1.1.1.14. SKIN BIOPSIES ARE FAIRLY SPECIFIC AND TYPICALLY SHOW LYMPHOCYTES WITHIN PERIVASCULAR STRUCTURES AND FULL THICKNESS EPIDERMAL DETACHMENT WITH A NORMAL IMMUNOFLUORESCENCE

8.1.1.1.15. THE MORTALITY RATE OF SJS IS ABOUT 10%

8.1.1.1.16. 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

8.1.2. GASTROENTEROLOGY

8.1.2.1. CELIAC SPRUE

8.1.2.1.1. CELIAC SPRUE (I.E. GLUTEN INTOLERANCE) IS AN IMMUNE-MEDIATED DESTRUCTION OF THE MUCOSA OF THE JEJUNUM

8.1.2.1.2. 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

8.1.2.1.3. CELIAC SPRUE HAS A STRONG HEREDITARY COMPONENT--HLA HAPLOTYPES DQ2 AND DQ8 ARE STRONGLY LINKED TO DISEASE

8.1.2.1.4. OTHER THAN DISEASE IN A FIRST-DEGREE RELATIVE, RISK FACTORS FOR CELIAC SPRUE INCLUDE:

8.1.2.1.5. FOR SUSPECTED CELIAC DISEASE, THE BEST INITIAL TEST IS A SERUM LEVEL OF IMMUNOGLOBULIN A ANTI-TISSUE TRANSGLUTAMINASE ANTIBODY (IGA TTG)

8.1.2.1.6. OTHER USEFUL LAB TESTS INCLUDE:

8.1.2.1.7. THE GOLD STANDARD IN DIAGNOSING CELIAC SPRUE IS A DUODENAL BIOPSY, WHICH SHOWS:

8.1.2.1.8. RADIOGRAPHIC STUDIES MAY BE USEFUL IN UNTREATED CELIAC SPRUE

8.1.2.1.9. THE PRIMARY TREATMENT OF CELIAC SPRUE IS THE AVOIDANCE OF GLUTEN-CONTAINING PRODUCTS, SUCH AS WHEAT, BARLEY AND RYE

8.1.2.1.10. CELIAC SPRUE MAY RESULT IN THE FOLLOWING LONG TERM COMPLICATIONS:

8.1.2.1.11. TROPICAL SPRUE

8.1.2.2. HEPATIC ENCEPHALOPATHY

8.1.2.2.1. IT OCCURS WHEN AMMONIA CLEARANCE IS COMPROMISED (DUE TO CHRONIC LIVER DYSFUNCTION) AND CONSEQUENTLY BUILDS UP AND CROSSES INTO THE CNS

8.1.2.2.2. PATIENTS PRESENT WITH

8.1.2.2.3. DIAGNOSIS IS BASED ON SERUM AMMONIA LEVELS, AND EVALUATING LIVER FUNCTION VIA THE FOLLOWING:

8.1.2.2.4. TREATMENT IS AIMED AT AMMONIA REDUCTION, WHICH CAN BE ACHIEVED THROUGH:

8.1.3. PULMONOLOGY

8.1.3.1. CYSTIC FIBROSIS

8.1.3.1.1. CYSTIC FIBROSIS (CF) IS AN AUTOSOMAL RECESSIVE INHERITED DISEASE CAUSED BY A MUTATION IN THE GENE CODING FOR A COMPLEX CHLORIDE CHANNEL

8.1.3.1.2. CF IS CAUSED BY MUTATIONS IN THE GENE THAT CODES FOR THE CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) PROTEIN

8.1.3.1.3. CF IS THE MOST COMMON LIFE-SHORTENING AUTOSOMAL RECESSIVE DISEASE IN CAUCASIANS, AND OCCURS ONCE IN EVERY 2000 TO 3000 LIVE BIRTHS

8.1.3.1.4. SYMPTOMS OF CYSTIC FIBROSIS USUALLY BEGIN TO PRESENT IN EARLY CHILDHOOD AND COMMONLY INCLUDE MECONIUM ILEUS, RESPIRATORY SYMPTOMS, AND FAILURE TO THRIVE

8.1.3.1.5. THE MAJORITY OF CYSTIC FIBROSIS CASES IN THE UNITED STATES ARE NOW DETECTED THROUGH NEWBORN SCREENING

8.1.3.1.6. IN ADULTS AND OLDER CHILDREN, TWO CRITERIA MUST BE MET FOR THE DIAGNOSIS OF CF:

8.1.3.1.7. 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

8.1.3.1.8. 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

8.1.3.1.9. THE COMPLICATIONS OF CYSTIC FIBROSIS ARE MANY AND VARIED

8.1.3.1.10. TREATMENT OF CF VARIES BASED ON THE SPECIFIC MUTATION AND SEVERITY OF DISEASE, BUT TYPICALLY INCLUDES:

8.1.3.1.11. CYSTIC FIBROSIS LUNG DISEASE EXACERBATIONS ARE TYPICALLY TREATED WITH AGGRESSIVE CHEST PHYSIOTHERAPY AND ADDITIONAL ANTIBIOTICS

8.2. OBSTETRICS

8.2.1. A HEALTHY PREGNANCY

8.2.1.1. PHYSIOLOGIC CHANGES OF PREGNANCY

8.2.1.1.1. CARDIOVASCULAR CHANGES THAT OCCUR DURING PREGNANCY INCLUDE AN INCREASE IN CARDIAC OUTPUT AND A DECREASE IN BLOOD PRESSURE, BOTH OF WHICH IMPROVE UTEROPLACENTAL PERFUSION

8.2.1.1.2. RESPIRATORY

8.2.1.1.3. RENAL CHANGES THAT OCCUR DURING PREGNANCY INCLUDE AN INCREASE IN RENAL BLOOD FLOW, INCREASED RENAL SIZE, AND URETERAL DILATION

8.2.1.1.4. ENDOCRINE

8.2.1.1.5. HEMATOLOGY

8.2.1.1.6. GASTROINTESTINAL CHANGES THAT OCCUR DURING PREGNANCY INCLUDE DELAYED STOMACH EMPTYING AND A DECREASE IN LOWER ESOPHAGEAL SPHINCTER TONE

8.2.1.1.7. LOW RISK ACTIVITIES THAT CAN CONTINUE DURING PREGNANCY INCLUDE:

8.3. PEDIATRICS

8.3.1. HEALTH SUPERVISION

8.3.1.1. OVERVIEW OF IMMUNIZATIONS

8.3.1.1.1. THERE ARE TWO MAIN TYPES OF VACCINES: LIVE ATTENUATED VACCINES AND INACTIVATED VACCINES

8.3.1.1.2. THE CENTER FOR DISEASE CONTROL (CDC) DISTRIBUTES AN ANNUAL IMMUNIZATION SCHEDULE FOR CHILDREN AND ADOLESCENTS, AS WELL AS A CATCH-UP SCHEDULE

8.3.1.1.3. IN GENERAL, A VACCINE IS CONTRAINDICATED IF AN ANAPHYLACTIC REACTION TO THAT VACCINE IS EXPERIENCED AND SHOULD BE DISCONTINUED

8.3.2. NEONATOLOGY

8.3.2.1. NEWBORN EXAM - SKIN

8.3.2.2. NEWBORN EXAM - CRANIOFACIAL

8.3.2.3. NEWBORN EXAM - NECK, CHEST, ABDOMINAL, GENITAL, EXTREMITIES

8.3.3. NEONATOLOGY (NICU)

8.3.3.1. NEONATAL RESPIRATORY DISTRESS SYNDROME (NRDS)

8.3.4. NORMAL GROWTH AND DEVELOPMENT

8.3.4.1. NEWBORN GROWTH RATE

8.3.4.2. NEWBORN CALORIC REQUIREMENT

8.3.4.3. BREAST FEEDING VS BREAST MILK JAUNDICE

8.3.4.3.1. 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

8.3.4.3.2. 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

8.3.4.3.3. TAKE HOME POINT:

8.3.4.4. FORMULA TYPES

8.3.4.5. GROWTH CHARTS

8.3.4.6. INTRAUTERINE FACTORS FOR GROWTH

8.3.4.7. TEETH

8.3.4.8. APPROACH TO A CHILD WITH MICROCEPHALY

8.3.4.9. FAILURE TO THRIVE

8.3.4.10. DEVELOPMENTAL MILESTONES: 1 MONTH

8.3.4.11. DEVELOPMENTAL MILESTONES: 2 MONTHS

8.3.4.12. DEVELOPMENTAL MILESTONES: 4 MONTHS

8.3.4.13. DEVELOPMENTAL MILESTONES: 6 MONTHS

8.3.4.14. DEVELOPMENTAL MILESTONES: 9 MONTHS

8.3.4.15. DEVELOPMENTAL MILESTONES: 12 MONTHS

8.3.4.16. DEVELOPMENTAL MILESTONES: 2 YEARS

8.3.4.17. DEVELOPMENTAL MILESTONES: 3 YEARS

8.3.4.18. DEVELOPMENTAL MILESTONES: 4 YEARS

8.3.4.19. DEVELOPMENTAL MILESTONES: 5 YEARS

8.3.4.20. PRIMITIVE REFLEXES

8.3.4.21. DEVELOPMENTAL DELAY

8.3.4.22. LEARNING DISABILITIES

8.3.4.23. SLEEP

8.3.4.24. FLUID MANAGEMENT OF THE PEDIATRIC PATIENT

8.3.4.25. BREAST FEEDING

8.3.4.25.1. 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

8.3.4.25.2. STAGES OF LACTOGENESIS

8.3.4.25.3. BENEFITS FOR THE INFANT

8.3.4.25.4. BENEFITS FOR THE MOTHER

8.3.4.25.5. COMPLICATIONS

8.3.4.25.6. CONTRAINDICATIONS

8.3.4.25.7. POSSIBLE VITAMIN DEFICIENCIES IN BREAST FED INFANTS REQUIRES THAT THESE INFANTS RECEIVE:

8.3.4.26. APPROACH TO A CHILD WITH MACROCEPHALY

8.3.4.27. DEVELOPMENTAL MILESTONES: 18 MONTHS

8.3.5. PEDIATRIC CARDIOLOGY

8.3.5.1. TRANSPOSITION OF THE GREAT VESSELS

8.3.5.2. ATRIAL SEPTAL DEFECT (ASD)

8.3.5.3. AORTIC COARCTATION

8.3.5.4. PATENT DUCTUS ARTERIOSUS

8.3.5.5. TETRALOGY OF FALLOT

8.3.5.6. VENTRICULAR SEPTAL DEFECT (VSD)

8.3.5.7. HYPOPLASTIC LEFT HEART SYNDROME

8.3.5.8. EBSTEIN'S ANOMALY

8.3.5.9. TRUNCUS ARTERIOSUS

8.3.5.10. TOTAL ANOMALOUS PULMONARY VENOUS RETURN

8.3.5.11. TRICUSPID ATRESIA

8.3.5.12. PULMONARY ATRESIA

8.3.5.13. PEDIATRIC AORTIC STENOSIS

8.3.6. PEDIATRIC DERMATOLOGY

8.3.6.1. STEVENS-JOHNSON SYNDROME/TOXIC EPIDERMAL NECROLYSIS

8.3.7. PEDIATRIC ENDOCRINOLOGY

8.3.7.1. CONGENITAL HYPOTHYROIDISM (CRETINISM)

8.3.7.2. PRECOCIOUS PUBERTY

8.3.7.3. MCCUNE ALBRIGHT SYNDROME

8.3.8. PEDIATRIC GASTROENTEROLOGY

8.3.8.1. ESOPHAGEAL ATRESIA

8.3.8.2. ESOPHAGEAL FOREIGN BODY

8.3.8.3. PEPTIC ULCER

8.3.8.4. PYLORIC STENOSIS

8.3.8.5. DUODENAL ATRESIA

8.3.8.6. INTUSSUSCEPTION

8.3.8.7. MECKEL'S DIVERTICULUM

8.3.8.8. CONSTIPATION

8.3.8.9. HIRSCHSPRUNG'S MEGACOLON

8.3.8.10. IMPERFORATE ANUS

8.3.8.11. GILBERT SYNDROME

8.3.8.12. CRIGLER-NAJJAR SYNDROME

8.3.8.13. ALAGILLE SYNDROME

8.3.8.14. ZELLWEGER SYNDROME

8.3.8.15. REYE SYNDROME

8.3.8.16. A1-ANTITRYPSIN DEFICIENCEY

8.3.8.17. HEPATOBLASTOMA

8.3.8.18. BACTERIAL ENTERITIS/ENTEROPATHOGENS

8.3.8.19. MALROTATION

8.3.8.20. CONSTIPATION

8.3.9. PEDIATRIC HEMATOLOGY & ONCOLOGY

8.3.9.1. PEDIATRIC SICKLE CELL ANEMIA

8.3.9.2. HEMOLYTIC DISEASE OF THE NEWBORN (ERYTHROBLASTOSIS FETALIS)

8.3.9.3. FANCONI ANEMIA

8.3.9.4. ANEMIAS IN THE PEDIATRIC POPULATION

8.3.9.5. INHERITED HEMATOLOGIC DISORDERS

8.3.10. PEDIATRIC INFECTIOUS DISEASE

8.3.10.1. BOTULISM

8.3.10.2. MENINGOCOCCEMIA

8.3.10.3. OCCULT BACTEREMIA IN CHILDREN

8.3.10.4. SEPSIS IN CHILDREN

8.3.10.5. HIV

8.3.10.6. RUBEOLA

8.3.10.7. RUBELLA

8.3.10.8. ERYTHEMA INFECTIOSUM

8.3.10.9. SCARLET FEVER

8.3.10.9.1. DEFINITION

8.3.10.9.2. SIGNS/SYMPTOMS

8.3.10.9.3. DIAGNOSIS/SCREENING

8.3.10.9.4. COMPLICATIONS

8.3.10.9.5. TREATMENT

8.3.10.10. VARICELLA

8.3.10.11. HAND-FOOT-MOUTH DISEASE

8.3.10.12. TORCH INFECTIONS

8.3.10.13. MUMPS

8.3.10.14. ROCKY MOUNTAIN SPOTTED FEVER

8.3.10.15. TOXIC SHOCK SYNDROME

8.3.10.16. COCCIDIODOMYCOSIS

8.3.10.17. HISTOPLASMOSIS

8.3.10.18. SCHISTOSOMIASIS

8.3.10.19. VISCERAL LARVA MIGRANS

8.3.10.20. ANIMAL BITES

8.3.10.21. NEONATAL SEPSIS

8.3.11. PEDIATRIC NEPHROLOGY

8.3.11.1. RENAL TUBULAR ACIDOSIS

8.3.11.2. WILMS TUMOR

8.3.11.3. RENAL DYSPLASIA

8.3.11.4. RENAL HYPOPLASIA

8.3.11.5. FANCONI SYNDROME

8.3.11.6. HORSESHOE KIDNEY

8.3.11.7. FEBRILE PROTEINURIA

8.3.11.8. RENAL VEIN THROMBOSIS IN INFANCY

8.3.11.9. CRYPTORCHIDISM

8.3.12. PEDIATRIC ORTHOPEDICS AND RHEUMATOLOGY

8.3.12.1. OSTEOGENESIS IMPERFECTA

8.3.12.2. DUCHENNE MUSCULAR DYSTOPHY

8.3.12.3. EHLERS-DANLOS SYNDROME

8.3.12.4. KAWASAKI'S DISEASE

8.3.12.5. TORUS FRACTURE

8.3.12.6. GROWTH PLATES

8.3.12.7. OSTEOMYELITIS

8.3.12.8. SEPTIC ARTHRITIS

8.3.12.9. TRANSIENT SYNOVITIS

8.3.12.10. OSGOOD-SCHLATTER DISEASE

8.3.12.11. LEGG-CALVE-PERTHES DISEASE

8.3.12.12. SLIPPED CAPITAL FEMORAL EPIPHYSIS

8.3.12.13. THE LIMPING CHILD

8.3.12.14. TODDLER'S FRACTURE

8.3.12.15. DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)

8.3.12.15.1. PREVIOUSLY KNOWN AS CONGENITAL HIP DYSPLASIA

8.3.12.15.2. DISORDER OF NEWBORNS WITH INSTABILITY IN THEIR HIP JOINTS, WHICH MAY PROGRESS TO A CHRONIC DISLOCATION IF IT IS NOT DIAGNOSED EARLY

8.3.12.15.3. ALTHOUGH THERE IS NO STRONG GENETIC RISK, THE “FOUR FS” ARE SEEN IN PATIENTS WITH DEVELOPMENTAL DYSPLASIA OF THE HIP:

8.3.12.15.4. DIAGNOSIS AND EXAM FINDINGS

8.3.12.15.5. OTHER CLINICAL FINDINGS AND WORKUP OF DDH

8.3.12.15.6. TREATMENT

8.3.12.16. OSTEOID OSTEOMA

8.3.12.17. SALTER-HARRIS FRACTURE CLASSIFICATION

8.3.12.18. GREENSTICK FRACTURE

8.3.12.19. SUBLUXATION OF THE RADIAL HEAD

8.3.12.20. PEDIATRIC OSTEOPETROSIS

8.3.12.21. JUVENILE IDIOPATHIC ARTHRITIS

8.3.12.21.1. 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

8.3.12.21.2. THE CRITERIA FOR CLASSIFICATION INCLUDE THE FOLLOWING:

8.3.12.21.3. JUVENILE IDIOPATHIC ARTHRITIS OCCURS IN ABOUT 22/100,00 CHILDREN AND AFFECTS GIRLS MORE THAN BOYS

8.3.12.21.4. THE MOST COMMON SUBTYPES IN DESCENDING ORDER ARE: OLIGOARTHRITIS, POLYARTHRITIS, AND SYSTEMIC-ONSET ARTHRITIS

8.3.12.21.5. THE ETIOLOGY OF JIA IS NOT COMPLETELY UNDERSTOOD BUT TWO COMPONENTS ARE CONSIDERED NECESSARY: IMMUNOLOGIC SUSCEPTIBILITY AND AN EXTERNAL TRIGGER

8.3.12.21.6. CLINICAL SYMPTOMS

8.3.12.21.7. A RARE BUT POTENTIALLY FATAL COMPLICATION IS MACROPHAGE-ACTIVATING SYNDROME THAT CAN PRESENT AT ANY TIME IN THE DISEASE COURSE

8.3.12.21.8. JIA IS A CLINICAL DIAGNOSIS OF EXCLUSION WITHOUT ANY DIAGNOSTIC LABORATORY TESTS

8.3.12.21.9. IMAGING

8.3.12.21.10. THE GOAL OF TREATMENT IS TO ACHIEVE REMISSION AND STOP JOINT DAMAGE

8.3.12.22. JUVENILE RHEUMATOID ARTHRITIS (JRA)

8.3.13. PEDIATRIC PULMONARY

8.3.13.1. CROUP

8.3.13.2. INHALED FOREIGN BODY

8.3.13.3. EPIGLOTTITIS

8.3.13.4. BACTERIAL TRACHEITIS (PSEUDOMEMBRANOUS CROUP)

8.3.13.5. PEDIATRIC PNEUMONIA

8.3.13.6. BRONCHIOLITIS

8.3.13.6.1. BRONCHIOLITIS IS INFLAMMATION OF THE BRONCHIOLES THAT RESULTS IN INFLAMMATORY BRONCHIOLAR OBSTRUCTION

8.3.13.6.2. BRONCHIOLITIS MOST COMMONLY OCCURS IN CHILDREN UNDER 2 YEARS OF AGE, WITH TWICE AS MANY GIRLS AFFECTED AS BOYS

8.3.13.6.3. RESPIRATORY SYNCYTIAL VIRUS (RSV) IS THE MOST COMMON CAUSE OF BRONCHIOLITIS, BUT OTHER COMMON RESPIRATORY VIRUSES MAY ALSO CAUSE BRONCHIOLITIS

8.3.13.6.4. SINCE BRONCHIOLITIS IS CAUSED BY INFECTION WITH VARIOUS RESPIRATORY VIRUSES, EPIDEMICS OCCUR DURING THE COLD AND FLU SEASON (NOVEMBER TO APRIL)

8.3.13.6.5. 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

8.3.13.6.6. PATIENTS TYPICALLY PRESENT WITH A GRADUAL ONSET OF UPPER RESPIRATORY SYMPTOMS SUCH AS:

8.3.13.6.7. PATHOPHYSIOLOGY

8.3.13.6.8. WHILE BRONCHIOLITIS IS A CLINICAL DIAGNOSIS, MANY HOSPITALS TEST ALL YOUNG CHILDREN WITH SYMPTOMS OF BRONCHIOLITIS FOR RESPIRATORY SYNCYTIAL VIRUS (RSV)

8.3.13.6.9. WORSENING AIRWAY OBSTRUCTION CAN LEAD TO HYPOXIA AND APNEA

8.3.13.6.10. TREATMENT IS PRIMARILY SUPPORTIVE AND INCLUDES SUCTIONING, BRONCHODILATORS, AND SUPPLEMENTAL OXYGEN

8.3.13.7. OTHER IMPORTANT PEDIATRIC PULMONOLOGY TOPICS

8.3.14. PEDIATRIC SYNDROMES

8.3.14.1. TRISOMY 18

8.3.14.2. TRISOMY 13

8.3.14.3. TURNER SYNDROME

8.3.14.4. INFANTILE SPINAL MUSCULAR ATROPHY

8.3.14.5. TRISOMY 21

8.3.14.6. VACTERL AND CHARGE

9. STEP 1

9.1. ORGAN SYSTEMS

9.1.1. CARDIOLOGY

9.1.1.1. LARGE VESSEL VASCULITIS

9.1.1.1.1. GIANT CELL (TEMPORAL) ARTERITIS

9.1.1.1.2. TAKAYASU ARTERITIS

9.1.1.2. PATHOLOGY

9.1.1.3. PHARMACOLOGY

9.1.1.3.1. ANTIHYPERTENSION DRUGS: ANGIOTENSIN AGENTS

9.1.2. ENDOCRINOLOGY

9.1.2.1. HYPOTHALAMIC-PITUITARY AXIS

9.1.2.1.1. ANTERIOR PITUITARY

9.1.2.2. ENDOCRINE PANCREAS

9.1.2.2.1. DIABETES MELLITUS

9.1.2.2.2. TYPE I DIABETES MELLITUS

9.1.2.2.3. TYPE II DIABETES MELLITUS

9.1.2.3. ENDOCRINE PHARMACOLOGY

9.1.2.3.1. DIABETES MELLITUS PHARMACOLOGY

9.1.2.4. OTHER PATHOLOGY

9.1.2.4.1. CARCINOID SYNDROME

9.1.3. GASTROENTEROLOGY

9.1.3.1. PATHOLOGY

9.1.3.1.1. CARCINOID

9.1.4. HEMATOLOGY/ONCOLOGY

9.1.4.1. HEMATOLOGICAL DISORDERS

9.1.4.1.1. OVERVIEW OF ANEMIA

9.1.4.1.2. THROMBOTIC MICROANGIOPATHIES

9.1.4.2. HEMATOLOGIC MALIGNANCIES

9.1.4.2.1. LYMPHOMA: NON-HODGKIN

9.1.4.3. HEMOSTASIS

9.1.4.3.1. THROMBOCYTOPENIA

9.1.4.3.2. ANTIPHOSPHOLIPID SYNDROME

9.1.5. ORTHOPEDICS & RHEUMATOLOGY

9.1.6. PULMONOLOGY

9.1.6.1. PATHOLOGY

9.1.6.1.1. NASOPHARYNGEAL DISORDERS

9.1.6.2. PHYSIOLOGY

9.1.6.2.1. OXYGEN-HEMOGLOBIN DISSOCIATION CURVE

9.1.7. REPRODUCTIVE

9.1.7.1. ANATOMY

9.1.7.1.1. PROSTATE

9.1.7.1.2. LIGAMENTS OF THE UTERUS

9.1.7.1.3. GONADAL DRAINAGE

9.1.7.1.4. UTERINE TUBES

9.1.7.1.5. VAGINA

9.1.7.1.6. TESTES

9.1.7.1.7. EXTERNAL GENITALIA - FEMALE

9.1.7.1.8. UTERUS

9.1.7.1.9. EXTERNAL GENITALIA - MALE

9.1.7.1.10. OVARIES

9.1.7.1.11. CERVIX

10. STANDARD ERROR OF THE MEAN (SEM) = Σ/√N

11. BLEEDING DIATHESIS (INCREASED TENDENCY TO BLEED, SECONDARY TO MALABSORPTION OF FAT-SOLUBLE VITAMIN K)

12. CONJUNCTIVITIS AND CORNEAL ULCERATIONS

13. CONJUNCTIVAL AND CORNEAL LESIONS ARE MORE SERIOUS COMPLICATIONS THAT CAN LEAD TO PERMANENT BLINDESS

14. → RECURRENT PSEUDOMONAS AND STAPH PNEUMONIAS, CHRONIC BRONCHITIS, BRONCHIECTASIS