Infection, Nutrition and Thyroid Disease

1
Infection, Nutrition and Thyroid Disease
2
Choose the correct statement about
community-acquired methicillin-resistant
Staphylococcus aureus (CA-MRSA).(A) Likely arose
from hospital strains that spread into the
community(B) Likely arose from de novo
acquisition of resistance by a methicillin-suscept
ible strain(C) Is genetically almost identical
to HA-MRSA(D) Is less susceptible to
non?-lactam antibiotics than HA-MRSA
3
Answer

• (B) Likely arose from de novo acquisition of
  resistance by a methicillin-susceptible strain

4
Data show the majority of pregnant women who
present with CA-MRSA are nulliparous.(A) True
(B) False
5
Answer

• (B) False

6
Which of the following is the first-line
treatment for uncomplicated skin and soft tissue
infection with MRSA?(A) Incision and drainage
(B) Daptomycin (C) Linezolid (D) Tigecycline
7
Answer

• (A) Incision and drainage

8
Which of the following is considered first-line
therapy for complicated skin and soft tissue MRSA
infection?(A) Co-trimoxazole (TMP/SMX) (B)
Clindamycin (C) Doxycycline (D) Vancomycin
9
Answer

• (D) Vancomycin

10
MRSA active surveillance cultures (ASC) that are
required in California

• They are required within 24 hr of admission for
  patients scheduled for inpatient surgery,
  discharged from acute care hospital during past
  30 days, admitted to ICU, receiving inpatient
  dialysis, or transferred from skilled nursing
  facility Rationale for ASCprevents
  patient-to-patient transmission (by using contact
  precautions, isolation, and/or decolonization)
• prevents subsequent infection of previously
  colonized patients
• enables appropriate modification of perioperative
  prophylaxis
• conflicting data supporting ASC led professional
  societies to conclude evidence insufficient to
  warrant routine or mandated use of ASC for
  detection of MRSA

11
Contact isolation

• supporting data inconclusive
• Potential adverse events associated with contact
  precautions (patients likely examined less
  frequently and for shorter periods, compared to
  nonisolated patients)
• patients more likely to experience preventable
  adverse events (eg, pressure ulcers, falls,
  electrolyte imbalances)
• increased rates of depression and anxiety
• trial currently ongoing to address question of
  whether intensive infection control strategies
  reduce transmission of pathogens

12
Origin of community-acquired MRSA (CA-MRSA)

• 4 deaths due to MRSA reported in previously
  healthy children in 1999
• outbreaks of CA-MRSA then reported in multiple
  diverse populations
• 2006 paper cited CA-MRSA as predominant cause of
  skin and soft tissue infection among patients
  presenting to 11 emergency departments
• likely arose de novo from acquisition of
  resistance by methicillin-susceptible strain
• CA-MRSA genetically distinct from
  hospital-acquired MRSA (HA-MRSA)
• Has novel staphylococcal chromosomal cassette
  element lacks multiple antibiotic resistance
  genes
• contains other genetic elements that may
  contribute to virulence

13
Spectrum of disease

• skin and soft tissue infections most common,
  followed by wound infections, urinary tract
  infections, and bacteremia
• CA-MRSA more susceptible to nonBeta-lactam
  antibiotics (compared to HA-MRSA)
• Cochrane Database of Systematic Reviews
  (2008)reported reduction of nosocomial S aureus
  infections in surgical and dialysis patients
• however, most patients had methicillin- sensitive
  S aureus (MSSA), and those with MRSA had HA
  strain
• studies of nonsurgical patients and MRSA
• carriers showed no benefit
• 2003 reviewtopical mupirocin and systemic
  antimicrobial therapy not effective in
  eradicating nasal or extranasal MRSA
• adverse events and development of resistance
  observed with oral systemic decolonization

14
MRSA carriage in pregnancy

• approximately one-third of women carriers (1
  colonized with MRSA both rates consistent with
  general population) 5 of infants carriers (lt1
  MRSA)
• no evidence of maternal-infant transmission
  vaginal- rectal colonizationprevalence 0.4 to
  3.5
• Conflicting data on association with Group B
  streptococcus carriage
• data looking at colonization and risk for
  vertical transmission showed no cases of
  early-onset invasive neonatal MRSA infections
• no evidence of substantial cost benefit with MRSA
  screening and decolonization, regardless of
  success of treatment
• perioperative prophylaxismeta-analysis of
  cardiac surgery patients treated with vancomycin
  or Beta-lactam showed no increased benefit from
  use of either drug
• vancomycin did appear to reduce rate of surgical
  site infection in subgroup of patients with MRSA
• threshold prevalence of MRSA infections for
  changing prophylaxis regimens not yet defined
• protocol at UCSFperform ASC on selected patient
  group
• focus on education of patient and health care
  personnel to reinforce standard precautions and
  hand hygiene

15
MRSA in pregnancy

• clinical presentationdata show majority of
  infected patients multiparous
• clinical infection mostly during second trimester
• mastitis and surgical site infection most common
  postpartum infections skin and
• soft tissue infections predominant clinical
  presentation
• data show no significant difference in obstetric
  outcomes between women with CA-MRSA and those
  without CA-MRSA
• postpartum mastitisdata show no difference in
  age, pregnancy history, clinical presentation, or
  prenatal or intrapartum risk factors
• patients more likely multiparous (may reflect
  increased prevalence of MRSA among children)
• no significant differences in clinical outcomes
  with antibiotic use
• MSSA predominant organism in women without
  abscess
• MRSA dominant organism in women with abscess
• MRSA and MSSA significant pathogens in
  nonpuerperal mastitis
• management of uncomplicated skin and soft tissue
  infectionsincision and drainage (I and D)
  primary treatment
• benefit of antibiotic beyond that of I and D
  unknown
• consider empiric treatment with systemic
  symptoms, severe local symptoms, or
  immunosuppression antibiotics may have more
  important role in patients treated with minimally
  invasive drainage techniques
• Empiric therapyif abscess present and antibiotic
  therapy indicated, consider coverage for CA-MRSA
  (pending culture)
• for mastitis without abscess, consider coverage
  for CA-MRSA based on local epidemiology or
  failure to respond to Beta-lactam therapy

16
Antimicrobial therapy

• co-trimoxazole (TMP/SMX)low rate of resistance
• covers MRSA and MSSA
• unreliable for group A streptococcal infection
  pregnancy category C or D in third trimester
• clindamycincovers MRSA, MSSA, and group A
  streptococci
• excellent tissue and abscess penetration
• potential for resistance
• risk for Clostridium difficile
• pregnancy category B
• doxycyclinelow resistance covers MRSA and MSSA,
  but unreliable for group A
• Streptococci
• pregnancy category D
• linezolidindicated for complicated skin and soft
  tissue infections
• Adverse events associated with long-term use (eg,
  potential bone marrow suppression, neurotoxicity)
• pregnancy category C
• inducible clindamycin resistancenot detected by
  standard broth microdilution testing
• consider with erythromycin-resistant but
  clindamycin-susceptible isolate
• If disk diffusion-test positive but patient
  improving, continue clindamycin
• change therapy with failure or moderately severe
  infection
• management of complicated skin or soft tissue
  infectionsempiric therapy for MRSA recommended
  (vancomycin first-line drug)

17
MRSA and breastfeeding

• one case report of transmission of MRSA via
  breast milk (mother asymptomatic)
• no clear data on whether woman with postpartum
  mastitis should continue breastfeeding
• breast emptying mainstay of therapy
• some experts recommend continuing breastfeeding
  if mother on antibiotics, unless draining wound
  or cellulitis in area
• another recommends breastfeeding on contralateral
  side and expressing on infected side

18
Vulvar abscesses

• data show MRSA dominant pathogen in 64 of women
  treated for vulvar abscess
• no distinguishing clinical signs or symptoms
• no difference in clinical outcomes perform I and
  D
• treat with TMP/SMX (covers MRSA and majority of
  other pathogens)

19
Study Lesser-known bug a bigger hospital threat

• March 20, 2010By MIKE STOBBE, AP Medical Writer
• 2010-03-20 061200 PDT Atlanta, , United States
  (03-20) 0612 PDT ATLANTA (AP) --
• As one superbug seems to be fading as a threat in
  hospitals, another is on the rise, a new study
  suggests.
• A dangerous, drug-resistant staph infection
  called MRSA is often seen as the biggest germ
  threat to patients in hospitals and other health
  care facilities.
• But infections from Clostridium difficile known
  as C-diff are surpassing MRSA infections, the
  study of 28 hospitals in the Southeast found.

20
C-Diff

• "I think MRSA is almost a household name.
• Everybody thinks of MRSA as a serious threat,"
  said Dr. Becky Miller, an infectious diseases
  specialist at Duke University Medical Center. She
  presented the research Saturday in Atlanta, at a
  medical conference on infection in health care
  facilities.
• "But C. difficile deserves more attention," she
  added.
• MRSA, or methicillin-resistant Staphylococcus
  aureus, are bacteria that can't be treated with
  common antibiotics. They are often harmless as
  they ride on the skin, but become deadly once
  they get in the bloodstream. They enter through
  wounds, intravenous lines and other paths.
• C-diff, also resistant to some antibiotics, is
  found in the colon and can cause diarrhea and a
  more serious intestinal condition known as
  colitis.
• It is spread by spores in feces. The spores are
  difficult to kill with most conventional
  household cleaners or alcohol-based hand
  sanitizers, so some of the disinfection measures
  against MRSA don't work on C-diff.
• Deaths from C-diff traditionally have been rare,
  but a more dangerous form has emerged in the last
  ten years.
• Still, MRSA is generally considered a more lethal
  threat, causing an estimated 18,000 U.S. deaths
  annually.

21
C-Diff

• The new study looked at infection rates from
  community hospitals in Virginia, North Carolina,
  South Carolina and Georgia in 2008 and 2009.
• It found the rate of hospital-acquired C-diff
  infections was 25 percent higher than MRSA
  infections.
• Here are the numbers The hospitals counted 847
  infections of hospital-acquired C-diff, and 680
  cases of MRSA.
• Miller also reported that C-diff was increasing
  at the hospitals since 2007, while MRSA has been
  declining since 2005.
• Last year, a government report noted a decline in
  MRSA infections in a study of 600 hospital
  intensive-care units.
• MRSA bloodstream infections connected with
  intravenous tubes fell almost 50 percent from
  1997 to 2007, according to data reported to the
  Centers for Disease Control and Prevention.
• C-diff has seemed to be increasing in recent
  years, but the trend is not uniform some
  hospitals report falling rates.
• The prevalence of different infections can vary
  in different parts of the country, said Dr. L.
  Clifford McDonald, a CDC expert who was not part
  of the Duke study.

22
What is a Hospital Acquired Infection

• An infection that is not present or incubating at
  the time healthcare services are delivered
• IT presents symptomatically 48 hours or more
  after admission or provision of care

23
HAI Frequency

• Each year in the US, five to ten percent of all
  patients admitted to the hospital develop HAIs
• This translates to almost two million cases of
  HAI each year, in hospitals alone.
• HAIs may also be acquired in the Ambulatory care
  setting and Home care setting

24
Overview thyroid nodules

• common found in 50 of patients on
  ultrasonography (US)
• About 10 of patients on palpation
• thyroid dysfunctionoccurs in up to 1 in 8
  patients, especially in elderly population
• thyroid conditions found predominantly in women

25
Thyrotropin (TSH) as monitoring tool

• only 0.04 of TSH in free bioactive form
• remainder bound (ie, inactive hormone) to
  thyroxine-binding globulin (TBG) and albumin
• therefore, never use total T4 to assess thyroid
  function

26
Factors affecting T4 levels, Use TSH in pregnancy

• estrogenincreases TBG
• pregnancytotal T4 can increase (to 14-16 g/dL),
  becauseo of increased binding proteins, and stay
  within normal range
• other estrogen sourcesreplacement therapy,
  contraception, and infertility treatments with
  follicle-stimulating hormone (FSH) injections
• long-term narcotic useelevates T4 leuprolide
  (eg, Lupron)lowers TBG and T4
• changes in pregnancyTGB levels rise quickly at
  start, plateau at 20 wk, then stabilize
• 50 increase in T4 during first 20 wk (eg, from 9
  to 13 µg/dL)
• estimate thyroid functions with TSH (levels
  decrease when thyroid hormone increases, and vice
  versa)
• 2-fold change in T4 levels results in 100-fold
  change in TSH
• TSH more sensitive, accurate, and can diagnose
  euthyroidism, hypothyroidism, and hyperthyroidism

27
Hypothyroid Prevalence

• In men it is 2 to 3 over decades,
• until gt70 yr of age (increases to 10 of men)
• womenstepwise increase starting at 30 yr of age
• by gt70 yr of age, 1 in 7 or 8 womem has
  unsuspected hypothyroidism

28
Screening

• TSHmost sensitive and specific test for
  hypothyroidism
• inexpensive

29
Causes

• Hashimoto disease most common
• other causes radioactive iodine therapy or
  thyroid surgery
• Hashimoto disease ask about family history of
  thyroid and other autoimmune diseases (eg, lupus
  erythematosus, colitis)
• environmental factors include pregnancy (presence
  of fetus can activate maternal immune system and
  initiate autoimmune disease)
• thyroperoxidase (TPO) antibody rises before onset
  of disease predicting disease
• measure TPO antibody levels rather than
  antithyroglobulin antibodies
• after destruction, TSH will rise
• Patient with mildly elevated TSH and positive
  antibody has 5 per year chance of developing
  hypothyroidism

30
TSH and TPO antibody in diagnosis

• slightly elevated TSH does not always lead to
  disease
• study of elderly patients with mildly elevated
  TSHin patients positive for TPO, 80 developed
  hypothyroidism after 4 yr (vs very few in
  negative TPO group)
• if hypothyroidism suspectedmeasure TSH if TSH
  lowpatient possibly hyperthyroid
• 0.3 to 3.5 g/dL considered restricted normal
  range
• if gt9 g/dLpatient hypothyroid requires
  treatment
• if 3.5 to 9 g/dLrepeat TSH 2 mo later (about 50
  of patients normalize) and measure TPO antibody
• treat if positive

31
Treatment

• levothyroxine standard treatment
• structure identical to that of natural thyroid
  hormone
• long half-life (7- 10 days)
• once-daily dosing (can take 2 next day if 1 dose
  missed)
• T350 to 100 times more active than T4
• dosedetermined by age and weight
• drastic weight loss may require reduction in dose
• younger patients need more thyroid hormone
  because of faster metabolism

32
Contraindications drugs

• estrogen therapy and antiseizure drugs increase
  binding protein
• may need more hormone to fill binding sites
• pregnancy50 to 80 of pregnant women taking
  thyroid hormone require 25 to 50 increase in
  dose
• interference with thyroid hormone absorption
• Levothyroxine locked by supplementation with iron
  or calcium, and sucralfate
• history of malabsorption (eg, celiac disease),
  and ingestion of high-fat foods
• Best time to take is on empty stomach one half
  hour prior to breakfast.

33
Importance of thyroid hormone brand

• study of patients using 4 brands of hormone
• normal thyroid function at start of study
• change in brand (not dose) increased risk for
  abnormal thyroid function by 40 to 50 (50 of
  affected patients hyperthyroid, 50 hypothyroid)
• Take home messagesspecify no substitution of
  brand
• Instruct patient to verify that same manufacturer
  used for each refill
• if manufacturer changes, patient must return for
  recheck of thyroid hormone levels after 1 mo

34
Maintenance of thyroid function

• study data show only 60 of patients taking
  thyroid hormone fall within normal range
• 20 have excess hormone 20 undertreated
• New England Journal of Medicine (NEJM) study
  found after initiation of oral contraceptives in
  25 women on thyroid hormone, 10 had elevated TSH
  levels
• Hashimoto diseaseadd 25 to 50 g of thyroid
  hormone (25 dose increase)
• no thyroid functionafter, eg, radioactive iodine
  or thyroid surgery, 50 dose increase required

35
Changes in thyroid function during pregnancy

• if untreated, increases risk of worsening of
  hypothyroidism and for preeclampsia, anemia,
  postpartum hemorrhage, and cardiac ventricular
  dysfunction
• effects on offspringincreased risk for
  spontaneous abortion, low birth weight, abnormal
  brain development, and lower intelligence
  quotient (IQ)
• Controversial NEJM studyIQ lt85 in 4 of children
  born to control women vs 13 born to women with
  hypothyroidism
• thyroid testing by primary care physicians
  recommended
• may see pregnant women earlier than obstetricians
  (in first trimester)
• Hypothyroidism may occur in first 20 wk (when
  TBGs rising)
• check TSH as soon as pregnancy confirmed
• check every 4 wk until week 20
• increase dose by 50 to 75 g/day
• after delivery, return to previous dose

36
Subclinical hypothyroidism

• signs and symptomsweight gain, fatigue, or TPO
  antibody positivity
• treatmentL-thyroxine (brand name or consistent
  generic manufacturer)
• taken on empty stomach
• avoid calcium and iron at the same time

37
Graves disease

• most common cause of thyrotoxicosis
• Autoimmune disease caused by thyroid-stimulating
  immunoglobulin (TSI)
• occurs predominantly in women 30 to 49 yr of age
• pregnancycondition exacerbated during first
  trimester
• improves in second and third trimesters (ie, can
  stop antithyroid medicine)
• worsens 1 to 6 mo postpartum
• fluctuations most likely due to changes in immune
  status

38
Treatment

• methimazole or propylthiouracil (PTU)interfere
  with thyroid hormone synthesis
• complicationspruritus occurs in 20 of patients
  (treat with antihistamines)
• 3 in 1000 have agranulocytosis
• if extreme sore throat or fever gt101F develop,
  stop medication and obtain complete blood count
  hepatitis and arthralgia (rare)
• dosage during pregnancy and breastfeedingPTU
  preferred (less transfer through placenta and
  breast milk) to decrease likelihood of fetal
  goiter
• Give lowest possible dose of antithyroid drug
• T3 and T4 in pregnancy
• maintain higher limits of normal, or slightly
  high (studies show no negative outcomes of mild
  thyrotoxicosis)
• check thyroid functions monthly in pregnant women
  taking antithyroid drugs
• TSIextremely high levels at end of pregnancy
  predict neonatal hyperthyroidism
• fetal US recommended, as large fetal goiter can
  cause asphyxiation during delivery
• if noncompliant or requiring high doses of
  antithyroid medication recommend surgery during
  second trimester

39
Alternative cause of low TSH during pregnancy

• Beta-human chorionic gonadotropin (Beta hCG)
  structurally similar to TSH
• Beta-hCG rises to maximal level at 12 wk, then
  falls to high but stable level Beta-hCG binds to
  TSH receptors and causes slight increase in
  thyroid hormone
• therefore, TSH drops during first trimester, then
  rises as Beta-hCG drops
• take-home message
• low TSH during pregnancy not always indicative of
  hyperthyroidism
• measure thyroid function at end of first
  trimester if TSH suppressed and T4 or free T4
  normal or slightly elevated, do not treat
• check levels next month

40
Which of the following statements about zinc is
CORRECT? AOral zinc improves healing of venous
and arterial ulcers of the legs.BNasal zinc
gel reduces the duration of symptoms of the
common cold.CMost zinc is absorbed in the
ileum and renally excreted.DRoutine zinc
supplementation is necessary in healthy
adults.ECitrus fruits are an excellent source
of zinc.
41
Answer

• B
• Nasal zinc gel reduces the duration of symptoms
  of the common cold.

42
Zinc

•  Zinc is an essential trace element and a
  component of many metalloenzymes. It is involved
  in alcohol, carbohydrate and nucleic acids
  metabolism. Zinc plays a role in DNA, RNA and
  protein synthesis and stabilization. It has a
  structural function in ribosomes and cell
  membranes and impacts polynucleotide
  transcription and genetic expression. Steroid
  hormone receptors depend on zinc for hormone
  binding. Zinc influences spermatogenesis,
  embryonic development and fetal growth.
  Additionally, zinc influences taste
  and smell, promotes wound healing and supports
  the immune system.
•  Vegetables, lean red meat, eggs, nuts and
  shellfish are all good sources for zinc. The
  recommended daily allowance (RDA) for zinc in
  males is 11 mg daily females require 9 mg daily
  with slightly more needed during pregnancy and
  lactation. Children 4-8 years old require 5 mg
  daily, while children 9-13 years need 8 mg per
  day. Supplementation is not necessary in persons
  who eat a regular diet.
•  Zinc is absorbed in the jejunum. Both dietary
  fiber and phytate found in whole grain can
  inhibit absorption. Copper, iron and oxalate may
  impair uptake. Drugs that decrease zinc
  absorption includepenicillamine, ethambutol and
  sodium valproate.
• Zinc is stored intracellularly, mostly in bone
  and muscle, with less stored in the liver and
  kidneys. The majority is excreted in stool,
  although 10 percent is lost in urine. Sweat and
  desquamated epithelial cells also contain zinc.
•  Zinc deficiency is seen with diets that are low
  in calories and proteins. Because pancreatic
  enzymes are required for absorption of dietary
  zinc, pancreatic disease can also cause zinc
  deficiency. Mild zinc deficiency is sometimes
  seen with diabetes mellitus, cirrhosis,
  inflammatory bowl disease (Crohns)
  andmalabsorption syndromes. Excess renal
  excretion of zinc due to renal disease also
  causes a deficiency.Acrodermatitis enteropathica i
  s a rare autosomal recessive condition in which
  zinc is not absorbed normally and results in a
  zinc deficit. Patients receiving
  total parenteral nutrition (TPN) develop zinc
  deficiency unless supplements are provided.
•  Clinical Findings with Zinc Deficiency
•  Abdominal pAlopeciAnorexia
• Anxiety Depression
• Dermatitis Diarrhea
• Glossitis,, Growth delay
• Impaired wound healing Night blindness
• Poor concentration
• Stomatitis
•  Measurement of zinc level is possible using
  either plasma or white blood cells. Plasma levels
  less than60mcg/dL are considered low. Because
  zinc is a cofactor for alkaline phosphatase (ALP),
  low ALP levels are confirmatory for zinc
  deficiency. Zinc 60 mg given twice daily is
  recommended for supplementation.
•  While zinc toxicity is uncommon, it is
  associated with overzealous use of supplements,
  contamination of food or absorption of fumes
  while welding using zinc. Symptoms include
  vomiting, diarrhea, fever and renal failure.
  Decreased serum copper, iron and HDL levels are
  also seen. Welding fumes specifically cause
  respiratory distress, excess salivation,
  headaches and sweating.
•  Zinc is purported to be effective for numerous
  medical problems. One randomized, controlled
  trial (RCT) involved medicating children and
  adolescents with zinc lozenges to treat the
  common cold. The lozenges were ineffective and
  made most subjects feel worse. Another RCT on the
  effectiveness of zinc nasal gel in treating the
  common cold found that zinc reduced the duration
  of cold symptoms by 1.7 days over placebo.
•  One Cochrane review found that oral zinc sulfate
  did not improve healing of arterial and venous
  ulcers of the legs. Zinc also was not effective
  for preventing type 2 diabetes mellitus in
  overweight women in another Cochrane review.
•  While routine zinc supplementation is not
  currently recommended, children with stunted
  growth and low plasma zinc concentrations may
  benefit from extra zinc. In a recent systematic
  review, zinc supplementation produced significant
  changes in height and weight in prepubertal childr
  en who were small for their age (SOR B Ref. 2).
•  Selected references     

43
A 32-year-old female presents to your office
after Roux-en-y gastric bypass surgery 3 months
prior for morbid obesity and hypertension. She
has lost weight rapidly after the surgery, but
she complains of persistent nausea and vomiting
with hand tingling for the previous 2 weeks. When
she called the surgeon?s office, she was
prescribed metoclopramide (generic, Reglan) and
advised to see her family physician. On
examination her gait is unsteady, she appears
slightly confused and forgetful and nystagmus is
noted her examination is otherwise unremarkable.
Select the most appropriate next step in her
management. AReassurance to continue oral
vitamin supplementation and oral
hydrationBReferral for endoscopy to treat
likely gastric outlet stenosisCRoutine
neurology referral for gastric bypass
neuropathyDUrine toxicology screen for illicit
drug useEEmergent admission for parental
thiamine treatment
44
Answer

• E
• Emergent admission for parental thiamine
  treatment

45
Wernicke Encephalopathy Following Bariatric Surger
y

• Obesity surgery provides benefits in treating the
  complications of obesity including diabetes,
  sleep apnea and hypertension. As obesity rates
  increase (two thirds of Americans are overweight
  or obese),bariatric surgery rates have increased,
  with more than 170,000 operations performed in
  2005. Given the number of cases, family
  physicians are caring for these patients along
  with bariatric surgeons, especially after the
  initial 30-day postoperative period when almost 1
  percent of patients die from pulmonary
  emboli, anastomotic leaks or respiratory failure.
•  
• In the long term, however, functionally diverting
  food past the stomach and duodenum (except for a
  20 ml stomach pouch) predisposes patients to a
  host of nutritional deficiencies to include iron,
  thiamine (Vitamin B1), pyridoxine (Vitamin B6),
  folic acid (Vitamin B9) and cobalamin (Vitamin
  B12). Despite use of lifelong vitamin
  supplements, poor absorption may cause
  complications such as peripheral neuropathy from
  B12 deficiency and Wernicke encephalopathy from
  B1 deficiency (as seen in this case).
  Characterized by a classic symptom triad of
  confusion, ataxia and nystagmus, Wernickeencephalo
  pathy was recently described in a systematic
  review of more than 30 obesity surgery cases.
  Most Wernicke cases were seen 1-3
  months postsurgery, occurred in women and were
  associated with abnormal vomiting (vomiting
  despite appropriately sized meals) and peripheral
  neuropathy. Of note, the classic symptom triad
  may be incomplete in one third of bariatric surgic
  al patients.
•  Clinicians need to maintain a high index of
  suspicion in bariatric surgery patients who
  present with neurological symptoms serum
  thiamine levels and erythrocyte transketolase leve
  ls may be normal and characteristic radiographic
  findings on magnetic resonance imaging (MRI)
   hyperintense signal around the thalamus and
  3rd/ 4th ventricles) may be absent. MRI has a
  sensitivity of 53 percent and a specificity of 93
  percent for the diagnosis of Wernicke encephalopat
  hy.
•  Patients suspected to have Wernicke encephalopath
  y need prompt thiamine replacement (at least 100
  mg daily) to reverse symptoms and prevent
  long-term sequelae, such as Korsakoffsyndrome
  (amnesia, apathy, ataxia and confabulation).
  Treatment response can be dramatic, with
  improvement seen in the first 24 hours (SOR A
  Ref. 2).
•  Urine toxicology drug screening could be helpful
  if the patient had no response to thiamine, but
  it would not be the initial indicated action,
  given the classic combination of Wernicke-like
  symptoms in a gastric bypass patient. Gastric
  bypass neuropathy can occur due to
  thiamine-deficiency-related defects in the myelin
  sheath, but thiamine replacement would be the
  best response, not delaying treatment for
  a neurologic consult. While nausea after obesity
  surgery is common, persistent vomiting is
  abnormal. Proceeding directly to
  therapeutic endoscopic dilatation would be
  premature without first performing a diagnostic
  upper gastrointestinal series.
•  Selected references
• 1. Sechi G, Serra A. Wernicke's encephalopathy
  new clinical settings and recent advances in
  diagnosis and management. Lancet Neurol 2007
  6(5)442-455.
• 2. Singh S, Kumar A. Wernicke encephalopathy
  after obesity surgery a systematic review.
  Neurology 2007 68(11)807-811.
• 3. Virji A, Murr MM. Caring for patients
  after bariatric surgery. Am Fam Physician 2006
  73(8) 1403-8.http//www.aafp.org/afp/20060415/140
  3.html  Accessed March 2008

46
Water-soluble vitamins are absorbed, transported
and quickly excreted. Because they are not
stored, water-soluble vitamins must be regularly
replaced. Which group of symptoms is correctly
paired with its causative vitamin deficiency?
AVitamin B3 (niacin) deficiency ? cheilitis,
stomatitis, glossitisBVitamin B2 (riboflavin)
deficiency ? scurvyCVitamin B1 (thiamine)
deficiency ? BeriberiDVitamin B6 (pyridoxine)
deficiency ? dermatitis, dementia,
diarrheaEVitamin C (ascorbic acid) deficiency
? elevated homocysteine levels
47
Answer

• C
• Vitamin B1 (thiamine) deficiency ? Beriber

48
Water Soluble Vitamins

•  Vitamin B1 (thiamine) is important for normal
  cardiac, muscle and nervous tissue function.
  Thiamine deficiency is associated with
  beriberi, Wernicke-Korsakoff syndrome and Leighs
  syndrome. Beriberi is a symmetric peripheral
  neuropathy. Dry beriberi is a combination
  sensory/motor neuropathy. Wet beriberi involves
  a combination of neuropathy and cardiac
  impairments (cardiomyopathy and congestive heart
  failure). Wernicke-Korsakoff syndrome is
  characterized by the triad of nystagmus,ophthalmop
  legia and ataxia. Leighs syndrome is a form
  of subacute necrotizing encephalomyopathy.
•  Vitamin B3 (niacin) is metabolized to active
  forms that are involved in the synthesis and
  metabolism of carbohydrates, fatty acids and
  proteins. Niacin deficiency is rare but is
  occasionally seen withcarcinoid syndrome, Hartnup 
  disease and prolonged use of isoniazid. Symptoms
  of niacin deficiency include diarrhea, dementia,
  delusions and dermatitis. The dermatitis is a
  symmetric, hyperpigmented, sunburn-like rash in
  sun-exposed areas.
•  Vitamin B2 (riboflavin) promotes development of
  skin and red blood cells through energy
  conversion of glucose. Riboflavin deficiency
  causes dry, cracked skin cheilitis stomatitis
  and glossitis. Anormocytic-normochromic anemia is
  often seen. While riboflavin deficiency is rare,
  certain groups are at risk. Persons with anorexia
  nervosa, lactose intolerance, malabsorption syndro
  mes, inborn errors of metabolism or long-term
  barbiturate use are at increased risk.
•  Vitamin B6 (pyridoxine) is necessary for the
  formation of amino acids, red blood cells and
  antibodies. Low levels of pyridoxine are
  associated with elevated homocysteine levels and
  increased risk for heart disease. Pyridoxine
  deficiency also causes stomatitis, glossitis, chei
  losis, confusion and depression.
•  Vitamin C (ascorbic acid) has several important
  functions. It helps build and maintain collagen
  and connective tissue. Vitamin C enhances iron
  and folic acid absorption, aids in wound healing
  and is an antioxidant. Scurvy, ecchymoses,
  bleeding gums, petechiae and impaired wound
  healing are all associated with vitamin C
  deficiency. Other symptoms include weakness,
  malaise, joint swelling,arthralgias and
  neuropathy. Routine vitamin C supplementation
  provides a consistent, statistically significant
  benefit, albeit small, on the duration and
  severity in the common cold (SOR B Ref. 2).
•  Selected references
• 1. Cervantes-Laurean N, McElvaney G, Moss J.
  Niacin. In Shils M, ed, Modern Nutrition in
  Health and Medicine.Philadelphia Lippincott,
  2000401.
• 2. Douglas R, Hemila H, Chalker E, et al. Vitamin
  C for preventing and treating the common
  cold. Cochrane DatabasSyst Rev 1998
  (1)CD000980. http//www.cochrane.org/reviews/en/a
  b000980.html  Accessed March 2008
• 3. Elsas LS, Longo N, Rosenberg LE. Inherited
  defects of membrane transport. In Fauci AS, Braun
  wald E, IsselbacherK, et al., eds, Harrisons
  Principles of Internal Medicine. 14th ed. New
  York McGraw-Hill, 19982203.
• 4. Jacob R. Vitamin C. In Shils M, Olson
  J, Shike M, et al., eds, Modern Nutrition in
  Health and Disease. PhiladelphiaLippincott,
  2000467.
• 5. Siegfried DR, Simmons K. Vitamins
  minerals. Arthritis Today. 2007 9-1069-71.
• 6. Tanphalchitr V. In Shils M, ed, Modern
  Nutrition in Health and Medicine.
  9th ed. Philadelphia Lippincott, 2000381.
• 7. Wilson JA. Vitamin deficiency and
  excess. In Fauci AS, Braunwald E, Isselbacher K, 
   et al., eds, Harrisons Principles of Internal
  Medicine. 14th ed. New York McGraw-Hill,
  1998481

49
A 75-year-old patient who resides in a nursing
home has just become your patient. She states
that her bones are brittle. She has a family
history of osteoporosis and hates taking
medications, although she has been on 1,500
milligrams of calcium citrate daily for years.
She wants to know whether vitamin D
supplementation, as recommended by her grandson
who is a nurse, would help her bones. Of the
following options, what dose and form of vitamin
D would be most likely to help prevent fractures
in this patient? A200 IU vitamin D3B400 IU
vitamin D2C800 IU 25-hydroxyvitamin DD800
IU vitamin D3E2,000 IU vitamin D of any form
50
Answer

• 800 IU vitamin D3

51
A 6-month-old infant girl is being evaluated for
recurrent vomiting, diarrhea and a relatively
rapid fall from the 50th percentile for weight to
the 10th percentile over a period of
approximately 6 weeks. She was the product of a
normal term pregnancy and delivery. Both parents
are healthy and have two other healthy children
ages 6 and 4 years. The baby was breast-fed
exclusively until very recently (after her
symptoms were noted). On examination she is
hypotonic, somnolent and does not play or smile.
She is pale and has fasciculations and sucking
movements of the tongue. Laboratory evaluation
reveals hemoglobin, 6.8 g/dL (normal, 11.2-16.5
g/dL) hematocrit, 24 percent (normal, 35-49
percent) MCV, 102 fL (normal, 80-96 fL) MCH, 32
pg/cell (normal, 26-34 pg/cell) MCHC, 32.8 g/dL
(normal, 32-36 g/dL) platelet count, 412 x 109/L
(normal, 150-400 x 109/L) and WBC, 5,500
/mm3 (normal, 4,500-11,000/mm3). The peripheral
blood film showed megaloblastic features
including oval macrocytosis, anisopoikilocytosis
and hypersegmented polymorphs. Additional
evaluation for her anemia reveals normal serum
iron and thyroid function tests. She has a normal
folate level however, her B12 is low at 75 pg/mL
(normal, 180-900 pg/mL). In a search for the
cause for the vitamin B12 deficiency, additional
questioning of the parents reveals that the
mother has been a strict vegetarian (no animal
products or byproducts) for almost 4 years. Which
of the following statements regarding Vitamin
B12 deficiency in infants is CORRECT?
AMaternal vitamin B12 serum levels normally
increase during pregnancy without vitamin
supplementation.BGuidelines recommend serum
testing of vitamin B12levels in infants of
pregnant women who are strict vegetarians.CPreg
nant vegetarians who consume milk in their diet
are not at risk for low vitamin
B12 levels.DMost infants born of mothers with
low vitamin B12 levels immediately show signs of
a neurological problem.EIntramuscular vitamin
B12 injections with iron and folate supplements
are the treatment of choice.
52
Answer

• E
• Intramuscular vitamin B12 injections with iron
  and folate supplements are the treatment of
  choice.

53
B12 Deficiency In Infants 

• Although the maternal vitamin B12 level is known
  to fall throughout pregnancy, this is not
  considered to be significant. However,
  correlation exists between maternal and neonatal
  vitamin levels and corresponding
  neonatal homocysteine levels. With severe
  maternal vitamin B12 deficiency, spontaneous
  abortions may occur, and, if this persists,
  infertility may ensue. With a mild deficiency, a
  normal pregnancy and delivery at term may occur,
  but such infants have low vitamin B12 levels at
  birth and may also be at risk of developmental
  defects. The situation of vitamin deficiency is
  perpetuated if the vitamin B12-deficient mother
  breast-feeds her infant. Vitamin B12 levels are
  very low in the milk of these mothers.
•  One of the causes of low maternal vitamin B12 is
  dietary deficiency. Vegans (vegetarians without
  intake of any animal products) have no vitamin
  B12 in their diet unless there is contamination
  by soil or bacteria. Vegetarians who also consume
  milk, milk products and eggs may also have low
  vitamin B12 levels. Vegetarians may mask the
  hematological effects of vitamin B12 deficiency
  due to their high folate (folic acid) intake and,
  therefore, have normal hemoglobin levels.
  Oral folatesupplement in the diet and the taking
  of folate preparations in pregnancy to prevent
  neural tube defects may also have a masking
  effect.
•  The clinical picture of vitamin B12 deficiency
  may appear in the infant several months after
  birth and after a period of normal development.
  The first signs of deficiency are irritability,
  anorexia, apathy, vomiting, weak cry and
  regression of motor development. The infant then
  fails to thrive and may develop neurological
  features such as head lag, hyporeflexia, hypotonia
   and choreoathetoidmovements. Heart failure may
  eventually develop. This may be associated
  with macrocytic anemia (which may be
  severe), hypersegmented polymorphonuclear leukocyt
  es and tissue evidence of vitamin B12 deficiency
  such as raised methylmalonic acid levels. Little
  information is available about long-term
  neurological sequelae. Intellectual impairment,
  gait disturbance and epilepsy may result.
•  can cause severe disease and since treatment is
  readily available and effective, screening of
  newborns of mothers who are vegetarian may be
  indicated. Guidelines for screening have not been
  established, although screening for increased
  urinary methylmalonic acid (a sign of
  B12 deficiency) at 3 weeks of age has been
  suggested but requires additional study.
  Treatment includes intramuscular vitamin
  B12administration as well as iron
  and folate supplementation.
•  Selected references
• 1. Campbell CD, Ganesh J, Ficicioglu C. Two
  newborns with nutritional vitamin B12 deficiency
  challenges in newborn screening for vitamin
  B12 deficiency. Haematologica 2005
  90(12 Suppl)ECR45.
• 2. Casella EB, Valente M, de Navarro JM, et
  al. Vitamin B12 deficiency in infancy as a cause
  of developmental regression. Brain Dev 2005
  27(8)592-594.
• 3. Simsek OP, Gonc N, Gumruk F, et al. A child
  with vitamin B12 deficiency presenting
  with pancytopenia andhyperpigmentation. J Pediatr 
  Hematol Oncol 2004 26(12)834-836.
•  

54
Ginger is a common spice and culinary herb. Which
of the following statements regarding ginger is
CORRECT? AGinger is approved by the U.S. Food
and Drug Administration for the treatment of
nausea associated with chemotherapy.BAt least
one randomized controlled study suggests that
ginger is effective in the treatment of nausea
associated with early pregnancy.CA common side
effect of ginger is constipation.DGinger tends
to elevate cholesterol levels.EGinger tends to
promote blood clotting.
55
Answer

• B
• At least one randomized controlled study suggests
  that ginger is effective in the treatment of
  nausea associated with early pregnancy.

56
Ginger

•  Ginger has been used for its medicinal effects
  since ancient times. Today, it is one of the most
  popular herbal supplements and is purported to be
  helpful for several medical conditions. The U.S.
  Food and Drug Administration categorizes ginger
  as a food additive. Ginger has been studied for
  the treatment for nausea and vomiting, especially
  during early pregnancy, and arthritis.
•  
• Ginger 250 mg PO QID has been proven effective in
  treating nausea and vomiting of early pregnancy.
  Human studies show no adverse effects on the
  fetus. Ginger has been found to suppress gastric
  contractions and increase gastrointestinal
  motility (SOR B Ref. 4). Six studies involving
  approximately 700 patients support the
  effectiveness of ginger on nausea and vomiting of
  early pregnancy. Ginger was superior to placebo
  in 4 of the studies and comparable to vitamin
  B6(pyridoxine) in 2 studies. One possible
  mechanism to explain gingers antiemetic property
  is that it appears to inhibit serotonin receptors
  of both the gastrointestinal and central nervous
  systems. Ginger has also been recommended for the
  treatment of motion sickness and
  chemotherapy-induced nausea and vomiting.
  However, evidence has not proved its
  effectiveness for these conditions.
•  
• Another common medicinal use of ginger is to
  decrease inflammation. Ginger has been shown to
  inhibit the activation of tumor necrosis factor
  alpha and cyclooxygenase-2 expression. It is used
  widely today for the treatment of osteoarthritis
  and ulcerative colitis. Studies of its efficacy,
  however, have concluded shown mixed results.
•  
• Ginger has also been reported to have a wide
  range of effects on the cardiovascular system. A
  few preliminary studies have suggested a
  protective effect on coronary artery disease by
  lowering cholesterol and preventing blood from
  clotting. In contrast, ginger may
  be inotropic and has been reported to cause
  arrhythmias. It should be used cautiously in
  patients taking warfarin (generic,Coumadin),
  since it may prolong bleeding time. Overall,
  ginger has few side effects. The most common ones
  are heartburn, diarrhea and irritation of the
  mucous membrane of the mouth.
•  
• Selected references
• 1. Altman RD, Marcussen KC. Effects of a ginger
  extract on knee pain in patients with
  osteoarthritis. Arthritis Rheum 2001
  442531-2538.
• 2. Chaiyakunapruk N, Kitikannakorn N, Nathisuwan S
  , et al. The efficacy of ginger for the
  prevention of postoperative nausea and vomiting
  a meta-analysis. Am J Obstet Gynecol 2006
  19495-99.
• 3. Frondoza CG, Sohrabi A, Polotsky A, et al. An
  in vitro screening assay for inhibitors
  of proinflammatory mediators in herbal extracts
  using human synoviocyte cultures. In Vitro Cell
  Dev Biol Anim 2004 4095-101.
• 4. Jewell D, Young G. Interventions for nausea
  and vomiting in early pregnancy. Cochrane
  Database Syst Rev2003(4)CD000145. http//www.coc
  hrane.org/reviews/en/ab000145.html  Accessed
  March 2008
• 5. University of Texas at Austin. Recommendations
  for the evaluation and management of nausea and
  vomiting of early pregnancy (lt20 weeks
  gestation). http//www.guideline.gov/guidelines/FT
  NGC-2454.html  Accessed March 2008
• 6. White B. Ginger an overview. Am Fam Physician
  2007 75(11)1689-1691.http//www.aafp.org/afp/200
  70601/1689.html  Accessed March 2008
•  

57
Which of the following statements regarding
high-density lipoprotein (HDL) cholesterol is
CORRECT? ALow HDL cholesterol level is defined
as less than 30 mg/dL.BThe use of
beta-blockers has been associated with an
increase in HDL serum levels.CElimination of
dietary trans fat can increase HDL serum
levels.DThe Mediterranean diet for improvement
of HDL serum levels consists of a relatively high
intake of red meat and alcohol with low
carbohydrate intake.EThirty to 60 minutes of
exercise on most days of the week will decrease
LDL serum levels but should not be expected to
change HDL levels.
58
Answer

• C
• Elimination of dietary trans fat can increase HDL
  serum levels.

59
HDL Diets

• A low-serum high-density lipoprotein (HDL)
  cholesterol level has been recognized as an
  independent risk factor for development of
  cardiovascular disease. HDL levels vary among
  different racial/ethnic groups, with African
  Americans having higher HDL levels in general
  than Caucasians. Up to half of the variability
  in HDL levels is related to genetic inheritance.
•  
• Every 1mg/dL increase in HDL level is associated
  with a 2-3 percent decrease in coronary artery
  disease risk. A low HDL is defined as lt40
  mg/dL and is often associated with elevated
  triglyceride levels, obesity, cigarette smoking,
  type II diabetes mellitus and ingestion of
  certain medications (e.g., beta-blockers,
  steroids and progestins). Lifestyle modification
  is the first line of treatment for low
  serum HDL levels. Thirty to 60 minutes of
  exercise on most days of the week can
  increase HDL. Elimination of dietary trans fatty
  acids can help decrease LDL levels and,
  simultaneously, increase HDL.Trans fat
  is monosaturated or polyunsaturated fat that has
  been commercially hydrogenated, making it
  chemically similar to saturated fats. The
  hydrogenation process increases the melting
  point, makingtrans fat easier to bake with, and
  the reduction in oxidation potential increases
  shelf life. Replacingtrans fats with
  healthy, monosaturated fats (canola oil,
  safflower oil, olive oil), polyunsaturated fats
  (corn oil, soybean oil) and monosaturated-rich
  nuts (hazelnuts, almonds, pecans, cashews,
  walnuts, macadamia nuts) can increase HDL levels.
  Although both monosaturated and polyunsaturated
  fats are preferred over trans fat, monosaturated f
  ats are recommended over polyunsaturated fats
  (which have been associated with increased
  platelet aggregation and incorporation
  of LDL into the arterial intima, leading to
  plaque formation). The addition of fiber
  (particularly soluble) or a fish oil supplement
  can add further gains in HDL levels. Moderate
  alcohol intake (up to 1 drink daily for women and
  2 drinks daily for men) has also been shown to
  increase HDL levels.
•  
• A Mediterranean diet, one that is rich in fruits
  and vegetables and includes healthy fat, is the
  best diet to increase HDL levels. The
  Mediterranean diet was first studied more than 50
  years ago when it was noticed that adults on
  the island of Crete lived longer and had fewer
  cardiovascular events than adults in the United
  States. While this is not a specific diet,
  general guidelines include high intake of
  vegetables, fruit, nuts, legumes and grains high
  intake of olive oil (but low intake of saturated
  fats) moderate intake of fish low to moderate
  intake of dairy products (primarily cheese or
  yogurt) limitation of eggs low consumption of
  poultry and very low consumption of red meat.
  Moderate alcohol consumption, primarily wine with
  meals, is also part of the diet. The food pyramid
  in Figure 2 gives a graphic representation of one
  interpretation of the diet.
•  

60
DIRECTIONS The following series of questions
deals with primary and secondary
hyperparathyroidism. For the following four
questions, select the answer most closely
associated with the statement. Surgery is the
primary form of treatment. Aif primary
hyperparathyroidism is associated with the
statement Bif secondary hyperparathyroidism is
associated with the statement Cif BOTH primary
hyperparathyroidism and secondary
hyperparathyroidism are associated with the
statement Dif NEITHER primary
hyperparathyroidism NOR secondary
hyperparathyroidism is associated with the
statement
61
Answer

•  A
• if primary hyperparathyroidism is associated with
  the statement

62
Treatment with 1,25-hydroxycholecalciferol
(1,25-dihydroxy vitamin D3, calcitriol) is
indicated. Aif primary hyperparathyroidism is
associated with the statement Bif secondary
hyperparathyroidism is associated with the
statement Cif BOTH primary hyperparathyroidism
and secondary hyperparathyroidism are associated
with the statement Dif NEITHER primary
hyperparathyroidism NOR secondary
hyperparathyroidism is associated with the
statement
63
Answer

•  B
• if secondary hyperparathyroidism is associated
  with the statement

64
Most commonly caused by chronic kidney disease
 Aif primary hyperparathyroidism is associated
with the statement Bif secondary
hyperparathyroidism is associated with the
statement Cif BOTH primary hyperparathyroidism
and secondary hyperparathyroidism are associated
with the statement Dif NEITHER primary
hyperparathyroidism NOR secondary
hyperparathyroidism is associated with the
statement
65
Answer

•  B
• if secondary hyperparathyroidism is associated
  with the statemen

66
May result in hypercalcemia  Aif primary
hyperparathyroidism is associated with the
statement Bif secondary hyperparathyroidism is
associated with the statement Cif BOTH primary
hyperparathyroidism and secondary
hyperparathyroidism are associated with the
statement Dif NEITHER primary
hyperparathyroidism NOR secondary
hyperparathyroidism is associated with the
statement
67
Answer

•  C
• if BOTH primary hyperparathyroidism and secondary
  hyperparathyroidism are associated with the
  statement

68
Hyperparathyroidism

•  Four parathyroid glands are located behind the
  thyroid gland. Through the secretion of
  parathyroid hormone (PTH), these small glands
  regulate calcium absorption from the gut, calcium
  secretion by the kidneys and calcium storage in
  bones. Calcium plays multiple roles within the
  human body including bone metabolism, nerve
  function and muscle activity. When serum calcium
  levels fall, PTH secretion increases. If serum
  levels of calcium are chronically low, the
  parathyroid glands may hypertrophy as they
  attempt to produce adequate amounts of PTH to
  maintain a normal calcium level.
•  Vitamin D also has an important role in calcium
  metabolism. PTH and vitamin D closely influence
  each other. Inadequate vitamin D leads to reduced
  calcium absorption, reduced serum calcium and a
  reactionary increase in PTH production. Vitamin D
  is not a true vitamin in the sense that it is not
  a required part of a human diet. Human skin when
  exposed to ultraviolet radiation creates vitamin
  D. In temperate climates and for those who spend
  most of their time indoors, dietary vitamin D or
  vitamin D supplements are usually necessary.
  Vitamin D has a confusing taxonomy. Vitamin D
  from dietary sources and the form of vitamin D
  used in nutritional supplements
  is cholecalciferol (vitamin D3). This form
  of vitamin D is metabolized in the liver to
  25-hydroxycholecalciferol (25-hydroxy vitamin
  D3). This in turn is metabolized by the kidney to
  produce 1,25-hydroxycholecalciferol (1,25-dihydrox
  y vitamin D3). This form is also
  called calcitriol and it is the most active form
  of vitamin D.
•  Primary hyperparathyroidism is caused by an
  adenoma of usually one but sometimes more that
  one parathyroid gland, producing excessive
  amounts of PTH. This results in hypercalcemia.
  The hypercalcemia may initially be asymptomatic,
  but as the serum calcium level increases,
  symptoms such as proximal muscle weakness,
  abdominal pain and generalized fatigue may occur.
  The serum level at which symptoms are noted
  partially depends on the rate of increase. With a
  relatively acute rise, symptoms may be noticed at
  a serum level of 12 mg/dL (normal, 8.4-10.6
  mg/dL). However, with a slow, chronic elevation,
  symptoms may not be noticed at a serum levels as
  high as 12-14 mg/dL. Prolonged hypercalcemia may
  result in nephrocalcinosis and or osteitis fibrosa
   cystica.
•  Primary hyperparathyroidism resulting in
  significant symptoms or complications is best
  treated by surgical excision of the hypertrophied
  gland. Criteria for surgery include age younger
  than 50 years, serum calcium gt12
  mg/dL, hypercalciuria (gt400 mg/day), nephrolithias
  is, impaired renal function, osteitis fibrosa cyst
  ica, reduced bone mass and neuromuscular symptoms
  including weakness, atrophy, hyperreflexia or
  gait disturbance. Minimally invasive procedures
  are now commonly used to remove parathyroid
  adenomas. In older patients who are asymptomatic,
  who have well-preserved renal function and who
  have no evidence of bone disease, it may be
  reasonable to follow the patient regularly and
  decide whether symptoms subsequently require
  surgery.
•  Secondary hyperparathyroidism is most often
  caused by renal disease that negatively impacts
  the conversion of 25-hydroxycholecalciferol to
  the more active 1,25-hydroxycholecalciferol. Insuf
  ficient 1,25-hydroxycholecalciferol leads
  initially to hypocalcemia. This results in
  increased PTH secretion. The increased PTH secreti
  on often results in hypercalcemia.
  Supplementation with 1,25-hydroxycholecalciferol (
  calcitriol) is the most effective means of
  treatment. In most cases calcitriol (generic, Roca
  ltrol) treatment results in decreased PTH levels
  and a normalization of serum calcium. Patients
  with a mild degree of renal impairment may have
  secondary hyperparathyroidism without their
  physicians being aware of it. Physicians who care
  for patients with renal impairment should measure
  1,25-hydroxycholecalciferol intermittently. In
  rare circumstanceshypertrophic parathyroid tissue
  may not respond to treatment with calcitriol,
  resulting in tertiary hyperparathyroidism. This
  may then require surgical treatment to remove one
  or more hypertrophicglands.
•  Selected references
• 1. Bailie GR, Massry SG. Clinical practice
  guidelines for bone metabolism and disease in
  chronic kidney disease an overview. Pharmacothera
  py 2005 25(12)1687-1707.
• 2. Carroll MF, Schade DS. A practical approach
  to hypercalcemia. Am Fam Physician 2003
  671959-1966. http//www.aafp.org/afp/20030501/195
  9.html  Accessed March 2008
• 3. Diaz-Corte C, Cannata-Andia J. Management of
  secondary hyperparathyroidism the gap between
  diagnosis and treatment. Am J Med Sci 2000
  320(2)107-111
• 4. Potts JT. Parathyroid hormone past and
  present. J Endocrinol 2005 187(3)311-325.
• 5. Taniegra ED. Hyperparathyroidism.
  Am Fam Physician 2004 69333-339,
  340. http//www.aafp.org/afp/20040115/333.html  Ac
  cessed March 2008 
•  

69
Many different types of infant formulas are
available. Parents often have questions
concerning infant formulas for their family
physicians. Which of the following is TRUE
concerning infant formulas? AWhey is the main
protein source in standard cow?s milk-based
formulas (e.g., Similar, Enfamil).BInfants
on formulas supplemented with docosahexaenoic
acid (DHA) and arachidonic acid (ARA) have been
shown to have greater growth parameters than
infants on formulas without DHA and ARA.CSoy
protein formulas (e.g., ProSobee, Isomil) are
hypoallergenic formulas.DSoy protein formulas
are recommended for infants weighing less than
1,800 grams.EElemental formulas (e.g.,
Neocate, EleCare) are recommended for infants
who cannot tolerate protein hydrolysate formulas.
70
Answer

• E
• Elemental formulas (e.g., Neocate, EleCare) are
  recommended for infants who cannot tolerate
  protein hydrolysate formulas

71
Infant Formulas

•  Most infant formulas are designed to approximate
  the nutritional value of human milk. Standard
  infant formulas are cows milk-based and are
  available with (Enfamil LIPIL, Good Start
  Supreme, SimilacAdvance) and without
  (Similac with Iron, Good Start
  Essentials) docosahexaenoic acid (DHA)
  andarachidonic acid (ARA) supplementation. DHA and
   ARA supplementation have been shown to improve
  visual acuity and cognitive development in some
  studies. There is no significant difference in
  growth parameters, however, with this
  supplementation. Formulas usually contain
  approximately 40-50 percent of calories from
  carbohydrates, 40-50 percent from fat and 5-10
  percent of calories from protein. Casein is the
  main protein source in standard infant formulas.
  Infants who cannot tolerate casein are given
  whey-predominant or whey-only formulas (e.g.,
  Good Start). All infant formulas are also
  fortified with iron as recommended by
  the American Academy of Pediatrics (AAP). While
  some formulas are labeled low iron, these are not
  recommended by AAP (SOR C Ref. 3).
•  Some formulas (ProSobee LIPIL, Good Start
  Supreme Soy, Similac Isomil Advance) are
  designed for infants who are allergic to standard
  formulas. Soy protein formulas are not true
  hypoallergenic formulas. Formulas are defined as
  hypoallergenic if randomized controlled trials
  show that they do not cause reactions in 90
  percent of infants or children with confirmed
  cows milk allergy. Although soy protein formulas
  are often used for infants with cows milk
  protein-induced enterocolitis, up to 60 percent
  of these infants will be equally sensitive to soy
  protein. The AAP does not recommend soy formulas
  for infants weighing less than 1,800 grams due to
  the potential for aluminum toxicity and
  inadequate weight gain in premature infants.
•  Protein hydrolysate formulas (Nutramigen LIPIL, 
  Pregestimil, Similac Alimentum) are
  hypoa