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SFM EXAM 2a/b 2020 > CIS: Nutrition > Flashcards

CIS: Nutrition Flashcards

1
Q

LO’s for CIS: Nutrition

A

uUpon completion of this CIS, the student should be able to:

  • Compare and contrast the physical signs associated with protein and calorie malnutrition states.
  • Summarize important information from a case history into a SOAP format.
  • Understand the criteria for metabolic syndrome in order to evaluate patients for the condition.
  • Understand the biochemistry of metabolic syndrome in order to summarize sequelae of the disease.
  • Evaluate the signs and symptoms of metabolic syndrome.
  • Compare and contrast types of inborn errors of metabolism.
  • Explain the need for and the logistics of newborn screening for inborn errors of metabolism.
  • Compare and contrast the clinical manifestations of vitamin deficiency, including Vitamins A, B1, B2, B3, B6, B12, C, D, E, and K.
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2
Q

How is BMI classified?

A
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3
Q

A 54 year old post menopausal Caucasian female presents for follow-up of her hypertension. She has noticed some shortness of breath with activity and some intermittent swelling of her ankles especially when she is on her feet for prolonged periods of time. Physical exam reveals a well developed and well nourished female 5‘ 6” and 190 lbs. Calculated BMI is 30.7, BP 145/92 mm Hg, heart rate is 86 BPM, temperature is 98.6 F, respiration is 18 breaths per minute. HEENT reveals xanthelasma palpebrarum and early corneal arcus. Chest is clear to auscultation and percussion. Cardiac exam reveals RRR without murmur and slightly decrease peripheral pulses. Abdomen is obese, liver is enlarged and non tender, well healed RUQ scar, and no other abnormalities. The remainder of the exam is unremarkable. Complete metabolic panel revealed the following abnormal results: Total cholesterol: 230 mg/dL, HDL: 30 mg/dL, LDL: 182 mg/dL, Triglycerides: 220 mg/dL, Glucose (fasting): 180 mg/dL. Which of the following is most likely in this scenario?

A.These findings are not supportive of a single diagnostic entity

B.Complications associated with cholecystectomy

C.Consistent with metabolic syndrome (Syndrome X)

D.Autosomal recessive inborn error of metabolism, autosomal recessive

E.Alcohol related cardiomyopathy with secondary liver “sclerosis”

A

C.Consistent with metabolic syndrome (Syndrome X)

WHY? —> Impaired fasting glucose, BMI >30, Dyslipidemia, Blood pressure >/= 140/90

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4
Q

A 54 year old post menopausal Caucasian female presents for follow-up of her hypertension. She has noticed some shortness of breath with activity and some intermittent swelling of her ankles especially when she is on her feet for prolonged periods of time. Physical exam reveals a well developed and well nourished female 5‘ 6” and 190 lbs. Calculated BMI is 30.7, BP 145/92 mm Hg, heart rate is 86 BPM, temperature is 98.6 F, respiration is 18 breaths per minute. HEENT reveals xanthelasma palpebrarum and early corneal arcus. Chest is clear to auscultation and percussion. Cardiac exam reveals RRR without murmur and slightly decrease peripheral pulses. Abdomen is obese, liver is enlarged and non tender, well healed RUQ scar, and no other abnormalities. The remainder of the exam is unremarkable. Complete metabolic panel revealed the following abnormal results: Total cholesterol: 230 mg/dL, HDL: 30 mg/dL, LDL: 182 mg/dL, Triglycerides: 220 mg/dL, Glucose (fasting): 180 mg/dL. Ultrasound guided liver biopsy is performed. Which finding is most likely?

A.Normal

B.Steatosis (fatty liver)

C.Iron deposition

D.Copper deposition

E.Increased fibrous tissue deposition

A

B.Steatosis (fatty liver)

WHY—> Increased insulin and insulin resistance increase fatty acid and triglyceride synthesis in the liver

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5
Q

What are inborn errors of metabolism?

A
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6
Q

Give a list of Abnormalities Suggesting Inborn Errors of Metabolism.

A
  • General
    • Dysmorphic features, deafness, hydrops, self-mutilation, abnormal body or urine odor, hepatosplenomegaly, abnormal hair growth
  • Neurologic
    • Hypo/hypertonia, coma, persistent lethargy, seizures
    • Not meeting developmental milestones
  • GI
    • Poor feeding, recurrent vomiting, jaundice
  • Eyes
    • Cataracts, Cherry red macula, dislocated lens, glaucoma
  • Muscles, joints
    • Myopathy, abnormal mobility
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7
Q

A 6 month old Caucasian female infant of European refugees presents for immunization. You notice social and cognitive delays. When questioned, mom says she does not reach for or hold on to toys, bring her hand to her mouth, push to her elbows when prone, and she does not sit up. She has noticed a “musty odor” to her daughter’s diapers with urination. On exam there are areas of skin hypopigmentation. Which of the following is most likely?

A.Hartnup disease

B.Cerebral palsy

C.MSUD

D.PKU

E.Albinism

A

D. PKU

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8
Q

What is Hartnup disease?

A

Effects absorption of nonpolar amino acids, particularly tryptophan

  • Treat with: High Protein diet
  • Symptoms (sx):
  • Diarrhea
  • Mood swings
  • Red, scaly skin rash

usually when exposed

to light

  • Photosensitivity
  • Short stature
  • Uncoordinated movements
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9
Q

What is Cerebral Palsy?

A
  • Movement disorder
  • Usually caused by brain damage occurring before birth, or in the first 5 years of life
  • Symptoms are variable
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10
Q

What is MSUD?

A

Maple syrup urine disease

  • Sweet smelling urine
  • Branched-chain ketoacid dehyrogenase deficiency (leucine, isoleucine, valine)
  • Treatment: Low protein diet
  • Sx:
  • poor feeding
  • Vomiting
  • Lack of energy (lethargy)
  • Abnormal movements
  • Delayed development
  • May lead to seizures, coma, death
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11
Q

What is PKU?

A

Phenylketonuria

  • Phenylalanine hydroxylase deficiency
  • Autosomal recessive
  • Sx:
  • Intellectual disorders, seizures
  • Musty smelling urine/sweat
  • phenylacetate
  • infants are normal at birth bc mother metabolizes the extra phenylalanine, usually detected during first newborn screen
  • Treatment: Low protein diet

Phenyllactate and to phenylacetate disrupt neurotransmission and block amino acid transport in the brain as well as myelin formation, resulting in severe impairment of brain function.

Usually by 6 months of life severe mental retardation becomes evident; fewer than 4% of untreated phenylketonuric children have IQs greater than 50 or 60. About one third of these children are never able to walk, and two thirds cannot talk.

Seizures, other neurologic abnormalities, decreased pigmentation of hair and skin, and eczema often accompany the mental retardation in untreated children.

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12
Q

What is Albinism?

A

Absence or defect of tyrosinase

  • Sx:
  • Sunburns/skin cancer
  • Photophobia, nystagmus, amblyopia
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13
Q

Describe a newborn screening.

A

Performed between 24-48 hours

Heel stick, hearing screen

Early detection of otherwise devastating diseases

Missouri – 2 pages of diseases tested >70 tested

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14
Q

A first time mom brings her 1 month old Caucasian male infant to the clinic with complaints of vomiting and weight loss. Birth weight was 8 pounds (3.6 kilograms). On exam the weight is 6.7 pounds (3.0 kilograms). The infant is displays yellow discoloration of skin and sclera. There is palpable hepatomegaly. HEENT reveals the findings in the photo. You favor a metabolic disorder that results in accumulation of galactose-1-phosphate. Which enzyme is most likely deficient?

A.Galactokinase

B.Dihydopteridine reductase

C.Galactosylceramidase

D.GALT (galactose-1-phosphate uridyl transferase)

E.galactitol

A

D.GALT (galactose-1-phosphate uridyl transferase)

WHY—>

A.Galactokinase – juvenile cataracts

B.Dihydopteridine reductase - malignant hyperphenylalaninemia

C.Galactosylceramidase – Krabbe’s disease – can’t make myelin properly

D.GALT (galactose-1-phosphate uridyl transferase)

E.Galactitol – not an enzyme

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15
Q

What happens in galactokinase deficiency?

A

Juvenile cataracts

Decreased conversion of galactose to galactose-1-phosphate by galactokinase

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16
Q

What is malignant hyperphenylalaninemia?

A

Dihydopteridine reductase deficiency

  • Impaired renewal of tetrahydrobiopterin
  • Decreased levels of dopamine, serotonin, and folate
  • Sx:

.psychomotor delay

.low muscle tone (hypotonia)

.Seizures

.abnormal movements

.Too much salivation

.Swallowing difficulties

  • Treatment:
    1. Supplement: BH4 and folate
    2. No phenylalanine
    3. Meds to restore neurotransmitters in the brain
17
Q

What is Krabbe’s disease?

A

Galactosylceramidase deficiency

  • Impairment of the GALC gene
  • Galactosylceramidase hydrolyzes galactosylceramide, an important component of myelin
  • Sx:

.Hypertonia/spasticity

.Impaired development

.Optic atrophy and blindness

.Unexplained fevers

.Seizures

.Irritability

.Eating problems

.Deafness

-Treatment:

.Anticonvulsant medication to stop seizures

.Muscle relaxer drugs (to help ease muscle spasms)

.Physical therapy to help slow deterioration of muscles

.Occupational therapy to help older children with common tasks, such as getting dressed and eating

.Bone marrow transplant

.Cord blood transplantation

18
Q

What happens in GALT (galactose-1-phosphate uridyl transferase) deficiency?

A
  • Failure to metabolize galactose/lactose into glucose
  • Back up of galactose causes symptoms
  • Sx:

.Feeding difficulties

.Lethargy

.Failure to thrive

.Jaundice

.Females – Premature ovarian insufficiency

.Liver damage

.Abnormal bleeding

.Sepsis

.Developmental delay

.Cataracts

-Tx:

.Eliminate lactose and galactose from the diet: Dairy products, avocados, sugar beets

19
Q

What is galactitol?

A

Galactitol is not an enzyme; it is the substance which causes cataracts in people with galactosemia.

20
Q

Describe Kwashiorkor- malnutrition

A
  • Severe protein deficiency
  • Sufficient calories, but insufficient protein
  • Usually occurs after weaning
  • Edema of hands and feet
  • Light-colored skin
  • Thinning hair
  • Distended abdomen
  • Shiny skin
  • Ulcerating dermatoses
  • Anemia
  • Irritable
  • Enlarged fatty liver
21
Q

Describe Marasmus- malnutrition

A
  • Protein-calorie deficiency
  • Emaciated
  • Chronic diarrhea
  • Respiratory infections
  • Intellectual disability
  • Stunted growth
  • Apathy
  • No energy
  • Weight is less than 62% of expected
22
Q

Compare Kwashiorkor vs Marasmus

A
23
Q

A 60 year old female presents to the office complaining of progressive fatigue, numbness in her feet, and a smooth tongue. She relates that she has had vague symptoms over the past 6 months. A couple of months ago, a physician told her that her blood cells were too big and she was anemic, but was rude to her, so she didn’t follow up for treatment. Which of the following deficiency would most likely present with these symptoms?

A.Vitamin A

B.Vitamin B1

C.Vitamin B12

D.Vitamin C

E.Vitamin K

A

C.Vitamin B12

24
Q

What happens in Vit. A deficiency?

A
  • Nyctalopia – night blindness
  • Xerophthalmia – failure to produce tears
  • Major player in phototransduction

.Changing light into electrical signals

25
Q

Describe Vit B1 (Thiamine) deficiency.

A

-Sx:

.Malaise

.Weight loss

.Confusion

.Beriberi

..Wet – fast heart rate, shortness of breath, difficulty moving the legs, pain

..Dry – numbness, confusion, difficulty moving the legs, confusion

.Wernicke-Korsakoff syndrome

..Vision changes, ataxia, impaired memory

26
Q

What happens in Vit. B12 deficiency?

A

-Sx:

.Fatigue

.Inflammation of the tongue

.Decreased taste

.Numbness/Tingling

-Sign:

.Megaloblastic anemia

27
Q

What happens in Vit. C deficiency?

A

-Sx:

.Fatigue

.Shortness of breath

.Dizziness

.Pale or yellowish skin

.Irregular heartbeats

.Weight loss

.Numbness or tingling in hands and feet

.Muscle weakness

.Personality changes

.Unsteady movements

.Mental confusion or forgetfulness

28
Q

What happens in Vit. K deficiency?

A

Sx:

  • Easy bruising
  • Oozing from nose or gums
  • Excessive bleeding from injuries
  • Heavy menstrual periods
  • Bleeding from the gastrointestinal (GI) tract
  • Blood in the urine and/or stool
  • Increased prothrombin time (PT)
29
Q

A 36 year old male presents to the office with complaints of numbness of his extremities and difficulty walking. He relates that he has recently had some difficulty with his vision. His past medical history includes Crohn’s disease and seasonal allergies. Which of the following deficiencies might be the cause of this patient’s symptoms?

●

A.Vitamin B2

B.Vitamin B3

C.Vitamin B6

D.Vitamin D

E.Vitamin E

A

E.Vitamin E

30
Q

What happens in Vit./ B2 (Riboflavin) deficiency?

A

Sx:

  • Stomatitis
  • Sore throat
  • Chapped/fissured lips
  • Oily/Scaly rashes on the scrotum, vulva, philtrum of the lip, nasolabial folds
  • Itchy, watery, bloodshot eyes
  • Sensitivity to light
  • Anemia (normocytic, normochromic)
31
Q

What happens in Vit. B3 (niacin) deficiency?

A

Mild deficiency Sx:

  • indigestion
  • fatigue
  • canker sores
  • vomiting
  • depression

Severe deficiency Sx:

  • Called Pellagra
  • Thick, scaly pigmented rash on skin exposed to sunlight
  • Swollen mouth and tongue
  • Vomiting and diarrhea
  • Headache
  • Apathy
  • Depression
  • Disorientation
  • Memory loss
32
Q

What happens in Vit. B6 deficiency?

A

Sx:

  • Microcytic anemia
  • Electroencephalographic abnormalities
  • Dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth)
  • Glossitis
  • Depression
  • Confusion
  • Weakened immune function
33
Q

What happens in Vit. D deficiency?

A

Sx:

-Subtle to none

Risks:

  • Increased risk of death from cardiovascular disease
  • Cognitive impairment in older adults
  • Severe asthma in children
  • Cancer
34
Q

What happens in Vit. E deficiency?

A

Digestive system requires fat to absorb Vitamin E

  • Abetalipoproteinemia
  • Crohn’s disease
  • Cystic fibrosis
  • AVED (Ataxia and Vitamin E Deficiency)

Sx:

  • Peripheral neuropathy
  • Ataxia
  • Skeletal myopathy
  • Retinopathy
  • Immune impairment
  • Infertility

SFM EXAM 2a/b 2020 (14 decks)

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