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USMLE > Nutrition > Flashcards

Nutrition Flashcards

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USMLE® Step 1 flashcards
1
Q

Water Soluble Vitamins that wash out easily?

A

All but B12 and folate which are stored in liver

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2
Q

B complex deficiencies result in

A

Dermatitis, Glossitis, Diarrhea

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3
Q 
VitA
General function 
Physiological role
Developmental role 
Role in cancer
Use as a medication 
Where is it found?
A

Antioxidant
Constituent of visual pigments (retinal)
Essential for normal differentiation of epithelial cells into specialized tissue (pancreatic cells, mucus-secreting cells)
Prevents squamous metaplasia
Used to treat measles, AML (subtype M3), wrinkles and acne
Found in liver and leafy vegetables

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4
Q

VitA
Deficiency
Excess

A

Night blindness and dry skin

Arthritis, Fatigue, Headache, Skin changes, Sore Throat, Alopecia, Teratogenic (cleft palate, cardiac abnormalities)

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5
Q

VitB1
Name
Enzymatic role

A

Thiamine
Part of Thiamine PyroPhosphate (TPP), a cofactor for decarboxylation reactions: “ATP Branch”
Pyruvate dehydrogenase (Glycolysis, TCA cycle), α-ketoglutarate dehydrogenase (TCA cycle), Transketolase (HMP shunt), Branched-chain AA dehydrogenase

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6
Q 
VitB1 Deficiency 
PathoPhys
What worsens it?
Which tissues affected?
Context
Names
A

Impaired glucose breakdown –> ATP Depletion worsened by glucose infusion
Highly aerobic tissue (brain and heart) affected first
Malnutrition or Alcoholism
Wernicke-Korsakoff, Beriberi

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7
Q

Wernicke-Korsakoff
Deficiency
Region damaged
Presentation

A

VitB1
Confusion, Ophthalmoplegia, Ataxia + Confabulation, Personality changes, Memory loss
Damage to medial dorsal nucleus of Thalamus, Mammillary bodies

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8
Q

Dry Beriberi
Deficiency
Presentation

A

VitB1

Polyneuritis, Symmetrical muscle wasting

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9
Q

Wet Beriberi
Deficiency
Presentation

A

VitB1

High output cardiac failure (Dilated Cardiacmyopathy), Edema

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10
Q

VitB2
Name
Function
Deficiency

A

Riboflavin
Cofactor in oxidation and reduction (FADH2). FAD and FMN are derived from B2 and yield 2 ATPs
“2 Cs of B2”
Cheilosis and Corneal vascularization

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11
Q 
VitB3
Name
Function 
Derived from...
Synthesis requires... 
Deficiency 
Excess 
Used as treatment for...
A

Niacin
Constituent of NAD+ and NADP+ used in RedOx reactions to produce 3 ATP (B3 –> 3 ATP)
Derived from Tryptophan
Synthesis requires VitB6 and VitB2
Glossitis, Pellagra
Facial flushing due to pharmacologic doses for treatment of hyperlipidemia

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12
Q

Pellagra
Causes
Presentation

A 
Hartnup Disease (↓ Tryptophan absorption), Malignant Carcinoid Syndrome (↑ Tryptophan metabolism), INH (↓ VitB6), VitB3 deficiency 
Diarrhea, Dermatitis, Dementia
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13
Q

VitB5
Name
Function
Deficiency

A

Pantothenate “PENTOthenate”
Essential component for CoA and Fatty Acid Synthase
Dermatitis, Enteritis, Alopecia, Adrenal insufficiency

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14
Q 
VitB6
Name
What is it converted into?
Kind of reactions it is involved with?
What molecules does it help synthesized?
Deficiency 
What can cause it?
A

Pyridoxine
Converted into Pyridoxal Phosphate
Cofactor for Transamination, Decarboxylation, Glycogen phosphorylase
Synthesizes Crystathionine, Heme, Niacin, Histamine, Neurotransmitters (5HT, Epi, NE, GABA)
Convulsions, Hyperirritability, Peripheral neuropathy, Sideroblastic Anemia (impaired hemoglobin synthesis and iron excess)
INH or oral contraceptives can lead to it?

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15
Q 
VitB7
Name
What kind of reactions 
Enzymes 
Deficiency 
What causes it?
A

Biotin
Cofactor for Carboxylation enzymes that add 1 carbon group
Pyruvate carboxylase, Acetyl-CoA carboxylase, Propionyl-CoA carboxylase
Rare, Dermatitis, alopecia, enteritis
Caused by antibiotics or ingestion of raw eggs

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16
Q 
BitB9 
Name
What is it converted into?
What kind of reactions?
What does it synthesize 
Where is it found?
Where is it stored in the body?
A 
Folic Acid
THF
Coenzyme for 1 carbon transfer/methylation 
Nitrogenous bases in DNA and RNA 
Leafy vegetables
Small reserve pool stored in liver
17
Q 
VitB9 deficiency 
What happens?
Frequency 
What can cause it?
When and why is it given as a treatment
A

Macrocytic, Megaloblastic anemia, No neurological symptoms (as opposed to B12)
Most common deficiency in US
Alcoholism, Pregnancy, Phenytoin, Sulfonamides, MTX
Given to prevent neural tube defects in early pregnancy

18
Q 
VitB12
Name 
Function 
Where is it found?
What synthesizes it?
Storage?
A

Cobalamin
Cofactor for homocysteine methyltransferase (transfers CH3 groups as methylcobalamin and methylmalonyl-CoA mutase)
Found in animal products
Synthesized by microorganisms
Very large reserve pool (several years) stored in liver

19
Q

VitB12 Deficiency
Presentation
Etiology
Test

A

Macrocytic Megaloblastic anemia, Hypersegmented PMNs, Neurological symptoms (paresthesia) due to abnormal myelin. Prolonged deficiency leads to irreversible nervous system damage
Malabsorption (sprue, enteritis, Diphyllobothrium latum), Lack of IF (pernicious anemia, gastric bypass surgery), Absence of terminal ileum (Crohn’s disease)
Schilling test to detect etiology of the deficiency

20
Q

VitB12 Reactions

A

Homocysteine + THF-CH3 –> [Homocysteine MethylTransferase w/ B12] –> Methionine + THF
Methionine gives CH3 for anabolic reactions
THF ->->-> dTMP pyrimidines
Odd # fatty acids –> Methylmalonyl-CoA –> [B12] –> Succinyl-CoA

21
Q

VitB6 Reactions

A

Homocysteine ->->-> [B6] –> Cysteine

Succinyl-CoA –> [B6] –> Hb

22
Q

Combined VitB12 and VitB6 Reactions

A

Odd # fatty acids –> Methylmalonyl-CoA –> [B12] –> Succinyl-CoA –> [B6] –> Hb

23
Q 
S-Adenosyl-Methionine 
What is it made of?
What is its function 
Basic Reaction 
Regeneration requires 
What reaction in neurons requires it?
A 
ATP + Methionine 
Transferes methyl units 
Methionine + ATP --> SAM --> CH3 (for anabolic pathways) + Homocysteine 
Regeneration requires B12 and Folate
Required for conversation of NE to Epi
24
Q

VitC
Name
Function
Where is it found?

A

Ascorbic Acid
Antioxidant, Facilitate iron absorption by keeping iron in reduced Fe2+ state
Necessary for hydroxylation of proline and lysine in collagen
Necessary for Dopamine-β-Hydroxylase to convert DA into NE
Found it fruits and Vegetables

25
Q

VitC
Deficiency
Excess

A

Weakened immune response, Scurvy due to collagen synthesis defect (swollen gums, bruising, hemarthrosis, anemia, poor wound healing)
Nausea, Vomiting, Diarrhea, Fatigue, Sleep Problems, and Risk of Iron Toxicity in predisposed individuals (transfusions, hemochromatosis)

26
Q

VitD
Names with Source
Storage form
Active form

A

D2 - Ergocalciferol - ingested from plants
D3 - Cholecalciferol - consumed in milk, sun exposure
25OH D3 is storage form
1,25, OH2 D3 is active form

27
Q

VitD
Function
Deficiency
Excess

A

Intestinal absorption of Ca and PO4, Increased bone mineralization
Rickets in children, Osteomalacia in adults,
HypoCa tetany. Decreased VitD in dark skinned pts.
HyperCa, Hypercalcinuria, loss of appetite, stupor. Seen in Sarcoidosis

28
Q

VitE
Function
Deficiency

A

“E is for Erythrocytes”
Antioxidant (protects erythrocytes and membranes from free radical damage)
Fragile erythrocytes leading to hemolytic anemia. Muscle weakness, posterior column and spinocerebellar tract demyelination

29
Q 
VitK
Function
What synthesizes it?
What enzymes are VitK dependent?
VitK antagonist 
Deficiency results in...
What causes deficiency?
When is it used as a medicine?
A

Catalyzes γ-carboxylation of glutamic acid residues on various proteins of blood clotting
Synthesized by intestinal flora
II, VII, IX, X, Proteins C and S
Warfarin –/ VitK
Neonatal hemorrhage with ↑ PT and ↑ aPTT but normal bleeding time
Infancy (because of sterile intestines) or broad spectrum antibiotics
Given to neonates because not in breast milk and prevents hemorrhage

30
Q

Zinc
Function
Deficiency
Predisposes pts to…

A

Enzyme activity. Zn fingers in transcription factors
Delayed wound healing, Hypogonadism, ↓ adult hair, Dysgeusia, Anosmia
Predispose to Alcoholic Cirrhosis

31
Q

Ethanol Hypoglycemia

A
  1. EtOH metabolism leads to ↑ NADH/NAD ratio in liver
  2. When NADH high, Pyruvate –> Lactate, Oxaloacetate –> malate
  3. This leads to inhibition of gluconeogenesis and stimulates Fatty Acid Synthesis
  4. Hypoglycemia and Hepatic Fatty Change
  5. Overproduction of lactate –> acidosis
  6. Depletion of oxaloacetate shuts down the TCA cycle, shunting acetyl-CoA into ketone production
  7. Excess malate ↑ NADPH and thus fatty acid synthesis
32
Q

Names of malnutrition syndromes

A

Kwashiorkor and Marasmus

33
Q

Kwashiorkor
Lack of what?
Presentation
Classic patient

A

Protein malnutrition
“MEAL” Malnutrition, Edema, Anemia, Liver
Skin lesions, edema, Liver malfunction (fatty change due to ↓ apolipoprotein synthesis)
Small child with a swollen belly

34
Q

Marasums
What is it?
Presentation

A

Energy malnutrition

Tissue and muscle wasting, loss of subcutaneous fat, edema

35
Q

EtOH Metabolism
Pathway
Limiting reagent
Kinetics

A

Cyto:
EtOH + NAD –> [Alcohol Dehydrogenase] –> Acetaldehyde + NADH
Mito:
Acetaldehyde NAD –> [Acetaldehyde Dehydrogenase] –> Acetate + NADH
NAD is limiting reagent
Zero-Order Kinetics

36
Q

Fomepizole
MoA
Use

A

Inhibits Alcohol Dehydrogenase

Antidote for methanol or ethylene glycol poisoning

37
Q

Disulfiram
MoA
Use
What does it produce

A

Inhibits Acetaldehyde Dehydrogenase
Alcoholism
Produces Hangover Symptoms

38
Q

Only vitamins not in breast milk?

A

D and K

USMLE (25 decks)

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