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Biochemistry Flashcards

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USMLE® Step 1 flashcards
1
Q

Vitamin D
*Purpose?:
*Acquired from:
*Storage & Active form?

A

*Purpose: Proper intestinal absorption of calcium & phosphate
- Estt’l for bone and teeth growth
- Stimulates osteoblastic activity

*Acquired from Sun + Food

*Storage: 25-OH-D3 (in liver)

*Active form: 1,25-OH2(D3) (in kidney)

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2
Q

Vitamin D XS

A

Stones, Thrones, Groans, Psychiatric Overtones

Tx: Saline + Calcitonin

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3
Q

Calcitonin
*Produced by what?

A

*A hormone produced by parafollicular C cells
in the thyroid
- Inhibits osteoclast activity and renal reabsorption of Ca2+ & phosphate to reduce serum Ca2+

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4
Q

Vitamin D Deficiency

A
  • Osteomalacia
  • Rickets
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5
Q

Rickets
*What?
*Findings

A

*What?: Genetic Defect in renal absorption of phosphate, leads to deficiency in vitamin D

*Findings: Bowing of legs

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6
Q

Osteomalacia
*What?:
*Findings?:

A

*What?: Deficiency of Vit. D
*Findings: bone + joint pain, muscle weakness, gait difficulties, muscle spasm/cramping
*Tx: Vit. D Supplement

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7
Q

Vitamin E
*What enzymes does it help with?
*Role in what function?
*Deficiency:
*XS:

A

*Glutathione pathway to make NADPH

*Role in neurologic function
- Deficiency = dec. proprioception, dec. vibration

*Deficiency:
- Dec. proprioception, Dec. Vibration
- Presents similar to Vitamin B12

*XS: Enterocolitis

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8
Q

Warfarin
- MOA:
- Reverse effects
- Monitor:

A
  • MOA: Inhibits Vitamin K dependent Co-factors: 2, 7, 9, 10
  • Reverse effects: Fresh frozen plasma & Vitamin K
  • Monitor: PT
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9
Q

Heparin
- MOA:
- Monitor:

A
  • MOA: Inhibits antithrombin 3 and activated factor X
  • Reverse effects:
  • Monitor: PTT
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10
Q

Factor V Leiden

*Description

*Mutation

A

*Clotting factor amplifies the production of thrombin

*Mutation: uncontrolled clotting

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11
Q

Vitamin A
*Role
*XS
*Deficiency
*Tx

A

*Role:
- Helps with vision
- Helps epithelial cells differentiate into specialized cells

*XS:
- N/V
- Dizziness
- Alopecia, Dry Skin,Liver toxicity, hyperlipidemia, renal failure
- Teratogenic effects

*Deficiency:
- Poor skin health
- Bitot spots (keratin spots in the eye)
- Dec. CSF production

*Tx:
- Help treat AML!

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12
Q

Pseudotumor Cerebri
*Cause:
*Findings:

A

*Cause: XS CSF Production

*Finding: Papilledema (increased intracranial pressure that leads to eye issues)
- Headache
- CT Scan demonstrates enlargement of ventricles

*Tx: Carbonic Anhydrase Inhibitors

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13
Q

Vitamin B1 (Thiamine)

*Reactions?:
*Deficiency

A

*Reactions: Dehydrogenase reactions

*Deficiency: seen in alcoholics
- Dry Beriberi : Peripheral neuropathy

  • Wet Beriberi: Neurologic findings + Cardiac Findings (CHF, edema, cardiomegaly)
  • Wernicke Korsakoff Syndromes:
    Acutely: Wernicke – Ophthalmoplegia, Nystagmus, Ataxia
    Chronically: Korsakoff – Memory loss, confabulations, nystagmus, ataxia
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14
Q

Vitamin B2 (Riboflavin)
*What Co-Factor is this?
*Deficiency

A

*What co-factor is this?: FAD
*Deficiency: Chelitis, Photosensitivity, Skin Dryness

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15
Q

Vitamin B3 (Niacin)
*Precursor to?:
*Treatment
*Deficiency

A

*Precursor to NAD, NADH, NADPH, NADP

*Tx: Can treat dyslipidemia = increases HDL, dec. VLDL, TGs,

*Deficiency:
- Pellagra: (4D’s) Dementia, Dermatitis, Diarrhea, Death
- Fatigue, restlessness, irritability, decreased concentration, anxiety, depression

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16
Q

Hartnup Disease
*Mutation?
*What is it?:

A

*Mutation in SCL6A19
- Gene encodes for neutral amino acid transporter

*Loss of Neutral amino acids in the urine = dec. amount of tryptophan leads to dec. niacin –> pellagra
- shift of remaining tryptophan produces XS serotonin

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17
Q

Vitamin B5 (Pantathoic Acid)
*Role?
*Deficiency:

A

*Role:
- Helps synthesize fatty acids, amino acids, cholesterol, steroids, plays a role in 1st step of citric acid cycle

*Deficiency:
- Burning feet syndrome (5 toes = burning feet)
- Disruption of vitamin, cholesterol, amino acids
- Impaired Heme Synthesis

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18
Q

Vitamin B6 (Pyridoxine)
*Rxns?:
*Deficiency

A

*Role in decarboxylation rxn’s

*Helps synthesize neurotransmitters, sphingolipids, converts tryptophan to niacin, homocysteine –> Cysteine

*Deficiency: isoniazid causes B6 deficiency & peripheral neuropathy

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19
Q

Vitamin B9 (Folic Acid)
*Reactions:
*Esst’l for?
*Deficiency

A

*Reactions: Can make tetrahydrofolate
*Esst’l for neural tube development
*Deficiency: can cause megloblastic anemia

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20
Q

Vitamin B12 Deficiency what acids are elevated?

A

Elevated Homocysteine & methylmalonyl CoA Levels

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21
Q

Vitamin B12
*Reactions
*Failure to reabsorb B12 leads to?

A

*Reactions:
- Helps odd-chain FA recycling, when it’s deficient causes issues with myelin = issues w/ corticospinal & dorsal columns
- Needed to produce mehionine & THF

*Pernicious Anemia

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22
Q

Vitamin C (Ascorbic Acid)
*What?:

A

*Vitamin C needed for hydroxylation of lysin & proline

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23
Q

How do you treat Iron XS

A

Deferoxamine

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24
Q

Hypokalemia
*Cause
*Signs + Sx’s

A

*Caused:
- Vomiting, diarrhea, Diuretic use, Renal disease

*Sx’s:
- Fatigue
- Muscle weakness
- Constipation
- Cardiac Arrhythmia
- Paralysis

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25
Q

Bartter Syndrome

A

*Defect in TAL, NKCC2 co-transporter (looks like Loop diuretic)

  • Loss of NaCl —> aldosterone stimulation –> loss of K+ and H+
  • Causes Metabolic Alkalosis
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26
Q

Digoxin MOA

*What does Digoxin compete w/?

A

Inhibits the Na+/K+ ATPase, traps Na+ reverse the Na+/ Ca2+ exchangers, increases intracellular Ca2+ = slows HR and ^ contractility

  • Digoxin competes with K+ for the same site on the ATPase,
  • So ^ Digoxin = ^ K+ levels
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27
Q

What can you get hyperkalemia from?
- How can you treat hyperkalemia

A

*Acidosis, burns, leukocytosis, crush injury, lack of insulin

*Treat:
- Insulin
- Glucose
- Beta-2 Agonist
- Thiazide diuretics
- Loop diuretics
- Cation exchange resin
- Metabolic acidosis: give Na+ Bicarb
-

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28
Q

Cell Cycle
- What makes up metaphase?
- What inhibits metaphase?

A

Interphase: G1 (protein), S (DNA synthesis), G2 (make more proteins), M (mitosis)

*Mitosis = prophase, metaphase, anaphase, telophase
- Inhibited by: vincristine, vinblastine, colchicine

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29
Q

Prophase, Metaphase, Anaphase, Telophase, Cytokinesis

A

*Prophase: Chromosomes pair up
*Metaphase: Chromosomes line up at the midline plate
*Anaphase: Chromosomes pull apart
*Telophase: Chromosomes start to create membrane
*Cytokineses: Separate cell membranes are made

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30
Q

PCR
*Use
*Steps

A

*Use: Amplifies DNA
*Steps: (1) Denatures protein– strand separation
(2) Annealing–binding of primers upon cooling
(3) Elongation (DNA polymerase works in 5’ –> 3’ direction)

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31
Q

What is on th 5’ end?
- What does it require?

A

7-methylguanosine cap
- GTP

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32
Q

What is on the 3’ end?
- What does it require?

A

Poly-A tail
- ATP

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33
Q

Glycine
*Size
*Charge
*MOA

A

*Size: Small
*Charge: Negative
*MOA: Opens chloride channels & leads to the influx of chloride channels

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34
Q

What does the restriction enzyme, chymotrypsin, recognize?

A

Aromatic Amino Acids: Phenylalanine, Tryptophan, Tyrosine

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35
Q

Tryptophan is a precursor for…

A

Niacin and Serotonin
(5HTP –> serotonin needs Vit. B6)
- Serotonin can be converted into melatonin

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36
Q

Basic AA’s
*Move towards anode or cathode?

A

Lysine & Arginine
- Move towards cathode

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37
Q

Acidic AA’s
*Move towards anode or cathode?
*Stimulate what type of receptor?

A

Glutamate or aspartate (have COOH-)
- Move towards anode
- NMDA receptor (leads to Ca2+ influx) – glutamate stimulates NMDA stronger

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38
Q

Sulfur AA’s
- Help build?

A

Cysteine & Methionine
- Help build: Insulin, GH, prolactin, inhibin

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39
Q

Nitrogen contining AA’s

A

Glutamine + Asparagine
- Helps build muscle

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40
Q

What is maple syrup urine disease?

A

Absence of Branched-chain alpha-keto acid DH, causes body to not be able to break down branched chain AA’s

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41
Q

Methylmalonic Acidemia

A

Occurs with Vitamin B12 or Methylmalonyl CoA defficiency! Can’t make Succinyl CoA.

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42
Q

Tyrosine is a precuror to…

A

NE, E (does have a methyl group), Dopamine

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43
Q

Ketogenic AA’s

A

Lysine + Leucine
- Broken down to yield Acetyl CoA –> Ketones

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44
Q

GLucogenic + Ketogenic AA’s

A

PITTT:
- Phenylalanine
- Isoleucine
- Tyrosine
- Tryptophan
- Threonine

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45
Q

Essential AA’s

A

PVT TIM HALL
*Phenylalanine
*Valine
*Threonine
*Tryptophan
*Isoleucine
*Methionine
*Histidine
*Arginine
*Lysine
*Leucine

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46
Q

PKU
*Involves?
*Deficiency of?

A

*Involves?: Phenylalanine
*Deficiency of?: Phenylalanine Hydroxylase (can’t make tyrosine)

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47
Q

Albinism
*Involves?
*Deficiency of?

A

*Involves?: Tyrosine
*Deficiency of?: Tyrosinase

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48
Q

Alkaptonuria
*Involves?
*Deficiency of?

A

*Involves?: Tyrosine & Phenylalanine
*Deficiency of?: Homogentistic Acid Oxidase
- AR
- Blue/Black discoloration of CT

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49
Q

Maple Syrup Urine Disease
*Involves?
*Deficiency of?

A

*Involves?: Build up of branched-chain AA’s
- Maple trees have branches = branched chain AA’s
*Deficiency of?:
- Branched chain Alpha Keto Acid DH

50
Q

G-protein S activates what? (say whole cascase)

A

Gs –> Adenylyl cyclase –> cAMP –> Protein Kinase A
- Protein Kinase A: phosphorylates serine & threonine
- Magnesium = Co-Factor

51
Q

Gq cascade

A

Gq –> phospholipase C –> PIP2 –> DAG & IP3 –> allows movement of Ca2+ into cytosol –> actions

52
Q

Receptors & their G-Proteins & Receptors action
“qiss & qiq siq sqs” = kiss & kick until you’re sick of sex

Alpha1
Alpha2
Beta1
Beta 2
M1
M2
M3
D1
D2
H1
H2
V1
V2

A

Alpha1: Gq ; SM contraction
Alpha2: Gi; Dec. NE release from pre-synpatic membrane
Beta1: Gs; ^ CO, HR, SV, Renin Release
Beta 2: Gs; SM relaxation
M1: Gq; Autonomic ganglia, CNS & Gastric Glands
M2: Gi; Heart & CNS
M3: Gq; SM of eye, viscera, exocrine glands + epithelium
D1: Gs; CNS
D2: Gi; Brain + Periphery
H1: Gq; SM, Vascular endothelial cells, heart, CNS
H2: Gs; Heart, CNS, PMN’s, vascular SM, Parietal Cells
V1: Gq; Vascular SM, platelets, heart, kidneys
V2: Gs; Kidney

53
Q

Nitrates MOA

A

Increase cyclic GMP –> vasodilation, intracellular cGMP = vascular relaxation
*Veins & Arteries both dilate = decrease preload

54
Q

Collagen Types

A

4 Types:
SCAB
- Type 1: Skin
- Type 2: Cartilage / Connective Tissue
- Type 3: Arteries
- Type 4: Basement Membrane

55
Q

What is needed for collagen production?

A

*Lysine + Proline (Vitamin C)
*Copper

56
Q

Glycosylation

A

Occurs in Golgi

57
Q

Hydroxylation

A

Occurs in RER

58
Q

Wound contractions happens with what?
- Abnormal connective tissue healing causes:

A

*Myofibrils & Fibrils
- Abnormal Healing: *Keloids & Desmoplasia

59
Q

Scurvy
*Cause
*Sx’s

A

*Results of Vitamin C deficiency
- Leads to inability to hydroxylate proline + lysine in RER
*Sx’s: Gingival bleeding, petechiae, ecchymoses, perifollicular hemorrhage, poor wound healing

60
Q

Ehler’s Danlos
*Cause
*Sx’s

A

*Cause: Faulty collagen synthesis
- Deficiencies of lysyl hydroxylase or pro-collagen peptidases
*Sx’s: Highly stretchable skin, hypermobile joints, easy bruising

61
Q

Osteogenesis Imperfecta

A

*Abnormal collagen type 1 production
- leads to brittle bones

*Sx’s
- Skin gets SO thin you can see through it
- See choroidal veins

62
Q

Keratin

A

*Proteinaceous structure rich in cysteine
- provides tensile strength to tissue

*Found in hair, nails, outer skin, cornea

*Epithelial cells:
- Tumors that stain (+) Keratin:
- Carcinomas, mesotheliomas, thymomas, sarcomas, trophoblastic tumors, desmoplastic small round cell tumors

63
Q

Elastin

A

*Needed for stretching and recoiling properties
*Contains Hydroxyproline
*Contains smallest amino acid glycine

64
Q

Anabolic Pathways take place in?

A

Cytoplasm/Cytosol

65
Q

Catabolic Pathways take place in?
*What pathway is the exception?

A

*Break down pathways

*Mitochondria
- Controlled by epinephrine & glucagon

*Glycolysis: cytosol

66
Q

What 3 pathways occur in cytoplasm & mitochondria?

A

(1) Heme Synthesis
(2) Gluconeogenesis
(3) Urea cycle

67
Q

Types of energy used by different structures?

A

*Brain: Glucose (normal conditions), glucose (stress conditions), ketones (extreme stress)
*Heart: Lipids
*Muscle: Glucose, Fatty Acids, FA’s
*RBC: Glucose

68
Q

Glucokinase
- Where does it work?
- Km

A
  • Where does it work?: Works in the liver + beta islet cells in the pancreas
  • Km: High Km, Low affinity
69
Q

Hexokinase
- Where does it work?
- Km

A
  • Where does it work?: Other tissues
  • Km: LOW Km, High affinity for glucose
70
Q

Rate limiting step of glycolysis

A

PFK-1
*Converts F-6-P —PFK-1—> F-1,6-BP

71
Q

2,3 BPG

A

Causes a conformational change in hemoglobin molecule and forces it to release oxygen

72
Q

Glycolysis produces how many net ATP’s? net NADH’s?

A

2 ATP’s ; 2 NADH’s/glucose

73
Q

Last step in glycolysis

A

Phosphenylpyruvate —pyruvate kinase–> Pyruvate

74
Q

2 methods for getting NADH into mitochondria

A

(1) Malate aspartate shuttle
- Alpha-KG–>OAA—-NADH-NAD+ & Malate DH—> Malate crosses mitochondria Malate –> OAA —> Alpha KG
(2) 3-phosphoglycerate shuttle (req. 2 ATP’s)

75
Q

Gluconeogenesis
*4 Uni-directional enzymes

A

(1) Pyruvate Carboxykinase (Pyruvate –> OAA)
(2) PEP Carboxykinase (OAA –> PEP)
(3) Fructose-1-6-Bisphophatase (Fructose-1,6-BP –> Fructose-6-P) Rate limiting enzyme
(4) Glucose-6-P (glucose-6-P –> glucose)

76
Q

The Cori Cycle

A

Shuttles lactate from muscle –> liver to make lactate –> pyruvate –> glucose

77
Q

Galactosemia
*What is the rate-limiting enzyme?
*Inheritance
*Sx’s
*Seen w/?

A

*Enzyme: Galactose-1-Phosphate Uridyltransferase Deficiency
*Inheritance: AR
*Sx’s: lethargy, N/V, failure to thrive, jaundice, hepatomegaly, intellectual disability, cataracts
*Seen in between bottle feedings

78
Q

Galactokinase Deficiency

A

*Galactokinase = kinder
Galactose accumulates
-Sx’s: see infantile cataracts

79
Q

Essential fructosuria
*Deficiency?

A

*Deficient enzyme: Fructokinase

80
Q

Fructosemia
*Enzyme deficiency?
*Seen when?
*Sx’s

A

*Enzyme deficiency: Aldose B deficiency
- Accumulation of F-1-P
*Seen w/ baby started on fruits
*Sx’s: hypoglycemia, jaundice, cirrhosis, vomiting

81
Q

Pyruvate –> Acetyl CoA
- Requires: 5 Co-Factors

A

*B Vitamins 1 - 5

82
Q

Antidote to methanol or ethylene glycol poisoning?

A

Fomepizole

83
Q

Citric Acid Cycle
*Mnemonic
*Main goal?
*Rate limiting step

A

*Mnemonic: Citrate is krebs starting substrate for making oxaloacetate
*Main goal: Produce NADH for ETC to make ATP
- NADH2 = 2.5 ATPs
- FADH2 = 1.5 ATPs
*Rate limiting step = isocitrate DH

84
Q

Do saturated fats have double bonds?

A

No

85
Q

Do unsaturated fats contain double bonds?

A

Yes

86
Q

How does fatty acid synthesis begin?
- Where does it get it’s NADPH’s from?

A

*Begins from citrate accumulation due from inhibition of PFK-1,

*Acetyl-CoA –ATP (via ACoA Carboxylase)—> Malonyl CoA

*NADPH’s come from HMP Shunt

87
Q

of rounds to make certain length of chain =

Number of NADPH’s needed / round =
Number of rounds to make certain length of chain =
# of ATP’s needed to make entire FA =
Number of FA breakdown to release NADH, FADH2, ACoA =

A

of rounds to make certain length of chain = (#C / 2) -1

Number of NADPH’s needed / round = # of carbons - 2
Number of roounds to make certain length of chain = (#C / 2 ) - 1
# of ATP’s needed to make entire FA = #C - 1
Number of FA breakdown to release NADH, FADH2, ACoA = (#C / 2 ) -1

88
Q

Fatty Acid synthesis steps

A

Acetyl CoA —–Acetyl CoA Carboxylase——> Malolnyl CoA —> Decarboxylation –> Addition of NADPH + Addition of NADPH

89
Q

How does fatty acid catabolism being?
- What is needed?
- Fatty acids > 12 carbons need?
- Steps of catabolism

A

Glucagon stimulates hormone sensitive lipase
- 2 ATP’s needed
- Fatty acids > 12 carbons need CAT-1 (cytosol) and CAT-2 (mito) to be transported
- Steps of catabolism:
Oxidation, hydrolysis, oxidation, thiolysis

90
Q

Deficiency of Cat-1 causes:

A

Adrenoleukodystrophy (X-linked Rec)
- Disrupts leydig cells, CNS , adrenal cortex

91
Q

What do you need in dealing with Odd chain fatty acids?

A

Propionate + Succinyl CoA –> TCA intermediate

92
Q

Ketone Synthesis
*What is the Rate Limiting Enzyme?
*What is the Reaction?

A

*Rate Limiting Enzyme?: HMG-COA Synthase

*Reaction:
Acetyl CoA –Thiolase–> Acetoacetyl CoA —–HMG-CoA Synthase–> Hydroxy-beta-methylglutaryl CoA —HMG-CoA Lyase–> Acetoacetate —D-Beta-hydroxybutyrate DH—> Acetone + CO2 & D-Beta-Hydroxybutyrate

93
Q

The phospholipid pathway

A

Phospholipids —> Arachidonic Acid —*–> COX1 & COX2
COX1 –> Homeostatic Functions
COX2 –> Inflammation

COX 1 & COX 2 –> Prostacyclin (PGI2), Thromboxane (TXA2), Prostaglandins (PGD2, PGE2)

*Can be inhibited by NSAIDs

Phospholipids —> Arachidonic Acid —> 5-Lipoxygenase –> 5-HPETE –> Lipoxin A4/B4
5-HPETE –> Leukkotrienes –> Vasoconstriction, ^ Vascular permeability, Bronchospasm

94
Q

(1) What irreversibly inhibits cox1 & cox 2?
(2) What reversibly inhibits cox1 & 2?
(3) What inhibits the cox enzyme?
(4) What reversibly inhibits Cox-2?

A

(1) Aspirin
(2) NSAIDs: Ibuprodfen & Naproxen
(3) Acetominophen
(4) Celecoxib

95
Q

What is the rate limiting enzyme of glycogen synthesis?
- What elongates the chain?

A

*Glycogen Synthase
- Chain elongates in alpha-1,4 direction & links via Alpha-1,6 linkage

96
Q

Von Gierke Disease
*Inheritance:
*Enzyme Defect:
*Clinical Findings:

A

*Inheritance: AR
*Enzyme Defect: Glucose-6-phosphatase
*Clinical Findings:
- Hepatomegaly
- Hypoglycemia (severe)
- Hyperlipidemia
- Hyperuricemia
- Failure to Thrive

97
Q

Pompe’s Disease
*Inheritance:
*Enzyme Defect:
*Clinical Findings:

A

*Inheritance: AR
*Enzyme Defect: Alpha-glucosidase
*Clinical Findings:
- Cardiorespiratory Failure

98
Q

What does ABCD stand for in terms of glycogen storage diseases?

A

A: Anderson
B: Branching enzyme
C: Cori
D: Debranching Enzyme

99
Q

Cori
*Inheritance:
*Enzyme Defect:
*Clinical Findings:

A

*Inheritance: AR
*Enzyme Defect:
- Debranching enzyme
*Clinical Findings:
- Similar to Von Gierke but less severe

100
Q

Anderson
*Inheritance:
*Enzyme Defect:
*Clinical Findings:

A

*Inheritance: AR
*Enzyme Defect: Branching Enzyme
*Clinical Findings:
- Cirrhosis of liver
- Death by liver failure

101
Q

McArdle
*Inheritance:
*Enzyme Defect:
*Clinical Findings:

A

*Inheritance: AR
*Enzyme Defect: Myophosphorylase
*Clinical Findings:
- Cramping during physical activity

102
Q

Hers
*Inheritance:
*Enzyme Defect:
*Clinical Findings:

A

*Inheritance: AR
*Enzyme Defect: Liver Phosphorylase
- issue w/ glycogen synthesis
*Clinical Findings:
- Increased Amount

103
Q

Pentose Phosphate Pathway
*Generates?
*Rate Limiting Enzyme?
*Occurs where?
*Two phases?

A

*Generates: NADPH & Ribose-5-Phosphate
*Rate Limiting Enzyme: Glucose-6-phosphate DH
*Occurs: Cytosol
*Two Phases: Oxidative & Non-Oxidative

104
Q

Glucose-6-Phosphate DH Deficiency
- Inheritance

A

*NADPH used by RBC to maintain reduced glutathione to counteract free radicals

*Inheritance: X-linked recessive

105
Q

Cholesterol Synthesis
*Rate-limiting enzyme:
*What acts at this enzyme?
*Pathway

A

*Rate-limiting enzyme: HMG-CoA Reductase

*What acts at this enzyme? Statins

*Pathway:
Acetoacetyl CoA + Acetyl CoA –> HMG-CoA –HMG-COA reductase–> Mevalonate –> Mevalonate –> Prequalene pyrophosphates –squalene synthase–> squalene –> Cholesterol

106
Q

Niacin
*What Vitamin is it?
*What does it do?

A

*Vitamin B3
*Decreases VLDL production in the Liver, Best HDL-raising ability, Uncomfortable skin flushing

107
Q

Urea Cycle (p. 125)
*What is it?
*Where does it work
*Rate limiting ezyme

A

*What is it?: Removes toxic ammonia that builds up during protein breakdown + makes urea

*Where does it work: cytosol & mitochondria

*Rate limiting enzyme: Carbamoyl phosphate synthetase 1 (CPS-1)

108
Q

Arginase Deficiency
*What is arginase used for?
*Sx’s of deficiency
*Management:

A

*What is arginase used for?: makes urea
*Sx’s: spaticity
*Management:
- Lower protein intake and eleminiate arginine from diet

109
Q

Liver Failure Tx
1. Management
2. Treatment

A
  1. Lower protein inake
  2. Lactulose: used to treat constipation + hepatic encephalopathy. Pulls in water to lumen, and traps ammonia
110
Q

Rate Limiting Enzymes

Glycolysis RLE

A

RLE of glycolysis: Phosphfructokinase-1 (PFK-1)

111
Q

Rate Limiting Enzymes
Gluconeogenesis RLE

A

RLE of gluconeogenesis: Fructose-1,6-Bisphosphatase

112
Q

Rate Limiting Enzymes
Citric Acid Cycle

A

RLE of Citric Acid Cycle: Isocitrate DH

113
Q

Rate Limiting Enzymes
Glycogen synthesis

A

RLE Glycogen Synthesis: Glycogen Synthase

114
Q

Rate Limiting Enzymes
Glycogenolysis

A

RLE of Glycogenolysis: Glycogen Phosphorylase

115
Q

Rate Limiting Enzymes
HMP Shunt

A

RLE HMP Shunt: G6PDH

116
Q

Rate Limiting Enzymes
Urea Cycle

A

RLE Urea Cycle: Carbamoyl Phosphate Synthetase 1 (CPS-1)

117
Q

Rate Limiting Enzymes
Fatty Acid Synthesis

A

Fatty Acid Synthesis RLE: Acetyl CoA Carboxylase

118
Q

Rate Limiting Enzymes
Fatty Acid oxidation

A

Fatty Acid Oxidation RLE: Carnitine acyltransferase 1

119
Q

Rate Limiting Enzymes
Ketogenesis

A

Ketogenesis RLE: HMG CoA Synthase

120
Q

Rate Limiting Enzymes
Cholesterol Synthesis

A

Cholesterol Synthesis RLE: HMG-CoA Reductase

121
Q
A

USMLE Success (6 decks)

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