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Step 1 USMLE/COMLEX > Biochemistry > Flashcards

Biochemistry Flashcards

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USMLE® Step 1 flashcards
1
Q

Respiratory acidosis:

a. pH (up/down)
b. pCO2 (up/down)
c. HCO3- compensation (up/down)

A

a. pH down
b. pCO2 up
c. HCO3- up with renal compensation

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2
Q

Respiratory alkalosis:

a. pH (up/down)
b. pCO2 (up/down)
c. HCO3- compensation (up/down)

A

a. pH up
b. pCO2 down
c. HCO3- down with renal compensation

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3
Q

Metabolic acidosis:

a. pH (up/down)
b. pCO2 compensation (up/down)
c. HCO3- (up/down)

A

a. pH down
b. pCO2 down with respiratory compensation
c. HCO3- down

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4
Q

Metabolic alkalosis

a. pH (up/down)
b. pCO2 compensation (up/down)
c. HCO3- (up/down)

A

a. pH up
b. pCO2 up with respiratory compensation
c. HCO3- up

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5
Q

Causes of respiratory acidosis

A

Respiratory depression

Pulmonary disease

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6
Q

Causes of respiratory alkalosis

A

Hyperventilation

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7
Q

Causes of metabolic acidosis

A

Diabetes

Renal failure

Methanol poisoning

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8
Q

Causes of metabolic alkalosis

A

Prolonged vomiting

Nasogastric suction

Antacids

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9
Q

Anion gap calculation

A

AG = Na - (HCO3 + Cl)

Normal = 12 +/- 4 mEq/L

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10
Q

What happens to anion gap in acidosis?

A

HCO3- is consumed (decreased). Anion gap increases.

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11
Q

How is RNA different to DNA?

A

U instead of T

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12
Q

What is a thalassemia?

A

Thalassemia = imbalance in Hb structure production. Must be 2 alphas and 2 beta in Hb

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13
Q

Sickle cell mutation

A

Glut -> Val

Position 6 in beta-globin chain

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14
Q

SSx of sickle cell disease

A

Hemolytic anemia

Sickle cell crises: severe pain in bones, chest, abdomen, often triggered by dehydration or infection

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15
Q

Tx for sickle cell disease

A

Hydroxyurea

MOA here = boosts Hb F (gamma-globin) expression.

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16
Q

Hb C disease mutation

A

Glut -> Lys

Position 6 in beta-globin chain (same as sickle cell dz)

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17
Q

SSx of Hb C disease

A

RBCs form crystals = mild to moderate hemolytic anemia

No episodic crises as in sickle cell disease

Occasional abdominal pain (splenomegaly, cholelithiasis)

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18
Q

Hb E disease mutation

A

Glut -> Lys

Position 26 in beta-globin

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19
Q

In what group is sickle cell and Hb C disease prevalent?

A

Africans, West African

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20
Q

In what group is Hb E disease prevalent?

A

Southeast Asian

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21
Q

SSx of Hb E disease

A

Mild thalassemia as beta-globin chain not synthesized effectively

Microcytosis, hypochromia, not significant or only very mildly anemic. Typically incidental finding.

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22
Q

CF inheritance

A

AR

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23
Q

Defect/pathogenesis in CF

A

Defect in CFTR gene encoding chloride channel

Mutation in Phe residue at position 508. Interferes with protein folding and glycosylation.

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24
Q

HD inheritance

A

AD

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25
Q

Pathogenesis in HD

A

CAG TNR repeat

Contains long stretches of glutamine residues. Misfolded protein aggregates in nuclei of neurons.

26
Q

Imaging findings in HD

A

Lateral ventricle enlargement

27
Q

Double reciprocal plot (aka Line-Weaver Burk) axes

A

X-axis: 1/[S]

Y-axis: 1/[v]

Where line intercepts with y-axis = 1/Vmax

Where line intercepts x-axis = -1/Km

28
Q

Vmax

A

Max rate of product formation by enzyme

29
Q

Vmax or Km is dependent or independent upon enzyme concentration?

A

Vmax is dependent upon enzyme concentration. Explained: more enzyme = higher rate of conversion to product.

Km is independent of enzyme concentration. Reflects physical properties of individual enzyme molecules.

30
Q

Km

A

Inversely related to the affinity of the enzyme for its substrate.

Km = 1/2 Vmax

31
Q

What will increasing concentration of inhibitor look like on a double reciprocal plot?

A

Increasing steepness of line = increased [inhibitor}

32
Q

What does reversible competitive inhibition look like on a double reciprocal plot? Describe changes to Km and Vmax.

A

Mnemonic = competitive scissors

Inhibitor and substrate compete for binding at same active site

Multiple lines of increased inhibitor concentration on plot with all lines going through same point on y-axis

Km: apparent Km increase

Vmax: unchanged

33
Q

What does reversible noncompetitive inhibition look like on a double reciprocal plot? Describe changes to Km and Vmax.

A

Inhibitor and substrate compete for binding at the active site

Multiple lines of increased inhibitor concentration on plot with all line going through different points on y-axis, arising from same point on x-axis.

Km: apparent Km unchanged

Vmax: decreased

34
Q

What does irreversible inhibition look like on a double reciprocal plot?

A

Same as for reversible non-competitive inhibition.

This is covalent modification of active site residue. Like you are taking enzyme out of the reaction. Difference = cannot wash or dilute the irreversible inhibitor out, whereas you can wash away the non-competitive inhibitor.

35
Q

Aspirin

A

Irreversible PG synthase inhibitor

36
Q

Ibuprofen

A

Competitive inhibitor of PG synthase

37
Q

Inhibitors of EF-2

A

Diphtheria toxin and pseudomonas exotoxin A

These ADP-ribosylate EF-2

38
Q

Inhibitors of 60 S subunit via removing adenine bases from 28s rRNA

A

Ricin, Shiga toxin

39
Q

Prenylation

A

Links G-proteins to hydrophobic residues in cell membrane

Statins interfere with this

40
Q

I cell disease

A

Defect in phosphorylation of mannose residue on enzyme directed to lysosome that is supposed to degrade molecules there. See accumulation of molecules in lysosome.

41
Q

Ways in which DNA is silenced/imprinted

A

DNA methylation &

Histone deacetylation

42
Q

What do PPAR transcription factors regulate?

A

Regulate lipid metabolism

43
Q

What transcription factor regulates immune system response?

A

NFkappaB

44
Q

What transcription factor regulates development and patterning in utero?

A

Homeodomain proteins (HOX)

45
Q

PEP carboxykinase

Where does this enzyme function?

A

Gluconeogenesis

46
Q

PEP carboxykinase

How is it expression of this stimulated?

A

Cortisol stimulates expression via cortisol receptor (nucleus)

Glucagon binds to membrane receptor and induces expression via cAMP/CREB

Epi binds to G-protein inducing expression

47
Q

Examples of water soluble hydrophilic hormones

A

Insulin, glucagon, epinephrine, oxytocin

48
Q

Examples of lipid soluble hormones

A

Steroid hormones, calcitriol, retinoic acid, thyroxine

49
Q

Describe activation of adenylate cyclase and downstream cascade

A

Heterotrimeric G protein (alpha subunit, beta, gamma)

Alpha subunit binds GTP and dissociates from beta, gamma

Alpha subunit activates adenylate cyclase = cAMP

cAMP activates PKA

PKA activates phosphorylase kinase

Phosphorylase kinase converts phosphorylase b into phosphorylase a, which is more active

50
Q

Describe phospholipase C second messenger system activation and downstream cascade

A

Hormone binds G-protein, which interacts with PLC

PLC cleaves PIP2 in membrane, generating IP3 and DAG (remains anchored into PM)

IP3 binds to receptor at endoplasmic reticulum inducing release of Ca

DAG + Ca activate protein kinase C

Protein kinase C regulates metabolic enzymes and control of gene expression

Calcium has other signaling roles

51
Q

Thiamine (B1) function

A

Decarboxylation of alpha-ketoacids (enzymes = pyruvate DH, alpha-ketoglutarate DH and branched-chain alpha-ketoacid DH)

Transketolase rxn (PPP)

52
Q

Thiamine deficiency disorders

A

Beriberi

Wernicke’s encephalopathy

53
Q

Beriberi

Deficiency?
SSx?

A

Deficiency in B1

SSx: pain, paresthesias, impaired cardiac energy metabolism, peripheral edema, peripheral neuritis, symmetric peripheral neuropathy

54
Q

Wernicke encephalopathy

Deficiency?
SSx?

A

Deficiency in B1

SSx: horizontal nystagmus, ophthalmoplegia, cerebellar ataxia, mental impairment

55
Q

Riboflavin (B2) function

A

Required for dehydrogenases needed to produce FAD

56
Q

SSx of riboflavin deficiency

A

Mucocutaneous involvement: smooth, swollen, magenta/red tongue, stomatitis, cheilosis

57
Q

Niacin (B3) function

A

Required for dehydrogenases needed to produce NAD and NADP

58
Q

Deficiency of niacin

A

Pellagra

59
Q

Pellagra

Deficiency?
SSx?

A

Deficiency in niacin

SSx: 4 Ds - dermatitis, diarrhea, dementia, death

60
Q

From what AA can niacin be synthesized?

A

Tryptophan. This requires B6.

61
Q

Pyridoxine (B6: Pyridoxal phosphate) function

A

Enzymes of AA metabolism

Heme synthesis (delta-aminolevulinate synthase)

62
Q

Deficiency of pyridoxine (B6)

A

Overlaps niacin deficiency (as it is used to convert tryptophan to niacin). Niacin deficiency = 4 Ds (dermatitis, dementia, diarrhea, death)

+

Heme synthesis impairment (sideroblastic anemia)

Step 1 USMLE/COMLEX (4 decks)

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