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Biochemistry Flashcards

(62 cards)

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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
Pathogenesis in HD
CAG TNR repeat Contains long stretches of glutamine residues. Misfolded protein aggregates in nuclei of neurons.
26
Imaging findings in HD
Lateral ventricle enlargement
27
Double reciprocal plot (aka Line-Weaver Burk) axes
X-axis: 1/[S] Y-axis: 1/[v] Where line intercepts with y-axis = 1/Vmax Where line intercepts x-axis = -1/Km
28
Vmax
Max rate of product formation by enzyme
29
Vmax or Km is dependent or independent upon enzyme concentration?
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
Km
Inversely related to the affinity of the enzyme for its substrate. Km = 1/2 Vmax
31
What will increasing concentration of inhibitor look like on a double reciprocal plot?
Increasing steepness of line = increased [inhibitor}
32
What does reversible competitive inhibition look like on a double reciprocal plot? Describe changes to Km and Vmax.
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
What does reversible noncompetitive inhibition look like on a double reciprocal plot? Describe changes to Km and Vmax.
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
What does irreversible inhibition look like on a double reciprocal plot?
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
Aspirin
Irreversible PG synthase inhibitor
36
Ibuprofen
Competitive inhibitor of PG synthase
37
Inhibitors of EF-2
Diphtheria toxin and pseudomonas exotoxin A These ADP-ribosylate EF-2
38
Inhibitors of 60 S subunit via removing adenine bases from 28s rRNA
Ricin, Shiga toxin
39
Prenylation
Links G-proteins to hydrophobic residues in cell membrane Statins interfere with this
40
I cell disease
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
Ways in which DNA is silenced/imprinted
DNA methylation & Histone deacetylation
42
What do PPAR transcription factors regulate?
Regulate lipid metabolism
43
What transcription factor regulates immune system response?
NFkappaB
44
What transcription factor regulates development and patterning in utero?
Homeodomain proteins (HOX)
45
PEP carboxykinase Where does this enzyme function?
Gluconeogenesis
46
PEP carboxykinase How is it expression of this stimulated?
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
Examples of water soluble hydrophilic hormones
Insulin, glucagon, epinephrine, oxytocin
48
Examples of lipid soluble hormones
Steroid hormones, calcitriol, retinoic acid, thyroxine
49
Describe activation of adenylate cyclase and downstream cascade
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
Describe phospholipase C second messenger system activation and downstream cascade
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
Thiamine (B1) function
Decarboxylation of alpha-ketoacids (enzymes = pyruvate DH, alpha-ketoglutarate DH and branched-chain alpha-ketoacid DH) Transketolase rxn (PPP)
52
Thiamine deficiency disorders
Beriberi Wernicke's encephalopathy
53
Beriberi Deficiency? SSx?
Deficiency in B1 SSx: pain, paresthesias, impaired cardiac energy metabolism, peripheral edema, peripheral neuritis, symmetric peripheral neuropathy
54
Wernicke encephalopathy Deficiency? SSx?
Deficiency in B1 SSx: horizontal nystagmus, ophthalmoplegia, cerebellar ataxia, mental impairment
55
Riboflavin (B2) function
Required for dehydrogenases needed to produce FAD
56
SSx of riboflavin deficiency
Mucocutaneous involvement: smooth, swollen, magenta/red tongue, stomatitis, cheilosis
57
Niacin (B3) function
Required for dehydrogenases needed to produce NAD and NADP
58
Deficiency of niacin
Pellagra
59
Pellagra Deficiency? SSx?
Deficiency in niacin SSx: 4 Ds - dermatitis, diarrhea, dementia, death
60
From what AA can niacin be synthesized?
Tryptophan. This requires B6.
61
Pyridoxine (B6: Pyridoxal phosphate) function
Enzymes of AA metabolism Heme synthesis (delta-aminolevulinate synthase)
62
Deficiency of pyridoxine (B6)
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)

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