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CMB > Drugs Exam 2 > Flashcards

Drugs Exam 2 Flashcards

1
Q

Chondroitin sulfate

A

covalently bound part of proteoglycans; contributes tonsil strength to cartilage, tendons, ligaments, etc

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2
Q

Hyaluronic acid

A

important for lubrication of synovial fluids and in joints

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3
Q

Proteoglycans

A

subclass of glycoproteins where carbohydrate subunits contain amino sugars (aka glycosaminoglycans) bound covalently to membrane or secreted protein. Usually have long unbranched polysaccharides whereas glycoproteins are usually shorter and more branched

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4
Q

GLUT Transporters

A
  • GLUT 1- in most tissues for basal glucose uptake
  • GLUT 2- liver, intestine, and pancreas for high capacity glucose uptake. Independent of insulin, but insulin activates glycolysis and facilitates glucose utilization*
  • GLUT 3- Brain for neuronal glucose uptake
  • GLUT 4- muscle, adipose, and heart tissue for insulin-dependent glucose uptake
  • In the small intestine, SLGT transporters are used to support glucose/galactose and Na+, but this process is inhibited when the chloride cystic fibrosis channels allow efflux of chloride when sodium follows, resulting in water loss. Can be fixed with water mixed with glucose and sodium.
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5
Q

fluoride

A
  • Enolase is inhibited by fluoride, which is used in toothpaste to strengthen tooth enamel and inhibit bacterial lactic acid production and subsequent tooth decay.
  • Sodium fluoride is also added to blood samples when obtaining a blood glucose reading to prevent metabolism of glucose within the sample
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6
Q

reactive oxygen species (ROS)

A
  • NADHP is used in oxidative bursts by phagocytic cells. The NADPH provides electrons to create reactive oxygen species (ROS) that are used.
    • NADPH oxidase is used to create superoxide radicals that are then turned into hydrogen peroxide through superoxide dismutase.
    • Some peroxide is then converted to HOCl (perchlorous acid; bleach) through myeloperoxidase
    • HOCl and peroxide are packaged in a vesicle that is released in the presence of bacteria that kills the cell along with many target bacteria.
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7
Q

anion gap

A

[Na+} - [HCO3-] - [Cl-]

  • It is used to diagnose metabolic acidosis*
    • usually about 12mEq/L +/-4mEq/L. If exogenous acid is present, then the anion gap increases indicating metabolic acidosis
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8
Q

Fluoroacetate

A

inhibits aconitase after being converted to fluorocitrate (used in rat poison)

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9
Q

Oligomycin

A

prevents ATP synthase (Complex V) causes the pumping action to stop because the buildup of H+ causes the pumps to be overloaded, like overfilling a tire

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10
Q

Amytal

A

inhibit complex I; so all the complexes remain oxidized

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11
Q

rotenone

A

inhibit complex I; so all the complexes remain oxidized

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12
Q

antimycin A

A

Complex III is inhibited by antimycin A

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13
Q

cyanide

A

Complex IV is inhibited by cyanide, azide, and CO

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14
Q

azide

A

Complex IV is inhibited by cyanide, azide, and CO

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15
Q

CO

A

Complex IV is inhibited by cyanide, azide, and CO

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16
Q

2,4-dinitrophenol (DNP)

A

Uncoupler

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17
Q

Chlorocarbonylcyanide phenylhywdrazone (CCCP)

A

Uncoupler

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18
Q

Aspirin

A

Aspirin and other salicylates are uncouplers

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19
Q

Thyroxin

A

physical Uncoupler

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20
Q

Uncoupling protein

A

Physical uncoupler; (UCPQ or thermogenin) protein that spans the membrane and creates a proton channel on purpose. Found in brown adipose tissue and used to generate heat, Brown fat is brown because it has higher than usual levels of mitochondria.

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21
Q

Myozyme

A

(alglucosidase α) supplementation can allow survival through infancy of Pompe disease. Must be given via IV biweekly. Complications can arise if the infant produces no enzyme; will recognize the enzyme as foreign and attack it. If they are at risk for this complication, must also be given immune modification treatment with Myozyme

22
Q

Hypoglycin A

A

toxin in the unripe akee fruit that causes vomiting, generalized weakness, altered consciousness, and death. Clincal features include hypoglycemia, lethargy, abdominal pain, and intractable vomiting. Hypoglycemia A is metabolized into a product that binds to and sequesters carnitine and CoA, leading to increased glucose utilization and decreased gluconeogenesis (due to inactivation of pyruvate carboxylase) and leading to increases in SCFAs and dicarboxylic acids; results in metabolic acidosis. Also may lead to increases in octanoic acid (mitochondrial poison) that may contribute to lethargy and CNS effects

23
Q

Ghrelin

A

released from the stomach during fasting; triggers hunger sensation

24
Q

gastric inhibitory peptide (GPI)

A

The other hormones cause satiety (full feeling); two of these released from the intestines stimulate insulin release: gastric inhibitory peptide (GPI) and glucagon-like peptide 1 (GLP1). These insulin releasing hormones are called incretins

25
Q

glucagon-like peptide 1 (GLP1

A

The other hormones cause satiety (full feeling); two of these released from the intestines stimulate insulin release: gastric inhibitory peptide (GPI) and glucagon-like peptide 1 (GLP1). These insulin releasing hormones are called incretins

26
Q

Leptin

A

Adipose cells also release leptin when they are “full” which acts on the hypothalamus to trigger suppression of appetite. Leptin or leptin receptor deficiency causes morbid obesity (rare). Leptin levels rise after a meal and are chronically high in obesity roughly proportional to the elevated adipose mass. Obesity is accompanied by leptin resistance, so leptin fails to prevent overeating

27
Q

diabetes diagnostic values

A
  • Diabetes can be diagnosed by urinalysis; when blood glucose exceeds 9-10mmol/L (160-180 mg/dL) glucose appears in the urine. Blood tests are quantitative to diagnose diabetes: fasting blood glucose levels higher than 7.8 mol/L (140 mg/dL) on two different occasions is used as diagnostic cutoff. Borderline cases can be evaluated by glucose tolerance test which involves measurement of blood glucose before and at different points after ingestion of a glucose solution
  • Hb A1C is used to assess long term management of diabetes. Glucose glycosylates termination amino groups of α and β chains of Hb, leading to the formation of abnormal Hb molecules. These normally make up 4-5.9% of Hb in normal individuals; levels are proportional to exposure to glucose
28
Q

Metformin

A

weak inhibitor of respiratory complex I in mitochondria that causes adaptive changes in metabolism to compensate; most important change is the inhibition of hepatic gluconeogenesis; decreased energy charge inhibits pyruvate crboxylae and F1,6BPase and AMP regulated protein kinase phosphorylates TFs that suppress gluconeogenic genes. Also leads to decreased FA synthesis in liver ad increased activity of GLUT 4 transporters

29
Q

Sulfonylureas

A
  • insulin releasers that bind to a component of KATP channel and cause it to close, triggering depolarization, Ca2+ entry, and release of insulin. These lead to weight gain as a result of increased insulin levels
30
Q

Thiazolidinediones (glitazones)

A

sensitizes cells to insulin by activation of TF PPAR-γ (peroxisomal proliferating activated receptor γ). Can increase risk of myocardial infarction by stimulating FA uptake by macrophages

31
Q

DPP-4 inhibitors (gliptins)

A

inhibit dipeptidyl peptidase 4; enzyme which inactivates incretins GLP-1 and GIP; deactivation leads to increased insulin secretion and reduced appetite, decreasing weight

32
Q

GLP-1 agonists

A

activate GLP1 receptor; also increase insulin and food intake/decrease weight

33
Q

SGLT2 inhibitors

A

block sodium glucose transporter 2 (responsible for reabsorbing glucose from proximal renal tubules), removing excess glucose

34
Q

Azaserine

A

glutamine analog and inhibit purine and pyrimidine synthesis by inhibiting glutamyl amidotransferases

35
Q

acivicin

A

glutamine analog and inhibit purine and pyrimidine synthesis by inhibiting glutamyl amidotransferases

36
Q

5-fluorouracil

A

used to treat colon, pancreas, stomach, esophagus, and breast cancers. It is processed to fluorodeoxyuridine monophosphate which tightly binds to thymidylate synthase, eventually reacting covalently with the enzyme to irreversibly inhibit it. 5-fluorouracil is also incorporated Ito RNA in the place of uracil

37
Q

amethopterin (methotrexate)

A

inhibits dihydrofolate reductase competitively, depleting THF; cells with high thimadylate synthase activity are susceptible to this drug

38
Q

colchicine

A

classic treatment for acute gout attack; not therapeutic for other forms of arthritis, so can be given as a diagnostic tool called a diagnosis ex juvantibus. Colchicine has intestinal side effects, so has been replaced with indomethacin, ibuprofen, and other NSAIDs

39
Q

probenecid

A

Uricosuric agents increase renal excretion of uric acid

40
Q

allopurinol

A

purine analog that is catabolized to alloxanthine by xanthine oxidase which competitively inhibits XO. There is also a noncompetitive option to inhibit XO: febuxostat

41
Q

Bertezomib

A
  • Causes G2-M cell cycle arrest and apoptosis. Proteasome inhibitor of the 20S subunit. Now used to treat multiple myeloma and mantle cell non-Hodgkin’s Lymphoma
42
Q

Pepsin

A

stomach peptidase; Cleaves after aeromatic amino acid or after leucine; secreted as pepsinogen

43
Q

trypsin

A

intestinal peptidase; secreted as trypsinogen and activated by enteropeptidase or autocatalysis by trypsin; cleaves after Arg or Lys. Secretin and cholecystokinin also stimulate pancreas to release digestive zymogens including trypsin, chymotrypsin, and proelastate. Entropeptidase converts these to trypsinogen and trypsin. Trypsin activates chymotrypsin, proelastese, and procarboxypeptidase to their active form

44
Q

chymotrypsin

A

intestinal peptidase; secreted as chymotrypsinogen; cleaves after aeromatic amino acids and leucine

45
Q

elastase

A

intestinal peptidase; secreted as proelastase; cleaves after small uncharged AAs like gly, ala, and ser

46
Q

Carboxypeptidase A

A

cleaves aeromatic AAs from

C terminal; secreted as procarboxypeptidase

47
Q

Carboxypeptidase B

A

Cleaves basic AAs from C terminal: procarboxypeptidase

48
Q

aminopeptidases

A

Cleave AA from N end

49
Q

Gastrin

A

causes the chief cells to release pepsinogen which activates itself through autocatalysis in the presence of low pH conditions (achieved through parietal cells producing HCl). Produces mixture of free amino acids and oligopeptides known as peptone

50
Q

Protein stability regulation

A
  • Regulated by susceptibility to proteolytic degradation which is influenced by the AA content of the N terminus:
    • Met, Ser, Gly, Ala, Thr, Val are stabilizing
    • Arg, Lys, Leu,Phe, Asp,Tyr
    • PEST: Proteins that contain regions rich in Pro, Glycerides, Set, and The have a short halflife

CMB (15 decks)

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