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106 Cards in this Set

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what are the sources of Energy?
• Proteins
• Fats
• Sugars
which one is easiest to mobilize?
sugars
describe the properties of a charged molecule ie. amino group (-NH4 +)
Amino Group (-NH4 +): Charged, more soluble, attracted to water
describe the properties of a uncharged molecule ie. acid group (-COOH)
Acid Group (-COOH): Uncharged, crosses membranes, reflection coefficient closer to zero, more
bioavailable
Buffers:
what is the intracellular buffer?, extracellular buffer and the best buffer?
• Intracellular: Protein (RBC's=hemoglobin)
• Extracellular: Bicarbonate
• Best Buffer: Histidine (pK = 6.0, sidechain closest to pH=7.4)
what is an Amino acids:
have an NH3+ and a COOH
Proline: where is it more abundant?
imino acid ⇨ think kinks, twists, bends, turns (Ex: GI, hair, blood vessels)
Dissociate
=> take H + away!
Bioavailable
=> neutral, can cross membranes, fat soluble
Soluble
=>charged or polar, water soluble (Sulphur, Oxygen, Nitrogen)
Acids
pKa<7, likes to give up hydrogen ions, dissociates early
Base:
pKa>7, likes to accept hydrogen ions, dissociates late
pKa 1-3
Strong acid
pKa 4-7
Weak acid:
pKa 7-9
Weak base:
pKa 10-14
Strong base:
pKa of 4-9
can be a weak acid or weak base
what happens when an acid dissociate:
gains negative charge, more soluble, less bioavailable
what happens when a bases dissociate:
loses a positive charge, less soluble, more bioavailable
Henderson-Hasselbach Equation
pH= pK -log Base/ Acid
what does it mean when pH= pK
Half acid and half base
• 50% dissociated
• 50% soluble
• 50% bioavailable
• 50% reflection coefficient close to 1
• 50% reflection coefficient close to 0
• 50% crosses BBB (bioavailable)
• 50% metabolized by liver (bioavailable)
pH: pK+2
Dissociated = Water Soluble:
Bioavailable=Fat Soluble:
for both acid/ base

pK+2 99% 1%
Dissociated = Water Soluble/
Bioavailable=Fat Soluble
99%/1% (acid), 1%/99%
pH: pK. + 1
Dissociated = Water Soluble:
Bioavailable=Fat Soluble:
Dissociated = Water Soluble/
Bioavailable=Fat Soluble
90%/10% (acid), 10%/90% (base)
pH:pK
Dissociated = Water Soluble:
Bioavailable=Fat Soluble:
Dissociated = Water Soluble:
Bioavailable=Fat Soluble
pH: pK. - 1
Dissociated = Water Soluble:
Bioavailable=Fat Soluble:
Dissociated = Water Soluble/
Bioavailable=Fat Soluble
50% "Best Buffer" 50%
pH: pK.- 2
Dissociated = Water Soluble:
Bioavailable=Fat Soluble:
Dissociated = Water Soluble/
Bioavailable=Fat Soluble
1%/99% (acid), base 99%/1% (base)
Rules to keep molecules neutral (bioavailable):
• To absorb more acid, place in a stronger acid
• To absorb more base, place in a stronger base
Common Acids
NH4Cl, ASA, Barbiturates, Myoglobin, Juice, Coke
Common Bases
Bicarb, Amphetamines, Baking soda, Activated charcoal, Milk
what are the anti-inflammatories?
Acetaminophen
NSAIDs: COX inhibitors
COX-2 Inhibitors
Acetaminophen: MOA, SE and toxicity tx
works at hypothalamus to decrease temp
• Liver toxicity: microsteatosis (highest levels in first 4 hours)
• Tx: N-acetylcystirte (absorbs free radicals)
NSAIDs: SE and what are the two types of NSAIDs and location
COX inhibitors => GI bleeding, interstitial nephritis
COX-1: on gut tissue
COX-2: on endothelial tissue
what are the COX-1 inhibitors
Indomethacin
Phenylbutazone
Ketorolac
Baclofen
Cyclobenzaprine
Naproxen
Ibuprofen
asa
Indomethacin
most potent => RTA, closes PDA, tx gout
Phenylbutazone
2nd most potent
Ketorolac
morphine-like, use w / drug addicts
Baclofen
tx back pain (GABA-ergic effect)
Cyclobenzaprine
anti-cholinergic effects (hot, dry skill)
Naproxen
tx dysmenorrhea
Ibuprofen
OTG
asa
acetylates COX-1/2 irreversibly=> most effective platelet inhibitor
why can we use aspirin in asthma patients
induces asthma sx because ⇧LT by blocking COX.
don't use aspirin w/ hyperthyroid pts?
displaces T4 from TBG
why can't gout patients use aspirin?
⇩urate excretion.
COX-2 Inhibitors advantage
decreased GI irritation
what are the cox 2 inhibitors
• Celecoxib
• Rofecoxib
• Valdecoxib
• Meloxicam
Platelet Haptens:
• Quinidine}
• ASA (>81mg}
• Heparin
which cox 2 inhibitor has sulfur?
Celecoxib
which cox 2 inhibitor was taken of the maket due to stroke increase?
Rofecoxib
which cox 2 inhibitor does not have sulfur?
Valdecoxib
ASA Toxicity
1) Resp Alkalosis (⇧RR)
2) Metabolic Acidosis (uncouples OP)
3) Mixed Acidosis (⇧GABA)
Sulfur Side Effects: CI
don't give to pregnant women
Sulfur Side Effects
Anaphylaxis
Rash
Interstitial nephritis
Hemolytic anemia
Met-Hemoglobin
Displaces stuff off of albumin Kidney stones
what are the Street Drugs: Uppers? and what effect do they have on the eyes?
dilated pupils
PCP
LSD
Amphetamines
Nicotine
Ecstasy
PCP "angel dust":
blocks NMDAr =>powerfully violent, nystagmus, ⇧CPK, ⇧SGOP
LSD "acid, trips":
5-HT agonist => laid back=> colorful hallucinating
Amphetamines "speed, ecstasy, ice=smoked":
hyperactivity, vertical nystagmus
Nicotine
⇩DA reuptake =>agitation, cotinine metabolites in urine
(Tx: Bupropion)
Ecstasy
very thirsty
Cocaine
"coke, snow, crack=smoked": ⇩DA reuptake
o Condescending, grandiose, big pupils, formication, HTN, ⇧TPR
Fetus: ⇩limbs, VSD, brain bleed, placenta abruptio
Cocaine Chest Pressure Tx:
1) BZ (⇩HR/BP)
2) Nitrate» (⇩vasospasm)
3) Aspirin (⇩thrombi)
Cocaine HTN Tx:
1) Lorazepam (anxiolytic)
2) Phentolamine (⇩BP)
3) Avoid β-blockers
Opiod Withdrawal Tx:
neonates
adults
Neonates: Paregori"
Adults: Clonidine /Methadone
Cocaine Rhabdomyolysis Tx:
1) IVF
2) Bicarbonate (keep Mb soluble)
what are the street downers:
Marijuana
Heroin
Alcohol
Heroin
"smack, shit": inhibits AC => constipation, pinpoint pupils
(Tx: naloxone, Methadone)
Alcohol
=> ataxia, euphoria, slurred speech, ⇧GGT, AST>ALT
(Tx: thiamine/glucose.+ BZ)
Marijuana
"dope, grass, weed, pot": Δ-9 THC => munchies, red eyes, impaired time orientation
Isoelectric Point (pi)
pH at which there is no net charge (pi= (pK1 + pK2)/2)
Zwitterions
have a negative carboxy and positive amino end
Cathode
where cations go, the negative electrode
Anode
where anions go, the positive electrode
Acidic aa
Asp, Glu
Basic aa
Lys, Arg
what enzyme cut basic aa?
Trypsin cuts basic aa
Sulfur aa
Cys, Met
what enzyme cuts aa that have sulfur in them?
β-ME cuts
0-Bonds aa?
significance of Tyr?
Ser, Thr, Tyr
Tyr makes catecholamines, melanin
N-Bonds aa?
significance?
Asn, Gln
Acid hydrolysis denatures
Branched aa?
significance?
Leu, Ile, Val
Maple syrup urine disease
what are Aromatic aa?
what enzyme cuts them?
Phe, Tyr, Trp
Chymotrypsin cuts "bulky word/ rings"
Smallest aa?
significance?
Gly
Spinal cord inhibitor
NMDA pathway excitatory aa?
Asp
Kinky (Imino)
significance?
Pro
Yellow on Nurhydrin reaction
Active sites aa
Ser
Ketogenic
significance
Lys, Leu
Broken down to Acetyl CoA
Glucogenic +Ketogenic
Phe, Iso, Thr, Trp
(Bulky)
"Mr. PITT never Tyrs"
who should avoid Ketogenic diet
Diabetes I
who should avoid glucogenic diet
Diabetes II
Reasons for Dialysis:
• Symptomatic Uremia
• Symptomatic Acidosis
• Hyperkalemia
Disulfide Bonds:
"PIGI"
• PRL
• Insulin
• GH
• lnhibin
what does Increased GABA levels lead to?
bradycardia, lethargy,
constipation, impotence, and memory loss. This means that anything or any disease that increases acidosis, urea, or ammonia will lead to an increase in GABA which will slow everything down.
NH3 + H+ ⇨ NH4+ αKG ⇨ Glu ⇨ GABA
Essential FA (must eat 'em):
Linolenic
Linoleic ⇨ AA ⇨ PG
Essential Amino Acids: you gotta eat 'em:
"PVT TIM HALL"
Phe, Val, Trp ⇨5HT, Thr, Ile, Met ⇨Cys, His, Arg, Leu, Lys
Newborn screening:
"Please Check Before Going Home"
PKY (Guthrie test)
Congenital adrenal hyperplsia
Biotiniase deficiency
Galactosemia
Hypothyroidism
Energy Utilization:
1) Plasma Glucose: 2-4 hr
2) Liver Glycogen: 24-48 hr
3) Proteolysis for Gluconeogenesis
4) Fats for Lipolysis
5) Ketones for Ketogenesis
AA Disorders (AD):
Met + ATP ⇨ SAM ⇨ Homocysteine ⇨ Cys + propionylCoA ⇨ MMCoA
PKU
Phe ⇨ Tyr ⇨ DOPA ⇨ DA ⇨ NE ⇨ Epi
DOPA ⇨T4 and Melanin (albinism)
Phenylketonuria:
presentation and test
No Phe ⇨ Tyr (via Phe-OHase)
• Mental retardation (can't make DA, NE, Epi)
• Pale, blond, blue eyes (no melanin)
• Musty odor (phenylacetate + phenylpyruvate)
• Nutrasweet sensitivity (Phe)
• Sclerodermatous plaques
• Test: Guthrie test (bacterial inhibition assay)
Albinism
No Tyr ⇨ Melanin (via Tyrosinase)
• Paleness, predisposed to skin cancer
Vitiligo:
• Anti-melanocyte AB
• Pale, predisposed to skin cancer
• Ex: Michael Jackson.
Alkaptonuria "Ochronosis":
• Kids w / osteoarthritis (black tendons), black urine
• Homogentisic acid oxidase deficiency
Maple Syrup Urine Disease:
"Life is sweet, so LIV it up!"
Defective renal transport of branced aa (Leu, Iso, Val) => aa leak out
Homocystenuria: mode of inheritance, pathogenesis
Homocysteinuria (AD): No homocysteine ⇨Cys⇨(via cystathione synthase)
>Defective amino acid transport
Homocystenuria is caused by?
presentation
>Caused by high fat diet: increased Met levels
>Dislocated lens from top "
>Recurrent kidney stones
what are the 4 Amino Acids show up in Urine in homocystenuria?
Defective amino acid transport "COLA"
• cystine stones⇦ + urine CN Nitroprusside
• ornithine
• Lysine - basic aa
• Arginine - basic aa