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135 Cards in this Set
- Front
- Back
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Opioids:
Toxicity |
Respiratory depression
ADdiction COnstipation Miosis (pinpoint pupils) |
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Tramadol:
MOA Use |
Weak opioid agonist; also inhibits 5HT and NE reuptake (works on multiple NTs--TRAM IT ALL)
Use in chronic pain |
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MAC:
What is it? How does it differ with solubility? |
MAC = minimal alveolar concentration at which 50% of populn is anesthitized; varies with age
High lipid solubility = Low MAC = High Potency (Low Km) High blood solubility = slow induction |
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Which inhaled anesthetics offer fast induction but low potency?
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N2O
Isofluvane |
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Which inhaled anesthetics offer high potency but slow induction?
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Methoxyflurane
Halothane, Enflurane |
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How does infection affect use of local anesthesia?
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Infected tissue is acidic; alkaline anesthetics are charged and cannot penetrate effectively. More anesthetic needed.
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Describe the order of nerve blockade in administration of local anesthesia.
Describe order of loss of sensation. |
Small diameter fibers > large diameter
Myelinated > unmyelinated Overall, size predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers Order of sensory loss: Pain > temperature > touch > pressure (lose last) |
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Why are vasoconstrictors given with local anesthetics?
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Enhacnes local action, decreases bleeding, inc'd anesthesia by dec'd systemic concentration
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Depolarizing vs Nondepolarizing anesthetics:
General Examples Antidotes |
Both used for muscle paralysis in surgery or mechanical ventilation; selective for motor nicotinic receptors
Depolarizing: Only depol drug is Succinylcholine Phase I--no antidote, induces prolonged muscle depolarization Phase II--repolarized muscle, but blocked; antidote = AchE-inhibitors (-stigmines) Nondepol: cuararium drugs; compete with ACh for receptors. Reverse w/stigmines |
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Dantrolene:
MOA Use |
Use in malignant hyperthermia caused by inhaled anesthetics and succinylcholine
Can also tx neuroleptic malignant syndrome MOA: prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle |
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Treatment of HD.
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Remember: HD = inc'd DA, low GABA, low ACh
So use: -Reserpine to deplete amines -Haloperidol to block DA receptors |
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What drugs comprise the inhaled anesthetics?
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SHINE
Sevoflurane Halothane Isoflurane Nitrous Oxide Enflurane |
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What are the endogenous agonists to the different opioid receptors?
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Mu receptor--morphine
Delta--enkephalin Kappa--dynorphin |
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Which drug:
Opioid cough suppressant commonly used with the expectorant guaifenesin |
Dextromethorphan
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Which drug:
Opioid used in the treatment of diarrhea |
Loperimide
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Which drug:
Opioid commonly used in the treatment of acute heart failure |
Morphine
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Which drug:
Opioid receptor antagonist |
Neloxone
Neltrexone |
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Which drug:
Non-addictive weak opioid agonist |
Tramadol
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Which drug:
Partial opioid agonist that causes less respiratory depression |
Butorphanol
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What 5 drug classes are used in treatment of glaucoma?
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alpha-agonists
beta-blockers Diuretics Cholinomimetic Prostaglandins |
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What drugs are known for causing Steven's Johnson syndrome?
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Seizure drugs
Sulfonamides -cillin drugs Allopurinol |
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How is barbiturate overdose managed?
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Treats symptomatically
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How is benodiazepene overdose managed?
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Flumazenil
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Which anesthetic:
IV, a/w hallucinations and bad dreams |
Ketamine
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Which anesthetic:
Inhaled, SE nephrotoxic |
Methoxyflurine
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Which anesthetic:
IV, most common drug used for endoscopy |
Medazolam
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Which anesthetic:
Inhaled, SE convulsions/seizures |
Enflurane
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Which anesthetic:
Inhaled, SE hepatoxic |
Halothane
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Which anesthetic:
IV, used for rapid anesthesia induction & short procedures |
Propofol
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Which anesthetic:
Inhaled, used for rapid anesthesia |
NO2
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Which anesthetic:
IV, decreases cerebral blood flow (important in brain surgery) |
Barbiturates (thiopentol for example)
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Which anesthetic:
IV, does not induce histamine release like morphine |
Fentanyl
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Which anesthetic:
High triglyceride content increases risk of pancreatitis with long-term use |
Propofol
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What agents are used in the treatment of Parkinson's Disease?
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BALSA
Bromocriptine Amantadine Levodopa with carbidopa Selegiline Antimuscarinics (benztropine) |
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What side effects are common to most anti-epileptics?
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Diplopia
Sedation Ataxia Nystagmus Dizziness |
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What are the side effects of phenytoin?
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Hirsutism
Gingival hyperplasia Fetal hydantoin syndrome Drug-induced lupus SJS (Stevens-Johnson) Induces CYP450 |
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What is the MOA of dantrolene?
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Prevents release of Ca2+ from Sarcoplasmic reticulum of skeletal muscle (shuts down contraction)
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What is the MOA of local anesthetics?
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Blocks Na+ channels
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Which nerve fibers are blocked first with local anesthesia?
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Pain fibers (or small myelinated)
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What drugs can be used to reverse neuromuscular blockade?
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Neostigmine
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What is the MOA of sumatriptan?
Contraindications? |
5HT 1B/1D agonist
Contraindications: CAD Prinzmetal's angina Pregnant |
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Kinase vs Phosphorylase
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Kinase - uses ATP to add phosphate group onto substrate
Phosphorylase - adds phosphate without ATP |
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Rate Limiting Enzyme:
Glycolysis |
Phosphofructokinase-1
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Rate Limiting Enzyme:
Gluconeogenesis |
Fructose-1,6-bisphosphatase
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Rate Limiting Enzyme:
TCA Cycle |
Isocitrate dehydrogenase
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Rate Limiting Enzyme:
Glycogen Synthesis |
Glycogen synthase
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Rate Limiting Enzyme:
Glycogenolysis |
Glycogen phosphorylase
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Rate Limiting Enzyme:
HMP Shunt |
Glucose-6-phosphate dehydrogenase (G6PD)
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Rate Limiting Enzyme:
De novo pyrimidine synthesis |
Carbamoyl phosphate synthetase II
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Rate Limiting Enzyme:
De novo purine synthesis |
Glutamine-PRPP amidotransferase
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Rate Limiting Enzyme:
Urea cycle |
Carbamoyl phosphate synthetase I
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Rate Limiting Enzyme:
Fatty Acid Synthesis |
Acetyl-CoA carboxylase (ACC)
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Rate Limiting Enzyme:
Ketogenesis |
HMG-CoA synthase
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Rate Limiting Enzyme:
Cholesterol synthesis |
HMG-CoA Reductase
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S-adenosyl-methionine:
Synthesis Functions |
ATP + methionine-->SAM
SAM transfers methyl units (SAM is the methyl donor man) Regeneration of methionine (and thus SAM), is dependent on Vitamin B12 and folate. Required for conversion of NE to Epi. |
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What receptor allows entry of glucose into cells?
How is glucose kept in the cell? |
GLUT-2 (facilitated diffusion)
After cell entry, hexokinase OR glucokinase (+ATP) phosphorylate glucose to Glucose-6-phosphate |
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Hexokinase vs Glucokinase
Role General differences |
Both do this:
Glucose + ATP-->glucose-6-phosphate Hexokinase: ubiquitous; high affinity (low Km), high capacity (high Vmax), induced by insulin Glucokinase: Liver and beta-cells of pancreas. Low affinity (high Km), high capacity (high Vmax), induced by insulin. GLUcokinase is a GLUtton. Has a high Vmax bc it cannot be satisfied. (also, want low affinity in liver so glucose spreads to other organs/tissues) |
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Glycolysis vs Gluconeogenesis:
Reactants vs Products |
Glycolysis: Glucose-->Pyruvcate
Gluconeogenesis: Pyruvate-->Glucose |
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Glycolytic enzyme deficiency:
Presentation Cause |
Hemolytic anemia due to inability to maintain Na/K/ATPase-->RBC swelling/lysis
Cause: Pyruvate kinase deficiency |
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Gluconeogenesis:
Irreversible enzymes and functions Include where in cell each step occurs |
Mitochondria:
Pyruvate-->Oxaloacetate via Pyruvate Carboxylase; requires biotin, ATP; stimulated by acetyl-CoA Cytosol: OAA-->phosphoenolpyruvate via PEP carboxykinase (kinase means requires GTP) In cytosol: Fructose,1,6-bisphosphate-->Fructose-6-phosphate via Fructose-1,6-bisphosphatase In ER: Glucose-6-P-->glucose Note: Pathway Produces Fresh Glucose: Pyruvate carboxylase, PEP carboxykinase, Fructose-1,6-bisphosphatase, Glucose-6-phosphatase |
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Gluconeogensis enzyme deficiency:
Presentation Where are most enzymes found? |
Results in hypoglycemia
Glucoengeogenesis enzymes found primarily in liver. (muscle cannot participate in gluconeogenesis bc lacks glucose-6-phosphatase) Can also use odd-chain fatty acids to yield propionyl-CoA (can enter TCA as succinyl-CoA) and undergo glucneo (even chain FAs can't do this) |
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In what two ways does the liver maintain blood sugar?
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Gluconeogenesis
Glycogenolysis |
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What is the rate limiting enzyme of glycogen synthesis?
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Glycogen synthase
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What are the two alpha bonds exhibited by glycogen?
How do they differ? How is this relevant to glycogen breakdown? |
alpha (1,6) forms branches
alpha (1,4) forms linkages During glycogenolysis: Glycogen phosphorylase breaks down alpha (1,4) bonds (linkages) Debranching enzyme breaks alpha-1,6 (AKA alpha-1,6-glucosidase) bonds |
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What is the rate limiting enzyme of glycogen breakdown?
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Glycogen phosphorylase (Breaks down linkages--alpha(1,5))
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Describe the steps required to store glucose as glycogen.
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Glucose-->Glucose 6-phosphate via GLUCOKINASE
G6P-->Glucose-1-phosphate via PHOSPHOGLUCOMUTASE G1P + UTP-->UDP-glucose UDP-glucose-->Glycogen synthetase-->Branching enzyme-->Glycogen |
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Describe the steps required to breakdown glycogen into glucose.
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Glycogen + Pi-->Glycogen Phosphorylase-->Debranching enzyme-->Glucose
BUT if you are delinking an alpha-1,4 link (no more branch) do this: Glycogen+Pi-->Glycogen phosphorylase -->Glucose-1-Phosphate -->Glucose-6-Phosphate via PHOSPHOGLUCOMUTASE G6P-->Glucose + Pi via GLUCOSE-6-PHOSPHATASE |
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VonGierke's Disease:
Pathophys Presentation |
Glucose-6-phosphatase deficiency (Can't let G6P escape from cell if need to)
Findings: Severe fasting hypoglycemia, inc'd glycogen in liver, blood lactate, hepatomegaly |
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Pompe's Disease:
Pathophys Presentation |
Lysosomal alpha-1,5-glucosidase deficiency; results in cardiomegaly and systemic findings lead to early death
Pompe's trashes the Pump (heart, liver, muscle) |
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Cori's Disease:
Pathophys Presentation |
Deficiency of debranching enzyme (alpha-1,6-glucosidase)
Presents as milder form of type I (Von Gierke's; G6Phosphatase deficiency); with normal blood lactate (and fasting hypoglycemia, and high liver glycogen) |
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McArdle's Disease:
Pathophys Presentation |
Skeletal muscle glycogen phosphorylase deficiency
Results in inc'd glycogen in muscle, but can't break it down Leads to painful muscle cramps, myoglobinuria with strenuous exercise |
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Which glycogen storage disease:
Glycogen phosphorylase deficiency |
McArdle's dz (Type V)
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Which glycogen storage disease:
Glucose-6-phosphatase deficiency |
Type I Von Gierke's
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Which glycogen storage disease:
Lactic acidosis, hyperlipidemia, hyperuricemia (gout) |
Type I Von Gierke's
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Which glycogen storage disease:
a-1 ,6-glucosidase deficiency |
Cori's (Type III)
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Which glycogen storage disease:
a-1 ,4-glucosidase deficiency |
Pompe's (Type II)
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Which glycogen storage disease:
Cardiomegaly |
Pompe's (Type II)
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Which glycogen storage disease:
Diaphragm weakness, respiratory failure |
Pompe's (Type II)
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Which glycogen storage disease:
Increased glycogen in liver, severe fasting hypoglycemia |
Von Gierke's (Type I)
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Which glycogen storage disease:
Hepatomegaly, hypoglycemia, hyperlipidemia (normal kidneys, lactate, and uric acid) |
Cori's (Type III)
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Which glycogen storage disease:
Painful muscle cramps, myoglobinuria with strenuous exercise |
McArdle's (Type V)
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Which glycogen storage disease:
Severe hepatosplenomegaly, enlarged kidneys |
Von Gierke's Dz (Type I)
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What are the four types of glycogen storage disease? (Type I-V)
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Very Poor Carbohydrate Metabolism
I- Von Gierke's II- Pompe's III- Cori's V- McArdle's idk what happened to IV :( |
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Describe the steps of the Cori cycle.
Under what conditions does it occur? |
Under anaerobic conditions:
Muscle/RBCs: Glucose + 2ATP-->2 pyruvate<---->2 lactate via LACTATE DH 2 lactate shuttled to liver Liver: 2 lactate<--->2 pyruvate via LACTATE DH 2 pyruvate + 12 ATP(!!!)-->Glucose-->shuttled to muscle/RBCs |
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What are alanine and glutamine found in such high concentrations in the blood?
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They are the two major carriers of nitrogen (from urea) from tissues.
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What is generally involved in transamination?
Enzymes required? |
Transfer of amino gorup of amino acid to alpha-ketoglutarate to form glutamate
Remaining deminated amino acid is a keto-acid such as pyruvate and is used in energy metabolism Require aminotransferase |
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How are aminotransferases named?
IN addition to substrates, what is required by ALL aminotransferases? |
Aminotransferases named by donor of amino group (alanine aminotransferase converts alanine to pyruvate and forms glutamate for ex)
IN addition ot substrates, al aminotransferases require PYRIDOXAL PHOSPHATE -- VITAMIN B6 |
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Pyridoxal phosphate:
Source Crucial to what process? |
Source = B6
Crucial to nitrogen excretion |
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What are the two most important aminotransferase enzymes and what reactions do they catalyze?
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ALT:
Alanine aminotransferase: alanine + alpha-ketoglutarate-->glutamate + pyruvate AST: aspartate aminotransferase: Glutamate + OAA-->alpha-ketoglutarate + aspartate |
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Pyruvate Dehydrogenase:
Required co-factors Reaction Activators |
Cofactors:
Tender Loving Care For No One Thiamine (TPP) Lipoic ACid CoA FAD NAD Pyruvate + NAD+ + CoA-->AcetylCoA + CO2 + NADH Activated by exercise: -Inc'd NAD+/NADH Ratio -Inc'd ADP -Inc'd Ca2+ |
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Arsenic:
Pathophys Presentaiton |
Arsenic inhibit lipoic acid (required for pyruvate dehydrogenase complex)
Findings: Vomiting, rice water stools, garlic breath |
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Pyruvate dehydrogenase deficiency:
Pathophys Causes Presentation Treatment |
Backup of pyruvate and alanine resulting in lactic acidosis
Can be due to alcoholism (B1 deficiency) or congenital Presents as neuro defects Tx: Inc'd intake of ketogenic nutrients (high fat content, or high lysine and leucine) Note: lysine nad leucine are the only purely ketogenic aa's |
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TCA cycle:
Products per cycle Products per glucose Where does it occur? |
1 cycle produces: 3NADH, 1 FADH2, 2CO2, 1 GTP per acetyl CoA, thus 12 ATP/acetylCoa
Multiply times 2 for per glucose bc one glucose yields 2 pyruvate This all occurs in mitochondria |
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NAD+ vs NADPH:
Functions |
NAD+ : used in CATABOLIC processes to carry reducing equivalents away as NADH
NADPH: used in anabolic processes (steroid and FA synthesis) as a supply of reducing equivalents, ex: respiratory burst (to kill bacteria), cyp450, glutathione reductase (~anti-oxidant) |
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HMP Shunt:
Function Reactions involved and enzymes required |
Source of NADPH from G6P--NADPH required for reductive reactions (glutathione reduction inside RBCs); yields ribose for nucleotide synthesis and glycolytic intermediates
Reactions: Oxidative (irreversible) G6P-->CO2 + 2NADPH + Ribulose-5-P via G6PD**** Nonoxidative (reversible): RIbulose-5-P-->RIbose-5-P via TRANSKETOLASES requires B1 (thiamine)--less impt |
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Respiratory burst:
Reactions involved |
Activation of membrane-bound NADPH oxidase (in nphils, macs)-->rapid release of reactive oxygen intermediates
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NADPH oxidase:
Function Associated Disease |
NADPH oxidase:
O2-->O2 radical (necessary for respiratory burst) Deficient in Chronic Granulomatous Disease |
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Glucose-6-Phosphate Dehydrogenase Deficiency:
Pathophys Presentation Hallmark Method of Inheritance |
G6PD:
G6P-->6PG + NADPH NADPH then reacts with glutathione to keep it reduced as GSH, which can then deactivate O2 radicals If low NADPH (due to low G6PD)-->hemolytic anemia bc RBCs have no defense against oxidizing agents (fava beans, sulfonamids, primquine, anti-tb drugs) Infection can also mediate this Hallmakr: Heinz bodies; Bite cells X-linked recessive |
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Essential fructosuria:
Pathophys Presentation |
Defect in fructokinase; benign (fructose doesn't enter cells)
Syx: Fructose in blood, urine |
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Fructose intolerance:
Pathophys Presenation Treatment |
Deficiency of ALDOLASE B*** (F1,P-->Dihydroxyacetone-P + Glyceraldehyde)
F1P accumulates-->dec'd in available phosphate-->inhibition of glycogenolysis, gluconeo Syx: hypoglycemia, jaundice, cirrhosis, vomiting Tx: dec'd intake of fructose and sucrose (glucose + fructose) |
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Galactokinase deficiency:
Pathophys Presentation |
Deficiency of galactokinase-->galactitol accumulates
Mild condition Galactose in blood/urine, infantile cataracts |
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Classic galactosemia:
Pathophys Presentation Treatment |
Absence of galactose-1-phosphate uridyltransferase
Accumuln of galactitol in lens of eye-->cataracts Syx: failure to thrive, jaundive, hepatomegaly, infantile cataracts, mental retardation Tx: avoid galactose and lactose (galactose + glucose) in diet |
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Describe ethanol metabolism.
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Cytosol:
EtOH-->acetaldehyde via Alcochol DH Mitochondria: Acetaldehyde-->Acetate via Acetaldehyde DH |
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Fomepizole:
MOA Use |
Inhibits alcohol DH (Ethanol-->Acetaldehyde)
Antidote for methanol or ethylene glycol poisoning (antifreeze) |
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Disulfiram:
MOA |
Inhibits acetaldehyde DH (acetaldehyde accumulates-->hangover syx)
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What fuels are produced and used in the post-absorptive period?
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Produced:
Glucose from liver FAs from adipose Used: Muscles, brain and other tissues use predominantly glucose |
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When does gluconeogenesis begin in the post-absorptive period?
When does it become fully active? |
Glucneo begins 4-6 hrs after last meal
Fully active when glycogen stores depleted (10-18 hours after last meal) |
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How does the pattern of fuel production and usage change in early starvation (24 hours after last meal)?
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Early starvation:
Produced: Glucose from glucneo with some glycogen from glycogenolysis FAs from adipose Used: Brain uses predom glucose Muscles and other tissues use some glucose but predom FAs |
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In intermediate starvation (48 hours after last meal), how does the pattern of fuel production and consumption change?
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Intermediate starvation:
Produced-- -Glucose from liver glucneo -no more glycogenolysis -FAs from adipose -Ketones from liver Used: Brain uses predom glucose but all some ketones Mm and other tissue use predom FAs but also some ketones |
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What metabolic scenarior favors the synthesis of ketone bodies?
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Excess of acetyl CoA from FA metabolism
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T/F: Ketone bodies can be used by all body tissues including the brain.
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False, RBCs can only use glucose, everything else can use ketones--even the brain
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What is the pattern of fuel utilization and production in prolonged starvation (5 days after last meal)?
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Prolonged starvation:
Produced-- Glucose from liver glucneo FAs from adipose Ketones from liver Use: Brain uses predom ketone MM and other tissues use predom FAs but also some ketones |
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Comparing an overnight fast to a 3 day fast, what percentage of energy comes from glucose and from ketone bodies?
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Overnight fast energy sources:
95% glucose 5% ketone bodies 3 day fast: 60% ketone bodies 40% glucose |
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How are ketone bodies produced?
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IN liver, FAs and aa's metabolized to acetoacetate and beta-hydroxybutyrate (to be used in mm and brain)--these are both ketone bodies
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Rate-limiting enzyme:
Ketone body synthesis |
HMG-CoA Synthase
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What are the major regulatory enzymes of the citric acid cycle?
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Citrate synthase
Isocitrate dehydrogenase alpha-ketoglutarate dehydrogenase |
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Rate-limiting enzyme:
Glycolysis |
PFK1 (phosphofructokinase 1)
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Rate-limiting enzyme:
Gluconeogenesis |
Fructose-1,6-bisphosphatase
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Rate-limiting enzyme:
Citric acid cycle |
Isocitrate dehydrogenase
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Rate-limiting enzyme:
Glycogenesis |
Glycogen synthase
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Rate-limiting enzyme:
Glycogenolysis |
Glycogen phosphorylase
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What is the functional role of S-adenosyl-methionine?
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Generation of phosphocreatine; methyl donor!!
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Activated carrier of:
CO2 |
Biotin
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Activated carrier of:
Glucose |
UDP glucose
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Activated carrier of:
Electrons |
NADH or FADH or NADPH
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Activated carrier of:
One-carbon units |
THF
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Activated carrier of:
Acyl |
CoA
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How many ATP are generated during aerobic metabolism?
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Aerobic:
Malate-aspartate shuttle--32 ATP Glycerol4-phosphate shuttle--30 ATP |
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How many ATP are generated during anaerobic metabolism?
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Anaerobic:
2 ATP + lactate molecule |
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What are the possible products of pyruvate?
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Acetyl CoA
Lactate Alanine OAA |
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What irreversible enzymes are involved in gluconeogenesis?
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Pyruvate Carboxylase
PEP carboxykinase F-1,6-Bisphosphatase (RATE LIMITING) Glucose-6-phosphatase |
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What is the primary energy source in a patient that has not eaten in two days?
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FAs
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What is the equation for Gibbs free energy?
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deltaG=deltaH-(TxdeltaS)
H = enthalpy (heat content; if difference is negative, rxn is spontaneous) S = entropy (disorder) T=298K |
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A stressed physician comes home from work, consumes 7 shots of tequila in rapid succession before dinner, and becomes hypoglycemic.
Why? |
Generating a lot of NADH, moving pyruvate and OAA to lactate/malate
No longer have pyruvate for glucneo More likely to become hypoglycemic |
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A woman commonly develops intense muscle cramps and darkening of her urine after exercise.
Diagnosis? |
McArdle's Dz
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