Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
171 Cards in this Set
- Front
- Back
|
Glucocorticoids |
- Modulate the HPA axis (hypothalamus, pituitary gland, adrenal glands) |
|
|
Birth control pills |
- Modulate hormonal control of the ovarian/menstrual cycle - Combination of Progesterone and Estrogen - Progesterone: negative feedback on GnRH, LH (result: no ovulation), and FSH (result: no egg) secretion |
|
|
Psychiatric drugs |
- Treats psychiatric disorders - Can cross blood-brain barrier (because lipid soluble) |
|
|
Antidepressants |
- Treats depression and anxiety disorders (ex. OCD, PTSD) - Affect serotonin and/or norepinephrine (monoamine) neurotransmitter systems - Monoamine hypothesis: depression is associated with low levels of serotonin and norepinephrine in brain) |
|
|
Monoamine Oxidase Inhibitors (MAOIs) |
- Inhibits monoamine oxidase which breaks down monoamines --> increasing the amount of norepinephrine and serotonin available for neurotransmission - avoid food/beverages with tyramine because tyramine is a monoamine --> increased levels of tyramine increases risk of hypertensive crisis - only used as a last resort |
|
|
Tricyclic Antidepressants (TCAs) |
- inhibits serotonin transporter (SERT) and norepinephrine transporter (NET) --> prevent their reuptake and increases amount available for neurotransmitter - have a high affinity for many other receptors leading to many side effects: anticholinergic effects, orthostatic hypotension, sedation, weight gain, cardiac arrhythmias |
|
|
Selective Serotonin Reuptake Inhibitors (SSRIs) |
- inhibits serotonin transporter (SERT) --> prevent serotonin reuptake - very selective, so less side effects thus first line treatment for depression): nausea, headache, drowsiness, sexual dysfunction |
|
|
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs) |
- inhibits SERT and NET --> prevent serotonin and norepinephrine reuptake - more selective than TCAs (less side effects) - similar side effects to SSRIs: nausea, headache, drowsiness, sexual dysfunction |
|
|
Bupropion |
- inhibits NET and dopamine active transporter (DAT) --> prevent norepinephrine and dopamine reuptake - less risk of weight gain and sexual dysfunction |
|
|
Mirtazapine |
- blocks presynaptic a2-adrenergic receptors and postsynaptic 5-HT2C receptors to enhance norepinephrine and serotonin release |
|
|
Trazodone |
- blocks postsynaptic 5-HT2A/2C receptors and inhibits SERT |
|
|
Schizophrenia |
- "positive" symptoms: hallucinations, delusions, disorganized thinking - resulting from overactivity of the mesolimbic pathway - "negative" symptoms: lack of motivation, social withdrawal, poverty of speech - resulting in a mesocortical pathway dysfunction |
|
|
Antipsychotic drugs |
- Treats schizophrenia and manic phase of bipolar disorder - Affects dopamine and/or serotonin neurotransmitter systems - Dopamine hypothesis: positive symptoms of schizophrenia are associated with excess dopamine signalling in the mesolimbic system |
|
|
Typical Antipsychotic drugs |
- All act by blocking dopamine D2 receptors to reduce dopamine activity - Effective against positive symptoms - Side effects: dystonia (abnormal, involuntary movements) |
|
|
Atypical Antipsychotic drugs |
- Blocks serotonin and to a lesser degree, dopamine activity (Dopamine D2 and serotonin 5-HT2A receptor antagonists) - Effective against positive and negative symptoms - Reduction in negative symptoms because they block 5-HT2a receptors on dopamine neurons to increase dopamine release/activity in mesocortical system - Side effects: metabolic related - weight gain, insulin resistance |
|
|
Mucous cells |
- Secrete mucous, bicarbonate ions |
|
|
Parietal cells |
- Secrete HCl - Ducts in apical surface to increase surface area |
|
|
Stomach acidity |
- Primary mechanism is via H+/K+ ATPase in apical membrane of parietal cells - Paracrine release of histamine from ECL cells • Responsible for basal secretion levels - Upon stimulus, acid release increased through: Neurocrine release of acetylcholine (parasympathetic. enteric nervous systems) and Endocrine release of gastrin (enteric nervous system peptide) - ACh and Gastrin also stimulate ECL cell-mediated acid release |
|
|
Stomach protection |
- Mucous resists acid and enzyme action - Bicarbonate ion secretion - Continuous epithelial cell replacement |
|
|
Prostaglandins |
- Derived from membrane phospholipids - Synthesized as needed because very short half-life - Prostaglandin E2 (PGE2) and I2 (PGI2) produced in gastric mucosa (production inhibited by NSAIDs) - PGE2 and PGI2 bind to receptors on parietal cells to inhibit H+/K+ ATPase protein, and to receptors on mucous cells to stimulate production/release of mucus and bicarbonate ions |
|
|
Peptic Ulcer Disease |
- Acid-induced erosion of stomach lining - Caused by Helicobacter pylori in the GI tract or NSAID-related inhibition of mucous/bicarbonate secretion - Treatment: Neutralize/reduce gastric levels of H+ or strengthen protective forces |
|
|
Antacids |
- Hydroxide and/or Carbonate salts - Direct chemical neutralization of excess acid - Doesn't affect future acid release, but cannot use while eating because acid is continuously produced - Side effects: altered gastric pH may affect solubility/absorption of other drugs, belching (carbonate-based salts), constipation (aluminum-based salts), diarrhea (magnesium-based salts) - use a mixture |
|
|
H2 Receptor Antagonists |
- the -tidines: Cimetidine - over the counter remedy - Competitive, selective block of histamine H2 receptors in epithelial parietal cells - Long-term treatment - Most effective for constitutive/nocturnal aid secretion (because food-induced aid release partially bypasses histamine pathway) - Little side effects: Diarrhea, headache, drowsiness - Avoided for pregnant women because it crosses placenta and enters breast milk |
|
|
Proton Pump Inhibitors |
- Inhibits the common pathway for all acid-release "triggers" - the -prazoles: Omeprazole - Ingested as prodrug, absorbed in intestine, diffuses into acidified compartments - Irreversible inactivation of H+/K+ ATPase enzyme via sulfenamide covalent binding - Accumulation in canaliculi can prolong effect - Requires new synthesis & membrane insertion (18-24 hrs) - Most common therapy for NSAID-related ulcers because fewer side effects, longer half-life |
|
|
Misoprostol |
- Mucous/Buffer stabilizing agent - PGE1 analogue - Reduces H+ release, increases mucous and bicarbonate secretion - Useful in NSAID-induced ulcers because it inhibits endogenous prostaglandin protection - Side effects: Diarrhea, abortion risk |
|
|
Sucralfate |
- Aluminum hydroxide sulfated sucrose complex - More effective as preventative measure - Reacts with HCl to form viscous, sticky protective gel that prevents mucous degradation - 4x daily dosing, empty stomach - Side effects: Reduces absorption of certain drugs, constipation (from aluminum) |
|
|
"Triple threat" |
- for H.Pylori-related ulcers - Proton pump inhibitor, clarithromycin (antibiotic) and amoxicillin/metronidazole for 14 days |
|
|
GERD |
- Gastroesophageal Reflex Disease - Reflux of stomach contents past lower esophageal sphincter causing inflammation/esophagitis (lack of mucous protection there) - Heartburn, mild regurgitation - Treatment: Lifestyle changes, reduction of acid release, prokinetic drugs |
|
|
Prokinetic drugs |
- Stimulate neurons of the enteric nervous system, facilitating gastric emptying and/or intestinal motility (reducing stomach volume) - Domperidone (dopamine receptor antagonist) |
|
|
Bulk Laxatives |
- Dietary fiber - Supplemental intake - Water retention properties which stimulates the GI tract to induce a bowel movement - No serious adverse effects |
|
|
Osmotic Laxatives |
- Poorly absorbed salts, fatty acids, and/or carbohydrates to increase water retention and colon fluid volume by osmosis - Side effects: abdominal cramps, diarrhea |
|
|
Stimulant/contact Laxatives |
- Senna preparations release anthracene compounds that directly stimulate myenteric plexus - Castor oil |
|
|
Fluid/electrolyte Management |
- Oral Na/glucose solution to facilitate reuptake |
|
|
Anti-infective Agents (Diarrhea treatment) |
- Rarely needed because most cases will resolve before drugs begin to take effect and side effects (of antivirals) can be more severe than initial diarrhea - Antibiotics: Use can lead to resistance |
|
|
Anti-motility Agents |
- Opiates diminish propulsive activity, allowing more time for water absorption - Loperamide is more selective for receptors in digestive tract than other opioids |
|
|
Pharmacogenomics |
- Relationship between your genotype and effects that drugs will have on you |
|
|
Adverse Drug Reactions |
- Caused by interactions between drugs since most common drugs go everywhere in the body |
|
|
Cisplatin |
- Important and effective drug for the treatment of liver, ovarian, brain, lung, bladder, head, and neck cancer - Side effect: Permanent hearing loss linked to a mutation in catechol-o-methyltransferase (COMT) |
|
|
Doxorubicin |
- Effective drug for the treatment of blood, breast and most childhood cancers - Compromises heart function, and in severe cases heart failure can occur - Highly variable response |
|
|
HER-2 Biomarker |
- Test if HER-2 is overexpressed in the patient's tumour, to determine whether Hercaptin (ntibody that binds to HER-2 protein) has an effect in treating metastatic breast cancer |
|
|
ALK Biomarker |
- Defective gene product of ALK drives cancer growth in non-small cell lung cancer - Xalkori (Crizotinib) inhibits it to shrink/stabilize tumours |
|
|
CFTR Biomarker |
- Defective CFTR gene causes Cystic Fibrosis - Kalydeco binds to a version of CFTR protein found in 3-5% of people with cystic fibrosis to improve function |
|
|
BRCA1 Biomarker |
- BRCA1 protein repairs damaged DNA or triggers cell death - Mutation in BRCA1 results in defective protein, thus allowing for uncontrolled cell proliferation |
|
|
Codeine (pharmacogenetics) |
- Codeine is converted to morphine by CYP2D6 - Variations of CYP2D6 have decreased metabolic activity so reduced conversion and analgesic effect |
|
|
Clopidogrel (Plavix) |
- Clopidogrel is converted into the active metabolite by CYP2C19 - Variations of CYP2C19 have a reduced ability to convert clopidogrel into its active metabolite, resulting in a diminished antiplatelet effect |
|
|
Warfarin (Coumadin) |
- Warfarin is metabolized by CYP2C9 - Variation in CYP2C9 gene causes slow metabolism of warfarin resulting in greater anticoagulant effect |
|
|
Health Products and Food Branch (part of Health Canada) |
- Legislates what products can be sold, level of control (prescription, OTC etc), issue of drug abuse - Price variations in different areas |
|
|
US Department of Health and Human Services |
- Review clinical research, ensure safety, efficacy and proper labeling, consult with experts, consumers and manufacturers - More centralized so same price everywhere |
|
|
Molecular Targeting |
- Drug targets a known protein involved in a disease process - High Throughput Screening: detect interaction between thousands of molecules and the target - Combinatorial Chemistry: allows rapid synthesis of different molecules for use in HTS - Molecular Modelling: 'create' the best drug candidate in silico and in vitro |
|
|
Steroid Hormones |
- Hydrophobic (derived from cholesterol) - Circulate in bloodstream bound to carrier proteins - Can permeate cell membranes - Bind to intracellular receptors to change transcription of target genes to elicit a response (slow) - Because bound to carrier proteins, breakdown is slow |
|
|
Peptide Hormones |
- Hydrophilic - Circulate in bloodstream without binding protein - Cannot permeate cell membranes - Bind to cell surface receptors. Conformational change of the receptor elicits a response (fast) - Rapid breakdown |
|
|
G-protein Coupled Receptors |
- Conformational change causes dissociation of heterotrimeric G-proteins and activation of downstream signaling cascades - Ex. glucagon receptor, TSH and FSH receptors - Catecholamines also bind to G-protein coupled receptors |
|
|
Receptor Tyrosine Kinases |
- Conformational change causes dimerization, autophosphorylation, followed by recruitment and activation of downstream signaling molecules - Ex. insulin receptor |
|
|
Feedback Regulation |
- Helps maintain homeostasis - Hormones released from endocrine glands following a stimulus - The hormone or physiological response exerts feedback regulation on the upstream control mechanism |
|
|
Tertiary Endocrine Disorder |
- Results from defect further upstream from the control gland |
|
|
Secondary Endocrine Disorder |
- Results from defect in an upstream control gland |
|
|
Primary Endocrine Disorder |
- Results from defect in primary hormone secreting gland |
|
|
Diuretic Drugs |
- Treats hypertension and edema - Results in removal of sodium and water |
|
|
Kidneys |
- Each kidney contains 1-2 million nephrons in 4 regions: glomerulus, proximal convoluted tubule, loop of Henle, distal convoluted tubule - Cleans extracellular fluid and maintains its volume and composition - Maintains pH - Excretes metabolic wastes and foreign substances |
|
|
Renal Processes |
- Filtration at the glomerulus - Reabsorption - Active tubular secretion at proximal convoluted tubule |
|
|
Diuretics |
- Blocks Na+ and Cl- reabsorption (keeping water in urine) - Greatest effect when targeting proximal tubule - Side effects: Hypovolemia, acid-base imbalance, electrolyte imbalances |
|
|
Carbonic anhydrase inhibitors |
- Present in proximal tubule - Weakest diuretic rarely used for CN diseases - Can form kidney stones - Ex. Acetazolamide |
|
|
Osmotic diuretics |
- Act on renal proximal tubule - Use in acute renal failure, decreasing intracranial and intraocular pressure - Ex. Mannitol |
|
|
Loop diuretics (Furosemide) |
- Acts on Loop on Henle to decrease Cl- and Na+ reabsorption - Strong but brief diuresis - Use for edema, congestive heart failure - Side effects: Loss of K+ (and Ca2+ and Mg2+), hypotension, volume loss - Many drug interactions with NSAIDs, digoxin etc |
|
|
Thiazides |
- Most widely used - Inhibits reabsorption of Na+, Cl-, K+ in distal convoluted tubule - Use in hypertension, mild heart failure, edema - Side effects: Loss of K+, enters breast milk |
|
|
Potassium-sparing diuretics |
- Blocks aldosterone in distal convoluted tubule, thus blocking reabsorption of Na+ and water - Retains K+ (Because no reabsorption of Na+) - Modest effects, use with other diuretics to reduce K+ loss - ex. Aldosterone receptor antagonists: Spironolactone |
|
|
Rapid-acting insulin |
- Rapid onset but short duration - Ex. insulin glulisine, lispro, insulin asp |
|
|
Short-acting insulin |
- Moderate onset, relatively short duration - Ex. Humulin-R |
|
|
Intermediate-acting insulin |
- Delayed onset, long duration - Ex. Humulin-N, Novolin-NPH |
|
|
Long-acting insulin |
- Very delayed onset, very long duration - Ex. Insulin glargine, insulin detemir |
|
|
Type 2 Diabetes |
- Insulin resistant - Beta cell dysfunction in the long term (causing programmed cell death) - No ketoacidosis |
|
|
Sulfonylureas |
- Promotes secretion of insulin |
|
|
Biguanides |
- Insulin sensitizers - Ex. Metformin |
|
|
Alpha-glucosidase inhibitors |
- Inhibits pancreatic alpha-glycosidase hydrolase enzymes (inhibiting breakdown of complex sugars) |
|
|
Thizaolidinedones |
- Insulin sensitizers |
|
|
Peroxisome proliferator-activator receptors (PPARs) |
- Nuclear receptors involved in expression of genes that regulate storage and catabolism of dietary fats - PPAR(gamma) activation leads to induction of adipocyte genes, improving insulin action in muscle and liver |
|
|
Glucagon-like peptide (GLP-1) |
- Metabolized by DPP-4 - Induces glucose-dependent insulin secretion |
|
|
GLP-1 agonist |
- Exenatide (resistant to DPP-4) thus can induce insulin secretion longer - Result in weight loss |
|
|
DPP-4 inhibitors |
- Ex. Sitagliptin - Prevents degradation of GLP-1 |
|
|
Macrovascular complications of diabetes |
- Coronary artery disease, peripheral vascular disease, cerebrovascular disease |
|
|
Microvascular complications of diabetes |
- Leading cause of blindness, kidney failure, amputations |
|
|
Hypertension |
- Primary (no identifiable underlying cause) - Secondary (underlying condition cause) |
|
|
Arterial pressure |
= cardiac output x peripheral resistance - cardiac output determined by: heart rate, contractility, blood volume, venous return - peripheral resistance determined by: arteriolar constriction |
|
|
Renin-angiotensin-aldosterone system (RAAS) |
- Kidneys produce renin, which converts angiotensinogen into angiotensin I - ACE converts angiotensin I into angiotensin II which causes vasoconstriction and induces the adrenal cortex to produce aldosterone |
|
|
Aldosterone |
- Increases sodium retention, fluid retention, and thus blood pressure |
|
|
ACE-inhibitor |
- Inhibits conversion of Angiotensin I to Angiotensin II - Side effect: Cough, from accumulation of bradykinin which is a bronchoconstrictor, since ACE also metabolizes bradykinin |
|
|
Preeclampsia |
- Hypertension and protein in urine during pregnancy - Cannot use ACE inhibitors. Only cure is delivery of baby |
|
|
Angina Pectoris |
- Acute chest pain resulting from insufficient blood supply to the heart (myocardial ischemia) - Treatment: nitrates, beta-blockers, calcium channel blockers Antiplatelet agents (ex. aspirin) Beta-blockers, BP control Cholesterol lowering, Converting enzyme inhibition, Cessation of smoking Diet, Diabetes control Exercise |
|
|
Congestive Heart Failure |
- Heart is unable to pump enough oxygenated blood with each contraction - Symptoms: Shortness of breath, fluid retention |
|
|
Replacement (category of drug action) |
- Drug replaces a physiological process |
|
|
Interruption (category of drug action) |
- Drug interferes with a physiological process |
|
|
Potentiation (category of drug action) |
- Drug stimulates a physiological process |
|
|
Agonists |
- Have affinity for the receptor - Binding elicits a response - Can be exogenous or endogenous, inhibitory or excitatory |
|
|
Antagonists |
- Have affinity for the receptor - Binding does not elicit a response |
|
|
Graded dose-response curves |
- Relates degree of effect to the amount of drug, often in a single individual |
|
|
Maximal efficacy |
- Maximal effect that drug can achieve |
|
|
Potency |
- Concentration/dose to produce 50% of drug's maximal effect |
|
|
Quantal dose-response curves |
- Relates dose to frequency of a predetermined effect - Yes/no response - Data collected for population of individuals |
|
|
Therapeutic index |
= TD50/ED50 - Larger the TI, safer the drug - Narrot TI means some dose might be therapeutic for some and toxic for others |
|
|
Pharmacokinetics |
- ADME: Absorption, distribution, metabolism, excretion - What the body does to the drug |
|
|
Volume of distribution |
- Compartments in which hydrophilic drugs can distribute - Total body water: 42L - Intracellular volume: 28L - Extracellular volume: 14L - Of 14L, interstitial volume: 10L and plasma volume: 4L - VD > 42L: drug distributes outside blood and body fluids into tissues - VD < 42L: drug has limited distribution |
|
|
Phase I metabolism |
- Cytochrome P450 enzymes add or uncover polar groups to increase drug's water solubility via oxidation/reduction/hydrolysis |
|
|
Phase II metabolism |
- Various non-P450 liver enzymes covalently add large, polar, endogenous molecules to parent drug or Phase I metabolite - Most phase II metabolites are inactive |
|
|
Steady state concentration |
- When rate of drug administration equals the rate of drug elimination (takes ~5 half-lives) - Goal is to have steady state fall within the drug's therapeutic range |
|
|
Gram Positive Bacteria |
- Ex. Staphylococcus - Has thicker cell wall |
|
|
Gram Negative Bacteria |
- Ex. E. Coli |
|
|
Anaerobes |
- Ex. Bacteroides - Don't need oxygen to survive |
|
|
B-Lactam Antibiotics |
- Inhibit synthesis of bacterial cell wall - Ex. Penicillins |
|
|
Macrolides |
- Inhibit bacterial protein synthesis by binding to 50S subunit of bacterial ribosomes - Inhibit RNA-dependent protein synthesis at the chain elongation step - Ex. Erythromycin |
|
|
Aminoglycosides |
- Interfere with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits - Ex. Gentamicin |
|
|
Tetracyclines |
- Inhibit bacterial protein synthesis by binding to 30S subunit (and possibly 50S subunit) of bacterial ribosomes - Ex. Tetracycline |
|
|
Quinolones |
- Inhibit relaxation of supercoiled DNA by inhibiting DNA gyrase/topoisomerase - Ex. Levofloxacin |
|
|
Glycopeptides |
- Inhibit cell wall synthesis in Gram Positive bacteria by binding to the D-alanyl-D-alanine terminus of cell wall precursor units - Ex. Vancomycin |
|
|
Oxazolidinone |
- Inhibits protein synthesis by binding at the P site of the 50S ribosomal subunit - Ex. Linezolid |
|
|
Alkylating Agents |
- Bind DNA by creating covalent bonds, preventing unwinding of DNA molecule - Ex. Cyclophosphamide |
|
|
Epipodophyllotoxins |
- Inhibit topoisomerase II - Ex. Etoposide |
|
|
Taxanes |
- Promote assembly and stabilization of microtubules - Ex. Docetaxel |
|
|
Antimetabolites |
- Incorporates into DNA or RNA and interferes with function/synthesis - Ex. 5-Fluorouracil (5-FU) |
|
|
Antitumour Antibiotics |
- Insert between DNA base pairs to uncoil DNA helix - Ex. Doxorubicin |
|
|
Streptozocin |
- Alkylating agent, antitumour antibiotic - Undergoes spontaneous decomposition and alkylates DNA to inhibit mitosis |
|
|
Camptothecins |
- Bind topoisomerase I - Ex. irinotecan |
|
|
Vinca Alkaloids |
- Prevent polymerization of tubule to form microtubules - Ex. Vincristine |
|
|
Biological response modifier |
- Ex. Interferon a - stimulates immune system against tumour cells |
|
|
Targeted Therapy (chemotherapy) |
- Ex. Monoclonal Antibodies - Targets a receptor |
|
|
Endocrine Therapy |
- Corticosteroids: Dexamethasone, Prednisone |
|
|
Screening Test Examples |
- Colonoscopy, mammography, pap smear, dermatology screening |
|
|
B2 agonist (to treat asthma) |
- Inhibits production of pro-inflammatory mediators - Short-acting: Salbutamol and Terbutaline - Long-acting: Salmeterol and Formeterol - Side effects: B2 receptor desensitization |
|
|
Cholinergic nerves |
- Releases Acetylcholine |
|
|
Adrenergic nerves |
- Releases epinephrine and norepinephrine |
|
|
Epinephrine receptor(s) are |
a1 = B1 = B2 = B3 |
|
|
Norepinephrine receptor(s) are |
a1 = B1 = B3 |
|
|
Phenylephrine receptor(s) are |
a1 |
|
|
Isoproterenol receptor(s) are |
B1 = B2 |
|
|
Salbutamol receptor(s) are |
B2 |
|
|
a1-Adrenoceptors |
Contraction |
|
|
B2-Adrenoceptors |
Relaxation; metabolic |
|
|
B1-Adrenoceptors |
Increase heart rate and contractility (cardiac stimulation) |
|
|
B3-Adrenoceptors |
Lipolysis |
|
|
a2-Adrenoceptors |
Decrease sympathetic nerve activity and release of norepinephrine |
|
|
Nicotinic receptor agonists |
Acetylcholine, nicotine |
|
|
Neuromuscular nicotinic receptor agonists |
Acetylcholine, nicotine - At neuromuscular junction of somatic nerves |
|
|
Ganglionic nicotinic receptor agonists |
Acetylcholine, nicotine - At autonomic ganglia |
|
|
Muscarinic receptor agonists |
Acetylcholine, muscarine - Parasympathetic postganglionic nerve terminals |
|
|
B1 effect on the heart |
- Increased heart rate and conduction velocity on SA/AV node - Increased heart rate, arrhythmias on etopic pacemakers - Increased contractile forces on ventricular muscle |
|
|
Muscarinic effect on the heart |
- Decreased conduction velocity and heart rate on SA/AV node |
|
|
a1 effect on the eyes |
- Pupil dilation on radial muscle |
|
|
Muscarinic effect on the eyes |
- More accommodation on ciliary muscle - Pupil constriction on circular muscle |
|
|
a1 effect on arterioles and veins |
- Vasoconstriction on skin, mucosa - if a1>>> B2, vasoconstriction at GI Tract - if a1>>> B2, vasoconstriction at veins |
|
|
B2 effect on arterioles |
- if B2 >>> a1, vasodilation at skeletal muscles |
|
|
B2 effect on bronchioles |
- Relaxation (bronchodilation) |
|
|
Muscarinic effect on bronchioles |
- Constriction (Bronchoconstriction) |
|
|
B2 effect on skeletal muscle |
- Tremors |
|
|
a1 effect on genitourinary |
- Constriction at sphincters - Ejaculation at penis |
|
|
B2 effect on genitourinary |
- Relax (decrease urgency) of bladder - Relaxation of uterus during pregnancy |
|
|
Muscarinic effect on gastrointestinal |
- Increase motility of smooth muscle wall - Relaxation of sphincters - Increase secretion |
|
|
Muscarinic effect on genitourinary |
- Contraction of bladder (increase urgency) - Relaxation of sphincters - Erection of penis |
|
|
B2 effect on metabolic |
- Increase glucose output at liver |
|
|
B3 effect on metabolic |
- Increase lipolysis of fat cells |
|
|
Muscarinic effect on sweat glands |
- Increase sweating * affecting sympathetic cholinergic |
|
|
a2 effect on CNS/nerve terminals |
- Decrease sympathetic nervous system activity and decrease norepinephrine release |
|
|
a1 effect on gastrointestinal |
- Constriction at sphincters |
|
|
B2, a2 effect on gastrointestinal |
- Relaxation (decreases motility) |
|
|
Physostigmine |
- Reversible anticholinesterase - Naturally occuring tertiary amine - Well absorbed and distributed to CNS |
|
|
Neostigmine |
- Reversible anticholinesterase - Quaternary ammonium - Does not penetrate CNS |
|
|
Malathion |
- Irreversible anticholinesterase - Insecticide |
|
|
Bethanecol |
- Choline ester - Limited use because not very selective - Muscarinic action, not susceptible to cholinesterase |
|
|
Antimuscarinic cholinergic blockers |
- Atropine and Scopolamine |
|
|
Antinicotinic cholinergic blockers |
- Tubocurarine competitively blocks N receptors in skeletal muscle (neuromuscular blocker) |
|
|
Cocaine |
- Local anesthetic, readily penetrates CNS - Blocks reuptake of norepinephrine causing increased BP/HR and dopamine causing euphoria and pleasure |
|
|
Amphetamine |
- Increase release of dopamine and norepinephrine reducing sleepiness and increase attention span of children (but cause growth problems) |
|
|
Ephedrine |
- Suppresses appetite |
