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156 Cards in this Set
- Front
- Back
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Which histamine receptor mediates allergic rhinitis?
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H1 receptor, causes increased capillary permeability and vasodilation
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Drug classes used to treat allergic rhinitis
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H1-receptor antagonists, corticosteroids, a1 antagonists (decongestants), and antimuscarinics
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H1-receptor antagonists
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Loratidine, Desloratadine, Cetirizine, Fexofenadine, Meclazine (all end in -ine)
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Side effects of H-1 antagonists
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Xerostomia, pharyngitis, headache, depression/sedation
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Actions of H-2 receptor
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Speed up sinus rhythm, stimulate gastric acid secretion, smooth muscle relaxation, inhibits antibody synthesis
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How does H1 receptor modulate sleep/wake cycles?
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Histaminergic neurons in the hypothalamus release histamine during alert state. This activates a G protein that leads to closure of K+ channels and depolarization of the cell (which increases its activity) and leads to wakeful state
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Where does respiratory gas excahnge occur?
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Across the respiratory bronchioles and alveoli
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How does pulmonary edema affect oxygen diffusion in the lungs?
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It increases the diffusion distance for oxygen absorption, decreasing uptake of oxygen
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How much blood is in the alveolar capillaries at any time?
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About 70 mL
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What is tidal volume?
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During periods of quiet breathing only about 500 mL of air is exchanged per breath. This is the tidal volume
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What is a capacity, when referring to ventillation?
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The sum of two or more volumes
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What is residual volume?
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The amount of air left in the lungs after maximal expiration (the lungs never fully empty)
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What is the expiratory reserve volume?
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The amount of air left in the lungs after a normal (sub-maximal) exhalation during quiet breathing
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What is the functional residual capacity?
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The expiratory reserve volume plus the residual volume. It is usually about 2.4L
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What is anatomical dead space?
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The amount of air that isn't taken into the alveoli during a tidal breath (about 150mL of the 500 mL tidal volume)
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Formula for alveolar ventillation
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Va = breaths/min x (Vt - Vd). So this equation removes the dead space (Vd) since that gas isn't exchanged in the alveoli
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Which volume of expired air most closely approximates the systemic arterial blood gas composition?
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The last half of the tidal volume, which is mostly alveolar air (not dead space air)
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At what point in exhalation do the expiratory muscles come in to play?
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When you get to the limit of the functional residual capacity (into the expiratory reserve volume). Above FRC, its all passive due to elastic recoil
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What are the most important muscles that raise the rib cage?
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The external intercostals
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What are the most important muscles that pull the rib cage down during expiration?
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Abdominus rectus. Internal intercostals contribute as well
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What is pleural pressure?
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The outward force exerted on the lungs by the inspiratory muscles. It is about -4 or -5 after expiration of a tidal breath (at FRC)
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What is transpulmonary pressure?
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The recoil pressure that tends to collapse the lung. It is about 5 cm H20
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When are transpulmonary pressure and pleural pressure equal?
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At the FRC
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How much additional pressure do the inspiratory muscles need to generate for a tidal breath?
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About 2.5 cm H20
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What is lung compliance?
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The volume of air that is exchanged per unit of pressure generated during inspiration (change in volume/change in pressure)
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What is the biggest factor affecting compliance?
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The surface tension of the think layer of fluid lining the alveoli. This must be overcome by surfactant
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How does emphysema affect lung compliance?
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Compliance is actually increased
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How does asthma affect lung compliance?
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It doesn't have much effect, its pretty close to normal.
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How does pulmonary fibrosis affect lung compliance?
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It is reduced significantly
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What is the major component of surfactant?
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Mainly phospholipids and some protein. The phophoslipid is mostly phosphatidylcholine
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What measurement is used to evaluate pulmonary disease?
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FEV1, which is the amount of a forced vital capacity expired in one second. Normal is about 80%
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What mediates the early response in asthma?
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Within 10-20 minutes, histamine, PAF, prostaglandins and leukotrienes lead to bronchoconstriction
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What mediates the late response in asthma?
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3 to 4 hours after exposure there is an influx of inflammatory cells, including PMNs and eosinophils. These produce many of the same mediators that mast cells produced early on
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Drug classes used to treat asthma
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Inhaled corticosteroids, non-catecholamine bronchodilators, anticholinergic agents, leukotriene receptor antagonists
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How do corticosteroids work to releive asthma symptoms?
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They reduce the inflammatory response by interfering with cytokine signaling
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What does muscarinic (M3) activation do in the airway?
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Stimulates the release of Ca from the SR of airway smooth muscle to promote vasoconstriction and bronchoconstriction
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Action of M3 antagonists
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Inhibits bronchoconstriction and vasoconstriction in the airway and reduces secretions
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Action of theophylline
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Relax bronchial smooth muscle and enhace effect of beta adrenergic stimulation (b2)
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What two drugs are combined in Advair?
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Fluticasone and salmeterol
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Side effects of bronchodilators
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Xerostomia, altered taste, nervousness, headaches, palpitations, and hypertension
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Chronic bronchitis
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Chronic inflammation of the alveolar epithelium caused by prolonged exposure to airway irritants (ie histamine, Ach)
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How do you treat emphysema?
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You can try Prolastin, which stops the proteolytic degradation of elastic tissue in the lungs. Thy will need oxygen therapy as well
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What percentage of American adults are afflicted with GI diseases?
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12%
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What type of medication can increase salivary flow?
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Muscarinic agonists like pilocarpine
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Process of saliva formation
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Primary secretion is nearly isotonic to plasma. In the striated ducts the saliva is modified and Na, Cl are reabsorbed and K, HCO are secreted
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Does a reduction in AQP 5 contribute to Sjogren's?
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No
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How does sympathetic stimulation decreases salivary flow?
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It causes vasocaonstriction so there is less blood flow to the glands and less ultrafiltrate available for secretion
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What medications can be used to reduce salivary flow?
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Muscarinic antagonists such as atropine, scopolamine, glycopyrrolate, and propantheline
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What controls swallowing?
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The swallowing center of the pons and medulla, which receives vagal afferernt signals from esophageal receptors
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GERD
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Transient relaxation of the lower esophageal sphincter not induced by swallowing. Common after meals, in pts with hiatal hernia, obesity, and slower gastric emptying
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Which refluxed fluids cause damage to esophageal mucosa?
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Acid, pepsin and bile
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Function of parietal (oxyntic)cells
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Secrete HCL
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Function of chief cells
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Secrete proteolytic enzymes
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What do surface epithelium of the stomach secrete?
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Protective mucous and bicarbonate
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How do NSAIDs lead to peptic ulcers?
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They inhibit production of prostaglandins that act as vasodilators. When PGE2 isn't present the bloodflow to the mucosa is decreased and mucous secretion decreases as well
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What membrane protein is responsible for H+ secretion in parietal cells?
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An H+/K+ ATPase in the apical membrane
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How does omeprazole become activated?
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It is inactive at neutral pH but its converted to the active form at low pH
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What happens systemically wheh the stomach over-prodcues acid?
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The blood and ECF can become transiently alkalotic, which is referred to as the alkaline tide.
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What are three end receptor types that can lead to stomach acid secretion?
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G protein receptors that bind gastrin, H2 receptor binding histamine, and M3 receptor binding Ach
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What is the common suffix for proton pump inhibitors?
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-PRAZOLE. Some drugs include lansoprazole, omeprazole, pantoprazole, etc
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What common chemical structure do all proton pump inhibitors share?
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An azole ring structure which contains nitrogen
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Side effects of proton pump inhibitors
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Diarrhea, headache, vomiting. HIgher gastric pH can lead to inactivation of pepsin, interfere with absorption of some drugs.
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Important drug interaction with omeprazole
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If diazepam is taken concurrently, the plasma concentrations of that drug can be increased by 15-25% due to activation of CYP enzymes
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Three classes of drugs used to treat gastric acid disorders
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H2 antagonists, M3 antagonists, and PPIs
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Common suffix for H2-antagonists
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-TIDINE. Some of the drugs include Cimetidine, Famotadine, Nizatidine, and Ranitidine
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Method of action of Misoprostol
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It is a prostaglandin analog so it inhibits acid secretion and stimulates mucous formation
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How does Sucralfate work to treat peptic ulcers?
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It coats and protects irritated mucosal tissues
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What medication used to treat peptic ulcers is an azole but not a PPI?
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Metronidazole, used with tetracycline for H. pylori infections
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What action of bismuth subsalicylate have?
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It is an antacid and an antimicrobial
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Helidac is a combo of what three meds used to treat H. pylori infections?
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Bismuth subsalicylate, metronidazole, and tetracycline
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Prevpac is a combo of what three meds used to treat H. pylori infections?
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Lansoprazole, amoxicillin, and clarithromycin
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What are the two components of the enteric nervous system?
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The myenteric (Aurbach's)plexus and the submucosal (Meissner's) plexus
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lWhere is Aurbach's plexus located?
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Spans the entire length of the GI tract and is found in the muscularis externa between the layers of circular and longitudinal muscle
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Where is Meissner's plexus found?
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It spans the entire length of the GI tract and is found in the submucosa
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What is the intrinsic reflex?
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Distension of the gut stimulates muscle contraction above and relaxation below a food bolus to mive it in an oral to anal direction
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What is the gastrocolic (or gastroenteric) reflex?
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An increase in motility of the colon caused by filling of the stomach
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What is the enterogastric reflex?
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A reduction of stomach emptying in response to distension associated with a full colon
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Innervation of the distal third of the transverse colon, descending colon, sigmoid, and rectum
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Pelvic nerves from the sacral spinal cord. Everything before that point is vagus nerve
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What happens in the rectum to cause the urge to poop?
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Reflex relaxation of the internal anal sphincter and reflex constriction of the external anal sphincter in response to filling of the rectum
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What medication is both an antacid and a laxative?
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Milk of magnesia. It is a laxative due to its osmotic properties as an inorganic salt
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Types of drugs used to treat diarrhea
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Opiates, anticholinergics, antibacterials, absorbent agents, and corticosteroids
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How do opiates work to treat diarrhea?
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They act on the mu opiod receptor in the myenteric plexus and cause decreased motility. Food stays in the gut longer and more water is thus reabsorbed
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What are two opiates that are used to treat diarrhea?
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Diphenoxylate and loperamide. The first one acts on CNS as well as gut and can be addictive
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Where is the vomiting center in the CNS located?
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In the lateral reticular formation of the medulla
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Pathways contributing to emesis
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CN 8 via vestibular apparatus and chemoreceptor trigger zone at the base of the 4th ventricle
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Action of antiemetics
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They inhibit receptor sites associated with emesis (ie in vestibular apparatus).
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Types of antiemetics
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Anticholinergics, antihistamines, dopamine and serotonin antagonists, and cannabinoids
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What receptor types are linked to emesis?
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Opiod receptors (all 3 kinds), dopamine2, histamine1, muscarinic, and serotonin receptors
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Which opiod receptors mediate antiemetic effect and which mediate emetic effect?
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Mu-receptors mediate antiemetic effect and delta and kappa mediate the emetic effect
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Side effects of antiemetics
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Possible syncope due to orthostatic hypotension
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Which spinal cord tract carries pain sensation coming from the periphery to the brain?
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The spinothalamic tract
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Inflammatory soup
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Damaged cells release K+, H+, and proteolytic enzymes that depolarize nociceptors
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Role of bradykinin in pain
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It makes free nerve endings more sensitive to stimulus
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How is bradykinin made?
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The enzyme kallikrein proteolytically cleaves bradykinin from HMWK following cellular damage
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Side effects of antiemetics
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Possible syncope due to orthostatic hypotension
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Which spinal cord tract carries pain sensation coming from the periphery to the brain?
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The spinothalamic tract
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Inflammatory soup
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Damaged cells release K+, H+, PGE2, and proteolytic enzymes that depolarize nociceptors
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Role of bradykinin in pain
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It makes free nerve endings more sensitive to stimulus
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How is bradykinin made?
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The enzyme kallikrein proteolytically cleaves bradykinin from HMWK following cellular damage
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Interaction between ACE inhibitors and bradykinin
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ACE degrades bradykinin. ACE inhibitors allow accumulation of bradykinin which can irritate the lungs and cause dry cough
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How is substance P released from free nerve endings?
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By antidromic release, where a signal travels toward the nerve ending from another branch
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Action of substance P
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Stimulates more bradykin formation, activates mast cells and platelets to produce histamine and serotonin. Also leads to vasodilation and extravasation
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Sensitization of free nerve endings
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Mediated by bradykinin, PGE2, histamine, and serotonin. Leads to hyperalgesia (increased sensitivity to pain)
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TRP channels
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Vanilloid receptors respond to heat and capsaicins. Melastatin receptors respond to cold and menthol.
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TRP channels and pain
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TRP channels are found in some pain receptors and can provide a soothing effect when stimulated by menthol or capsaicin
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Aside from being released at the free nerve endings, where else is PGE2 and substance P released?
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It is released from the primary nociceptor into the synapse with the secondary neuron, and thus also contributes to transmission of pain signals
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Which brain stem nucleus has synapses for nociceptors of the head?
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The nucleus caudalis. After this synapse, the secondary neuron carries the signal to the brain via the trigeminothalamic tract
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How do NSAIDs alleviate pain?
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They interfere with COX so prostaglandins don't get produced. No PGE2 means less sensitization and less pain signal transmission
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Which neurotransmitter is released by primary nociceptors to stimulate secondary neurons?
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Substance P
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What do inhibitory interneurons release to modulate pain response?
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Enkephalins
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Endogenous algesia system
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Inhibitory interneurons release enkephalins that block substance P and modulate pain signals to the brain
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Which AA on the enkephalin peptide chain is thought to give them their morphine-like effects?
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The tyrosine moiety, probably corresponds to the OH group on morphine
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Mechanism of action of opiods
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They act on inhibitory Ga proteins. Their activation leads to decreased intracellular Ca and increased K+. This lowers substance P release and hyperpolarizes the cell
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Sites of action of opiods
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Periaqueductal grey matter, rostroventral medial medulla, and dorsal horn
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Permebility of lidocaine
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It is a weak base so it gets protonated in acidic or neutral media. Only the neutral form can diffuse across the cell membrane
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Equation for amounts of charged/uncharged lidocaine
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pH - pKa = log ([L]/[LH+])
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How does pH of ECF effect lidocaine?
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Lower pH will result in more charged form that can't diffuse into the cells
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How does pKa of a local anasthetic effect its diffusability?
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Those with higher pKa will have less in the neutral form and so onset will be slower
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What is an opiate?
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A synthetic morphine-like drug with nonpeptidic structure
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What is an opioid?
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Any substance, endogenous or synthetic, that produces morphine-like effects
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Which opioid receptor are most clinical opiods selective for?
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The mu receptor, which has receptor sites in the brain, spinal cord, and periphery
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Which opioid receptor are the enkephalons selective for?
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The delta receptor
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Which endogenous opiod is selective for the mu receptor?
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Endomorphin1 and 2
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Aside from oral administration, what other method is commonly used to administer opiod analgesics?
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Intramuscular
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What moleucle conjugates opioids in the plasma?
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Glucuronic acid
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When is an opiate combined with a peripherally acting analgesic indicated?
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For cases of moderate to severe dental pain
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Drug interactions with opioid analgesics
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CNS depressants like anxiolytics, antidepressants, and antipsychotics. Also beta adrenergic blockers because it can lead to narcotic toxicity
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Oxycodone + ASA
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Schedule 2 drugs. Percodan has 5mg oxycodone and 325mg ASA. 10mg (2 tablets) is the dose
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Oxycodone + Acet
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Schedule 2 drugs. All contain 5mg of oxycodone. Drugs are Percocet, Tylox, Roxilox, Roxicet, and Oxycontin
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Codeine + ASA
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Schedule 3 drugs. Empirin/Tylenol comes in 2,3, and 4 doses. 4 has 60mg codeine, 3 has 30, 2 has 15. All have 325mg ASA
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Hydrocodone + ACET
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Schedule 3 drugs. Most have 5mg of hydrocodone and 500 mg ACET. Drugs are Vicodin, Lortab, Hydrogesic/Co-gesic
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Which schedule 3 drug has 10 mg Hydrocodone and 650mg of Acet?
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Lorcet, its the only one of its class that has 10 instead of 5 mg of hydrocodone
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Propoxyphene + ASA
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Schedule 4 drugs, called Darvon and Darvocet. Contain 100 mg D-propoxyphene.
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Which schedule 4 drug is now banned by the FDA?
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Propoxyphene, due to weak pain killing abilities, addictiveness, related deaths and arrhythmias
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What is an alternate drug to propoxyphene since it is now banned?
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Tramadol HCl, not a scheduled drug but is capable of producing dependence. Ultracet has tramadol 37.5mg and APAP 325mg in it
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Pentazocine
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Schedule 4 drug, comes in combo with ASA, Acet, and Naloxone. 50mg is equilavent to 60mg Codeine
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Describe the reward pathway that is implicated in addiction
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Dopaminergic neurons in the ventral tegmental area project into the nucleus accumbens. They are under inhibition by GAGA normally. Any release of dopamine from these neurons produces positive reinforcement
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Inhibitory mechanism of GABA
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GABAergic neurons release GABA thats binds to GABA A receptor, which is a chloride channel. Entry of Cl- hyperpolarizes the post-synaptic cell leading to decreased excitability
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Mechanism of endogenous opiates
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They inhibit GABA release so the dopaminergic neurons become more active and stimulate the reward pathway
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What drug is an opiate receptor antagonist?
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Naloxone. It is given to people who have overdosed on narcotics
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Genetic basis for addiction
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Based on finding of single nucleotide polymorphism commonly found in addicts. These people may be predisposed to addiction
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Mechanism of action of cocaine
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It inhibits reuptake of neurotransmitters, including dopamine and serotonin, from the synaptic space
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Mechanism of action of methamphetamine
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It causes massive release of vessicles containing dopamine, then reuptake into vesicles is inhibited
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Mechanism of benzodiazepines
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They increase GABA inhibition
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Of the 5 dopamine receptors, which are excitatory and which are inhibitory?
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D1 and D5 are coupled to a Gs protein that stimulates adenylyl cyclase. D2-D4 are couple to an inhibitory G protein.
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What dopamine receptor is targeted in schizophrenia meds?
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D2 antagonist. This can lead to Parkinson's-like symptoms due to inhibition of dopamine.
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Function of the basal ganglia
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Assists the motor cortex in coordinating fine motor control
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Which receptors in the basal ganglia are excitatory?
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Glutamate receptors
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Which drugs enhance GABA binding to enhace inhibitory effect?
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Benzodiazepines
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What is the name of the benzodiazapine antagonist?
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Flumazenil
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Mechanism of action of propofol
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It works on GABA like benzos, but also inhibits sodium channels to block depolarization. It also blocks nicotinic receptors
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What effect do prostaglandins have in the stomach?
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They inhibit acid secretion. So, if you take an NSAID that reduces prostaglandins, acid secretions will increase
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What H2 antagonist can have an interaction with bupivicane?
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Ranitidine, causes decreased metabolism of bupivicane that can lead to toxic levels
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What part of the GI tract responds to opiates in treating diarrhea?
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Mu receptors in the myenteric plexus
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Where is the chemical trigger zone responsible for stimulating vomiting?
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Near the caudal end of the fourth ventricle
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What neurotransmitter is involved in the final common pathway leading to emesis?
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Substance P
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