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169 Cards in this Set

  • Front
  • Back
What is allergic rhinitis?
Histamine released from mast cells and basophils, bind H1 receptors and cause vasodilation and increased capillary permeability
What are the two types of allergic rhinitis?
Seasonal caused by pollen and Perennial caused by a variety of allergens like dust or animal dander.
How can you medically manage allergic rhinitis?
A course of desensitization injectios, H1-receptor blocking agents, Nasal corticosteroids, Decongestants (alpha-1 agonists), Antimuscarinics (Ipratropium nasal spray)
How do H1 receptor antagonists work?
They compete with histamine at the H1 receptor on effector cells in the respiratory system, blood vessels, and the GI tract.
What are the indications for H1-receptor antagonists?
Perennial and seasonal allergies and Uticaria (hives).
What are 5 H1-recetor antagonist drugs?
Loratadinie(Claritin), Desloratadine (Clarinex), Cetirizine (Zyrtec), Fexofenadine (Allegra), and Meclazine (Meclazine)
What are some of the clinical issues with H-1 antagonists?
Xerostomia, Pharyngitis, Headache, and depression/sedation.
What 4 things do H1 receptors do?
They mediate daily wake-sleep cycles/ circadian rhythms, ileum contraction, Systemic vasodilation, and bronchoconstriction.
How many different Histamin receptor types are there?
Four, H1-H4
How does Histamine promote an alert/awake state?
It bindes H1 receptors that activate a G protein that stimulates events to close K+ channels and depolarize the cell, increasing their activity causing an alert state.
What occurs to histamine release while asleep?
Histaminergic neurons are less active and histamine release is lower so histamine stimulated cells become hyperpolarized and less active. This is why H-1 antagonists cause drowsiness and can be used as sedatives.
Where does respiratory exchange occur?
Across the respiratory bronchioles and the alveoli.
How does pulmonary edema affect gas exchange at the alveoli?
It increases the diffusion distance for oxygen absorption.
What does smooth muscle in the bronchioles do?
It can contract to constrict the air flow to the alveoli.
What is the area of gas exchange like in the alveoli?
There are 300 milion alveoli and they provide about 140 m^2 for gas exchangeabout the size of a tennis court.
What drives the ventilation exchange at the alveoli?
The partial pressure gradients for O2 delivery and CO2 removal from the blood.
What is the partial pressure of O2 in the pulmonary artery vs. the pulmonary vein?
Opposite that of the systemic partial pressure.
What is the volume of blood in the alveolar capillaries when at rest?
70 ml…..spread over the tennis court.
What is the stroke volume at rest?
About 70 ml/beat….the same as the volume of blood in the alveoli, thus the blood is replaced about once per second
What was the traditional way to measure lung volume?
Using a spirometer, recorded as an ink tracing on a rotating drum.
What does volume refer to in respiration?
Air movements due to a specific change in ventilation
What does capacity refer to with respiration?
The sum of two or more volumes.
What is a tidal volume?
Around 500 ml of air above functional residual capacity (FRC) is exchanged during quiet breathing
What is the FRC?
Forced residual capacity about 2.4 L
Do we ever completely empty the lungs?
No even with forced expiration.
How much of the tidal volume of 500 ml do we actually use?
About 150 ml is termed anatomical dead space Vd which is the volume of air not taken into the alveoli.
What is the functional Reserve capacity?
The expiratory reserve volume and the residual volume
How much of the 500 ml tidal volume enters the alveoli and exchange air with the alveolar air?
350 ml
What is the alveolar ventilation (Va)?
Breaths/min X (Vt-Vd)
What portion of the tidal volume approximates the systemic arterial blood gas composition?
The last half to be expired. The first volume is the dead space and mixed alveolar and dead space air.
What is the minute volume?
Breaths/min x Vt.
What is the passive process of expiration above the FRC due to?
The elastic recoil of the chest wall and alveoli
What do you need for expiration that utilizes the Expiratory reserve volume?
Contraction of the expiratory muscles.
Which muscles are used for inspiration?
Mostly the external intercostals, but also aided by the sternocleidomastoid, the anterior serrate, the scalene. The diaphragm lowers the floor of the thoracic cavity to draw air into the airway.
What are the muscles that pull the ribs down during forced expiration?
The abdominal recti mostly, along with the other ab muscles and then the internal intercostals also lower the ribs.
What is the pressure in the alveoli after expiration of a tidal breath?
It is equal to the ambient atmospheric pressure.
How is negative pressure in the alveoli created?
Air is drawn into the airway as the thoracic cavity expxpands.
What is the parietal pleura?
The outer membrane of the lung or inner lining of the thoracic cavity
What fills the space between the parietal and visceral pleura?
The thin space is filled with lymphatic fluid.
What prevents collapse of the lungs under normal circumstances?
The inspiratory muscles overcome the inward force due to the elasticity of the visceral pleura. This outward force by the inpiratory muscles is called the pleural pressure and is about -5 cm H2O at FRC.
What is the transpulmonary pressure?
The positive recoil pressure that tends to collapse the lung.
At FRC, what opposes the pleural pressure?
The relaxed thoracic muscles….there is no difference between alveolar air pressure and atmospheric pressure.
How much additional negative pressure is generated by a tidal inspiration?
-2.5 cm H2O to give a -7.5 cm H2O pleural pressure and thus a -2.5cm H2O negative alveolar pressure….drawing air into the alveoli.
What generates the positive pressure to expire the alveolar air?
Inspiratory muscles relax and the recoil of elastic elements. Here transpulmonary pressure can be seen as a positive pressure.
What is the natural tendency of the lungs?
To collapse….with 5 cm H2O
What opposes the lungs collapsing?
The negative pressure exerted by the chest wall (-5 cm H20) at FRC.
What occurs in pneumothorax?
Open chest wounds that can lead to lung collapse.
What is the mediastinum?
The compartment between the lungs.
What is lung compliance?
The amount of filling per unit of pressure gradient….with normal compliance, reducing the pressure by 2.5 cm H20 will move .5L of air.
What are four common diseases that affect the Va?
Asthma, Pulmonary Fibrosis, Emphysema, and Respiratory Distress Syndrome.
How does asthma affect Va?
Airway smooth muscles constrict, increasing airway resistance and thus Va.
How does pulmonary fibrosis affect the lungs?
You have a loss of elastic elements of alveoli
How does emphesema affect the lungs?
The fusion of alveoli occurs due to smoking or other irritant.
How does respiratory distress syndrome affect the lungs?
Common in premature babies, due to a lack of surfactant, will reduce alveolar compliance.
What is the largest factor in lung compliance?
Due to the surface tension of the thin layer of fluid lining the alveoli (2/3)…so even with a large pressure, very little inspiration occurs.
What overcomes the surface tension on the fluid lining the alveoli?
Surfactant…this greatly increases the compliance
Where is surfactant made?
Type II alveolar cells during late gestation….thus premies have RDS
What is surfactant made from?
85-90 % lipids (85-90% phospholipids (70-80% phosphatidylcholine), 5-10% glycolipids and 5% neutral lipids) and 10-15% protein
What is compliance like with emphysema?
Lungs are more compliant, but gas exchange is greatly reduced and expiration is difficult.
What is lung compliance like in asthma?
Compliance is near normal, but airway smooth muscle is constricted. (can be relaced by sympathetic neurotransmitters binding Beta-2 receptors.
How can you evaluated pulmonary disease?
FEV-1 or forced expiratory volume at one second. Measured as a percentage of the forced vital capacity.
What causes the early (20-30 min) response in asthma?
Mast cell mediators like histamine, PAF, prostaglandins and leukotrienes.
What mediates the late asthmatic phase?
3-12 hours caused by the chemotactic recruitment of eosinophils and neutrophils and other inflammatory cells that will also increase the bronchoconstrictive reactions.
What is BHR?
Bronchial hyperreactivity…refers to an increased contractile response of airway smooth muscles.
What is reactive airway disease?
Asthma…reversible airway obstruction.
What are the characteristics of asthma?
Cellular (eosinophil and lymphocytic) infiltration, Inflamation and edema of the respiratory mucosa, increased mucous secretion, and the spasm of respiratory smooth muscles.
What things can cause reactive airway disease/asthma?
Allergens, exercise, cold air, cigarette smoke, environmental irritants, viral and bacterial infections, and genetic factors.
What are the signs and symptoms for asthma?
SOB, Coughing, Wheezing, tightness in chest, use of accessory muscles of respiration.
What are the 4 common treatments for asthma?
Inhaled corticosteroids, noncatecholamine bronchodilators, anticholinergic agents, and leukotriene receptor antagonists.
How do leukotirene synthesis inhibitors and receptor antagonist help the asthma patiens?
They work to block the synthesis of leukotrienes by the inflammatory cells and thus block the inflammatory response which is what induces asthma.
What do most leukotriene synthesis inhibitors inhibit?
5-lipoxygenase thus decreasing inflammation and the need for steroid use.
What does muscarinic stimulation to the airway?
It releases Ca from the SR or the smooth muscle to activate MLK and promote vasoconstriction.
What can be used to reduce the effects of muscarinic induced vasoconstriction of the airway?
M3 antagonists.
What does epinephrine do to the airway during exercise?
It is released to dilated the airway via Beta-2 receptors.
What do Beta-2 agonists and methyl xanthenes like theophylline do to the airway?
Dilation like with Epi and Beta-2 receptors.
What is the trick to making Beta-2 agonists?
Making one that is Beta-2 specific and resistant to COMT degredation.
What are the adverse affects of using B-adrenergic agonists or non-selective adrenergic agonists for asthma?
May cause tachycardia or tremor
What are the negative side effects to using antimuscarinic agents for asthma?
Tachycardia or xerostomia.
What are the adverse side effects of methylxanthines as asthma drugs?
Anorexia, naseau, vomiting, arrhythmias eg. Theophyline. Eg. Epinephrine, albuteral, salmeterol.
What is advair?
A long term oral medicine for the treatment of COPD that combines two common treatments, a corticosteroid and a beta 2 agonist….these work better than the two drugs individuallysynergistic.
What are bronchodilators used for?
Asthma and COPD
What are some clinical ADE’s for broncodilators?
Xerostomia, altered taste, nervousness, headaches, palpitations and HTN.
What is chronic bronchitis/COPD?
Chronic inflammation of the alveolar epithelium caused by prolonged exposure to airway irritants that promote acetylcholine, histamine, and inflammatory mediators.
What are 6 characteristics of chronic bronchitis/ COPD?
Increased pulmonary secretions, bronchospasms, narrowed airways, epithelial proliferation, loss of ciliated epithelium, and Fibrosis.
What are 3 main signs/symptoms of chronic bronchitis/ COPD?
Productive cough, Hypoxic hopoxemia (CO2 retention and Polycytemia) , and right heart failure (cyanosis)
How do you manage Chronic Bronchitis associated with COPD?
Inhaled corticosteroids, Noncatecholamine bronchodilators (albutero and salmeterol), Anticholinergic agents (Ipratopium), Leukotriene receptor agonists (Montelukast)
What is Emphysema?
A COPD that is usually preceded by chronic bronchitis or due to a genetic defect that causes a lack of protease inhibitor and the proteases digest the pulmonary elastic tissues leading to irreversible obstructive disease with dilation and destruction of acini walls.
How do you manage emphysema medically?
Reverse or prevent proteolytic destruction of lung tissue with alph1-protease inhibitor…..also use oxygen therapy @ 2L/minute.
How common are GI diseases?
The afflict 12% of all Americans and account for 16% of all absences from work.
What are some of the drugs used to treat GI diseases?
Anticholinergics, antihistamines, antacids, proton pump inhibitors, antiemetics, laxatives, anti-diarrheal or antispasmodic drugs, stimulants etc.
What are the two stages of salivary formation?
Primary secretion by acini and then the ductal modification by the striated ducts.
What are people with inadequate salivary flow given to increase saliva?
Muscarinic agonists like pilocarpine stimulate primary secretion
Where does the modification of ion content of the saliva take place?
The striated and excretory ducts.
What is aquiporin 5?
It is found in the apical membrane of acinar cells even in conditions like sjogren’s syndrome.
What does sympathetic stimulation do to salivary flow?
It initially stimulates primary secretion,but also reduces blood flow to the salivary glands so less ultrafiltrate is available and salivary flow is reduced = dry mouth when nervous.
What are antisialogogues?
They are muscarinic antagonists that can also reduce sweating and increased heart rate.
What is the first reflex involving movement along the gut?
The swallowing reflex.
How does the swallowing nervous control function?
Pressure on pharynx and esophagus is sensed by receptors and afferent impulses are carried by the Vagus nerve to the swallowing centers in the Pons and medulla and then vagal efferent stimulation of the esophageal muscles occurs..
What propels the food to the stomach?
Peristaltic waves propel food into the stomach as the lower esophageal sphincter opens and then quickly closes, the stomach relaxes and the food enters.
What is GERD?
Gastroesophageal reflux disease…due to transient relaxation of the lower esophageal sphincter not induced by swallowing.
What can increase/induce GERD?
Common after meals, slow gastric emptying, Hiatus hernia, Obesity, and Smoking.
What will determine the extent of the damage due to GERD?
Intrinsic resistance of the esophageal epithelium to gastric acid and the characteristics (acid, pepsin, bile) of the refluxed fluids, and the duration of the contact with the mucosa ( number of episodes, efficiency of esophageal peristalsis to remove the refluxed bolus of gastric acid)
What do the parietal cells in the stomach do?
Secrete HCl
What do the Chief cells of the stomach do?
Secrete proteolytic enzymes.
What does the surface epithelium of the stomach do?
Secretes mucous and bicarbonate.
What is secreted to help protect the stomach lining?
Mucous rich glycoproteins (mucin) and HCO3
How can carbonic acid become strong enough to drop the stomach pH to 2?
CO2 forms carbonic acid which dissociates and the proton pump pumps protons out and shifts the equilibrium from a weak acid to the formation of the strong acid, the proton gets pumped out and then combines with Cl.
What is an imidazole like omeprazole?
It inhibits the K-ATPase that inhibits the proton pump that acidifies the gastric secretion. This decrease the acidity of the stomach. These are good drugs because they are inactive at neutral pH.
What is alkaline tide?
The transient alkalotic blood and ECF that is due to normal HCl secretion that causes a shift of acid into the stomach and away from the blood. This alkalotic condition can also be produce by vomiting.
What do PPI’s do?
They inhibit proton pumps in the parietal cells to decrease acid secretion and reduce irritation during episodes of acid reflux.
What are Azoles?
They have a ring structure with a nitrogen incorporated and they can be tailored to bind a variety of receptors to inhibit ergosterol synthesis in fungi or inhibit the proton pumps that acidify the stomach.
What are two indications for PPI’s?
GERD and Peptic ulcer disease (PUD)
What are some of the ADE’s of PPI’s?
Diarrhea, headache, and vomiting, also higher pH with inactivate pepsin and can interfere with apsorption of some drugs, these drugs can also inhibit CYP enzymes and produce an increase of plasma concentration of some drugs…eg. Omeprazole can increase plasma diazepam concentration.
What might alter the mucosal defense mechanisms and cause peptic ulcer disease?
Hlicobacter pylori, NSAIDs, Stress, Alcohol, Cigarrette smoking, Genetic factors.
How do you treat peptic ulcers?
Gastrin can increase Ca ion concentration, M3-receptors interact with acetylcholine increase Ca ions concentration, and H2-receptors interact with histamine to increase cAMP.
What are four factors that regulate HCl secretion?
Preostaglandins and somatostatins inhibit acid secretion, ECL cells (enterochromaffin like cells) , Parasympathetic NS, and the G-cells in antrum and duodenum.
Why are histamine receptor antagonists used to treat PUD?
Because histamine is a potent stimulator of gastric acid secretion and Histamine receptor antagonists will decrease gastric acid secretion.
Which histamine receptors mediate gastric acid secretion?
H-2 receptors.
What is a potential drug-drug reaction with the H2 antihistamine Ranitidine (Zantac) used to treat gastric ulcers?
It can decrease the metabolism of bupivacaine  possible bupivacaine toxicity.
What type side effects are common with the H2 antihistamine cimetidine (tagamet)?
It inhibits CYP enzymes and has CNS side effects.
What do prostaglandin analogs do to the stomach secretions?
They inhibit acid secretion and stimulate mucus formation so NSAIDS that inhibit prostaglandins will cause an increase in acid secretion.
What controls the motility and secretions of the gut?
The sympathetic an parasympathetic nervous systems.
What does the sympathetic system do to the GI?
Decreases motility and closes sphincters as opposed to the heart where it increases heart rate. PS does the opposite.
Where does the enteric nervous system run?
Along the entire lenth of the GI.
What is the myenteric plexus?
Aka aurbachs plexus that lies in the muscularis layer that coordinates peristalsis.
What is the submucosal plexus?
Aka meisners plexus that lies in the submucosa and does more local stimulation of glands.
What is the intrinsic reflex of the GI?
Distension of the gut stimulates muscle contraction above and relaxation below the food bolus to move bolus from oral to anal direction.
What is the gastrocolic reflex?
Aka gastroenteric reflex is an increase in motility of the colon caused by filling of the stomach.
What is the enterogastric reflex?
It is the reduction of stomach emptying due to a full colon.
What stimulates motility in the colon?
The parasympathetic NS.
What stimulates the parasympathetic reflex to relax the internal anal sphincter(smooth muscles) and reflex constriction of the external anal sphincter (skeletal muscle) and cause the urge to defacate?
The filling of the rectum.
Where is the integrating center for the defacation reflex?
In the sacral spinal cord and it is modulated by higher centers in the brain.
What types of things might cause constipation?
Functional abnormalities, colonic disease, neurological disease, metabolic conditions, antimuscarinic drugs, and Opiates (pain meds)
4 ways to treat constipation?
Fiber diet, bulk forming and saline laxatives ( inorganic salts), irritants, and lubricants.
What are some bulk forming treatments for constipation?
Psylium and methylcellulose
What are two examples of stimulants/irritants to treat constipation?
Bisacodyl and senna
What are some examples of Saline (osmotic) treatments for constipation?
Magnesium hydroxide aka milk of magnesia, and lactulose.
What are two examples of wetting agents for the treatment of constipation?
Docusate and mineral oil.
What are 6 things that might cause acute diahhrea?
Infection, toxins, drugs, secretory diarrhea, osmotic diarrhea, and functional abnormalities.
What is the range of the amount of GI secretions/day?
7 liters/day normally but as much as 20 L/day with E. coli or cholera toxin effects.
What are the typical fluid intake and GI secretions like vs. the amount reabsorbed by the small intestines and colon?
2000 ml/day ingested then another 7000 ml/day in gastric and intestinal secretions . 8500 ml reabsorbed in small intestines and 400 ml reabsorbed in colon = 100 ml/day excreted.
What are 6 causes of chronic diarrhea?
Laxative abuse, Lactose intolerance, Inflammatory bowel disease, Malabsorption syndromes, Endocrine disorders, and irritated bowel syndrome.
What is Lomotil?
Aka diphenoxylate, an opiate that acts in cns and myenteric plexus plus a sub therapeutic dose of atropine (muscarinic inhibitor) used to treat diarrhea.
What is Imodium?
Aka Loperamide, an opiate that works on opiate receptors in the myenteric plexus, but not the CNS.
What is emesis and what can it cause?
Protracted vomiting that can cause electrolyte imbalance (metabolic alkalosis), dehydration, malnutrition syndrome, mucosal laceratioin, and upper GI hemorrhage.
Where is the chemoreceptor trigger zone for emesis?
The area postrema at the caudal end of the fourth ventricle, external to the BBB. that is accessible to humoral stimuli I in the blood or in the CSF. .
Where do the impulses originate from that cause emesis?
The Pharynx, the GI tract, or the cerebral cortex.
Where is the vomiting center of control?
In the lateral reticular formation of the medulla, the final common pathway along with different impulses induce emesis.
What is nausea for?
To prevent food intake.
To where are signals transmitted from the vomiting center in the brain?
Respiratory muscles, ab muscles, esophageal sphincters, and esophageal musculature.
How do antiemetics work?
By inhibiting receptor sites associated with emesis like anticholinergics, antihistamines, dopamine antagonists, serotonin antagonists, and cannabinoids- R all antiemetics
What plays a major role in motion sickness?
The Vestibulocochlear nerve, CN VIII which is rich in muscarinic and Histamine H-2 receptors.
Can the CNS cause vomiting?
Yes, due to psychiatric disorders and stress
What type of receptors are found in the chemoreceptor trigger zone for emesis?
Dopamine D2 receptors, Serotonin 5-HT receptors, Opiod receptors, acetylcholine receptors and substance P receptors.
What appears to be involved in the final common pathway for emesis stimulation?
Substance P.
How does vomiting occur?
Begins with a wave of reverse peristalsis from small intestine to duodenum, Pyloric sphincter and stomach relax to receive intestinal contents, intra abdominal pressure increases by tightening ab muscles to drive gastric contents into the esophagus the LES relaxes and the stomach contracts, the rapid propulsion of gastric contents causes the UES to relax and out come the cookies.
What occurs in a dry heave?
The UES remains closed and then the respiratory and ab muscles relax and a secondary peristalsis empties back into the stomach.
What are emetics?
Substances that induce vomiting.
Which 5 receptor types are related to emesis?
Opioid receptors, Dopamine D2 receptors, Histamine1-receptors, Muscarinic receptors, and Serotonin (5HT) receptors.
What can you give an emetic patient?
Opiods, dopamine D2 receptor antagonists, Histamin1-receptor antagonists, Muscarinic-receptor antagonists, serotonin receptor antagonists, corticosteroids that block prostaglandin, benzodiazepines, and cannabinoids.
What should you watch for with a patient on antiemetics?
Syncope, instruct your patients to rise from supine positions with caution…they may get orthostatic hypotension which could become a medical emergency.
What are Bonine and Dramamine?
They are OTC antiemetic drugs that are both Histamine receptor antagonists
What is promethazine?
A H1 antagonist (phenergan)…sometimes coupled with codeine
What is metoclopramide?
A dopamine D2 blocker
What type of drugs are those that end in prazole?
Proton pump inhibitors. Many are used to treat ulcers.
Why would antibiotic be used to treat ulcers?
Metronidazole or amoxicillin are commonly used to kill any H. Pylori that might be contributing to the ulcer.
How do antacids work?
They have high pH which neutralizes the acid in the stomach.
What is flagyl?
Metronidazole…not a PPI and can be used for some protozoan infections. For H. pylori it is given with tetracycline.
What are most antacids?
Aluminum, Calcium, Magnesium, or Sodium carbonates, bicarbonates, or hydroxides.