Reading...
Play button
Play button
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;
46 Cards in this Set
- Front
- Back
|
Name all sources of histamine.
|
Endogenous – mast cells, basophils(major sites); epidermis, neurons, gastic mucosa (minor)
Exogenous – consumed, formed by bacteria |
|
|
Discuss different ways that trigger histamine release.
|
Antibodies – IgE primarily, IgD in atopic animals
Inflamatory mediators – prostaglandin, heparin, leukotrienes, cytokines Compunds – radiographic contrast media Theraputic agents – amphotericin B, morpheine, Doxorubicin |
|
|
Discuss the different histamine receptors, where they reside, and the physiological response that they mediate when stimulated.
|
H1 – smooth muscle (bronchi, vasculature, GI); endothelium, CNS
H2 – Parietal cells (HCl release) H3 – CNS, |
|
|
What are classic uses for antihistamine agents?
|
Allergy prevention, motion sickness, anti-emesis
|
|
|
Discuss the identifiable features that distinguish first generation and second generation antihistamine agents (don’t worry about chemical names/structures).
|
1st gen. – block H1, muscarinic, serotonin, and α adrenergic receptors
Crosses B/B barrier 2nd gen. – Does not readily cross B/B barrier (less CNS effect) |
|
|
Name the components of the vomiting reflex, where they are located, their role in vomiting, and the receptors responsible for each.
|
a. Emetic center
i. Lateral reticular formation of medulla ii. Receives info )afferent) from other components and sends info out (efferent) b. Chemoreceptor trigger zone(CRT) i. Area postremia in the floor of the 4th ventricle ii. Senses toxins in the blood iii. Receptors – dopamine, H1/2 (more important in dogs than cats), serotonin, acetylcholine(muscarinic) c. Higher centers i. Cerebral cortex and limbic centers ii. Mediate sensory input, sense head trauma/inc. intracranial pressure iii. Acetylcholine(muscarinic), H1 d. Pharynx i. Mediates gag reflex via CN 5 & 9 to the Nucleus solitarius ii. Serotonin, ACh(musc), dopamine, H! e. Peripheral structures i. Heart, testis, GI ii. Afferent signals in response to toxins etc. iii. Serotonin, Dopamine, ACh f. Vestibular apparatus i. Motion sickness ii. CN 8 to cerebellum and emetic center iii. ACh, H1 |
|
|
Which species can/cannot vomit?
|
a. Can
i. Carnivores (cats, dogs) ii. Omnivores b. Can not i. Horses ii. Ruminants iii. Rabbits iv. rodents |
|
|
Name peripheral acting emetics and the properties of each agent.
|
a. Salt – salt poisoning
b. H2O2 – stimulates CRT c. Syrup of ipecac – inc lacrimation, salivation, bronchial secretions |
|
|
Name central acting emetics and the properties of each agent, especially which receptor they act upon
|
a. Apomorphine – not used in cats; revers w/ naloxone; D2 and musc. Receptors
b. Xylazine, medotomidine – A2 adrenergic receptors |
|
|
Name the agents and their site of action, the major receptor targeted for each type.
|
a. Metoclopramide – Dopamine receptor(D2) antag.
i. Also Serotonin and muscarinic b. Phenothiazines – D2 recetor antag. i. chlorpromazine, prochlorperazine, perphenazine, acepromazine, mepazine Also serotonin H2, muscarinic and a2 adrenergic c. Butyrophenones - D2 receptor haloperidol, droperidol d. α2 adrenergic antag prochlorperazine, yohimbine e. antihistamines – H1 antagonists Diphenhydramine, dimenhydrinate tripelennamine, chlorphenaramine, cyclizine, terfenadine, clemastine, astemizole, meclizine f. anti muscarinc g. serotonin receptor blockers |
|
|
Discuss causal factors and defense mechanisms involved in gastric mucosa related to GI ulcer formation.
|
a. Cause
i. Gastric acid ii. Pepsin production iii. Bacteria (Helicobacter pylori) b. Defense i. Bicarb ii. Mucous secretion iii. prostaglandin |
|
|
Name the agents used and the receptor or pump that they are targeted against; discuss how they work.
|
a. H2 receptor antagonists –
i. Cimetidine ii. Ranitidine iii. famotidine b. Proton pump inhibitors i. omeprazole c. Antacids i. Aluminum, magnesium , or calcium salts d. Gastric cytoprotective agents i. Sucralfate |
|
|
Name all sources of histamine.
|
Endogenous – mast cells, basophils(major sites); epidermis, neurons, gastic mucosa (minor)
Exogenous – consumed, formed by bacteria |
|
|
Discuss different ways that trigger histamine release.
|
Antibodies – IgE primarily, IgD in atopic animals
Inflamatory mediators – prostaglandin, heparin, leukotrienes, cytokines Compunds – radiographic contrast media Theraputic agents – amphotericin B, morpheine, Doxorubicin |
|
|
Discuss how each cytoprotective agent works, receptors if any and potential side effects.
|
a. Antacid, reduce H+
b. Sucralfate, forms viscous film over mucosa, must have pH lower than 4 c. Prostaglandins |
|
|
Discuss the different histamine receptors, where they reside, and the physiological response that they mediate when stimulated.
|
H1 – smooth muscle (bronchi, vasculature, GI); endothelium, CNS
H2 – Parietal cells (HCl release) H3 – CNS, |
|
|
What are classic uses for antihistamine agents?
|
Allergy prevention, motion sickness, anti-emesis
|
|
|
Discuss the identifiable features that distinguish first generation and second generation antihistamine agents (don’t worry about chemical names/structures).
|
1st gen. – block H1, muscarinic, serotonin, and α adrenergic receptors
Crosses B/B barrier 2nd gen. – Does not readily cross B/B barrier (less CNS effect) |
|
|
Name the components of the vomiting reflex, where they are located, their role in vomiting, and the receptors responsible for each.
|
a. Emetic center
i. Lateral reticular formation of medulla ii. Receives info )afferent) from other components and sends info out (efferent) b. Chemoreceptor trigger zone(CRT) i. Area postremia in the floor of the 4th ventricle ii. Senses toxins in the blood iii. Receptors – dopamine, H1/2 (more important in dogs than cats), serotonin, acetylcholine(muscarinic) c. Higher centers i. Cerebral cortex and limbic centers ii. Mediate sensory input, sense head trauma/inc. intracranial pressure iii. Acetylcholine(muscarinic), H1 d. Pharynx i. Mediates gag reflex via CN 5 & 9 to the Nucleus solitarius ii. Serotonin, ACh(musc), dopamine, H! e. Peripheral structures i. Heart, testis, GI ii. Afferent signals in response to toxins etc. iii. Serotonin, Dopamine, ACh f. Vestibular apparatus i. Motion sickness ii. CN 8 to cerebellum and emetic center iii. ACh, H1 |
|
|
Which species can/cannot vomit?
|
a. Can
i. Carnivores (cats, dogs) ii. Omnivores b. Can not i. Horses ii. Ruminants iii. Rabbits iv. rodents |
|
|
Discuss indications and contraindications of emetic therapy.
|
a. Indications
i. Non-corrosive poisons ii. Pre gen. anesthesia b. Contra i. Corrosives ii. Seizures (possible asporation) iii. Animals that cant vomit iv. Situations that predispose to aspiration |
|
|
Name peripheral acting emetics and the properties of each agent.
|
a. Salt – salt poisoning
b. H2O2 – stimulates CRT c. Syrup of ipecac – inc lacrimation, salivation, bronchial secretions |
|
|
Name central acting emetics and the properties of each agent, especially which receptor they act upon
|
a. Apomorphine – not used in cats; revers w/ naloxone; D2 and musc. Receptors
b. Xylazine, medotomidine – A2 adrenergic receptors |
|
|
Discuss indications and contraindications of antiemetic therapy.
|
a. Indications
i. Vomiting is disadvantageous b. Contra i. GI infection ii. GI blockage iii. GI toxicity iv. Systemic hypotension v. Epilepsy |
|
|
Name the agents and their site of action, the major receptor targeted for each type.
|
a. Metoclopramide – Dopamine receptor(D2) antag.
i. Also Serotonin and muscarinic b. Phenothiazines – D2 recetor antag. i. chlorpromazine, prochlorperazine, perphenazine, acepromazine, mepazine Also serotonin H2, muscarinic and a2 adrenergic c. Butyrophenones - D2 receptor haloperidol, droperidol d. α2 adrenergic antag prochlorperazine, yohimbine e. antihistamines – H1 antagonists Diphenhydramine, dimenhydrinate tripelennamine, chlorphenaramine, cyclizine, terfenadine, clemastine, astemizole, meclizine f. anti muscarinc g. serotonin receptor blockers |
|
|
Discuss causal factors and defense mechanisms involved in gastric mucosa related to GI ulcer formation.
|
a. Cause
i. Gastric acid ii. Pepsin production iii. Bacteria (Helicobacter pylori) b. Defense i. Bicarb ii. Mucous secretion iii. prostaglandin |
|
|
Name the agents used and the receptor or pump that they are targeted against; discuss how they work.
|
a. H2 receptor antagonists –
i. Cimetidine ii. Ranitidine iii. famotidine b. Proton pump inhibitors i. omeprazole c. Antacids i. Aluminum, magnesium , or calcium salts d. Gastric cytoprotective agents i. Sucralfate |
|
|
Discuss how each cytoprotective agent works, receptors if any and potential side effects.
|
a. Antacid, reduce H+
b. Sucralfate, forms viscous film over mucosa, must have pH lower than 4 c. Prostaglandins |
|
|
Discuss any special pharmacokinetic parameters of each class of drug that may affect how it is administered
|
Lidocaine: : must be continuous IV drip
|
|
|
What is the difference between cathartics and laxatives?
|
Cathartics are more severe than laxatives and cause “bowel evacuation, usually of liquid feces.” Laxatives promote a soft-formed stool in order to encourage evacuation.
|
|
|
Discuss indications for use of each class.
|
Cathartics - Relieve constipation by promoting defecation
Laxatives - promote a soft-formed stool Caution: overuse can lead to severe dehydration, colic, and shock |
|
|
What are 2 osmotic cathartic compounds, their mechanism of action and side effects?
|
* Magnesium sulfate (milk of magnesia)
- osmotic response to poorly absorbed Mg2+ (draws things into the GIT) - inhibits absorption of Na+ - increases secretion of Cl- - overdose of Mg2+ causes CNS signs such as depression * Mannitol - given orally, not absorbed increases osmotic P in GIT lumen - do NOT use in dehydrated animals (very potent in pulling fluids into GIT lumen) * Magnesium sulfate (milk of magnesia) - osmotic response to poorly absorbed Mg2+ (draws things into the GIT) - inhibits absorption of Na+ - increases secretion of Cl- - overdose of Mg2+ causes CNS signs such as depression * Mannitol - given orally, not absorbed increases osmotic P in GIT lumen - do NOT use in dehydrated animals (very potent in pulling fluids into GIT lumen) |
|
|
Name one cathartic compound, its mechanism of action and side effects?
|
other laxative tre* Castor oil
- can cause severe colitis and diarrhea - evacuates when atments have failed - can titrate to effect (to some degree) |
|
|
What are 4 laxatives their method of action, etc.....
|
- Mineral oil
* used for impaction colic in horses * typically administered via ng tube – expect transit time to be ~ 12 h * caution: inadvertent placement into lungs causes severe pneumonia that may cause death - Dioctyl sodium sulfosuccinate (DSS) * used for impaction colic in horses that are refractory to mineral oil (try mineral oil for 2-3 d first, then switch to DSS) * it’s like a detergent that breaks up the impaction * not recommended if abdominal sx is imminent (b/c it could leak out when GIT is cut open and it’s very irritating to the peritoneum, etc) - Psylliumhydrophilic mucilloid (Metamucil) * increases bulk of intestinal content by absorbing water more contents promotes reflex motility * used for sand impactions in horses * must be tubed - Dietary fibers * bran or prunes * increases bulk in GIT to absorb more water (draw it into the lumen) |
|
|
Discuss indications for emetic therapy.
|
i. Non-corrosive poisons
ii. Pre gen. anesthesia |
|
|
Discuss contraindications for emetic therapy.
|
i. Corrosives
ii. Seizures (possible asporation) iii. Animals that cant vomit iv. Situations that predispose to aspiration |
|
|
Discuss indications of antiemetic therapy.
|
It is disadvantageous to vomit
|
|
|
1. Discuss the anatomy of the upper and lower respiratory tract and the defense mechanisms used in each case.
|
Nares – trachea – upper
Bhronchi – alveoli - |
|
|
2. Know, in detail, each receptor required for control of the bronchial diameter and the steps that follow their stimulation to cause relaxation or constriction.
|
Alpha 1, musc, H1 –constrictor
B2 – dilation - decrease cyclic AMP |
|
|
3. Discuss each class of bronchodilator agents, mechanism of action, peculiarities of each drug.
|
Adrenergic – albuterol(bronchospasm in dog, COPD in Horse), clenbuterol(Horses COPD), terbutylene – increase cyclic AMP
Contraindications - Seizure, hypertension, hyperthyroid, diabetes Methylxanthine – aminophiline(IV), theophiline(oral) – inhibit phosphodiesterase, indirect or direct affect on intracellular Ca. Anticholinergic – Atropine, ipratopium bromide Cyproheptacine - cats |
|
|
4. Name each type of mast cell stabilizer
|
B – adrenergic
Chromalyn |
|
|
5. Discuss indications/contraindications of antitussive agents.
|
Indication – prevent coughing (tracheal collapse, canine bronchitis)
Non productive Contra – productive cough |
|
|
6. Know the difference between peripheral and central acting antitussive agents and examples of each.
|
Peripheral – bronchodilator(relieve bronchospasm)
Central – Dextromethorphan(alleviate threshold for cough) - Diphenoxylate – w/ atropine in Lamotil - codeine - butorphanol – alalgesic, antitusive in dogs - hydrocodone – dogs (more potent) |
|
|
7. Be able to list examples of expectorant and mucolytic agents and how they work.
|
- systemic fluid therapy
- Iodide salts – irritates mucous glands, C/I hypothyroid, preg., lactating; - Guaifenesin – - Acetylcystine – treat acetominophin toxicity, mucolytic; can be very irritating |
|
|
8. List examples of anti-inflammatory, decongenstants, diuretics, respiratory stimulants.
|
- Glucocorticoids – feline asthma, allergic resp. disease, COPD
- NSAIDS – heartworm, comfort, steroids more effective - Antihistamines – small animals, NOT COPD - Decongestants – i. H1 receptor blockers ii. a-adrenergic agonist - Diuretics – pulmonary edema, - Resp stim. – apnea in neonates, drug induced medullar depression i. Doxapram ii. accupuncture |
|
|
9. Discuss indications of oxygen therapy and how this can be achieved.
|
- alveolar ventilation is critically compromised
- provides oxygen directly to alveoli - administration – mask, endotrach. Tube, nasal catheter, respirator, oxygen cage - 95% O2, 5% CO2 |
