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GI Drugs > GI drugs > Flashcards

GI drugs Flashcards

1
Q

where is histamine stored from

A

mast cells, basophils, brain, stomach in enterochromaffin like cells

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2
Q

conditions that cause histamine release

A

tissue injury, allergic reactions, drugs, foreign substances

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3
Q

what type of reaction is degranulation of mast cells?

A

type I sensitivity

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4
Q

H1 receptors

A

throughout the body, smooth muscles, vascular, heart, CNS, endothelial cells. Increase vascular permeability and vasodilation, bronchoconstriction, itching. Symptoms are allergic: rhinitis, conjunctivitis, urticarial, bronchospasm, vasodilation, CNS: sleep/arousal, motion sickness

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5
Q

H2 receptors

A

mainly gastric parietal cells to a lesser extent vascular smooth muscle, neutrophils, CNS, heart, uterus. Gs receptors. Increased release of gastric acid, tachycardia, smooth muscle relaxation. Symptoms of GERD

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6
Q

H3 receptors

A

found in the CNS, primarily in the thalamus, caudate nucleus and cortex. Some in the small intestine and prostate. G protein coupled.

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7
Q

H4 receptors

A

recently discovered and present throughout the immune system, spleen, thymus, leukocytes, likely G protein, but mechanism is unknown.

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8
Q

wheal and flare

A

local response or wheal and flare is H1. If you were to inject histamine locally, you will see a red spot with an erythematous red base and central flare. Erythema is caused by vasodilation within a few seconds. Flare is the spread of erythema more than 1 cm beyond this site caused by dilation of vessels- itching begins here. Wheal forms within a few minutes and is localized edema a raised area due to increased capillary permeability.

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9
Q

allergies

A

vasodilation and edema lead to inflamed mucosal tissues which can cause paroxysms of sneezing, rhinorrhea, nasal obstruction, and nasal itching. The same mechanism can inflame conjunctival tissue, leading to scleral injection, watery eye drainage, and itching

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10
Q

uticaria

A

similar but present on the skin. Diagnostic criteria is itchy raised lesions that migrate.

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11
Q

external urticaria causes

A

new topical exposures, medications, foods, infections

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12
Q

internal urticaria causes

A

often the cause behind chronic urticarial no single cause could be isolated yet prolonged over six month duration of hives

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13
Q

what is cause of large local reaction

A

insect bite, sting, plant based reaction, will not migrate to hives

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14
Q

anaphylaxis- criteria

A

scheduled antihistamines are important because there is often an acute or delayed hypersensitivity reaction. Criteria is acute onset and many different things on different systems

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15
Q

cardiovascular symptoms of anaphylaxis

A

hypotension from decreased BP from H1 receptors and tachycardia- hypotension causes reflex tachycardia.

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16
Q

pain and itching in anaphylaxis

A

nerves with H1. H3 reduce the release of acetylcholine, amine, peptide transmitters in various areas of the brain and peripheral nerves

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17
Q

allergy induced asthma

A

histamine causes bronchoconstriction from H1

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18
Q

H1 receptor antagonists

A

antihistamines compete for histamine at the receptor binding site, but will not remove already bound histamine

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19
Q

first generation H1 blockers

A

for seasonal allergies, medication associated allergies, hives, itching, anaphylaxis, or vomitting. They are readily absorbed through oral mucosa administration with peak blood concentrations at 1-2 hours. They have lots of side effects. This molecule allows first generation antihistamines to cross the BBB. They have anti-cholinergic adverse effects.

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20
Q

ethylenediamines

A

significant anticholinergic side effects and sedation less GI side effects. H1 first generation blockers

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21
Q

diphenhydramine

A

helpful with allergies, anaphylaxis, hives, nausea, and sedation. Used in many over the counter sleep aids. Can cause agitation in children. It is H1 first generation blocker. ethylenediamines

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22
Q

dimenhydrinate

A

anti-emetic with strong sedation properties often used for motion sickness. This is an H1 first generation. Eryhlenediamines

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23
Q

alkylamines

A

less sedating and GI advise effects, more CNS effects- it is a first generation H1 blocker

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24
Q

chloropenamine

A

allergies and a common ingredient in OTC cold medications. Inhibits serotonin activity. It is from alkyl amine class of H1 first generation antagonists

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25
Q

piperazine

A

significant effects so used for motion sickness, nausea, vertigo. Generation 1 of H1 blockers

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26
Q

hydroxyzine

A

used for itching but for anti-anxiety- piperazine- Generation 1 of H1 blockers

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27
Q

meclizine

A

antiemetic used for vertigo- piperazine- generation 1 of H1 antagonists

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28
Q

cetirizine

A

common allergic rhinitis medication, available for over the counter and used in kids. It is piperazine generation 1 of H1 antagonist

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29
Q

tricyclics

A

related to the anti-depressants- first generation H1 blocker

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30
Q

promethazine

A

used as an anti-emetic or sedative due to an extremely strong anti-cholinergic and sedative effect. This can be used for migraines with a NSAID. cocktail with other drugs. It is a tricyclic

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31
Q

cyproheptadine

A

antihistamine and antiserotonin; helps with allergies and migraines but is mainly used for appetite stimulation. Tricyclic class

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32
Q

ketotifen

A

primarily used as an ophthalmic form for allergic conjunctivitis. it is tricyclic.

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33
Q

second generation H2 blockers

A

these are newer drugs are more selective for the peripheral antihistamine receptors involved in allergies os they spare many of the sedating side effects of the first generation. They are bulkier and less lipophilic so don’t cross the blood brain barrier as readily. They may also have an anti-inflammatory activity that helps in allergic asthma- may be due to H4 receptors

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34
Q

loratidine

A

the first second generation available with over the counter daily dosing. H2 second generation antagonist

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35
Q

azelastine

A

mast cell stabilizer, nasal spray and eye drop. H2 second generation antagonist

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36
Q

olopatadine

A

ophthalmic drip for allergic conjunctivitis. H2 second generation antagonist

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37
Q

Third generation H2 blockers

A

derived from second generation antihistamines.

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38
Q

levocetirizine

A

active isomer of cetirizine with fewer side effects- less drowsy. Not metabolized, so will not cute drug interactions. Helpful in asthmatics. H2 third generation antagonist

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39
Q

desloratidine

A

active metabolite of loratadine- no evidence that it is more effective. h2 third generation antagonist

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40
Q

fexofenadine

A

anti-allergy medication. H2 third generation antagonist

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41
Q

emesis

A

holdover mechanism to protect from inested toxins. It is from excessive vestibular stimulation or psychological stimuli such as fear, dread,or obnoxious stimuli like sites and odors

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42
Q

nucleus tractus solitaris

A

located in the medulla and receives input from the GI tract, vestibular system and area pastrema. Vagal afferents work here from mechanical stimulation, chemical stimulation, acetylcholine, dopamine, serotonin, histamine, neurokinins. Projects to the other medullary nuclei and coordinated vomiting response

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43
Q

vestibular system

A

CNVIII responsible for vertigo induced nausea

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44
Q

area postrema

A

next to NTS but outside the blood brain barrier in the fourth ventricle, so responds to many substances that may not cross the BBB

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45
Q

substance P

A

activates many NK1 receptors

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46
Q

efferents of the vomit reflex

A

vagus and phrenic nerves when they are stimulated, they relax the funds and body of the stomach and lower esophageal sphincter and retrograde giant contractions occur in the small intestine. Diaphragmatic and abdominal muscle contractions compress the stomach and together this produces vomiting

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47
Q

serotonin antagonists

A

these antagonize the 5HT-3 receptors on the vagal afferents in the IG tract leading to the brain. They are one of the more effective anti-emetics for chemo but good for gastroenteritis-induces nausea and emesis. Ondasetron

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48
Q

ondansetron

A

the most commonly used but still expensive can come in IV, sublingual, and oral form- serotonin antagonists- antagonize 5HT-3 receptors on the vagal afferents

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49
Q

substance P/Neurokinin antagonists

A

antagonists the the neurokinin1 receptors in the CNS inhibiting the action of substance P in the CTZ. They augment the effects of steroids and helpful for chemo and serotonin antagonists- post operative nausea. Aprepitant

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50
Q

aprepitant

A

substancep/neurokinin1 antagonist- an inhibitor or liver enzyme CYP and inducer of 29, so it decreases the clinical effect of warfarin

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51
Q

antidopaminergic agents

A

D2 dopamine receptor antagonists in the CTZ. They inhibit dopaminergic stimulation of the CTZ. Anti-psychotics doses for nausea are 1/3 of dose required for psychosis. Used for nausea from drugs and surgery. Metoclopramide, phenothiazine, procholrperzane

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52
Q

metoclopramide

A

at higher doses, acts as 5HT-3 receptor antagonist. It increases the tone of the gastroesophageal sphincter and enhances gastric emptying and small intestine motility. This allows to work well as a pro kinetic gastroperesis. It can cause diarrhea, it is contraindicated if there is obstruction because it can cause perforation. Extrapyramidal symptoms like dystonia, akthesia, tradeoff dyskinesia, neurologic malignant syndrome, fever, rigidity, mental status change, rhabdo. Pre-treat with migraine cocktail. sedation, depression, increased prolactin, and increased QT interval. Anti-dopanergic

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53
Q

phenothiazine- procholrperzane

A

possesses anti-muscarinic activity so its is helpful with vestibular disorders. Often used as migraine abortifactant. anti-dopaminergic

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54
Q

butyrophenones

A

haloperidol, antidopaminergic. same side effects as metoclopramide

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55
Q

scopolamine

A

antimuscarinic that works on the vestibular system via M1 receptors. Muscarinic receptors are involved in the visceral afferent input from the gut to vomiting center and in the tract that CNVIII takes from the labryinth to the CTZ via the vestibular nucleus. Great for motion sickness. Anticholinergic side effects: dry mouth, blurred vision, drowsiness, available orally, trandsermally, parentally

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56
Q

H1 antihistamines

A

first generation anti-histamines so they easily cross into the CNS. These CNS effects help the motion sickness/vestibular nausea but can cause sedation and muscarinic receptor blocking: dimeydridate, meclizine, promethazine

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57
Q

promethazine

A

blocks 5HT-3 commonly used in pregnancy, used for refractory hiccups

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58
Q

corticosteroids

A

not approved for nausea/vomiting but commonly used for chemo induced vomiting both alone, they work bettie in combination with other anti-emetics: methylpredisolone, dexamethasone

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59
Q

methylprednisolone

A

IV formulation for corticosteroids. Can be used for chemo induced vomiting alone or in other combinations

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60
Q

dexamethasone

A

longer lasting steroid- oral and IV- chemo induced vomiting alone or in combination

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61
Q

benzodiazepines

A

these have no intrinsic anti-emetic properties but will sometime help with amnesia during emetogenic period or anticipatory nausea can cause sedatiion and amnesia of vertiginous episodes, so can cause sedation and amnesia of vertiginous episodes so may be paired with meclizine: lorazepam and diazapam

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62
Q

lorazapam

A

benzo for chemo during or before

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63
Q

diazepam

A

longer acting- bento for chemo during or before anticipatory nausea

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64
Q

cannabinoids

A

synthetic derivatives of tetrahydrocannabinol or THC. Unclear mechanism of action- possible inhibition of cortical activity and anyphylaxis. Helpful wit chemo induced vomiting if given prior to chemo. Uncertain about potential for abuse adverse effects: dry mouth, sedation, vertigo, ataxia. In elderly it can cause delirium, disorientation, hallucinations: dronabinol

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65
Q

dronabinol

A

cannabinoid that is helpful if used before chemo. Uncertain abuse potential.

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66
Q

pregnancy induced emesis

A

easting modification, and other pharmacologic means are attempted prior to medications for morning sickness and treating any contributing symptoms like GERD: pyridine, antihistamines, domapine antagonists, sertonin antagonists

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67
Q

pyroxidine

A

combined with doxylamine for pregnancy

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68
Q

antihistamines in pregnancy

A

diphenhydramine, dimenhydramine, and mecxline

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69
Q

motion sickness drugs

A

scopolamine, preomethazine, prochlorperzine, meclizine, lorazapam, diazepam

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70
Q

postoperative vomiting

A

scopolamine, metclopramide, prochloperazine, ondansteron, promethazine

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71
Q

drug induced vomiting

A

prochlorperazine, metoglopramide, ondansteron

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72
Q

cytotoxic drug induced vomiting

A

procholorperazine, metocholpramide, dropabinol, nabilone, ondansterone, solumedroel, lorazapeam,

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73
Q

pregnancy induced vomiting

A

promethazine, metoclopramide, procholperazine, pydridozine, doxylamine, diphenhyrdramine, meclizine

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74
Q

GERD and Peptic Ulcer Disease-treatment goals

A

relieve pain, promote healing, prevent recurrence, prevent complications, (hemorrhage, obstruction, perforation)

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75
Q

vagus nerve in relation to upper Gi

A

releases acetylcholine which binds to M3 receptors to power the proton pump. Releases gastrin releasing peptide, which activates G cells enterochromaffin like cells to release histamine

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76
Q

histmaine for upper GI

A

it directly activated the proton pump and the ECL/histamine action is the primary way that gastrin causes increased gastric acidity. Gastrin directly binds to parietal cells to release gastric acid

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77
Q

H. pylori

A

it is responsible for a majority of peptic ulcer disease and almost all duodenal ulcers. The organism attacks the epithelial cells and releases enzymes that damage mucosal cells induces inflammation and tissue destruction. Eradication of h.pylori heals most peptic ulcers and significantly reduces recurrence rate for gastric and duodenal ulcers, so exclusion of H.pylori and treatment if needed is crucial to PUD treatment

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78
Q

h.pylori treatment- triple therapy

A

triple therapy- PPI+two of the following (clarithromycin/amoxicillin, metronidazole, tinidazole, tetracycline) Used to be standard therapy- rabeprazole and amoxicillin for five days followed by rabeprozole, clarithro, metronidazole,tinidazole for another five days

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79
Q

h.pylori treatment- quadruple therapy

A

PPI+clarithromycin, amoxicillin/metronidazole+bismuth. If cannot tolerate, PPI, H2 blockers_antibiotics for at lest four weeks can be used but its less effective

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80
Q

H2 blockers

A

reversible block of histamine H2 receptors leading to decreased hydrogen ion secretin by parietal cells. Sometimes used for allergic reaction to provide some excess histamine antagonism. Good for dyspepsia and GERD. These really help with nighttime secretion but only offer moderate relief during meal time surge. They decrease pepsin. the half life is typical for needing twice a day dosing: Randitine, famotidine, cimetidine, nizatidine

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81
Q

cimetidine

A

anti-androgenic side effects: impotence, gynecomastia, galactorrha, CYP inhibitor, so can have medication side effects- H2 blocker

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82
Q

randitine, famotidine, cimetidine, nizatidine

A

H2 blockers used for reversible histamine blocking of H2 so can reduce parietal acid secretion.

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83
Q

PPI

A

these block the protein pump directly by forming a covalent disulfide bond. Better for nocturnal symptoms. These are delayed release so easier for adherence. Once a day dosing can make this easier. Some people are rapid metabolizers so have failure without increasing the dose

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84
Q

indications for PPI

A

first line for PUD because it blocks everything happening upstream so good acid suppression, NSAID gastritis, gastronomes, part of treatment for Pylori, stress ulcer prophylaxis

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85
Q

adverse effects of PPI

A

decreased acidic environment can lead to increased risk of diff, patient in the ICU are increased risk of nosocomial pneumonia, decreased absorption of food bound materials. This can lead to increased risk of osteoporosis with chronic use, hypo magnesia, iron deficiency

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86
Q

PPI drugs

A

omeprazole, esomprazole, lansonprazole, pantropazole

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87
Q

octreotide

A

somatistatin analog- great for gastronomes will inhibit the release of gastrin and histamine by ECL. Helps with diarrhea in VIPomas and carcinoid tumors can used for esophageal varies acutely in the ICU, for chronic use it should be subcutaneous

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88
Q

misprostol

A

prostaglandin E1 agonist that inhibits gastric acid secretion of mucus and bicarbonate by epithelial cells. Can be used for PUD and prevention of gastric ulcers in long term NSAIDs. Must be four times daily so not very well tolerated also causes diarrhea and cramping. Cytoprotective

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89
Q

sulcradate

A

viscous polymer or sucrose octasulfate and aluminum hydroxie. usually is a suspension. Can coat the stomach adhering to ulcers and it inhibits pepsin-catalyzed hydrolysis or mucosal proteins. It also impedes absorption of other drugs

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90
Q

calcium carbonate

A

constipation very large doses can lead to rebound acid secretion

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91
Q

aluminum hydroxide

A

constipation

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92
Q

magnesium hydroxide

A

diarrhea from the magnesium often aluminum magnesium combination controls the GI side effects like Mylanta

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93
Q

Milk Alkalai

A

increased milk ingestion or overuse of antacids causing increased calcium, alkalosis, hypophophatemia, and mild acute kidney injury

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94
Q

IBS

A

can be constipation or diarrhea predominant and sometimes alternating. Many patients have chronic and idiopathic constipation. Most drugs are orally administered

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95
Q

acute constipation

A

can be from trauma, surgery, pain medications, hypthyrodism

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96
Q

chronic constipation cause

A

its from lasting changes

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97
Q

non-pharmacologic treatment for constipation

A

should be first-line. Fruits, whole grains, vegetables, adequate hydration, and regular exercise.

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98
Q

biggest issue with laxatives

A

electrolyte derangement are the biggest issue they alter the water in the colon, so it messes with the ion concentrations of the body

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99
Q

bulk forming laxatives

A

resembles dietary fiber, absorbs and retains water in the intestinal lumen to increase the mass. This causes mechanical distention of the intestinal wall which stimulates peristalsis. They need to be taken with a full glass of water for the appropriate hydration of the fiber. These come in pills, powders. there are some in other forms. They are some side effects but are fool proof. The worst that usually happens is gas or bloating. If a great deal of bulk forming laxatives are used without enough water, it can cause an impaction can also be used for diarrhea: psyllium, calcium polycarbophil, wheat dextrin, methyl cellulose

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100
Q

psyllium, calcium polycarbophil, wheat dextrin, methyl cellulose

A

bulk forming laxatives

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101
Q

osmotic laxatives

A

These work by increasing moisture and causing intestinal distention to facilitate peristalsis. Polyethylene glycol, laceless, magnesium agents

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102
Q

polyethylene glycol

A

PEG- tasteless, odorless, liquidform. Usually bowel preparation prior to colonoscopy. Can cause some nausea, bloating, and cramping

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103
Q

lactulose

A

an osmotic agent to help with constipation. its other indication is hepatic encephalopathy in cirrhotics. It is coverted in the colonic bacteria. Can cause bloating and flatulence

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104
Q

magnesium agents

A

can cause hypermagnesiumia in renal failure patients. Magnesium oxide or magnesium citrate

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105
Q

magnesium oxide

A

milk of magnesia- poorly absorbed salt that becomes osmotic. Sometimes given for chronic hypomasgnesia can cause diarrhea

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106
Q

enemas

A

will have osmotic agents, soap suds, SMOG, sodium phosphate. There is somewhat of a risk of electrolyte derangement with repeated saline enemas. Enemas can come in over the counter, small, plastic bottles, hanging to gravity attached that goes up there

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107
Q

glycerine suppositories

A

tend to be used for infants with constipation

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108
Q

docusate

A

surfactant lacatives- stool softeners because they actually incorporate water into the fatty intestinal issue and make the stool softer and help lubricate the intestinal lumen. Occasional absorption issues or rashes

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109
Q

stimulants for laxatives

A

composed of natural or synthetic compounds that alter the fluid secretion to stimulate peristalsis. the amount of peristalsis generated can cause cramping, electrolyte, abnormalities, gastric, rectal irritation. Senna, bisacodyl

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110
Q

Senna

A

stimulant laxatives, it is used for natural combines with decussate in the formulation called D. Started to prevent opioid, overuse of this can cause melanosis coli

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111
Q

bisacodyl

A

this is the other stimulant laxative. synthetic or suppository

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112
Q

prokinetics

A

serotonin is the big player in treating motility issues. It is produced and released by enterochromaffin cells in the gut where it activates 5HT3 and HT4 receptors on cholinergic neurons and enhance peristalsis. Drugs that activated 5HT receptors increase motility and have been used in treating constipation. 5HT3 are used for diarrhea

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113
Q

metoclopramide

A

prokinetic- dopamine antagonist that prevents relaxation of the GI smooth muscle. It generated increased tone in the esophagus and stomach creating propulsion machine. It helps with gastroparesis by accelearing gastric emptying. It is sometimes used for GERD, refractor constipation due to decreased motility and emesis

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114
Q

lubiprostone

A

prokinetic- chloride CIC2 chanel agonist- chronic idiopathic constipation or IBS with constipation. Low systemic absorption. It can cause nausea but it improved

115
Q

erythromycin

A

prokinetic- an antibiotic that forms as a prokinetic

116
Q

opioid antagonists

A

these can help with constipation due to opioid use or bowel resection. They only antagonize opioids at the periphery. Will block entrance of opioids to the bowel

117
Q

methylnaltrexone

A

contraindicated in bowel obstruction can cause GI upset and constipation. It is an opioid antagonist

118
Q

cholestryramine

A

inhibits enteroheaptic repute of bile salts

119
Q

bismuth subsalicylate, activated charcoal

A

absorbants- these coat the walls of the IG tract and can bind to any causative bacterias or toxins which will then be eliminated through the stool

120
Q

antispasmodics

A

typically used for IBS, with associated diarrhea or other chronic cases of diarrhea. They work by decreasing intestinal muscle tone and peristalsis to slow the movement of fecal matter through the GI tract: atropine, hyoscyamine, scopolamine, dicyclomine

121
Q

atropine- muscarine antagonist not used because it leads to blurred vision and bladder retention

A
  • muscarine antagonist not used because it leads to blurred vision and bladder retention- antispasmodics
122
Q

hyocyamine

A

anticholinergic- commonly used in IBS-D- used as antispasmodic

123
Q

dicylomine

A

used in IBS-D- antispasmodic

124
Q

Mu agonists

A

Mu opiod receptors are located in the GI tract. When activated, they cause colonic phase segmental activity. This is different than typical peristalsis and increased the colonic transit time. Since stool is in the colon longer, ti allows for more water absorption. These can be helpful for chronic diarrhea either from a needed medication or other causes such as IBS: loperamide, diphenoxylate

125
Q

loperamide

A

mu opioid receptor agonist- no ability to cross the BBB so no abuse potential. Help increase water reabsorption

126
Q

dipehoxylate

A

some ability to cross the BBB in high doses. It is with atropine with over the counter. Can have a high with a high dose, but thats why atropine is given with it.

127
Q

IBS-D

A

most common complaints are cramping, pain, diarrhea, bloody stool, these can wax and wane as disease remits and flares. Medications can be used for these symptoms as well as underlying inflammation. Mild to moderate disease can be approached from top down or step up. With most potent therapies have the most side effects. The purpose of this is to control the disease before it worsens and to minimize the total amount of steroids required. treatment is different fro chronic vs. acute

128
Q

ulcerative colitis

A

begins at the rectum and proceeds continuously through the colon. If there is only disarm disease,e some of the medications can be used rectally for direct absorption without systemic side effects

129
Q

crohns

A

can occur anywhere through the immune system; not only in lower GI tract although it is usually in the terminal ileum. It is important for colonoscopies.

130
Q

aminosalicylates

A

these are helpful to insure and maintain remission of ulcerative colitis but are less effective in Crohns disease. The verdict is out of what the exact mechanism is but there is anti-inflammatory modulation at work. These are mainstay and starting point of treatment of mild-moderate disease. Topical are used for ulcerative colitis. don’t give if sulfa allergy is present. Can cause folate deficiency

131
Q

sulfasalazine

A

combination of sulfapuramidine+5ASA. It is not well abosobed systemically so works great for GI disease- aminosalicylates

132
Q

mesalamine

A

active metabolite of sulfasalazine; 5ASA rectal suspension or delayed release oral tablet. Less side effects as administerred locally- aminosalicylates

133
Q

glucocoritcoids

A

mainstay for mild to moderate disease flare without complete resolution after aminosalicylates. They must be tapered off slowly and even so rebound symptoms may arise. Prolonged usage has host of side effects so alternative agents may be required.

134
Q

methylpredisonolone

A

severe disease IBS

135
Q

predinsone

A

most common for IBS but must be tapered off

136
Q

budesonide

A

controlled ill release formation with high first pass metabolism so is great for ileitis in Crohns if they can’t tolerate glucocorticoids.

137
Q

hydrocortisone

A

suppository or foam for distal ulcerative colitis

138
Q

cyclosporine

A

immunosuppressant- when steroids +%ASA fail to induce remission or with fistulizing disease, cyclosporine can be used as a bridge while awaiting longer acting medications to work. Really not sued much any longer now that biologics are existence so can lad to high relapse rate

139
Q

azanthioprine

A

inhibits mitosis which helps to suppress the immune response. Prior to treatment TPMT genotype can be checked and it will be immediately started at full dose instead of half with titration. Hepatic, renal and blood side effects. 6-mercaptopurine is the active metabolite

140
Q

methotrexate

A

dihydrofolate reductase inhibitor intramuscular while getting disease under control then changed to weekly oral dose. Nausea, vomiting and folic acid deficiency are common. Given with folic acid

141
Q

infliximab, adalimumab

A

monoclonal antibodies against TNF-alpha receptors. Severe crohns disease they don’t help with non-active disease. Can cause GI upset, decompensation of heart failure, hypersensitivity reactions, fever, headache, pancytopenia, these can increase TB and other infections.

142
Q

thiamine B1-diet

A

grains, legumes, meat and fortified grains

143
Q

thaimine reactions

A

oxidative decarboxylations, these function in energy metabolism transitioning from glycolysis to TCa. Thiamine is central in production of acetyl coA and a central metabolic hub involved in energy processes. It is used to synthesize neurotransmitter, acetyl choline. Thiamine is carbonyl career in carbon assimilation reactions, It functions in the non-oxidative phase of pentose phosphate pathway operating to synthesize NADPH and pentose phosphates used in nucleotide synthesis

144
Q

thaimine deficiency- causes

A

dietary deficiencies are observed in regions where refined rice is a dietary staple in north America. The refining process removes thiamine found in rice husks. Can also be from thiamine deficiency is associated with changes in GI absorption due to chronic alcoholism, liver damage may also affect conversion to thiamine pyrophosphate

145
Q

beriberi- wet vs. dry

A

o Beriberi is cardiovascular manifestations rapid heartbeat, pathogenic remodeling of the heart and congestive heart failure.
• Cardio is wet beriberi
o Neurological features are weakness, apathy, nerve tingling, poor coordination, paralysis linked to heavy relianc of brain on glucose metabolism and acetyl COA needed for acetlychoiine synthesis- dry beriberi

146
Q

Wernicke-Korsakoff

A

specific neurological features associated with thiamine deficiency linked to alcoholism- confusion, psychosis, memory problems, coma

147
Q

Riboflavin B2- diet

A

found in milk and dairy, meats, whole na denriched grains, vegetables. Flavin gets its name from yellow in oxidized state

148
Q

riboflavin B2- reactions

A

electron carrier- oxidation/reductions. Functins in energy metabolism as part of pyruvate and alpha ketoglutarate dehdrogenases and as an electron carrier in the TCA cycle and electron transport chain.

149
Q

riboflavin- deficiency causes

A

• Causes- found in association with other decreased B vitamins- chronic alcoholsm but can be found in other parts of the world where dairy and meat are low

150
Q

ariboflavinosis

A

• Ariboflavinosis- inflammation of eyes, skin, lips, mouth, and tongue- seborrheic dermatitis becoming red, scaly, and greasy.
o Can influence iron absorption and mobilization and as a consequence can affect the production and function of red blood cells.

151
Q

why is milk stored in opaque plastic

A

riboflavin is broken down by sunlight

152
Q

Niacin B2- diet

A

found in meat and fish, legumes, bran, peanuts. The addition of niacin to enriched flours provides much of this vitamin in north American diets

153
Q

niacin B2 reactions

A

• Reactions- electron carrier, oxidation/reduction. Functions as either a co-enzyme or substrate in energy metabolism, glycolysis, TC cycle, transport chain, breakdown and synthesis of fats, cholesterol synthesis, and many other reactions

154
Q

niacin deficiency causes

A

• Causes- dietary- it can be synthesized in small ammounts in the human body from tryptophan. It is low in corn, so it can be issue in southestern USA when diet was rich in corn. It is seen in Hartnups disease with neutral amino acid transported due to inefficient absortion of tryptophan (W) from the gut and resportion in the kidney

155
Q

pellagra

A

diarrhea, dermatitis, dementia can lead to death

156
Q

niacin supplementation

A

• Can be used to reduce cardiovascular events and mortality. It causes skin flushing, GI side effects, and itching.

157
Q

Biotin B4- diet

A

liver, egg yolks, yogurt, and nuts. It is not found in large amountsi n fruits and meats, but it can also be made by intestinal bacteria and absorbed into the body

158
Q

biotin B4- reactions

A

only used for carboxylation reactions. Biotin is needed for gluconeogenesis, fatty acid synthesis, and the catabolism of certain amino acids

159
Q

biotin B4- deficiency causes

A

dietary are uncommon but could be from absorption or feeding tubes.• Acquired deficiency- biotin was discorved when rats were only fed raw egg whites which prevents biopn from binding by avidin binding.
• Inborn errors of metabolism- for enzyme to use biotin, they must be liberated from natural sources b biotinidase and then bonded to relevant enzymes. Can show carboxylase deficiency

160
Q

biotin deficiency symptoms

A

brittle fingernails, hair loss, skin rashes, neurological deficits, tingling of extremities

161
Q

pantothenic acid (B5)-diet

A

pantothenic acid gets its name from wide range of foods

162
Q

pantothenic acid B5- reactions

A

pantothenic acid functions as an acyl carrier, acetyl CoA being the most familiar and various others are found in nature.

163
Q

pantothenic acid B5- deficiency causes

A

rare but severely malnourished

• Alcoholics seen with it

164
Q

pantothenic acid B5- deficiency symptoms

A

• Numbness and painful burning and tingling in extremities

165
Q

pyridoxine B6- diet

A

it is found in meats, whole grains, brown rice, and some fruits and vegetables. It is inactivated by heat and light therefor it is not used to fortify grain products but it used to fortify breakfast cereals

166
Q

pyridoxine B6 reactions

A
  • Reactiosn- it is involved in amny different aspects of protein and amino acid metabolism
  • Transamination reactiosn- all transaminases use this as a coenzyme
  • X-linked sideroblastic anemia- enzyme affects gamma amino levulinic acid synthase, defect in heme synthesis
  • Homocysteinuria- enzume affected, cystathionine synthase so issue in methionine catabolism
  • Ornithineamia with gyrate atrophy- enzyme affected orniting gamma amino tranferase- proline
  • Pyridoxine-dependent epilepsy- enzyme is aminoadipic semialdehyde dehydrogenase which is involved in lysine breakdown.
  • Hypophosphatasia- non-tissue specific alkaline phosphatase, needed for pyridoxal entry into the brain. The disease is characterized by convulsions and epilepsy
  • Pyridoxal phosphate is in a lot of neurotransmitter metabolism
167
Q

pyridoxine deficiency causes

A

o Nutritional are rare except in alcoholics
o Drug interactions –certain drugs can inactivate pyridoxine and its derviatives. Thes drugs can therefore induce a B6 deficiency. B6 supplements are often recommended when using these durgs to avoid neuropathy and other symptoms of B6 deficiency.
• Cycloserine
• Isoniazid
• Hydralazine
• Theophylline
• Penicillamine
• Monoamine oxidase inhibiotrs
• L-DOPA- limiting bioavailability of B6
o pyridoxine is destroyed by light and heat so can be from overheating infant formula

168
Q

pyridoxine deficiency symptoms

A 
o	neuroplogical deatures- infants consuming the formula were abdominal problems, convulsions. Reversed when their diet was resolved.
o	Anemia
o	Seborrheic dermatitis
o	Glossitis
o	Cheilosis
o	Sideoblastic anemia
169
Q

pyridoxine toxicity

A

o Long term high doses can lead to sensory neuropathy

170
Q

high dose pyridoxine inhibits which medications

A

L-dopa, phenytoin, phenobarbitol

171
Q

what does pyridoxine not help with

A

carpal tunnel

172
Q

folate (B9)-diet

A

lentils and green vegetables. It is now in refined grains. Fortified foods are more bioavailable.

173
Q

folate reactions

A
  • Reactions- tetrahydrofolate and its one carbon dreviateives are involved n many reactions in one carbon metabolism. It is very important for dividing cells and pregnant women have higher requirement becuaseo fthis.
  • Purine synthesis
  • Thymidine synthesis
  • Methionine synthesis from homocysteine- can create dead-end intermediates.
174
Q

folate deficiency causes

A

dietary deficiencies of folate are common before food was fortified. It is also in chronic alcoholism

175
Q

folate deficiency symptoms

A

o Megaloblastic anemia
o Neural tube defects- folate deficiency in pregnancy
o Elevated homocysteine- cardiovascular disease and could decrease risk of HA if the supplements were taken

176
Q

folate trap and relationship with B12

A

• Folate trap so fole supplementation can mask B12 deficiency. A vitamin B12 deficiency traps folate in the methyl tetrahydrofolate state. With B12 unavilable to convert, the usable folate level in the body drops and leads to macrocytic anmia.

177
Q

is folate or folic acid better absorbed in food

A

folic acid

178
Q

cobalamin B12- diet

A

cobalamin is found in aminal products so issue with vegans

179
Q

cobalamin B12- reactions

A
  • Methionine synthase- methyl cobalamin is used to emthylate homocysteine to methionine by the enzyme methionine synthase. Cbalamine formed in this reaction is coverted back to methyl-cobalamine by the same enzyme using tetrahydrofolate as the methyl group donor. Isnce this is the only reaction that tetrahydrofolate is returned to the folate pool, this reaction forms the folate trap.
  • Metyhlmalony-COA-mutase- adenosyl cobalamin participates in this mutase reaction nwhere methylmalonyl-CoA is rearranged into succinyl CoA in a late step in catabolism f certain amino acids and odd chain fatty acids.
180
Q

cobalamin deficiency- cause

A

• Causes- dietary deficiency is rare, but can take months to years to develop because of storage and recycling
• Malabsorption-
o Pernicious anemia- autoimmune disorder- destroys the parietal cells involved in the synthesis of intrinsic factor needed for B12 absortion in the ileum. Pernicious anemia can be effectively treated by B12 injections or mega-doses
o Atrophic gastritis- affects acid decretion from the stomach which decreases the release of B12 from dietary proteins, so reduced absorption. Atrophic gastritis can lead to bacterial overgrowth, which affects other nutrients
o Celiac disease or tropical sprue can effect it
o Surgical resection of terminal ileum or parts of stomach can decrase the intrinsic factor production
o Drug interactions- PPI reduce stomach acid can affect B12 absorption- prolonged use is necessary for B12 deficiency to develop.
• Nitrous oxide- it inactivates B12
• Metformin- it decreases absorption by influencing calcium levels
• Tetracyclin- take them at different times

181
Q

cobalamin deficiency clinical features

A

o Macrocytic anemia- caused by the folate trap where a cobalamin deficiency prevents tetrahydrofolate from being converted to usable forms so folate deficiency develops.
o Neurological symptoms- numbness and tingling in hands and feet, difficulty walking, memory loss, disorientation, and dementia. B12 deficiency leads to damage to myelin sheaths covering various nerves.

182
Q

ascorbic acid (c)- diet

A

ascorbic acid is rich in fruits and citrus fruits and veggies. It is destroyed by oxygen, lights, and heat

183
Q

ascorbic acid deficiency cause

A

• Inadequate fresh fruits and vegetables in the diet, rare but poor with inadequate access

184
Q

ascorbic acid deficiency clinical symptoms

A 
o	Fragile blood vessels, pinpoint hemorrhages, bleeding gums, bruising
o	Poor wound healing,
o	Bone fractures
o	Loose teeth
o	Joint pain and swelling
185
Q

what does ascorbic acid do to iron uptake

A

increased in the Gi tract so be careful with hemochromatosis

186
Q

retinoids (A)- diet

A

liver, fish, egg yolks, dairy for preformed retinoids. Carotinoids- vegetable and fruits that have yelloe/orange pigments that are converted to retinoids in mucosal cells of the liver

187
Q

retinoids- reactions

A

• Visual cycle- six membered ring with hydrocarbon tail that have a number of double bonds, mosstof which are trans except a double bond which is cis that is converted to trans when photon hits it. This change in retinal is transmitted to opsin a G protein which transmits information to the brain.All transrentianl goes from the photoreceptor cell to the pigment epithelium where it is coverted back to 11-cis retinal and returned to the photoreceptor cell
• Signal transduction- retinoid acid derivatives are retinoids involved in controlling gene expression at the transcriptional level. This regulation occurs htorugh retinoic acid receptors that function as transcription factors via this regulation, retinoic acid controls both cell fate and function.
o Development- retinoic acid derivatives play critical roles in human development affecting the formation of cardiovascular system, nervous system, respiratory system, and skeletal growth
o Immune system- retinoic acid derivatives control cell fate decidisons during erythropoiesis.
o Epithelial tissue-retinoic acid plays a role in the differentiation of epithelial layers
• Eyes- mucus secreting cells of the eye require retinoic acid signaling for appropriate function.
• Skin- retinoic acid plays an important role in controlling the differentiation of hair follicles and mucus secreting glands
o Bone growth and remodeling

188
Q

retinoids-deficiency causes

A
  • Causes- inadequate sources of preformed
  • Inadequate fat intake which limits the solubalization of retinoid
  • Inadequate dietary protein/amino acids- needed for retinol binging protein involved in transport mechanism
  • Inadequate zinc- interferes with metabolism and absorption
189
Q

retinoids- deficiency symptoms

A

o Xerophthalmia- spectrum of eye problems linked to vitamin A deficiency including night blindnesss, extreme dryness, and softnening of the cornea is referred to as keratomalacia. If untreated it is leading to blindness
o Susceptibility to infectious diseses because of immune controlled heamatopoesis
• It is considered nutritional immunodeficiency
o Follicular hyperkeratosis- hard dru skin surfaces with lesions on extremities
o Microcytic anemia

190
Q

retinoids toxicities

A

o Preformed only
o Adults- nausea, headache, blurred vision, cerebral edema, lack of muscle coordination
o Chronic- eight loss, muscle and joint pain, liver dmage, bone abnormalities, visual defcts, anemia, and skin rashes
o Infants- bulging fontanels
o Pregnancy- excess consumptions leading to birth defects

191
Q

retinoids drug uses

A

psoriasis, acnes, retinitis pigmentosa, acute promylocytic leukemia with Philadelphia chromosome

192
Q

cholecalciferol D3- diet

A

salmon, liver, egg yolks. Fortified milk and cereals

193
Q

cholecalciferol D3- synthesis

A

can be made by the human body. It is derived from cholesterol by a series of rearrangements and it induced by the cunlight. Activation ccurs by a second hydroxylation at position 1 carried out by an enzyme in the kidney. Vitamin D derivatives are transported through the circulation bong to the vitamin D bidning protein and to a lesser extent by albumin

194
Q

cholecalciferol- reactions

A

• Regulates levels of calcium and phosphorous in the blood so central to bone metabolism. The PTH releases parathyroid hormone which stimulates activity of kidney hydroxylase involved in converting 25-hydroxy vitamin D3 to 1,2 dihydroxy vitamin D3
• Active vitamin D binds to nuclear receptors and targets gene expression in responsive tissues to increase blood calcium
o Low levels of active D act in intestine to increase Ca
o Active D stimulates Ca reabsopriton. In absocenecs to Ca from diet, high active D stimulates Ca from the bone
• It is also an immune modulator acting at the level of antigen presenting cells and regulatory T cells.

195
Q

cholecalciferol- deficiencies causes

A

o Environmental conditions, latitiude, length, and strength of sunlight exposure
o Clothing that blocks the skin
o Sunscreen and protection measures
o Infants who only breast feed and receive limited fortification
o Indicidueals with darker skin
o Chronic kidney disease
o Fat malabsorption syndromes- individuals with cystic fibrosis tend to have low levels of D as do individuals with cholestatis and non-cholestatic liver disease
o Obesity- vitamin D can be absorbed into fat stores limiting its availability for other functions
o Elderly- reduced capacity to synthesis active vitamin D with age and more limited exposure to sun.

196
Q

rickets

A

vitamin D deficiency reduces calcium uptake limiting the amount available for bone formation thereby causing abnormal bone growth. Rickets is characterized by narrow rib cages and bowed legs

197
Q

osteomalacia

A

o Osteomalacia- adults where bones are already formed, vitamin D feficiency can weaken bones leading to fractures in weight beraing bones. Osteomalacia can also promote osteoporosis or make it worse

198
Q

cholecalciferol over-supplementation

A

high blood calcium and calcium deposition in blood vessels, kidney, and cardiovascular system

199
Q

which drugs increase vitamin D supplement catabolism

A

phenytoin, carbamazepine, rifampin

200
Q

tocopherol (E)- diet

A

alpha tocopherol is the active form of the vitamin. Nuts and vegetable oils are good sources of vitamin E in diet. Smaller amounts are found in certain vegetables. Vitamin E is found in dietary supplements and fortified foods are inactive thereby overstating the amount of active alpha tocopherol being consumed.

201
Q

tocopherol E- reactions

A

the primary function of vitamin E is as a fat soluble antioxidant.
• Being fat soluble, vitamin E serves as a critical function in neutralizing oxidatively damaged unsaturated fats in cell membranes, a function that cannot be effectively performed by water soluble antioxidants. Protecting cell membranes from oxidative damages is of vital importance in RBS, nerves and cells in the immune system
• Vitamin E protects VLDLs and other lipoproteins from oxidation and are thought to be protective for cardiovascular disease
• Vitamin E is oxidized in performing its antioxidant functions, it needs to be recycliced, receiving electrons from other antioxidants like vitamin C

202
Q

tocopherol- E- deficiency cause

A

dietary are rare, but associated with malnutrition
o Fat malabsortion syndromes
o Genetics- defects in alpha tocopherol transfer protein needed for the transfer of alpha tocpherol to lipoportiens for delivery to cells
o Birth- little transfer to vitamin E occurs from omother to fetus until late pregnancy. This means premature infants can have damaged red blood cell membranes and suffer hemolytic anemia due to vitamin E deficiency

203
Q

tocopherol- symptoms of deficiency

A

o Neurologic- impaired balance and coordination, damage to sensory nerves, muscle weakness, and damage to the eye
o Hemolytic anemia- premature infants

204
Q

tocopherol supplement drug interactions

A
  • Vitamin E supplements can inhibit the gamma carbxylation of clotting factors, so should not be taken with warfarin because it can increase serious bleeding
  • Cholesterol sequesterants should not be taken at the same time as vitamin E supplements
  • Drugs like phenytoin, carbamazepine and rifampin increase vitamin E catabolism
205
Q

phylloquinone (K)- diet

A

phyllloquinones are rich in leady green plants and vegetable oils. Some forms of vitamin K are formed by bacteria in the digestive tract and absorbed.

206
Q

phylloquinone- reactions

A

active forms of vitamin K serve as an essential co-enzyme for gamma glutamyl carboxylase which is the enzyme responsible for forming gamma glutamyl residues in coagulation factos. This modification is essential for full activity of coagulation factors.
• Vitamin K is an electron donor in the reaction an is recycled back to the reduced state by vitamin K epoxide reductase (VKOR)
• This recycling is targeted by the anticoagulant warfarin

207
Q

phylloquinone deficiency cause

A

dietary are rare in adults, but are common in newborns as there is little transfer of vitamin K from mother to fetus and the neuborn GI tract is essentially free of bacteria nd breast milk is vitamin K poor. Most infants receive a vitamin K shot after birth around six hours post birth
o Fat malabsorption syndromes can affect vitamin K absorption.
o Antibiotics that kill off GI bacteria couples with a diet low in vitamin K can lead to vitamin K deficiency

208
Q

symptoms of phylloquinone deficiency

A

excessive bleeding.

209
Q

phylloquinone drug interactions

A

it counteracts warfarin

210
Q

chronic, mild elevations ALT/AST

A 
o	Alpha1 antitrypsin deficiency
o	Autoimmune hepaptitis
o	Chronic viral hepatitis (B,C,D)
o	Hemochromatosis
o	Medications and toxins
o	Steatosis and steatohapatitis
o	Wilsons disease
o	Non-hepatic (celiac or hyperthyroidism)
211
Q

severe acute elevations ALT/AST

A 
o	Acute bile duct obstruction
o	Acute Bud Chiari syndrome- portal venous thrombus
o	Acute viral hepatitis
o	Autoimmune hepatitis
o	Drugs and toxins
o	Hepatic artery ligation
o	Ischemic hepatitis
o	Wilsons disease
212
Q

chronic mild elevations AST>ALT

A

o Alcohol related liver injury
o Cirrhosis
o Non-hepatic- hypothyroid, myopathy, strenuous exercise
o Virtually any injury

213
Q

severe acute elevation AST>ALT

A

o Medications or toxins in patient with underlying alcoholic liver disease
o Non-haptic cause- acute rhadomyolysis

214
Q

GGT

A

found in hepatocytes and billiard epithelial cells as well as kidneys, seminal vesicles, pancreas, spleen, heart, and brain. It can be elevated with many things but its sensitive but not specific

215
Q

elevated GGt and elevated alk phos

A

liver origin

216
Q

normal GGT and elevated alk phos

A

bone issue

217
Q

direct hyperbillirubinemia

A
  • Dubin Johnson- lifelong mild jaundice
  • Rotor syndrome- genetic mild jaundice
  • Structural issues
  • Alagailes- paucity of bile ductsleading to butterfly vertebrae and triangular facise
  • Familial hepatocellular cholestasis
218
Q

indirect hyperbilirubinemia

A
  • Gilberts syndrome- have not been eating well and is dehydrated causing mild jaundice
  • Crigler najjar I
  • Criget Najjar II
  • Hemolysis
  • Multiple drugs
  • Congestive heart failure
  • Portocaval shunt
  • Ineffective erythropoiesis
  • Neonatal jaundice
  • Sepsis
219
Q

alk phos elevation

A

o Partial bile duct obstruction, infiltration, ofr focal liver mass
o If its elevated along with bilirubin, and/or mild elevated of transminases, intrahepatic or extrahaptic cholestasis

220
Q

LDh

A

lactate dehydrogenase is a cytoplasmic enzyme present in tissues and can be separated by isoenzymes

221
Q

obstructive jaundice symptoms and labs

A

o Abdominal pain, fever, rigos, prior biliary surgery, acholic stools,
o High fever, abdominal tenderness, palpable abdominal mass, abdominal scar
o Predominant elevation of serum billirunin and alkaline phosphatase, prothrombin time that is normal or normalizes with vitamin , elevated serum amylase

222
Q

parenchymal liver disease

A

o Anorexia, malaise, myalgias, viral prodrom, infectious exposure, injection durg use or coke, exposure to hepatotoxin, family history of jaundice
o Ascites, stigmata of liver disease,
o Predominant elevation od serum aminotransferases, prolonged prothrombin time that does not correct with vitamin K administration, blood tests for specific liver disease

223
Q

what are tests that can measure synthetic liver function

A

INR, ammonia, albumin

224
Q

MELD score

A

predictor of five year mortality. Creatine is from how congested the liver is causes kidney ischemia

225
Q

chronic hepatitis pattern

A
  • Haptocellular AST/ALT
  • Cholestatis (alkphos, bilirubin)
  • Mixes picture of these is possible
226
Q

high liver enzymes

A
  • Drugs (tylonol)
  • Ischemic hepatitis
  • Viral hepatitis
  • Heaptive artery ligation
  • Autoimmune hepatitis
  • Acute- budd chiari
  • Rare- obstruction, wilsons disease
  • Features of cirrhosis
227
Q

features of cirrhosis

A
  • AST>ALT
  • Decreased platelets
  • Decreased albumin
  • Increased bilirubin
  • Increased PT/INR
228
Q

chromium- diet

A

liver, processed meats, while grain cereals, brewers yeast and nuts

229
Q

chromium- functions

A

exact function of chromium within the human body. It has been proposed that trivalent chromium functions as a cofactor for an oligopeptide called chromomdulin. Biologically active chromomodulin is reported to enhance the effects of insulin on target tissues

230
Q

chromium toxicities

A

hexavalent chromium exposure is more likely to occur in industrial setting as chromium has been used in paint and dye

231
Q

copper diet

A

organ meats, shellfish, whole grain cereals, fruits, and certain vegetables

232
Q

copper functions

A

these are cytochrome C oxidase, superoxide dismutase, lysyl oxidase, ceruloplasmin, and tyrosinaase

233
Q

copper deficiency- diet

A

one of the most common sings of copper deficiency is anemia linked to the role of copper containing ferrioxidases like ceruloplasmin in iron mobilization. Such anemias are unresponsive to iron but to respond to copper. Individuals at risk for copper deficiency include infants fed couws milk, individuals with malabsorption symptoms, or iatrogenically through strict, but incomplete dietary

234
Q

copper deficiency-inheritted

A

• Inherited- menkes disease is causes by a deficiency of a copper-transporting ATPase found in many cells throughout the body, including enterocytes where copper becomes trapped and fials to enter the circulation. The clinical features of Menkes disese include intractable seizures connective tissue disorders, subdural hemorrhage and hair abnormalities

235
Q

copper toxicities

A

copper toxicities have been reported in contaminated water supplies and in beverags stored in coppr containing containers. Symptoms typically involve abdominal pain, nausea, vomiting, and diarrhea. Individuals with Wilons disease caused by a defect in copper excretion from the body in the bile are at risk for copper toxicity. Copper accumulation in the liver of patietns wit hWilsons disease can lead to liver failure. Copper accumulation in the brain of wilsons syndrome patients can lead to neuropsychiartirc symptoms

236
Q

fluorine diet

A

seafood tea, fluorinated water

237
Q

fluorine function

A

fluoride does not function as a enzme cofactor, but instead is incorporated into mineralized tissues of bones and teeth displacing OH groups of hydroxyapatite in forming fluoroapatie hardening tooth enamel and stabilizing mineralized bone

238
Q

fluorine deficiencies

A

inadequate fluoride intake leads to an increased risk of rental caries. There is little evidence to suggest that fluorination of water is effective for bone mineralization

239
Q

fluorine toxicities

A

fluoride is toxic in high doses. Can cause nausea and abdominal pain in high doses from toothpaste too much. Fluorosis can also be characterized by mottling and pitting of permanent teeth in adults.

240
Q

iodine diet

A

seafood, iodized salt, eggs, cheese

241
Q

iodine function

A

iodine is important substituent of the thyroid hormones thyroxine and triiodothyronine. Iodine is taken from the blood into the thyroid gland where it is incorporated into thyroglobulin. Breakdown of thyroglobulin is by lyosomal enzymes produced by the thyroid homrones that are stored and released as needed. Thyroid hormones regulate growth, development, metabolism, and reproductive function

242
Q

iodine deficiency

A

mental retardation, hypothyroidism, and goiter. Iodine is considered treatable brain damage

243
Q

iodine toxicities

A

acute iodine toxicity is associated with ingestion of large amounts of iodine can cause burning of mouth, throat, stomach, and subsequent nausea, vomiting, and diarrhea. Acute toxicitiy can result in cyanosis and coma. Excess iodine intake can lead to hyperthyroidism characterized by weight loss, tachycardia, muscle weakness, and warm skin

244
Q

iron diet

A

meats, fish, enriched grains, and cereals.

245
Q

iron function

A
  • iron is critical component of hemecontaining proteins and iron sulfur proteins
246
Q

iron deficiency

A

tends to be common in children pre-menopausal women, and in pregnant women. Other symptoms incluse pica, glossitits, angular cheilosis

247
Q

iron toxicity

A

excess iron leads to hemochromatosis which hcan be characterized by liver cirrhosis, diabetes mellitus, cardiomyopathy, bronze skin, hypogonashism. Iron overload have have genetic or too many chronic perfusions. Accidnetal overdose associated wit hingestion or iron containing products. Initial symptoms of acute toxicity include abdominal pain, nausea, vomiting, and tarry sstools but may progress to CNS damage, cirrhosis, other organ damage with time

248
Q

manganese diet

A

whole grain cereals, pineappele, nuts, tea, tomatoes

249
Q

manganese function

A

manganese is a component of a relatively small number of enzymes: glycosyl-transferases, phophoenopyructate, carboxykinase and manganese superoxide dismutatse

250
Q

manganese deficiency

A

naturally occurring manganese deficiency has nto been in humans. Growth retardation, congential bone malformations, and defects in carbohydrate and fat metabolism

251
Q

manganese toxicities

A

manganese toxicities have been reported in welders and smelters who inhale manganese dust. Symptoms are similar to Parkinsons disease including tremors and difficulty walking. Psychiatric symtoms have been observed with manganese toxicitiy

252
Q

molybdenum diet

A

milk, legumes, whole grin bread, cerelas, dark green vegetables

253
Q

molybdenum functions

A

is a component of xanthine oxidase, sulfite oxidase and aldehyde oxidase

254
Q

molybdenum deficiency- inherited

A

• Inherited deficiencies in formation of the cmolybdenum cofactor used by the enzymes above have been reported with the major impact on the activitiy of sulfite oxidase which palys a role in the metabolism of cysterine and methionine. Defects in the formation of Moco cause severe neurological dysfunction characterized by cerebral atrophy, mental retardation, and intractable seizures

255
Q

molybdenum deficiency acquired

A

acquired are patients wit hCrohns disease on total parenteral nutiriton without adequate molybdemiun. Tachycardai, tachypnea, headache, nausea, vomiting, and coma

256
Q

selenium- diet

A

meats, seafood, nuts, plant-based foods

257
Q

selenium- functions

A

it is a component glutathione peroxidase and thyroid hormone iodinase

258
Q

selenium- deficiency

A

insufficient selenium may negatively effect antioxidant responses but does not give rise to overt clinical symptoms except under certain physiological stresses. Kashin Beck disease in SE asia in regions where the selentium content of soil is low. His disese results in degeneration of articular cartilage and is thought ot occur from the loss of antioxidant protection against certain mycotozins in the diet. Keshan disease is another associated with selenium. Keshan disease is dilated cardiomyopathy first reported in a region of China where selium content of the soil is low. In keshan disease selenium deficiency appears to enhance the virulence of coxackie virus B3 which is responsible for myocarditis

259
Q

selenium- toxicities

A

selenium is high doses is toxic. Symptoms of selenosis include hair and nail brittleness, GI distress, fatigue, irritability, and include neurological disorders. Clincially significant selenosis was observed in inidviduals taking excessively high doses of selenium in supplements due to a manufacturing error

260
Q

zinc- diet

A

meats, seafood, fortified cereals, whole grains

261
Q

zinc- functions

A

zinc is a cofactor for over 300 different enzymes. Zinc can also have structural and regulatory

262
Q

zinc- deficiency

A

most of what is known about zinc deficiency comes from pateints born with acrodermatitis enteropathica, associated with deficient uptake. The symptoms of this zinc deficiency include the slowing or cessation of growth and development, delayed sexual maturation, characteristic skin rashes, chronic and severe diarrhea, immune deficiency impaired wound healing, diminished appetite, impaired taste sensation, night blindness, swelling and clouding of the corneas, and behavioral disturbances. While such a severe forms of dietary zinc deficiency are rare, it is now thought that almost 2 billion people have milder forms of zinc deficiency, which may contribute to a host of helath problems, including compromised immune function and susceptibility to infections

263
Q

zinc toxicities

A

arise from contamination of food and beverage containers made of galvanized metal. Abdominal pain, diarrhea, nausea, vomiting. Individuals ingesting large quantities zinc induces the intestinal synthesis of metallothionein which traps copper limiting its availability and inducing copper deficiency

264
Q

zinc in the immune system

A

helps you get over colds faster

265
Q

what is a dietary supplement?

A

a product inded for ingestion that ciantinas a dietary ingredient intded to add further nutriotional calue to the diet. A dietary ingredient may be one or any combination of vitmains, minerals, herbs, amino acid, dietary substance used by people to supplemtn the diet by increasing the total dietary intake, a concentrate, metabolite, constituent or extract

266
Q

what is a botanical

A

herb, root, leaf or flower that has some properties to treat disease

267
Q

nutriceuticals

A

• Not a food or a drug, but in between and not regulated

268
Q

regulation of supplements

A

neither botanicals or dietary supplements are FDA approved. Their manufacturer are responsible for ensuring that the ingredient is reasonably sade. If the FDA wants to investigate they give ten days notice. There are standards of what must be on the label, but the manufacturer is responsible for the truth and accuracy of the statement but its not approve. They must have name, quantitiy and weight.

269
Q

FDA approved folate

A

neural tube defects

270
Q

FDA approved- Ca

A

osteoporosis

271
Q

FDA approved Na-

A

HTN

272
Q

FDA- fruits and veggies

A

cancer

273
Q

FDA- dietary lipids

A

cancer

274
Q

FDA- saturated fat/cholesterol

A

coronary artery disease

275
Q

licorice

A

peptic ulcers are meant to be treated. It causes pseudoaldosteronism,
• Interactions- digoxin, furosemide

276
Q

ephedra

A

taken for decongestant and anorexiant can lead to palpitations, MI, death
• Drug interactions- thropylline, digoxin, caffeine

277
Q

kava

A

taken for anxiety, stress, sleep. Adverse effect is hepatotoxicity
• Drug interactions- do not use over 4 weeks

278
Q

warfarin- increased INR

A

ginger, garlic, feverfew

279
Q

warfarin decreased INR

A

st. jonhs wort

280
Q

ginkgo biloba

A

leaves from trees, improves blood flow, and inhibits platelet activating factor, dementia, HSN, GI side effects
• Interacts with Coumadin, and antiplatelts and insulin

281
Q

ginseng

A
  • several types but the root is active part. Improve cognition, control DM2
    • Adverse- nervousness, insomnia, excitation, palpitations, lowers blood glucose, alters immune function
    • Interactions- antidiabetic drugs, warfarin
282
Q

echinacea

A

purple cornflower
• Indirect antiviral activity, stimulates immune system
• Reduce symptoms of viral URI if started when symptoms apprear.
• Allergic reactions, fever, nausea, vomiting, unpleasant taste, dizziness
• Drug interactions- immunosuppressants and biologics

283
Q

what should you not do before surgery

A

take supplements

284
Q

who takes the most supplements

A

women with higher education that tend to take more pharmaceuticals and want to feel in control of their health

GI Drugs (1 decks)

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