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Year 3 > Block 32 PPT > Flashcards

Block 32 PPT Flashcards

1
Q

GI bleed with melaena?

A
  • 1st: fluids via cannula - IV fluid resus
  • compound sodium lactate/ Hartmann’s solution
  • or sodium chloride 0.9% solution
  • blood transfusion
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2
Q

investigation for a GI bleed w melena?

A
  • definitive: endoscopy
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3
Q

management of an ulcer?

A
  • Pantoprazole first IV as a bolus and then IV infusion
  • PPI
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4
Q

drugs to withhold in a hypotensive patient?

A

rampiril and amlodipine

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5
Q

gastroduodenal mcusoal injury

A
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6
Q

Gastroduodenal mucosal injury mechanism?

A
  • inhibition of COX -> reduced GI protection through reduced prostanoid secretion
  • prostanoids stimulate mucus secretion and mantain gastric blood flow
  • promote platelet aggregation
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7
Q

test for H pylori?

A

CLOtest

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8
Q

drug therapy for H pylori eradication?

A
  • Lansoprazole
  • amoxicillin
  • clarithromycin - macrolide
  • metronidazole - anaerobes
  • combination antibiotics used to avoid selecting for resistance
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9
Q

lansoprazole in H pylori eradication therapy?

A

to raise pH, H pylori thrive in acidic environments

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10
Q

H pylori eradication for penicillin allery?

A

clarith and metronidazole

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11
Q

H pylori eradication when there isn’t a penicillin allergy?

A
  • no allergy: amoxicillin plus either clarith or metronidazole as a first line
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12
Q

clarithromycin + ? increases risk of hypotension

A

amlodepine

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13
Q

clarithromycin can’t be prescribed with? due to risk of rhabdomyalysis

A

simvastatin - statins

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14
Q

bulk forming laxatives?

A

isphalga husk

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15
Q

osmotic laxatives?

A

lactulose and macrogols

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16
Q

irritant and stimulants (constipation)?

A

bisacodyl, docusate laxatives

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17
Q

(constipation) - faecal softners?

A

co-danthrusate and docusate sodium

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18
Q

which laxatives are safe in pregnancy?

A
  • senna (stimulant laxative)
  • docusate (stimulate)
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19
Q

which constipation drugs are suitable for the elderly or for the terminally ill with opioid induced constipation ?

A
  • bisadocyl
  • co-danthramer
  • co-danthrusate
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20
Q

what is lactulose good for?

A
  • good for hepatic encephalopathy related constipation
  • broken down into lactic acid which neutralises ammonia from bacteria
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21
Q

laxative choice?

A
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22
Q

anti-diarrhoeals?

A
  • codeine phosphate - opiod
  • diphenoxylate - binds to mu receptors without causing a central effect
  • loperamide - opiod with no central affect
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23
Q

pathophys of IBS?

A
  • visceral hypersensitivity: common
  • exaggerated resp to cholecystokinin
  • altered resp to meal injection
  • increased bowel motility and low grade inflammation
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24
Q

RF for pathophys?

A

psychological stressors: anxiety, stress, depression

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25
Q

drug classes for IBS ?

A
  • Antimuscarinics
  • antispasmodics
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26
Q

Antimuscarinics e.g.?

A
  • dicycloverine
  • propantheline
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27
Q

IBS - other antispasmodics?

A
  • mebeverine
  • peppermint oil
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28
Q

UC drug classes?

A
  • aminosalicyclates
  • corticosteroids
  • cytokine modulators
  • immunosuppressants
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29
Q

aminosalicyclates?

A
  • mesalazine
  • olsalazine
  • sulfasalazine
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30
Q

corticosteroids?

A
  • hydrocortisone
  • predinosolone
  • budenoside
    • used initiallty, to induce remission
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31
Q

cytokine modulators in IBD?

A
  • anti TNFa antibodies
  • adalimumab
  • infliximab
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32
Q

Immunosuppressants in IBD?

A
  • azathioprine
  • methotrexate
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33
Q

Ab used in IBD?

A

metronidazole

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34
Q

Biologics for IBD - be careful of?

A

latent TB

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35
Q

Proctitis/ left sided IBD?

A
  • localised therapy
  • e.g.e enema
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36
Q

when giving high dose steroids, protect?

A
  • when giving high dose steroids: protect GI using PPIs and protect bones using bisphosphonates
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37
Q

2 serious interactions of azathioprine?

A

allopurinol and febuxostat which slow the elimination of 6-MP by inhibiting xanthine oxidase

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38
Q

what needs to be measured before azathioprine can be prescribed?

A

TPMT levels

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39
Q

Infilimab mechanism?

A
  • high spec for TNF-a, inhibits the binding of TNFa to receptors, neutralizing its activity
  • infliximab can also stimulate apoptosis of activated lymphocytes in gut mucosaa
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40
Q

adalimumab mechanism?

A

TNF-a inhibitor

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41
Q

Tx of C diff associated diarrhoea?

A

vancomycin

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42
Q

pain pathways?

A
  • tissue injury leads to release of inflammatory mediators w nonciceptor stimulation
  • pain impulses transmitted to the dorsal horm of the SC where they contact 2nd order neurons that deccussate
  • ascend via the spinothalamic tract to the RAS and thamus
  • pain localization occurs at somatosensory cortex
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43
Q

peri-operative pain management options?

A
  • opiods
  • bupivacaine
  • paracetamol
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44
Q

acute side effects of opiods?

A
  • nausea, flushing/ sweating,
  • hypotension,
  • urticaria,
  • myoclonus/ muscle rigidity.
  • resp depression,
  • visual distrubance
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45
Q

opiod antagonist?

A
  • naloxone (competitive antagonist)
  • but it has a shorter half life than most opiods so enough needs to be given to correct respiratory rate - resus dose
  • IV dose, IM if IV not feasible
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46
Q

bupivacaine?

A
  • sodium channel blocker
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47
Q

paracetamol?

A

acts on spinal receptors through action of its breakdown product NAPQI acting on TPRA1 receptors

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48
Q

vomiting center?

A
  • nucleus of tractus solitarius
  • H1, M1, NK1, 5-HT3
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49
Q

5-HT3 receptor antagonist?

A

ondansteron

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50
Q

ondansteron works on ? receptors?

A
  • 5-HT3 antagonism peripherally and chemoreceptor trigger zone
  • preventative
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51
Q

ondansteron causes?

A

QT interval prolongation

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52
Q

drugs for post op nausea and vomiting - steroids?

A
  • dexamethasone
  • prevantative
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53
Q

anticholinergic used in post op nausea and vomiting?

A
  • scopolamine
  • preventative
  • sedating, not to be used in patients w narrow angle glaucoma
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54
Q

neurokinin receptor antagonist used in post op nausea and vomiting?

A
  • aprepitant
  • blocks neurokinins effect at receptor site
  • preventative
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55
Q

metoclopramide and domperidone both cause?

A

QT prolongation

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56
Q

metroclopramide?

A
  • acute dystonia espec in young women
  • procyclidine hydrochloride can be given for acute dystonia
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57
Q

domperidone?

A
  • doesn’t cross BBB so doesn’t cause same dystonic reactions as metroclopramide
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58
Q

co-amoxiclav?

A
  • clavaunic acid and amoxicillin = to inhibit beta lactamase in bacteria
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59
Q

vomiting, not eating for several days, bowel cancer ->

A

think bowel obstruction

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60
Q

isotonic fluids?

A
  • sodium chloride
  • compound sodium lactate (Hartmann’s solution)
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61
Q

mixed fluids?

A
  • mixtures w Na + glucose e.g. glucose saline
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62
Q

glucose containing fluids?

A
  • 5% glucose isotonic
  • 10, 20,50% are hypertonic
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63
Q

50% glucose can cause ? as a side effect

A

if 50% glucose gets out of the cannula will cause an area of skin necrosis

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64
Q

how much hartmans solution can be given?

A
  • up to 2L of either Hartmann (contains K+) or NaCl fluids can be given
  • give 500ml fluid at a time
  • fluid resus algorithm >
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65
Q

why is harmann’s preferred to sodium chloride?

A
  • Hartmanns is better than sodium chloride bc less risk of hyperchloremic metabolic acidosis bc NaCl comtains more Cl- than plasma
  • Hartmanns lactate acts as a buffer & has a higher pH
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66
Q

maintenance fluids?

A
  • 0.9% sodium chloride
  • hartmanns
  • 5% glucose
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67
Q

pharmacokinetics =

A

what the body does to the drug

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68
Q

pharmacodynamics =

A

what the drug does to us

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69
Q

volume of distribution =

A

amount of drug in the body (dose)/ plasma conc of drug

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70
Q

massive volume of distribution tells us?

A
  • massive VoD tells u that the drug is conc somewhere usually binding to proteins or in fat reserves
  • vol of 5L in circ only
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71
Q

amount in body =

A

volume of distrubution x plasma concentration

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72
Q

usually takes how many half lives to reach a steady state?

A
  • usually takes 5 half lives to reach the steady state then the conc comes up and down to the steady state level
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73
Q

larger vs small VoD?

A
  • larger volume of distribution means less peaks in conc bc it distributes out into thr wider space of the body
  • small VoD (water soluble drugs) more peaks
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74
Q

Long half life generally requires a longer?

A

dosing interval

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75
Q

phase 1 of a clinical trial?

A

drug tested in healthy ppl

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76
Q

phase 2 of a clinical trial?

A

drug tested in healthy ppl to find the right dosing interval

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77
Q

phase 3 of a clinical trial?

A

drug used in intended patient group against placebo

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78
Q

phase 4 of a clinical trial?

A

pick up rarer side effects when its being used in the population

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79
Q

drugs that require monitoring?

A
  • gentamicin is given IV and then monitored (6-14 hours after dose blood sample is taken)
  • lithium requires monitoring - above 3.5mmol/L regarded as a medial emergency
  • has a narrow therapeutic index (short window between it working and it becoming toxic)
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80
Q

oral availability of drugs?

A
  • oral availability = the fraction of drug that reaches the systemic circulation after oral ingestion
  • oral availability is determined by absorption and first pass metabolism
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81
Q

first pass metabolism?

A
  • FPM: pre-systemic drug metabolism
  • occurs in the brush border of gut wall, portal vein or liver
82
Q

ionised drugs don’t ? easily?

A
  • ionised drugs don’t cross the PM easily
  • ionised drugs are more water soluble so are more easily excreted
83
Q

what can help aspirin excretion in the case of aspirin overdose?

A
  • alkalisation of urine using sodium bicarb in the case of aspirin overdose - this favours excretion of aspirin in the urine
84
Q

physiochemical factors affecting drug abs?

A
  • pH partition theory
  • lipid solubility
  • salts
  • crystal form
  • drug stability and hydrolysis in GIT
  • complexation - does it concrete together with other drugs
  • abs
85
Q

100% oral bioavailability would be when?

A

when u get the same conc when taking the drug orally as injecting the drug

86
Q

how does cirrhosis affect drug metabolism?

A
  • cirrhosis increases bioavailability by affecting FPM
  • Avoid oral preparations in the cases of hepatic impairment
87
Q

IM injections can cause issues due to?

A
  • IM injections can cause issues due to coagulopatheis assoc w hepatic impairment or those on AC
88
Q

oral drugs peak ? bc they have to be?

A
  • Oral drugs peak slow bc they have to be abs
  • giving an intial larger loading dose gets u in the TR quicker, then give smaller maintenance doses
89
Q

hypoproteinaemia due to liver disease causes a higher ?

A
  • proportion of free drug
90
Q

physiological liver function?

A
  • fenestrations in the endothelium, allows ready access to ECF
  • rapid diffusion across the space of Disse
  • brush border on hepatocytes allows rapid uptake
91
Q

what happens in cirrhosis?

A
  • fenestrations lost
  • diffusion across space of Disse reduced
  • brush border lost
  • enzyme activity reduced
  • intrahepatic vascuar shunts may reduce perfusion of hepatocytes
92
Q

which drug is heavily renally excreted?

A

codeine

93
Q

which drug is heavily hepatically metabolised?

A

fentanyl

94
Q

first order kinetics?

A
  • amount of drug that is eliminated per unit time is proportional to the drug conc - so a constant % of the drug is eliminated per unit time
95
Q

zero order kinetics?

A
  • amount of drug eliminated is constant per unit time and not related to conc - no matter how much drug there is, body can only eliminate a certain absolute amount
  • this is saturation kinetics
96
Q

when can drugs move from first to zero order kinetics?

A
  • drugs can move from first to zero order kinetics when the enzyme metabolizing them becomes saturated
97
Q

first vs 0 order kinetics

A
98
Q

most drugs in the therapeutic range are in which type of kinetics?

A
  • first order
  • exceeding a certain dose can cause them to move to 0 order - small changes in dose can largely inc blood levels
99
Q

GI side effects of chemotherapy?

A
  • diarrhoea, sore mouth, nausea and vomiting
100
Q

bone marrow side effects of chemo?

A
  • myelosuppression, can lead to anemia, neutropenia and thrombocytopenia
101
Q

tumour lysis syndrome from cancer chemo?

A
  • rapid breakdown of malignant cells can cause
  • hyperuricaemia,
  • hyperkalaemia and high phosphate
  • hypocalcaemia with renal damage/ arrhythmias
102
Q

capecitabine is used for?

A
  • CRC, gastric cancer and breast cancer
103
Q
A
104
Q

mercaptopurine?

A

purine antagonist

105
Q

what makes sure that chemotherapy is prescribed safely?

A
  • electronic prescribing helps make sure that chemotherapy is prescribed safely - keeps a record of what has been prescribed and makes it so that only certain users can prescribe it
106
Q

Oxaliplatin drug class?

A
  • alkylating agent - inhibits DNA synthesis
  • platinum compound
107
Q

what are the platnium compounds?

A
    • oxiplatin, cisplatin, carboplatin - drugs ending in platin
  • used for solid malignancy
108
Q

side effects of chemo?

A
  • severe nausea and vomiting
  • nephrotoxicity (hydration is esssential)
  • ototoxicity
  • peripheral neuropathy
  • myelosuppression
109
Q

if chemo is given via cannula, what can happen?

A

extravasation

110
Q

anastrazole?

A
  • aromatase inhibitor
  • given to post menopausal women
  • aromatase converts test produced by the ovaries into oestradiol
111
Q

why is anastrazole only given to post menopausal women?

A
  • giving anastrazole to a pre-menoposal woman would trigger release of more FSH meaning more oestrogen production - pointless
  • post-menopausal women have generally stopped producing oestrogen but still some test and oestrodiol (conversion in peripheral tissues)
  • androgens -> estradiol by aromatase in the breast tissue
  • this conversion is enough to stimulate an oestrogen responsive BC
112
Q

general side effects of anastrazole?

A
  • drowsiness - affects ability to drive or operate machinery
  • asthenia
  • hot flushes
  • hair thinning
113
Q

steven jonson syndrome?

A
  • severe skin reaction, mucous membranes freq involved
  • blisters. fever, flu like syndromes
  • can progress to sepsis and multi organ failure untreated
114
Q

tamoxifen?

A
  • SERM - selective estrogen receptor modulator
  • completitively binds at the oestrogen receptor inhibiting transcription of oestrogen receptive genes
  • strongly antiestrogenic on mammary epithelium, used in prevention and Tx of BC
115
Q

who can tamoxifen be used in?

A
  • Effective in pre and post menopausal women w ER+ breast cancer
  • once a day for 5 yrs
116
Q

tamoxifen interacts with?

A
  • WARFARIN through inhibition of CYP3A4 increasing risk of bleeding
  • SSRIs e.g. fluoxetine possibly inhibit metaboism of tamoxifen
117
Q

signs of leukemia?

A
  • sig raised leucocytes - raised in 40-50s rarely occurs w infection
  • marked leukoblastosis
118
Q

stages of leukemia treatment?

A
  1. induction
  2. consolidation
  3. maintenance
119
Q
  1. induction (leukemia treatment)
A
  • intestive therapy aimed at destroying as many leukemia cells as possible and achieving remission (no leukemia cells on bone marrow biopsy)
  • lasts 4-6 weeks
120
Q
  1. consolidation (leukemia treatment)
A
  • aimed at remission and preventing spread
  • often involves intra-spinal injections then tablets (looks for cancer cells hiden behind BBB)
  • usually a month and a half
121
Q
  1. maintenance in the treatment in leukemia?
A
  • lasts 2 years (girls) or 3 yrs (boys) from the start of interim treatment
  • regular tablets +/- injections
122
Q

Chemotherapy combination of drugs ?

A
  • reduced development of drug resis
  • rapidly dividing so can undergo new mutations which are advantageous
123
Q

cyclophosphamide mechanism?

A
  • alkylating agent causing cross linking between DNA strands leading to cell apoptosis
  • binds to DNA preventing synthesis
  • binds to proteins blocking DNA repair processes
124
Q

side effects of cyclophosphamide?

A
  • impaired fertility in the future
  • bone marrow suppression and neutropenia
  • can develop other malignancies like AML or bladder cancer
125
Q

reducing risk of bladder cancer from cyclophoshamide?

A
  • bladder cancer risk reduced by giving mesna (mercaptoethane sulphonic acid) prior to treatment
  • causes haemorrhagic cystitis - mesna
126
Q

vincristine mechanism?

A
  • vinca alkaloids
  • miotic inhibitors
  • binds to tubulin molecules preventing formation of microtubules preventing chromosome separation
  • eventually leads to cell death
127
Q

? vincristine is fatal

A
  • intrathecal vincristine is fatal
128
Q

vincristine is used for?

A

leukemias

129
Q

doxorobucin drug class?

A
  • cytotoxic antibiotic
  • anthracycline
  • prevention of DNA double helix from being resealed
130
Q

side effect of doxorubicin?

A

dilated cardiomyopathy - can happen many yrs later

131
Q

methotrexate mechanism?

A
  • folic acid antagonist
  • immunosuppressant
132
Q

uses of methotrexate?

A
  • DMARD used in RA and psoriasis
  • used in abortion and molar pregnancy
133
Q

methotrexate toxicties?

A
  • nephrotoxic, hepatotoxic, bone marrow toxic
  • requires reg monitoring
134
Q

oral mucositis ?

A
  • sore mouth is mostly associated with fluorouracil, methotrexate and anthracyclines
  • saline mouthwashes
135
Q

hyperuricaemi may be present in?

A
  • may be present in high-grade lymphoma and leukaemia, can be markedly worsened by chemotherapy and is associated with acute renal failure
136
Q

treatment of hyperuricaemia?

A
  • allopurinol
  • or febuxostat
  • rasburicase
137
Q

which chemotherapy agents cause bone marrow suppression?

A
  • All cytotoxic drugs exceptvincristine sulfateandbleomycincause bone-marrow suppression.
  • This commonly occurs 7 to 10 days after administration
138
Q

drugs used for low risk of emesis from chemo?

A

dexamethasone or lorzepam

139
Q

high risk of emesis from chemo Tx?

A
  • serotonin antagonist with dexamethasone
  • neurokinin receptorantagonistaprepitantis effective
140
Q

treatment of methotrexate induce mucositis or myelosuppression?

A
  • Folinic acid
  • (given as calcium folinate) is used to counteract the folate-antagonist effects- methotrexate-induced mucositis or myelosuppression (‘folinic acid rescue’).
141
Q

urethral toxicity from chemo?

A
  • from cyclophosphamide and ifosfamide
  • mesna used to treat
142
Q

acute pain Mx ladder?

A
  • step 1: paracetamol
  • step 2: swap paracetamol for ibuprofen
  • if the person can’t take NSAIDs, use weak opioids like coedine phosphate
  • step 3: add paracetamol to the ibuprofen or weak opiod
  • step 4: continue with paracetamol and replace ibuprofen with other NSAID like naproxen
  • step 5: add weak opiod to the paracetamol and/or nSAID
143
Q

WHO analgesic ladder

A

Step 1: non opiods - NSAIDs, paracetamol

Step 2: weak opiods - codeine

Step 3: strong opiods

144
Q

chronic pain management?

A
  • Acceptance and commitment therapy
  • CBT
  • acupuncture or dry needling
145
Q

antidepressants used in chronic pain management?

A
  • antidepressants: amitriptyline, citalopram, duloxetine, fluoxetine, paroxetine, sertraline
146
Q

lifestyle advice for chronic pain?

A
  • diet, weight, alcohol use, smoking, exercise for improving health
147
Q

neuropathic pain Mx?

A
  • trycyclic antidepressant or with antiepileptic drugs
  • amitriptyline and pregabalin are effective for neuropathic pain
  • can be used in combination if there’s an inadequate response to either drug
148
Q

what else can be used for neuropathic pain>

A
  • nortriptyline
  • gabapentin
  • opiod analgesics: tramadol, morphine, oxycodone
149
Q

management of drug induced especially opiate induced vomiting ?

A
  • anti-emetics e.g. cyclizine, ondansteron, prochlorperazine
  • ondansteron has the advantage of not producing sedation
150
Q

management of motion sickness?

A
  • hycosine hydrobromide
  • anti-histamines
151
Q

what are the less sedating antihistamines?

A

cinnarizineand cyclizine

152
Q

more sedating antihistamines?

A

include promethazine hydrochloride andpromethazine teoclate.

153
Q

management of post op nausea and vomiting

A
  • 5-HT3 receptor antagonists e.g. ondansteron
  • dexamethasone
  • droperidol
  • cyclizine
  • prochlorperazine
154
Q

cytotoxic drug induced vomiting?

A
  • 5-HT3 antagoist
  • dexamethasone may also be needed
  • delayed symptoms: dexamethasone is the drug of choice, used alone with metoclopramide hydrochloride - high risk of neuro side effects
155
Q

drugs used for pregnancy induced nausea and vomiting?

A
  • cyclizine
  • prochlorperazine
  • promethazine hydrochloride
  • ondansteron
156
Q

Supplementation

hyperemesis gravidrarum management?

A
  • severe/ persistent hyperemesis gravidrarum -> supplementation of thiamine to reduce risk of Wernicke’s encephalopathy
157
Q

indications for IV fluids?

A
  • management of adult patient requiring IV fluid resus - including treatment of hypovolaemia
    • patient NBM e.g. bowel obstruction, ileus, post op
  • vomiting or severe diarrhoea
  • hypovolaemic as a result of blood loss
158
Q

Types of fluids/

A
  • crystalloids: solutions of molecules in water (e.g. solutions of small molecules in water, Hartmann’s, dextrose)
  • colloids: solutions of larger organic molecules e.g. albumin, gelofusine
  • crystalloids superior for initial resusicitation
159
Q

hartman’s solution?

A
  • sodium chloride 0.9%
  • used for resus/ maintenance
160
Q

sodium chloride 0.18%

A
  • dextrose
  • for maintenance
161
Q

Resus - fluids?

A
  • 500ml bolus of crystalloid soidum - NaCl/ Hartmannls over less than 15 mins
  • if patient still has evidence of hypovolaemia - give further 250-500ml bolus
  • repeat until you’ve given 2L then seek expert help
162
Q

fluid resus in more complex patients?

A

If patients havecomplex medical comorbidities(e.g. heart failure, renal failure) and/or areelderlythen you should apply a morecautious approachto fluid resuscitation (e.g. giving fluid boluses of 250 ml rather than 500 ml and seeking expert help

163
Q

IV fluids indicated for the management of an adult patient with hypokalaemia.

A
  • potassium chloride with sodium chloride IV infusion is the initial treatment for correction of severe hypokalaemia when enough potassium can’t be taken by mouth
  • initial potassium replacement shouldn’t involve glucose transfusions bc glucose can cause a further decrease in plasma potassium conc
164
Q

relationship between drug dose and resp?

A
  • describes the magnitude of theresponseof anorganism, as afunctionof exposure (ordoses) to astimulusorstressor(usually achemical) after a certain exposure time
165
Q

changes in receptor sensitivity?

A
  • when receptor sensitivity changes, the same conc of a drug will produce a greater or lesser physiological response
  • changes in sensitivity occur e.g. after prolonged stimulation of cells by agonists, the cell becomes refractory to further stimulation - desensitisation
166
Q

TI?

A
  • measurement of the relative safety of a drug
  • The therapeutic index (TI) isthe range of doses at which a medication is effective without unacceptable adverse events.
167
Q

Explain receptor desensitisation?

A
  • underlying mechanisms may involve receptor changes like phosphorylation or the receptor may be concealed within the cell so that it’s no longer exposed to the ligand
168
Q

tolerance?

A
  • tolerance - e.g. accelerated metabolism
  • tolerance leads to increasing doses of a drug being needed to produce the same effect
  • Other possible mechanisms are a decrease in binding affinity between a drug and receptor and a decrease in the number of receptors
169
Q

impact of pharmacokinetics on drug dosing schedule?

A
  • drug half life can be used to determine dosing schedule and the time to attain a steady state concentration
  • short half life requires more frequent dosing
170
Q

common medicines that are likely to cause harm to patients with impaired liver function ?

A
  • rifampicin and fusidic acid are excreted in bile unchanged
  • hypoproteinaemia - increased toxicity of highly protein bound drugs like phenytoin and prednisolone
  • reduced clotting - warfarin
171
Q

drugs that can cause harm to ppl w impaired liver function - hepatic encephalopathy?

A
  • hepatic encephalopathy - all sedative drugs, opioid analgesics, those diuretics that produce hypokalaemia, and drugs that cause constipation.
172
Q

drugs that can harm ppl w impaired liver cuntion - fluid overload

A
  • fluid overload - oedema and ascites exacerbated by drugs that cause fluid retention like NSAIDs and corticosterouds
173
Q

First and second line in constipation?

A
  • first-line laxative: bulk-forming laxative first-line, such as ispaghula
  • second-line: osmotic laxative, such as a macrogol
174
Q

inducing remission in crohns?

A
  • glucocorticoids first line
  • mesalazine second line
  • azathioprine or mercaptopurine can be added on
175
Q

infliximab in CD?

A

infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate

176
Q

maintaining remission in crohns?

A
  • azathioprine or mercaptopurine first line
  • stop smoking
177
Q

Inducing vs remaining remission in CD?

A
  • Inducing - steroids
  • maintaining - azathioprine/ mercaptopurine
178
Q

inducing remission in UC - procitis?

A
  • topical (rectal) aminosalicyclate
  • add oral amino if this doesn’t work
  • add topical/ oral steroid if this doesn’t work
179
Q

Left sided colitis - inducing remission?

A
  • topical aminosalicyclate
  • 2: high dose oral amino
  • 3: add steroid
180
Q

inducing remission in extensive UC?

A
  • topical amino and a high dose aminosalicyclate
181
Q

severe colitis?

A
  • should be treated in hospital
  • IV steroids are usually given first-line
182
Q

maintaining remission in UC?

A
  • proctitis: topical amino
  • left sided/ extensive: oral amino
182
Q
A
182
Q
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182
Q
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182
Q
A
182
Q
A
182
Q
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182
Q
A
182
Q

UC - Following a severe relapse or >=2 exacerbations in the past year

A

oral azathioprine or oral mercaptopurine

182
Q

Methotrexate in UC?>

A

methotrexate is not recommended for the management of UC (in contrast to Crohn’s disease)

182
Q
A
182
Q
A
182
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182
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182
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182
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182
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182
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183
Q
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Year 3 (45 decks)

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