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YEAR 3 > PHARM DECK > Flashcards

PHARM DECK Flashcards

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1
Q

gray baby syndrome

A

caused by administration of CHLORAMPHENICOL during pregnancy.

causes altered respiration, abdoninal distension, hypothermia and flaccid limbs

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2
Q

tooh discoloration

A

caused by doxycyline use in children < 12 years

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3
Q

chloramphenicol adverse effects

A
  • haematological toxicity: leukopenia, anaemia and thrombocytopenia. in worse cases can cause idiosyncratic anaemia, which results in aplastic anaemia and fatal pancytopenia
  • gray baby syndrome – caused by administration of CHLORAMPHENICOL during pregnancy.

causes altered respiration, abdoninal distension, hypothermia and flaccid limbs

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4
Q

doxycycline adverse effects and 2 key things to note affecting its absorption

A

tooth discoloration
-caused by doxycyline use in children < 12 years

  1. not to be administered with antacids or iron pills as the divalent cations can compete for absorption, leading to reduced absorption
  2. enzyme inducers such as rifampicin, phenytoin and carbamezepine increases its metabolism, leading to decreased drug concentration
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5
Q

what are the 6 protein synthesis inhibitors (antibiotic version)

A
  1. tetracyclines (doxy) - 30
  2. aminoglycosides (amikacin, gentamicin) - 30
  3. chloramphenicol - 50
  4. macrolides (erythromycin, clarithromycin) - 50
  5. lincosamides (clindamycin) - 50
  6. oxazolidinones (linezolid) - 50
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5
Q

what are the 4 groups of penicillins

A
  1. penicillin G/V
  2. penicillinase resistant (e.g. methicillin, fluoxicillin)
  3. aminopenicillins (e.g. amoxicillin, ampicillin) ++ beta-lactamase inhibitors (e.g. clauvunate)
  4. extended spectrum penicillins (got 2, carboxypenicillins and ureidopenicillins - piperacillin)
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6
Q

what are the types of betalactams

A
  1. penicillins
  2. cephalosporins
  3. carbapenems
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7
Q

what are the generations of cephalosporins

A
  1. cephalexin - GP settning
  2. cefaclor
  3. ceftriaxone, ceftizidine, cefotaxime - hospital setting
  4. cefepime
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8
Q

examples of carbapenems

A

imipenem + cilastatin (renal dehydropeptidase inhibitor, inhibiting its breakdown)
meropepnem
aseotreonam

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9
Q

pk of aminoglycosides

A

very large structure hence poorly absorbed via PO (only IV), inadequate CSF penetration and renal elimination

post antibioitc effect - is the reason why we gotta do the extended interval dosing since the drug concentration can drop to below the MIC already but there will be still residual bacteria

concentration dependent

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9
Q

examples of aminoglycosides, moa and selectivity

A

amikacin
gentamicin

bacteriocidial
30S subunit, only G-s

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10
Q

key a/e of aminoglycosides and something important we gotta do

A

therapeutic drug monitorin g

nephrotoxic and ototoxic (same as glycopeptides)

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11
Q

sulphonamides MOA and the 3 examples

A

bacteriostatic inhibiting folic acid synthesis via inhibitng the enzyme dihydropteroate synthase

  1. sulfamethoxazole + trimethaprim (downstream of the THF synthesis, inhibiting dihydrofolate reductase) = co-trimaxole - for pnuemocystis jiroverci

2.sulfapyridine + mesalazine = sulfasalazine (ibd)

  1. suladoxine + pyrimethamine = fansidar for malaria
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12
Q

sulphonamides important a/e and pk

A

bone marrow suppression

increasing warfarin, sulfynourea and phenytoin concentrations by competeign with them for the plasma binding protein (? albumin i assume)

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13
Q

quinolones/fluouroquinolones MOA and some eXamsPLES

A

inhibits the topoisomerases
- bacterial DNA gyrase (topo II) for G-s
- topo IV for G+s

ciprofloxacin
levofloxacin

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14
Q

key a/e for quinolones

A

ACHILLES TENDON RUPTURE and tendinitis inpatients > 60y, solid organ transplant patients or on corticosteroids

QT prolongation (moxifloxacin)
pseudomembranous coliis (cipro)

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15
Q

is quinolones (cipro) enz inducer or inhibitor

A

enz inhibiotrs
1A2 inhibitor, causing increased concentratino of THEOPHYLLINE

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16
Q

why is probenecid important in the setting of antibiotics

A

it is a uricosuric
so it inhibits the tubular secretion of penicillin increaisng its levels / conc

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17
Q

chloramphenicol pk

A

prodrug, metabolised by esterases in the body
inactived by acetyltransferases (resistant mechanism)

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18
Q

examples of macrolides and their PKS

A

clarithromycin
erythromycin
azithromycin

clari/ery - cyp 450 inhibitrs
clari/ery/azi - pgp inhiibtors (increasing concentrations of doacs and digoxin, increasing bleeding risk)

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19
Q

key a/e of macrolides

A
  • QT prolongation (as with fluoroquinolones)
  • hepatotoxicity (cholestatic hepaptis with erythromycin)
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20
Q

what can clindamycin be used for

A

almost all G-s are resistant, so only for G+sand anaerobes

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21
Q

what can linezolid be used for

A

G+ organisms
poor activity against G-

used of rtreatment of infections caused by MDR organisms, e.g. penicilllin resistant s. pneumoniae, MRSA, VRE

should not be used if other antibiotics can be used

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22
Q

major side effects of linezolid

A

SEROTONIN syndrome (MAO-i), when administered with SSRIs
BM suppresion
Peripheral neuropathy, optic neuritis and lactic acidosis
Pseudomembranous colitis

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23
is linezolid bacteriostatic or bacteriocidial
bacteriostatic - staph, enterococci bactericidial - strep
24
examples of glycopeptide and their MOAs
inhibiting the transglycosylase reactions, inhibiting bacterial cell wall synthesis, hence bacteriocidial vancomycin teicoplanin G+ only G- are resistant
25
importnat (many) a/es of glycopeptides
hypersensitivty reactions (REDMAN SYNDROME) flushing, tachycardia and hypotension - NB not really a allergic reaction, but direct toxic effects on the mast cells instead nephro and ototoxicty (as with aminoglycosides) neutropeia
26
what causes the RED MAN SYNDROME
vancomycin glycopeptide
27
what casuses the SEROTONIN SYNDROME
linezolid
28
what causes peripheral neuropathy, optic neuritis and lactic acidosis
linezolid
29
what causes bone marrow suppresion
linezolid, sulfonamdies
30
what is sulphonamides metabolised by
acetylation
31
therapy for hyperPRL
1 DA agonists (carbegolline and bromcriptine) 2 Transphenoidal resection (but only 30% cure rate)
32
Carbegolline, bromcriptine use
DA agonists binding to D2 receptors in pitruitary lactotrophs, decreasing PRL secretion for hyperPRL
33
SIde effects of carbegolline and bromcriptine
- N&V*D use at night - gambling and sex addiction - avlvaular heart diseases bromcriptine shorter half life than carbegolline (2 pills a weak) and not assciated with valvular heart disease. pregnancy bromcriptine beteer tho both can
34
how to measure acromegaly
OGTT - give glucose, which will increase the somatostatin secretion from hypothalamus, which is supposed to suppress GH. normal/rise in GH suggests
35
treatment for high GH
1. transphenoidal resection (gold standard) + 1 radioteherpay 2. frist line: somatostatin analogues (SSA) - octreoride, lanreotide second line: pegvisomant seconda line alt: SSA + DA agonist (e.g. carbegoline)
36
octeoride, lanreotide pegvisomant use and adverse effects
1. somatostatin analogue, decreases GH secretion and also acts to suppress pancreas endocrine and exocrine functions A/Es: N&V*faltulence, cholelithiasis and suppression of glucose metabolism + injection site (SC) 2. GH analogue, but bind and block the receptor, so GH antagonist. A/E: hepatitis so monitor the LFTs
37
therapy to manage Cushing's disease
1. TSS 2. Medical therapy targeting the - Pituitary (inhibting ACTH secertion, e.g. carbegolline, pasireotide - Adrenals - inhibitnig steroidogenesis (like metyrapone, ketoconazole), or adrenolytics (miltotane) Miltotane inhibits the 11-B hydroxylase, required for steroid generation - GR antagonists, e.g. milfepristone
38
what investigations required for diagnosis and screening of Cushing's disease
screening: 1. low dose DMT - 1mg at 11pm and measure cortisol before 9am 2. 24h urinary cortisol levels 3. Midnight salivary cortisone levels diagnosis: - plasma ACTH - high dose DMT ( can differentiate the pituitary or ectopic causes, e.g. from SCLC) - CRH stimulation test
39
what is cushings disease and syndrome CUSHINGOID is what
cushing disease is the ACTH-secreting tumour nad cushing syndrome is the effect of increased ACTH stimualtion on the adrenasl increasing the cortisol levels Cushingoid symptoms - Cataracts - Ulcer - Striae/skin thinning - Hirsutism, hyperL, hypertension - Infection - Necrosis (of femoral head) - GIT disturbance / Glucose - Obesity / Osteoporosis - Immunosuppression - Diabetes / depression
40
what is primary adrenal insufficiency
caused by addison's disease (autoimmune destruction of the adrenal glands, leading to decreased MC and GC) high ACTH, but low cortisol/adosterone autoimmune antibodies against the21-hydroxylase or others like genetic AIRE gene, post infection or meningitis
41
symptoms of addisons'
1. elevated ACTH = pigmentation (buccal / mucosal) 2. hypoGC d 3. hypoMC = hyperK (met acidosis), hypoNa FBC can show anaemia, lymphocytosisand oesinophilia due to lower GC and MC levels
42
diagnosing addison's
1. plasma ACTH and cortisol 2. Synacthen stmulation test (ACTH stimulation) then measure the cortisol lvesl
43
treatment of addisions
1. GC replacement - hydrocortisone (insomnia) 2. MC replacement - fludrocortisone (hypert, hypoK, fluid retention) emergency kit of 100mg IM hydrocortisone and steroid atlert card
44
what can cause excess MC but low ACTH
1. Conn's - MC-producing adrenal carcinoma - elevated aldosterone, suppressed renin 2. bilateral adrenal hyperplasia - adrenal MRI tro, adrenal vein sampling for aldosterone levees
45
investingations for conn's
elevated aldosterone, suppressed rening presenting as hypoK (met alk), hyperNa, resistant hypertension and fluid retention plasma renin activty (low) aldosterone renin ratio (ARR) - high aldosterone, low rening, suggesting primary hyper ald
46
treatment for conn's
1. spirinolactone 2. epleronone both act to block AR-mediated actions, e.g. Na+ reabsorption and K+ secretion reduced. Increased K+ levels. NB can cause breast complaints, e.g. men gynaecomastia, C/I in pregnancy as it leads to feminisation ofo foetus
47
what is pheochromocytoma and what does it cause
chromaffin cells of medulla adrenaline secreting
48
diagnosing pheochromocytoma
1. plasma free metanephrines 2. 24h catecholamine collection 3. CT / MRI for mass NB classic triad: episodic headaches, sweating, tachycardia 10% rule: 10% malignany, 10% bilateral, familial and extra-adrenal
49
What are the drug treamtents for Parkinson's disease
By enhancing dopamine activity 1. levodopa + dopadecarboxylase inhibitor (carbidopa) 2. dopamine receptor agonists (ergot / non-ergot derived) ergot - e.g. carbegoline, bromcriptine ; non-ergot - pramipexole 3. MAO-Bi - e.g. selegiline 4. COMT inhibitors - e.g. entcaptone 5. Amantadine, Apomorphine, Adenosine A2A receptor antagonists
50
which is centrally acting mnuscle relaxant - dantrolene - baclofen - diazepam
Used for relief of chronic muscle spasms / spasticity associated with MS Dantrolene acts peripherally Diazepam, Baclofen acts centrally (binding to GABA receptors on afferent nerve terminal, reducing NT release)
51
what are the side effects of ocreolizumab
- infusion related reactions (pretreat with antihistamines and steroids) - infections (e.g. RTIs, oral herpetic infections) - neoplasms
52
53
why is ocreolizumab different from the other MS drugs
most MS drugs (e.g. natalizumab and fingolimod) target teh T cells, but ocreolizumab is a humanised mAb specifically depleting CD20 levels, preventing B cell reconstituition and pre-existing humoral immuntity. most target relapsing remitting MS, but ocreolizumab can also target primary progressive MS trials: OPERA, ORATOARIO
54
how often is ocreolizumab administered
6 monthly
55
what is ocreolizumab indicated for
RRMS Pri progressive MS
56
which MS drugs have autoimmune side effects
Alemtuzumab, human mAb, has immunomodulatroy effects. autoimmune side effects include ITP, thyroid dysfuction adn nephropathies
57
what is fingolimod MOA
fingolimod is a spingosphine-1 phosphate receptor modulator, preventing lymphocyte from exiting the LNs, decreasing recirculation of autoregressive lymphocytes, decreasing inflammatory reaction related to demyelination. indicated for highly acitve MSwh
58
what is the S/E of fingolimod
- infections - neoplasms (BCC, melanoma) - bradycardia, AV heart blockw
59
what study supports fingolimod
TRANSFORM Study demonstrated the superiority of fingolimod wrt to relapse rates and MRI outcomes in paitents with MS as compared to intramuscualr injections of interferon beta 1a
60
which MS drug i s the first oral MS drug
fingolimod
61
what is one key side effect of natalizumab
- hypersensitivity but also - Progressive multifocal leukoencephalopathy (PML), 1 in 1,000 with significantly mortality
62
can antimuscarinic agents be used to treat PD?
NO! Used to reduce the effects of central cholinergic excess occurring from the dopamine deficiency. NOT indicated for PD, but useful in drug-induced Parkinsonism (e.g. antipsychotics, metoclopramide) Not for PD as they are less effective than dopaminergic drugs and are associated with cognitive impairment S/E: worsens tardive dyskinesia
63
which is an non-ergot derived dopamine receptor agonist? - bromcriptine - carbegoline - lisuride - pergolide - pramipexole
pramipexol (the preferred ones)
64
why are ergot derived dopamine receptor agonists not preferred over non-ergot derived?
S/Es: associated with pulmonary, retroperitoneal and pericardial fibrosis (hence non-ergot > ergot) Recent studies suggesting that valvular regurgitation linked too
65
what are the common side effects of all the drugs used to treat PD?
- hallucinations / behavioural issues - orthostatic hypotension - confusion - dykinesia (levodopa)
66
how do levodopa and pramipexol differ in efficacy
pramipexole has fewer motor complications (e.g. dykinesia), but lower effectiveness in treating. levodopa associated with dykinesia, has fluctuating response (on and off times) with end of dose deteriortationa dn decrease in length of on time after a few years (like 4) pramipexole has neuropsych side effects, so contraindicated with dementia as it can produce hallucinations. may be first line, but in advanced can alos be used in combinations with levodopa
67

YEAR 3 (10 decks)

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