CNS Flashcards
(134 cards)
1
Q
What are central analgesics?
A
drugs which relieve pain by central action without impairing consciousness or other sensations
2
Q
What are central analgesics classified into?
A
- non-steroidal anti-inflammatory drugs (NSAIDs) = analgesic antipyretic drugs
- opioid (narcotic) analgesic drugs
3
Q
What do NSAIDs do?
A
- relieve low intensity pain (e.g. headache, neuralgia, myalgia)
- act subcortical on thalamus
- no euphoria or drowsiness
- non addictive
- no tolerance
4
Q
What do opioids do?
A
- relieve any type of pain (except itching)
- cortical and subcortical
- produce euphoria and addiction
5
Q
What are peripheral analgesics?
A
include physical protectives, local and surface anaesthetics, obtundents, astringents and counter-irritants
6
Q
What is the function of NSAIDs?
A
inhibit COX (cyclo-oxygenase) enzyme which inhibits prostaglandin (PG) synthesis
7
Q
What are the types of COX enzymes and their function?
A
- COX 1: mainly constitutive (present normally in tissue regulation in physiologic functions), responsible for forming protective PGs in GIT and kidney
- COX 2: inducible in inflammation, constitutive in endothelium and kidney
- COX 3: newly discovered and under investigation, mainly CNS
8
Q
What are some characteristics of PGs?
A
- made in cells in body normally
- stimulate nerve impulse and pain sensation
- induce fever
- not an enzyme or hormone
- found all around the body
9
Q
What breaks down phospholipids?
A
phospholipase A2
10
Q
What is the product of phospholipid breakdown by phospholipase A2
A
- fatty acids (mainly arachidonic acid)
- glycerol
11
Q
How is prostaglandin secreted by arachidonic acid?
A
- by COX enzyme (90%)
- by lipoxygenase (LOX) enzyme which releases leukotrienes (10%)
12
Q
What happens if there is excessive leukotrienes present in the lungs?
A
bronchospasm which develops to bronchial asthma
13
Q
What is the function of leukotrienes?
A
- inflammatory mediator
- has a function in the immune system
14
Q
What are the general functions of PGs?
A
- induce pain, fever and inflammation
- contract uterus (during labour and pregnancy)
- prevent peptic ulcer (protects stomach lining)
- maintain patency of ductus arteriosus in the foetus
- increase renal blood flow
- thromboxane A2 (released from platelets) produces VC and increase platelet aggregation during injury
- prostacyclin produces VD and reduces platelet aggregation
15
Q
What are the therapeutic uses and side effects of aspirin-like drugs (NSAIDs)?
A
- analgesic, antipyretic and anti-inflammatory (paracetamol has no anti-inflammatory action)
- can be used in dysmenorrhea (pain during menstruation), patent ductus arteriosus and tocolytic (relax uterus) in premature labour
- affect platelet function and can be used as antithrombotic (decrease thrombosis and thromboxane A2)
- can induce gastric or intestinal ulcerations
- may induce bronchospasm and urticaria in susceptible patients due to increase in leukotrienes (product of LOX pathway)
- have little effect on renal function in normal subjects but may decrease renal blood flow and glomerular filtrate in renal diseases and could lead to neuropathy (they produce salt and water retention)
- use of aspirin-like drugs in pregnant women is not recommended but if there is need, aspirin is te safest anti-inflammatory while paracetamol is the safest analgesic antipyretic
- most of the NSAIDs bind firmly to plasma proteins and can displace other drugs as warfarin, oral hypoglycaemics, inducing serious drug interactions
16
Q
Why does paracetamol have no anti-inflammatory effects?
A
because it inhibits COX 3 enzyme only which works centrally
17
Q
What does antipyretic mean?
A
decrease temperature to normal
18
Q
What is the classification of analgesic antipyretic drugs?
A
- non-selective COX inhibitors
- selective COX 2 inhibitors
- selective COX 3 inhibitors
19
Q
What are examples of non-selective COX inhibitors?
A
- salicylates (aspirin)
- indomethacin
- ibuprofen
- ketoprofen
- diclofenac
- piroxicam
20
Q
What is a selective COX 2 inhibitor example?
A
celecoxib
21
Q
What is a selective COX 3 inhibitor example?
A
paracetamol
22
Q
What are the characteristics of salicylates?
A
- derived from salicylic acid which is highly irritant
- example is aspirin
23
Q
What are the pharmacokinetics of non-selective COX inhibitors?
A
- effective orally
- complete absorption in upper part of small intestine
- excreted in urine
- alkaline urine increases excretion by sodium bicarbonate
24
Q
What are the local actions of non-selective COX inhibitors?
A
- salicylic acid: keratolytic (remove dead cells), antifungal and antiseptic
- -methyl salicylate (oil of winter green): counter-irritant
25
What are the systemic actions of non-selective COX inhibitors on the CNS?
- analgesic action by inhibiting PGs synthesis (they have central action elevating pain threshold and peripheral action due to anti-inflammatory effect)
- effective in low intensity pain without drowsiness, tolerance or addiction
- antipyretic action: by inhibiting PGs synthesis causing resetting of hypothalamus thermostat to normal and increase heat loss by cutaneous VD and sweating
- however, salicylate in large dose may lead to hyperthermia due to uncoupling of oxidative phosphorylation
26
What are the peripheral actions of non-selective COX inhibitors?
- anti-inflammatory
- anti-rheumatic
- due to inhibition of COX enzyme so inhibits PGs synthesis and inhibition of other inflammatory mediators
27
What are the CVS action of non-selective COX inhibitors?
- therapeutic dose has little effect
- large dose can produce hypotension
28
What are the actions on uric acid of non-selective COX inhibitors?
- salicylates in small dose inhibit uric acid secretion (not good for patients with gout)
29
What are the actions of aspirin in small dosein blood (therapeutic dose)?
- inhibits platelets aggregation
- prolongs bleeding time
- needs to be stopped 1 week before surgery
30
What are the actions of aspirin in large dose?
- due to dicoumarol like action, they compete with vitamin K leading to hypoprothrombinaemia (act as anti-vitamin K)
- in patients with G6-PD deficiency, they produce haemolytic anaemia
31
What are the actions on GIT of non-selective COX inhibitors?
- epigastric distress
- nausea
- vomiting
- ulceration
32
What are the actions on kidney of non-selective COX inhibitors?
- salicylates can cause sodium retention and reduce renal function especially in patients with H.F. or hypovolemia
- reduce renal blood flow
- bad for patients with renal failure
33
What are the actions on respiratory center of non-selective COX inhibitors?
large dose case increase in respiratory center and washing of CO2 which can lead to respiratory acidosis or alkalosis
34
How is non-selective COX enzyme inhibitors administered?
- orally after meals to avoid gastric irritation
- sodium salicylate should be given enteric coated
35
What are the local uses of non-selective COX inhibitors?
- salicylic acid: keratolytic and fungistatic
- methyl salicylate: counter-irritant
36
What are the systemic uses of non-selective COX inhibitors?
- fever
- analgesic in headache, arthritis, neuralgia, common cold
- acute rheumatic fever (when there is continuous streptococcal infection)
- rheumatoid arthritis (auto-immune disease in joint)
- to prevent intravascular thrombosis (antithrombotic and prevents platelet aggregation)
37
What are the side effects of non-selective COX inhibitors?
- gastric irritation, ulceration perforation and bleeding
- allergic reaction: urticaria, skin rash, angioneurotic oedema
- precipitate an attack of asthma in predisposed patients as it blocks COX pathway with increase in leukotrienes which produce bronchoconstriction
- idiosyncrasy: in patient with G6-PD deficiency leading to haemolytic anaemia
- Reye's syndrome if used in children with viral infection (increase hepatic necrosis with severe virus infection in children)
- prolonged use may lead to hypoprothrombinaemia
- salicylism (chronic use): headache, mental confusion, vertigo, ringing in ears (timitus), sweating, nausea, vomiting
37
What is the result of acute aspirin toxicity?
- hyperpyrexia
- convulsions
- hyperventilation
- dehydration
- decrease B.P.
- acidosis or alkalosis
-hyperglycaemia
38
How is acute aspirin toxicity treated?
- cold fomentation
- stomach wash (NaHCO3)
- vitamin K
- alkalinise urine
39
What are the contraindications of non-selective COX inhibitors?
- peptic ulcer
- bronchial asthma
- idiosyncrasy (in patients with G6-PD deficiency)
- allergy
- virus infection if children , bleeding tendency
- pregnancy (early and late)
- small dose in gout
40
What happens to cells during aspirin toxicity?
- convert ATP to heat
- hyperventilation (huge loss of CO2 from body
- respiratory alkalosis
41
What are the interactions with non-selective COX enzyme inhibitors?
- ammonium chloride enhances toxicity (acidify urine)
- alcohol and glucocorticoids increase GIT bleeding by salicylates
- can displace drugs from plasma proteins (e.g. hypoglycaemics and oral antibiotics)
42
Which drug does indomethacin act like?
aspirin but it has stronger anti-inflammatory effect and serious side effects
43
What is an example of selective COX 2 inhibitor?
clecoxib
44
What is the mechanism of action of selective COX 2 inhibitors?
- COX 2 isoenzyme induced at site of inflammation, selective COX 2 inhibitor have analgesic antipyretic and anti inflammatory effect
- weak effect on COX 1 isoenzyme with few gastrointestinal side effects and without affecting platelets
45
Why do we use ibuprofen and ketoprofen more than aspirin?
- longer duration
- 20 times more potent than aspirin
46
What are some characteristics of clecoxib?
- selective COX 2 inhibitor (analgesic)
- not antiplatelet or antithrombotic
- for peptic ulcer
- anti-inflammatory
- antipyretic
47
What is an example for selective COX 3 enzyme?
paracetamol
48
What are some characteristics of paracetamol?
- safe analgesic
- works centrally only
49
Is selective COX 3 absorbed orally?
yes
50
What are the actions of selective COX 3 enzyme
- analgesic
- antipyretic
- not anti-inflammatory
- decreases PG synthesis centrally and not peripherally
- no effect on platelets
- no uric acid effect
- no bronchospasm
- no peptic ulcer effect
51
Does paracetamol cause drug-drug interactions?
no
52
What happens if paracetamol is used in high doses?
- accumulation of toxic metabolite in liver and kidney
53
How is paracetamol toxicity detoxified?
- glutathione
- acetyl cysteine is used to treat the toxicity as it increases glutathione secretion in the body
54
What are the uses of paracetamol?
- all contraindications of aspirin are indicated in paracetamol
- allergy or intolerance to aspirin
- in pregnancy
- patients with haemophilia or bleeding tendency
- history of peptic ulcer
- bronchial asthma
- viral infection in children
- gout
55
Is paracetamol not tolerated in therapeutic doses?
no
56
What is the toxic dose of paracetamol?
more than 4g/day
57
What re the characteristics of opioid analgesic drugs?
- CNS depressants
- prolonged use leads to addiction
- act cortically as analgesic
- agonist on opioid receptors
- prevent secretion of substance P
- have euphoric effect
58
What are examples of opioid agonists?
- morphine
- codeine
59
Does morphine have a spasmogenic action on smooth muscles?
yes
60
What are the characteristics of papaverine?
- negligible CNS action
- spasmolytic action of smooth muscles
61
What are some characteristics of morphine?
- stimulate opioid receptors
- inhibit heat regulatory centre
- inhibit respiratory centre --> hypoventilation
- cause severe miosis and constipation
62
What is the mechanism of action of morphine?
stimulation of opioid receptors located in brain and spinal cord regions inhibit the release of substance P (inhibit pain sensation
63
What does aspirin toxicity cause?
hyperthermia
64
What does morphine addiction cause?
hypothermia
65
What are the types of opioid receptors?
- mu receptors: mostly found in brain
- kappa receptors: mostly found in spinal cord
66
What is the action of mu receptors?
- respiratory centre inhibition (hypoventilation and accumulation of CP2)
- euphoria
- supraspinal analgesia
- miosis
- reduced gastrointestinal motility
67
What is the action of kappa receptors?
- spinal analgesia
- miosis
- less sedation than me receptor
- less R.C. inhibition than mu receptor
68
What is the CNS action of morphine?
- analgesia (without loss of consciousness), drowsiness, mood changes, mental clouding and may produce euphoria
- relieves pain without affecting other sensations
- change affective response as anxiety and fear
- itching is not relieved because it releases histamine
69
What happens when morphine is given IV in large doses?
may produce convulsions
70
What are the stimulant actions of morphine?
- euphoria
- miosis
- vagal centre stimulation (bradycardia)
- increase ADH
- increase CTZ
- increase monosynaptic reflexes (stretch reflex)
- lower seizure threshold (epilepsy)
71
What is the depressant action of morphine?
- analgesia
- narcosis
- inhibit respiratory centre
- inhibit cough centre
- inhibit VMC (causes VD)
- inhibit HRC --> hypothermia
- decrease ACTH, FSH, LH
- decrease polysynaptic spinal reflexes (withdrawal reflex)
72
What i hypotension caused by?
- stimulation of vagal centre and inhibition of VMC
73
What is the respiratory action of morphine?
- decreases sensitivity of RC to CO2
- inhibits cough center
- releases histamine
- induces bronchospasm
74
What is the CVS action of morphine?
- no major actions in therapeutic doses
- large doses produce hypotension
75
What is the smooth muscle action of morphine?
- increase tone of muscles and spasm of sphincter
- decreases peristaltic propulsive movement and inhibits defecation reflex
- all these factors produce constipation
- biliary tract: spasm of wall of gall bladder and sphincter which increases intrabiliary pressure
- urinary tract: spasm of muscles and internal sphincter which may lead to urine retention
- uterus passes placental barrier and may produce neonatal asphyxia
- bronchi: large doses produce bronchospasm due to histamine release
76
What does asphyxia do?
- inhibition of RC in baby and prolong labour
77
What is the skin action of morphine?
- sweating
- -itching
- wheal formation due to histamine release
78
When does tolerance occur for morphine tolerance?
depressant actions after 10-14 days but no tolerance develops to miosis and constipation
79
Does morphine achieve cross tolerance?
no, other CNS depressant does
80
Is morphine tolerance reversible?
yes
81
What happens if a patient takes overdose of morphine?
death
82
What are the therapeutic indications of morphine?
- analgesic to relieve severe pain as in terminal cancer, myocardial infarction, post-operative pain except after cholecystectomy (relieve any type of pain except itching)
- acute left ventricular failure and pulmonary oedema (give IV), it reduces fear and apprehension, venodilator action, reduce work of heart
- preanesthetic medication (meperidine is better)
83
What are the contraindications of morphine?
- very old, very young (no metabolism --> accumulation --> toxicity)
- acute abdominal pain (interferes with diagnosis)
- head injury (increased CSF pressure)
- respiratory diseases as bronchial asthma (central and peripheral action on bronchi)
- pregnancy, delivery and lactation
- alone in biliary and renal colic and in pancreatitis
- advanced liver diseases (myxoedema)
- history of addiction
- epilepsy
- acute alcoholism
- patients that don't have gall bladder
84
What are the adverse effects of morphine?
- respiratory depression
- nausea
- dizziness
- mental clouding
- dysphoria
- pruritus constipation
- increased biliary pressure
- urine retention
- hypotension
85
What happens in acute morphine poisoning?
- depressed respiration
- hypotension
- hypothermia
- coma
- pin-point pupils (severe miosis)
86
What is the treatment of acute morphine poisoning?
- gastric wash by potassium permanganate followed by purgative (MgSO4)
- artificial respiration with O2
- specific antidote: naloxone IV (during emergency) or naltrexone (antagonist)
87
What happens in chronic morphine toxicity?
- addiction
- sudden withdrawal induces abstinence syndrome (yawning, dilated pupils, urination, mydriasis, diarrhoea, excitation, tremors, increase HR and BP, aches, sweating salivation, convulsions and coma)
88
What is the treatment of chronic morphine toxicity?
- hospitalisation, psychotherapy, gradual withdrawal until stabilising dose
- transfer patient from short acting opioid into a long acting one as methadone (opioid agonist, better than morphine and taken orally) then gradual withdrawal of methadone
- naltrexone can be used after detoxification for patients with high motivation to remain opioid free
89
What are the characteristics of codeine compared to morphine?
- less potent
- less addictive
- less RC depressant
- inhibits cough center and produces excitation in large doses
90
What is the use of codeine (methyl morphine)?
- analgesic
- central antitussive (cough centre inhibitor)
91
What is an example of semi-synthetic derivatives?
heroin (diacetyl morphine)
92
What are the characteristics of semi-synthetic derivatives?
- more potent
- more addictive
- hydrolysed into morphine
93
What is an example of synthetic derivative?
- meperidine
- fentanyl
94
What is the administration of meperidine?
- orally or by injection
- metabolised into meperidinic acid normeperidine
- excreted in urine
95
What are the characteristics of meperidine compared to morphine?
- analgesic action 1/10th potency of morphine
- less addiction
- shorter duration (2-4 hours)
- less or no hypnotic effect
- less RC depressant
- no antitussive action
- weak atropine-like action
- less spasmogenic on smooth muscle (no constipation and may cause mydriasis)
96
Do we treat morphine addiction with opioid blockers?
no
97
What are the therapeutic uses of meperidine?
- analgesic in obstetrics, renal or biliary colics
- preanesthetic medication (labour and delivery)
98
What are the characteristics of fentanyl?
- 80 times more potent than morphine with shorter duration
- used combined with droperidol to produce neurolept-analgesia IV
- can be used as skin patch to relieve pain
99
What does it mean when a drug produces neurolept analgesia?
non-responsive patient without losing their consciousness
100
What is tramadol?
- weak agonist
- inhibit noradrenaline and 5HT (serotonin) uptake
101
What are examples of opioid antagonists?
naloxone and naltrexone
102
What are the clinical uses of opioid antagonists?
- treatment of acute opioid poisoning and neonatal asphyxia caused by opioid
- for diagnosis of opioid addiction (induce withdrawal symptoms)
- naltrexone has higher oral efficacy and longer duration (t1/2 is 10 hours), used orally to prevent return to opioid use
103
What is the classification of antibacterial chemotherapy according to spectrum?
- narrow spectrum (gram positive OR gram negative bacteria)
- broad spectrum (gram positive AND gram negative bacteria
104
What is the classification of antibacterial chemotherapy according to whether they kill or inhibit growth??
- bacteriostatic drugs: inhibit bacterial growth and allows for natural immunity to deal with microbe (suitable for patients with normal immune system)
- bactericidal drugs: kills bacteria and are selected when host defence mechanism is impaired
105
Bactericidal drugs can be divided into...?
- concentration dependent killing drugs: quinolones and aminoglycosides
- time dependent killing drugs: beta lactams antibiotics and vancomycin
106
What is post-antibiotic effect?
persistent suppression of bacterial growth after limited exposure to anti-microbial agents
107
What are inhibitors of cell wall synthesis antibiotics?
- beta lactams
- vancomycin
108
What are the characteristics of inhibitors o cell wall synthesis antibiotics?
- require proliferating organisms: little or no effect on non-growing bacteria
- no effect on organisms devoid of cell walls (e.g. mycoplasma)
- less toxic on human cells (mammalian cells have no cell wall)
109
What are the types of beta lactams?
- penicillin
- cephalosporin
-carbapenems (e.g. imipenem and meropenem
- monobactam (e.g. aztreonam)
110
What is the mechanism of action of beta lactams?
- bactericidal by inhibiting cell wall synthesis (all beta lactam antibiotics)
- affects growing organisms that are not resting
- inactive against mycobacteria, viruses and fungi
- they bind to penicillin-binding proteins (PBP)
- PBP inhibit transpeptidation and cross links peptide chain
- overactivated autolytic enzymes: lysis of bacterial cell
111
What are the classifications of penicillin?
- short acting penicillin (penicillin G/benzyl-penicillin)
- long acting penicillin
- acid resistant penicillin (penicillin V)
- penicillinase resistant penicillin
- broad spectrum penicillin
- anti-pseudomonas penicillin (extended spectrum penicillin)
112
What are the characteristics of short acting penicillin?
- acid sensitive so given IV or IM/6 hours
- narrow spectrum
- penicillinase sensitive (beta lactamase sensitive)
- short duration due to rapid renal excretion by tubules (90%) and glomeruli
- probenecid inhibits renal tubular secretion so increase level of penicillin in blood
113
What are the characteristics of long acting penicillin?
- procaine penicillin G/12-24 hours (procaine + penicillin G)
- benzathine penicillin G/4 weeks
- acid sensitive so given IM
- narrow spectrum
- penicillinase sensitive
114
What are the characteristics of acid r resistant penicillin?
- oral absorption
- short duration
- penicillinase sensitive
- narrow spectrum
115
What are the characteristics of penicillinase resistant penicillin?
- oxacillin, cloxacillin, dicloxacillin, flucloxacillin orally
- nafcillin has incomplete oral absorption (taken IM)
- methicillin IM (acid sensitive) is nephrotoxic (rarely used)
- some strains of staphylococci become resistant to methicillin (MRSA)
116
What are the characteristics of broad spectrum penicillin?
- active against many gram negative bacteria
- ampicillin and amoxycillin orally
amoxycillin produces higher blood level than ampicillin and no affected by food
- penicillinase sensitive
- can be combined with penicillinase-resistant penicillin or penicillinase enzyme inhibitor clavulanic acid or sulbactam
- ampicillin esters = prodrugs e.g. pivampicillin, talampicillin. They are better absorbed orally than ampicillin (so have less side effects on gut) and must be de-esterified in gut mucosa or liver to release ampicillin
117
Which antibiotic has less side effects: amoxycillin or ampicillin?
amoxycillin as it has better distribution and absorption than ampicillin
118
What are the characteristics of anti pseudomonas penicillin?
- broad spectrum includes pseudomonas and many gram negative bacilli
- penicillinase sensitive and are synergistic with aminoglycosides (but not mixed in one syringe)
- carbenicillin and piperacillin
- can be combined with beta lactamase inhibitors
- more active and more tolerated
also used in anaerobic infections
119
What can be the cause of penicillin resistance?
- lack of peptidoglycan structure (in mycoplasma)
- decreased permeability to drug
- altered penicillin binding sites or beta lactamase activity
120
What are the pharmacokinetics of penicillin?
- after absorption, they are distributed to all tissues
- low level in CSF except in inflammation (meningitis)
- can cross placenta
- excreted by tubules and glomeruli
121
What are the therapeutic uses of penicillin?
- amoxicillin is used alone or with metronidazole in acute necrotising alcerative gingivitis, dentoalveolar abscess, osteomyelitis of mandible
- meningitis (pass to CSF in inflammation)
- prophylaxis of streptococcal infection in rheumatic fever by benzathine penicillin and in subacute bacterial endocarditis by procaine penicillin
122
What are the characteristics of penicillin toxicity?
- hypersensitivity reaction: major cause is penicilloic acid which reacts with
protein and serves as hapten to cause immune reaction (urticaria, angioedema,
and anaphylaxis). cross allergy with beta lactam antibiotics
- diarrhoea by disruption of normal balance of intestinal microorganisms with
incompletely absorbed penicillin and superinfection may occur.
- high concentration produces local pain, induration, and thrombophlebitis
- nephrotoxicity
- platelets dysfunction and decreased agglutination with carbenicillin
- with high doses or intrathecal administration may produce seizures and epilepsy
123
Is penicillin a safe drug?
yes
124
What is cephalosporin?
bactericidal as penicillin and resistant to penicillinase to some extent
125
What is the classification of cephalosporins?
- 1st generation (narrow spectrum)
- 2nd generation (intermediate spectrum)
- 3rd generation (broad spectrum)
- 4th generation (broad spectrum)
- 5th generation (parenteral ceftaroline)
126
What are the characteristics of generation 1?
- taken oral and parenteral
- activity: Gram+ve > Gram-ve
127
What are the characteristics of generation 2?
- taken oral and parenteral
- activity: gram positive less than first generation and gram-negative greater than first generation
- they can not pass to CNS
- used in anaerobic infections (cefoxitin)
128
What are the characteristics of generation 3?
- oral and parenteral absorption
- decreased activity against gram positive organisms
- gram negative: further increased activity against gram negative organisms
- they are also able to penetrate CNS
- ceftriaxone (Parentral, longest t1/2)
- bone: good penetration into bone
- BBB: cross BBB, can be given in meningitis
- bile: excreted in bile (40%), used in biliary infection and renal dysfunction
129
What are the characteristics of generation 4?
- parenteral route only
- more resistant to beta lactamase
- they have good activity against most penicillin non-susceptible strains
- they penetrate the CNS
130
What are the pharmacokinetics of cephalosporins?
- they are distributed to body fluid, adequate level in CSF with third generation
(except cephoperazone) and fourth generation
- excreted by tubules and glomeruli (probenecid reduces their secretion)
- ceftriaxone is excreted in bile and faeces and has long duration, so can be given once daily
131
What happens in cephalosporin toxicity?
- allergy: less than penicillin, cross allergy with penicillin (5% - 10%)
- nephrotoxicity: renal tubular necrosis with cephaloridine and increased toxicity
by loop diuretics and aminoglycosides
- thrombophlebitis after I.V. administration-pain after I.M. injection, gut upset, diarrhoea, superinfection with oral preparation
- ceftriaxone with calcium will precipitate in gall bladder --> biliary sludge (rare)
-Cefamandole, cefoperazone and cefotetan may produce hypoprothrombinemia
due to anti-vitamin K effect
- they also cause disulfiram like action so alcohol must be avoided
132
What is an example of a 3rd generation cephalosporin?
ceftriaxone
133
What is an example of 2nd generation cephalosporin?
cefoxitin
