SESSION 5: PAEDS & OBGYN Flashcards
Missed pill rules for traditional POP?
If pill was less than 3 hours late take pill and no action required
If pill missed is >3 hours late then take the most recent missed pill asap and use additional contraception for 48 hours after correct pill-taking has started.
If there was UPSI from the time the first pill was missed until correct pill taking has resumed for 48 hours then consider EC
Note if cerazette is the POP then no action is needed until pill is >12 hours late
Missed pill rules for COCP?
If 1 pill is missed take the last pill even if it means taking 2 pills in one day and then continue taking pills daily. no additional contraceptive protection needed
If 2 or more pills missed: take the last pill even if it means taking 2 pills in 1 day, leave any earlier missed pills and then continue taking pills daily, one each day. use condoms or abstain from sex until taken pills for 7 days in a row.
if pills are missed in week 1: emergency contraception should be considered if she had unprotected sex in the pill-free interval or in week 1
if pills are missed in week 2: after 7 consecutive days of taking the COC there is no need for emergency contraception
if pills are missed in week 3: she should finish the pills in her current pack and start a new pack the next day; thus omitting the pill free interval
Which common drugs have anticholinergic SE?
Antimuscarinics e.g. glycopyrronium, ipratropium, tiotropium, oxybutinin, tolterodine, hyoscine
TCAs
Antipsychotics
Antihistamines
Neuromuscular drugs e.g. baclofen, procyclidine, atropine, cyclopentolate, tropicamide
Antiarrhythmics e.g. dispyramide, propafenone
Amantadine
Which drugs can worsen HF?
NSAIDs
CCBs - particuarly non-hydropyridine
Diabetes medications e.g. glitazones, SGLT2i
Antiarrhythmic meds e.g. flecainide and propafenone
Glucocorticoids e.g. pred and dex can cause fluid retention
Some oncology drugs e.g. doxorubicin
Alpha blockers
Why can NSAIDs worsen HF?
the vasoconstriction effects of noradrenaline and angiotensin 2 are usually antagonised by prostaglandins and prostaglanin usually maintains vasodilation of the afferent arteriole to help preserve the GFR under conditions where renal perfusion is compromised e.g. HF = NSAIDs inhibit COX enzymes which are necessary for prostaglandin synthesis = NSAIDs reduce the kidneys ability to maintain afferent arteriole dilation = increased resistance in afferent arteriole (and efferent to some degree) reduces the GFR = less filtration so less Na+ and water excretion by the kidneys = fluid retention = increases pre-load and after-load of the heart adding strain to an already compomrised heart and exacerbating HF Sx
Why do non-dihydropyridone CCB worsen HF?
Because of their negative inotropic effects - they inhibit the influx of Ca2+ into myocardial cells = reduced force of contraction = exacerbates the problem of the heart being able to pump blood effectively
They also decrease the HR by slowing conduction though SAN and AVN = can reduce CO in HF pts
This effect is less pronounced in Dihydropyridine CCBs but they can still cause peripheral vasodilation = oedema
How does total body water vary as we grow from newborns to adults?
Term neonates are 80% TBW whereas a 1 year old & adult man is 60% TBW and 50% in adult women
How do the proportions of our TBW which make up ECF and ICF vary as we grow from neonates to adults?
The proportion of ECF decreases and ICF increases
Term neonates 45% of TBW is ECF
1 year olds 25% and adult men 20%
What is considered a term infant in the international classification for different age groups?
0-27 days old
What is considered an infant/toddler in the international classification for different age groups?
28 days - 23 months
What is considered a child in the international classification for different age groups?
2-11
What is considered an adolescent in the international classification for different age groups?
12-16 or 18 - no agreement on this
Which routes of administration of drugs undergo hepatic first-pass metabolism?
Predominantly oral drugs
This is why IV/nasal/buccal/others drugs have a faster onset of action
Why are drugs barely ever given IM in neonates (usually limited to vaccines)?
As they have reduced skeletal muscle blood flow and inefficient muscular contractions due to their limited movements which may reduce the rate of absorption of drugs
They are also very painful!
What are the physiological changes throughout childhood that affect drug absorption?
Neonates have immature biliary systems = less bile acid = reduces fat absorption and therefore lipophilic drugs
Immature gut motility at birth, smaller bowel length, different intestinal flora, prolonged gastric emptying time
Neonates - high pH due to presence of amniotic fluid still in stomachs - increase in absorption of weak base drugs and decreased absorption of acidic drugs so higher/lower doses respectively may be needed
Absorption through intestinal walls is considered fully developed by 4 months
Developmental changes in lung structure and capacity - this is why kids should always use a mask and spacer
Babies have larger SA of skin compared to adults relative to body weight = better skin absorption. They also have thinner skin - makes them more prone to systemic absorption of drugs and SE
What factors affect drug distribution?
Body composition - younger children have higher TBW% so larger volume of distribution means they need higher doses of water-soluble drugs and smaller doses for fat-soluble drugs as they have less adipose tissue
Binding protein - newborns have less albumin and glycoproteins so plasma binding proteins levels are lower, lower affinity of foetal albumin for drugs, presence of endogenous compounds e.g. bilirubin competing for protein binding
Differences in regional blood flow, organ perfusion, permeability of cell membranes, changes in acid-base balance, cardiac output changes
Drug factors - pH, drug formulation and protein-binding capacity
What are phase 1 reactions in drug metabolism?
Reactions which alter the structure of the drug
E.g. oxidation, reduction, hydrolysis, demethylation
CYP enzymes from birth to adulthood?
CYP enzyme levels change throughout life - there are age-dependant differences in the abundances of these hepatic CYp enzymes
E.g. CYP3A7 is expressed in the foetal liver and then rapidly declines after birth, CYP1A2 is expressed by the liver a little while after birth, CYP3A4 levels are absent in new burns but reach adult level by 1 Lear of age
What are phase 2 reactions in drug metabolism?
Reactions which allow conjugation of the drug with other molecules to make the drug more water-soluble
E.g. sulphation, glycine conjugation, methylation, glucuronidation, acetylation
Why are babies less prone to liver damage following an OD of paracetamol?
Less glucoronidation occurs in babies and more sulphation. This means there is less CYP450 which converts paracetamol to its toxic metabolite NAPQI
This leads to more production of the non-toxic metabolite instead which can be excreted
What is grey baby syndrome?
Toxicity of chloramphenicol in babies which gives them this grey colour to their skin.
It happens because neonates have a deficiency in UDP-glucuronyltransferase (due to underdeveloped liver enzymes) that converts chloramphenicol to chloramphenicol glucuronate = build up of the drug
Outline the genetic differences in codeine metabolism?
10% of Caucasians and 2% of Asians are poor metabolisers of codeine as they have no expression of the genes that produce CYp2D6 - they get no response from codeine as an analgesic
1-7% of the population are ultra-rapid metabolisers of codeine who convert it to morphine much faster and are therefore more at risk of morphines toxic SE. This is because they have duplication of CYp2D6.
Which ethnicity has the highest rates of being ultra-rapid metabolisers of codeine?
North african and Ethiopian
Why is drug elimination worse in neonates?
At birth the renal system is immature due to incomplete glomerular development, low renal perfusion pressures and an inadequate osmotic load to produce the full counter-current effects
What are the 2 types of adverse drug reactions?
Type A augmented reaction - exaggerated effects of the medicines known pharmacological action. Usually dose dependant. E.g. hand tremor in beta agonist therapy or renal failure with high serum concentration of gentamicin
Type B Bizarre reaction - an unexpected result of the medication unrelated to the medicines known pharmacology e.g. urticaria during penicillin therapy or intractable vomiting during erythromycin therapy
Which classes of medications do the yellow card scheme indicate are most frequently associated with fatalities?
Anticonvulsants, cytotoxic drugs, anaesthetic agents and antibiotics
First line antiemetics in pregnancy?
Doxylamine and pyridoxine - this is the only drug that is actually licensed for NVIP
Cyclizine
Prochlorperazine
Promethazine
Chlorpromazine
Which antibiotics are considered safe in pregnancy?
Beta lactam antibiotics - penicillins, cephalosporins
Macrolides - particuarly erythromycin
Adverse effects of ACEi in pregnancy?
Renal dysgenesis
Foetal and neonatal bp control issues
Skull defects and other craniofacial abnormalities
Oligohydramnios
IUGR
PDA
Adverse effects of atenolol in pregnancy?
IUGR
Neonatal hypoglycaemia and bradycardia
Adverse effects of Carbimazole in pregnancy?
Neonatal hypothyroidism
(Avoid in first trimester)
Adverse effects of lithium in pregnancy?
Ebsteins anomaly - avoid in first trimester
Adverse effects of methotrexate in pregnancy?
Medical termination
Adverse effects of NSAIDs in pregnancy?
Premature closure of ductus arteriosus
Oligohydramnios from foetal renal dysfunction
PPHN
Avoid prescribing from week 20/40. If used for > a few days additional monitoring may be required
