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s4 - Repro, Develop, Ageing, Pharm > PHARM > Flashcards

PHARM Flashcards

1
Q

Gastrointestinal absorption of drugs in newborn is implicated as:
they have less gastric acid which is ph~7..
give 3 other reasons

A
  • peristalisis is reduced in first 6months
  • reduced production of bile
  • GI disorders e.g. gastroschisis, NEC that reduce absorption so need to deliver via TPN
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2
Q

How will absorption of acid labile medicines e.g. penicilin be affected by the gastric acid in a newborn?

A

As the gastric acid is more alkaline (ph 7) you will get more absorption

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3
Q

IV for drugs in babies is commonly used as it has 100% bioavailability, give 2 disadv of this method of administration:

A
  • difficult line access
  • drug compatibility
  • infection risk
  • longer hospital stay, $$$
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4
Q

Why is intramuscular administration of drugs in babies discouraged?

A
  • absorption form injection site is erratic/variable
  • depends on vascular perfusion there, muscle mass and contraction
  • too painful
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5
Q

In what 2 pathologies is intramuscular administration of drugs in babies esp. discouraged due to the variable blood flow?

A

Hypotension

Sepsis

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6
Q

Caution should be taken with percutaneous administration of drugs into the skin of neonates in terms of absorption. Why?

A
  • thinner s.corneum
  • increased skin hydration
  • larger SA so enhanced absorption
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7
Q

What are the risks associated with the following drugs admisistered percutaneously in neonates?

  • topical corticosteroids
  • topical aminoglycosides
A
  • Corticosteroids may reach high systemic levels –> Cushingoid symptoms
  • Aminoglycosides can lead to hearing loss
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8
Q

Rectal administration of drugs to babies/children is useful in 2 instances in particular…when? What can lead to erratic absorption here?

A
  • vomiting/nil by mouth patients
  • children reluctant to take orally
  • variation in rectal venous drainage
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9
Q

Vd is the degree to which a drug is distributed in….. rather than…..

A

distributed in…..body tissue rather than…..plasma

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10
Q

Suggest 3 `things that affect the degree of drug distribution (once within circulation) out of plasma.

A
  • size of body water compartments
  • how much drug binds to p.proteins
  • degree of development of BBB
  • metabolic disturbances e.g acidosis
  • specificity of drug to receptor sites
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11
Q

How does total body water and adipose % in neonates compare to adults? Hence water-soluble drug distribution…?

A
  • higher body water (92 vs 60%) and less adipose in neonates

- higher loading doses of water-soluble drug needed to reach steady state

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12
Q

How does the fact that neonates have less plasma protein with lower binding affinities affect Vd?

A

-less bound drug so more free fraction so more distribution out from plasma

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13
Q

The drug phenytoin is 98% protein bound, how does it cause kernicterus + long-term neuro damage in neonates?

A
  • phenytoin can displace bilirubin

- more free bilirubin which can cross BBB –> kernicterus

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14
Q

Hypoalbuminea can affect protein binding. Suggest 2 conditions this can occur with.

A
  • malnutrition
  • sepsis
  • nephrotic syndrome
  • hepatic disease
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15
Q

What is different about the BBB in neonates? What 2 factors determine the rate of drug transfer to the CNS?

A
  • BBB is functionally incomplete so more enters CNS

- lipid solubility and ionisation of drug affect it

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16
Q

How is hepatic metabolism of drugs in neonates?
Phase I hydroxylation
Phase II Sulfation/Methylation/Glucoronidation

A

Immature as enzyme functioning esp CYP has delayed maturity (phase I)
Phase II Sulfation/Methylation = normla
Glucoronidation = immature until ~1yr

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17
Q

What syndrome can the antibiotic chloramphenicol or idomethacin cause in a baby due to immature hepatic metabolism?

A

Grey Baby Syndrome

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18
Q

Nephrogenesis is from wk9-34 gestation but renal function is still immature at birth. In children what can further compromise function, give 2 e.g.s.

A
  • sepsis
  • dehydration
  • nephrotoxic drugs
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19
Q

Suggest why ADRs are more common in neonates.

A
  • lack of clinical trial data

- immature liver function–>lack of detoxification and excretion so drug accumulates

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20
Q

What is dosage in paedatric units based on?

A

-weight/SA

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21
Q

The myometrium has 3 smooth muscle layers, what are the fibre orientations?

A
  • outer: longitudinal fibres
  • middle: figure of 8 fibres
  • inner: circular fibres
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22
Q

How does the myometrrium sm organisation act like a ligature preventing blood loss in birth?

A
  • contraction of the fibres increases the uterine pressure

- forces the contents towards the cervix

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23
Q

The myometrium is spontaneously active/myogenic. What modulates contractions? (increases/decreases?)

A
  • NTs influence
  • Oestrogen increases contractions
  • Progesterone inhibits activity
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24
Q

-In the non-pregnant uterus why do they experience weak contractions early in the MC and strong contractions during menstruation? (horomones..)

A
  • progesterone starts high then decreases (inhibitory)

- prostoglandins increases at menstuation

25
Q

The myometrium is myogenic but has ANS innervation, symp/para? Receptors? Effects?

A

Sympathetic
Alpha receptor stimulation causes contraction
B receptor -> relaxation

26
Q

What pacemaker cells set the myogenic activity of the mypometrium?

A

ICC-Interstitial Cells of Cajal, initiate and coordinate contractions

27
Q

ICCs generate electrical activity. Via what do they pass to SM cells?, what proteins make this pathway?

A
  • via gap junctions made of connexin proteins

- makes low resistance pathways

28
Q

How does oestrogen increases the contractions of the myometrium?…think GJs

A

-increases the expression of gap junctions so more activity from ICCs pass to SMs promoting contraction

29
Q

ICCs generate “slow wave” depolarisations that generate APs. APs to SM via gap junctions..what is the Ca2+ mechanism of contraction?

A

AP causes Ca2+ influx via VGCC opening

the increases intracellular [Ca2+] causes contraction

30
Q

What are type of GPCRs does the myometrium have for oxytocin? What happens when oxytocin binds?

A
  • Gaq so stimulates PLC which hydrolyses PIP2 to IP3 and DAG
  • Ca2+ release from SR and more depolarisation, VGCC open more, Ca2+ influx
  • Ca2+ & calmodulin activates MLCK -> cross bridge
31
Q

At low conc, of ICC stimulants e.g. oxytocin, there is little slow wave activity and SM contraction. High conc –> sustained contractions, what about [v. high]?

A

Hypertonus (incomplete relaxation) as Ca2+ extrusion process cant keep up

32
Q

What is the benefit of hypertonus in birth vs. danger if baby still inside?

A

stops haemorage if baby out. If baby in, cuts blood supply -> foetal distress

33
Q

Oxytocin is a nonapeptide released in response to suckling and cervical dilation. Where is it made? Where is it released from?

A

Made in hypothalamus

Released from post. pituitary

34
Q

Syntocinon and Pitocin are synthetic versions of which hormone?

A

Oxytocin

35
Q

How is oxytocin action dependent on oestrogen release(in late stages of birth)?

A
  • oestogen produces a rise in oxytocin release

- oestrogen increases oxytocin receptors and GJs

36
Q

Give 2 uses of oxytocin clinically:

A
  • induce labour at TERM to increase contractions (but wont soften cervix)
  • used with ergot to prevent post. p. haemorrage by acting like ligature on vessels, less bleeding
37
Q

Syntometrtine is the name of the drug with which 2 hormones? What are their effects?

A

Oestrogen-rapid acting
Ergot-prolonged action
Prevent post.partum haem.

38
Q

Oestrogen promotes the synthesis of what?

Clue: made in endometrium, have role in dys/menorrahgia and partruition

A

-prostoglandins

39
Q

Name 3 functions of protoglandins in birth

A
  • coordinate and increase frequency/force of contractions
  • increases GJs present
  • increases oxytocin synthesis
  • SOFTENS CERVIX
40
Q

Dinoprostone and Carboprost are analougues of what?

A

Dinoprostone = PGE2 (v.dilates)
Carboprost - PGF2a (v.constricts)
prostoglandins

41
Q

Give 2 uses of prostoglandin analogues clinically:

A
  • induce labour BEFORE TERM (receptors always present)
  • induce abortion
  • prevent p.p.haem
  • soften the cervix
42
Q

What is the risk of using prostoglandin analogues in labour clinically if it enters circulation?

A
  • Dinoprostone will cause systemic v.dilation and huge BP drop -> CV collapse
  • Carboprost can cause too much contraction -> hypertonus ->f oetal distress
43
Q

How are prostoglandin analogues in labour clinically administered to reduce systemic effects?

A

-as a cervical gel/vaginal insert to act locally

44
Q

The fungus ergot can produce powerful uterine contractions only if myometrium starts relaxed. What is it used for clinically?

A

-prevent post partum haemorrhage

45
Q

Why may myometrial relaxants be admistered? What can be done in the time?

A

In premature labour to delay deliver 48hrs

-transfer to specialist, give corticosteroids for lung maturation, improve survival

46
Q

Give 3 examples of c;lasses of myometrial relaxants

A
  • Ca2+ channel antagonists (eg. nifedipine)
  • Oxytocin receptor antagonists (eg. Retosiban)
  • COX inhibitors (eg. NSAIDS)
47
Q

How may the absorption of drugs in older adults be affected?

A
  • influenced by food/lack of food
  • gastric transit time longer
  • pH increases a bit (further alkaline if taking PPIs)
48
Q

What changes to the body of older adults affect distribution of drugs?

A
  • sarcopaenia
  • less body water, less mean body mass,
  • increase body fat
49
Q

How does less body water and more body fat affect the Vd of hydrophilic and lipophlic drugs?
(less lean body mass..and digoxin VD..?)

A

-hydrophilic drugs e.g. lithium have reduced Vd
-lipophilic drugs e.g. bezos have increased VD
(digoxin binds to muscle so Vd decreases with age)

50
Q

What changes in the liver cause metabolism of drugs in older adults to change?

A
  • liver mass decreases and hepatic b.flow decreases

- (enzyme activity unchanged)

51
Q

What age-related changes affect pharmacodynamics of e.g. opiates, digoxin..

A
  • more sensitive to sedation & psychomotor impairment as BBB leaky (e.g. benzo, opiates)
  • more intensity and longer duration of opiates
  • more cardiac sensitivity to digoxin
52
Q

What changes in the kidney cause elimination chof drugs in older adults to change?

A
  • smaller kidneys as basement membrane changes
  • less renal BF as artery resistance increased
  • poorer nephron functioning (sclerosis)
  • reduced GFR
53
Q

What is optimal pharmacotherapy for older adults?

A
  • balance of over/under prescribing
  • correct drug and dose for condition
  • specific to that patient
54
Q

What 2 criteria are in place to screen for inappropriate prescriptions in older adults?

A
  • STOPP START criteria

- Beers criteria

55
Q

10% of over 75yrs patients have an ADR…what are some risk factors in older adults?

A
  • multiple medications
  • multi-morbidity
  • previous ADRs
  • lower BMI (sarcopaenia)
  • renal/liver impairment
  • compliance
56
Q

Drug interactions can cause confustion, cognitive impairment, hypotension, acute renal faliure…what 2 classes of drugs most commonly interact?

A

-cardiovascular and psychotropic drugs

57
Q

What 3 factors/impairments affect compliance of taking medications in older adults?

A
  • impaired cognition
  • impaired vision
  • impaired manual dexterity
58
Q

Suggest 4 ways we can improve compliance in older adults:

A
  • communication, simplify regimes
  • readable labels, specific instructions
  • easy openable containers
  • blister packs/Dosset boxes
  • involve carers/family
  • recognise side effects

s4 - Repro, Develop, Ageing, Pharm (14 decks)

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