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PA30325 > Pharmacology and Therapeutics > Flashcards

Pharmacology and Therapeutics Flashcards

1
Q

What are some of the risk factors for CKD progression?

A

CVD

Hypertension

Diabetes

Smoking

AKIs

African origin

Chronic use of NSAIDs

Urinary tract outflow obstruction

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2
Q

What are the indications for starting RRT?

A

Uremia starting to effect daily life

Biochemical measures (hyperkalemia/acidosis)

Fluid overload

eGFR of 5-7ml/min/1.73m2

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3
Q

What are the 2 different types of dialysis?

A

Haemodialysis –> Transfer of uraemic solutes from the blood by diffusion via a semi-permeable membrane

Requires a fistula, or a line/graft (which has an increased risk of infections)

LMWHs are added to prevent clots, and bicarbonate is added to the blood

Peritoneal –> Access to the peritoneal cavity allows continuous dialysis whilst at home, with only the bags needing to be changed 4 times per day

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4
Q

What 3 vaccines are compulsory before starting dialysis?

A

Hep B

Influenza

Pneumonia

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5
Q

What is the effect of volume of distribution on the removal of drugs by dialysis?

A

Over 2L/Kg –> Not removed

Under 1L/Kg –> Removed significanlty by dialysis

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6
Q

What is the effect of protein binding in dialysis?

A

Only the unbound (free) drug can be removed in dialysis

Over 80% bound means that no drug will be dialysed

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7
Q

What is the “Triad of General Anasthesia”?

A

Unconsiousness

Analgesia

Muscle Relaxation

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8
Q

Name some of the key characteristics of the ideal general anaesthetic

A

Stable and potent

Controllable –> So it can be turned off if needed

Minimal cardio/resipiratory depressent

Non-irritant

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9
Q

What are the 4 stages of anasthesia?

A

Stage 1 (Analgesia) –> Consiousness and drowsiness

Stage 2 (Excitement) –> Loss of consiouness, but delirium occurs, spaciticity, gagging and vomiting

This stage needs to be minimised!

Stage 3 (Anasthesia) –> Regular respiration, loss of reflex and muscle tone

Stage 4 (Medulllary Paralysis) –> Cardiorespiration depression and so death

Dont want to push it this far!!

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10
Q

What are the 2 types of general anasthetic?

A

Inhalation –> Controllable with rapid blood-gas exchange

Stable and potent

Usually halogenated ethers or hydrocarbons

Used to maintain unconsiousness

Intravenous –> Rapid and short acting. Normally used for the induction of anasthesia

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11
Q

Explain the difference between the lipid and protein theory of anasthesia

A

Lipid –> Anasthetic potency is proportional to lipid solubility

The drug binds to lipid membranes and causes the shape of Na+ channels to change, meaning they’re less effective

Protein –> States that anasthetics bind to membrane proteins and receptors

Eg, potency correlates with luciferase inhibition

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12
Q

How does halothane affect K+ channels?

A

Cause them to open, meaning that APs are less likely to occur

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13
Q

In what stage of anaesthesia are muscle spasms most likely?

A

Stage 2

‘Excitement stage’

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14
Q

What is a motor unit?

A

The motor neuron and the muscle fibre that it innervates

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15
Q

What is the make up of nicotinic receptors in skeletal muscle?

A

2 alpha

1 beta

1 delta

1 gamma

2 moleucles of ACh must bind to activate it (with Na+ going in and K+ going out….cause end plate depolarisation)

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16
Q

What is the mechanism of muscle contraction?

A

ACh binds to Na+ channels, causing depolarisation at the end plate. This causes VG Na+ channels to open, causing APs to fire further into the muscle

This depolarisation causes VG Ca2+ to open, causing calcium-dependent calcium release from the SR. This calcium then binds to troponin which causes muscular contraction

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17
Q

What are the 2 types of Neuromuscular Junction blocking drugs?

A

Non-Depolarising (competitive antagonists) –> Acts by blocking ACh

Reversible by increase ACh levels (neostigmine)

Depolarising –> Weak nicotinic agonists

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18
Q

What % of ACh receptors needs to be blocked to prevent synaptic transmission at NMJs?

A

90% of receptors

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19
Q

What determins the rate of recovery, in terms of non-depolarising NMJ blockers?

A

Susceptibility to cholinesterases and clearance

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20
Q

What are the 3 main side effects of non-depolarising NMJ blockers?

A

Hypotension –> Due to the blockade

Histamine release from mast cells

Respiratory faliure

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21
Q

What type of molecules are depolarising NMJ blockers?

A

Symmetrical bisquarternary ammonium compounds

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22
Q

How do depolarising NMJ blockers work?

A

Bind and activate the nicotinic receptor, opening Na+ channels and causing depolarisation

They are slowly hydrolysed by cholinesterases, but the depolrisation is kept at the end plate

The Na+ channels become refractory, and so further binding of nictonic agonists has no effect, causing Ca2+ to build up….making the muscles flacid

The persistant stimulation that also occurs causes the receptors to desensitise. Therefore when the muscle does partially repolarise it has no effect (transmission is still blocked)

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23
Q

What are the main problems with depolarising NMBs?

A

Initial Muscle Twitching –> Due to initial depolarisation

Bradycardia

Post-op pain

Prolonged paralysis –> ONLY in cholinesterase deficinet patients

Hyperkalemia

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24
Q

What is the train of 4?

A

A way of assessing anasthetic depth

Usually 4 stimulatons would cause 4 APs, but when done with NMBs the response is reduced

Non Depolarising produces a greater first reponse due to the higher ACh levels (due to ACh block)

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25
Q

What is Suxamethonium?

A

A depolarising NMB

Doesn’t cross the placenta as ionized

Has a rapid onset and short duration of action

26
Q

What’s Neostigmine?

A

An acetylcholinesterase inhibitor

Reverse non-depolarising NMBs… but potentiates depolarising NMBs!!

27
Q

What’s Sugammadex?

A

Chelates aminosteroids, such as rocurnium (a non-depolarising NMB)

Will NOT bind to atracurium

28
Q

What is Phenylketonuria?

A

An inherited deficinecy of Phenylalanine Hydroxylase (PAH) (an allosteric liver enzyme) which converts S-Phe to S-Tyr

Causes an increase in S-Phe, and deficinecy in S-Tyr

This causes neurological defects such as smaller brains and mental retardation (in children)

29
Q

What is the normal metabolic pathway for phenylalanine?

And where does it occur?

A

Occurs in the liver

30
Q

What are the consequences of Phenylketonuria?

A

Mental retardation

Prone to fractures due to poor bone metabolism –> due to strict diet that needs to be adhered to

Increases inflammation –> Due to ROS stimulation

Less NO levels

31
Q

How can we treat Phenylketonuria via dietary means?

A

Restrict S-Phe intake, such as meats (high AA content) and aspartate!

Must also take S-Tyr and other supplements

Very expensive foods!

32
Q

How can Large Neutral Amino Acids (LNAAs) and Sapropterin (BH4) help treat Phenylketonuria?

A

LNNAs –> Decrease the absorbance of S-Phe and competes for amino acid transporters (increasing AA levels in the brain)

Glycomacropeptdies are often a source of LNNAs

Sapropterin –> Acts as a co-substrate to PAH, creating more S-Tyr

Need some PAH to be avaliable to work, so milder PKU has the better outcomes

Often means diet can go back to normal (which is tempting for patients!)

Very expensive (over £100k per annum!)

33
Q

How can we treat PKU with gene, enzyme and probiotic therapy?

A

Gene –> Using an adenovirus to replace the genes in the tissue

This vector is only effective for a few weeks before the immune response renders it useless

Female mice needed 3x more of the vector, due to androgen signalling

Enzyme –> Directly replace PAH, or use enzymes (such as Phenylalanine Ammonia Lyase (PAL)) to degrade S-Phe

Must be given IV to prevent side effects in the HI

Probiotics –> Contain recombinant enzymes that are released in the small intestines (due to the bacteria being lysed). The enzmye breaks down S-Phe

Given IV and very expensive

34
Q

Define Safeguarding

A

Protecting peoples health, wellbeing and human rights, and enabling them to live free from harm, abuse and neglect. It’s fundemental to high-quality health and social care

35
Q

When does a child become an adult, in terms of safeguarding?

A

18 years old

36
Q

What could cause somebody to be a vunerable adult?

A

Elderly or frail

Has learning diabilities

Mental illnesses (dementia etc)

Physical disability

Substance misuser

Homeless

37
Q

What are the 10 different types of possible abuse?

A

Physical

Domestic

Sexual

Psychological

Finanical/Material

Modern Slavery

Discriminatory

Organisational

Neglect and Acts of Omission

Self-Neglect

38
Q

When abouts do the 3 trimesters occur in pregnancy?

A

1st –> Up to 13 weeks….the embryo is forming

2nd –> 13-28 weeks…..bodily systems are being refined

3rd –> After 28 weeks…..The body is growing

39
Q

What are some of the changes in absorption and distribution that occur in pregnancy?

A

Absorption –> Morning sickness can cause tablets not to be absorbed!

Progesterone slows gastric empyting, causing slower and less absorption

Distribution –> Total body water volume increases to 8L, which means drug concs are reduced due to dilation

Serum albumin decreases, so there is more free drug for highly bound drugs

40
Q

What do we measure in pregnancy to check thyroid function?

A

TSH due to protein binding changes

41
Q

What are some of the metabolism and excretion changes that occur during pregnancy?

A

Metabolism –> Quicker breakdown of pro-drugs and active drugs due to liver CYP450 changes

Eg, lamotrigene needs an increased dose in the 3rd trimester

Excretion –> Cardiac output and GFR increases, so renally excreted drugs are removed quicker

42
Q

In reference to pregnancy, why do we get less side effects of B-blockers and why are CCBs less effective?

A

B-Blockers –> Tachycardia occurs naturally in pregnancy, so the side effect of bradycardia is less likely to occur

CCBs –> The total peripheral resistance is already reduced, so CCBs are unlikely to futher decrease this

43
Q

How do most drugs pass through the placenta?

A

Simple diffusion

So dependent on MW and concentration gradient

44
Q

How is diabetes dealt with in pregnancy?

A

Glucose levels go all over the place during pregnancy due to glucose tolerence arising from anti-insulin effects

Lots of finger pricking is needed to check glucose levels

Insulin often needs to be administered

45
Q

What type of antihypertensives can be used in pregnancy?

A

Alpha-Methyl Dopa

Nifedipine

Labetalol

Hydralazine

46
Q

When is a baby known as a pre-term new born?

A

<37 weeks gestation

47
Q

What is the use of the IM, percutanous and rectal routes in neonates?

A

IM –> Not often used due to low muscle mass and blood flow, as well as distress to the patient

Percutaneous –> High absorption occurs due to the thin SC

Rectal –> Useful when other routes are inavaliable. However there is varaible blood supply to the rectum, and so absorption can be slow/incomplete

48
Q

What are the 2 different metabolic pathways for paracetamol in neonates and children/adults?

A

Neonates –> Sulphonation

Children/Adults –> Glucuronidation

49
Q

Why does a lower dose of Theophylline need to be given to neonates?

A

Because it is broken down to caffiene (which is active) is neonates, whereas in children/adults it is broken down to inactive metabolites

50
Q

What are the 3 different types of licence of drugs?

A

Licenced –> Shown to be safe and effective

Has suitable quality control

Unlicenced –> Not licenced for any age group or condition (eg, imports, specials or extemp)

Expensive but only some quality control

Off-Label –> Used outside of the drugs licence

Most common in the paediatric community

51
Q

What is a PUMA?

And what was the first drug to get one?

A

Paediatric Use Marketing Authorisation (PUMA)

Buccolam (Buccal Midazolam) –> 3 months to 18 years

52
Q

What type of IV formulations are contraindicated in pre-term neonates?

A

Benzyl Alcohol

Polyoxyl Castor Oil

Propylene Glycol (unless properly diluted)

53
Q

What type of antibody is given to babies via colostrum breastmilk?

A

IgA

54
Q

What type of drugs will pass into breastmilk?

A

Weak Bases

Low protein bound drugs

Drugs with high lipid solubility

MW of less than 300

Those with much longer half lives –> accumulation more likely

55
Q

How long does WHO recommend that women should breastfeed for?

A

First 6 months of the babies life

56
Q

What percentage of men and women are predicted to be obese by 2020?

A

80% of men

70% of women

57
Q

When can people be allowed to have bariatric surgery?

A

BMI of 40 or over…..or 35-40 and a co-morbitidity like T2DM

All non-surgical methods have been tried

Generally fit for anasthesia and the surgery

Commits to long term follow up

58
Q

Name 2 types of reversible and 2 types of non-reversible baratric surgeries

A

Reversible –> Intra-gastric balloon and Gastric band

Irreversible –> Gastric sleeve and Gastric bypass

59
Q

What is the peri-operative diet that patients must do when having bariatric surgery?

A

Liquid diet –> Pureed foods –> Soft foods –> Solid foods

Normal foods return after around 4-6 weeks

Often needed to reduce the size of the patients liver, which normally is very large…making surgery difficult

60
Q

What are the main physiological changes that occur after bariatric surgery?

A

Reduction in the surface area of the stomach –> Means disintergration takes longer

Reduced gastric volume –> Means many liquid preperations cant be taken, and solids may get stuck

Bypass of main areas of absorption –> sites of absorption for many drugs (like the duodenum) can be totally bypassed

pH changes –> Decreased HCl secretion means different salts for drugs (eg, calcium citrate instead of carbonate) that are not pH effected need to be used

Potentially rapid weight loss –> Alters volume of distribution

61
Q

What are the main post-op considerations that need to be made for bariatric surgery?

A

Review drugs with GI side effects (eg, NSAIDs and bisphosphonates)

Ensure monthly Vit B12 injections

Calcium and iron supplements (due to deficiency in bypass patients)

PA30325 (5 decks)

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