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IPP/Drug Action > Drugs > Flashcards

Drugs Flashcards

1
Q

Statins MoA and S/E

A

Statins work by inhibit HMG-CoA reductase (rate limiting step for cholesterol synthesis in liver)
Can cause liver function impairment, muscle aches
Test baseline liver function
Oral administration overnight cause liver most active at night

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2
Q

Sodium nitroprusside MoA and Tx

A

Release NO to increase cAMP/cGMP

But molecule has cyanide so only used in emergency hypertension

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3
Q

PDEI is suitable for what type of hypertension

A

Pulmonary

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4
Q

What drug can interact with nitrates

A

PDEI esp if poor vascular health and with angina

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5
Q

How does cardiac glycoside work

A

Block Na/K ATP to make cell more excitatble to increase calcium levels and facilitate binding of troponinC to ca -> increase contractility

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6
Q

Vasodilation drugs

A 
Ca blockers - nifedipine (DHP) 
CGMP modulator - PDE I to prevent cGMP breakdown, GTN -> GC substrate spontaneous breakdown to NO
Organic nitrates (amyl nitrates) 
K activators - (ATP sensitive channels), minoxidil
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7
Q

CTZ area include

A

DRG NTS postrema

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8
Q

Postrema is part of what and where is it

A

Part of CTZ that is outside the BBB

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9
Q

Antiemetics for general purposes

A 
Aprepitant -NK1 antagonist 
Ondansetron - 5-HT3 antagonist 
Steroids (dexamethasone)
Cannabinoids - nabilone 
Neuroleptics - dirty drugs - haloperidol, domperidone metaclopromide 
BDZ- diazepam, lorazepam
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10
Q

Vasodilators

A 
K activators - amilodarone , minoxidil 
Ca blockers - nifedipine 
PDE3I or PDE5I 
Organic nitrate (amyl nitrate) 
GTN
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11
Q

Inotropics

A

Beta agonists (esp beta 1 - dobtamine)
Cardiac glycosides (digoxin) - block NaK/Katpase
PDE3I
Atropine (paraNS antagonist)

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12
Q

Antiarrhythmics

A 
Class I-IV
Na blockers - lidocaine (also block K)
Beta blockers - metaprolol, atenolol
K activator - amiodarone
Ca L type blocker - verapamil
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13
Q

Motion sickness is due to

A

The activation of the LVC pathway

Labyrinthe-vestibular-cerebellum pathway (received from vestibular system in inner ears)

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14
Q

Tx for motion sickness

A

Antimuscurinics - mAChR blockers - scopolamine

Antihistamines -H1R antagonist - cinnarizine

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15
Q

Opioids acute OD Tx

A

Naloxone - IV over hrs (5 min halflife)

Mu receptor antagonist to prevent drug activity on GABA neurones

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16
Q

Opioid Tx long term

A

Methadone (mu receptor agonist)

  • decrease dose overtime
  • doesn’t get as much of a awarding effect
  • help with withdrawal symptoms
  • log halflife (1 day) - oral
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17
Q

Symptoms of opioid OD

A

Myosis - pinpoint pupil (activate paraNS)

Unconsciousness

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18
Q

Why do we vomit

A

To get rid of toxic substances and to prevent further ingestion thereby minimising toxin uptake

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19
Q

Define emesis

A

Emesis is a combination of vomiting and nausea. Of which the former is beneficial whilst the latter is not

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20
Q

3 levels of action in preventing toxin uptake

A

1) sight and smell - avoidance - prevent encountering with the substance
2) spit - slight ingestion but limited
3) vomit - empty gastric content to prevent further uptake of substance

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21
Q

Do rodents vomit?

A

No they feel nauseous but doesn’t vomit

Their body can digest the toxin and make use of t

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22
Q

Emesis associated with diseases

A

Uraemia - high urea in plasma alters metabolism
Infections
Gastroduodenal reflex - gut wall damages

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23
Q

Iatrogenic emesis types (CDMA)

A

Chemo drug induced - cisplatin induced
Dopamine induced
Morphine induced
Alcohol induced

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24
Q

How does cisplatin induced emesis occur?

A

Cisplatin target cells via creating interstrand or intrastrand cross link which makes it hard for cells to unwind DNA during replication thereby inducing apoptosis. However, cisplatin targets all dividing cells meaning more rapidly turnover cells are more susceptible. Hence cisplatin result in great nephro/GI/BM toxicity and the gut wall is so severely damaged that the patient can tip their oesophagus

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25
Q

Dopamine induced emesis is associated with what type of drug

A

L-DOPa given to Parkinson’s

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26
Q

Morphine is an emetic drug because

A

It acts on GABAa receptor to prevent the GABA neurone from firing. This disinhibits the break on dopaminetgic neurones therefore the increase in dopamine results in emesis

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27
Q

What drug is administrated in conjunction with morphine administration during first infusion

A

Anti emetic

- metaclopromide

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28
Q

Opiates example

A

Apomorphine
Morphine
Heroin

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29
Q

Alcohol induced emesis is due to what mechanism

A

Increase in plasma concentration will stimulate brain to provoke vomit reflex
Also alcohol prevent PG synthesis, which is a trophic factor for gut lining secretion and thus gut wall is damaged and 5-HT is released into the bloodstream and via the X afferent to the CTZ

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30
Q

Anticipatory emesis

A

Imitated due to past experience

Controlled by higher sensory centre of brain

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31
Q

Motion sickness emesis is due to

A

Activation of LVC pathway

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32
Q

Post operative emesis often due to

A

Stimulation of vagus nerve

General anaesthetics

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33
Q

Pregnancy emesis is due to

A

High hCG levels - indicate good pregnancy

In extreme cases dehydration can cause metabolite imbalances which result in vomiting

34
Q

Where is the emetic centre

A

Medulla

35
Q

Dorsal bit of the medulla consist of what structure that control vomit reflex

A

Reticular formation

36
Q

CTZ consist of

A

Postrema, NTS, DRG which are anatomically close to each other

37
Q

NTS is filled with (majority) what type of emetic receptors?

A

NK1 which uses substance P

38
Q

Fenestration can be see at which bjtnof the CTZ

A

Postraema

39
Q

What part of CTZ is outside BBB and why

A

Postrema and to sense toxins before they get into brain. Toxins tends to be polar which mean they can’t cross BBB

40
Q

What would happen if we have an universal antiemetic

A

It will also repress RE or CVS function due to the similarity in neuronal phenotype

41
Q

S/E of antiemetics

A

Sometimes sedative
EPS (extrapyrimidal motor side effects) if block dopamine receptors
Depression
Cushings if give steroids

42
Q

How do we get High off substances and how is it regulated

A

Accumulation of extra cellular DA in the nucleus accumbens (Mesolimbic pathway). The high the plasma is saturated, the greater the high/rush/reward

43
Q

What are we tolerant against

A

The rewarding effect produced by drug

44
Q

Can dependence and tolerance be treated?

A

Yes and no respectively

45
Q

Hyperlipidaemia drugs classes

A 
Statins 
Vibrates 
PCSK9 inhibitor 
Bike acid binding resin 
Ezetimib - NPC1L1 blocker 
Fish oil 
Nicotine is acid
46
Q

What type of hyperlipidaemia drug is not suitable for type IIb patients

A

Fish oil

47
Q

S/E of bile binding resins

A

GI side effects
Very uncomfortable
Increase TG but decrease bile and cholesterol levels

48
Q

Lorsartan belongs to what class of drug

A

ATI inhibitor

49
Q

ACEI example

A

Captopril

50
Q

DHPS are used for

A

Ca blockers used for Hypertension to decrease vasoconstriction

51
Q

NON DHPS used for (e.g verapamil, diltiazem

A

Cardiac arrhythmia

52
Q

What is an atheroma

A

Build up of fatty deposits

53
Q

Where does atheroma tends to form

A

At bifurcations

54
Q

What other haemodynamic factors contribute to intima thickening

A

Shear stress impacting on EC making them cobblestone like and upregulate VCAM1 which recruits WBC

55
Q

FIBRATES MoA

A

Activate nuclear receptor and increase LDLR and lipoprotein lipase
Esp prescribed for type IIb

56
Q

Hyperglycaemic fasting glucose level

A

> 7 mM

57
Q

HbA1c levels for hyperglycaemia patient and normal person

A

DM > 48 mmol/mol and < 38 for normal

58
Q

Chylomicron consist of

A

Cholesterol/ TG and FA

59
Q

Hormone sensitive lipase can be stimulated by what and induce what process

A

Glucagon

Induce lipolysis to increase FA into bloodstream (bound to albumin)

60
Q

Where does lymphatic drain

A

L/R thoracic duct and enter bloodstream via subclavian veins

61
Q

Apoproteins binds to what receptor

A

LDLR, part of outer chylomicron (polar structure)

62
Q

What is cholesterol synthesised from

A

Acetyl co A

63
Q

VLDL is

A

FA + chylomicron remnants - made in liver

64
Q

What is endogenous cholesterol used for

A

Bile synthesis

65
Q

LDLR stimulate uptake of what

A

Cholesterol

66
Q

Why is LDL good indicator of disease

A

More likely to be taken up by hepatocytw

67
Q

Increase HDL aids uptake of

A

LDL from plasma

68
Q

What inhibits the Rate limiting step of cholesterol synthesis in liver

A

Statins

69
Q

Fibrates activate what receptor

A

PPARa/RXR

70
Q

Fibrate MoA

A

Activate PPARa receptor which increase transcription of lipoprotein lipase expression in PNS to remove TG from VLDL and chylomicron
Increase HDL thereby promote LDLuptake by increasing LDLR

71
Q

Type IIb prescription esp needs

A

FIBRATES

72
Q

Which hyperlipidaemia drug affects fat soluble vit D uptake

A

Bike acid binding resins

73
Q

What can be substitute Rx for bike acid binding resins

A

Ezetemib
- inhibit NPC1L1 receptor which is more precise and inhibits cholesterol absorption in gut. Doesn’t affect fat bit uptake

74
Q

PSCK9 inhibitor MoA

A

Normally they bind to LDLR and promote internalisation of receptor in hepatocytes and promote degradation
Inhibitor prevent this and hence more LDLR expressed to take up LDL

75
Q

Problems with using thiazolidinedione

A

Water retention and weight gain

76
Q

Thiazolidinedione MoA

A

Binds to PPAp gamma receptor which result in sensitisation of cells to insulin
Inhibiton of Angiogenesis, decrease TG and increase HDL to promote LDL uptake

77
Q

What is the bainbridge reflex

A

Increase SNS activity to the heart when blood volume increase
Might be protective reflex to prevent volume overload

78
Q

What is the mesolimbic pathway (where does it run)

A

Aka the motivated pathway (dopaminergic)
Runs via the medial forebrain bundle from the VTA (ventral segmental area) of the midbrain to nucleus accumbens and limbic region

79
Q

Long acting insulin

A

Glargine, determir

80
Q

Rapid acting insulin

A

Aspart, lispro, glulisine

81
Q

Intermediate insulin

A

NPH

IPP/Drug Action (5 decks)

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