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

Drugs Flashcards by Celine Chen

Statins MoA and S/E

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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Sodium nitroprusside MoA and Tx

Release NO to increase cAMP/cGMP

But molecule has cyanide so only used in emergency hypertension

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PDEI is suitable for what type of hypertension

Pulmonary

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What drug can interact with nitrates

PDEI esp if poor vascular health and with angina

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How does cardiac glycoside work

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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Vasodilation drugs

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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CTZ area include

DRG NTS postrema

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Postrema is part of what and where is it

Part of CTZ that is outside the BBB

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Antiemetics for general purposes

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

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Vasodilators

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

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Inotropics

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

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Antiarrhythmics

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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Motion sickness is due to

The activation of the LVC pathway

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

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Tx for motion sickness

Antimuscurinics - mAChR blockers - scopolamine

Antihistamines -H1R antagonist - cinnarizine

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Opioids acute OD Tx

Naloxone - IV over hrs (5 min halflife)

Mu receptor antagonist to prevent drug activity on GABA neurones

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Opioid Tx long term

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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Symptoms of opioid OD

Myosis - pinpoint pupil (activate paraNS)

Unconsciousness

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Why do we vomit

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

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Define emesis

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

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3 levels of action in preventing toxin uptake

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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Do rodents vomit?

No they feel nauseous but doesn’t vomit

Their body can digest the toxin and make use of t

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Emesis associated with diseases

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

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Iatrogenic emesis types (CDMA)

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

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How does cisplatin induced emesis occur?

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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Dopamine induced emesis is associated with what type of drug

L-DOPa given to Parkinson's

Morphine is an emetic drug because

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

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

Anti emetic | - metaclopromide

Opiates example

Apomorphine Morphine Heroin

Alcohol induced emesis is due to what mechanism

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

Anticipatory emesis

Imitated due to past experience | Controlled by higher sensory centre of brain

Motion sickness emesis is due to

Activation of LVC pathway

Post operative emesis often due to

Stimulation of vagus nerve | General anaesthetics

Pregnancy emesis is due to

High hCG levels - indicate good pregnancy | In extreme cases dehydration can cause metabolite imbalances which result in vomiting

Where is the emetic centre

Medulla

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

Reticular formation

CTZ consist of

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

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

NK1 which uses substance P

Fenestration can be see at which bjtnof the CTZ

Postraema

What part of CTZ is outside BBB and why

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

What would happen if we have an universal antiemetic

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

S/E of antiemetics

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

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

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

What are we tolerant against

The rewarding effect produced by drug

Can dependence and tolerance be treated?

Yes and no respectively

Hyperlipidaemia drugs classes

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

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

Fish oil

S/E of bile binding resins

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

Lorsartan belongs to what class of drug

ATI inhibitor

ACEI example

Captopril

DHPS are used for

Ca blockers used for Hypertension to decrease vasoconstriction

NON DHPS used for (e.g verapamil, diltiazem

Cardiac arrhythmia

What is an atheroma

Build up of fatty deposits

Where does atheroma tends to form

At bifurcations

What other haemodynamic factors contribute to intima thickening

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

FIBRATES MoA

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

Hyperglycaemic fasting glucose level

> 7 mM

HbA1c levels for hyperglycaemia patient and normal person

DM > 48 mmol/mol and < 38 for normal

Chylomicron consist of

Cholesterol/ TG and FA

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

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

Where does lymphatic drain

L/R thoracic duct and enter bloodstream via subclavian veins

Apoproteins binds to what receptor

LDLR, part of outer chylomicron (polar structure)

What is cholesterol synthesised from

Acetyl co A

VLDL is

FA + chylomicron remnants - made in liver

What is endogenous cholesterol used for

Bile synthesis

LDLR stimulate uptake of what

Cholesterol

Why is LDL good indicator of disease

More likely to be taken up by hepatocytw

Increase HDL aids uptake of

LDL from plasma

What inhibits the Rate limiting step of cholesterol synthesis in liver

Statins

Fibrates activate what receptor

PPARa/RXR

Fibrate MoA

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

Type IIb prescription esp needs

FIBRATES

Which hyperlipidaemia drug affects fat soluble vit D uptake

Bike acid binding resins

What can be substitute Rx for bike acid binding resins

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

PSCK9 inhibitor MoA

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

Problems with using thiazolidinedione

Water retention and weight gain

Thiazolidinedione MoA

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

What is the bainbridge reflex

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

What is the mesolimbic pathway (where does it run)

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

Long acting insulin

Glargine, determir

Rapid acting insulin

Aspart, lispro, glulisine

Intermediate insulin

NPH