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Flashcards in Drugs Deck (81):
1

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

2

Sodium nitroprusside MoA and Tx

Release NO to increase cAMP/cGMP
But molecule has cyanide so only used in emergency hypertension

3

PDEI is suitable for what type of hypertension

Pulmonary

4

What drug can interact with nitrates

PDEI esp if poor vascular health and with angina

5

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

6

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

7

CTZ area include

DRG NTS postrema

8

Postrema is part of what and where is it

Part of CTZ that is outside the BBB

9

Antiemetics for general purposes

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

10

Vasodilators

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

11

Inotropics

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

12

Antiarrhythmics

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

13

Motion sickness is due to

The activation of the LVC pathway
Labyrinthe-vestibular-cerebellum pathway (received from vestibular system in inner ears)

14

Tx for motion sickness

Antimuscurinics - mAChR blockers - scopolamine
Antihistamines -H1R antagonist - cinnarizine

15

Opioids acute OD Tx

Naloxone - IV over hrs (5 min halflife)
Mu receptor antagonist to prevent drug activity on GABA neurones

16

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

17

Symptoms of opioid OD

Myosis - pinpoint pupil (activate paraNS)
Unconsciousness

18

Why do we vomit

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

19

Define emesis

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

20

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

21

Do rodents vomit?

No they feel nauseous but doesn't vomit
Their body can digest the toxin and make use of t

22

Emesis associated with diseases

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

23

Iatrogenic emesis types (CDMA)

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

24

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

25

Dopamine induced emesis is associated with what type of drug

L-DOPa given to Parkinson's

26

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

27

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

Anti emetic
- metaclopromide

28

Opiates example

Apomorphine
Morphine
Heroin

29

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

30

Anticipatory emesis

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

31

Motion sickness emesis is due to

Activation of LVC pathway

32

Post operative emesis often due to

Stimulation of vagus nerve
General anaesthetics

33

Pregnancy emesis is due to

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

34

Where is the emetic centre

Medulla

35

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

Reticular formation

36

CTZ consist of

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

37

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

NK1 which uses substance P

38

Fenestration can be see at which bjtnof the CTZ

Postraema

39

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

40

What would happen if we have an universal antiemetic

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

41

S/E of antiemetics

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

42

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

43

What are we tolerant against

The rewarding effect produced by drug

44

Can dependence and tolerance be treated?

Yes and no respectively

45

Hyperlipidaemia drugs classes

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

46

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

Fish oil

47

S/E of bile binding resins

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

48

Lorsartan belongs to what class of drug

ATI inhibitor

49

ACEI example

Captopril

50

DHPS are used for

Ca blockers used for Hypertension to decrease vasoconstriction

51

NON DHPS used for (e.g verapamil, diltiazem

Cardiac arrhythmia

52

What is an atheroma

Build up of fatty deposits

53

Where does atheroma tends to form

At bifurcations

54

What other haemodynamic factors contribute to intima thickening

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

55

FIBRATES MoA

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

56

Hyperglycaemic fasting glucose level

> 7 mM

57

HbA1c levels for hyperglycaemia patient and normal person

DM > 48 mmol/mol and < 38 for normal

58

Chylomicron consist of

Cholesterol/ TG and FA

59

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

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

60

Where does lymphatic drain

L/R thoracic duct and enter bloodstream via subclavian veins

61

Apoproteins binds to what receptor

LDLR, part of outer chylomicron (polar structure)

62

What is cholesterol synthesised from

Acetyl co A

63

VLDL is

FA + chylomicron remnants - made in liver

64

What is endogenous cholesterol used for

Bile synthesis

65

LDLR stimulate uptake of what

Cholesterol

66

Why is LDL good indicator of disease

More likely to be taken up by hepatocytw

67

Increase HDL aids uptake of

LDL from plasma

68

What inhibits the Rate limiting step of cholesterol synthesis in liver

Statins

69

Fibrates activate what receptor

PPARa/RXR

70

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

71

Type IIb prescription esp needs

FIBRATES

72

Which hyperlipidaemia drug affects fat soluble vit D uptake

Bike acid binding resins

73

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

74

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

75

Problems with using thiazolidinedione

Water retention and weight gain

76

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

77

What is the bainbridge reflex

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

78

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

79

Long acting insulin

Glargine, determir

80

Rapid acting insulin

Aspart, lispro, glulisine

81

Intermediate insulin

NPH