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phar24 > Week 12 > Flashcards

Week 12 Flashcards

1
Q

What type of drugs are rosuvastatin & atorvastatin

A

Satins - lower cholesterol

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2
Q

What type of drug are pantoprazole & esomeprazole

A

Protein pump inhibitors - decrease acid secretion in the stomach

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3
Q

What type of drug is perindopril

A

ACE inhibitor

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4
Q

What type of drug are cefalexin & metformin

A

Antibiotics - help stop bacterial infections

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5
Q

What is metformin used for

A

First line drug for diabetes type II

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6
Q

What type of drug are escitalopram & Sertraline & what is the target

A

Serotonin - antidepressants = drug target transporter

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7
Q

Define dyslipdaemia

A

Abnormal amount of lipids in the blood

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8
Q

About how much of the plasma lipoproteins are synthesised in the liver

A

2/3rds

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9
Q

What do lipoproteins contain

A

Cholesterol

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10
Q

What is the effect of therapy that lowers LDL & raises HDL on coronary atherosclerosis

A

Reduce the progression of the disease

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11
Q

Define the disease coronary atherosclerosis

A

Cholesterol crystals & fat that gets into the vessel walls narrowing them and restriction blood flow, sometimes can rupture. If happens in the heart can decrease blood flow causing issues such as angina or even heart attack

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12
Q

Why are lipoproteins essential

A

Transport fat in the blood

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13
Q

What leads to lower density lipoproteins & why are LDLs smaller and denser

A

Higher fat content & lower protein. LDLs are smaller and denser because formed from VLDL after fatty acids/glycerol are cleaved off by lipases

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14
Q

Summary of the motion of chylomicrons

A
  1. Fat broken down to fatty acids & glycerol
  2. Absorbed by small intestine via transporter NPC1L1
  3. Packaged into chylomicrons
  4. Travels through circulatory
  5. Remnants go to liver where synthesised into Cholesterol
  6. Then packed into VLDL, liver can also release HDL
  7. VLDL can be broken down into LDL by lipoprotein Lipase in vascular endothelium once leaves liver
  8. LDL will deliver more cholesterol whilst circulating and will also be taken back up by the liver via LDL receptors
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15
Q

Define rate limiting enzyme

A

Slowest step in metabolic pathway

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16
Q

Simple enzyme used in the liver to synthesise cholesterol

A

HMG-CoA reductase = the rate limiting enzyme in the pathway

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17
Q

Where does HDL come from

A

Cholesterol turn over from cells - HDL takes cholesterol from cells and decreases tissue cholesterol = that’s why it’s kinda good

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18
Q

What is the primary target of lipid-modifying therapy

A

LDL-C

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19
Q

The higher the LDL-C and the lower the HDL-C, the higher the risk of…

A

ischemic heart disease

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20
Q

What are the classes of lipid lowering drugs

A
  • HMG-CoA reductase inhibitors - statins (most common)
  • Fibrates (fabric acid derivatives)
  • Bile acid-binding resins
  • cholesterol absorption inhibitors
  • nicotine acid —> rarely used
  • PCSK9 inhibitors —> new
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21
Q

Mechanism of action of bile acid-binding resins

A

Sequestrate bile acids in the intestine & prevent their reabsorption & enteropathy recirculation

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22
Q

when are bile acid-binding resins used

A

Hypercholesterolaemia = increased cholesterol in the blood stream

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23
Q

Adverse effects of bile acid-binding resins (dose related)

A
  • common is GI disturbances ( e.g., constipation, abdominal pain, flatulence, nausea)
  • Rare is fat-soluble vitamin deficiency
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24
Q

Effects of bile acid-binding resins on LDL, HDL, triglycerides

A

LDL - decreases
HDL - minimal increase if any
Triglycerides - minimal increase which is unwanted

25
Q

example of bile acid-binding resin

A

cholestyramine

26
Q

mechanism of action of cholesterol absorption inhibitor

A

blocks cholesterol transport protein in the brush border of enterocytes (intestinal wall), without affecting the absorption of fat solvable vitamins, triglycerides or bile acids

27
Q

when are cholesterol absorption inhibitors used

A

hypercholesterolaemia

28
Q

adverse effects of cholesterol absorption inhibitor

A

common - headache, diarrhoea
infrequent - myalgia, raised liver enzymes
rare - myopathy, raised creative kinase levels

29
Q

cholesterol absorption inhibitor effect on LDL, HDL, triglyceride

A

LDL- decreases
HDL - negligible
Triglyceride - negligible

30
Q

example of cholesterol absorption inhibitor drug

A

ezetimibe

31
Q

mechanism of action of fibrates

A

agonist of PPARaplha (nuclear receptor) leading to increase transcription of genes for lipoprotein lipase, apoA1 and apoA5

32
Q

fibrates effects on LDL, HDL, Triglycerides

A

LDL - 1 arrow decreases
HDL - 2 arrows increases
Triglycerides - 3 arrows decreases (plasma triglycerides)

33
Q

when are fibrates used

A
  • severe hypertriglyceridaemia with risk of pancreatitis
  • second line for mixed hyperlipidaemia and dyslipidaemia associated with diabetes
  • second line for hypercholesterolaemia
34
Q

adverse effects of fibrates

A

common - GI disturbances

rare - myopathy, rhabdomyolysis (muscle cells die and content released into bloodstream)

35
Q

example of fibrates

A

fenofibrate and gemfibrozil

36
Q

examples of PCSK9 inhibitors

A

evolocumab & alirocumab

37
Q

do PCSK9 inhibitors have high or low bioavailability and why

A

low because they are monoclonal antibodies so that have low VD and BA and high elimination half life

38
Q

mechanism of action of PCSK9 inhibitor

A

human monoclonal antibody that binds to PCSK9 = increase the number of LDL receptors by inhibiting their degradation by PVSK9

39
Q

when is PCSK9 used

A
  • homozygous and heterozygous familial hypercholesterolaemia
  • primary hypercholesterlaemia and pre- existing ischaemic CVD after inadequate response or intolerance to statins
  • when statin doesn’t work
40
Q

adverse effects from PCSK9 inhibitor

A

common - injection site reaction, rash

rare - hypersensitivity reactions

41
Q

effects of PCSK9 inhibitor drugs on LDL HDL and triglycerides

A

majorly decreases LDL

unsure about other 2

42
Q

normal bodily function of PCSK9

A
  • PCSK9 binds to same receptor as LDL receptor in liver cell
  • creating a complex that is broken down including the LDL receptor therefore few LDL receptors are recycled and more are needed to be made to reach membrane = takes a while
43
Q

how does the PCSK9 inhibitor work

A

it inhibits PCSK9 binding to LDL receptor so more LDL receptors recycle to absorb more LDL into liver cell to be broken down = remove LDL from plasma

44
Q

how does statin work to decrease cholesterol

A

indirectly decreases cell cholesterol which leads to increase expression of LDL receptors

45
Q

define primary compared to secondary hypercholesterolaemia

A

primary - high cholesterol due to genetics

secondary - mostly related to environment and other diseases such as diabetes

46
Q

mechanism of action of statins

A

inhibiting of HMG-CoA reductase, the rate limiting enzyme in cholesterol synthesis

47
Q

examples of HMG-CoA reductase inhibitor drugs

A

atorvastatin, fluvastatin, pracastatin, rosuvastatin, simvastatin

48
Q

when are statins used

A

hypercholesterolaemia

high risk of coronary heart disease with or without hypercholesterolaemia

49
Q

adverse effects of statins (dose related)

A

common - myalgia, sleep disturbances, mild GI symptoms, elevated aminotransferase concentrations

rare - myopathy, rhabdomyolysis, renal failure, hep, liver failure

50
Q

effects of statins on LDL, HDL, triglycerides

A

LDL - majorly decrease
HDL -slight increase
triglycerides - slight decrease

51
Q

what was the first statin in the market and is it inactive or active

A

simvastatin and inactive = metabolised in the liver to the active form

52
Q

what are the best drugs to treat dyslipidaemia

A

statins

53
Q

what factors increase the risk of statin-related adverse effects

A

pre-exisiting muscle, liver or kidney disease, high dose or high potency therapy, concurrent drugs, concurrent illness, frailty and advanced age

54
Q

is simvastatin an active or inactive drug

A

inactive - metabolised in the liver to the active form

55
Q

drug interactions with simvastatin

A

can lead to serious adverse affects

56
Q

what does simvastatin inhibit

A

HMG-CoA reductase

57
Q

what increases the risk of simvastatin inverse effects

A

preexisting muscle, liver or kidney disease, high-dose or high-potency therapy, concurrent drugs, concurrent illness, frailty and advanced age

58
Q

suffix of -sartan

A

angiotensin II receptor antagonist (ARB)

phar24 (12 decks)

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