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Pharmacology > Week 9 & 10 > Flashcards

Week 9 & 10 Flashcards

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1
Q

Medications that can cause ulcers

A

NSAID -> These inhibit the arachidonic acid that produces prostaglandin that inhibits the action of gastrin, histamine and ACh in the production of gastric acid

Gram-negative bacterium: negative bacterium e.g. Helicobacter pylori

Hereditary factors: susceptibility of H pylori

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2
Q

General drug physiological function for treating Ulcers:

A

Drugs that affect gastric acid secretion and antibiotics for H pylori

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3
Q

H2 Receptor antagonists

A

Ranitidine (zantac)

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4
Q

Proton pump inhibs.

A

Omeprazole
Lansoprazole

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5
Q

Brief description of Omeprazole

A

▪ First and older drug, very effective
▪ Enteric coated capsules
▪ Irreversibly binds and inhibits H/K ATPase (proton pump)

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6
Q

Anticholinergics:

A

Atropine

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7
Q

Uses of Atropine for ulcers:

A

Reduces parasymp drive by blocking muscarinic receptors.

Not first line treatment.

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8
Q

Cytoprotective Prostaglandin analogues used with NSAIDs treatment which can cause ulcers

A

o Misoprostol PGE2
▪ Prostaglandin analogue which takes on the role of PGE2 and directly inhibits the proton
pump
▪ NSAIDs block all prostaglandin production and by taking PGE2 you are taking away the
suppression of gastric acid secretion but you’ll still get suppression of other prostaglandins
involved in inflammation in order to overcome it

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9
Q

what ions does H. Pylori produce?

A

bicarbonate ions (HCO3) from urea (urease enzyme)

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10
Q

What is responsible for most non-NSAID related bowel ulcers?

A

H. Pylori

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11
Q

2 ways that H. Pylori can cause peptic ulcer

A

H pylori disturbs the mucus layer predisposing a person to peptic ulcer disease: Urease activity -> releases ammonia and bicarbonate -> inc. pH -> stimulates Gastrin secretion -> inc. gastric acid secretion

Inflammation of the mucus layer by T-cells and cytokine release tends to suppress mucus secretion

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12
Q

why isnt monotherepy typically used to treat H. Pylori?

A

30% success rate

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13
Q

What therapy is used to treat H. Pylori peptic ulcers?

A

Triple therapy

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14
Q

example of Trip therapies used for H. Pylori peptic ulcers?

A

Antibiotic, proton pump inhibitor, bismuth subsalicylate (antacid)

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15
Q

examples of each individual drug for triple therapy

A

Bismuth is is toxic to H. pylori

metronidazole (antibiotic) and tetracycline (antibiotic) or amoxycillin
(antibiotic) -> typically effective A. biotics

Proton pump inhibitor (omeprazole), clarithromycin (antibiotic), amoxycillin . (reduce gastric secretion)

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16
Q

Why isnt triple therapy always succesful?

A

sometimes H. Pylori can get AB resistance.

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17
Q

What is cholesterol typically used for?

A

steroid hormone synthesis, bile acid and vitamin D.

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18
Q

What are chylomicrons ?

A

big bundles of triglycerides and cholesterol with a coat of phospholipids and proteins

-These go into lymphatic ducts (lacteals) - empty into the venous circulation

-They require a transport system because they are not soluble in blood

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19
Q

Can Chylomicrons cause atherosclerosis ?

A

No.. too large to burrow into endothelial walls of blood vessels.

Unless they are broken down by lipase. Free fatty acids will be released and the core of the chylomicron will be mostly cholesterol meaning it can be atherogenic.

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20
Q

VLDL meaning

A

Very-low-density-lipoprotiens.

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21
Q

where are left over chylomicrons typically taken?

A

to Liver

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22
Q

What happens to chylomicrons in the liver?

A

Combined with liapse to become a IDL and removed from circulation or further broken down into LDL

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23
Q

Why are LDL most dangerous for atherogenisis?

A

Whilst they are mostly protein they dont have as higher affinity for receptors as IDL and HDL, so theres more chance for them to build up and cause plaque.

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24
Q

Which type of LDL is the most problematic?

A

oxidised : it can get into smooth muscle layer and deposit

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25
What happens when LDL move through the endothelial lining to the smooth mm.?
Sets of alarm bells: attracts WBCs (monocyte macrophage system) to the area due to cytokines releasing chemical signals - They engulf the oxidised LDL and remain under the endothelium and become engorged with LDL named foam cells - They attract more macrophages which is the start of the plaque formation
26
what function does HDL do that IDL and LDL do not?
They readily absorb cholesterol and take it to be processed in liver whereas the others deposit cholesterol into cells (bad)
27
Other HDL benefits?:
* Other benefits of HDL: ** Anti-thrombotic effects ▪ Problem when atherosclerotic plaque is fully developed as it causes ruptures of these plaques ▪ But generally very useful **Endothelial anti-apoptotic effects ▪ Apoptosis - genetically programmed self-destruction ▪ Protects cells against dying ▪ Also increases production of NO (nitric oxide) by endothelium * Vasodilator * Anti-inflammatory effects * Stimulates repairing cells of the endothelium
28
How is LDL broken down in the body?
LDL in the circulation can be taken in by various cells (as a vesicle) -> breaks down -> various components released into cell -> receptors recycled (back into the membrane to wait for some more LDL)
29
Examples of statins
Atorvastatin, Fluvastatin, Pravastatin, HMG-coA reductase (enzyme) inhibitors
30
What are statins typically used for?
CVD
31
How do Statins work?
HMG-CoA is an enzyme involved in the synthesis of mevalonic acid which is further synthesised to form cholesterol in the liver cell * Decreasing HMG-CoA and therefore cholesterol levels stimulates the production of LDL receptors that are inserted into the membrane of liver cells to catch passing LDL and bring them into the cell. This is good for the health of the blood vessels. * Low intracellular levels of cholesterol means you get less production by the same hepatic cells of VLDL which also decreases arthrosclerosis risk
32
Adverse affects of statins
Muscle related - myalgia, myositis, myopathy, myolysis - creatine kinase increases o May even cause rhabdomyolysis * More likely to occur in the elderly and those with renal impairment * Known to be an increase in diagnoses of diabetes with people on statins (usually because they are already a high risk from other factors)
33
Examples of fibrates
Fenofibrate, Gemfibrozil, Activators of PPAR's * Activating receptors known as PPAR's
34
PPAR meaning
= Peroxisome proliferator-activated receptors
35
where are PPAR receptors typically located
nuclear membrane of cells
36
What do PPAR do?
o Cause changes in gene expression and various different proteins o Nutritional sensors ▪ Involvedinmodulationoflipidandglucosemetabolism * Both alpha and beta PPAR receptors exist - fibrates activate alpha o Increase fatty acid breakdown rates
37
Adverse effects of fibrates
In order of most common * GIT effects e.g. Abdominal pains, dyspepsia (indigestion) * Gall stones, pancreatitis * Jaundice, anaemia * Myopathies, rhabdomyolysis
38
What do ezetemibes do?
= inhibitor of intestinal transport of dietary cholesterol
39
How do ezetemibes work?
Agent on its own, not a class of drugs * Used for people who experienced adverse effects from statins * Inhibits uptake of cholesterol from the gut Reduces amount of chylomicrones in blood CAUSES AN UPTAKE OF LDL CELL RECEPTORS
40
what is an evolocumab
= monoclonal antibody against Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) (an enzyme, notice convertase)
41
How to use PCSK9?
When PCSK9 is involved, you don't get the LDL receptor returned to the membrane because everything is destroyed. When it is not present, LDL gets recycled and returns to the membrane. If you can remove PCSK9, you can make more of the LDL receptors recycled which is what the monoclonal antibody is doing. * Effective in increasing LDL receptors * Problems: expensive and a monoclonal antibody so must be injected * Used as second, third or fourth line of agents used to lower LDL levels (statins always first line)
42
adverse affects of evolocumab / PCSK9?
Injection site reactions * RTI (respiratory tract infections) and flu like illnesses * Infrequently, anything can be reported: headache, nausea, fatigue, joint pain, back pain, mm pain, infections in other organ systems, neurological systems, confusion, delirium etc
43
Name all the things needed to have metabolic disease? and how many of the listed are needed to have metabolic disease?
* Abdominal obesity * HTN * Elevated blood glucose (suggesting insulin resistance) * High triglycerides * Low HDL Need any 3 of these
44
What is the principle of chemo?
Chemotherapy = the treatment of disease by means of chemicals which have a selective effect on the disease- causing organisms or cancer cells (selective toxicity)
45
Antimicrobal meaning
Antimicrobial = general term for drug which acts on microbes (bacteria, fungi, protozoa etc.)
46
Antibacterial meaning
Antibacterial = drug which acts on bacteria
47
Antibiotic meaning
Antibiotic = substance produced by another microorganism, which has antibacterial or antimicrobial properties * Antibiotics - not as appropriate to call them this anymore because initially anti-bacterials were antibiotics because we collected them from e.g. Mould and substances that produced it but now it's a lot more synthetic
48
What is gram positive and negative used for?
Distinguishes between two major groups of bacterial - depends on whether or not they take up the gram stain (gram positive do, gram negative don't)
49
Describe peptidoglycan
absorbs the stain o Peptidoglycan = a polymer (sugars and amino acids) that forms a mesh-like layer on the outside of the plasma membrane of most bacteria, forming the cell wall o Much thicker layer in gram positive whereas gram negative has a much thinner layer and is hiding between an inner and outer membrane layer
50
Lipopolysaccardies and gram
(endotoxin) in the outer layer of the gram negative cell are antigenic (stimulate an immune response) for humans so should gram negative cells be broken down they can cause serious illnesses o Gram positive cells do not have these endotoxin bacteria (they do have exotoxins however) To summarise:
51
Bacteriostatic meaning
stop reproduction/ perliforation of bacterium
52
examples of bariostatics
* Tetracyclines * Macrolides * Sulfonamides * Trimethoprim * Oxazolidinones
53
Example of bacterialcidals
* B-lactams * Vancomycin * Aminoglycosides * Quinolones * Imidazoles * Polymyxins * Rifamycins There is some cross over between the bac. -cidals/statics (depends on levels and selective to some bacteria more than others)
54
Drawbacks of anti-microbals
Killing of normal flora -> superinfection o I.e. Killing the normal bacteria that complete your body (remember, most bacteria are helpful rather than pathological) o Superinfection because there is a constant competition between all the bacteria keeping them all at a reasonable level. If you knock some of them out, others will proliferate and overgrow potentially causing problems e.g. Diarrhoea, thrush * Resistance -> multi-drug resistance o Multi-drug resistance strains are being developed by the disease causing bacteria o Increase in the number of deaths due to infection that we haven't seen for a long time
55
what does Clostridium Difficile typically cause?
Overgrowth of this resident bacterium in the gut causes pseudomembranous colitis (yellow lumps in the large intestine), with risk of toxic megacolon (the colon becomes paralysed, gut motility reduces, becomes larger and actually burst)
56
Main problem with B- lactams
Main problems = bacterial resistance (bacteria produce B-lactamase -> breakdown B-lactams) and allergic reactions
57
what type of drug is B-lactams?
Bacterialcide
58
What drugs do B-lactams include?
penicillins, cephalosporins and monobactams
59
What type of drug is glycopeptides
bacterialcidal
60
what drugs are examples of glycopeptides
Vancomycin, teicoplanin
61
main uses of glycopeptides
Main problems = narrow spectrum (Gram pos bacteria), and toxicity Used only against resistant microbes or when pt is allergic to B-lactams
62
examples of penacilin
penicillin G, procaine penicillin, ampicillin, flucloxacillin
63
main drawback of penacilins ?
narrow spectrum of activity
64
Amoxycillin and ampicillin are useful for what and why
broader spectrum and effective against Gram neg bacteria
65
Flucloxacillin and dicloxacillin main use and drawback
Beta lactamase resistant (still effective on bacteria that produce B-lactamase) = can be used against MRSA
66
What can be combined with broad spectrum -cilins to aid with B-lactam resistancy
can be protected by combining with clavulanic acid (an inhibitor of B-lactamase)
67
What can also occur with -cilin allergy
Cross-sensitivity to cephalosporins and other B-lactams may also occur
68
How many generations of cephalosporins?
4: cephalexin1, cefamandole2, ceftriaxone3, cefepime4
69
What are cephalosporins derived from?
cephalosporium (mould).
70
cephalosporins have a narrower spectrum of action vs -cillins. T or F?
false - they are broader.

Pharmacology (6 decks)

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