Vasoprotective drugs, angio-protectors. Dyslipidemic drugs.

Question 1

Classification of vaso protective drugs?

Answer 1

1. CAPILLAROTONIC - TROXEVASIN
2. VENTONIC - PEFLAVIT C
3. HEMORRHOIDAL - DETRALEX

Question 2

Explain the vaso protective drugs.

Answer 2

Decrease capillary permeability, increase tone in veins and treat dilated veins. Therapeutic use: venous thrombosis, allergy, radiation sickness. Good oral/topical administration, hepatic metabolism and urinary excretion. ADR’s: topical application – local irritation and allergy. Oral application – GI disturbance

Question 3

Classification of Dyslipidemic drugs?

Answer 3

Aim is to decrease LDL and increase HDL in the plasma.

1. Drugs that inhibit cholesterol synthesis:
   - STATINS
   - FIBRATES
   - NICOTINIC ACID
2. Drugs enhancing cholesterol elimination:
   - BILE ACID-BINDING RESINS
   - PHYTOPREPARATIONS
3. INHIBITORS OF INTESTINAL ABSORPTION OF CHOLESTEROL e.g. Ezetimibe
4. PREPARATIONS CONTAINING POLYUNSATURATED ESSENTIAL OMEGA-3 FATTY ACIDS e.g.
   Flax oil
5. MONOCLONAL ANTIBODIES (PCSK9) INHIBITORS e.g. Evolocumab

Question 4

Explain the “Statin” Dyslipidemic drugs.

Answer 4

Inhibit HMG CoA reductase which increases LDL receptors on cell membrane so more LDL can be
removed from the plasma. (Interaction of LDL with its receptor causes internalisation of LDL). PhK: variable oral absorption. Significant 1st pass metabolism, Lipophilic statins have larger volume of distribution. Some statins like Simvistatin require activation by liver. Elimination :Bile, faeces mainly but urinary excretion.

Therapeutic use: all hyperlipidemias.

ADR: myositis, rhabdomyositis, liver damage (monitoring of enzymes needed), GI disturbances.

Adverse drug reactions: Don’t combine with Fibrates and nicotinic acid due to increased risk of muscle damage

Question 5

Explain the “Fibrates” Dyslipidemic drugs.

Answer 5

Acts on “peroxisome proliferator-activated receptor alpha” (PPAR-alpha), a type of receptor which which regulates lipid metabolism.

PhK:
Absorption: Good oral absorption, highly bound to plasma proteins. Hepatic metabolism and urinary excretion. Therapeutic use: hypertriglyceridemias. Fenofibrate has uricosuric effect ( increased uric acid excretion in the urine.

ADR: Myositis, myopathy, rhabdomyolysis, GI disturbance.

Drug interactions: increase effects of Warfarin by displacing it from plasma proteins

Contraindications: liver or renal dysfunction.

Question 6

Explain the “NICOTINIC ACID (NIACIN) Dyslipidemic drugs.

Answer 6

Inhibits lipolysis and decreases triglycerides. Most potent for increasing HDL

PhK:
- Absorption: Good oral absorption, metabolised into nicotinamide adenine dinucleotide (NAD+), urinary excretion.

Therapeutic use: familial hyperlipidemias and severe hypercholesterolemias

ADR: flushing, hyperuricemia, impaired glucose tolerance and hepatatoxicity.

Question 7

Explain “Bile acid binding resins”, 2nd subtype of dyslipidemic drugs.

Answer 7

Binds to bile acids and prevents their absorption into enterohepatic circulation. They are excreted in the faeces. As a result there is an increased excretion of cholesterol containing bile acid, reducing the amount of LDL.

Therapeutic use: type IIA and IIB hyperlipidemias.

ADR: nausea, flatulence and constipation.

Contraindications: patients with hypertriglyceridemia (drugs cause increased triglycerides)

Question 8

Explain “EZETIMIBE” (3rd dyslipidemic subtype)

Answer 8

Function to inhibit cholesterol absorption by interfering with specific transport protein in intestinal mucosa.

PhK: no absorption. Acts locally in GIT.

Therapeutic use: Used to treat hyperlipidemias but should be used in combination with other drugs due to its weak effects.

ADR’s are uncommon (Like paracetamol).

Question 9

Explain “Omega 3 fatty acids” (4th subtype)

Answer 9

• Decrease serum triglyceride levels
• Given in combination with other drugs
• Therapeutic use: hypertriglyceridemias

Question 10

Explain the “Monoclonal antibody inhibitors” (EVOLOCUMAB)

Answer 10

• Block PCSK9 on liver and increase LDL receptor expression

PhD: decrease LDL