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Yr 3 Cardiovascular > CVD Pharmacology > Flashcards

CVD Pharmacology Flashcards

(62 cards)

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1
Q

What is a lipoprotein

A

Lipids and cholesterol transported in blood as complexes of lipids and proteins
Hydrophobic core of lipid
Hydrophilic phospholipids, cholesterol and apoprotein

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2
Q

What are the types of lipoproteins

A

Chylomicrons (biggest) TG
Very low density lipoproteins TG
Low density lipoproteins TG and cholesterol
Intermediate density lipoproteins cholesterol
High density lipoproteins (smallest) proteins

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3
Q

How are cholesterol and TGs absorbed

A

From diet-> ileum -> chylomicrons-> lymph->blood-> muscle and adipose tissue
TG hydrolysed by lipoprotein lipase -> glycerol and fatty acids
Cholesterol stored if remaining chylomicrons

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4
Q

What lipoproteins are absorbed and in what stage?

A

Cholesterol and new TG travel as VLDL
Lipoproteins get smaller but keep cholesterol esters and become LDL and bind to receptors
Cholesterol deposited in tissues
Cholesterol can return to plasma via HDL (reverse cholesterol transport)
Cholesterol esterified with LCFA in HDL and transferred to VLDL or LDL by cholesterol ester transfer protein

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5
Q

How are cholesterol esters up taken by cells by the LDL receptors

A

Coated pit -> vesicle -> endosome -> recycling vesicle -> coated pit again

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6
Q

What is reverse cholesterol transport

A

Cholesterol from tissues back to liver
HDL made in liver- protein rich and no cholesterol
When circulating- takes up cholesterol
Forms spherical HDL3
CETP transfers cholesterol esters and HDL taken back to liver where hepatocytes excrete the cholesterol it contains

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7
Q

What is CETP

A

cholesteryl ester transfer protein
Transfers cholesteryl ester between HDL to IDL or VLDL

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8
Q

What is dyslipidaemia

A

Disorder of lipid metabolism (lipoprotein over production and deficiency)

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9
Q

What are the stages of atherosclerosis

A

Injury in endothelial cells of blood vessels
Adhesion molecules and monocytes bind
Blood vessels take up oxidised LDL and combines with macrophages (FORMS FOAM CELLS)
Foam cells under endothelial layer cause plaque - immune response!
More plaque causes necrotic core and fibrous cap on top forms
If ruptures then heart attack/stroke

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10
Q

What is the target for cholesterol

A

less than 5mmol/l
But 40% decrease in Non-HDL is the aim

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11
Q

What are some non-pharmalogical treatments of dyslipidaemia

A

Decrease sat and trans fats, increase unsat. fats= decr. LDL and incr. HDL
Oily fish
Plant sterols to decrease cholesterol abs.
Incr. fibre
Weight loss
smoking
30mins 5x a week activity
decrease alcohol

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12
Q

What do statins do

A

HMG-CoA reductase
Competitive and reversible
Decreases cholesterol synthesis
Increases LDL receptors
Decrease blood LDL as increases cholesterol uptake

RLS- catalyses conversion of HMG-CoA to mevalonic acid - prevents mevalonate production

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13
Q

What is simvastatin and pravastatin metabolised by

A

CYP450

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14
Q

What protective effects do statins offer

A

plaque stability
Anti thrombotic
Anti-oxidant - decreases NADPH oxidase
Anti-inflammatory - decreases NF-kB

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15
Q

What are fibrates and how do they work

A

-fibrate usually
agonists for PPARalpha
Increases APOA1, APOA11,ABCA1, APOC111, acyl-CoA synthase

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16
Q

What inhibits cholesterol absorption?

A

Ezetimibe
plant stanols and sterols

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17
Q

What does ezetimibe do

A

blocks NPC1L1- blocks abs of cholesterol without affecting vitamins, TGs or bile acids

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18
Q

What is the niacin MOA

A

Decreased TG synthesis as decreases mobilisation of FFA
Decreases VLDL and ApoB in hepatocytes

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19
Q

What is PCSK9

A

Proprotein convertase subtilisin/kexin type-9 (pcsk9)
Binds to hepatic LDL receptors and promotes lysosomal degradation of LDL particles
prevents recycling of LDL receptors back onto hepatocyte surface and therefore limits LDL uptake into liver

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20
Q

What is alirocumab and evolucumab

A

MAB that inhibit PCSK9 increasing receptor number and LDL uptake.
Anti-pcsk9 antibody binds to pcsk9 preventing it from binding to LDL receptor, allowing recycling of expression of LDL receptor

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21
Q

What is Inclisiran

A

small interfering RNA that inhibits translation of PCSK9 mRNA -> gene silencing!!
Interacts with RISC complex (RNA induced silencing complex)
which degrades mRNA of PCSK9
Less PCSK9 therefore less likely to interfere with LDL receptor expression

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22
Q

What is atherosclerosis

A

Damage to endothelial cells
LDL cross endothelial layer and accumulates/ oxidises
Markers expressed for immune response
Immune cells pass thru endothelial layer and destroy oxidised LDL
Immune cells -> foam cells
causes smooth muscle cells to form a FIBROUS CAP to stop access to necrotic core
Fibrous cap- plaque can thin and rupture causing blood clot

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23
Q

What is haemostasis

A

stopping blood loss from damaged blood vessels

wound
vasoconstriction
platelet activation and adhesion
coagulation (haemostatic plug)
Fibrinolysis (resolve coagulation)

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24
Q

What is thrombosis

A

formation of a clot

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25
What causes platelet activation and adhesion
Damage! Collagen exposure Thromboxane A2 and ADP can also activate platelets Platelet aggregation Fibrin/fibrinogen von willebrand factor prostacyclin nitric oxide
26
What do antiplatelets do
decrease platelet aggregation and inhibit thrombus formation
27
Name some antiplatelets
Aspirin Thienopyridines (clopidogrel) Ticagrelor
28
How does aspirin have anti-platelet activity
Irreversibly inactivates COX (cyclooxygenase) Prevents thromboxane A2 production in platelets therefore less clotting Also decreases prostaglandin formation COX1 IN PLATELETS-| decreases Thromboxane A2 decreasing platelet aggregation COX2 IN ENDOTHELIUM-| decreases prostaglandins but increases platelet aggregation Net effect = 0 HOWEVER- endothelial cells synthesize new COX 2 , platelets cant! Low doses only inhibit platelets, high dose inhibits both COX.
29
How do thienopyridines (clopidogrel) work as an antiplatelet
Inhibits ADP induced aggregation Antagonise platelet P2Y12 receptor
30
How does ticagrelor work as an antiplatelet
Nucleoside analogue - adenosine Blocks P2Y12 ADP receptors on platelets Allosteric inhibitor
31
How do Glycoprotein 11B and 111A receptor antagonists work
Binds to glycoprotein 11b/111a blocking fibrinogen preventing aggregation of platelets
32
How does coagulation work
Platelets attach to endothelium They release fibrin and seal endothelium Fibrin network traps RBC and seals endothelium Fibrin clot
33
What is the coagulation cascade
Intrinsic- damaged surface *xII-> xIIa *xI-> xIa *Ix-> Ixa *x-> xa * prothrombin(II) -> Thrombin (IIa) * Fibrinogen (I) -> Fibrin (Ia) * XIIIa *Cross linked fibrin clot Extrinsic -trauma *VII-> VIIa * tissue factor causes x-> xa * prothrombin(II) -> Thrombin (IIa) * Fibrinogen (I) -> Fibrin (Ia) * XIIIa *Cross linked fibrin clot
34
What is the role of thrombin
Cleaves fibrinogen producing insoluble fibrin Activated XIII strengthens fibrin links Platelet aggregation
35
Role of the liver and coagulation
Koagulation vitamin- VIT K Makes clotting factors makes bile salts
36
Anti-coag agents
warfarin and heparin
37
How do heparins work
Activates anti thrombin 111 Inactivates thrombin and Xa
38
What are the types of heparin
Unfractionated (inhibits thrombin and Xa) Low molecular weight (Mainly inhibits Xa- more predictable)
39
What are the advantages of Low molecular weight heparin
Binds less to endothelium so has better bioavailability and half life Predictable dose response Decreased frequency of dosing Less side affects- can be used at home
40
How does warfarin work
Inhibits vitamin K reductase Competitive therefore Anticoagulation factors and protein C cant be made
41
Does warfarin have direct action on clots?
No Acts indirectly via vitamin K
42
What are the pharmacokinetics of warfarin
Readily absorbed thru GIT Binds to plasma proteins Long half life! 37 hrs Metabolised by cytochrome P450 Hard to control drug
43
What is fibrinolytics
where clots are resolved and removed to restore blood flow Degrades fibrin polymers into smaller products (done by plasmin)
44
What is plasmin formed by and by what enzymes?
Plasminogen by: *Tissue plasmin activators (tPA) *Urokinase Plasminogen activator (uPA) *Kallikrein
45
What drugs stimulate fibrinolysis
streptokinase Urokinase- less useful/selective Recombinant human tPA: *reteplase *alteplase *tenecteplase
46
What is alteplase used for
'Clot selective' as active for fibrin bound plasminogen rather than plasma bound Acute ischaemic stroke, PVT and PE
47
What 3 classes of drugs are used for angina
Nitrates Beta blockers CCBs
48
What is angina pectoris
its a symptom Oxygen supply to myocardium is insufficient due to partial blockage or artery spasm
49
What are angina triggers
Increasing O2 needs and reducing O2 supply by increasing cardiac workload or having a restricted coronary perfusion
50
What decreases afterload of the heart
Arterial dilators- CCB and nitrates
51
What decreases pre-load
Venodilator eg nitrates
52
How to improve oxygen supply
CCB and nitrates Surgery- bypass , stent etc Decrease atherosclerosis
53
What drugs are used for angina
Organic nitrates CCBs B-adrenoreceptor antagonists (slows HR) Potassium channel activators (vasodilators)
54
What are some organic nitrates and whats the MOA
Glyceryl trinitrate (nitroglycerin) Isosorbide mononitrate Nitric oxide relaxes smooth muscle by Myosin Light Chain- mainly effects heart, decreases pre-load Low doses good- high doses can mess with BP and causes headache etc nitrates->Activates guanylate cyclase->cGMP-> Activation of Myosin Light Chain-> vasodilation-> decr. pre-load
55
What is shear stress
Frictional force parallel to wall
56
How do BBlockers work for angina
Decreases oxygen consumption Slows heart Secondary prevention Blocks calcium ions entering cells by blocking Voltage gated L-type Calcium channel. Binds to alpha1 subunit of cardiac L-type CaChannels
57
What BBlocker is contraindicated for heart failure
Verapamil
58
What do class 1 agents do and what are they
Na transporter blockers can lengthen, shorten or intensify the action potential in muscle cells in ventricles
59
What do class 2 agents do and what are they
B-Blockers Decreases Hr, usually affects SA node Prevents tachyarrhythmias
60
What do class 3 agents do and what are they
Potassium Channel blockers Widen duration of action potential Also can use sotalol
61
What do class 4 agents do and what are they
Calcium channel blockers Works on AV node
62
How does digoxin work
Inhibits Na/K ATPase Increases Na inside myocytes/ cells Increases exchange of Na for Ca Increases intracellular Ca Increases contractility of cardiac muscle

Yr 3 Cardiovascular (9 decks)

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