Cardiac Pharmacology Flashcards
What is usually seen in the ribs In case of aortic coarctation?
(birth defect of narrowing of aorta)
We see the Notching on the ribs (inferior side as the intercostal rteries run there)
the nothing is due to the increased pressure in the IC arteries due to the coarctation of aorta.
What are the two types of hypertension?
Primary (idiopathic causes)
treatnment- lifestyle changes, low salt, lose weight,Excersise,
Secondary (some previous underlying cause)
Name the classes of druugs used to treat Hypertension.
Sympatholytics
Direct Vasodilators
Calcium Channel blockers
RAAS modulators
Diuretics
What is Fenoldopam?
fan of Dopamine) D1 receptor is a Gs GPCR (that means increase cyclic AMP
class - sympatholytic (peripheral acting)
Selective D1 partial agonists (dopamine receptor 1 agonists)
helps vasodilationused in hypertensive crisis
What is a Partial agonist?
In pharmacology, partial agonists are drugs that bind to and activate a given receptor, but have only partial efficacy at the receptor relative to a full agonist.
What is Reserpine
Class - Sympatholytic
Blocks VMAT. no epinehrine formation. no release
VC is prevented
Heart rate Can not go up
no release of renin from JG cells
what do you mean by Sympatholytic drugs.
Sympatholytic drugs stops or oppose the physiological results of sympathetic nervous activity or of sympathomimetic drugs.
such as opposing vasoconstriction done by sympathetic NS.
what is VMAT ?
Vesicular Monoamine transporter
Phenylalanine to tyrosine to dopa to dopamine.
once dopamine is formed into the sympathetic neuron it is then inserted into the vesicle through VMAT and then converted to Norepinephrine.
What is the diffrence between centrally acting and peripheral acting sympatholytics?
central = Doesnt allow release of neurotransmitters peripheral = transmitter released from synapse but inhibiting the receptors so the NT doesnt act
What will happen if you Inhibit the sympathetic Nervous system?
centrally - sedation,drowsiness,depression and libido occurs
peripheral- alpha1 blocks=postural hypotension and low TPR (afterload)
(alpha1 is on vessels and Beta 2 is on heart muscle)
beta2 = decrease heart rate
now when sym is blocked parasym works more
that means doarrhoea, high secretion and high urination
high gastric acid secretion can worsen PUD
what type of receptor is alpha 1?
Gq (calcium increase and vasoconstriction)
Explain the Lipid lowering agents.
statins - HMG CoA reductase inhibitors
Fibrates- Lipoprotien lipase Activator
Cholsyramine- bile acid resins
Niacin- Hormone synthesis lipase inhibiot
Ezetimibe- Cholesterol uptake ing=hibitor
PCSK inhibiotrs
Bempedoic acid
Explain metabolism of cholesterol :)o
Eat cheeseburger =Dietary cholesterol= stomach=intestine = gets absorbed= gets packed into chylomicrons=hets to lymph=goes to portal venous system= goes to liver= liver synthesize Cholesterol=secrete in systemic venous system
Explain Niacin’s Two functions.
In lower doses - Vitamin B3
In Higher doses acts as anti-hyperlipidemic drug
how many Lipoprotiens do we have?
lipid+protiens
chylomicrons (low protien high lipid)
vLDL (low Protien high lipid)
LDL (comparatively high protien but lipid ratio is still high)
HDL (ratio of both protiens and lipids are equal) (good cholesterol)
total cholesterpl = HDL+LDL + Triglycerides/5
Explain Ezetimibe.
It doesnt let the cholesterol absorb through Intestine :)
Inhibits dietary cholesterol from getting absorbed.
it can cause Diarrhoea and greasy stool.
How ezetimibe stops dietary cholesterol from getting absorbed into the intestine?
There is a cholesterol transporter in GIT and the Liver called the Niemann pick C1 like protien.
this drug inhibits this transporter
How statins works? (HMG CoA reductase inhibitors)
HMg coa in liver is converted to the Mevalonic acid which then is further converted to cholesterol in liver.
by inhibiting the HMG Coa reductase these drugs stops the cholesterol formation within the liver.
low cholesterol in liver= liver cells increase the number of LDL transporter for compensation= more LDL comes to liver from blood= low cholesterol in blood.
side effect can include liver toxicity and rhabdomyalisis (breakdown of muscle cell)
used in MI and prevention of Strokes
why do we need cholesterol?
Cholesterol is a fat-like, waxy substance that helps your body make cell membranes, many hormones, and vitamin D. The cholesterol in your blood comes from two sources: the foods you eat and your liver. Your liver makes all the cholesterol your body needs.
Cholesterol and other fats are carried in your bloodstream as spherical particles called lipoproteins. The two most commonly known lipoproteins are low-density lipoproteins (LDL) and high-density lipoproteins (HDL).
diff in vldl and ldl
The main difference between VLDL and LDL is that they have different percentages of the cholesterol, protein, and triglycerides that make up each lipoprotein.
VLDL contains more triglycerides. (fatty acids)
LDL contains more cholesterol.
VLDL and LDL are both considered types of “bad” cholesterol.
liver makes VLDL====gets converted to IDL=======gets converted to LDL=======plaques
how Fibrates drugs help lower cholesterol?
Fibrates activates the LPL enzyme that converts vLDL to IDL.
since they increase the catabolism of vLDL and vldl are rich in triglycerides they are basically lowering the amount of tgs present
since the metabolism is increased these dugs can cause gallstones as the cholesterol after metabolism goes to the bile :)
