Cholesterol (normal levels), Statins, Beta blockers

Why is it important that nitric oxide and endothelin be released?

the tunica media needs to dilate or constrict to control blood pressure

atherosclerosis

plaque in the arteries

foam cells

macrophages that become laden with lipids after ingesting LDLs

what happens if nitric oxide is not released?

the arteries won’t dilate and foam cells build up; plaque continues to grow until it clogs the artery completely

Why does hypertension cause atherosclerosis?

Because hypertension is constrictive and makes it harder for blood to go through the arteries

factors of endothelial injury related to atherosclerosis

inflammatory reaction is incited and WBCs are brought to damage site → WBCs engulf and phagocytose lipids in the region to form foam cells → lack of NO release decreases the vasodilation ability in the BV → Excess of von Willebrand factor

how many liters of blood circulates in the body?

5 L

cardiac output

the amount of blood that flows from the heart’s left ventricle per minute

Peripheral vascular resistance (PVR)

resistance caused by blood vessels within the circulatory system

systole

when the ventricles are contracting (active part of BP)

diastole

when the heart muscles relax

lipids are composed of…

cholesterol

cholesterol is synthesized where?

in the liver

triglycerides

large lipid molecules acquired through diet and stored as fat tissue

Low density lipoproteins

bad cholesterol, deposited on artery walls usually in areas where inflammation is occurring; they form foam cells when being phagocytosed by WBCs and contribute to atherosclerosis

high density lipoproteins

good cholesterol that is cardioprotective because it carries cholesterol away from the artery walls to be excreted

Why does exercise combat cholesterol?

Increased metabolism makes body more efficient at removing cholesterol

Why must you give diet restrictions for statin meds?

so people don’t think they can eat whatever they want; If they do, they will gain weight, which will increase triglycerides and the meds can’t keep up

When should statins be taken?

at night because liver works better at night when making cholesterol

what should a patient not have when taking statins?

grapefruit because it interferes with the enzyme that breaks down certain drugs, so the dose will not work properly and will cause issues

What are statins?

drugs that are HMG-CoA reductase inhibitors that are recommended if diet and exercise are ineffective at lowering bloodstream lipids

How do statins work?

they block the liver enzyme that assists in cholesterol manufacturing; they can reverse atherosclerotic plaque formation

what is HMG-CoA reductase?

an enzyme in the liver that synthesizes cholesterol

actions of statins (AKA HMG-CoA reductase inhibitors)

inhibition of HMG-CoA,

decreses serum cholesterol, LDLs, and triglyceride levels

increases HDL levels

Indications of statins (AKA HMG-CoA reductase inhibitors)

used in addition to diet in the treatment of high cholesterol, LDLs, and triglycerides

pharmacokinetics of statins (AKA HMG-CoA reductase inhibitors)

absorbed in GI tract, undergoes first-pass metabolism by liver

excreted in urine and feces

Contraindications of statins (AKA HMG-CoA reductase inhibitors)

allergy

active liver disease or history of alcoholic liver disease

pregnancy and lactation

cautions of statins (AKA HMG-CoA reductase inhibitors)

impaired endocrine function

adverse effects of statins (AKA HMG-CoA reductase inhibitors)

GI symptoms: flatulence, cramps, nausea, vomiting, constipation

CNS symptoms: headache, dizziness, blurred vision, insomnia, fatigue

liver failure

rhabdomylosis (muscle break down)

Prototype of statins

atorvastatin

atorvastatin route

oral route

atorvastatin onset

slow onset

atorvastatin peak

1-2 hrs

atorvastatin duration

20-30 hrs

total cholesterol desired

<200 mg/dL

total LDL cholesterol desired

<100 mg/dL

total HDL cholesterol desired

≥ 60 mg/dL

total triglycerides desired

< 150 mg/dL

target organs of HTN

heart - left ventricular hypertrophy

brain - hemorrhagic stroke

extremities - PAD

retina - retinopathy

kidney - damage of glomeruli

actions of beta-blockers

competitively blocks beta receptor sites in heart and kidneys

decrease heart rate and cardiac output

indications of beta blockers

treatment of supraventricular tachycardia and premature ventricular contractions

adverse effects of beta blockers

cardiac: bradycardia, heart failure, cardiac arrhythmias, heart blocks, cerebrovascular accident, pulmonary edema

GI: cramps, flatulence, nausea, vomiting, diarrhea

Other: impotence, decreased exercise tolerance

prototype for beta blockers

propranolol

propranolol routes

oral, IV

propranolol oral onset, peak, and duration

Onset: 20-30 mins

Peak: 60-90 mins

Duration: 6-12 hrs

propranolol IV onset, peak, and duration

Onset: immediate

Peak: 1 min

Duration: 4-6 hrs

How do Beta blockers control BP?

leads to decrease in HR, strength of contraction, and vasodilation

Symptoms of PAD; 5 Ps

palpable coolness

pain (intermittent claudication)

paresthesias (tingling/numbness)

pulselessness

paresis (weakness of extremities)

(honorable mention is pallor)

why does diabetes cause PAD?

uncontrolled diabetes can cause endothelial injury → decreased sensation in the feet → decreased blood flow to feet → decreased wound healing in feet