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MS2 exam1 > atherosclerosis > Flashcards

atherosclerosis Flashcards

1
Q

pathophysiology

A

-an abnormal characterized by disorders of the heart and blood vessels
common causes: HTN, coronary heart disease, stroke, CHF, smoking
-process begins as soft fatty deposits and hardens with age
-can occur in any artery but prefers coronary artery

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2
Q

patho cont.

A
  • focal deposits of cholesterol, lipids, cellular wastes, calcium, & other substances within the intima wall of an artery
  • build up referred to as plaque
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3
Q

endothelial injury theory

A
  • endothelium injury
  • hyperlipidemia (nondenuding); HTN (denuding); chemical irritants(infections)
  • 1) factor release into subendothelium
  • 2) smooth muscle cells move into intima
  • 3) initaites synthesis of collagen, lastic fiber protein, and protepglycans
  • 4) platelets ad clotting factors accumulate
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4
Q

developmental variable

A
  • takes many years, may start in childhood(15)
  • stage 1: fatty streak formation (reversable)–collateral circulation formation
  • stage 2: raised fibrous plaque–progressive changes (age 30 and up), chronic endotheial injury–HTN, elevated cholesterol, heredity, carbon monoxide, immune reactions, toxic substances
  • stage 3: complicated lesion: rigidity and hardening (atheromas)
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5
Q

formed plaque

A

hemorrhage into the plaque
thrombus formation on the plaques surface
total occusion
once occurred: myocardial infarction, stroke

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6
Q

unmodifiable risk factors

A

age
gender
genetic predisposition
ethnicity

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7
Q

modifiable risk factors

A 
elevated serum lipids and cholesterol correlated with : obesity, physical inactivity, high alcohol intake, intake of trans fatty acids, HDLs, LDLs, VLDLs
HTN
Smoking
physical inactivity [decreases HDLs, decreases fibrinolytic activity, stifles collateral formation]
obesity
Diabetes
stress/behavior patterns
elevated cholesterol
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8
Q

lipid synthesis: to utilize lipids

A

must become water soluble by combining with proteins
-lipoproteins provide vehicles for fat mobilization & transport
HDLs, LDLs, VLDLs

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9
Q

High density lipoproteins

A 
HDLs--healthy or good
contains more protein by weight and less lipids
carry lipids away from arteries
increase with physical exercise
decreased with age and Hx of CAD
>60= negative risk
45-59=average risk
36-44=moderate risk
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10
Q

Very low density lipoproteins

A

VLDLs
lethal or bad
leads to LDL
elevation may increase the risk of premature atherosclerosis with other risk factors (DM, HTN, smoking)

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11
Q

triglycerides

A

made of fatty acids (saturated or unsaturated)

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12
Q

low density lipoproteins

A 
lethal or bad
-contain more cholesterol than protein
--have an affinity for arterial walls
-decreased level is desirable 
160= high risk
>190= very high risk
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13
Q

cholesterol

A

liver manufacture cholesterol directly from foods we eat
-specifically from foods we eat: egg yolks, poultry, meat, fish, seafood(shrimp and shell fish), whole-milk dairy products, organ meats (liver, gizzards, etc.)

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14
Q

foods that do not contain cholesterol

A

fruits, veggies, grains (esp whole grains), nuts and seeds(except peanuts- have lots of oil)
typically the body makes all the cholesterol it needs, people do not need to consume it

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15
Q

cholesterol levels

A
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16
Q

saturated fats

A

major reason for elevated blood cholesterol
trans fats also do this
AHA says daily cholesterol intake

17
Q

primary prevention

A

Patient education:-reduce intake of saturated fats and cholesterol
-increase physical activity
-control weight
-smoking cessation
-decrease stress or alter behavioral patterns
evaluate dietary patterns

18
Q

secondary prevention

A

medication therapy

goals: increase lipoprotein removal
- restrict lipoprotein production
- decrease cholesterol absorption

19
Q

HGM CoA reductase inhibitors

A
  • STATINS
  • block synthesis of cholesterol
  • increase removal of LDLs and triglycerides
  • increase HDLs
  • administered at bedtime
  • require monitoring of liver function
  • side effects mild-severe, but subside as therapy continues
  • generally GI-constipation, abdominal pain and cramps
  • statins: Atorvastatin, pravastatin, simvastatin, lovastatin, fluvastatin
20
Q

benefits of statins

A
  • reduction of CHD mortality
  • overall reduction of coronary events
  • reduction of coronary procedures (PTCA/CABG)
  • reduction of strokes
  • reduction of overall mortality
21
Q

bile acid sequestrants

A
  • binds with bile acids in the intestine
  • forms an insoluble complex
  • excreted through the stool: loss of bile acids lowers cholesterol & LDL levels in liver by converting them, tends to increase triglyceride levels
  • side effects decreae over time: GI (consipation, nausea), interferes with absorption of other drugs: digoxin, beta-adrenergic blockers, coumadin, synthroid
22
Q

bile acid sequestrants

A
  • cholestyramine
  • colestipol
  • colesevelam
  • give before meals
  • mix with applesauce or a beverage (unpleasant gritty taste)
23
Q

nicotinic acid (niacin)

A
  • inhibits synthesis of VLDLs & triglycerides; decreasing LDL & cholesterol levels
  • increase HDL levels
  • Side effects: flushing, hyperglycemia, hyperuricemia, upper GI distress, hepatotoxicity( watch liver enzymes)
  • take with food but do not crush or chew
  • contraindications: liver disease, severe gout, peptic ulcer
24
Q

fibric acids (fibrates)

A 
reduce triglycerides by decreasing VLDLs
-decreases liver synthesis of VLDLs
-increases HDL
-may enhance the effects of anticoagulants and hypoglycemia
-give 30 mins before meals
-gemfibrozil, fenofibrate
side effects: dyspepsia, gallstones
-avoid grapefruit juice
25
Q

additional therapies

A
  • further intensify LDL lowering therapy
  • therapeutic options: higher dose of statin, Statin+bile acid sequestrant, statin + nicotinic acid
  • return visit in 6 weeks
26
Q

tertiary intervention

A

-initiate moderate physical activity and advance
-begin by reducing saturated fats and cholesterol
-weight management
-referral to a dietitian
return for follow up

27
Q

nursing diasnoses

A
  • not noted until client is symptomatic
  • symptoms dont start until arteries are 60-65% occluded
  • alteration in comfort/acute pain
  • anxiety
  • activity intolerance
  • lack of knowledge
  • ineffective therapeutic regime managment

MS2 exam1 (10 decks)

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