Test #4 Flashcards
where is atherosclerosis found
in any arteries but most commonly the coronary arteries.
how long does atherosclerosis take to develop
years and years.
ppl usually do not seek medical attention until the pt has symptoms which means the arteries have been hardened and narrowed for some time
why do pts have chest pain with atherosclerosis
because of the ischemia and the decreased perfusion to the heart.
what happens to the body in response to the plaque beginning to grow
it stimulates macrophages to come to the sight- an inflammatory response -
this then triggers inflammation
so there is increasing plaque formation in conjunction with inflammation causing stenosis
what are the non modafiable risk factors for CAD
age-
greatest among white middle aged med
>65 yrs in females
ethnicicty-
African Americans- early onset CAD (35-64yrs more than twice of caucasians)
Native Americans- <35 yrs
Genetics- contribution as high as 40-60%
What are the modifiable risk factors for CAD
HTN- puts greater demand on the heart to pump and increased BP causes strain on the vessels endothelial layer causing vessel injury, inflammation & dislodging of plaque
Diabetes- higher cholesterol and triglyceride levels
Tobacco use-causes increased HR and vasoconstriction increasing BP, decreases HDL, increases LDL & triglycerides. vessel inflammation
physical inactivity- diminishes lipid metabolism production of HDL, increases Cardiac workload
Obesity- high LDL & triglycerides, low HDL
what are the two forms of lipids
Triglycerides and Cholesterol
what are triglycerides and where do they come from
The major storage form of fat.
it is made in the liver but we also get from diet.
our body will convert any unnecessary calories into triglycerides
why do we need triglycerides
provides fuel for our body
helps release energy between meals
what to high levels of triglycerides indicate
an excessive amount of calorie intake
what is cholesterol and where does it come from
waxy fat like substance that occurs naturally in our body
our liver secretes it into our bloodstream
why do we need cholesterol
building block for:
hormones-cortisol, estrogen, cell membranes
bile acids
insulation of nerve fibers
why do we only need a small amount of cholesterol in our diet
because our liver can synthesize more if our body needs it
what food is cholesterol found in
meat
poultry
whole fat dairy
why are anti lipemic meds recommended for night
because our synthesis of these lipids are highest at night.
what are characteristics of lipoprotiens
lipid molecules
combo of protein and lipids
dont dissolve in blood.
have to be packaged and transported through the blood stream
how are lipoproteins classified
by their composition size and density
what are the lipoproteins
high density lipoprotein
low density lipoprotein
very low density lipoprotein
what do the lipoproteins do
to mobilize and transport lipid molecules (fat)
why is HDL better than LDL
because HDL has more protein (45-50% protein and 20%cholesterol) we want the high protein
while LDL has 45% cholesterol and only 25% is protein
is protein or fat more dense
protein is more dense than fat
what is the cholesterol and protein % in VLDL
55-65% triglycerides, 10-15% cholesterol , 5-10% protein
what are triglycerides associated with
High levels are associated with atherosclerosis
what makes HDL good
it contains up to 50% protein, contains less fat
we want HDL because it is a scavenger and carries away bad cholesterol from body’s tissues and arteries and carries it back to the liver for metabolism
helps protect the arteries of lipid accumulation
what does LDL do
carries cholesterol to places in our body where we need it such as cell membranes, cortisol, insulation of nerve fibers,
however
when there is too many LDLs it is carried to the arteries where we DONT need it
what is the role of VLDL
primary transport of triglycerides in the blood
from the liver to be stored in our fat tissue
what is the problem with VLDL
it migrates towards the fat tissue so we gain fat
and fat can be a risk factor for CAD as well as resistant to insulin possibly resulting in diabetes and CHO metabolism issues.
it also deposits cholesterol directly in the arterial walls
what are the levels for total cholesterol
<200–Desirable
200-240– borderline
>240– High
LDL levels
<100 Optimal
100-129 borderline
>130 High
HDL levels
<60 low
>60 optimal
VLDL levels
5-30
Triglyceride levels
<150 normal
150-199 Borderline
>200 high
what dietary approach should a person maintain when trying to control cholesterol
low caloric intake to avoid conversion of triglycerides in storage of fat
heart healthy- fruits, veggies, whole grains, lean meats, low fat dairy
limiting red meats and high sugary food items
decrease or eliminate saturated fat
avoid trans fat
increase mono and polyunsaturated fats (do not raise LDL levels and does increases good cholesterol, anti inflammatory effect)
increase omega 3 fatty acids (reduce risk of CAD & decrease mortality of MI and stroke)
increase fiber
what is the most contributing factor to dyslipidemia
saturated fats
what is the recommendation of saturated fats of total caloric intake
<30%
what does trans fat do
increases risk for CAD
raises LDL leves
lowers HDL
increase risk of BM type II
what foods are mono and poly unsaturated fats
olive oil, avocados peanut butter nuts seeds
what foods contain omega 3 fatty acids
tofu soy bean canola oils fish flaxseed
how does fiber lower cholesterol
it binds to cholesterol and eliminates it via feces
fiber makes us fuller faster therefore decrease in caloric intake
what is something a person can take to decrease cholesterol (that usually isn’t given to lower cholesterol)
metamucil
what can saturated fat do
raise bad cholesterol
raise good cholesterol
increases risk of heart disease
sources of saturated fats
beef pork chicken fat cheese butter tropical oils
food sources of trans fat
partially hydrogenated oils
fried foods
baked goods
margarine
what do the “statin” drugs do
enzyme that helps regulate cholesterol biosynthesis
goal: effect the enzyme that normally helps us produce cholesterol- this drug interferes with this synthesis.
interferes with hydroxymehtylglutaryl coEnzyme A
causing interference with production of cholesterol
why are liver enzymes monitored when on statin drugs
because these drugs are extensively metabolized by the liver so we want to make sure they aren’t effecting the liver
why would statins be recommended at night
because cholesterol biosynthesis is higher at night
what are the outcomes of “statin” therapy
decrease total cholesterol and LDL
decreasing plaque formation
thus decreased risk of MI and Stroke
increase HDL
what is the enzyme that synthesizes cholesterol
hydroxymethylglutaryl CoEnzyme A
what is a statin
a hydroxymethylglutaryl CoEnzyme A reductase inhibitor
what are the adverse effects of statins
abd cramps constipation diarrhea flatus heartburn
LT: rhabdomyolosis- if occurs d/c meds- condition is reversible after d/c meds
what is rhabdomyolysis and s/s
breakdown of muscle protein
s/s muscle pain, weakness, dark urine (kindeys having to break down and excrete myoglobin) which can lead to acute renal failure
what do we need to monitor for on pts taking statins
liver enzymes
and s/s of rhabdomyolosis
what can increase the risk of rhabdomyolysis
taking with grapefruit juice or grapefruit
or using statins with other anti-lipemic drugs
what is the only drug safe to use with statins
Cholestryamine
a bile acid sequestrant
what is the implimentation requirements for cholestyramine
it needs to be mixed with 4-6 ounces of fluid
dissolved thoroughly
can be given in applesauce- needs to be swallowed well
if it is not dissolved well in water (given too dry) it can cause a GI obstruction b/c this mixture has the ability to swell
administer other meds 1 hour before OR 4 hours after cholestyramine administration
what is cholestyramine used for
used for management of hypercholesterolemia
what do bile acids do
bile acids are re-absorbed in the small intestines and they return back to the liver and get recycled and become part of the bile acids
help us break down fat
but also they have the ability to carry cholesterol in high concentrations
how does cholestyramine work
eliminates cholesterol from circulating in our body by binding to the bile acid cholesterol complexes(forming an insoluble complex) BEFORE they are absorbed into the sm intestines and then it is excreted in feces
what is the goal of cholestyramine therapy
decrease cholesterol and LDL
what are adverse effects of cholestyramine
abd discomfort, constipation, nausea
what is niacin and what does it do
a nicotinic acid derivative
vit b3
lowers cholesterol in large doses
what happens when niacin is taken in large doses
250mg-2000mg in 2-3 divided doses
decreases VLDL, LDL, triglyceride synthesis
and MAY increase HDL
what are side effects of niacin
flushing of the face and neck
feeling like you are on fire/burning
itching
GI upset
why is niacin not the first choice
because of the adverse effects
if niacin is needed what can the pt do to reduce the severity of the side effects
take an aspirin 300mg 30 minutes before each dose
what is used in combination with niacin for dislipidemia
simvastatin + niacin = SIMCOR
however the risk for rhabdomylosis is increased
what is fibric acid derivatives used for
hyperlipidemia
pts who present with low HDL and high LDL and triglycerides
who DO NOT have CAD
and pts who have tried to correct levels with diet and exercise and other agents
what medication is the fabric acid derivative
gemfibrozil
what is the effect of gemfibrozil
decrease of triglyceride production by the liver and decrease triglyceride carrier protein (VLDL)
what is the goal of gemfibrozil
decrease triglycerides and increase HDL
side effects of gemfibrozil
abd pain
diarrhea
epigastric pain
what type of medication is ezetimibe
cholesterol absorption inhibitor
how does ezetimibe work
it inhibits absorption of cholesterol in the small intestines by up to 50%
causing less cholesterol to enter the blood stream
what can ezetimibe be used in conjunction with
statin drugs
what are the adverse effects of ezetimibe
NONE
what is CRP
c reactive protein
protein produced by liver- non specific that increases in the presence of inflammation in the body
-increases with CAD- because of the macrophages that are trying to eat up the fatty streaks on the lumen of the artery
-chronic elevation can be indicators of unstable plaques.
may also see increased CRP wth bacterial infections
what are the heart disease risks r/t crp levels
low risk <1mg
average risk 1-3mg/L
High risk >3.0mg/L
what is troponin
myocardial muscle protein
released into circulation AFTER cardiac injury or infarction
what is the biomarker of choice for myocardial infarctions
troponin
what are the ranges for troponin
<0.05=normal
0.05-2.3 = suspicion of MI
>2.3 = myocardial injury
what is the rise, peak and return to baseline time of troponin markers
rise 4-6 hours after MI onset
peak 10-24 hours
return to baseline 10-14 days
how often should a troponin be drawn
as a serial sampling
every 6-8 hrs for 24 hrs
because this allows to differentiate between an acute infarction compared to chronic troponin elevation
what is creatine kinase
enzyme found in muscle cells in the body such as skeletal muscle, brain, heart and nervous system
what would cause creatine kinase levels to rise
MI skeletal muscle injury strenuous excercise and taking certain medications such as statin d/t incidence of rhabdomylosis
what creatine kinase level is more specific to cardiac
ck-mb
what is the range levels for males and females for CK
males-50-204units/L
females- 36-160units/L
what is the rise peak and return of CK
rise-3-6 hours after onset
peaks 12-24 hrs
returns to baseline 12-48 hours
what two tests are ran to assess for MI
serial sampling of troponin and CK
what is myoglobin
a muscle protein that is released into circulation 2 hours after an MI
peaks of 3-15 hrs
what do the kidneys regulate
- regulate bp (RAAS)
- maintain fluid and electrolyte balance
- regulate acid base balance (reabsorb bicarb excrete H-vice versa)
what do the kidneys excrete
waste products of protein metabolism
-filter metabolic waste, toxins, excess ions and water from the blood
what endocrine functions do the kidneys have
- they secrete erythropoietin- hormone that stimulates bone marrow to produce RBCs & hgb
- secrete renin(regulate bp via RAAS)
- activates vitamin D3 to calcitriol to increase Ca levels.
what stimulates the kidneys to secrete erythropoietin
decreased perfusion to the kidneys
what does renin do
Renin is secreted by the kidneys when they sense low bp, low ecf, low Na+,
-it converts agniotensinogen to angiotensin I
(from there angiotensin I converts to angiotensin II from ACE and BP and fluid volume is increased)
what happens as CKD progresses
the kidneys are unable to excrete waste
- unable to respond to acid base imbalance
- unable to control BP or fluid vol.
what are the non modifiable risk factors
-family hx of kidney disease, DM, HTN, CVD
-age->60 have gradual loss of kidney function
-ethnicity-higher in African Americans d/t greater incidence of HTN and complications r/t htn
Hispanics
what are the modifiable risk factors for ckd
HTN- can cause arteries around kidneys to narrow, weaken and harden, deterioration of glomerulus altering filtering abilities
Diabetes- causes nephrons to slowly thicken and become scarred. damage glomeruli increasing permeability
what characterizes diabetic nephropathy
a progressive decline in GFR and proteinuria(confirmed on 2 different occasions 3-6months apart)
what is urea nitrogen
a waste product from the breakdown of protein in the body
what does a BUN reveal
indicates how well the kidneys and liver are working
(urea is made in the liver and excreted through kidneys via urine)
non specific to kidney function
what is BUN range
5-25mg/dL
what is creatinine range
0.5-1.2mg/dL
what is creatinine
a waste product of muscle metabolism
what does the creatinine test reveal
it is sensitive indicator of kidney function because creatinine is filtered out by the glomerulus
what do increased levels of creatinine indicate
diabetic nephropathy
what is the range for GFR
90-120
what does the GFR determine
how well the kidneys are filtering wastes from the blood.
what happens to GFR as BUN and creatinine levels increase
GFR decreases
because the glomerulus is no longer able to filter these out efficiently so they accumulate in the blood
what is the creatinine clearance
the total amount of creatinine that appears in urine
what does a decline in creatinine clearance indicate
a low GFR and impaired renal function
(there is less creatinine in the urine which means the glomerulus is unable to filter out the waste product indicating renal dysfunction)
what can cause an increase in creatinine clearance
increased meat consumption
what is the purpose of a 24 hr urine collection
to assess how much creatinine, protein and electrolytes are excreted in a 24 hr period.
can serve as an indicator of renal disease
-more accurate than a UA because certain substances are excreted at different rates throughout the day
what is the GFR in ckd stage 1
> or equal to 90 (can be as high as 120)
what is the goal management of CKD stage 1
manage and treat the underlying conditions causing kidney damage
slow progression and
reduce risks
what symptoms are associated with stage 1 CKD
patients are often symptom free
what is the GFR of stage 2 CKD
60-89
what are the symptoms of stage 2 CKD
pts are often symptom free
what is the GFR for stage 3 CKD
30-59
what begins to happen in stage 3 CKD
*complications arise and ckd progresses
hormones become imbalanced leading to anemia (lack of erythropoietin) and weak bones (lack of vit d3 conversion to cacitriol so calcium is not absorbed in sm intestines. )
what is the management of CKD stage 3
complications of stage 3 are evaluated and treated
what is the GFR of stage 4 CKD
15-29
what is the management of CKD stage 4
dialysis
possible kidney transplant
what is the GFR of stage 5 CKD
Kidney failure! (end stage kidney disease)
<15
what is the management of Stage 5 CKD
dialysis or kidney transplant is necessary to maintain life
what is renal osteodystrophy
a mineral and bone disorder/defective bone development
d/t renal disease
why does renal osteodystrophy occur in CKD patients
because less vitamin D is converted to calcitriol thus less Ca+ and phosphorus is absorbed in the gi tract-
this leads to defective bone development and hypocalcemia
what is the management for renal osteodystrophy
calcitriol and calcium supplements
how does osteomalacia occur in CKD pts
d/t the hypocalcemia from the decreased conversion of vit d3 to calcitrial
that signals the parathyroid gland to secrete more PTH that will stimulate the kidneys to form more calcitriol
it also causes demineralization of bone to increase the calcium and phosphorus levels thus leaving the bones softened
what would a pt want to avoid if they had hypocalcemia and hyperthyroidism 2ndary to CKD
they would want to avoid aluminum based products such as Milk of Magnesia and Mylanta
these can also contribute to osteomalacia
why would a CKD pt want to avoid aluminum products
because aluminum inhibits the influx of calcium to bones and suppresses the secretion of PTH
why would a CKD pt have hyperphosphatemia
high levels of phosphate are d/t bone demineralization
and
d/t decreased phosphate secretion
what can hyperphosphatemia cause
can lead to vascular and soft tissue calcifications
as well as
neuromuscular excitability such as cramps
what is the goal of treating hyperphosphatemia and how will it be acheived
to lower phosphate levels
by using phosphate binders such as PhosLo sevelamer
what do you need to keep an eye on when administering PhosLo
-it contains calcium so it can raise the calcium levels.
why would HTN be a clinical manifestation of CKD
because CKD kidneys sense a decreased perfusion and thus secrete more renin
via the RAAS system
the BP rises
-aldosterone also increases Na+ and water retention thus
The BP rises
why does proteinuria occur with CKD
The glomeruli are damaged and so their permeability is increased allowing larger particles such as proteins to escape.
why does peripheral edema occur in CKD
because the RAAS system is activated and thus aldosterone is secreted by the adrenal glads which causes Na+ and water retention
leading to hypervolemia thus edema in the lower extremities
why would a CKD pt need to worry about HF
d/t the chronic HTN caused from the CKD as well as the hypervolemia caused from the increased aldosterone and renin from the RAAS system
what is a consequence of hyperinsulinemia in CKD pts
alterations in lipoprotein metabolism
it suppresses lipoprotein lipase production by the liver
thus unable to break down VLDL and LDL
as well as hyperinsulinemia stimulates liver to produce triglycerides
the 3 of these(high LDL, VLDL and triglycerides) are causes of atherosclerosis and eventually lead to CVD
what does lipoprotein lipase do
breaks down lipoproteins LDL and VLDL
why is anemia associated with CKD
d/t the erythropoietin deficiency because the kidneys cannot secrete enough.
therefore bone marrow makes less RBC and hgb
the lower the RBC and Hgb the less perfusion the kidneys get thus the further deterioration of the kidneys
what is a possible management for anemia 2ndary to CKD
erythropoietin stimulating agents.
epoetin alpha
when would you hold epoeitn alpha
if their Hgb is > or equal to 10
what is a black box warning for epoeitin alpha
increased risk for cv and thromboembolic events
what must the pt have in order to take epoetin alpha
a functioning bone marrow and sufficient iron stores
what happens to the acid base balance in CKD
Metabolic acidosis occurs
bicarb is not able to be reabsorbed and is excreted.
H+ ions are not excreted and begin to accumulate in the acid dropping the pH level
what does the body to to attempt to correct metabolic acidosis
it tries to blow off CO2
which represents Kussmaul breathing
what does the excess H+ ions in the blood do
they move into the cell replacing K+, therefore there becomes an abundance of K+ in the circulation leading to hyperkalemia - cardiac dysrhythmias
what is an intervention for hyperkalemia 2ndary to metabolic acidosis
sodium polystyrene sulfonate(kayexalate)
for mild to moderate hyperkalemia
what is necessary for the pt to have in order for sodium polystyrene sulfonate administration
normal bowel function with active bowl sounds and normal bowel movements
DO NOT give to pt with chronic constipation, IBS, hx of bowel obstruction or bowel resection
what is the goal of sodium polystyrene sulfonate
normalized K+ levels
what are lifestyle modifications for pts with CKD
Manage HTN- ACE inhibitors(renoprotective/ ARBs(ckd)/ Losartan(diabetic nephropathy)
DASH diet- heart healthy
more fruits, veggies, fat free/low fat milk, whole grains, fish poultry beans seads, nuts
lower cholesterol - “statins” to lower LDL, triglycerides and raise HDL
maintain glucose control(hgba1c <7%)
exercise
avoid nephrotoxic drugs/drugs primarily excreted by kidneys (vanco)
avoid alcohol (causes kidneys to not be able to filter blood)
smoking cessation
what is a healthy level of sodium
less than 2300mg/day
