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202D > Test #4 > Flashcards

Test #4 Flashcards

1
Q

where is atherosclerosis found

A

in any arteries but most commonly the coronary arteries.

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2
Q

how long does atherosclerosis take to develop

A

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

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3
Q

why do pts have chest pain with atherosclerosis

A

because of the ischemia and the decreased perfusion to the heart.

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4
Q

what happens to the body in response to the plaque beginning to grow

A

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

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5
Q

what are the non modafiable risk factors for CAD

A

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%

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6
Q

What are the modifiable risk factors for CAD

A

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

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7
Q

what are the two forms of lipids

A

Triglycerides and Cholesterol

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8
Q

what are triglycerides and where do they come from

A

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

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9
Q

why do we need triglycerides

A

provides fuel for our body

helps release energy between meals

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10
Q

what to high levels of triglycerides indicate

A

an excessive amount of calorie intake

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11
Q

what is cholesterol and where does it come from

A

waxy fat like substance that occurs naturally in our body

our liver secretes it into our bloodstream

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12
Q

why do we need cholesterol

A

building block for:
hormones-cortisol, estrogen, cell membranes
bile acids
insulation of nerve fibers

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13
Q

why do we only need a small amount of cholesterol in our diet

A

because our liver can synthesize more if our body needs it

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14
Q

what food is cholesterol found in

A

meat
poultry
whole fat dairy

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15
Q

why are anti lipemic meds recommended for night

A

because our synthesis of these lipids are highest at night.

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16
Q

what are characteristics of lipoprotiens

A

lipid molecules
combo of protein and lipids

dont dissolve in blood.
have to be packaged and transported through the blood stream

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17
Q

how are lipoproteins classified

A

by their composition size and density

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18
Q

what are the lipoproteins

A

high density lipoprotein
low density lipoprotein
very low density lipoprotein

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19
Q

what do the lipoproteins do

A

to mobilize and transport lipid molecules (fat)

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20
Q

why is HDL better than LDL

A

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

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21
Q

is protein or fat more dense

A

protein is more dense than fat

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22
Q

what is the cholesterol and protein % in VLDL

A

55-65% triglycerides, 10-15% cholesterol , 5-10% protein

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23
Q

what are triglycerides associated with

A

High levels are associated with atherosclerosis

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24
Q

what makes HDL good

A

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

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25
Q

what does LDL do

A

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

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26
Q

what is the role of VLDL

A

primary transport of triglycerides in the blood

from the liver to be stored in our fat tissue

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27
Q

what is the problem with VLDL

A

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

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28
Q

what are the levels for total cholesterol

A

<200–Desirable
200-240– borderline
>240– High

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29
Q

LDL levels

A

<100 Optimal
100-129 borderline
>130 High

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30
Q

HDL levels

A

<60 low

>60 optimal

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31
Q

VLDL levels

A

5-30

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32
Q

Triglyceride levels

A

<150 normal
150-199 Borderline
>200 high

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33
Q

what dietary approach should a person maintain when trying to control cholesterol

A

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

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34
Q

what is the most contributing factor to dyslipidemia

A

saturated fats

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35
Q

what is the recommendation of saturated fats of total caloric intake

A

<30%

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36
Q

what does trans fat do

A

increases risk for CAD
raises LDL leves
lowers HDL
increase risk of BM type II

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37
Q

what foods are mono and poly unsaturated fats

A

olive oil, avocados peanut butter nuts seeds

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38
Q

what foods contain omega 3 fatty acids

A 
tofu
soy bean
canola oils
fish
flaxseed
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39
Q

how does fiber lower cholesterol

A

it binds to cholesterol and eliminates it via feces

fiber makes us fuller faster therefore decrease in caloric intake

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40
Q

what is something a person can take to decrease cholesterol (that usually isn’t given to lower cholesterol)

A

metamucil

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41
Q

what can saturated fat do

A

raise bad cholesterol
raise good cholesterol
increases risk of heart disease

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42
Q

sources of saturated fats

A 
beef
pork
chicken fat
cheese
butter
tropical oils
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43
Q

food sources of trans fat

A

partially hydrogenated oils
fried foods
baked goods
margarine

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44
Q

what do the “statin” drugs do

A

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

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45
Q

why are liver enzymes monitored when on statin drugs

A

because these drugs are extensively metabolized by the liver so we want to make sure they aren’t effecting the liver

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46
Q

why would statins be recommended at night

A

because cholesterol biosynthesis is higher at night

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47
Q

what are the outcomes of “statin” therapy

A

decrease total cholesterol and LDL
decreasing plaque formation
thus decreased risk of MI and Stroke
increase HDL

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48
Q

what is the enzyme that synthesizes cholesterol

A

hydroxymethylglutaryl CoEnzyme A

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49
Q

what is a statin

A

a hydroxymethylglutaryl CoEnzyme A reductase inhibitor

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50
Q

what are the adverse effects of statins

A 
abd cramps
constipation
diarrhea
flatus
heartburn

LT: rhabdomyolosis- if occurs d/c meds- condition is reversible after d/c meds

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51
Q

what is rhabdomyolysis and s/s

A

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

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52
Q

what do we need to monitor for on pts taking statins

A

liver enzymes

and s/s of rhabdomyolosis

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53
Q

what can increase the risk of rhabdomyolysis

A

taking with grapefruit juice or grapefruit

or using statins with other anti-lipemic drugs

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54
Q

what is the only drug safe to use with statins

A

Cholestryamine

a bile acid sequestrant

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55
Q

what is the implimentation requirements for cholestyramine

A

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

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56
Q

what is cholestyramine used for

A

used for management of hypercholesterolemia

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57
Q

what do bile acids do

A

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

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58
Q

how does cholestyramine work

A

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

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59
Q

what is the goal of cholestyramine therapy

A

decrease cholesterol and LDL

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60
Q

what are adverse effects of cholestyramine

A

abd discomfort, constipation, nausea

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61
Q

what is niacin and what does it do

A

a nicotinic acid derivative
vit b3

lowers cholesterol in large doses

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62
Q

what happens when niacin is taken in large doses

A

250mg-2000mg in 2-3 divided doses

decreases VLDL, LDL, triglyceride synthesis
and MAY increase HDL

63
Q

what are side effects of niacin

A

flushing of the face and neck
feeling like you are on fire/burning
itching
GI upset

64
Q

why is niacin not the first choice

A

because of the adverse effects

65
Q

if niacin is needed what can the pt do to reduce the severity of the side effects

A

take an aspirin 300mg 30 minutes before each dose

66
Q

what is used in combination with niacin for dislipidemia

A

simvastatin + niacin = SIMCOR

however the risk for rhabdomylosis is increased

67
Q

what is fibric acid derivatives used for

A

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

68
Q

what medication is the fabric acid derivative

A

gemfibrozil

69
Q

what is the effect of gemfibrozil

A

decrease of triglyceride production by the liver and decrease triglyceride carrier protein (VLDL)

70
Q

what is the goal of gemfibrozil

A

decrease triglycerides and increase HDL

71
Q

side effects of gemfibrozil

A

abd pain
diarrhea
epigastric pain

72
Q

what type of medication is ezetimibe

A

cholesterol absorption inhibitor

73
Q

how does ezetimibe work

A

it inhibits absorption of cholesterol in the small intestines by up to 50%
causing less cholesterol to enter the blood stream

74
Q

what can ezetimibe be used in conjunction with

A

statin drugs

75
Q

what are the adverse effects of ezetimibe

A

NONE

76
Q

what is CRP

A

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

77
Q

what are the heart disease risks r/t crp levels

A

low risk <1mg
average risk 1-3mg/L
High risk >3.0mg/L

78
Q

what is troponin

A

myocardial muscle protein

released into circulation AFTER cardiac injury or infarction

79
Q

what is the biomarker of choice for myocardial infarctions

A

troponin

80
Q

what are the ranges for troponin

A

<0.05=normal
0.05-2.3 = suspicion of MI
>2.3 = myocardial injury

81
Q

what is the rise, peak and return to baseline time of troponin markers

A

rise 4-6 hours after MI onset
peak 10-24 hours
return to baseline 10-14 days

82
Q

how often should a troponin be drawn

A

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

83
Q

what is creatine kinase

A

enzyme found in muscle cells in the body such as skeletal muscle, brain, heart and nervous system

84
Q

what would cause creatine kinase levels to rise

A

MI skeletal muscle injury strenuous excercise and taking certain medications such as statin d/t incidence of rhabdomylosis

85
Q

what creatine kinase level is more specific to cardiac

A

ck-mb

86
Q

what is the range levels for males and females for CK

A

males-50-204units/L

females- 36-160units/L

87
Q

what is the rise peak and return of CK

A

rise-3-6 hours after onset
peaks 12-24 hrs
returns to baseline 12-48 hours

88
Q

what two tests are ran to assess for MI

A

serial sampling of troponin and CK

89
Q

what is myoglobin

A

a muscle protein that is released into circulation 2 hours after an MI
peaks of 3-15 hrs

90
Q

what do the kidneys regulate

A
  • regulate bp (RAAS)
  • maintain fluid and electrolyte balance
  • regulate acid base balance (reabsorb bicarb excrete H-vice versa)
91
Q

what do the kidneys excrete

A

waste products of protein metabolism

-filter metabolic waste, toxins, excess ions and water from the blood

92
Q

what endocrine functions do the kidneys have

A
  • 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.
93
Q

what stimulates the kidneys to secrete erythropoietin

A

decreased perfusion to the kidneys

94
Q

what does renin do

A

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)

95
Q

what happens as CKD progresses

A

the kidneys are unable to excrete waste

  • unable to respond to acid base imbalance
  • unable to control BP or fluid vol.
96
Q

what are the non modifiable risk factors

A

-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

97
Q

what are the modifiable risk factors for ckd

A

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

98
Q

what characterizes diabetic nephropathy

A

a progressive decline in GFR and proteinuria(confirmed on 2 different occasions 3-6months apart)

99
Q

what is urea nitrogen

A

a waste product from the breakdown of protein in the body

100
Q

what does a BUN reveal

A

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

101
Q

what is BUN range

A

5-25mg/dL

102
Q

what is creatinine range

A

0.5-1.2mg/dL

103
Q

what is creatinine

A

a waste product of muscle metabolism

104
Q

what does the creatinine test reveal

A

it is sensitive indicator of kidney function because creatinine is filtered out by the glomerulus

105
Q

what do increased levels of creatinine indicate

A

diabetic nephropathy

106
Q

what is the range for GFR

A

90-120

107
Q

what does the GFR determine

A

how well the kidneys are filtering wastes from the blood.

108
Q

what happens to GFR as BUN and creatinine levels increase

A

GFR decreases

because the glomerulus is no longer able to filter these out efficiently so they accumulate in the blood

109
Q

what is the creatinine clearance

A

the total amount of creatinine that appears in urine

110
Q

what does a decline in creatinine clearance indicate

A

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)

111
Q

what can cause an increase in creatinine clearance

A

increased meat consumption

112
Q

what is the purpose of a 24 hr urine collection

A

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

113
Q

what is the GFR in ckd stage 1

A

> or equal to 90 (can be as high as 120)

114
Q

what is the goal management of CKD stage 1

A

manage and treat the underlying conditions causing kidney damage
slow progression and
reduce risks

115
Q

what symptoms are associated with stage 1 CKD

A

patients are often symptom free

116
Q

what is the GFR of stage 2 CKD

A

60-89

117
Q

what are the symptoms of stage 2 CKD

A

pts are often symptom free

118
Q

what is the GFR for stage 3 CKD

A

30-59

119
Q

what begins to happen in stage 3 CKD

A

*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. )

120
Q

what is the management of CKD stage 3

A

complications of stage 3 are evaluated and treated

121
Q

what is the GFR of stage 4 CKD

A

15-29

122
Q

what is the management of CKD stage 4

A

dialysis

possible kidney transplant

123
Q

what is the GFR of stage 5 CKD

A

Kidney failure! (end stage kidney disease)

<15

124
Q

what is the management of Stage 5 CKD

A

dialysis or kidney transplant is necessary to maintain life

125
Q

what is renal osteodystrophy

A

a mineral and bone disorder/defective bone development

d/t renal disease

126
Q

why does renal osteodystrophy occur in CKD patients

A

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

127
Q

what is the management for renal osteodystrophy

A

calcitriol and calcium supplements

128
Q

how does osteomalacia occur in CKD pts

A

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

129
Q

what would a pt want to avoid if they had hypocalcemia and hyperthyroidism 2ndary to CKD

A

they would want to avoid aluminum based products such as Milk of Magnesia and Mylanta

these can also contribute to osteomalacia

130
Q

why would a CKD pt want to avoid aluminum products

A

because aluminum inhibits the influx of calcium to bones and suppresses the secretion of PTH

131
Q

why would a CKD pt have hyperphosphatemia

A

high levels of phosphate are d/t bone demineralization
and
d/t decreased phosphate secretion

132
Q

what can hyperphosphatemia cause

A

can lead to vascular and soft tissue calcifications
as well as
neuromuscular excitability such as cramps

133
Q

what is the goal of treating hyperphosphatemia and how will it be acheived

A

to lower phosphate levels

by using phosphate binders such as PhosLo sevelamer

134
Q

what do you need to keep an eye on when administering PhosLo

A

-it contains calcium so it can raise the calcium levels.

135
Q

why would HTN be a clinical manifestation of CKD

A

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

136
Q

why does proteinuria occur with CKD

A

The glomeruli are damaged and so their permeability is increased allowing larger particles such as proteins to escape.

137
Q

why does peripheral edema occur in CKD

A

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

138
Q

why would a CKD pt need to worry about HF

A

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

139
Q

what is a consequence of hyperinsulinemia in CKD pts

A

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

140
Q

what does lipoprotein lipase do

A

breaks down lipoproteins LDL and VLDL

141
Q

why is anemia associated with CKD

A

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

142
Q

what is a possible management for anemia 2ndary to CKD

A

erythropoietin stimulating agents.

epoetin alpha

143
Q

when would you hold epoeitn alpha

A

if their Hgb is > or equal to 10

144
Q

what is a black box warning for epoeitin alpha

A

increased risk for cv and thromboembolic events

145
Q

what must the pt have in order to take epoetin alpha

A

a functioning bone marrow and sufficient iron stores

146
Q

what happens to the acid base balance in CKD

A

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

147
Q

what does the body to to attempt to correct metabolic acidosis

A

it tries to blow off CO2

which represents Kussmaul breathing

148
Q

what does the excess H+ ions in the blood do

A

they move into the cell replacing K+, therefore there becomes an abundance of K+ in the circulation leading to hyperkalemia - cardiac dysrhythmias

149
Q

what is an intervention for hyperkalemia 2ndary to metabolic acidosis

A

sodium polystyrene sulfonate(kayexalate)

for mild to moderate hyperkalemia

150
Q

what is necessary for the pt to have in order for sodium polystyrene sulfonate administration

A

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

151
Q

what is the goal of sodium polystyrene sulfonate

A

normalized K+ levels

152
Q

what are lifestyle modifications for pts with CKD

A

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

153
Q

what is a healthy level of sodium

A

less than 2300mg/day

202D (6 decks)

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