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Step 1 Complete > Biochem 3 USMLE > Flashcards

Biochem 3 USMLE Flashcards

1
Q

NADPH is a procatabolicduct of this pathway

A

HMP shunt

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2
Q

NAD+ is generally used in _______ processes to carry reducing equivalents away as NADH

A

catabolic

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3
Q

NADPH is used in _____ processes (steroid and fatty acid synthesis) as a supply of reducing equivalents

A

anabolic

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4
Q

NADPH is used in these 3 ways:

A

1) anabolic processes
2) respiratory burst
3) P-450

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5
Q

where is hexokinase found

A

throughout the body

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6
Q

where is glucokinase found

A

liver

mneu: gLucokinase in Liver

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7
Q

describe the Km and Vmax of glucokinase in comparison to hexokinase

A

glucokinase has a lower affinity [higer Km] but higher capacity [ higher Vmax]

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8
Q

which one hexokinase or glucokinase is feedback inhibited by G6P

A

hexokinase

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9
Q

which one hexokinase or glucokinase phosphorylates excess glucose (e.g., after a meal) to sequester it in the liver as G6P

A

glucokinase

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10
Q

give the irreversible enzymes in glycolysis regulation

A

hexokinase/glucokinase
phosphofructokinase-1 (RLS)
pyrovate kinase
pyruvate dehydroginase

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11
Q

hexokinase/glucokinase converts D-glucose into what?

what is this inhibited by?

A

Glucose-6-P

Glucose-6-P(inh by product)

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12
Q

phosphofructokinase-1 (RLS) converts fructose 6-phosphate into what?
what is it inhibited by?
stimulated by?

A

Fructose-1,6-BP
inh by: ATP, citrate
stim by: AMP,Fructose-2,6-BP

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13
Q

pyrovate kinase converts phosphoenolpyruvate into what?
what is it inhibited by?
stimulated by?

A

pyruvate

stim: fructose-1,6-BP
inh: ATP, alanine

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14
Q

pyruvate dehydroginase converts pyuvate into what?

what is it inhibited by?

A

Acetyl CoA
inh: ATP, NADH
Acetyl-CoA

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15
Q

Glycolyc enzyme deficiencies such as hexokinase, glucose phosphate isomerase, aldolase, triosephosphate isomerase, phosphate glycerate kinase, enolase, and pyruvate kinase deficiencies are associated with what condition

A

hemolytic anemia

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16
Q

why do glycolytic enzyme deficiencies result in hemolytic anemia

A

RBCs metabolize glucose anaerobically (no mitochondria) and thus depend solely on glycolysis

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17
Q

The pyruvate dehydrogenase complex contains 3 enzymes that require 5 cofactors. What are these cofactors.

A

1) pyrophosphate (B1, thyamine; TTP)
2) FAD (B2, riboflavin)
3) NAD (B3, niacin)
4) CoA (B5, pantothenate)
5. Lipoic acid

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18
Q

Pyruvate dehydrogenase complex is similar to what other complex (same cofactors, similar substrate and action)

A

alpha ketoglutarate

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19
Q

give thee pyruvate dehydrogenate reaction.

A

pyruvate + NAD+ + CoA

-> acetyl CoA + CO2 + NADH

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20
Q

pyruvate dehydrogenase complex is activated by exercise because it increases these three things

A

NAD+/NADH ratio
ADP
Ca++

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21
Q

pyruvate dehydrogenase deficiency causes a backup of substrate which is?

A

pyruvate and alanine

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22
Q

pyruvate dehydrogenase deficiency results in this

A

lactic acidosis

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23
Q

pyruvate dehydrogenase deficiency is often seen in alcoholics due to a deficiency of this vitamen

A

B1

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24
Q

someone with a pyruvate dehydrogenase deficiency may present with this deficit

A

neurologic

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25
Q

what is the tx for pyruvate dehydrogenase deficiency

A

increase intake of ketogenic nutrients (e.g., high fat content or high lysine and leucine)

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26
Q

name the only purely ketogenic amino acids

A

lysine and leucine

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27
Q

how many ATP equivalents are needed to generate glucose from pyruvate

A

6

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28
Q

this AA serves as a carrier of amino groups form mm to liver

A

alanine

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29
Q

this can be used to replenish TCA cycle or in gluconeogenesis

A

oxaloacetate

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30
Q

This cycle transfers excess reducing equivalents from RBCs and mm to liver, allowing muscle to funcction anaerobically (net 2 ATP)

A

cori cycle

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31
Q

TCA cycle enzymes

A 
Citrate
Isocitrate
alpha-Ketogluterate
Succinyl-CoA
Succinate
Fumarate
Malate
Oxaloacetate

mneu: Can I Keep Selling Sex For Money, Officer?

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32
Q

What does the TCA cycle produce per Acetyl-CoA?

how much do we multiply these numbers by if we are dealing with glucose?

A 
3NADH,
1FADH2
2CO2
1GTP
12 ATP

2x w/ glucose

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33
Q

in the electron transport cha in 1 NADH gives how many ATP

A

3

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34
Q

in the electron transport cha in 1 FADH gives how many ATP

A

2

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35
Q

name 4 electron transport inhibitors that directly inhibit electron transport, causing a decrease of proton gradient and block ATP synthesis

A

rotenone, antimycin A, CN-, CO

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36
Q

This ATPase inhibitor directly inhibits mitochondrial ATPase, causing an increase of proton gradient, but no ATP is produceed because electron transport stops

A

oligomycin

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37
Q

Uncoupling agents like this increase the permeability of the membrane, causing a decrease of proton gradient and increase O2 consumption. ATP synthesis stops. Electron transport continues.

A

2,4 DNP

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38
Q

irreversible enzymes in gluconeogenesis

A

pyruvate carboxylase
PEP carboxykinase
Fructose-1,6-biphosphatase
Glucose-6-phosphate

mneu: Pathway Produces Fresh Glucose

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39
Q

pyruvate carboxylase is found here and converts this to this
It requires this
& is activated by this

A

mitochondria
pyruvate ->oxaloacetate
biotin, ATP
Acetyl-CoA

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40
Q

PEP carboxykinase is found here and converts this to this

It requires this

A

cytosol
oxaloacetate
->phosphoenolpyruvate
GTP

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41
Q

Fructose-1,6-biphosphatase is found here and converts this to this.

A

cytosol
fructose-1,6 bisphosphate
->fructose-6-P

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42
Q

where does gluconeogenesis occur

A

liver, kidney, intestinal epithelium

note: mm cannot participate in gluconeogenesis

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43
Q

deficiency of key gluconeogenic enzymes results in this

A

hypoglycemia

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44
Q

this dz is caused by a lack of glucose 6 phospatase in the liver

A

Von Gierke’s

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45
Q

This pathway produces ribose-5-P for nucleotide synthesis
and produces NADPH from NADP+ for fatty acid and steroid biosynthesis and for maintaining reduced glutathione inside RBCs

A

Pentose Phosphate Pathway (HMP shunt)

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46
Q

All pentose Phosphate Pathway (HMP shunt) reactions occur here

A

cytoplasm

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47
Q

Is ATP used or produced in Pentose Phosphate Pathway (HMP shunt)

A

no

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48
Q

give sites of Pentose Phosphate Pathway (HMP shunt)

A

all sites of fatty acid or steroid synthesis (e.g., lactating mammary glands, liver, adrenal cortex

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49
Q

this is the rate-limiting enzyme in HMP shunt (which yields NADPH)

A

G6PD

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50
Q

NADPH is necessary to keep this reduced, which in turn detoxifies free radicals and peroxides

A

glutathione

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51
Q

decreased NADPH in RBCs lead to this due to poor RBC defense against oxidizing agents (fava beans, sulfonamides, primaquine) and antituberculosis drugs

A

hemolytic anemia

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52
Q

G6PD deficiency is more prevelent amun this racial group

A

blacks

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53
Q

this sign of G6PD deficiency describes when hemoglobin precipitates within RBCs

A

Heinz bodies

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54
Q

G6PD deficiency has this inheritance

A

x-linked recessive

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55
Q

This is a hereditary deficiency of aldolase B (recessive) Fructose-1-phosphate accumulates causing a decrease in available phosphate, which results in inhibition of glycogenolysis and gluconeogenesis.
Symptoms include hypoglycemia,jaundice, cirrhosis, vomiting

A

fructose intolerance

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56
Q

what is the tx for fructose intolerance

A

decrease intake of both fructose and sucrose (glucose + fructose)

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57
Q

this d/o involves a defect in fructokinases and is a benign, asymptomatic condition.
Symptoms: fructose appears in blood and urine.

A

essential fructosuria

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58
Q

essential fructosuria is a deficiency in this enzyme

A

fructokinase

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59
Q

fructose intolerance is a deficiency in this enzyme

A

aldolase B

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60
Q

This d/o is an absense of galactose-1-phosphate uridyltransferase. It is autosomal recessive. Damage is caused by accumulation of toxic substances (including galactitol) rather than absense of an essential compound.
Symptoms: cataracts, hepatosplenomegaly, mental retardation

A

galactosemia

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61
Q

tx of galactosemia

A

exclude galactose and lactose (galactose + glucose) from diet

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62
Q

this enzyme deficiency causes galactosemia and galactosuria, galactosuria, galactitol accumulation if galactose is present in ddiet.

A

galactokinase deficiency

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63
Q

this is an age dependent or hereditary intolerance to dairy often seen in blacks and asians. Symptoms include bloating, cramps and osmotic diarrhea.
Tx includes avoiding milk or adding lactase pills to diet

A

lactase deficiency

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64
Q

give the ketogenic essential amino acids

A

leucine, lysine

All essential amino acids: PriVaTe TIM HALL

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65
Q

give the glucogenic/ketogenic essential amino acids

A

Ile, Phe, Trp

All essential amino acids: PriVaTe TIM HALL

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66
Q

give the glucogenic essential amino acids

A

Met, Thr,Val, Arg, His

All essential amino acids: PriVaTe TIM HALL

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67
Q

which 2 AA are required during periods of growth

A

Arg

His

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68
Q

what are the acidic amino acids

A

Asp, Glu

mneu: Asp=aspartic ACID, Glu=glutamic ACID

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69
Q

At body pH (7.4) acidic amino acids (Asp, Glu)are _____ charged

A

negatively

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70
Q

what are the basic amino acids

A

arg, lys, his

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71
Q

At body pH (7.4) basic amino acids (Arg, lys)are _____ charged, but _____ has no net charge

A

positively

his

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72
Q

arg and lys have an extra _____ group

A

NH3

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73
Q

the MOST basic amino acid

A

arginine

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74
Q

thise 2 AA are found in high amounds in histones, which bind to negatively charged DNA

A

arg, lys

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75
Q

this cycle degrades amino acids into amino groups. It accounts for 90% of the nitrogen in the urine.

A

urea cycle

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76
Q

urea cycle occurs in this organ

A

liver

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77
Q

in what part of the cell does the urea cycle occur

A

carbamoyl phosphate incorporation occurs in the mitochondria; the remaining steps occur in the cytosol

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78
Q

urea cycle image p. 94

A

ornithine, Carbamoyl phosphate, Citrulline, Aspartate, Argininosuccinate, Fumarate, Arginine, urea

mneu: Ordinarily, Careless Crappers Are Also Frivolous About Urination

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79
Q

give the amino acid derivative of epinephrin

A

phenylalanine

80
Q

give the amino acid derivative of thyroxine

A

phenylalanine

81
Q

give the amino acid derivitive of NAD+/NADP+

A

tryptophan

82
Q

give the amino acid derivative of melanin

A

phenylalanine

83
Q

give the amino acid derivative of serotonin

A

tryptophan

84
Q

give the amino acid derivative of melatonin

A

tryptophan

85
Q

give the amino acid derivative of histamine

86
Q

give the amino acid derivative of heme

87
Q

give the amino acid derivative of creatine

88
Q

give the amino acid derivative of urea

89
Q

give the amino acid derivative of nitric oxide

90
Q

give the amino acid derivative of GABA

91
Q

give the amino acid derivative of dopamine

A

phenylalanine

92
Q

give the amino acid derivative of norepinephnine

A

phenylalanine

93
Q

In normal metabolism phenylalanine is converted into _____

94
Q

in PKU there is decreased ________ or decreased tetrahydrobiopterin cofactor

A

phenylalanine hydroxylase

95
Q

findings of phenylketonuria

A

mental retardation, growth retardation, fair skin, eczema, musty body odor.

mneu: d/o of AROMATIC amino acid metabolism -> musty body ODOR

96
Q

tx of PKU

A

no phenylalanine in diet (e.g., aspartame, nutrasweet) and increase in tyrosine

97
Q

when should you screen for PKU

98
Q

name the 3 phenylketones

A

phenylacetate
phenyllactate
phenylpyruvate

99
Q

what is the inheratiance of PKU & incidence

A

autosomal-recessive dz

1:10,000

100
Q

this is a congenital deficiency of homogentisic acid oxidase in the degradative pathway of tyrosine.

A

alkaptonuria

101
Q

in alkaptonuria, these cause the urine to turn black on standing

A

alkapton bodies

102
Q

in alkaptonuria, in addition to dark urine this is also dark

A

connective tissue

103
Q

pts w/ alkaptonuria may have debilitating

A

arthralgias

104
Q

this d/o is a congenital deficiency of either of the follwoing:
1) tyrosinase (inability to synthesize melanin from tyrosine)
2) Defective tyrosine transporters (decrease amounts of tyrosine and thus melanin)
It can result from lack of migration of neural crest cells

105
Q

lack of melanine results in an increase risk of this CA

106
Q

this dz results in excess homocysteine in the urine. Cysteine becomes essential. It can cause mental retardation, osteoporosis, tall stature, kyphosis, lens subluxation (downward and inward) and atherosclerosis (stroke and MI

A

homocystinuria

107
Q

there are three forms of homocystinuria. Name the enzyme deficiency and give the dietary txs if there is one

A

1) cytathionine synthase deficiency (tx: decrease Met & increase Cys in diet)
2) decrease affinity of cystathionine synthase for pyridoxal phosphate (tx: increase vit. B6 in diet)
3) Methionine synthase deficiency

108
Q

This is a common(1:7000) inherited defect of renal tubular amino acid transporter for Cystine, Ornithine, Lysine, and Arginine in kidneys. Excess cystine in urine can lead to the precipitation of cystine kidney stones

A

Cystinuria

mneu: COLA in the urine

109
Q

this is a congenital deficiency of homogentisic acid oxidase in the degradative pathway of tyrosine.

A

alkaptonuria

110
Q

in alkaptonuria, these cause the urine to turn black on standing

A

alkapton bodies

111
Q

in alkaptonuria, in addition to dark urine this is also dark

A

connective tissue

112
Q

pts w/ alkaptonuria may have debilitating

A

arthralgias

113
Q

this d/o is a congenital deficiency of either of the follwoing:
1) tyrosinase (inability to synthesize melanin from tyrosine)
2) Defective tyrosine transporters (decrease amounts of tyrosine and thus melanin)
It can result from lack of migration of neural crest cells

114
Q

tx for Cystinuria

A

acetazolamide to alkalinize the urine

115
Q

this dz results from blocked degradation of BRANCHED AA (Ile, Val, Leu) due to decreease alpha ketoacid dehydrogenase. It causes increased alpha ketoacids in the blood, esp Leu. It causes severe CNS defects, mental retardation, and death.

A

maple syrup urine dz

mneu: urine smells like maple syrup. I Love Vermont maple syrup

116
Q

tx for Cystinuria

A

acetazolamide to alkalinize the urine

117
Q

this dz results from blocked degradation of BRANCHED AA (Ile, Val, Leu) due to decreease alpha ketoacid dehydrogenase. It causes increased alpha ketoacids in the blood, esp Leu. It causes severe CNS defects, mental retardation, and death.

A

maple syrup urine dz

mneu: urine smells like maple syrup. I Love Vermont maple syrup

118
Q

what does SCID stand for?
What is the enzyme deficiency?What immune cells are involved?
Who does it effect

A 
Severe combined (T and B) immuodeficiency dz.
Adenosine deaminase (ADA)deficiency 
happens to kids

mneu: bubble boy

119
Q

pathophysiology of SCID

A

excess ATP and dATP imbalances nucleotide pool via feedback inhibition of ribonucleotide reductase. This prevents DNA synthesis and thus decreases lymphocyte count.

120
Q

This dz results from a purine salvage problem owing to absense of HGPRTase, which vonverts hypoxanthine, to inosine monophosphate (IMP) and guanine to guanosine monophosphate (GMP)

A

Lesch-Nyyhan syndrome

mneu: LNS- Lacks Nucleotide Salvage (purine)

121
Q

inheratance of Lesch Nyhan syndrome

A

X-linked recessive.

122
Q

LNS results in excess of this acid

123
Q

patient manifestation of Lesch-Nyhan syndrome

A

retardation, self-mutilation, aggression, hyperuricemia, gout, choreoathetosis

124
Q

is the fasting state phosphorylated or non-phosphorylated

A

phosphorylated

mneu: in the fasting state phosphorylate

125
Q

this hormone is required for adipose and skeletal mm uptake of glucose

A

insulin

mneu: INsulin moves glucose INto cells

126
Q

where is insulin made (cells/organ)

A

Beta cells of pancreas

127
Q

what receptors are found in the beta cells

128
Q

what receptors are found in mm and fat

129
Q

insulin inhibits the release of this hormone by alpha cells of pancreas

130
Q

is serum C-peptide present w/ exogenous insulin intake

131
Q

what are the anabolic effects of insulin

A

1) glucose transport
2) glycogen synthesis and storage
3) triglyceride synthesis and storage
4) Na+ retention (kidneys)
5) protein sytnesis (mm

132
Q

Name the tissues that don’t need insulin for glucose uptake

A 
Brain
RBCs
Intestine
Cornea
Kidney
Liver

mneu: BRICK L

133
Q

Glucagon ______ (phosphorylates/Dephosphorylates), turns glycogen sytnase _____ and phosphorylase ____

A

phosphorylates
OFF
ON

134
Q

Insulin______ (phosphorylates/Dephosphorylates), turns glycogen sytnase _____ and phosphorylase ____

A

dephosphorylates
ON
OFF

135
Q

there are 12 types of these diseases all resulting in abnormal glycogen metabolism and accumulation of glycogen within cells

A

glycogen storage diseases

136
Q

In this glycogen storage disease, there is a glucose 6-phosphatase deficiency

A

Von Gierke’s dz (GSD type I)

137
Q

Give some clinical findings of Von Gierke’s dz (GSD type I)

A

severe fasting hypoglycemia, increased glycogen in the liver, hepatomegly, increased blood lactate

hint: the liver becomes a mm

138
Q

In this glycogen storage disease, there is a lysosomal alpha 1,4-glucosidase deficiency

A

Pompe’s dz (type II)

139
Q

Give some findings of Pompe’s dz

A

cardiomegly and systemic findings, leading to early death

mneu: Pompe’s trashes the Pump
heart, liver mm

140
Q

In this glycogen storage disease, there is a deficiency of debranching enzyme alpha 1,6 glucosidase

A

Cori’s dz (type III)

141
Q

give some clinical findings of Cori’s dz

A

milder form of type I w/ normal blood lactate levels

142
Q

In this glycogen storage disease, there is a deficiency of skeletal mm glycogen phosphorylase deficiency

A

McArdle’s dz (type V)

mneu: McArdle’s: Muscle

143
Q

Give some findings of McArdle’s dz

A

increased glycogen in mm but cannot greak it down, leading to painful cramps, myoglobinuria w/ strenuous exercise

144
Q

this classification of dz is caused by a deficiency in one of the many lysosomal enzymes

A

lysosomal storage diseases

145
Q

clinical findings are peripheral neuropahty of hands/feet, antiokeratomas, CV/renal dz. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Fabry’s dz
alpha-galactosidase A
Ceramide trihexoside
XR

146
Q

clinical findings are hepatosplenomegly, aseptic necrosis of femur, bone crises. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Gaucher’s dz
B-glucocerbrosidase
Glucocerebroside
AR

147
Q

clinical findings are progressive neurodegeneration, HSM, cherry red spot on macula What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Niemann-Pick dz
Sphingomyelinase
Sphingomyelin
AR

mneu:NO MAN PICS (NIEMANN-PICK) his nose w/ his SPHINGER(SPHINGomylenase

148
Q

clinical findings are progressive neurodegeneration, developmental delay, cherry-red spot, lysozymes w/ onion skin. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Tay-Sachs dz
Hexosaminidase A
GM2 ganglioside
AR

mneu: Tay-SaX (Tay-Sachs) lacks heXosaminidase

149
Q

clinical findings are peripheral neuropathy, developmental delay, optic atrophy. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Krabbe’s dz
B-galactosidase
Galactocerebroside
AR

150
Q

clinical findings are central and peripheral demyelination w/ ataxia, dementia. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Metachromatic leukodystophy
Arylsulfatase A
Cerebroside sulfate
AR

151
Q

clinical findings are developmental delay, gargoylism, airway obsxn, corneal clouding, HSM What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Hurler’s syndrome
alpha-L-iduronidase
Heparan sulfate & dermatan sufate
AR

152
Q

clinical findings are mild Hurler’s w/ aggressive behavior, no corneal clouding. What is the dz? deficient lysosomal enzyme? Accumulated substrate? Inheritance?

A

Hunter’s syndrome
Iduronate sulfatase
heparan sulfate, dermatan sulfate
XR

mneu: HUNTERS aim for the X (X-linked recessive)

153
Q

Where does fatty acid degradation occur

A

mitochondria

where its products will be consumed

154
Q

in the liver, fatty acid and amino acids are broken down into ______ to be used by _____ & ______

A 
ketone bodies (acetoacetate + hydroxybuterate
To be used in mm & brain).
155
Q

when are ketone bodies found

A

prolonged starvation and diabetic ketoacidosis

156
Q

how are ketone bodies excreted

157
Q

what are ketone bodies made from

158
Q

Ketone bodies are metabolized by the brain to 2 molecules of _______

A

acetyl-CoA

159
Q

how do ketone bodies smell on the breath

A

like acetone (fruity odor)

160
Q

What is the rate-limiting step in cholesterol synthesis

A

HMG-CoA reductase, which converts HMG-CoA to mevalonate.

161
Q

What cholesterol drug inhibits HMG CoA reductase

A

Lovastatin

162
Q

2/3 of plasma cholesterol is esterified by this

A

lecithin-cholesterol acyltransferase (LCAT)

163
Q

this lipase is responsible for degradation of dietary TG in the small intestine

A

pancreatic lipase

164
Q

this lipase is responsible for degradation TG circulating in chylomicrons and VLDLs

A

lipoprotein lipase

165
Q

this lipase is responsible for degradation TG remaining in IDL

A

Hepatic TG lipase

166
Q

this lipase is responsible for degradation of TG stored in adipocytes

A

hormone sensitive lipase

167
Q

this major apolipoprotein Activates LCAT

168
Q

this major apolipoprotein Binds to LDL receptor

169
Q

this major apolipoprotein is a Cofactor for lipoprotein lipase

170
Q

this major apolipoprotein mediates Extra (remnant) uptake

171
Q

the cells in this part of the body convert FFA back to TG and package it in chylomicrons

A

intestines

172
Q

give the 5 lipoproteins

A

chylomicrons, VLDL, IDL, LDL, HDL

173
Q

this lipoprotein delivers dietary triglycerides to peripheral tissues and dietary cholesterol to the liver. It is secreted by intestinal epithelial cells. Excess causes pancreatitis, lipemia retinalis, and eruptive xanthomas

A

chylomicron

174
Q

Apolipoprotein ____ mediates secetion of chylomicrons

175
Q

Apolipoprotein ____ are used for formation of new HDL

176
Q

Apolipoprotein ____ activates lipoprotein lipase

177
Q

Apolipoprotein ____ mediates remnant uptake by liver

178
Q

These lipoproteins deliver hepatic triglycerides to peripheral tissues.

179
Q

VLDL is secreted by this organ

180
Q

excess VLDL causes this dz

A

pancriatitis

181
Q

this apolipoprotein mediates secretion of VLDL

182
Q

this apolipoprotein mediates remnant uptake of VLDL by the liver

183
Q

this lipoprotein is formed in the degradation of VLDL. It delivers triglycerides and cholesterol to the liver, where they are degraded to LDL

184
Q

This lipoprotein delivers hepatic cholesterol to peripheral tissues It is formed by a lipoprotein lipase modification of VLDL in the peripheral tissue. It is taken up by target cells via receptor-mediated endocytosis. Excess causes atherosclerosis, xanthomas, and arcus cornae

185
Q

this LDL apolipoprotein mediates binding to cell surface receptor for endocytosis

186
Q

This lipoprotein mediates centripetal transport of cholesterol (reverse cholesterol transport, from perhiphery to liver). It acts as a repository for apoC and apo E (which are needed for chylomicron and VLDL metabolism). It is secreted from both liver and intestine

187
Q

this HDL apolipoprotein helps form HDL sx

188
Q

this HDL apolipoprotein in particular activates LCAT (which catalyzes esterification of cholesterol)

189
Q

this HDL apolipoprotein mediates transfer of cholesterol esters to other lipoprotein particles.

190
Q

LDL & HDL carry most cholesterol. ___ transports cholesterol from liver to tissue; ____ transports it from periphery to liver

191
Q

This type of familial dyslipidemia results from a lipoprotein lipase deficiency or altered apolipoprotein CII. It results in increased chylomicrons which leads to elevated blood levels of TG & cholesterol

A

type I - hyperchylomicronemia

192
Q

This type of familial dyslipidemia results from a decrease in LDL receptors. It results in an increase of LDL which leads to elevated cholesterol.

A

type IIa hypercholesterolemia

193
Q

This type of familial dyslipidemia results from a hepatic overproduction of VLDL leading to an increase in LDL and VLDL leading to elevated TG & cholesterol

A

type IIb-combined hyperlipidemia

194
Q

This type of familial dyslipidemia results from altered apolipoprotein E leading to an increase in IDL & VLDL resulting in elevated TG & cholesterol

A

type III-dysbetalipoproteinemia

195
Q

This type of familial dyslipidemia results from hepatic overproduction of VLDL resulting in increased VLDL levels leading to elevated TGs in the blood

A

type IV-hypertriglyceridemia

196
Q

This type of familial dyslipidemia results from increased production and decreased clearance of VLDL and chylomicrons leading to increased VLDL and chylomicrons resulting in elevated blood levels of TGs & cholesterol

A

type V-mixed hypertriglyceridemia

Step 1 Complete (29 decks)

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