Biochemistry Flashcards
(152 cards)
1
Q
DNA exists in the ——— form to fit into the ———
A
- Condensed, chromatin
- Nucleus
2
Q
DNA loops —(number)— around a ——— to form a ——— (nicknamed ———)
A
- twice
- histone octamer
- nucleosome
- (“beads on a string”).
3
Q
——— binds to the nucleosome and to ———, thereby stabilizing the chromatin fiber
A
- H1
- “linker DNA”
4
Q
DNA has ——— charge from ———
A
- negative
- phosphate groups
5
Q
Histones are ——— and have ———charge from ———
A
- large
- positive
- lysine and arginine (Note: LARge)
6
Q
In mitosis, DNA ——— to form ———
A
- condenses
- chromosomes
7
Q
DNA and histone synthesis occurs during:
A
S phase
8
Q
Mitochondria have their own DNA, which is ——— and ———
A
- circular
- does not utilize histones
9
Q
Heterochromatin is ———, and appears ——— on EM
A
- condensed
- darker
(HeteroChromatin = Highly Condensed)
10
Q
Heterochromatin is sterically ———, and thus transcriptionally———, ——— methylation and ———acetylation
A
- inaccessible
- inactive
- increased
- decreased
11
Q
Barr bodies are ———, categorized as —(heterochromatin or euchromatin)—, and may be visible on the ———
A
- inactive X chromosomes
- heterochromatin
- periphery of nucleus
12
Q
Euchromatin is ———, and appears ——— on EM
A
- less condensed
- lighter
13
Q
Euchromatin is transcriptionally ———, and sterically ———
A
- active
- accessible
(Euchromatin is Expressed)
14
Q
DNA methylation changes the ——— without changing the ———
A
- expression of a DNA segment
- sequence
15
Q
Name 5 processes DNA methylation is involved with :
A
aging, carcinogenesis, genomic imprinting, transposable element repression, and X chromosome inactivation (lyonization)
16
Q
Methylation within gene promoter (——— ) typically ———
A
- CpG islands
- represses (silences) gene transcription
17
Q
Dysregulated DNA methylation is implicated in ——— syndrome
A
Fragile X
18
Q
Histone methylation usually causes ———, but can also cause ——— depending on ———
A
- reversible transcriptional suppression
- activation
- location of methyl groups
19
Q
——— and ——— residues of histones can be methylate
A
Lysine and arginine
20
Q
Histone acetylation results in ———, which yields ——— and thus ———
A
- removal of histone’s positive charge
- relaxed DNA coiling
- increased transcription
(Histone Acetylation makes DNA Active)
21
Q
——— hormone synthesis is altered by acetylation of ——— receptor
A
- thyroid
- thyroid hormone
22
Q
Histone deacetylation (removal of acetyl groups) results in ———, and thus ———
A
- tightened DNA coiling
- decreased transcription
23
Q
Histone deacetylation may be responsible for altered gene expression in ——— disease
A
Huntington
24
Q
What is uniparental disomy?
A
Offspring receives 2 copies of a chromosome from 1 parent and no copies from the other parent
25
What are the two types of uniparental disomy, and what do they each indicate about when a genetic error occurred?
1. HeterodIsomy (heterozygous) indicates a meiosis I error
2. IsodIsomy (homozygous) indicates a meiosis II error or postzygotic chromosomal duplication of one of a pair of chromosomes, and loss of the other of the original pair
26
What might be suggested by an individual manifesting a recessive disorder when only one parent is a carrier?
Consider isodisomy
27
Would someone with uniparental disomy be euploid (correct number of chromosomes)?
Yes
28
Most occurrences of uniparental disomy result in what type of phenotype?
Normal
29
Describe genomic imprinting, and disorders of imprinting:
- Genomic imprinting = One gene copy is silenced by methylation, and only the other copy is expressed (parent-of-origin effects)
- Disorders of imprinting: If expressed copy mutated, not expressed, or deleted altogether
30
What causes Prader-Willis syndrome?
Maternally derived genes are silenced; Disease occurs when the paternal allele is deleted or mutated
31
Name 5 symptoms of Prader-Willis syndrome?
Hyperphagia, obesity, intellectual disability, hypogonadism, hypotonia
32
Which chromosome is involved in Prader-Willis syndrome?
Chromosome 15 of paternal origin
33
How often is uniparental disomy responsible for Prader-Willis syndrome and Angelman syndrome?
Prader-Willis syndrome: 25% of cases are due to maternal uniparental disomy
Angelman syndrome: 5% of cases are due to paternal uniparental disomy
34
What do the mnemonics POP and MAMAS stand for Prader-Willis syndrome and Angelman syndrome?
- POP: Prader-Willis, Obesity/overeating, Paternal allele deleted
- MAMAS: Maternal allele deleted, Angelman syndrome, Mood, Ataxia, Seizures
35
What causes Angelman syndrome?
Paternally derived UBE3A is silenced Disease occurs when the maternal allele is deleted or mutated
36
Name 5 symptoms of Angelman syndrome?
Hand-flapping, Ataxia, severe Intellectual disability, inappropriate Laughter, Seizures
(HAILS the Angels)
37
Which chromosome is involved in Angelman syndrome?
UBE3A on maternal copy of chromosome 15
38
If disease is autosomal recessive,
what is the probability that an unaffected individual with an affected sibling is a carrier?
2/3 probability
39
Cystic fibrosis is the most common lethal genetic disease in patients with:
European ancestry
40
What is the genetic cause of cystic fibrosis?
Autosomal recessive; defect in CFTR gene on chromosome 7 (deletion; ΔF508)
41
What does the CFTR gene encode and what is its function?
CFTR encodes an ATP-gated Cl− channel (secretes Cl− in lungs/GI tract, reabsorbs Cl− in sweat glands)
42
Describe the pathophysiology of cystic fibrosis:
- Phe508 deletion —>
- misfolded protein —>
- improper protein trafficking —>
- protein absent from cell membrane—>
- decreased Cl− (and H2O) secretion->
- increased compensatory Na+ reabsorption via epithelial Na+ channels (ENaC) —>
- increased H2O reabsorption —>
- abnormally thick mucus secreted into lungs/GI tract
43
In cystic fibrosis, more ———reabsorption = more ——— transepithelial potential difference
- Na+ reabsorption
- negative transepithelial potential difference
44
Name 3 clues for cystic fibrosis diagnosis:
1. Increased Cl− concentration in pilocarpine-induced sweat test
2. Can present with contraction alkalosis and hypokalemia (ECF effects analogous loop diuretic effect) due to ECF H2O/Na+ losses via sweating and concomitant renal K+ /H+ wasting
3. Immunoreactive trypsinogen (newborn screening) due to clogging of pancreatic duct
45
List 4 key pulmonary manifestations of cystic fibrosis:
1. Recurrent pulmonary infections (eg, S aureus [infancy and early childhood], P aeruginosa [adulthood], allergic bronchopulmonary aspergillosis [ABPA])
2. Chronic bronchitis and bronchiectasis —> reticulonodular pattern on CXR, opacification of sinuses
3. Nasal polyps
4. Nail clubbing
46
List 7 key GI manifestations of cystic fibrosis:
1. Pancreatic insufficiency
2. Malabsorption with steatorrhea
3. Fat-soluble vitamin deficiencies (A, D, E, K)
4. Progressing to endocrine dysfunction (CF-related diabetes)
5. Progressing to biliary cirrhosis
6. Progressing to liver disease
7. Meconium ileus in newborns
47
List key male and female reproductive manifestations of cystic fibrosis:
- Infertility in males (absence of vas deferens, spermatogenesis may be unaffected)
- Subfertility in females (amenorrhea, abnormally thick cervical mucus).
48
List 3 treatments for improved mucus clearance in cystic fibrosis:
1. Chest physiotherapy
2. Aerosolized dornase alfa (DNase)
3. Inhaled hypertonic saline
49
List treatment to prevents acute exacerbations in cystic fibrosis:
Azithromycin
50
List treatment used for anti-inflammatory effect in cystic fibrosis:
Ibuprofen
51
List a treatment for pancreatic insufficiency in cystic fibrosis:
Pancreatic enzyme replacement therapy (pancrelipase)
52
Describe the overall use and 2 mechanisms/examples of CFTR modulators:
- Can be used alone or in combination for treatment of cystic fibrosis
- Efficacy varies by different genetic mutations (pharmacogenomics)
Mechanisms:
- Potentiators (hold gate of CFTR channel open —> Cl− flows through cell membrane; eg, ivacaftor)
- Correctors (help CFTR protein to form right 3-D shape —> moves to the cell surface; eg, lumacaftor, tezacaftor)
53
Name a condition that would make females more likely to have an X-linked recessive disorder
Turner syndrome (45,XO)
54
Describe X-inactivation (lyonization), and what can happen if skewed inactivation occurs:
Description:
During development, one of the X chromosomes in each XX cell is randomly deactivated and condensed into a Barr body (methylated heterochromatin)
If skewed inactivation occurs:
XX individuals may express X-linked recessive diseases (eg, G6PD); penetrance and severity of X-linked dominant diseases in XX individuals may also be impacted
55
What is the mode of inheritance for Duchenne muscular dystrophy?
X-linked recessive disorder
56
Duchenne muscular dystrophy is typically due to ——— or ———, resulting in ——— protein and ——— damage
(Can also result from ———)
- frameshift deletions or nonsense mutations
- truncated or absent dystrophin protein and progressive myofiber damage
- splicing errors
(Duchenne = Deleted Dystrophin)
57
Why is the gene involved in Duchenne muscular dystrophy susceptible to spontaneous mutations?
Dystrophin gene (DMD) is the largest protein-coding human gene; thus has an increased chance of spontaneous mutation
58
What is the usual role of the protein involved in Duchenne muscular dystrophy, and what does this proteins loss lead to in this disease?
- Dystrophin helps to anchor muscle fibers to the extracellular matrix, primarily in skeletal and cardiac muscles
- Loss of dystrophin leads to myonecrosis
59
How can Duchenne muscular dystrophy be diagnosed?
- Elevated creatine kinase and aldolase
- Genetic testing confirms diagnosis
60
List 5 key symptoms of Duchenne muscular dystrophy:
- Weakness that begins in pelvic girdle muscles and progresses superiorly
- Pseudohypertrophy of calf muscles due to fibrofatty replacement of muscle
- Waddling gait
- Lordosis
- Thigh atrophy
61
In what age range does Duchenne muscular dystrophy typically onset?
Onset before 5 years of age
62
The common cause of death in Duchenne muscular dystrophy is:
Dilated cardiomyopathy
63
List a classical sign of Duchenne muscular dystrophy, and list a few other conditions that may also have this sign:
- Gowers sign—patient uses upper extremities to help stand up (eg, pushes on legs to stand)
- Also seen in other muscular dystrophies and inflammatory myopathies (eg, polymyositis).
64
What is the mode of inheritance for Becket muscular dystrophy?
X-linked recessive disorder
65
Becket muscular dystrophy is typically due to ——— in ——— gene (leading to ——— instead of ———)
- non-frameshift deletions
- dystrophin gene
- partially functional instead of truncated
66
Contrast the severity of Becker and Duchenne muscular dystrophy:
Becker less severe than Duchenne
(Becker is Better)
(Deletions can cause both Duchenne and Becker muscular dystrophies. 2 ⁄3 of Becker cases have large deletions spanning one or more exons.)
67
In what age range does Becker muscular dystrophy typically onset?
Onset in adolescence or early adulthood
68
What is the mode of inheritance for myotonic dystrophy?
Autosomal dominant
69
In what age range does myotonic dystrophy typically onset?
Onset 20–30 years
70
Myotonic dystrophy caused by ——- in the ——— gene leading to abnormal expression of ———
- CTG trinucleotide repeat expansion
- DMPK gene
- Myotonin protein kinase
71
List 6 key symptoms of myotonic dystrophy:
- myotonia (eg, difficulty releasing hand from handshake)
- muscle wasting
- cataracts
- testicular atrophy
- frontal balding
- arrhythmia
(CTG = Cataracts, Toupee (early balding in males), Gonadal atrophy)
72
In the electron transport chain/ oxidative phosphorylation, NADH electrons are transferred to ——— FADH2 electrons are transferred to——— (—NADH or FADH2— at a lower energy level than —NADH or FADH—)
- complex I (NADH to NAD+)
- complex II (succinate dehydrogenase) (FADH2 to FAD)
- FADH2
-NADH
73
In the electron transport chain, the passage of ——— results in the formation of a ——— that, coupled to oxidative phosphorylation, drives ———
- electrons
- proton gradient
- ATP production
74
——— can be coupled to energetically unfavorable reactions
ATP hydrolysis
75
Uncoupling proteins (found in ——— fat, which has more mitochondria than ——— fat) produce ——— by ——— which ——— (——— stops, but ——— continues)
- brown
- white
- heat
- increasing inner mitochondrial membrane permeability
- decreased the proton gradient
- ATP synthesis stops
- electron transport continues
76
How many ATP are produced by 1 NADH? How many ATP are produced by 1 FADH2?
1 NADH produces 2.5 ATP
1 FADH2 produced 1.5 ATP
77
NADH electrons from glycolysis enter mitochondria via the ——— or the ———
malate-aspartate or glycerol-3-phosphate shuttle
78
Aerobic metabolism of one ——— molecule produces ——— net ATP via ——— shuttle (in ———), ——— net ATP via ——— shuttle (in ———)
- glucose
- 32
- malate-aspartate
- heart and liver
- 30
- glycerol-3-phosphate
- muscle
79
Anaerobic glycolysis produces ———net ATP per ——— molecule.
- 2
- glucose
80
——— overdose can also cause uncoupling of oxidative phosphorylation resulting in ———
- Aspirin
- hyperthermia
81
Mitochondrial diseases are rare disorders arising 2° to failure in ———
- oxidative phosphorylation
82
Among mitochondrial diseases, tissues with ——— are preferentially affected (eg, ——— and ——— tissue)
- increased energy requirements
- CNS, skeletal muscle
83
List two key mitochondrial myopathies:
MELAS (mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes)
MERRF (myoclonic epilepsy with ragged red fibers)
84
What is observed in mitochondrial myopathies (MELAS and MERRF) on light microscopy with stain and electron microscopy?
- Light microscopy with stain: ragged red fibers (due to compensatory proliferation of mitochondria)
- Electron microscopy: mitochondrial crystalline inclusions
85
Leber hereditary optic neuropathy is caused by:
mutations in complex I of ETC
86
Leber hereditary optic neuropathy results in —(cell type)— death in ——— and ———, which results in main symptom of ——— in —(age group)—
- neuronal
- retina and optic nerve
- subacute bilateral vision loss
- teens/young adults
87
Is Leber hereditary optic neuropathy more common among males or females?
Is it usually transient or permanent?
What type of dysfunction is it usually accompanied by, and list 2 examples of such dysfunction?
- males > females
- usually permanent
- neurologic dysfunction (eg, tremors, multiple sclerosis–like illness)
88
Rett syndrome is a sporadic disorder caused by:
de novo mutation of MECP2 on X chromosome
89
Rett syndrome is seen most with which gender, and why?
Seen mostly in females.
Embryonically lethal in males.
90
Describe the developmental timeline for Rett syndrome, and name 4 key symptoms:
Developmental timeline:
Initial normal development (6–18 months) followed by regression (“RETTurn”) in motor, verbal, and cognitive abilities
Key symptoms:
Ataxia, seizures, scoliosis, and stereotypic hand-wringing.
91
What is the mode of inheritance in Fragile X syndrome?
X-linked dominant inheritance
92
Fragile X syndrome is caused by a ——— in ——— with ——— residues resulting in ——— expression
- Trinucleotide repeat expansion [(CGG)n]
- FMR1
- hypermethylation of cytosine residues
- decreased expression
93
What is the most common genetic cause of intellectual disability?
What is the most common inherited cause of intellectual disability?
Down syndrome is most common genetic cause, but most cases occur sporadically
Fragile X syndrome is the most common inherited cause of intellectual disability
94
What is the cause of Fragile X syndrome and when does it occur?
Trinucleotide repeat expansion [(CGG)n] occurs during oogenesis
95
For Fragile X syndrome, what are the number of repeats and symptoms associated with premutation and full mutation?
Premutation (50–200 repeats): tremor, ataxia, 1° ovarian insufficiency
Full mutation (>200 repeats): postpubertal macroorchidism (enlarged testes), long face with large jaw, large everted ears, autism, mitral valve prolapse, hypermobile joints
96
In Fragile X syndrome, —(symptom)— is common and can be confused with ——— syndrome
- Self-mutilation
- Lesch-Nyhan syndrome
97
Trinucleotide repeat expansion diseases may show genetic anticipation meaning that:
disease severity increases and age of onset decreases in successive generations
98
For Huntington disease, Myotonic dystrophy, Fragile X syndrome, Friedreich ataxia, what is the associated trinucleotide repeat expansion, mode of inheritance, and mnemonic?
Huntington disease:
- (CAG)n
- Autosomal Dominant
- CAG =Caudate has decreased ACh and GABA (increased dopamine)
Myotonic dystrophy:
- (CTG)n
- Autosomal Dominant
- CTG = Cataracts, Toupee (early balding in males), Gonadal atrophy in males, reduced fertility in females
Fragile X syndrome:
- (CGG)n
- X-linked Dominant
- CGG = Chin (protruding), Giant Gonads
Friedreich ataxia:
- (GAA)n
- Autosomal Recessive
- ataxic GAAit
99
Autosomal trisomies are screened in ——— trimesters with noninvasive prenatal tests
first and second
100
Relative incidence of trisomies 13, 18, and 21:
Down (21) > Edwards (18) > Patau (13)
101
Why are autosomal monosomies not seen?
Incompatible with life (high chance of recessive trait expression)
102
Name 10 key findings in Downs Syndrome:
- intellectual disability
- flat facies
- prominent epicanthal folds
- single palmar crease
- incurved 5th finger
- gap between 1st 2 toes
- duodenal atresia
- Hirschsprung disease
- congenital heart disease (eg, AVSD)
- Brushfield spots (whitish spots at the periphery of the iris)
103
Name 3 conditions that individuals with Downs Syndrome are at higher risk of developing:
- Early-onset Alzheimer disease (chromosome 21 codes for amyloid precursor protein)
-AML
-ALL
104
When nondisjunction occurs in meiosis I vs meiosis II, what are the results in terms of chromosome numbers?
Nondisjunction in meiosis I:
- 2 monosomy
- 2 trisomy
Nondisjunction in meiosis II:
- 2 normal
- 1 monosomy
- 1 trisomy
105
95% of cases of Down syndrome are due to ———, most commonly ——— ( with increased risk associated with ———); 4% of cases due to ———, most typically between ———; and, 1% of cases due to ———
- meiotic nondisjunction
- during meiosis I
- advanced maternal age
- unbalanced Robertsonian translocation
- chromosomes 14 and 21
- postfertilization mitotic error
-
106
What is a Robertsonian translocation?
(One of the most common types of translocation)
Occurs when the long arms of 2 acrocentric chromosomes (chromosomes with centromeres near their ends) fuse at the centromere and the 2 short arms are lost
107
Balanced translocations result in ———, and relative to phenotype ———
- no gain or loss of significant genetic material
- normally do not cause abnormal phenotype
108
Unbalanced translocations result in ———, and relative to phenotype ———
- missing or extra genes
- can result in miscarriage, stillbirth, and chromosomal imbalance (eg, Down syndrome, Patau syndrome)
109
Robertsonian translocation commonly involves which 5 chromosome pairs?
21, 22, 13, 14, and 15
(Note: 1, 2, 3, 4, 5)
110
What is the most common viable chromosomal disorder and most common cause of genetic intellectual disability?
Down syndrome
111
With Down syndrome, first-trimester ultrasound commonly shows which two findings?
- increased nuchal translucency and hypoplastic nasal bone
112
Markers for Down syndrome:
Increased hCG and increased inhibin
(hi up)
113
With Down syndrome, there is an increased risk of what type of hernia?
- umbilical hernia (incomplete closure of umbilical ring)
114
List the 5 A’s of Down syndrome:
- Advanced maternal age
- Atresia (duodenal)
- Atrioventricular septal defect
- Alzheimer disease (early onset)
- AML (<5 years of age)/ALL (>5 years of age)
115
List 10 key features of Edwards syndrome (trisomy 18):
- Prominent occiput
- Rocker-bottom feet
- Intellectual disability
- Nondisjunction
- Clenched fists with overlapping fingers
- low-set Ears
(PRINCE Edward)
- micrognathia (small jaw)
- congenital heart disease (eg, VSD)
- omphalocele
- myelomeningocele
116
In Edwards syndrome (trisomy 18), death usually occurs by age———
One
117
What are the two most common autosomal trisomy resulting in live birth?
Most common Down syndrome followed by Edwards syndrome
118
List 11 key features of Patau syndrome (trisomy 13):
- severe intellectual disability
- rockerbottom feet
- microPhthalmia
- microcePhaly
- cleft liP/Palate
- holoProsencephaly
- Polydactyly
- cutis aPlasia
- congenital heart (Pump) disease
- Polycystic kidney disease
- Omphalocele
119
In Patau syndrome (trisomy 13), death usually occurs by age———
One
120
Patau syndrome associated with defect in fusion of ——— resulting in ———
- prechordal mesoderm
- midline defects
121
Name 2 important 1st trimester screening tests for trisomy 21, 18, and 13; and their findings for each trisomy:
β-hCG:
- increased with Down syndrome
- decreased with Edward and Patau syndrome
PAPP-A:
- decreased with Down, Edward, and Patau syndrome
(In EDwards syndrome, every prenatal screening marker Decreases )
122
Name 4 important 2nd trimester screening tests for trisomy 21, 18, and 13; and their findings for each trisomy:
hCG:
- increased with Down syndrome
- decreased with Edward syndrome
- unchanged with Patau syndrome
Inhibin A:
- increased with Down syndrome
- decreased or unchanged with Edward syndrome
- unchanged with Patau syndrome
Estriol:
- decreased with Down and Edward syndrome
- unchanged with Patau syndrome
AFP:
- decreased with Down and Edward syndrome
- unchanged with Patau syndrome
(In EDwards syndrome, every prenatal screening marker Decreases )
123
What is the full name of vitamin D3 vs D2 and where is each produced?
D3 Name: cholecalciferol
D3 Produced from: exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants
D2 Name: ergocalciferol
D2 Produced from: ingestion of plants, fungi, yeasts
124
Vitamin D2 and D3 are both converted to ——— (storage form) in ——— (associated enzyme ———) and to the active form ——— (called ———) in ———(associated enzyme ———)
- 25-OH D3
- liver
- 25-hydroxylase
- 1,25-(OH)2 D3 (called calcitriol)
- kidney
- 1α-hydroxylase
125
List the 3 key functions of vitamin D:
- increase intestinal absorption of Ca2+ and PO4 3– (increased release from bone, increased absorption in intestines, and increased reabsorption in renal tubular cells (thus decreased in urine))
- increase bone mineralization at low levels (calcium and phosphate when present together in the blood bond very well to each other and they then mineralise or precipitate into the bone)
- increase bone resorption at higher levels
126
Low calcium and low phosphate stimulates ———; When calcium is low, it triggers ——— to be released, which activates the ———
- 1 alpha hydroxylase
- parathyroid hormone (PTH)
- 1 alpha hydroxylase
127
1,25-(OH)2D3 production is increased by what and decreased by what:
- increased by: increased PTH, and decreased Ca2+, PO4 3–
- decreased by: 1,25-(OH)2D3 feedback (inhibits its own production)
128
Increased PTH has what effect on reabsorption in the kidneys?
Increased Ca2+ reabsorption and decreased PO4 3– reabsorption in the kidney
129
List 3 conditions that result from vitamin d deficiency:
- Rickets in children (deformity, such as genu varum “bowlegs”)
- osteomalacia in adults (bone pain and muscle weakness)
- hypocalcemic tetany
130
List 5 causes of vitamin d deficiency:
- malabsorption
- lack of sun exposure
- poor diet
- chronic kidney disease (CKD)
- advanced liver disease
131
List 2 factors that predispose to vitamin d deficiency:
Darker skin and prematurity
132
Provision of oral vitamin D is important for:
breastfed infants
133
Excess vitamins d cause what 4 findings:
- hypercalcemia
- hypercalciuria
- loss of appetite
- stupor
134
Vitamin d excess is observed in ——— (due to increased activation of vitamin D by ———)
- granulomatous diseases
- epithelioid macrophages
135
Lipoproteins are composed of varying proportions of —(4 components)—; LDL and HDL carry the most ———
- proteins, cholesterol, TGs, and phospholipids
- cholesterol
136
List 4 key functions of cholesterol:
- maintain cell membrane integrity
- synthesize bile acids
- synthesize steroids
- synthesize vitamin D
137
Chylomicron are secreted by:
intestinal epithelial cells
138
Chylomicron deliver ——— to ———, as well as delivering ——— to ——— in the form of ———, which are mostly depleted of their ———
- dietary TGs
- peripheral tissues
- cholesterol
- liver
- chylomicron remnants
- TGs
139
VLDL are secreted by:
liver
140
VLDL deliver ——— to ———
- hepatic TGs
- peripheral tissue
141
IDL is formed from:
degradation of VLDL
142
IDL delivers ——— to ———
- TGs and cholesterol
- liver
143
LDL is formed by ——— modification of ——— in the ———
- hepatic lipase
- IDL
- liver and peripheral tissue
144
LDL delivers ——— to ———; Taken up by target cells via ———
- hepatic cholesterol
- peripheral tissues
- receptor-mediated endocytosis
145
HDL is secreted from both ———; ——— increases synthesis
- liver and intestine
- alcohol
146
HDL mediates ——— transport from ——— to ———
- reverse cholesterol
- peripheral tissues
- liver
147
HDL acts as a repository for ——— and ——— (which are needed for ———)
- apoC
- apoE
- chylomicron and VLDL metabolism
148
List function of apoE and where it is present:
Function:
Mediates remnant uptake (everything except LDL)
Present on:
Chylomicron, Chylomicron remnant, VLDL, IDL, HDL
149
List function of apoA1 and where it is present:
Function:
Found only on alphalipoproteins (HDL), activates LCAT (lecithin-cholesterol acyltransferase = Catalyzes esterification of 2 ⁄3 of plasma cholesterol (ie, required for HDL maturation))
Present on:
HDL
150
List function of apoCII and where it is present:
Function:
Lipoprotein lipase Cofactor that Catalyzes Cleavage
Present on:
Chylomicron, VLDL, IDL, HDL
151
List function of apoB48 and where it is present:
Function:
Mediates chylomicron secretion into lymphatics; Only on particles originating from the intestines
Present on:
Chylomicron, Chylomicron remnant
152
List function of apoB100 and where it is present:
Function:
Binds LDL receptor; Only on particles originating from the liver (I hope I live to Be 100)
Present on:
VLDL, IDL, LDL
