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MCBM Exam 4 > Review > Flashcards

Review Flashcards

1
Q

When is a positive nitrogen balance seen?

A

Rapid tissue growth; growing children, pregnancy, illness/trauma recovery

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2
Q

When is a negative nitrogen balance seen?

A

Starvation

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3
Q

When is kwashiorkor seen?

A

Generally in children under starvation conditions - muscle wasting

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4
Q

What is the major nitrogen excretion product in humans?

A

Urea

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5
Q

What is the 1st step in nitrogen metabolism? What cofactor is required?

A

Transamination

Vitamin B6

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6
Q

What is the 2nd step of nitrogen metabolism?

A

Bimolecular ping pong

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7
Q

What is the intermediate of nitrogen metabolism? The final product?

A

alpha-ketoglutarate

Glutamate

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8
Q

Where does the 1st portion of the urea cycle occur?

A

In the mitochondrial matrix

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9
Q

What is the rate limiting step of the urea cycle?

A

Carbamoyl phosphate synthetase I

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10
Q

In what organ does the urea cycle take place?

A

In liver (hepatocyes)

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11
Q

Why does an elevated level of ammonia result in decreased ATP production, thus hampering brain function?

A

Excess ammonia is “cleaned up” by the TCA cycle intermediate alpha-ketoglutarate, that depletes NADH production.

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12
Q

What amino transmitters does an elevated level of ammonia deplete?

A

Glutamate

GABA

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13
Q

How does a build up of ammonia cause the brain to swell?

A

It causes a build up of Glutamine that increases intracellular osmotic balance, causing water to enter astrocytes, causing brain swelling

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14
Q

The 5 carbon amino acids are metabolized to glutamate before their final product. What are the 4 amino acids that do so?

A

Glutamine
Proline
Argenine
Histidein

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15
Q

To metabolize histidine to glutamate what is required?

A

THF transfer

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16
Q

What is required to transaminate glutamate to alpha-ketoglutarate?

A

OAA tranaminase

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17
Q

How is glutamine converted into glutamate?

A

By adding NH4

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18
Q

What is the metabolism of argenine to alpha-ketoglutarate?

A

Argenine -> Ornithine -> Glutamate -> alpha-ketoglutarate

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19
Q

Maple syrup urine disease is associated with what?

A

Branched-chain alpha-keto acid dehydrogenase complex

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20
Q

The conversion of propionylCoA to succinylCoA requires what two enzymes?

A

Biotin

Cobalamin

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21
Q

What are the two enzymes that are strictly ketogenic?

A

Lysine

Leucine

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22
Q

What is lysine converted into?

A

AcetoacetylCoA

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23
Q

What is leucine converted into?

A

AcetylCoA

Acetoacetate

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24
Q

What amino acids are both ketogenic and glucogenic?

A

The aromatics:
Phe
Tyr
Trp

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25
Q

Which enzyme requires tetrahydrobiopterin?

A

Phenylalanine hydroxylase

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26
Q

In which reaction is phenylalanine hydroxylase important?

A

The conversion of phenylalanine to tyrosine

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27
Q

What does tryptophan break down into?

A

Pyruvate and acetoacetyl CoA

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28
Q

How is phenylketonuria passed genetically?

A

Autosomal recessive

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29
Q

Phenylketonuria stems from a deficiency in what?

A

Phenylalanine hydroxylase

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30
Q

What is the result of untreated PKU?

A

Severe mental retardation

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31
Q

A defect in alkaptonuria is called what?

A

Homogentisate oxidase

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32
Q

Maple syrup urine diseases comes from a defect in what?

A

Branched chain amino acid DH

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33
Q

A defect in methymalonylCoA mutase causes what?

A

Methylmalonic acidemia

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34
Q

What causes homocystinuria?

A

A defect in cystathione synthase

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35
Q

Which amino acid is insufficient in infants?

A

Argenine

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36
Q

What are the 10 essential amino acids?

A

Phe, Trp, Lys, His, Arg, Ile, Leu, Val, Thr, Met

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37
Q

Which amino acid can be recycled?

A

Met

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38
Q

What is the transamination precursor to alanine?

A

Pyruvate

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39
Q

What is the transamination precursor to aspartate?

A

OAA

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40
Q

How is asparagine made from aspartate?

A

By adding NH4

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41
Q

Which amino acid is broken down to make tyrosine?

A

Phenylalanine

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42
Q

Alpha-ketoglutarate is a precursor for what three amino acids?

A

Glutamate
Glutamine
Proline

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43
Q

How is glutamine made from glutamate?

A

By adding NH4

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44
Q

Homocistanuria is caused by a lack of what?

A

Cystathionine B-synthetase

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45
Q

Cystathionine B-synthetase is important in the synthesis of ___ from ___.

A

Cysteine from serine

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46
Q

Elevated serum levels of what is a known risk factor of cardiovascular disease?

A

Homocysteine

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47
Q

Elevated serum levels of homocysteine may result from deficiencies in what?

A

THF
B12
B6

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48
Q

What do hydroxylases and oxidases do?

A

Add OH groups

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49
Q

What cofactors can be required for hydroxylases and oxidases?

A

Tetrahydrobiopterin

Ascorbate

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50
Q

What do decarboxylases do?

A

Remove COO- groups

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51
Q

What cofactor is required in decarboxylase reactions?

A

Pyridoxine (PLP) (B6)

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52
Q

What do methyl transferases do?

A

Add methyl groups

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53
Q

What cofactors can be required in methyl transferase?

A

Tetrahydrofolate

SAM

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54
Q

What cofactor is needed to methylate epinephrine?

A

SAM

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55
Q

What are the three catecholamine neurotransmitters?

A

Dopamine
Norepinepherine
Epinephrine

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56
Q

Serotonin is synthesized from which amino acid?

A

Tryptophan

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57
Q

In the pineal gland, serotonin can be converted into what?

A

Melatonin

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58
Q

What does prozac do?

A

Inhibits the re-uptake of serotonine

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59
Q

Serotonin is also important in what?

A

Vasoconstriction

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60
Q

Thyroid hormones come from which amino acid?

A

Tyrosine

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61
Q

Thyroid hormones are amine hormones, but act like ___ hormones.

A

Steroid hormones

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62
Q

How does the hypothalamus communicate with the anterior pituitary gland?

A

Via the portal vein system

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63
Q

How does the hypothalamus communicate with the posterior pituitary?

A

Direct innervation

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64
Q

What type of hormones does the anterior pituitary release?

A

Tropic hormones

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65
Q

What are the 6 tropic hormones released by the anterior pituitary?

A 
Corticotropin (ACTH)
Follicle stimulating hormone (FSH)
Luteinizing hormone (LH)
Thyrotropin
Somatotropin
Prolactin
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66
Q

What are the 4 classifications of ligands?

A

Peptide
Eicosanoid
Amine
Steroid

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67
Q

All signaling molecules use cell membrane associated receptors except for:?

A

Steroids

Thyroid hormones

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68
Q

Most neurotransmitters are which classification of ligand?

A

Amines

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69
Q

What are the 5 major concepts of cell signals?

A 
Signals are:
Specific
Amplified
Desensitized
Integrated
Transient
70
Q

How are signals self-limiting?

A

By breakdown, endocytosis, phosphatases, GTPases and Ca pumps used to limit the signal

71
Q

How does desensitization occur?

A

Beta arrestin removes some of the beta adrenergic receptors

72
Q

How does the ubiquitin/proteosome pathway work?

A

Ubiquitin ligases attach ubiquitin to lysine side chains of the proteins;
Ubiquitin acts as a targe for the 26S proteosome

73
Q

What are the 6 major hormone receptor classes?

A 
Gated ion channels
Receptor enzymes
Serpentine
Adhesion
Steroid
"Orphan"
74
Q

What is an example of an adhesion receptor?

A

Integrins

75
Q

How does an adhesion receptor function?

A

Binds molecules in extracellular matrix, changes conformation and alters its interaction with the cytoskeleton

76
Q

How do serpentine receptors work?

A

External ligand binding to receptor activates an intracellular GTP-binding protein (G) which regulates an enzyme that generates an intracellular second messenger

77
Q

How is inositol released?

A

Protein Gq stimualtes phospholipase C which releases inositol

78
Q

What are the three major classes of G-proteins?

A

Gs
Gi
Gq

79
Q

What does Gs stimulate?

A

Adenylate cyclase

80
Q

What does Gi do?

A

Inhibits adenylate cyclase

81
Q

How does the cholera toxin interfere with G proteins?

A

ADP-ribosylates Gs-alpha, making it permanently active

82
Q

If the cholera toxin causes Gs-alpha to be permanently active what is the result?

A

High cAMP in intestinal epithelium causing secretion of Cl, HCO3 and water into the lumen

83
Q

How does the pertussis toxin interfere with G proteins?

A

ADP-ribosylates Gi so that adenylate cyclase is not inhibited

84
Q

What does the pertussis toxin cause?

A

Increased cAMP in the lung epithelium resulting in increased mucous secretion

85
Q

With adenylate cyclase, what is the 2nd messenger, and the kinase that it activates?

A

cAMP

Protein Kinase A

86
Q

With guanylate cyclase, what is the 2nd messenger, and the kinase that it activates?

A

cGMP

Protein kinase G

87
Q

With phospholipase C, what is the 2nd messenger, and the kinase that it activates?

A

IP3, DAG, Ca++

Protein kinase C

88
Q

What is Cushing’s syndrome?

A

Having excess cortisol causing changes in skin and fat deposit

89
Q

What is cortisol supposed to do?

A

Mobilize fuel in response to stress

90
Q

What is the pathway to achieve cortisol secretion?

A

Hypothalamus secretes CRH into portal system
A. pituitary secretes ACTH into circulation
Adrenal cortex secretes cortisol

91
Q

What does ACTH come from?

A

A large precursor protein that stems from the POMC gene

92
Q

What are the effects of cortisol?

A

Elevates blood glucose
Mobilizes fat
Increases muscle protein catabolism
Anti-inflammatory

93
Q

How does cortisol act as an anti-inflammatory?

A

It is a steroid hormone that blocks NFKB signaling by entering the nucleus and changing gene expression

94
Q

What are some symptoms of Cushing’s syndrome?

A 
Upper body weight gain
Skin darkening, bruising, stretching
Excess hair growth or acne in women
Fatigue & muscle weakness
Mood swings
Menstrual disorder
95
Q

Addison’s disease results from what?

A

A cortisol deficiency

96
Q

What are symptoms of Addison’s disease?

A 
Changes in BP/heart rate
Chronic diarrhea
Patchy darkening of skin
Weakness/fatigue
Loss of appetite
Mouth lesions - buccal mucosa
Salt craving
Slow movement
Weight loss
97
Q

What causes the brown patches in Addison’s disease?

A

Excess ACTH - causes melanocyte stimulating hormone

98
Q

What hormones regulate basal metabolic rate?

A

T3, T4

99
Q

Why is iodine necessary in the body?

A

To iodinate tyrosine to get thyroid hormones

100
Q

Are thyroid hormones lipophilic or hydrophilic?

A

Lipophilic (act like steroids)

101
Q

What are symptoms of hypothyroidism?

A 
Cold sensitive
Unintentional weight gain
Fatigue
Brittle hair
Constipation
Depression
102
Q

What are other names for hypothyroidism?

A

Myxedema

Hashimoto’s syndrom

103
Q

What are symptoms of hyperthyroidism?

A 
Heat sensitive
Weight loss
Exophthalmia
Racing/irregular heart
Insomnia
Diarrhea
Tremor
104
Q

What is another name for hyperthyroidism?

A

Grave’s disease

105
Q

What is the role of leptin?

A

To shut down the hunger response so that there is less adipose - regulates body weight

106
Q

Where does leptin come from?

A

Adipose

107
Q

As adipose tissues decreases, what happens to adiponectin?

A

It increases

108
Q

What does adiponectin activate?

A

AMPK

109
Q

Why is AMPK important, especially in diabetes?

A

It allows us to bypass the insulin dependence of GLUT4 receptors

110
Q

What does exercise do to AMPK?

A

Activates it so that it will bring GLUT4 to the membrane

111
Q

What activates Toll receptors?

A

PAMPs - Pathogen associated molecular patterns

112
Q

What are examples of PAMPs?

A

Lipopolysaccharide or flagella proteins

113
Q

What do Toll receptors activate?

A

2 major pro-inflammatory transcription factors:
AP-1
NFkB

114
Q

What is the “master switch” for inflammation?

A

NFkB

115
Q

How is NFkB activated?

A

IkB is phosphorylated, ubiquintinated and degraded, allowing NFkB to enter the nucleus

116
Q

What do glucocorticoids do?

A

Interfere with NFkB

117
Q

How does the thromboxane A2 receptor work?

A

Hormone binds receptor and activates Gq
Gq activates phospholipase C
Phospholipase C catalyzes the hydrolysis of phosphatidylinositol -4,5-bisphosphate to release diacylglyceral (DAG) and inositol trisphosphate (IP3)
IP3 opens Ca++ channels and DAG activates PKC

118
Q

What activates the two different types of guanylate cyclase?

A

ANF

NO

119
Q

What does guanylate cyclase do?

A

It is a secondary messenger that activates cGMP

120
Q

What are the two types of gyanylate cyclase?

A

Integral membrane proteins

Cytosolic protein w/associated heme

121
Q

What activates PKG?

A

cGMP

122
Q

What does PKG target in the kidneys?

A

Na+ channels; enhances Na+ excretion (along with water)

123
Q

What does PKG target in the vasculature?

A

Ca++ channels; lowers cytosolic Ca++, decreases smooth muscle contraction
*Ultimately decreases blood pressure

124
Q

What secretes atrial natriuretic factor? What does it cause to increase?

A

Heart (acting as an endocrine gland)

By binding to guanylate cyclase receptor, it increases cGMP

125
Q

Why is nitroglycerin used for ischemia near the heart?

A

It degrades to NO, which binds GC and increases cGMP, that activates PKG which results in relaxation of the heart muscle

126
Q

What are the 3 types of diabetes mellitus?

A

Type I - Insuline dependent (juvenile)
Type II - Non-insulin dependent (adult-onset)
Gestational

127
Q

What happens in type I diabetes?

A

Autoimmune destructions of beta cells - lack of insulin production

128
Q

What is the normal value for the fasting plasma glucose test?

A

Below 100 mg%

129
Q

What is the normal HbA1c level?

A

6 or lower

130
Q

What is the direct target of insulin?

A

Muscle

Adipose

131
Q

What is the direct target of binguanides?

A

AMPK activator - enhances glucose uptake

132
Q

When is adiponectin activated?

A

Extended fasting or starvation - reduced triacylglycerols

133
Q

What does AMPK activate?

A

GLUT4 transporter

134
Q

What is a key substrate in both purine and pyrimidine synthesis?

A

PRPP

135
Q

What does PRPP do?

A

Activates C1 on ribose

136
Q

What is the committed step in de novo purine biosynthesis?

A

Formation of 5-physphoribosyl-1-amine

137
Q

What catalyzes the formation of 5-phosphoribosyl-1-amine?

A

Glutamine-PRPP amidotransferase

138
Q

Where does the formation of carbamoyl phosphate in de novo pyrimidine biosynthesis take place?

A

In the cytoplasm

139
Q

What is the committed step in de novo pyrimidine biosynthesis?

A

Formation of N-Carbamoylaspartate from aspartate

140
Q

What is needed to synthesize deoxyribonucleotides?

A

Nucleoside diphosphate

Ribonucleotide reductase

141
Q

What inhibits dihydrofolate reductase?

A

Methotrexate
Aminopterin
Trimethoprim

142
Q

What energy source is required for the synthesis of dTMP?

A

NADPH

143
Q

What is the precursor for dTMP synthesis?

A

dUMP

144
Q

Which base is more often recycled, purines or pyrimidines?

A

Purines

145
Q

If you don’t have any HGPRT, what disease do you get?

A

Lesch-Nyhan

146
Q

A deficiency in HGPRT causes what?

A

Gout

147
Q

Guanine and hypoxanthine are formed from what?

A

Adenine

148
Q

What does ribonucleuotide reductase do?

A

Converts ribose to deoxyribose - provides deoxyribose for DNA synthesis

149
Q

If you don’t have adenosine deaminase, what disease do you have?

A

SCID (bubble boy)

150
Q

To prevent gout, what would you block?

A

Xanthine oxidase

151
Q

How is SCID treated?

A

Gene therapy - no real treatment

152
Q

What enzyme is needed to produce uric acid?

A

Zanthine oxidase

153
Q

What did Hershey and Chase prove?

A

Viruses inject DNA

154
Q

What is the DNA “melting” temperature dependent upon?

A

CG base pairs - more H bonds, so they are a little stronger than AT bonds

155
Q

What components are in mRNA?

A

Transcriptional start site
Initiation codon
Exons
*No introns!

156
Q

The sense strand and mRNA are both ___ to the template strand.

A

Complementary

157
Q

What chromosomes make up the nucleolus?

A

13, 14, 14, 21, 22

158
Q

Ribosome RNA genes are found where?

A

On the nucleolus

159
Q

What are the levels of DNA compaction from biggest to smallest?

A 
Coil
Rosette
Loop
Solenoid
Nucleosome
160
Q

What are telomeres?

A

Buffers at the end of chromosomes

161
Q

What are centromeres?

A

The part that links the sister chromatids

162
Q

What happens if an alkylating agent donates alkyl groups to bases?

A

Changes the pairing properties, causing transitions, transversions and/or frameshifts

163
Q

What are the 4 major repair systems?

A

Mismatch repair
Base-excision repair
Nuclotide-excision repair
Direct repair

164
Q

Which type of mutation repair is for bigger lesions?

A

Nucleotide excision

165
Q

What is the most specific type of mutation repair?

A

Direct repair

166
Q

What type of damage does base-excision repair fix?

A

Abnormal bases
Alkylated bases
Pyrimidine dimers

167
Q

What type of damage does nucleotide-excision repair fix?

A

DNA lesions that cause large structural changes

168
Q

What type of damage does direct repair fix?

A

Methylated stuff

169
Q

Xeroderma pegmentosum results from what?

A

Defect in nucleotide excision repair - specifically the thymine dimer repair system

170
Q

What phenotype is caused by hereditary nonpolyposis?

A

Colon cancer - due to ineffectivity of mismatch repair

MCBM Exam 4 (5 decks)

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