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Pass Program > Chapter 9: Catabolic Pathways > Flashcards

Chapter 9: Catabolic Pathways Flashcards

1
Q

What do epinephrine, glucagon, cortisol and growth hormone have in common?

A

all catabolic hormones (in state of starvation/stress)

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2
Q

What is the only purely catabolic pathway that goes on in the cytoplasm?

A

glycolysis

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3
Q

What kind of energy do brain, muscles and RBCs use in normal state?

A

glucose

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4
Q

What is the energy source for the heart in a normal state?

A

FFA (free fatty acids)

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5
Q

What is the energy source for brain, heart, and RBCs in a stressed state?

A

glucose

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6
Q

What is the energy source for muscles in a stressed state?

A

FFA

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7
Q

What is the energy source for RBCs always?

A

glucose

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8
Q

What is the energy source for brain in extreme stress?

A

ketones

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9
Q

What is the second messenger of epinephrine and glucagon?

A

cAMP

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10
Q

What is the first regulatory step of glycolysis?

A

G6P (because glucose is trapped inside cell)

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11
Q

Which two organs use glucokinase to trap glucose inside its cells?

A

liver and pancreas

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12
Q

What do other cells use to trap glucose?

A

hexokinase

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13
Q

Rate limiting enzyme of glycolysis?

A

PFK-1

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14
Q

F1,6 DP splits into what via Aldolase A

A

DHAP and G3P

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15
Q

Which two organs run gluconeogenesis?

A

liver (90%) and adrenal glands

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16
Q

What is the rate limiting step of gluconeogenesis?

A

pyruvate carboxylase

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17
Q

What does pyruvate carboxylase do?

A

It turns pyruvate into oxaloacetate (OAA)–OAA turns into aspartate via AST–aspartate into cytoplasm and becomes OAA again–OAA turns into PEP then glycolysis can be reversed until F1,6 DP where it needs F16DPase to continue to G6P

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18
Q

What does pyruvate carboxylase do?

A

It turns pyruvate into oxaloacetate (OAA)–OAA turns into aspartate via AST–aspartate into cytoplasm and becomes OAA again–OAA turns into PEP then glycolysis can be reversed until F1,6 DP where it needs F16DPase to continue to F6P then G6P

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19
Q

What enzyme is deficient in galactosuria?

A

galactokinase

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20
Q

What enzyme can fill in for galactokinase?

A

hexokinase

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21
Q

What are the symptoms of galactokinase deficiency?

A

polyuria, polydipsia, UTIs

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22
Q

What enzyme is deficient in galactosemia?

A

galactose 1 phosphate uridyltranserase

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23
Q

What is the clue to galactosemia?

A

cataracts in both eyes (galactose turned into galactitol by aldose reductase in neuronal tissue)

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24
Q

What are other symptoms of galactosemia?

A

nausea, vomiting after meals, seizures

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25
Q

4 main causes of secretory diarrhea (plasma secreted into bowel):

A

ETEC, VIPoma, Vibrio cholera, cryptosporidium (AIDS pts)

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26
Q

Why is fructosuria fairly asymptomatic?

A

because hexokinase can fill in for fructokinase deficiency

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27
Q

When does fructosemia manifest?

A

6 mo. old when fruits are introduced into diet

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28
Q

What is the deficiency in fructosemia?

A

aldolase B

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29
Q

What are the five pathways pyruvate can take?

A

Alanine pathway, OAA (gluconeogenesis); AcCoA (Kreb’s); Etoh; lactate

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30
Q

When does pyruvate shift to lactate pathway?

A

low or no oxygen state, pyruvate turned into lactate

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31
Q

Why does the body make lactate?

A

helps regenerate NAD+ which drives glycolysis at the G3P dehydrogenase step

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32
Q

If too much lactic acid, pyruvate will be switched to which pathway?

A

alanine via alanine transaminase (ALT)

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33
Q

In which kind of organism is pyruvate turned into alcohol (EtOH)?

A

yeast

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34
Q

What happens if a person drinks methanol?

A

turns into formic acid, toxic to retina

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35
Q

What happens if a person drinks ethylene glycol (anti-freeze)?

A

turns into glycoxalate (kidney stones)

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36
Q

antidote for anti-freeze or methanol

A

fomepizole

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37
Q

What happens if a person drinks ethylene glycol (anti-freeze)?

A

turns into glyoxalate (kidney stones that damage kidneys)

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38
Q

What does alcohol produce a lot of in our bodies?

A

NADH

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39
Q

What will too much NADH do?

A

turn of gluconeogenesis causing hypoglycemia (low energy state)

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40
Q

Why can’t alcoholics use the NADH for energy?

A

the NADH will be stuck in the cytoplasm, can’t get to mitochondria for conversion to energy

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41
Q

What will alcoholics use for energy then?

A

fatty acids causing high triglycerides and ketosis

42
Q

Which drugs besides Disulfram can cause a disulfram-like reaction?

A

Metronidazole, Cefotetan, cefamandole, etoperidone, moxalactam, chlorpropamide

43
Q

What kind of genetic inheritance is pyruvate dehydrogenase deficiency?

A

X linked dominant (dad’s give to all daughters)

44
Q

What enzyme allows pyruvate to become Acetyl CoA?

A

pyruvate dehydrogenase

45
Q

What must be present for pyruvate to become acetyl CoA?

A

oxygen

46
Q

What cofactors does pyruvate dehydrogenase and alpha ketoglutarate DH and branched chain ketoacid DH need?

A

Tender Loving Care For Nancy
Thiamine PP (vita B1)
Lipoic Acid (vita B4)
CoA (vita B5)
FAD (vita B2)
NAD (Vita B3)

47
Q

How many ATP does once around Kreb cycle yield?

A

10 (3 NADHs (32.5), 1 FADH2 (11.5), 1 GTP

48
Q

How many ATPs does 1 glucose molecule yield?

A

30-32 ATPs

49
Q

What is the rate limiting step of the Kreb’s cycle?

A

isocitrate dehydrogenase

50
Q

Which shuttle can move NADH from cytoplasm to the mitochondria?

A

Malate-Aspartate shuttle (1 NADH used and 1 NADH gained, no loss of energy; shut down in alcoholics so they cannot use NADH in the cytoplasm

51
Q

During periods of rapid growth, glycerol3-phosphate shuttle runs for a net energy loss of how many ATPs?

A

1 ATP net loss

52
Q

What are the 4 periods of rapid growth and when can rapid growth be turned back on?

A

0-2 years old
4-7 years old
puberty
pregnancy
turned back on: cancer (KI-67); chronic disease (TNF); burn pts; crush injury

53
Q

Which enzymes are involved in protein breakdown?

A

transaminases

54
Q

What are the three main aminotransferases in the body?

A

GGT(90% of transanimations in mitochondria), AST (malate/aspartate shuttle), ALT(cytoplasm)

55
Q

All transaminases require which Vitamin?

A

B6 (pyridoxal-phosphate)

56
Q

In which liver disease will there be a rise in both ALT and AST on a 1:1 ratio?

A

hepatitis

57
Q

In which liver disease will there be a rise in both AST and ALT to a 2:1 ratio?

A

alcoholic hepatitis

58
Q

What is the main fatty acid the body makes?

A

16 C palmitic acid

59
Q

Short, medium, long fatty acid chains, which ones can cross the mitochondrial barrier?

A

short and medium

60
Q

Long chain fatty acids require which shuttle to get it into mitochondrial membrane?

A

Carnitine Shuttle (CAT1)

61
Q

What happens to fatty acids in the mitochondria?

A

They undergo beta oxidation to break down and give off energy.

62
Q

What are the 4 steps of beta oxidation (OHOT)?

A

O=oxidation yields NADH
H=hydration yields H2O
O=oxidation yields FADH2
T=Thiolysis yields AcCoA
(OHOT occurs every time a pair of carbons are removed from the FA) 16C Palmitic acid, each time 2 carbons removed=7 times each beta oxidation of 16 C palmitic acid yields 108 ATP- 2 ATP cost of glycolysis)=106 net ATP

63
Q

What is Adrenoleukodystrophy?

A

defect in carnitine shuttle; LCFA accumulate in cytoplasm; adrenal gland failure; early white matter involvement

64
Q

What if there are odd numbered fatty acids?

A

every 2 broken down as above;
last 3 carbon unit is Propionyl-CoA which is carboxylated to make Methyl Malonyl CoA which mutated to Succinyl CoA and goes into Kreb’s cycle

65
Q

What vitamin does Methyl-malonyl mutase require?

A

Vita B12

66
Q

What energy pathway is run during extreme starvation (more than 48 hours)?

A

ketogenesis

67
Q

How is a ketone made?

A

2 or 3 acetyl CoA together made into HMG-CoA by HMG CoA synthase and then remove one acetyl CoA becomes acetoacetate.

68
Q

What is the most abundant ketone and how is it made?

A

beta hydroxybutyrate made from reducing acetoacetate by NADH

69
Q

Which ketone can cross the blood brain barrier?

A

beta hydroxybutyrate

70
Q

Tx of DKA?

A

do not give bicarb!
fluids and when anion gap is normal, insulin

71
Q

How do we correct Sodium in DKA?

A

(serum glucose-100/100)*1.6+measured Na
Do not correct Na faster than .5mEq/ hour
do not correct glucose no faster than 100ml/h
when anion gap is normal, add insulin (watch electrolytes, esp. K)

72
Q

What is the #1 cause of death during treatment of DKA?

A

arrythmias from very low K+ levels
give K+ in first bag of saline (before insulin)!!!

73
Q

What about phosphate in DKA pts?

A

very low, administer phosphate in first bag of IV fluids!!!

74
Q

What about sodium in DKA pts?

A

dilutional hyponatremia because ketones and glucose pull water into plasma use formula: (serum glucose-100/100)*1.6+measured sodium to find the true Na level (do not correct faster than 0.5mEq/h)

75
Q

What could happen if you correct Na too fast?

A

central pontine demyelinolysis

76
Q

Why do DKA pts have abdominal pain?

A

ketones irritate visceral organs

77
Q

Why do DKA pts. have false high creatinine?

A

Ketones interfere with creatinine assay

78
Q

What do we add to IV in DKA pts when glucose hits 250 or less?

A

D5

79
Q

5 reasons never to give bicarb to DKA patient:

A

1.corrects numbers without correcting problem
2. exacerbates low potassium
3. decreases cardiac output (acidosis causes increased cardiac output to get rid of acid)
4. shifts hemoglobin dissociation curve to left (when it needs to go to right for acidosis)
5. does not prevent GABA accumulation

80
Q

What is hyperosmolar hyperglycemic state in NIDDM?

A

hyperglycemia without ketoacidosis: dehydration, weakness, vision problems, altered mental state

81
Q

Why should all DM2 pts be on statins?

A

because hyperglycemia glycosylates the endothelial cells leading to more risk of clot and bleeding; statins can protect endothelial cells

82
Q

How do DM2 pts develop nephropathy?

A

high viscosity pokes holes in glomerulus; proteins leak out; microalbuminuria; nodular glomerulosclerosis (Kimmelsteil-Wilson)

83
Q

What medication could reduce proteinuria in DM2?

A

ace inhibitors (esp for diabetics with HTN); why? ACEi dilate efferent flow allows afferent flow to bypass filtration

84
Q

How does Metformin work for DM2 patients?

A

stops gluconeogenesis

85
Q

main SE of metformin

A

metabolic acidosis

86
Q

contraindication to Metformin?

A

renal dysfunction/failure

87
Q

Which drugs are incretin mimetics?

A

exanatide, semaglutide (the “tides”

88
Q

How do incretin mimetics work?

A

up insulin release, inhibits glucagon release, inhibits GI secretion and motility, inhibits appetite and food intake, weight loss

89
Q

SE incretin mimetics

A

cardiotoxic, pancreatitis, MEN2

90
Q

What are the most common insulins given together?

A

regular and NPH

91
Q

When serum glucose is raised by the morning effect of epinephrine, glucagon, and cortisol it is called

A

dawn effect

92
Q

How should you regulate insulin intake for dawn effect?

A

increase morning glucose

93
Q

When you have hypoglycemia in early morning (2-3am) and reactive hyperglycemia in late morning (6-7 am) that is called:

A

Somogyi effect

94
Q

How should you regulate insulin if you experience Somogyi effect?

A

decrease evening NPH insulin

95
Q

Which enzyme is deficient in Andersen’s Disease?

A

branching enzyme (can only make straight chains of glycogen which accumulate in hepatocytes)

96
Q

Which enzyme is deficient in Von Gierke’s disease?

A

glucose 6 phosphatase

97
Q

Which enzyme is deficient in Cory’s disease?

A

Debranching enzyme

98
Q

Which enzyme is deficient in Her’s disease?

A

liver phosphorylase (hepatomegaly)

99
Q

Which enzyme is missing in McArdle’s?

A

muscle phosphorylase (muscle cramps during exercise)

100
Q

Which enzyme is missing in Pompe’s?

A

cardiac alpha 1,4 glucosidase (heart cannot get enough energy, heart failure before 1st birthday) “Pompe’s trashes the pump”

101
Q

What do all glycogen storage diseases have in common?

A

hypoglycemia and low energy state

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