Chapter 9: Catabolic Pathways Flashcards
(101 cards)
1
Q
What do epinephrine, glucagon, cortisol and growth hormone have in common?
A
all catabolic hormones (in state of starvation/stress)
2
Q
What is the only purely catabolic pathway that goes on in the cytoplasm?
A
glycolysis
3
Q
What kind of energy do brain, muscles and RBCs use in normal state?
A
glucose
4
Q
What is the energy source for the heart in a normal state?
A
FFA (free fatty acids)
5
Q
What is the energy source for brain, heart, and RBCs in a stressed state?
A
glucose
6
Q
What is the energy source for muscles in a stressed state?
A
FFA
7
Q
What is the energy source for RBCs always?
A
glucose
8
Q
What is the energy source for brain in extreme stress?
A
ketones
9
Q
What is the second messenger of epinephrine and glucagon?
A
cAMP
10
Q
What is the first regulatory step of glycolysis?
A
G6P (because glucose is trapped inside cell)
11
Q
Which two organs use glucokinase to trap glucose inside its cells?
A
liver and pancreas
12
Q
What do other cells use to trap glucose?
A
hexokinase
13
Q
Rate limiting enzyme of glycolysis?
A
PFK-1
14
Q
F1,6 DP splits into what via Aldolase A
A
DHAP and G3P
15
Q
Which two organs run gluconeogenesis?
A
liver (90%) and adrenal glands
16
Q
What is the rate limiting step of gluconeogenesis?
A
pyruvate carboxylase
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
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
19
Q
What enzyme is deficient in galactosuria?
A
galactokinase
20
Q
What enzyme can fill in for galactokinase?
A
hexokinase
21
Q
What are the symptoms of galactokinase deficiency?
A
polyuria, polydipsia, UTIs
22
Q
What enzyme is deficient in galactosemia?
A
galactose 1 phosphate uridyltranserase
23
Q
What is the clue to galactosemia?
A
cataracts in both eyes (galactose turned into galactitol by aldose reductase in neuronal tissue)
24
Q
What are other symptoms of galactosemia?
A
nausea, vomiting after meals, seizures
25
4 main causes of secretory diarrhea (plasma secreted into bowel):
ETEC, VIPoma, Vibrio cholera, cryptosporidium (AIDS pts)
26
Why is fructosuria fairly asymptomatic?
because hexokinase can fill in for fructokinase deficiency
27
When does fructosemia manifest?
6 mo. old when fruits are introduced into diet
28
What is the deficiency in fructosemia?
aldolase B
29
What are the five pathways pyruvate can take?
Alanine pathway, OAA (gluconeogenesis); AcCoA (Kreb's); Etoh; lactate
30
When does pyruvate shift to lactate pathway?
low or no oxygen state, pyruvate turned into lactate
31
Why does the body make lactate?
helps regenerate NAD+ which drives glycolysis at the G3P dehydrogenase step
32
If too much lactic acid, pyruvate will be switched to which pathway?
alanine via alanine transaminase (ALT)
33
In which kind of organism is pyruvate turned into alcohol (EtOH)?
yeast
34
What happens if a person drinks methanol?
turns into formic acid, toxic to retina
35
What happens if a person drinks ethylene glycol (anti-freeze)?
turns into glycoxalate (kidney stones)
36
antidote for anti-freeze or methanol
fomepizole
37
What happens if a person drinks ethylene glycol (anti-freeze)?
turns into glyoxalate (kidney stones that damage kidneys)
38
What does alcohol produce a lot of in our bodies?
NADH
39
What will too much NADH do?
turn of gluconeogenesis causing hypoglycemia (low energy state)
40
Why can't alcoholics use the NADH for energy?
the NADH will be stuck in the cytoplasm, can't get to mitochondria for conversion to energy
41
What will alcoholics use for energy then?
fatty acids causing high triglycerides and ketosis
42
Which drugs besides Disulfram can cause a disulfram-like reaction?
Metronidazole, Cefotetan, cefamandole, etoperidone, moxalactam, chlorpropamide
43
What kind of genetic inheritance is pyruvate dehydrogenase deficiency?
X linked dominant (dad's give to all daughters)
44
What enzyme allows pyruvate to become Acetyl CoA?
pyruvate dehydrogenase
45
What must be present for pyruvate to become acetyl CoA?
oxygen
46
What cofactors does pyruvate dehydrogenase and alpha ketoglutarate DH and branched chain ketoacid DH need?
Tender Loving Care For Nancy
Thiamine PP (vita B1)
Lipoic Acid (vita B4)
CoA (vita B5)
FAD (vita B2)
NAD (Vita B3)
47
How many ATP does once around Kreb cycle yield?
10 (3 NADHs (3*2.5), 1 FADH2 (1*1.5), 1 GTP
48
How many ATPs does 1 glucose molecule yield?
30-32 ATPs
49
What is the rate limiting step of the Kreb's cycle?
isocitrate dehydrogenase
50
Which shuttle can move NADH from cytoplasm to the mitochondria?
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
During periods of rapid growth, glycerol3-phosphate shuttle runs for a net energy loss of how many ATPs?
1 ATP net loss
52
What are the 4 periods of rapid growth and when can rapid growth be turned back on?
0-2 years old
4-7 years old
puberty
pregnancy
turned back on: cancer (KI-67); chronic disease (TNF); burn pts; crush injury
53
Which enzymes are involved in protein breakdown?
transaminases
54
What are the three main aminotransferases in the body?
GGT(90% of transanimations in mitochondria), AST (malate/aspartate shuttle), ALT(cytoplasm)
55
All transaminases require which Vitamin?
B6 (pyridoxal-phosphate)
56
In which liver disease will there be a rise in both ALT and AST on a 1:1 ratio?
hepatitis
57
In which liver disease will there be a rise in both AST and ALT to a 2:1 ratio?
alcoholic hepatitis
58
What is the main fatty acid the body makes?
16 C palmitic acid
59
Short, medium, long fatty acid chains, which ones can cross the mitochondrial barrier?
short and medium
60
Long chain fatty acids require which shuttle to get it into mitochondrial membrane?
Carnitine Shuttle (CAT1)
61
What happens to fatty acids in the mitochondria?
They undergo beta oxidation to break down and give off energy.
62
What are the 4 steps of beta oxidation (OHOT)?
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
What is Adrenoleukodystrophy?
defect in carnitine shuttle; LCFA accumulate in cytoplasm; adrenal gland failure; early white matter involvement
64
What if there are odd numbered fatty acids?
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
What vitamin does Methyl-malonyl mutase require?
Vita B12
66
What energy pathway is run during extreme starvation (more than 48 hours)?
ketogenesis
67
How is a ketone made?
2 or 3 acetyl CoA together made into HMG-CoA by HMG CoA synthase and then remove one acetyl CoA becomes acetoacetate.
68
What is the most abundant ketone and how is it made?
beta hydroxybutyrate made from reducing acetoacetate by NADH
69
Which ketone can cross the blood brain barrier?
beta hydroxybutyrate
70
Tx of DKA?
do not give bicarb!
fluids and when anion gap is normal, insulin
71
How do we correct Sodium in DKA?
(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
What is the #1 cause of death during treatment of DKA?
arrythmias from very low K+ levels
give K+ in first bag of saline (before insulin)!!!
73
What about phosphate in DKA pts?
very low, administer phosphate in first bag of IV fluids!!!
74
What about sodium in DKA pts?
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
What could happen if you correct Na too fast?
central pontine demyelinolysis
76
Why do DKA pts have abdominal pain?
ketones irritate visceral organs
77
Why do DKA pts. have false high creatinine?
Ketones interfere with creatinine assay
78
What do we add to IV in DKA pts when glucose hits 250 or less?
D5
79
5 reasons never to give bicarb to DKA patient:
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
What is hyperosmolar hyperglycemic state in NIDDM?
hyperglycemia without ketoacidosis: dehydration, weakness, vision problems, altered mental state
81
Why should all DM2 pts be on statins?
because hyperglycemia glycosylates the endothelial cells leading to more risk of clot and bleeding; statins can protect endothelial cells
82
How do DM2 pts develop nephropathy?
high viscosity pokes holes in glomerulus; proteins leak out; microalbuminuria; nodular glomerulosclerosis (Kimmelsteil-Wilson)
83
What medication could reduce proteinuria in DM2?
ace inhibitors (esp for diabetics with HTN); why? ACEi dilate efferent flow allows afferent flow to bypass filtration
84
How does Metformin work for DM2 patients?
stops gluconeogenesis
85
main SE of metformin
metabolic acidosis
86
contraindication to Metformin?
renal dysfunction/failure
87
Which drugs are incretin mimetics?
exanatide, semaglutide (the "tides"
88
How do incretin mimetics work?
up insulin release, inhibits glucagon release, inhibits GI secretion and motility, inhibits appetite and food intake, weight loss
89
SE incretin mimetics
cardiotoxic, pancreatitis, MEN2
90
What are the most common insulins given together?
regular and NPH
91
When serum glucose is raised by the morning effect of epinephrine, glucagon, and cortisol it is called
dawn effect
92
How should you regulate insulin intake for dawn effect?
increase morning glucose
93
When you have hypoglycemia in early morning (2-3am) and reactive hyperglycemia in late morning (6-7 am) that is called:
Somogyi effect
94
How should you regulate insulin if you experience Somogyi effect?
decrease evening NPH insulin
95
Which enzyme is deficient in Andersen's Disease?
branching enzyme (can only make straight chains of glycogen which accumulate in hepatocytes)
96
Which enzyme is deficient in Von Gierke's disease?
glucose 6 phosphatase
97
Which enzyme is deficient in Cory's disease?
Debranching enzyme
98
Which enzyme is deficient in Her's disease?
liver phosphorylase (hepatomegaly)
99
Which enzyme is missing in McArdle's?
muscle phosphorylase (muscle cramps during exercise)
100
Which enzyme is missing in Pompe's?
cardiac alpha 1,4 glucosidase (heart cannot get enough energy, heart failure before 1st birthday) "Pompe's trashes the pump"
101
What do all glycogen storage diseases have in common?
hypoglycemia and low energy state
