Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Biochemistry > Biochemistry final exam study deck > Flashcards

Biochemistry final exam study deck Flashcards

1
Q

What is the best source of immediate energy and why?

A

Glucose (from carbohydrates) can readily diffuse into the blood to be used quickly via fast pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do the highest overall stores of energy come from for metabolism

A

Fats–> they ultimately produce much more ATP, but it takes longer to transport them into the blood and break them down in the cell.
Fat undergoes Beta oxidation and creates much more ATP than any other pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the makeup of fatty acids and phospholipids (what is hydrophobic and hydrophillic in their makeup?)

A

Hydrophillic head with a phosphate group
Hydrophobic tails that are tucked into membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which point in glycolysis does glycerol enter metabolism?

A

Glycerol is converted to Glyceraldehyde 3-phosphate and then turned into DHAP (which is an intermediate of glycolysis and can be readily used).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens to glycerol if blood sugar is low

A

It is used in gluconeogenisis and turned directly into glucose in a liver cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What breaks down triglycerides and what are they broken into?

A

Triglycerides are broken down by lipases into glycerol and 3 fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens to glycerol after lipase breaks up triacylglycerol?

A

Glycerol can be converted to G3P and then DHAP to enter glycolysis (in cytoplasm of a liver cell)
Or
Glycerol can enter gluconeogenesis to turn into glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens to the Fatty acids that are broken down from triacylglycerol

A

Fatty acids are turned into Acyl CoA to get into the mitochondrial membrane.
- Long chain fatty acids are transferred to carnitine (in exchange for Acetyl CoA off of carnitine) to get into the mitochondrial matrix. Cartinine acyltransferase goes through a carnitine transporter channel, and then once into the matrix, the carnitine swaps the fatty acyl-CoA for ACOA. Once this happens, the long chain fatty acids can then undergo B-oxidation to acetyl CoA and then enter the Kreb’s cycle.

-Short chain fatty acids can get directly into the inner membrane without carnitine, and then are turned into acyl-COA–>B-oxidation–>Acetyl CoA–>Kreb’s cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens to odd-number carbon chains that undergo B-Oxidation

A

They are converted to Succinyl-CoA and enter the CAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does insulin do to lipases? What do Lipases do?

A

Insulin deactivates lipases.
Lipases break down triglycerides to be used for fuel. Insulin is released when the body has glucose already, so lipases are inactivated because the body doesn’t need more fuel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does glucagon and epinephrine do to lipases

A

Activate lipases- Stimulate fatty acid release and B-oxidation.
Blood sugar is low when glucagon and epinephrine are released, so lipases must be activated to break down triaglycerides into fuel and trigger the start of metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is CJD caused by

A

Caused by prions (misfolded proteins that cause the misfolding and aggregation of other, healthy proteins). This inhibits protein function in the brain, causes neuronal damage and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which other disease is CJD often mistaken with

A

Alzheimer’s disease– the early symptoms are often similar, with loss of memory, changes in visual perception, and unstable mental status.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does prion infection cause CJD

A

When a misfolded protein or prion is present, it aggregates with other, healthy proteins, and causes the healthy proteins in the brain to aggregate as well. In CJD, the prions overtake the proteins in the brain, causing damage to the brain tissue, and leading to cell death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why is CJD often misdiagnosed and what is it commonly misdiagnosed as?

A

Often misdiagnosed as Alzheimer’s disease.
Early symptoms (loss of memory, visual field changes, mental decline) are similar in both. CJD symptoms are nonspecific in early stages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

If a patient had a defect in Glucose-6-phosphatase, what would happen to blood serum levels upon administration of fructose?

A

G6Pase is needed to get a phosphate off of G6P to get it out of the cell and out of glycogen stores. Ultamately, glycogen builds up.
Normally, if fructose is administered, it is turned into G6P, and G6Pase turns it into glucose.
If there is a G6PAse defect, if fructose is administered, there wouldn’t be a glucose level rise after the patient gets fructose, because G6Pase can’t turn the fructose into glucose. It would stay as G-6-P, and be converted to glycogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why does hypoglycemia following stimulation with epinephrine and glucagon indicate a diagnosis of Von Gierke’s Disease?

A

Epinephrine and glucagon stimulate glycogen breakdown into glucose and stimulate the process of glucose getting into muscles and heart.
If someone has VGD, and stimulate with epinephrine and glucagon, their blood glucose levels won’t rise because G6-Pase is dysfunctional, so glucose can’t get into the blood and out of stores.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

List three potential physical symptoms a child with Von Gierke’s Disease would present with

A

Extreme fatigue, easy bruising/frequent nosebleeds, Doll-like face with very puffy cheeks and thin extremities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Tangier’s Disease big picture?

A

Rare genetic disorder where the body has a deficiency in HDL (good cholesterol) in the blood.
HDLs are needed to remove cholesterol out of arterial walls, so with low HDL, cholesterol will buildup on arterial walls and in other locations/on other organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tangier Disease is a genetic disorder characterized by a deficiency in what?

A

HDL (High Density lipoproteins in the blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is most characteristic of a patient who has Tangier Disease?

A

Yellow or orange tonsils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If you have a patient who has yellow or orange tonsils, what possible disease are they suffering from?

A

Tangier disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Vitamin C needed for in collagen?

A

Vitamin C is a coenzyme needed for collagen to form its secondary folding structure to be as strong as it is
- Coenzyme for the hydroxylation of proline (which gives collagen its secondary structure of a triple helix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does a vitamin C deficiency lead to

A

Scurvy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are common symptoms of scurvy
bleeding and spongy gums, swollen joints, skin hemorrhages because with less properly formed collagen→ loose and fragile connective tissues
26
What are common symptoms of Osteogenesis imperfecta
Genetic disease that causes abnormal formation of collagen→ bones don't have correct tensile strength so they break easily
27
What is the post-translational modification that happens to the proline residues in collagen?
Hydroxylation of proline residues which makes hydroxyproline
28
Briefly explain the role of Vitamin C in the structure and function of collagen.
Vitamin C is a key coenzyme in the hydroxylation of proline in collagen. The hydroxylation allows collagen to form its secondary folding for its triple helix structure. This is what gives collagen its strength
29
List three hallmark signs of Scurvy and explain in one sentence why a patient with a Vitamin C deficiency will exhibit these symptoms.
Scurvy symptoms are bleeding spongy gums, swollen joints and skin hemorrhages. Patients with low Vitamin C develop these symptoms because without vitamin C they cannot produce collagen. Without the collagen as connective tissue the tissues are weak and fragile.
30
Define the term anemia in 1 sentence
Anemia is a blood disorder that is caused because the body makes blood cells that are too large, misshapen, or immature, leading to inefficient oxygen delivery to tissues. Lack of RBCs
31
Explain the role folic acid plays in the body’s ability to transfer oxygen from the lungs to the tissues
Folic acid is involved in the production of healthy cells, including the production of red blood cells. When there is a deficiency of folic acid, the body has insufficient numbers of healthy red blood cells, so there is not enough transfer of oxygen into tissues. Decreased red blood cells that are healthy means there are essnentially not enough carriers to get oxygen into tissues from the lungs.
32
Why is alcoholism considered an aggravating factor in megaloblastic anemia?
Alcoholism decreases the amount of folic acid metabolism in the body, which inhibits the production of healthy red blood cells. Thus, it contributes to anemia development, because it decreases the folic acid that is essential in healthy red blood cell production.
33
List three potential causes of folate deficiency
-Alcoholism can lead to a lack of healthy RBC creation because of decreased metabolism of folate (necessary to create the healthy RBCs) -Folate deficiency simply because of the lack of intake through diet (such as not eating enough folate rich foods in vegetables). -Taking medications that impair absorption of folic acid can lead to a folate deficiency, similar to the way that alcoholism leads to it.
34
Why is HIV able to be dormant in our bodies
It makes inactive viral proteins that are very harmful when active, but these proteins remain inactive while constantly multiplying and creating a very large issue for when HIV proteases do ultamately turn on
35
What is the main reason for differences in substrate specificity between different proteases like Trypsin and Chymotrypsin?
Trypsin and Chymotrypsin have the same active sites but they both have different binding pockets. Trypsin binds to a C terminal of lysine and arginine Chymotrypsin cleaves the C terminal of bulky, nonpolar side chains
36
Which molecule acts as a nucleophile for HIV protease
aspartyl protease Aspartic acid deprotonates a water molecule and uses the OH as a nucleophile
36
Which enzymes in the Citric Acid Cycle require Thiamine?
Pyruvate Dehydrogenase and a-ketoglutarate dehydrogenase Without pyruvate dehydrogenase, pyruvate will never become acetyl CoA for the citric acid cycle This will cause lactic acidosis
37
Which two metabolites will build up if Thiamine levels are insufficient?
Pyruvate and a-ketoglutarate
38
Briefly describe Beriberi disease
Beriberi disease is when patients have a severe deficiency of thiamine. Their cells are unable to run the citric acid cycle without Thiamine and will therefore have a build up of pyruvate that leads to a buildup of lactic acid, leading to a range of symptoms. The most concerning of which are decreases in mental function and progressive weakness due to the hyperlactatemia.
39
Give two examples of clinical situations where thiamine deficiency can result in lactic acidosis.
-A thiamine deficiency can result in lactic acidosis as a direct result of the metabolite (pyruvate) buildup, increasing the pH in the body. - People who eat lots and lots of rice or who are in nutrient deficiency can get it too -People who have alchoholism (creating a thymine deficiency) and who haven't been eating food will end up in lactic acidosis if they eat glucose because the glucose will be immediately built up very quickly.
40
Biotin carries an active form of which molecule?
CO2 Needed in carboxylation reactions, moves CO2 from one thing to another
41
In gluconeogenesis, which enzyme requires biotin?
pyruvate carboxylase (Catalyzes pyruvate to oxaloacetate) requires biotin
42
List the three most common pathways that utilize biotin.
Gluconeogenesis PEP synthesis Amino Acid metabolism
43
Glycerol and fatty acids have different paths in the metabolism of triglycerides. How does glycerol enter metabolism of glycolysis?
As G3P (GAP) Can be used in gluconeogenesis if blood sugar is low Fatty acids turned into Acyl Coa to get into membrane, LCFAs in carnitine--> Beta oxidation (In mitochondria) ---> Acetyl CoA-->Kreb's cycle
44
The urea cycle secretes nitrogen from amino acids as what
Urea
45
The urea cycle creates urea from what
Excretes nitrogen released from amino acids as urea
46
What molecule is required to complete the Urea cycle
CO2
47
What are NAGs and how are they releated to the urea cycle
NAGS are N-acetyl glutamate synthase Controller of urea cycle, high presence of arginine signals that ammonia levels are high, so urea runs
48
Your patient presents to your office with a distorted mental affect, vision problems, memory problems, and issues with speech. Which 2 diseases come to mind?
Alzheimer's disease and prion disease Often misdiagnosed because Prion disease is not specific to start. Very rapid onset, often mistaken for AD.
49
What type of genetic inheritance is GSD (Von Gerke's disease)
Genetically recessive Von Gereks is a type of GSD
50
What is the main concern with Von Gerekes disease
Cannot get glucose out of stores because there is a defect in G6P. You can still glucose that enters the body after eating, but cannot go back the other way from Glycogen to glucose or from turning fructose to glucose.
51
G6Pase catalyzes which reaction
From G6P to Glucose (final step of gluconeogenesis)
52
You have a patient who is complaining of severe nausea, light-headedness, and vomitting. They say their symptoms get better immediatly after eating, and are worse inbetween meals. Which disease could this be?
Von Gereks disease Cannot do gluconeogenesis, so are stuck with glycogen stores and buildup of glycogen of all the food you intake. Severe hypoglycemia
53
Which tests would you do to rule out von gereks disease?
1. See if the patient feels better after eating (they should, their body can still use glucose). 2. Administer fructose to see if there is a spike in glucose (there should be normally) 3. You stimulate with epinephrine and glucagon and see if there is increase in BG levels (there should be--> this should get glycogen out of storage in liver, glycogen should turn to Glucose in epi or glucagon stimulation).
54
You have a patient with doll-like face and puffy cheeks, thin extremities, and extreme fatigue. Which disease is at the top of your DD?
Von Gerkes disease
55
If your patient has chronic HTN with enlarged and yellow tonsils, which disease are you automatically suspicious of?
Tangier's disease--> buildup of fat deposits all over body - HDL deficiency
56
Your patient has hepatomegaly and splenomegaly with enlarged lymph nodes. They also have elevated triglyceride levels. Which disease are you cocnerned about?
Tangier's diseaese--> not enough HDL to move triglycerides into stores. Fatty acids will accumulate in the tonisls and around the body.
57
What is the coenzyme needed for collagen to form its secondary folding
Vitamin C - Deficiency can lead to Scurvy--> bleeding and spongy gums, swollen joints, improperly formed triple helix of collaen.
58
What is the post-translational modification that happens to the proline residues in collagen?
Hydroxylation of proline residues which makes hydroxyproline
59
Briefly explain the role of Vitamin C in the structure and function of collagen.
Vitamin C is a key coenzyme in the hydroxylation of proline in collagen. The hydroxylation allows collagen to form its secondary folding for its triple helix structure. This is what gives collagen its strength
60
Briefly explain the mutation to collagen seen in Osteogenesis imperfecta, and why that mutation results in decreased bone strength.
The syndrome is caused by mutations of genes that encode for type 1 collagen, leading to bones that fracture easily. In the common form of it, there is a mutation that replaces glycine with bulky side chains. This means that there are abnormal shaped alpha chains, leading to improperly formed helical conformations in the triple helices. Ultimately, the chains simply are bound together in bones improperly, leading to them being structurally less sound.
61
You have a patient who has bleeding and spongy gums, swollen joints, and skin hemmorrhages enter your clinic. What is the first disease that you are concerned about?
Scurvey--> caused because of improperly formed collagen because of vitamin C deficiency
62
You have a patient who breaks around 2 bones a year come to your office asking why it is that they are so accident prone. Which disease is possible?
osteogenesis imperfecta--> brittle bone disease--> abnormal formation of collagen. Nothing to do with vitamin C.
63
What is anemia
Lack of red blood cells/oxygen being delivered to tissues because of improperly formed RBCs
64
Which process is folic acid crucial for in the body
Making healthy RBCs--> needed to deliver oxygen to tissues. Body has insufficient numbers of healthy RBCs so not enough transfer of oxygen to tissues.
65
You have a patient who has AUD. How would you explain to them that their alcohol consumption is causing their megaloblastic anemia?
Alcohol prevents proper breakdown of folic acid in the body (not enough to make RBCs) Inhibits production of healthy RBCs.
66
You are informing your patient about issues that could lead to a foic deficiency. What are 4 things you tell them?
Alcoholism Surgery to stomach or intestines Intesttinal disorder like Crohn's Insufficient absorption of folic acid
67
Which cells do HIV proteins target
Attack host T-cells and symptoms begin. HIV makes millions of viral proteins that are harmful to cells after activated by HIV proteases.
68
What is the mechanism of HIV inhibitors?
They are HIV protease inhibitors--> deactivate proteases so that inactive proteins are never spliced and can't cause harm to the host
69
What is the main difference between Trypsin and Chymotrypsin
Trypsin and Chymotrypsin have different binding pockets (Trypsin cleaves C terminal of lysine and arginine, Chymotrypsin cleaves C-terminal of bulky nonpolar side chains)
70
What do trypsin and chymotrypsin have in common
Same active sites
71
What does Trypsin cleave
C terminal of Lysine and Arginine (LYS, ARG)
72
What does Chymotrypsin cleave
Bulky, nonpolar side chains, F/W/Y (Phenylalanine, Tryptophan, Tyrosine, Alanine, Leucine, Phenylalanine, Methionine)
73
Which molecule acts as a nucleophile for HIV protease
Aspartyl protease - Aspartic acid is a bad nucleophile, so the first one deprotonates water, and the OH serves as a nucleophile
74
Briefly explain how HIV is able to remain in a dormant form for potentially extended periods of time after host infection.
Proteins are made that are inactive, and these are not flagged by the immune system. They build up. When HIV Protease starts cutting them to activate them, it attacks T cells and causes symptoms
75
What is Thiamine needed for
Pyruvate Dehydrogenase and alpha ketoglutarate dehydrogenase need thiamine Thiamine is a water soluble vitamin Without pyruvate dehydrogenase, pyruvate levels will build up and alpha ketogluterate. This can cause lactic acidosis
76
Which 2 metabolites will build up if thiamine levels are low
Pyruvate (because pyruvate dehydrogenase doesnt work) and Alpha ketoglutarate (because alpha ketoglutarate dehydrogenase doesnt work).
77
Describe BeriBeri disease
Severe thiamine deficiency Cells cannot run the CAC without thiamine, so have a buildup of pyruvate that leads to a buildup of Lactic acid, leading to mental function decrease and weakness due to hyperlactic buildup.
78
Give 2 cases where someone might develop lactic acidosis
1. In areas where people are consuming mostly rice (very low in thiamine) 2. In people who stay in the hospital for a long time with insufficient nutrients
79
You have a patient who comes to you complaining of mental decline and weakness. They said they were in the hospital for almost 3 months and just recently left. What is a possible differential?
Thiamine deficiency--> weakenss and mental decline are signs of lactic acidosis. Being in the hospital puts you at a decreased nutrient state and you may become thiamine deficient.
80
Which enzyme needs biotin to work in gluconeogenesis?
Pyruvate carboyxlase (the enzyme that catalyzes pyruvate-->oxaloacetate
81
List 3 pathways that use biotin
Gluconeogenesis ( Needed to get PEP) Fatty acid synthesis Amino acid metabolism Biotin is the active form of Carbon Dioxide. Critical to move CO2 around.
82
Vitamin K converts which factor to which factor in the coagulation cascade
Prothrombin to thrombin, which initiates the coagulation cascade
83
What is the enzyme that facilitates the conversion of prothrombin to thrombin
Gamma glutamyl carboxylase
84
Which glutamic acid residue is formed in the conversion from prothrombin to thrombin
Gamma carboxyglutamic acid
85
An infant gets poked for their newborn test and cannot stop bleeding. Which disease are you primarily concerned about?
Hemmorhagic disease of the newborn/ Vitamin K deficiency bleeding--> not enough vitamin K, so cannot convert prothrombin to thrombin.
86
Which 2 drugs inhibit the function of vitamin K
Warfarin and dicourmarol
87
What is the desired product of the pentose phosphate pathway
NADPH From G6P using G6P Dehydrogenase
88
Symptoms of someone who has botin deficiency
Skin, hair nails brittle.
89
If you have a patient who has moderate hypoglycemia and is in a state of lactic acidosis, which disease is possible/which nutrient is deficient?
Thiamine--> need administration of thiamine, because pyruvate dehydrogenase and alpha keto gluterate require thiamine to function in the citric acid cycle.
90
Which nutrient do you administer to a patient who has beriberi disease
Thiamine
91
If your body has a lot of sugar in it already, what happens to glycerol
Goes to liver cell and enters glycolysis

Biochemistry (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions