BSI EXAM 3 Flashcards
Where does glycolysis take place?
cytosol
Where does Krebs cycle take place?
mitochondria
Where does ETC take place?
inner mitochondrial membrane
Where glycogenesis stored?
liver and muscle
Where does glyconeogenesis take place?
liver and kidneys
Where does glycogenolysis take place?
liver and muscle
Exception is glucose 6 phosphotase only happens in liver
What is the net ATP and net NADH from oxidation of glucose into pyruvate?
2ATP
2NADH
How many molecules of pyruvate do you end up with when partially oxidizing one molecule of glucose?
2
What are the rate limiting enzymes of glycolysis?
Hexokinase
phosphofructose kinase
pyruvate kinase
What is the function of NAD+ and FAD+?
to carry electrons
What are 3 conditions in which the conversion of pyruvate to lactate will increase?
- no oxygen
- mitochondria dysfunction
- pyruvate is accumulating faster than mitochondria
How is lactate handled by the body? (in other words, how is it removed?)
other cells and tissues that are better oxygenated can take up and use it for energy.
lactose oxidized back to pyruvate–> acetyl coA–> krebs cycle
In this case, cell with mitochondria will take advantage by making the lactate to convert to pyruvate and then enter to mitochondria
What is the definition of lactic acidosis?
build up of lactate
Is the build-up of lactate causing the acidosis?
no, acidosis is build up of protons
Name 4 molecules that will directly stimulate the rate of glycolysis.
ADP, Pi, insulin, epinephrine
Name 2 molecules that will directly inhibit or decrease the rate of glycolysis.
ATP, Glucogon
What enzyme catalyzes the conversion of pyruvate into acetyl-CoA? In this reaction, what is being oxidized and what is being reduced?
Pyruvate dehydrogenase= pyruvate+NAD + coA—> acetyl coA+ CO2+ NADH + H+
Pyruvate reduced
Acetyl coA oxidized
When completely oxidizing 1 molecule of glucose, how many molecules of acetyl-CoA will go through the Krebs Cycle?
2
How many ATP, NADH, and FADH2 do you get with one turn of the Krebs Cycle?
1ATP
3NADH
1FADH
What are the rate limiting enzymes of the Krebs Cycle? What molecules regulate their activity?
- Pyruvate dehydrogenase
- citrate synthase
- Isocitrate dehydrogenase
- alpha- ketoglutarate
Where in the cell does Krebs Cycle take place?
mitochondria
What does NADH and FADH2 do with their electrons they are carrying?
both carry 2H+ when oxidized
What is the path of electron flow through the ETC from NADH?
NADH: 1–> coQ–>3–> cyto c–> 4
What is the path of electron flow through the ETC from FADH2?
FADH: 2–>CoQ–>3–>cyto C–> 4
Why does the electrons coming from NADH produce 2.5 ATP?
10H+ pumped out and 4H+ required to make 1 ATP
10/4= 2.5ATP
Why does the electrons coming from FADH2 produce 1.5 ATP?
6H+ pumped out and 4H+ required to make 1 ATP
6/4= 1.5ATP
If there is lack of oxygen, why does the ETC shut down?
YES
If there is lack of oxygen, why does the Krebs Cycle shut down?
YES
If there is lack of oxygen, why does the glycolysis shut down?
Because mitochondria need oxygen to produce ATP. No ATP= no glycolysis
what happens in dihydroxyacetone phosphase?
it converted to glyceraldehyde 3 phosphate
what is the function of NAD+?
1) To carry oxygen to mitochondria
2) to carry electrons
3) its an enzyme and catalyze various rxn
2) to carry electorns
Pyruvate—–> lactate
Under what condition this happens?
1) lack of oxygen- only applies maxiumum level of intensity
2) catholigcal reason- mitochondria dysfunction- diease states that no produce proteins from mitochondria
3) pyruvate is accumumlating gaster than mitochondria- glycolysis and pyruvate exceeded the pathway
What rxn is pyruvate—> Lactate
what is the enzyme?
what is oxidized
reverse reaction
lactate dehydrogenase
NADH to NAD+
Lactic acidosis is a cause for muscle fatigue and “stingly” of the muscles during high intensity exercise
T or F?
T
Lactic acidosis is a cuase for delayed onset muscle soreness after exercise
T or F?
F; due to inflammation response
Pyruvate—> Krebs cycle oxidized
what is net NADH?
4
How many NADH produce with 1 acetyl coA?
3
How many net ATP, NADH, FADH2 in the process of completely oxidized krebs cycle?
4ATP
10NADH
2FADH2
How lack O2 stops ATP synthase?
electron flows= maintain proton gredients missing -> cant have ATP synthase
Damage mitochondria DNA, how does it lead to lactic acidosis?
mitochondrial dysfunction= proton is building up
How does mitochondria DNA damage cause mitochondrial dysfunction?
Remember 13 proteins in ETC
Dysfunction will shut dow ETC and lead to shut down in ATP and Krebs cycle
No mitochndria= no pyruvate= accumulate lactose instead of protons= going faster than its suppose to
What is the difference between glucokinase and hexokinase?
glucokinase= in liver hexokinase= not in liver
What effect does insulin and glucagon have on glycogenesis? Glycogenolysis?
increase glucogon
decrease insulin
Does glucagon affect glycogenesis and glycogenolysis in skeletal muscle? Liver?
liver
During a state of starvation, is glycogenesis in the liver stimulated or inhibited? What about the fed state?
Starvation: inhibit
Fed: stimulate
During a state of starvation, is glycogenolysis in the liver stimulated or inhibited? What about the fed state?
Starvation: stimulates
Fed: inhibit
Define gluconeogenesis. What substrates can be used for gluconeogenesis?
Forming new glucose aa lactase gylcerol oaa
For what purpose does the liver release glucose into the blood?
so brain can function
Why don’t you become hypoglycemic in the middle of the night when you are sleeping and haven’t eaten in several hours? What happens to your insulin and glucagon levels in the middle of the night?
glycogenesis and glyconeogenesis is in the liver provides glucose to dump in to the blood
What effect does insulin and glucagon have on gluconeogenesis?
Glycogenolysis
Stimulate glucogon
Inhibit insulin
Glycogenesis
Stimulate insulin
Inhibit glucagon
What happens to gluconeogenesis right after you eat a meal (is it stimulated or inhibited)?
inhibit
metformin decreases the activity of glucose 6 phosphate. what effect this have on the body?
1) it will inhibit glycolysis in all tissues
2) it will inhibit glycogenolysis in muscle tissue
3) it will inhibit glyconeogenesis in muscle
4) it will inhibit glyconeogenesis in the liver
4
why skeletal muscle is not taking glucose?
insulin stimulate anabolic pathway
it stimulate uptake of glucose
since decreased in insulin, there is no insulin to uptake the glucose
brain does not insulin to take it up
glycolysis: oxidized sugar
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon inhibits
insulin stimulates
glycogenesis: forming glycogen trees
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon inhibits
insulin stimulates
glycogenolysis: breaking down glycogen trees
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon stimulates
insulin inhibits
glyconeogenesis: forming new glucose and move along to blood
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon stimulates
insulin inhibits
lipolysis
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon stimulates
insulin inhibits
Lipogenesis
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon inhibits
insulin stimulates
ketogenesis
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon stimulates
insulin inhibits
krebs cycle
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon inhibits
insulin stimulates
b-oxidation
glucagon inhibits? stimulates?
insulin inhibits? stimulates?
glucagon stimulates
insulin inhibits
why can’t the brain use fat for energy?
- neurons don’t express b-oxidation enzymes
2. free fatty acids bound to albumin cannot cross the blood-brain barrier
why can’t fats used for energy under anaerobic conditions or any other condition that will shut dow the ETC?
if ETC shuts down, NADH and FADH2 cannot be recycled back to NAD+ and FAD+.
B-oxidation will shut dow—> fatty acid will never tranfer to the mitochondria matrix and will accumulate in cytosol.
same does to mitochondrial dysfunction
B-oxidation is the process of cleave the bond between a fatty acid and glycerol backbone in the trigylceride molecule
T or F?
False; this is definition of lipolysis
B-oxidation is 4 steps process of cleaves off 2c from fatty acids coA in the form of acetyl coA
Insulin increases phosphodiesterase activity in adipocytes. What effect this have on lipolysis
- stimulate lipolysis
- inhibit lipolysis
- no effect
- inhibit lipolysis
insulin stimulates anabolic and inhibits catabolic
Why?
incerased phosphodiesterase activity will decrease the amount of cAMP, therefore decrease activity of hormone sensitive lipase and decrease lipolysis
What are the main functions of epithelial tissue?
protection, absorption, secretion, ion transport, filtration plus “slippery when wet.”
Cillia do what?
propel stuff (eggs, sperm and mucus)
Villi do what?
↑surface area (for absorption).
Which of these cell types is considered to be connective tissue?
- oesteoblasts
- adipocytes
- goblet cells
- mast cells
- RBC’s
all but Goblets.
Fibroblasts secrete which fiber types?
all 3; collagen, elastic and reticular
Dense irregular connective tissue cannot?
withstand ↑tension in one direction
Dense regular connective tissue cannot?
withstand ↑tension in multiple directions.
What type of connective tissue forms the vertebral discs?
fibrocartilage
Is the statement “the terms dorsal and posterior are synonymous in four-legged animals” true or false?
false
The elbow is more what relative to the wrist?
proximal
A rostral to caudal brain section not along the midline is what type of section?
sagittal
The thorax is what to the abdomen?
superior
Are the serous membranes just to reduce friction of moving organs?
no, in the lungs they also link the alveoli to the thoracic wall
Do the body’s systems try to maintain exact physiological values such as body temperature?
not an exact value but a narrow range depending on variable.
Significant variations in all physiological parameters can be tolerated; true or false?
False; depends on variable- ↑BP can be tolerated for years but a significant change in body temperature or especially pH cannot.
What is the normal mechanism for limiting change and restoring homeostasis?
negative feedback.
Where is the best place to control metabolic pathways?
: at the first step/first enzyme.
What is vital if utilizing positive feedback for physiological processes?
: to have a separate, limiting mechanism (not self-limiting like negative feedback).
What are the 4 types of tissue? (histologically speaking).
epithelial, connective, muscle and nervous.
Why do you need to stain tissues?
most tissue is colorless (Caucasians only really have a pink tinge due to blood!) so without the contrast afforded by specific dyes you would find it very difficult to discern anything down a microscope.
Where did the first histological stains originate from? (developed from?).
the first stains were dyes used to stain material woven for clothes.
What are the resolving limits of normal/light microscopy?
: about the size of a small bacterium (~1m to 100nm); limited by the wavelength of visible light.
What are the main problems with normal/light microscopy?
in most situations the processing; impregnating the tissue with wax so it can be cut requires treatment with harsh chemicals, etc. Additionally, the microscope must be set up carefully (“critical illumination”) to get the correct stain colors especially for photography.
What are the resolving limits of electron microscopy?
almost down to single atoms! (~0.1nm/electrons).
What are the main problems with electron microscopy?
the processing even more so. Electron microscopy requires that the tissue be in a vacuum (where no one can hear you scream- see below!) and it is therefore totally dehydrated which is even more likely to introduce artifacts (something added by the experiment/observation/whatever which confounds your results and/or observations) than preparing tissue for light microscopy.
mitochondrial dysfunction in the liver can cause ketoacidosis
T or F?
False; acetyl coa is produced in mitochondria so when mitochondria shut down at the acetyl coa will not formed. so cant synthisize ketone bodies
if mitochondria shut dow, then ketogensis cannot occur
Anaerobic conditions can cause high rish of ketoacidosis
T or F?
False
anaerobic condition–> no o2–> etc shut down–> krebs cycle shut down–> cannot use fat because no b-oxidation and no ketoacidosis
a common adverse side effect of Zidovudre is ketoacidosis
T or F?
False
Lack of insulin and high secretion of glycogen is a common cause if ketoacidosis
T or F?
True
example= uncontrolled type 1 diabetes
Ketosis
example= fasting, or eating high fat and low carb
high rate of b-oxidation and low krebs –> high glucagon and low insulu=in
common
ketoacidosis
example= uncontrolled type 1 diabetes
very very very high level of b-oxidation
glucagon
high level of glucagon will attack bodies such as pancreases when it have “0” insulin
Because glucagon is high, glyconeogenesis is going to happen even though its not suppse to becasue we do not have insulin to uptake glucagon
OAA will deplet–> accumulation of acetyl coa
Tolbutamine and glyburide (drugs to treat diabetes) can inhibit carnitine palmotoyl transferase 1 ( as a side effect) which leads to muscle weakness, pain and exercise intolerance. why would this cause exercise intolerance?
- they inhibit use of glucagon as a fuel source
- they inhibit use of blood glucose as fuel source
- they stimulate ketogenesis
- they inhibit use of fats as a fuel source.
4
why?
cannot transport fatty acids into the mitochondrial matrix for b-oxidation, so cannot use fats a fuel course which can lead to weakness and exercise intolerance
the pain is due to accumulation of lipid droplets in the cytosl of the cell. Accumulation fo lipids cell (except adipocytes) cause dyfunction or death of the cell
accumulations in cytosol are bad!!
Zidovudine can deplete mitochondrial DNA. How can this lead to steatosis?
(accumulation of lipids in the cell)
Damage mitochondria–> no ETC
Depletion of mtDNA (low mtDNA) will lead to dysfunctional ETC and it will shut down. Therefore, B-oxidation will shut down. If B-oxidaiton shut down, then the fatty acids will not be transported into the mitochondria and will then accumulate in the cytosol. Steatosis can cause dyfunction or death to thecell
mtDNA does not encoded bust some of ETC
What tissue does ketogenesis take place?
liver
what are ketone bodeis made from?
acetyl coa
what is ketoacidosis cause from?
accumulation of ketone bodies
how are most of the ROS/RNS produced in the body of external source?
in the mitochondria of most cells via ETC
what is Doxorubicin?
cause damage in health heart cell
cancer drug stimulate HO* to heard
increase H2O2 and increase irons to the heart
What is Dexrazoxane?
prevent doxorubicin
when patient is given binds to free ions
ion is not free it can react
this helps reduce OH*
4 main cell types of epidermis
Keratinocytes, melanocytes, Merkel cell, and langerhans cell
Nailed are modified epithelial tissue composed of what?
Hard keratin
First degree burn?
Second degree burn?
Third degree burn?
First= only epidermis Second= epidermis and dermis Third= all
Melanomas
Developed from moles
Arise from melanocytes
Psoriasis
Due to excessive growth of keratinocytes and like eczema
It has inflammation
Homeostasis
Dynamic mechanism that detect and response to deviations
Afferent
Sensory information going in
Efferent
Muscle response
Example of positive effect
Blood clots and child birth
Positive effect is non self limited
Example of negative feedback
Alosteric modulators
Negative feedback is self limiting
