Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiological concepts > Wk13 - endo & metabolism > Flashcards

Wk13 - endo & metabolism Flashcards

1
Q

Catabolism:

a. ) This is mostly through what chemical process?
b. ) This mostly results in production of what?

A

a. ) Oxidation of the larger molecule, breaking it into a smaller molecule.
b. ) ATP.

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

State some broad purposes of anabolism. (2)

A
  1. Structure.

2. Storage.

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

t/f: AA’s can be used directly to generate energy.

A

FALSE - AA’s must first be converted into CHO/ lipids before they can be used for energy. This sort of gluconeogenic reaction often occurs in the liver.

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

State the 2 main complications relating to food metabolism. Briefly explain.

A
  1. Diet means intermittent supply: excess energy during feeding must be stored (saved) for fasting. For example, glycogen and triglyceride formation.
  2. Brain requires glucose: meaning other tissues must use other sources (like FFA’s or AA’s) for energy.
    (note: under normal conditions the brain only metabolises glucose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The brain demands blood glucose remains within what range?

A

~70 - 110 mg/ 100ml.

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

State the source of glucose for:

a. ) Short fasting.
b. ) Longer fasting.

A

a. ) Glycogen (muscle, liver).

b. ) Gluconeogenic processes (FFA’s, AA’s,) as well as lipolysis. Occurs in many tissues.

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

State the 2 functional metabolic states related to fasting/ eating cycles. Explain breifly.

A
  1. Absorbitive state: during meal when nutrients are ingested, body absorbing them.
  2. Postabsorbitive state: Some time after meal when body is no longer really absorbing energy, but instead metabolising the energy stores within.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does the body know when to switch from net anabolism, to net catabolism and glucose sparing?

A

HORMONAL LEVELS - particularly pancreatic hormones:
Insulin - fed state.
Glucagon - fasted state.

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

Where are the islands of langerhans found?

A

Pancrease.

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

State the 2 types of cells and the respective hormones they release, from the islets of langerhans.

A

α cells - glucagon.
β bells - insulin.
(hint: glucagon has an ‘a’ indicating alpha cells)

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

State the main actions of insulin. (4)

Is this hormone prevalent in fed, or fasting state?

A

Insulin DECREASES BLOOD SUGAR, increasing:
1. Protein synthesis.
2. Glycogen synthesis.
3. Fat synthesis.
4. Glucose oxidation (removing glucose from the blood thus further decreasing levels.
Insulin is prevalent in FED STATE.

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

State the main actions of glucagon. (3)

Is this hormone prevalent in fed, or fasting state?

A

Glucagon INCREASES BLOOD SUGAR, increasing:

  1. Glycogenolysis (glycogen breakdown).
  2. Gluconeogenesis (glucose made from AA/ fats).
  3. Ketogenesis (fatty acid breakdown producing ketones).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which hormone is dominant in the absorptive phase?

A

Insulin.

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

Insulin promotes the cellular uptake of nutrients, so that they can be stored. This DECREASES the concentration of what substances? (3)

A
  1. Glucose.
  2. FFA’s.
  3. AA’s.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Broadly, how is it that insulin is achieves it’s functions (on a cellular level)? (2)

A
  1. Alters enzymatic activity.

2. Affects cell transport.

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

Explain the influence of INSULIN on the following:

Carbohydrates. (4)

A
  1. Facilitates glucose transport into cells.
  2. Stimulates glycogenesis.
  3. Inhibits glycogenolysis.
  4. Inhibits gluconeogenesis (decreasing blood [AA]).
    (explanation for (4): Insulin is the hormone responsible for packaging away molecules. To understand why inhibiting gluconeogenesis will decrease blood [AA], look at insulin’s effect on proteins - insulin inhibits protein degradation + promotes AA transport into other tissues. Thus, the purpose of inhibiting gluconeogenesis using AA’s is so that these can be packaged away, thus decreasing blood [AA])
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Some tissues are not dependant on insulin - provide 2 examples.

A
  1. Brain.

2. Liver.

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

Explain the influence of INSULIN on the following:

Proteins. (3)

A

“PIE”

  1. P - promotes AA in blood to move into muscle/ other tissues.
  2. I - inhibits protein degradation (so less free AA’s are about).
  3. E - enhances protein synthesis at ribosome level (so less free AA are about).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain the influence of INSULIN on the following:

Fat. (4)

A

“PAPI”

  1. P - promotes glucose uptake so it can be used as a lipid precursor.
  2. A - activates enzymes converting glucose to AA.
  3. P - promotes entry of FA from blood into adipose tissue.
  4. I - inhibits lipolysis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

State all possible factors for control of insulin release.

A

“DIGS”

  1. D - direct negative feedback on B cells (high BS stimulates insulin release).
  2. I - Increased [AA] from meal increases insulin.
  3. G - GIT hormones.
  4. S - SNS and adrenaline decreases insulin (so that theres more blood sugar for fight or flight).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Briefly explain how direct negative feedback controls insulin secretion.

A
  1. Stimulus = high blood glucose.
  2. Response = insulin release and its effects.
  3. Effect = decreased blood glucose, exerts negative feedback on B cells so less insulin is released.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Briefly explain how GIT hormones control insulin secretion.

A
  1. Presence of food triggers ANS activity.

2. Vagus nerve fires to increase GIT hormones, however also increases insulin secretion (parasympathetically).

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

State the dominant hormone of the post-absorbitive phase.

A

Glucagon.

24
Q

Where is the major site of glucagon activity?

A

Liver.

25
Q

t/f: glucagons actions are the opposite of insulin.

A

True.

26
Q

State all possible factors for control of glucagon release.

A
  1. Direct negative feedback on α cells (low blood sugar stimulates glucagon release).
  2. Decrease FFA’s stimulates increased glucagon release.
27
Q

Explain the effect of GLUCAGON on the following:

Carbohydrates. (3)

A
  1. Promotes glycogenolysis.
  2. Promotes gluconeogenesis.
  3. Inhibits glycogen synthesis.
28
Q

Explain the effect of GLUCAGON on the following:

Proteins. (2)

A
  1. Inhibit HEPATIC protein synthesis.
  2. Promote HEPATIC protein breakdown.
    (note: NO EFFECT on muscle protein, key here is that glucagon only effects liver protien)
29
Q

Explain the effect of GLUCAGON on the following:

Lipids. (3)

A
  1. Promote lipolysis.
  2. Promote ketone production.
  3. Inhibit triglyceride synthesis.
30
Q

t/f: glucagon released into the bloodstream stimulates breakdown of muscle protein.

A

FALSE - hepatic protein only.

31
Q

Insulin and glucagon are antagonistic hormones. This is true apart from one exception - state this stimulus.

A

Increased blood [AA] stimulates release of BOTH glucagon and insulin.

32
Q

Why is it that both insulin and glucagon are released post a protein-rich meal?

A

Usually only insulin is released during the absorptive state. However, if a meal is rich in proteins (which can’t be used as fuel directly), their is a risk of hypoglycaemia; as the insulin further reduces blood glucose levels. To counter this, glucagon is released, raising blood sugar levels.

33
Q

What other, non-pancreatic hormones may influence fuel metabolism?

A
  1. Stress hormones (cortisol, adrenaline).
  2. GH + cortisol.
  3. GH individually.
34
Q

State the effect of the following hormone(s) on fuel metabolism:
Cortisol + adrenaline.

A
  1. Increased blood [glucose].

2. Increased blood [AA] (cortisol specifically induces protein catabolism).

35
Q

State the effect of the following hormone(s) on fuel metabolism:
GH + cortisol.

A

Help maintain [glucose] during starvation.

36
Q

State the effect of the following hormone(s) on fuel metabolism:
GH individually.

A

Protein anabolism resulting in muscle growth.

37
Q

Diabetes is a metabolic disorder caused by lack of what hormone?

A

Insulin.

38
Q

State the types of diabetes mellitus.

A

Diabetes Mellitus comes in 2 forms:
Type 1 - Insulin Dependant (IDDM).
Type 2 - Non-Insulin Dependant (NIDDM)

39
Q

IDDM is AKA? Why is it so named?

A

Juvenile-onset diabetes, as onset of IDDM occurs in individuals <30 who are not obese.

40
Q

IDDM pateints are prone to what condition? What do they require as a result of this?

A

Ketosis (due to oxidation of ketone bodies, as glucose cannot enter cells). As a result of the condition insulin injections are required.

41
Q

Describe the likely cause(s) of IDDM.

A

IDDM involves B cell destruction (resulting in reduced mass of B cell’s of pancrease, meaning less insulin produced). This may occur due to:

  1. Genetic predisposition.
  2. Auto-immune reactions.
  3. Infection.
  4. Environmental factors.
  5. Viruses (viral infections often precede IDDM).
42
Q

NIDDM is AKA? Why is it so named?

A

Adult-onset diabetes, where onset occurs in individuals >30 years, with 70-80% of those individuals being obese.

43
Q 
IDDM = \_\_% total DM. 
NIDDM = \_\_% total DM.
A 
IDDM = 20%. 
NIDDM = 80%.
44
Q

Physiologically, how is NIDDM characterised?

A

Individuals with type 2 DM have some levels of insulin (but not enough), or the cells of the body are not sensitive enough to it.

45
Q

In terms of control, how does NIDDM differ to IDDM?

A

NIDDM can be controlled through diet.

46
Q

State the clinical manifestations of type 2 DM.

A
  1. Polyuria.
  2. Polyphagia.
  3. Polydipsia.
  4. Weight loss.
  5. Weakness.
47
Q

The predominant pathophysiology of diabetes is due to what 3 factors?

A
  1. Impaired use of glucose by cells.
  2. Increased mobilisation, abnormal metabolism and deposition of fats.
  3. Depletion of protein in body tissues.
48
Q

The predominant pathophysiology of diabetes is due to what 3 factors?

A
  1. Impaired use of glucose by cells.
  2. Increased mobilisation, abnormal metabolism and deposition of fats.
  3. Depletion of protein in body tissues.
49
Q

What % of individuals with NIDDM are obese?

A

70 - 80%.

50
Q

Which of the following options requires MORE INSULIN:
a.) Level of insulin required to transport glucose into fat cells.
b.) Level of insulin required to prevent lipolysis and release of fatty acids.
Explain the EVIDENCE behind your answer.

A

A - more insulin is required to transport glucose into fat cells, then the amount required to prevent lipolysis/ release of FFA. Evidence for this is that individuals with type 2 diabetes usually have some (low) level of insulin within the blood, which is enough to prevent lipolysis, but NOT enough to lower blood sugar levels by transporting excess glucose into adipocytes.

51
Q

What is the overall major or primary concern of the body in terms of energy metabolism? Briefly, how is such concern addressed (in fasting states, as during feeding glucose is obviously already in the bloodstream)?

A

The major concern is keeping a steady glucose supply to the brain. This is ensured (in fasting states) by GLUCOSE SPARING of other tissues, which use FFA’s or AA’s (via gluconeogenesis) to generate glucose - instead of taking it from the glucose pool reserved for the brain.

52
Q

Why does the brain have a constant demand for glucose? (2)

A
  1. As the brain lacks glycogen stores, and (under normal conditions) only metabolises glucose for energy. Neurons are unable to store glucose (in the form of glycogen) like other cells.
  2. FFA’s cannot be used for fuel to the brain as they travel in the blood bound to albumen; which cannot cross the BBB.
    (note: brain can oxidise ketones in emergency situations, however this may lead to ketosis and isn’t the preferrable option)
53
Q

What ~% of blood glucose utilisation does the brain undergo at rest?

A

~50%.

54
Q

How does mild hypoglycaemia affect the brain, and why? (brief)

A

Mild hypoglycaemia -> CNS dysfunction:
1. Incoordination.
2. Slurred speech.
As the brain struggles for energy supplies.

55
Q

Explain how RBC’s obtain energy.

A

RBC’s contain no mitochondria, so their ATP is derived from glycolysis. ????

56
Q

t/f: erythrocytes contain many mitochondria.

A

FALSE - they contain none.

Physiological concepts (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions