Physiology 4 Flashcards

1
Q

Objectives of absorption and storage: during & after meal

A

1) fill glycogen stores (from carbos)
2) Don’t spill much glucose in urine
3) Utilize ingested carbos and fat for energy
4) Package excess carbos & fats as TAG
AAs as protein

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

Objectives of absorption and storage: between meals

A

1) keep glucose about constant for CNS
2) dec. glucose utilization (except CNS)
3) keep some glycogen reserves
4) burn fats for energy (FA, KB)
5) utilize “sparable” proteins (AAs) (& glycerol, lactate) for gluconeogenesis

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

Most efficient energy storage form?

A

fat

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

Glucose can be used by?

A

all tissues

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

How much glycogen stores?

A

more than glucose

enough for 1/2 day fuel

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

Tissues that must have glucose?

A

brain (nerves)
RBC
WBC
renal tubules

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

Carbohydrate processes during feeding?

A
  • inc glucose uptake & utliz.
  • inc. glycolysis
  • inc. glycogen stores
  • dec. glyconeogenesis
  • dec. glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Carbohydrate processes during fasting?

A
  • dec. glucose uptake & utli.
  • dec. glycolysis
  • small dec. in glycogen stores
  • small dec. glycogenesis
  • inc. gluconeogenesis
  • inc. glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Fat processes during feeding?

A
  • inc. lipogenesis
  • inc. fat stores
  • dec. lipolysis
  • dec. ketogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Fat processes during fasting?

A
  • dec. lipogenesis
  • dec. fat stores
  • inc. lipolysis (inc FFA)
  • inc. ketogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Protein processes during feeding?

A
  • inc PS
  • inc. protein stores

-dec. PD

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

Protein processes during fasting?

A
  • dec PS
  • dec. protein stores (especially in muscle & lymph)

-inc PD

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

Glucose-Fatty Acid Cycle

A

-glucose goes to Glucose-6-P in Muscle
-goes to energy,
-FFA inhibit glucose utilization b/w meals
(from fat cells)

-glucose goes to triglycerides in fat cells

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

Short acting hormones

A
  • insulin
  • epinephrine
  • norepinephrine
  • glucagon

-rapid onset, brief action

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

Long acting hormones

A
  • GH
  • Thyroid hormone
  • Glucocorticoids
  • Sex steroids

-delayed onset, prolonged action

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

Short acting hormone mechanism

A

-inc/dec enzyme or protein activity

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

Long acting hormone mechanism

A

inc/dec amount of enzymes or other problems

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

Change in Cortisol during a meal?

A

none

few effects: slight dec. in glucose uptake & utilization; glycostatic

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

Change in Cortisol during fasting?

A

none

effects: allow inc. gluconeogenesis & lipolysis
dec. in glucose uptake & utilization

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

Change in GH during a meal?

A

none

effects: inc PS

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

Change in GH during fasting?

A

none
effects: dec in glucose utilization
dec lipolysis
slows protein loss (glycostatic)

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

Change in T3 during a meal?

A

none
effects: inc PS
inc glycolysis - from residual hormones

23
Q

Change in T3 during fasting?

A

none

effects: permissive, to inc. lipolysis, synergizes with GH

24
Q

Largest effect to raise plasma glucose?

A

glucagon + epinephrine + cortisol

25
Lipolytic Substances
- epinephrine - norepinephrine *T4, cortisol, GH make theme more effective
26
Antilipolytic Substances
-insulin
27
What do Glucocorticoids do?
-
28
Change in Glucagon during meal?
- may dec. | effects: few
29
Change in Glucagon during fasting?
- may inc. effects: inc. glycogenolysis inc. gluconeogenesis inc. ketogenesis dec. glycogen synthesis dec. glycolysis
30
Change in Epi&NE during a meal?
decrease | effects: few
31
Change in Epi&NE during fasting?
tend to increase effects: inc. glycogenolysis + lipolysis inc. gluconeogenesis dec. insulin secretion mild dec. of glucose uptake
32
Change in Insulin during a meal?
INCREASE effects: increase many anabolic & anticatabolic processes and decrease catabolic processes (except glycolysis & TCA cycle)
33
Change in Insulin during fasting?
DECREASE - decrease in many anabolic & anticatabolic precesses - allows catabolic ones to dominate
34
Normal Growth
-increase in height and mass -several phases: fetal (rapid at end of gestation) postnatal (early childhood) pubertal (adolescent growth spurt) adulthood senescent - may be decline in stature
35
Normal Growth Requires
- proper nutrition, including energy, essential amino acids, fatty acids, vitamins, & minerals (Ca, Fe) - sufficient hormones at proper times - good physchosocial environment (psychosocial deprivation)
36
Catch-up Growth
-after illness in childhood
37
Compensatory Growth
Kidney Liver Adrenal - hormone involved (ACHT, CRH)
38
Hormones involved in normal somatic growth
- Insulin - Thyroid Hormones - Crotisol - GI hormones - Vit D - Sex hormones (androgens (male & female), estrogens) * after stimulating pubertal spurt, they shut down growth zones - probably certain "growth factors" - GROWTH HORMONE
39
How much does GH change height?
-20-30%
40
To much GH?
- giantism or gigantism - increase to maximal genetic potential - increase linear growth - normal skeletal maturation
41
To little GH?
- dwarfism (one type of -) - hyposomatotropic dwarfism - decrease linear growth - delayed skeletal maturation
42
Somatotropin
Growth Hormone (GH)
43
Somatomedin
SM-C, probably mediates some of GH actions, particularly on bone elongation and adipocytes -also known as IGF-1
44
Somatostatin
-hypothalamic peptide that inhibits GH secretion | = SS, SRIH
45
Somatocrinin
-hypothalamic peptide that stimulates GH secretion | =GHRH
46
Acromegaly
- bone thickening | - excess GH for years
47
T3 interactions with growth hormone
1) increased sensitivity to GH-RH 2) increased synthesis of GH 3) increased responsiveness of target cells
48
Insulin & growth hormone
-insulin needed for GH to be able to work
49
Physiological Factors that Increase GH
- GHRH - decrease SS - spontaneous incr. - deep sleep - exercise - acute stress - thyroid hormone - puberty (estrog./ androg.) - post-prandial decr. glucose
50
Physiological Factors that Decrease GH
- SS - decrease GHRH - spontaneous decr. - light sleep & waking - elevated GH - IGF-1 - aging - postprandial hyperglycemia - inc. free fatty acids
51
Effect of excess Thyroid Hormone on Growth
excess: increase linear growth, advanced skeletal maturation, minimal effect on adult stature deficiency: decreased linear growth, delayed skeletal maturation, decreased adult stature
52
Effect of Cortisol on Growth
-excess: decreased linear growth, delayed skeletal maturation, decreased effect on adult stature
53
Effect of Androgen of Growth
- excess: decreased linear growth, advanced skeletal maturation, decreased adult stature - deficiency: increase linear growth, delayed skeletal maturation, "eunuchoidal" adult stature - tall long arms & legs