Metabolism Flashcards

(36 cards)

1
Q

Glucogon is stimulated by

A

Low blood glucose levels which stimulates glycogen breakdown in liver

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2
Q

Insulin is stimulated by

A

High blood glucose levels which stimulates glycogen formation in lver and glucose uptake by tissue cells

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3
Q

In absense of insuline signal (diabetes)

A

Body mobilizes fats, but no glucose can be made. Build up of ketone bodies in the blood (could lead to ketoacidosis as loss of acetyl-CoA acceptor molecules)

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4
Q

3 P’s of diabetes mellitus

A
  1. Polyuria (excess glucose in urine=inhibitation of water resorption by kidney)
  2. Polydipsia (Dehydration stimulates hypothalamic thirst centers)
  3. Polyphagia (Excessive hunger: starving due to inability to use ingested carbs)
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5
Q

Type 1 diabetes

A

No insulin production–> due to autoiummune reaction (molecular mimicry - Bcells as intruders)

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6
Q

Type 2 diabetes

A

Reduction in insulin secretion+/ target cell sensitivity. Ketoacidosis less of a problem for type 2

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7
Q

Liver functions

A
  1. Carb metabolism (glucose store…glycogenolysis- release glucose, gluconeogenesis- conv)
  2. Fat metabolism (beta oxidativea
  3. Protein metabolism (site of amino acid deamination (forms urea for removal of ammonia). Major site of generation of non-essential amino acids by transamination
  4. Vitamin storage (1-2yr vit A, 1-4m, vit D,B12)
  5. Biotransformation (“ionactivates” ethanol, drugs, actives some drugs)
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8
Q

4 major types of lipoproteins (triglycerides and cholesterol)

A
  1. Chylomicrons (mostly lipids= lowest density)
  2. VLDL (triglycerides to adipose tissue. VLDL–>LDL)
  3. LDL (Deliver cholesterol to tissues
  4. HDL (cholesterol to liver)
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9
Q

Trans fats

A

Unsaturated, stimulate an increaes in LDL, decrease HDL. REALLY BAD

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10
Q

Unsaturated-Cis

A

Promote catabolism and excretion of chlosterol

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11
Q

Saturated

A

“not that good” makes more chlosterol

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12
Q

Anatomy of thyroid gland

A

Composed of follicles. Follicle cells produce thyroglobin. Iodinated thyroglobin serves as precursor for thyroid hormone. Parafolicular cells produce calcitonin.

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13
Q

Thyroid hormone derived from:

A
  1. Throxine (T4)- secreted by thyroid follicles. contains 4 iodine molecules
  2. Triiodothyronine (T3) More active thyroid homrone. Derived from T4 at target cells
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14
Q

6 steps of synthesis of thyroid hormone

A
  1. Thryroglobin into follicle
    and Iodide transported from capillary in
  2. Thyroglobin in through packaged exocytosis and iodide oxidized into iodine
  3. Tyrosines (from thryoglobin) and iodine attache forming T1 and T2. We call out for this when we need it.
  4. T1 and T2 are linked together to form T3 and T4
  5. These are endocytosed and combined with a lysosome
  6. Lysomsomal enzymes cleave T3 and T4 and hormones diffuse into bloodstream!
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15
Q

Why is T3 so much more potent?

A

Active form. Higher affinity to receptors than T4

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16
Q

Regulation of thyroid hormone.

A

Falling thyroid hormone levels lead to secretion of TSH (thryroid stimulating hormone) in the anterior pituitary. This released stored thyroid hormone (from follicules) and resynthesizes more.

17
Q

TH affects every cell in the brain except

A

adult brain, spleen, testes, uterus and thyroid gland

18
Q

Major function of TH

A

Regulate BMR, heat production (can do this in part by stimulating enzymes involved in glucose oxidation. Maintaining blood pressure, regulates tissue growth and dev.

19
Q

Nervous system. Hypo and hypersecretion of TH

A

Hypo: “slow stuff”. slowed brain dev. mental dulling, depression, memory impairment.

Hyper: “fast stuff”. Irritarbility, restlessness, insomnia

20
Q

Muscular system: Hypo and Hyper

A

Hypo- “slow stuff”, sluggish, muscle cramps

Hyper- Muscle atrophy and weakness

21
Q

Sketelal system: Hypo and hyer

A

Hypo- Growth redardation, skeletal stunting, in adults- joint pain

Hyper- Child- excessive growth at first, then short stature and early epiphyseal closure. Adults- demineralization of skeleton

22
Q

Hypothyrodism

A

If inadequate dietary iodine, the follicle cells try to make colloid but annot iodinate it, TSH increases to try to induce it but leads to an enlarged and protruding thyroid gland (endemic goiter)

23
Q

Hyperthyroidism

A

Grave’s disease- autoimmune (antibodies that mimic TSH). Elevated BMR, sweating, raphid heatbeat…

24
Q

Calcitonin

A

Lowers calcium, inhibits bone resorption, stimulates Ca2+, uptake and incorportation into bone.

Increase blood levels of calcium

25
BMR is influenced by
1. Body surface area (greater SA= more heat loss) 2. Age (decreases with age, loss of muscle mass) 3. Higher BMR in males (more muscle, less fat) Stress can also increase metabolic rate (norepinephrine and epinephrine increase fat catabolism, generate heat as a byproduct) Increases oxygen consumption by accelerating metabolic rate.
26
Total metabolic rate (TMR) definition
BMR is most of this. Work done by skeletal muscle produce the largest increases
27
4 Mechanisms of heat exchange
1. Radiation (50% ie cool room with warm people) 2. Conduction (Transfer of heat between direct contact, heat to body from warm tub) 3. Convection (warm air rises, ie fan) 4. Evaportation (regulate body temp. perspiration to shed heat)
28
Role of hypothalamus
2 thermoregulatory centers - heat loss - heat promoting Receives input from peripheral thermoreceptors (just under skin) and central thermoreceptors (in core- blood temp) Perserve core temp!!
29
Heat conservation mechanisms
1. Vasoconstriction of cutaneous vessels (supply skin)- frostbite if prolonged 2. Shivering (stimulate stretch receptors- involuntary shuttering) 3. Increase in metabolic rate (cold stimulus) 4. Enhanced thyroxine release (lowering of external temp. increased secretion of TSH) 5. Behavioural modifications (warmer clothing, drinking warm fluids)
30
Heat-loss mechanisms
1. Vasodilation of cutaneous blood vessels (increased blood flow) 2. Enhanced sweating (activated by sympathetic nervous system) 3. Behavioral modifications
31
Hyperthermia
Increased temp, increased metabolic rate, incrased heat production
32
Fever
Pyrogens (body secretes this to increase body temp) released by macrophages. Vasoconstriction
33
Short term regulation of appetite
Neural signals- Stretch receptors in GI tract inhibits appetite. Protein and carbohydrates stimulate vagal afferents to inhib appetite: protein stimulates longer response 1. During eating- plasma glucose levels rise, activate glucose receptors in brain- then eating is depressed 2. Elevated plasma AAs depress and low plasma AAs stimulate eating 3. Blood concentrations of FFA and glycerol play a simialr role.
33
Mechanisms of appetite regulation
Arcuate nucleus in hypothalamus! Neuropeptide Y/ agouti-related Peptide (NPY/AGRP) secretion stimulates appetite Proopiomelanocortin/cocaine and amphetamine-regulated transcript (POMC/CART) neurons release melanocortins- sippress appetite via corticotropin releasing hormone by the VMH
34
Short term reg. of appetite HORMONES
Insulin- in response to food intake, known to depress hunger Cholecystokinin- released by small intestine during food digestion, depreses hunger Glucagon- levels rise during fasting and stimulates hunger Ghrelin- released from stomach, potent stimulator of hunger
35
Long term regulation of appetite (ie months and years)
Leptin- peptide hormone secreted by adipose tissue (more=more) - serves as a sensor for adipose stores, binds to receptors in the ACR nuceleaus (inhibs NPY secretion and increases CART expression). Leads to inhibirtion of appetite until adipose stores decrease