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Biochemistry/Physiology > Quiz 7 - Hormones, Fatty Acid Metabolism, Regulation of Metabolism, Musculoskeletal system, Diabetes, Bone Physio > Flashcards

Quiz 7 - Hormones, Fatty Acid Metabolism, Regulation of Metabolism, Musculoskeletal system, Diabetes, Bone Physio Flashcards

1
Q

Homeostasis

A

Physiologic ability to maintain a relative stable internal environment despite external changes.

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2
Q

4 features of feedback mechanisms

A
  1. System Variable
  2. Set Point
  3. Detector
  4. Corrective mechanism
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3
Q

Hormones

A

Chemical messengers secreted into the blood to alter rates of processes in target organs and cells.
Low concentrations produce effects.
Control long-term homeostatic processes of growth, development, metabolism, reproduction and internal environment regulation.

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4
Q

Endocrinology

A

Study of endocrine system and hormone action

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5
Q

Where do hormones bind?

A

Receptors on or in target cells

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6
Q

What do hormones control?

A
  1. Rates of enzymatic reactions
  2. Movement of ions or molecules across membranes
  3. Gene expression and protein synthesis.
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7
Q

Where are hormones produced?

A

Endocrine cells and organs

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8
Q

Where are hormones released?

A

Endocrine glands

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9
Q

Thyroid hormone

A

Made in thyroid, controls basal metabolism

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10
Q

Cortisol

A

Made in adrenal cortex, controls energy metabolism and stress responses.

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11
Q

Mineralcorticoids

A

Made in adrenal cortex, regulate plasma volume via effects on serum electrolytes

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12
Q

Vasopressin

A

Made in the posterior pituitary, regulates plasma osmolality via effects on water excretion

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13
Q

Parathyroid hormone

A

Made in the parathyroids, regulates calcium and phosphorus levels.

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14
Q

Insulin

A

Made in the B cells of the pancreas, regulates plasma glucose concentration.

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15
Q

Neurocrine

A

Secretion of hormones into the bloodstream by neurons

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16
Q

Endocrine

A

Secretion of hormones into the bloodstream by endocrine glands

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17
Q

Paracrine

A

Hormone molecules secreted by one cell affects adjacent cells

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18
Q

Autocrine

A

Hormone molecule secreted by a cell affects the secreting cell.

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19
Q

Three chemical classes of hormones

A
  1. Steroid hormones
  2. Peptide and protein hormones - 50 aas is a protein
  3. Amine hormones (tyrosine derivatives)
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20
Q

Lipophilic hormones

A

Fat-soluble
Steroid and thyroid hormones
Bind to intracellular receptors

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21
Q

Hydrophilic hormones

A

Water-soluble
All other hormones
Bind to extracellular receptors and trigger signaling cascades

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22
Q

Amine hormones

A

Thyroid hormones and Catecholamines (epinephrine, norepinephrine)
Derived from amino acid tyrosine

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23
Q

Thyroid hormones

A

Thyroxine
Derived from Tyrosine (Amine hormone)
Bind to nuclear receptors

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24
Q

Catecholamines

A

Epinephrine and Norepinephrine
Derived from Tyrosine
Bind to cell surface receptors

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25
Q

Peptide and Protein hormones

A

Water soluble
Most numerous hormones
Often produced as preprohormones that are cleaved and modified
Often carried inactively bound to a protein to carry it though the blood

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26
Q

Modification of Peptide hormones

A
  1. Genes code for mRNA, translated into preprohormone
  2. Preprohormone formed in ER, broken into prohormone in the Golgi
  3. After posttranslational modification in the Golgi, peptide hormone is secreted
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27
Q

Prohormones exist for which hormones?

A 
Insulin
Somatostatin
Glucagon
Enkephalin
ADH (Vasopressin)
Gastrin
Parathyroid hormone
Calcitonin
ACTH
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28
Q

Signal transduction/Extracellular Hormone Receptor Pathway

A

Hydrophilic hormone binds to cell surface GPCR, G-protein activates second messenger (like cAMP), 2nd messenger activates other effects

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29
Q

Steroid hormones

A

Derived from Cholesterol
Lipid Soluble
Must be carried in plasma by plasma blinding globulins
“Bound” steroid hormones serve as a reservoir

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30
Q

Plasma binding globulins

A

Bind to steroid hormones in the plasma

Albumin, testosterone binding globulin, thyroxine binding globulin

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31
Q

Intracellular Hormone Receptor Pathway

A

Lipid soluble hormones cross membrane, bind to intracellular receptors (hormone-receptor complex), HRC binds to DNA and acts as transcription factor, directing protein synthesis

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32
Q

Aromatase Enzyme/Aromatization

A

Enzyme that converts “Free” androgen hormones into estrogens.
Occurs in trophoblastic tumors
Occurs normally in adipocytes, liver, brain.

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33
Q

5 Factors that effect circulating hormone levels

A
  1. Synthesis and secretion rate
  2. Rates of degradation and uptake
  3. Receptor binding/availability of receptors
  4. Affinity of hormone for plasma carriers
  5. Free hormones equilibrate with bound hormones
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34
Q

Negative feedback regulation of hormones

A

Hormone shuts down stimulating or releasing factors, ending hormone action

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35
Q

Positive feedback regulation of hormones

A

Uncommon, hormones enhance releasing and stimulating factors

Occurs in childbirth (parturition)

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36
Q

Long-loop feedback

A

Target gland hormone may feedback and inhibit its production

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37
Q

Short-loop feedback

A

Stimulating hormone (trophic hormone) inhibits hormone production

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38
Q

Pituitary gland anatomy

A
  1. Anterior pituitary - pars anterior
  2. Intermediate lobe - pars intermedia
  3. Posterior pituitary - neurohypophysis/pars nervosa
  4. Infundibulum - stalk that links to hypothalamus
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39
Q

Hypothalamo-hypophysial portal system

A

Capillary system that links secretory neurons of hypothalamus with storage portion of anterior pituitary

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40
Q

Pituitary hormone

A

Ocytocin
ADH
Adrenocorticotrophic hormon (ACTH)

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41
Q

Hypothalamic-Pituitary-Adrenal Axis (HPA)

A

Responsible for adaptation of stress response, regulates many body functions

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42
Q

Feedback control of Osmolality

A

Vasopressin/ADH made in hypothalamus, secreted from neurohypophysis/Posterior pituitary. Hypothalamic osmoreceptors control release of ADH. ADH causes aquaporins to be inserted into collecting duct of renal tubules to reabsorb water

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43
Q

Adrenal gland hormones

A
  1. Mineralcorticoids - Aldosterone, secreted by zona glomerulosa (top layer of adrenal cortex)
  2. Glucocorticoids - Cortisol, secreted by zona faciculataa (Middle layer)
  3. Adrenal androgens - Dehydroepiandrosterone (DHEA), secreted by zona reticularis (bottom layer)
  4. Epinephrine (80%) and Norepinephrine (20%) - secreted by adrenal medulla
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44
Q

Aldosterone

A

Mineralcorticoid
Promotes sodium reabsorption and potassium excretion by renal tubules
Imbalanced increase causes hypokalemia and muscle weakness
Imbalanced decrease causes hyperkalemia and cardiac toxicity
Aldosterone escape - persistent elevated EC fluid volumes causes loss of excessive Na+ and water, causing dehydration

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45
Q

Cortisol

A

Glucocorticoid
Stimulates gluconeogenesis, increasing serum glucose
Has anti-inflammatory effects, adversely affects immunity, eosinophil and lymphocyte counts decreasae

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46
Q

Adrenal androgens

A

DHEA, DHEAS, androstenedione, 11-hydroxyandrostenedione
Formation of progesterone and estrogen via aromatization
Development of sex organs
ACTH effects androgen release, so secretion parallels cortisol

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47
Q

Acute stress

A

Fight or flight response
Epinephrine and norepinephrine
Blood glucose rises, BP rises, Bronchioles dilate

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48
Q

Chronic stress

A

Steroid hormones secreted
Immune suppressed
Water retention
Eventual exhaustion

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49
Q

Cortisol regulation

A

Negative feedback loop

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50
Q

Endocrine gland hyposecretion

A

Hormone deficiency (Ex. Type 1 Diabetes)

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51
Q

Hormone resistence

A

Ex.) Type 2 Diabetes

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52
Q

Hormone Excess

A

Tumors of glands produce excessive hormone
Ex.) Acromegaly - gigantism, too much growth hormone. Treated with somatostatin
Ex.) Graves disease - antibodies bind to hormone receptors causing thyroid hormone release

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53
Q

Addison’s Disease

A

Adrenal insufficiency, leads to hypoglycemia, weight loss, postural hypertension, weakness, GI distubances

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54
Q

Cushing’s Syndrome

A

Excess ACTH causes excess cortisol

Moon face, buffalo hump, buisability, poor wound healing

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55
Q

Hypothyroidism

A

Insufficient thyroid hormone
Fatigue, constipation, dry skin, depression, enlarged thyroid
Hashimoto’s disease - autoimmune hypothyroidism

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56
Q

Hyperthyroidism

A

Excess thyroid hormone
Weight loss, fast heart rate, exopthalmos (bulging eyes), enlarged thyroid
Grave’s disease - autoimmune hyperthyroidism

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57
Q

Dietary Lipid processing

A
  1. Bile salts emulsify dietary fats in the small intestine, forming mixed micelles
  2. Intestinal lipases degrade trigycerides
  3. Fatty acids and other breakdown products taken into intestinal mucosa, converted into triglycerides
  4. Triglycerides incorporated with cholesterol and apolipoproteins into chylomicrons
  5. Chylomicrons move through lymphatic system and into blood vessels
  6. Lipoprotein lipase in blood vessels converts triglycerides into fatty acids and glycerides. Fatty acids enter cells
    (C chains 14C or longer need protein to transport across membrane)
  7. Fatty acids are oxidized as fuel or reesterified into storage
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58
Q

How are fatty acids transported?

A

Albumin carries free fatty acids in serum

Lipoproteins carry triglycerides and cholesterol (Chylomicrons)

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59
Q

4 classes of Lipoproteins

A
  1. Chylomicrons - take triglycerides from gut to muscle, liver, etc.
  2. Very Low Density Lipoprotein - created in liver, sent to tissues
  3. Low Density Lipoprotein - made from VLDL when triglycerides are removed at body cells
  4. High Density Lipoprotein - has low triglyceride content, collects lipids from vasculature
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60
Q

Triacylglycerol cycle

A

Triacylglycerol (triglycerides) cycles between adipose tissue, blood and liver to mobilize fatty acids for energy. Imbalanced towards triglycerides and storage rather than free fatty acids for energy

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61
Q

Adipose triglyceride mobilization

A

Glucagon binds to adipose cell surface receptor, triggars G protein, adenylyl Cyclase, cAMP cascade. Protein Kinase A triggers Triglyceride breakdown into free fatty acids that are released into the bloodstream.
Fatty acids are brought into body cells via a transporter, then are used for Beta Oxidation.

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62
Q

Lipid Catabolism

A

Glycerol enters glycolysis, produces 5% of energy from fatty acids
Fatty acids form Acyl-CoAs, generate 95% of energy from fatty acids

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63
Q

Acyl-Carnitine/Carnitine Transporter

A

Carnitine used as carrier to bring Carbon chains from cytosol, across intermembrane space and into matrix of mitochondria

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64
Q

3 stages of fatty acid oxidation

A
  1. Beta Oxidation - breaks fatty acids into acetyl-CoAs and generates NADH and FADH2
  2. Citric Acid Cycle - Utilizes acetyl-CoAs to generate NADH and FADH2
  3. Oxidative Phosphorylation - Utilized NADH and FADH2 to generate ATP. Generates 108 ATP from one 16C chain
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65
Q

Fatty Acid Beta Oxidation

A

Removes a 2 carbon piece at the Beta carbon, producing 1 NADH and 1 FADH per Acetyl-CoA produced

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66
Q

What happens to Acetyl-CoA after production in Beta Oxidation?

A
  1. Enters Citric Acid Cycle
  2. Converted into Ketone Bodies to use for energy production when glucose is low.
  3. Formed back into fatty acids
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67
Q

Citrate shuttle

A

Acetyl-CoA is produced in mitochondria matrix, but lipid synthesis occurs in the cytoplasmic space. OXA is converted into Citrate using Acetyl-CoA. Citrate leaves the mitochondria and is converted back into OXA, releasing Acetyl-CoA into the cytoplasm.

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68
Q

Acetyl-CoA Carboxylase

A

Adds a CO2 to Acetyl-CoA, creating Malonyl-CoA, which is used to create fatty acid chains

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69
Q

Fatty Acid Synthase

A

Enzyme binds Malonyl-CoA to Acetyl-CoA, releasing CO2 and using NADPH. Creates a 4 Carbon chain. Repeats to add 2C at a time.
Creates palmitate - 16:0 fatty acid. Further processing can create an 18:1 fatty acid
NADPH is an electron donor

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70
Q

Essential Fatty Acids

A

18:2 and longer chains cannot be created by mammals and must be ingested. Linoleate is first essential fatty acid

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71
Q

Regulation of Fatty Acid Synthesis and breakdown

A

Insulin promotes phosphatase activation of Acetyl-CoA Carboxylase, promoting Fatty Acid Synthesis.
Glucagon promotes PKA inactivation of ACC, suppressing fatty acid synthesis.
Production of Malonyl-CoA via ACC suppresses carnitine acyl-transferase I which initiates Beta Oxidation, thus suppressing Beta Oxidation

72
Q

Phosphatidic acid

A

Precursor to phospholipids and triglycerides

73
Q

What is Cholesterol formed from?

A

Acetyl-CoA

74
Q

Cholesterol uses

A

Lipoprotein and steroid hormone formation

75
Q

Atherosclerotic Plaque formation

A

Cholesterol accumulates in macrophages (foam cell), which apoptoses and deposits cholesterol-rich plaque in artery lumens.

76
Q

Autonomic Nervous System

A

Sympathetic and Parasympathetic control of organ function. Direct contact from nervous system to organs

77
Q

Neuroendocrine system

A

Hormone control of organ function. Indirect control via the HPA axis - Hypothalamus, Pituitary, Adrenals

78
Q

Hypothalamus methods of control

A
  1. Direct - autonomic - innervation of pre-ganglionic neurons
  2. Indirect - Hormonal - release of pituitary and adrenal cortex hormones
79
Q

3 Parts of the Autonomic Nervous System

A
  1. Sympathetic - fight or flight
  2. Parasympathetic - rest and digest
  3. Enteric nervous system - digestive system
80
Q

Carotid Body

A

Site of chemoreceptors that detect blood O2/CO2 composition. Autonomic control of cardiac function

81
Q

Autonomic control of cardiac function

A

Chemoreceptors and baroreceptors analyze blood
Sympathetic - norepinephrine - increases heart rate and vasoconstricts
Parasympathetic - cholinergic - decreases heart rate and vasodilates
Increased BP inhibits tonic sympathetic activity and activates vagal parasympathetic activity

82
Q

Baroreceptors

A

Detect blood pressure. Autonomic control of cardiac function

83
Q

What does the liver regulate?

A

Blood sugar
Carbohydrate storage (glycogen) and regulation
Amino acid content
Lipid formation and mobilization
First pass metabolism - blood enters directly from gut

84
Q

What does the pancreas regulate?

A

Insulin release during high blood sugar
Glucagon release during low blood sugar
Duodenum pH buffering
Protease release

85
Q

What does the gallbladder regulate?

A

Bile salts release to degrade lipids

86
Q

What’s important about Glucose-6-Phosphate

A

It is the branching point - can become glucose, glycogen, go down pentose phosphate pathway, become acetyl-CoA

87
Q

Leptin

A

Triggers satiety signals in the hypothalamus. Eat less, metabolize more

88
Q

Grehlin

A

Triggers hunger signals in the hypothalamus. Eat more, metabolize less

89
Q

Insulin release pathway

A

Beta Cells maintain voltage potential. Increasing concentration of ATP leads to blockage of K+ out. Depolarization results, opening Ca2+ channels in. Ca2+ triggers release of insulin granules

90
Q

Glucagon release pathway

A

Alpha cells work just like Beta cells, only ADP concentration increase blocks K+ channels

91
Q

Superior/Cranial/Rostral

A

Head end

92
Q

Inferior/Caudal

A

Feet end

93
Q

Proximal

A

Toward main body

94
Q

Distal

A

Away from main body

95
Q

Median

A

Midline, divides right from left

96
Q

Medial

A

Close to midline to side

97
Q

Lateral

A

Away from midline to side

98
Q

Coronal

A

Divides front from back

99
Q

Anterior/Ventral

A

Front

100
Q

Posterior/Dorsal

A

Back

101
Q

Saggital

A

Median plane in skull

102
Q

Transverse

A

Cross section cut parallel to ground

103
Q

Axial

A

Transverse plane in skull

104
Q

Extension of neck

A

Tilt head back

105
Q

Flexion of neck

A

Tilt head forward

106
Q

Rotation

A

Circular motion around a joint

107
Q

Axial skeleton

A

Head, vertebrae, ribs, sternum

108
Q

Appendicular skeleton

A

Everything else, including the pelvis and scapula and clavicles

109
Q

Numbers of ribs

A

7 pairs of true ribs
3 pairs of false ribs
2 pairs of floating ribs

110
Q

Scapula landmarks

A

Superior angle, supraspinous fossa, scapular spine, acromion, coracoid process, intraspinous fossa, medial border, subscapular fossa

111
Q

Pelvic bones

A

Os Coxae - 3 bones fused

Ilium, Ischium, Pubis

112
Q

Synarthroses

A

Immovable joints

Fibrous - Skull sutures, Gomphoses (teeth)

113
Q

Diarthroses

A

Freely movable

Synovial

114
Q

Limits to joint movement

A

Bones, Muscles, ligaments, other tissue

115
Q

Superficial back muscles

A 
Trapezius
Levator scapulae
Rhomboid major and minor
Latissimus dorsi
Innervated by ventral rami
116
Q

Trapezius

A

Spinal accessory nerve
Rotation of scapula for abduction of arm beyond 90 degrees
Extends neck

117
Q

Levator Scapulae

A

Dorsal scapular nerve

Elevates scapula

118
Q

Rhomboid major and minor

A

Dorsal scapular nerve

Retracts, adducts scapula

119
Q

Latissimus dorsi

A

Thoracodorsal nerve

Adducts humerous

120
Q

Deep back muscles

A 
Spenius muscles
Erector Spinae muscles
Transversospinalis muscles
Suboccipital muscle group
Innervated by dorsal rami
121
Q

Splenius muscles

A

From back of head to spinal column

122
Q

Erector Spinae muscles

A

Iliocostalis muscles - from ilium of pelvis to ribs
Longissimus muscle - from lumbar all the way to cervical
Spinalis muscle - along spinous processes in thoracic region

123
Q

Tranversospinalis muscles

A

Semispinalis - Along spinous processes from Occipital to thoracic
Multifidus - Along spinous processes from sacrum to ribs - lower back pain muscle

124
Q

Suboccipital muscles

A 
Rectus Capitis Posterior Minor and Major
Obliquus Capitis Inferior and Superior
Suboccipital nerve dorsal ramus of C1
Bilateral contraction extends head/neck
Unilateral contraction rotates head to same side
125
Q

Obliquus Capitis Superior muscle

A

Contraction tilts head like a curious dog

126
Q

Deltoid

A

Axillary nerve

Abduction of arm from 15 degrees to 90

127
Q

Subscapularis

A

Upper and lower subscapular nerves

Glenohumeral internal rotation

128
Q

Supraspinatus

A

Suprascapular nerve

Glenohumeral abduction to 15 degrees

129
Q

Infraspinatus

A

Suprascapular nerve

Genohumeral external rotation

130
Q

Pectoralis major

A

Lateral and medial pectoral nerves

131
Q

Pectoralis minor

A

Medial pectoral nerve

Glenohumeral adduction

132
Q

Subclavius

A

Nerve to subclavius

Glenohumeral adduction

133
Q

Serratus Anterior

A

Long thoracic nerve

Scapula protraction

134
Q

Brachial plexus

A 
Ventral rami from C5-T1
Meet in 3 trunks
Divide
Separate into 2 anterior cords and one posterior cord
Many nerves branch from here
135
Q

What brachial plexus nerves branch in what region?

A

Roots - Dorsal Scapular Nerve off C5, Long Thoracic Nerve off C5-C7, Nerve to Subclavius off C5-C6
Trunks - no nerves
Divisions - no nerves
Posterior Cord - Upper Subscapular nerve, Thoracodorsal nerve, Lower subscapular nerve, axillary nerve
Lateral Cord - Lateral Pectoral Nerve
Medial cord - Medial pectoral nerve

136
Q

Diabetes Mellitus

A

Inability of the body to regulate glucose through insulin

137
Q

Type 1 Diabetes

A

Autoimmune loss of insuline-producing B-cells
Genetically Linked
Juvenile onset
Insulin-dependent

138
Q

Type II Diabetes

A

Insensitivity to insulin
Lifestyle and genetics - weight gain and obesity
Adult onset (though becoming common in juveniles)
Non-insulin dependent

139
Q

Gestational Diabetes

A

Develops during pregnancy
Fetus induces changes in metabolism
Causes a predisposition to Type II later in life

140
Q

Frequency of Diabetes in the US

A

29.1 million with disease - 9.3% of US population

141
Q

Symptoms of Type I diabetes

A 
Polyuria and Thirst
Weakness
Polyphagia and weight loss
Blurred Vision
Peripheral Neuropathy
Nocturnal Enuresis
Sweet smelling breath and urine
Impaired wound healing
142
Q

Symptoms of Type II diabetes

A 
Polyuria and thirst
Weakness
Blurred Vision
Peripheral Neuropathy
Sweet smelling breath and urine
Impaired wound healing
143
Q

What does Type I diabetes ultimately cause?

A

Lack of insulin leads to a dysregulated metabolic state of extreme fasting and starvation

144
Q

Pathogenesis of Type I diabetes

A

Loss of insulin signaling - Glucose not taken into cells, remains in blood
Systemic mimicry of prolonged fasting - Cells unable to take in glucose, glucose release from glycogen and adipose increases, ketone bodies created and released

145
Q

Ketoacidosis

A

Uncontrolled Type I causes ketoacidosis by release of ketone bodies in attempt to “feed” body cells. Leads to osmotic diuresis –> Dehydration –> Electrolyte imbalance –>Coma and tachycardia

146
Q

Treatment of Type I diabetes

A
  1. Insulin administration - Injections or pump
  2. Glucose monitoring
  3. Diet - low carbohydrate
147
Q

Insulin administration

A

Different types
Basal insulin - maintains low-level systemic insulin
Bolus - Given when food is consumed

148
Q

Pathogenesis of Type II diabetes

A

Progressive increase in fasting glucose due to reduced insulin sensitivity followed by a degeneration of insulin production
As insulin resistance increases, B-cells try to compensate, experience stress
B-cells fatigue, fail and degenerate

149
Q

How might adipose signaling drive type II diabetes?

A

Enlargement of adipocytes releases protein (MCP-1) that brings in macrophages. Macrophages release TNF alpha, releasing fatty acids. Lipids deposit in improper places, interfering with glucose movement, producing insulin resistance.

150
Q

Type II diabetes management

A
  1. Lifestyle - reduced carbohydrate and sugars, increase physical activity, maintain healthy body weight
  2. Oral Hypoglycemics - increase insulin secretion, increase insulin sensitivity, decrease carbohydrate absorption
  3. Insulin - required when B-cell mass degenerates
151
Q

Type II drugs

A
  1. Sulfonylurease - increase B-cell insulin secretion by binding close K+ channels
  2. Metformin - Uncouples Oxidative Phosphorylation, reduces liver gluconeogenesis and lipogenesis
  3. Peroxisome Proliferator-activated receptor agonists - increase glucose transporter expression
  4. Alpha-glucosidase inhibitors - Prevent carbohydrate absorption
  5. Drug combinations
152
Q

How is diabetes detected

A
  1. Urinalysis
  2. Glucose monitoring
  3. HBA1c - measure of glycolated hemoglobin
  4. Glucose tolerance test
  5. C-peptide test - cleavage product of proinsulin
153
Q

Hypoglycemia

A

Low blood sugar

154
Q

Hyperglycemia

A

High blood sugar

155
Q

Long-term diabetic complications

A

Cardiovascular Disorder - heart disease, stroke, peripheral vascular disease
Blindness - glaucoma, retinopathy
Kidney disease
Neurologic Complications - Peripheral neuropathy, autonomic neuropathy, erectile dysfunction
Impaired wound healing and amputation

156
Q

Plasma calcium

A

Vital 2nd messenger, necessary for muscle contraction, coagulation, nerve function

157
Q

Bone Calcium

A

99% of body calcium

  1. Readily exchangeable reservoir
    - – 500 mmol/day in and out
  2. Slowly exchangeable stable calcium
    - – Bone remodeling, 7.5 mmol/day exchanged with ECF
158
Q

What does phosphate do?

A
  1. Component of ATP
  2. Biological buffer
  3. Modify proteins
159
Q

How is phosphate regulated?

A

Many of the same systems that regulate Ca2+ regulate phosphate, but sometimes in reciprocal fashion.

160
Q

Body Phosphorus

A

500-800 g
85-90% in skeleton
300 mg/d in and out of bone per day

161
Q

What foods are high in phosphate?

A

Dark greens, beans, shellfish, lean meat

162
Q

NaPi-lla

A

Sodium dependent Phosphate cotransporters
Absorb Pi in the duodenum and small intestine
Stimuli that increase Ca absorption including vitamin D increase these transporters in the intestine

163
Q

Parathyroid hormone function

A

Secreted by Chief Cells of Parathyroid Glands

Mobilize calcium and bone and increase urinary phosphate excretion

164
Q

1,25-Dihydroxycholecalciferol (1,25 (OH)2D)

A

Steroid hormone formed from Vit. D in skin via sun processed in liver and kidneys
Increases calcium absorption from the intestine and increase Ca2+ in bone
Downregulates PTH formation and release

165
Q

Calcitonin

A

Secreted by parafollicular cells in the thyroid gland
Lowers free calcium by:
1. Inhibiting Ca2+ reabsorption in intestines
2. Inhibiting osteoclast activity
3. Stimulating Osteoblast activity
4. Inhibits Ca2+ reabsorption in the kidneys

166
Q

Vitamin D

A

Sterols produced by the action of ultraviolet from the sun on certain provitamins
Fatty fish
90% obtained through exposure to sunlight
Hydroxylation reactions activate it

167
Q

Other hormones that act on Ca

A

Glucocorticoids - lower plasma Ca levels by inhibiting osteoclast formation and activity
Growth hormone - increases Ca excretion in urine, but has greater increase of intestinal Ca absorption
Estrogens - Prevent osteoporosis by inhibiting the stimulatory effects of cytokines on osteoclasts
Insulin - Increases bone formation

168
Q

Compact/Cortical bone

A

Makes up outer layer of bone

80% of bone in body

169
Q

Trabecular/spongy bone

A

Inside cortical bone

remaining 20% of bone

170
Q

Epiphyses

A

Specialized areas at end of long bones
Epiphysial plate - site of actively proliferating cartilage
Width of the epiphysial plate is proportional to the rate of growth and is affected by hormones
Growth ceases with epiphysial closure

171
Q

Osteoclasts

A

Erode and absorb previously formed bone
Attach to bone via integrins, creating sealing zones.
Acidify area to dissolve hydroxyapatites
Proteases break down collagen
Digested products endocytosed, then released

172
Q

Osteoblasts

A

Modified fibroblasts that lay down Type 1 Collagen to form new bone

173
Q

Osteopetrosis

A

Osteoclasts are defective and unable to resorb bone
Osteoblasts opperate unopposed
Bone density increases and growth becomes distorted, few foramina for nerves

174
Q

Osteoporosis

A

Relative excess of osteoclast function results in loss of bone matrix and high risk of fractures
Involutional osteoporosis - as age increases, bone loss increases
Treatment: bisphosphonates - inhibit osteoclasts

175
Q

Rickets/Osteomalacia

A

Vitamin D and/or Ca2+ deficiency
Rickets in children - bowing of weight-bearing bones, dental defects
Osteomalacia in adults - muscle weakness and bone pain, enamel hypoplasia

Biochemistry/Physiology (10 decks)

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