Quiz 7 - Hormones, Fatty Acid Metabolism, Regulation of Metabolism, Musculoskeletal system, Diabetes, Bone Physio Flashcards
(175 cards)
1
Q
Homeostasis
A
Physiologic ability to maintain a relative stable internal environment despite external changes.
2
Q
4 features of feedback mechanisms
A
- System Variable
- Set Point
- Detector
- Corrective mechanism
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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.
4
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Endocrinology
A
Study of endocrine system and hormone action
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Where do hormones bind?
A
Receptors on or in target cells
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What do hormones control?
A
- Rates of enzymatic reactions
- Movement of ions or molecules across membranes
- Gene expression and protein synthesis.
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Where are hormones produced?
A
Endocrine cells and organs
8
Q
Where are hormones released?
A
Endocrine glands
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Thyroid hormone
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Made in thyroid, controls basal metabolism
10
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Cortisol
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Made in adrenal cortex, controls energy metabolism and stress responses.
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Mineralcorticoids
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Made in adrenal cortex, regulate plasma volume via effects on serum electrolytes
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Vasopressin
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Made in the posterior pituitary, regulates plasma osmolality via effects on water excretion
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Parathyroid hormone
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Made in the parathyroids, regulates calcium and phosphorus levels.
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Insulin
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Made in the B cells of the pancreas, regulates plasma glucose concentration.
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Neurocrine
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Secretion of hormones into the bloodstream by neurons
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Endocrine
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Secretion of hormones into the bloodstream by endocrine glands
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Paracrine
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Hormone molecules secreted by one cell affects adjacent cells
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Autocrine
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Hormone molecule secreted by a cell affects the secreting cell.
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Three chemical classes of hormones
A
- Steroid hormones
- Peptide and protein hormones - 50 aas is a protein
- Amine hormones (tyrosine derivatives)
20
Q
Lipophilic hormones
A
Fat-soluble
Steroid and thyroid hormones
Bind to intracellular receptors
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Hydrophilic hormones
A
Water-soluble
All other hormones
Bind to extracellular receptors and trigger signaling cascades
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Amine hormones
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Thyroid hormones and Catecholamines (epinephrine, norepinephrine)
Derived from amino acid tyrosine
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Thyroid hormones
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Thyroxine
Derived from Tyrosine (Amine hormone)
Bind to nuclear receptors
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Catecholamines
A
Epinephrine and Norepinephrine
Derived from Tyrosine
Bind to cell surface receptors
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Peptide and Protein hormones
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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Modification of Peptide hormones
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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Prohormones exist for which hormones?
```
Insulin
Somatostatin
Glucagon
Enkephalin
ADH (Vasopressin)
Gastrin
Parathyroid hormone
Calcitonin
ACTH
```
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Signal transduction/Extracellular Hormone Receptor Pathway
Hydrophilic hormone binds to cell surface GPCR, G-protein activates second messenger (like cAMP), 2nd messenger activates other effects
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Steroid hormones
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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Plasma binding globulins
Bind to steroid hormones in the plasma
| Albumin, testosterone binding globulin, thyroxine binding globulin
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Intracellular Hormone Receptor Pathway
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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Aromatase Enzyme/Aromatization
Enzyme that converts "Free" androgen hormones into estrogens.
Occurs in trophoblastic tumors
Occurs normally in adipocytes, liver, brain.
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5 Factors that effect circulating hormone levels
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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Negative feedback regulation of hormones
Hormone shuts down stimulating or releasing factors, ending hormone action
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Positive feedback regulation of hormones
Uncommon, hormones enhance releasing and stimulating factors
| Occurs in childbirth (parturition)
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Long-loop feedback
Target gland hormone may feedback and inhibit its production
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Short-loop feedback
Stimulating hormone (trophic hormone) inhibits hormone production
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Pituitary gland anatomy
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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Hypothalamo-hypophysial portal system
Capillary system that links secretory neurons of hypothalamus with storage portion of anterior pituitary
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Pituitary hormone
Ocytocin
ADH
Adrenocorticotrophic hormon (ACTH)
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Hypothalamic-Pituitary-Adrenal Axis (HPA)
Responsible for adaptation of stress response, regulates many body functions
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Feedback control of Osmolality
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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Adrenal gland hormones
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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Aldosterone
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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Cortisol
Glucocorticoid
Stimulates gluconeogenesis, increasing serum glucose
Has anti-inflammatory effects, adversely affects immunity, eosinophil and lymphocyte counts decreasae
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Adrenal androgens
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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Acute stress
Fight or flight response
Epinephrine and norepinephrine
Blood glucose rises, BP rises, Bronchioles dilate
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Chronic stress
Steroid hormones secreted
Immune suppressed
Water retention
Eventual exhaustion
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Cortisol regulation
Negative feedback loop
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Endocrine gland hyposecretion
Hormone deficiency (Ex. Type 1 Diabetes)
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Hormone resistence
Ex.) Type 2 Diabetes
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Hormone Excess
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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Addison's Disease
Adrenal insufficiency, leads to hypoglycemia, weight loss, postural hypertension, weakness, GI distubances
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Cushing's Syndrome
Excess ACTH causes excess cortisol
| Moon face, buffalo hump, buisability, poor wound healing
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Hypothyroidism
Insufficient thyroid hormone
Fatigue, constipation, dry skin, depression, enlarged thyroid
Hashimoto's disease - autoimmune hypothyroidism
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Hyperthyroidism
Excess thyroid hormone
Weight loss, fast heart rate, exopthalmos (bulging eyes), enlarged thyroid
Grave's disease - autoimmune hyperthyroidism
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Dietary Lipid processing
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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How are fatty acids transported?
Albumin carries free fatty acids in serum
| Lipoproteins carry triglycerides and cholesterol (Chylomicrons)
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4 classes of Lipoproteins
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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Triacylglycerol cycle
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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Adipose triglyceride mobilization
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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Lipid Catabolism
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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Acyl-Carnitine/Carnitine Transporter
Carnitine used as carrier to bring Carbon chains from cytosol, across intermembrane space and into matrix of mitochondria
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3 stages of fatty acid oxidation
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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Fatty Acid Beta Oxidation
Removes a 2 carbon piece at the Beta carbon, producing 1 NADH and 1 FADH per Acetyl-CoA produced
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What happens to Acetyl-CoA after production in Beta Oxidation?
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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Citrate shuttle
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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Acetyl-CoA Carboxylase
Adds a CO2 to Acetyl-CoA, creating Malonyl-CoA, which is used to create fatty acid chains
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Fatty Acid Synthase
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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Essential Fatty Acids
18:2 and longer chains cannot be created by mammals and must be ingested. Linoleate is first essential fatty acid
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Regulation of Fatty Acid Synthesis and breakdown
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
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Phosphatidic acid
Precursor to phospholipids and triglycerides
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What is Cholesterol formed from?
Acetyl-CoA
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Cholesterol uses
Lipoprotein and steroid hormone formation
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Atherosclerotic Plaque formation
Cholesterol accumulates in macrophages (foam cell), which apoptoses and deposits cholesterol-rich plaque in artery lumens.
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Autonomic Nervous System
Sympathetic and Parasympathetic control of organ function. Direct contact from nervous system to organs
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Neuroendocrine system
Hormone control of organ function. Indirect control via the HPA axis - Hypothalamus, Pituitary, Adrenals
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Hypothalamus methods of control
1. Direct - autonomic - innervation of pre-ganglionic neurons
2. Indirect - Hormonal - release of pituitary and adrenal cortex hormones
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3 Parts of the Autonomic Nervous System
1. Sympathetic - fight or flight
2. Parasympathetic - rest and digest
3. Enteric nervous system - digestive system
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Carotid Body
Site of chemoreceptors that detect blood O2/CO2 composition. Autonomic control of cardiac function
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Autonomic control of cardiac function
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
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Baroreceptors
Detect blood pressure. Autonomic control of cardiac function
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What does the liver regulate?
Blood sugar
Carbohydrate storage (glycogen) and regulation
Amino acid content
Lipid formation and mobilization
First pass metabolism - blood enters directly from gut
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What does the pancreas regulate?
Insulin release during high blood sugar
Glucagon release during low blood sugar
Duodenum pH buffering
Protease release
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What does the gallbladder regulate?
Bile salts release to degrade lipids
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What's important about Glucose-6-Phosphate
It is the branching point - can become glucose, glycogen, go down pentose phosphate pathway, become acetyl-CoA
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Leptin
Triggers satiety signals in the hypothalamus. Eat less, metabolize more
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Grehlin
Triggers hunger signals in the hypothalamus. Eat more, metabolize less
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Insulin release pathway
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
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Glucagon release pathway
Alpha cells work just like Beta cells, only ADP concentration increase blocks K+ channels
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Superior/Cranial/Rostral
Head end
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Inferior/Caudal
Feet end
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Proximal
Toward main body
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Distal
Away from main body
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Median
Midline, divides right from left
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Medial
Close to midline to side
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Lateral
Away from midline to side
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Coronal
Divides front from back
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Anterior/Ventral
Front
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Posterior/Dorsal
Back
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Saggital
Median plane in skull
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Transverse
Cross section cut parallel to ground
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Axial
Transverse plane in skull
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Extension of neck
Tilt head back
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Flexion of neck
Tilt head forward
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Rotation
Circular motion around a joint
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Axial skeleton
Head, vertebrae, ribs, sternum
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Appendicular skeleton
Everything else, including the pelvis and scapula and clavicles
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Numbers of ribs
7 pairs of true ribs
3 pairs of false ribs
2 pairs of floating ribs
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Scapula landmarks
Superior angle, supraspinous fossa, scapular spine, acromion, coracoid process, intraspinous fossa, medial border, subscapular fossa
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Pelvic bones
Os Coxae - 3 bones fused
| Ilium, Ischium, Pubis
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Synarthroses
Immovable joints
| Fibrous - Skull sutures, Gomphoses (teeth)
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Diarthroses
Freely movable
| Synovial
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Limits to joint movement
Bones, Muscles, ligaments, other tissue
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Superficial back muscles
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Trapezius
Levator scapulae
Rhomboid major and minor
Latissimus dorsi
Innervated by ventral rami
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Trapezius
Spinal accessory nerve
Rotation of scapula for abduction of arm beyond 90 degrees
Extends neck
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Levator Scapulae
Dorsal scapular nerve
| Elevates scapula
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Rhomboid major and minor
Dorsal scapular nerve
| Retracts, adducts scapula
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Latissimus dorsi
Thoracodorsal nerve
| Adducts humerous
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Deep back muscles
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Spenius muscles
Erector Spinae muscles
Transversospinalis muscles
Suboccipital muscle group
Innervated by dorsal rami
```
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Splenius muscles
From back of head to spinal column
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Erector Spinae muscles
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
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Tranversospinalis muscles
Semispinalis - Along spinous processes from Occipital to thoracic
Multifidus - Along spinous processes from sacrum to ribs - lower back pain muscle
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Suboccipital muscles
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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
```
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Obliquus Capitis Superior muscle
Contraction tilts head like a curious dog
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Deltoid
Axillary nerve
| Abduction of arm from 15 degrees to 90
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Subscapularis
Upper and lower subscapular nerves
| Glenohumeral internal rotation
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Supraspinatus
Suprascapular nerve
| Glenohumeral abduction to 15 degrees
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Infraspinatus
Suprascapular nerve
| Genohumeral external rotation
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Pectoralis major
Lateral and medial pectoral nerves
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Pectoralis minor
Medial pectoral nerve
| Glenohumeral adduction
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Subclavius
Nerve to subclavius
| Glenohumeral adduction
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Serratus Anterior
Long thoracic nerve
| Scapula protraction
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Brachial plexus
```
Ventral rami from C5-T1
Meet in 3 trunks
Divide
Separate into 2 anterior cords and one posterior cord
Many nerves branch from here
```
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What brachial plexus nerves branch in what region?
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
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Diabetes Mellitus
Inability of the body to regulate glucose through insulin
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Type 1 Diabetes
Autoimmune loss of insuline-producing B-cells
Genetically Linked
Juvenile onset
Insulin-dependent
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Type II Diabetes
Insensitivity to insulin
Lifestyle and genetics - weight gain and obesity
Adult onset (though becoming common in juveniles)
Non-insulin dependent
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Gestational Diabetes
Develops during pregnancy
Fetus induces changes in metabolism
Causes a predisposition to Type II later in life
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Frequency of Diabetes in the US
29.1 million with disease - 9.3% of US population
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Symptoms of Type I diabetes
```
Polyuria and Thirst
Weakness
Polyphagia and weight loss
Blurred Vision
Peripheral Neuropathy
Nocturnal Enuresis
Sweet smelling breath and urine
Impaired wound healing
```
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Symptoms of Type II diabetes
```
Polyuria and thirst
Weakness
Blurred Vision
Peripheral Neuropathy
Sweet smelling breath and urine
Impaired wound healing
```
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What does Type I diabetes ultimately cause?
Lack of insulin leads to a dysregulated metabolic state of extreme fasting and starvation
144
Pathogenesis of Type I diabetes
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
Ketoacidosis
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
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Treatment of Type I diabetes
1. Insulin administration - Injections or pump
2. Glucose monitoring
3. Diet - low carbohydrate
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Insulin administration
Different types
Basal insulin - maintains low-level systemic insulin
Bolus - Given when food is consumed
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Pathogenesis of Type II diabetes
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
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How might adipose signaling drive type II diabetes?
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
Type II diabetes management
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
Type II drugs
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
How is diabetes detected
1. Urinalysis
2. Glucose monitoring
3. HBA1c - measure of glycolated hemoglobin
4. Glucose tolerance test
5. C-peptide test - cleavage product of proinsulin
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Hypoglycemia
Low blood sugar
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Hyperglycemia
High blood sugar
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Long-term diabetic complications
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
Plasma calcium
Vital 2nd messenger, necessary for muscle contraction, coagulation, nerve function
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Bone Calcium
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
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What does phosphate do?
1. Component of ATP
2. Biological buffer
3. Modify proteins
159
How is phosphate regulated?
Many of the same systems that regulate Ca2+ regulate phosphate, but sometimes in reciprocal fashion.
160
Body Phosphorus
500-800 g
85-90% in skeleton
300 mg/d in and out of bone per day
161
What foods are high in phosphate?
Dark greens, beans, shellfish, lean meat
162
NaPi-lla
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
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Parathyroid hormone function
Secreted by Chief Cells of Parathyroid Glands
| Mobilize calcium and bone and increase urinary phosphate excretion
164
1,25-Dihydroxycholecalciferol (1,25 (OH)2D)
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
Calcitonin
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
Vitamin D
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
Other hormones that act on Ca
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
Compact/Cortical bone
Makes up outer layer of bone
| 80% of bone in body
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Trabecular/spongy bone
Inside cortical bone
| remaining 20% of bone
170
Epiphyses
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
Osteoclasts
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
Osteoblasts
Modified fibroblasts that lay down Type 1 Collagen to form new bone
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Osteopetrosis
Osteoclasts are defective and unable to resorb bone
Osteoblasts opperate unopposed
Bone density increases and growth becomes distorted, few foramina for nerves
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Osteoporosis
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
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Rickets/Osteomalacia
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
