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- 1True or false, nervous system becomes more excitable when extracellular Ca2+ levels dropTrue. Causes membranes to become increasingly permeable to Na+
- 2What happens when nervous system becomes hyperexcitableTetanic contractions
HYPOCALAEMIC TETANY - 3What is a classic symptom of hypocalcaemic tetanyTrossaus sign, clenched fist because of muscle contraction
- 4What are the forms of extracellular calcium50% in free unbound form
10% in anion complex (bicarbonate, citrate and phosphate)
40% protein bound (albumin and globulins) = albumin most abundant - 5What makes up filterable calciumfree form and anion form (60%) filterable at kidney
- 6Describe rapidly exchangable pool of calciumRight on surface of bone. Doesn't stay on surface of bone. Moves either from extracellular fluid to bone (bone formation)
OR out of bone to extracellular fluid (bone reabsorption) - 7Role of kidney in Ca2+Filtration and reabsorption
- 60% reabsorbed in kidneys through an active mechanism in proximal tubule
- 30% absorbed paracellularly in loop of henle
- 9% absorbed in distal tubule via an active transcellular mechanism ***most important for regulation
(1-2% excreted) - 8Role of intestines in Ca2+absorption and secretion
- 9Role of bone in ca2+Formation and resorption
- 10Describe the parcellular pathway in the for CA2+ absorption1) Paracellular transport pathway between cells. PASSIVE PATHWAY, MAINLY IN LOWERE GI TRACT (ILEUM
- NO rate limiting step (larger gradient, more absorption) however doesn't work if no gradient (if lumen is below 2.4mm) - 11Describe the trancellular pathway of Ca2+ absorption- Calcium taken into epethelial cells in duodenum, jejunum
- CaBP (Ca2+ binding protein/ vit D metabolites) in cells prevents this free Ca2+ activating any pathways
- released out of cell ca2+ pumps or Na+/Ca2+ (pumps) = RATE OF PUMP E.G. SATURATION = RATE LIMITING STEP
CA2+ MUST MOVE AGAINST CONC GRADIENT = active
- This pathway never stops
- It can be regulated - 12Describe action of parathyroid hormone on kidneysActs on distal tubule to increase ca2+ absorption. Stimulates reabsorption
- Acts directly on kidney to stimulate activity of 1alpha-hydroxilase which catalyses the formation of 1,25 DHCC (hypercalcaemic hormone) - 13Where does bone formation occurSpongey/ trabecular bone because of greater surface area for calcium exchange
- 14Role of osteoclastsLarge multinucleated cells derived from monocytes whose function is to resorb bone. Release enyzmes that dissolve bone to release calcium into extracellular (regulated by plasma calcium)
- 15Role of osteocytesMature bone cells enclosed in bone matrix. Connected to surface cells and each other via canaliculi to allow for nutrient and ion exchange
- 16Role of osteoblastsDifferentiated bone forming cells that secrete organic bone matrix (OSTEOID -made of collagen protein) on which Ca3(PO4)2 precipitates prior to full mineralisation
- 17Structure of bone
- 18What type of cell does parathyroid hormone act on and what is the effectActs on osteoclasts which dissolve bone and increase Ca2+ in blood
(bone resorption) - 19Non-Hormonal method of regulation of extracellular Ca2+ concRapidly exchangeable pool, fast but limited so not used
- 20Which 3 hormones are used to regulate calcium1) Parathyroid hormone
2) 1, 25 dihydroxycholecalciferol (1,25 DHCC) VitaminD metabolite - VitD = cholecaliferol
3) Calcitonin - 21Describe synthesis of parathyroid hormoneChief cells in parathyroid gland (behind thyroid) synthesize parathyroid hormone
Peptide hormone = transcribed into INACTIVE preprohormone
cleavage of prosequence to make active form
Increases plasma calcium
Stimulus for release is a decrease in calcium levels - 22Mechanisms of action of Parathyroid on bone- Acts directly on bone to stimulate Ca2+ (increases osteoclast number and activity)
- Decreases collagen synthesis by osteoblasts (i.e. decreases bone formation)
Increased net transfer of Ca2+ into plasma - 23Affect of parathyroid hormone on GI tractNO DIRECT EFFECT ON CA2+ ABSORPTION
Indirect effect by stimulating 1,25 DHCC (in kidney) which does increase Ca2+ in kidney - 24ArthritisInflammation of the foot
- 25Arthralgia Arthopathy RheumatismInflammation of joint
Joint pain
Joint problem - 26Inflammatory arthritis (Rheumatoid)Rheumatoid
Immune
Can genetic or environmental - 27Properties of DHCC- DHCC is similar structure to DHCC
- From diet (oily fish)
- Produced in skin by action of UV light from the BASE MOLECULE IS (2/3)rd produced via this method
CHOLESTEROL (similar to all steroid hormones) - 28Production of DHCCConverted from Vitamin D3
Goes to hepatic circulation
Hydroxyl group added to 25carbon
Goes to kidneys where 1 - alpha hydroxylase*** adds carbon to 1 position
makes 1,25DHCC
Stimulated by parathyroid horomone - 29Mechanism of action of DHCCInduces the production of intracellular calcium binding proteins (CaBP) which sequester Ca2+ thereby buffering the high intracellular Ca2+ that arise during initial absorption. They allow Ca2+ to be absorbed against a high Ca2+ gradient
- Minor effect on kidneys by increasing calcium reabsorption in distal tubule
- In bone, promotes the action of parathyroid hormone - 30DHCC similar properties to steroid hormones- based off cholesterol
- increases protein expression - 31Calcitonin properties- Only hypocalcaemic hormone we have
- synthesised and secreated by c cells in parathyroid gland (parafollicular cells)
- stimulated by hypercalcaemia
- Physiological antagonist to parathyroid hormone
- Not that important for overall calcium balance (chronic excess of calcitonin does not cause hypocalcaemia and removal of parafollicular cells doesnt cause hypercalcaemia) - 32Action of calcitonin- Main target is the osteoclasts (cell type for bone resorption)
- Calcitonin inhibits this process (prevents bone resorption)
- No effect on kidneys
- Weak effect on kidneys (decreases tubular reabsorption) - 33Osteoporosis- reduced bone density and mass
- equal loss of mineral and organic matrix
- increase risk of fractures
- Equilibrium shifts to bone resorption
- either too much resorption or too little formation
- female = major risk factor
- testosterone deficiency and steroid use are also risk factors
(bone present = biochemically normal) - 34Effect of oestrogen on osteoporosisOestrogen is a potent stimulator of bone formation
post menopause, oestrogen levels decline and then osteoporosis develops - 35Treatment of osteoporosisReplace sex steroids (adrogens in menopause)
Calcium and vitamin D in diet
Exercise - 36Osteomalacia (adults) and Rickets- Biochemically distinct from osteoporosis
- Inadequate mineralisation of new bone = ratio of MINERAL TO ORGANIC MATRIX is lower than normal = too much organic phase and not enough mineral phase
- Symptoms = bowed legs because of weight of torso - 37Cause of Rickets/ Ostoemalacia- Commonly caused by deficiency in vitamin D (hypocalaemic)
inability of 1,25 DHCC to act on target tissue e.g. vitamin D-dependent rickets type ii (despite high levels of 1,25 in blood)
cannot convert vit D to 1,25 DHCC - 38Treatment of rickets/ osteomalaciavit d analogs
dietary calcium - 39Hypercalaemia- May be present without other symptoms (mild)
- Moderate to sever = symptoms of neuromuscular supression
- symptoms include kidney stones, dehydration (calcium urea), weight loss, nausea, vomiting and fatigue - 40Primary hypercalcaemia- Most common cause of mild hypercalcaemia
- Ca2+ homeostatic loss due to excessive PTH secretion
May be from benign parathyroid tumour or hyperplastic parathyroid tissue (bigger thyroid than normal)
- Combined effect of PTH induced bone resorption, intestinal Ca2+ and renal tubular reabsorption
- increased PTH = increased 1,25 DHCC - 41What is the result of primary hyperthyroidsimDeposition of Ca2+ in heart, lung + soft tissue
= Stone formation - 42Treatment of hypercalcaemia- Antiresoptive agents
- Salmon calcitonin = more potent that calcitonin (prevents absorption)
- Surgery to remove tumour or plastic tissue - 43True or false, patients with severe hypercalcaemia have cancerTrue
Malignant cells in bone cause destruction of gone and release Ca2+
local osteolytic hypercalcaemia = tumour secretes factors that activate osteoclasts that dissolve bone
Sometimes metasteses not in bone synthesis
Sign is in blood levels of PTH are low - 44Difference between malignant disease and primary hypercalcaemia?Malignant disease = lower blood levels of PTHY
- 45Other causes of Hypercalcaemia- Vitamin D-Dependent hypercalcaemia due to overdose (too much 1,25DHCC)
- Hyperthyroidism = increase bone turnover (osteoclast activity, usually asymptomatic)
- Acromegaly = stimulation of 1alpha hydroxylase in kidney by elevated levels of growth hormone
- Milk ingestion (Ca2+ - containing antacids) - 46Hypercalcaemic Crisis- End stage of hypercalcaemia
- May lead to coma and death, associated with malignancy
- Usually dehydrated (due to kidneys trying to secrete calcium) - 47HypocalcaemiaInadequate response of PTH-vitamin D axis to hypocalcaemic stimuli
- NOT due to calcitonin
- results in neuromuscular excitability - 48Causes of hypocalcaemia?Hypoparathyroidsm (HPT)
1) PTH-deficient HPT 1 reduced or absent synthesis of PTH = Low levels of PTH results in low 1,25 DHCC
2) PTH - ineffective HPT = biologically inactive PTH produced
3) PTH - resistant HPT = PTH produced is not recognised by target tissue (pseudohypothyroidism)
4) Seocndary hyperparathyroidsism = malabsorption of vit D in tract = low 1,25DHCC, decrease in plasma Ca2+ stmulates PTH - 49How is hypercalcaemia treated- Ca2+ (for malabsorption in GI tract) and Calcitirol long term
- can be injected - 50How to determin a Ca2+ homeostatic problem- Determin serum Ca2+ concentration
- determin circulating levels of PTH and Vit D
- In practice, Vit D conc determined by levels of DHCC - 51What does primary hyperthyroidism look like on a graph- Hypercalcaemic = Ca2+ blood levels are high
- High PTH = due to excessive secreton
This leads to high levels of 1,25 DHCC - 52What does non PTH - Hypercalcaemia look like- Low levels of parathyroid hormone
- High levels of Ca2+ (hypercalcaemic) moderate to severe
- Due to malignant disease
- Vit D overdose
- Acromegaly (Excess 1,25 DHCC)
- Endocrine disorder (hyperthyroidism)
- Granulocyte disorder TB/ Leprocy - 53What does hypoparathyroidism look like- Hypocalcaemic (low levels of Ca2+
- Low levels of parathyroid hormone
Due to underperforming parathyroid gland
(e.g. parathyroid deficient or ineffective parathyroidism) - 54What does pseuodohyperthyroidism look likeHigh level of parathyroid hormone
Low levels of Ca2+ (hypcalcaemic)
- Biologically active PTH but receptors dont respone
- Also due to vit D deficiency (OSTEOMALACIA/ RICKETS) - 55Calcitonin pathophysiologyE.g. due to tumours of parafollicular cells producing excess = hypercalcitonaemia
- but normal levels of bone density and plasma calcium - 56What happens during pregnancy= Elevated levels of Calcitonin, PTH, 1,25DHCC
- Placenta also syntesises 1,25 DHCC
Increased levels of Ca2+ from GI tract - 57What type of crystals are in bone (mineralised matrix)Hyroxyapatite
- 58Describe the structure of boneDense outer cortex of compact cortical bone
Inner cavity meshwork of trabecular/ spongy bone with spaces between occupied by marrow
Epiphysis at the end, Diaphysis in the middle - 592 Phases of bone development1) Woven bone (immature, irregular, collagen fibrils)
2) Lamellar bone (plate like) (mature, arranged in layers, compact or trabecular) - 60Describe woven boneImmature, first layer laid in bone formation
- Persists in adults in tooth sockets, cranial suture, May be formed in fracture repaire - 61Describe the basic structure of compact and tracbecular bone
- 62Describe the haversian (lamellar bone)Can be arranged and compact and trabecullar bone
Arranged in a circle
External = two layers of periosteum
1) outer = collagen and blood vesells
2) inner = osteoprogenitor cells
Internal = Endosteum (osteoprogenitor cells, reticular fibres) - 63Describe the detail of the osteon/ haversian system
- 64What defines a single haversian systemA cement line. Surrounded by outer lamellae + interstitial lamellae
- 65What part of the bone are ostocytes inIn the lacunae, canaliculi link the lacunae
- 66What other structures form connections within the haversian systemVolkmans cannals are perpendicular
Sharpey's fibres connect - 67Where are the osteoprogenitor cellsIn the endosteum (medulla) of bone
- 68Describe bone mineralisationOsteoblasts secrete osteoid collagen and vesicles deposite hydroxyapitite which along with proteoglycans and proteins produce mineralisation
Occurs in matrix vesicles, requires Calcium - 69Organic vs Inorganic components of boneOrganic = osteoid, collagen fibres, proteins and proteoglycans
Inorganic = hydroxyapatite and other molecules - 70What are the 2 main proteins in bone matrixOsteocalin + Osteopontin
- 71True or false, osteoblasts secrete hydroxyapatite?False vesicles secrete hydroxyapatite, osteoblasts secrete osteoid collagen
- 72Osteoprogenitor cellsStem cells that can differntiate into other bone cell types
- 73True or false, osteocytes are the inactive form of osteoblasts and can regulate osteoclastsTrue
- 74True or false, osteoclasts are differentiated from osteoprogenitor cellsFalse, they are differentiated from blood monocytes
- 75Describe bone remodelling- During development woven bone is eroded by osteoclast activity (secretion of HCL + Cathepsin K protease into suosteoclastic compartent to degrade collagen proteins)
and remodelled. Stimulated by PTH and inhibited by Calcitonin - 76What are the 2 methods of ossification1) intramembranous (condensation of mesenchyme forms bone blastema) e.g. skull, mandible and clavical
2) endochondrol (cartilage to bone) most bones. Involves chondrocytes and bone cells - 77Describe the structures in a synovial joint- Hyaline cartilage (articular surfaces)
- Synovial membrane (non articular surface)
- Fibrous membrane (dense connective tissue) = capsule - 78What type of cell produces collagen- Fibroblasts
- In a triple helix
- high tensile stregnth
(also produce collagen) - 79What structures are made of loose connective tissue?Adipose (white and brown)
- Synovial
Reticular (in liver, endocrine, spleen)
Areola (these are low in collagen) - 80What structures are made of dense connective tissueIrregular = dermis (fibroblasts)
Regular = tendon and ligaments and fibrous capsule
high in collagne - 81Describe properties of cartilage- Not in direct contact with nerves or blood
Nutrients from diffusion through synovial fluid
- Accelerated diffusion when pressure is put during walking - 82Describe the make up of collagen30% glycine, 30% proline/ hydroxyprolein
It is a proteoglycan
Procollagen to tropocollagen (many moleules) put together to form Type II Trans Helix Structure (Vit C is a Co-Factor) for making hydrogen bonds - 83Describe structure of Trans HelixCovalent Cross links stabalise collagen along with hydrogen bonds
- 84What is Ehlers-Danlos Syndrome= Loose skin, collagen not formed properly because Type II Trans helix structure is not formed
- 85Describe a proteoglycan- Low in proteins, High in CHO
- Repeating disaccharide
- Highly negatively charged = hold a lot of water
- contains glycosaminoglycans
- Key ones are AGGRECAN
- Susceptible to proteolytic deggregation - 86Describe features of aggrecan?Hyaluronan core (important in bone + joint development), aggregates glycosaminoglycans (repeating dipeptides with negative charge)
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- TSM Karteikarten am TSM Extra, erstellt von Wannie Chisala am 04/01/2018.
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