Homeostasis Word Stimulants Flashcards
Homeostasis
Constant internal conditions
Physiological control system
Organisms functions independent to external environment
Improve survival chance
Conditions kept constant
Blood glucose concentration
Blood and tissue fluid pH and water potential
Core temperature
Blood glucose concentration
Cellular respiration
Maintains water potential
Blood and tissue fluid pH and water potential
Cells strink/expand
Core temperature
Fat - insulator
Optimum temperature and pH
Enzymes most active (sensitive - denature)
Rate of enzyme-catalysed reactions maximum
Metabolism of cells most efficient
Feedback Mechanisms
Self regulating system Information about system changes effects future changes 1. Optimum 2. Stimuli 3. Receptors 4. Coordinator 5. Effectors 6. Feedback
Stimuli
Deviation from optimum
Receptors
Detect deviation
Coordinator
Receives info from receptors
Sends instructions to effectors
Effectors
Bring about response
Return system to optimum
Feedback
Informs receptors of system changes
Caused by effectors
Negative feedback
Reverses direction of change towards stimulus
Maintains stability
Conditions fluctuate around optimum
Self adjusting
Eg Blood glucose (high - insulin; low - glucagon)
Positive feedback
Causes more and more change away from optimum
Reinforces original change
Does not maintain stability
Chain reaction develops - could run out of control&destroy itself - (negative feedback prevents)
Eg Damaged tissues - continuous platelets - blood clot (breaks chain reaction)
Eg Neurones - Na+ influx = increases Na+ permeability
Glycogen
Glucose store
Liver and muscle tissue
Hormones
First messenger molecules
Bind to receptors (proteins)
Receptors
Embedded in phospholipid biplayer of plasma membrane of target cells
Endocytosis
Hormone-substrate complex > Cytoplasm (target cells)
Insulin combines with receptor passage
Hormone-substrate complex > Cytoplasm (target cells) > Golgi apparatus > Cell Surface > Plasma membrane
Insulin/Receptor Golgi apparatus
Bud off portions of material (glucose carrier proteins)
Insulin/Receptor Plasma membrane
Increase no. of glucose carrier proteins
Uptake of glucose increases
Glucagon & Adrenaline combines with receptor passage
Activates Adenylate cyclase
Adenylate cyclase
ATP > cyclic AMP (cAMP)
cyclic AMP (cAMP)
Secondary messenger molecule
Activates glycogen phosphorylase (glycogen > glucose)
Insulin
Secreted by B cells of islets of Langerhan (pancreas)
Responds to high glucose conc (reduces conc)
Liver/Muscle Plasma membrane more permeable to glucose > more uptake
Glucose > glycogen
Glycogenesis
Insulin
Glucose > Glucogen
Glucogen synthase
Condensation
Glucogen synthase
Glucose > Glucogen
Glucagon
Secreted by A cells of islets of Langerhan (pancreas)
Responds to low glucose conc (increases conc)
Reduces liver plasma membrane permeability to glucose > less glucose uptake
Glycogen > Glucose
Inhibits glycogen synthase
Glycogenolysis
Activates glycogen phosphorylase
Glycogen > Glucose
Glycogen phosphorylase
Glycogen > Glucose
Glyconeogenesis
Activates fructose biphophate
Non carbohydrate substances (glycerol & amino acid) > glucose
Adrenaline
Secreted by adrenal glands Responds to low glucose conc (increases conc) Inactivates glycogen synthase Activates glycogen phosphorlyase Glycogen > Glucose
Diabetes Type 1
Insulin deficient diabetes
Pancreas does not produce enough insulin
B cells destroyed (autoimmune disease)
Genetic disorder - children, fast development
Diabetes Type 1 Treatment
Healthy balanced diet
Daily injections (GM bacteria produce insulin; dose - biosensors)
Transplant (insulin producing cells - B cells)
Immunotherapy (T cells prevent autoimmunity)
Diabetes Type 2
Non insulin deficient
Pancreas does produce enough insulin
Body tissue insensitive/resistant to insulin
Adult, slow development
Diabetes Type 2 Resistance
Body tissue insensitive/resistant to insulin
Glycoprotein receptors lost
Cannot use blood glucose (energy)
B cells produce more insulin (eventually unable to produce)
Liver release more insulin - increase in blood glucose conc
Diabetes Type 2 Treatment
Balanced, healthy diet
Regular exercise
Weight control
Drugs - if necessary
Symptoms of hyperglycemia/excess glucose
Bloody supply to extremities reduced - Gangrene (derived of O2 and nutrients)
Increase in urine vol (excessive)
pH fall (Acidosis)
Nephron Structure
Renal artery; afferent arteriole; Bowmen’s capsule; glomerulus; malphigan body; efferent arteriole; vesa recta (blood capillaries); renal vein; proximal convulated tubule; loop of henle (descending-left/ascending-right); distal convulated tubule; collecting duct
Top of nephron
Cortex
Bottom of nephron
Medulla
Glomerulus
Malphigan body
Knot of blood capillary
Efferent arteriole
Diameter smaller
Maintain pressure
Rein vein
Carries clean blood
Collecting Duct
> Ureter
Malphigan body
Bowmen’s (renal) capsule
Glomerulus
Filters wastes
Kidney Structure
Renal vein; Renal artery; Ureter; pelvis; medulla; cortex; fibrous capsule (protects); nephron
Osmoregulation
Maintains balance between water potential of cells and tissue fluid
Ultrafiltration location
Malphighan body
Endothelium lining structure
Between blood vessel of glomerus and Bowmen lumen
Fenestrations (pres)
Podocytes (projections, gaps, Bowmen capsule cells)
Filter
Small molecules - Blood plasma to lumen of Bowmens capsule (fenestrations, caps between podocytes)
Large molecules stopped
Hydrostatic pressure
Blood capillaries of glomerulus
Forces substrates out of blood
Water potential
Lower in Bowmens than blood
No proteins
Osmotic pressure
Water into blood
Oncotic pressure
Less than hydrostatic pressure
Proximal Convulted Tubule wall cells
Contain mitochondria
Cilitated
Metabolically active
Specialised
Reabsorption by proximal convulated tubule purpose
Adjust ion concentration
Secrete urea into liquid
Secreted liquid to blood
Active Transport of glucose, amino acids and mineral ions
pH regulation
Removal of H+
Uptake of HCO3-
Reabsorption by distal convulated tubule purpose
Fine tune ion concentration
Secrete blood to tubule
Cells forming wall actively transport :
K+ , H +, NH4+
Secrete liquid to blood
Cells forming wall actively transport :
Na+
Rate of exchange varies
Ion concentration in blood regulated
Maintains pH
Urine - pH 6 (contains NH4+, H+)
Loop of Henle
Liquid enters from proximal convulated tubule
Leaves to collecting duct
Counter-current multiplier
Ascending limb
Na+, Cl- actively transported from, diffuse into descending limb
- Conc in tissue fluid of medulla increases
Lose more as liquid moves up the limb
Impermeable to H2O - thick walls
Descending limb
Cl-, Na+ conc increases
Conc greatest at bottom of loop
Diffuse into medulla tissue
Water lost to medulla tissue (osmosis) - carried away in vena recta (blood)
Countercurrent multiplier
Short - less Na+ Cl- build up - less conc urine
Energy to generate an osmotic gradient - conc of ions decrease up limb
Maintains water potential gradient
Antidiveretic Hormone (ADH)
Effects permeability of collecting ducts
Negative feedback
Osmoreceptors of hypothalamus
Water potential of blood more negative
Hypothalamus secretes ADH > down axon in neuroscretory cells > pituitary gland > released into blood > collecting duct
Collecting ducts more permeable to H20 > Osmosis into medulla tissue > blood
Small volume of urine, concentrated
Water potential of blood less negative
Neurosecretory cells in hypothalamus secrete less ADH
Collecting ducts less permeable > less H2O (osmosis) out of collecting duct to medualla
Large volume of urine, dilute
