General Physiology Flashcards
Homestasis: Nervous system
Afferent to fibres link receptors to the brain and spinal cord (Coordinating centres)
Efferent fibres carry information from centres out to effector organs
Somatic nervous systems uses the skeletal muscle as effectors
Autonomic system: Uses organs such as heart, blood vessels , glands as effectors via efferent fibres
Homestasis: Hormonal system
Endocrine glands use hormones as efferent signal to effect change
Generally slower than the nervous system
Under nervous system control via the Hypothalamo-pituitary-adrenal axis under negative feedback
Homestasis: Thermoregulation
Balance of heat gain and heat loss.
Small heat changes are created by changes in blood flow
Large heat changes are created by shivering and sweating
Heat production methods:
- Shivering
- Increased voluntary effort
- Hypothalamic control
Heat loss methods:
- Controlled by sympathetic nervous system and hypothalamus
- Sweating
- Altering skin blood flow
Homestasis: Regulation of body temperature
Peripheral thermoreceptors
- Respond to warm and cold stimuli
- Connect centrally to the cortex (conscious sensation and hypothalamus)
Temperature sensitive receptors are situated in the anterior hypothalamus
HOT Activation:
-Skin vasodilation and sweating
COLD Activation:
- INHIBITS heat sensitive neurons
- Vasoconstriction
- Shivering
Reflex vasoconstriction (Ipsi and contralateral)
Direct contact with a cold surface:
- Afferent neuron: cutaneous nerve
- Signal to the coordinating center: Spinal cord and hypothalamus
- Efferent neuron: Sympathetic nerves
Reflex vasoconstriction (Ipsi and contralateral)
Direct contact with a cold surface:
- Afferent neuron: cutaneous nerve
- Signal to the coordinating center: Spinal cord and hypothalamus
- Efferent neuron: Sympathetic nerves
Reflex vasodilation (Ipsi and contralateral)
Radiant heat to part or whole of body
- Afferent neuron: cutaneous nerve
- Signal to the coordinating center: Above C5 of spinal cord
- Efferent neuron: Sympathetic nerves (Inhibit activity)
homeostasis of body temperature
Rectal temperature best for core temperature
0.5 degrees higher than mouth and axilla
In menstruation 0.5 degrees higher in latter half
Diurnal variation-higher in evening c.f. morning
Peripheral temperature mechanisms of loss:
- Conduction and evaporation
- Convection: skin to air movement
- Radiation
Aspirin returns the set point temperature in the hypothalamus to normal-pt will often feel hot as the core temperature is higher than it should be (once hypothalamus resets itself)
Heat stroke and Hypothermia
Heat stroke >41 degrees
Hypothermia <30 thermoregulation completely fails therefore no response to increase the temperature
Death from cardiac arrhythmias
Factors affecting thermoregulation
Anaesthetics
- Depress hypothalamus
- Vasocilation
- Lack of shivering
- Subsequent drop in temp
Exercise
- Raises temp faster than body can lose
Circulatory shock
- True shock: Drop in temp due to reduced perfusion
- Septic shock raises temp due to vasodilation causing skin to feel hot
Spinal Injuries:
- Thermoregulation lost below spinal injury
- Vasoconstriction lost therefore increased heat loss
- Shivering ceases
Hyperthyroidism
- Patient hot
Hypothyroidism
-Patient cold
Neonates
- Increased heat loss
Composition of body water
60% body water
1) Intracellular and extracellular
Extracellular –> A) Intravascular e.g. blood plasma
Extravascular (Interstitial fluid, transcellular fluid)
Diuresis
1) Water diuresis
Intake of water–>inhibits ADH, collecting tubules become impermeable, water loss with minimal solute loss
2) Osmotic
High solute intake, tubules cannot reasborb causing loss of water along with solute e.g. diabetes, mannitol, drugs
Sources of water loss
1) Evaporation via respiratory system (500mls)
2) Urine obligatory loss (500mls)
3) Insensible loss e.g. skin (400mls)
4) Faeces (100mls)
1. 5l loss per day
Osmolality control
Normal serum osmolality 285-295mOsm/L
Main mechanisms of control include
1) Thirst
2) ADH release
Plasma perfusing nuclei in the hypothalamus control thirst and ADH release. ADH releasing nuclei have 10mOsm/L lower threshold than thirst releasing nuclei-ensures ADH retains water first before increasing intake.
Sub mechanisms include (>in hypovolaemia)
1) Arterial blood pressure (Aortic and carotid baroreceptors)
2) Central venous pressure (atrial and low pressure receptors)
3) Angiotensin II
Sodium
Major cation in ECF
Renal control 1) 99% reabsorbed 2) 65% in proximal tubule 3) 25% in loop of Henle 4) 10% in distal and collecting ducts Determined by GFR, Renin-angiotensin (reabsorbs Na+ and vasoconstricts glomerular arterioles)
Extrarenal control
1) AldosteroneNa+ reabsorbed from distal tubule and collecting ducts, colon, salivary and sweat glands
2) ANP (In response to stretch)increases GFR, inhibits reabs in collecting duct, inhibits renin and aldosterone
3) Ang IIaldosterone release from ZG of adrenals
Hypernatraemia
1) Excess IV fluids containing sodium
2) Conns syndrome
3) Cushings
4) Steroid therapy
5) CCF
6) Cirrhosis
Hyponatraemia
1) Low intake
2) Excess loss (Diarrhoea, fistula, obstruction, sweating, burns, diuretics)
3) Addisons
4) SIADH
Potassium
Chief intracellular cation
Extracellular changes can have profound effects
1) Aldosterone Increases excretion via distal tubule
2) Insulin promotes K+ entry into cells
3) Acidosis increases plasma K+ by inhibiting cell entry and reduced urinary excretion (alkalosis opposite effect)
