General Physiology Flashcards
Reflex vasoconstriction: afferent, centre and efferent.
Which limbs?
Afferent: cutaneous nerve
Centre: hypothalamus and spinal cord
Efferent: sympathetic neurones
Bilateral limbs effected (ie cold stimulus R leg causes R+L)
Reflex vasodilatation: afferent, centre and efferent
Afferent: cutaneous nerve
Centre: above C5 of spinal cord
Efferent: sympathetic nerves (inhibition, reduce activity)
Which internal surfaces have thermoreceptors?
Resp & GI tracts
Inhalation of cold air causes shivering during inspiration
Hot food causes
Difference between core and mouth/axillary temp?
Variation throughout day?
Change throughout menstrual cycle?
0.5 C
Higher in evening
0.5 C higher latter half
7 causes of pyrexia?
Illness
Exercise
Heatstroke
Anterior hypothalamic lesion (neoplasm/surgery/ischamia)
Hyperthyroidism
Malignant Hyperpyrexia (anaesthesia)
Failure of heat-loss mechanism (e.g. dehydration)
3 methods of heat loss from body?
Conduction/evaporation from skin
Convection due to air movement (e.g. from lungs via convection of tidal air flow)
Radiation from naked skin
Heatstroke:
- above which temperature?
- 4 Potential complications?
41 C
Circulatory failure, cerebral oedema, hepatic failure, renal failure
Regulatory systems fail below which temp in hypothermia?
30 C (often fatal <32 C)
Symptoms of hypothermia?
What causes death?
Shivery
Bradycardia/Hypotension
Resp depression
Muscle stiffness
Metabolic abnormalities
Arrhythmias, esp VF
How anaesthesia affects temp?
Depresses hypothalamic function
Vasodilatation with increased heat loss
Lack of shivering
How circulatory shock affects temp?
Reduced tissue perfusion
Reduced cellular metabolism
Compensation:
Vasoconstriction piloerection, secretion of catecholamines
(exception is endotoxic (septic) shock - skin feels hot)
How spinal injuries affect temperature?
Thermoregulation lost below level of injury
- Cannot vasoconstrict/shiver
- Cannot sweat
Approximate fluid compartment volumes in 70kg man?
60% of weight
25L intracellular
19L extracellular:
- 3L plasma
- 15L interstitial fluid
- 1L transcellular (CSF, peritoneal, intraocular)
What is water diuresis?
Excess water ingested
ADH secretion suppressed, collecting ducts relatively impermeable, excrete more water without affecting solutes
What is osmotic diuresis?
More solute presented to tubule than can reabsorb (e.g. glucose in diabetes)
Water stays with the solutes
Or in diuretics which block rebasorption of NaCl in tubule
Approx water loss routes and volumes daily?
Evaporation (respiratory) 500ml
Skin (insensible) 400ml
Faeces 100ml
Urine (obligatory) 500ml
Total 1.5L
(in practice 1.5L urine daily from drinking water to maintain fluid balance)
Normal serum osmolality?
What regulates this?
Normal solute excretion daily in urine?
285-296 mosmol/L
Adjustments in ADH secretion and thirst-mediated water intake
600 mosmol
Relationship between osmolality, ADH release and thirst?
Thirst and ADH release determined by osmolality of plasma-perfusing nuclei in hypothalamus
Receptors indicating thirst have an osmotic threshold of 10mosmol higher than osmoreceptors in ADH release
Therefore, thirst not experience until ADH release has ensured water retention from kidneys
Apart from osmolality, 2 other mechanisms for thirst and ADH release?
Reduced arterial BP (signals via carotid and aortic baroreceptors)
Reduced central venous pressure (signals via ATRIAL low pressure receptors)
Increased angiotensin II in brain
All indicate reduced circulating blood volume
Sodium urine concentration in dehydration?
LOW despite hypernatraemia (retaining sodium to retain fluid)
Clinical manifestations of hypernatraemia?
Occur >160mmol/L
CNS depression, lethargy, coma
Max water excretion volume per hour in healthy adults?
750ml/hr
Causes of water intoxication?
-Renal failure with excessive fluid intake
-Cardiac failure
-Liver disease
-Hypoalbuminaemia
-ADH secreting tumours
-Excessive administration of 5% dextrose in post-op period when ADH secretion is high
Renal regulation of Na+?
- 99% filtered is reabsorbed (65% PCT, 25% LoH, 10% distal)
- Determined by GFR, RAAS and several prostaglandins
- Angiotensin II stimulates Na+ reabsorption throughout nephron and constricts arterioles
Extrarenal regulation of Na+?
- RAAS: angiotensin II releases aldosterone from zona glomerulosa which promotes Na+ reabsorption in distal tubule and collecting ducts, as well as colon epithelium, salivary ducts and sweat glands
- ANP released from atria in response to stretch. This increases excretion of Na+ by increasing GFR, inhibiting reabsorption in ducts and reducing RAAS
Causes of sodium excess leading to hypernatraemia?
- Excessive IV infusion (e.g. post-op)
- Conn’s (hyperaldosterone)
- Cushing’s
- Steroid therapy
- Chronic CCF
- Cirrhosis
Causes of water depletion leading to hypernatraemia?
- Reduced intake (coma/confusion)
- Renal (osmotic diuresis, diuretic phase acute renal failure, post-relief obstructive uropathy, diabetes insipidus)
- Fever, burns, diarrhoea, fistulae
Causes of Na+ deficiency?
- Low intake (coma/dysphagia/dextrose)
- GI loss (diarrhoea obstruction, fistulae, ileus)
- Excessive sweating (eg fever)
- Burns
- Drainage of ascites
- Addison’s disease
- Diuretics
- SIADH (meds, lung Ca, head injury etc)
What regulates K+ levels?
Aldosterone - increases excretion in distal tubule
Insulin - promotes K+ entry into cells
Acid-base - acidosis results in reduced K+ entry into cells and reduced urinary excretion (alkalosis opposite)
- Hydration - K+ lost from cells when dehydrated
- Catabolic states (trauma, surgery, infection) K+ lost from cells
Causes of hyperkalaemia?
- Excess administration
- Renal failure
- Haemolysis
- Crush injuries
- Tissue necrosis (burns, ischaemia)
- Metabolic acidosis
- Adrenal insufficiency (addison’s)
ECG changes hyperkalaemia?
Peaked T waves
Loss of P waves
Wide QRS complex
Hypokalaemia ECG changes?
Low, broad T waves
Presence of U waves
Causes of hypokalaemia?
Inadequate intake (dextrose/saline, coma, dysphagia)
Excessive loss:
- Renal (diuretucs, renal tubular disorders)
- GI (D&V, fistulae, laxatives, villous adenoma)
- Endocrine (Cushing’s, steroid, hyperaldosteronism prim and sec)
