urinary Flashcards
what is the main function of aldosterone?
- reabsorption of sodium and water
- excretion of potassium
- this increase blood volume
6y/o has facial and limb oedema. on admission she weighs 30kg and is discharged at 28.5kg. how much fluid has she lost, assuming the difference in weight is due to fluid?
1500mL
54y/o with syncopal episode. sweating profusely in the heat and not had anything to eat or drink in the last 7 hrs. BP= 102/88. plasma sodium high, plasma potassium fine, plasma glucose fine. what is the cause of syncope?
hypovolaemia
- hypernatriaemia is due to increased loss of hypo-osmotic fluid in sweat and failure of water balance.
- contracture of circulating volume lead to syncope
55y/o with hypertension. BP = 140/90 so prescribed with a thiazide diuretic. three days later has muscle cramps, BP of 135/78 and a low potassium level. what has contributed to the loss of serum potassium
- Inhibition of Na+/ Cl- symporter in the DCT
- this diuretic inhibits this symporter allowing increased delivery of sodium to CD causing increased NA uptake from lumen by apical epithelial Na channels (ENaCs)
- causes basolateral NA/K exchanger to more actively exchange NA for K, which is then passively seceded into the lumen through apical channels, resulting in K loss.
what is an action of ADH?
vasoconstriction
- activation of V1 receptor on VSM to cause vasoconstriction triggering the thirst response in the hypothalamus
how would you define the cause of dipsogenic diabetes insipidus (psychogenic polydipsia)?
defect/ damage to the hypothalamus causing malfunction of the thirst mechanism
loss of which renal function is most likely to be identified by lab measurements of the urine specific gravity following water deprivation?
concentration
which hormones are stored in the post pituitary gland?
oxytocin and ADH
28 y/o presents with diabetes inspidius 10 days after basilar skull fracture. haematoma in the post lobe of the pituitary gland but no lesions in the hypothalamus or pituitary stalk. release of which hormone has been affected?
ADH
diagnosed with hyponatraemia due to SIADH. what physiological response is the primary cause of hyponatraemia in this patient?
excess water reabsorption in the collecting duct
70y/o works in the heat for 12 hrs. loss of 1.5kg body weight and plasma sodium is within normal range. urine osmolality max conc at 1800 mosmol/kg. stimulation of what physiological response will best help to restore his extracellular volume?
thirst
- ADH already at max conc of urine
68y/o with orthostatic hypotension . in this patient on standing what acute compensatory mechanism will occur in the nephron?
- increase in glomerular filtration rate of the same nephron
- on standing, BP falls this reduces the pressure to the afferent arterioles and it will relax- allow more blood to glomerulus
- cells of the macula densa sensitive to conc of NaCl in the late thick ascending limb. decrease in conc causes signals to:
- decrease resistance to blood flow in afferent arterials via vasodilation- increases golumerular capillary hydrostatic pressure and helps return GFR
- increases renin release from Juxtaglomerular cells of the afferent and efferent arterioles
- therefore decrease in NaCl= vasodilation of afferent arterioles, increased paracrine stimulation of JGCs.
what is the effect of aldosterone on BP, where is it produced and where does it act?
- aldosterone increases salt reabsorption therefore increases BP
- is a steroid hormone
- acts at the distal tubule and CD
- synthesised in the adrenal glands
- major site is at the distal nephron (DCT)
sample of fluid from a nephron obtained- very low sodium, very low potassium, no glucose and a low osmolality. what features of the tubule that the fluid has most recently passed through has resulted with this?
permeable to ions but impermeable to water
- fluid is hypo osmotic to plasma
- this has occurred while moving through the ascending loop of Henle
55 y/o with hypertension. what adaptations in the kidney will have occurred in response to change in BP?
decreased release of renin
goes for a swim and needs to urinate. what actual effect is being mimicked by the increased pressure on her peripheral circulation due to being immersed in water?
effective circulating fluid volume increased
- increased external pressure of periphery tricks the body sensors into perceiving an increase in BP
28y/o feeling light headed and dizzy. BP = 90/50 mmHg. what chemical messenger will her juxtagolmerular cells release in an attempt to compensate for her hypotension?
Renin
Granular cells of the JGA secrete renin in response to 3 stimuli:
1. decrease in arterial BP as detected by baroreceptors
2. decrease in NaCl levels in the ultra filtrate of the nephron- flow measured by the macula densa of JGA
3. sympathetic nervous system activity - b1 adrenergic receptors
what class of hormone is aldosterone?
steroid hormone
- derived from cholesterol
30y/o feeling light headed and nauseated for the last 2 days. BP= 90/50
what is the most appropriate physiological response by her macula densa cells?
stimulate JG cells to secrete renin
35y/o has urinary incontinence. activation of which nerves will cause detrusor contraction?
parasympathetic neurones from the spinal cord to the urinary bladder
decreased AP along which pathway will lead to relaxation of the external urethral spinchter?
somatic motor neurones
- EUS is under conscious control