Urinary Anatomy Flashcards
anuria
absence of urine formation
bacteriuria
bacteria in the urine
dysuria
painful urination
enuresis
involuntary discharge of urine (bedwetting)
glycosuria
glucose in the urine
hematuria
blood in the urine
incontinence
loss of control (urine or feces)
ketonuria
acetone bodies (ketones) in the body
micturition
the physical action involved in active urination
oliguria
urine output < 30 ml/hr or < 400 ml/day
polyuria
excessive urine output
proteinuria
protein, usually albumin, in the urine
pyuria
pus in the urine
urgency
a sudden, uncontrollable need to urinate
Kidney function
fluid and electrolyte balance, acid base balance, regulate arterial BP (RAAS), excrete waste products
acid base balance
HPO4 buffer system
NH3 buffer system
regulate arterial BP (RAAS)
renin, angiotensin 2, aldosterone
excrete waste products
urea, creatinine
kidney structure outer to inner
cortex -> medulla -> renal pelvis -> nephron
kidney cortex
outer layer, glomeruli and tubules
kidney medulla
middle layer, renal pyramids
kidney renal pelvis
inner layer, calyces
kidney nephron
functional unit. Filters (glomerulus), reabsorbs (tubule), secretes (tubule)
glomerulus
in the nephron
afferent arteriole
tuft (capillary structure)
efferent arteriole
tubule
in the nephron
Bowman capsule, proxial convoluted tubule, loop of henle, distal convoluted tubule
where is the collecting tubule?
in the nephron of the kidney
where is urine filtration?
glomerulus
where is urine reabsorption?
proximal tubule
where is urine secretion?
distal tubule
ureters
conveys urine from the pelvis of the kidneys to the bladder, scant smooth muscle, gently moves by peristalsis + gravity
bladder
detrusor muscle tone expels urine or stores it until it is time to void
urethra
conveys urine from the bladder to the outside of the body during voiding
Is the urinary tract sterile?
yes
why does scant mucus secretion occur in the bladder?
to prevent incidental bacterial colonization
neural control of the urinary system
external urinary sphincter is under voluntary control
increased activity of the sympathetic nervous system (adrenergic receptors) and causes the detrusor muscle to relax, bladder tone decreases and the internal urinary sphincter tightens (urinary retention occurs)
increased activity of the parasympathetic nervous system (cholinergic/muscarinic receptors), causes the detrusor muscle to contract, bladder tone increases, and the internal urinary sphincter relaxes (micturition can happen now)
general impact of diuretic therapy
reduces intravascular volume, reduces mechanical strain on the heart, reduces serum potassium levels (thiazides and loop diuretics only), augments renal function
Reduction of intravascular volume
lower BP, reduce interstitial fluid (dependent edema, cerebral edema)
reduction of mechanical strain on the heart
can help reduce cardiac workload in heart failure, can help prevent complications of heart failure
reduction of serum potassium levels
can be used therapeutically in hyperkalemia, needs to be watched as a critical side effect
augmenting of renal function
can’t fix true renal function, must be used under careful supervision in renal disease states
where do potassium sparing diuretics act in the kidneys?
on the terminal end of the distal convoluted tubule (DCT)
potassium sparing diuretics
weakest class of diuretics
inhibit the sodium-potassium pump (sodium stays in the tubule -> flushed out, potassium is reabsorbed from the tubule -> reclaimed, spironolactone inhibits aldosterone to achieve this effect)
sodium get flushed out and water follows (more urine volume is secreted/cleared)
where do thiazide diuretics act on the kidneys?
proximal end of the distal convoluted tubule (DCT)
Thiazide diuretics on urine formation
moderately aggressive diuretic class
blocks sodium channels in the DCT (sodium stays in the tubule -> flushed out),
sodium gets flushed out and water follows (more urine volume is secreted/cleared)
where do loop diuretics act on the kidney?
loop of henle
Loop diuretics on urine formation
strong, rapid effect -> significant increase in urine output
stops activity of the sodium-potassium-chloride transporter in the thick limb of the loop of henle (significantly increases tubule clearance of sodium, potassium, and chloride. increases clearance of trance calcium and magnesium)
lots of sodium gets flushed out + water follows (much more urine volume is secreted/cleared)
where does the CAI impact the kidneys?
proximal convoluted tubule (PCT)
Carbonic anhydrase inhibitors (CAI) on urine formation
mild diuretic
blocks the carbonic anhydrase; normally allows for bicarbonate to be reabsorbed
bicarbonate stays in the tubule -> sodium, bicarbonate, and chloride is flushed out
sodium and bicarbonate gets flushed out + water follows (more urine volume is secreted and cleared)
watch for acidosis - less bicarbonate to act as a buffer
osmotic diuretic impact on urine formation
carry water into the nephron, do not alter nephron physiology
depends on normal kidney function and nephron activity
many osmotic diuretics cross the basement membrane of the glomerulus (pulls water from tissues into vascular space)
more water is held in the tubule -> more water clears the nephron
RAAS
pathway activated by a decrease in BP, usually related to decreasing circulating volume (intravascular fluid)
RAAS start to finish
START - renin is secreted by the juxtaglomerular cells in the kidney, renin enzymatically converts angiotensinogen to angiotensin 1
angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzyme (ACE) in the lungs (angiotensin 2 is a vasoactive peptide -> directly causes vasoconstriction) (angiotensin 2 stimulates the adrenal cortex to secrete aldosterone)
aldosterone induces sodium resorption within the distal convoluted tubule (Where salt goes, water goes)
FINISH - when BP and intravascular fluid has sufficiently increased -> renin secretion is inhibited; RAAS ‘turns off’
electrolyte excess
hyperkalemia, hypernatremia, hyperphosphatemia
hyperkalemia
too much potassium
hypernatremia
too much sodium
hyperphosphatemia
too much phosphorus
fluid volume excess
increased circulatory volume (mechanical strain on the heart and blood vessels) and elevated BP (increased hydrostatic pressure)
waste accumulation
elevated levels of urea (neurotoxic effects, impairs the clotting cascade)
urinary lifespan considerations
older adults (>65 yrs) have more adiposity and a lower fluid mass ration (higher risk of dehydration and electrolyte derangement)
nephron function gradually decreases naturally with age (higher risk of kidney disease and elevated BP, decreased renal clearance of drugs)
how do diuretics work?
shifting sodium (salt) out of the nephron and water follows
what do thiazide and loop diuretics promote? What should you watch for?
potassium loss
hypokalemia
