W1 Urology and Nephrology Fundamentals (Joey) Flashcards
Inner lining of ureter is __________. This is important because it is often an area of __________. and __________.
Inner lining of ureter is transitional epithelium. This is important because it is often an area of bleeding and bladder cancer
Describe the circulation of blood flow in the kidney lobe
Renal artery → segmental artery → interlobar artery → arcuate artery → cortical radiate artery → afferent arteriole → glomerulus → efferent arteriole leaves the glomerulus → peritubular capillaries surround the nephron
→ venule → cortical radiate vein → arcuate vein → interlobar vein → renal vein
SAIC = segmental, interlobal, arcuate, cortical
Kidneys are located between the ________ vertebra, partially protected by ribs ________ and are considered ________ organs.
The ________ kidney is lower
They filter ________ litres of blood per day.
Approximately ________ litres are produced every day in a healthy adult
Water is reabsorbed in ________, ________ and ________ — NOT the ________
60-70% Ca++ is reabsorbed in the ________ and _______
Kidneys are located between the T12 and L3 vertebrae, partially protected by ribs 11 and 12 and are considered retroperitoneal organs.
The right kidney is lower
They filter 150 litres of blood per day.
Approximately 1-2L are produced every day in a healthy adult
Water is reabsorbed in PCT, descending limb of the loop of Henle and collecting ducts — NOT the ascending limb
60-70% Ca++ is reabsorbed in the PCT and collecting duct
Hyper-precision of Ca++ in the DCT, only 5-10% but the exchange is very high
Up to date: approximately two-thirds of the filtered calcium is reabsorbed in the PCT.
In the PCT ______, ______, ______, ______, ______, ______ and ______ are reabsorbed, whereas ______ , ______ and many ______ secreted (secreted = into the lumen of the tubule)
Aldosterone (salt retaining hormone, draws water in) acts on the ______ and the ______
Aldosterone promotes expression of ______.
In the PCT sodium, chloride, potassium, GLUCOSE, AA, urea and H2O are reabsorbed, whereas H+, creatinine and many drugs secreted (secreted = into the lumen of the tubule)
Aldosterone (salt retaining hormone, draws water in) acts on the late distal convoluted tubule and the collecting duct
Aldosterone promotes expression of Na/K+ symporter.
Na+ out of the nephron (reabsorption), water follows, K+ secreted into nephron (to then be excreted)
3 Na+ into the interstitial space and 2 K+ into the lumen
Go back through Loop of Henle:
Descending Limb: MAJOR site of _______ reabsorption
Ascending Limb: Reabsorption of _______, _______, _______
DCT:
Reabsorption of _______, _______, _______, ________, _______ and _______
Although 90% of _______ is reabsorbed in the PCT via the ______ mechanism
Secretion of _______ and _______ back into the tubule lumen
Note that Na+ reabsorption and K+ secretion is mediated in the DCT via a Na+/K+ exchange transporter
Loop of Henle:
Descending Limb: MAJOR site of H2O resorption
Ascending Limb: Reabsorption of sodium, chloride and potassium
DCT:
Reabsorption of sodium, chloride, potassium, calcium, magnesium and bicarb (HCO3-)
Although 90% of bicarb is reabsorbed in the PCT via the carbonic anhydrase mechanism
Secretion of H+ and potassium back into the tubule lumen
Note that Na+ reabsorption and K+ secretion is mediated in the DCT via a Na+/K+ exchange transporter
Collecting duct:
Reabsorption of ______, ______, ______, ______, and very little ______
Reabsorption of ______ is also very important and is the second site of urine ______
Collecting Duct:
Reabsorption of sodium, chloride, H20, Urea, and very little Ca++
Note that in addition to the H2O reabsorption in the descending loop of henle, H2O reabsorption here is also extremely important and the secondary major site of urine solute concentration
What is Anuria?
What is it NOT?
Failure of the kidneys to produce urine
— Note that this is not the same as a person not being able to urinate (failure to eliminate urine from the bladder, also known as urinary retention). True anuria is a failed process more upstream at the level of the kidneys, and can be thought of as failure of the kidneys themselves at producing any volume of urine throughout the renal filtration process
— May occur in severe / complete renal failure
— If you catheterize a patient and you get return of urine, this patient is not anuric (may be oliguric vs urinary retention)
What is Oliguria?
True (cc per hour and 24hr)
and rough definition
True definition:
urinary formation / output of
< 400 cc / 24 hours
or < 20 cc / hr
normal is ~1.5L
Normal elimination = 1-2L of urine per day
—More rough definition: decreased urogenesis / output compared to what should be expected based on their expected volume status and renal perfusion
—May be a sign of hypovolemia, poor renal perfusion, severe renal failure, or early sign of complete renal failure
Urinary retention is?
Inability to empty bladder when attempting to void (either not voiding at all, or only partially emptying bladder)
Bladder scan or straight cath to see if urinary retention or anuria
—-Urinary retention may be acute (typically presents as inability to void at all) or chronic (typically presents as ability to void, but having incomplete bladder emptying) - more on these later
Average healthy adult eliminates how much?
The average “healthy” adult eliminates about 1-2 L of urine per day (when taking in the approximate average recommended adult PO fluid intake of 2 - 2.5 L / day)
When the amount of urine that is produced in a day on average does not get eliminated in a day is when urinary retention or “incomplete bladder emptying” picture should be on your mind (as in examples: underactive bladder, or an obstructive uropathy (like BPH, a hypertonic pelvic floor, or another cause of bladder outlet / UT obstruction)
ADH, aka _______ is a hormone produced by the _______, though stored & released by _______, in response to _______ / _______, as well as hyperosmotic states (most commonly _______)
ADHʼs physiologic function is to promote expression of _______ in the _______ & _______, which leads to diffusion mediated _______ from the collecting duct lumen back into the vasculature, thereby > _______ and < _______
ADH has a second mechanism which is to promote ______ which helps to increase BP
______ is the only other major hormone to be released from the posterior pituitary gland
Anti-diuretic Hormone (ADH), aka Vasopressin is a hormone produced by the hypothalamus, though stored & released by posterior pituitary gland, in response to low plasma volume / hypotension, as well as hyperosmotic states (most commonly hypernatremia)
ADHʼs physiologic function is to promote expression of aquaporin channels in the DCT & Collecting Duct, which leads to diffusion mediated reabsorption of H2O from the collecting duct lumen back into the vasculature, thereby > intravascular pressure and < serum osmolarity & osmolality
ADH has a second mechanism which is to promote vasoconstriction which helps to increase BP
Oxytocin is the only other major hormone to be released from the posterior pituitary gland
RAAS system — walk through the steps
— Drop in blood pressure
— Liver releases angiotensinogen
— Kidneys release renin which
— Converts angiotensinogen to angiotensin I
— Lungs release ACE which converts angiotensin I to angiotensin II
— angiotensin II goes wild:
1. Acts on the adrenal glands to release aldosterone
—Aldosterone promotes expression of Na+ / K+ pump in the collecting duct in the kidneys : sodium absorbed, water follows
2. Acts on the blood vessels stimulating vasoconstriction
3. Acts on posterior pituitary gland to stimulate ADH secretion which leads to H20 reabsorption
4. Increases SNS activity
What do these anti-HTN medications do?
ACEI
ARBs
Aldosterone receptor antagonists
ACEIs (~prils)
—Inhibit pulmonary ACE, leading to decrease formation of angiotensin II and further downstream effects….
Angiotensin Receptor Blockers (“-sartans):
—Directly block the angiotensin II receptor, preventing release of aldosterone from adrenal cortex
—They also block AT2 receptors on the systemic vasculature, preventing vasoconstriction
Aldosterone receptor antagonists (spironolactone)
—prevents expression of Na+/K+ transporter (that normally draws in Na+ and secretes K+ into the tubule)
—this can lead to hyperkalemia
Loop diuretics:
—Block the ______ on the _______ symporter in the ______, inhibiting reabsorption of all, promoting ______ excretion
—Which one do you need to know?
What about thiazide diuretics:
—Block the “thiazide mediated” ______, preventing ______ and ______ reabsorption, promoting ______ excretion
Which electrolyte do they spare?
Loop Diuretics (“-semides” * -”amides”)
—Block the chloride binding sites on the Na+/K+/2Cl- symporter in the ascending LOH, inhibiting reabsorption of all, promoting H2O excretion
⭐️ KNOW LASIX (Furosamide)
Thiazide Diuretics (HCTZ, Chlorthalidone)
—Block the “thiazide mediated” Na+/Cl- symporter, preventing Na+ and Cl- reabsorption, promoting H2O excretion
—“Calcium Sparing Diuretics” (can be both helpful & harmful d/o situation)
Aldosterone receptor blockers block the expression of ______ in the ______
Commonly associated with ______
ADH secretion blockers cause a decrease in expression of ______
Aldosterone Receptor Blockers:
—Directly blocks the Aldosterone receptor whose agonism by Aldosterone normally promotes expression of the collecting duct Na+/K+ transporter), leading to increased Na+ loss, K+ retention, and increased H2O excretion
—Commonly a/w HyperKalemia
ADH Secretion Inhibitors:
—Just a note that EtOH, can prevent ADH release from the posterior pituitary, leading to < aquaporin surface channel expression, leading to decreased H2O reabsorption
Fish bone electrolyte diagram, know the values roughly
BMP: main electrolytes?
Which is reflective of bicarb?
BUN:
—produced where?
—From which metabolic process?
—elevated levels could indicate?
Creatinine
—product of?
—levels go up when?
Glucose
—increase or decrease could mean?
What do you add on to get a “Chem 8” ?
What about a chem 10?
Na: 135 - 145
K+ : 3.5 - 5
Cl: 95 - 105
CO2 is reflective of bicarb: 22 - 38
Creatinine: 0.5-1.2:
—renal function.
—Best friend regarding kidney injury.
—Byproduct of muscle breakdown.
—Usually cleared by kidneys.
—Either not producing enough urine or not getting enough blood flow = Creatinine will go UP
BUN: 7-18
—“blood urea nitrogen”
— produced by liver in the Urea cycle.
— Elevated in GI bleeds, hemolysis, dehydration, HF, KF
Glucose: 70-110
—too much = diabetes/pre diabetes
—too little = hypoglycaemia
Chem 8 includes Ca++
Chem 10 includes Mg++ and Phos
AKI
What is it defined as?
What are the criteria?
Which metabolite level are you watching?
What are the 3 criteria that defines AKI?
AKI:
—Acute/short term
—Can be on top of chronic kidney disease
—term used when speaking to the impairment of the renal functions of filtration, urogeneis, ion balance, acid/base function, etc
Normal creatinine is 0.5-1 (basically <1 to keep it simple, is normal
AKI is defined as (meeting at least 1 of the following criteria):
○ 1. Increase in sCr by >0.3 mg/dl within 48 hours
○ 2. Increase in sCr to ≥1.5x b/l sCr over course of 1 wk
○ 3. Urine volume <0.5 ml/kg/hr for duration of >6 hrs
0.3 - 48 - 1.5 - 1 - 0.5 - 6
clinically however the definition is more loose
Chronic Kidney Disease defined as?
Over what period of time?
What common condition can arise from CKD?
—CKD is defined more loosely than AKI and represents a broader spectrum of renal dysfnx & chronic sequelae
—CKD is the same criteria as AKI but over weeks to months to years (rather than AKI which is more days to week(s)
—CKD → decrease in EPO → not making enough RBCs → can become anemic
Micturition
Bladder sends signal to where in the spinal cord?
time to void:
Which muscle contracts? Which NT sand receptor ?
What do the sphincters do? Under which control?
—collecting a volume of urine that eventually leads to both a chemical & physical stretch receptor response
— bladder sends signals to afferent neurons of the spinal cord S2, S3 and S4 and brain (pontine micturition center)
—brain processes and sends a response via efferent pathways to the detrusor muscle and pelvic floor muscles signalling them that it is soon time to void
—when both the autonomic and somatic nervous systems agree that itʼs
time to void:
a. The detrusor muscle (autonomic, PNS ACh on M3 receptor in bladder) contracts
b. The internal urethral sphincter (autonomically mediated) relaxes
c. The external urethral sphincter (skeletal muscle - somatically mediated) relaxes
think M3, M=micturate
Which part of the brain is sending a signal to the pontine micturition center (PMC) to hold off voiding until the time is right?
—SNS efferent output from T10 - L2 to the ______ muscle via ______ (NT) agonism of ______ receptors (superior & posterior aspects of the bladder wall) which promotes detrusor ______
—Also SNS norepi agonism of ______ receptors → ______ of the ______ urethral sphincter
—when the cortex decides it’s okay to void, it ______ the inhibitory influences on the PMC leading to ______ detrusor ______
—the cortex of the brain provides an inhibitory signal to the PMC telling it to hold off until itʼs safe / time is right
—SNS efferent output from T10 - L2 to the detrusor muscle via norepi agonism of β-3 receptors (superior & posterior aspects of the bladder wall) which promotes detrusor relaxation
—Also SNS norepi agonism of 𝝰-1(a) receptors → contraction of the internal urethral sphincter
—when the cortex decides it’s okay to void, it **withholds the inhibitory influences on the PMC leading to increased detrusor contraction
Understand the terminology
Note the difference between frequency and polyuria: polyuria is an objective sign captured by measuring urine output. Frequency is pt reported feeling of going more often
Note stranguria:
weak stream w/ discomfort or tightness
Incomplete emptying: objective
PVR = post void residual
Urinary retention
Acute vs chronic
How many mls for each
What potential sequela you get with chronic that you probably won’t see w/ acute?
Chronic:
—usually not very symptomatic, or progressively symptomatic
—able to void
—partial/intermittent obstruction
—no pain
— >800ml
— + hydronephrosis (excess fluid in a kidney due to a backup of urine.)
Acute:
—suddenly and highly symptomatic
—a/w pain
—drainage volume < 800ml
—cannot void
—complete obstruction
— +/- hydronephrosis if acute on chronic urinary retention
Hydronephrosis
What is it?
Dilation of the kidney 2/2 dilation of the ______.
Occurs from some sort of ________ process
Water on the kidney
Dilation of the kidney 2/2 dilation of renal pelvis.
Occurs from some sort of obstructive process
Can get uni/bilateral depending on where the obstruction is
When to use a catheter: Foley 3
Acute urinary retention
Peri/post operative
Need to collect a urinary sample and pt is unable to provide
External catheters for?
Ureteral stents?
PCNs?
external catheters
—chronically incontinent
—concern for indwelling foley a/w infectious risk
—skin irritation is a draw back
ureteral stents
—placed to help the draining of urine from the upper tracts to the bladder
percutaneous nephrostomy tubes
—external
—need to divert urine away from kidney urgently and concerned patient can’t void when urine reaches the bladder
