CM Renal Flashcards
what is the total body sodium?
why is this an approximation?
amount of sodium measure in the ECF, it is a approximation because although most of the Na is in ECF, some is still in the ICF, and the total body sodium doesn’t account for this
what are the 3 mechanisms that are used to regulate Na in the body?
- renin-angiotensin-aldosterone system: receptors in juxtaglomerular cells of the kidney sense renal perfusion and respond by releasing renin leading to angiotensin II production and aldosterone which causes Na/H2o reabsorption at the kidneys
2. volume receptors: in atria and great veins sensitive to small changes in venous and arterial pressure, if the volume gets too high they secrete atrial natriuretic factor that promotes Na secretion
3. pressure receptors: in the aorta and carotid sinus, pressure drop it activates these to activate the sympathetic nervous system and leads to renal retention of sodium
what happens to the excretion of Na in these senarios:
- if ECFV increases?
- if ECFV decreases?
if ECFV increases: activation of mechanism to increase Na excretion
if ECFV decreases: activation of mechanism to decrease Na excretion
volume overload
what is it caused by and what is the main influencer? what are four things you might find on PE?
what are two conditions this is common with?
increase in total body f_luid/Na, mostly controlled by sodium_ TOO MUCH SODIUM
PE: increase weight, edema, ascites, pulmonary edema
often seen with HF, cirrohsis
volume depletion
what is this caused by and what is the main thing that influences this? what are 6 things you can find one PE? what are 3 main causes of this?
H2o/Na lost, TOO LITTLE SODIUM so fluid follows
PE: weight loss, tachycardia, postural hypotension, thirst from stimulation of ADH, dry membranes, decreased skin tugor
causes: vomiting/diarrhea, sweating
dehydration
what is this and waht does it cause?
volume depletion with disproportionate free water deficit, can lead to increase Na osmolarity
what is the most common cause of dehydration worldwide?
diarreah
osmolarity
what is this determined by?
what are the three main contributors and how does each one influence osmolarity?
determined by the total solute concentration in a fluid compartment
three maine solutes considered in renal:
Na: increased ADH and thirst
glucose: severely elvated in uncontolled diabetes mellitus causes increase in hyperonicity of serum and so causes fluid to leave the cells into intravascular
urea: doesn’t move water, but contributes to TOTAL osmolarity of the blood
what is the equation for OSMOLARITY?
what is the biggest influencing component of this equation?
what does it tell you?
osmolarity= 2 [Na] + [glucose]/18 + [BUN]/2.8
sodium concencentration is the major contributor in this equation so most accurately reflect the serum osmolarity
abnormalities in the Na levels tell us there are abnormalities in the regulation of the amount of water in the ECF
tonicity
what is this a measure of? what does it cause?
if this increases what does it most likely reflect an increase in? why?
ability of the combined effect of all the solutes to generate an osmotic driving force that causes water movement from one compartment to another “aka a concentration gradient”
if tonicity increases it means that the concentration of Na has increased, because this is one of the main driving factors for this concentration gradient
why does a hyptonic/hypertonic solution important when talking about brain cells?
rapid increase in ECFV (hypotonic): causes brain cells to swell
rapid decrease in ECFV (hypertonic): causes brain cells to shrink
**this is really important because these cells are influenced heavily by ECF and are the first to be effected so neurological changes are what you are concerned with here!**
increased serum tonicity
what happens to Na?
What happens to H20 excretion?
urine?
hypertonic solution
increased Na
decreased H20 excretion
urine becomes relatively concentrated (since the water is being sucked out!)
decreased serum tonicity
what happens to Na?
What happens to H20 excretion?
urine?
hypotonic blood
has decreased Na
increase H20 excretion
urine is relatively dilute (since more water is being excreted)
the process of adjusting the tonicity/osmolarity (concentrating/diluting) of the serum is dependent on which four things?
- adequate eGFR
- filtrate delivery to the concentrating and diluting segments of the loop of henle and distal nephron
- appropriate turning on/off of ADH
- ADH responsiveness to the kidney
glomerular filtration rate (GFR)
what does this represent?
what percent to kidneys start having issues doing both?
if low what does this lead to?
what is it effected by?
represents the ability of the kidneys to concentrate and dilute the urine
20% is where kidney start to have issues with BOTH adequate concentration and dilution
if low, leads to azotemia
affected by age, sex, weight, fluid status
explains what happens in the renal concentrating (refers to what happens in the urine) mechanism? what allows this to happen?
occurs when water needs to be reabsorbed
- 20-30% of Na is reabsorbed in the ascending limb of the loop of henle creating a hypertonic medullary interstitium and concentration gradient that is necessary to concentrate the urine
- the hypertonic medullary interstitium allows for water to be pulled out from the descending limb of henle and the the collecting tubule
- as water is pulled out, esp from the collecting tubule, the filtrate becomes more concentrated
renal diluting (urine) mechanism
what causes this to occur?
ascending loop of henle and distal convoluted tubule transport Na from the tubule to the lumen to the blood
net result is more dilute urine because you are taking the Na out of it
creatinine
what is creatinine? is this a good test?
what are the levels you should know?
when does this go up quickly?
.06-1.2
breakdown of muscle energy metabolism
good indicator of glomerular filtration
better test than bun
if greater than 40 indicates prerenal axotemia
if less than 20 indicates intrinsic renal failure
**creatinine goes up quickly in acutre renal failure due to ischemia and radiocontrast**
blood urea nitrogen (BUN)
what is this a product of?
why isn’t this as good of a test as creatinine?
8-20
end product of protein metbolism
some gets reabsorbed after being filtered so not such a great test as creatinine
explain the relationship between creatinine and BUN?
BUN and creatinine both measure kidney function because they are a measure of the f_iltration at the glomerulus_
these are both blood tests! so if these increase it means that they aren’t being filtered by the kidneys and something is wrong
creatinine is the better measure of this because it isn’t reabsorbed after being filtered
what is the most common symptoms you see with electrolyte imbalances?
neuromuscular
if you have a pt with neuromuscular symptoms, what should you always check?
electrolytes!!
what are four things you must include as part of your clinical evaluation if suspecting electrolyte imbalances?
EVALUATE:
- neurological status
- volume status
- metabolic/renal status
- osmolarity
hyponatremia
what is this defined by?
what are two things you need to access?
what volemias can this occur with?
what is the most common cause of this?
definition: Na less than 130
volune status and osmolarity essential for clarification
can be hypo, hyper, euvolemic hyponatremia
**most often results from H20 imbalance (from increase ADH secretion) not Na imblanace AKA, you increase water so the Na looks more**
ADH/vasopressin
what does this do? where does it alter permeability?
when is it released (3)? what does it decrease?
how does it effect the urine?
regulates the body’s retention of water by increasing water reabsorption in the kidney collecting ducts
increases the permeability of the renal collecting tubule and allows water to freely move down its concentration gradient into the hypertonic medullary interstitium
released in response to:
- decrease in blood volume
- decrease in BP
- increase in ECF osmolarity
this increases water reabsorption and a decrease in the tonicity of ECFV
concentrates the urine since all the water has been pulled out
what are the two main drivers of ADH/vasopressin release?
explain what happens in each
- osmolarity
a. if small increase in osmolarity of the EVFC (# of particles in serum)-ADH secreted to decrease osmolarity and Na (increasing the reabsorption of water a little bit)
b. similarly if you have too much water in the blood and a decrease in osmolarity, then ADH will stop secreting, get a brief diuresis and will return osmolarity to normal
2. intravascular pressure
if large decrease in intravasular volume (5-10%) with decrease in BP also results in ADH release mediated by baro-receptors in circulation and free H2o is retained leading to hypoNa because there is an rapid increase in the proportion of water to Na
****this OVERIDES osmolarity since maintaining BP and profusion is the most important!!!****
explain how loops and thiazides work?
what do each excrete?
where do they work?
what happens to ECF?
are they contracindicated in anyone?
Both block Na reabsorption, resulting in sodium loss from the body, since fluid follows sodium, you also get a decrease in the ECFV
LOOPS:
- greater loss of BOTH Na and H20 than Thiazides
- block Na in the ascending loop of Henle where 20-30% of Na is reabsorbed
3 cause proportional loss of Na/H20 so ECF is left undisturbed
THIAZIDES:
- block Na in the distal convoluted tubule where 5-10% of Na is reabsorbed
- more Na is excreted than H20
- since more H20 left in the ECF, this means there is a increased H20 to Na ratio and can lead to hyponateremia (by dilution)
**this is why thiazides are contraindicated in people with hyponateremia**
suggestions for clinical evaluation:
if abnormal volemia:
if abnormal Na concentration:
**where do you look for the problem?**
if abnormal volemia: look for issues with the Na
if abnormal Na concentration: look for issues with failed water control mechanisms
***Take away: identify the abnormality and then look for the reason in the opposit branch…this is likely where you will find it***
hypertonic saline injection
what does this do?
increases sodium concentration in the blood, causes water to leave from the cells into the intravasculature to dilute the increased sodium load and prevent hypernatremia
hypotonic saline injection
what does this cause?
dilutes the intravasculature, so it moves out and into the cells causing the cells to swell and prevents hyponatermia in the blood
isotonic saline injection
what does this cause?
same concentration as the cells so it doesn’t cause a fluid shift and the intravascular volume will simply increase, typically use this type
what is important to consider when selecting an IV solution?
if you choose the wrong one what is the worst case senario that this can cause?
Because if they are corrected to rapidly with IV fluids the brain does not have time to re-equilibrate this is known as osmotic demyelination syndrome where there are dramatic fluid shifts that take place between the cells in the brain and the surrounding fluid***
how are volemias accessed?
ON PHYSICAL EXAM BY LOOKING AT THE PATIENT!!!
**this explains why euvolemic patients, despite the movement of fluid, aren’t hypovolemic or hypervolemic because it must be enough that you can SEE it on physical exam….slightly misleading**
hypervolemia
what is this caused by?
what are 2 senarios that cause this in relationship to Na?
secondary to fluid overload
- IV solution generated hypernatremia
- internally generated hyponatremia from CHF, cirrohosis, or nephrotic syndrome
“giving the patient too much Na because it causes the H20 to come back and increase volume or a condition that causes there to be too much fluid in the patient from failed organs”
hypovolemia
what are the PE of a patient with this?
what are the two general categories of causes?
1
4
how do you distinguish between these two causes?
dry mucous membranes, tenting
can be either renal or extra renal cauess
renal causes: diuretics
extra-renal causes: diarreah, sweating, blood loss, fluid shifts
****distinguish between these two via urine [Na] test, if urine Na is low then it means the kidneys are functioning properally and the loss is from someplace else, if it is high it means that the kidneys arent functioning properally****
euvolemic
what are two things that contribute to this?
what causes hyperNa (3)?
what causes hypoNa (2)?
what do you need to remember with euvolemic?
aberrancies in ADH or changes in water consumption
hyperNa: diabetes insipidus, central diabetes (decrease ADH secretion), nephrogenic (decrease response to ADH)
hypoNa: increased ADH secretion (SIADH), polydipsia
***keep in mind the volumes are actually changing, however not enough for you to be able to pick it up objectively on PHYSICAL EXAM****
hypovolemic hypotonic hyponatremia
what do you loose in this?
what is the mechanism that causes a increase in ADH?
what are the two branches of causes?
2
2
what do you use to determine the cause and the values?
what are the two tx options and who are they appropriate for?
Loss of water AND Na, but more Na loss than water
“decreased Na with decreased ECF”
ADH SECRETION INCREASED TO MAINTAIN INTRAVASCULAR VOLUME WHICH OVERIDES THE NEED TO MAINTAIN OSMOLARITY
must determine if:
1. renal: diuretics/salt wasting
2. non-renal: GI loss vomiting, diarrhea
**determine this based on urine!!**
less than 10= Na retention of kidneys working, so NOT KIDNEYS
greater than 20= renal Na wasting, so KIDNEYS
Tx:
- Isotonic fluids IV (normal saline .9% or ringers lactate) +KCL(it will stay in the intravascular space to maintain BP and shut off ADH secretion via intravascular pressure)
- electrolyte drink “gatorade” +KCL (if mild and oral intake intact)
hypervolemic hypotonic hyponatremia
explain what happens in this and what it is associated with for conditions (3)? what makes this worse? is this difficult to treat? why? what are the 3 tx options?
hyponatremia caused by INCREASE IN EXTRACELLULAR FLUID
“body basically tricked into thinking it need more volume since the kidneys aren’t being profused, so it activates RAAs and ADH which makes the problem worse”
Edema related conditions: CHF, cirrhosis, nephrotic syndrome
total body Na/H2O are increased but circulating blood volume is sensed as inadequate by baroreceptors because of decreased CO and decreased BP decreased renal perfusion leads to increased ADH and activation of RAA system
TX: difficult since associated with organ failure
1. water restriction
2. treat underlying condition
- diuretics
explain how
HF
cirrhosis
nephrotic syndrome
cause
hypervolemic hypotonic hyponatremia
***whats something you would see in the urine***
HF: less forward flow so causes a decrease in BP and intravascular pressure
cirrhosis: blood pools in the blood mesenteric
nephrotic syndrome: stenosis so less profusion
urine: less Na in the urine since all of it is being absorbed
euvolemic hyptonic hyponatremia
why is this euvolemic?
what 2 things do yo uneed to dx?
what are the 3 requirements?
what are 7 causes of this?
decreased Na with slight changes in volume that can’t be detected on PE
NEED URINE Na AND OSMOALITY TO DX
1. hyponatremia
2. decreased serum osmoality less than 280
3. high urine osmoality greater than 150
**peeing it out when it should be absorbed**
- syndrome of inappropriate ADH (SIADH)
- post-op hyponatremia
- psychogenic polydipsia
- stroke
- tumors
- pulmonary lesions (TB, lung abcess)
- SSRIs
syndrome of inappropriate ADH (SIADH)
what is this and when does it happen?
what happens to the urine?
what is the urine concentration of Na?
what two tests are low?
tx if symptomatic (1) or asymptomatica (2)?
if ADH secretion is occurring to a point of creating hyponatremia (absorbing too much) then it is clearing being inappropriately over secreted
absence of cardiac, liver, renal, adrenal or thyroid disease
urine becomes extremely concentrated since the over secretion of ADH causes the water to be reabsorbed in the collecting duct
urine Na>20 since water being absorbed and urine is concentrated
serum BUN and UA are low since increased clearance
TX:
symptomatic with Na <120
MEDICAL EMERGENCY
1. hypertonic saline (has a lot of Na), monitor Na every 2 hours, no MUST DO SLOWLY <10-12 a day
- if asymptomatic:
H20 restriction
demeclocycline/tolvaptan(clock ADH receptors so you stop getting water)
post-op hyponatremia
what is this caused by?
what makes this situation worse?
what is the tx? (2)
post-up pain increases ADH secretion (dilutes Na)
to make it worse: if patient receives inappropriate administration of hypotonic fluids, results can be severe symptomatic hyponatremia (N, HA, seizures, etc)
tx:
pain control with administration of isotonic fluids until patient can take adequate fluids orally
psychogenic polydipsia causing euvolemic hyponatremia
what is is this caused by?
how do they maintain euvolemic?
ADH levels, urine osmolarity?
Na in urine?
drink excessive amounts of water because of psych >10 L/d
despite drinking excess amounts of fluids, they just pee out the excess because their kidneys work
becomes a problem if they take SSRIs that block te water excretion
ADH levels low, urine osmolarity low(dilute from peeing so much)
urine Na >20
how do you determine between increase urination from diabetes insipidus and psychogenic polydipsia?
both have increased urinary frequency
******NEED TO CHECK THE SERUM Na CONCENTRATION***
polydipsia: leads to INCREASE in plasma volume leads to HYPONATREMIA, however since peeing function works still peeing off the volume
diabetes insipidus: leads to DECREASED intravascular volume and thus INCREASED serum sodium levels HYPERNATEREMIA
hypertonic hyponatremia
what 4 things can cause this?
what is this and how does it relate to the osmolarity equation?
why is this unlike the other types of hyponatremia?
osmarlity in the serum is dependent on Na, glucose and urea based on the osmolarity equation= 2x[Na] +[glucose]/18+ [urea]/2.8, under NORMAL circumstances the Na plays the biggest role in determining osmolarity
EXCEPTION: an increase in GLUCOSE (think diabetics), lipids, proteins or urea could raise the serum osmolality pulling water into the intravascular space to re-equilibrate things
although Na doesn’t change in these situations, because of the increase of other particles, as the water moves into the space it
****This is an exception because****
hyponatremia is caused by a osmolarity INCREASE (others caused by decrease)
hypertonic hyponatremia caused by diabetic circumstances
what causes this?
how does this cause hyponatremia?
what blood sugar do you worry about this?
what is the Tx for this?
the rapid increase in glucose causes the osmolarity in the blood to increase according to the osmolarity increase
acute rise inf BS increases osmolarity water is drawn from cells into extracellular space resulting in dilution of Na and hyponatremia
glucose above 200 Na
levels start to fall
TX:
insulin infusion and volume expansion
hyponatremia and HIV/AIDS
what percent of hospitalized with AIDS have hypoNa?
what is this often seen with?
50% of pts hospitalized with AIDS have hypoNa
often comes from CNS/pulmonary involvment seen with HIV infections
hypernatremia
what is a common demoninator in nearly all of these cases?
what is the serum Na level associated with this?
who does this often occur in?
why can they be confused or lethargic?
generally doesn’t develop in an alert person since they have intact thirst mechanism and access to water, inadequate intake of water is therefore a common denominator in nearly all cases of hyperNa
serum sodium greater than 145
often occurs in elderly since they have diminished sensitivity to thirst as older, esp in setting of pulmonary or UTI
as water is lost, Na concentration increases so water shifts out of the brain cells to establish osmotic equilibrium and brain cells shrink, pt can become lethargic or even comatosed
hypernatremia:
explain the two main branches of this?
1.
hallmark
why don’t this work?
3 main causes?
2.
what does it decrease?
4 causes?
what can’t person do?
hypernatremia
renal cause with dilute urine
hallmark: polyuria with greater than 3L in 24 hours
inability of kidneys to conserve water appropriately
- diabetes insipidus
- central diabetes insipidus
- nephrogenic diabetes insipidus
hypernatremia with extrarenal cause concentrated urine
MOST COMMON and get decrease ECFV
causes: fever, profuse sweating, diarrheah, hyperventialation
greater deficiency in water increases the concentration of the sodium and the person can’t appropriately replace water loss
hypernatremia with concentrated urine
(hypovolemic)
what is the typical presentation of a pt with this?
why can’t the pt fix this?
what are two signs?
what is the urine osm? ADH?
how do you tx and over how long?
why do you need to be cautious?
“stranded in dessert/lost at sea”
unusual with intact thirst mechanism and access to H20, but in this case no H2o intake possible, even with increased ADH levels
signs: orthostatic hypotension, dehydration comes from excessive sweating, GI, and respiratory tract without a way to replenish
lab: greater than 400 urine osm with intact renal function, ADH levels increased
TX:
- replace water and electrolytes over 48-72 hours
- .9% saline followed by .45% saline
***replace water slowly to prevent cerebral edema since brain has been adapted to hyperosmolality, theyve gotten used to being shrunk so don’t want to give them too much water too quickly because they will swell quickly***
hypernatremia with dilute urine (euvolemic)
what is the hallmark of this?
what happens in this?
what 3 conditions is this seen in?
what is the Uosm?
2 tx options?
hallmark: greater 3L urine in 24 hours
inability of kidneys to conserve water appropriately so you urinate more than you should witout uptaking enough to equal out the hyperNa
seen in:
- central diabetes insipidus
- nephrogenic diabetes insipidis
- congenital nephrogenic insipidis
decreased osmolarity less than 250 uosm
Tx:
- D5W-replace H20 without Na
- .45% saline- for hyperNa and hyperglycemia
hypernatremia with dilute urine
central diabetes insipidus
what causes this?
why does hyperNa occur?
what 4 things is this associated with?
what is the diagnostic test?
treatment?
lack of ADH/AVP production by the posterior pituitary or loss of ADH action
hypernatremia due to free water loss
associated with severe CNS structual lesions or infections, head trauma, or pituiatary surgery
Dx: give them person ADH and see if it increases their H2o intake and equalizes their osmolarity and decreases their urinary frequency, this is a DIAGNOSTIC TEST
Rx: ADH
hypernatremia with dilute urine
nephrogenic diabetes insipidus
what causes this?
what are 5 things that can cause a person the acquire this?
how do you tx?
acquired
renal insensitivity to ADH
see after relief of prolonged UT obstruction, renal interstitial disease, hypercalcemia, lithium or demeclocycline
**giving ADH doens’t do anyhting for it**
Rx: increase response to ADH
hypernatremia with dilute urine
congenital nephrogenic disease
what do they lack?
absence of ASH receptors
hypokalemia
what is K levels maintained by?
what are 5 causes of this?
what are 5 signs of this?
2 tx options?
K is the major INTRACELLULAR cation with the gradient maintained by the Na/K pump
oral intake=renal output in a steady state
Causes of hypokalemia:
1. insulin: insulin cause K to move into the cell, so excessive amounts cause hypokalemia
2. RAA systemactivation**: ALDOSTERONE facilitates K excretion **most important regulator of body K conten
- diuretics
- vomiting/diarrhea/sweat
- digoxin
signs: weakness, muscle cramps, fatigue, constapation EKG NSST-T changes and U waves, PVCS
tx:
- mild to mod=oral KCL
- severe= IV admin of KCL slowly with cardiac monitoring
hyperkalemia
what are 3 causes of this?
what do you need to confirm?
what are 3 signs you see?
what tx can you give in lifethreatening?
what are 4 other txs?
causes:
1. patients with renal insufficiency are at risk
2.renal insufficiency + K sparking diuretics
3. KCl and K sparing diuretics
important to confirm lab results because can be from hemolysis
signs: diarreah, weakness
ekg: PEAKED T waves, widening QRS, increased intervals and loss of P waves KEY!!
TX:
- if lifethreatening k greater than 6.6 can give infusion of insulin to drive the K inside to buy time
- eliminate KCL or K sparing diuretics
- cation exchange resins that exchange Na for K
- dialysis for severe renal failure
why is calcium important?
where is it mostly found?
50% of it is ionized to help with muscle and nerve function
40% is bound to protein mostly albumin
why is it important to measure serum albumin to determine if Ca is truly deficient?
if there is a deficiency of Ca reported it could reflect either the ionized Ca (the one we care about) or the amount bound to albumin
if we check the albumin levels and it is low, it means that the Ca bound to this is low which is the likely source of the Ca deficiency
if the albumin is normal, then it is likely the ionized Ca is low, which is what we care about
**we care about this because it is what allows for muscle and nerve function**
hypocalcemia
what are three causes of this and what is most common?
5 signs of this?
2 ways to test for it?
what EKG changes you see?
what are the 2 tx?
MOST COMMON CAUSE IS RENAL FAILURE
(DECREASED VIT D3, INCREASED PHOSPHORUS)
other causes:
- hypoparathyroidism
- malabsorption
signs: increased excitation of nerve and muscle cells, cramps, tetant, paresthesias, convulsions
chvosteks sign:tap on facial nerve and you will start twitching on the side of the face you tapped
trousseaus sign: BP cuff inflate for over a min, if you inflate all the way your hand willl start twitching if over 1 minute
EKG: Prolonged QT, arrythmias
ionized Ca less than 4.5
tx:
asymptomatic: oral calcium/vit D
symptomatic: IV calcium gluconate
hypercalcemia
what are 3 cauess of this?
what are 3 signs of this?
what are 3 txs?
what can make this worse and should be prevented?
causes:
1. hyperparathyroidism
2. malignancy produce PTH
3. milk-alkali syndrome Ca antacids + vitamind D excess
signs:
- polyuria- H20 reabsorption is blocked by hypercalcemia
- neuro changes: lethargy, weakness, dowsiness
- shorted QT, PVCs
TX:
- treat underlining cause
- promote Na rich diuresis because Ca will follow
- IV infusion 0.9% saline with IV furosemide
**avoid thiazide diuretics, can worsen hypercalcemia**
hypomagnesemia
who is this common in?
why is this a big deal?
what are 4 signs?
2 things it is often associated with?
what are 2 tx?
what should you do in hospitalized pts?
very common in hospitalized patients esp for those on diuretics who are receiving continuous IV support
Low Mg potentiates dangerous ventricular cardiac arrythmia esp if K is low
signs: weakness muscle cramps tremors, neuromuscular and CNS hyperirritability
often associated with: hypoK and hypoCa
Tx:
- important to check Mg levels in hospitalized pts
- IV therapy with MgSO4
- oral Mg oxide can be given as supplement
another name for acute renal failure is?
acutre renal injury
another name for chronic renal failure is?
chronic kidney disease
another name for end stage renal disease is?
end stage kidney disease
explain what falls under the two categories of uncomplicated UTI (2)
and
complicated UTI? (6)
uncomplicated UTI
- acute cysitits
- acute pyelonephritis
complicated UTI
- something that makes the more likely to fail treatment
- obstruction
- anatomic abnormality
urologic dysfunction
- MDR uropathogen
2. pregnant
3. elderly
4. children
5. males
6. recurrent
Complicated UTI
Pregnancy
what are 3 things its assocaited with?
do you screen?
if positive what must you do (2)?
what is one really key thing to remember about UTI and pregnant women?
associated with preterm birth, low birth weight, prenatal mortality
screen in 1st trimester with UC
admit them since dangerous with baby
always check urine culture if asymptomatic because the bacteria in the urine can cause the things under A, if + treat with abx
if they get 2+ positive tests with greater than 100,000 positive tests they they will be on suppressive abx for the remainder of the pregnancy
Complicated UTI
eldery
what are two groups of peopel that are esp susceptible?
what are three things that contribute to the first?
postmenopausal women
- bladder/uterine prolapse
- loss of lactobacilli in vaginal flor allos for E. coli to take over
- diabetes (sugar)
benign prostatic hypertrophy
complicated UTI
children
who is this more common in?
3 symptoms?
what is the DOC?
how long do you treat for, two options?
white children more common than black children
fever, hematuria, abdominal pain
DOC: 2nd-3rd line cephalosporin
7-14 days if febrile
5 days if immune competent and afebrile
complicated UTI
males
what are two risk factors?
urethra length?
unusual for men 15-50
RF: uncircumcised, anal intercourse
antibacterial material in prostatic fluid
18-20 cm urethra
who are UTIs most common in?
what is the most common route of infection?
what are most from?
what isthe pathogenisis of this and what does it RARELY come from?
30:1 ratio women to men because women have a significantly short urethra
route of infection: ascending from the urethra
UTI most commonly from uncomplifcated acute cystitis
pathogenisis:
- colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder CYSTITIS
- uropathogens ascend from bladder to kidney via ureters
RARELY CAUSED BY SEEDING OF BACTERIA
what are 5 RF for UTI?
female sex
frequent sexual intercourse
diaphragm/spermicide use
delayed post-coital micturition (not urinating after intercourse)
hx of UTI
what are four bacteria that cause UTI and which is by far the most common? what percent?
e.coli most common 75-95%
proteus mirabilis
klebsiella pneumoniae
enterococcus
what are the difference in symptoms for
cystitis (6)
vs
pyelonephritis? (5)
cystitis:
- dysuria or burning while urination
- increased frequency/urgency
- suprapubic pain/discomfort
- hematuria
- voiding small amounts
- AFEBRILE
pyelonephritis
- FEBRILE
- chils
- flank pain
- costovertebral tenderness
- CBC with left shift
what 3 lab tests are important to do when diagnosiing a UTI?
what do you find on each?
1. UDIP
+ leukocyte esterase (product of baceteria)
+ nitrites (conversion of nitrates to nitrites via bacteria)
+WBC
+WBC casts (INDICATES KIDNEY ORIGIN!***)
2. hematuria
3. culture greater than 100,000
what are the DOC fo acute cystitis (4) vs pyelonephritits (2)?
what do you need to note?
acute cystitis
DOC1: TMP-SMX
DOC2: CIPRO
DOC3 if pregnant/allergic: Nitrofurantoin
***add pyridium***
acute pyelonephritis
DOC1: ciprofloxacin
DOC2: TMP-SMX
*****NOTE THE DOC FOR FOR THESE TWO ARE DIFFERENT!!!*****
what is the DOC for an inpatient with UTI/pyelonphritis?
CIPROFLOXACIN!!
others:
fluoroquinolone, amp+gentamycin, ceftriaxone
what is the most common nosocomial infection in the US? what is the tx protocol with this?
cathertized associated UTI
if asymptomatic don’t need to treat with abx
screen urine 48 hours after removing catheter
recurrent UTIs
what are the two definitions of this?
what should you consider?
what about in women with decrease in lactobacillis?
3 or more episodes per year confirmed UC OR 2 UTIs in last 6 months
consider self treatment at first sign (urine cup for UC)
vaginal estrogen in women since they have a decrease in lactobacillus
in asymptomatic bacteremia who do you treat (3) and who do you not treat (3)? *key!*
treat:
- pregnant
- before urologic procedures
- after renal transplant
DONT TREAT
- diabetics
- elderly
- patients with spinal cord injury or indwelling urethral catheter
do you tx UTI empirically while waiting for culture?
YES! then adjust abx as appropriate! :)
Nephrolithiasis
what are the two things you need for the formation of crystals?
what are four risk factors that allows this to happen?
what are the four types of stones?
formation is dependent on supersaturation and an environment that allows the stone to grow!
supersaturation risk:
heredity- cystinuria SLC3A1/SLC7A9
environmental
diet
obesity
four types of stones:
- calcium oxalate
- struvite
- uric acid
- cystine
nephrolithiasis
calcium oxalate stones
can you see it on a xray?
what is it usually associated with?
what are 4 associated factors?
3 tx options in general?
MOST COMMON TYPE OF STONE
- RADIOOPAQUE
- usually associated with high calcium levels in the blood and urine
- contributing factors: excessive bone reabsorption, bone disease, hyperparathyroidism and renal tubular acidosis predispose for these stones
TX:
treat underlying conditions
increased fluid intake
thiazide diuretics
(70-80%)
nephrolathiasis
struvite stone
what 2 things is this associated with?
4 bacteria?
can you pass them?
when do they get bigger?
3 tx options?
“staghorn” stones that always associated with UTI and alkaline urine
- produced by UTI with urease producing bacteria
- proteus, klebsiella, pseudomonas, enterobacter
- made of magnesium ammonium
- usually too large to pass and require lithotripsy or surgical removal
- they enlarge as the bacterial count increases
Tx:
- prevent UTIs
- lithrotripsy
- surgical removal
nephrolithiasis
uric acid stone
what is this caused by?
can you see on xray?
what are 2 RF?
2 tx options?
caused by low Ph (acidic) urine <5.6 for greater than 24 hours
- radiolucent cant be seen on xray
- caused by high levels of uric acid in the urine or gout
- RF: obesity/diabetic or both
Tx:
- decrease uring PH below 6 (more alkaline) using potassium citrate
- allopurinol with decrease purine diet (fish, shellfish, and meats)
nephrolithiasis
cystine stones
what type of disorder is this and who is it common in?
what is the appearance of the stones?
what are the two treatement options?
autosomally recessive inherited abnormalities CYSTINURIA
“childhood caliculi”
1.smooth-edged ground glass appearence
TX:
- increase urine volumes to 3 L a day and increase urine pH to greater than 7
- occasionally chelating agents
what are 6 RF for nephrolithiasis in general?
high humidity
high temp
sedentary
high animal protein and high salt
FH for calcium stones
hyperthyroidism/hypothyroidism
what are the 4 most common symptoms with nephrolithiasis? and less common symtpoms? (4)
Most common:
- unilateral flank pain
- sudden onset
- renal colic
- hematuria
Less common:
- vague abdominal pain
- acute abdominal/flank pain
- difficulty urinating
- penile or testicular pain
what is the most important test when suspecting nephrolithiasis? what do you expect to see for each of the stones? 4 types of labs you should consider ordering?
- non-contrast CT (gold standard)
used to identify the size, location and type of stone
- low density (aka can’t see): uric acid, cystine
- high density: calcium oxalate, struvite
- struvite: laminar, rugged apperance, full of casts with “stag horn apperance”
*****do renal US for pregnant people who can’t have the CT****
- labs
- urinalysis (stone type/blood)
- BMP (calcium and creatinine if worried about kidney function)
- 24 hour urine for the amount excreted
- thyroid function test
chart that puts it all together
:)
what is the most common cause of recurrent calcium stones?
most common abnormality elevated Ca excretion, decreased serum Ca
stone passage
- explain how size and location effect the ability to pass the stone?
- what are two meds you can give to help during the passage?
size
<5 mm pass spontaneously
5-10 mm less likely to pass on their own
>10 mm won’t pass on their own
location
stones in proximal ureter less likely to pass
ureterovesicular junction more likely to pass
Meds to help pass:
alpha blocker (tramsulosin)
CCB (nifedipine)
if you txing a pt with nephrolithiasis what are 3 things you want to do to help manage the pt?
when do you consider hospitalization (2)?
- most managed conservatively with pain management Nsaids and Opoids (BETTER USED TOGETHER!!)
- hydration
- strain urine
consider hospitalization:
uncontrolled pain/fever
can’t tolerate oral intake
what are 6 things that would qualify for urologist referral in a patient with nephrolithiasis?
acute renal failure
urosepsis
urinary obstruction
concomitant pyelonephritis
>10 cm
haven’t passed for 4-6 weeks
what are the 5 tx options for nephrolithiasis?
1. NSAIDS and opoids!!
1.5. increased fluid intake key!
2. shock wave lithotripsy (small renal caliculi)
3. precutaneous nephrolithotomy
4. rigid and flexible ureterscopy +/- stent placement
(tx of choice for maority of middle and distal urethral stones or those who failed shock wave lithrotripsy)
5. diet changes for Ca oxalate stones (decrease spinach, animal protein, Na intake)
why is it important to educate your patient on recurrence for nephrolithiasis?
⅓ will experience stone recurrence within 5 years
½ experience stone reccurence within 10 years
explain the blood flow through the kidneys?
9 steps
renal artery
segmental artery
interlobar arteries
arcuate arteries (communicate with each other0
interlobular branches (extend into the cortext)
afferent arteriole to glomerulus to efferent arteriole
interlobar veins
and reverse with the same name as the veins (these go to the inferior vena cava
explain the difference between the two capillary beds found in relationship to the nephron?
glomerular capillary bed
- brings blood to the glomerulus
- high pressure system at 60 mmHg
allows for FILTRATION
peritubular capillaries
- surround all portions of the tubules, and are in an arrangement that permits rapid movement of solutes and water between the fluid in the tubular lumen and the blood in the capillaries
- low hydrostatic pressure around 13 mmHg
allow for ABSORPTION
what is the rate of blood flow through the glomerulus?
1200 ml/min
explain the two different types of nephrons found in the kidney?
where are they?
what is their function?
cortical nephrons
85% of them
originate in the superficial part of the cortex, short, thick loops of Henle that penetrate only a short distance into the medulla
juxtamedullary nephrons
less common
originate deeper in the cortex and have longer thinner loops of henle that penetrate the entire length of the medulla
largely concerned with concentrating the urine
what are the two major mechanisms for maintaining renal blood flow and eGFR effecting both the efferent and afferent renal blood flow?
- myogenic mechanism
- tubuloglomerular feedback menchanism
myogenic mechanism
what is this mechanism sensitive to?
what intrinsic mechanism does it rely on?
what happens as the pressure changes in the afferent arteriole to maintain pressure in the glomerulus?
- pressure sensitive mechanism
- relies on intrinsic mechanism of vascular smooth muscle that cause it to contract when stretched
- as arterial pressure rises and the
afferent arteriole is stretched=__the smooth muscle contracts
when the afferent pressure falls= it relaxes
tubuloglomerular feedback mechanism via juxtaglomerular apparatus
what is the ulimated end point of this apparatus?
where does it occur?
what are the two main cells that play a role here and where are they located?
what are thet wo things this apparatus is thought to measure?
what are the two things that are linked here?
- NaCl concentration in the tubular fluid is sensed by the juxtaglomerular apparatus in the distal tubule
- occurs where the distal tubule extends back to the glomerulus and then passes between the afferent and efferent arterioles
- includes a group of sensing cells called the macula densa in the distal tubule and a group of secretory cells in the wall of the afferent and efferent arterioles called juxtaglomerular cells or granular cells that secrete renin
- the juxtaglomerular apparatus is located right between the afferent and efferent arterioles and is though to play an essential feedback role in linking the arterial BP and renal flow tothe GFR and the composition of distal flow, thought to measure both the stretch of the afferent arteriole and the concentration of NaCl as it passes through in the tubular filtrate through the macula densa in distal tubule=determines how much renin is released
eGFR
marathon runner analogy
what happens in these:
- constricting afferent arteriole
- constricting efferent arteriole
- dilating efferent arteriole
- dilating afferent arteriole
constricting afferent arteriole= decreases pressure in glomerular capillary pressure decreasing eGRF
constricting efferent arteriole=increases pressure in glomerular capillary pressure increasing eGFR
dilating efferent arteriole= decreases pressure in glomerular capillary pressure decreasing eGFR
dilating afferent arteriole= increases pressure in the glomerular capillary pressure increasing eGFR
what effect do these have on the arteriole system of the glomerulus?
prostaglandin
angiotensin II
prostaglandin: dilates the afferent arteriole
angiotensin II: constricts efferent areteriole
- explain the blood flow as it moves through the glomerulus and out of the kidney?
- where do the two greatest drops in BP occur? what is this area known as? what is it nessacary to maintain?
- what medication works in the above area?
afferent arteriole, to glomerular capillary, to efferent arteriole, to peritubular capillary to intrarenal vein, to renal vein
greatest drops in pressure are the afferent arteriole and efferent arteriole
are the sites of greatest resistance
this is why the pressure is higher in the glomerular capillary than in the peritubular capillary that allows for filtration!
this is where ACE/ARBS works because they have the most effect
what are the 4 main function of the kidneys?
- filtration
- reabsorption
- secretion
- excretion
kidney filtration
when does this occur?
what is this caused by?
what do you use to measure it?
what is normal amounts?
- first step in urine formation
- bulk movement of fluid from blood into kidney tubule
- isosmotic filtrate
- blood cells and larger proteins don’t filter - caused by hydralic pressure
- Glomerular filtration rate: amount of filtrate produced in the kidneys each minute
125 mL/min=180L per day
kidney reabsorption
what is this the process of?
what percent of filtrate is reabsorpbed?
what can aid in this process?
what is totally reabsorbed?
process of returning filtered material to bloodstream
99% of what is filtered is reabsorbed
may involve transport proteins
normally glucose is totally reabsorbed
kidney secretion
what is this?
what are two things that rely on active transport?
material added to the lumen of kidney tubule from blood
active transport (usually) of toxins and foreign substances
- saccharine
- penicillin
kidney excretion
what is this?
what is the equation for amount of solute excreted?
loss of fluid from body in form of urine
excreted means=as urine
amount of solute excreted= (amount filtered +amount secreted) - amount reabsorbed
glomular filtration rate is regulated by what 3 mechanisms?
the amount of plasma that is filtered each minute
provides information about the kidneys ability to filter and reabsorb/secrete substances
- renal autoregulation
- neural regulation
- hormonal regulation
GFR:
renal autoregulation
what pressure range does this have a modest effect on?
when does it have a great effect?
what is the goal of this regulation?
what two mechanisms allow you to accomplish this?
what is the end point?
between 80-170 mmHG, autoregulation of blood flow and GFR only modestly rise as renal perfusion increases
outsides of this range, the changes are much greater
purpose: maintain a relatively constant GFR and allow for precise regulation of solute and water excretion
accomplished by:
- myogenic mechanism (response to pressure changes in the afferent arteriole)
- tubuloglomerular feedback
(response to Na concentration in the distal renal tubule)
causes RENIN release
GFR:
neural regulation
the afferent and efferent arterioles are innervated by which types of fibers? when is it stimulated? what are the three effects of this?
sympathetic nerve fibers from renal plexsus of autonomic nervous system innervate SM afferent and efferent arterioles at the hilus
sympathetic stimulation causes constriction of the afferent and efferent arterioles and thus decreases renal blood flow
Effects:
- reduce the GFP and GFR through contracting the afferent and efferent arterioles through alpha receptors
- increase Na resorption in proximal tubules B receptors
- increase the release of renin B receptors
normally sympathetic stimulation is low so the arteries are dilated except during exercise and hemorrhage where the blood is decreased here
what are the three neural nerve reflexes that contribute to BP regulation by the kidneys?
what does the last one cause and what is its significance?
- cardiopulmonary reflex
- baroceptor reflex
- renorenal reflex
a. sensory nerves located in the renal pelvic wall are activated by stretch of the renal pelvis wall
- leads to increase of bradykinin which activates protein kinase C causing pelvic release of PGE2 by activation of COX2 and activates calcium channels in renal pelvic wall
b. causes afferent renal nerve activity to increase, efferent activity to decrease, which causes increase in flow rate and urinary sodium excretion
GFR:
hormonal regulation
6 things
angiotensin II: produced by renin released by JGA cells is a potent vasoconstrictor of the efferent arteriole increases GFR
ANP: released by the atria when stretched increases GFR by increasing capillary surface area available for filation
NO
endothelian
postaglanding E2: dilates the afferent arterioles
glomerular filterability
what are the two characteristics that make things able to get into the glomerular filtrate?
what are 3 things that can filter freely? 3 things that can get some across?
what are the 1 favoring and 2 opposing forces of glomerular filterability?
what does this movement occur in response to?
1. molecular weight
2. charge of the molecules
urea, glucose, and insulin can filter freely across the membrane, some myoglobin (75%) can get through
albumin and hemoglobin may be present in small amount (3-1%)
DRIVEN BY:
favoring force: capillary blood pressure (BP)
opposing forces:
- blood colloid osmotic pressure (COP)
- capsulre pressure (CP)
moves out based on glomerular hydrostatic pressure
what are the three tests you use can use to measure GFR?
- inulin
- creatinine
- Blood urea nitogen
measurement of GFR:
inulin
5 characteristics that make this work
- freely filtred at the glomerulus
- biologically inert
- not synthesized or metabolized by the kidney
- does not alter renal function
- can be accurately quantitfied
GFR measurement
creatinine
what is this a product of?
why is this effective in measuring GFR?
is it an over or underestimate of the damage?
how do you interpret results?
what do you need to keep in mind as the serum creatinine rises?
end product of muscle metabolism
its formation and release is relative constant and proportional to the amount of muscle mass present, since it is freely filtered by the kidneys and is not reabsorbed from the tubules its levels are used to measure the eGFR
small amount secreted from the tubule in a healthy person, so you area actually underestimating the amount of kidney dysfunction
interpretation: if the serum level rises it means that kidneys are unable to filter it and they aren’t working correctly
**keep in mind, the as the serum creatinine gets higher the GFR is less helpful the GFR calculations are**
GFR measurement
blood urea nitrogen (BUN)
what is this a product of?
what are 3 things that can cause this to rise?
better or worse than creatinine?
what is an important thing this measurement can be used for? (values)
product of protein metabolism and is eliminated entirely by the kidneys
also rises with protein intake, gastrointestinal bleeding, and hydration status so is less effective than creatinine since effected by more things
BUN-creatine ratio is more helpful than BUN alone
normally 10:1
greater than 12/1 indicates prerenal issues like CHF and blleding
what percent is:
filtered
reabsorbed
excreted
what is the reabsorption of:
glucose
Na
water
creatine
20% of bllod is filtered
19% reabsorbed
1% excreted
glucose: all reabsorbed
Na and water: nearly all reabsorbed 99%
creatinine: none reabsorbed
what are the two absorption pathways?
transcellular: from lumen through the cell
paracellular: from lumen between the cells
what are the four mechanisms of transport seen in the nephron?
1
2
1
1
- primary active transport: uses ATP to move solutes against their concentration gradient, used by K, Na, H
Ex: Na/K pump (Na out, K in)
-
secondary active transport
a. cotransport/symport: moves solutes in the same direction
b. counter-transporters (antiporters): move solutes opposit directions
3. pinocytosis: proximal tubule reabsorb lage molecules such as proteins by pinocytosis
4. passive transport: diffusion
proximal convoluted tubule
what 5 main things are absorbed here (5)?
what percent?
what is the main vechicle for Na, Cl, and H20?
what occurs in the first half of PCT?
what occurs in the second half of PCT?
65% Na, Water, K, HCo3 and Cl reabsorption from proximal convoluted tubule to thick descending segment of loop of henle
reabsorption of Na, Cl, and water main absoprtion vechicle is sodium-potassium pump
first half of PCT:
- Na reabsorbed by co-transport with glucose and amino acids
second half of PCT:
- Na and Cl reabsorbed: think about it, in the first half of PCT there was no reabsorption of Cl so now it is highly concentrated which facilitates it reabsorption
explain the process of glucose and amino acid reabsorption in the proximal convoluted tubule?
what is this limited by? what concentration in the blood causes this? what is this caused? what are the values?
typically amino acids and glucose are reabsorbed
glucose/amino acids: reabsorbed by secondary transport symport with Na
since removed by secondary active transport, the transport reaches a transport maximum or the maximum amount of substance the transport system can reabsorb per unit time, relates to the number of carriers and is usually sufficient to remove all the glucose from the urine
when this is exceeded, the urine glucose level rises because the amount in the urine exceeds the workload of the pumps putting it back into the blood
renal threshold is the plasma level at which the glucose appears in the urine and indicates the amount filtered exceeds the transport maximum
200 mg/dl arterial glucose
180 mg/dl venous glucose
secretion of H+, acids, and bases bicarbonate
where are the three main places this occurs?
explain wha happens in the proximal tubule? (2)
explain what happens inteh late distal tubule? (4)
what is this imporant for?
occurs at proximal tubules, loop of henle, and early distal tubule
-
proximal tubule
- 90% bicarbonate reabsorbed
- secretion of H+ through secondary active transport
2. late distal tubule and the rest
- primary active transport
- occurs at the luminal membrane of tubular cell
- H ions are transported directly by a specific protein Hydrogen-transport ATPase (proton pump)
- decreases the pH of tubular fluids
**important in forming maximally acidic urine
loop of henle:
think descending loop
what happens here and why?
highly permeable to water
little to not active reabsportion
the interstitial area around this is HYPERTONIC, which means the water wants to move out and get into the interstitial space to balance this out!
loop of henle:
thick ascending limb
what percent is absorbed here? what is absorbed (6) what is secreted? why does this happen?
reabsorbed 25% of filtered loads of Na, Cl, and K as well as large amounts of calcium, bicarbonate, and Mg
secretes hydrogen ions into the tubule
***the fluid in the lumen is hyposmotic meaning there is a high concentration of particles since all the water has been taken out, the particles therefore want to move out into the interstitial space***
urine concentration and dilution
what happens when-
osmolarity of the serum decreases:
osmolarity of serum increases:
what are two KEY features taht must be present to allow the concentration/dilution of urine to occur?
osmolarity of the serum/ECF decreases: loose water and get dilute urine
osmolarity of serum/ECF increases: water reabsorbtion and get concentrated urine
***this is sensed by osmoreceptors in the hypothalmus sensing high ECF osmolarity…tells posterior pituitary to release ADH and alter collecting duct permeability***
Mechanism that allows this to happen:
- controlled secretion of ADH from posterior pituitrary glandwhich regulates the permeability of medullary collecting ducts to water in response to osmoreceptors in the hypothalamus sense high ECF osmolarity, causes more water reabsorption and concentrates the urine
- a high osmolarity of the renal medullary interstitial fluid, which provides an osmotic gradient necessary for water reabsorption to occur in the presence of high level ADH (if the concentration gradient wasn’t high in solute or non existent, if ADH made the tubule more permeable, the fluid wouldn’t go anywhere)
BOTH ARE KEY! ADH, osmolarity of interstital
how is hyperosmotic renal medullary interstitium maintained by the:
- thin descending limb
- thick ascending limb
- collecting ducts
what this this produced by?
countercurrent mechanism produces hyperosmotic renal medullary
1. thin descending limb
permeable to water, not solutes
water reabsorption occurs because of the Na leaving the thick ascending limb
2. thick ascending limb
permeable to solutes, not water
active transport of NaCl into interstitium
3. collecting ducts
only papillary duct is permeable to urea to this concentrates the urea in the medulla and accounts for ⅓ the solutes in the deepest portions of the medula
water movement:
obligatory water reabsorption
what is this largely dependent on?
what are the two ways this occurs by?
using water and other solutes
water follows solute to the interstitial fluid (transcellular and paracellular methods)
largely influenced by Na reabsorption “if more sodium is reabsorbed then so will water because water follows sodium”
water movement:
facultative (selective) water reabsorption
what is this regulated by?
what are the 4 steps?
where does this most often occur?
occurs mostly in the collecting ducts through portes or water channels
regulated by ADH:
1. ADH binds to membrane receptor
2. receptor activates cAMP second messanger
3. cell inserts aquaporin 2 water pores into the apical membrane or the side next to the lumen
4. water is absorbed by osmosis into blood
water movement:
solute/osmotic dieuresis
what is this caused by?
what happens?
what type of kidney?
large amounts of poorly absorbed solute like glucose, mannitol, or urea…this would be in the filtrate if the kidney wasn’t working properally
highly osmolarity filtrate, so water rushes in and causes a hypotonic saline
aldosterone
what type of componet is this?
what cause it cause and where?
what are two things it does and where does it take place?
steroid hormone synthesized in the adrenal cortex
causes: reabsorption of Na/H2O in distal convoluted tubule** **and collecting ducts (also K excretion)
acts primarily on the principal cells of the corticla colllecting ducts and
1.stimulates the Na/K ATPase pump on the baslolateral side of the cortical collecting tubule
2. increase Na permeability of the luminal side of the membrane
**in the pic note that Na is being reabsorbed and K is excreted**
micturation
where does this originate?
what are the two main motor functions that are coordinated here?
-what do they each cause? via which nerve?
2
1
originates in sacral S1-S4
combination of Motor function:
- Stimulation of parasympathetic neurons=contraction of detrusor muscle and internal urterthral spincter (involuntary) via pelvic nerve
- inhibition of somatic neurons=relaxation of external spincter (voluntary) via pudenal nerve
tubular disorders:
autosomal dominant polycystic dieases
what age group do you find this in?
what is this characterized by?
what are the 5 most common symptoms and which one is most reported by pts?
what genes are responsible?
Test of choice?
Tx? 2 things to consider?
most common of all inherited kidney diseases
uncommon before 40 years old, 40% dx before 45
3rd-4th decade
multiple expanding expanding cysts of both kidneys that destroy the surround kidney structures and cause kidney failure
kidneys are englarged/enormous with “straw colored” fluid
Symptoms:
- flank pain from ruptured cyst
- gross episodes of hematuria from bleeding into cysts
- infected cysts from ascending UTIS (most common thing reported by pt)
- HTN
- stones 15-20%
CALCIUM OXALATE, URIC ACID
Genes:
PKD1: 85% of cases
PKD2: 15% of cases
DX: ULTRASOUND TEST OF CHOICE
Tx:
SUPPORTIVE
controll HTN and prevent/ TX UTIs AGGRESIVELY!!
what are 3 assoiated findings that are important to look for in autosomal dominant polycystic kidney disease?
***all of these were in porth and dr, reiserts lecture!**
- cysts in the liver
- mitral valve prolapse 20-25%
- cerebral aneurysm from weakness in the cerebral arteries 20%
autosomal recessive polycystic disease
who does this present in?
what becomes abnormal?
what gene is responsible?
what are 5 symptoms?
what is the tx?
CHILDHOOD polycystic kidney disease
cystic dilation of the cortical and medullary collective tubules
perinatal and infantile types most common
PKHD1 gene: produces fibrocystin that is involved in cell proliferation and adhesion
Sxs:
present at birth
renal failure
billateral flank masses
portal HTN
imparied lung development
Tx:
supportive
ventilatory support
nephrotic syndrome
what is the patho of this?
what are the 7 main symptoms of this and which is the hallmark?
is this a disease on its own?
what are the 3 main causes?
**not a specific disease by a characterization of symptoms**
the glomular membrane acts as a filter, this increased permability allos proteins to ecape into the urine leading to excessive loss of albumin
as the solutes move out of the ECF, it becomes hyposmotic and so it moves into the tissues and cells where there is a higher concentration of solutes and causes the generalized edema
characterized by:
- massive proteinuria more than 3.5 a day
2. lipiduria with fatty casts
3. hypoalbuminemia
4. generalized edema HALLMARK starts in dependent parts like extremeities but spreads to become generalized
5. hyperlipidemia LDL and Tri
- high cholesterol!!
- HYPERCOAGUBILITIES….so at increase risk for clots/DVT
three main causes:
- minimal change disease
- membraneous glomerulonephritis
- focal segmental glomerulosclerosis
nephrotic syndrome:
minimal change disease
what happens in this?
who is it most comon in?
what do they have a hx of?
what 4 things are they predisposed for?
tx?
diffuse loss of podocytes or foot processes of the visceral epithelial cells of the glomeruli
most common in children 2-6 but can occur in adults
child has hx of URI
predisposition to infection with gram + organisms, thrombotic events, hyperlipidemia, and protein malnutrition
TX:
short dose of glucocorticoids
nephrotic syndrome:
membraneous glomerulonephritis
what is the patho?
what is this caused by? (5)
what are the 3 main symptoms?
tx?
most common cause of primary nephrosis in adults
“think THICK BGM without infllammation”
diffuse thickening of the glomerular basement membrane from deposition of immune complexes that create “spikes”
causes: SLE, chronic Hep B, DM, thyroiditis, gold compounds
SXS:
- peripheral edema
- hypoalbuminemia
- hyperlipidemia
Tx:
controversial since often times the pt has spontaneous remission and it is relatively benign
hematuria disease #1:
IgA nephropathy
what is the nickname for tihs?
who is it most common in?
what is the patho of this?
what are the 2 ways to diagnose this?
tx?
“Berger disease”
“THIN GBM DISEASE”
BENIGN HEMATURIA
MC GLOMERURPATHY WORLDWIDE
most common in asians, 3-4th decade of life
primary glomerulonphritis characterized by presence of glomerular IgA immune complex deposits which causes inflammation
DX:
discovered during routine testing, find elevated IgA levels
- gross hematuria preceded by URI
50% have single episode
- diagnostic findings: mesangial staining for IgA tat is more intense than staining for IgG or IgM
TX:
NO TREATMENT
hydronephrosis
what is this and what does it cause?
characteristics?
who should this be susepcted in?
if caught early?
if caught late?
urine filled dilation of the renal pelvis and calyces associated with progressive atrophy of kidney due to the obstruction of urine flow, usually unilateral but can be bilateral with hyperplasia
acute or chronic
partial or complete
unilateral or billateral
**the stasis of urine/obstruction encourages microorganism growth and should be suspected in people with recurrent UTI**
if recognized early: can be reversible
if recognized late: can lead to UTI, urosepsis, and end stage renal disease
hydronephritis
what determines presentation?
what are the 5 symptoms?
how do you DX and what do you see?
presentation depends on site of obstruction, degree, and speed at which obstruction occurs
SYMPTOMS
- pain
- change in urine output
- HTN
- Hematuria
- increased serum creatine
DX:
TEST OF CHOICE: RENAL ULTRASOUND
**dilation of renal collecting system in one or both kidneys**
renal artery stenosis
what is this caused by?
what does this cause (3)?
who should you suspect this in (4 key attributes)?
what is the gold standard?
but what do you use?
persistent and progressive decreased GFR from reduction of blood flow from atherosclerotic ishchemia
results in CKD (increased serum creatinine and BUN)
consider in pts with severe or resistant HTN, less than 30 years old, and with no family history of HTN or obesity, acute rise in serum creatinine after starting ACE or ARBS
DX:
- renal angiography is gold standard
- less invasive test is TEST OF CHOICE: doppler US, STA, MRA
renal cell carcinoma
who is this most common in?
where does it grow specifically?
how does it grow and what does it look like?
where can it grow into?
fast? slow?
what are 5 types?
northern european descent
MOST COMMON KIDNEY CANCER
grows spherically and is well circumscribed mass in the CORTEX of the kidney
arises in the epithelial lining of the proximal tube**, and **grows into the renal vein, inferior vena cava, occlude right side of heart
slow growing and doesn’t present until advances
Many types:
- clear cell
- papillary
- chromophobe
- collecting
- unclassified
wilms tumor
what is another name for this?
what age group?
what type of cells are cancerous?
what are three random associated findings?
what are the four most common sxs?
which is most important?
MOST COMMON RENAL CANCER IN CHILDREN
“nephroblastoma”
dx 3-5 years old most common
primitive cells of renal cortex
associations:
- absense of iris
- enlargement of the side of face
- genituiatry complications
SX:
- abdominal mass/swelling w/o other symptoms (parents find while dressing)
- hematuria 20-25%
- HTN IN CHILD!! HUGE KEY
- fever, abdominal pain less common
wilms tumor
what do you find on PE?
test of choice? two others?
3 tx options?
PE:
firm, nontender, smooth mass that is eccentrically located and rarely crosses the midline
tests:
-
CT scan test of choice, US, MRI
tx: surgery, chemo, radiation
IT IS RESPONSIVE TO CHEMO/RAD
expain the 4 stages of transitional cell cancer/urothelial carcinoma?
Stage 0: inner lining of bladder
Stage I: spreads to bladder wall
stage II: penetrated inner wall and is present in the muscle of the bladder wall
Stage III: gets into fat surrounding bladder
Stage Iv: spreads to pelvis wall or abdomen, lymph nodes, lungs, liver bones etc
bicarbonate buffer system
what are the two levels we really care about?
what is the equation?
what produces them?
acid/bases?
normal ranges?
HCO3: weak base, regulated by the kidneys, 22-28 normal comes from dissociated NaHCO3 which is a salt, so Na pops off
CO2: acid, regulated by the lungs, 35-45 mmHg
pH 7.35-7.45
on bicarb buffer system, which component is regulated by lungs and kidneys?
what do primary disturbances cause? can it fix it?
Primary respiratory disorders affect PCO2
primary metabolic disorders affect HCO3
primary disturbances cause: compensatory changes
Compensatory can’t fully compensate for primary disorder but can help!
respiratory acidosis
ph? 1st thing? comp?
where does equation shift?
important buffering system involved?
what is the primary cause?
4 condition causes?
4 symtpoms
3 tx?
pH decreases, CO2 increases, HCO3 increases (comp)
equation shifts to the right: H is buffered by the intracellular phosphate and protein buffers NOT NaHCO3…this system is essential because it uses the H and combines it with phosphate so don’t get a massive decrease in pH that could cause organ/system failure
primary defect: decreased alveolar ventilation
acute and chronic forms
Conditions that cause this:
1. COPD
2. ASTHMA who tires
3. DRUG OD with supressive of ventilatory drive
4. neuromuscular disease
SXS:
- somulence
- coma
- confusion
- respiratory arrest
Tx:
- *1. VENTILLATORY SUPPORT
2. Naloxone/Narcan**
3. benzodiazepen antagonists: flumazenil
Respiratory Alkalosis
ph? CO2? comp? equation shift?
what is the primary defect?
what are 7 causes of this?
what are 3 sxs?
what are the two tx?
pH increases, PCO2 decreases, HCO3 decreases (comp)
equation shifts to the left (wants to make more acidic)
acute and chronic forms
primary defect: decreased PCO2 from increased alveolar ventilation rate
Causes:
1. hyperventilation
2. anxiety
3. panic attacks
4. sepsis
5. cirrhosis
6. progesterone
7. mechanical overventilation
SXS:
- lightheadedness
2. parenthesia
- tetany
TX:
1. TREAT UNDERLYING CAUSES
2. breath into brown paper bag for short term only
metabolic acidosis
ph? HCO3? PCO2? shift?
explain the patho of this?
what must you sure or consider?
what are the two main subcategories?
2
1
pH decreases, HCO3 decreases, PCO2 decreases (comp)
shifts to the left
MOST COMMON OF ACID/BASE DISORDERS
here there is a increase in the H (acid) in the body, which is buffered by the HCO3, since this is coupled with the HCO3 to make the intermediate H2CO3, with causes the decrease HCO3
H IS BUFFERED IN THIS CASE BY THE BICARB BUFFER SYSTEM
EXCESS FIXED ACIDS OF ENDOGENOUS (INSIDE THE BODY CAUSES) IS THE MOST COMMON ACID-BASE DISORDER
**must measure anion gap**
categories:
1. increased anion gap metabolic acidosis
- lactic acidosis
- DKA
2. normal anion gap metabolic acidosis
metabolic acidosis:
Increased anion gap acidosis
ph? HCO3? comp? Cl? effects on anion gap?
shift?
what is increasing?
what are the four causes? explain what each one causes?
3 tx?
pH decrease, HCO3 decreased, Cl normal
ANION GAP: greater than 10
pH: lower than 7.25
cause increase in H, which then combines with HCO3 and decreases the levels
4 causes:
1. lactic acidosis: cardiogenic shock or arrest, lactatic acid unmeasured anion produced due to inadequate tissue profusion or hypoxia
2. dibetic ketone acidosis (DKA): hyperglycemia with lack of insulin causing increased production of B-hydroxybutric acid and acetoacetic acid KETO acids, if no insulin the fats break down abonromal and produce more acid or H
3. toxins: ethylene glycol, salicyclates, methanol
4. uremia: severe renal failure leads to endoenous acids
TX:
- insulin
- electrolyte replacement
- volume expansion
metabolic acidosis:
normal anion gap acidosis
what is the hallmark findings for this?
what increases that causes the normal anion gap?
what are the two main cases of this?
explain the first.
hallmark:
decreased pH, decreased HCO3, HYPERCHLOREMIA
***the increase in Cl compensates for the loss of HCO3 so the anion gap appeares normal***
causes:
- massive secretory diarrhea: massive loss HCO3 (NaCl and K loss as well)
a. causes Na and Cl retention at the kidney since significant VOLUME DEPLETION
b. as HCO3 secretion in the small/large bowel causes _Cl absorption VIA COUNTERTRANSPORT!!! **this is why you see increase in the Cl which makes the anion gap appeare nromal_***
think: bicarb levels go down (acidosis), Cl levels go up=normal anion gap - renal tubular acidosis
metabolic acidosis:
normal anion gap acidosis
Renal tubular acidosis
explain the three types!
decreased pH, decreased HCO3, increased Cl in the ABSENCE OF DIAHREAHH
1.distal renal tubular acidosis:deficiency in H secretion by distal nephron, can’t acidify the urine and so the H stays in the blood; enhanced K secretion
2. proximal renal tubular acidosis: can’t adequately reabsorb filtered HCO3
3. hyporeninemic hypoaldosterone renal tubular acidosis: impaired Na reabsorption, impaired K and H secretion hypercholeremic acidosis with hyperkalemia
if any of these suspected get nephrology consult
metabolic alkalosis
what are the hallmarks of this?
ph? hco3? pco2? shift?
what is the one thing that causes this?
what are 2 things you loose?
explain the two perpetuation factors?
Tx?
hypokalemia
hypochloremia metabolic alkalosis
pH increases, HCO3 increases, PCO2 increases (comp)
causes: SEVERE VOMITING causes HCl and Nacl loss from stomache initiates alkalosis and volume contraction
1. Cl loss sustains the alkalosis because increase in renal Na absorption to maintain volume is accompanied by HCO3 REABSORPTION
2. actiation of RAA systems to maintain volume causes hypokalemia (increase in Na cause decrease in K and H losses)….so as more Na is absorbed, so is HCO3
TX:
1. 0.9% saline (isotonic) with SUPPLEMENTAL KCL
why must you ALWAYS treat metabolic alkalosis?
***MUST TREAT BECAUSE THE PROBLEM SELF PERPETUATES UNTIL NA/K/CL AND H20 ARE REPLENISHED***
think about how the increase Cl loss causes HCO3 reabsorption that maintains alkalosis, volume depletion causes Na reabsorption and K loss, the more it is activated the more K you loose
what are the stages and values for eGFR of CKD?
