CM Renal

Question 1

what is the total body sodium?

why is this an approximation?

Answer 1

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

Question 2

what are the 3 mechanisms that are used to regulate Na in the body?

Answer 2

1. 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

Question 3

what happens to the excretion of Na in these senarios:

1. if ECFV increases?
2. if ECFV decreases?

Answer 3

if ECFV increases: activation of mechanism to increase Na excretion

if ECFV decreases: activation of mechanism to decrease Na excretion

Question 4

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?

Answer 4

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

Question 5

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?

Answer 5

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

Question 6

dehydration

what is this and waht does it cause?

Answer 6

volume depletion with disproportionate free water deficit, can lead to increase Na osmolarity

Question 7

what is the most common cause of dehydration worldwide?

Answer 7

diarreah

Question 8

osmolarity

what is this determined by?

what are the three main contributors and how does each one influence osmolarity?

Answer 8

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

Question 9

what is the equation for OSMOLARITY?

what is the biggest influencing component of this equation?

what does it tell you?

Answer 9

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

Question 10

tonicity

what is this a measure of? what does it cause?

if this increases what does it most likely reflect an increase in? why?

Answer 10

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

Question 11

why does a hyptonic/hypertonic solution important when talking about brain cells?

Answer 11

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!**

Question 12

increased serum tonicity

what happens to Na?

What happens to H20 excretion?

urine?

Answer 12

hypertonic solution

increased Na

decreased H20 excretion

urine becomes relatively concentrated (since the water is being sucked out!)

Question 13

decreased serum tonicity

what happens to Na?

What happens to H20 excretion?

urine?

Answer 13

hypotonic blood

has decreased Na

increase H20 excretion

urine is relatively dilute (since more water is being excreted)

Question 14

the process of adjusting the tonicity/osmolarity (concentrating/diluting) of the serum is dependent on which four things?

Answer 14

1. adequate eGFR
2. filtrate delivery to the concentrating and diluting segments of the loop of henle and distal nephron
3. appropriate turning on/off of ADH
4. ADH responsiveness to the kidney

Question 15

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?

Answer 15

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

Question 16

explains what happens in the renal concentrating (refers to what happens in the urine) mechanism? what allows this to happen?

Answer 16

occurs when water needs to be reabsorbed

1. 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
2. the hypertonic medullary interstitium allows for water to be pulled out from the descending limb of henle and the the collecting tubule
3. as water is pulled out, esp from the collecting tubule, the filtrate becomes more concentrated

Question 17

renal diluting (urine) mechanism

what causes this to occur?

Answer 17

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

Question 18

creatinine

what is creatinine? is this a good test?

what are the levels you should know?

when does this go up quickly?

Answer 18

.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**

Question 19

blood urea nitrogen (BUN)

what is this a product of?

why isn’t this as good of a test as creatinine?

Answer 19

8-20

end product of protein metbolism

some gets reabsorbed after being filtered so not such a great test as creatinine

Question 20

explain the relationship between creatinine and BUN?

Answer 20

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

Question 21

what is the most common symptoms you see with electrolyte imbalances?

Answer 21

neuromuscular

Question 22

if you have a pt with neuromuscular symptoms, what should you always check?

Answer 22

electrolytes!!

Question 23

what are four things you must include as part of your clinical evaluation if suspecting electrolyte imbalances?

Answer 23

EVALUATE:

1. neurological status
2. volume status
3. metabolic/renal status
4. osmolarity

Question 24

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?

Answer 24

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**

Question 25

ADH/vasopressin ## Footnote what does this do? where does it alter permeability? when is it released (3)? what does it decrease? how does it effect the urine?

Answer 25

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: 1. decrease in blood volume 2. decrease in BP 3. 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_

Question 26

what are the two main drivers of ADH/vasopressin release? explain what happens in each

Answer 26

1. osmolarity ## Footnote 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!!!\*\*\*\*

Question 27

explain how loops and thiazides work? ## Footnote what do each excrete? where do they work? what happens to ECF? are they contracindicated in anyone?

Answer 27

Both block Na reabsorption, resulting in sodium loss from the body, since fluid follows sodium, you also get a decrease in the ECFV **LOOPS:** 1. greater loss of _BOTH_ Na and H20 than Thiazides 2. 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:** 1. block Na in the _distal convoluted tubule where 5-10%_ of Na is reabsorbed 2. _more Na_ is excreted than H20 3. 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\*\*

Question 28

suggestions for clinical evaluation: if abnormal volemia: if abnormal Na concentration: \*\*where do you look for the problem?\*\*

Answer 28

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\*\*\*

Question 29

hypertonic saline injection ## Footnote what does this do?

Answer 29

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

Question 30

hypotonic saline injection ## Footnote what does this cause?

Answer 30

dilutes the intravasculature, so it moves out and into the cells causing the cells to swell and prevents hyponatermia in the blood

Question 31

isotonic saline injection ## Footnote what does this cause?

Answer 31

same concentration as the cells so it doesn’t cause a fluid shift and the intravascular volume will simply increase, typically use this type

Question 32

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?

Answer 32

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\*\*\*

Question 33

how are volemias accessed?

Answer 33

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\*\*

Question 34

hypervolemia ## Footnote what is this caused by? what are 2 senarios that cause this in relationship to Na?

Answer 34

secondary to fluid overload 1. IV solution generated hypernatremia 2. 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"

Question 35

hypovolemia ## Footnote 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?

Answer 35

**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\*\*\*\*

Question 36

euvolemic ## Footnote what are two things that contribute to this? what causes hyperNa (3)? what causes hypoNa (2)? what do you need to remember with euvolemic?

Answer 36

**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\*\*\*\*

Question 37

hypovolemic hypotonic hyponatremia ## Footnote 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?

Answer 37

**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: 1. _**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) 2. **_electrolyte drink "gatorade" +KCL_** (if mild and oral intake intact)

Question 38

hypervolemic hypotonic hyponatremia ## Footnote 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?

Answer 38

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_** 3. diuretics

Question 39

explain how HF cirrhosis nephrotic syndrome cause _hypervolemic hypotonic hyponatremia_ \*\*\*whats something you would see in the urine\*\*\*

Answer 39

**_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

Question 40

euvolemic hyptonic hyponatremia ## Footnote why is this euvolemic? what _2 things do yo uneed to dx?_ what _are the 3 requirements_? what are 7 causes of this?

Answer 40

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\*\*** 1. **_syndrome of inappropriate ADH (SIADH)_** 2. **_post-op hyponatremia_** 3. **_psychogenic polydipsia_** 4. stroke 5. tumors 6. pulmonary lesions (TB, lung abcess) 7. **SSRIs**

Question 41

syndrome of inappropriate ADH (SIADH) ## Footnote 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)?

Answer 41

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_** 2. if asymptomatic: _H20 restriction_ _demeclocycline/tolvaptan_(clock ADH receptors so you stop getting water)

Question 42

post-op hyponatremia ## Footnote what is this caused by? what makes this situation worse? what is the tx? (2)

Answer 42

**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

Question 43

psychogenic polydipsia causing euvolemic hyponatremia ## Footnote what is is this caused by? how do they maintain euvolemic? ADH levels, urine osmolarity? Na in urine?

Answer 43

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_

Question 44

how do you determine between increase urination from diabetes insipidus and psychogenic polydipsia?

Answer 44

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

Question 45

hypertonic hyponatremia ## Footnote 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?

Answer 45

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)

Question 46

hypertonic hyponatremia caused by diabetic circumstances ## Footnote what causes this? how does this cause hyponatremia? what blood sugar do you worry about this? what is the Tx for this?

Answer 46

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**

Question 47

hyponatremia and HIV/AIDS ## Footnote what percent of hospitalized with AIDS have hypoNa? what is this often seen with?

Answer 47

_50% of pts hospitalized with AIDS have hypoNa_ often comes from _CNS/pulmonary involvment_ seen with HIV infections

Question 48

hypernatremia ## Footnote 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?

Answer 48

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

Question 49

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?

Answer 49

hypernatremia renal cause with dilute urine hallmark: _polyuria with greater than 3L in 24 hours_ inability of kidneys to conserve water appropriately 1. diabetes insipidus 2. central diabetes insipidus 3. 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_

Question 50

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?

Answer 50

"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: 1. replace water and electrolytes over _48-72 hours_ 2. .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\*\*\*

Question 51

hypernatremia with dilute urine (euvolemic) ## Footnote what is the hallmark of this? what happens in this? what 3 conditions is this seen in? what is the Uosm? 2 tx options?

Answer 51

_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: 1. central diabetes insipidus 2. nephrogenic diabetes insipidis 3. congenital nephrogenic insipidis decreased osmolarity less than 250 uosm Tx: 1. D5W-replace H20 without Na 2. .45% saline- for hyperNa and hyperglycemia

Question 52

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?

Answer 52

lack of ADH/AVP production by the posterior pituitary or loss of ADH action ## Footnote 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

Question 53

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?

Answer 53

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

Question 54

hypernatremia with dilute urine congenital nephrogenic disease what do they lack?

Answer 54

absence of ASH receptors

Question 55

hypokalemia ## Footnote what is K levels maintained by? what are 5 causes of this? what are 5 signs of this? 2 tx options?

Answer 55

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_** 3. diuretics 4. vomiting/diarrhea/sweat 5. digoxin signs: **weakness, muscle cramps, fatigue, constapation _EKG NSST-T changes and U waves, PVCS_** tx: 1. mild to mod=oral KCL 2. severe= IV admin of KCL slowly with cardiac monitoring

Question 56

hyperkalemia ## Footnote 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?

Answer 56

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: 1. if lifethreatening k greater than _6.6_ can give _infusion of insulin to drive the K inside_ to buy time 2. eliminate KCL or K sparing diuretics 3. _cation exchange resins that exchange Na for K_ 4. _dialysis for severe renal failure_

Question 57

why is calcium important? where is it mostly found?

Answer 57

50% of it is ionized to help with muscle and nerve function 40% is bound to protein mostly albumin

Question 58

why is it important to measure serum albumin to determine if Ca is truly deficient?

Answer 58

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\*\*

Question 59

hypocalcemia ## Footnote 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?

Answer 59

**_MOST COMMON CAUSE IS RENAL FAILURE_** (DECREASED VIT D3, INCREASED PHOSPHORUS) other causes: 1. hypoparathyroidism 2. 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

Question 60

hypercalcemia ## Footnote 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?

Answer 60

causes: **_1. hyperparathyroidism_** **_2. malignancy_** produce PTH **_3. milk-alkali syndrome_** Ca antacids + vitamind D excess signs: 1. **polyuria**- H20 reabsorption is blocked by hypercalcemia 2. **neuro** changes: lethargy, weakness, dowsiness 3. **shorted QT, PVCs** TX: 1. treat underlining cause 2. promote _Na rich diuresis because Ca will follow_ 3. IV infusion 0.9% saline with IV furosemide \*\*avoid thiazide diuretics, can worsen hypercalcemia\*\*

Question 61

hypomagnesemia ## Footnote 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?

Answer 61

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: 1. important to check Mg levels in hospitalized pts 2. IV therapy with MgSO4 3. oral Mg oxide can be given as supplement

Question 62

another name for acute renal failure is?

Answer 62

acutre renal injury

Question 63

another name for chronic renal failure is?

Answer 63

chronic kidney disease

Question 64

another name for end stage renal disease is?

Answer 64

end stage kidney disease

Question 65

explain what falls under the two categories of uncomplicated UTI (2) and complicated UTI? (6)

Answer 65

**uncomplicated UTI** - acute cysitits - acute pyelonephritis **complicated UTI** 1. 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

Question 66

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?

Answer 66

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_**

Question 67

Complicated UTI eldery what are two groups of peopel that are esp susceptible? what are three things that contribute to the first?

Answer 67

**postmenopausal women** 1. bladder/uterine prolapse 2. loss of lactobacilli in vaginal flor allos for E. coli to take over 3. diabetes (sugar) **benign prostatic hypertrophy**

Question 68

complicated UTI children who is this more common in? 3 symptoms? what is the DOC? how long do you treat for, two options?

Answer 68

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

Question 69

complicated UTI males what are two risk factors? urethra length?

Answer 69

unusual for men 15-50 RF: **uncircumcised, anal intercourse** antibacterial material in prostatic fluid **18-20 cm urethra**

Question 70

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?

Answer 70

**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: 1. colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder **CYSTITIS** 2. uropathogens ascend from bladder to kidney via ureters RARELY CAUSED BY SEEDING OF BACTERIA

Question 71

what are 5 RF for UTI?

Answer 71

female sex frequent sexual intercourse diaphragm/spermicide use delayed post-coital micturition (not urinating after intercourse) hx of UTI

Question 72

what are four bacteria that cause UTI and which is by far the most common? what percent?

Answer 72

**e.coli most common 75-95%** proteus mirabilis klebsiella pneumoniae enterococcus

Question 73

what are the difference in symptoms for cystitis (6) vs pyelonephritis? (5)

Answer 73

cystitis: ## Footnote 1. dysuria or burning while urination 2. increased frequency/urgency 3. suprapubic pain/discomfort 4. hematuria 5. voiding small amounts 6. AFEBRILE pyelonephritis 1. FEBRILE 2. chils 3. flank pain 4. costovertebral tenderness 5. CBC with left shift

Question 74

what 3 lab tests are important to do when diagnosiing a UTI? what do you find on each?

Answer 74

**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**

Question 75

what are the DOC fo acute cystitis (4) vs pyelonephritits (2)? what do you need to note?

Answer 75

**_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!!!\*\*\*\*\*

Question 76

what is the DOC for an inpatient with UTI/pyelonphritis?

Answer 76

CIPROFLOXACIN!! others: fluoroquinolone, amp+gentamycin, ceftriaxone

Question 77

what is the most common nosocomial infection in the US? what is the tx protocol with this?

Answer 77

cathertized associated UTI ## Footnote _if asymptomatic don’t need to treat with abx_ screen urine 48 hours after removing catheter

Question 78

recurrent UTIs ## Footnote what are the two definitions of this? what should you consider? what about in women with decrease in lactobacillis?

Answer 78

_3 or more episodes per year confirmed UC_ OR _2 UTIs in last 6 months_ ## Footnote consider self treatment at first sign (urine cup for UC) vaginal estrogen in women since they have a decrease in lactobacillus

Question 79

in _asymptomatic bacteremia_ who do you treat (3) and who do you not treat (3)? \*key!\*

Answer 79

**_treat:_** 1. pregnant 2. before urologic procedures 3. after renal transplant **_DONT TREAT_** 1. diabetics 2. elderly 3. patients with spinal cord injury or indwelling urethral catheter

Question 80

do you tx UTI empirically while waiting for culture?

Answer 80

YES! then adjust abx as appropriate! :)

Question 81

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?

Answer 81

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: 1. calcium oxalate 2. struvite 3. uric acid 4. cystine

Question 82

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?

Answer 82

MOST COMMON TYPE OF STONE 1. **_RADIOOPAQUE_** 2. usually associated with high calcium levels in the blood and urine 3. 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%)

Question 83

nephrolathiasis struvite stone what 2 things is this associated with? 4 bacteria? can you pass them? when do they get bigger? 3 tx options?

Answer 83

**_"staghorn" stones that always associated with UTI and alkaline urine_** 1. produced by UTI with urease producing bacteria 2. _proteus, klebsiella, pseudomonas, enterobacter_ 3. made of magnesium ammonium 4. usually too large to pass and require lithotripsy or surgical removal 5. they enlarge as the bacterial count increases Tx: 1. prevent UTIs 2. lithrotripsy 3. surgical removal

Question 84

nephrolithiasis uric acid stone what is this caused by? can you see on xray? what are 2 RF? 2 tx options?

Answer 84

**_caused by low Ph (acidic) urine \<5.6 for greater than 24 hours_** 1. **_radiolucent_** cant be seen on xray 2. caused by high levels of uric acid in the urine or gout 3. RF: obesity/diabetic or both Tx: 1. decrease uring PH below 6 (more alkaline) using _potassium citrate_ 2. allopurinol with decrease purine diet (fish, shellfish, and meats)

Question 85

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?

Answer 85

**_autosomally recessive inherited abnormalities CYSTINURIA_** "childhood caliculi" 1.**_smooth-edged ground glass appearence_** TX: 1. increase urine volumes to 3 L a day and increase urine pH to greater than 7 2. occasionally chelating agents

Question 86

what are 6 RF for nephrolithiasis in general?

Answer 86

high humidity high temp sedentary high animal protein and high salt FH for calcium stones hyperthyroidism/hypothyroidism

Question 87

what are the 4 most common symptoms with nephrolithiasis? and less common symtpoms? (4)

Answer 87

**Most common:** 1. unilateral flank pain 2. sudden onset 3. renal colic 4. hematuria **Less common:** 1. vague abdominal pain 2. acute abdominal/flank pain 3. difficulty urinating 4. penile or testicular pain

Question 88

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?

Answer 88

1. non-contrast CT (gold standard) used to identify the size, location and type of stone ## Footnote - _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\*\*\*\* 2. labs 1. urinalysis (stone type/blood) 2. BMP (calcium and creatinine if worried about kidney function) 3. 24 hour urine for the amount excreted 4. thyroid function test

Question 89

chart that puts it all together

Answer 89

:)

Question 90

what is the most common cause of recurrent calcium stones?

Answer 90

most common abnormality elevated Ca excretion, decreased serum Ca

Question 91

stone passage ## Footnote 1. explain how size and location effect the ability to pass the stone? 2. what are two meds you can give to help during the passage?

Answer 91

**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)

Question 92

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)?

Answer 92

1. most managed conservatively with pain management Nsaids and Opoids (BETTER USED TOGETHER!!) 2. hydration 3. strain urine **consider hospitalization:** uncontrolled pain/fever can’t tolerate oral intake

Question 93

what are 6 things that would qualify for urologist referral in a patient with nephrolithiasis?

Answer 93

acute renal failure urosepsis urinary obstruction concomitant pyelonephritis \>10 cm haven’t passed for 4-6 weeks

Question 94

what are the 5 tx options for nephrolithiasis?

Answer 94

**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)

Question 95

why is it important to educate your patient on recurrence for nephrolithiasis?

Answer 95

⅓ will experience stone recurrence within 5 years ½ experience stone reccurence within 10 years

Question 96

explain the blood flow through the kidneys? 9 steps

Answer 96

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

Question 97

explain the difference between the two capillary beds found in relationship to the nephron?

Answer 97

**glomerular capillary bed** 1. brings blood to the glomerulus 2. _high pressure system at 60 mmHg_ allows for FILTRATION **peritubular capillaries** 1. 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 2. _low hydrostatic pressure around 13 mmHg_ allow for ABSORPTION

Question 98

what is the rate of blood flow through the glomerulus?

Answer 98

1200 ml/min

Question 99

explain the two different types of nephrons found in the kidney? where are they? what is their function?

Answer 99

**_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_

Question 100

what are the two major mechanisms for maintaining renal blood flow and eGFR effecting both the efferent and afferent renal blood flow?

Answer 100

1. myogenic mechanism 2. tubuloglomerular feedback menchanism

Question 101

myogenic mechanism ## Footnote 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?

Answer 101

1. pressure sensitive mechanism 2. relies on intrinsic mechanism of vascular smooth muscle that cause it to _contract when stretched_ 3. as arterial pressure rises and the _afferent arteriole is stretched=__the smooth muscle contracts_ _when the afferent pressure falls= it relaxes_

Question 102

tubuloglomerular feedback mechanism via juxtaglomerular apparatus ## Footnote 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?

Answer 102

1. _NaCl_ concentration in the tubular fluid is sensed by the **_juxtaglomerular apparatus in the distal tubule_** 2. occurs where the _distal tubule_ extends back to the glomerulus and then _passes between the afferent and efferent arterioles_ 3. 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_** 4. 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

Question 103

eGFR marathon runner analogy what happens in these: 1. constricting afferent arteriole 2. constricting efferent arteriole 3. dilating efferent arteriole 4. dilating afferent arteriole

Answer 103

**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

Question 104

what effect do these have on the arteriole system of the glomerulus? prostaglandin angiotensin II

Answer 104

**prostaglandin**: dilates the afferent arteriole **angiotensin II:** constricts efferent areteriole

Question 105

1. explain the blood flow as it moves through the glomerulus and out of the kidney? 2. where do the two greatest drops in BP occur? what is this area known as? what is it nessacary to maintain? 3. what medication works in the above area?

Answer 105

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

Question 106

what are the 4 main function of the kidneys?

Answer 106

1. filtration 2. reabsorption 3. secretion 4. excretion

Question 107

kidney filtration ## Footnote when does this occur? what is this caused by? what do you use to measure it? what is normal amounts?

Answer 107

1. first step in urine formation 2. bulk movement of fluid from blood into kidney tubule - isosmotic filtrate - blood cells and larger proteins don't filter 3. caused by **_hydralic pressure_** 4. **Glomerular filtration rate:** amount of filtrate produced in the kidneys each minute 125 mL/min=180L per day

Question 108

kidney reabsorption ## Footnote what is this the process of? what percent of filtrate is reabsorpbed? what can aid in this process? what is totally reabsorbed?

Answer 108

process of returning filtered material to bloodstream **99%** of what is filtered is reabsorbed may involve **transport proteins** normally _glucose_ is totally reabsorbed

Question 109

kidney secretion ## Footnote what is this? what are two things that rely on active transport?

Answer 109

material added to the lumen of kidney tubule from blood active transport (usually) of toxins and foreign substances 1. saccharine 2. penicillin

Question 110

kidney excretion ## Footnote what is this? what is the equation for amount of solute excreted?

Answer 110

**loss of fluid from body in form of urine** excreted means=as urine _amount of solute excreted_= (amount filtered +amount secreted) - amount reabsorbed

Question 111

glomular filtration rate is regulated by what 3 mechanisms?

Answer 111

**the amount of plasma that is filtered each minute** provides information about the kidneys ability to filter and reabsorb/secrete substances 1. renal autoregulation 2. neural regulation 3. hormonal regulation

Question 112

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?

Answer 112

**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: 1. myogenic mechanism (response to pressure changes in the afferent arteriole) 2. tubuloglomerular feedback (response to Na concentration in the distal renal tubule) causes RENIN release

Question 113

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?

Answer 113

sympathetic nerve fibers from _renal plexsus_ of autonomic nervous system innervate SM afferent and efferent arterioles at the hilus ## Footnote sympathetic stimulation causes constriction of the afferent and efferent arterioles and thus decreases renal blood flow Effects: 1. reduce the GFP and GFR through contracting the afferent and efferent arterioles through _alpha receptors_ 2. increase Na resorption in proximal tubules _B receptors_ 3. 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_**

Question 114

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?

Answer 114

1. cardiopulmonary reflex 2. baroceptor reflex 3. 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_**

Question 115

GFR: hormonal regulation 6 things

Answer 115

**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

Question 116

glomerular filterability ## Footnote 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?**

Answer 116

**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**: 1. blood colloid osmotic pressure (COP) 2. capsulre pressure (CP) moves out based on glomerular hydrostatic pressure

Question 117

what are the three tests you use can use to measure GFR?

Answer 117

1. inulin 2. creatinine 3. Blood urea nitogen

Question 118

measurement of GFR: inulin 5 characteristics that make this work

Answer 118

1. freely filtred at the glomerulus 2. biologically inert 3. not synthesized or metabolized by the kidney 4. does not alter renal function 5. can be accurately quantitfied

Question 119

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?

Answer 119

**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\*\*

Question 120

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)

Answer 120

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

Question 121

what percent is: filtered reabsorbed excreted what is the reabsorption of: glucose Na water creatine

Answer 121

20% of bllod is filtered 19% reabsorbed 1% excreted glucose: all reabsorbed Na and water: nearly all reabsorbed 99% creatinine: none reabsorbed

Question 122

what are the two absorption pathways?

Answer 122

transcellular: from lumen through the cell paracellular: from lumen between the cells

Question 123

what are the four mechanisms of transport seen in the nephron? 1 2 1 1

Answer 123

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) 2. **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

Question 124

proximal convoluted tubule ## Footnote 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?

Answer 124

**_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:** 1. _Na_ reabsorbed by _co-transport with glucose and amino acids_ **second half of PCT:** 1. _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

Question 125

explain the process of glucose and amino acid reabsorption in the proximal convoluted tubule? ## Footnote what is this limited by? what concentration in the blood causes this? what is this caused? what are the values?

Answer 125

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

Question 126

secretion of H+, acids, and bases bicarbonate ## Footnote 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?

Answer 126

occurs at **proximal tubules, loop of henle, and early distal tubule** 1. **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

Question 127

loop of henle: think descending loop what happens here and why?

Answer 127

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!

Question 128

loop of henle: thick ascending limb what percent is absorbed here? what is absorbed (6) what is secreted? why does this happen?

Answer 128

**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\*\*\*

Question 129

k excretion..how much do you loose a day so how much do you need to replace?

Answer 129

oose 12% a day so need to take in this much or 92 mEq to replace daily losses

Question 130

Ca regulation ## Footnote what hormone controls this? what happens to Ca? where does this occur (2)?

Answer 130

both filtered and reabsorbed in the kidneys but not excreted only 50% of plasma calcium is ionized with the remainder bound to plasma proteins, excretion is adjusted to meet body’s needs **_parathyroid hormone (PTH) increases calcium reabsorption_** in the **_thick ascending loop of henle_** and **_distal tubules_** and reduces urinary excretion of Ca

Question 131

urine concentration and dilution ## Footnote 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?**

Answer 131

**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: 1. controlled secretion of **_ADH_** **_from posterior pituitrary gland_**which 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** 2. **_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

Question 132

explain the presence or absence of ADH effect on urine concentration?

Answer 132

ADH PRESENT: water absorbed leaving concentrated urine ADH ABSENT: no water absorbed leaving dilute urine

Question 133

how is hyperosmotic renal medullary interstitium maintained by the: 1. thin descending limb 2. thick ascending limb 3. collecting ducts what this this produced by?

Answer 133

**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

Question 134

what are three ways that water is reabsorbed/excreted?

Answer 134

1. obligatory water reabsorption 2. facultative (selective) water reabsorption 3. solute/osmotic diuresis

Question 135

water movement: obligatory water reabsorption what is this largely dependent on? what are the two ways this occurs by?

Answer 135

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”

Question 136

water movement: facultative (selective) water reabsorption what is this regulated by? what are the 4 steps? where does this most often occur?

Answer 136

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**

Question 137

water movement: solute/osmotic dieuresis what is this caused by? what happens? what type of kidney?

Answer 137

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

Question 138

aldosterone ## Footnote what type of componet is this? what cause it cause and where? what are two things it does and where does it take place?

Answer 138

**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\*\*

Question 139

atrial Natriuretic Peptide (ANP) ## Footnote when is this released? what does it inhibit? (3) what does it promote (2)

Answer 139

released by atrium in response to atrial stretching due to increased blood volume inhibits Na and water reabsorption, and ADH secretion promotes increased sodium excretion (natriuresis) and water excretion (diuresis) in urine

Question 140

what do these cause: **_Angiotensin II, ADH, and endothelians_** and what about these: **_Dopamine, NO, PGE2, PGI2_**

Answer 140

**_Angiotensin II, ADH, and endothelians:_** **VASOCONSTRICTION** to maintain pressure \*\*think about it, angiotensin II and ADH are released when decreased profusion so if less fluid the afferent and efferent arterioles must constrict to maintain the pressure in the glomerular capillaries\*\* **_Dopamine, NO, PGE2, PGI2_** **VASODILATION** to maintain pressure \*\*think about it....ASA and NSAIDS inhibit prostaglandins so thats why you get constriction and increase BP\*\*

Question 141

micturition ## Footnote what is this? what are the 3 steps that occur?

Answer 141

once urine enters the renal pelvis, it flows through the ureters and enters the bladder where urine is stored micturition is the process of emptying the urinary bladder processes: 1. fills progressively until the tension in the wall rises above threshold level then 2. a nervous reflex called micturition reflex that empties that bladder 3. automatic spinal cord reflex, however, it can be inhibited or facilitated by centers in the brainstem and cerebral cortex

Question 142

micturation ## Footnote 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

Answer 142

**originates in sacral S1-S4** combination of Motor function: 1. Stimulation of _parasympathetic neurons_=contraction of _detrusor muscle and internal urterthral spincter (involuntary) via pelvic nerve_ 2. inhibition of _somatic_ neurons=_relaxation of external spincter (voluntary) via pudenal nerve_

Question 143

explain the process of an AP that causese micturitiion? what are the four main steps? what if its an ok time to urinate? what if not ok time to urinate?

Answer 143

1. APs generated by stretch receptors 2. reflex arc generates AP that stimulate smooth muscle lining bladder 3. relax internal urethral sphincter 4. stretch receptors also send AP to pons **if appropriate time to urinate:** APs from pons excite smooth muscle of bladder and relax Internal urethral sphincter relax external urethral sphincter **if not appropriate time to urinate:** APs from pons keep external urethral sphincter contracted

Question 144

Elderly what happens to number of functional nephrons? what happens to GFR? what happens to sensitivity to ADH? what about micturition?

Answer 144

1. decline in the number of functional nephrons 2. reduction of GFR based on number of function nephrons 3. reduced sensitivity to ADH of those that are left, so elderly have more dilute urine 4. problems with micturition reflex

Question 145

tubular disorders: ## Footnote _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?

Answer 145

_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: 1. _flank pain_ from ruptured cyst 2. gross episodes of hematuria from bleeding into cysts 3. _infected cysts from ascending UTIS (most common thing reported by pt)_ 4. HTN 5. 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!!_

Question 146

what is improtant to do if you have a patient with confirmed polycystic kidney disease?

Answer 146

SCREEN IN ASYMPTOMATIC FAMILY MEMBERS!!!

Question 147

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!\*\*

Answer 147

1. cysts in the _liver_ 2. _mitral valve prolapse_ 20-25% 3. _cerebral aneurysm_ from weakness in the cerebral arteries 20%

Question 148

autosomal recessive polycystic disease ## Footnote who does this present in? what becomes abnormal? what gene is responsible? what are 5 symptoms? what is the tx?

Answer 148

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

Question 149

tubular disease: _renal tubular acidosis (RTA)_ TYPE 1 what does this alter? pH? what type of metabolic acidosis is it characterized by? tx?

Answer 149

**_alteration of H+ transport_** urine pH high greater than 5.5 hypercalcemia **_hypokalemic, hyperchloremic non-anion gap metabolic acidosis_** Tx: **_alkalinize urine-NaHCO3_**

Question 150

tubular disease: _renal tubular acidosis_ TYPE 2 what is this a defect in? pH? what is it characterized by?

Answer 150

proximal **_defective bicarbonate reabsorbtion_** urine pH less than 5.5 **_hypokalemic, hyperchloremic non anion gap metabolic acidosis_**

Question 151

tubular disease _renal tubular acidosis_ TYPE 4 what is this caused by? what are 3 causes? what are 3 tx options?

Answer 151

**_hyperchloremic distal RTA_** acidic urine **_hypercholoremic hyperkalemic acidosis_** **_abnormal tubular secretion of K and H, abnormal aldosterone production or aldosterone resistance_** causes: 1. NSAIDS 2. ACE-I 3. renal disease like DM nephropathy Tx: 1. low K diet 2. stop offending meds (K sparing diuretics like spirolactone, amiloride, and tiameterence 3. minteralcorticoids

Question 152

acute nephritic syndrome ## Footnote what is this? what are the 4 things it is characterized by? what are the two main causes?

Answer 152

**_acute inflammation that occludes the glomerular capillary lumen and damages the capillary wall_** characterized by: 1. inflammation 1. suddent onset **hematuria** **(RBC casts)** active urinary sediment 2. HTN 2. diminished GFR 3. oliguria (decreased urine) 4. signs of impaired renal function two main causes: 1. acute postinfectious glomerulonephritis 2. rapidly progressing glomerulonephritis

Question 153

nephritic syndrome: Immune complex nephropathies: acute postinfectious glomerulonephritis who is this common in? when does it occur? what is the most common organism to cause this? two ways this can occur? what is the damage caused by? (3)

Answer 153

**This is an immunecomplex nephropathy** **Post streptococcal glomular nephritis is the most common immune complex nephropathies** most common in children but can be in anyone, most commonly follows a strep infection by **_10 days_** most commonly **_Group A strep pharngitis_** but can be **_impetigo skin_** infection as well **_after 2 weeks_** characterized: 1. acute 2. oliguric 3. decreased GFR 4. focal or diffuse in kidney other causes: staph, viral chickenpox, measles, mumps Caused by deposition of immune complexes in the kidneys, rare in industerialized areas deposition causes swelling of endothelial cells and swelling, proliferation, and leukocyte infiltratation obliterates the glomerular capillary lumens

Question 154

nephritic syndrome: immune complex nephropathies: acute postinfectious glomerulonephritis what are the 6 symptoms associated with this? tx option? how do you dX:what sometimes occurs?

Answer 154

1. _oliguria_ from decrease GFR, one of the first symptoms 2. _proteinuria and hematuria_ follow from increased glomerular capillary wall permeability from damage 3. _cola colored urine_ 4. _edema_ of hands and face _5. HTN_ 6. elevated anti strep antibodies DX: _circulating levels of antrstreptolysin antibodies_ TX: 1. abx and supportive 2. many have spontaneous remission in 6-8 weeks prognosis is good!

Question 155

nephritic syndrome: anti-glomerular basement membrane disease: rapidly progressive glomerulonephritis what is the characterized by? what are 2 causes of this? how do you dx this? how do you tx this?

Answer 155

subacute used interchangeably with "crescentric glomular nephritis"-moon shaped lesions in bowmans space antibodies against type IV collagen called anti GBM antibodies glomerular ijury without a specific cause, occurs within a matter of months proliferation of glomerular cells and recruitment of monocytes and macrophages destroy bowmans space Causes: SLE, Goodpastures syndrome DX: renal bx to show IgG along GBM Tx: **_immunosupressants_**

Question 156

nephritic syndrome: rapidly progressive glomerulonephritis: _Goodpasture syndrome_ what is this caused by? what else can it cause in a unrelated system? what is the hallmark? do we know the cause? associated with (2)? 2 tx options?

Answer 156

uncommon and aggressive form of glomerulonephritis **_antibodies to glomerular basement membrane_** antibodies cross react with the lungs so cause renal failure _associated with pulmonary hemorrhages_ **HALLMARK: _diffuse linear staining of glomerular basement membrane for IgG_** DON'T KNOW CAUSE: ASSOCIATION WITH _INFLUENZA AND PAINT_ TX: 1. plasmapharesis to remove IgG 2. immunosuppresive therapy (corticosteroids/cyclophosphamide)

Question 157

what are the three types of Pauci immune glomerular nephritis? what is it characterized by?

Answer 157

characterized by: **glomerulonephritis without IG** Idiopathic renal limited crescentic GN Microscopic polyarteritis nodosa (PAN) Wegener’s Granulomatosis

Question 158

nephritic syndrome: idiopathic crescentic glomerular nephritis

Answer 158

middle aged men crescent involvement of the kidneys Tx: steroids

Question 159

what are the serum tests you want to do to help dx nephritis/RPGN?

Answer 159

bx often required! immunoflorescence serum testing: 1. C3 2. anti GBM 3. antineutrophilic cytoplasmic antibodies (ANCA)

Question 160

nephrotic syndrome ## Footnote 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?

Answer 160

\*\*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: 1. _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 6. high cholesterol!! 7. HYPERCOAGUBILITIES....so at increase risk for clots/DVT three main causes: 1. minimal change disease 2. membraneous glomerulonephritis 3. focal segmental glomerulosclerosis

Question 161

what is the general tx for proteinuria ?

Answer 161

1. dietary protein restriction 2. ACE-inhibitor 3. NSAIDS

Question 162

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?

Answer 162

**_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

Question 163

nephrotic syndrome: membraneous glomerulonephritis what is the patho? what is this caused by? (5) what are the 3 main symptoms? tx?

Answer 163

**_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: 1. peripheral edema 2. hypoalbuminemia 3. hyperlipidemia Tx: controversial since often times the pt has spontaneous remission and it is relatively benign

Question 164

nephrotic syndrome: focal segmental glomerulosclerosis what occurs in this? who is this the most common in? what are 4 secondary causes of this? tx?

Answer 164

**sclerosis and increase in collagen deposition** in some but not all of the glomeruli GENETIC leading cause of nephrotic syndrome in **_African Americans_** causes: idiopathic or secondary including: reduced o2 in the blood from sickle cell, CHF, HIV, IV drug use Tx: corticosteroids

Question 165

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?

Answer 165

"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 1. _gross hematuria preceded by URI_ 50% have single episode 2. diagnostic findings: **_mesangial staining for IgA_** tat is more intense than staining for IgG or IgM TX: NO TREATMENT

Question 166

hereditary nephritis "alport syndrome" what happens in this? what is the inheritance? how do you dx it and how is it normally found? what are 2 random things associated with it?

Answer 166

hereditary child defect of the glomerular basement membrane that results in hematuria and may progress to chronic renal failure as adults _X linked autosomal dominant trait_ 1. heavy microscopic _hematuria_ that progresses to _proteinuria_ 2. usually picked up from checking urine of family with known dx 3. **_sensorineural deafness, billateral_** **_4. eye disorders_** lense dislocation, post cataracts, corneal dystrophy

Question 167

inherited glomerulopathies Fabry's disease what is this a disorder of? what accumulates? what type of inhertiance? what are 6 abnormal findings you would see?

Answer 167

**_Lysosomal storage disease_** accumulation of _globotraoslyveramide (Gb3)_ _X-linked_ Abnormalities: 1. 50% in ESRD 2. neurological (stroke, TIA) 3. telegenctasis 4. skin deposits 5. corneal lesions 6. cardiac (LVH, CAD, valvular disease)

Question 168

chronic glomerulopathies: systemic immune disease: _polyarteritis nodosa_ what is this? 4 features? 2 tx options?

Answer 168

systemic disorder features: 1. HTN 2. urine sediment 3. renal insufficiency 4. negative ANCA Tx: glucocorticoids chemo agents

Question 169

chronic glomerulopathies: systemic lupus erythematous glomerulonephritis what is this caused by? what should all SLE pts do? what are the 2 tx options?

Answer 169

"lupus nephritis" **most common complication from SLE** caused by deposition of immune complexes with the glomerular wall all patients with SLE should undergo _routine urine analysis_ to monitor for _hematuria_ and _proteinuria_ DX: + ANA low complement Tx: _1. glucocorticoids_ _2. chemo_

Question 170

Chronic Glomerular disease: diabetic nephropathy what is this? what does it occur with? pathophys of it? why does sugar play a role? DX (2)? 5 tx options?

Answer 170

**_most common cause of kidney failure treated by renal replacement therapy in the US_** occurs with: T1DM (30%), T2DM (20%) Mechanisms: HYPERGLYCEMIA, INTRAGLOMERULAR HTN, AND GLOMERULAR HYPERTROPHY widespread _thickening of glomerular basement membrane_ with diffuse _increase in mesangial matrix_ and _proliferation of these cells_=**impinge capillary lunem**, reducing the SA available for filtration _REISERT_: INJURED FILTRATION BARRIER WITH THICKENED GLOMERULAR BASEMENT MEMBRANE - pores bigger - electrical barrier favors passage of protein screen DM every year for this if TYPE II and after 5 years of type 1!! inappropriate incorporation of glucose into these noncellular components of the glomerular structures DX: increased GFR with _microalbuminuria_ TX: 1. **_control BS_** _2. ACE/ARB to decrease glomerular pressure_ 3. _control BP **Goal less than 130/80**_ 4. smoking cessation 5. weight loss

Question 171

what are 3 deposition diseases that cause glomerulopathy?

Answer 171

**1. amyloidosis** a. abnormal protein in the glomerulus b. biopsy shows green apple befringence under polarized light using congo red stain c. tx unsuccesfful **2. light chain disease** **3. wldenstroms macroglobinemia** -due to IGM secreting plasma cell clone

Question 172

name four drugs that can induce nephropathies?

Answer 172

1. NSAIDS 2. Gold 3. penicillamine 4. IV heroin

Question 173

stress urinary incontinence ## Footnote who is this common in? why does it occur? explain the pressure differences? what actions might bring this on? what are 3 things that could cause this in a person?

Answer 173

common problem in **women** of all ages and results from **weakness or disruption in the pelvic floor muscles** leading to poor support of the **vesicourethral sphincters** usually: the i_ntraurethral pressure is greater than the intravesicular pressure_ which is called the urethral closure pressure if i_ntra-abdominal pressure increases_ from things like coughing, laughing, or sneezing and the pressure isn’t equally distributed to the urethra then incontinence occurs causes of decreased muscle tone: aging, child birth, surgical procedures

Question 174

urge urinary incontinence ## Footnote what does the pt feel? what is this associated with? what is the definition of this? what are 2 contributing factors? 3 symptoms?

Answer 174

overactive, nocturia, urinary frequency, detrusor overactivity ## Footnote loss of urine associated with _strong desire to void URGENCY,_ often associated with **overactive bladder** **definition:** urgency, frequency with or without incontinence in the absence of UTI or obvious pathology Two contributing factors to overactive bladder: 1. CNS and neural control of bladder sensation and emptying, ex: stroke, Parkinsons, MS 2. smooth muscle of the bladder itself (myogenic)

Question 175

incomplete emptying "overflow" urinary incontinence ## Footnote what are 7 signs of this? what are two causes? what are 2 causes in women? what are 2 causes in men?

Answer 175

intravesical pressure exceeds the maximal urethral pressure because of _bladder distension_ dribbling, weak urinary stream, frequency, and nocturia, hesitancy, frequency, nocturia, nocturnal enuresis (bedwetting), **_detrusor underactivity_** or **_bladder outlet obstruction_** **women** causes: uterine prolapse, previous incontinence surgery **men**: most common is enlarged prostate gland

Question 176

what are the 3 PE tests you want to do with someone with urinary incontinence? what are the 4 workup tests you would do?

Answer 176

**PE:** 1. pelvic exam 2. digital rectal exam (masses, prostate) 3. neuro exam if sudden loss (think cauda equina) **Workup:** 1. urinalysis 2. prostate specific antigen 3. post void bladder scan 4. urology consult

Question 177

although urinary incontince tx is dependent on the type, what are 5 tx options you could consider?

Answer 177

1. fluid management 2. timed voiding 3. bladder retraining 4. keagle/pelvic floor exercises 5. surgical intervention

Question 178

obstruction in UT ## Footnote what are some causes of this? what are the two big things this causes? concerns with each? 2 1

Answer 178

many things can cause obstruction: caliculi, cancer, pregnancy, stones, defects etc. Key points of things that it causes: 1. stasis of urine: predisposes to **_infection and stone function_** **_infection:_** urea splitting bacteria like **_proteus and staph_**, these increase the _ammonia levels_ and cause urine to become more _alkaline_ **_alkaline urine:_** calcium salts are able to precipitate in alkaline urine better so obstruction predisposes to stone formation 2. dilation progressive dilation of the renal collecting ducts and renal tubular structures from backflow which causes atrophy of the renal tissue

Question 179

hydronephrosis ## Footnote what is this and what does it cause? characteristics? who should this be susepcted in? if caught early? if caught late?

Answer 179

**_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**

Question 180

hydronephritis ## Footnote what determines presentation? what are the 5 symptoms? how do you DX and what do you see?

Answer 180

presentation depends on site of obstruction, degree, and speed at which obstruction occurs SYMPTOMS 1. pain 2. change in urine output 3. HTN 4. Hematuria 5. increased serum creatine DX: TEST OF CHOICE: RENAL ULTRASOUND **\*\*dilation of renal collecting system in one or both kidneys\*\***

Question 181

renal artery stenosis ## Footnote 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?

Answer 181

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: 1. renal angiography is gold standard 2. less invasive test is **TEST OF CHOICE: doppler US, STA, MRA**

Question 182

urethrovesicular reflux ## Footnote when does it occur? what happens? why is this a bad thing?

Answer 182

urine from the urethra moves into the bladder ## Footnote occurs during activites like **coughing** or **squatting** where the i_ntraabdominal pressure increases_ and causes the urine to be squeezed into the urethra and the _flow backwards into the bladder as the pressure decreases_ the urethra is contaminated with bacteria so this increases the likelyhood for infection in the bladder

Question 183

vesicoureteral reflux ## Footnote where does this occur? what does this cause?

Answer 183

occurs are the level of the _bladder and the ureter_ and allows urine and bacteria to ascend from the bladder to the kidney and can cause _pyelonephritis_

Question 184

what is the most common cause of renal cancer?

Answer 184

renal cell carcinoma

Question 185

renal cell carcinoma ## Footnote 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?

Answer 185

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: 1. clear cell 2. papillary 3. chromophobe 4. collecting 5. unclassified

Question 186

what are the 5 metastasis place for renal cell carcinoma?

Answer 186

lung, lymph nodes, bone, liver, brain

Question 187

what are the 6 RF for **_renal cell carcinoma_**?

Answer 187

1. **_SMOKING!!_** 2. **50-70 year olds** 3. **_Von Hipple-lindau:_** family hx, can transfer into _malignant pathology_ of _CNS_ brain spinal cord and kidneys most common **4. _tuberous sclerosis_**: can become large, benign 5. long term dialysis 6. obesity

Question 188

renal cell carcinoma ## Footnote what are the 3 most classic symptoms? what are 4 other symptoms?

Answer 188

**CLASSIC TRIAD:** **1. flank pain** **2. PAINLESS hematuria** **3. palpable flank abdominal renal mass:** firm, homogenous, and nontender (few have all of these) also intermittent fever night sweats anorexia weight loss fatigue

Question 189

renal cell carcinoma ## Footnote 3 tests to work up? 1 tx option and 2 subgroups? what is NOT effective!!!

Answer 189

**WORKUP:** often find incidently for routine work up for something else **1. urinalysis: microscopic hematuria _retest if suspcicious_** **2. _CT_** or US **3. MRI** if concerned with mets, PET to confirm **TX:** **first line: surgical eradication only cure!!!** **1. resection** **2. ablation with cryotherapy or embolization** **_CHEMO/RADIATION NOT EFFECTIVE!!!_**

Question 190

how does the staging of renal cell carcinoma effect tx options? what are the two staging methods?

Answer 190

stage I-III: resection Stage IV: pallative TNM and Robson staging

Question 191

what are the two most common types of renal cell carcinoma? what do they look like?

Answer 191

1. clear cell renal celll carcinoma 7/10: clear or pale under microscope MOST COMMON ## Footnote 2. papillary renal cell carcinoma: 10%, finger like projections on the tumor

Question 192

what are the 5 differnt types of rencal cell carcinoma?

Answer 192

**1. clear cell renal cell carcinoma**: clear/pale **2. papillary renal cell carcinoma:** finger like projections **3. chronophobe renal cell carcinoma:** large **4. collecting duct renal cell carcinoma:** irregular tubes **5. unclassified**

Question 193

what type of renal cancer effect the blood vessels or connective tissue?

Answer 193

renal sarcomas

Question 194

wilms tumor ## Footnote 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?

Answer 194

**MOST COMMON RENAL CANCER IN CHILDREN** "nephroblastoma" dx 3-5 years old most common primitive cells of _renal cortex_ associations: 1. absense of iris 2. enlargement of the side of face 3. genituiatry complications SX: 1. abdominal mass/swelling w/o other symptoms (parents find while dressing) 2. hematuria 20-25% 3. **_HTN IN CHILD!! HUGE KEY_** 4. fever, abdominal pain less common

Question 195

wilms tumor ## Footnote what do you find on PE? test of choice? two others? 3 tx options?

Answer 195

PE: firm, nontender, smooth mass that is _eccentrically located_ and rarely crosses the midline tests: 1. _CT scan test of choice_, US, MRI tx: surgery, chemo, radiation IT IS RESPONSIVE TO CHEMO/RAD

Question 196

what do you want to make sure you NEVER do to a patient with suspected wilms tumor? ## Footnote prognosis?

Answer 196

you NEVER biopsy because it runs risk of _RUPTURE_ which allows it to spread! ## Footnote STAGING OCCURS AFTER RESECTION!!! prognosis good before METS!

Question 197

transitional cell cancer or urothelia carcinoma ## Footnote what population do you see this in (2)? what is this a cancer of? where else can you find it (3)? one additional type? danger?

Answer 197

_55+, 50% cases SMOKERS!!!!!!_ cancer of the _mucosal lining_ of the _bladder_, _papillary growth_ also in renal pelvis, ureters, urethra where these transitional cells are found **urothelial carcinoma in situ (CIS) does not invade the submucosa** irregular red sports on cytoscopy but **_CAN PROGRESS TO INVASIVE CARCINOMA_**

Question 198

what are the 3 RF for urothelial carcinoma/transitional cell cancer?

Answer 198

1. smoking 50% of pts 2. aniline dyes 3. leather woodwork

Question 199

Transitional cell cancer/urothelial carcinoma ## Footnote what are the 3 symptoms of this? _hallmark?_ what are the two test you run if suspecting this? how do you dx (2)?

Answer 199

1. _painless hematuria typical_ ## Footnote 2. may have back pain 3. may have dysuria tests: **_1. KUB: kindey ureter bladder_**: xray of choice, do pregnancy test first **_2. intravenous pyelogram_**: dye injected into kidney to highlight mass \*do post micturition view DX: 1. **_CYSTOSCOPY_** **_2. biopsy_**

Question 200

how do you tx transitional cell cancer/urothelial carcinoma? ## Footnote (4) what must you do?

Answer 200

1. carcinoma in situ-BCG vaccine/TB vaccine injected into site 2. resect part of the involved bladder for recurrent carcinoma in situ or invasive urothelial carcinoma 3. create new bladder from intestine, store in ostomy bag 4. _resection and chemo, monitor for annual regrowth via cytology!!_

Question 201

what do you need to educate your patient about if they have transitional/urothelia carcinoma?

Answer 201

80% will have reoccurance

Question 202

expain the 4 stages of transitional cell cancer/urothelial carcinoma?

Answer 202

**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

Question 203

what is antoher name for wilms tumor?

Answer 203

nephroblastoma

Question 204

what is the typical prognosis for a child dx with wilms tumor?

Answer 204

5 years 90% survival so pretty good

Question 205

what is the most common neoplasm arising in the kidney?

Answer 205

renal cell carcinoma 9/10 cases

Question 206

what are the two major groups of malignant tumors under renal cell carcinoma?

Answer 206

clear cell and papillary

Question 207

what type of pattern would you descibe a renal cell cancer that has proliferation alon fibrovascular core?

Answer 207

papillary

Question 208

what is the gold standard first line tx for renal cell carcinoma?

Answer 208

RESECTION radiation and Chemo aren't effective for renal cell carcinoma!!!!!!!!!!!!!

Question 209

transitional cancer has a high rate of recurrence? true or false?

Answer 209

true!!! 80%

Question 210

what are the two staging methods used for renal cell carcinoma?

Answer 210

1. robson 2. TNM

Question 211

what is the #1 risk factor for bladder cancer?

Answer 211

SMOKING

Question 212

bicarbonate buffer system ## Footnote what are the two levels we really care about? what is the equation? what produces them? acid/bases? normal ranges?

Answer 212

**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**

Question 213

how do you measure total venous CO2 on arterial blood gas?

Answer 213

the venous CO2 is approximately equal to the HCO3 on the blood gass because most CO2 is carried as HCO3

Question 214

on bicarb buffer system, which component is regulated by lungs and kidneys? what do primary disturbances cause? can it fix it?

Answer 214

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!_**

Question 215

what is the most common acid/base disturbance of all?

Answer 215

metabolic acidosis

Question 216

snapshot: respiratory acidosis pH? PCO2? HCO3? think of?

Answer 216

pH decreases, _PCO2 increase_s (acid), HCO3 increased (comp), acute and chronic forms \*think not breathing enough\*

Question 217

snapshot: respiratory alkalosis pH? PCO2? HCO3? think of?

Answer 217

pH increases, _PCO2 decreases_, HCO3 decreases (comp), acute and chronic forms \*think breathing too much\*

Question 218

snapshot: metabolic acidosis pH? PCO2? HCO3? think of?

Answer 218

pH decreases, _HCO3 decreases,_ PCO2 decrease (comp) \*think increase resp to blow off more CO2 to decrease the levels since it becomes more acidic with loss of HCO3\*

Question 219

snapshot: metabolic alkalosis pH? what happems? comp?

Answer 219

pH increases, _HCO3 increases_, PCO2 increases (comp)

Question 220

respiratory acidosis ## Footnote ph? 1st thing? comp? where does equation shift? important buffering system involved? what is the _primary cause_? _4 condition causes?_ _4 symtpoms_ _3 tx?_

Answer 220

**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: 1. somulence 2. coma 3. confusion 4. respiratory arrest Tx: * *1. VENTILLATORY SUPPORT 2. Naloxone/Narcan** **3. benzodiazepen antagonists: _flumazenil_**

Question 221

how long does it take HCO3 to compensate for a respiratory acid/base disturbance?

Answer 221

about 3 days

Question 222

how much does the pH decrease for every 10mmHG in CO2?

Answer 222

.08 units this is consistent and you can count on this!

Question 223

acid base case: Billy got into some of his dads pain meds. He has suffered a significant mental status depression and his respiration rate is 4. You see him in the ED and a blood gas is obtained: pH 7.16, PCO2: 70mmHG, HCO3-24 meq/L. what does he have?

Answer 223

**uncompensated respiratory acidosis** PH is acidic PCO2 is elevated (showing respiratory fault, decreased breathing, PCO2 build up causing the acidosis) HCO3 is normal (compensation hasn’t occurred yet)

Question 224

if a patient has respiratory acidosis from drug OD, what do you need to keep in mind if you give them Naxolone/narcan?

Answer 224

_very hsort halflife_ ## Footnote they could wake up start breathing, and then go back into their respiratory acidosis and might need to keep giving this every half hour until it is completely out of the system

Question 225

if patient has respiratory acidosis from drug OD and you give them benzodiezepine antagonist _flumazenil_, what do you need to be cautious of?

Answer 225

if rapidly removed can cause seizures so don’t use too big of a dose

Question 226

Respiratory Alkalosis ## Footnote 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?

Answer 226

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: 1. _lightheadedness_ _2. parenthesia_ 3. tetany TX: **_1. TREAT UNDERLYING CAUSES_** **_2. breath into brown paper bag for short term only_**

Question 227

why are most cases of respiratory alkalosis self sustained?

Answer 227

because of muscle fatigue, the person gets too tired so they are unable to keep breathing off the CO2 so they don't reach syncope

Question 228

what happens to the pH as the PCO2 DECREASES by 10 mmHg?

Answer 228

pH increases .08 units

Question 229

in respiratory sources of acid/base rxns, how do you predict the pH? ## Footnote what happens as this increases or decreases?

Answer 229

by measuring the changes in PCO2 increase in PCO2: decrease in pH of .08 units decrease in PCO2: increase in pH of .08 units

Question 230

metabolic acidosis ## Footnote ph? HCO3? PCO2? shift? explain the patho of this? what must you sure or consider? what are the two main subcategories? 2 1

Answer 230

**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**

Question 231

what acid/base condition is it important to consider anion gap? explain? what is this?

Answer 231

metabolic acidosis ## Footnote fictious number that is only helpful in classifying the type and metabolic acidosis theory states: anion gap=Na-(Cl+HCO3) in the body there are an equal amount of cations and anions. cations: Na Anions: Cl, HCO3 we don't really measure the others. if we had the CL and the HCO3, and subract from Na, the range hsould be **_4-10_** **_in metabolic acidosis_**: usually the anion gap _increases_ since the _HCO3 decreases_, so the difference between the cations and the anions increases or gets larger

Question 232

metabolic acidosis: ## Footnote _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?

Answer 232

**_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: 1. insulin 2. electrolyte replacement 3. volume expansion

Question 233

explain what things you lose if you have a lot of vomiting and diarrhea?

Answer 233

**gastric acid:** has a lot of Na and a high Cl levels, if a lot of vomiting loose Na, Cl, and a lot of H **diarrhea:** has a lot of Na, Cl, and a lot of HCO3

Question 234

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.

Answer 234

**_hallmark:_** **_decreased pH, decreased HCO3, HYPERCHLOREMIA_** \*\*\*the increase in Cl compensates for the loss of HCO3 so the anion gap appeares normal\*\*\* causes: 1. 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 2. renal tubular acidosis

Question 235

metabolic acidosis: normal anion gap acidosis _Renal tubular acidosis_ explain the three types!

Answer 235

**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

Question 236

case: JR has intermittent vomiting and severe diarrhea for 4 days. He has been unable to keep fluids down and has not urinated in 8 hours. He has cardiomyopathy and compensated HF. Appears lethargic and cool to the touch. pH 7.3, PCO2=28 mmHG, HCO3=14, Na=136, K=3, Cl 110

Answer 236

pH=acidosis HCO3= decreased, metabolic PCO2=decreased, compensatory elevated chloride Na, K=normal DX: compensatory metabolic acidosis, slightly increased anion gap add Na-(HCO3+Cl) should be between 4-10, his is 12

Question 237

metabolic alkalosis ## Footnote 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?

Answer 237

**_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_**

Question 238

why must you ALWAYS treat metabolic alkalosis?

Answer 238

\*\*\*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

Question 239

case: a 27 year old is brought to the ED by his gf after found obtunded at home. RR 6, BP 100/60, PH 7.26 PCO2: 65 mmHG, PO2: 68 mmHg, HCO3 31 what is this? tx? how long has it been going on?

Answer 239

acidosis HCO3 elevated PCO2: elevated compensated respiratory acidosis been going on for a few days tx: support ventilation

Question 240

**case**: following a alcoholic binge, a 54 year old make presents to the ED with severe nausea and vomiting for 3 days. He has only had water in the last 36 hours. PH 7.5 PCO2: 48 mmHg HCO3 36, Na 129, K2.7, CL84. what is this? how do you tx?

Answer 240

alkalosis compensated metabolic alkalosis low Na low Cl low K compensated metabolic alkalosis, hypochloremia, hypokalemia (from activation of the RAA activation) tx: saline 0.9% and KCL

Question 241

case: 16 yo with DM is brought to ED after collapsing at home. he is dehyrdated, disoriented and hypotensive and his breath has a sweet odor. Urine has high specific gravity and positive for glucose and ketones. pH 7.24. PCO2 25 mmHg. HCO3 10. Glucose 700 mg/dl. Na 124. K 5.2. Cl 98. Creatine 1.0. BUN 24 mg/dl.

Answer 241

acidosis **compensated metabolic acidosis** low Na elevated K normal Cl glucose elevated **increased anion gap acidosis** HCO3-down to buffer H PCO2- down showing compensation

Question 242

case: 24 year old med student becomes extremely anxious prior to his board exams. He is brought to the ED with light-headedness and muscle cramps.pH 7.52. PCO2 25. HCO3: 24

Answer 242

**respiratory alkalosis** PCO2 decreased HCO3 normal tx: breath into paper bag, deal with the anxiety

Question 243

case 7 part 1: ## Footnote case: a hospitalized man is discovered by nursing staff unconscious with no pulse or respirations. a code is called. they start IV and start CPR. pH 7.01. PCO2 65. HCO3 12. PO2 43HC.

Answer 243

PH: acidosis (should be 7.2… but it is 7.01… so what else is contributing to respiratory acidosis… also metabolic acidosis is contributing because HCO3 is low and Lactic acid building up! PCO2: rise HCO3: low initially both respiratory acidosis (since not breathing CO2 build up and metabolic acidosis (lactic acid build up)

Question 244

case 7 part 2: ## Footnote he is intubated and given 100%O2. CPR is condinued and ABG is done 3 minutes later. PH 7.21. PCO2 41 mmHG HCO3 13, PO2 280.

Answer 244

PCO2: breeathing for patient! So Co2 is better! Blown off the high Pco2 and correctd the respiratory acidosis but his bicarb is still low so he still has a **METABOLIC ACIDOSIS GOING ON!** HCO3: low O2: high

Question 245

case 7 part 3: ## Footnote following defib he stabilizes. He is placed on ventilator. PH 7.5 PCO2 26 HCO3 22 PO2 160

Answer 245

respiratory alkalosis over ventilating him decrease the rate of the ventilator \*\*blowing off too much CO2\*\*

Question 246

what are the time frames for acute or chronic?

Answer 246

acute: days to weeks chronic: months to years

Question 247

what is oliguria characterized by?

Answer 247

less thatn 400 cc in 24 hours

Question 248

uremia what is this?

Answer 248

decreased renal function, axotemia, symptoms

Question 249

creatinine clearance ## Footnote what is this? what equation is us? when is this used?

Answer 249

involves 24 hour urine test mated with serum creatinine fairly accurate and easy can be measured by inulin (usually in research) _cockcroft-gault equation, tells the creatinine clearance_ replaced by eGFR used in hospital with IV antibiotic dosing

Question 250

renal failure _azotemia_ what is this? due to? symptomatic?

Answer 250

**_excess of urea and nitrogenous compounds in the blood_** due to breakdown of proteins metabolism of carbohydrates and fats yields water and CO2 if symptoms are present use the term **_uremia_**

Question 251

renal failure ## Footnote 3 test you should consider ordering for renal failure 4 2 1

Answer 251

1. US ## Footnote you can see obstructions and size very well!! so this is good! non invasive no risky dye contrast dye readily avaliable 2. plain Xray pyelogram retrograd pyelogram 3. CT probally better but risk of dye and raising creatinine

Question 252

pyelogram

Answer 252

inject dye cleared through the kidney viewed with plain view

Question 253

retrograde pyelogram

Answer 253

inject dye inside urinary collection system using a cytoscope viewed with plain xray

Question 254

should you avoid contrast dye in ARF or CRF if not on diaylsis?

Answer 254

yes

Question 255

what might be needed to dx intrinsic renal failure?

Answer 255

biopsy

Question 256

what is the benefit of doing an US?

Answer 256

no radiation or dye easy and helpful

Question 257

what are 6 complications of acute renal faillure?

Answer 257

**1. volume overload** decreased sodium and water excretion resultant weight gain, heart failure, and edema **2. hyponatremia** **3. hypocalcemia** paresthesias, cramps, seizures, confusion **4. hyperkalemia (increases), phosphatemia (increases), magnesem**ia 5. metabolic acidosis 6. HTN

Question 258

what are the 5 tx of acute renal failure?

Answer 258

**1. prevention!!!** (avoid nephrotoxins, diabetes control etc) **2. reverse poisons** (ETOH, bicarbonate in acidosis) **3. restore fluid volume and electrolyte balance** (saline/crystalloids, colloids, blood) **4. dialysis when needed** (acute if responsive or dialyzable toxin or CRF) **5. relieve obstruction** (easiest way to fix ARF)

Question 259

how long does it take acute renal failure to come on? are there symptoms?

Answer 259

hours to days ## Footnote typically little symptoms found randomly on lab tests

Question 260

what are the 3 classifications of acute renal failure? what one is most common?

Answer 260

**1. prerenal renal failure (renal hypoprofusion) 55%** **2. renal/parenchyma/intrinsic 45%** **3. post renal (obstructive) 5%** **pre renal azotemia (failure) most common**

Question 261

acute renal failure _prerenal azotemia_ what are the two things that cause this the most often? permanent/reversible? damage to kidney? 3 things that cause the first? 4 things that cause the second

Answer 261

**_due to renal hypoprofusion and Hypovolemia_** ## Footnote usually _reversible_ if restoring renal blood flow (RBF) parenchyma usually not damaged in severe cases, ischemia/injury **1. hypovolemia** **a. fluid loss** **b. decreased cardiac output** **c. decreased systemic vasculature** causing: - epi relase and vasoconstriction - RAA activation - arginine vasopressin rlease 2. renal hypoprofusion **a. vasoconstriction from epi** **b. cycloxygenase inhibitors** **c. hyperviscosity syndrome** **d. hepatorenal syndome**

Question 262

acute kidney failure prerenal azoturia: **_hepatorenal syndrome causing hypoprofusion of kidneys_** what is this? what does it do?

Answer 262

**_cirrhosis leads to intrarenal vasoconstriction_** **_sodium retention_** precipitated by: bleeding paracentesis diuretics vasodilation cycloocygenase inhibitors

Question 263

acute renal failure prerenal azouremia 2 signs 4 symptoms 2 tests and 1 result

Answer 263

**symptoms** thirst dizzy **signs** low BP tachycardia orthostasis low urine output **lab evaluation** urine volume urine microscopy hyaline/bland casts due to concentrated urine

Question 264

acute renal failure: intrinsic renal failure what are the two main categories of this? 2 in fist 6 im second **WHAT ONE IS THE MOST COMMON CAUSE OF intrinsic renal disease?**

Answer 264

1. renovascular cause ## Footnote a. obstructed renal artery (atherosclerosis/thrombus) b. renal vein obstruction 2. glomerular/microvascular disease a. glomerulonephritis b. vasculitis c. acute tubular necrosis \***MOST COMMON CAUSE OF INTRINSIC RENAL FAILURE\*** d. ischemia/neprotoxin e. intersitial nephritis

Question 265

what are 6 nephrotoxins that can cause acute intrinsic renal failure?

Answer 265

1. radioconstrast dye 2. aminoglycosides 3. cyclosporine 4. chemo 5. solvents (ETOH) 6. endogenous nephrotoxin (things in the body taht can be toxic if too much is present, rhabdomylosis, hemolysis, UA etc.

Question 266

Acute intrinsic renal failure nephrotoxins: _radiocontrast dye_ what does this cause? how long after exposure? what are the 4 features? how can you prevent this? tx?

Answer 266

**_intrarenal vasoconstriction resulting in acute tubular necrosis (ATN)_** **_24-48 hours after contrast exposure_** FEATURES: 1. decrease eGFR 2. sediment 3. reversible 4. elevation of BUN **HOW TO AVOID:** **use _NON IONIC contrast_, more expensive** resolves 1-2 weeks

Question 267

what are 7 RF for having a negative rxn to contrast dye and having it cause acute intrinsic renal failure?

Answer 267

age over 80 CKD diabetes CHF hypovolemia multiple myeloma chemotherapy, antibiotics

Question 268

acutre intrinsic renal failure ## Footnote 1. are there symptoms? 2. signs? 3. what might you see on labs (5) 4. tx?

Answer 268

often no sxs ## Footnote signs: **_azotemia on lab tests_** labs: 1. muddy brown casts (ischemia/nephroxic) 2. red cell cats (nephritis/acute glomerular) 3. eosinophilic cats (allergic nephritis) 4. white cell casts (interstitial nephritis) 5. proteinuria

Question 269

what are the 4 signs of nephritic syndrome?

Answer 269

1. olioguria 2. edema 3. HTN 4. urine sediment

Question 270

acute postrenal kidney failure ## Footnote what is this? what are 6 things that can cause it?

Answer 270

**_urinary outflow obstruction_** single kidney or urethral obstruction leading to **_anuria_** causes: 1. prostate disease 2. neurogenic bladder (spinal cord injuries) 2. anticholinergics 3. blood clots 4. stones 5. tumor or other extrarenal obstruction

Question 271

acute postrenal failure ## Footnote what are 4 signs of this? what are the 2 tx options?

Answer 271

SIGNS: 1. **bladder distension** **2. abdominal pain-colic** **3. renal distension** (check with US) **4. hx of RF** (prostate disease, stones etc) TREATMENT: fix the plumbing! 1. **urologist** **2. nephrostomy tube or suprapubic catherer**

Question 272

what might dopamine promote?

Answer 272

water and sodium excretion

Question 273

what are 5 conditions that might warrent dialysis?

Answer 273

1. uremia 2. hypervolemia 3. hyperkalemia 4. acidosis 5. toxins (multiple, digoxin)

Question 274

end stage chronic renal failure characterized by what 3 things?

Answer 274

1. proteinuria 2. hematuria 3. _3 month of disease and eGFR less than 60/ml_

Question 275

what are the stages and values for eGFR of CKD?

Answer 275

Question 276

currently what are the two most common causes of end stage CKD/uremia?

Answer 276

1. diabetes 2. HTN

Question 277

uremia what is this?

Answer 277

azotemia + syndrome of anemia, malnuitrition, and metabolic problem

Question 278

what are 5 sxs of end stage CKD?

Answer 278

anorexia (weight loss/loss of appetite) nausea/vomiting malaise headache itching

Question 279

what is important to keep in mind with creatinine/bun? ## Footnote explain this in relationship to eGFR/

Answer 279

they follow disease not symptoms ## Footnote greater 50: normal 35-50 usually BUN and creatinine normal 20-30 usually symptoms or signs or uremia with decreased stress threshold

Question 280

what are 3 metabolic effects you see with chronic kidney disease?

Answer 280

1. **_hypothermia_**: decreased Na transport; source of energy/head 2. **_impaired carbohydrate metabolism: “pseudodiabetes”_**, slower handling of glucose load to insulin resistance 3. increased **_triglycerides_**

Question 281

when does decreased K excretion occur? what does this leave the chronic kidney disease patient at risk for?

Answer 281

typically occurs if GFR less than 10 cc/min ## Footnote at risk for hyperkalemia

Question 282

why does CKD cause calcium disorders? ## Footnote what is the nickname for this? what two things contribute to fracture risk? explain the process?

Answer 282

"renal osteodystrophies" osteomalacia and osteitis fibrosa cystica due to hyperthyroidism increase fracture risk Reasoning: 1. decreased conversion of vitamin D to 1,25 dihydroxy (activated) vitamin D 2. decreased calcium in serum since less active vitamin D to absorb it 3. increase in PTH in response to low Ca 4. results in weakness of bones because it sucks the the Ca out

Question 283

phosphorus disorders seen in CKD why is this increased? what is the domino effect of increase phosphorus? what are 3 tx options?

Answer 283

decreased phosphorus excretion in CKD so it accumulates in the blood Domino effect of bad things: 1. causes low calcium 2. increase in PTH 3. bone reabsorption 4. weak bones/fractures TX: 1. decrease serum phosphate - diet restriction of _proteins, dairy, colas_ _-calcium carbonate_ _-selevemer_

Question 284

what is the goal level of calcium phophorus (calcium \* phosphours) levels in the body?

Answer 284

below 70 else solid organs/arteries/joints calcification (calciphylaxis)

Question 285

what is the most common complication of end stage renal disease?

Answer 285

hypertension

Question 286

what are 7 random other things you can see with CKDs?

Answer 286

1. pericarditis (toxin induced) 2. anemia 3. metabolic acidosis 4. thrombocytopenia 5. bruising/bleeding 6. platelet dysfunction 7. infection

Question 287

anemia in CKD ## Footnote what are 5 causes of this? what helped to sove this problem? decreased need for?

Answer 287

**Causes:** 1. bone marrow toxins 2. decreased eryhtropoetin 3. hemolysis 4. hemodilution 5. decreased RBC \*\*this used to be aa HUGE problem in CKD patients, but now with _ERYTHROPOETIN_ we can fight it!! REVOLUTION!\*\* and helps to limit the need for transfusion

Question 288

explain what sxs you would see in CKD for: neuromuscular gastro \*don't memorize just read it\*

Answer 288

**_neuromuscular_** decreased concentration drowsiness insomnia hiccups cramps/twitches periphreal neuropathy/restless leg syndrome more severe **_stupor_** **_seizure_** **_coma_** **_gastrointestinal_** anorexia N/V hiccups **_uremic fetor/ bad breath_** mucosal irritation

Question 289

when is transplant or dialysis appropriate? where can you get it from?

Answer 289

creatinine greater than 8 creatinine clearance less than 10 donor cadaver

Question 290

hemodialysis ## Footnote what are the three ways you can accomplish this? what alows you to accomplish this? what are the 2 requirements? what are 2 things you must monitor?

Answer 290

1. requires a shunt that connects artery and vein, "must ripen", allow for _diffusion across semipermeable membrane_ ## Footnote 2. artificial options 3. IV cathertic into IJ REQUIREMENTS: 300-450 ml/min blood flow 9-12 hour commitment a week MONITOR: _KT/V_ _urea pre and post dialysis_

Question 291

what are complications of hemodialysis? what must they have?

Answer 291

required to take heparin cause the blood can clot outside of the body in machine ## Footnote complications: anemia poor flow rates plugged grafts infection aneurysm disequilibrium arrhythmia hypotension infection

Question 292

peritoneal dialysis ## Footnote what is this process? what are 3 advantges?

Answer 292

catheter- can use immediately, goes in the stomach, put catheter in the belly dump fluid in there with certain osmolarity and you keep doing it over and over again and it comes out, makes you less likely to be able to receive a kidney push fluid for 4-6 hours intermittent tx can do at night, cyclic Advantages: 1. no heparin 2. independence 3. no vascular acess

Question 293

what are 3 disadvantes of periotoneal dialysis?

Answer 293

1. _DONT USE IN LUNG DISEASE_ _2. PERITONITIS major risk_( may be so risky that they can be disqualified from recieving a kidney transplant) 3. need to be trained

Question 294

which is better hemodyalysis or peritoneal dialysis?

Answer 294

hemodyalysis does better

Question 295

what is the most effective way to tx CKD? ## Footnote what must they be? time frame? success/

Answer 295

transplant! ## Footnote must be _HLA compatible on chromosome 6_ 24-48 hour timeframe for transplant family donor higher success rate!

Question 296

can you get live vaccines in transplant? what do you need to be careful of?

Answer 296

no live vaccines hew zoster vaccine is LIVE!!

Question 297

explain the chronic and acute rejection symptoms? what are two things you need to check for to determine if this is occuring?

Answer 297

**Acute rejection:** fever swelling pain **Chronic rejection:** nephrosclerosis renal ischemia, HTN, fibrosis \*\*need to check creatinine and get a biopsy to confirm after ruling out ostruction via arteriogram/US\*\*

Question 298

what is the most common cause of death in CKD patient?

Answer 298

ATHEROSCLEROSIS

Question 299

PROTEINURIA ## Footnote microablumemia albumin levels explain!!

Answer 299

some urine excretion of protein is normal but not a lot! Urine tests for protinuria are used to detect abnormal filtering ofalbumin in the glomerulus or abnormal absorption in the proximal tubule 1. a rapid dipstick can be used to detect small amounts of urine in the blood just tells PRSENCE 2. once protein is present then run 24 hour urine to quantify the amount **_ALBUMIN IS THE SMALLEST PROTEIN_** so it filters before others when there is the begining stages of damage. **_1. MICROALBUMEMIA_** tends to occur long before clinical proteinura, so we can screen for this using a microalbumemia dipstick only tells us PRESENCE not how much 2. **24 hr albumin to quantify** greater than 30 is abnormal

Question 300

what albumin level is conistent with tubular damage? glomerular damage?

Answer 300

tubular: 1000 mg 24 hr glomerular: 1000-3000 24 hr

Question 301

the source of most proteinurias is.....

Answer 301

glomerular proteins, like albumin!

Question 302

what are two other things that contribute to the total urine protein other than albumin?

Answer 302

IgA Tamm-horsfall proteins

Question 303

what are three conditions that can lead to proteinuria?

Answer 303

**1. _acute tubular necrosis_** **2. _multiple myeloma_** -light chain protein in the urine bence jones **_3. nephrotic syndrome_** - greater than 3500 - _hypoalbumemia_ (refers to loss of it from blood into urine) - edema - hyperlipidemia - hypercoagulabiliy

Question 304

what are the 4 tests used to asses for proteinuria?

Answer 304

**_1. standard dipstick_** (tests for protein total of all types) **_2. microalbumin_** dipstick for albumin between 30-300 (should be less than 30) **_3. albumin_** total 24 hour urine amount! **_4. albumin to creatinine ration_** takes into account the amount of urine that was produced

Question 305

hematuria ## Footnote what is this classificed by? options for presentation? 3 test to order?

Answer 305

2-5 RBC per high power field can either be: 1. gross (visible) 2. microscopic tests: UA cytology US

Question 306

if a patient has hematuria without specific cause what MUST YOU DO EVERY SINGLE TIME!?!?!

Answer 306

RULE OUT MALIGNANCY!!!!! YOU MUST DO THIS.

Question 307

what is the most common glomerulonopathy?

Answer 307

IgA nephropathy

Question 308

if thinking nephrotic syndrome....think....

Answer 308

HIGH PROTEIN!!!