CM Renal Flashcards

Question 1

Q

what is the total body sodium?

why is this an approximation?

Answer

A

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

Q

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

Answer

A

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

Q

what happens to the excretion of Na in these senarios:

if ECFV increases?
if ECFV decreases?

Answer

A

if ECFV increases: activation of mechanism to increase Na excretion

if ECFV decreases: activation of mechanism to decrease Na excretion

Question 4

Q

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

A

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

Q

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

A

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

Q

dehydration

what is this and waht does it cause?

Answer

A

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

Question 7

Q

what is the most common cause of dehydration worldwide?

Question 8

Q

osmolarity

what is this determined by?

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

Answer

A

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

Q

what is the equation for OSMOLARITY?

what is the biggest influencing component of this equation?

what does it tell you?

Answer

A

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

Q

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

A

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

Q

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

Answer

A

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

Q

increased serum tonicity

what happens to Na?

What happens to H20 excretion?

urine?

Answer

A

hypertonic solution

increased Na

decreased H20 excretion

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

Question 13

Q

decreased serum tonicity

what happens to Na?

What happens to H20 excretion?

urine?

Answer

A

hypotonic blood

has decreased Na

increase H20 excretion

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

Question 14

Q

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

Answer

A

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

Question 15

Q

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

A

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

Q

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

Answer

A

occurs when water needs to be reabsorbed

20-30% of Na is reabsorbed in the ascending limb of the loop of henle creating a hypertonic medullary interstitium and concentration gradient that is necessary to concentrate the urine
the hypertonic medullary interstitium allows for water to be pulled out from the descending limb of henle and the the collecting tubule
as water is pulled out, esp from the collecting tubule, the filtrate becomes more concentrated

Question 17

Q

renal diluting (urine) mechanism

what causes this to occur?

Answer

A

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

Q

creatinine

what is creatinine? is this a good test?

what are the levels you should know?

when does this go up quickly?

Answer

A

.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

Q

blood urea nitrogen (BUN)

what is this a product of?

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

Answer

A

8-20

end product of protein metbolism

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

Question 20

Q

explain the relationship between creatinine and BUN?

Answer

A

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

Q

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

Answer

A

neuromuscular

Question 22

Q

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

Answer

A

electrolytes!!

Question 23

Q

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

Answer

A

EVALUATE:

neurological status
volume status
metabolic/renal status
osmolarity

Question 24

Q

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

A

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

Q

ADH/vasopressin

what does this do? where does it alter permeability?

when is it released (3)? what does it decrease?

how does it effect the urine?

Answer

A

regulates the body’s retention of water by increasing water reabsorption in the kidney collecting ducts

increases the permeability of the renal collecting tubule and allows water to freely move down its concentration gradient into the hypertonic medullary interstitium

released in response to:

decrease in blood volume
decrease in BP
increase in ECF osmolarity

this increases water reabsorption and a decrease in the tonicity of ECFV

concentrates the urine since all the water has been pulled out

Question 26

Q

what are the two main drivers of ADH/vasopressin release?

explain what happens in each

Answer

A

osmolarity

a. if small increase in osmolarity of the EVFC (# of particles in serum)-ADH secreted to decrease osmolarity and Na (increasing the reabsorption of water a little bit)
b. similarly if you have too much water in the blood and a decrease in osmolarity, then ADH will stop secreting, get a brief diuresis and will return osmolarity to normal
2. intravascular pressure

if large decrease in intravasular volume (5-10%) with decrease in BP also results in ADH release mediated by baro-receptors in circulation and free H2o is retained leading to hypoNa because there is an rapid increase in the proportion of water to Na

****this OVERIDES osmolarity since maintaining BP and profusion is the most important!!!****

Question 27

Q

explain how loops and thiazides work?

what do each excrete?

where do they work?

what happens to ECF?

are they contracindicated in anyone?

Answer

A

Both block Na reabsorption, resulting in sodium loss from the body, since fluid follows sodium, you also get a decrease in the ECFV

LOOPS:

greater loss of BOTH Na and H20 than Thiazides
block Na in the ascending loop of Henle where 20-30% of Na is reabsorbed

3 cause proportional loss of Na/H20 so ECF is left undisturbed

THIAZIDES:

block Na in the distal convoluted tubule where 5-10% of Na is reabsorbed
more Na is excreted than H20
since more H20 left in the ECF, this means there is a increased H20 to Na ratio and can lead to hyponateremia (by dilution)

**this is why thiazides are contraindicated in people with hyponateremia**

Question 28

Q

suggestions for clinical evaluation:

if abnormal volemia:

if abnormal Na concentration:

**where do you look for the problem?**

Answer

A

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

Q

hypertonic saline injection

what does this do?

Answer

A

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

Q

hypotonic saline injection

what does this cause?

Answer

A

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

Question 31

Q

isotonic saline injection

what does this cause?

Answer

A

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

Q

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

A

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

Q

how are volemias accessed?

Answer

A

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

Q

hypervolemia

what is this caused by?

what are 2 senarios that cause this in relationship to Na?

Answer

A

secondary to fluid overload

IV solution generated hypernatremia
internally generated hyponatremia from CHF, cirrohosis, or nephrotic syndrome

“giving the patient too much Na because it causes the H20 to come back and increase volume or a condition that causes there to be too much fluid in the patient from failed organs”

Question 35

Q

hypovolemia

what are the PE of a patient with this?

what are the two general categories of causes?

1

4

how do you distinguish between these two causes?

Answer

A

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

Q

euvolemic

what are two things that contribute to this?

what causes hyperNa (3)?

what causes hypoNa (2)?

what do you need to remember with euvolemic?

Answer

A

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

Q

hypovolemic hypotonic hyponatremia

what do you loose in this?

what is the mechanism that causes a increase in ADH?

what are the two branches of causes?

2

what do you use to determine the cause and the values?

what are the two tx options and who are they appropriate for?

Answer

A

Loss of water AND Na, but more Na loss than water

“decreased Na with decreased ECF”

ADH SECRETION INCREASED TO MAINTAIN INTRAVASCULAR VOLUME WHICH OVERIDES THE NEED TO MAINTAIN OSMOLARITY

must determine if:

1. renal: diuretics/salt wasting

2. non-renal: GI loss vomiting, diarrhea

**determine this based on urine!!**

less than 10= Na retention of kidneys working, so NOT KIDNEYS

greater than 20= renal Na wasting, so KIDNEYS

Tx:

Isotonic fluids IV (normal saline .9% or ringers lactate) +KCL(it will stay in the intravascular space to maintain BP and shut off ADH secretion via intravascular pressure)
electrolyte drink “gatorade” +KCL (if mild and oral intake intact)

Question 38

Q

hypervolemic hypotonic hyponatremia

explain what happens in this and what it is associated with for conditions (3)? what makes this worse? is this difficult to treat? why? what are the 3 tx options?

Answer

A

hyponatremia caused by INCREASE IN EXTRACELLULAR FLUID

“body basically tricked into thinking it need more volume since the kidneys aren’t being profused, so it activates RAAs and ADH which makes the problem worse”

Edema related conditions: CHF, cirrhosis, nephrotic syndrome

total body Na/H2O are increased but circulating blood volume is sensed as inadequate by baroreceptors because of decreased CO and decreased BP decreased renal perfusion leads to increased ADH and activation of RAA system

TX: difficult since associated with organ failure

1. water restriction

2. treat underlying condition

diuretics

Question 39

Q

explain how

HF
cirrhosis

nephrotic syndrome

cause

hypervolemic hypotonic hyponatremia

***whats something you would see in the urine***

Answer

A

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

Q

euvolemic hyptonic hyponatremia

why is this euvolemic?

what 2 things do yo uneed to dx?

what are the 3 requirements?

what are 7 causes of this?

Answer

A

decreased Na with slight changes in volume that can’t be detected on PE

NEED URINE Na AND OSMOALITY TO DX

1. hyponatremia

2. decreased serum osmoality less than 280

3. high urine osmoality greater than 150

**peeing it out when it should be absorbed**

syndrome of inappropriate ADH (SIADH)
post-op hyponatremia
psychogenic polydipsia
stroke
tumors
pulmonary lesions (TB, lung abcess)
SSRIs

Question 41

Q

syndrome of inappropriate ADH (SIADH)

what is this and when does it happen?

what happens to the urine?

what is the urine concentration of Na?

what two tests are low?

tx if symptomatic (1) or asymptomatica (2)?

Answer

A

if ADH secretion is occurring to a point of creating hyponatremia (absorbing too much) then it is clearing being inappropriately over secreted

absence of cardiac, liver, renal, adrenal or thyroid disease

urine becomes extremely concentrated since the over secretion of ADH causes the water to be reabsorbed in the collecting duct

urine Na>20 since water being absorbed and urine is concentrated

serum BUN and UA are low since increased clearance

TX:

symptomatic with Na <120

MEDICAL EMERGENCY

1. hypertonic saline (has a lot of Na), monitor Na every 2 hours, no MUST DO SLOWLY <10-12 a day

if asymptomatic:

H20 restriction

demeclocycline/tolvaptan(clock ADH receptors so you stop getting water)

Question 42

Q

post-op hyponatremia

what is this caused by?

what makes this situation worse?

what is the tx? (2)

Answer

A

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

Q

psychogenic polydipsia causing euvolemic hyponatremia

what is is this caused by?

how do they maintain euvolemic?

ADH levels, urine osmolarity?

Na in urine?

Answer

A

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

Q

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

Answer

A

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

Q

hypertonic hyponatremia

what 4 things can cause this?

what is this and how does it relate to the osmolarity equation?

why is this unlike the other types of hyponatremia?

Answer

A

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

Q

hypertonic hyponatremia caused by diabetic circumstances

what causes this?

how does this cause hyponatremia?

what blood sugar do you worry about this?

what is the Tx for this?

Answer

A

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

Q

hyponatremia and HIV/AIDS

what percent of hospitalized with AIDS have hypoNa?

what is this often seen with?

Answer

A

50% of pts hospitalized with AIDS have hypoNa

often comes from CNS/pulmonary involvment seen with HIV infections

Question 48

Q

hypernatremia

what is a common demoninator in nearly all of these cases?

what is the serum Na level associated with this?

who does this often occur in?

why can they be confused or lethargic?

Answer

A

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

Q

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

A

hypernatremia

renal cause with dilute urine

hallmark: polyuria with greater than 3L in 24 hours

inability of kidneys to conserve water appropriately

diabetes insipidus
central diabetes insipidus
nephrogenic diabetes insipidus

hypernatremia with extrarenal cause concentrated urine

MOST COMMON and get decrease ECFV

causes: fever, profuse sweating, diarrheah, hyperventialation

greater deficiency in water increases the concentration of the sodium and the person can’t appropriately replace water loss

Question 50

Q

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

A

“stranded in dessert/lost at sea”

unusual with intact thirst mechanism and access to H20, but in this case no H2o intake possible, even with increased ADH levels

signs: orthostatic hypotension, dehydration comes from excessive sweating, GI, and respiratory tract without a way to replenish
lab: greater than 400 urine osm with intact renal function, ADH levels increased

TX:

replace water and electrolytes over 48-72 hours
.9% saline followed by .45% saline

***replace water slowly to prevent cerebral edema since brain has been adapted to hyperosmolality, theyve gotten used to being shrunk so don’t want to give them too much water too quickly because they will swell quickly***

Question 51

Q

hypernatremia with dilute urine (euvolemic)

what is the hallmark of this?

what happens in this?

what 3 conditions is this seen in?

what is the Uosm?

2 tx options?

Answer

A

hallmark: greater 3L urine in 24 hours

inability of kidneys to conserve water appropriately so you urinate more than you should witout uptaking enough to equal out the hyperNa

seen in:

central diabetes insipidus
nephrogenic diabetes insipidis
congenital nephrogenic insipidis

decreased osmolarity less than 250 uosm

Tx:

D5W-replace H20 without Na
.45% saline- for hyperNa and hyperglycemia

Question 52

Q

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

A

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

hypernatremia due to free water loss

associated with severe CNS structual lesions or infections, head trauma, or pituiatary surgery

Dx: give them person ADH and see if it increases their H2o intake and equalizes their osmolarity and decreases their urinary frequency, this is a DIAGNOSTIC TEST

Rx: ADH

Question 53

Q

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

A

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

Q

hypernatremia with dilute urine

congenital nephrogenic disease

what do they lack?

Answer

A

absence of ASH receptors

Question 55

Q

hypokalemia

what is K levels maintained by?

what are 5 causes of this?

what are 5 signs of this?

2 tx options?

Answer

A

K is the major INTRACELLULAR cation with the gradient maintained by the Na/K pump

oral intake=renal output in a steady state

Causes of hypokalemia:

1. insulin: insulin cause K to move into the cell, so excessive amounts cause hypokalemia

2. RAA systemactivation**: ALDOSTERONE facilitates K excretion **most important regulator of body K conten

diuretics
vomiting/diarrhea/sweat
digoxin
signs: weakness, muscle cramps, fatigue, constapation EKG NSST-T changes and U waves, PVCS

tx:

mild to mod=oral KCL
severe= IV admin of KCL slowly with cardiac monitoring

Question 56

Q

hyperkalemia

what are 3 causes of this?

what do you need to confirm?

what are 3 signs you see?

what tx can you give in lifethreatening?

what are 4 other txs?

Answer

A

causes:

1. patients with renal insufficiency are at risk

2.renal insufficiency + K sparking diuretics

3. KCl and K sparing diuretics

important to confirm lab results because can be from hemolysis

signs: diarreah, weakness
ekg: PEAKED T waves, widening QRS, increased intervals and loss of P waves KEY!!

TX:

if lifethreatening k greater than 6.6 can give infusion of insulin to drive the K inside to buy time
eliminate KCL or K sparing diuretics
cation exchange resins that exchange Na for K
dialysis for severe renal failure

Question 57

Q

why is calcium important?

where is it mostly found?

Answer

A

50% of it is ionized to help with muscle and nerve function

40% is bound to protein mostly albumin

Question 58

Q

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

Answer

A

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

Q

hypocalcemia

what are three causes of this and what is most common?

5 signs of this?

2 ways to test for it?

what EKG changes you see?

what are the 2 tx?

Answer

A

MOST COMMON CAUSE IS RENAL FAILURE

(DECREASED VIT D3, INCREASED PHOSPHORUS)

other causes:

hypoparathyroidism
malabsorption
signs: increased excitation of nerve and muscle cells, cramps, tetant, paresthesias, convulsions

chvosteks sign:tap on facial nerve and you will start twitching on the side of the face you tapped

trousseaus sign: BP cuff inflate for over a min, if you inflate all the way your hand willl start twitching if over 1 minute

EKG: Prolonged QT, arrythmias

ionized Ca less than 4.5

tx:

asymptomatic: oral calcium/vit D
symptomatic: IV calcium gluconate

Question 60

Q

hypercalcemia

what are 3 cauess of this?

what are 3 signs of this?

what are 3 txs?

what can make this worse and should be prevented?

Answer

A

causes:

1. hyperparathyroidism

2. malignancy produce PTH

3. milk-alkali syndrome Ca antacids + vitamind D excess

signs:

polyuria- H20 reabsorption is blocked by hypercalcemia
neuro changes: lethargy, weakness, dowsiness
shorted QT, PVCs

TX:

treat underlining cause
promote Na rich diuresis because Ca will follow
IV infusion 0.9% saline with IV furosemide

**avoid thiazide diuretics, can worsen hypercalcemia**

Question 61

Q

hypomagnesemia

who is this common in?

why is this a big deal?

what are 4 signs?

2 things it is often associated with?

what are 2 tx?

what should you do in hospitalized pts?

Answer

A

very common in hospitalized patients esp for those on diuretics who are receiving continuous IV support

Low Mg potentiates dangerous ventricular cardiac arrythmia esp if K is low

signs: weakness muscle cramps tremors, neuromuscular and CNS hyperirritability

often associated with: hypoK and hypoCa

Tx:

important to check Mg levels in hospitalized pts
IV therapy with MgSO4
oral Mg oxide can be given as supplement

Question 62

Q

another name for acute renal failure is?

Answer

A

acutre renal injury

Question 63

Q

another name for chronic renal failure is?

Answer

A

chronic kidney disease

Question 64

Q

another name for end stage renal disease is?

Answer

A

end stage kidney disease

Answer 64

A

uncomplicated UTI

acute cysitits
acute pyelonephritis

complicated UTI

something that makes the more likely to fail treatment
- obstruction
- anatomic abnormality

urologic dysfunction

MDR uropathogen
2. pregnant
3. elderly
4. children
5. males
6. recurrent

Answer 65

A

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

Answer 66

A

postmenopausal women

bladder/uterine prolapse
loss of lactobacilli in vaginal flor allos for E. coli to take over
diabetes (sugar)

benign prostatic hypertrophy

Answer 67

A

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

Answer 68

A

unusual for men 15-50

RF: uncircumcised, anal intercourse

antibacterial material in prostatic fluid

18-20 cm urethra

Answer 69

A

30:1 ratio women to men because women have a significantly short urethra

route of infection: ascending from the urethra

UTI most commonly from uncomplifcated acute cystitis

pathogenisis:

colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder CYSTITIS
uropathogens ascend from bladder to kidney via ureters

RARELY CAUSED BY SEEDING OF BACTERIA

Answer 70

A

female sex

frequent sexual intercourse

diaphragm/spermicide use

delayed post-coital micturition (not urinating after intercourse)

hx of UTI

Answer 71

A

e.coli most common 75-95%

proteus mirabilis

klebsiella pneumoniae

enterococcus

Answer 72

A

cystitis:

dysuria or burning while urination
increased frequency/urgency
suprapubic pain/discomfort
hematuria
voiding small amounts
AFEBRILE

pyelonephritis

FEBRILE
chils
flank pain
costovertebral tenderness
CBC with left shift

Answer 73

A

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

Answer 74

A

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!!!*****

Answer 75

A

CIPROFLOXACIN!!

others:

fluoroquinolone, amp+gentamycin, ceftriaxone

Answer 76

A

cathertized associated UTI

if asymptomatic don’t need to treat with abx

screen urine 48 hours after removing catheter

Answer 77

A

3 or more episodes per year confirmed UC OR 2 UTIs in last 6 months

consider self treatment at first sign (urine cup for UC)

vaginal estrogen in women since they have a decrease in lactobacillus

Answer 78

A

treat:

pregnant
before urologic procedures
after renal transplant

DONT TREAT

diabetics
elderly
patients with spinal cord injury or indwelling urethral catheter

Answer 79

A

YES! then adjust abx as appropriate! :)

Answer 80

A

formation is dependent on supersaturation and an environment that allows the stone to grow!

supersaturation risk:

heredity- cystinuria SLC3A1/SLC7A9

environmental

diet

obesity

four types of stones:

calcium oxalate
struvite
uric acid
cystine

Answer 81

A

MOST COMMON TYPE OF STONE

RADIOOPAQUE
usually associated with high calcium levels in the blood and urine
contributing factors: excessive bone reabsorption, bone disease, hyperparathyroidism and renal tubular acidosis predispose for these stones

TX:

treat underlying conditions

increased fluid intake

thiazide diuretics

(70-80%)

Answer 82

A

“staghorn” stones that always associated with UTI and alkaline urine

produced by UTI with urease producing bacteria
proteus, klebsiella, pseudomonas, enterobacter
made of magnesium ammonium
usually too large to pass and require lithotripsy or surgical removal
they enlarge as the bacterial count increases

Tx:

prevent UTIs
lithrotripsy
surgical removal

Answer 83

A

caused by low Ph (acidic) urine <5.6 for greater than 24 hours

radiolucent cant be seen on xray
caused by high levels of uric acid in the urine or gout
RF: obesity/diabetic or both

Tx:

decrease uring PH below 6 (more alkaline) using potassium citrate
allopurinol with decrease purine diet (fish, shellfish, and meats)

Answer 84

A

autosomally recessive inherited abnormalities CYSTINURIA

“childhood caliculi”

1.smooth-edged ground glass appearence

TX:

increase urine volumes to 3 L a day and increase urine pH to greater than 7
occasionally chelating agents

Answer 85

A

high humidity

high temp

sedentary

high animal protein and high salt

FH for calcium stones

hyperthyroidism/hypothyroidism

Answer 86

A

Most common:

unilateral flank pain
sudden onset
renal colic
hematuria

Less common:

vague abdominal pain
acute abdominal/flank pain
difficulty urinating
penile or testicular pain

Answer 87

A

non-contrast CT (gold standard)
used to identify the size, location and type of stone

low density (aka can’t see): uric acid, cystine
high density: calcium oxalate, struvite
struvite: laminar, rugged apperance, full of casts with “stag horn apperance”

*****do renal US for pregnant people who can’t have the CT****

labs
urinalysis (stone type/blood)
BMP (calcium and creatinine if worried about kidney function)
24 hour urine for the amount excreted
thyroid function test

Answer 88

A

most common abnormality elevated Ca excretion, decreased serum Ca

Answer 89

A

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)

Answer 90

A

most managed conservatively with pain management Nsaids and Opoids (BETTER USED TOGETHER!!)
hydration
strain urine

consider hospitalization:

uncontrolled pain/fever

can’t tolerate oral intake

Answer 91

A

acute renal failure

urosepsis

urinary obstruction

concomitant pyelonephritis

>10 cm

haven’t passed for 4-6 weeks

Answer 92

A

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)

Answer 93

A

⅓ will experience stone recurrence within 5 years

½ experience stone reccurence within 10 years

Answer 94

A

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

Answer 95

A

glomerular capillary bed

brings blood to the glomerulus
high pressure system at 60 mmHg

allows for FILTRATION

peritubular capillaries

surround all portions of the tubules, and are in an arrangement that permits rapid movement of solutes and water between the fluid in the tubular lumen and the blood in the capillaries
low hydrostatic pressure around 13 mmHg

allow for ABSORPTION

Answer 96

A

1200 ml/min

Answer 97

A

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

Answer 98

A

myogenic mechanism
tubuloglomerular feedback menchanism

Answer 99

A

pressure sensitive mechanism
relies on intrinsic mechanism of vascular smooth muscle that cause it to contract when stretched
as arterial pressure rises and the

afferent arteriole is stretched=__the smooth muscle contracts

when the afferent pressure falls= it relaxes

Answer 100

A

NaCl concentration in the tubular fluid is sensed by the juxtaglomerular apparatus in the distal tubule
occurs where the distal tubule extends back to the glomerulus and then passes between the afferent and efferent arterioles
includes a group of sensing cells called the macula densa in the distal tubule and a group of secretory cells in the wall of the afferent and efferent arterioles called juxtaglomerular cells or granular cells that secrete renin
the juxtaglomerular apparatus is located right between the afferent and efferent arterioles and is though to play an essential feedback role in linking the arterial BP and renal flow tothe GFR and the composition of distal flow, thought to measure both the stretch of the afferent arteriole and the concentration of NaCl as it passes through in the tubular filtrate through the macula densa in distal tubule=determines how much renin is released

Answer 101

A

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

Answer 102

A

prostaglandin: dilates the afferent arteriole

angiotensin II: constricts efferent areteriole

Answer 103

A

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

Answer 104

A

filtration
reabsorption
secretion
excretion

Answer 105

A

first step in urine formation
bulk movement of fluid from blood into kidney tubule
- isosmotic filtrate
- blood cells and larger proteins don’t filter
caused by hydralic pressure
Glomerular filtration rate: amount of filtrate produced in the kidneys each minute

125 mL/min=180L per day

Answer 106

A

process of returning filtered material to bloodstream

99% of what is filtered is reabsorbed

may involve transport proteins

normally glucose is totally reabsorbed

Answer 107

A

material added to the lumen of kidney tubule from blood

active transport (usually) of toxins and foreign substances

saccharine
penicillin

Answer 108

A

loss of fluid from body in form of urine

excreted means=as urine

amount of solute excreted= (amount filtered +amount secreted) - amount reabsorbed

Answer 109

A

the amount of plasma that is filtered each minute

provides information about the kidneys ability to filter and reabsorb/secrete substances

renal autoregulation
neural regulation
hormonal regulation

Answer 110

A

between 80-170 mmHG, autoregulation of blood flow and GFR only modestly rise as renal perfusion increases

outsides of this range, the changes are much greater

purpose: maintain a relatively constant GFR and allow for precise regulation of solute and water excretion

accomplished by:

myogenic mechanism (response to pressure changes in the afferent arteriole)
tubuloglomerular feedback

(response to Na concentration in the distal renal tubule)

causes RENIN release

Answer 111

A

sympathetic nerve fibers from renal plexsus of autonomic nervous system innervate SM afferent and efferent arterioles at the hilus

sympathetic stimulation causes constriction of the afferent and efferent arterioles and thus decreases renal blood flow

Effects:

reduce the GFP and GFR through contracting the afferent and efferent arterioles through alpha receptors
increase Na resorption in proximal tubules B receptors
increase the release of renin B receptors

normally sympathetic stimulation is low so the arteries are dilated except during exercise and hemorrhage where the blood is decreased here

Answer 112

A

cardiopulmonary reflex
baroceptor reflex
renorenal reflex
a. sensory nerves located in the renal pelvic wall are activated by stretch of the renal pelvis wall
- leads to increase of bradykinin which activates protein kinase C causing pelvic release of PGE2 by activation of COX2 and activates calcium channels in renal pelvic wall
b. causes afferent renal nerve activity to increase, efferent activity to decrease, which causes increase in flow rate and urinary sodium excretion

Answer 113

A

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

Answer 114

A

1. molecular weight

2. charge of the molecules

urea, glucose, and insulin can filter freely across the membrane, some myoglobin (75%) can get through

albumin and hemoglobin may be present in small amount (3-1%)

DRIVEN BY:

favoring force: capillary blood pressure (BP)

opposing forces:

blood colloid osmotic pressure (COP)
capsulre pressure (CP)

moves out based on glomerular hydrostatic pressure

Answer 115

A

inulin
creatinine
Blood urea nitogen

Answer 116

A

freely filtred at the glomerulus
biologically inert
not synthesized or metabolized by the kidney
does not alter renal function
can be accurately quantitfied

Answer 117

A

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**

Answer 118

A

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

Answer 119

A

20% of bllod is filtered

19% reabsorbed

1% excreted

glucose: all reabsorbed

Na and water: nearly all reabsorbed 99%

creatinine: none reabsorbed

Answer 120

A

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

Answer 121

A

primary active transport: uses ATP to move solutes against their concentration gradient, used by K, Na, H

Ex: Na/K pump (Na out, K in)

secondary active transport
a. cotransport/symport: moves solutes in the same direction
b. counter-transporters (antiporters): move solutes opposit directions

3. pinocytosis: proximal tubule reabsorb lage molecules such as proteins by pinocytosis

4. passive transport: diffusion

Answer 122

A

65% Na, Water, K, HCo3 and Cl reabsorption from proximal convoluted tubule to thick descending segment of loop of henle

reabsorption of Na, Cl, and water main absoprtion vechicle is sodium-potassium pump

first half of PCT:

Na reabsorbed by co-transport with glucose and amino acids

second half of PCT:

Na and Cl reabsorbed: think about it, in the first half of PCT there was no reabsorption of Cl so now it is highly concentrated which facilitates it reabsorption

Answer 123

A

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

Answer 124

A

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

proximal tubule
- 90% bicarbonate reabsorbed
- secretion of H+ through secondary active transport

2. late distal tubule and the rest

primary active transport
occurs at the luminal membrane of tubular cell
H ions are transported directly by a specific protein Hydrogen-transport ATPase (proton pump)
decreases the pH of tubular fluids

**important in forming maximally acidic urine

Answer 125

A

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!

Answer 126

A

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***

Answer 127

A

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

Answer 128

A

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

Answer 129

A

osmolarity of the serum/ECF decreases: loose water and get dilute urine

osmolarity of serum/ECF increases: water reabsorbtion and get concentrated urine

***this is sensed by osmoreceptors in the hypothalmus sensing high ECF osmolarity…tells posterior pituitary to release ADH and alter collecting duct permeability***

Mechanism that allows this to happen:

controlled secretion of ADH from posterior pituitrary glandwhich regulates the permeability of medullary collecting ducts to water in response to osmoreceptors in the hypothalamus sense high ECF osmolarity, causes more water reabsorption and concentrates the urine
a high osmolarity of the renal medullary interstitial fluid, which provides an osmotic gradient necessary for water reabsorption to occur in the presence of high level ADH (if the concentration gradient wasn’t high in solute or non existent, if ADH made the tubule more permeable, the fluid wouldn’t go anywhere)

BOTH ARE KEY! ADH, osmolarity of interstital

Answer 130

A

ADH PRESENT: water absorbed leaving concentrated urine

ADH ABSENT: no water absorbed leaving dilute urine

Answer 131

A

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

Answer 132

A

obligatory water reabsorption
facultative (selective) water reabsorption
solute/osmotic diuresis

Answer 133

A

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”

Answer 134

A

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

Answer 135

A

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

Answer 136

A

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**

Answer 137

A

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

Answer 138

A

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**

Answer 139

A

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:

fills progressively until the tension in the wall rises above threshold level then
a nervous reflex called micturition reflex that empties that bladder
automatic spinal cord reflex, however, it can be inhibited or facilitated by centers in the brainstem and cerebral cortex

Answer 140

A

originates in sacral S1-S4

combination of Motor function:

Stimulation of parasympathetic neurons=contraction of detrusor muscle and internal urterthral spincter (involuntary) via pelvic nerve
inhibition of somatic neurons=relaxation of external spincter (voluntary) via pudenal nerve

Answer 141

A

APs generated by stretch receptors
reflex arc generates AP that stimulate smooth muscle lining bladder
relax internal urethral sphincter
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

Answer 142

A

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

Answer 143

A

most common of all inherited kidney diseases

uncommon before 40 years old, 40% dx before 45

3rd-4th decade

multiple expanding expanding cysts of both kidneys that destroy the surround kidney structures and cause kidney failure

kidneys are englarged/enormous with “straw colored” fluid

Symptoms:

flank pain from ruptured cyst
gross episodes of hematuria from bleeding into cysts
infected cysts from ascending UTIS (most common thing reported by pt)
HTN
stones 15-20%

CALCIUM OXALATE, URIC ACID

Genes:

PKD1: 85% of cases

PKD2: 15% of cases

DX: ULTRASOUND TEST OF CHOICE

Tx:

SUPPORTIVE

controll HTN and prevent/ TX UTIs AGGRESIVELY!!

Answer 144

A

SCREEN IN ASYMPTOMATIC FAMILY MEMBERS!!!

Answer 145

A

cysts in the liver
mitral valve prolapse 20-25%
cerebral aneurysm from weakness in the cerebral arteries 20%

Answer 146

A

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

Answer 147

A

alteration of H+ transport

urine pH high greater than 5.5

hypercalcemia

hypokalemic, hyperchloremic non-anion gap metabolic acidosis

Tx:

alkalinize urine-NaHCO3

Answer 148

A

proximal

defective bicarbonate reabsorbtion

urine pH less than 5.5

hypokalemic, hyperchloremic non anion gap metabolic acidosis

Answer 149

A

hyperchloremic distal RTA

acidic urine

hypercholoremic hyperkalemic acidosis

abnormal tubular secretion of K and H, abnormal aldosterone production or aldosterone resistance

causes:

NSAIDS
ACE-I
renal disease like DM nephropathy

Tx:

low K diet
stop offending meds (K sparing diuretics like spirolactone, amiloride, and tiameterence
minteralcorticoids

Answer 150

A

acute inflammation that occludes the glomerular capillary lumen and damages the capillary wall

characterized by:

inflammation
suddent onset hematuria (RBC casts) active urinary sediment
HTN
diminished GFR
oliguria (decreased urine)
signs of impaired renal function

two main causes:

acute postinfectious glomerulonephritis
rapidly progressing glomerulonephritis

Answer 151

A

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:

acute
oliguric
decreased GFR
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

Answer 152

A

oliguria from decrease GFR, one of the first symptoms
proteinuria and hematuria follow from increased glomerular capillary wall permeability from damage
cola colored urine
edema of hands and face

5. HTN

elevated anti strep antibodies

DX:

circulating levels of antrstreptolysin antibodies

TX:

abx and supportive
many have spontaneous remission in 6-8 weeks

prognosis is good!

Answer 153

A

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

Answer 154

A

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:

plasmapharesis to remove IgG
immunosuppresive therapy (corticosteroids/cyclophosphamide)

Answer 155

A

characterized by:

glomerulonephritis without IG

Idiopathic renal limited crescentic GN

Microscopic polyarteritis nodosa (PAN)

Wegener’s Granulomatosis

Answer 156

A

middle aged men

crescent involvement of the kidneys

Tx:

steroids

Answer 157

A

bx often required!

immunoflorescence

serum testing:

C3
anti GBM
antineutrophilic cytoplasmic antibodies (ANCA)

Answer 158

A

**not a specific disease by a characterization of symptoms**

the glomular membrane acts as a filter, this increased permability allos proteins to ecape into the urine leading to excessive loss of albumin

as the solutes move out of the ECF, it becomes hyposmotic and so it moves into the tissues and cells where there is a higher concentration of solutes and causes the generalized edema

characterized by:

massive proteinuria more than 3.5 a day

2. lipiduria with fatty casts

3. hypoalbuminemia

4. generalized edema HALLMARK starts in dependent parts like extremeities but spreads to become generalized

5. hyperlipidemia LDL and Tri

high cholesterol!!
HYPERCOAGUBILITIES….so at increase risk for clots/DVT

three main causes:

minimal change disease
membraneous glomerulonephritis
focal segmental glomerulosclerosis

Answer 159

A

dietary protein restriction
ACE-inhibitor
NSAIDS

Answer 160

A

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

Answer 161

A

most common cause of primary nephrosis in adults

“think THICK BGM without infllammation”

diffuse thickening of the glomerular basement membrane from deposition of immune complexes that create “spikes”

causes: SLE, chronic Hep B, DM, thyroiditis, gold compounds

SXS:

peripheral edema
hypoalbuminemia
hyperlipidemia

Tx:

controversial since often times the pt has spontaneous remission and it is relatively benign

Answer 162

A

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

Answer 163

A

“Berger disease”

“THIN GBM DISEASE”

BENIGN HEMATURIA

MC GLOMERURPATHY WORLDWIDE

most common in asians, 3-4th decade of life

primary glomerulonphritis characterized by presence of glomerular IgA immune complex deposits which causes inflammation

DX:

discovered during routine testing, find elevated IgA levels

gross hematuria preceded by URI

50% have single episode

diagnostic findings: mesangial staining for IgA tat is more intense than staining for IgG or IgM

TX:

NO TREATMENT

Answer 164

A

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

heavy microscopic hematuria that progresses to proteinuria
usually picked up from checking urine of family with known dx
sensorineural deafness, billateral

4. eye disorders lense dislocation, post cataracts, corneal dystrophy

Answer 165

A

Lysosomal storage disease

accumulation of globotraoslyveramide (Gb3)

X-linked

Abnormalities:

50% in ESRD
neurological (stroke, TIA)
telegenctasis
skin deposits
corneal lesions
cardiac (LVH, CAD, valvular disease)

Answer 166

A

systemic disorder

features:

HTN
urine sediment
renal insufficiency
negative ANCA

Tx:

glucocorticoids

chemo agents

Answer 167

A

“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

Answer 168

A

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:

control BS

2. ACE/ARB to decrease glomerular pressure

control BP Goal less than 130/80
smoking cessation
weight loss

Answer 169

A

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

Answer 170

A

NSAIDS
Gold
penicillamine
IV heroin

Answer 171

A

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

Answer 172

A

overactive, nocturia, urinary frequency, detrusor overactivity

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:

CNS and neural control of bladder sensation and emptying, ex: stroke, Parkinsons, MS
smooth muscle of the bladder itself (myogenic)

Answer 173

A

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

Answer 174

A

PE:

pelvic exam
digital rectal exam (masses, prostate)
neuro exam if sudden loss (think cauda equina)

Workup:

urinalysis
prostate specific antigen
post void bladder scan
urology consult

Answer 175

A

fluid management
timed voiding
bladder retraining
keagle/pelvic floor exercises
surgical intervention

Answer 176

A

many things can cause obstruction: caliculi, cancer, pregnancy, stones, defects etc.

Key points of things that it causes:

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

dilation

progressive dilation of the renal collecting ducts and renal tubular structures from backflow which causes atrophy of the renal tissue

Answer 177

A

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

Answer 178

A

presentation depends on site of obstruction, degree, and speed at which obstruction occurs

SYMPTOMS

pain
change in urine output
HTN
Hematuria
increased serum creatine

DX:

TEST OF CHOICE: RENAL ULTRASOUND

**dilation of renal collecting system in one or both kidneys**

Answer 179

A

persistent and progressive decreased GFR from reduction of blood flow from atherosclerotic ishchemia

results in CKD (increased serum creatinine and BUN)

consider in pts with severe or resistant HTN, less than 30 years old, and with no family history of HTN or obesity, acute rise in serum creatinine after starting ACE or ARBS

DX:

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

Answer 180

A

urine from the urethra moves into the bladder

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

Answer 181

A

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

Answer 182

A

renal cell carcinoma

Answer 183

A

northern european descent

MOST COMMON KIDNEY CANCER

grows spherically and is well circumscribed mass in the CORTEX of the kidney

arises in the epithelial lining of the proximal tube**, and **grows into the renal vein, inferior vena cava, occlude right side of heart

slow growing and doesn’t present until advances

Many types:

clear cell
papillary
chromophobe
collecting
unclassified

Answer 184

A

lung, lymph nodes, bone, liver, brain

Answer 185

A

SMOKING!!
50-70 year olds
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

long term dialysis
obesity

Answer 186

A

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

Answer 187

A

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!!!

Answer 188

A

stage I-III: resection

Stage IV: pallative

TNM and Robson staging

Answer 189

A

clear cell renal celll carcinoma 7/10: clear or pale under microscope MOST COMMON

papillary renal cell carcinoma: 10%, finger like projections on the tumor

Answer 190

A

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

Answer 191

A

renal sarcomas

Answer 192

A

MOST COMMON RENAL CANCER IN CHILDREN

“nephroblastoma”

dx 3-5 years old most common

primitive cells of renal cortex

associations:

absense of iris
enlargement of the side of face
genituiatry complications

SX:

abdominal mass/swelling w/o other symptoms (parents find while dressing)
hematuria 20-25%
HTN IN CHILD!! HUGE KEY
fever, abdominal pain less common

Answer 193

A

PE:

firm, nontender, smooth mass that is eccentrically located and rarely crosses the midline

tests:

CT scan test of choice, US, MRI
tx: surgery, chemo, radiation

IT IS RESPONSIVE TO CHEMO/RAD

Answer 194

A

you NEVER biopsy because it runs risk of RUPTURE which allows it to spread!

STAGING OCCURS AFTER RESECTION!!!

prognosis good before METS!

Answer 195

A

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

Answer 196

A

smoking 50% of pts
aniline dyes
leather woodwork

Answer 197

A

painless hematuria typical

may have back pain
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:

CYSTOSCOPY

2. biopsy

Answer 198

A

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

Answer 199

A

80% will have reoccurance

Answer 200

A

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

Answer 201

A

nephroblastoma

Answer 202

A

5 years 90% survival so pretty good

Answer 203

A

renal cell carcinoma 9/10 cases

Answer 204

A

clear cell and papillary

Answer 205

A

papillary

Answer 206

A

RESECTION

radiation and Chemo aren’t effective for renal cell carcinoma!!!!!!!!!!!!!

Answer 207

A

true!!! 80%

Answer 208

A

robson
TNM

Answer 209

A

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

Answer 210

A

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

Answer 211

A

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!

Answer 212

A

metabolic acidosis

Answer 213

A

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

Answer 214

A

pH increases, PCO2 decreases, HCO3 decreases (comp), acute and chronic forms *think breathing too much*

Answer 215

A

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*

Answer 216

A

pH increases, HCO3 increases, PCO2 increases (comp)

Answer 217

A

pH decreases, CO2 increases, HCO3 increases (comp)

equation shifts to the right: H is buffered by the intracellular phosphate and protein buffers NOT NaHCO3…this system is essential because it uses the H and combines it with phosphate so don’t get a massive decrease in pH that could cause organ/system failure

primary defect: decreased alveolar ventilation

acute and chronic forms

Conditions that cause this:

1. COPD

2. ASTHMA who tires

3. DRUG OD with supressive of ventilatory drive

4. neuromuscular disease

SXS:

somulence
coma
confusion
respiratory arrest

Tx:

*1. VENTILLATORY SUPPORT
2. Naloxone/Narcan**

3. benzodiazepen antagonists: flumazenil

Answer 218

A

about 3 days

Answer 219

A

.08 units

this is consistent and you can count on this!

Answer 220

A

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)

Answer 221

A

very hsort halflife

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

Answer 222

A

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

Answer 223

A

pH increases, PCO2 decreases, HCO3 decreases (comp)

equation shifts to the left (wants to make more acidic)

acute and chronic forms

primary defect: decreased PCO2 from increased alveolar ventilation rate

Causes:

1. hyperventilation

2. anxiety

3. panic attacks

4. sepsis

5. cirrhosis

6. progesterone

7. mechanical overventilation

SXS:

lightheadedness

2. parenthesia

tetany

TX:

1. TREAT UNDERLYING CAUSES

2. breath into brown paper bag for short term only

Answer 224

A

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

Answer 225

A

pH increases .08 units

Answer 226

A

by measuring the changes in PCO2

increase in PCO2: decrease in pH of .08 units

decrease in PCO2: increase in pH of .08 units

Answer 227

A

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

Answer 228

A

metabolic acidosis

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

Answer 229

A

pH decrease, HCO3 decreased, Cl normal

ANION GAP: greater than 10

pH: lower than 7.25

cause increase in H, which then combines with HCO3 and decreases the levels

4 causes:

1. lactic acidosis: cardiogenic shock or arrest, lactatic acid unmeasured anion produced due to inadequate tissue profusion or hypoxia

2. dibetic ketone acidosis (DKA): hyperglycemia with lack of insulin causing increased production of B-hydroxybutric acid and acetoacetic acid KETO acids, if no insulin the fats break down abonromal and produce more acid or H

3. toxins: ethylene glycol, salicyclates, methanol

4. uremia: severe renal failure leads to endoenous acids

TX:

insulin
electrolyte replacement
volume expansion

Answer 230

A

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

Answer 231

A

hallmark:

decreased pH, decreased HCO3, HYPERCHLOREMIA

***the increase in Cl compensates for the loss of HCO3 so the anion gap appeares normal***

causes:

massive secretory diarrhea: massive loss HCO3 (NaCl and K loss as well)
a. causes Na and Cl retention at the kidney since significant VOLUME DEPLETION
b. as HCO3 secretion in the small/large bowel causes _Cl absorption VIA COUNTERTRANSPORT!!! **this is why you see increase in the Cl which makes the anion gap appeare nromal_***
think: bicarb levels go down (acidosis), Cl levels go up=normal anion gap
renal tubular acidosis

Answer 232

A

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

Answer 233

A

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

Answer 234

A

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

Answer 235

A

***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

Answer 236

A

acidosis

HCO3 elevated

PCO2: elevated

compensated respiratory acidosis

been going on for a few days

tx: support ventilation

Answer 237

A

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

Answer 238

A

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

Answer 239

A

respiratory alkalosis

PCO2 decreased

HCO3 normal

tx: breath into paper bag, deal with the anxiety

Answer 240

A

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)

Answer 241

A

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

Answer 242

A

respiratory alkalosis

over ventilating him

decrease the rate of the ventilator

**blowing off too much CO2**

Answer 243

A

acute: days to weeks
chronic: months to years

Answer 244

A

less thatn 400 cc in 24 hours

Answer 245

A

decreased renal function, axotemia, symptoms

Answer 246

A

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

Answer 247

A

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

Answer 248

A

US

you can see obstructions and size very well!! so this is good!

non invasive

no risky dye contrast dye

readily avaliable

plain Xray

pyelogram

retrograd pyelogram

CT

probally better but risk of dye and raising creatinine

Answer 249

A

inject dye cleared through the kidney

viewed with plain view

Answer 250

A

inject dye inside urinary collection system using a cytoscope

viewed with plain xray

Answer 251

A

no radiation or dye

easy and helpful

Answer 252

A

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), magnesemia

metabolic acidosis
HTN

Answer 253

A

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)

Answer 254

A

hours to days

typically little symptoms found randomly on lab tests

Answer 255

A

1. prerenal renal failure (renal hypoprofusion) 55%

2. renal/parenchyma/intrinsic 45%

3. post renal (obstructive) 5%

pre renal azotemia (failure) most common

Answer 256

A

due to renal hypoprofusion and Hypovolemia

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

Answer 257

A

cirrhosis leads to intrarenal vasoconstriction

sodium retention

precipitated by:

bleeding

paracentesis

diuretics

vasodilation

cycloocygenase inhibitors

Answer 258

A

symptoms

thirst

dizzy

signs

low BP

tachycardia

orthostasis

low urine output

lab evaluation

urine volume

urine microscopy

hyaline/bland casts due to concentrated urine

Answer 259

A

renovascular cause

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

Answer 260

A

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

Answer 261

A

intrarenal vasoconstriction resulting in acute tubular necrosis (ATN)

24-48 hours after contrast exposure

FEATURES:

decrease eGFR
sediment
reversible
elevation of BUN

HOW TO AVOID:

use NON IONIC contrast, more expensive

resolves 1-2 weeks

Answer 262

A

age over 80

CKD

diabetes

CHF

hypovolemia

multiple myeloma

chemotherapy, antibiotics

Answer 263

A

often no sxs

signs:

azotemia on lab tests

labs:

muddy brown casts (ischemia/nephroxic)
red cell cats (nephritis/acute glomerular)
eosinophilic cats (allergic nephritis)
white cell casts (interstitial nephritis)
proteinuria

Answer 264

A

olioguria
edema
HTN
urine sediment

Answer 265

A

urinary outflow obstruction

single kidney or urethral obstruction leading to anuria

causes:

prostate disease
neurogenic bladder (spinal cord injuries)
anticholinergics
blood clots
stones
tumor or other extrarenal obstruction

Answer 266

A

SIGNS:

bladder distension

2. abdominal pain-colic

3. renal distension (check with US)

4. hx of RF (prostate disease, stones etc)

TREATMENT:

fix the plumbing!

urologist

2. nephrostomy tube or suprapubic catherer

Answer 267

A

water and sodium excretion

Answer 268

A

uremia
hypervolemia
hyperkalemia
acidosis
toxins (multiple, digoxin)

Answer 269

A

proteinuria
hematuria
3 month of disease and eGFR less than 60/ml

Answer 270

A

diabetes
HTN

Answer 271

A

azotemia

+

syndrome of anemia, malnuitrition, and metabolic problem

Answer 272

A

anorexia (weight loss/loss of appetite)

nausea/vomiting

malaise

headache

itching

Answer 273

A

they follow disease not symptoms

greater 50: normal

35-50 usually BUN and creatinine normal

20-30 usually symptoms or signs or uremia with decreased stress threshold

Answer 274

A

hypothermia: decreased Na transport; source of energy/head
impaired carbohydrate metabolism: “pseudodiabetes”, slower handling of glucose load to insulin resistance
increased triglycerides

Answer 275

A

typically occurs if GFR less than 10 cc/min

at risk for hyperkalemia

Answer 276

A

“renal osteodystrophies”

osteomalacia and osteitis fibrosa cystica due to hyperthyroidism increase fracture risk

Reasoning:

decreased conversion of vitamin D to 1,25 dihydroxy (activated) vitamin D
decreased calcium in serum since less active vitamin D to absorb it
increase in PTH in response to low Ca
results in weakness of bones because it sucks the the Ca out

Answer 277

A

decreased phosphorus excretion in CKD so it accumulates in the blood

Domino effect of bad things:

causes low calcium
increase in PTH
bone reabsorption
weak bones/fractures

TX:

decrease serum phosphate
- diet restriction of proteins, dairy, colas

-calcium carbonate

-selevemer

Answer 278

A

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

Answer 279

A

hypertension

Answer 280

A

pericarditis (toxin induced)
anemia
metabolic acidosis
thrombocytopenia
bruising/bleeding
platelet dysfunction
infection

Answer 281

A

Causes:

bone marrow toxins
decreased eryhtropoetin
hemolysis
hemodilution
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

Answer 282

A

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

Answer 283

A

creatinine greater than 8

creatinine clearance less than 10

donor

cadaver

Answer 284

A

requires a shunt that connects artery and vein, “must ripen”, allow for diffusion across semipermeable membrane

artificial options
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

Answer 285

A

required to take heparin cause the blood can clot outside of the body in machine

complications:

anemia

poor flow rates

plugged grafts

infection

aneurysm

disequilibrium

arrhythmia

hypotension

infection

Answer 286

A

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:

no heparin
independence
no vascular acess

Answer 287

A

DONT USE IN LUNG DISEASE

2. PERITONITIS major risk( may be so risky that they can be disqualified from recieving a kidney transplant)

need to be trained

Answer 288

A

hemodyalysis does better

Answer 289

A

transplant!

must be HLA compatible on chromosome 6

24-48 hour timeframe for transplant

family donor higher success rate!

Answer 290

A

no live vaccines

hew zoster vaccine is LIVE!!

Answer 291

A

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**

Answer 292

A

ATHEROSCLEROSIS

Answer 293

A

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

a rapid dipstick can be used to detect small amounts of urine in the blood just tells PRSENCE
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

24 hr albumin to quantify

greater than 30 is abnormal

Answer 294

A

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

Answer 295

A

glomerular proteins, like albumin!

Answer 296

A

IgA

Tamm-horsfall proteins

Answer 297

A

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

Answer 298

A

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

Answer 299

A

2-5 RBC per high power field

can either be:

gross (visible)
microscopic

tests:

UA

cytology

US

Answer 300

A

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

Answer 301

A

IgA nephropathy

Answer 302

A

HIGH PROTEIN!!!