IM Nephro

Question 1

Best initial test in nephrology

Answer 1

a ua and the bun and creatinine

Question 2

UA

Answer 2

protein

wbc (direct microscopic examination) or leukocyte esterase (dipstick)

RBC

Specific gravity and pH

nitrites (indicates gram neg bacteria)

Question 3

UA is 2 parts

Answer 3

1. dipstick and if thats positive

2. microscopic analysis

Question 4

dont be worried about

Answer 4

normal lab values bc they are provided on the test

Question 5

severe proteinuria means

Answer 5

glomerular damage

Question 6

standing and physical activity increases urinary

Answer 6

protein excretion

Question 7

urine dipstick for protein detects

Answer 7

only albumin

Question 8

normal protein per 24 hours

Answer 8

<300mg

Question 9

biopsy determines the cause of

Answer 9

proteinuria

Question 10

Normal protein in urine

Answer 10

the tubules secrete slight amounts of protein normally known as tamm-horsfall protein. this should be less than 30-50 mg per 24 hours

Question 11

very large of proteins can only be excreted with

Answer 11

glomerular disease

Question 12

Trace Proteinuria

Answer 12

the problem with using trace through 4+ is that you are only getting a snapshot of that moment in the day.

Question 13

transient proteinuria

Answer 13

occurs in 2-10% of the population, with most of this being benign without representing pathology. if the proteinuria persits and is not related to prolonged standing (orthostatic protineuria) then do a kidney biopsy

Question 14

1+ protein =

2+ protein =

Answer 14

1 gram per 24 hours

2 gram per 24 hours

Question 15

2 methods to assess total amount of protein in a day are

Answer 15

1. single protein to creatinine ratio
2. 24 urine collection

these tests are condisdered equal in accuracy

Question 16

to assess proteinuria

Answer 16

ua is the inital test

protein to creatinine ratio is more accurate at determing the amount

Question 17

Protein to Creatinine ratio

Answer 17

can be superior in accuracy to a 24 hour urine bc of difficulties in collecting a 24 hour urine sample

Question 18

what test do you choose for proteinuria if both a protein/creatinine ratio and 24 urine are choices?

Answer 18

chose pr/cr bc it is faster and easier

Question 19

Microalbuminuria=

Answer 19

30-300 mg/24 hours

Question 20

kidney biopsy is especially important in

Answer 20

kidney disease in a diabetic pt with no ophthalmic findings

Question 21

Bence-Jones protein

Answer 21

in mm is not detectable on a dipstick, use electrophoresis

Question 22

nsaid induced renal disease doe not show

Answer 22

eosinophils

Question 23

IgA nephropath is common for

Answer 23

mild recurrent hematuria

Question 24

Microalbuminura

Answer 24

the presence of tiny amounts of protein that are too small to detect on the UA is called microabluminuria.

this is important to detect in diabetic pts. long term microalbuminuria leads to woresning renal function in a diabetic pt and should be treated

Question 25

best initial tratement for any degree of proteinuria in a diabetic pt

Answer 25

acei or arb they decrease the progression of proteinuria and delay the devlopment of renal insufficinecy

Question 26

WBC on UA

Answer 26

Detect inflammation, infection, or allergic interstitial nephritis cannot distinguish neutros from eos neutros indicate infection eos indicate allergic or acute interstitial nephritis

Question 27

wright and hansel stains

Answer 27

detect eos in the urine answer for allergic interstitial nephritis

Question 28

Hematuria normal UA

Answer 28

<5 RBCs per high power field

Question 29

Hematuria indicative of

Answer 29

stones in bladder, ureter, or kidney hematologic disorders that cause bleeding (coagulopathy) infection (syctitis, pyelonephritis) cancer of bladder, ureters, or kidney treatment (cyclophosphaimde gives hemorrhagic cystitis) trauma: simply banging the diney or bladder makes the shed red cells glomerulonephritis

Question 30

what causes false positive tests for Hematuria on dipstick

Answer 30

hemoglobin or myoglobin, there will be no rbc on smear

Question 31

abdominal xray shows

Answer 31

smoll bowel obstruction (ileus)

Question 32

Renal ct is the most accurate test for

Answer 32

tones

Question 33

intraneous pyelogram is always q

Answer 33

wrong for Hematuria, renal toxic and too slow

Question 34

when dysmorphic rbcs are described on smear

Answer 34

the correct answe is glomeulonephritis

Question 35

cytoscopy is the most accurate test of

Answer 35

the bladder

Question 36

Hematuria when is cytoscopy the answer

Answer 36

hemature w/o infection or prior trauma and the renal us or ct does not show anetilogy or bladder sonography show a mass for possible biopsy

Question 37

Casts

Answer 37

microscopic collections of material clogging up the tubules and being excreted in the urine

Question 38

Red Cell cast

Answer 38

glomerulonephritis

Question 39

White cell cast

Answer 39

pyelonephritis

Question 40

Eosinophil cast

Answer 40

acute (allergic) intersititial nephritis)

Question 41

Hyaline cast

Answer 41

dehydration concetrnates the urin and the normal Tamm-horsfall protein precipiates or concentrates into a cast

Question 42

Borad, waxy casts

Answer 42

chronic renal disease

Question 43

Granula muddy brown casts

Answer 43

acute tubular necrosis, they are collection of dead tubular cells

Question 44

Acute Kidney Injury (AKI) definition

Answer 44

formely called acute renal failure degined as a decrease in creatining clearance resulting in a sudden rise in BUN and creatining not based on a specific number for BUN and creatinine

Question 45

Acute Kidney Injury (AKI) etiology

Answer 45

3 types ``` prerenal azotemia (decreased perfusion) postrenal azotemia (obstruction) intrinsic renal disease (ischemia and toxins) ```

Question 46

Prerenal azotemia overview

Answer 46

problems of inadequate perfusion of the kidney in which the kidney itself is normal. any cause of hypperfusion or hypovolemia will raise the BUN and creatinin, with the BUN rising more than the creatinine

Question 47

Prerenal azotemia etiology (8)

Answer 47

Hypotension (systolic below 90 mm Hg) from sepsis, anaphylaxis, bleeding, dehydration Hypovolemi: diuretics, burns, pancreatitis renal artery stenosis: even thorugh the bp may be high, the kidney is underperfused relative hypovolemia from decreased pump function: CHF constrictive pericarditis, tamponade hypalbuminemia cirrhosis nsaids constrict the afferent arteriole acei cause effert arteriole vasodilation

Question 48

Postrenal Azotemia overview

Answer 48

obstruction of any cuase damages the diney by blocking filtration at the glomerulus,

Question 49

Postrenal Azotemia etiology (6)

Answer 49

prostate hypertrophy or cancer stone in the ureter cervical cancer urethral stricture neurogenic (atonic) bladder retroperitoneal fibrosis (look for bleomycin, methylsergide, or radiation in the hx)

Question 50

are prerenal and postrenal azotemia reversivel

Answer 50

most of them are

Question 51

how to fix pre and postrenal azotemia

Answer 51

correct the underlying cause

Question 52

with obstruction what cuases creatining to rise

Answer 52

must obstruct both kidneys

Question 53

the kidney in prerenal and postrenal disease would function

Answer 53

normally if transplanted into another person

Question 54

Intrinsic renal disease overview

Answer 54

most common cause is acute tubular necrosis from tosins or prolonged ischemia of the kidney. glomerulonephritis is rarely acute, but when the kidney is injured from any cuase, there is always a reater risk of AKI. for example a few hours of hypotension might not damage a normal kidney at all, but with underlying renal damage it may cuase AKI

Question 55

Intrinsic renal disease etiology (6)

Answer 55

acute (allergic) interstitial nephritis (commonly from medications such as penicillin) rhabdomyolysis from hemoglobinuria contrast agents, aminoglycosised, cisplatin, amphotericin, cyclosporin and nsaids: most common toxins causing aki from atn crystals such as hyperuricemia, hypercalcemia, or hyperoxaluria proteins such as bence jones protein from myeloma postrsptococcal infection

Question 56

Prerenal AKI etiologies from hypotension

Answer 56

sepsis anaphylaxis bleeding dehydration

Question 57

Prerenal AKI etiologies from hypovolemia

Answer 57

``` diuretics burns pancreatitis dec pump function lowealbumin cirrhosis ```

Question 58

Prerenal AKI etiologies from other

Answer 58

renal artery stenosis

Question 59

Intrinsic Renal AKI etiologies from ATN

Answer 59

``` toxins nsaids aminoglycoside antibiotics, amphotericin cisplatin, cyclosporin prolonged ischemia ```

Question 60

Intrinsic Renal AKI etiologies from AIN

Answer 60

penicillin sulfa drugs

Question 61

Intrinsic Renal AKI etiologies from other

Answer 61

``` rhabdomyolysis/hemoglobinuria contrast crystals bence-jones proteins poststerptococcal infection ```

Question 62

PostRenal AKI etiologies

Answer 62

``` BPH/Prostate cancer ureteral stone cervial cancer urethral stone neurogenic bladder retroperitoneal fibrosis (chemo or radiation) ```

Question 63

AKI presentation

Answer 63

may present with only an asymptomatic rise in BUN and creatinine

Question 64

AKI presentation with symptomatic

Answer 64

nauseated and vomiting tired/malaise weak short of breath and has edema from fluid overload

Question 65

AKI presentation with symptomatic very severe disease

Answer 65

confusion arrhythmia from hyperkalemia and acidosis sharp, pleuritic chest pan from pericarditis

Question 66

there is no pathognomonic physical finding of

Answer 66

AKI

Question 67

Presentation of postrenal azotemia

Answer 67

enlargment of bladder (distention) and massive diuresis after Foley (urinary) catheter placement are specific to urinary obstruction. this is the closest you will get to a specific presentation for any form of AKI

Question 68

Best initial test of AKI

Answer 68

BUN and creatinine with completely dead kidneys the creatinine will rise about one point (1mg/Dl) a day.

Question 69

BUN to creatinine ratio above 20:1

Answer 69

either prerenal or postrenal

Question 70

Bun to creatinine ratio around 10:1

Answer 70

intinsic

Question 71

Best initial imaging in AKI

Answer 71

renal sonogram, does not need contrast, need to avoid contrast in renal insufficiency

Question 72

Prerena azotemia dx

Answer 72

BUN to creatinin above 20:1 clear hx of hypoperfusion or hypotension

Question 73

postrenal azotemia dx

Answer 73

BUN to creatinin above 20:1 distended bladder or massive release of urine with catheter placement bilateral or unilateral hydronephrosis on sonogram

Question 74

AKI kidney biopsy

Answer 74

rarely the right answer, although biopsy is the most accurate test for allergic interstitial nephritis or poststreptococcal glomerulonephritis

Question 75

next diagnostic test for AKi of unclear etiology

Answer 75

ua urine sodium fractional excretion of na urine osmolality go with ua first

Question 76

prerenal azotemia test results

Answer 76

Low una (<20)=low fena (<1%)

Question 77

urine sodium and fractional excretion of sodium

Answer 77

decreased blood pressure (or decreased intravascular volume) normally will increase aldosteron. increased aldosterone increases sodium reabsorption. it is normal for urine sodum to decrease when there is decreased renal perfusion bc aldosterone levels rise

Question 78

Urine Osmolality (1) when intravascular volume is low

Answer 78

normally adh levles hould rise. a healthy kidney will rebsorb more water to fill the vasculature an dincrase renal perfusion

Question 79

Urine Osmolality (2) when more water is reabsorbed from the urine,

Answer 79

will the urine be concentrated or dilute? increased reabsorption leads to an increase in urine osmolality: more concentrated urine

Question 80

Urine Osmolality (3) normal tubule cells reabsorb water, in ATN,

Answer 80

the urine cannot be concentrated bc the tubule cells are damaged. the urin produced in ATN is similar in osmolality to the blood (about 300 mOsm/L). this is called isosthenuria. urine osmolality in ATN is inappropriately low. isothenuria is espceially prolematic when th pt is dehydrated

Question 81

Urine Osmolality (4) isosthenuria means

Answer 81

the urine is the same strenth as the blood. the term isosthenuria is used interchangeably with the phrase renal tubular concentrating defect

Question 82

Urine Osmolality (5) Dehydration should normally

Answer 82

increase the urine concentration (osmolality). if there is damage to the tubular cells from ischemia or toxins, the kidney loses the ability to absorb sodium and water bc a live, functioning cell is necessary to absorb sodium and water. in ATN, the body inappropriatly loses sodium (una above 20) and water (uasm bleow 300) into the hurin

Question 83

healthy person fluid overload > healthy person dehydration >

Answer 83

low urine osmolality or dilute urine high urine osmolality or concentrated urine

Question 84

the only significant manifestation of sickle cell trati

Answer 84

is a defect in rneal concentrating ability or isosthenuria, these pts will continue to produce dilute urine even in dehydration

Question 85

high uosm=

Answer 85

high specific gravity

Question 86

classification of acute renal failure by lab testing Prerenal azotemia BUN:creatinine Urine sodium (uNA) fractinal excretion of sodium (feNa) urin osmolality (Uosm)

Answer 86

BUN:creatinine >20:1 Urine Sodium (Una) <20meq/L fractinal excretion of sodium (feNa) <1% urin osmolality (Uosm) >500 mosm/kg

Question 87

classification of acute renal failure by lab testing acute tubular necrosis BUN:creatinine Urine Sodium (Una) fractinal excretion of sodium (feNa) urin osmolality (Uosm)

Answer 87

BUN:creatinine <20:1 Urine Sodium (Una) >20meq/L fractinal excretion of sodium (feNa) >1% urin osmolality (Uosm) <300 mosm/kg

Question 88

Acute tubular necrosis (ATN) Definition

Answer 88

ATN is an injry to the kidneys from ischemia and/or toxins resulting in sloughing off of tubular cells into the urine. sodium and water reabsorptive mechanisms are lost iwth the tubular cells. proteinurua is not significant since protein, not tubules, spills into the urine when glomeruli are damaged

Question 89

Acute tubular necrosis (ATN) etiology significance

Answer 89

knowing the ause of ATN is ciritical since there is no specific diagnostic test to prove the etiology, you dannot do a blood level of a drug or a biopsy to prove that a particulare toxin caused the renal failure

Question 90

acute renal faulre and a toxin in the hx are your clues to the what is the most likely cause of

Answer 90

ATN

Question 91

radiographic contrast ATN

Answer 91

occurs rapidly (within 36 hours)

Question 92

ATN and vanco genamicin and amphotericin

Answer 92

takes 5-10 days to kick in ATN

Question 93

what prevents contrast induced nephrotoxicity

Answer 93

saline hydration

Question 94

contrast induced renal failure lab values

Answer 94

contrast causes spasm of the afferent arteriole leading to renal dysfunction. so you reabsorb sodium and water leading the specific gravity to become very high and giving you a very low urine sodium

Question 95

creatinine rising after chemo

Answer 95

bc of lumor lysis syndrome leading to hyperuricemia, occurs in a couple of days so give allopurinol hydration ad rasburicase prior to chemo to prevent renal failure from tls

Question 96

ATN from ethylene glycol

Answer 96

bc oxalic acid and oxalate preciitate within the kidneys and cause stones (envelope shaped) the calcium level will be low bc of these sotnes

Question 97

methanol causes inflammation of

Answer 97

the retina

Question 98

opiates by injection are associated with

Answer 98

focal segmented glomulonephritis

Question 99

how much renal function do you lose every year past 40

Answer 99

1%

Question 100

summary or causes of ATN meds

Answer 100

nonoliguric renal injury is caused by aminoglycoside antibiotics, amphotericin, cisplatin, vancomycin, acyclovir, and cyclosporin slower onset: usually 5-10 days dose dependant: the more administered, the sicker the pt gets low mg level may increase risk of aminoglycoside or cisplatin toxicity

Question 101

summary or causes of ATN contrast

Answer 101

cause immediate renal toxicity. this can best be prevented with saline hydration. n acteylcystein and sodium bicarb are not consistently proven as beneficial

Question 102

summary or causes of ATN hemogloin and myoglobin

Answer 102

from rhabdomyolysis for myoglobin

Question 103

summary or causes of ATN hyperuricemia

Answer 103

from tumor lysis syndrome acutely. long standing hyperuricemia from gout can cause chronic renal failure

Question 104

summary or causes of ATN ethylene glycol overdose

Answer 104

precipitation of calcium oxalate int eh renal cortex

Question 105

summary or causes of ATN bence jones

Answer 105

mm directly toxic to renal tubules

Question 106

summary or causes of ATN nsaids

Answer 106

cause afferent arteriole constriction

Question 107

Rhabdomyolysis

Answer 107

caued by trauma, prolonged immobility, snake bites, seizures, and crush injuries. best initial test is ua, it iwll be positive only on dipstick for large amounts of blood, but no cells will be seen on microscopic examination creatinine levels are markedly elevated but is is the findings on ua that tell you myoglovin is spilling into the urine

Question 108

most specific test for rhabdomyolysis

Answer 108

urine test for myoglobin

Question 109

rhabdomyolysis hyperkalemia

Answer 109

occurs from the release of potassium from damaged cells bc 95% of potassium in the body is intracellular

Question 110

rhabdomyolysis hyperuricemia

Answer 110

occurs for the same reason it does in tumore lysis syndrome. when cells break down, nucleic acids are released from the cell's nuclei and are rapidly metabolized to uric acid

Question 111

damaged muscle also releaases

Answer 111

phosphate

Question 112

rhabdomyolysis hypocalcemia

Answer 112

occurs from increased calcium binding to damaged muscle

Question 113

rhabdomyolysis treatment

Answer 113

saline hydration mannitol as an osmotic diuretic bicarbonate, which drives potassium back into cells an dmay prevent precipiation of myoglobin in the kidney tubule the concept is that myoglibin is a severe oxidant stress on the tubular cells. saline and mannitol increase urine flow rates to decrease the amount of contact time between the myoglobin and the tubular cells

Question 114

why doesnt hemolysis cause hyperuricemia

Answer 114

rbcs have no nuclei

Question 115

dont treat hypcalcemia in rhabdo if

Answer 115

asymptomatic, in recovery the calcium will bome back out of the muscles

Question 116

why do an ekg after fluid replacement in rhabdo?

Answer 116

to detect life-threatening hyperkalemia

Question 117

ATN treatment

Answer 117

there is no therapy proven to benefit ATN. Patients should be managed with hydration, if they are volume depleted, and correction of electrolyte abnormalities. diuretics increase urine output, but do not change overall outcome try to correct the underlying cause

Question 118

ATN treatment wrong answers

Answer 118

low-dose dopamine diuretics mannitol steroids

Question 119

ATN treatment when is dialysis hte answer

Answer 119

initiate dialysis if: fluid overload encephalopathy pericariditis metabolic acidosis hyperkalemia

Question 120

initiating dialysis in ATN is not based on a specific level of BUN or creatinine

Answer 120

it is based on the development of life-threatening conditions like these that cannot be corrected another way

Question 121

ATN treatment of hypcalcemia

Answer 121

give viramin D and calcium can cause seizures and prolonged QT intervals

Question 122

furosemid causes

Answer 122

otoxicity

Question 123

Hepatorenal syndrome definition

Answer 123

renal failure devloping secondary to liver disease, the kidneys are intrinsically normal

Question 124

Hepatorenal syndrome look for

Answer 124

severe liver disease (cirrhosis) new-onset renal failure with no other explanation very low urine sodum (less than 10-15 meq/dl) FENA below 1% elevated BUN:creatinine ratio (greater than20:1)

Question 125

Hepatorenal syndrome treatment

Answer 125

midodrine octreotide albumin (albumin is less clear)

Question 126

Hepatorenal syndrome lab values

Answer 126

fit in with prerenal azotemia

Question 127

Atheroemboli etiology

Answer 127

Cholesterol plaques in the aorta or near the coronary arteries are sometimes large and gragile enough that thye can be borken off whn these vessels are manipulated during catheter prceures. cholesterol emboli lods in the kidny, leading to aki.

Question 128

Atheroemboli look for

Answer 128

blue/purplish skin lesions in fingers and toes livedo reticularis ocular lesion

Question 129

Atheroemboli diagnostic tests

Answer 129

eosinophilia low complement levels eosinophiluria elevated ESR

Question 130

Atheroemboli most accurate test

Answer 130

biopsy of one of the purplish skin lesions is the most accurate diagnostic test. it shows choleterol crystals, but this does not change management bc there is no specific therapy to reverse atherobemolic dz

Question 131

Atheroemboli peripheral pulses

Answer 131

normal, bc they are too small to occlude vessels such as the radial or brachial artery

Question 132

Acute (allergic) interstitial nephritis definition

Answer 132

a form of acute renal failure that damages the tubules occurring on an idiosyncratic (idiopathic) basis. antibodies and eosinophils attack the cells lining the tubules as a reaction to drugs (70%), infection, and autoimmune disorders

Question 133

Acute (allergic) interstitial nephritis etiology

Answer 133

an medication can cause it but most common are: ``` penicillins/cephalosporins sulfa drugs (furosemide and hctz) phenytoin rifampin quinolones allopurinol ppi's ```

Question 134

the drugs that cause AIN are the same as those that cause:

Answer 134

drug allergy and rsh stevens-johnson syndrome toxic epidermal necrolysis hemolysis

Question 135

Allergenic substances affect

Answer 135

skin kidney red cells

Question 136

what else causes Acute (allergic) interstitial nephritis

Answer 136

sle sjogren sarcoidosis

Question 137

Acute (allergic) interstitial nephritis presentation/what is the most likely dx

Answer 137

acute renal failure (rising BUN and creatinine) with: fever (80%) rash (50%) arthralgias eosinophilia and eosinophiluria (80%)

Question 138

Acute (allergic) interstitial nephritis diagnostic tests

Answer 138

elevated BUN and creatinine with ratio below 20:1 white and red cells in the urine the ua is not accurat enought o determine that htey are eosinophils

Question 139

Acute (allergic) interstitial nephritis most accurate test

Answer 139

hansel or wright stain which is how you determine whether eosinophils are present

Question 140

Acute (allergic) interstitial nephritis treatment

Answer 140

usually resolves spontaneously with stopping the drug or controlling the infection. severe disease is managed wih dialysis, which may be temporary. when creatinine continues to rise after stopping the drug, giving glucocorticoids (prednisone, hydrocorticortisone, methylprenisolone) is the answer.

Question 141

eosinophilia is not found in the urine with aki from

Answer 141

nsaids

Question 142

urine sodium and osmolality are not uniformly up or down in

Answer 142

ain, they cannot help establish dx

Question 143

analgesic nephropathy presents with

Answer 143

atn from direct toxicity to the tubules ain membranous glomerulonephritis vascular insufficiency papillary necrosis

Question 144

analgesic nephropathy vascular insufficiency

Answer 144

vascular insufficiency of the kidney from inhibiting prostaglandins. prostaglandins dilate the afferent arteriole. nsaids constrict the afferent arteriole and decrease renal perfusion. this is symptomatic in healthy pts. when pts are older and have underlying renal insufficinecy from diabetes and/or htn, then nsaids can tip them over into clincally apparent renal insuficiency

Question 145

tere is no specific diagnsotic test to determine nsaids cause atn

Answer 145

exclude other cuases and look for nsaids in the hx

Question 146

papillary necrosis definition

Answer 146

a sloughing off of the renal papillae caused by nsaids or sudden vascular insufficiency leading to death of the cells in the papillaie and their dropping off the internal structure of the kidney. must have a reason for underlying renal damage, even if the baseline BUN and creatinine levels are normal

Question 147

how much renal function must be lost before creatinine begins to rise

Answer 147

60-70%

Question 148

papillary necrosis look for

Answer 148

extra nsaid use with hx of: sickle cell dz diabetes urinary obstruction chronic pyelonephritis

Question 149

papillary necrosis presentation

Answer 149

papillary necrosis can be very hard to distinguish from pyelonephritis. look for the sudden onset of flank pain, fever, and hematuria in a pt with one of the disease previously listed.

Question 150

papillary necrosis best initial test

Answer 150

ua that shows re and white cells and may show necrotic kidney tissue. the urine culture will be normal (no growth).

Question 151

papillary necrosis most accurate test

Answer 151

ct scan that shows the abnormal internal sturctures of the kidney from the loss of the papillae

Question 152

papillary necrosis treatment

Answer 152

no specific therapy you cannot reattach the sloughed off par tof the kidney

Question 153

papillary necrosis can give grossly visible

Answer 153

necrotic material passed in the urine, which are renal papillae

Question 154

Pyelonephritis onset - sx - urine culture - Ct scan - treatment -

Answer 154

onset - few days sx - dysuria urine culture - positive Ct scan - diffusely swollen kidney treatment - abs such as ampicillin/gentamicin or fqs

Question 155

Papillary necrosis onset - sx - urine culture - Ct scan - treatment -

Answer 155

onset - few hours sx - necrotic material in urine urine culture - negative Ct scan - bumpy contour of interior where papillae were lost treatment - none

Question 156

summary or tubular disease

Answer 156

gnerally, they are acute cause by toxins (drugs, myoglobin, hemoglobin, oxalate, urate, NSAIDS, contrast) non of them ever cause nephrotic syndrome or give massive proteinuria biopsy is not needed to establish dx they are not treated with steroids (susually clear up spontaneously like all drug allergies) additional immunosuppressive meds (cyclophosphamid, mycophenolate) are not used treat tubular dz by correcting hypoperfusion and removing the toxin

Question 157

Tubular dz

Answer 157

``` acute toxins none nephrotic no biopsy usually no steroids never additional immunosuppressive agents ```

Question 158

acuTe=

Answer 158

Tubular=Toxin

Question 159

Glomerular Diseases General answers

Answer 159

Glomerular Diseases are generally chronic Glomerular Diseases are generally not caused by toxins or by hypoperfusion all of them can cause nephrotic syndrome

Question 160

Glomerular Diseases most accurate test

Answer 160

biopsy is the most accurate but it not always needed

Question 161

Glomerular Diseases often treated with

Answer 161

steroids addititonal immunosuppressive meds (cyclophosphamide, mycophenolate) are frequently used

Question 162

Glomular=

Answer 162

slow=sample=steroids=immunosuppressives

Question 163

Glomerular Diseases diagnostic tests

Answer 163

ua with hematuria dysmorphic red cells (deformed as they squeeze through an abnormal glomerulus) red cell casts urin sodium and FeNa are low proteinuria

Question 164

what is the main difference between glomerulonephritis and nehprotic syndrome

Answer 164

degree or amount or proteinuria

Question 165

Glomerular Diseases overview

Answer 165

chronic not from toxins/drugs all potentially nephrotic biopsy sample steroids often

Question 166

Individual glomerular diseases

Answer 166

every type of glomerulonephritis causes proteinuria, red cells, red cell casts in urine, htn, and edema, so you will need to know what is different or unique about each disease. it is like an IQ test: which of these is different from the others?

Question 167

Goodpasture syndrome also presents with

Answer 167

lung and kidney involvement but not upper respiratory like Wegener Granulomatosis or systemic vasculitits so no skin joint GI eye or neuro involvement

Question 168

Goodpasture Syndrome Diagnostic tests

Answer 168

best initial test is antiglomerular basement membrane antibodies. most accurate test is a lung or kidney biopsy anemia is often present from chornic lood loss from hemoptysis cxr is abnormal but insufficient to confirm diagnosis

Question 169

Goodpasture Syndrome treatment

Answer 169

plasmapharesis and steroids cyclophosphamid can be helpful

Question 170

kidney biopsy in goodpasture syndrome shows

Answer 170

linear deposits

Question 171

IgA Nephropathy (berger disease)

Answer 171

most common cause of acute glomerulonephritis in the US. look for an Asian pt with recurrent epidosed of gross hematuria 1 to 2 days after an upper resp tract infection (synpharyngitic). This actually helps, bc IgA disease is the most common cause of glomerulonephritis and all other causes have some specific physical findings

Question 172

poststreptococcal glomerulonephritis followed pharyngitis by

Answer 172

1 to 2 weeks

Question 173

Unique physical findings in IgA Nephropathy (berger disease)

Answer 173

there are none, this is how you answer the most likely question

Question 174

IgA Nephropathy (berger disease) diagnostic tests

Answer 174

iga levels are increased in only 50% most accurate test is a kidney biopsy proteinuria levels correspond to severity of disease and likelihood of progression (more proteinuria=worse progression)

Question 175

IgA Nephropathy (berger disease) treatment

Answer 175

There is no treatement to reverse the disease. thirty percent will completely resolve. between 40-50% will lsowly progress to end-stage renal disease severe proteinuria is treated with ACE inhibitors and steroids, fish oils is of uncertain benefit

Question 176

Postinfectious glomerulonephritis

Answer 176

the omst common organism leading to postinfectious glomerulonephritis is (PIGN) is streptococcus, but almsot any infection can lead to abnormal acitvation of the immune system and PIGN. it follows a throat or skin infection (impetigo) by 1 to 3 weeks.

Question 177

Postinfectious glomerulonephritis presentation

Answer 177

dark (cola colored) urine edema that isoften periorbitl htn oliguria

Question 178

Postinfectious glomerulonephritis diagnostic tests

Answer 178

a ua with proteinurai, red cells, red cell casts telsl you that glomerulonephritis ispresents. PSGN from group A beta hemolytic strep (pyogenes) is confirmed first by antistreptolysin O (ASO) titers and anti-DNAse antibody titers. biopsy is the most accurate tes but you should not routinely do a biopsy bc the blood test is sufficiently accurate and the disorder usually resolves spontaneously

Question 179

what is low in Postinfectious glomerulonephritis

Answer 179

complement levels

Question 180

Postinfectious glomerulonephritis treatment

Answer 180

management does not reverse Postinfectious glomerulonephritis. use supportive therapies like: antibiotics diuretics to control fluid overload

Question 181

how many of those with Postinfectious glomerulonephritis will progress

Answer 181

<5%

Question 182

Alport Syndrome

Answer 182

congenital defect of collagen that results in glomerular disease combined with: sensorineural hearing loss visual disturbance from loss of the collagen fibers that hold the lens of the eye in place no specific therapy to reverse this defect of type IV collagen

Question 183

Polyarteritis Nodosa definition

Answer 183

systemic vasculitis of snall and medium sized arteries that most commonly affects the kidney. virtually every organ in the body can be affected, but it tends to spare the lung. although it is of unknown etiology it can be assocaited with hepatitis B and all patietns with PAN should be tested.

Question 184

Polyarteritis Nodosa presentation

Answer 184

besided the presentation of glomerulonephritis, PAN presents with nonspecific sx of fever, malaise, weight loss, myalgias, and arhtralgia developing over weeks to months-asdoes almost ever type of vasculitis.

Question 185

Polyarteritis Nodosa Gastrointestinal

Answer 185

abdominal pain, bleeding, nausea, and vomiting occur paoin can be worsened by eating bc ofmesentericvasclitit

Question 186

Polyarteritis Nodosa neurologic

Answer 186

vasculitis damages the blood vesselssurrounding larger periopheral nerves such as the peroneal, ulnar, radial, and brachialnerves. when more than one large peripheral nerve isinvolved, it is call "mononeuritis multiplex". wen presented with strok ina young person you should look for vasculitits

Question 187

Polyarteritis Nodosa skin

Answer 187

vasculitits of any cuase leads to purpura (large) and petechiae (small). pan also gives ulcers, digital gangrene, and livedo reticularis

Question 188

Polyarteritis Nodosa cardiac disease

Answer 188

preent in about 1/3 of pts

Question 189

Polyarteritis Nodosa diagnostic tests: blood test

Answer 189

will show: anemia elevated esr and c reactive protein anca, not present in most cases ana and rf, sometimes present in low titer

Question 190

Polyarteritis Nodosa diagnostic tests: angiogrpahy

Answer 190

angiography of the renal, mesenteric, orhepatic artery showing aneurysmal dilation in assocation iwth new-onset htn and characteristic symptoms is the best initial test that has specificity for Polyarteritis Nodosa. angiography is a clear answer as a diagnostic test when the most invovled organ is not easily accessible for a biopsy (such as the kidney)

Question 191

Polyarteritis Nodosa most accurate diagnostic test

Answer 191

biopsy of a symptomatic site such as skin, nervs, or muscles

Question 192

Polyarteritis Nodosa treatmeent

Answer 192

prenisone and cyclophosphamide ar the standard of care and they lower mortality treate hep b when it is found

Question 193

damage to small blodo vesels around nerves startves them into

Answer 193

neuorpathy

Question 194

pan is nonspecifice

Answer 194

there is no single finding that allows youto answer the most likely diagnosis question

Question 195

stroke or Mi in young person suggests

Answer 195

Polyarteritis Nodosa

Question 196

there is no blood test to confirm

Answer 196

Polyarteritis Nodosa

Question 197

any form of glomerular disease can produce

Answer 197

nephrotic syndrome

Question 198

Lupus Nephritis presentation

Answer 198

sle can give any degree of renal involvement. the kindeys in sle can be normal or present with mild, asymptomatic proteinuria. severe disease presents with membranous glomerulonephtitis. long stading sle may simple scar the kidneys and biopsy will show glomerulosclerosis, which has no active inflammatory componenet but may lead to such damage as to require dialysis

Question 199

Lupus Nephritis mosta ccurate test

Answer 199

biopsy it is indispensible in determing therapy base on the stage

Question 200

Lupus Nephritis treatment

Answer 200

mild inflammatory changes may respond to glucocoritcoids. severe, proliferative disease such as membranous nephropathy is treatd with glucocroticoids combined with either cyclophosphamide or mycophenolast

Question 201

biopsy is ont permored to diagnose lupus but rather to

Answer 201

guide intesnity of therapy

Question 202

Amyloidosis

Answer 202

an abnormal protein produced in assocation with ``` myeloma chornic inflammatory disease rheumatoids arthirtis inflammatory bowel disease crronic infections ``` there is also a primary form of amyloidsosis in which hte protein is produced for unknown reasons.

Question 203

Amyloidosis what is the primary target of the proteins

Answer 203

kidney

Question 204

Amyloidosis omst accurate test

Answer 204

biopsy. you will se green birefringence with congo red staining

Question 205

Amyloidosis treatment

Answer 205

treate by trying to contorl the underlying disease.when this is unsuccessful or there is no primary disease to control, the treatment of amyloidosis is with melphalan and prednisone

Question 206

what gives large kidneys on sonogram

Answer 206

Amyloidosis hiv nephropathy polycystic kidneys

Question 207

massive proteinuria leads to:

Answer 207

edema hyperlipidemia thrombosis: from urinary loss of the nautral anticoagulatns protein C, protein S, and antirthrombin

Question 208

Nephrotic syndrome is not based on the etiology it is base on the

Answer 208

severity

Question 209

Nephrotic syndrome Etiology

Answer 209

overall, diabetes andhtnare the most commoncuases of nephrotic syndorome. any of the glomerular disease just described may lead to such massive protein loss that nephrotic syndrome developes

Question 210

Nephrotic syndrome cancer (solidorgan)

Answer 210

membranous

Question 211

Nephrotic syndrome children

Answer 211

minimal change disease

Question 212

Nephrotic syndrome | injection drug use and AIDS

Answer 212

focal-segmental

Question 213

NSAIDS

Answer 213

minimal change disease and membranous

Question 214

Major diff between nephritic and neprhotic syndrome

Answer 214

amount of protein

Question 215

Nephrotic syndrome presentation

Answer 215

nephrotic syndrome presetns with generalized edema. ingections are more prequent bc of increased urinary loss of immunoglobulins and complement. clots are more common from loss of antithormibn, protein c and s

Question 216

CHF leads to edema of dependent areas like the legs. nephrotic pts are edematous

Answer 216

everywhere

Question 217

Nephrotic syndrome best initial test

Answer 217

ua, but bc renal fucntion varies with the time of day as well as posture the ua is not sufficiently accurate

Question 218

Nephrotic syndrome albumin/creatinine

Answer 218

gives a measure of the average protein produced over 24 hours. a ration of 2:1 means 2 grams of protein excreted over 24 hours. aratio of 5.4:1 means 5.4 grams excreted over 24 hours

Question 219

Nephrotic syndrome most accurate test

Answer 219

renal biopsy, only test that can determine between the different form of Nephrotic syndrome

Question 220

Nephrotic syndrome by definition

Answer 220

hyperproteinuria (more than 3.5 grams per 24 hours hypoproteinemia hyperlipidemia edema

Question 221

ua only detects what as protein

Answer 221

albumin

Question 222

what is characteristic of Nephrotic syndrome

Answer 222

periorbital edema

Question 223

maltese corsses

Answer 223

seen in Nephrotic syndrome they are lipid depostis in sloughed off tubular cells

Question 224

Nephrotic syndrome lipid levels

Answer 224

lipid levels rise bc the liporptein signals that turn off the production of circulating lipid ar enow lost in the urine. with the loss of these ;iporptoeins that surround chylomicrons and VLDLs, all lipid levels in the blood iwll rise. Iron, copper, and zinc are low bc their carrier protein is lost in the urine.

Question 225

anything iwth a carrier proteins can be lost in

Answer 225

urine

Question 226

Nephrotic syndrome best initial therapy

Answer 226

glucocorticoids, if there is no response after several weeks of therapy, other immunosuppressive medications such as cyclophosphamide are used

Question 227

Nephrotic syndrome ACEi/ ARBS

Answer 227

are used to try anc control proeinuria

Question 228

Nephrotic syndrome edema treatment

Answer 228

is managed with salt restiction and diuretics.

Question 229

Nephrotic syndrome hyperlipidemia treatmenet

Answer 229

statins

Question 230

End Stage Renal Disease definition

Answer 230

or chronic renal failure, is defined as that form of kidney failure so severe as to need dialysis or renal transplantation. ESRD is not defined as a particular BUN or creatinine. ESRD is defined as the lsos of renal function leading to ac collection of sx and laboratory abnormalities also known as uremia. uremia is a term interchagable with the dondtions for which dialysis is the answer as therapy.

Question 231

End Stage Renal Disease Etiology

Answer 231

any form of tubular or glomerular damage canc ause ESRD. Overall, diabetes and htn are, by far, more common than all the other causes of renal failure compbined. ESRD usually iomplies disease that has been present for years; however, rapidly progressive glomerulonephritis is so named bc it can lead to ESRD over weeks.

Question 232

End Stage Renal Disease Uremia (so how ESRD presents)

Answer 232

metabolic acidosis fluid overload encephalopathy hyperkalemia pericarditis each of these is an indiication for dialysis

Question 233

Most common causes of End Stage Renal Disease

Answer 233

diabetes and htn

Question 234

what is better peritoneal dialysis or hemodialysis

Answer 234

they are equally effective

Question 235

Manifestations of renal failure

Answer 235

anemia hypocalcemia osteodystrophy bleeding infection pruritis hyperphosphatemia hypermagnesemia accleerated atherosclerosis and hypertension endocrinopathy

Question 236

Manifestations of renal failure anemia

Answer 236

loss of epo leads to normocromic, normocytic anemia

Question 237

Manifestations of renal failure hypocalcemia

Answer 237

the diney transorms the less active 250hvitd into the much more active 1,25ohvitd. w/o 1,25ohvitd, thebody will not absorb enough calcium from the gut

Question 238

Manifestations of renal failure osteodystropohy

Answer 238

low calcium leads to secondary hyperparathyroidsim. hgigh parathyroid hoemrone levels remove calcium from bones, making then soft and weak

Question 239

Manifestations of renal failure bleeding

Answer 239

platelets do not work nomrally in a uremic environement, they do not degranulate, if a platelet does not release the ocntents of its granlues is will no work

Question 240

Manifestations of renal failure infection

Answer 240

the same defect occurs with neutrophils. without degrnuatlion neutros will not effectively combat infection

Question 241

Manifestations of renal failure pruritus

Answer 241

unclear reasonin, urea accumulating in skin causes itching

Question 242

Manifestations of renal failure hyperphosphatemia

Answer 242

phosphate is normally excreted through kidneys. high parathyroid hormone levels release phosphate from bones, but the body is unable to excrete it

Question 243

Manifestations of renal failure hypermagnesemia

Answer 243

from loss of excretory ability

Question 244

Manifestations of renal failure accelerated atherosclerosis and hypertension

Answer 244

the immune system (lymphocytes) helps keep arteries clear of lipid accumulations. white cells dont work normally in a uremic environment. this is the most common cause of death in those on dialysis

Question 245

Manifestations of renal failure endocrinopathy

Answer 245

women are anovulatory. men havce low testosterone. Erectile dysfucntion is common. insulin levels tend to go up bc insuling is ecrested renally howevere insulin resitance also increases. glucose levels therefore canbe up or down

Question 246

cardiac disease kills

Answer 246

triple the amount of people that infection does in ESRD

Question 247

aneima from ESRD is the only time

Answer 247

erythropoitin is always used

Question 248

Treatment of manifestations of ESRD Anemia

Answer 248

erythropoietin replacement and iron supplementation

Question 249

Treatment of manifestations of ESRD hypocalcemia and osteomalacia

Answer 249

replace vitamin D and calcium

Question 250

Treatment of manifestations of ESRD bleeding

Answer 250

ddavp incrases platelet function; use only when lbeeding

Question 251

Treatment of manifestations of ESRD pruritus

Answer 251

dialysis and uv light

Question 252

Treatment of manifestations of ESRD hyperphospatmia

Answer 252

oral binders: see treatment of hyperphosphatemia

Question 253

Treatment of manifestations of ESRD hypermagnesemia

Answer 253

restriction of high-magnesium foods, laxative, and antacids

Question 254

Treatment of manifestations of ESRD atherosclerosis

Answer 254

dialysis

Question 255

Treatment of manifestations of ESRD endocrinopahty

Answer 255

dialysis, estrogen and testosterone replacement

Question 256

Treatment of hyperphosphatemia

Answer 256

oral phosphate binders will prevent phosphate absorption form the bowel. treatment of hypocalcemia will also help bc it is the hyperparathyroidism that causes increase sphosphate release from bone. when vitamin D is replaced to control hypcalcemia it is critical to also give phosphate binders; otherwise vitamine D will increase GI absorption of phosphate

Question 257

oral phosphate binders

Answer 257

calcium acetate calcium carbonate sevelamer lanthanum

Question 258

when do you use sevelamer and lanthanum to bind phosphate

Answer 258

when the calcium levle is high

Question 259

why dont you use aluminum-containing phosphate binders

Answer 259

aluminum cause dementia

Question 260

Kidney Transplantation

Answer 260

only 50% of ESRD pts will be suitable for transplantation. the donor does not have to be alive or related, although these are both better

Question 261

how long do HLA identical related donor dineys lst

Answer 261

24 years on average

Question 262

Kidney Transplantation living rleated donor

Answer 262

1 year 95% 3 year 88% 5 years 72%

Question 263

Kidney Transplantation deceased donor

Answer 263

1 year 90% 3 years 78% 5 years 58%

Question 264

Kidney Transplantation Dialysis alone

Answer 264

variable for 1 and 3 years survival | 5 year 30-40%

Question 265

Kidney Transplantation diabetics on dialysis

Answer 265

variable for 1 and 3 year | 5 years 20%

Question 266

Thrombotic Thrombocytpenic purpura and hemolytic uremic syndrome

Answer 266

diff variants of what is probablyt he same disease

Question 267

ttp is mor ecommon with

Answer 267

hiv and cancer and drugs like cyclosporine ticlopidine and clopidogrel

Question 268

HUS is more common in

Answer 268

children and the most frequently tested association is E coli 0157 h7 and shigella

Question 269

Thrombotic Thrombocytpenic purpura and hemolytic uremic syndrome are both associated with

Answer 269

intravasculate hemolysis (visible on smeare with schistocytes, helmet cells, and fragmented red cells rneal insufficiency thromocytopenia

Question 270

ttp is associated with

Answer 270

neurological symptoms fever

Question 271

pt and aptt in hus/ttp

Answer 271

normal

Question 272

Thrombotic Thrombocytpenic purpura indispensible finding

Answer 272

intravascular hemolysis

Question 273

Thrombotic Thrombocytpenic purpura and hemolytic uremic syndrome treatment

Answer 273

most cases of hus from e coli will resolve spontaneously. plasmapheresis is generally urgen in TTP severe hus also needs urgent plasmapheresis. if plasmapheresis is not one of the choices, use infusions of fp. steroids do not help.

Question 274

when do you do platelet transfusion in hus and ttp

Answer 274

never

Question 275

Cystic Disease

Answer 275

the sinlge most important point in cystic disease is how to recognize a cyst that is potentioally malignant and needs to be aspirated. if the qualities of a complex cyst are found , it should b easpirated to exclude malignancy

Question 276

cystic disease simple cyst

Answer 276

echo free smooth,thin sharp (demarchation) good thorugh to back (transmision)

Question 277

cystic disease complex cysts (potential malignancy)

Answer 277

mixed echogenicity irregular,thick lower density on back wall debris in cyst

Question 278

Polycystic Kidney Disease presents with

Answer 278

``` pain hematuria stones ingestion hypertension ```

Question 279

most common cause of death from PCKD

Answer 279

renal failure

Question 280

associated with PCKD

Answer 280

liver cysts (most common site outside of the kidney) ovarian cysts mitral valve prolapse anuerysms diverticulosis

Question 281

PCKD treatmeent

Answer 281

no thereapy of any kind to reverse cysts of any type

Question 282

Hypernatremia etilogy

Answer 282

occurs when there is loss of free water. Examples are: sweating burns fever pneymonia: from insensible losses from hyperventilation diarrhea diuretics Diabetes insipidus

Question 283

Diabetes insipidus central

Answer 283

leads to high olume water loss from insufficient or ineffective antidiuretic hormone (ADH). Any CNS disorder (stroke, tumore, trauma, hypxoia, infection) can damage the production of adh in the hypthalamus or storage int he posterior pituitary leading to central diabetes insipidus

Question 284

DI nephrogenic

Answer 284

a loss of ADH efect on the collecting duct of the kidney, this is much less common. nephrogenic DI is causes by lithium or demeclocycline, chornic kidny disease, hypokalmeia, or hypercalcemia. they make adh infeffecitve at the tubule

Question 285

first clue to DI

Answer 285

high volume nocturia

Question 286

Hypernatremia presentation

Answer 286

di and hypernatremia of any cause presents with neurological sx such as confusion, disorientation, lethargy, and seizures. if uncorrected, severe hypernatremia causes coma and irreversible brain damage.

Question 287

sodium disorders cause

Answer 287

CNS disorders

Question 288

Hypernatremia diagnostic tests

Answer 288

high serum sodium is nearly equivalent to hyperosmolality since the majority of osmolality is sodium. fluid losses form the skin, kidneys, or stool generally lead to: decreased urine volume (high urine volume in DI) increased urine osmolality (decreased urine osmolality in DI) decrease urine sodium

Question 289

Best initial test for DI

Answer 289

water deprivation test, prevent the patient from drinking, then observeing urine output and urine osmolality. with di, urine volume stays high and urine osmolality stays low depsite viforous urine productiona nd despite developing hydration.

Question 290

DI response to ADH administration

Answer 290

CDI: sharp decrease in ruine olume, increase in osmolality NDI: no change in urine volume or osmolality with ADH administartion

Question 291

DI ADH levels

Answer 291

ADH level is low in CID and markedly elevated in NDI

Question 292

What does a postiive water deprivation test mean

Answer 292

urine volume statys high depsite withholding water

Question 293

CDI overview polyuria and nocturia: urine osmolality and sodium: positive water deprivation test: repsonse to adh: adh level:

Answer 293

polyuria and nocturia: yes urine osmolality and sodium: low positive water deprivation test: yes repsonse to adh: yes adh level: low

Question 294

NDI overview polyuria and nocturia: urine osmolality and sodium: positive water deprivation test: repsonse to adh: adh level:

Answer 294

polyuria and nocturia: yes urine osmolality and sodium: low positive water deprivation test: yes repsonse to adh: no adh level: high

Question 295

hypernatremia treatement fluidl osso

Answer 295

replace fluid and correct hte underlying cause

Question 296

cdi treatment

Answer 296

replace ADH (vasopressin also known as DDAVP)

Question 297

ndi treatment

Answer 297

correct k and calcium stop lithium or demeclocycline give hydrochlorothiazide or nsaids for those still having ndi despite these inteventrions

Question 298

hyperntremia complications of therapy

Answer 298

if sodium levels are brougth down too rapidly, cerebral dema will occur this is formt he shift of lfuids from the basculare space into the cells of the brain. cerebral edema presnts with worsening confusion and seizures

Question 299

hypernatremia diagnosti ctests

Answer 299

best initial: water deprivation, if corrects then sphycogenic polydipsia if doesnt correct hte di and the best next test and most oaccurate test is adh administration test

Question 300

hyponatremia etiology

Answer 300

hyponatremia is characterized accoreding to overall volume status of the body hypervolemia euvolemia hypovolemia

Question 301

hyponatremia Hypervolemia

Answer 301

the most common causes are CHF nephrotic syndrome and cirrhosis these are cases in which intravascular volume depletion leads to increased ADH levels. pressure receptors in the atria and carotids sense the decrease in volume and stiulate ADH production and release. although the sodium level drops, it is more important to maintain vascular volume and organ perfusion

Question 302

Hyponatremia hypvolemia causes

Answer 302

sweating burns fever pneymonia: from isnsible losses from hyperventilation diarrhea diuretics all of these are also causes of hypernatremia; however, they cause hyponatremia if thre is chornic replacemnt with free water. a little sodium and a lot of water are lost in urine, which is then replaced with free water that has no sodium. over time, this process depletes the body of sodium and the serum sodium level drops addison disease

Question 303

Addison disease

Answer 303

is loss of adrenal function also causes hypnatremia bc of loss of aldosterone. aldosterone causes sodium reabsorption. if the body loses ldosterone, it loses sodium

Question 304

Hyponatremia Euvolemia

Answer 304

the most common causes of hyponatrmiea with euovlemia are: psydohyponatrmiea (hyperglycemia) psychogenic polydipsia hypothryodism syndrome of inappreopriate ADH relsease (SIADH)

Question 305

Hyponatremia Euvolemia hyprglycemia

Answer 305

very high glucose levels lead to a decrease in sodium levels. hyperglycemia acts as an osmotic draw on fluid inside the cells. free water leaves the cells to correct he hyperosmolar serum. this drops the sodium level. the management is to correct he glucose level for ever 100 mg/dl of glucose above normal, there is a 1.6meq/l decrease in sodium

Question 306

Hyponatremia Euvolemia psychogenic polydipsia

Answer 306

massive ingestion of free water above 12 to 24 liters a day will overhwelm the kidney's ability to excrete water. the minimum urine osmolality is 50 mosm/kg. the body can produce 12 to 24 liters of urine a day, depending on whether you can get the urine osmolality down to 50 or 100 mosm/kg

Question 307

look for a hx of wahtto diagnose spychogenic polydipsia

Answer 307

bipolar disorder

Question 308

what is more importatnt than normal sodium

Answer 308

perfusion

Question 309

Hyponatremia Euvolemia Hypthyroidism

Answer 309

thyroid hormone is needed to excrete water. if the thyroid hormone level is low, free water excretion is decreaed

Question 310

Hyponatremia Euvolemia SIADH

Answer 310

any lung or brain disease can cause SADH for unclear reasons. certain drugs such as SSRI's sulfonylureas, vincristine , cyclophospamide, or tcas can cause siadh. certain cancers, especially samll cell cancer of the lung, produce adh pain also causes siadh

Question 311

Hypernatremia persentation

Answer 311

CNS sx: confusion lethargy disorientation seizures coma if the sodium levels drop very fast the pt can immediately seize, slow dorp may be entirrely asymptomatic even if the level is very low

Question 312

hypernatremia diagnosti ctests

Answer 312

in siadh, the urine is inappropriately concentrated (high urine osmolality) the urine sodium is inapproprietely high in siadh. the uric acid level and bun are low in siadh the most accurate test is a high adh

Question 313

urine osmolality levels with hyponatremia

Answer 313

usually below 100 with siadh it is higher

Question 314

urine sodium with hyponatremia

Answer 314

usually below 20 by will get hight than 40

Question 315

mild hyponatremia clincial manifestations

Answer 315

no symptoms just restrict fluids

Question 316

modearte hyponatremia clinical manifestations

Answer 316

minimal confusion saline and loop diuretic

Question 317

severe hyponatrmeia clnicial manifestation

Answer 317

lethargy, seizures, and coma use hypertonic saline, conivaptain, tolvaptan

Question 318

symptoms of yponatremia are dependent on

Answer 318

how fast it occurs

Question 319

sodium means

Answer 319

cns sx

Question 320

in siadh what makes it worse

Answer 320

saline wihtout diuretic

Question 321

treatmeent for hyponatremia

Answer 321

depnds on sx not severeity

Question 322

ADH antagonists for hyponatremia

Answer 322

tolvaptan and conivaptan are antagnosits of ADH. they are the answer as part of urgent therpy for severe, sympmtomatic siadh. they are only for urgen treatment inhospital . no oral version is available

Question 323

Chronic SIADH treatment

Answer 323

siadh can be from an underlying disorder that cannot be corrected such as metastatic cancer. demeclocycline treats chronic SIADH. demeclocycline blocks the action of ADH at the collecting duct of the kidney tubule

Question 324

Complications of SIADH treatment

Answer 324

correction of sodium must occur slowly. slowly is defines as under 0.5 to 1 meq per hour or 12 to 24 meq per day. if the sodium level is brought up to normal too rapidly, the neurological disorder known as central ponint myelinolysis or osmotic demylinization occurs.

Question 325

Hyperkalemia

Answer 325

high potassium levels are an absolutely indispnsable portion of your knowledge bc of the life-thretening nature of potassium diroserds

Question 326

Hyperkalemia pseudohyperkalemia (falsely elevated elvels) etiology

Answer 326

hemolysis repeated first cldingin with tourniquet in place thrombocytosis or leukocytosis will leak out of cells in the lab specimen none of these causes of heyprkalemia needs further treatment or investivation beyond repeating the sample

Question 327

Hyperkalmeia decreased excretion etiology

Answer 327

renal failure aldosteron decrease - ace inhibitores/arbs - type 4 renal tubular aidosis (hyporeninemic, hypaldosteronism0 - spironolactone and eplerenone (aldosterone inhibitors - triamteren and amiloride (potassium-sparing diuretics - addison disease

Question 328

hyperkalemia releas of potassium from itssues etiology

Answer 328

any tissue destruction, such as hemolysis, rhabdomyolysis, or tumor lysis syndrome, can release potassium decreased insulin: insulin normally drives potassium into cells acidosis: cells will pcik up hydrogen ions (acid) and release potassium in exchange beta blockers and digoxin: these drugs inhibit the sodium.potassium atpase that normally brinds potassium into the cells heparin increases potassium levles, presumably throuhg increased itssue release

Question 329

severe hyperkalemia can do what

Answer 329

stop theheart in seconds if the level is high enough

Question 330

hyperkalemia presentation

Answer 330

potassium disorders interfere with muscle contraction and cardiac conductionancd, look for: weakness paralysis when svere ileus (paralyzes gut muscles) cardiac rhythm disorders

Question 331

Hyperkalemia diagnosit ctests

Answer 331

besides a k level, testing is aimed at looking for causes, the most urgen test in severe hyperkalmia is an ekg the ekg in severe hyperkalmia shws: peaked T waves wide qrs pr interval prolongation

Question 332

hyperkalemia treatment life threatening hyperkalemia (abnormal ekg)

Answer 332

calcium choloide or calcium gluconate insulin and glucose to drive k back into cells bicarbonate: drivesk into cells but sould be used most when acidosis causes hyperkalemia

Question 333

hyperkalemia treatment removing potassium from the body

Answer 333

sodium polystyrene suflonate (kayexalate; sanofi-aventis, bridgewater, newjersey) removes poassium from the body through the bowel. the patient ingests kayexalate orally and ove rseveral hours it will bind potassium in the gut and remove it from the body

Question 334

hyperkalemia insulin and bicarb

Answer 334

lower the potassium level through the redistribution into the cells

Question 335

other methods to lower potassium

Answer 335

inhaled beta agnosists (albuterol) loop diuretics dialysis

Question 336

when there is hyperkalmeia and an abnormal ekg the most appropriate next step is

Answer 336

calcium chloride or bluconate

Question 337

hyperkalemia does not cause

Answer 337

seizures

Question 338

how much potassium is in the cells

Answer 338

95%

Question 339

when do use calcium with hyperkalemia

Answer 339

when the ekg is abnormal to protects the heart bc it does not lower the k level

Question 340

insulin does not remove what fromt he body

Answer 340

potassium

Question 341

sodium=

Answer 341

cns sx

Question 342

hyperkalemia=

Answer 342

muscular and cardiac sx

Question 343

hyperkalemia with no ekg changes treatment

Answer 343

kayexalate and loop diuretics

Question 344

hyperkalmiea iwth ekg changes

Answer 344

calcium cholirde or gluconate insuling and glucose, inhaled beta agnoist g ive bicarb if acidosis is the cause consider hemodialysis

Question 345

Hypokalemia decreased intake etiology

Answer 345

this is unusal bc the kdiney can decrease potassium excretion to extremely small amounts

Question 346

Hypokalemia shift into cells etiology

Answer 346

alkalosis (hydrogen ions come out of the cell in exchange for potassium entering) increased insulin beta adrenergic stimulation ( acccleatares sodium/k atpase)

Question 347

Hypokalemia renal loss etiology

Answer 347

loop diuretics increased aldosterone - primary hyperaldosteronism (conn syndrome) - volume dpeletion raises alodsoterone - cushing syndome - bartter sydrome (genetic disease causing salt loss in loop of henle) - licorice hypomagnesmia: there are magnesium-dependant potassium channels. when magnesium is low, they open and spill potassium intot he urine renal tubular acidosis (RTA) both proximal and distal

Question 348

Hypokalemia etiology gi loss

Answer 348

vomiting diarrhea laxative abuse

Question 349

Hypkalemia presentation

Answer 349

hypokalemia leads to problems with muscular contraction and cardiac conduction. potassium is essential for proper neuromuxcular contraction presents with: weakness paralysis loss of reflexes

Question 350

Hypokalemia ekg finding

Answer 350

u waves ar ethe mos tcharacteristic finding of hypkalmiea other findings are ventricular extopy (PVCs), flattened T waves, and ST depression

Question 351

Hypokalemia treatment

Answer 351

there is no maximum rate of oral potassium rpelacement. the gi system cannot absorb potasium faster than the kdineys can excrete it, s o you cannot go too far too fast. iv potasskum replacement, however, can ccause fatal arrhythmia if it is done too fast. you must allow time for epotassium to equilibaret into the cells

Question 352

muscular abnomralities may be so severe as to cause what hyperkalmia

Answer 352

rhabdomyolysis

Question 353

iv potassium replacement must be very

Answer 353

slow

Question 354

what do you protect first in ptoassium disorders

Answer 354

heart

Question 355

Renal tubular acidosis definition

Answer 355

a metabolic acidosis with a normal anion gap. the anion gap is defined as sodium minus choloide plus bicarb na minus cl and bicarb a normal anion gap is between 6 and 12. the difference between the cations and the anions is predominalty from the negative charges that are no albumin

Question 356

2 most importatn causes of a metablic acidosis with a normal anion gap

Answer 356

rta and diarrhea the anion gap is noraml bc the chloride level rises. hence, theya re also referred to as hyperchloremi metabolic acidosis.

Question 357

what causes anion gap acidosis

Answer 357

M — Methanol U — Uremia (chronic kidney failure) D — Diabetic ketoacidosis P — Propylene glycol ("P" used to stand for Paraldehyde but this substance is not commonly used today) I — Infection, Iron, Isoniazid, Inborn errors of metabolism L — Lactic acidosis E — Ethylene glycol (Note: Ethanol is sometimes included in this mnemonic as well, although the acidosis caused by ethanol is actually primarily due to the increased production of lactic acid found in such intoxication.) S — Salicylates

Question 358

Distal RTA

Answer 358

type I the distal tubule is responsible fore genrearting new bicarb under the influecne of aldosterone. drugs such as amphotericin and autoimmune disease such as SLE or sjogren syndrome can damage the distal tubule. if new bicarb cannot be genreated at the distal butuble, then acid cannot be excreted into the tubule, raising the PH of the urine in an alkaline urine, thre in increased formation of kienys stones from calcium oxalate

Question 359

Distal RTA diagnostic tests

Answer 359

the best initial test is a ua looking for an abnomrally high PH above 5.5 the most accurate test is to infuse acid intot he blood awith ammonium chloride. a healthy person will be able to excrete the acid and will decrease the urine PH. those with distal RTA cannot excrete the acid and the urine pg will remain basic (over5.5) despite an icnreasinly acidic serum.

Question 360

Distal RTA treatment

Answer 360

replace icar that will be abosrbed at the proximal tubule. since the majority of bicarb is absorbed at the proximal tubule.Distal RTA is relatively easy to correct. just give more bicarb and the proximal tubule will absorb it and correct teh acidosis

Question 361

Proximal RTA

Answer 361

type II normally 85 to 90% of filtered biacrb is reabosrbed at the proximal tubule. damae to the proximal tubule from amyloidosis, myeloma, fanconi syndrome, acetazoliame, or heavy metals decreases the ability of the kdiensy to reabsorb most of the filtered bicarb. biacrb is lost int he urine untilt he body is so depelted of biacrb ethat the distal butulbe can absorb the rest. when it dhappens, the urine pg will become low (at or abelow 5.5) chornic metabolic aidosis leaches calcium out fot he bones and they become osteomalacia)

Question 362

no acid into the tubule

Answer 362

makes the urine basic

Question 363

Diatal rta calcifices

Answer 363

the kidney parenchyma (nephrocalcinosis)

Question 364

RTA does not mean

Answer 364

the tubule is always acidic

Question 365

both proxima and distal rta are

Answer 365

hypokalemic, k is lost in the urine

Question 366

Proximal RTA diagnostic tests

Answer 366

the urine ph is avriable in proxima rta. first, it is basic (above5.5) untilmost of the biarb is lost from the body, then it is low (below 5.5) the mos taccurate test is to evaluate bicarb malabsorption in the kidney y giving bicarb and testin the urine ph. bc the kidney cannot abosrb iarb, teh urine ph will rise

Question 367

Proximal RTA treatment

Answer 367

bc bicarb is not absorbed well in hte Proximal RTA it is difficult to treate it with bicarb prelacement and masive doeses are necesary. thiazide diuretics casue volume dpeletion. volume depletion will enhane bicarb reabosrption

Question 368

Hypertensive Crisis

Answer 368

defines as high blood pressure in assocaiton with confusion blurry vision dyspnea chest pain

Question 369

Hypertensive Crisis therapy

Answer 369

best initial therapy is labetolol or nitroprusside. bc nistroprusside neds montoring with an arterial line, this is not usually the first choice other acceptable forms of treatment are: enalapril ccbs: dilt and verapamil esmolol hhydralazine any iv medication is acceptable. the specific drug available is not as important as giving enough of it to conttrol the blood pressure

Question 370

Htn definition

Answer 370

Systolic pressure above 140 distolic pressure above 90

Question 371

Htn diagnosis

Answer 371

nin order to establisht he diagnosis of thn blood pressure measuremnt must be preeated in a calm state over time. the precise interval between measuremtn over what period of time isot clear

Question 372

htn is:

Answer 372

the most common disease in the us the most common risk factore for the most common cause of death: mi

Question 373

HTN etiology

Answer 373

95% of htn hasno clear etiology and can be called essential hn. know causes are: renal artery stenosis glomerulonephritis coarctation of the aorta acromegaly obstructive sleep apnea pheo hyperaldosteornism cushing syndrome or any cause o hypercotisolism including meds cah

Question 374

JNC 8 says:

Answer 374

in diabetes goal is 140/90 thiazided ar enot better than ccb ace or arb bp 150/90 over age 60

Question 375

HTN presnetation

Answer 375

the vast majority of cases ar efound on routine screening of asymptomatic pts. when htn does have symptoms, they are from end organ damage from atherosclerosis like: ``` cad verebrovascular disease chf visual disturbance renal insufficiency pad ```

Question 376

Presentation of secondary htn

Answer 376

renal artery stenosis: buirt is auscultated at the flank. the bruit is continuous thorugh tsytole and diastole glomerulonerphirits coarctation of the aorta:upper extremity>lower extremity blood pressure acromegaly pheo: episodi htn with flusign hyperaldosteronism: weakness from hypokalemia

Question 377

HTN diagnostic tests

Answer 377

repeated in office measuremnt or home ambulatory measuremnts carry equal significancen also test with ekg urinalysis glucose measurement to exclude concomitant diabetes cholesterol screening

Question 378

HTN best initial therapy

Answer 378

wieght loss (most effective) sodium restiction dietary modifications (less fat and red meat, more fish and vegetables) exercie tobacco cessation doesnot stop htn but beomes improtant to prevent cardiovascular disease

Question 379

summary of jnc 8 managemetn of hypertension

Answer 379

blood pressure goal in diabetes is 140/90 initial management is with eith thiazides or ccb or ace inhbitor or arbs. diuretics are not considered specifically better as the intial therapy the main point is to controlt he bp the specici agent is not as improtant with age above 60 the goal is 150/90

Question 380

HTN drug therapy best initial therapy

Answer 380

thiazide diuretic, ccb, acei or arb sixty to 70 percent of patients are controlled by a single medication. if blood pressure is very high on presentation (above160/90), 2 medications should be used at the outset

Question 381

if diuretics do not control bp the most approiate next stp is

Answer 381

acei arb bb ccb

Question 382

meds not considered first line or second line for htn

Answer 382

central actin alpha agonsits (alpha mehtyldopa, clonidine) periphera acting alpha antagonists (prazosin, terazonin, doxazosin) direct acting vasodiltors (hydralazine, minoxidil

Question 383

what percentage of htn pts will be ctonrolled by 2 meds

Answer 383

90

Question 384

pregnancy safe htn drugs

Answer 384

bb use first ccb hydralzaine alpha methyldopa

Question 385

Treatment for htn with cad

Answer 385

bb ace arb

Question 386

Treatment for htn with diabetes

Answer 386

ace arb (goal 140/90)

Question 387

Treatment for htn with bph

Answer 387

alpha blockers

Question 388

Treatment for htn with depression and asthma

Answer 388

just avoid bb

Question 389

Treatment for htn with hyperthyroidism

Answer 389

bb first

Question 390

Treatment for htn with osteoporosis

Answer 390

thiazides

Question 391

Nephrolithiasis

Answer 391

the most common cause of kidney stones is calcium oxalate, which forms more frequently in an alkaline urine. the most common risk factor is the overexcretion of calcium in the urine

Question 392

what is the most appreirate next tep in Nephrolithiasis after it is diagnosed

Answer 392

ketorlolac

Question 393

most accurate test for Nephrolithiasis

Answer 393

CT scan, does not need ontract and is more accurat ethan xray or us

Question 394

what is alway swrong for Nephrolithiasis

Answer 394

ivp

Question 395

what disease causes Nephrolithiasis

Answer 395

crohn bc it causes increased reabsorption of calcium oxalate

Question 396

what stones are not seen on xray

Answer 396

uric acid

Question 397

Nephrolithiasis treatment best inital therapy for acute renal colic

Answer 397

analgesics and hydration ct and sonography to detect obstruction such as hdronephrosis stones <5mm pass spontaneously sotnes 5-5 mm get nifedipine an dtamsulosin to help them pass

Question 398

Nephrolithiasis etiology of the stone is determined with

Answer 398

sonte analysis serum calcium, sodium, uric acid, magneium and phosphate levels 24 hour urine for volume, calcium, oxalate, citrate, cystine, ph, uric acid, phophate, and magneium

Question 399

cystine sotnes are managed with

Answer 399

surgical removal, alkalinixin urine

Question 400

Fat malabsorption increases

Answer 400

stone formation

Question 401

sontes 5-7 mm get what for treatment

Answer 401

nifedipine and tamsulosin to help them pass

Question 402

uti givves what kind of stones

Answer 402

struvite sontes (mangesium/ammonium/phosphate) rmeove them surgically

Question 403

management of stones that are .5cm to 2-3 cm

Answer 403

lithotripsy

Question 404

management of stones that are greater than 2-3 cm

Answer 404

surgically, place a stent to remove hydronephrosis, stones in the upper half of ureter get lithotrips those half down are removed with a basket

Question 405

Lont term management with stones

Answer 405

50% of those with kidney stones will have a recurrecne ove rthe next 5 years hctz removes calcium from the urine by increasing dital tubule reabsorption of calcium furosemid eincreased calcium excretion anc can make themm wor calcium restriction doesnt help and can actually make it worse when calcium injestion is low ther is increased oxalate absortpion int he gut c there is no calcium to bind it in the gut the risk of stone formation is incresed if there is a dietary decrease in calcium, increase in oxalatae or decrease in citrate

Question 406

Metabolic acidosis and stone formation

Answer 406

metabolic acidosis removes calcium from bones and increases stone formation. in addition, metabolic acidosis decreases citrate levels. citrate binds calcium, making it unavailable for stone formation

Question 407

Stress incontinence symptoms

Answer 407

older woman with painless urinary leakage with coughing, laughin or lifitn heavy objects

Question 408

Stress incontinence test

Answer 408

havve pt stand and cough; observe for leakage

Question 409

Stress incontinence treatment

Answer 409

kegel exercises local estrogen cream surgial tightenin of urethra

Question 410

Urge incontinence symptoms

Answer 410

sudden pain in the bladder followed immediately by the overwhelming urge to urinate

Question 411

Urge incontinence test

Answer 411

pressure measuremnt in half full bladder; manometry

Question 412

Urge incontinence treatment

Answer 412

bladder training exercises local anticholinergic therapy oxybutynin tolteradin solifenacin dariferancin surgical tightneing of the urethra

Question 413

Metabolic Alkalosis definition

Answer 413

elevated serum bicarb elvel. the compensation for this is resp acidosis. there will be a relative hypoventilationt aht will increse the pco2 to compensate for metabolic alkalosis

Question 414

Metabolic Alkalosis etiology

Answer 414

GI loss: vomiting or ng suction increase aldosterone: primary hyperaldosteronism, cushing syndrome, ectopic acth, volume contraction, licorice diuretics milk-alkali syndrome: high volume liquid antacids hypkalemia: hydrogen ions move into cells so potassium can be released

Question 415

Metabolic Alkalosis abg

Answer 415

increase ph>7.40 increase pco2 indicating repiratory acidosis as compensation increased bicarb

Question 416

Resp acidosi and alkalosis

Answer 416

they are easy to understank bc they come down to the single pathway of the effect on minute ventilation minute ventilation=respiratory ratextidal volum

Question 417

Respiratory alkalosis overview

Answer 417

decreased pco2 increased minute ventilation metaboli acidosis as compensation ``` anemaia anciety pain fever interstitial lung diease pe ```

Question 418

respiratory acidosis overview

Answer 418

increased pco2 decreased minute ventilation metabolic alkalosis as compensation ``` copd/emphysema drowning opiate overdose alpha 1antitrypsin deficiency kyphoscoliosis sleap apnea/morbid obesity ```

Question 419

Metabolic acidosis anion gaps

Answer 419

noraml 6-12 elevated above 12 the anion gap is incresed if there are unmeasured anions driving eh bicarb levels down

Question 420

Metabolic acidosis causes of increased anion gap

Answer 420

lactate ketoacids oxalic acid formic acid uremia salicylates

Question 421

Metabolic acidosis lactate

Answer 421

hyptension or hypperfusion blood lactate level correct hypperfusion

Question 422

metabolic drangements kill patients with

Answer 422

cardiac arrhythmia. they also alter ptoassium elvels

Question 423

minute ventialtion is more accurate than

Answer 423

rr

Question 424

hyperventilation may occure with

Answer 424

a tiny tidal vomume. this does not increase mnute venilation

Question 425

Metabolic acidosis ketoacids

Answer 425

dka and starvation acetone level insulin and lfuids

Question 426

Metabolic acidosis oxalic acid

Answer 426

ethylene glycole overdose crystals on UA fomepizole and diaylsys

Question 427

Metabolic acidosis formic acid

Answer 427

methanol overdose inflamed retina fomeizple and dialysis

Question 428

Metabolic acidosisuremia

Answer 428

renal failure bun and creatinine dialysis

Question 429

Metabolic acidosis salicylates

Answer 429

aspirin overdose aspirin level alkalinize urine

Question 430

Metabolic acidosis abg

Answer 430

decreased ph below 7.4 decreased pco2 indicating respiratory alkalosis as compensation decreased bicarb

Question 431

resp alkaloiss from hypeventialtion compensates for

Answer 431

all fomrs of metabolic acidosis

Question 432

Urin anion gap definition

Answer 432

the urine anion gap is a way to distinguish between diarrhea and RTA as causes of normal anion gap metaboli c acidosis UAG= sodium minus chloride or na minus cl

Question 433

Urin anion gap process

Answer 433

acid excreted by the diney is buffered off as nh4cl or ammonium chloride. the more acid excreted, the greater the amount of chloride found in the urine. in rta there is a defec tin acid excretion into the urine, so the amount of chloride in the urin is diminshed. this gives a positive number when calculating na minus cl

Question 434

Urin anion gap in diarrhea

Answer 434

the ability to excrete acid theought he diney remains intacts. bc diarrhea is associated with metabolic acidosis, the kidney tries to compesate by incresing acid excretion. hence,, in diarrhea there is more acid in the urine. acid (H) is excreted with cholide. so, in diarrhea, more acid in theurine means more choliride in the urine. na minus cl will become a negative number in diarrhea

Question 435

rta has a positive

Answer 435

uag

Question 436

diarrhea has a negative

Answer 436

uag

Question 437

Hyporeninemia, hypaldosteronism (type IV RTA)

Answer 437

occurs most often in diabetes. there is a decreased amount or effect of aldosterone at the kidney tubule. this leads to loss of socium and retention of k and hydrogen ions. test for type IV RTA by finding a persistently high urine sodium despite a sodium depleted diet. in addtion, hyperkalemia is a main clue to answering "what is the most likely diagnosis"

Question 438

what streoid has the highest meneralocorticoid or aldosteronlike effect

Answer 438

fludrocortisone

Question 439

Proximal (type II) RTA Urine ph: blood potassium level: nephrolithiasis: diagnostic test: treatment:

Answer 439

Urine ph: variable blood potassium level: low nephrolithiasis: no diagnostic test: administer bicarb treatment: thiazides

Question 440

Distal (type I) RTA Urine ph: blood potassium level: nephrolithiasis: diagnostic test: treatment:

Answer 440

Urine ph: high >5.5 blood potassium level: low nephrolithiasis:yes diagnostic test: administer acid treatment:bicarb

Question 441

Type IV RTA Urine ph: blood potassium level: nephrolithiasis: diagnostic test: treatment:

Answer 441

Urine ph: <5.5 blood potassium level: high nephrolithiasis: no diagnostic test:urine salt loss treatment: fludricortisone