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OMS III > IM Nephro > Flashcards

IM Nephro Flashcards

1
Q

Best initial test in nephrology

A

a ua and the bun and creatinine

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2
Q

UA

A

protein

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

RBC

Specific gravity and pH

nitrites (indicates gram neg bacteria)

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3
Q

UA is 2 parts

A
  1. dipstick and if thats positive

2. microscopic analysis

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4
Q

dont be worried about

A

normal lab values bc they are provided on the test

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5
Q

severe proteinuria means

A

glomerular damage

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6
Q

standing and physical activity increases urinary

A

protein excretion

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7
Q

urine dipstick for protein detects

A

only albumin

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8
Q

normal protein per 24 hours

A

<300mg

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9
Q

biopsy determines the cause of

A

proteinuria

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10
Q

Normal protein in urine

A

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

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11
Q

very large of proteins can only be excreted with

A

glomerular disease

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12
Q

Trace Proteinuria

A

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

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13
Q

transient proteinuria

A

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

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14
Q

1+ protein =

2+ protein =

A

1 gram per 24 hours

2 gram per 24 hours

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15
Q

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

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

these tests are condisdered equal in accuracy

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16
Q

to assess proteinuria

A

ua is the inital test

protein to creatinine ratio is more accurate at determing the amount

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17
Q

Protein to Creatinine ratio

A

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

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18
Q

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

A

chose pr/cr bc it is faster and easier

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19
Q

Microalbuminuria=

A

30-300 mg/24 hours

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20
Q

kidney biopsy is especially important in

A

kidney disease in a diabetic pt with no ophthalmic findings

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21
Q

Bence-Jones protein

A

in mm is not detectable on a dipstick, use electrophoresis

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22
Q

nsaid induced renal disease doe not show

A

eosinophils

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23
Q

IgA nephropath is common for

A

mild recurrent hematuria

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24
Q

Microalbuminura

A

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

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25
Q

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

A

acei or arb

they decrease the progression of proteinuria and delay the devlopment of renal insufficinecy

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26
Q

WBC on UA

A

Detect inflammation, infection, or allergic interstitial nephritis

cannot distinguish neutros from eos

neutros indicate infection

eos indicate allergic or acute interstitial nephritis

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27
Q

wright and hansel stains

A

detect eos in the urine

answer for allergic interstitial nephritis

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28
Q

Hematuria

normal UA

A

<5 RBCs per high power field

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29
Q

Hematuria

indicative of

A

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

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30
Q

what causes false positive tests for Hematuria on dipstick

A

hemoglobin or myoglobin, there will be no rbc on smear

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31
Q

abdominal xray shows

A

smoll bowel obstruction (ileus)

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32
Q

Renal ct is the most accurate test for

A

tones

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33
Q

intraneous pyelogram is always q

A

wrong for Hematuria, renal toxic and too slow

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34
Q

when dysmorphic rbcs are described on smear

A

the correct answe is glomeulonephritis

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35
Q

cytoscopy is the most accurate test of

A

the bladder

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36
Q

Hematuria

when is cytoscopy the answer

A

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

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37
Q

Casts

A

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

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38
Q

Red Cell cast

A

glomerulonephritis

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39
Q

White cell cast

A

pyelonephritis

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40
Q

Eosinophil cast

A

acute (allergic) intersititial nephritis)

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41
Q

Hyaline cast

A

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

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42
Q

Borad, waxy casts

A

chronic renal disease

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43
Q

Granula muddy brown casts

A

acute tubular necrosis, they are collection of dead tubular cells

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44
Q

Acute Kidney Injury (AKI)

definition

A

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

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45
Q

Acute Kidney Injury (AKI)

etiology

A

3 types

prerenal azotemia (decreased perfusion)
postrenal azotemia (obstruction)
intrinsic renal disease (ischemia and toxins)
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46
Q

Prerenal azotemia

overview

A

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

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47
Q

Prerenal azotemia

etiology (8)

A

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

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48
Q

Postrenal Azotemia

overview

A

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

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49
Q

Postrenal Azotemia

etiology (6)

A

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)

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50
Q

are prerenal and postrenal azotemia reversivel

A

most of them are

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51
Q

how to fix pre and postrenal azotemia

A

correct the underlying cause

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52
Q

with obstruction what cuases creatining to rise

A

must obstruct both kidneys

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53
Q

the kidney in prerenal and postrenal disease would function

A

normally if transplanted into another person

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54
Q

Intrinsic renal disease

overview

A

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

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55
Q

Intrinsic renal disease

etiology (6)

A

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

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56
Q

Prerenal AKI etiologies

from hypotension

A

sepsis
anaphylaxis
bleeding
dehydration

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57
Q

Prerenal AKI etiologies

from hypovolemia

A 
diuretics
burns
pancreatitis
dec pump function
lowealbumin
cirrhosis
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58
Q

Prerenal AKI etiologies

from other

A

renal artery stenosis

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59
Q

Intrinsic Renal AKI etiologies

from ATN

A 
toxins
   nsaids
   aminoglycoside antibiotics, amphotericin
   cisplatin, cyclosporin
prolonged ischemia
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60
Q

Intrinsic Renal AKI etiologies

from AIN

A

penicillin sulfa drugs

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61
Q

Intrinsic Renal AKI etiologies

from other

A 
rhabdomyolysis/hemoglobinuria
contrast
crystals
bence-jones proteins
poststerptococcal infection
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62
Q

PostRenal AKI etiologies

A 
BPH/Prostate cancer
ureteral stone
cervial cancer
urethral stone
neurogenic bladder
retroperitoneal fibrosis (chemo or radiation)
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63
Q

AKI presentation

A

may present with only an asymptomatic rise in BUN and creatinine

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64
Q

AKI presentation with symptomatic

A

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

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65
Q

AKI presentation with symptomatic

very severe disease

A

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

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66
Q

there is no pathognomonic physical finding of

A

AKI

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67
Q

Presentation of postrenal azotemia

A

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

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68
Q

Best initial test of AKI

A

BUN and creatinine

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

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69
Q

BUN to creatinine ratio above 20:1

A

either prerenal or postrenal

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70
Q

Bun to creatinine ratio around 10:1

A

intinsic

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71
Q

Best initial imaging in AKI

A

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

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72
Q

Prerena azotemia dx

A

BUN to creatinin above 20:1

clear hx of hypoperfusion or hypotension

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73
Q

postrenal azotemia dx

A

BUN to creatinin above 20:1

distended bladder or massive release of urine with catheter placement

bilateral or unilateral hydronephrosis on sonogram

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74
Q

AKI kidney biopsy

A

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

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75
Q

next diagnostic test for AKi of unclear etiology

A

ua
urine sodium
fractional excretion of na
urine osmolality

go with ua first

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76
Q

prerenal azotemia test results

A

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

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77
Q

urine sodium and fractional excretion of sodium

A

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

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78
Q

Urine Osmolality (1)

when intravascular volume is low

A

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

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79
Q

Urine Osmolality (2)

when more water is reabsorbed from the urine,

A

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

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80
Q

Urine Osmolality (3)

normal tubule cells reabsorb water, in ATN,

A

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

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81
Q

Urine Osmolality (4)

isosthenuria means

A

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

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82
Q

Urine Osmolality (5)

Dehydration should normally

A

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

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83
Q

healthy person fluid overload >

healthy person dehydration >

A

low urine osmolality or dilute urine

high urine osmolality or concentrated urine

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84
Q

the only significant manifestation of sickle cell trati

A

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

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85
Q

high uosm=

A

high specific gravity

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86
Q

classification of acute renal failure by lab testing

Prerenal azotemia

BUN:creatinine

Urine sodium (uNA)

fractinal excretion of sodium (feNa)

urin osmolality (Uosm)

A

BUN:creatinine >20:1

Urine Sodium (Una) <20meq/L

fractinal excretion of sodium (feNa) <1%

urin osmolality (Uosm) >500 mosm/kg

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87
Q

classification of acute renal failure by lab testing

acute tubular necrosis

BUN:creatinine

Urine Sodium (Una)

fractinal excretion of sodium (feNa)

urin osmolality (Uosm)

A

BUN:creatinine <20:1

Urine Sodium (Una) >20meq/L

fractinal excretion of sodium (feNa) >1%

urin osmolality (Uosm) <300 mosm/kg

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88
Q

Acute tubular necrosis (ATN)

Definition

A

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

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89
Q

Acute tubular necrosis (ATN)

etiology significance

A

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

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90
Q

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

A

ATN

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91
Q

radiographic contrast ATN

A

occurs rapidly (within 36 hours)

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92
Q

ATN and vanco genamicin and amphotericin

A

takes 5-10 days to kick in ATN

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93
Q

what prevents contrast induced nephrotoxicity

A

saline hydration

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94
Q

contrast induced renal failure lab values

A

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

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95
Q

creatinine rising after chemo

A

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

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96
Q

ATN from ethylene glycol

A

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

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97
Q

methanol causes inflammation of

A

the retina

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98
Q

opiates by injection are associated with

A

focal segmented glomulonephritis

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99
Q

how much renal function do you lose every year past 40

A

1%

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100
Q

summary or causes of ATN

meds

A

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

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101
Q

summary or causes of ATN

contrast

A

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

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102
Q

summary or causes of ATN

hemogloin and myoglobin

A

from rhabdomyolysis for myoglobin

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103
Q

summary or causes of ATN

hyperuricemia

A

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

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104
Q

summary or causes of ATN

ethylene glycol overdose

A

precipitation of calcium oxalate int eh renal cortex

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105
Q

summary or causes of ATN

bence jones

A

mm

directly toxic to renal tubules

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106
Q

summary or causes of ATN

nsaids

A

cause afferent arteriole constriction

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107
Q

Rhabdomyolysis

A

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

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108
Q

most specific test for rhabdomyolysis

A

urine test for myoglobin

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109
Q

rhabdomyolysis hyperkalemia

A

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

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110
Q

rhabdomyolysis hyperuricemia

A

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

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111
Q

damaged muscle also releaases

A

phosphate

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112
Q

rhabdomyolysis hypocalcemia

A

occurs from increased calcium binding to damaged muscle

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113
Q

rhabdomyolysis

treatment

A

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

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114
Q

why doesnt hemolysis cause hyperuricemia

A

rbcs have no nuclei

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115
Q

dont treat hypcalcemia in rhabdo if

A

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

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116
Q

why do an ekg after fluid replacement in rhabdo?

A

to detect life-threatening hyperkalemia

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117
Q

ATN treatment

A

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

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118
Q

ATN treatment

wrong answers

A

low-dose dopamine

diuretics

mannitol

steroids

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119
Q

ATN treatment

when is dialysis hte answer

A

initiate dialysis if:

fluid overload

encephalopathy

pericariditis

metabolic acidosis

hyperkalemia

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120
Q

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

A

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

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121
Q

ATN treatment of hypcalcemia

A

give viramin D and calcium

can cause seizures and prolonged QT intervals

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122
Q

furosemid causes

A

otoxicity

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123
Q

Hepatorenal syndrome

definition

A

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

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124
Q

Hepatorenal syndrome

look for

A

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)

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125
Q

Hepatorenal syndrome

treatment

A

midodrine

octreotide

albumin (albumin is less clear)

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126
Q

Hepatorenal syndrome

lab values

A

fit in with prerenal azotemia

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127
Q

Atheroemboli

etiology

A

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.

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128
Q

Atheroemboli

look for

A

blue/purplish skin lesions in fingers and toes

livedo reticularis

ocular lesion

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129
Q

Atheroemboli

diagnostic tests

A

eosinophilia

low complement levels

eosinophiluria

elevated ESR

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130
Q

Atheroemboli

most accurate test

A

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

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131
Q

Atheroemboli

peripheral pulses

A

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

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132
Q

Acute (allergic) interstitial nephritis

definition

A

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

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133
Q

Acute (allergic) interstitial nephritis

etiology

A

an medication can cause it but most common are:

penicillins/cephalosporins
sulfa drugs (furosemide and hctz)
phenytoin
rifampin
quinolones
allopurinol
ppi's
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134
Q

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

A

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

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135
Q

Allergenic substances affect

A

skin
kidney
red cells

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136
Q

what else causes Acute (allergic) interstitial nephritis

A

sle

sjogren

sarcoidosis

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137
Q

Acute (allergic) interstitial nephritis

presentation/what is the most likely dx

A

acute renal failure (rising BUN and creatinine) with:

fever (80%)
rash (50%)
arthralgias
eosinophilia and eosinophiluria (80%)

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138
Q

Acute (allergic) interstitial nephritis

diagnostic tests

A

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

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139
Q

Acute (allergic) interstitial nephritis

most accurate test

A

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

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140
Q

Acute (allergic) interstitial nephritis

treatment

A

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.

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141
Q

eosinophilia is not found in the urine with aki from

A

nsaids

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142
Q

urine sodium and osmolality are not uniformly up or down in

A

ain, they cannot help establish dx

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143
Q

analgesic nephropathy

presents with

A

atn from direct toxicity to the tubules

ain

membranous glomerulonephritis

vascular insufficiency

papillary necrosis

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144
Q

analgesic nephropathy

vascular insufficiency

A

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

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145
Q

tere is no specific diagnsotic test to determine nsaids cause atn

A

exclude other cuases and look for nsaids in the hx

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146
Q

papillary necrosis

definition

A

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

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147
Q

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

A

60-70%

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148
Q

papillary necrosis

look for

A

extra nsaid use with hx of:

sickle cell dz

diabetes

urinary obstruction

chronic pyelonephritis

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149
Q

papillary necrosis

presentation

A

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.

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150
Q

papillary necrosis

best initial test

A

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

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151
Q

papillary necrosis

most accurate test

A

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

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152
Q

papillary necrosis

treatment

A

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

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153
Q

papillary necrosis can give grossly visible

A

necrotic material passed in the urine, which are renal papillae

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154
Q

Pyelonephritis

onset -

sx -

urine culture -

Ct scan -

treatment -

A

onset - few days

sx - dysuria

urine culture - positive

Ct scan - diffusely swollen kidney

treatment - abs such as ampicillin/gentamicin or fqs

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155
Q

Papillary necrosis

onset -

sx -

urine culture -

Ct scan -

treatment -

A

onset - few hours

sx - necrotic material in urine

urine culture - negative

Ct scan - bumpy contour of interior where papillae were lost

treatment - none

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156
Q

summary or tubular disease

A

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

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157
Q

Tubular dz

A 
acute
toxins
none nephrotic
no biopsy usually
no steroids
never additional immunosuppressive agents
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158
Q

acuTe=

A

Tubular=Toxin

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159
Q

Glomerular Diseases

General answers

A

Glomerular Diseases are generally chronic

Glomerular Diseases are generally not caused by toxins or by hypoperfusion

all of them can cause nephrotic syndrome

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160
Q

Glomerular Diseases

most accurate test

A

biopsy is the most accurate but it not always needed

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161
Q

Glomerular Diseases

often treated with

A

steroids

addititonal immunosuppressive meds (cyclophosphamide, mycophenolate) are frequently used

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162
Q

Glomular=

A

slow=sample=steroids=immunosuppressives

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163
Q

Glomerular Diseases

diagnostic tests

A

ua with hematuria

dysmorphic red cells (deformed as they squeeze through an abnormal glomerulus)

red cell casts

urin sodium and FeNa are low

proteinuria

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164
Q

what is the main difference between glomerulonephritis and nehprotic syndrome

A

degree or amount or proteinuria

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165
Q

Glomerular Diseases

overview

A

chronic

not from toxins/drugs

all potentially nephrotic

biopsy sample

steroids often

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166
Q

Individual glomerular diseases

A

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?

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167
Q

Goodpasture syndrome

also presents with

A

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

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168
Q

Goodpasture Syndrome

Diagnostic tests

A

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

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169
Q

Goodpasture Syndrome

treatment

A

plasmapharesis and steroids

cyclophosphamid can be helpful

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170
Q

kidney biopsy in goodpasture syndrome shows

A

linear deposits

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171
Q

IgA Nephropathy (berger disease)

A

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

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172
Q

poststreptococcal glomerulonephritis followed pharyngitis by

A

1 to 2 weeks

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173
Q

Unique physical findings in IgA Nephropathy (berger disease)

A

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

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174
Q

IgA Nephropathy (berger disease)

diagnostic tests

A

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)

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175
Q

IgA Nephropathy (berger disease)

treatment

A

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

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176
Q

Postinfectious glomerulonephritis

A

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.

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177
Q

Postinfectious glomerulonephritis

presentation

A

dark (cola colored) urine

edema that isoften periorbitl

htn

oliguria

178
Q

Postinfectious glomerulonephritis

diagnostic tests

A

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

179
Q

what is low in Postinfectious glomerulonephritis

A

complement levels

180
Q

Postinfectious glomerulonephritis

treatment

A

management does not reverse Postinfectious glomerulonephritis. use supportive therapies like:

antibiotics
diuretics to control fluid overload

181
Q

how many of those with Postinfectious glomerulonephritis will progress

A

<5%

182
Q

Alport Syndrome

A

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

183
Q

Polyarteritis Nodosa

definition

A

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.

184
Q

Polyarteritis Nodosa

presentation

A

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.

185
Q

Polyarteritis Nodosa

Gastrointestinal

A

abdominal pain, bleeding, nausea, and vomiting occur

paoin can be worsened by eating bc ofmesentericvasclitit

186
Q

Polyarteritis Nodosa

neurologic

A

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

187
Q

Polyarteritis Nodosa

skin

A

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

188
Q

Polyarteritis Nodosa

cardiac disease

A

preent in about 1/3 of pts

189
Q

Polyarteritis Nodosa

diagnostic tests: blood test

A

will show:

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

190
Q

Polyarteritis Nodosa

diagnostic tests: angiogrpahy

A

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)

191
Q

Polyarteritis Nodosa

most accurate diagnostic test

A

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

192
Q

Polyarteritis Nodosa

treatmeent

A

prenisone and cyclophosphamide ar the standard of care and they lower mortality

treate hep b when it is found

193
Q

damage to small blodo vesels around nerves startves them into

A

neuorpathy

194
Q

pan is nonspecifice

A

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

195
Q

stroke or Mi in young person suggests

A

Polyarteritis Nodosa

196
Q

there is no blood test to confirm

A

Polyarteritis Nodosa

197
Q

any form of glomerular disease can produce

A

nephrotic syndrome

198
Q

Lupus Nephritis

presentation

A

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

199
Q

Lupus Nephritis

mosta ccurate test

A

biopsy

it is indispensible in determing therapy base on the stage

200
Q

Lupus Nephritis

treatment

A

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

201
Q

biopsy is ont permored to diagnose lupus but rather to

A

guide intesnity of therapy

202
Q

Amyloidosis

A

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.

203
Q

Amyloidosis

what is the primary target of the proteins

A

kidney

204
Q

Amyloidosis

omst accurate test

A

biopsy. you will se green birefringence with congo red staining

205
Q

Amyloidosis

treatment

A

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

206
Q

what gives large kidneys on sonogram

A

Amyloidosis
hiv nephropathy
polycystic kidneys

207
Q

massive proteinuria leads to:

A

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

208
Q

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

A

severity

209
Q

Nephrotic syndrome

Etiology

A

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

210
Q

Nephrotic syndrome

cancer (solidorgan)

A

membranous

211
Q

Nephrotic syndrome

children

A

minimal change disease

212
Q

Nephrotic syndrome

injection drug use and AIDS

A

focal-segmental

213
Q

NSAIDS

A

minimal change disease and membranous

214
Q

Major diff between nephritic and neprhotic syndrome

A

amount of protein

215
Q

Nephrotic syndrome

presentation

A

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

216
Q

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

A

everywhere

217
Q

Nephrotic syndrome

best initial test

A

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

218
Q

Nephrotic syndrome

albumin/creatinine

A

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

219
Q

Nephrotic syndrome

most accurate test

A

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

220
Q

Nephrotic syndrome

by definition

A

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

221
Q

ua only detects what as protein

A

albumin

222
Q

what is characteristic of Nephrotic syndrome

A

periorbital edema

223
Q

maltese corsses

A

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

224
Q

Nephrotic syndrome

lipid levels

A

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.

225
Q

anything iwth a carrier proteins can be lost in

A

urine

226
Q

Nephrotic syndrome

best initial therapy

A

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

227
Q

Nephrotic syndrome

ACEi/ ARBS

A

are used to try anc control proeinuria

228
Q

Nephrotic syndrome

edema treatment

A

is managed with salt restiction and diuretics.

229
Q

Nephrotic syndrome

hyperlipidemia treatmenet

A

statins

230
Q

End Stage Renal Disease

definition

A

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.

231
Q

End Stage Renal Disease

Etiology

A

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.

232
Q

End Stage Renal Disease

Uremia (so how ESRD presents)

A

metabolic acidosis

fluid overload

encephalopathy

hyperkalemia

pericarditis

each of these is an indiication for dialysis

233
Q

Most common causes of End Stage Renal Disease

A

diabetes and htn

234
Q

what is better peritoneal dialysis or hemodialysis

A

they are equally effective

235
Q

Manifestations of renal failure

A

anemia

hypocalcemia

osteodystrophy

bleeding

infection

pruritis

hyperphosphatemia

hypermagnesemia

accleerated atherosclerosis and hypertension

endocrinopathy

236
Q

Manifestations of renal failure

anemia

A

loss of epo leads to normocromic, normocytic anemia

237
Q

Manifestations of renal failure

hypocalcemia

A

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

238
Q

Manifestations of renal failure

osteodystropohy

A

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

239
Q

Manifestations of renal failure

bleeding

A

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

240
Q

Manifestations of renal failure

infection

A

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

241
Q

Manifestations of renal failure

pruritus

A

unclear reasonin, urea accumulating in skin causes itching

242
Q

Manifestations of renal failure

hyperphosphatemia

A

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

243
Q

Manifestations of renal failure

hypermagnesemia

A

from loss of excretory ability

244
Q

Manifestations of renal failure

accelerated atherosclerosis and hypertension

A

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

245
Q

Manifestations of renal failure

endocrinopathy

A

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

246
Q

cardiac disease kills

A

triple the amount of people that infection does in ESRD

247
Q

aneima from ESRD is the only time

A

erythropoitin is always used

248
Q

Treatment of manifestations of ESRD

Anemia

A

erythropoietin replacement and iron supplementation

249
Q

Treatment of manifestations of ESRD

hypocalcemia and osteomalacia

A

replace vitamin D and calcium

250
Q

Treatment of manifestations of ESRD

bleeding

A

ddavp incrases platelet function; use only when lbeeding

251
Q

Treatment of manifestations of ESRD

pruritus

A

dialysis and uv light

252
Q

Treatment of manifestations of ESRD

hyperphospatmia

A

oral binders: see treatment of hyperphosphatemia

253
Q

Treatment of manifestations of ESRD

hypermagnesemia

A

restriction of high-magnesium foods, laxative, and antacids

254
Q

Treatment of manifestations of ESRD

atherosclerosis

A

dialysis

255
Q

Treatment of manifestations of ESRD

endocrinopahty

A

dialysis, estrogen and testosterone replacement

256
Q

Treatment of hyperphosphatemia

A

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

257
Q

oral phosphate binders

A

calcium acetate

calcium carbonate

sevelamer

lanthanum

258
Q

when do you use sevelamer and lanthanum to bind phosphate

A

when the calcium levle is high

259
Q

why dont you use aluminum-containing phosphate binders

A

aluminum cause dementia

260
Q

Kidney Transplantation

A

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

261
Q

how long do HLA identical related donor dineys lst

A

24 years on average

262
Q

Kidney Transplantation

living rleated donor

A

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

263
Q

Kidney Transplantation

deceased donor

A

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

264
Q

Kidney Transplantation

Dialysis alone

A

variable for 1 and 3 years survival

5 year 30-40%

265
Q

Kidney Transplantation

diabetics on dialysis

A

variable for 1 and 3 year

5 years 20%

266
Q

Thrombotic Thrombocytpenic purpura and hemolytic uremic syndrome

A

diff variants of what is probablyt he same disease

267
Q

ttp is mor ecommon with

A

hiv and cancer and drugs like cyclosporine ticlopidine and clopidogrel

268
Q

HUS is more common in

A

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

269
Q

Thrombotic Thrombocytpenic purpura and hemolytic uremic syndrome are both associated with

A

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

rneal insufficiency

thromocytopenia

270
Q

ttp is associated with

A

neurological symptoms

fever

271
Q

pt and aptt in hus/ttp

A

normal

272
Q

Thrombotic Thrombocytpenic purpura indispensible finding

A

intravascular hemolysis

273
Q

Thrombotic Thrombocytpenic purpura and hemolytic uremic syndrome

treatment

A

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.

274
Q

when do you do platelet transfusion in hus and ttp

A

never

275
Q

Cystic Disease

A

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

276
Q

cystic disease

simple cyst

A

echo free

smooth,thin

sharp (demarchation)

good thorugh to back (transmision)

277
Q

cystic disease

complex cysts (potential malignancy)

A

mixed echogenicity

irregular,thick

lower density on back wall

debris in cyst

278
Q

Polycystic Kidney Disease

presents with

A 
pain 
hematuria
stones
ingestion
hypertension
279
Q

most common cause of death from PCKD

A

renal failure

280
Q

associated with PCKD

A

liver cysts (most common site outside of the kidney)

ovarian cysts

mitral valve prolapse

anuerysms

diverticulosis

281
Q

PCKD treatmeent

A

no thereapy of any kind to reverse cysts of any type

282
Q

Hypernatremia

etilogy

A

occurs when there is loss of free water. Examples are:

sweating

burns

fever

pneymonia: from insensible losses from hyperventilation

diarrhea

diuretics

Diabetes insipidus

283
Q

Diabetes insipidus

central

A

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

284
Q

DI

nephrogenic

A

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

285
Q

first clue to DI

A

high volume nocturia

286
Q

Hypernatremia

presentation

A

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.

287
Q

sodium disorders cause

A

CNS disorders

288
Q

Hypernatremia

diagnostic tests

A

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

289
Q

Best initial test for DI

A

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.

290
Q

DI response to ADH administration

A

CDI: sharp decrease in ruine olume, increase in osmolality

NDI: no change in urine volume or osmolality with ADH administartion

291
Q

DI ADH levels

A

ADH level is low in CID and markedly elevated in NDI

292
Q

What does a postiive water deprivation test mean

A

urine volume statys high depsite withholding water

293
Q

CDI overview

polyuria and nocturia:

urine osmolality and sodium:

positive water deprivation test:

repsonse to adh:

adh level:

A

polyuria and nocturia: yes

urine osmolality and sodium: low

positive water deprivation test: yes

repsonse to adh: yes

adh level: low

294
Q

NDI overview

polyuria and nocturia:

urine osmolality and sodium:

positive water deprivation test:

repsonse to adh:

adh level:

A

polyuria and nocturia: yes

urine osmolality and sodium: low

positive water deprivation test: yes

repsonse to adh: no

adh level: high

295
Q

hypernatremia treatement

fluidl osso

A

replace fluid and correct hte underlying cause

296
Q

cdi treatment

A

replace ADH (vasopressin also known as DDAVP)

297
Q

ndi treatment

A

correct k and calcium

stop lithium or demeclocycline

give hydrochlorothiazide or nsaids for those still having ndi despite these inteventrions

298
Q

hyperntremia complications of therapy

A

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

299
Q

hypernatremia diagnosti ctests

A

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

300
Q

hyponatremia

etiology

A

hyponatremia is characterized accoreding to overall volume status of the body

hypervolemia

euvolemia

hypovolemia

301
Q

hyponatremia

Hypervolemia

A

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

302
Q

Hyponatremia

hypvolemia causes

A

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

303
Q

Addison disease

A

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

304
Q

Hyponatremia

Euvolemia

A

the most common causes of hyponatrmiea with euovlemia are:

psydohyponatrmiea (hyperglycemia)

psychogenic polydipsia

hypothryodism

syndrome of inappreopriate ADH relsease (SIADH)

305
Q

Hyponatremia

Euvolemia

hyprglycemia

A

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

306
Q

Hyponatremia

Euvolemia

psychogenic polydipsia

A

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

307
Q

look for a hx of wahtto diagnose spychogenic polydipsia

A

bipolar disorder

308
Q

what is more importatnt than normal sodium

A

perfusion

309
Q

Hyponatremia

Euvolemia

Hypthyroidism

A

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

310
Q

Hyponatremia

Euvolemia

SIADH

A

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

311
Q

Hypernatremia persentation

A

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

312
Q

hypernatremia

diagnosti ctests

A

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

313
Q

urine osmolality levels with hyponatremia

A

usually below 100 with siadh it is higher

314
Q

urine sodium with hyponatremia

A

usually below 20 by will get hight than 40

315
Q

mild hyponatremia clincial manifestations

A

no symptoms just restrict fluids

316
Q

modearte hyponatremia clinical manifestations

A

minimal confusion

saline and loop diuretic

317
Q

severe hyponatrmeia clnicial manifestation

A

lethargy, seizures, and coma

use hypertonic saline, conivaptain, tolvaptan

318
Q

symptoms of yponatremia are dependent on

A

how fast it occurs

319
Q

sodium means

A

cns sx

320
Q

in siadh what makes it worse

A

saline wihtout diuretic

321
Q

treatmeent for hyponatremia

A

depnds on sx not severeity

322
Q

ADH antagonists for hyponatremia

A

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

323
Q

Chronic SIADH treatment

A

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

324
Q

Complications of SIADH treatment

A

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.

325
Q

Hyperkalemia

A

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

326
Q

Hyperkalemia

pseudohyperkalemia (falsely elevated elvels)

etiology

A

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

327
Q

Hyperkalmeia

decreased excretion

etiology

A

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
328
Q

hyperkalemia

releas of potassium from itssues

etiology

A

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

329
Q

severe hyperkalemia can do what

A

stop theheart in seconds if the level is high enough

330
Q

hyperkalemia

presentation

A

potassium disorders interfere with muscle contraction and cardiac conductionancd, look for:

weakness

paralysis when svere

ileus (paralyzes gut muscles)

cardiac rhythm disorders

331
Q

Hyperkalemia diagnosit ctests

A

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

332
Q

hyperkalemia treatment

life threatening hyperkalemia (abnormal ekg)

A

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

333
Q

hyperkalemia treatment

removing potassium from the body

A

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

334
Q

hyperkalemia

insulin and bicarb

A

lower the potassium level through the redistribution into the cells

335
Q

other methods to lower potassium

A

inhaled beta agnosists (albuterol)

loop diuretics

dialysis

336
Q

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

A

calcium chloride or bluconate

337
Q

hyperkalemia does not cause

A

seizures

338
Q

how much potassium is in the cells

A

95%

339
Q

when do use calcium with hyperkalemia

A

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

340
Q

insulin does not remove what fromt he body

A

potassium

341
Q

sodium=

A

cns sx

342
Q

hyperkalemia=

A

muscular and cardiac sx

343
Q

hyperkalemia with no ekg changes treatment

A

kayexalate and loop diuretics

344
Q

hyperkalmiea iwth ekg changes

A

calcium cholirde or gluconate

insuling and glucose, inhaled beta agnoist
g
ive bicarb if acidosis is the cause

consider hemodialysis

345
Q

Hypokalemia

decreased intake etiology

A

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

346
Q

Hypokalemia

shift into cells etiology

A

alkalosis (hydrogen ions come out of the cell in exchange for potassium entering)

increased insulin

beta adrenergic stimulation ( acccleatares sodium/k atpase)

347
Q

Hypokalemia

renal loss etiology

A

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

348
Q

Hypokalemia

etiology

gi loss

A

vomiting

diarrhea

laxative abuse

349
Q

Hypkalemia

presentation

A

hypokalemia leads to problems with muscular contraction and cardiac conduction. potassium is essential for proper neuromuxcular contraction

presents with:

weakness

paralysis

loss of reflexes

350
Q

Hypokalemia

ekg finding

A

u waves ar ethe mos tcharacteristic finding of hypkalmiea

other findings are ventricular extopy (PVCs), flattened T waves, and ST depression

351
Q

Hypokalemia

treatment

A

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

352
Q

muscular abnomralities may be so severe as to cause what hyperkalmia

A

rhabdomyolysis

353
Q

iv potassium replacement must be very

A

slow

354
Q

what do you protect first in ptoassium disorders

A

heart

355
Q

Renal tubular acidosis

definition

A

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

356
Q

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

A

rta and diarrhea

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

357
Q

what causes anion gap acidosis

A

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

358
Q

Distal RTA

A

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

359
Q

Distal RTA

diagnostic tests

A

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.

360
Q

Distal RTA

treatment

A

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

361
Q

Proximal RTA

A

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)

362
Q

no acid into the tubule

A

makes the urine basic

363
Q

Diatal rta calcifices

A

the kidney parenchyma (nephrocalcinosis)

364
Q

RTA does not mean

A

the tubule is always acidic

365
Q

both proxima and distal rta are

A

hypokalemic, k is lost in the urine

366
Q

Proximal RTA

diagnostic tests

A

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

367
Q

Proximal RTA

treatment

A

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

368
Q

Hypertensive Crisis

A

defines as high blood pressure in assocaiton with

confusion

blurry vision

dyspnea

chest pain

369
Q

Hypertensive Crisis

therapy

A

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

370
Q

Htn

definition

A

Systolic pressure above 140

distolic pressure above 90

371
Q

Htn

diagnosis

A

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

372
Q

htn is:

A

the most common disease in the us

the most common risk factore for the most common cause of death: mi

373
Q

HTN

etiology

A

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

374
Q

JNC 8 says:

A

in diabetes goal is 140/90

thiazided ar enot better than ccb ace or arb

bp 150/90 over age 60

375
Q

HTN

presnetation

A

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
376
Q

Presentation of secondary htn

A

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

377
Q

HTN

diagnostic tests

A

repeated in office measuremnt or home ambulatory measuremnts carry equal significancen also test with

ekg

urinalysis

glucose measurement to exclude concomitant diabetes

cholesterol screening

378
Q

HTN

best initial therapy

A

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

379
Q

summary of jnc 8 managemetn of hypertension

A

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

380
Q

HTN drug therapy

best initial therapy

A

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

381
Q

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

A

acei
arb
bb
ccb

382
Q

meds not considered first line or second line for htn

A

central actin alpha agonsits (alpha mehtyldopa, clonidine)

periphera acting alpha antagonists (prazosin, terazonin, doxazosin)

direct acting vasodiltors (hydralazine, minoxidil

383
Q

what percentage of htn pts will be ctonrolled by 2 meds

A

90

384
Q

pregnancy safe htn drugs

A

bb use first

ccb

hydralzaine

alpha methyldopa

385
Q

Treatment for htn with cad

A

bb ace arb

386
Q

Treatment for htn with diabetes

A

ace arb (goal 140/90)

387
Q

Treatment for htn with bph

A

alpha blockers

388
Q

Treatment for htn with depression and asthma

A

just avoid bb

389
Q

Treatment for htn with hyperthyroidism

A

bb first

390
Q

Treatment for htn with osteoporosis

A

thiazides

391
Q

Nephrolithiasis

A

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

392
Q

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

A

ketorlolac

393
Q

most accurate test for Nephrolithiasis

A

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

394
Q

what is alway swrong for Nephrolithiasis

A

ivp

395
Q

what disease causes Nephrolithiasis

A

crohn bc it causes increased reabsorption of calcium oxalate

396
Q

what stones are not seen on xray

A

uric acid

397
Q

Nephrolithiasis

treatment

best inital therapy for acute renal colic

A

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

398
Q

Nephrolithiasis

etiology of the stone is determined with

A

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

399
Q

cystine sotnes are managed with

A

surgical removal, alkalinixin urine

400
Q

Fat malabsorption increases

A

stone formation

401
Q

sontes 5-7 mm get what for treatment

A

nifedipine and tamsulosin to help them pass

402
Q

uti givves what kind of stones

A

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

403
Q

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

A

lithotripsy

404
Q

management of stones that are greater than 2-3 cm

A

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

405
Q

Lont term management with stones

A

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

406
Q

Metabolic acidosis and stone formation

A

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

407
Q

Stress incontinence

symptoms

A

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

408
Q

Stress incontinence

test

A

havve pt stand and cough; observe for leakage

409
Q

Stress incontinence

treatment

A

kegel exercises

local estrogen cream

surgial tightenin of urethra

410
Q

Urge incontinence

symptoms

A

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

411
Q

Urge incontinence

test

A

pressure measuremnt in half full bladder; manometry

412
Q

Urge incontinence

treatment

A

bladder training exercises

local anticholinergic therapy
oxybutynin
tolteradin

solifenacin

dariferancin

surgical tightneing of the urethra

413
Q

Metabolic Alkalosis

definition

A

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

414
Q

Metabolic Alkalosis

etiology

A

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

415
Q

Metabolic Alkalosis

abg

A

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

416
Q

Resp acidosi and alkalosis

A

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

417
Q

Respiratory alkalosis

overview

A

decreased pco2

increased minute ventilation

metaboli acidosis as compensation

anemaia
anciety
pain
fever
interstitial lung diease
pe
418
Q

respiratory acidosis

overview

A

increased pco2

decreased minute ventilation

metabolic alkalosis as compensation

copd/emphysema
drowning
opiate overdose
alpha 1antitrypsin deficiency
kyphoscoliosis
sleap apnea/morbid  obesity
419
Q

Metabolic acidosis

anion gaps

A

noraml 6-12

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

420
Q

Metabolic acidosis

causes of increased anion gap

A

lactate

ketoacids

oxalic acid

formic acid

uremia

salicylates

421
Q

Metabolic acidosis

lactate

A

hyptension or hypperfusion

blood lactate level

correct hypperfusion

422
Q

metabolic drangements kill patients with

A

cardiac arrhythmia. they also alter ptoassium elvels

423
Q

minute ventialtion is more accurate than

A

rr

424
Q

hyperventilation may occure with

A

a tiny tidal vomume. this does not increase mnute venilation

425
Q

Metabolic acidosis

ketoacids

A

dka and starvation

acetone level

insulin and lfuids

426
Q

Metabolic acidosis

oxalic acid

A

ethylene glycole overdose

crystals on UA

fomepizole and diaylsys

427
Q

Metabolic acidosis

formic acid

A

methanol overdose

inflamed retina

fomeizple and dialysis

428
Q

Metabolic acidosisuremia

A

renal failure

bun and creatinine

dialysis

429
Q

Metabolic acidosis

salicylates

A

aspirin overdose

aspirin level

alkalinize urine

430
Q

Metabolic acidosis

abg

A

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

431
Q

resp alkaloiss from hypeventialtion compensates for

A

all fomrs of metabolic acidosis

432
Q

Urin anion gap

definition

A

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

433
Q

Urin anion gap

process

A

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

434
Q

Urin anion gap

in diarrhea

A

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

435
Q

rta has a positive

A

uag

436
Q

diarrhea has a negative

A

uag

437
Q

Hyporeninemia, hypaldosteronism (type IV RTA)

A

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”

438
Q

what streoid has the highest meneralocorticoid or aldosteronlike effect

A

fludrocortisone

439
Q

Proximal (type II) RTA

Urine ph:

blood potassium level:

nephrolithiasis:

diagnostic test:

treatment:

A

Urine ph: variable

blood potassium level: low

nephrolithiasis: no

diagnostic test: administer bicarb

treatment: thiazides

440
Q

Distal (type I) RTA

Urine ph:

blood potassium level:

nephrolithiasis:

diagnostic test:

treatment:

A

Urine ph: high >5.5

blood potassium level: low

nephrolithiasis:yes

diagnostic test: administer acid

treatment:bicarb

441
Q

Type IV RTA

Urine ph:

blood potassium level:

nephrolithiasis:

diagnostic test:

treatment:

A

Urine ph: <5.5

blood potassium level: high

nephrolithiasis: no

diagnostic test:urine salt loss

treatment: fludricortisone

OMS III (21 decks)

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