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internal medicine ishani > nephrology > Flashcards

nephrology Flashcards

1
Q

types of acute kidney injury

A

prerenal AKI
Intrinsic AKI
postrena AKI

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2
Q

falsely elevated BUN

A

drugs steroids
git / soft tissue bleeding
protein intake

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3
Q

low bun

A

malnutrition
liver ds
siadh

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4
Q

how is gfr measuresd

A

creatinine clearence sighlt overestimatesbecause it is secreated
inulin

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5
Q

if a person is anuric the rate of rise of creatinine will be

A

0.5-1 / day and also depends on muscle mass

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6
Q

causes of prerenal azotemia

A 
hypovolemia 
hypotension 
drugs NSAIDS, ACE inhibitor 
CHF 
renal artery obstruction 
cirrhosis
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7
Q

parameters to find out cause of azotemia

A

FeNa

 BUN /Cr

Uosm

 Urine NA

 urinanalysis
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8
Q

change in parameters in prerenal azotemia

A

urinalysis Hyaline casts
Bun/Cr Ratio ⬆️
Fena ⬇️
urine osmolality >500mosmol
urine Sodium ⬇️

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9
Q

change in parameters in intrinsic kidney injury

A

urinalysis abnormal
Bun/Cr Ratio ⬇️
Fe Na ⬆️
urine osmolality ⬇️
urine Sodium ⬆️

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10
Q

diagnosis of hepatorenal syndrome

A

exclide renal failure first

no improvement after 1.5l of colloid
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11
Q

role of PG in kidney

A

dilates the renal afferent inhibits by NSAIDS

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12
Q

how do ACE inhibitor prevent renal failure

A

short term inc in bun/creatinine by dec in GFR

long term dec intraglomerular pressure

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13
Q

can there be renal failure with obstruction to 1 kidney

A

No

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14
Q

retroperitoneal fibrosis caused by drugs

A

bleomycin

methylsergide

methotrexate

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15
Q

MCC of neurogenic bladder

A

diabetes and multiple sclerosis

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16
Q

most common complication of oliguric phase

A

hypokalemia

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17
Q

ATN causes

A

ischemic

 dec in blood flow to the kidney 
shock, sepsis,DIC

#toxic
  Causes include
antibiotics(aminoglycosides,vancomycin),
radio contrast agents
,NSAIDs(especially in the setting of CHF),
poisons,
myoglobinuria(from muscle damage,rhabdomyolysis,strenuous exercise), hemoglobinuria(from hemolysis),
chemotherapeutic drugs(cisplatin),and
kappa and gamma lightchains produced in multiplemyeloma.
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18
Q

phases of ATN

A

oliguric phase

  •Azotemia and uremia—average length10 to14days 
  •Urine output # •Diuretic phase
    •Begins when urine output is>500mL/day 
   •High urine output due to the following:
            fluid overload(excretion of retained salt,water,other           solutes that were retained during oliguric phase);
           osmotic diuresis due to retained solutes during oliguric phase;
            tubular cell damage(delayed recovery of epithelial cell function relative to GFR)
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19
Q

treatment of ATN

A

general measures
no specific RX

  1.hydration to prerenal component no effects of diuretics , mannitol, dopamine 
   2.  intrinsic cause 
              supportive treatment 
 3.   postrenal 
            stone removal catherisation
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20
Q

wht is azotemia and uremia

A

azotemia refers to the elevation of BUN.

# •uremia  refers to the signs and symptoms associated with accumulation of nitrogenous wastes due to impaired renal function.
 It is difficult to predict when uremic symptoms will appear,but i trarely occurs unless theBUN is >60mg/dl.
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21
Q

how to differentiate between intrarenal causes of AKI

A

Acute tubular necrosis

Intrarenal

      “Muddybrown”casts,renal tubularcells/ casts,granular casts
    preotein trace
     blood -ve 
       Dysmorphic RBCs,RBCs with casts,WBCs with casts,fatty casts 
     protein 4+
      blood 3+
             WBCs,WBCs with casts,eosinophils 
                   protein  1+
                    blood    2+
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22
Q

causes of steven johnson syndrome

A

penicillin
sulfadrug
rifampin
quinolones

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23
Q

causes of allergic interstial nephritis

A

drugs ( most commonl
infection
autoimmune ds

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24
Q

characteristic finding of allergic interstitial nephritis

A

drug rash
fever
eosinophiluria
eosinophilia

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25
Q

best initial test for allergic interstitial nephritis

A

urinanalysis

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26
Q

best initial test to for rhabdomyolysis

A

urinary dip stick
+for blood
- for cells

other test are
CPK levels

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27
Q

why does chrons ds causes hyperoxaluria

A

because chrons ds decreases fat absorbtion
⬇️
fat binds with calcium which was to bind with oxalte
⬇️
this leads to increased absorbption of oxalate
⬇️
hyperoxaluria

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28
Q

pappilary necrosis diagnostic test

A

CT scan ill show “bumpy” contours in the renal pelvis where the papillae have sloughed off.

There is no specific therapy for papillary necrosis.

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29
Q

pt of sickle ds comes with sudden flank pain and history of NSAIDS use wht is diagnostis

A

pappillary necrosis

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30
Q

wht can u do prevent contrast induced nephropathy

A

hydration
bicarbonate
acetylcystine

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31
Q

cause of red cell casts

A

glomerulonephritis

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32
Q

granular casts

A

ATN

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33
Q

white cell casts

A

pyleonephritis

interstitial nephritis

34
Q

waxy cast in urine

A

chronic kidney failure

35
Q

gross painless hematuria is a sign of

A

bladder or kidney cancer untill proven otherwise

36
Q

defination of hematuria

A

> 3erythrocytes / HPF

37
Q

most sensitive test for microalbuminuria

A

radioimmunoassay

38
Q

2 normal anion gap metabolic acidosis

A

RTA

diarrhoea

39
Q

man comes with envelope shaped crystals in urine wht could be the most possible cause

A

ethylene glycol antifreeze

40
Q

best initial test for ethylene glycol antifreeze suicide attempt

A

urinanalysis showing envelope shaped crystals in urine of oxalate

41
Q

cause of elevated metabolic acidosis

A

LA MUD PIE (Mnemonic)
Lactate (sepsis, ischemia, etc.)

Aspirin

Methanol

Uremia

Diabetic ketoacidosis (DKA)—Beta hydroxybutyric acid (BHB) and acetoacetate, which are formed from fatty acids, are an alternate fuel source because the cells cannot absorb glucose because there is a deficiency of insulin

Paraldehyde, Propylene glycol
Isopropyl alcohol,
Ethylene glycol (antifreeze, low calcium)

42
Q

analgesic nephropathy

A 
This patient's abnormal urinalysis 
        painless hematuria.
         sterile pyuria
        white blood cell casts,
        trace proteinuria

suggests a non-glomerular disorder affecting the
tubulointerstitium or lining of the urinary tract. Given his chronic low back pain treated
with over-the-counter analgesics, he likely has analgesic nephropathy.

Chronic analgesic use with 1 or more analgesics (eg, nonsteroidal anti-inflammatory drug
such as aspirin) can cause chronic kidney disease due to chronic tubulointerstitial
nephritis.
Patients are typically asymptomatic with an elevated creatinine found
incidentally. Patients can also develop painless and prominent hematuria due to
papillary ischemia from analgesic-induced vasoconstriction of medullary blood vessels
(vasa recta). Significant papillary necrosis and sloughing may cause renal colic.

43
Q

most common cause of drug induced chronic renal failure

A

analgesic nephropathy

44
Q

most common pathologies seen with analgesic nephropathy

A

tubulointerstitial nephritis

pappikary necrosis

45
Q

urinalysis finding of intrinsic renal failure

A

Her serum BUN and Cr ratio is less than 20:1.

Other
findings that support this diagnosis are:
1. Urine osmolality of 300-350 mOsm/L (but never <300)
2. Urine Na of >20 mEq/L
3. FE-Na ->2%

46
Q

urinalysis finding of prerenal azotemia

A

bun / cr <20:1
urinary Na <1%
urine Osm >500

47
Q

features of crystal-induced acute kidney injury

A

Clinical features of crystal-induced acute kidney injury

Common causes 
• Acyclovir ♧♧♧♧
• Sulfonamides  
• Methotrexate 
• Ethylene glycol 
• Protease inhibitors 
• 
Clinical features
Usually asymptomatic 
• Elevated creatinine within 1-7 days of starting drug 
• Urinalysis can show hematuria, pyuria &amp; crystals presentation 
• t Risk with underlying volume depletion, chronic 
kidney disease 
• 
Treatment

Discontinue drug, volume repletion
• Concurrent volume repletion while giving drug can
prevent kidney injury

The patient’s presentation is most likely consistent with crystal-induced acute k

48
Q

alport syndrome♧♧♧♧♧♧

A

familial disorder which usually presents in childhood as ▪recurrent gross hematuria and
▪proteinuria
.▪ Sensorineural deafness usually occurs.
▪Electron microscopy findings
include alternating areas of thinned and thickened capillary loops with splitting of the
glomerular basement membrane

49
Q

Most common cause of nephrotic syndrome in children;

A

minimal change ds

50
Q

lipoid nephrosis

A

minimal change ds

51
Q

finding of minimal change ds
biopsy
EM
immunofloresence

A

biopsy Structurally normal glomeruli; positive fat stains in glomerulus and tubules
Negative IF
EM shows fusion of podocytes and no electron-dense deposits

52
Q

Most common cause of nephrotic syndrome in adults

A

focal segmental glomerulosclerosis

53
Q

finding of FOCAL SEGMENTAL GLOMERULOSCLEROSIS

A

Negative IF;
EM shows focal damage of VECs
biopsy ¿

54
Q

Diffuse membranous glomerulopathy biopsy ,EM,IF finding

A

Diffuse thickening of membranes;
silver stains show “spike and dome” pattern beneath VECs (subepithelial deposits)

Subepithelial ICs with granular IF

55
Q

type 1 MPGN

A

Subendothelial ICs with granular IF
; ICs activate the classical and alternative complement pathways;
EM shows tram tracks caused by splitting of the GBM by an ingrowth of mesangium

56
Q

type 2 MPGN finding

A

Diffuse intramembranous deposits (“dense deposit disease”); EM shows tram tracks

57
Q

dense deposit ds

A

type 2 MPGN

58
Q

causes of minal change ds

A

T-cell cytokines cause the GBM to lose its negative charge; selective proteinuria (albumin not globulins)
Secondary causes: Hodgkin lymphoma

Often preceded by an upper respiratory infection or routine immunization
Usually normotensive (90% of cases), unlike other types of nephrotic syndrom
59
Q

cause of focal segmental glomerulosclerosis

A

primary or secondary disease
; secondary causes—
HIV (most common glomerular disease; mainly in young black males) and
intravenous heroin abuse

60
Q

cause of diffuse membranous glomerulopathy

A

Primary and secondary types;
secondary causes:
Drugs: e.g., captopril, gold therapy
Infections: HBV, Plasmodium malariae, syphilis
Malignancy: carcinomas, Hodgkin lymphoma
Autoimmune disease: SLE (nephrotic presentation)

61
Q

causes of nephrotic syndrome

A

Common causes of nephrotic syndrome in adults are
, ,
minimal change disease,
focal segmental glomerulosclerosis
membranous glomerulopathy
amyloidosis.
membranoproliferative glomerulonephritis type1 and type2

62
Q

pathgnonomic finding of diabetic nephropathy

A

Hyalinosis that affects both afferent and efferent arterioles i

63
Q

most common cause of AA and AL amyloidosis

A

Multiple myeloma is the most common cause of AL amyloidosis, and

rheumatoid arthritis is the most common cause of AA amyloidosis.

64
Q

salicylate toxicity causes which acid base disturbance

A

acute salicylate toxicity leads to respiratory alkalosis by
stimulating the respiratory center in the medulla and causing tachypnea (with resultant
low PaC02 as the C02 is blown off)

. It then causes an* anion gap metabolic acidosis *by
uncoupling of oxidative phosphorylation in the mitochondria leading to anaerobic
metabolism (with resultant low HCO; from acid buildup).

The arterial blood gas (ABG) in salicylate toxicity is most likely to show a
▪ low PaC02 (due
to primary respiratory alkalosis and respiratory compensation for metabolic acidosis) and
▪low HCO; (due to primary metabolic acidosis and metabolic compensation for respiratory
alkalosis).
▪In addition, the arterial pH is usually in the normal range as the 2 primary acid-
base disturbances shift the pH in opposite directions. As a result, this patient’s ABG is
most likely to show a near-normal pH with mixed respiratory alkalosis and metabolic
acidosis▪

. The low HC03- in this answer choice suggests a metabolic acidosis. Based on
the corresponding formula for respiratory compensation (Winter’s formula), the
expected PaC02 = [1 .5 • HCO;) + 8 ± 2 = [1 .5 • 12] + 8 ± 2 = 26 ± 2 mm Hg. Because
the observed PaC02 (20 mm Hg) is lower than the expected value (26 ± 2 mm Hg), there
is a coexisting primary respiratory alkalosis. If the patient had a process causing only
metabolic acidosis (and appropriate respiratory compensation), a low HCO;, low PaC02 ,
and acidic pH (pH <7.35) would have been expected as the compensatory processes do
not perfectly correct the pH to normal.

65
Q

appropriate compensation for metabolic acidosis

A

PaC02 = 1.5 (serum HCo3·) + 8 _+ 2

66
Q

appropriate compensation for metabolic alkalosis

A

⬆️PaC02 by 0.7 mm Hg for every 1 mEq/L rise

in serum HC03.

67
Q

appropriate compensation for acute respiratory acidosis

A

⬆️ Serum HCo3· by 1 mEq/L for every 10 mm Hg

rise in PaC02

68
Q

appropriate compensation for acute respiratory alkalosis

A

⬇️ Serum HC03·by 2 mEq/L for every 10 mm Hg

decrease in PaC02

69
Q

wht is asymptomatic bacteriuria

A

Asymptomatic bacteriuria

Definition
>:100,000 CFU/mL bacteria

Risk factors
• Pre-gestational diabetes mellitus  
• History of urinary tract infection 
• Multiparity 
• Escherichia coli (most common) 
Common pathogens 
        • Klebsiella 
       • Enterobacter 
       • Group B Streptococcus 
         • Cephalexin

First-line treatment
• Amoxicillin-clavulanate
• Nitrofurantoin
• Fosfomycin

70
Q

most common type of genitourinary cancer

A

transistional bladder carcinoma

71
Q

kehr sign

A

, irritation of the peritoneal lining of the right or left hemidiaphragm may cause
referred pain to the ipsilateral shoulder (Kehr sign) as sensory innervation to the
shoulder originates from the C3 tQ C5 spinal roots; these roots are also the origin of the
phrenic nerve innervating the diaphragm.

72
Q

extraperitoneal bladder rupture presentation

A

extraperitoneal bladder injury (EPBI), which may consist of
either contusion or rupture of the neck, anterior wall, or anterolateral wall of the
bladder. In
the case of rupture, extravasation of urine into adjacent tissues causes
localized pain in the lower abdomen and pelvis. Pelvic fracture is almost always
present in EPBI, and sometimes a bony fragment can directly puncture and rupture the
bladder.
Gross hematuria is also usually present, and urinary retention (evidenced
by suprapubic fullness in this patient) may occur, especially in the case of injury to the
bladder neck.

73
Q

intraperitoneal bladder rupture presentation

A

the setting of blunt abdominal trauma, spillage of blood, bowel contents, bile,
pancreatic secretions, or urine into the peritoneal cavity can cause acute chemical
peritonitis, which is evidenced by diffuse abdominal pain and guarding. The superior
and lateral surfaces of the bladder compose the dome of the bladder and are bordered
by the peritoneal cavity. Therefore, rupture of the dome of the bladder causes urine
to spill into the peritoneum, leading to peritonitis. Bladder rupture after blunt trauma is
due to a sudden increase in intravesical pressure and most likely occurs following a blow
to the lower abdomen when the bladder is full and distended.
In addition, irritation of the peritoneal lining of the right or left hemidiaphragm may cause
referred pain to the ipsilateral shoulder (Kehr sign) as sensory innervation to the
shoulder originates from the C3 tQ C5 spinal roots; these roots are also the origin of the
phrenic nerve innervating the diaphragm.

74
Q

most common site of urethral injury

A

The bulbomembranous junction ie junction of the anterior and posterior urethra is the most common site of urethral injury.

75
Q

cause of bleeding in chronic renal failure

A

platelet dysfunction due to uremic coagulopathy
platelets donot degranulate
uremic toxins cause platelet dysfunction but count is normal

76
Q

most common cause of chronic renal

insufficiency/failure in children.

A

Posterior urethral valves

77
Q

diagnostic modalities of vesicourethral reflux

A

The definitive diagnosis of VUR is made by contrast voiding cystourethrogram.
Renal ultrasound is performed to screen for hydronephrosis.

Recurrent and/or chronic
pyelonephritis can lead to blunting of calices (calyceal clubbing) and focal parenchymal
scarring.

Renal scintigraphy with dimercaptosuccinic acid is the preferred modality for
long-term evaluation for renal scarring. Renal function should be followed by serial
creatinine. Patients should be monitored closely for complications of chronic renal
insufficiency, such as hypertension and anemia.

78
Q

acid base disturbance due to AKI

A

AKI can also cause an anion gap acidosis due to
retention of unmeasured uremic toxins which can also cause encephalopathy. However
the normal anion gap suggests that the elevated blood ure.a nitrogen can be due to other cause like
Gl bleed (ie, metabolism of blood proteins to urea) and there is not likely to be
an excessive concentration of other unmeasured uremic toxins.
and if thr pt has mental status
changes tht are therefore less likely to be due directly to her AKI.

79
Q

most common cause of death in dialysis pt

A

CARDIOVASCULAR disease

80
Q

most common cause of death in renal transplant pt

A

CARDIOVASCULAR disease

internal medicine ishani (9 decks)

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