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Clin Med GU > GU Exam > Flashcards

GU Exam Flashcards

1
Q

How do you estimate GFR?

A

Creatinine clearance

GFR is inversely related to serum creatinine

GFR = (Urine Cr x V)/ PCr

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2
Q

What is a urogram?

A

CT Scan used for urinary obstructions, polycystic disease, and masses

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3
Q

What does foamy urine indicate?

A

foamy or frothy indicates proteinuria

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4
Q

What is the definition of microscopic hematuria?

A

> 3RBCs/hpf in 2/3 specimens

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5
Q

What is the next step for someone with microscopic hematuria?

A

blood culture

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6
Q

All hematuria (gross and microscopic) get urologic evaluation except….

A

history of vigorous exercise

leukocyte esterase or nitrate (most likely due to an infection so just go ahead and treat)

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7
Q

What is the most common reason to see hematuria in pts under the age of 20?

A

glomerulonephritis, UTI, congenital

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8
Q

What is the most common reason to see hematuria in pts over the age of 60?

A

BPH (if male)
UTI
Cancer

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9
Q

What is the most common reason to see hematuria in pts between 20-60?

A

UTI
Stone
Cancer

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10
Q

Characteristics of glomerular urine analysis

A

acanthocytes
RBC casts
Cola colored urine
NO blood clots

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11
Q

Characteristics of non-glomerular urine analysis

A

WBC casts
Brown muddy casts
blood clots
pink or red colored urine

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12
Q

Brown muddy casts

A

non-glomerular

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13
Q

RBC cast

A

glomerular

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14
Q

Blood clots found in urine

A

non-glomerular

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15
Q

What is the most common nosocomial infection?

A

UTIs

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16
Q

What pathogens are responsible for hospital acquired pyelonephritis?

A

klebsiella

pseudomonas

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17
Q

What is the most common pathogen in UTIs of younger females?

A

S. saprophyticus

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18
Q

What is the most common pathogen in UTIs of older men?

A

S. epidermidis

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19
Q

What is the Tamm-Horfall protein?

A

host defense

it binds to the E.coli preventing it from attaching to the epithelium

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20
Q

Pyelonephritis clinical presentation?

A 
flank pain 
fever 
CVAT 
dysuria 
urgency 
frequency 
\+/- N/V, chills, diarrhea, tachycardia
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21
Q

Cystitis clinical presentation?

A 
suprapubic pain 
dysuria 
urgency 
frequency 
usually afebrile 
NO vaginal discharge
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22
Q

What is pyuria?

A

6-10 WBC/hpf

will see more pyruria with pyelonephritis than cystitis

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23
Q

Why does a negative dipstick test not rule out cystitis?

A

the dipstick is negative in 20% of patients with cystitis

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24
Q

If a pt has a UTI secondary to an obstruction, what might you see on US?

A

hydronephrosis

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25
Q

Children under 2 with a UTI present with what type of sxs?

A

fever, vomiting, failure to thrive

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26
Q

What makes something a complicated UTI?

A

functional, anatomical, or metabolic abnormalities of the urinary tract

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27
Q

WBC casts are dx for…?

A

Upper UTI

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28
Q

How do you treat pyelonephritis?

A

Start strong with ABX until cultures come back
10-14 days
Cipo (x7d)
Bactrim

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29
Q

For which UTI are you going to get a urine culture?

A

Pyelonephritis
Complicated UTIs

you dont have to get a culture for women with sxs and no vaginal discharge –> just treat

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30
Q

What are the predisposing factors to recurrent UTIs?

A

Stones
VUR
obstruction
incomplete bladder emptying

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31
Q

How do you treat acute cystitis?

A

ABX 3-5 days
Nitrofurantoin x 5 days
Bactrim x 3 days

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32
Q

When do you treat asymptomatic bacteruria?

A

pregnancy
before urologic procedure
young children with high incidence of VUR

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33
Q

What is the treatment for complicated cystitis?

A

Cipro (any FQ)
Aminoglycocides
for 7-10 days (which is longer than the 3-5 days for uncomplicated)

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34
Q

Which UTI do you see WBC casts with?

A

pyelonephritis

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35
Q

CUTE DIMPLES

A

DDx for high anion gap metabolic acidosis

Citrate
Uremia
Toluene
Ethanol

DKA 
Iron 
Methanol 
Paraldehyde 
Lactate 
Ethylene Glycol 
Salicylate
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36
Q

What are the hallmark findings for nephrotic syndrome?

A

Proteinuria
Hypoalbuminemia
Edema
Hyperlipidemia –> Lipiduria

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37
Q

What is the most common cause of nephrotic syndrome?

A

Diabetic nephropahty

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38
Q

Is there a change in GFR with nephrotic syndrome?

A

NO

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39
Q

Is there a change in GFR with nephritic syndrome?

A

yes

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40
Q

When do you see oval fat bodies?

A

nephrotic syndrome

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41
Q

What is the treatment for Minimal Change GN?

A

prednisone for 8 weeks with gradual tapering over 1 - 2 months

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42
Q

What do you do if a pt does not respond to treatment for minimal change GN?

A

relapse for the first time just treat the same
if they continue to relapse switch to Cyclophosphamide
if it is STILL not responding –> rituximab

for kids we assume their nephrotic sxs are minimal change so we start them on steroids, unless they dont respond, then we get biopsy

for adults we get biopsy

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43
Q

What is the hallmark findings for nephritic syndrome?

A

Remember that nephritic syndrome is also called acute GN and is due to immune and inflammation crap

HTN 
Hematruia 
RBC casts 
Edema (periorbital + dependent) 
Azotemia
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44
Q

How do you dx most nephrotic and nephritic syndromes?

A

renal biopsy

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45
Q

What is the gold standard for dx nephrotic syndrome?

A

24 hour urine protein collection

>3.5 g/day

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46
Q

Which drugs might help with proteinuria reduction?

A

ACEI or ARB

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47
Q

Which, nephrotic or nephritic, are you more likely to see uremia?

A

Nephritic
this is because nephritic occurs more globally in the kidneys (glomerulus)
and the thickening due to inflammation that decreases GFR, thus an increase in BUN and creatinine –> uremia

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48
Q

Minimal change GN is commonly associated with ….?

A

Hodgkin’s Lymphoma

MC in kids

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49
Q

What is the most common cause of ESRD?

A

DM

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50
Q

FSGS

A

focal segmental GS (FSGS) –> scarring of some parts of some nephrons

nephrotic
MC in AA
asymptomatic

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51
Q

What signs and sxs will you see with someone who has FSGS?

A

hypoalbuminemia
proteinuria
lipiduria

most likely will be asymptomatic

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52
Q

FSGS is associated with…?

A

HIV
Morbid Obestity
Sickle cell disease

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53
Q

What is different about minimal change GN from FSGS in regards to prognosis?

A

Minimal change, once treated, is likely to regress

FSGS can progress to ESRD

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54
Q

What causes membranous nephropathy?

A

nephrotic syndrome

immune complexes get deposited into GBM making it thick and inflamed –> inflammatory complex leads to damage

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55
Q

What will you see on electron microscopy or membranous nephropathy?

A

spike and dome deposits on the subepithelium

effacement of podocytes

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56
Q

What is the prognosis of membranous nephropathy?

A

33% progress to ESRD
33% remain –> years of proteinuria
33% regress

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57
Q

Most common cause of nephrotic syndrome in adults?

A

diabetic nephropathy

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58
Q

What is the most common cause of ESRD?

A

diabetic nephropathy

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59
Q

When might you see “tram track”?

A

splitting of the basement membrane with membranoproliferative GN

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60
Q

What are the clinical presentations and findings of poststreptococcal GN?

A

impetigo
sore throat
edema

hematuria 
proteinuria 
HTN 
Oliguria 
low serum C3

immune “humps”

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61
Q

What is the prognosis of poststreptococcal GN?

A

some progress to ESRD

25% get RPGN

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62
Q

What titer can you get for poststretococcal GN?

A

ASO titer

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63
Q

What titer can you get for Lupus Nephritis?

A

Anti-DNA titer

ANA

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64
Q

What is the Anti-GBM titer used for?

A

goodpasture

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65
Q

What are the clinical presentations and findings for lupus?

A

Malar rash

Low C3
hematuria
proteinuria

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66
Q

What is the most common GN worldwide?

A

IgA

MC in children

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67
Q

What is IgA nephropathy?

A

mutated IgA so that body doesn’t recognize it as self and send IgG to attack

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68
Q

What is goodpasture’s syndrome?

A

autoimmune disease that targets lungs and GBM

type 2 hypersenitivity –> activation of complement pathways

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69
Q

What clinical presentation and findings would you see with goodpastures?

A 
flu like sxs 
myalgia 
hemoptysis 
dyspnea 
rales, bronchi 
CXR: infiltrates

hematuria
proteinuria

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70
Q

How do you dx goodpasture?

A

renal biopsy preferred

anti-GBM titer

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71
Q

What is microscopic polyangiitis?

A

small vessel vasculitis
inflammation of blood vessels

presents with flu like sxs and purpura of the skin

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72
Q

How do you dx microscopic polyangiitis?

A

ANCA titer

positive P - microscopic
positive C - granulomatosis

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73
Q

RPGN

A

rapidly progressive GN
a complication of nephritic syndrome

presents with nephritis and acute renal failure

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74
Q

What is type one RPGN?

A

goodpastures

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75
Q

what is type 2 RPGN?

A

SLE, post-infective GN, IgA nephropathy

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76
Q

What is type 3 RPGN?

A

microscopic polyagniitis

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77
Q

ANCA

A

anti-neutrophilic-cytoplasmic-antibody
a titer you use for microscopic polyangiitis
the pauci-immune type 3 RPGN

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78
Q

What is the prognosis for RPGN?

A

progress to ESRD in weeks to months if untreated

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79
Q

What is a common site of lodgment for bladder stones?

A 
ureterovesical junction (UVJ) 
more likely to be bladder stones
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80
Q

What is the MC cause of obstructive uropathy in children’s?

A

anatomical abnormalities

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81
Q

What is the MC cause of obstructive uropathy in young adults?

A

Kidney stones

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82
Q

What is the MC cause of obstructive uropahty in older pts?

A

BPH, prostate CA, pelvic tumors, kidney stones

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83
Q

What should you suspect if you have periods of anuria or oliguria followed by polyuria?

A

obstructive uropathy

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84
Q

When should a pt be catheterized?

A

anuria, distended bladder, or suprapubic pain

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85
Q

What does the VCUG show?

A

Voiding cystourethrography

shows the neck of the bladder and urethral obstruction and the urine that remains in the bladder after voiding

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86
Q

What is the initial imaging test for obstructive uropathy?

A

abdominal US (aimed at detecting hydronephrosis)

per the American Urological Association its non-contrast CT (more sensitive for obstructive nephropathy)

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87
Q

What is renal colic pain?

A

excruciating and intermittent pain lasting 20-60 minutes

can radiate to groin/anteriorly

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88
Q

What are the risk factors for Calcium oxalate stones?

A

hypercalcuria
hypocituria
renal tubular acidosis

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89
Q

Rank the types of stones from most common to least common

A

Calcium oxalate > uric acid stones > Struvite stone > cystine stones

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90
Q

Struvite stones are associated with …..

A

UTI caused by urea-splitting bacteria like proteus or klebsiella

more likely to be alkalouria

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91
Q

What is the path behind kidney stones?

A

slow urine flow causing super saturation of urine forming crystals that later become stones

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92
Q

When do you send a stone in for stone analysis?

A

when it was collected by strainer

i think normally they just assume it is a calcium oxalate stone since they’re the most common

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93
Q

What is the treatment for kidney stones <5mm?

A

Flomax or tamsulosin

An alpha receptor blocker –> facilitates passage (shortens explusion duration by 3 days by relaxing smooth muscle)

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94
Q

What are the side effects of alpha blockers?

A

given for kidney stones to help passage

SE include HA, dizziness, postural hypotension, palpitations

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95
Q

What are the contraindications for stone manipulation (removal)?

A

active, untreated UTI
pregnancy
blood thinning or coagulation problems (uncorrected bleeding diathesis)

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96
Q

What is a percutaneous nephrostilithotomy?

A

useful in stones >2cm, staghorn

gold standard = percutaneous nephrostomy tube

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97
Q

What is the treatment of choice for stones <2cm and lodged in the upper or middle calyx?

A

shockwave lithotripsy

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98
Q

When is ureteroscopy used?

A

when the stone is directly visualized
typically 1-2cm in size and lodged in the lower calyx or below

stent must be placed to prevent obstruction form ureter spasm or edema

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99
Q

Shockwave lithotripsy is contraindicated in….?

A

Pregnancy
uncontrolled bleeding disorders

this is used to treat stones that are <2cm and lodged in upper or middle calyx
least invasive

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100
Q

When do symptoms typically begin for kidney stones?

A

once the stone starts moving down the urinary tract

until obstruction or infection is usually when symptoms begin

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101
Q

What are the risk factors for kidney stones?

A 
decreased fluid intake 
medications (loop diuretics, chemo drugs) 
hypercalcemia 
polycystic kidney disease 
UTIs (urea-splitting organisms)
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102
Q

explain the work up for a pt you suspect has a kidney stone

A 
get UA (hematuria ---culture if signs of infection) 
non-contrast CT

depending on size will determine treatment
most likely start with an alpha antagonsits such as tamsulosin as well as giving fluids and something for the pain

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103
Q

What is the prevention for kidney stones?

A

decrease proteins and salt intake
increase fluid intake

an increase in protein can precipitate stones just like calcium

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104
Q

What does urinary incontinence mean?

A

involuntary loss of urine

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105
Q

What is the most common type of incontinence in the elderly?

A

urge incontinence

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106
Q

What is the second MC type of incontence in women?

A

stress incontinence

107
Q

What is the second MC type of incontinence in men?

A

overflow incontinence

108
Q

What causes stress incontinence?

A

increase in intra-abdominal pressure

more severe in obese pts

109
Q

A women post-childbirth is likely experiencing which type of incontinence?

A

stress incontinence

laxity of pelvic floor

110
Q

Dribbling is a common complaint in pts with what type of incontinence?

A

overflow incontinence

111
Q

What is functional incontinence?

A

urine loss d/t cognitive or physical impairments or environmental barriers that interfere w/ control of voiding

might be a person that know they have to urinate but lack the mental ability, like with delirium or dementia?

112
Q

Small volume voids are seen with which types of incontinence?

A

urge and overflow

113
Q

What are the most common mixed incontinence?

A

stress + urge

stress + functional

114
Q

____ doubles the risk of incontinence in elderly pts?

A

CVA

115
Q

Which types of brain lesions can cause incontinence?

A

cortical lesions

116
Q

What are some causes of incontinence?

A

delirium, acute confusion, infection, atropic vaginitis, psych disorders, restricted mobility, stool impaction
Meds –> think drugs that cause too much relaxation or drugs that cause too much urine
Pharm (anticholinergics, antidepressants, alpha blockers, alpha agonists, diuretics, CCB, ACEI, sedatives, anti-parkinsons)

117
Q

What PE should you do for a pt with incontinence?

A

neuro, rectal, pelvic

118
Q

What does the workup look like for a pt with urinary incontinence?

A

UA, UC
Serum BUN/Cr
Post-void residual volume
urodynamic testing

119
Q

What are the pharm and non pharm treatments for incontinence?

A

bladder training –> timed voiding while awake
kegel exercise
avoid caffeine or other fluids that irritate the bladder
TCAs, antispasmodics

120
Q

What is interstitial cystitis?

A

noninfectious bladder inflammation that causes pain (mostly pain when the bladder is full)
the bladder wall gets more damaged and scarred overtime causing more pain

unknown etiology
90% occur in women

121
Q

What food make interstitial cystitis pain worse?

A

foods high in potassium
EtOH
tabacco

122
Q

What does the workup look like for a pt with interstitial cystitis?

A

rule out other more common dz

CYSTOSCOPY is necessary to dx

123
Q

A pt comes in complaining of lower abdominal pain that goes away after she has peed. She notices the pain gets worse when she drinks wine. What are you suspicious of?

A

interstitial cystitis

124
Q

What is polycystic kidney disease?

A

a hereditary disorder causing renal cysts (in the cortex and medulla) that cause gradual enlargement of both kidneys
can lead to renal failure
can be a systemic disease (cysts on liver, etc) but more commonly affects the kidneys

125
Q

What is the difference between autosomal dominant and recessive for polycystic kidney disease?

A

dominant is the MC, typically found in adulthood (dx in 4th decade of life) and affects both kidneys

the recessive is typically seen in children and has a worst prognosis

126
Q

What is the MC mutation associated with polycystic kidney disease?

A

PKD1 –> polycystin 1 on chromosome 16

127
Q

What is the path behind polycystic kidney disease?

A

tubules dilate and fill with glomerular filtrate –separating from the functioning nephron —impair kidney function

128
Q

How do pts with polycystic kidney disease usually present?

A

for something else
this is an incidental finding, typically, asymptomatic

might have low grade flank and back pain
40-50% have HTN
+/- palpable kidneys

129
Q

What does the work up look like for a pt with polycystic kidney disease?

A

UA - hematuria, proteinuria, +/- signs of UTI
FAT OVAL BODIES (also seen in nephrotic syndrome)

start with abdominal US
get CT if US is unclear

130
Q

What is the dx criteria for polycystic kidney disease?

A

2 kidney cysts on either kidney (like you could have one on each) before 30 y/o
2 kidney cysts on the same kidney at age 31-59
4 kidney cysts in 1 kidney after 60

131
Q

What is the treatment for pts with polycystic kidney disease?

A 
symptomatic control (might have to get nephrectomy if pt gets infections and pain) 
control HTN to prevent progression to ESRD
132
Q

What is the equation for urine anion gap?

A

Urine (Na+ K) - Cl

133
Q

What does a positive urine anion gap indicate?

A

RTA

134
Q

What does a negative urine anion gap indicate?

A

diarrhea

135
Q

What is the equation for delta gap?

A

change in AG/change in HCO3

136
Q

What does a delta gap <1 mean?

A

normal anion gap metabolic acidosis

137
Q

What does a delta gap >2 mean?

A

metabolic alkalosis co-exists

138
Q

What is considered a normal delta gap?

A

between 1-2

139
Q

What can urine Cl- levels tell you?

A

if the alkalosis is responsive or resistant to chloride

140
Q

Urine [Cl-] <20 means…

A

chloride responsive alkalosis –> hypovolemia

141
Q

Urine [Cl-] >40 means

A

chloride resistant alkalosis –> HTN, aldosterone problems, cortisol

142
Q

What medications can you use for PKD?

A

RAAS inhibitors
Somatostatin
Tolvaptan (ADH antagonist)

143
Q

What is the most common type of kidney cancer in adults?

A

Renal Cell Carcinoma (RCC)

144
Q

What is the most common type of renal tumor in children?

A

Wilms tumor (malignant)

145
Q

Which gender and age are more likely to have RCC?

A

Men ages 50 -70

146
Q

What are risk factors for RCC?

A 
Smoking!!!!
Obesity (especially in women) 
ESRD, dialysis 
HTN 
Family hx of Von Hipple Lindau Sydnrome 
Horse shoe shaped kidney
147
Q

Which type of RCC is MC?

A 
Clear cell (60%) 
Followed by papillary cell (10-15%)
148
Q

What is the “classic triad” for RCC?

A 
Flank pain 
Macroscopic hematuria (MC finding) 
palpable abdominal mass
149
Q

What are the signs and sxs of RCC?

A 
Classic triad (flank pain, hematuria, palpable abdominal mass) 
HTN 
weight loss 
fever of unknown origin 
swelling in veins around testicles

parencoplastic syndrome seen in 20% of pts
less commonly seen is polycythemia, excessive hair growth in women, visual problems

150
Q

How are most RCC normally dx?

A

accidentally, on abdominal imaging

Confirmed with CT or MRI (wow contrast) –> circumscribed mass with sharp margins
bright yellow/orange d/t lipid + glycogen content

151
Q

Solids lesions of the kidney are ____ unless proven otherwise

A

RCC

152
Q

What does the workup for a pt with RCC look like?

A

UA, CBC, CMP (w/ LFTs), CXR

if alkaline phosphatase is elevated or pt has bone pain –> get bone scan

153
Q

How are RCC tumors staged?

A

AJCC
1 = <7 cm in diameter, confined to the kidney
2 = >7 cm in diameter, confined to the kidney
3 = extension to the renal capsule, confined to Gerota’s fascia
4 = invasion to other organs, involve multiple lymph nodes, distant metastasis

154
Q

What is the treatment for localized RCC?

A

radical nephrectomy

155
Q

What is the treatment for advanced RCC?

A

palliative surgery, radiation therapy, targeted drug therapies, and/or interferon alpha 2b or IL-2

THERE IS NO EFFECT CHEMOTHERAPY FOR RCC

156
Q

What factors are seen to have poor prognosis for RCC?

A

low Hb
higher corrected Ca
abnormal LDH

157
Q

What is the most likely first location for metastasis of RCC?

A

lungs

that is why you have to get CXR during your initial work up!

158
Q

What is the path behind Wilms tumor?

A

arise from primitive metanephric bastema (precursor of normal kidney)

159
Q

What is the age range for Wilms tumors?

A

typically 2-5 years (lecture says 3-3.5 years)

95% hve been dx by the age of 10

160
Q

What is the clinical presentation of Wilms tumor?

A

Palpable abdominal mass that doesn’t cross the midline is the most common finding –> because 90-95% are unilateral tumors

abdominal pain
fever
HTN
hematuria

161
Q

What is the best initial test for Wilms tumor?

A

abdominal US

162
Q

What other structures must you check in a pt you suspect has Wilms tumor?

A

chest and inferior vena cava

the tumor could have extended from the kidney

163
Q

What is the DDx for Wilms tumor?

A

PKD
RCC
hydronephrosis
other renal tumors

164
Q

What is the treatment for Wilms tumor?

A

controversial

immediate nephrectomy followed by adjuvant chemotherapy

165
Q

Which incontinence has nocturia?

A

urge incontinence

166
Q

“underactive bladder”

A 
overflow incontinence 
urinary retention (incomplete bladder emptying)
167
Q

“overactive bladder”

A

urge incontinence

urine leakage + detrusor muscle overactivity

168
Q

What is the treatment for stress incontinence?

A

pelvic floor exercises
kegel exercises
alpha agonists (Midodrine)

169
Q

What is the treatment for urge incontinence?

A

Bladder training (timed voiding during the day)
anticholinergics (are first line) –oxybutynin, tolterodine
TCA - imipramine

170
Q

What is the treatment for overflow incontinence?

A

bladder atony (intermittent or indwelling catheterization is 1st line)

cholinergics (bethanacol)

BPH –> Flomax (alpha 1 antagonists)

171
Q

Bladder cancer is the ___ most common cause of cancer in men

A

4th

M > F 3:1

172
Q

What is the most common type of bladder cancer?

A

Transitional cell

173
Q

What are the risk factors for bladder cancer?

A 
SMOKING 
old age (60-80) 
occupational exposures 
chronic analgesic use 
heavy cyclophosphamide use (chemo drug that is also used for nephrotic)
174
Q

What are the signs and sxs for bladder cancer?

A

painless hematuria = classic sxs

frequency, urgency, dysuria (resembles a UTI)

hydronephrosis

175
Q

What are the 2 types of urothelial carcinomas?

A

Flat and papillary

papillary is MC and less progressive

176
Q

What is the gold standard for bladder cancer?

A

cytoscopy

+/- transurethral resection of visible tumors to confirm w/ biopsy

177
Q

What is the definition of AKI?

A

abrupt decrease in GFR that causes retention of nitrogenous waste products

178
Q

What is the most common cause of AKI?

A

Pre-renal (decreased RBF and thus hypoperfusion)

179
Q

Of the intrinsic causes for AKI, what is the most common cause?

A

acute tubular necrosis

180
Q

Where do nephrotic and nephritic syndromes fall under AKI?

A

Intrinsic –make up GN which is 5%

181
Q

What is the most common cause of AKI in hospital setting?

A

Acute tubular necrosis

182
Q

What are the sxs for mild to moderate AKI?

A

asymptomatic

183
Q

FENa <1% suggests?

A

pre-renal

184
Q

What are the 3 different guidelines for staging AKI?

A

KDIGO
AKIN
RIFLE

185
Q

What is the difference between AKIN and RIFLE AKI guidelines?

A

RIFLE includes changes in GFR in addition to Cr

AKIN scores 1-3
RIFLE is risk, injury, failure, loss, esrd

186
Q

What is the treatment for any AKI?

A

treat the underlying problem and restore the hemodynamic balance

if serum Cr is greater than 5 –> short term dialysis

187
Q

What are some of the causes for pre-renal AKI?

A

vomiting, diarrhea, low fluid intake, HF, diuretics
liver dysfunction
septic shock
anesthesia (in surgery this decreases effective blood volume and can decrease RBF)

188
Q

What is the “hallmark” of intrinsic AKI?

A

Cellular cast formation

189
Q

Muddy brown casts

A

Acute tubular necrosis
also referred to as “brown granular casts”

makes up 85% of AKI

190
Q

WBC casts are pathognomonic for?

A

AIN - acute interstitial nephritis

191
Q

If you are given a case study and the UA mentions casts, what automatically can you start thinking of?

A

Intrinsic causes for AKI

post and pre-renal dont have casts

192
Q

BPH can cause what?

A

post-renal AKI via obstruction

193
Q

_____ is associated with Berry aneurysms, mitral valve prolapse and hepatic cysts

A

Adult Polycystic Kidney disease

194
Q

What is the treatment for acute tubular necrosis?

A

Stop the offending agent + supportive therapy (IV fluids)

195
Q

Which part of the tubule is more likely to be affected by acute tubular necrosis?

A

PCT > DCT

196
Q

You have a pt complaining of a fever, with a small rash, and some side and lower back pain. She recently had a UTI and was prescribed a PCN. What might be causing these symptoms?

A 
Allergic Interstitial nephritis 
AKI post drug exposure 1-2 weeks 
Fever 
Skin rash 
Eosinophilia 
flank pain 
oliguria
197
Q

How do you dx AIN?

A

Acute interstitial nephritis

regardless of if it is drug induced or due to an infection
Renal Biopsy is dx

198
Q

You have a concern parent in front of you stating her son just got over having diphtheria but now seems tired, not eating well, N/V, not urinating often. What do you suspect?

A

Infectious AIN

199
Q

What is the treatment for allergic AIN?

A

stop the offending agent and watch Cr levels for 5-7 days

if Cr doesn’t improve start them on prednisone

200
Q

What are some of the offending pathogens that can cause infectious AIN?

A 
Diphtheria (children)
legionella
histoplasmosis
TB
CMV
EBV
201
Q

WBC casts are seen with….

A

AIN and pyelonephritis

202
Q

What are risk factors for multiple myeloma nephropathy?

A

Low urine flow
hypercalcemia
IV contrast
Volume depletion

203
Q

What is multiple myeloma nephropathy?

A

When there is an overproduction of Ig light chains that then get into the lumen and cause obstruction and toxicity

Bence Jones proteins can precipitate in the lumen as well

204
Q

What are the signs and sxs for multiple myeloma nephropathy?

A

elevated serum Cr
tace albumin on UA
NO hematuria
WBCs in urine

205
Q

Multiple myeloma nephropahty is a type of….

A

AIN

206
Q

BenceJones Proteins or light chains lead to

kidney failure through

A

direct tubular toxicity

tubule cast formation

207
Q

Fanconi Syndrome is associated with…

A

multiple myeloma nephropathy

208
Q

What is the next step for someone you suspect has multiple myeloma nephropathy?

A

Hematology eval for bone marrow biopsy

kidney biopsy

209
Q

What is the treatment for multiple myeloma nephropathy?

A

chemotherapy
bone marrow transplant

controversial is plasmaphoresis

210
Q

What is the most common inherited kidney disease?

A

Polycystic Kidney Disease

211
Q

Livedo Reticularis

A 
Skin lesions (pupura, mottling - lower legs, toes, feet) 
see in pts with atheroembolic renal disease
212
Q

Hollenhorst plaques

A

can be found in the eye of pts with atheroemoblic renal disease

whitish yellow flecks that are often asymptomatic but can cause transient visual field defects

213
Q

What is atheroembolic renal disease?

A

post arterial manipulation (say from a CABG), cholesterol emoblizes from athersceloritc plaques getting stuck in renal artery

systemic embolization can cause gangreen or ischemia

214
Q

Cholesterol emboli are pathognomonic for…

A

atheroemoblic renal disease

215
Q

What is the treatment for atheroembolic renal disease?

A

avoid future vascular procedures

avoid anticoagulation to prevent dissolution and embolization of thrombus

216
Q

When do you see eosinphilia?

A

atheroembolic renal disease

allergic interstitial nephritis

217
Q

When should you suspect VUR?

A

in a child less than 5 with UTI
repeat UTIs
a boy of any age with UTI

218
Q

VUR can present as ….

A

nephrotic syndrome

+/- polyuria, nocturia, HTN, proteinuria

219
Q

What two kidney diseases can cause chronic interstitial nephritis?

A

analgesic nephropathy

VUR reflux nephropathy

220
Q

What offending agents can cause analgesic nephropathy?

A

Aspirin
NSAIDs
Acetaminophen
Caffeine

221
Q

What is the most common type of chronic interstitial nephritis worldwide?

A

Analgesic nephropathy

222
Q

What gender and age group is most likely to present with analgesic nephropathy?

A

women ages 60-70

223
Q

What do the kidneys look like for someone with analgesic nephropathy?

A

small
bumpy contours/indentations on the kidney
microcalcifications at papillary tips

224
Q

What is renal artery stenosis?

A

narrowing of the renal artery most likely due to atherosclerosis –> decrease in GFR

the decrease in GFR causes the RAAS to increase BP and GFR –>HTN

225
Q

What is a typical pt for renal artery stenosis going to look like?

A

HTN <30years old that is hard to control
hx of CAD
recurrent and unexplained flash pulmonary edema
abdominal bruits

226
Q

What imaging confirms the dx of renal artery stenosis?

A

CT angiography
MR angiography
Duplex US

227
Q

What is the treatment of renal artery stenosis?

A

CONTROL BP (ACEI/ARB)

statin to lower lipid level
lifestyle modifications

intervention is controversial –> renal artery stenting + clopidogrel PPx

228
Q

Henoch-Schonlein purpura is associated with what….

A

IgA nephropathy (Berger’s)

deposits of IgA in the glomerulus post viral URI or something auto immune

229
Q

Hep B and C is associated with what glomerularnephritis?

A

Membranous and membranoproliferative

230
Q

positive p-ANCA titer

A

microscopic polyangiitis

231
Q

What is the daily maintenance dose needed?

A

5D 1/2 NS + KCl 20 mEq at 2 L/day

232
Q

How does Ron Swanson play a role in potassium balance?

A

He is the quintessential hypokalemic pt.

Ron doesn't eat bananas 
Has DM --> takes insulin --> increases Na/K pump increasing K into the cell 
Has asthma --> beta agonists increase Na/K pump 
Has BPH --> alpha blocker (prazosin) blocks calcium dependent K channel from allowing K leaving the cell 
Metabolic alkaloisis (can be caused by vomiting) this is because the body sends out H+ from the cells to counter the high pH, using a K/H pump

CHF –> takes loops + HCTZ diuretics
hyperaldosteronism

233
Q

What is refeeding?

A

When a pt who has been starved eats for the first time,
they have hypokalemia and when they get glucose and release insulin they increase Na/K pump and take in more K into the cells – further causing their hypokalemia –> leading to tachyarrythmia and DEATH

234
Q

What are the consequences of hypokalemia?

A 
weakness 
paralysis 
poor GI motility (cramps) 
tachyarrythmias 
Rhabdo (your body trying to compensate for hypokalemia by rupturing the cells and letting K+ out) 
nephrogenic DI
respiratory depression
235
Q

What occurs to the action potential with hypokalemia?

A

decrease the resting membrane potential so that it hyperpolarizes and is thus less reactive

236
Q

What are the EKG changes for hypokalemia?

A 
long QT 
U wave 
prolonged PR 
increased P amplitude 
T wave flattening

tachyarrythmias

237
Q

What is the treatment for hypokalemia?

A

treat underlying cause

be sure to check the Mg level

238
Q

What is the ROMK?

A

the potassium channel on the basolateral side of the principal cell that allows potassium to be excreted into the urine

blocked by Mg

239
Q

What do you expect to see with a pt who has acute tubulointertitial nephritis?

A 
fever 
sin rash 
eosinophilia 
oliguria 
flank pain 
WBC casts 
increase BUN and Cr (low BUN:Cr) (unable to filter as well)
240
Q

What are the internal balance shifts for hyperkalemia?

A

Insulin deficiency
metabolic acidosis
beta blockers
alpha agonists
hyperosmolarity of the blood (extracellular fluid)
cell lysis (burns, rhabdo, chemo)
exercise (decrease ATP keeping K out of the cell)

241
Q

What are external shifts affecting hyperkalemia?

A

adrenal insufficency
hypoaldosterone
AKI
Meds (ACE-I, ARBs, NSAIDs)

242
Q

What happens to the membrane potential in hyperkalmeia?

A

it goes up making the cell more excitable

243
Q

What are the EKG changes for hyperkalemia?

A

Bradyarrythmias

At first:
peaked T waves, shorted AT interval, ST depression

SEVERE:
prolonged PR
absent P
wide QRS

244
Q

What is the treatment for hyperkalemia?

A 
calcium - stabilize myocardial membrane 
bicarb (for the acidosis) 
k+ wasting diuretics 
resin binding K+ 
beta agonists (albuterol) 
insulin + glucose
245
Q

What is happening to your water and sodium in hypotonic isovolemic hyponatremia?

A

you are gaining free water

246
Q

What are the causes of hypotonic isovolemic hyponatremia?

A

SIADH
hypothyroidism
crotisol issues
meds

247
Q

What is the treatment for hypotonic isovolemic hyponatremia?

A

water restriction
give NS

if its chronic also give loop + anti ADH meds + tolvaptan (vasopressin antagonist)

248
Q

What is happening to your sodium and water in hypotonic hypovolemic hyponatremia?

A

loosing Na + H20 just more Na

249
Q

What is the cause of hypotonic hypovolemic hyponatremia?

A 
vomiting 
diuretic 
decrease in ADH 
ACEI 
diuretics

the magic number is urine [Na] >20 = renal

250
Q

What is the treatment for hypotonic hypovolemic hyponatremia?

A

NS
treat the underlying cause

be careful about speed of correction d/t cerebral edema

251
Q

What is the cause of hypotonic hypervolemic hyponatremia?

A

increase in sodium and water, just more water

252
Q

What is the cause of hypotonic hypervolemic hyponatremia?

A

cirrhosis
CHF
Nephrotic
intravascular volume depletion

renal failure

253
Q

What is the treatement for hypotonic hypervolemic hyponatremia?

A

prevent ADH/aldosterone effects
restrict H20 + Na
give loop diuretic

254
Q

What is the cause of hypovolemic hypernatremia?

A 
non renal: 
sweating 
diarrhea 
insensible loss with/ inability to get H20 (like dehydrated old pts) 
[Na] <10
renal:
osmotic diuresis (mannitol) 
post obstruction [Na] >20
255
Q

What is the treatment of hypovolemic hypernatremia?

A

NS

256
Q

What is happening in hypervolemic hypernatremia?

A

increase in water and sodium but more increase is sodium

most commonly due to over resuscitation with NS or d/t mineralocorticoid excess (cushings)

257
Q

What is the treatment for hypervolemic hypernatremia?

A

diuretics + free h2o

258
Q

What is happening in isovolemic hypernatremia?

A

decrease in H20 while Na stays the same

259
Q

What is the cause of isovolemic hypernatremia?

A

DI (decrease in ADH)

260
Q

What is DI?

A

Diabetic insipidus

central:
due to the body not producing enough ADH

nephrogenic:
due to the body not responding to ADH

dx by H2O deprivation test and checking their urine —if it stays dilute DI
then to see which DI give them ADH and see if they respond

261
Q

What is the treatment for isovolemic hypernatremia?

A

for nephrotic DI
give HCTZ and restrict Na

for central DI
give ADH

262
Q

What does a pt with chronic SIADH look like?

A

might be asymptomatic

might be anorexic

263
Q

What does demeclocycline do?

A

its an antibiotic that is given for isovolemic hyponatremia to cause nephrogenic DI??

Clin Med GU (1 decks)

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