APE 3 :

Pre-APE

1) What doesn’t cause hypokalemia

Aldosterone antagonist

2) What cell is central to pathophysiology in nephrotic syndrome?

Podocyte

3) What doesn’t have diminished C3?

IgA Nephropathy
NOT Lupic glomerulonephritis, or post-infectious glomerulonephritis

4) What is main cause of infection in nephrotic syndrome?

Loss of IgG (hypogammaglobulinemia)

5) Where is site of action of furosemide?

Ascending Anse of Henle

6) Normal proteinuria levels

100-150mg (ie : Tamm-Horsefall proteins) – not detectable, but present

Problem

1) Why does William’s head turn?

Orthostatic hypotension

2) Why did William develop a pulmonary embolism?

Urinary loss of antithrombin III in nephrotic syndrome

3) Which is not a mechanism implicated in William’s metabolic alkalosis?

Tachypnea
Bicarbonate reabsorption in proximal tubule
Intracellular H+ shift
H+ secretion in proximal and distal tubule

4) Why are William’s legs painful (cramping)?

Hypovolemia (hypokalemia..also…)
- Why? Idk

5) Why ,anifestation acould have been apparen with mixed syndrome?

Tension 120/80 mmHg (esp considering hypovolemia) and hematuria
Lipid cylinders and hyaline cylinders
Lowered C3

6) Which could have been a part of DDX of LMM

Hyalinose focale et segmentaire (pathologically, can resemble LMM at beginning)

T1 diabetes
Lupus
Alport (not nephrotic)

7) How do we explain 15mm/day urinary sodium?

Activation of RAA

Low salt diet

ADH stimulation (only absorbs water)
Lowered filtration

8) By what mechanism does nephrotic syndrome cause hyperlipidemia

Non-specific stimulation of hepatic lipoprotein synthesis

APE 4

1) Why don’t we attempt sevrage de sonde?

BECAUSE HE’S IN IRA  send him to surgery right away
Taking out a sonde at that age is morbid

2) Once we install sonde, we have debacle urinaire (200ccr x 2 heures consecutives), what is the
physippathology of this?
a) perte de pouvoir de concentration
b) appropriate elimination of hydrosodic charge accumulated
c) osmotic diuresis
ALL OF THEM ARE TRUE

3) What does phimosis signify?

- usually acquired
- hygiene is related to penis cancer (circumcision eliminates risk of penis cancer if done at
REALLYYYY young age)
(circumcision is rarely necessary, esp in oldies….as a matter of fact, topical corticosteroids are
enough 99% of time – keep in mind that phimosis is usually in inflammatory cause)

4) Masse scotale deoite – fluctuates and transilluminates

masse benign
spermatocele
hydrocele
5) How do we explain tht sus-pubic palpation does not provoke the need to urinate

if we obstruct, slowly, the vessie gets accustomed to being chronically stretched, and thus loses
proprioception

6) Why is creaining @ 200?

Because intrarenal pressure is increased

7) What type of incontinence is the dude suffering of?

Incontinence par trop plein (esp. due to obstruction)

APE 5
Questions

1) leucocyturie peut se retrouver dans tout sauf :

a) cystite
b) néphrites intertitielle allergique
c) pyélonéphrite
d) syndrome néphrotique pur

2) Which is true concerning hypercalciuria and calcic lithiases?

a) we must diminish Ca intake (only works for secondary calcic lithiase)
b) alcanalise urine with sodium bicarbonate (no, will form CaPOH4)
c) thiazide diuratic can diminish calciuria (reduce distal Na R, which will increase prox R of Na
& Ca)
d) diruetic of anse will diminish calciuria (no, will decrease prox Na and C reabsroption, which
increases risk of calcic lithiase.

3) Absence of réflux vésico-utrétérl, dû à ?

longue implantation de l’uretère terminal au niveau e la paroi musculaire de la vessie

4) Clairance de la créatinine d’une femme

don’t forget that women have 85% of creatinin clearance due to correction for women having
less muscle mass0

5) detect a renal lithiase at echography that was radio-transparent..

therefore, it’s a uric acid lithiase, and which depends on pH, urinary volume, hyperuriciuria
not calciuria

Problems :

1) Why do we use the estimation formla to etimate renal function

because we want to adjust the medical posology
keep in mind that : if not in equilibirum (creatine creation = creatin elimination), then your
formula sucks

2) How do we interpret urine density?

Suggests a risk factor for lithiasis****
LE FACTEUR PRINICIPAL FOR ALL KIDNEY STONES***

3) Why do we treat asymptomaic bacturia during grossesse?

Risque de travail pré-terme

4) Mais reason that woman is more susceptible to infection than her husband?
A :because she’s a woman
- Because she had a lithiasis (we need a persisting, or recurrent lithiase…in vessie..so no)

5) Why is pain less intense in pyelonephritis?

Distention is not as rapid as in colic nephritis…

APE 6

1) Which Symptom isn’t a part of uremic syndrome?

Tremblements au repos
Frottement péricardiqe
Nausée
Prurit

2) Which is true concerning chronic renal failure?

Reduction in # of nephrons increases kidney filtration (increases neprhon filtration, not kidney)
Tubular hypertrophy increases golmerular filtration…wtf no
Vd of aff and eff arterioles increases bloodflow to nephrons
We can detect CRF in diagnostic tests as soon as 20% of nephrons are lost

3) Concerning exprimental models for renovascular hypertion, which is true?

HTa un-rein-un-clip is volume dependent

4) which slows dow CRF?

Use of AINS
Treat hyperkalemia
Treat alcalosis (acidosis does however)
Use IECE and ARA
Problem

All mechanisms may have contributd to the dude’s hypocalcemia, except one :
a) Deficit in 1-25-OH vitamin D
b) Metabolic acidosis
c) Hyperphosphatemia
d) Reduced intestinal calcium absorption

Least probable Dx for 1st part of problem

a) Ischemic nephropathy
b) Diabetic nephropathy (normal glycemia)
c) Atteinte obstructive dans le cadre d’une hypertrophie bénigne de la prostate (bc no
hydronephrosis)
d) Néphroangiosclérosis

Why did dude g into ARF after IECA?

a) Increased glomerular filtration is due to angiotensin
b) Patient has a bilateral stenosis

Difference : patient that has good kidneys, or patient that has shitty kidneys

APE 7
Pre-APE

Most sensible test to Dx vesical neoplasia:

a) uroscan
b) CT abdo-pelv (if bladder isn’t empty and fully distened, you won’t see shit)
c) echography (WORST test….MD-dependent ; if vessie full of pus, it sucks)
d) Cystoscopy (use ur fken head)

2) Which is true about vesical cancers (keep in mind : main risk factors : age and tabacco)
a) the most prevalent risk factor is use of anilin dyes
b) most common presentation is a vesical pain that looks like a cystitis
c) presented as a silent hematuria macro
d) women are 3x more susceptible to have bladder cancer

3) Which is true about adenocarcinoma

a) pronostoic est souvent sombre (no, because thanks to echo, we find a lot of them when they
small)
c) there’s no genetic predisposition
d) most frequent histology is papillary carcinoma (no it’s clear cell carcinoma mofo)

which is the most specific for glomerular hematuria?

 a) Caillots (that’s a fken lesion, not a fken glomerular bleeding)
b) Urine de teinte brun coca-cola (old blood)
c) Cylinder erthrocytaires

5) Whciih is true about aut dominant renal polykysose?

a) maladie rare (nope, 1/500 white ppl)
b) all nephrons are dilated (nope, only 5%)
c) 10% of all CRF (TRUE BETCH)
d) enfants porteurs ont multitude des kystes cortico-médulaires (nope, affects adults)

Problem

Which are is the use for pyeloscan?

a) Verify local spread of tumour
b) Search for metastases Gg and visceral
c) Search presence of urothelial tumours and synchronous renal tumours
d) all of the above
pyeloscan pretty much is a Ct with and without contrast…bae

What does presence of caillots indicate?

a) Saignement est d’origine vésiculaire (could come from everywhere…)
b) Saignement n’origine pas d’un kyste rénal (wtf?)
c) Saignement est abondant…depends on caillot size
d) Saignement n’est pas d’origine urinaire

What is risk of pyeloscan?

ARF

What indicates that hematuria is total?

a) No signification if hematuria is abundant