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DT3-Exam 3 > IL Renal Review & Cystic Diseases--Leah** > Flashcards

IL Renal Review & Cystic Diseases--Leah** Flashcards

1
Q

Vertebral level of the kidneys?

A

T12-L3
ONE TWO THREE; THERES THE KIDNEE!
*Note that left kidney is slightly higher than right and that left renal vein is longer than right.

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2
Q

Renal Blood Flow is ______% of total cardiac output?

A

20%

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3
Q

Outermost two parts of kidney

A

-cortex, then columns which are BETWEEN the pyramids.

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4
Q

Describe flow of urine from the medullae to the ureters

A

medullas –> pyramids –> calyces –> pelvis –> ureter

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5
Q

Within the renal pelvis there are _____.

A

renal papillae

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6
Q

Describe the 7 parts of a nephron:

A

-glomerulus/ bowmans capsule –> PT –> thin descending loop –> thick asecending loop –> Distal convoluted tubule –> connecting tubule –> collecting duct

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7
Q

Vascular system surrounding the loops of henle:

A

vasa recta, collects any H2O secreted from thin descending loop

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8
Q

artery that feeds into the afferent arteriole?

A

arcuate artery

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9
Q

Vessels that enter and exit the glomerulus?

A
  • afferent enters glomerulus

- efferent exits

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10
Q

microscopic structures seen in the renal cortex?

A

glomeruli

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11
Q

microscopic structures seen in the renal medullae?

A

straight portions of tubules and collecting ducts

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12
Q

Definition of azotemia

A

-decreased GFR –> elevated Cr and BUN

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13
Q

Definition of uremia

A

-essentially azotemia, but must have manifestation of renal disease in OTHER organ systems as well

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14
Q

three types of azotemia

A

pre-renal, renal, post-renal

  • pre: reduced renal perfusion, not renal malfunction
  • renal: intrinsic renal disease
  • post: downstream urine obstruction
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15
Q

Two examples of post-renal azotemia

A

-BPH, stone

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16
Q

Two examples of pre-renal azotemia

A

-hypovolemic shock, CHF

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17
Q

Example of uremia

A

fibrinous pericarditis secondary to presence of circulating nitrogenous compounds in blood

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18
Q

Rapidly progressive glomerulonephritis is assc with what change?

A

-rapid GFR decrease

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19
Q

How does acute kidney injury manifest?

Reversible?

A
  • rapid GFR decrease
  • oliguria, anuria
  • azotemia
  • usually reversible
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20
Q

Chronic Kidney Disease definition

A
  • common end point of renal disease

- GFR less than 60 for at least 3 months

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21
Q

End Stage Renal Disease definition

A

GFR five or less, will need dialysis

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22
Q

Renal Tubular Diseases cause

A

electrolyte derangement, polyuria

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23
Q

What is a UTI called if it effects the kidney? The bladder?

A
  • kidney: pyelonephritis

- bladder: cystitis

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24
Q

What is Nephrolithiasis?

How does it present?

A
  • kidney stone

- pain and hematuria

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25
Q

Four tissue types that may be effected by renal disease?

A
  • tubules
  • glomeruli
  • interstitium
  • vasculature
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26
Q

Diffuse, focal, segmental, and global are used to describe?

A
  • location of disease involvement
  • diffuse vs focal refers to location in kidney
  • segmental vs global refers to location in glomeruli
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27
Q

Three methods of examining renal tissue and their uses?

A
  • light micro: determines disease process/ cells present
  • ImmunoF: determines etiology; ie presence of Abs
  • electron micro: determines structural changes
28
Q

What do the kidneys look like in fetal life/ childhood? Adulthood?

A
  • kids: lobulated kidneys
  • adult: smooth
  • Asx if adult retains lobules, NOT the same as ADPKD
29
Q

Bilateral renal agenesis is not compatible with life. Describe the outcome of unilateral renal agenesis.

A
  • compatible with life BUT

- get compensatory hypertrophy and possible glomerulosclerosis –> chronic disease

30
Q

What is oligohydraminos and what can cause it?

A
  • low levels of amniotic fluid
  • fluid is either LEAKING or not being produced
  • not being produced= baby isn’t peeing = kidney’s absent or not functional
31
Q

What are symptoms of oligohydraminos?

A 
POTTER
P- pulm hypoplasia 
O- oligohydraminos 
T- twisted face
T- twisted skin 
E- extremity defects 
R- renal agenesis 
*Also: Breech Position
32
Q

What is dangerous to patients with unilateral renal agenesis?

A 
Any systemic disease with potential for renal damage
-DM, pregnancy, HTN, CHF, others 
-chemo, drugs
-renal disease
(many others)
33
Q

Ddx for a small kidney?

A
  • congenital hypoplasia

- atrophy secondary to some systemic disease

34
Q

In horseshoe kidney, where do the kidneys fuse?

How common is it?

A
  • inferior pole 90%, upper in 10%

- 1:500-1k

35
Q

Where does horseshoe kidney get stuck in development?

Is horseshoe kidney clinically relevant?

A
  • IMA (L3)

- not clinically relevant, usually incidental finding

36
Q

Disease to assc with horseshoe kidney?

A

Turners, although definitely not all horseshoe kidney patients have Turners, incidence is just higher in that population.

37
Q

Cause of 5-10% chronic kidney disease?

A

ADPKD, just as common as horseshoe kidneys

38
Q

polycystin 1 + 2 are what type of proteins and cause which diseases?

A

polycsystin 1 mutation = PKD type 1
polycystin 2 mutation = PKD type 2
*Both code for integral membrane proteins and lead to poor cell-cell/ cell-matrix interactions = POOR TUBULAR GROWTH + ABNORMAL ECM = TUBULAR CYSTS

39
Q

What chromosome is assc with PKD1? PKD2?

A

PKD1-chromosome 16p (more common, higher number)

PKD2- chromosome 4 (2X2=4)

40
Q

PDK1/2
Which is more severe?
More common?
Has older age of onsent?

A

PKD1: earlier onset severe disease (50s), more common AND more severe
PKD2 severe disease presents in late 60s

41
Q

Result of tubular cysts in ADPKD (3)

A
  • interstitial inflammation
  • vascular damage
  • enlarged cystic kidneys w/ functioning tubules b/n cysts
  • Cysts seen on EXTERNAL surface
42
Q

ADPKD PE findings:

What is the cause of the pain?

A
  • palpable kidneys
  • hematuria (hemorrhaging into cysts) and CVA tenderness
  • pain is caused by enlarging/ clot passing cysts
43
Q

Three extrarenal findings that MAY BE assc with ADPKD

A

-liver cysts
-Berry aneurysms
-heart valve anomalies
(only in smaller percentages of patients)

44
Q

Gene assc with childhood polycystic disease/ ARPKD

A

PKHD1, fibrocystin, chromosome 6

45
Q

Describe the appearance of childhood ARPKD:

A
  • enlarged SMOOTH kidneys
  • COLLECTING DUCT cysts = SPONGY cut surface
  • ALWAYS liver cysts/ fibrosis assc (40% in ADPKD)
46
Q

Four categories of ARPKD?
Which are more common?
What is the result?

A
  • perinatal, neonatal, infantile, juvenile
  • *more common are perinatal, neonatal
  • see death in utero/ sometimes at birth due to - **PULMONARY HYPOPLASIA ensues
47
Q

Medullary Sponge Kidney: two changes in the kidney

A
  • medullary cysts

- collecting duct dilation

48
Q

Medullary Sponge Kidney clinical findings:

A
  • asx, calculi, infections, hematuria etc

- No impairment of kidney function

49
Q

Most common cause of genetic renal disease in children and young adults

A

Nephronophthisis

group of disorders

50
Q

Three variants nephronophthisis:

Which is most common?

A 
sporadic, familial juvenile, renal-retinal 
#1 = familial juvenile
51
Q

nephronophthisis:
inheritance pattern
number of genes involved?
genes assc with familial juvenile form?

A

AR
7 genes
NPH1-3 assc with most common form, familial juvenile

52
Q

Where are cysts located in nephronophthisis?
Gross appearance of kidneys?
End result?

A
  • SMALL kidneys
  • corticomedullar jxn cysts
  • causes chronic renal failure
53
Q

Three histo findings assc with nephronophthisis

A
  • tubular atrophy
  • BM thickening in Distal + proximal tubules
  • interstitial fibrosis
54
Q

Three early clinical findings assc with nephronophthisis

A

polyuria (dilute urine), tubular acidosis, sodium wasting

55
Q

How long after onset does nephronophthisis cause renal failure?

A

5-10 years

56
Q

Four extra-renal findings assc with nephronophthisis

A
  • liver fibrosis
  • cerebellar and ocular abnormalities (extra ocular mm’s)
  • retinal dystrophy
57
Q

Describe the appearance of multicystic renal dysplasia (2):

Treatment and prognosis if unilateral/ bilateral

A
  • islands of undifferentiated mesenchyme/ cartilage
  • immature collecting ducts
  • baby gets renal failure if bilateral, can surgically remove affected kidney if unilateral
58
Q

Acquired cystic kidney disease:

  • cause
  • location of cysts
  • symptoms
A
  • chronic dialysis –> tubular obstruction by fibrosis or oxalate crystals
  • cortical and medullary cysts
  • asx or hematuria
59
Q

Rare outcome of acquired cystic kidney disease

A

-7% get renal squamous cell carcinoma

60
Q

Two renal cystic disease effecting children

A

ARPKD, nephronophthisis

61
Q

How to distinguish tumor v cyst on imaging

A

cysts always AVASCULAR, have fluid lines, and appear smooth

62
Q 
Where are cysts located in:
ADPKD
ARPKD 
Sponge Kidney
Nephronophthisis
Cystic Kidney Disease
A

-ADPKD: tubular
(Note: tubular can also be called “cortex + medulla”, because that’s where tubules are.)
-ARPKD: collecting ducts
-Sponge: medulla
-Nephronophthisis:corticomedullar jxn
-Cystic Kidney Disease: cortex AND medulla

63
Q

Renal condition causing ocular/ retinal anomalies?

A

Nephonrophthisis, also causes cerebellar and hepatic anomalies.

64
Q

Disease assc with pulmonary hypoplasia and neonatal death?

A

ARPKD

65
Q

Disease that causes renal failure within 5-10 years of onset?

A

nephronophthisis

66
Q

Baby with Portal HTN should make you put what cystic kidney disease on your Ddx?

A

ARPKD- almost always presents with hepatic cysts/ fibrosis –> portal HTN

DT3-Exam 3 (9 decks)

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