Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin med sem 2 > Nephrology- Peds > Flashcards

Nephrology- Peds Flashcards

1
Q

CKD- pathophysiology

A

GFR <60ml/min for >3min
GFR >60ml/min + evidence for structural damage
- albuminuria, proteinuria, pathologic abnormalities on histology or imaging

Staging - if below 1 standard deviation - more concerned

Reversible Causes
Dec Perfusion to Kidneys
- Hypotension
- Volume depletion - vomiting, diarrhea
- Meds that dec kidney perfusion - NSAIDs, ACE, ARB
Nephrotoxic drugs - NSAIDs, contrast, aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CKD- cause

A

Congenital disease - 60%

  • obstructive uropathy
  • renal hypoplasia
  • Renal dysplasia
  • Reflux nephropathy
  • PKD

Glomerular disorders - 2nd most common

  • > 12yo
  • FSGS
  • membranoproliferative glomerulonephritis
  • Minimal change disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CKD- S/S & PE

A

Nonglomerular

  • Polyuria
  • Elevation in serum creatinine
  • poor growth

Glomerular

  • Tea colored/colar colored urine
  • Edema
  • Inc serum creatinine
  • Inc BP for age
  • systemic findings of concurrent systemic disease that affect kidney function - SLE

Stage 3

  • anorexia, N/V, Fatigue
  • pericarditis
  • bone and mineral disease
  • dec neuro function
PE: 
Growth parameters
HTN
Hypervolemia
Pericardial rub
Pallor
Deformities or extremities - CKD bone-mineral disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CKD- diagnosis

A

U/S - widely used

  • measure size of kidneys against nl values for age
  • look for deformities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

CKD- labs & imaging

A 
Serum Cr
UA
Serum Ca
Sphphorous
Vit D
PTH
- if suspect bone and minilaral issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

CKD- treatment

A

Treat reversible kidney dysfunction
Prevent or slow progression
- BP control - ACEI/ARB - HTN + Proteinuria
- Don’t limit protein intake
- No data to support lipid lowering or anemia correction
Treat complications
Identify and prepare kids/families if RRT needed

Mineral/Bone Disease

  • growth failure, avascular necrosis, skeletal fractures/deformities/pain, vascular calcification
  • Control - PO4, Ca, PTH, VitD
  • Tx: diet, binders (sevalemer, Ca, Iron), Vit D2/D3, Vit D analogs

Renal Replacement Therapy (RRT)

  • GFR <30 - start preparing family/child
  • 1st line - Kidney transplant preferred for best survival
  • 2nd line - Paranteral Diaylsis
  • 3rd line - Hemodyalisis
  • Start before GFR 10-15 if - poor calarie intake, Symptomatic uremia, delay in psychomotor development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CKD- prognosis

A 
Inc M&M
Inc Hosp
Inc Depression
Worse QOL for pts, and family
\: More likely unemployed
Leading cause of death - CV and infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Obstructive uropathy- pathophysiology

A

Stricture
Stenosis
Stones

In posterior urethral valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Obstructive uropathy- treatment

A

Refer to Urology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Reflux Nephropathy/ Vesicoureteral Reflux (VUR)- pathophysiology

A

Retrograde passage of urine from bladder -> upper urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Renal Dysplasia- pathophysiology

A

Malformed kidneys

Microscopic level:

  • disorganized nephron elements
  • Dec # of nephrons
  • maldifferentiation of mesenchymal and epithelial elements
  • Transformation of tissue to cartilage and bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Renal Dysplasia- cause

A

Kidney’s variable in size - usually small
Unilateral or bilateral
Multicystic - nonfunctioning dysplastic kidney w/ multiple cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Renal Hypoplasia- pathophysiology

A

Low number of structural nl nephrons -> small kidneys

Reduce renal size by 2 SD of mean size by age
AND
Exclusion of renal scaring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Renal Hypoplasia- cause

A

Genetic

No damage or malformations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Renal agenesis- pathophysiology

A

Congenital absence of renal parenchymal tissue - only have 1 kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Renal agenesis- epidemiology

A

M>F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Renal agenesis- S/S & PE

A 
Asymptomatic 
Incidental finding on U/S 
- antenatally - during preg 
- part of UTI eval 
- postnatally in dysmorphic kid

Impaired renal function at birth & progressive renal failure

Associated urologic abnormalities - jrenal pelvis, calyces (congenital hydronephrosis), and ureters (Stenosis,VUR, megaureter)
- can lead to complications - UTI, hematuria, fever, abdominal pain

Non renal anomalies - malformations of heart, genitals, bones, GI tract, respiratory tract

18
Q

Renal agenesis- diagnosis

A

Ranal U/S
Frequent association of dysplasia w/ a collecting system anomaly
- get voiding cystourethrography as well

19
Q

Renal agenesis- treatment

A

Monitor

Transplant/RRT

20
Q

Focal Segmental Glomeruloscerosis (FSGS)- pathophysiology

A

Most common Glomerular disorder

Sclerosis in parts/segments of 1 glomerulus in entired kidney biopsy

21
Q

Focal Segmental Glomeruloscerosis (FSGS)- cause

A

Genetic
Injury to podocytes and/or direct toxicity from drugs or viral infections
2nd to - obesity, HTN, HIV, chronic urinary reflux, analgesic or bisphospbonate exposure

22
Q

Focal Segmental Glomeruloscerosis (FSGS)- S/S & PE

A

Acute onset - Most common

  • Peripheral Edema
  • Hypoalbuminemia
  • Proteinuria - >3.5 g/day

Dec GFR
ESRD - develop in 6-8 yr

23
Q

Focal Segmental Glomeruloscerosis (FSGS)- diagnosis

A

Renal biopsy

Genetic testing

24
Q

Focal Segmental Glomeruloscerosis (FSGS)- treatment

A

Diuretics - edema
ACEI/ARB - HTN/proteinuria
Statin/niacin - HLD – controversial

Prednisone
Immunosuppressants - cyclosporine, tacrolimus
Plasma exchange - prior to renal transplant - lower risk of graft loss
- good for those who are about to relapse

25
Q

Membranoproliferative Glomerulonephritis- pathophysiology

A

Pattern of glomerular injury on biopsy w/ characteristic changes on light microscopy

Rare

26
Q

Membranoproliferative Glomerulonephritis- cause

A

Immune - complex mediated

Complement mediated - less common

27
Q

Membranoproliferative Glomerulonephritis- S/S & PE

A

Spectrum of nephritidies:

  • asymptomatic glomerular hematuria
  • Gross hematuria
  • Rapidly progressive glomerulonephritis
28
Q

Membranoproliferative Glomerulonephritis- diagnosis

A

Renal biopsy

29
Q

Membranoproliferative Glomerulonephritis- labs & imaging

A

Cr - nl or inc
Complement levels - low
Hematuria -dysmorphic red cells and red cell casts
Proteinuria - variable

30
Q

Membranoproliferative Glomerulonephritis- treatment

A

Mild - ACEI/ARB
Severe - cyclophosphamide or MMF + steroids or rituximab

ESRD - develop in most even w/ treatment
Kidney transplant - still may recur

31
Q

Minimal Change Disease- pathophysiology

A

Most common nephrotic syndrome

32
Q

Minimal Change Disease- cause

A 
Idiopathic
After Viral URI
Neoplams - Hodgkin
Meds - lithium
Hypersensitivity reaction
33
Q

Minimal Change Disease- S/S & PE

A

Nephrotic syndrome symptoms
Even though inc fluid vol -> will have s/s of dec effective circulating volume
- tachy, peripheral vasoconstriction, oliguria, dec GFR, inc plasma renin, aldosterone, and norepinephrine

Susceptible to infection - gram +

Tendency toward thromboembolic events

Severe hyperlipidemia

34
Q

Minimal Change Disease- diagnosis

A

Clinical
Biopsy - rare
- no changes on light microscopy
- electron microscopy - effacement of podocyte foot processes

35
Q

Minimal Change Disease- treatment

A

Prednisone

  • 4m to respond
  • cont several weeks after proteinuria is resolved

Cyclophosphamide or Retuximab
- resistant to steroids or relapse

Prog to ESRD - rare

36
Q

Horseshoe Kidney- pathophysiology

A

Most common kidney fusion anomaly

One pole of each kidney fuses to the other - 5-9w gestation

1/2 have another congenital anomaly

  • urological or genital
  • syndromes - turner, trisomny 13, 18, 21

Inc risk for Wilms tumor

37
Q

Horseshoe Kidney- S/S & PE

A

Asymptomatic
Pain and/or hematuria - obstruction or infection
Hydronephrosis - 80%
Renal calculi - 20%
Inc inf risk - inc urinary stasis and impaired drainage

38
Q

Horseshoe Kidney- diagnosis

A

Incidental

39
Q

Horseshoe Kidney- labs & imaging

A

Cr
U/S
Voiding cystourethrogram

40
Q

Horseshoe Kidney- treatment

A

Good prognosis w/out intervention
VUR - prophylactic abx for prevention of UTI
Obstruction - refer to urology

Clin med sem 2 (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions