Renal Pathophysiology Flashcards Preview

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Flashcards in Renal Pathophysiology Deck (28)
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1
Q

Presentation of renal disease:

A
azotemia
uremia
proteinuria
hematuria
altered naturesis (leading to HTN)
edema
circulatory congestion
2
Q

Azotemia:

A

elevated blood urea nitrogen and creatinine level

decreased glomerular filtration rate

3
Q

uremia:

A

excess of urea and other nitrogenous waste in the blood

  • failure of renal excretory function, host of metabolic and endocrine altercation
  • secondary gastrointestinal, neuromuscular, and cardiovascular involvement
4
Q

Acute kidney disease/injury/failure

A

-abrupt decrease in GFR or creatinine clearance
-RIFLE classification
-based on anatomical area of injury or malfunction:
prerenal
intrinsix
postrenal

5
Q

RIFLE

A

-risk, injury, failure, loss of kidney function, and end-stage kidney disease

6
Q

prerenal

A

decreased renal blood flow

7
Q

intrinsic

A

structure within kidney damaged

8
Q

postrenal

A

obstruction present within the urine collection system

9
Q

chronic kidney disease

A

progressive loss of function over several months to years

gradual replacement of normal kidney with parenchymal fibrosis

10
Q

hemodialysis

A
  • perfusion of blood and dialysate on opposite side of semipermeable membrane
  • substances removed by diffusion or convection
  • excess water removed via ultrafiltration
11
Q

peritoneal dialysis

A

instillation of dialysate into peritoneal cavity by permanent peritoneal catheter

  • substances removed from blood across peritoneum via diffusion and ultrafiltration
  • excess water removed by ultrafiltration created by osmotic pressure generated by various dextrose or icodextrin concentrations
12
Q

drug-induced kidney disease

A

drug causes immune reaction, inflammation causes damage to structures of kidney

  • antibiotics
  • NSAIDs (analgesic nephropathy)
13
Q

chronic glomerulonephritis

A
  • most common causes of renal failure in humans

- divided into primary and secondary

14
Q

secondary GN

A

associated with a number of systemic disease:

  • SLE (systemic lupus erythrometitis-attack joints, skin lesions, kidney and spleen))
  • diabetes (diabetic neuropathy)
  • etc.
15
Q

antibody-mediated glomerular injury (3)

A

1) immune complex (antibody/antigen) deposition- sub endothelial deposit, deposit in basement membrane:protein and blood leak out
2) anti-GBM (glomerular basement membrane) antibody
3) antibody against glomerular antigen (membranous nephropathy)

16
Q

cell mediated

A

T-cell immune reaction: macrophages, mesangial cells

17
Q

nephrotic syndrome

A

protein leakage only:

  • proteinuria
  • hypoalbuminemia
  • edema
  • hyperlidemia and lipiduria
18
Q

nephritic syndrome

A

protein and RBC leakage

  • hematuria
  • oliguria (not enough urine)
  • azotemia
  • HTN
19
Q

3 major glomerular syndrome

A
  • nephrotic syndrome
  • nephritic syndrome
  • chronic glomerulonephritis
20
Q

Chronic glomerulonephritis

A
  • nephrosis

- nephritis

21
Q

nephrosis

A

1) nephropathy (any disease of the kidney)

2) degeneration of renal tubular epithelium

22
Q

nephritis

A

inflammation of the kidney

23
Q

acute pyelonephritis pathways

A

1) hematogenous infection-bacterial spread (staphylococcus, E.coli)
2) ascending infection :urinary bladder infection, vesicoureterial reflux, intrarenal reflux

24
Q

APKD acronym

A

autosomal dominant (adult) polycystic kidney disease

25
Q

APKD definition

A

multiple expanding cyst of both kidneys, destroys intervening parenchyma

26
Q

APKD pathogenesis

A
inherited mutation of PKD1 or PKD2 gene in renal tubular cells
-abnormal cyst formation in both kidneys
intermittent gross hematuria
HTN and urinary infection
ultimately fatal
renal transplantation necessary
27
Q

Autosomal recessive (childhood) PKD pathogenesis

A

autosomal recessive inheritance

mutation in PKHD1-fibrocystin (polyductin)

28
Q

Autosomal recessive PKD clinical features

A
  • serious manifestation usually present at birth
  • young infants dies quickly from pulmonary or renal failure
  • patients who survive infancy develop liver cirrhosis (HTN)