Renal dysfunction Flashcards

1
Q

what is creatinine

A
  • waste product derived from muscle metabolism in the body
  • present in bloodstream
  • excreted in urine
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2
Q

define acute kidney injury (AKI)

A

defined as any of the following:

  • increase in creatinine by >0.3mg/dl within 48h OR
  • increase in creatinine to >1.5x baseline, which is known or presumed to have occured within prior 7 days OR
  • urine vol <0.5ml/kg/h for 6 hours
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3
Q

types of AKI

A
  1. non-oliguric AKI -> AKI with urine output > 400ml/day
  2. oliguria -> <400ml/day
  3. anuria -> 100ml/day
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4
Q

what are the criteria of stage 1 AKI

A

1.5-1.9x baseline SCr OR
>0.3mg/dl increase in SCr

<0.5ml/kg/h urine output for 6-12h

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5
Q

what are the criteria of stage 2 AKI

A

2-2.9x baseline SCr

<0.5ml/kg/h urine output for >12h

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6
Q

what are the criteria of stage 3 AKI

A

3x baseline SCr OR
>4.0mg/dl increase in SCr OR
initiation for RRT OR
decrease in eGFR to <35ml/min per 1.73m^2

<0.3ml/kg/h for >24h OR
anuria for >12h

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7
Q

define chronic kidney disease

A
abnormalities of kidney structure OR 
renal function present for more than 3months with implications for health: (either of the following)
- albuminuria
- urine sediment abnormalities
- electrolyte and other abnormalities due to tubular disorders
- abnormalities detected by histology
- history of kidney transplant
- GFR <60ml/min/1.73m^2
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8
Q

possible causes of AKI

A

pre-renal
- inadequate perfusion -> not enough blood at sufficient pressure to allow filtering

renal
- cellular damage/intrinsic -> damage to the cells that make filtering mechanism possible

post-renal
- obstruction -> urine unable to drain adequately resulting in system “back up”

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9
Q

possible renal causes of AKI

A

small vessel disease
- inflammation (vasculitis)

glomerular disease
- inflammation (glomerulonephritis)

acute tubular necrosis

  • toxins
  • ischaemia

acute interstitial nephritis

intratubular obstruction

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10
Q

explain what pre-renal AKI will result in

A

due to the lack of blood flow to the kidneys, it will result in ischemia, which will result in endothelial injury. this activates vasoconstrictors and impair vasodilation, and increase leukocyte adhesion which leads to inflammation (inflammation = endothelial injury)

vasoconstriction + leukocyte adhesion will lead to capillary obstruction and continued ischemia eventually.

ischemia will lead to tubular injury, followed by desquamation of cells and then tubular obstruction.

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11
Q

explain what post-renal AKI will result in

A

system back up will cause build up in waste, ureteric and tubular pressure which compromises urinary blood flow and decrease in glomerular filtration, affecting function of kidney

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12
Q

what is radiation nephropathy

A

renal injury and loss of function caused by ionising radiation
damage to renal blood vessels resulting in ischemic insult to the kidneys
patients who develop acute radiation nephritis can progress to chronic kidney disease and subsequently end stage renal failure

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13
Q

explain the pathophysiology of radiation therapy on kidney function

A

ionising radiation of sufficient energy disrupts chemical bonds and knocks electrons out of atoms,
this generates oxygen radicals that cause prompt DNA injury within ms of irradiation
this can cause death of cancer cells and/or injury to irradiated normal tissues

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14
Q

explain the radionuclide therapy on kidney function

A

radioisotope protein conjugate filtered at glomeruli and reabsorbed by tubular epithelium. this acts as a radioemitter when it is lodged in the kidney and result in injury to renal tissue

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15
Q

what is the accepted threshold dose of photon irradiation for radiation nephropathy

A

exposure of both kidneys to a total dose of 23Gy, fractionated in 20 doses over 4 weeks

renal failure from radiation nephropathy will not occur if only one kidney is irradiated with a threshold or higher dose though radiation injury will occur in that kidney

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16
Q

explain what will CKD result in

A

systemic hypertension -> elevated intraglomerular pressure -> progressive glomerular and tubulointerstitial damage -> proteinuria

damage -> loss of nephrons -> afferent arteriole dilation and activation RAAS (to increase systemic hypertension) -> efferent arteriole constriction -> elevate intraglomerular pressure

17
Q

function of kidney

A

regulation of RBC production
regulation of BP
regulation of bone-mineral-metabolism
influence on blood pH acid-base-metabolism
excretion of metabolic waste products and water

18
Q

complications of renal failure

A

A- anemia; acidosis
B- blood pressure (hypertension); bone (mineral bone)
C- cardiovascular complications; constitutional
D- diet (nutrition)
E- electrolytes (hyperkalaemia)
F- fluid overload

19
Q

explain anemia in CKD patients

A

RBC have decreased lifespan (to 60-90 days)
reduced synthesis of erythropoietin hormone responsible for bone marrow stimulation for RBC production
uraemic toxins induced platelet dysfuntion and increases bleeding tendencies

20
Q

explain metabolic acidosis in CKD patients

A

kidneys are unable to produce enough ammonia in the PCT to excrete the endogenous acid (H+) into the urine in the form of ammonium
aggravates bone disease, protein/muscle wasting, CKD progression and mortality

21
Q

what is the constitutional symptom present in CKD

A

itch related to uremic toxic accumulation

22
Q

hyperkalaemia vs hyperphosphataemia vs hypocalcaemia

A

hyperkalaemia: reduced excretion of potassium from the kidneys
hyperphosphataemia: reduced excretion of phosphate from the kidneys

hypocalcaemia:

  • decreased intestinal calcium absorption due to low vitamin D (calcitriol) levels
  • increased calcium-phosphate binding caused by elevated serum phosphate levels
23
Q

benefits and risk of renal transplant

A

benefits:

  • improved patient survival
  • correction of metabolic abnormalities
  • avoidance of complications related to dialysis access and treatment
  • improved quality of life
  • reduced healthcare cost

risks:

  • surgical risks
  • rejection
  • cancer
  • infections
  • cardiovascular disease
  • transplant failure
  • aggravation of pre-existing comorbidities
  • toxicities of drugs
24
Q

classification of deceased donor

A

standard criteria donor (SCD)

expanded criteria donor (ECD)

  • > 60 years old
  • 50-59 years of age with any 2 criteria: terminal Cr >1.5mg/dl; death due to CVA; hypertension
  • diabetes mellitus of any age

donor after cardiac death (DCD)

25
Q

what is peritoneal dialysis

A

PD catheter is inserted permanently at the abdomen
approx 2L of the PD solution is filled and drained out of the peritoneum or abdominal cavity which is surrounded by the peritoneal membrane
peritoneal membrane then filters waste and fluids from blood into the solution
the replacing of fresh PD solution with the used PD solution is called an exchange
each exchange takes about 30 mins: inflow 10 mins, outflow 20 mins

26
Q

benefits of peritoneal dialysis

A

home based therapy
can also be performed at work or on trips but requires more careful supervision
allows more flexibility and patient ownership
family play an important role should patients not be able to perform therapy themselves
daily therapy makes it a gentler treatment, lesser food restrictions
painless with no needling involve unlike hemodialysis

27
Q

what is hemodialysis

A

performed 3 times a week, with each session lasting about 4 hours, depending on body size and medical condition
2 needles inserted into the vascular access: one to remove blood, one to return cleansed blood to body
patient is connected to the dialysis machine through a vein in the arm
blood is pumped from the body to a special filter called dialyser, which i made of tiny capillaries
blood is continuously pumped through the dialyser, where waste products and excess water are removed
blood becomes purified when the waste products diffuse from the blood across the membrane of the tiny capillaries
blood is then returned to the patient’s body through larger tubes

28
Q

hemodialysis access

A
  1. vascular catheters:
    - temporary non tunneled vascular catheter
    - tunneled vascular catheter
  2. ateriovenous fistula
    - radiocephalic
    - brachiocephalic
    - brachiobasilic
  3. ateriovenous graft
    - loop graft
    - straight graft
29
Q

drug dosing in renal impairment

A

chronic kidney disease affects renal drug elimination
- may lead to accumulation of metabolite as well as parent compound
drug absorption, bioavailability, protein binding, distribution volume and nonrenal clearance can also be altered
- increase in volume of distribution may be the result of decreased protein binding, increased tissue bind, or alteration in body composition (eg fluid overload)
- CKD may lead to alterations in the activities of uptake and efflux transporters as well as cytochrome P450 in the liver and other organs
- inappropriate dosing in renal patients can cause toxicity or ineffective therapy
- dosages of drugs cleared renally should be adjusted according to the glomerular filtration rate of the patinet
- loading doses usually do not need to be adjusted but maintenance dose will require dose reduction and lengthen dosing intervals
- in patients on dialysis, will need to consider clearance of drug by dialysis therapy