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HSC2008 Pathophysiology & Pharmacology > Renal System > Flashcards

Renal System Flashcards

1
Q

How are the control of fluid balance regulated?

A

Thirst mechanism

Hormone
- ADH (increase ADH = decrease H20 = > reabsorption; decrease ADH = increase H20 = < reabsorption)
- Aldosterone (increase H20 = decrease Aldo.)

Atrial Natriuretic Peptide

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2
Q

What are the mechanical causes of edema?

A

Increase capillary hydrostatic pressure
- high BP, pregnancy

Decrease plasma osmotic pressure due to loss of plasma protein
- loss of albumin lead to decrease plasma osmotic pressure

Obstruction of lymphatic system
- tumor

Increase capillary permeability
- due to inflammatory response (V.D)

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3
Q

What are the causes of fluid deficits/ dehydration?

A

Can be due to both inadequate intake / excessive loss OR both
- losses are more common & affects the extracellular compartment

  • vomiting / diarrhea
  • excessive sweating (decrease Na+ & H20)
  • diabetic ketoacidosis (glucose in urine)
  • insufficient fluid intake
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4
Q

What is the definition of Acute Kidney Injury (AKI)?

A

Increase in SCr more than or equals to 0.3mg/dL (more than or equals to 26.5) within 48hr OR

Increase in SCr more than or equals to 1.5x baseline, which is known to / presumed to occur within previous 7 days OR

Urine volume less than 0.5ml/kg/hr for 6 hours

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5
Q

What are the types of AKI?

A
  • Non-oliguric AKI - AKI with urine output >400ml/day
  • Oliguria - <400ml/day of urine
  • Anuria - <100ml/day of urine
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6
Q

What are the stages of AKI (KDIGO staging)?

A

Stage 1
- SCr 1.5-1.9x baseline OR more than 26 milli mol/L
- Urine output <0.5ml/kg/hr for 6-12 hrs

Stage 2
- SCr 2-2.9x baseline
- Urine output <0.5ml/kg/hr for more than or equals to 12hrs

Stage 3
- SCr higher than 3x baseline OR initiation of RRT OR patients younger than 18y/o with eGFR <35ml/min/1.73m2

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7
Q

What is the definition of CKD?

A

Abnormalities in structure or function of the kidney for > 3 months with implications for health

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8
Q

What are the criteria for CKD?

A

Presence of albuminuria
- A1 - normal to mild increase; <30mg/g; <3mg/mmol
- A2 - moderately increased; 30-300mg/g; 3-30mg/mmol
- A3 - severely increased; >300mg/g; >30mg/mmol

GFR - <60ml/min/1.73m2; category G3a - 5
- G3a - 45-59ml/min (mildly to moderately decreased)
- G3b - 30-44ml/min (moderately to severely decreased)
- G4 - 15-29ml/min (severely decreased)
- G5 - <15ml/min (kidney failure)

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9
Q

What are the possible kidney injury areas?

A

Pre-renal - inadequate perfusion resulting in not enough blood to sustain pressure to allow filtering

Renal - cellular / intrinsic damage which makes filtering mechanism not possible

Post-renal - obstruction of ureter leading to issues with urine drainage (system backed up)

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10
Q

What are the 5 renal causes?

A

Small vessel disease - inflammation (vasculitis)
Glomerular disease - inflammation to glomeruli
Acute tubular necrosis - toxins / ischemia
Acute interstitial nephritis
Intratubular Obstruction

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11
Q

What are the sequence of events that occur during AKI?

A

Ischemia -> initiation of cell injury (tubular obstruction) -> extension (coagulopathy & inflammation) -> maintenance (proliferation, migration, differentiation) -> recovery

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12
Q

What is the pathophysiology of post-renal AKI?

A

Back-up of system leads to increase ureteric & tubular pressure

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13
Q

What is the definition of Radiation Nephropathy?

A

Renal injury & loss of function caused by ionising radiation

  • Acute radiation nephritis can progress to CKD & subsequently ESRF
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14
Q

What is the accepted threshold dose of photon irradiation that can cause radiation nephropathy?

A

Exposure of both kidney to a total dose of 23Gy, fractioned in 20 doses over 4 weeks

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15
Q

What is the criteria to be met for CKD to occur due to radiation nephropathy?

A
  • CKD would not occur if irradiated volume is <30% of both kidneys
  • Constant exposure to low radiation can cause kidney injury after many years of follow up
  • Renal failure from radiation nephropathy would not occur if only 1 kidney is irradiated with a threshold / higher dose BUT radiation injury will still occur
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16
Q

What are the clinical presentation of external beam radiation?

A

Acute radiation nephropathy - 6-12 months

Chronic radiation nephropathy - more than or equals to 18 months

Malignant hypertension - 12-18 months

Benign hypertension - more than or equals to 18 months

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17
Q

What is the definition of Contrast Induced Nephropathy (CIN)?

A

A generally reversible form of AKI that occurs soon after administering radio contrast media

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18
Q

What is the typical presentation of CIN?

A

Acute decline in renal function that occurs 48-72 hrs (SCr peaks at 3-5 days) after IV injection of contrast medium w/o an alternative explanation

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19
Q

What are the risks of CIN?

A

Patient related risks
- CKD
- Diabetes mellitus
- Intravascular volume depletion
- Reduced cardiac output
- Concomitant nephrotoxins

Procedure related risks
- Increased dose of radiocontrast
- Multiple procedures within 72 hours
- Intra-arterial administration
- Type of radio contrast

20
Q

What are the preventive measures of CIN?

A

eGFR >/= 60ml/min - very low risk (avoid dehydration)

eGFR 45-59ml/min - low risk (preventive measure for patients receiving IA contrast media

eGFR <45ml/min - moderate risk (IV hydration)

eGFR <30ml/min - high risk (IV hydration)

21
Q

What is the most prevalent cause of CKD?

A
  1. Diabetes
  2. HBP
  3. Others
22
Q

Describe the pathophysiology of CKD

A

Systemic hypertension -> increase intraglomerular pressure -> proteinuria -> progressive glomerular & tubulointerstitial damage -> loss of nephrons -> RAAS activated -> AA dilation & EA constriction -> increase intraglomerular pressure

To prevent CKD progression - prescribe ACEi, angiotensin receptor blockers to decrease proteinuria

23
Q

What are the areas of evaluation to diagnose renal failure?

A

Checking history - family, drug, past medical history, symptoms of complications of renal failure

Physical examination - swelling, signs of uraemia, distended bladder

Investigation - blood, urine, imaging, renal biopsy

24
Q

What are the functions of kidney?

A
  • Regulation of RBC production
  • Regulation of BP
  • Acid-base metabolism
  • Regulation of bone-mineral metabolism (Ca2+)
  • excretion of metabolites waste products & water
25
Q

What are the complications of renal failure?

A

Acidosis
Anemia
Blood pressure
Bone (mineral bone)
Cardiovascular complications
Constitutional factos
Diet
Electrolyte imbalance (Hyperkalemia)
Fluid overload

26
Q

How does kidney failure lead to anemia?

A
  • Kidney fail to reduce erythropoietin hormone -> affect bone marrow stimulation for RBC production
  • RBC lifespan decrease (60-90 days)
  • Uraemic toxins induce platelet dysfunction & increase bleeding tendency
  • Treatment - SC erythropoietin injections; iron supplement
27
Q

How does kidney failure lead to metabolic acidosis?

A

Kidney unable to prices enough ammonia in Proxima tubules to excrete acid into urine -> aggravated bone disease, protein/muscle wasting, CKD progression

Treatment - sodium bicarbonate to reduce acid level in blood -> reduce CKD progression rate

28
Q

How does kidney failure lead to blood pressure complications?

A

Damaged kidney cannot excrete waste & fluid which lead to a buildup in the body (increases BP)

RA system activated to maintain BP to to sustain GFR

Treatment
- Low salt diet
- Medications - ACEi, beta blocker
- Calcium channel blockers
- Diuretic

29
Q

How does kidney failure lead to mineral bone disease?

A

Decrease in GFR -> low Vit. D activity & high PO43- ->low Ca2+ -> high PTH -> increase bone reabsorption -> increase Ca2+ & PO43- -> increase soft tissue calcification

  • Increase bone reabsorption lead to increase risk of fractures
  • Increase soft tissue calcification -> CVS risk, endocrine failure, tendon rupture
  • Treatment - supply calciferol, restrict PO43-, PO43- binders, dialysis
30
Q

How does kidney failure lead to electrolyte complications?

A

Hyperkalemia
- reduce excretion from kidney due to EA constriction
- require low K+ diet

Hyperphosphatemia
- reduce excretion from kidney
- require phosphate binder to reduce absorption of phosphate

Hypocalcemia
- decrease intestinal absorption of Ca2+ due to low calcitrol levels from decrease do Vit. D activity

31
Q

Describe the transition from CKD to ESRF

A

CKD -> Stage 4 CKD (long term plan) -> Stage 4 CKD (GFR <20) -> ESRF

32
Q

What are the options for CKD & ESRF?

A
  • Peritoneal dialysis
  • Haemodialysis
  • Kidney transplant
33
Q

What is the importance of renal replacement therapy timing?

A
  1. Avoid unplanned initiation of RRT
    - might have infective complications associated with vascular catheters
    - increase morbidity
  2. Allow for timely dialysis access placement
  3. Allows transplantation referral for consideration of preemptive renal transplant
34
Q

What are the types of renal transplantation?

A
  1. Living donor renal transplant
  2. Deceased donor renal transplant
    - Standard criteria - kidney considered to be of good quality & suitable for transplantation
    - Expanded criteria - kidney considered to be of lower quality & may have higher risk of complications after transplantation
    - Donation after cardiac death
35
Q

How does dialysis work?

A
  • Fluid moves through semi-permeable membrane (dialyzer / peritoneal membrane)
  • Dialysate solution contains electrolyte level that resembles the level in the human body
36
Q

How does peritoneal dialysis work?

A
  • PD catheter is inserted permanently into the abdomen
  • ~2L of PD solution is filled into & drained out of the abdominal cavity
  • Each exchange takes ~30 minutes (10 mins inflow; 20 mins outflow); can dwell up to ~1.5-4 hrs depending on PD formed
  • Dialysis fluid consist of glucose which creates the tonicity of dialysate solution
37
Q

What are the types of PD?

A

Continuous Ambulatory PD
- dialysis exchange up to 3-4x during the day
- PD solution allowed to dwell up to 4-6 hrs in abdomen before draining
- either ‘cap-up’ at night or have a night dwell

Automated PD
- performed using a cycler when patient sleep at night
- attached to the machine for ~8-10 hrs
- Continuous cycling PD - dialysis with day dwell
- Intermittent PD - dialysis with ‘day dry’

38
Q

What are the complications of PD?

A

Infective complications - PD peritonitis, exit site infection, tunnel infection

Non-infective complications
- Metabolic - hyperglycaemia (due to fluid containing glucose), insulin resistance, weight gain, dyslipidaemia
- Mechanical - hernias, leaks, catheter obstruction, abdominal pain
- Membrane complications - encapsulating peritoneal sclerosis, membrane failure

39
Q

How does Haemodialysis work?

A
  • Performed up to 3-4x a week with each session lasting ~4hrs depending on patient size & medical condition
  • Method - 2 needles inserted into vascular access
  • Patient is connected via tubing to the dialysis machine through a vein in the arm
40
Q

What are the different vascular access to haemodialysis?

A
  1. Vascular catheters - temporary non-tunnelled vs tunneled
  2. Arteriovenous Fistua (AVF)
    - Brachiobasilic
    - Brachiocephalic
    - Radiocephalic
  3. Arteriovenous Graft - looped vs straight
41
Q

What are the complications of vascular catheters?

A
  • Catheter related bloodstream infection
  • Exit site/tunnel tract infection
  • Central Venous stenosis
  • Right atrium / mural thrombosis
  • Occlusion - blood clot/ fibrin sheath/ kink
42
Q

What are the complications of AVF / graft?

A

Non-infection complications
- High outflow to the heart -> cardiac failure
- Steal syndrome - inadequate blood flow to the hands & finger
- Central vein stenosis
- Thrombosis
- Primary failure

43
Q

What are the types of HD?

A

Intermittent HD
- 3 times a week in centre for ~4 hrs

Nocturnal HD
- 3 times a week in centre for ~6-8 hrs

44
Q

What are the interdialytic complications?

A
  • BP - hyper / hypo
  • Cardiac arrhythmia - due to electrolyte shift
  • Dialysis disequilibrium syndrome - decrease urea in blood ->fluid shift into brain -> cerebral edema
  • Air embolism
  • Haemolysis
  • Muscle cramp
  • Dialyser reaction
45
Q

What are the implications of drug dosing for renal impairment?

A
  • Fluid accumulation affect Vd of drug (lower Vd)
  • Increase Vd may be a result to decrease protein binding
  • May lead to non renal clearance of medication

Dosing should be adjusted to GFR of patient; adjust maintenance dose
- reduce dosing & lengthen dosing intervals

46
Q

What are the types of renal drug dosing?

A
  • Diuretics - to increase urine output
  • Antimicrobials - different types of antibiotics
  • Oral hypoglycemic agents - to manage blood glucose levels in patients with type II diabetes
  • Analgesics - to manage pain

HSC2008 Pathophysiology & Pharmacology (4 decks)

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