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Inflammation block > Intro to CKD > Flashcards

Intro to CKD Flashcards

1
Q

Which stages of kidney disease are represented by acute renal failure

A

Aka acute kidney injury

stages 1-3

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2
Q

Which stages of kidney disease are represented by chronic renal failure

A

aka chronic kidney disease

stages 1-5

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3
Q

How do kidneys control the production of RBCs

A

create erythropoietin to control the production of RBCs

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4
Q

How can we classify renal disease ?

A
  1. ) Pre-renal: due to problems with arterial supply (and venous drainage)
  2. )Intrinsic renal: due to problems within the renal interstitium/tubules
  3. )Post-renal: due to problems with the outflow tract of the kidney
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5
Q

Outline the renal arterial supply & venous drainage and what it may be susceptible to

A

Single blood supply and venous drainage

  1. )susceptible to pre-renal insults:
    - hypovolaemia
    - heart failure
    - vasodilation (sepsis/shock)
    - arterial dissection
  2. )susceptible to renal artery stenosis:
    - atherosclerosis
    - fibromuscular dysplasia
  3. ) Susceptible to sludging &hyperviscosity
  4. ) Susceptible to large vessel vasculitis
    - giant cell arteritis
    - Takayasu’s arteritis
  5. )Susceptible to venous thrombosis
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6
Q

What are the signs of mild and severe dehydration

A
  1. ) MILD:
    - thirst
    - dry mouth
    - fatigue
    - headache
  2. )SEVERE:
    - rapid breathing
    - rapid heartbeat
    - severe dizziness or lightheadedness
    - unconsciousness or delirium
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7
Q

What are the different types of acute renal failure that are classes as pre-renal?

A
  1. ) Absolute decrease in effective blood volume:
    - Haemorrhage
    - volume depletion
  2. )Relative decrease in blood volume (ineffective arterial volume)
    - congestive heart failure
    - decompensated liver cirrhosis
  3. )Arterial occlusion or stenosis of renal artery
  4. ) Haemodynamic form:(can cause serious problems when coupled with dehydration)
    - NSAIDs
    - ACE inhibitors or angiotensin II receptor antagonists in renal artery stenosis of congestive heart failure
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8
Q

What are the different types of acute renal failure that are classes as intrinsic renal?

A
  • Vascular
  • Acute glomerulonephritis eg post infectious causes by ab to GBM
  • Acute interstitial nephritis (drug associated)
  • Acute tubular nephritis
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9
Q

What are the different types of acute renal failure that are classed as post-renal?

A

Obstruction of collecting system or extrarenal drainage

  1. )Bladder-outlet obstruction
    - Bilateral ureteral obstruction
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10
Q

What are the different types & causes of acute tubular nephritis

A

1.) Ischaemic
2.) Nephrotoxic:
can be a.) exogenous:
-abx(gentamacin)
-radio constrast agents
-Cisplatin
b.)Endogenous:
-Intratubular pigments (myeloma)
-Intratubular crystals (uric acid, oxalate)

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11
Q

State the indications for when to have a renal biopsy

A
  • Progressive or unexplained renal impairment regardless of urine sediment
  • Nephrotic and diffuse nephritic syndrome
  • Significant proteinuria with normal BP
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12
Q

State the contra-indications for when to have a renal biopsy

A
  • No likely change in management
  • Severe co-morbidity
  • Small kidneys
  • Uncontrolled BP or coagulopathy
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13
Q

Which kidney do we usually perform a renal biopsy on?

A

left

This is a local anaesthetic procedure, we put some locally in their back with ultrasound guidance

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14
Q

Outline the pre/intra-renal pathology

A
  • The Bowman’s capsule& glomerulus depend on regulated BP to maintain health of ‘sieve’ & GFR
  • Can be overwhelmed by severe sudden hypertension
  • Susceptible to scarring of the sieve with long term hypertension
  • Susceptible to injury from drugs that affect afferent and efferent BP ( ACE inhibitors & NSAIDs)
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15
Q

Which drugs affect the afferent arteriole in renal physiology

A

you are going to the glomeruli so more blood flow via vasodilation will mean more gets filtered

  1. )Vasodilation:
    - Prostaglandins= increased GFR
  2. )Vasoconstriction
    - NSAIDs=decreased GFR
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16
Q

Which drugs affect the efferent arteriole in renal physiology

A

you are coming from the glomeruli so more blood flow via vasodilation will mean more leaves (opposite to afferent)
(think of it as to do with urine and water retention RAAS system)
1.) Vasodilation:
-ACE inhibitors/angiotensin receptor blockers
2.) Vasoconstriction:
-Angiotensin II=increased GFR

NB: ACE/ARB inhibition can be harmful acutely, but beneficial long term

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17
Q

Outline the intra-renal pathology (glomeruli)

A
  • Requirement for intricate network of defined pore size and high surface area
  • Can be injured by sludging and embedding of immune complexes
  • SLE
  • Cryoglubulinaemia
  • Other immune complex GNs
  • Microorganisms
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18
Q

Outline the glomerular pathology (GN)

A
  • Limited capacity for healing
  • Tends to scar easily
  • Different histological patterns
  • severe injury leads to rupture and thrombosis in the Bowman’s capsule i.e crescent formation
  • loss of function & heavy proteinuria
  • If insidious then proteinuria may be only feature
  • glomerular injury from systemic disease is difficult to recover from
  • Often the aim is to preserve the less damaged glomeruli
19
Q

Outline the intra-renal (tubular) pathology

A

1.)Narrow convoluted tubular system with significant changes in osmolality and pH
-susceptible to precipitation of solutes and luminal obstruction (light chain disease; uric acid; myoglobin(rhabdomyolysis)
2.)Highly metabolically active with a dependence on oxygen supply
susceptible to acute tubular necrosis:
-hypoperfusion (pre-renal)
-tubular toxins
-aminoglycosides
-cisplatin
-ethylene glycol
-IV contrast

20
Q

Outline the clinical pattern seen in tubular pathology

A

-Most commonly ATN (or ATI)
-More robust than glomeruli
-Better capacity for recovery
clinical pattern:
-usually loss of tubular function (eg failure to absorb filtered solute esp Na) with an AKI
-oliguria/anuria
-recovery usually accompanied by polyuria &saluria
-scarring can’t be recovered by dehydration can

21
Q

Outline the pathology of the interstitum/vascular

A

-Large volume of interstitial tissue with intricate blood supply
Susceptible to inflammatory infilitration (tubulo-interstitial nephritis)
-Drugs(allergic-like reaction)
-Infections(pyelonephritis, viral eg CMV,HIV; fungal/parasitic)
-Autoimmune(SLE, Sjogren, Sarcoid)
-Alloimmune (transplant rejection)
-Idiopathic

22
Q

Outline the characteristics of acute interstitial nephritis

A
  • Important to establish cause (often drug related)

- steroids can aid recovery in some cases

23
Q

Outline the characteristics of chronic interstitial nephritis

A
  • insidious in onset
  • Less inflammation, more scarring
  • important to establish cause(but frequently idiopathic)
  • steroids unhelpful
  • less capacity for recovery
24
Q

Outline the outflow tract in renal physiology & what it may be susceptible to

A 
Single drainage pathway
susceptible to obstruction:
1.)URETERIC:
-stones
-retroperitoneal fibrosis
-gynae malignancy
2.)BLADDER OUTFLOW:
-stones 
-bladder cancer
-Prostatic (BPH/cancer) 
3.) URETHRAL:
-stones
-urethral stricture
25
Q

What is hydronephrosis

A
  • Swelling of a kidney due to a build-up of urine.
  • When urine cannot drain out from the kidney to the bladder from a blockage or obstruction. -Can occur in one or both kidneys.
  • The back pressure on your kidneys(pushing back on the parenchyma-if for long enough the parenchyma can get thinner and you lose kidney function) can cause this
26
Q

How is the GFR affected with ageing

A

Declines

27
Q

What can be the consequence of AKI without recovery

A

-Severe sepsis

28
Q

How can we measure kidney function

A
  • GFR=approx percentage kidney function
  • Insulin clearance
  • Isotopic EDTA-GFR
  • Creatinine

-Creatinine clearance
(UCr x V)/PCr
24 hr urine collections
overestimates GFR by 10-40%

-GFR estimating equations

29
Q

Outline the characteristics of urea

  • source
  • constancy of production
  • renal handling
  • value as marker of GFR
  • correlation with uraemic symptoms
A
  1. ) Source=hepatic breakdown of protein: endogenous or exogenous (NB meat, GI bleed; malnutrition)
  2. ) Constancy of production=variable
  3. ) Renal handling= completely filtered; significant tubular reabsorption
  4. ) value as a marker of GFR=modest
  5. ) Correlation with uraemic symptoms=good
30
Q

Outline the characteristics of creatinine

  • source
  • constancy of production
  • renal handling
  • value as marker of GFR
  • correlation with uraemic symptoms
A
  1. )Source= non-enzymatic hydrolysis of creatine released from skeletal muscle
  2. )constancy of production= more stable
  3. ) renal handling=completely filtered; some tubular secretion (up to 20% clearance)
  4. ) value as a marker of GFR= good in steady state
  5. ) correlation with uraemic symptoms=poor
31
Q

State the functions of the kidneys

A
  • regulation of water and electrolyte balance
  • Excretion of metabolic waste (H+ as NH4+)
  • Excretion of bioactive substances that affect body function
  • Regulation of arterial blood pressure
  • Regulation of RBC production
  • Regulation of vitamin D production
  • Gluconeogenesis
32
Q

Outline management of CKD

A
  • specific disease management
  • water balance, BP & cardiac risk factors
  • electrolytes
  • acid/base balance
  • erythropoesis
  • Bone management
  • Assessment of uraemic symptoms
  • planning & initiation of renal replacement therapy or conservative management
33
Q

at what level of an estimated GFR should an immediate referral be carried out

A

<15ml/min/1.73m^2

34
Q

Outline the specific disease management for renal co-morbidities

A
  1. ) Immunosuppression eg lupus nephritis
  2. )Chemotherapy eg Myeloma
  3. )Blood sugar control i.e diabetes
35
Q

Outline the BP& volume management

A

-Assess fluid status: weight, JVP, oedema
-Correct volume then BP(i.e if overloaded start with diuretic)
-Use ACEI or A2B in almost all cases for BP control
-Targets-130/80 probs consensus in CKD
(see lecture for list of drugs)

36
Q

Outline the characteristics of erythropoetin

A
  • Synthesised by interstital fibroblasts in the kidney
  • Stimulated by low oxygen tension
  • HIF1(alpha) protein degraded in normoxia
  • HIF complex stimulates transcription of epo genes
  • Epo binds to receptors on erythroid precursors
37
Q

Outline renal anaemia management

A
  • Check Hb and ferritin regularly
  • Check B12(>187) and folate(>3.1)
  • Iron stores need to be super-normal ( Tsats>30%; ferritin >500 (normally 22-275))
  • Use epo (often earlier in diabetics). This stimulates the body to produce RBCs
  • Target Hb 100-115g/l (normal 130-170)
  • Some pts may benefit from higher Hb
38
Q

How can renal impairment affect the bones

A

-Normally your kidneys should make active vit D & rid the body of phosphate

  1. )FGF23 is made in your bones& normally makes your kidneys get rid of more phosphate but they get less responsive to this due to kidney failure
    - your kidneys excrete FGF23
  2. ) Renal disease results in high PTH
    - main triggers are low calcium (low vit D) and high phosphate (poor renal clearance)
39
Q

What is calciphylaxis?

A
  • A result of high calcium and phosphate
  • Very painful
  • High mortality (sepsis)
40
Q

What happens if calcium and phosphate are put in your blood vessels

A
  • ‘chalk pipes’

- calcium phosphate pipes

41
Q

Outline CKD-MBD management

A
  • Previously known as mineral bone disease
  • Mineral and bone disorder in chronic kidney disease
  • reduce dietary phosphate
  • bind dietary phosphate with drugs then excreted in faeces (calcium containing eg calcichew; non-calcium containing eg sevelemer)
  • Restore active vitamin D eg with alfacalcidol to suppress PTH
  • Consider calcimimetic eg cinacalcet
  • parathyroidectomy if not winning
  • Identify target levels
42
Q

Outline acid-base management in CKD and the benefits of it

A
  • Aim for serum bicarbonate>20
  • Use NaHCO3 tablets (your bones will dissolve if your blood is too acidic so these tablets are needed)
  • Theoretical benefit for bones and CV system
  • Proven benefit to slow CKD progression and improve nutritional status
43
Q

Explore the different options for renal replacement therapy

A
  1. ) Pre-emptive living transplantation
  2. )Deceased donor transplantation
  3. ) Transplant work-up required during advanced CKD(anasthetic,anatomy,immunology)
  4. )Haemodialysis
    - AV fistula created in good time
    - HD can be done at home or self care in hospital
    - should be as close to home as possible (‘satellite’)
  5. )Peritoneal dialysis
    - high level of independence
    - should be continued for>5 years
  6. ) conservative management
    - RRT may not prolong life and may severely impact on the quality of remaining life

Inflammation block (27 decks)

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