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Urinary > AKI & CKD > Flashcards

AKI & CKD Flashcards

1
Q

What are the 3/4 major causes of CKD?

A
  • diabetes
  • hypertension
  • glomerular nephritis
  • adult polycystic kidney disease
    also infection, alports and vascular changes like atherosclerosis, in many cases the cause is unknown
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2
Q

What are the 4 major causes of AKI?

A
  • infections/ sepsis
  • inflammatory conditions
  • hypovolaemia (inc heart failure)
  • nephrotoxins
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3
Q

What are the presentations of CKD?

A
  • Abnormal urine or blood results (but asymptomatic)
  • fatigue/ malaise
  • nausea, vomiting
  • headache
  • loss of appetite and weight
  • acute illness/ recent infection
  • ankle swelling
  • haematuria and nocturia
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4
Q

How may AKI present?

A
  • preceeing illness/ infection
  • history of volume depletion
  • fatigue/ malaise
  • Nausia and vomiting
  • side effect of a drug
  • loin/ suprapubic pain
  • changes to urine amount and colour
  • dysuria
  • fever
  • odema (rasied JVP, ankle swelling)
  • fluid depleted (postural hypotension)
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5
Q

Define acute kidney injury

A

a clinical syndrome characterised by abrupt decline in actual GFR, with upset of ECF volumes, U&Es and acid base homeostasis

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6
Q

Why can eGFR not be used in AKI?

A

In AKI creatinine increases slowly, but actual GFR has changed quickly, since creatinine is used to calculate eGFR, eGFR wont change till later on

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7
Q

How can AKI be diagnosed? (3)

A
  • Urine volume of <0.5ml/kg/hr for 6hrs
  • increase in serum creatinine by >26.5mmol/l over 48 hrs
  • increase in serum creatinine by >1.5 times baseline in 7days
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8
Q

What are the most common causes of AKIs in developed vs undeveloped countries?

A

In developed countries its generally hospital aquired and seen in older ppl, most common causes are dehydration and hypovolaemia.
In poorly developed countries its seen more in younger ppl, coming in with infections causing diarrhoea and vomiting or toxins from bites.

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9
Q

What causes pre renal failure?

A

Reduced blood flow- blood loss (hypovolaemia), systemic vasodilation (sepsis, cirrhosis, anaphylaxis) and cardiac failure

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10
Q

What drugs may precipitate pre renal AKI and why?

A

NSAIDS and ACEi because these inhibit glomerulotubular feedback meaning the EA and AA cannot vasodilate/ constrict to maintain GFR

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11
Q

Below what systolic pressure does autoregulation of GFR fail?

A

<80mmHg- if BP drops below this you get very sharp decline in GFR

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12
Q

Why is serum osmolarity very high in prerenal AKI but not renal AKI?

A

Because in prerenal your nephrons are still intact so work very hard to recover salt to try and recover as much water as possible. But in renal AKI you have some kind of cell damage so they cant recover the salt and so water.

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13
Q

What is acute tubular necrosis and what causes it?

A

If under perfusion goes too far (usually due to ischamia, nephrotoxins, sepsis ect). The cells are not actually necrosed but very damaged meaning you cant recover salt or excrete excess water.

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14
Q

Why does aggressive fluid resuscitation cause fluid overload when someone has ATN?

A

Because the nephrons cannot expell this excess water any more as the cells are basically non functional- meaning urine is excreted at a constant rate and this cannot be increased.

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15
Q

Where in the nephron is ATN most likely to occur?

A

PCT and TAL as this is where energy demand is highest

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16
Q

Nephrotoxins damage epithelial cells of the nephrons, and can cause (but usually only contribute) to renal AKI. Give some examples of nephrotoxins

A
  • myoglobin, urate and bilirubin (endogenous)
  • endotoxins
  • xray contrast
  • drugs (many- NSAIDs, gentamicin ect)
  • Poisons (eg antifreeze)
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17
Q

What is rhabdomyolysis, when does it occur and how does it lead to AKI?

A

It is muscle necrosis, often occuring in crush injuries, drug users (unconscious-> dont move-> muscle crushed and dies) and elderly (fall and cant get up).
The dying muscle cells release myoglobin, which is nephrotoxic.

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18
Q

What colour will the myoglobin (released in rhabdomyolysis) turn urine?

A

back/ cocacola coloured

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19
Q

What causes acute interstital nephritis and how does this cause renal AKI?

A

Antibiotics, NSAIDS, PPIs ect

It is not the drug/ toxin directly causing nephron damage but the inflammatory response it triggers.

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20
Q

Other than ATN and acute interstitial nephritis, what else can cause renal AKI?

A
  • intratubular obstruction
  • glomerular disease (any glomerular nephropathy)
  • Small vessel diseases affecting the AA and EA- vasculitis, emboli
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21
Q

How do you get post renal AKI?

A

obstruction–> rise in intraluminal pressure-> dilation of renal pelvis (hydronephrosis)-> rise in bowmans capsule pressure–> drop in net filtration pressure–> drop in GF
Both kidneys need to be affected/ only one

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22
Q

What can cause obsturctions leading to post renal AKI?

A
  • Stuff in the lumen (stones, tumours)
  • Stuff in the wall (usually cause CKD as slower process)
  • pressure from outside (enlarged prostate, tumours, AAA, ligation or ureter, trauma )
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23
Q

Why does AKI often result in metabolic acidosis?

A

less reabsorbtion and creation of bicarbonate

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24
Q

What investigations should be done when AKI is suspected?

A
  • bloods
  • urine dipstick (blood/protein suggest intrinsic renal cause)
  • urine culture if leucocytes ++
  • CXR to look for fluid overload and infection
  • USS if obstruction suspected
  • Kidney biopsy if pre and post renal AKI ruled out or confident ATN diagnosis cant be made
25
Q

How should AKI be treated?

A
  • treat any volume overload w/ fluid restriction
  • give fluids if prerenal cause
  • treat any hyperkalaemia with calcium gluconate, change diuretics, give dextrose and insulin, sodium bicarbonate, B2 agonists ect
  • support acidosis (NaHCO3 not usually given as it may contribute to fluid overload, the acidosis usually reverses as the hyperkalaemia reverses)
  • dialysis if the above doesnt work
26
Q

When is dialysis implicated in AKI? (5)

A
  • K+ high and refractory to treatment
  • metabolic acidosis not fixing
  • fluid overload refractory to treatment
  • pericarditis, reduced consciousness ect due to uraemia
  • a dialyzable nephrotoxin is the cause (aspirin overdose, ethylene glycol ect)
27
Q

What is the prognosis for AKI?

A

30-80% mortality

if they do recover it takes 2-3 weeks

28
Q

How can AKI be prevented?

A
  • identify risk factors (old age, ckd, heart disease, diabetes, cancer, dehydration, sepsis, burns, trauma, GN, nephrotoxins)
  • monitor at risk pts closely
  • ensure theyre well hydrated
  • avoid nephrotoxins
29
Q

Define chronic kidney disease

A

the irreversible and sometimes progressive loss of renal function over a period of months to years

30
Q

What genetic mutation causes adult polycystic disease?(APCKD)

A

Mutations in PKD1 or 2 genes (auto dominant)

31
Q

What secondary complications can the cysts cause in APCKD

A

Pain, bleeding, infections, stones

32
Q

How is APCKD diagnosed?

A

USS or a genetic test

33
Q

How is CKD staged?

A

The stage depends on how low GFR has dropped and also how much albumin is present in urine

34
Q

How is CKD investigated?

A
  • Bloods (U&E, FBC, Iron, PTH, LFT, bone biochem, CRP)
  • Find cause: complement levels and autoantibody screening, anti- neutrophil cystoplasmic antibody (ANCA vasculitis) ect
  • USS for size of kidney and hydronephrosis
  • Kidney biposy is kidney isn’t enlarged
  • CT, MRI to look for stones or masses
  • MR angiogram to look for renal artery stenosis
35
Q

Why do 85% of ppl with CKD have hypertension and odema?

A

GFR has dropped so you filter much less so you cannot excrete as much, if you cant excrete excess fluid then it builds up as odema and also causes hypertension

36
Q

Why do ppl with CDK get nocturia?

A

They loose their response to ADH and so their ability to dilute urine. They actually have polyuria but tend to present with nocturia.

37
Q

How do you treat hypertension/ odema as a result of CKD?

A
  • Loop or thiazide diuretics (avoid K+ sparing due to risk of hyperkalaemia)
  • fluid restriction
  • Antihypertensives- Ca2+ channel blockers or ACEi
38
Q

Why do ppl with CKD get acidosis? How do you treat it?

A

Reduced ability to reabsorb and create bicarbonate.

Treat w/ oral sodium bicarbonate tablets

39
Q

Why do ppl with CKD get hyperkalaemia?

A

If GFR below 20ml/min, filtrate flow slows, decreased distal delivery of Na+, so decreased secretion of K+. Also acidosis leads to hyperkalaemia.

40
Q

How is hyperkalaemia treated in CKD?

A
  • Thiazide or loop diuretics
  • Stop ACEi or angiotensin 2 inhibitors
  • Avoid food (banana) and drugs (trimethoprim) which increase K+
41
Q

Why can you get puritis with CKD?

A

less filtration= less removal of waste products eg urea, uraemia causes itching as well as confusion, headaches, nausia, vomiting

42
Q

How does CKD cause anaemia?

A
  • Increased hepcidin levels= less iron absorption
  • loss of appetite= less iron intake
  • loss of EPO production in kidneys
  • blood loss, meds like ACEi, bone disorders, uraemia also suppresses bone marrow
43
Q

What effect will CKD have on drug metabolism?

A

It may reduce its elimination rate. It may also increase drug sensitivity even if elimination isnt affected. This means drug dose changes are often needed.

44
Q

How do you treat anaemia in CKD?

A
  • Check iron levels and replace with oral or IV iron
  • When iron stores are ok, recheck Hb. If they’re still anaemia give EPO stimulating agent
  • Aim for Hb of 100-120 g/L (slightly low)
45
Q

Why does CKD lead to mineral bone disease? What 3 effects are seen as a result of this bone disease?

A

It leads to low vit D and high phosphate, both of which decrease Ca2+. This leads to hyperparathyoidism, however the high Ca2+ reduces the sensitivity of the PTH. Overall this leads to:

  • Erosion of terminal phalanges
  • Rugger jersey spine
  • Calcification of non bone structures because the high phosphate can complex with the calcium and calcify joints (esp shoulder) and blood vessels
46
Q

How is mineral bone disease managed in CKD?

A
  • reduce phosphate intake
  • phosphate binders
  • 1 a calcidol
  • give vit D
47
Q

List the complications of CKD

A
  • hypertension and odema
  • acidosis
  • hyperkalaemia
  • accumulation of waste products
  • altered drug metabolism
  • anaemia
  • mineral bone disease
48
Q

How is CKD generally managed?

A
  • lifestyle changes
  • stop smoking and loose weight
  • increase exersize
  • stop PPIs and NSAIDs
  • control diabetes and hypertension
  • control protein urea with ACEi
  • control lipids (statins)
49
Q

When is renal replacement therapy indicated?

A

When GFR <15ml/min and youve hit endstage renal failure

50
Q

What are the features of ESRD/ dialysis?

A 
tiredness
insomnia
difficult concentrating 
volume overload (SOB, odema)
restless legs and cramps
puritus
sexual dysfunction 
infections
51
Q

How often do you need to go in for haemodialysis?

A

3 times a week for 4 hrs

52
Q

What are the adv and disadv for haemodialysis?

A

ADV: less personal responsibility, days off
DISADV: travel and waiting time, tied down to dialysis time and location, big restrictions on food and fluid intake, 19 pills per day avg

53
Q

When can haemodialysis not be done?

A
  • failed vascular access
  • heart failure
  • coagulopathy
54
Q

What are the 2 types of peritoneal dialysis?

A

CAPD- you carry bags with you and have to change them daily

APD- overnight dialysis

55
Q

What are the ADV and DISAVD of peritoneal dialysis?

A

ADV: self sufficient, less fluid and food restrictions, travel is easier, initially preserves renal function better
DISADV: frequent daily changes and over night, your responsbility

56
Q

When cant you do peritoneal dialysis?

A

failure of peritoneal membrane, adhesions, obese or very muscular

57
Q

What are the complications of peritoneal dialysis?

A

peritonitis, ultrafiltration failure, leaks, hernia development

58
Q

What is the ideal renal replacement therapy and why?

A

TRANSPLANT- reduces morbidity and mortality, better QoL. But operation and immunosurpression risks, also the meds can give you hypertension and diabetes.

Urinary (9 decks)

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