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Urinary > 10 > Flashcards

10 Flashcards

1
Q

What is Acute Kidney injury?

A
  • decline in the GFR that occurs during a short period of time
  • decline in GFR is currently measured by an increase in serum creatinine ALTHOUGH creatinine is not an ideal marker
  • an acute change in renal function in comparison to CKD
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2
Q

What is the NICE guideline for detecting acute kidney injury?

A
  • rise in serum creatinine of 26 or greater within 48 hours
  • a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  • fall in urine output to less than 0.5ml/kg/hour for more than 6 hours in adults and more than 8 hours in children and young people
  • 25% or greater fall in eGFR in children and young people within the past 7 days
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3
Q

What is anuria?

A

-usually indicates a blockage of urine flow or very severe damage to the kidneys, and is a less common form of AKI

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4
Q

What is oliguria?

A
  • diagnosed by examining the obligatory amount of cellular waste products that need to be excreted from an average sized individual
  • approximates to 600mOsmol/day
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5
Q

What is uraemia?

A
  • defined as the clinical signs and symptoms of kidney failure
  • results in a lack of secretory as well as excretory function in the kidneys
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6
Q

How do you measure renal function?

A
  • creatinine endogenous product in muscle cells at a constant rate
  • creatinine excretion rate of excretion is relatively fixed
  • MDRD formula used to give eGFR
  • rise in creatinine rate means kidney function has dropped
  • normal creatinine: 100-120 mmol/L
  • eGFR >90ml/min

See session 10 AKI slide 12-15

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7
Q

What is CKD?

A
  • chronic kidney disease is a progressive loss of function over a period of months or years
  • functioning renal tissue is replaced by ECM and gives rise to glomerulosclerosis and tubular interstitial fibrosis
  • progressive loss of both excretory and hormone functions of kidney
  • development of proteinuria and systemic hypertension
  • symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing reduced appetite

See session 10 CKD slide 9-10

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8
Q

List the stages of CKD

A
  • CKD 1: eGFR > 90, with proteinuria/haematuria
  • CKD 2: eGFR > 60, with proteinuria/haematuria
  • CKD 3: eGFR 30-60 (P)
  • CKD 4: eGFR 30-15
  • CKD 5: eGFR <15
  • end stage renal failure ESRF

See session 10 CKD slide 11

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9
Q

What are the causes of CKD?

A
  • diabetes nephropathy
  • hypertension
  • glomerulonephritis
  • UTI
  • polycystic kidney disease
  • renal vascular disease
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10
Q

What is the staging of AKI?

A

-stage 1: creatinine is 1.5-1.9 times the baseline
-stage 2: creatinine is 2.0-2.9 times the baseline
Stage 3: creatinine is 3.0 times the baseline

See session 10 AKI slide 19-24

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11
Q

How does pre-renal disease cause AKI?

A
  • most common cause of AKI
  • defined as decreased renal perfusion
  • if BP falls beneath a threshold level, the kidney is unable to maintain blood flow and the GFR declines
  • kidneys themselves are not yet impaired, just unable to maintain blood flow and hence GFR
  • pre-renal failure is reversible
  • commonest cause: Acute Tubular Injury
  • if not treated kidney cells are eventually starved of oxygen
  • PCT are at most risk since they are less well perfused
  • if pre-renal AKI is sustained for long enough intrinsic ATI can occur
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12
Q

What are some causes of hypo-perfusion in regards to AKI?

A
  • septic shock
  • hypovolaemic shock
  • cardiogenic shock
  • medications
  • AKI marker picks up pt’s with CVS disease
  • AKI is not a marker of kidney disease
  • cannot maintain perfusion to kidneys due to these types of shocks

See session 10 AKI slide 26-28

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13
Q

What renal problems can cause AKI?

A
  • drugs: antibiotics, NSAIDS, ACE inhibitors (best solution for kidney disease but may cause hypotension)
  • sepsis
  • rhabdomyolysis
  • myeloma
  • tubulointestitial diseases
  • glomerulonephritis

See session 10 AKI slide 32-34

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14
Q

How does post-renal disease cause AKI?

A
  • indicates obstruction to urine flow after urine has left the tubules
  • bladder outlet obstruction
  • bilateral pelvic retreat obstruction
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15
Q

How would you treat and manage AKI?

A
  • dictated by the cause of the AKI
  • pre-renal: restoration of renal perfusion by restoring volume or treating pump failure
  • post-renal: if urinary tract obstruction then urological intervention is necessary to re-establish urine flow
  • manage fluid balance
  • recovery can take many weeks and treatment is supportive
  • maintain good kidney perfusion, avoid nephrotoxic restricting various solutes and providing nutritional support
  • dialysis is initiated if the kidneys can no longer excrete salt, water, potassium or other waste products or if acid-base balance is no longer maintained
  • URINE DIPSTICK TEST IS VITAL
  • prevention is better than cure

See session 10 AKI slide 35-43

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16
Q

What is adult polycystic kidney disease (ACKD)?

A
  • autosomal dominant
  • mutation in either PKD 1 gene or PKD 2 gene
  • cysts grow with age, generally presents in adulthood
  • diagnosed with ultrasound (can’t exclude if < 30 years old)
  • genetic testing (not widespread)
  • prognosis depends on rate of increase in kidney size and age

See session 10 CKD slide 3-4

17
Q

What is the clinical disease in APCKD?

A
  • cysts fluid filled an can cause secondary complications: pain, bleeding into cyst, infection, renal stones (stasis)
  • hypertension very common (before renal function changes)
  • rate of decline in function variable even between families
  • increased incidence of intra-cranial aneurysms
  • increased incidence of heart valve abnormalities

See session 10 CKD slide 5

18
Q

How can we manage APCKD?

A
  • treat hypertension block RAAS
  • diet: drink plenty of fluid (will slow progression of disease), low salt, normal but not excessive protein
  • tolvaptan: is a vasopressin 2 receptor antagonist which stop you from reabsorbing water so you pee a lot
  • others such as somatostatin analogues

See session 10 CKD slide 6

19
Q

What is the incidence of CKD?

A

-CKD is often asymptomatic so hard to measure

See session 10 CKD slide 12-15

20
Q

What is the aetiology of CKD?

A
  • CKD is often associated with old age, diabetes, hypertension, obesity and CVD
  • common causes:
  • diabetes
  • arteriopathic renal disease
  • hypertension
  • immunologic (ex. Glomerulonephritis)
  • other systemic diseases (ex. Lupus)
  • infection (ex. Pyelonephritis)
  • obstructive and reflux nephropathies
  • genetic family history of stage 5 CKD or hereditary kidney disease

See session 10 CKD slide 16-17

21
Q

What are the risk factors of CKD?

A
  • any form of AKI
  • proteinuria
  • hyperlipidaemia

See session 10 CKD slide 26-27

22
Q

How do we investigate CKD?

A
  • define degree of renal impairment
  • define cause of renal impairment
  • provide patient with diagnosis and prognosis
  • identify complications of CKD
  • plan long term treatment
  • must ALWAYS MEASURE BP AND URINE DIPSTICK
  • not helpful to just look at creatinine
  • look at eGFR and blood tests
  • USS, kidney biopsy, CT scan, MRI scan, MR angiogram

See session 10 CKD slide 18-20, 24

23
Q

What restrictions are there with using eGFR as investigation method for CKD?

A
  • only accurate in adults, doesnt work in kids or pregnant women
  • correction needed for black patients (not Asians)
  • it defines chronic kidney disease and isn’t useful in acute kidney injury
  • because it takes time for creatinine to change, so takes time for eGFR to change

See session 10 CKD slide 21

24
Q

What would you check for in a blood test investigating CKD?

A
  • urea and electrolytes
  • bone biochemistry
  • LFT
  • FBC
  • CRP
  • iron levels
  • PTH
  • check for auto-immune disease

See session 10 CKD slide 22-23

25
Q

How is regulation of water and salt affected in CKD?

A
  • 80-85% of CKD patients are hypertensive
  • treatment: anti-hypertensives, diuretics, fluid restriction
  • amount of urine produced depends on GFR
  • CKD causes reduced GFR
  • lose ability to maximally dilute and concentrate urine
  • small GFR but same solute load causes osmostic diuresis
  • nocturia common because they are insensitive to ADH secretion in order to get rid of the solute load
  • low volume of filtrate reduces maximum ability to excrete urine therefore max urine volume much smaller

See session 10 CKD slide 28-30

26
Q

How does hyperkalaemia occur in CKD?

A
  • occurs once eGFR <20ml/min
  • less likely when good urine output maintained
  • may require: stopping ACE inhibitor, avoidance of other drugs that can increase K+, altering diet to avoid foods with high potassium
  • can potentially lead to acidosis which would be treated with oral NaHCO3 tablets

See session 10 CKD slide 31-32

27
Q

What are some causes of anaemia in CKD and how can we treat it?

A

Causes

  • high hepcidin level: stops you from absorbing iron
  • absolute iron deficiency
  • blood loss
  • decreased EPO production

Treatment

  • important to treat because need to improve Hb and ultimately reduce mortality
  • just giving EPO without any iron is ineffective
  • so much replace iron first
  • when iron supplies ok, re-check Hb and if Hb is still low then give EPO

See session 10 CKD slide 33-35

28
Q

HOw does CKD cause mineral bone disease and how can it be treated?

A
  • decrease in Klotho-FGF 23
  • decreased vitamin D which leads to bone resorption
  • increased osteoclastic activities
  • stimulating Parathyroid glands leading to hyperplasia
  • non bone calcification occurs in wrong places such as joints, vessels, skin
  • can cause significant morbidity
  • management: reduce phosphate intake, phosphate binders (to prevent malnutrition), 1-a-calcidol, vitamin D

See session 10 CKD slide 36-38

29
Q

What are the main symptoms of CKD?

A
  • tiredness
  • breathlessness
  • restless legs
  • sleep reversal
  • aches and pains
  • nausea and vomiting
  • itching
  • chest pain
  • seizure
30
Q

What is end stage renal disease?

A
  • CKD can progress to this
  • reduced life expectancy
  • reduced QoL
  • transplant is best hope for survival
  • when death is likely without renal replacement therapy
  • eGFR <15ml/min
31
Q

What is renal replacement therapy?

A
  • required when native renal function declines to a level no longer adequate to support health
  • usually when eGFR 8-10ml/min

See session 10 CKD slide 41-42

32
Q

What symptoms occur with ESRD/dialysis?

A
  • tiredness: overwhelming fatigue, physically and mentally incapacitated, feelings of guilt at needing rest
  • difficulty sleeping
  • difficulty concentrating
  • CKD stage 5
  • symptoms and signs of volume overload (oedema)
  • nausea and vomiting/reduced appetite
  • restless legs/cramps
  • pruritis
  • sexual dysfunction/reduced fertility
  • increased infections

See session 10 CKD slide 43-44

33
Q

What options do you have when kidneys fail?

A
  • haemodialysis
  • peritoneal dialysis
  • conservative care (for older patients)
  • transplants
34
Q

What are the advantages/disadvantages of haemodialysis?

A

Advantages

  • do not need to be responsible for own treatment
  • can remain on haemodialysis for years
  • 4 days free from treatment

Disadvantages

  • fluid and diet restriction
  • limited ability to travel
  • CVS instability
  • high capital cost
  • hospital based

-nocturnal /home HD are better option as you need fewer meds, allows more dialysis hours, patients feel better

See session 10 CKD slide 46-50

35
Q

What are the advantages and disadvantages of peritoneal dialysis?

A

Advantages

  • low technology
  • home technique
  • easily learn
  • allows mobility
  • CVS stability better for elderly and diabetic
  • little dietary restriction

Disadvantage

  • frequent exchange
  • unable to do long-term
  • frequent treatment failure
  • peritonitis
  • limited dialysis dose rang
  • high revenue cost
  • body image problem

See session 10 CKD slide 51

36
Q

What are the advantages/disadvantages of a kidney transplant?

A

Advantages

  • freedom from dialysis
  • restoration of near normal renal function
  • improved quality and quantity of life
  • cheap

Disadvantages

  • requires immunosuppressive drugs
  • operative mortality
  • limited supply of organs
  • not suitable for all
  • still left with CKD
  • new kidneys don’t last forever

-most transplants attach to iliac vessel so sit in pelvis

See session 10 CKD slide 52-57

Urinary (11 decks)

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