Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Chronic kidney disease > Flashcards

Chronic kidney disease Flashcards

1
Q

Stags of CKD based on eGFR

A

With added proteinuria/abluminurea = worse outcome

None/mild/Heavy (A1-A3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Definition of chronic kidney disease

A

Must have kidney damage or eGFR <60 for greater than three months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of CKD

A

Glad shop

Chronic glomerulonpehritis - 20%, Chronic refluxnephropathy -15%

Lupus

Analgesiacs

DM - 20% Most common recognised cause

Systemic vascular disease

Hypertesion

Obstruction

Polycystic kidney disease

Renovascular (including hypertension - 15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Screening

A

Intervening early in CKD can reduce the progression to ESRF and so screening is recommended for at risk patients with:

  • DM
  • hypertension
  • CV disease
  • structural renal disease
  • recurrent UTS or childhood history of Vesicoureteric reflux
  • family history of ESRF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

History in known/suspected CKD

A
  • Possible cause -
    • ​Ask about previous UTI, LUTS
    • PMH of increased BP, DM, IHD
    • check drug history and family history
    • systemic review: malignancy>
  • Current state:
    • ​Uraemic symptoms such as anorexia, vomitting, restless legs, fatigue, weakness, pruritis, bone pain
    • in women ask about ammeonorhoea and impotence in men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Examination in patient with suspected or known CKD

A

Look for

  1. cause of ESRF/CKD e.g polycystic kineys, signs of IHD, DM
  2. current mode of renal replacement therapy and any complications
  3. previous types of RRT and any compliations

Periphery- hypertension, ateriovenous fistula, signs of previous transplant- bruising from steroids, skin malignancy

Face- pallor of anaemia, yellow tinge of uraemia, gum hypertrophy from cicilosporin, cushingoid appearance

neck- current or previous tunnelled line inserstion , scar from parathyroidectomy

Abdomen: PD catheter or previous catheter (small midline scar just below umbilicus and small rund scar to sife of midline from exit site), signs of previous transplant (hockey-tick scar, palpable mass), ballotable polycystic kidneys

Elsewhere: signs of diabetic nephropahty, retinopathy, cardiovascular or periphieral vascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Symptoms

A

Rare in the early stages of disease

usually only occur once stage 4 is reached

Late stage disease

  • fatigue
  • metallic tase
  • restless legs
  • low urine output
  • anorexia - loss of apetite
  • shortness of breath pulmonary odema
  • ankle swelling - fluid overload
  • confusion - severe uraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Signs

A
  • increased BP- fluid overload + release of vasoactive hormones
  • oedema- peripheral and pulmonary
  • pallor/yellow skin pigmentaiton - increased blood urea
  • exoriations- pruritis
  • pericardial rub- pericarditis
  • tachypnea- metabolic acidois
  • tetany- hyperphosphataemia
  • coma- severe uraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What worses with each stage of CKD

A

Cardiovascular risk factors and should be adressed even in teh early stages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management of chronic renal failure

A

Blood pressure control (aim for <130/80mmhg)

  • ACE i
  • other hypertensives
  • diuretics

Reduction in proteinuria- ACE i

Treatment of anaemia

  • IV iron
  • erythropoetin

Diet

  • low salt intake
  • low potassium intake
  • high calorie intake

Treatment of hyperphosphataemia and hypocalcaemia (renal bone disease)

  • phosphate binders
  • alpha caclidol

glucose control in diabetes

Hyperlipidaemia control

Volume status monitoring

Avoid nephrotoxic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical presentation of chronic renal failure

A

RESIN and 8 Ps

Retinopathy

E exoriations (scatch marks)

S skin is yellow

i increased blood pressure

N nails are brown

Pallor,

purpura and brusing

pericarditis

pleural effusions

pulmonary oedema

peripheral oedema

proximal myopathy

peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Salt Losing vs Salt retaining

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Investigations

A

Bloods

  • ↓Hb – normochromic & normocytic – ↓Epo
  • ↑Urea & ↑Creatinine
  • ↓ Calcium & ↑Phosphate
  • ↑Parathyroid Hormone– due to low Calcium
  • increased alk phos (renal osteodystrophy)

Urine

  • Microscopy, Culture & Sensitivity
  • Dipstick – proteinurea, haematuria
  • 24 Hour Urinary Protein

Imaging

  • Renal ultrasound – exclude obstruction, assess kidney size (small in CRF)
  • CXR – Cardiomegaly, Pleural or Pericardial effusions, Pulmonary Oedema
  • Renal biopsy – if cause is unclear & kidneys are normal size
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anti-proteinuric action of ACE inhibitors

A
  • Reduction of systemic blood pressure
  • Relaxation of efferent arteriole from glomerulus (so additional reduction of intraglomerular pressure)
  • Gradual reduction in glomerular permeability to protein ?cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Response of kidneys to blood pressure

A

Hypotensive

  • kidneys respond by releasing renin (activating RAS), leading to release of angiotensin II which causes contriction of the efferent arteriole
  • Also causes release of prostaglandins to dilate the afferent arteriole
  • ultimately maintaining pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Functions of the kidney, effect of failure and management

A
17
Q

Calcium and phosphate metabolism in chronic kidney disease

A
  • When a patient has chronic kidney disease (esp 4 or 5) leads to r
    • Reduced production of 1,25(OH)2D3
    • Malabsoprtion of calcium
    • Hyperphosphataemia (failure of excretion as kidneys not working(
  • This triggers the parathyroid to increase PTH (secondary hyperthyroidism)
  • Causes increased bone disease (source of calcium) and increased demand on kidney

Softens the bones and hardens the arteries

18
Q

Clinical features of renal osterodystrophy

A
  • osteoporosis
  • osteomalacia
  • areas of osteosclerosis
19
Q

Treatment of renal osteodystrophy

A

Prevention

  • phosphate binders (calcium acetate)
  • vitamin D (alpha-calcidol)

Treatment

  • parathyroidectomy
  • cinacalcet
20
Q

Uraemia

A

Urea accumulates, leading to axotaemia and ultimatlely uraemia. Symptoms can be non-sepcific. However, with rising uaemia the patient may develop severe sympoms and complications like:

  • pericarditis
  • encephalopathy
  • pulmonary oedema
  • confusion
  • coma
  • seizures
21
Q

Key signs to identify in patients suspected of CKD and possible uraemia are:

A
  • uraemic fetor- uraemic fetor is a urine-like odor on the breath of persons with uraemia
  • Uraemic frost- crystallized urea deposits that can be fpund on the skin of those affected by chronic kidney disease
22
Q

Complications of CKD

A

CKD compromises the physiology of the kidney. The GFR is reduced therefore reabsorption in the tubules are reduced. Also the kidenys loses its ability to produce hormones

  • Rise in BP - due to fluid overload and production of vasoactive hormones created by the kidney via RAAS leass to increased risk of hypertension and congestive HF
  • Hyperkalaemia - due to reduced clearance
  • anaemia - due to reduced production of EPO
  • pulmonay oedema or pitting oedema - fluid overload
  • hyperphosphataemia - reduced phosphate excretion, follows the decrease in glomerular filtration
  • hypocalcaemia - due to 1,25 dihydroxyvitamin D3 deficiency. Later this progresses to secondary hyperparathyroidsimm, renal osteodystrophy and vascular calcification that further impair cardiac function
  • metabolic acidosis (due to accumulationof sulfates, phosphates, uric acid etc)
23
Q

Treatment: Lifestyle advice

A

lifestyle changes

  • smoking cessation
  • diet-healthy balance diet (low fat)
  • restricting salt intake
  • limitng NSAID use
  • moderate alcohol intake so i is within recommended limitis
  • losing weight if overweight or obese
  • regular exercise

Medical therapy

*

24
Q

Treatment: Medical

A
  • anti-hypertensives (ACEi/ARB)
  • medication to reduce cholesterol - statins
  • treatment of anaemia - daily ferrous sulphate tablets, injections of erythropoetin
  • correction of phosphate balance - reduce food containing phosphate (red meats, eggs), phosphate binders (sevelamer hydrocholride)
  • Vitamin D supplements
25
Q

Supportive therapy

A

Supportive treatment includes, medical, physciological and practical care for both the eprson with kidney failure and their family, including discussion about how they fell and planning for the end of life

26
Q

Why might patients choose supportive therapy:

A
  • unlikely to benefit or have the quality of life with treatment
  • do not want to go through the inconvenience of treatment with dialysis
  • are advised against dilaysis because they have other serious illnesses that will shorten their life, and the negative aspects of reatment ouweigh any likely benefits
  • have been on dialysis but have decided to stop

Renal (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions