condition part 1 Flashcards

1
Q

definition for AKI

A

a significant deterioration in renal function occurring over hours-days

KDIGo definition

  • inc in SCr by > 03.mg within 48 hours
  • inc in SCr to >1.5 times baseline
  • urine volume <0.5ml/Kg for 6 hours
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2
Q

what are the different stages of AKi

A

Stage 1

  • SCr 1.5-1.9 times baseline or >0.3mh inc
  • Urine - <0.54ml/kg for 6-12 hrs

Stage 2

  • SCr 2-2.9 times baseline
  • urine < 0.5ml/kg for > 12hrs

Stage 3

  • 3 times baseline or inc >4.0mg or initiation of renal replacement therapy
  • urine - <0.3ml/kg for > 24hrs or anuria for > 12hrs
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3
Q

how common is AKI

A

affect 18% of hospital patients in the UK
incidence of hospital-acquired AKI has Inc
incidence of commnity-acquired AKI on admission to hospital is 3-5% in the UK

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4
Q

who is affected the most by AKi

A

elderly and hospitalised pt

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5
Q

causes of AKI

A

pre-renal (40-70% of cases)

  • due to renal hypotensions
  • hypovolaemia
  • hypotension
  • sepsis (systemic vasodilation)
  • congestive cardiac failure
  • liver cirrhosis
  • renal artery stenosis
  • NSAIDs
  • ACEi (interfere with blood flow)

Intrinsic ( 10-50%)

  • due to damages in the kidney
  • tubular - acute tubular necrosis, nephrotoxins eg drugs, radiological contrasts, heavy metal poisoning, HB in haemolysis, myoglubinuria in rhabdomyolysis, crystal and protein (Ig)
  • glomerular - glomerulonephritis, autoimmune conditions (SLE, HSP)
  • interstitial - acute interstitial nephritis (drugs, infection, autoimmune)
  • vascular - vasculitis, malignant hypertension, thrombus, cholesterol emboli, large vessels occlusion

post-renal (10-25%)

  • due to urinary tract obstruction
  • luminal - stones, clots, sloughed papillae
  • mural - malignancy ( ureteric, bladder, prostate)
  • extra-luminal - malignancy in the pelvic
  • retroperitoneal fibrosis
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6
Q

RF for AKi

A
>65yrs 
HF
Liver disease 
CKD
past history of AKI
diabetes 
poor fluid intake 
inc fluid loss -diarrhoea, bleeding 
Oliguria (production of abnormal small amount of urine) 
haematological malignanacy
- urinary symtoms 
spesis
nephrotoxic drugs
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7
Q

symptoms of AKI

A

usually result of underlying causes, but could be

  • oliguria/anuria
  • polyuria
  • N+V
  • dehydration
  • confusion
  • palpitations - cardiac arrhythmia due to altered K+ level
  • rash/bruising - vascular disease
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8
Q

signs on exam for AKI

A
HTN
skin turgor - dec with dehydration and inc in oedema 
raised JVP 
palpable bladder 
postural hypotension 
pulmonary and peripheral oedema
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9
Q

differenital for AKI

A

CKD

acute on chronic renal failure

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10
Q

investigation for AKI

A

ABCDE - C - check BP, JVP, skin turgor, cap refill, urine poutput, check urgent K+ and ECG

history - looking for RF

examination - full systemic examination, abdo masses, renal bruits, rashes

urinalysis - leukocytes and nitrites indicating infection, blood and protein indicating glomerular disease, send culture for infection

bloods - FBC, U+E, creatinine, LFT, clotting, ESR, CRP
- creatine kinase - (rhabdomyolysis), ABG, blood film and renal immunology

imaging - renal USS, CTKUB, CXR

need to variefy if pt has CKD or actually AKI

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11
Q

mangement for AKI

A

general measure

  • euvolaemia - correct any fluid imbalance (avoid potassium containing fluids unless hypokalaemic
  • stop nephrotoxic drugs
  • stop exacerbating factors - hypovolaemia, sepsis, high BP

monitor

  • consider transfer to ICU.HDU
  • hourly obs
  • daily fluid balance and weight chart
  • daily U+Es

nutrition - aim for normal calorie intake, consider NG tube if intake is poor

treating underlying causes

  • pre-renal - fluids for volume depletion, antibiotics for sepsis, ICU referral if in shock
  • intrinsic - refere to nephrology
  • post-renal - cather for obstruction
  • refer to urology for cystoscopy/stents/nephrostomy

managing complications

  • hyperkalaemia - IV calcium gluconate over 2 mins for cardioprotectivity, IV insulin and glucose stimulates intracellular uptake of K+ to buy time to lower K+
  • pulmonary oedema - high flow O2, IV flurosemide, venous vasodilator
  • uraemia - dialysis maybe if severe of complication eg encephalopathy
  • acidaemia - dialysis maybe or IV bicarb

Renal replacement therapy
- haemodialysis - requires patient to be haemodynamically stable, allows good clearance of solutes in short periods
haemofiltration - slower at clearing solutes, less significant shift so BP likely to drop
indication for acute dialysis - refractory pulmonary oedema, perisistnet hyperkalaemia, severe meabolic acidosis, uraemic encephalopathy, uraemic pericarditis

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12
Q

definition of CKD

A

presence of kidney damage or dec in kidney function for 3 months or more or

GFR <60 for 3 months or more with or without evidence of kidney damage or

GFR > 60 for 3 months or more together with evidence of kidney damage

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13
Q

what are the different stage of CKD

A

1 - >90, normal or inc GFR with other evidence of renal damages

2 - 60-89, slight dec GFR with other evidence of renal damage

3A&B - A(45-59) & B (30-44) with moderate dec GFR +/- evidence of renal damage

4- 15-29, severe dec GFR +/- evidence of renal damage

5 - <15, established renal failure (ERF)/End stage renal disease (ESRD)

evidence of renal damage = proteinuria, haematuria, evidence of disease

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14
Q

how common is CKD

A

8.8% of UK population have symtpomatic CKD

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15
Q

who is affected the most by CKD

A

4x more common in African-American deut to increase prevalence of HTN
CKD due to atherosclerotic renal disease more common in elderly
>70% of all CKD are due to DM, atherosclerosis and HTN

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16
Q

what are some screening questions for CKD

A

duration of symptoms
drugs eg NSAIDs, analgesia, herbal remedies
previous medial and surgical history -chemo, multisystem disease such as SLE, malaria
previous occasions on which urinalysis (urea and creatinine) might have been performed

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17
Q

causes for CKD

A

congenital and inherited - PCKD, medullary cystic disease, tuberous sclerosis, oxalosis, cystinosis, congenital obstructive uropathy

glomerular disease - primary glomerulonephritis incl focal glmoerulosclerosis, secondary glomerular disease ((systemic lupus, polyangitis, Wegener’s granulomatosis, amyloidosis, diabetic glomerulosclerosis, accelerated HTN, haemolytic uraemic syndrome,

vascular disease - hypertensive nephrosclerosis (inc BP), reno-vascular disease, smale and medium-sized vessel vasculitis, DM

tubulointersitial disease - Tubulointerstitial nephritis – idiopathic, due to drugs (especially nephrotoxic analgesics), immunology related, reflux nephropathy, tuberculosis

Urinary tract obstruction - calculus disease, prostatic disease, pelvic tumours, retroperitoneal fibrosis

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18
Q

RF for CKD

A

DM, age > 60, recurrent UTIs, urinary obstruction, systemic illness that affects the kidneys

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19
Q

symptoms for CKD

A

early CKD often asymptomatic

when urea is >40ml
- malaise, loss of energy
loss appetite/anorexia
insomnia
nocturia/polyuria (loss of concentrating ability)
-N+V and diarrhoea
- metallic taste
- paraesthesiae due to neuropathy
-restless legs snydrome (overwhelming need to frequently alter position of lower limbs)
bone pain due to metabolic bone disease
paraesthesiae and tetany due to hypocalcaemia
symptoms due to salt and water retention - peripheral or pulmonary oedema
symptoms due to anaemia
amenorrhoea in women, erectile dysfunction in men
oliguria

[urea] > 60mmol/L = more severe uraemic symptoms and CNS involvement eg mental slowing, confusion, clouding of consciousness, seizures, myoclonic twitching, encephalopathy, coma
Urine output is not a useful guide to kidney function as though GFR decreases => oliguria; tubular resorption is also less so high vols of urine may still result

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20
Q

signs on exam for CKD

A

short stature (if CKD in childhood)
pallor due to anaemia or yellow pigmentation (uraemic syndrome)
bruising or purpura
inc photosensitivity prigmentation
brown discolouration of nails
scratch marks due to uraemic puritis
signs of fluid overload eg pleural effusion
pericardial friction rub
mitral regurgitation due to overload or annular calcification
glove and stocking peripheral sensory loss
high BP

impalpable kidneys unless enlarged due to PCKD, tumours or obstruction

signs of an underlying condition that has lead to CKD

  • cutaneous vasculitis lesion in systemic vasculitides
  • retinopathy in DM
  • evidence of peripheral vascular disease
  • evidence of spina bifida or other causes of neruogenic bladder
  • should assess hydration status (JVP and skin turgor, BP lying and standing)
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21
Q

differential for CKD

A

AKI

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22
Q

investigation for CKD

A

bloods - FBC (Hb dec), eosinophilia (vasculitis, allergic tubulointerstitial nephritis), fragmented RBC +/- thrombocytopenia (accelerated HTN, haemolytic uraemic syndrome)
ESR inc
Uand E inc - inc PTH
immnunology - autoantibody screening in SLE, antibodies to HBV,HCV,HIV

urinalysis

urine microscpy, culture and sensitivity

  • WCC (infection)
  • eosinophiluria 0 allergic tubulointersititial nephritis
  • casts - Granular casts formed from abnormal cells within the tubular lumen, and indicate active renal disease. Red-cell casts are highly suggestive of glomerulonephritis.

radiology - USSm AXR, CT (retroperitoneal fibrosis), MRI and IV urography

renal biopsy

bone scan and DXR

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23
Q

treatment for CKD

A

transplant ultimate choice, RRT

monitoring - ultimately need ed dialysis
reduce use of drug that are excreted in the kidney - heparin, lithium, digoxin, ehtnambutol, cephalosporins, sulfmethoxazole, procainaminde, tetracycline, opiates

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24
Q

definition of hydronephrosis

A

aseptic distension and dilation of the renal pelvis and calyces usually caused by urinary tract obstruction

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25
Q

how common is hydronephrosis

A

1 in 300 in the uk per year
1 in 600 have bilateral hydronephrosis
1 in 100 pregnanacies affected by antenatal hydornephrosis and is one of the most common abrno detected on antenatal screening

26
Q

causes of hydronephrosis

A

unilateral hydronephrosis

  • intraluminal - calculi, embolus, congenital PUJ onstruction
  • intrinsic/mural - ureteric stricture, BPH, malignancy (Kidney, prostate, bladder), ureterocele (ongenital abnormality found in the ureter. In this condition the distal ureter balloons at its opening into the bladder, forming a sac-like pouch), neurogenic bladder
  • extraluminal - pregnancy, malignancy in the pelvic organs, lymphadenopathy

bilaterial

  • congenital - strictures, Primary vesicoureteral reflux – dysfunctional valves between ureter and bladder allowing retrograde flow of urine, posterior urthral valves, phimosis (non retractibility of the foreskin)
  • acquired - bladder neck hypertrophy, BPH, prostate cancer, malignancy, urinary strictures
27
Q

symptoms of hydronephrosis

A

vary depending whether the obstruction being acute or chronic and the severity of the blockage

acute - pain in flank (intense, often caused by renal stone), suprapubic pain, haematuria, N+V, palpable kidney

chronic - not much symptoms

28
Q

differentials for hydronephrosis

A

renal stones, BPH

29
Q

investigation for hydronephrosis

A

bloods - U+E, creatinine

imaging- USS, CT pr IVU
urine dipstick, MSU MC+S, bladder scan

30
Q

management for hydronephrosis

A

nephrostomy (an artificial opening created between the kidney and the skin which allows for the urinary diversion directly from the upper part of the urinary system (renal pelvis)

ureteric stent

pyeloplasty

uretheral or suprabubic catheter

Weight, fluid balance and U+Es must be closely monitored as a temporary salt-losing nephropathy may occur due to large diuresis after relief of obstruction.

31
Q

definition for Benign prostatic hyperplasia

A

non-malignant inc in size of the prostate gland which happens with ages

32
Q

how commons is BPH

A

<45s - unusual
50s - 40%
90s - 90%

33
Q

who is affected the most by BPH

A

men over 50s less common in asians

34
Q

pathology of BPH

A

both glandular epithelial cells, muscle fibres and stromal cells undergo hyperplasia. stromal hyperplasia predominates

Majority of the growth occurs in the transitional zone and also the posterior urethral glands but the peripheral zone is less involved

35
Q

causes to BPH

A

aetiology unknown

suggested that it might be mediated by testosterone and oestrogen. Dihydrotestosterone which is a metabolite of testosterone is thought to have a role in this

inc oestrogen with age and also inc DTH and so mediate prostatic growth

36
Q

RF for BPH

A

DM

HTN

37
Q

symptoms of BPH

A

LUTS - lower urinary tract symptoms - without haematurai and dysuria unless presenting with other problems

38
Q

signs of BPH on examination

A

PR exam - smooth, symmetrical, flattened sulcus
palpable bladder
dec urinary outflow

39
Q

differenital diagnosis of BPH

A

prostate cancer - prostate might feel bumpy/asymmetrrical on PR, raised PSA

UTI - dysuria, systemic symptoms, resolves

urinary tract stones - haematuria, pain

detrusor muscle weakenss - no pain/dysuria. incontinence

chronic prostatitis - abdo/plvice/perineal pain, post-ejaulatory pain

40
Q

what are some questions for asking for BPH

A
incomplete emptying? 
frequency?
intermittency 
urgency 
weak stream 
straining 
nocturia
41
Q

treatment for BPH

A

watchful waiting

medical therapy

  • tamsulosin (alpha blockers) - 1st line
  • finasteride (5alpha-reducatase inhibitors)

surgical treatment

  • transurethal resectino of the prostate
  • transurethal incision of the prostate
  • retropubic prostatectomy
  • transurethral lasser-induced prostatectomy
42
Q

what are lower urinary tract symptoms

A

storage symptoms

  • frequency
  • urgency
  • nocturia
  • overflow incontinence

voiding symptoms

  • hesitancy
  • intermittency
  • poor stream
  • incomplete voiding
  • dysuria

Post-micturition symptoms

  • terminal dribling
  • haematuria
43
Q

how common is prostatic carcinoma

A

7% of all cancer affecting men and most common cancer in men in the UK

44
Q

who is affected the most by prostatic carcinoma

A

80% of men >80 yrs, risk inc with age

45
Q

pathogenesis of prostatic carcinoma

A

most of the prostate cancers are adenocarcinomas which are usually well-differentiated

Mostly this occur in the peripheral zone
begins as carcinoma in situ or PIN (prostate intraepithelial neoplasia) - clumps of cancer cells remain confined to otherwise normal prostate glands

ZIP1 is a tumour suppressor gene whcih codes for a protein that actively transport zinc into the prostate glands for production of semen and when this is silence by carcinoma, the cancer cells can save all this energy on active transport to grow and proliferate instead

spread maybe local to seminal vesicles, bladder or rectum via lymph or haematogenously into sclerotic bone lesions

46
Q

RF for prostatic carcinoma

A

age
FH - 2-3x higher risk with 1st degree relateive
FH of breast cancer - BRCA1 and BRCA2 found to have been implicated in some cases
- highest incidence inAfrican Americans, lowest incidence in aisan and Oriental men
smoking - inc risk of fatal prostate cancer

47
Q

symptoms of prostatic carcinoma

A
2/3 asymptomatic 
1/3 LUTS 
erectile dysfunction 
painful ejaculation 
metastatic spread - back pain, bone pain, weight loss, anaemia, lymph node enlargement
48
Q

signs of prostatic cancer

A

PR exam - asymmetry, nodules, adhesion to surrounding tissue, hard gland, palpable seminal vesicles, obliteration of median sulcus

49
Q

differential for prostate cancer

A

BPH
UTI/UT stones
chronic prostatitis

50
Q

investigations for prostate cancer

A

urinalysis - to rule out bladder/renal patholgy
MSU MC+S - to rule out infection
bloods - U+Es, creatinine - to rule our renal disease
PSA
Biopsy
CT
Bone scan - if metastases suspected

51
Q

management for prostate cancer

A
watchful waiting 
active surveillance 
radial prostatectomy 
radiotherapy 
brachytherapy - transperineal implantation of radioactive seeds into the prostate 
High-Intensity Focused Ultrasound (HIFU)
hormone therapy
52
Q

definition for urinary tract calculi

A

renal stones consisting of crystal aggregates

53
Q

what is pyelonephritis

A

infection within the renal pelvis (with or without infection of the renal parenchyma)

54
Q

what are the most common pathogens that cause pyelonephritis

A

EKPPE

E.coli 
Klebsiella pneumoniae 
Proteus 
Pseudomonas 
enterococcus
55
Q

RF for pyelonephritis

A

female, FH

sexual intercourse, exposure to spermicide, menopause, pregnancy, uncircumsized

immunosuppression, urinary tract obstruction/stone/malformation, prostate enlargement, DM, catheter, fistulas, spinal cord/nerve damages

56
Q

presentation of pyelonephritis

A
rigors 
fever 
N+V
rapid onset 
loin pain - radiate to groin 
suprapubic pain 
diarrhoea 

may have lower UTI infection symptoms eg frequency, dysuria, gross haematuria, hesitancy

57
Q

signs of pyelonephritis

A

tender to palpaite
general ill
fever

58
Q

differentials for pyelonephritis

A
UTI
MSK 
renal calculi 
ectopic pregnancy 
endometriosis 
prostatitis 
appendicitis 
AAA
abdo abscess 
diverticulitis
59
Q

investigation for pyelonephritis

A

FBC, U+Es, ESR, CRP
urinalysis - nitriles, WBC
MSU culture and sensitivity
CTKUB - if renal calculi suspected

60
Q

treatment for pyelonephritis

A

ciprofloxacin, co-amoxiclav

paracetamol
fluids