Nephrology Flashcards
(181 cards)
1
Q
what is the definition of CKD?
A
A glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 on at least two occasions separated by a period of at least 90 days (with or without markers of kidney damage).
Markers of kidney damage such as urinary albumin:creatinine ratio (ACR) greater than 3 mg/mmol, urine sediment abnormalities, electrolyte and other abnormalities due to tubular disorders, abnormalities detected by histology, structural abnormalities detected by imaging, and a history of kidney transplantation.
2
Q
what are the risk factors for CKD?
A
HTN
DM - most common cause
glomerular disease - such as acute glomerulonephritis
patients with previous AKI
nephrotoxic medication
px radiotherapy
conditions associated with obstructive uropathy
SLE/meyloma/HIV
gout
FHx of CKD
3
Q
what are some complications of CKD?
A
AKI
HTN
Dyslipidaemia
CVD
ESRD
Hyperkalaemia
pulmonary oedema - secondary to fluid overload
anaemia
mineral and bone disorder
peripheral neuropathy
malnutrition
risk of renal Ca
stroke
4
Q
what initial investigations should be organised in CKD?
A
If eGFR<60 – repeat the test within 2 weeks to ensure not acute
If eGFR is still < 60 but stable, repeat again within 3 months + arrange ACR
If ACR between 3-70 mg/mmol - repeat the test again within 3 months to confirm.
If ACR > 70 – no repeat needed, refer to renal.
Arrange urine dipstick – check for haematuria – if persistent on x2 dipsticks – refer via 2ww.
5
Q
when would you suspect deteriorating CKD?
A
If accelerated fall – sustained decrease in eGFR of 25% or more and change in CKD category within 12 months OR sustained decrease in eGFR of 15 mL/min in 12 months
6
Q
what investigations should be carried out in deteriorating CKD?
A
Repeat serum eGFR three times over minimum of 3 months
If progression evident then:
Arrange renal USS
Check for nephrotoxic meds / reversible causes
Refer to renal for specialist input
ALSO arrange FBC – if renal anaemia suspected – refer to renal team.
7
Q
what is the management of stable CKD?
A
repeat bloods yearly - or as soon as recommended based on category
Manage lifestyle factors
Optimise blood pressure -
If ACR <30, manage as per non-ckd HTN
If ACR >30 – trial of ACE-I or ARB (not together) , then add in other anti-hypertensives
Start atorvastatin 20mg OD
Offer antiplatelet to all people with CKD to prevent CVD
Consider SGLT-2 inhibitor – offer to T2DM with CKD
8
Q
what are some symptoms of CKD?
A
oedema: e.g. ankle swelling, weight gain
polyuria
lethargy
pruritus (secondary to uraemia)
anorexia, which may result in weight loss
insomnia
nausea and vomiting
hypertension
9
Q
what factors can affect eGFR result?
A
pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken
10
Q
when would you suspect renal artery stenosis?
A
refractory hypertension, recurrent pulmonary oedema with normal left ventricular function, or an increase in serum creatinine of 20% or more when started on an angiotensin-converting enzyme [ACE] inhibitor.
11
Q
what is renal artery stenosis?
A
Renal artery stenosis (RAS) is a significant cause of secondary hypertension and can lead to chronic kidney disease (CKD). It occurs due to narrowing of the renal arteries, often caused by atherosclerosis or fibromuscular dysplasia.
12
Q
how does renal artery stenosis cause hypertension?
A
RAS reduces renal perfusion pressure, stimulating the renin-angiotensin-aldosterone system (RAAS), leading to increased blood pressure and sodium retention. Over time, this can result in nephron damage and progressive CKD.
13
Q
what are the causes of anaemia in CKD?
A
reduced EPO secretion from the kidneys
reduced absorption of iron
14
Q
what is the mechanism leading to reduced EPO secretion in CKD?
A
EPO is produced in the kidneys, usually in response to hypoxia. In CKD, the nephrons are destroyed, leading to less production of EPO resulting in decreased erythropoesis in the bone marrow - this contributes to a nromocytic normochromic anaemia
15
Q
at what eGFR level do you tend to see anaemia secondary to CKD?
A
tends to occur when eGFR <35
16
Q
what is the mechanism behind anaemia in CKD due to reduced absorption of iron?
A
hepcidin is an acute-phase reactant
in CKD, hepcidin levels are often increased due to inflammation and reduced renal clearance
elevated hepcidin levels lead to decreased iron absorption from the gut and impaired release of stored iron from macrophages and hepatocytes, reducing the iron available for erythropoiesis
additionally, metabolic acidosis, a common condition in CKD, can inhibit the conversion of ferric iron (Fe³º) to its absorbable form, ferrous iron (Fe²º), in the duodenum → reduced iron absorption.
17
Q
what is the target haemoglobin for patients with anaemia secondary to CKD?
A
10-12 g/dl
18
Q
what is the management of anaemia secondary to CKD?
A
refer to renal team
usually - commenced on epoetin alfa
also can commence on iron if needed
19
Q
what is glomerulonephritis?
A
inflammation of the glomeruli of the kidneys leading to impaired filtration. This can be either acute or chronic.
20
Q
what are some causes of acute glomerulonpehritis?
A
Infections - post strep glomerulonephritis (most common), IE, viral ix
autoimmune - lupus, goodpasture syndrome, IgA Nephropathy
Vasculitis - Wengers granulomatosis, microcytic polyangiitis
Others - i.e. toxins/medications/blood disorders such as TTP/HUS
21
Q
what are some acute infective causes of glomerulonephritis?
A
post strep glomerulonephritis
bacterial endocarditis
viral infections - hep B, hep C, HIV
22
Q
what is post strep glomerulonephritis?
A
acute glomerulonephritis that occurs after infection with group A strep bacteria - usually skin (impetigo) or throat
23
Q
what is the pathophysiology of post strep glomerulonephritis?
A
strep infection (impetigo or throat) causes immune system to produce antibodies to fight the infection, this leads to the formation of antibody-antigen complexes that get trapped within the glomeruli, which triggers inflammation - leading to kidney damage + impaired infiltration
24
Q
what are the symptoms of PSGN?
A
haematuria - dark urine
oedema
HTN
oliguria
fatigue + weakness
mild fever in some cases
25
which patient group is most commonly affected by glomerulonephritis?
paediatrics - 5-15 year olds
26
what investigations would you do for PSGN?
urinalysis - protein + , haematuria +
bloods - ASO tier high, complement C3 low
renal function
throat/skin culture
27
management of PSGN?
usually supportive
antibiotics (usually penicillin) - for remaining infection
blood pressure management
salt and fluid restriction - reduce swelling and high blood pressure
28
explain the renin - angiotensin - aldosterone system?
Renin converts angiotensinogen (from the liver) into angiotensin I.
Angiotensin I is converted into angiotensin II by an enzyme (ACE).
Angiotensin II narrows blood vessels (vasoconstriction) and stimulates the release of aldosterone from the adrenal glands.
Aldosterone signals the kidneys to retain sodium and water, increasing blood pressure.
29
what are the five different types of diuretics?
loop diuretics
thiazide diuretics
potassium sparing diuretics
carbonic anhydrase inhibitors
osmotic diuretics
30
what is the main role of diuretics?
1. blood pressure management - lower blood pressure
2. offload excessive fluid - CCF, fluid retention in liver cirrhosis, renal disease
3. hypercalacemia - increase Ca excretion
4. reduce intracranial pressure
31
what is MOA of loop diuretics?
act on the loop of henle (ascending limb)
block the Na/K/cl co-transporter - preventing Na, K and Chloride being reabsorbed
this leads to more sodium and water being excreted
32
what are some examples of loop diuretics?
furosemide
bumetanide
33
what are loop diuretics most commonly used for?
CCF
severe oedema
34
what are some examples of thiazide diuretics?
Indapamide. Bendroflumethiazide
35
what is the MOA of thiazide diuretics?
act on the distal convoluted tubule
block the Na/Cl co-transporter
this reduces sodium and water re-absorption
36
what are thiazide diuretics commonly used for?
used for HTN control as they cause moderate diuresis (not as much as loop diuretics)
37
what are some exmaples of potassium sparing diuretics?
spironolactone
eplerenone
amiloride
38
how do potassium sparing diuretics work?
spironoloactone + eplerenone - block the aldosterone receptors, reducing Na reabsorption and potassium loss
amiloride - block Na channels, preventing Na reabsorption
39
what are potassium sparing diuretics most commonly used for?
often used in combination with other diuretics to prevent K loss, as they are weaker diuretics
40
MOA of carbonic anhydrase inihibitors?
Act on the proximal tubule.
Inhibit carbonic anhydrase, reducing bicarbonate reabsorption and increasing urine output.
41
what is an example of carbonic anyhdrase inhibitors?
acetazolamide
42
what is acetazolamide used for?
glaucoma
altitude sickness
43
how do osmotic diuretics work?
Work throughout the nephron, primarily in the proximal tubule and loop of Henle.
Increase the osmotic pressure in the filtrate, pulling water into the urine.
44
what is an example of an osmotic diuretic?
mannitol
45
when is mannitol used?
emergency - raised ICP
46
what is an ASO titre?
ASO Titer (Antistreptolysin O Titer) is a blood test that measures the level of antistreptolysin O (ASO) antibodies in the blood. These antibodies are produced by the immune system in response to an infection with group A Streptococcus bacteria (which cause strep throat and skin infections like impetigo).
47
what are complement C3 levels and why are they low in post-strep glomerulonephritis?
Complement C3 levels refer to the amount of C3 protein in the blood, which is part of the complement system—a group of proteins that help the immune system fight infections and clear damaged cells.In Post-Streptococcal Glomerulonephritis (PSGN), C3 levels are typically low due to excessive consumption of complement proteins in the immune response.
The immune system mistakenly attacks the kidneys, activating the complement system and leading to C3 depletion.
48
how does acute bacterial endocarditis cause acute glomerulonephritis?
infection causes antibodies to be made against the bacterial antigens - they then circulate through the bloodstream and get treapped in the glomruli causing inflammatio.
the immune system aslo activates the complement system which worsens inflammation and leads to glomerular injury.
IE also causes septic emboli - which can lodge in the blood vessels leading to ischaemia.
49
how are nephritic syndrome and nephrotic syndrome different?
nephritic syndrome - due to inflammation of the glomeurli, causes oedema, haematuria and some degree of protein loss.
nephrotic syndrome - due to non-inflammatory damage to the glomerular filtration barrier.- causes severe protein loss and massive oedema, but NO haematuria
50
what is SLE?
systemic autoimmune disease that affects a wide range of bodily tissues. Leads to immune complex dysregulation, with leads to the formation of antibody-immune system complexes. They then deposit into any organs, including kidney, skin, heart, and brain. The deposits then cause local inflammation and damage.
51
what type of hypersensitivity reaction is SLE?
type 3 hypersensitivity reaction
52
what genes is SLE associated with?
HLA B8
DR2 DR3
53
who is SLE most common in?
F:M - 9:1
more common in afro-caribbeans and asian communities
54
what age does SLE typicially appear?
20-40 years
55
what are the investigations for SLE?
ANA - 99% are positive
RF - 20% are positive
anti-dsDNA - highly specific > 99%, but less sensitive
anti-smith - highly specific > 99%, nut sensitivity 30%
also anti- ro and anti-la
ESR
56
what are the features of SLE?
malar rash - butterfly rash on the face in response to sun
discoid rash - plaque like , chronic
photosensitive skin
ulcers of mouth/nose
pleuritis / pericarditis
arthritis - 2 or more joints
renal disorder - diffuse proliferative glomerulonephritis
blood disorders - anaemia/thrombocytopenia
seizures/psychosis
57
what is the most common type of lupus nephritis?
diffuse membranous glomerulonpehritis
58
what is diffuse membranous glomerulonephritis?
Diffuse membranous glomerulonephritis (DMGN) is a type of kidney disorder that primarily affects the glomeruli, which are the tiny filtering units of the kidneys. The term "diffuse" means that the condition affects most of the glomeruli, and "membranous" refers to the thickening of the glomerular basement membrane, which is a key structure in the filtration process
59
what is the pathophysiology of diffuse membranous glomerulonephritis?
antibodies form targeting the glomerular basement membrane, leading to immune complex formation whcih deposit in the basement membrane, this causes thickening of the membrane and loss of function.
60
how do you diagose diffuse membranous glomerulonephritis?
renal biopsy - classical findinting of immune complex deposits along the glomerular basement membrane and electron microscopy shows "spike and dome" appearance
61
management of diffuse glomerulonephritis?
usually immune suppression - with corticosteroids or immune supressants i.e. cyclophosphamide, mycophenolate
62
what is goodpasture syndrome?
rare autoimmune disease where antibodies attack the type 4 collagen found in the lungs and kidneys. This leads to small vessel vasculitis causing bleeding in the lungs and renal failure.
63
what is goodpasture syndrome also known as?
anti-glomerular basement membrane disease
64
symptoms of goodpasture syndrome?
abrupt onset of cough with haemoptysis, SOB, peripheral oedema, dark urine and oliguria
65
what is seen on renal biopsy with goodpasture disease?
cresenteric glomerulonephritis
66
investigations for goodpasture disease?
Anti-GBM antibody titre - useful confirmatory diagnostic test in addition to the renal biopsy.
Anti-neutrophil cytoplasmic antibodies (ANCA) - positive in up to 30% of patients with anti-GBM disease.
Urea & electrolytes - high urea and creatinine
67
management of goodpasture disease?
secondary care
intensive plasmapheresis to remove all the antibodies - 4L per day for 10-14 days
then prednisolone 3 month course
or cyclophosphamide
68
what is the most common cause of glomerulonephritis worldwide?
IgA nephropathy
69
what is the pathophysiology of IgA nephropathy?
immune system goes into overdrive after upper resp tract infection
produces IgA immune complexes
deposit in the glomeruli
70
what are the clinical features of IgA nephropathy?
usually young male
recurrent episodes of macroscopic haematuria
associated with URTI 1-2 days after
71
management of IgA nephropathy?
typically - supportive
manage HTN - needs early and aggressive management with aCE-I or ARB
steroids - needed for 6 months
72
what is granulomatosis with polyangitis?
Granulomatosis with polyangiitis (GPA, formerly known as Wegener's granulomatosis) is an antineutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis, typically affecting small and medium sized blood vessels.
73
what is the classic triad of symptoms for granulomatosis with polyangitis?
upper resp tract infection
lowe resp tract infection
glormerulonpehritis
74
investigations for granulomatosis with polyangitis?
cANCA positive in > 90%, pANCA positive in 25%
chest x-ray: wide variety of presentations, including cavitating lesions
renal biopsy: epithelial crescents in Bowman's capsule
75
management of granulomatosis with polyangitis?
needs admission - risk of deterioration is high without aggressive management
76
what medications commonly cause glomerulonephritis?
NSAIDs
antibiotics - penicillins, cephalosporins, sulfonamides
PPI
diuretics
allopurinol
lithium
hydralazine
77
what are some causes of chronic glomerulonephritis?
IgA nephropathy
focal segmental glomerulosclerosis
membranous nephropathy
SLE
diabetic nephropathy
HTN nephropathy
Alport syndrome
chronic interstitial nephritis
vasculitis
78
what is focal segmental glomerulosclerosis?
typically causes nephrotic syndrome, but can cause nephritic
thought to be caused by an initial glomerular injury, which then leads to loss of podocytes, and scar formation
79
how to diagnose focal segmental glomerulosclerosis>
renal biopsy - segmental sclerosis and effacement of foot processes on electron microscopy
80
management of FGS?
steroids +/- immunosupression
81
what is alport syndrome?
X linked inherited dominant disease
defect gene which codes for type IV collagen
leads to formation of abnormal glomerular basement membrane
82
what are the features of alport syndrome?
renal failure
haematuria
bilateral sensorineural deafness
lenticonus/retinitis pigmentosa
83
what is seen on renal biopsy for alport syndrome?
splitting of the lamina densa resulting in basket weave appearance
84
why would a patient with alports have a failing renal transplant
caused by the presence of anti-GBM antibodies, leading to a goodpasture syndrome type picture
85
what is the triad of nephrotic syndrome?
1. Proteinuria (> 3g/24hr) causing
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema
86
what is the most common cause of nephrotic syndrome in children
minimal change glomerulonephritis - 80%
87
what are the causes of nephrotic syndrome?
minimal change glomerulonephritis
membranous glomerulonephritis
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis
systemic disease - DM, SLE, amyloidosis
88
what is minimal change disease?
autoimmune condition where there is T-cell medicated damage to the glomerular basement membrane, causing increased glomerular permeability and loss of albumin
89
what is seen on biopsy for minimal change disease?
normal glomeruli
electron miscoscopy shows fusion of podocytes and effacement of foto processes
90
what is the prognosis of minimal change disease?
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
91
how is minimal change disease managed?
oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases
92
what are some complications of nephrotic syndrome?
thromboembolism
hypercholesterolaemia
infection
progress to CKD / renal failure
93
what is the most common renal cancer?
hypernephroma/renal cell cancer - arising from the proximal renal tubular epithelium
94
what are the symptoms of renal cancer?
haematuria
loin pain
abdominal mass
pyrexia of unknown origin
95
what are the endocrine effects of renal cell cancer?
may secrete EPO - causing polycythemia
PTH - causing hypercalcaemia
96
what are the risk factors for renal cell carcinoma?
smoking
high BMI
HTN
occupational hazard - asbestos
polycystic kidney disease
chronic hep C infection
97
where does renal cell carcinoma commonly spread?
lung
liver
bone
98
what can be seen on CXR with mets from renal cell carinoma?
cannon ball metastases
99
what are the two types of bladder cancer?
transitional cell cancer
squamous cell cancer
100
which type of bladder cancer is the most common in the UK?
transitional cell cancer
101
where does transitional cell bladder ca arise from?
arises from the urothelium - the transitional lining of the bladder
102
which type of bladder cancer is the most common in the world?
squamous cell cancer
103
which type of bladder ca has a poorer prognosis?
generally SCC - as it tends to present at a more advanced stage than TCC
104
what are the risk factors for bladder cancer?
smoking
schistosomiasis infection
stasis of urine
chronic UTI
textile/rubber industry exposure
105
how does bladder cancer tend to present?
haematuria typically painless
but can present with loin pain, back pain, frequency, recurrent UTI symptoms
106
what are the different stages of bladder cancer
T1 - only the epithelium
T2 - invades into the connective tissue surrounding the bladder
T3- invasion through the muscle into the fat layer
T4 - spread beyond the bladder
107
how is T1 bladder cancer treated
TURBT +/- chemo
108
how is T2 bladder cancer treated?
same as for t1 - TURBT +/- chemo
109
how is T3 bladder cancer treated?
radial cystectomy +/- radiotherapy
110
what is the CKS guidelines for referral to TWR suspected bladder malignancy?
anyone aged 45 and over:
- unexplained visible haematuria without UTI
- visible haematuria that persists after treatment for UTO
anyone aged 60 and over:
- unexplained non-visible haematuria AND either: dysuria or raised WBC
111
first choice and second choice abx for UTI in pregnancy?
1st - nitrofurantoin 100mg MR BD for 7/7 (avoid in third trimester)
2nd - cefalexin 500mg BD for 7/7 OR amoxicillin 500mg TDS for 7/7
112
first choice abx for UTI in non-pregnant woman?
nitrofurnatoin 100mg MR BD for 3/7
trimethoprim 200mg BD for 3/7
113
what is the second line choice of abx for UTI in non-pregnant woman?
nitrofurnatoin 100mg MR BD for 3/7 (if not tried as first line)
Pivmecillinam 400mg one dose, then 200mg TDS for 3/7
Fosfomycin one sachet 3g
114
what abx are used for prophylaxis of recurrent UTI with obvious trigger ie post coital ?
single dose nitrofurantoin 100mg OD
OR since dose trimethorpim 200mg
second line - can use single dose amox (but off label) or cefalexin 500mg once only
115
what abx are used for daily prophylaxis for recurrent UTI?
trimethorpim 100mg ON if low risk for resistance or nitrofurantoin 50-100mg ON
116
what can be offered for prophylaxis of UTI in women alternative to abx?
hipprex - methenamine hippurate (1g twice daily)
117
what is hipprex?
methenamine hippurate - urinary antiseptic - works on urea-degrading bacteria such as pseudomonas or proteus
118
abx first line treatment for catheter associated UTI?
Nitrofurantoin 100 mg modified-release twice a day for 7 days, or
Trimethoprim 200 mg twice a day for 7 days (if low risk of antimicrobial resistance), or
Amoxicillin 500 mg three times a day for 7 days (only if urine culture results show susceptibility).
119
abx second line for catheter associated UTI?
Pivmecillinam 400 mg initial dose, then 200 mg three times a day for a total of 7 days.
120
what is the abx management for men with a UTI?
nitro or trimethoprim for 7 days
121
which men should be referred to urology who have had UTI?
Have ongoing symptoms despite appropriate antibiotic treatment.
May have an underlying cause or risk factor for the UTI.
Have recurrent episodes of UTI (for example, two or more episodes in a 6-month period).
122
mx of suspected UTI in <3 months?
refer to paeds ED - needs IV
123
mx of suspected pyelonephritis in > 3 months old child?
if clinically stable and well - can treat with cefalexin
arrange USS
send urine for mc+ s
review after 48 hours - needs ED if no improvement
124
first line mx of lower UTI in children 3 months or older?
trimethoprim or nitrofurantoin abx
125
second line mx of lower UTI in children 3 months or older?
switch to nitro, amox or cefalexin
arrange USS
send urine mc+s
126
which children should have a DMSA scan?
atypical UTI - non e.coli organisms
failure to respond to abx in 48 hours
sepsis
puur urinary flow
abdominal or bladder mass
raised creatinine
127
which children should be referred for a ultrasound scan when have had UTI?
During the acute infection in all children with atypical infection.
Within 6 weeks, for all children younger than 6 months of age with first-time UTI that responds to treatment.
In babies and children with a non-E. coli UTI that is responding well to antibiotics and has no other features of atypical infection, a non-urgent ultrasound can be requested, to happen within 6 weeks.
128
what is recurrent UTI defined as in children?
Two or more episodes of UTI with acute pyelonephritis/upper urinary tract infection, or
One episode of UTI with acute pyelonephritis/upper urinary tract infection plus one or more episode of UTI with cystitis/lower urinary tract infection, or
Three or more episodes of UTI with cystitis/lower urinary tract infection.
129
management of recurrent UTI in children?
refer al children to paeds outpatients if well
130
what are the most common UTI organisms?
ecoli
pseudomonas
proteus
streptococci
staph
131
management of acute pyelonephritis?
cefalexin 500mg BD for 7-10 days
co-amoxiclav TDS for 7-10 days
Trimethoprim 200mg BD for 14 days
Ciprofloxacin 500mg BD - only if others are not appropriate
132
management of acute pyelonephritis in women who do not need admission and are pregnant?
cefalexin 500mg BD
133
what is autosomal dominant polycstic kidney disease?
genetic disorder characterised by the formation of numerous cysts in the kidneys
134
what is the genetic mutation responsible for ADPKD?
primarily mutations on PKD1 gene (chromosome 16)
or
PKD2 gene (chromosome 4)
135
which genetic mutation is most common in ADPKD?
PKD1 chr 16 - 85% of cases
136
what are the symptoms suggestive of ADKPD?
hypertension - early sign, due to increased renin secretion
abdominal pain - due to enlarged cyst
haematuria
progressive renal failure
137
how to diagnose ADPKD?
ultrasound primary diagnostic tools
138
what is the diagnostic criteria for ADPKD by ultrasound?
If < 30 years - 2 cysts, unilateral or bilateral
If > 30 years - 2 cysts, both kidneys
If > 60 years - 4 cysts both kidneys
139
what is the prognosis for ADPKD?
Approximately 50% of people with ADPKD have
established renal failure by 60 years of age, but one third will reach 70 years
of age with some preservation of renal function.
140
what are some extra-renal manifestations of ADPKD?
liver cysts - 70%
berry aneurysms 8%
CVD
cysts in other organs
141
management of ADPKD?
Referral all pt to renal
Blood pressure control with antihypertensives
Treatment of UTIs:
This should be achieved using antibiotics according to culture and sensitivity results and local guidelines
A 7-14 day course of antibiotics is recommended
Treatment of kidney stones:
This is achieved with analgesia and appropriate surgical techniques depending on the composition and size of the stone
142
what is a urethral stricture?
narrowing in a segment or segments of the urethra as it runs its course from the bladder to the urethral meatus
143
causes of urethral strictures?
Iatrogenic (45%) - transurehtral interventions, traumatic catheter insertions, prostatectomy, radiotherapy
Idiopathic (30%) - can be from minor trauma to perineum
Infection (20%) - chlamydia/gonorrhoea
Lichen sclerosis / pelvic trauma / congenital urethra stricture
144
symptoms of urethral stricture?
Weak flow of urine (also includes reduced force of ejaculation)
Straining to pass urine
Terminal dribbling
A double stream or spraying of urine (particularly if the stricture is more distal).
145
what are posterior urethral valves?
obstructive membranes that have developed in the urethra close to the bladder - only occurs in boys, and is picked up usually neonatally
146
what are symptoms of PUV?
abdominal mass - palpation of bladder
urinary tract infections (UTIs)
difficulty urinating
a weak stream of urine
unusually frequent urination
bed wetting after toilet training has been successful
poor weight gain
147
Ix for PUV?
refer for USS + MCUG if suspected
refer to paeds
148
what is vesicoureteric reflux?
abnormal back flow of urine from the bladder into the ureter and kidney
149
how common is vesicoureteric reflux?
common - occurs in 30% of children with UTI + fever
150
what is the pathophysiology of VUR?
ureters are displaced laterally, entering the bladder at a more perpendicular angle, this leads to a shortened intramural course for the ureter, and so the vesicoureteric junction cannot functional adequately
151
how is VUR diagnosed?
MCUG - shows reflux of urine
152
how is VUR managed?
Observation: For low-grade reflux in asymptomatic children.
Antibiotic prophylaxis: To prevent urinary tract infections (UTIs).
Surgery: Indicated for high-grade reflux or recurrent UTIs despite prophylaxis, often via ureteral reimplantation.
153
symptoms of renal stones?
renal colic
vomiting
nausea
haematuria
154
what are the different types of renal stones?
calcium oxalate
cystine
uric acid
calcium phosphate
struvite
155
which is the most common type of renal stone?
caclium oxalate
156
what investigations should be done for patients with suspected renal stones?
non-contrast CT KUB within 24 hours
157
what is the management of renal stones based on their size?
watchful waiting if < 5mm and asymptomatic
5-10mm shockwave lithotripsy
10-20 mm shockwave lithotripsy OR ureteroscopy
> 20 mm percutaneous nephrolithotomy
158
what is the management of ureteric stones?
shockwave lithotripsy +/- alpha blockers if < 10 mm
if > 10mm - uretoscopy
159
what is shockwave lithotripsy?
A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone fragmentation
The passage of shock waves can result in the development of solid organ injury
Fragmentation of larger stones may result in the development of ureteric obstruction
The procedure is uncomfortable for patients and analgesia is required during the procedure and afterwards.
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what is ureteroscopy?
A ureteroscope is passed retrograde through the ureter and into the renal pelvis
It is indicated in individuals (e.g. pregnant females) where lithotripsy is contraindicated and in complex stone disease
In most cases a stent is left in situ for 4 weeks after the procedure.
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what is percutaneous nephrolithotomy?
Percutaneous nephrolithotomy
In this procedure, access is gained to the renal collecting system
Once access is achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed.
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how to prevent calcium renal stones from forming?
high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate may be beneficial NICE
thiazides diuretics (increase distal tubular calcium resorption)
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what is cystinuria?
Autosomal recessive condition - Cystine stones are due to an inherited defect in the transport of the amino acid cystine, leading to excessive excretion in the kidney, causing cystinuria.
164
what analgesia should be offered to patients with renal stones?
NSAIDS - diclofenac / ibu
if nsaids not appropriate - IV paracetamol
do not offer antispasmodics
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complications of renal stones?
hydronephrosis
abscess formation
rupture
sepsis
obstruction
UTI
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which medications should be avoided in renal failure?
antibiotics: tetracycline, nitrofurantoin
NSAIDs
lithium
metformin
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which medications require dose adjustment in CKD as they can accumulate?
most abx - including penicillins, cephalosporins, vancomycin, gent
digoxin , atenolol
methotrexate
sulphonyulreas
furosemide
opioids
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which antibiotics can be used at normal dose in renal failure?
erythromycin
rifampicin
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what other medications can be used at normal dose in renal failure?
diazepam
warfarin
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what are the two different types of dialysis?
haemodialysis and haemofiltration
peritoneal dialysis
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how long do haemodialysis sessions last?
3- 6 hours
in CKD - minimum 12 hours split over 2-3 days per week
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how can the efficiency of dialysis be estimated?
from the urea clearance of the dialyser
173
what are short dialysis times associated with?
risk of cardiovascular complications
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what are some complications of dialysis treatment?
hypotension
anaphylactic reactions
HTN
hyperkalaemia
amyloidosis
infection
malnutrition
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how do the clearance rates of haemodyalisis compare to peritonal dialysis?
Haemodialysis achieves clearance rates of 100 ml/min compared to values of 25-30 ml/min for peritoneal dialysis. Thus, peritoneal dialysis becomes increasingly inadequate with:
increasing uraemia
increasing body weight
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what are the complications of peritoneal dialysis?
peritonitis
leakage around the site
local infection
poor drainage
mechanical effects of increased pressure - i.e. abdominal herniae, back pain, haemorrhoids
hypovolaemia
electrolyte disturbance
weight gain
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who is peritoneal dialysis first choice for?
children 2 years old or younger
people with residual renal function
adults without significant associated comorbidities
178
benefits of peritoneal dialysis?
can be delivered at home or another location
patients can administer it themselves
can do this overnight while they sleep
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what are electrolyte abnormalities in CKD and how do they occur?
CKD leads to low vit D
kidneys normally excrete phosphate -> in CKD you get high phosphate levels
phosphate in turn "drags" calcium from the bones, resulting in osteomalacia
low calcium due to lack of vit D
this can lead to secondary hyperparathyroidism - due to low Ca, high phos and low Vit D
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alkalinising agents such as potassium citrate reduce the effectiveness of which antibiotic?
nitrofurantoin
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