Flashcards in Week 4 Deck (173):
1
What bacteria are usually present in the urine?
None- it is sterile.
2
What part of the urinary tract has bacteria?
The lower end of the urethra is colonised by coliforms and enterococci from the bowel.
3
What is the definition of a UTI?
The presence of micro-organisms in the urinary tract that are causing clinical infection (PATIENT MUST HAVE SYMPTOMS TO HAVE A UTI)
4
Upper UTI
Infection involving the kidneys (pyelonephritis) and/or ureters
5
Lower UTI
Infection involving the bladder (cystitis) and/or urethra.
6
What is a complicated UTI?
UTI complicated by systemic sepsis or urinary structural abnormality or stones.
7
Bacteruria
The presence of bacteria in the urine (does not mean infection especially with elderly patients or patients with catheters)
8
Cystitis?
Inflammation of the bladder (not always due to infection)
9
Why do more women get UTI's than men?
Short, wide urethra
Proximity of urethra to anus
Increased risk with sexual activity and pregnancy.
10
What makes you more susceptible to UTI's?
Women
Catheterisation
Congenital abnormalities of the urinary tract.
11
What is the most common route of infection?
Ascending infection- bacteria from the bowel enters the urethra and goes up.
12
How else (not ascending infection) can you get a UTI?
Haematogenous spread- patient with bacteraemia/septicaemia from another focus of infection
Bacteria in blood- seeded in the kidneys- multiple small abscesses- urine bacteria.
13
What are coliforms?
A class of bacteria found in the gut.
14
Causative coliforms for UTI?
E coli- main one (70%)
Klebsiella and enterobacter also.
Proteus is less common.
15
What is proteus infection in urinary tract associated with?
Formation of stones (calculi). Also foul smelling.
16
What does proteus produce?
Produces urease which breaks down urea to form ammonia which increases urinary pH and precipitation of salts.
17
What are enterococci and which enterococci cause UTI's?
They are a type of streptococci found in the gut.
Commonly enterococci faecalis and enterococcus faecium.
18
What UTI infection are women of childbearing age likely to get?
Staphylococcus saphrophiticus (coagulase negative staph)
19
What other type of staph (other than saphrophiticus) can cause UTI's?
staph aureus.
20
Which causative organism of a UTI is associated with catheters and instrumentation?
Pseudomonas aeruginosa.
21
What symptoms do UTI's present with?
Dysuria
Frequency of urination/nocturia
haematuria
22
What symptoms suggest an upper UTI?
Loin pain
Fever
Rigors.
23
Describe the precautions you should take when obtaining a specimen for microscopy?
Do not take the first pass urine- likely to be contaminated. You want a midstream sample.
Get the urine to the lab within 2 hours if it is in a universal bottle or within 24 hours if it is in a boricon container.
24
What does leukocyte esterase in the urine tell you?
Indicates the presence of leukocytes (WBC)
However you can have an increased number of pus cells in the urine in non-uTI patients e.g. those with a catheter in.
25
Why do nitrites indicate the presence of bacteria in the urine?
Some bacteria reduce nitrates to nitrites- mainly coliforms.
26
What coliform will not test positive for nitrites on dipstick?
Enterococcus.
27
Describe Kass's criteria for UTI organisms. Who does it apply too?
>10^5 organisms- significant- probably UTI
10^4 organisms- contaminated? test again
<10^3 organisms- Not significant bacteruria.
Women of childbearing age.
28
Is mixed growth of organisms significant?
Probably not significant- even if greater than 10^5 organisms.
29
What is ESBL and what is the significance of it?
Extended spectrum beta lactamase.
Resistant to all cephalosporins and almost all penicillins.
30
All cephalosporins start with...
Cef, ceph or kef
31
Which antibiotics may be useful against extended spectrum beta lactamase?
Nitrofurantoin (oral)
Pivmecillinam (oral)
Fosfomycin (Oral)
Temocillin (IV)
Meropenem (IV)
Ertapenem (IV)
32
Where does ESBL come from?
Imported chicken.
33
What are carbapenemase producing enterobactericaei?
They are gram negative coliforms bacilli that are resistant to meropenem.
34
What is the significance of CPE?
They are effectively resistant to all current antibiotics. Resistance is plasmid mediated and spreads easily.
35
How do people get CPE?
Some strains are associated with travel to Indian subcontinent. Hospitals in London and Manchester now affected.
36
For an antibiotic to be effective to treat UTI, what should it be?
Excreted in the urine in high concentrations
Oral
Inexpensive
Few side effects.
37
How long should the course of antibiotics be for men and women in an uncomplicated UTI?
Women- 3 days
Men- 7 days
38
How would you treat an uncomplicated female lower UTI?
Nitrofurantoin 50mg qds or 100mg MR
Or
Trimethoprim 200mg BD. (3 days)
39
How would you treat an uncomplicated male UTI?
Nitrofurantoin 50mg qds or 100mg MR
Or
Trimethoprim 200mg BD. (7 days)
40
When would you not use trimethoprim?
Safe other than in the 1st trimester of pregnancy.
41
How else can trimethoprim be given? (hint- in combination)
As co-trimoxazole (oral or IV)- combination of sulphamexazole and trimethoprim- risk of Steven Johnson syndrome.
42
How would you treat complicated UTI or pyelonephritis in GP?
Co-amoxiclav or co-trimaxozole for 14 days.
43
How would you treat complicated UTI or pyelonephritis in hospital?
Amoxicillin and gentamicin for 3 days.
(use co-trimaxozole if penicillin allergic).
44
When would you not use nitrofurantoin?
In 2nd and 3rd trimester of pregnancy (can cause neonatal heamolysis)
Breast feeding
Children < 3months old.
45
If pregnant women have an asymptomatic bacteruria, would you treat- if so what with?
Yes you would.
And with nitrofurantoin early in pregnancy and trimethoprim late in pregnancy.
46
How is gentamicin administered?
IV
47
Why is gentamicin only used for 3 days?
Its toxic- can cause renal and VIIIth nerve damage (deafness and balance problems)
48
When should antibiotics be given in catheterised patients?
Only be given if there is supporting evidence of UTI (fever, rigors ect)
49
What is abacterial cystitis/ urethral syndrome?
Pus cells present in the urine but no significant growth on culture.
50
Why would you have abacterial cystitis?
Early phase of UTI
Urethral trauma- honeymoon cystitis
Could be due to urethritis caused by STI (chlamydial or gorrnorhoeal)
51
How would you treat a patient with abacterial cystitis?
Alkalinisng the urine may help with symptoms.
52
Cause of acute urinary retention?
Benign prostatic hypertrophy.
53
What does it mean by precipitated acute urinary retention?
When there has been some sort of surgery, catheterisation or instrumentation that predisposes you to acute urinary retention.
54
How is acute urinary retention treated?
Catheterisation.
In BPH- add an alpha blocker (tamsulosin)
55
What is post obstructive diuresis? Who gets it?
Once the catheter has been removed- high urine output after obstruction is relieved.
Patients with chronic outflow obstruction, uraemia, oedema, CCF or hypertension.
56
Is it worrying if you get haematuria in acute urinary retention?
Nope- usually settles within 24 hours (catheter can cause bleeding)
57
Differential of acute loin pain?
AAA
Ureteric colic secondary to calculus.
58
How would you treat acute renal stones?
Fluids, pain control and anti-emetics
Surgery- either renal stenting or if there is a radiologist around then do percutaneous nephrostomy
59
For stones less than 10mm what is the management?
For stones greater than 10mm what is at the management?
Medical expulsive therapy
Use an alpha blocker
Extracorporeal shock wave therapy or ureteroscopy.
Very large stones (greater than 15mm)- percutaneous antegrade uretoscopy
60
Where are renal stones likely to get stuck?
Where the ureter crosses the iliac vessels.
61
When would you want to treat renal stones urgently?
Pain is unrelieved
Pyrexia
Persistent nausea/vomiting
High grade obstruction.
62
How would you treat renal stones urgently?
Ureteric stent or stone fragmentation/removal if no infection.
Percutaneous nephrostomy for infected hydronephrosis.
63
What can cause frank haematuria?
Infection (infective cystitis is a really common cause)
Stones
Tumours
BPH
Polycystic kidneys
Trauma
Coagulation/platelet deficiencies
64
How would you treat clot retention?
Use a 3 way irrigating haematuria catheter.
Investigate using a CT urogram and cystoscopy.
65
Describe spermatic cord torsion?
Usually occurs at puberty. Can be due to sport but most often is spontaneous.
66
Presentation of spermatic cord torsion?
Adolescent often woken from sleep.
Sudden onset of pain (sometimes previous episodes of self limiting pain due to torsion sorting itself out)
May have nausea/vomiting
Pain may be referred to the lower abdomen.
67
Examination of spermatic cord torsion
Testis high in the scrotum
Transverse lying
Absence of cremasteric reflex (stroking the inner thigh causes the testis to retract)
Acute hydrocele and oedema may obliterate landmarks.
68
Investigations into spermatic cord torsion
Could do ultrasound. Will tell you if there is blood supply to the testis.
69
Treatment of spermatic cord torsion
Prompt exploration. Irreversible ischaemic injury may begin as soon as 4 hours.
2-3 point fixation with non-absorbable stitches. Need to do the same to the other side too.
If testes are necrotic then remove.
70
How would someone with appendage torsion present?
Could be more insidious in onset than spermatic cord torsion or could present very similarly.
If seen early may have localised tenderness to the upper pole and 'blue dot' sign.
71
How would you differ between spermatic cord torsion and appendages torsion?
Cremasteric reflex is present in appendage torsion and the testis are more mobile.
72
How would you treat appendage torsion?
Will resolve spontaneously.
73
Describe epipydidimitis presentation?
Also what pre-dipsoses you to this?
Will present similarly to spermatic cord torsion however likely to be pyrexial.
History of UTI, urethritis, catheterisation and instrumentation.
74
On examination of epidydidimitis what would you expect to find?
Cremasteric reflex present
Suspect if pyuria (presence of pus in the urine)
75
Investigations and what you would expect to see in epidydimitis?
Doppler US- swollen epididymis and increased blood flow.
Send urine for culture and chlamydia PCR.
76
How would you treat epidydimitis?
Scotal support, analgesics and bed rest
Ofloxacin 400mg/day for 14 days.
77
How does idiopathic scotal oedema present?
Swollen scrotum. May be itchy
Unknown cause
No fever and tenderness is minimal.
78
What is paraphimosis?
Painful swelling of the foreskin distal to the phimotic ring.
79
When does paraphimosis occur?
Often happens after the foreskin has been retracted for procedures e.g. catheterisation and staff members forget to put it back in its natural position.
80
Treatment of paraphimosis?
Iced glove and granulated sugar for 1-2 hours- to draw fluid out.
Multiple punctures in oedematous skin.
Manual compression of glans with distal traction on oedematous foreskin.
Or a procedure- dorsal slit.
81
What is priapism?
Prolonged erection for greater than 4 hours. Often painful and not associated with sexual arousal.
82
Why does priapism occur?
Could be due to trauma
Intracorporeal injection for erectile dysfunction.
Haematological dycrasias
Idiopathic
Neurogenic
83
How can priapism be classified?
Ischaemic and non-ischaemic
Ischaemic- vascular stasis in penis and decreased venous outflow. Like compartment syndrome
Non-ischaemic- traumatic disruption of penile vasculature results in unregulated blood entry and filling of the corpora.
84
Treatment of priapism
Ischaemic- aspiration +/- irrigation with saline
Injection of alpha agonist e.g. phenylephrine every 5-10mins.
Surgical shunt
Needs to be within 48 hours for treatment to work. If greater than 72 fit penile prosthesis.
Non-ischaemic
Observe- may resolve spontaneously.
Selective arterial embolisation with non-permanent materials.
85
What is Fourniers gangrene?
a type of necrotising fasciitis on the male genitalia. Most commonly arising from skin, urethral or rectal origin.
86
Predisposing factors to fourniers gangrene?
Diabetes
Local trauma
Periurethral extravasation
Perianal infection
87
Pathogenesis of Fourniers gangrene?
Usually starts as cellulitis- swollen, oedematous, tender.
Marked pain, fever, toxicity.
Swelling and crepitus of the scotum (crackles can be heard), dark purple areas.
88
How would you investigate fourniers gangrene?
Plain Xray or US may confirm gas in tissues
89
Treatment of Fourniers gangrene?
Antibiotics and aggressive surgical debridement.
90
What is emphysematous pyelonephritis?
An acute necrotising parenchymal and perirenal infection caused by gas forming uropathogens (usually E coli)
91
Who usually gets emphysematous pyelonephritis?
Diabetics
People with ureteric obstruction
92
Symptoms of emphysematous pyelonephritis?
Fever, vomiting, flank pain.
See gas on KUB
CT defines extent.
93
Treatment of emphysematous pyelonephritis?
Often requires nephrectomy.
94
How do perinephric abscesses occur?
Usually result from rupture of an acute cortical abscess. into the perinephric space or from seeding from sites of infection.
95
Presentation of perinephric abscesses?
Flank mass in 50%
High WCC
High serum creatinine
96
Investigations into perinephric abscess
CT
97
Treatment of perinephric abscess
Antibiotics and percutaneous/surgical drainage
98
Classification of renal trauma
1- haematoma, sub capsular, non expanding with no parenchymal expansion.
2-laceration less than 1cm parenchymal depth
3-Laceration greater than 1cm parenchymal depth- no collecting system rupture or extravasation
4-Laceration through cortex, medulla and collecting system.
5-shattered kidney- avulsion of hilum.
99
When are imaging (CT with contrast) indicated in renal trauma?
Frank haematuria in adult
Frank or occult haematuria in child
Occult haematuria + shock (systolic<90mmhg)
Penetrating injury with any degree of haematuria.
100
Treatment of renal trauma?
98% of blunt renal injuries can be managed non-operatively via angiography or embolisation.
Surgery indicated in - persistent renal bleeding, expanding perirenal haematoma, pulsatile perirenal haematoma.
101
What fracture commonly causes bladder injury?
Pelvic fractures.
102
How do bladder injuries present?
Suprapubic/abdominal pain
Inability to urinate.
Guarding/rigidity
Diminished bowel sounds
103
Treatment of bladder injury?
Catheterisation in most cases.
If it doesn't pass easily or blood at external meatus then perform retrograde urethrogram.
104
what imaging would you do in bladder injury?
CT cystography
105
What will an extra peritoneal injury look like on CT?
Flame shaped collection of contrast in pelvis.
106
Treatment of exztraperitoneal injury?
Large bore catheter
Antibiotics
Repeat imaging in 14 days.
107
What often causes posterior urethral injury?
Fracture to the pubic rami.
108
On examination- how will a urethral injury present?
Blood at the external meatus. Inability to urinate. Palpably full bladder. Butterfly perineal haematoma (awful looking bruise on the perineum)
109
How would you investigate urethral injury?
Retrograde urethrogram
110
How would you treat urethral injury?
Suprapubic catheter.
Delayed reconstruction after at least 3 months.
111
How does a penile fracture occur?
Typically occurs during intercourse- buckling injury when penis slips out of the vagina and hits pubis.
112
How does penile fracture present?
Cracking or popping sound followed by pain, rapid detumescence, discolouration and swelling.
113
How would you treat a penile fracture?
Rapid exploration and repair
Circumcision incision to expose all 3 compartments.
114
What is glomerular nephritis?
An immune mediated disease of the kidneys affecting the glomeruli (with secondary tubulointerstitial damage)
115
Where are the antibodies targeted at in glomerular nephritis? what does it cause?
Could be an intrinsic tissue (e.g. podocytes, endothelium). Could be an implanted antigen.
Causes T cell activation- release of inflammatory mediators (complement).
116
What is the function of mesangial cells?
Act as a structural matrix that holds the capillaries together.
117
Normal glomerular wall filters by:
1: Propels negative ions.
2:size selective- only small ions can get through.
118
Glomerular nephritis disturbs normal filtering function meaning patients present with:
Haematuria and/or proteinuria.
119
Damage to endothelial and mesangial cells leads to.. lesion
A proliferative lesion (inflammatory cells and red cells leak out)
120
Damage to the podocytes leads to a... lesion
Non- proliferative lesion (no inflammatory cascade) and protein in the urine.
121
How to podocytes respond to injury?
They atrophy and shrink back- allowing big proteins to leak through.
122
How do mesangial cells respond to injury?
They proliferate and inflammatory cells come in (release ang2, chemokine and attract inflammatory cells)
123
How do endothelial cells respond to injury?
If you damage the endothelial cells you get inflammation of the vascular epithelium (vasculitis). The capillary wall gets damaged- holes with bursting out blood vessels and inflammatory cells leak out.
124
What allows you to differ between mesangial damage and endothelial damage?
If you damage the endothelial cells you will have a high creatinine. Also really significant renal impairment.
125
What investigations would you do to determine cause of glomerular nephritis?
Urinalysis- proteinuria, haematuria.
Urine microscopy- dysmorphic red cells, lipiduria
Urine protein:creatinine ratio- quantify proteinuria.
126
How would someone with glomerular nephritis present?
Haematuria (painless)- could be micro or macroscopic
Proteinuria: could be:
-microalbuminurea- 30-300mg albuminuria/day)
-asymptomatic proteinuria (<1g/day)
-heavy proteinuria (1-3g/day)
-nephrotic syndrome (>3g/day)
-impaired renal function (AKI or CKD)
-hypertension
-nephrotic syndrome
-nephritic syndrome
-nephrotic nephritic syndrome
127
Why do you get dysmorphic red cells?
During microscopy: the red cells that have to squeeze through the glomeruli will be strange in shape.
128
What do red cell casts tell you?
Whether their are inflammatory and red cells in the glomeruli.
129
What is nephritic syndrome?
Acute renal failure
Oligouria- pass less urine
Oedema/fluid retention
Hypertension
Active urinary sediment- RBCs, RBC and granular casts
130
What is nephritic syndrome indicative of?
A proliferative process affecting endothelial cells
131
What is nephrotic syndrome?
Proteinuria >3g/day
Hypoalbuminaemia
Oedema (more than nephritic)
Hypercholesterolaemia
Usually normal renal function.
132
What is nephrotic syndrome indicative of?
Non-proliferative process affecting podocytes.
133
Complications of nephrotic syndrome?
Infection- due to loss of opsonising antibodies
Renal vein thrombosis (due to hyperlipidaemia and hypercholesterolaemia)
Pulmonary emboli
Volume depletion (overaggressive use of diuretics- may lead to pre renal ARF)
134
What are the three types of biopsy you can do for glomerular nephritis?
Microscopy
IgG staining (good for good pastures)
Electromicrscopy.
135
What are the principles of treatment of GN?
Reduce degree of proteinuria
Induce remission of nephrotic syndrome
Preserve long term renal function
136
Non-immunosuppressive treatment of glomerular nephritis?
Anti-hypertensives- ACE inhibitors/ARBs to reduce proteinuria
Diuretics- lose oedema
Statins- protect cardiovascular risk in long term
Anticoagulate if they are nephrotic.
137
Immunosupressive treatment of glomerular nephritis?
Drugs-
-corticosteroids (prednisolone)
-Azathioprine
-Alkylating agents- cyclophosphamide/chlorambucil
-Calcineurin inhibitors (cyclosporin)
-Mycophenolate Mofetil (MMF)
Plasmapheresis- removal of large volumes of plasma and replacing it- used in really aggressive vasculitis that you know is being mediated by a circulating antibody.
IV immunoglobulin- antibodies that attack the autoantibodies
138
General treatment of nephrotic patients
Fluid restriction
Salt restriction
Diuretics
Ace/ARB
Anticoagulation
IV albumin (only if volume depleted)
then immunosupress them
Aim is to induce sustained remission (remission proteinuria <300mg/day. Partial remission proteinuria<3g per day)
139
Where do minimal change GN autoantibodies target? Will they suffer from nephritic or nephrotic syndrome?
Target the antigen on part of the podocyte.
Causes nephrotic syndrome
140
Who normally gets minimal change nephropathy?
Commonest cause of nephrotic syndrome in children.
141
What will investigations into minimal change nephropathy show?
Normal renal biopsy on light microscopy and IF with foot process fusion showing on electron microscopy.
142
How would you treat minimal change nephropathy?
94% have complete remission with oral steroids.
Some are steroid resistant/dependent or have relapses. In this case use cyclophosphamide or CSA.
143
Can minimal change nephropathy lead to progressive renal failure.
NOPE
144
What might minimal change nephropathy be associated with?
IL 13
145
Who gets focal segmental glomerulosclerosis?
Commonest form of nephrotic syndrome in adults.
146
What can FSGS be secondary too?
HIV, Heroin use, obesity, reflux nephropathy
147
How does FSGS present on investigations:?
Light microscopy- presents as focal segmental glomerulosclerosis (scarring on the glomerulus)
On IF- minimal Ig/complement depositation.
148
Can FSGS be a primary disease?
Yes- it usually presents as this.
149
How would you treat FSGS?
60% get remission with steroids.
50% progress to end stage renal failure.
150
Where are the autoantibodies directed against in FSGS?
What occurs due to this?
Against an antigen in the podocytes. Causes podocyte damage and foot process shrinking back and atrophy.
Parietal epithelial cells try to help out and plug holes- this works to an extent but due to ongoing injury and inflammation- it forms scar tissue.
151
Who gets membranous nephropathy?
Second commonest cause of nephrotic syndrome in adults.
152
Membranous nephropathy can be primary or secondary, what are the secondary causes?
Infections- Hep B/parasites
Connective tissue diseases (lupus)
Malignancies (carcinomas/lymphomas)
Drugs- gold/penicillamine
153
What will a renal biopsy show?
Subepithelial immune complex depositation in the basement membrane.
154
How would you treat membranous nephropathy?
Steroids/alkylating agents/ B cell monoclonal Ab.
155
How common is it that patients progress to end stage renal disease from membranous nephropathy?
30%.
156
What antigen is it that causes membranous nephropathy?
Phospholipase A2 receptor is targeted by anti-PLAR2r antibody
Surface receptor on the podocyte.
The podocytes atrophy when you target them- therefore they shrink down giving a thicker BM.
157
What is the most common nephropathy in the world?
IgA nephropathy.
158
How does IgA nephropathy present?
Asymptomatic microhaematuria +/- non nephrotic range proteinuria.
Macroscopic haematuria after resp/GI infection
Acute kidney disease/chronic kidney disease.
159
What is IgA nephropathy associated with?
Heuloch Schonlein Purpura (HSP)
-arthritis, colitis and purpuric skin rash
160
What will a renal biopsy of IgA nephropathy show?
Mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on IF.
161
How many progress to end stage renal failure with IgA nephropathy?
25%
162
How would you treat IgA nephropathy?
BP control/ ACE inhibitors/ARBs/Fish oil
163
What is the typical presentation of IgA nephropathy?
Young person with tonsillitis- blood in pee and kidney pain.
164
Why is IgA nephropathy a multi system disease?
IgA deposits are not just in the kidney. Vasculitis effects everywhere.
165
How is IgA nephropathy different from other nephropathies?
Antigen is not from the kidney. They have abnormal IgA-IgG antibodies. Immune complexes form causing local injury.
166
What is rapidly progressive glomerular nephritis?
A treatable cause of acute renal failure.
Involves rapid detoiration of renal function over days/weeks.
Active urinary sediment (RBC's, RBC and granular casts)
May be part of systemic disease
167
How does rapidly progressive glomerular nephritis present on biopsy?
Glomerular crescents.
168
What causes rapidly progressive glomerular nephritis?
Can be either ANCA positive or ANCA negative.
ANCA +ve- systemic vasculitis. Wegners granulomatos (GPA) and microscopic polyangititis.
ANCA-ve- Goodpastures disease-GBM
Henoch Scholein Purpura/IgA
SLE
169
What is ANCA?
Anti-nuclear cytoplasmic antibodies- behave like bombs- become much more sticky and stick to vascular endothelium and cause inflammation.
170
Where do good pastures antibodies target against?
Type 4 collagen in BM.
171
What is the treatment of rapidly progressive glomerular nephritis?
Prompt- consist of strong immunosuppression with supportive care including dialysis.
Immunosuppression consists of steroids- prednisone oral or methylprednisolone IV.
Cytotoxics (cyclophosphamide, mycophenolate/azathioprine)
Or plasmapharesis.
172
Scenario- 74 year old lady. Hypoxic. Haemoptysis. Creatinine 430. Blood and protein on dip. Red cell casts on microscopy. Purpuric rash.
Thinking vasculitic cause because of purpuric rash.
Goodpastures- due to the haemoptysis because type 4 collagen damage in alveoli.
Or could be ANCA positive vasculitis
Tests to be done would be biopsy to differentiate between the two.
173