Genitourinary Flashcards
(378 cards)
1
Q
What is testicular torsion?
A
sudden onset of pain in one testis, making walking uncomfortable
2
Q
At what age are you most likely to acquire testicular torsion?
A
11-30 years
3
Q
What symptoms can accompany pain in testicular torsion?
A
Abdominal pain, nausea and vomiting
4
Q
What is the appearance of a testis in testicular torsion?
A
inflamed, hot, tender, swollen in one testis (can be intermittent)
5
Q
How will the testis lie in testicular torsion, in mild and severe?
A
Mild - high and transversely
Severe - horizontal
6
Q
What investigations would you do for testicular torsion?
A
Doppler US - shows lack of blood flow to testis
Surgical exploration - the sooner the better to save the testis
7
Q
What is the treatment for testicular torsion?
A
ask for consent for possible orchiectomy and bilateral fixation
expose and untwist testes and fix to scrotum
8
Q
DD for testicular torsion?
A
epididymo-orchitis, idiopathic scrotal oedema, tumour, trauma, acute hydrocycle
9
Q
What is benign prostatic hyperplasia?
A
hyperplasia of the epithelial and stromal cells of the prostate gland in the transitional zone
10
Q
What part of the prostate undergoes hyperplasia in benign prostatic hyperplasia?
A
The transitional zone
11
Q
Who most commonly gets benign prostatic hyperplasia?
A
males over 60
12
Q
What complications does benign prostatic hyperplasia lead to?
A
Distorts the urethra and obstructs bladder outflow causing urinary retention, recurrent UTI, impaired renal function and haematuria
13
Q
What are the symptoms of benign prostatic hyperplasia?
A
frequency and urgency of micturition, nocturia, hesitancy, intermittent flow, poor urine stream/dribbling, incomplete bladder emptying, enlarged smooth rostate, haematuria, bladder stones, UTI
14
Q
What causes benign prostatic hyperplasia?
A
Androgen dihydrotesterone
15
Q
What will a rectal examination show in benign prostatic hyperplasia?
A
enlarged and smooth prostate with a palpable midline sulcus
16
Q
What investigations should you do for benign prostatic hyperplasia?
A
urine dipstick, microscopy and culture, FBC, U and E, creatinine, LFTs, increased PSA, US of urinary tract and transrectl and renal
17
Q
What are the 4 zones in the prostate?
A
fibro-muscular, transitional, central and peripheral
18
Q
Where is the most common place for prostate cancer to occur?
A
In the peripheral zone
19
Q
What is the management of benign prostatic hyperplasia?
A
watchful waiting if mild
complete international prostate symptom score
complete voiding diary
selective a1 adrenoreceptor antagonists e.g.tamsulosin
5-a-reductase inhibitor e.g. finasteride
urethral catheterisation if retention
prostatectomy or permanent catheter
avoid caffeine and alcohol
relax when voiding and train bladder
prostate resection
incision of prostate
20
Q
How do selective a1 adrenoreceptor antagonists e.g.tamsulosin help treat benign prostatic hyperplasia?
A
They relax smooth muscles in bladder neck and prostate to increase flow rate and reduce symptoms
21
Q
How to 5-a-reductase inhibitor e.g. finasteride help treat benign prostatic hyperplasia?
A
They block the conversion of testosterone to dihydrotesterone to reduce dihydrotestosterone
22
Q
What is an epididymal cyst?
A
A non malignant scrotal disease just above the testis that contains spermatocele fluid
23
Q
When are you most likely to get an epididymal cyst?
A
in adulthood
24
Q
What is the treatment of an epididymal cyst?
A
No treatment unless symptomatic, then remove
25
What is hydrocele?
Fluid within the tunica vaginalis
26
What are the causes of hydrocele?
primary - patent processus vaginalis
| secondary - tumour, trauma, infection
27
What is the treatment of hydrocele?
Primary can resolve spontaneously, aspirate or surgery of placating the tunica vaginalis or inverting the sac
28
What is a varicocele?
Dilated veins of the pampiniform plexus, normally on the left, appear as dilated scrotal blood vessels, will a dull ache
29
What are potential complications of a varicocele?
Can be associated with subfertility and a dull ache
30
What is the treatment of a varicocele?
repair via surgery or embolization
31
How common is testicular cancer?
It is the most common malignancy in men aged 15-44
32
What is the cause of testicular cancer?
undescended testis (even after ochidopexy), infant hernia, infertility
33
What are the 4 types of testicular cancer?
seminoma
non seminomatous germ cell tumour
mixed germ cell tumour
lymphoma
34
What is the most common testicular cancer?
seminoma
35
What is the more common testicular cancer in 20-30 year olds?
non seimnomatous germ cell tumour
36
What are the symptoms of testicular cancer?
testis lump, haemospermia, secondary hydrocele, pain, dyspnoea, abdominal mass, effects of secreted hormones (testosterone), metastases
37
What are the 4 stages of testicular cancer?
1 - no metastases
2 - infradiaphramatic node involvement spread via para aortic nodes
3 - supradiaphramatic node involvement
4 - lung involvement
38
What investigations should be done in testicular cancer?
CXR, CT and US of testis, excision biopsy, a-FP, B-hCG mildly raised, increased serum LDH
39
What is the treatment of testicular cancer?
radical orchiectomy, surgery, radiotherapy, chemotherapy, self examination education
stage 3 - cycles of bleomycin and etoposide and cisplatin
40
What is involved in a radical orchiectomy?
Inguinal incision to occlude spermatic cord before mobilisation to reduce risk of intra operative spread
41
What is the prognosis of testicular cancer?
>90% 5 yr survival
42
What is the most common age to get prostate cancer?
72
43
What are risk factors for prostate cancer?
age, family history, african
44
What are the symptoms of prostate cancer?
weight loss, malaise, fatigue, bone pain and fracture, normocytic anaemia, hypercalcaemia, purpura, immune suppression, anorexia, thirst, confusion, collapse, hard irregular gland
45
What will a per rectum examination show in prostate cancer?
enlarged prostate gland, uninodular or multinodularr, midline sulcus is not palpable
46
What is protein specific antigen?
It is expressed from normal and neoplastic prostate tissue and secreted into the blood stream?
47
What is an abnormal PSA level and what level is seen in 50% of men with prostate cancer?
>4ng/ml
| >10ng/ml
48
What percentage of people with elevated PSA levels do not prostate cancer?
6%
49
What investigations should be done for prostate cancer?
FBC, U and E, creatining, LFTs, transrectal US, transrectal prostate biopsy, endorectal coil MRI for staging, TNM staging, urine dipstick, microscopy, PCA3, gene fusion products
50
What is used for prostate cancer grading?
The Gleason grading score form the biopsy, add the two most common together, and the higher the more aggressive
51
What does the prostate cancer screening involve?
annual measurement of serum PSA and digital rectal examination
52
Where is the most common site for metastases from the prostate?
The bone, leading to bone pain and fracture
53
What are some disadvantages of the prostate cancer screening?
cost, variable intervals of testing, increased anxiety, overdiagnosis
54
What is the treatment for prostate cancer?
macmillan nurses and psychological support
radiotherapy with external beam and brachytherapy
watchful waiting
high intensity US
Goserelin - a LHRH agonist
Antiandrogens e.g. cyproterone
Transuretheral resection of prostate (TURP)
Laparoscopic radical prostatectomy
55
How does androgen deprivation therapy work in the treatment of prostate cancer?
Uses GnRH agonists e.g. goserline, leuprorelin, orchidectomy to lower circulating androgens
56
What does androgen deprivation therapy for prostate cancer have to be used with?
Needs an antiandrogen e.g. flutamide in the 1st phase due to the initially increase LH and testosterone which could cause a flare in metastases.
The antiandrogen inhibits CYp17 for androgen production to prevent flare
57
What should be used for prostate cancer treatment if resistant?
2nd line hormone therapy e.g. abiratone which inhibits adrenal androgen synthesis
cytotoxic chemo
bisphosphonates
5-a-reductase inhibitors
58
What is the treatment of prostate cancer if no metastases?
Androgen deprivation therapy and radiotherapy
59
What parts of the body are lined with transitional cell epithelium?
calyces, renal pelvis, bladder, urethra
60
What is another name for bladder cancer?
Transitional cell carcinoma
61
How common is bladder cancer?
4th most common in men
8th most common in women
9th overall
62
Who is most likely to get bladder cancer?
men in the 80s
63
What is the mortality of bladder cancer?
50%
64
Why is an elderly women with UTI symptoms cause suspicion for bladder cancer?
As UTIs are common in the young, and it is rare she has just become sexually active or changing partners
65
What are risk factors for bladder cancer?
smoking, occupational exposure to carcinogens e.g. rubber, leather, plastics, azo dyes, fishing, exposur to industrial chemicals e.g. phenacetin, cyclophosphamide, schitosomiosis (chronic inflammation), chronic infection
66
What are the two types of bladder cancer and which is most common?
urothelial - 95%
| squamous cell - 5%
67
What are the clinical features of bladder cancer?
haematuria (usually painless), dysuria, urgency, frequency, flank pain, pain to a metastases
68
What does grade mean in terms on cancer?
indicator of invasiveness
69
What does stage mean in terms of cancer?
extent of the cancer
70
What are the 4 grades of bladder cancer?
Low grade - 70% - recurrence and bleeding
Medium grade
Invasive high grade - 2.5%
Carcinoma in situ - 5% - high rate of progression - poorly differentiated
71
What investigations should be done in bladder cancer?
urine dipstick, blood tests, flexible cystoscopy, upper tract imaging
72
What is an advantage and disadvantage of using CT over US?
CT is more detailed but uses more radiation
73
Why is a transurethral resection used instead of a biopsy in bladder cancer?
To show histological grade and stage
74
What is the treatment of a non muscle invasive bladder cancer?
resection and intravesical chemotherapy. Use mitmoycin , mmc and BCG
75
How does MMC work in bladder cancer treatment?
reduces risk of recurrence and causes cell lysis
76
How does BCG work in bladder cancer treatment?
reduces risk of progression to muscle invasive and upregulates cytokines
77
What is the treatment of a muscle invasive bladder cancer?
radical surgery of cystoprostatectomy and urethrectomy with neoadjuvant chemotherapy and radical radiotherapy
78
What is the treatment of a locally advanced bladder cancer?
radical surgery with neoaduvant/adjuvant chemotherapy, radical radiotherapy
79
What is the difference between adjuvant and neoadjuvant chemo?
adjuvant aims to kill cancer cells and neo adjuvant aims to shrink it before surgery
80
What is a BCG?
A bacilli Calmette Guerum, which is a bladder installation
81
What is haematuria and how is it detected?
blood in the urine found by MSSU or dipstick, it is >3RBC/HPF
82
What is the difference between macroscopic and microscopic haematuria?
macroscopic can be seen and microscopic appears normal
83
What does a urine dipstick detect?
RBC, free Hb and myoglobin
84
How sensitive is a urine dipstick for RBC?
97% so many false positives
85
What is the difference between uniform and dysmorphic in MSSU?
```
uniform = non glomerular origin
dysmorphic = glomerular origin
```
86
If there is RBC and dysmorphic in urine tests, what does this suggest?
a glomerular disease
87
What does the presence of leucocytes and bacteria in a urine test suggest?
stones of infection
88
What can cause a false positive blood test?
menstruation and exercise
89
What does red urine but MSSU negative suggest?
porphyria, rifampicin, beetroot, veg dyes
90
What does a positive dipstick but negative MSSU suggest?
haemolysis myoglobinuria, vit C excess
91
What does haematuria and dysuria and frequency suggest?
UTI
92
What does haematuria and bilate loin pain suggest?
glomerulonephritis
93
What does haematuria and uteteric colic suggest?
stone disease
94
What investigations should be done in haematuria?
urine analysis, urine cytolody, abdomen US, abdomen CT, cytoscopy, renal biopsy
95
Rare causes of haematuria?
sport, renal artery embolism, renal vein thrombosis, loin pain haematuria syndrome, idiopathic
96
What do negative urological tests in haematuria suggest?
nephrological cuase
97
In who is renal cell carcinoma most common?
male, ages >60
98
Risk factors for renal cell carcinoma?
smoking, obesity, hypertension, asbestos
99
Signs and symptoms of renal cell carcinoma?
haematuria (40%), flank pain, paraneoplastic, weight loss, fever, malaise
100
Causes of renal cell carcinoma?
Von Hippel Lindau disease, dialysis, familial traits, smoking, heavy meals, obesity
101
What is the mutation in Von Hippel Lindau disease that causes renal cell carcinoma?
lose short arm of chromosome 3, causing inactivation of VHL gene which is a tumour suppressor gene, and then there is over expression of VEGF antagonist
102
How willVon Hippel Lindau syndrome present?
phaeochromocytoma, renal and pancreatic cysts, cerebellar haemangioblastoma
103
Treatment of renal cell carcinoma?
nephrectomy, exploration is IVC is involved, mutli-tyrosine kinaseinhibitors eg. sumirtinab and sarefinib
104
How do multi-tyrosine kinase inhibitors treat renal cell carcinoma?
block kinase that usually phosphorylates proteins and cause proliferation
105
What will investigations show in renal cell carcinoma?
liver dysfunction, abnormal LFTs, cholestasis, nephrogenic hepatomegaly
106
What is the difference between a simple and a complex cyst?
simple is benign, complex can be benign or cancer
107
What classification is used in cystic lesions?
Bozniak Classification
108
What is the Bozniak classification?
1-simple septations, thin wall
2-irregular wall, no enhancement
3-thick, irregular wall enhancement
4-irregular walls, ca and enhancement
109
What investigations are done in a cystic lesion?
classification, spatial observation, renal biopsy, surgery, bone scan if raised Ca, DMSA renogram if concerned about renal fucntion, CT chest and abdo with contrast, MRI if other organs/IVC affected or poor renal function
110
What are the histological subtypes in renal cell carcinoma?
clear cell (80-90%)
papillary (10-15%)
chromophobe (4-5%)
sarcomatoid
111
What is involved in small renal mass surveillance?
can progress to cancer so should be managed with serial imaging to follow progression
112
What is involved in cryotherapy?
2 freeze cycles using helium and argon,
113
What is involved in radiofrequency ablation?
heating, percutaneously or laparoscopically
114
When is cryotherapy and radiofrequency ablation used?
in small cystic lesions, in patients with VHL, solitary kidneys, unsuitable for partial/full nephrectomy
115
When is surgery used for renal cell carcinoma treatment?
preferably nephron sparing, T1 and
116
Treatment of metastatic renal cell carcinoma?
palliative nephrectomy, surgical resection if can do complete resection and has good performance status, radiotherapy to symptomatic bone and brain metastases
117
Where does metastatic renal cell carcinoma develop from and what do they have high levels of?
proximal tubules, high levels of expression of the mulitiple drug resistance protein, so resistant to chemo.
118
What is the multiple drug resistance protein expressed in high levels in renal cell carcinoma?
P-glycoprotein
119
How does sporadic clear cell renal cell carcinoma cause neoangiogenesis?
hypoxia inducible factor accumulation from VHL inactivation causes increased VEGF and PDGF to promote neoangiogenesis
120
Palliative treatment in renal cell carcinoma?
palliative nephrectomy, macmillan, embolisation, palliate bleeding, radiotherapy to alleviate bleeding, node pain, bone pain, cerebral mass
121
What is polycystic kidney disease?
mutations leading to cyst formation, full of fluid, leading to kidney enlargement
122
What is the main form of polycystic kidney disease?
autosomal dominant
123
What are the 2 main mutations in autosomal dominant polycystic kidney disease?
PKD1 gene (c16) which codes for the polycystin 1 protein which regulates tubular and vascular development
PKD2 gene (c4) is less cases
124
Symptoms of polycystic kidney disease?
acute loin pain from cyst haemorrhage, infection, or urinary stone formation
abdominal discomfort from renal enlargement
flank pain/back pain
hypertension
renal impairment
mitral valve prolapse
cerebral aneuryms, subarachnoid haemorrhage,
125
Diagnosis of polycystic kidney disease?
kidney US shows large, irregular kidneys, multiple fluid filled cysts
hypertension, hepatomegaly
creatinine
head imaging
FH +2cysts 60
126
How does age affect polycystic kidney disease?
cysts increase in size with age, leading to more kidney tissure destruction and loss of renal function
127
Treatment of polycystic kidney disease?
monitor BP, ACE-I, dialysis, renal transplant, familial screening, geneic counselling, gene linkage analysis, laproscopic cyst removal, increase water, decrease sodium, avoid caffiene, target sites of action of PKD1/2
128
How do renal cysts form?
cysts grow in planar polarity then proliferate and multiply so grow outwards of lumen, destroys surrounding tissue and is disconnected from lumen, fluid secretion and apicobasal polarity, causing obstruction and hydronephrosis
129
What is the difference in presentation of polycystic kidney disease in men and women?
men - haematuria
| women - pain
130
When is mutation analysis indicated in polycystic kidney disease?
```
potential LRD under 40
older patient and no FH
atypical cystic disease
prenatal testing for early onset of disease
pre implantation genetic diagnosis
```
131
What is autosomal recessive polycystic kidney disease and how does it present?
1/40000, on chromosome 6, variable signs, may present in infancy with multiple renal cysts and congenital hepatic fibrosis, no specific therapy
132
What is medullary sponge kidney?
dilation of collecting ducts in papillae, with occasional cystic change, small caliculi form within the cysts
133
How does medullary sponge kidney present?
renal colic, haematuria, hypercalciuria, renal tube acidosis, medullary sponge like appearance
134
What is meduallary cystic disease?
autosomal recessive mutation in NPHP1-4 genes, mutating the proteins nephrocystin and inversin in the cilia of the renal tubules
135
Causes of polycystic kidney disease?
simple, acquired, CKD, lithium, congenital: ADPKD, ARPKD, TS. VHL, OFDS1
136
What is orofacial digital 1 syndrome?
in females (as it is lethal to males), abnormalities to dental and roof of mouth, extra digits and renal cysts
137
What is tuberous sclerosis?
adenomasebations, spots around the nose, hyperpigmented patches
138
What is Von Hippel Lindaw?
a pre renal cell carcinoma syndrome, increased renal cancer ris, inherited germline mutations and can devlop brain tumours and hermangioblastomas
139
What is a typical GFR?
120ml/min, 20% of cardiac output
140
Examples of creatinine secretion inhibitors?
trimethoprim, cimetidine, ritonavir
141
How do you predict creatinine generation?
based on age, race, gender
142
Where is most stuff reabsorbed in the kidney?
in the proximal tubule, reabsorbing Na, glucose, Hco3-, amino acids
143
What does the descending loop of Henle reabsorb?
Na, K, Cl
144
What does the distal convoluted tubule reabsorb?
Na and Cl
145
What does the collecting duct reabsorb?
sodium, regulated by aldosterone and secretes potassium and hydrogen ions
146
What dirves cellular K+ uptake in the kidney?
insulin and catechloamines
147
Treatment of hypokalaemia?
loop diuretics and thiazide diuretics
148
Treatment of hyperkalaemia?
spironolactone, amiloride, ace-i, arbs, trimethoprim, calcineruin
149
What does a increase in aldosterone cause?
sodium retention and potassium excretion
150
When are ACE-I and ARB used in CKD treatment?
in glomeular hypertension which causes proteinuric CKD
151
How is circulating active vitamin D produced?
by 1a hydroxylation in the proximal tubule
152
How does CKD affect vitamin D production?
increased FGF-23 production which inhibits 1a-hydroxylation, inhibiting vitamin D production
153
Function of calcitrol?
increases calcium and phosphate absorption from the gut and suppresses the parathyroid hormone
154
What causes calcitrol deficiency?
advanced CKD, leading to secondary hyperparathyroidism
155
What nerves drive detrusor contraction?
PNS s3-5 (cholegenic)
156
What nerves inhibit detrusor contraction?
SNS t10-l2 (noradenergic)
157
How much fluid can a full bladder hold?
400-600ml
158
How much is in an empty bladder?
159
Who is more likely to become incontinent and why?
women, due to a shorted urether, so less resistance and higher pressure
160
What is acute renal failure?
a reversible decrease in GFR caused by damage to the kidneys, leading to a rise in serum urea and creatinine and loss of normal water and solute homeostasis
161
Main causes of acute renal failure?
pre renal (40-70%) - failure of cardiac/liver/skin/vascular, sepsis, infection, haemorrhage, thrombosis
intrarenal (10-15%) - renal vascular, glomerulinephritis, nephrotic syndrome, nephrotoxis drugs, microangiopathy, hypertension, inflammation, autoimmune disease
post renal (10-25%) - urinary tract obsturction, stones, tumour, prostatic hypertrophy, extrinsic compression
162
Stages of acute renal failure with serum creatinine and urine output?
early - creatinine >26.5umol/L or 1.5-2xrise - urine output 6h
moderate - creatinine 2-3x baseline - urine output 12h
severe - creatinine >3x baseline or >350u/mol/L or start RRT - urine output 24h or >12h anaemia
163
In who is acute renal failure common?
hospital admissions, elderly, critically ill
164
Mortality of acute renal failure?
25-30%
165
Risk factors of acute renal failure?
>75yrs, CKD, HF, Chronic liver disease, diabetes, new drugs, spesis, poor fluid intake, history of urinary symptoms, blockage of urinary tract, dehydrated, infection, aminoglycosides
166
Most common cause of acute renal failure and types of this?
intra renal
acute glomerularnephritis - from SLE, erythromyetosis
acute tubular necrosis (50% of AKI)
acute interstitial nephritis - in allergic reactions and infection
vascular
167
Pathophysiology of acute renal failure?
vascular change causes inflammation and tubular change causes back leakage of urine
168
What do investigations show in acute renal failure?
decrease GFR and urine output, increase nitrogenous waste in blood (urea, creatinine)
apoptosis, loss of adhesion
pericardial rub, suprapubic percussion dull
CT, CXR, avoid imaging with contrast, US (priotity if anuric)
169
Symptoms of acute renal failure?
lethargy, nausea, anorexia, itch, confusion, rash, joint pain, red eyes, nasal stiffness, GI bleeding, haemoptysis, reduced urine output, impaired platelet function, abdominal flank pain, oedeme, pruritis
170
Treatment of acute renal failure?
treat underlying cause, stop nephrotoxins, fluid, electrolytes, improve perfusion, restrict sodium and potassium, prevent pressure sores, antibiotics, dialysis, nutrition, sequele, prevent further complications, MDT, catheter if obstruction, percutanous nephrostomy, prevent ischemic renal injurt
171
When should you use dialysis in acute renal failure?
AEIOU
```
acidosis -metabolic
electrolyte abnormalities e.g. K
ingestions of toxins - salicylates, methanol, barbityrates
overload of fluid
uremic symptoms e.g. pericarditis
```
172
What is the classification of acute renal failure?
RIFLE
risk, injury, failure, loss, end stage
173
When would you do a urology referral in acute renal failure?
infected or obstructed urinary tract, renal stone, urological malignancy, renal trauma, frank haematuria,
174
Management of pulmonary oedema?
o2, diureticsm nitrates, opiates, venesection, haemodialysis, ventilatory support
175
What complications can acute renal failure lead to?
metabolic acidosis, hyperkalaemiam hyperphosphataema, pulmonary oedema
176
What does prognosis of acute renal failure depend on?
underlying cause, most common cause of death is sepsis from impaired immune defence from uaemia, malnutrition or dialysis//catheters
it is reversible
cortical necrosis can heal with scar tissues, tubule regenerate
177
What can you use to determine pre renal or intra renal acute renal failure?
urine specific gravity and urine osmolarity are higher in pre renal, urine sodium and fractional excretion of sodium are less in pre renal
178
What is the onset like in post renal AKI?
insidious rather than acute
179
What are the 2 phases in acute tubular necrosis?
initialoliguric phase from decrease GFR, microvascular vasoconstriction, ischemia, but then tubular cells can regenerate , reversing it
diuresis during recovery phase - improved GFR but still impaired tubular reabsorpton
180
How does acute tubulointerstitial nephritis cause acute renal failure?
interstitial inflammation with oedema and tubular damage, occurs do to infection (acute pyelonephritis) or hypersensitivity reaction to drugs (penicillin, NSAIDs)
181
How does hyperkalaemia appear in ECG and what is the treatment?
tall tented t waves
small absent p waves
increase PR interval
wide QRS
IV calcium gluconate, Iv insulin and dextrose, ion exchange resins
182
NICE definition for acute renal failure?
rise in serum creatinine of 26+mmol/L in 48hrs
50% rise in serum creatinine in past 7 days
drop in urine output to 0.5ml/kg/h for 6 hours
(different for children)
183
What is glomerulonephritis?
disease of the glomeruli, inflammation
184
What is the most common cause of end stage renal failure?
glomerulonephritis
185
How does glomerulonephritis present?
leaky glomeruli, haematuria, proteinuria, hypertension, decreased kidney function, end stage kidney failure, oedema, low urine sodium and fractional excretion of sodium
186
Why is urine sodium low in glomerulonephritis?
due to congestion of afferent arterioles, so kidney perceives there to be less blood coming to the kidneys
187
What tests should be done in glomerulonephritis?
urines and bloods, complete metabolic profile, azotemia, elevated creatinine, 24 hr urine protein, renal biopsy
188
What is the difference between nephritic and nephrotic syndome?
all glomerulonephritis cause nephritic syndrome (RBC in urine), and have the ability to cause nephrotic syndrome if proteinuria is severe enough (>3.5g/day) which can then lead to hypoalbuminaemia and hyperlipidaemia
189
Causes of glomerulonephritis?
autoimmune with glomerular (anti-GBM) or non glomerular (immune complexes) antigens
non immunological e.g. DM
190
What is acute nephritic syndrome and how does it present?
AKI with rapid deterioration in function, presenting with oliguria, hypertension, oedema and increased intravascular fluid
191
What are the causes of acute nephritic syndrome?
ANCA associated vasculitis
goodpastures syndrome (antiglomerular basement membrane disease)
SLE, systemic sclerosis
post streptococcal infection
crescentric IgA
nephropathy/Henoch Schonlein purpura (variant of IgA nephropathy)
192
How does acute nephritic syndrome appear on histology?
acute, severe, rapidly progressive
proliferative, membranous, membranoproliferative, cresecnteric
Bowman's space filled with fibrin, epithelial cells and inflammatory cell matrix to form crescents
compress glomerulus
193
What are the 4 types of glomerular disease and how do they differ?
diffuse - all glomeruli
focal - some glomeruli
global - all of the glomerulus
segmental - part of the glomerulus
194
What can cause proteinuria?
transient, orthostatic, glomerula abnormalities, increased GFR, reduced renal mass, hypertension, tubular proteinuria
195
How does nephrotic syndrome present?
heavy proteinuria, hypoalbuminaemia, periorbital edema (especially on walking), hyperlipidaemia, scrotal vulvul leg and ankle edema, ascites, breathlessness
196
Causes of nephrotic syndrome?
primary, DM, amyloidosis, infections, SLE, drugs, malignancy, malaria
197
What are the 3 types of primary nephrotic syndrome and who are they most common in?
minimal change - children and adults
membranous - caucasian adults
focal segmental glomerulosclerosis - black adults
198
Management of nephrotic syndrome?
treat complications of fluid state and clotting abnormalities, treat underlying cause, diuretics, ACE-I, ARBs, spironalactone, anticoagulation, salt restriction, NSAIDs
199
How does minimal change nephrotic syndrome appear?
normal biopsy, but fused podocytes of ECM
200
Treatment of minimal change nephrotic syndrome?
steroids
201
How does membranous nephrotic syndrome appear?
thickened basement membrane due to immune complex formation or drugs, antiphospholipase A2 receptor antibody positive
202
Treatment of membranous nephrotic syndrome?
supportive, immunosuppresives
203
How does focal segmental nephrotic syndrome appear?
scarring focal to only some glomeruli involved and segmental
204
Treatment of focal segmental nephrotic syndrome?
steroids, immunosuppression
205
What is IgA nephropathy?
abnormality in IgA glycosylation leading to mesangium deposition and mesangeum proliferation
206
What is the most common cause of asymptomatic glomerulonephritis?
IgA nephropathy
207
Treatment of IgA nephropathy?
BP control, ACE-I and ARBs, immunosuppression if aggressive
208
What are the two causes of asymptomatic glomerulonephritis?
iga nephropathy and thin membrane disease
209
How will asymptomatic glomerulonephritis present?
incidental haematuria and proteinuria, kidney function and BP are normal
210
3 main functions of the kidney?
water regulation, salt regulation, acid/base regulation
211
What happens to JVP in fluid overload?
becomes more visible and increases
212
What should be done for fluid management?
fluid input and output chart, weight and stool chart, oral fluid if able, IV if unable
213
What are the two types of IV fluid?
crystalloid and colloid
214
What is crystalloid fluid?
small molecules pass through cell membrane form intravascular to extravascular, if fluid contains salt, it stays in intravascular space a bit longer than 5% dextrose e.g. isotonic solutions
215
What is colloid fluid?
large molecules which do not pass through cell membrane, remains in intravascular compartment and expands the intravascular volume through higher oncotic pressure
216
What patients are at risk of hypovolaemia?
elderly, ileostomy, short bowel syndrome, bowel obstruction
217
What patients are at risk of hypervolaemia?
CKD, heart failure, liver failure
218
What is euvolaemia?
no signs or symptoms of hypo or hypervolaemia
219
How to treat a rise in creatinine?
reduce diuretics or relax fluid restriction
220
What are the 3 methods of renal replacement therapy?
haemodialysis, peitoneal dialysis, transplant
221
How does haemodialysis work?
exchange out side the body, it is removed for cleansing, dialysed then returned to the body via and AV fistula
222
What is an AV fistula?
joining of an artery to a vein to provide permanent and easy access for insertion of needle with good blood flow, 2 needles, one to add and one to remove
223
How long does it take for an AV fistula to be mature?
pressure from the artery makes the vein bigger, taking 4-8 weeks
224
How is haemodialysis used in urgent situations?
on right atrium and one other side of chest, using a cuffed haemodialysis catheter
225
How often is haemodialysis done?
in hospital 4hrs 3x a week or 2-3hrs 4-5x a week at home
226
What drug is also given during haemodialysis?
heparin as an anticoagulant as foreign bodies would activate the clotting cascade
227
Side effects of haemodialysis?
hypotension from excessive extracellular fluid removal, cramps, nausea, headache, chest pain, fever, rigors
228
What are the potential risks in haemodialysis?
blocked dialysis or catheter, infection, fistula aneurym, removal too fast, amyloidosis
229
What is peritoneal dialysis?
uses the peritoneum as a membrane to exchange fluids and solutes in the blood in the lower abdomen, waste products move down conc gradient into dialysis fluid
230
What type of catheter is used in peritoneal dialysis?
Tenckoff
231
What is the difference between continuous ambulatory peritoneal dialysis (CAPD) and APD?
capd - done every 3-4 hours for about 30 minutes
apd - done at night
232
When would peritoneal dialysis be the preferred choice?
young, full time work, want control and responsibility, severe HF
233
When would haemodialysis be the preferred option?
live alone, frail, elderly, scared of operating machienes, previous abdominal surgery, hernia, lack of space at home
234
Long term complications of dialysis?
CV disease, sepsis, peritonitis, amyloidosis
235
Why is amyloidosis caused by dialysis?
accuulation and polymerisation of B2 microglobulin as it is not excreted by the kidney but not dialysis
236
Benefits of renal transplant?
increased survival over dialysis (80% at 10yr)
can get pregnant
economic advantage
increased QoL, can go abroad
237
Treatment of stage 5 CKD?
renal transplant
238
Which is better, living or deceased donor and why?
living as increases survival and graft half life, reduces mortality by CV, infection, malignancy, treatment withdrawal
239
Surgical complications of renal transplant?
bleeding, infection, blood clot in renal artery, need immuno suppression
240
What is cross matching?
final step before any transplant, to see if donors lymphocytes and recipients serum to see any attack, a better match is better survival
241
What is a total match and total mismatch score?
```
match = 000
mismatch = 222
```
242
What are the types of match and which is most important?
A, B, DR
A is most important, each one has two subtypes
243
What is erectile dysfunction/impotence?
the inability to achieve and maintain an erection for sexual performance
244
In who is erectile dysfunction commonly seen?
in elderly due to erectile capacity decreasing with age
245
What causes erectile dysfunction?
vascular, neurogenic, iatrogenic, anatomical, hormonal, psychogenic
DM, hypertension, MS, nerve damage, hormonal imblances, atherosceloris, heart disease, unhealthy lifestyle, oebese, alcoholic, smoking, drug abuse, medications, antihypertensive, antipsychotics, antidepressant
246
What psychological factors can cause erectile dysfunction?
stress, fear, gloom, uncertainty, sadness, relationship problems
247
Lifestyle choices to help erectile dysfunction?
quit smoking, reduce alcohol, dont abuse drugs, exercise regularly, psychotherpay, talk to partner
248
What is erectile function?
neurovascular phenomenon under hormonal control causing arterial dilation, smooth muscle relaxation and activation of the corporeal veno occlusive mechanism
249
Anatomy of the penis?
left and right corpora cavenosa covered by and fused together by tunica albuginea, containing spongy vascular erectile tissue with trabeculated smooth muscle lined by endothelial cells
corpus spongiosum has thinner tunica and contains the urethra, glans penis and bulb of penis
250
Blood supply of the penis?
internal iliac supplies the internal pudendal which supplied the
dorsal penile - glans penis
cavernosal - spongy tissue of corpora
bulbar - bulb, spngiosum, glans
251
Venous drainage of the penis?
sinusoids to subtunieal plexus to circumflex veins and deep dorsal veins
corpora cavernosa to cavernous veins to crural veins to internal pudendal veins
252
Nerve supply of the penis?
```
erection = s2-s4
relax = t11-l2
```
cavernous never carries both fibres
253
Physiology behind an erection?
NO release causes cGMP build up
cGMP dependent pKa activates large conductance, K+ channels open, so hyperpolarising and relaxing vascular and trabecular smooth muscle cells allowing engorment
254
What is the difference between psychogenic and organic erectile dysfunction?
organic is gradual, no erection in any circumstances and morning erections are effected
psychogenic is sudden, situational and unaffected by morning erections
255
Causes of hypogonadism?
testicular dysfunction (high LH, low testosterone), hypothalamic dysfunction (low LH as cant produce any), pituritary dysfunction, chronic illness, age
256
Tests for erectile dysfunction?
nocturnal penile tumescence and rigidity, intracavernosal injection test, duplex USS of penile arteries, arteriography, morning testosterone, fasting glucose, lipid profile
257
Treatment of erectile dysfunction?
lifestyle, psychosexual counselling, PDE5 inhibitors, ampomorphine SL, intracavernous injections, intraurethral aloprostadil, vacuum device, testosterone replacement, monitor for hepatic and prostatic disease, viagra, change BP meds, start satin, penile prosthesis implantation
258
How do PDE5 inhibitors treat erectile dysfunction?
increase blood flow, vasodialation and erection via action on NO
259
What are the 3 types of oral pharmacology for erectile dysfunction?
sildenafil (viagra), tadalafil (Cialis) and vardenafil
260
How does sildenafil (viagra) work?
60 minute wait after administration, effected by food and alcohol, reduced efficacy after fatty meal, increased erections in diabetics, successful intercourse, cheap and can be prescribed
261
How does tadalafil work in erectile dysfunction?
30 min wait, maintained for 36 hours, 2 a week, last long time
262
How does varenafil treat erectile dysfunction?
30 min wait, less effective after fatty meal
263
When is oral pharacology contraindicated in erectile dysfunction?
concurrent use of nitrates, hypertension, degenerative retinal disorders, unstable angina, stroke, MI, bleeding, peptic ulcer, renal/hepatic impairment
264
Side effects of oral pharmacology in erectile dysfunction?
headache, flushing, dyspepsia, nasal congestion, dizziness, visual disturbance, back pain, myalgia
265
Side effect of alpha blockers ?
orthostatic hypotension
266
How does sublingual apomorphine treat erectile dysfunction?
centrally acting dopamine agonist, sublingual, no CI with nitrates, lower efficacy than PDE5 inhibitors, limited to mild-moderate ED
267
How does a vacuum constriction device treat erectile dysfunction?
passive engorgment with constricton ring, 90% efficacy and reduced efficacy over time, keeps the blood in the penis due to pressure, causing penis enlargement, use for 30 mins, it is a cold erection
268
Side effects of a vacuum constriction device for ED?
painful, inability to ejeculate, petechiae, bruises, numbness, expensive
269
Contraindications of vacuum constriction device for ED?
bleeding disorder or anticoagulants
270
How do intracavenosal injections treat ED?
inject into copra cavernosa e.g. alprostadil
271
Side effects of intracavenosal injections for ED?
pain, prispism, fibrosis, leading to a high drop out rate
272
What is a priapism?
a prolonged erection for more than 4 hours, risk of permanent ischemic damage to the copara
273
Treatment of priapism?
aspirate coproa with 19 gauge needed, inject phenylephrenine if that fails
274
How does intraurthral alprostadil treat ED?
void, then massage pellet into urethra
SE pain, dizzines and urethral bleeding
275
How does a malleable prosthesis treat ED?
2 rods, placed in corpora cavernosa surgically, so it is always hard and you just postion it yourself, but can cause penis shortening
276
How does a mechanical implant treat ED?
2 empty cylinders into corpra cavernosa and pump is placed in scrotum, reservoir placed in abdomen
277
What is urinary incontinence?
involuntary passage of urine which is sufficient enough to be a health or social problem
278
What is voiding?
relaxing sphincters and contracting detrusor muscle, overall control and coordinate of micturition is by higher brain centres
279
In who is urinary incontinence seen?
common in elderly >65, 25% of women, 15% of man
280
Under what control are the bladder sphincters under?
```
internal = involuntary
external = voluntary
```
281
What happens in an empty bladder?
decrease in stretch fibres in the bladder, causing the SNS to cause the detrusor muscle to relax and internal spincter contract via the hypogastric nerve and causes the pontine micturition centre to release a PSNS fibre to inhibit M3 and have detrusor relaxation, also activates pudendal nerve to activate skeletal muscle of external sphincter
282
What happens when the bladder is full?
increase in stretch fibres to cause sphincter relaxation and detrusor muscle contraction
283
What are the 4 types of incontinence?
urge, stress, overflow, functional
284
What is urge incontinence?
overactivity of detrusor so it thinks it full, causing it to leak , causing urgent urination (detrusor instability)
285
What can cause urge incontinence?
bladder infection, stones, stroke, dimentia, Parkinsons
more common in women
286
Treatment of urge incontinence?
treat underlying cause, absorbant pad, condom catheter, incontinence chat, bladder training
287
What is stress incontinence?
due to increased intra abdominal pressure causing sphincter weakness and degeneration of pelvic floor and urethral sphincter, leads to urethral atrophy
288
Causes of stress incontinence?
women after childbirth, cough, sneeze, weak pelvic floor, neurogenic or iatrogenic in men
289
Treatment of stress incontinence?
pelvic floor exercises, intravaginal electrical stimualtion, oestrogen creams, prostatectony, male sling, transurethral injections with autologous myoblasts
290
What is overflow incontinence?
due to a full distended bladder leading to leakage of small amounts of urine
291
Cause of overflow incontinence?
men with prostatic obsturction or post spinal cord injury or women with cystoceles
292
Treatment of overflow incontinence?
catheterisation
293
What is functional incontinence?
unable to get to the toilet due to disability e.g. stroke, trauma, dementia, diuretic treatment
294
Treatment of functional incontinence?
improve facilities, regular urine voiding, absorbent padding
295
How can autonomic neuropathy cause urinary incontinence?
decreased detrusor excitability causing distended atonic bladder with a large residual volume urine which is liable to infection so may need permanent chatheterisation
296
Treatment of an overactive bladder?
behaviour therapy - frequency volume chat, caffeine, alcohol
physio - pelvic floor exercise, biofeedback, electrical stimulation
drugs - anticholinergic agents e.g.oxybutynin, tolterodine, tropium chloride, B 3 adrenergic agonist
intravesical botox - causes muscular paralysis
neuromodulation - prelimary tiral then permanent implant if >50% improved
bladder augmentation - detrusor myectomy and cystoplasty
bladder reconstruction
topical oestrogens
surgery
297
Neurogenic stress incontinence managment?
artificial sphincter, autologous sling, synthetic tapes
298
Neurological causes of incontinence?
brainstem damage leads to incoordination or detrusor muscle activity and sphincter relaxtion
299
What happens to incontinence in a spastic spinal cord injury?
supra conal lesion, loses coordination and completion of voiding
reflex bladder contractions, detrusor sphincter dysynergia, poorly sustained bladder contractions, potentially unsafe and poor sustained bladder contraction
conus is functioning but not controlled by the brain
involunatry urination and defaecation
300
What happens to incontinence in a flaccid spinal cord injury?
conus lesion with decentralised bladder, loser reflex bladder contraction, guarding reflex and receptibe relaxation
areflexic bladder, stress incontinence, risk of poor compliance
bladder overflows e.g. spina bifida, sacral fracture, transverse myelitis, ischemic injuries, cauda equina
301
What is autonomic dysreflexia?
lesions above T6 from overstimulation of SNS below level of lesion in response to a noxious stimulus, giving symptoms of headache, severe hypertension and flushing
302
What is reflex bladder?
harness reflexes to empty bladder into incontinence device, suppressed reflexes converting bladder to flaccid type and then empty regularly, suppress with anticholinergics, botox, cystoplasty
303
What is C5 tetraplegia?
no movement or sensation below upper chest and minimal hand function, has spasm and is at risk for autonomic dysrefelexia, reflex bladder, reflex bowel and reflex erections
manage with suprapubic indweling catheter, coveen drainage, SARS and urostomy
304
What is coveen drainage?
no indwelling catheter, needs monitoring, develop incomplete bladder emptying in the long term, make the sphincter safe with sphincterotomy and intersphincteric botox
305
What is SPC?
inserted under anaesthetic, preferably spinal, for infections, stones, autonomic dysreflexia, use clip and release and use large catheters
306
What is paraplegic?
paralysed from waist down with normal upper body function, has spasm, reflex bladder, reflex bowel and reflex erections
manage with suprapubic catheter, coveen or suppresses reflexes
307
How does MS cause incontinence?
demyelinated nerves cause damage and prevent transmission, causing overactive bladder syndrome, urinary urgency, frequency or incomplete bladder emptying
308
What is renal calculi?
stones in the renal tract
309
What are renal calculi made of?
small masses of minerals when they are very concentrated and become crystallised: calcium, strivite or uric acid crystals
310
Symptoms of renal calculi?
lower abdominal pain, painful and frequent urination, haematuria, nocturia, UTI, dark urine
311
Main causes of bladder stones?
enlarged prostate, damaged nerves to the bladder, weakened bladder wall, diverticular, inflammed bladder, UTI, radiation to urinary tract, catheters, hypercalcaemia, hyperuricaemia, from kidney stones travelling down
312
Risk factors for bladder stones?
dehydration, infection, low protein, older men, rare in the young, neurogenic bladder
313
What is renal colic?
caused by kidney stones, rapid onset of unilateral loin pain, unable to get comfortable, radiates to groin and ipsilateral testis with nausea, vomiting, fluid loading, flank pain, back pain
314
Investigations for renal calculi?
distended stomach
24 hr urinalysis of calcium, uric acid, oxalate and citrate
CT KUB (kidney, ureter, bladder) for radiopaque stnes
US/IVU
chemical analysis for stone composition
KUBXray
NCCT KUB
315
Treatment of renal calculi?
small ones are observed, intravenous pyelogram to detect stones, litholapasty, surgical removal, extracororeal shock wave lithotripsy if large, antegrade uteric stent insertion, nephrostomy insertion, allopurinol, low oxalate diet, stop diuretics, low calcium diet, antiemetics, IV fluids, analgesics and tamsulosin, antibiotics
316
Complications of renal calculi?
recurrent UTI, recurrent calculi, obstruction, trauma, bleed
317
Prevention of renal calculi?
hydrate, low Na diet, normal dairy, healthy protein, reduce BMI, exercise, deacidify urine/alkalisation, cysteine binders (captopril, penicillamine)
318
What is piyonephrosis?
combination of infection and obstruction which can lead to loss of renal function in 24 hours and systemic sepsis and septic shock, treat with IV antibiotics, IVI, o2 and drainage
319
DD of renal calculi?
ruptured AA, bowel, gynae, testicular torsion, MSK
320
What is congenital COLA?
where you cant keep aminoacids, and cystine renal calculi form
321
Prevention of uric acid stones?
deacidification
322
Prevention of cystine stones?
excessive overhydration, urine alkalinisation, cysteine binders, genetic counselling
323
Consequences of urospesis?
20 digit gangrene
324
How big are kidney stones?
most are relatively small but can grow large, leading to increased pressure and pain
325
Pathophysiology of urinary tract obstruction?
severity is based on size, rise in intraluminal pressure, dilation proximal to obsturction, compression and thinning of renal parenchyma, progressing to a thin rim and resulting in a decrease size of kidney
326
Effect of urinary tract obstruction on tubular function?
dysregulation of aquaporin water channels in the proximal tubule, thin descending loop and collecting tubule, leads to polyuria and impaired concentrating capacity
decreased sodium transport leading to impaired ability to concentrate and dilute urine
greater sodium and water excretion after release of BUO than UUO, due to retention of Na, water, urea nitrogen and increased ANP which stimulate a profound naturesis
altered potassium and phosphate excretions
deficit in urinary acidification
327
Gross pathological changes to the kidney due to obstruction?
dilation of pelvis and ureter, blunting of papillary tips, heavier kidney, edematous parenchyma, cortex and medullary tissues have thinned, cysts appearing
328
Microscopic pathological changes to the kidney due to obstruction?
lymphatic dilation, interstitial oedema, tubular and glomerular preservation, collecting duct and tubular dilataton, widening of Bowman's space, tubular basement membrane thickening, cell flattening, papillary tip necrosis, regional tubular destruction, inflammatory cell response, widespread glomerular collapse, tubular atrophy, interstitial fibrosis, proliferation of connective tissue in collecting duct
329
What is SIRS?
severe inflammatory response syndrome which as two of:
| >38c/90, RR>20, pCO212000or
330
What is sepsis?
2xSIRS and confirmed suspicion
331
What is severe sepsis?
sepsis and end organ damage, hypotension with SBP2mmol
332
What is septic shock?
severe sepsis with perisitant hypotension
333
Management of urosepsis?
diagnose with screening sepsis tool, treat with sepsis 6, manage systemic factors, relieve pressure with catheter and nephrostomy
334
What is the sepsis 6 treatment?
high flow o2, blood cultures, iv antibiotics, iv fluid resuscitation, check lactate, monitor hourly urine output
must do this within one hour then critical care support to complete early goal directed therapy
335
What is asymptomatic bacteriuria?
normal urine is sterile but is coming increasing common and may need treatment in pregnancy and children, bacteria ispresent in all catheterised patients
336
Why should you not treat asymptomatic bacteriuria?
increases antibiotic resistant organisms and does no sterilise the system or reduce the number of bacterial species, should only be done if symptoms occur
337
Why are intermittent self catheters preferred?
lowest risk of catheter related complications, and provides max protection for kidneys and better QoL
338
What is a UTI?
inflammatory response of urothelium to bacterial invasion associated with bacteruria and pyuria
339
What is the main organism to cause UTIs?
E.coli
coagulated proteus sp., enterococci, Kiebsiella sp.
340
What is bacteriuria?
prescence or bacteria in the urine that can be asmyptomatic or symptomatic
341
When does bacteriuria need treating?
in pregnancy due to the risk of pyelonephritis and preterm labour risk
342
What is the difference between pathogenic and contaminant bacteriuria?
pathogenic is single isolate and contaminant is mixed growth
343
In who is bacteriuria most common?
over 70s, females, catheters, less common in those who have been circumcised
344
What is pyruria?
prescence of leukocytes in urine, appearing as pus in the urine, associated with infection as it is the hosts tissue response
345
Causes of pyruria?
treated UTI, appendicitis, calculi, bladder tumour, papillary necrosis, PKD, chemical cystisis, tubulointerstitial nephritis
346
Symptoms of cystisis?
dysuria, frequency, urgency, pain, haematuria, cloudy, smell
347
Treatment of cystisis?
hydration, cranberry, ibuprofen, antibiotics
348
Diagnosis of cystisis?
urine multistix dipstick
nitrates and leucocytes means UTI in 98.5% of cases as nitrates are a product of bacteria
haematuria
pH >8 in urea splitting infections
S9 raised in concentrated/protein rich urine
proteinuria
glucose - DM increases UTI risk
ketones - raised in catabolic states
MC+S, clean catch
349
What is classed as a complicated UTI?
males, pregnant, children, reucrrent infection, immunocompromised, nasocomial infection, structural/functional abnormality, SIRS, urosepsis, associated disease
350
Treatment of uncomplicated UTI?
antibiotics e.g. trimethoprim, nitrofuratoin
increased fluids, void pre and post sex
hygiene
351
Causes of antibiotic resistance?
extended spectrum B lactamase production reduces effectiveness of penicillins and cephalosporins
DNA changes e.g. plasma mediated, altered binding sires, altered permeability
repeated antibiotic course or not finished antibiotics
352
What is classed as a recurrent UTI?
>2 episodes in 6 months or >3 in 12 months
caused by reinfection, bacterial persistance or unresolved infection
can be same or different organism >2 weeks after stopping antibiotics
353
What is a UTI relapse?
recurrance of bacteriuria with the same organism within 7 days of completing treatment
354
Treatment of complicated UTI?
MSU needed, longer antibiotics course, USS scan, avoid spemicides and perfumed soaps, vaginal oestrogen replacement, prosnthrocyadins (cranberry), prophylaxis, GAG replacement, urovaxom for Ecoli infection
355
How many pregnant women will develop pyelonephritis?
20%
356
What complications can complicated UTIs lead to?
renal papillary necrosis, renal or perinephric abscess with gram negative septicaemia
357
Who is most likely to get prostatitis?
men of all ages, most common one in men
358
What is the NIDDK/NIH classification for prostatitis?
1 - acute bacterial with s.faecalis and ecoli and chlamydia, presents with systemically unwell, fevers, rigors, significant voiding, pelvic pain, swollen prostate, treat with analgesia and levofloxacin
2 - chronic bacterial or non bacterial, symptoms >3 months, recurrent, pelvic pain, voiding LUTS, uropathogens and blood in urine, treat with anti inflammatorys and a blockers
3 - chronic pelvic pain syndrome and can be inflammatory or non inflammatory
4 - asymptomatic inflammatory prostatitis
359
Treatment of prostatitis?
1 - antibiotics e.g. gentamicin and co-amoxycillin
once well, 2-4 weeks quinolone
IRUSS guided abscess drainage if >1cm
2 - 4-6 weeks quinolone and a blocker and NSAIDs
360
What causes urethritis and the symptoms?
Neisseria gonorrhoea - urethral pus, dysuria, tenesmus, proctitis, discharge
nongonococcal urethritis - thinner discharge caused by c.trachomatis
non infective urethritis - traumatic, chemical, cancer
361
Treatment of urethritis?
mainly STI causes so managed by GUM
362
What causes epididymoorchitis?
chlamydia if
363
Symptoms of epididymoorchitis?
hot, red swollen testicular pain
364
Treatment of epididymoorchitis?
```
GUM if STI
quinolone if >35 or no STI
Deoxycycline and azithromycin if STI likely as it can lead to infertlity
supportive underwear
NSAIDs
drainage of abscess
ceftriaxone is gonorrhoea suspected
```
365
What is pyelonephritis?
infection of the renal parenchyma and soft tissues of the renal pelvis/upper ureter with neutrophil infiltration
366
How does pyelonephritis present?
tender loin pain, fever, pyuria, small cortical abscessses and streaks of pus in renal medulla
367
Who does pyelonephritis affect?
women
368
Treatment of pyelonephritis?
IV Gentamicin/co amoxicillin +/- HDU, increase fluid intake, drain obstructed kidney, catheter is compromised, analgesics, oral antibiotics once well, complete 10-14 days of antibiotics
369
What can pyelonephritis lead to?
renal abscess and emphysematous pyelonephritis
370
What is vesicouretic reflux?
incompetent valve between bladder and ureter, allowing reflux or urine during bladder contraction and voiding, causing dmaage of scarring and hypertension
371
Who is most likely to get reflux?
children, caused by structural or functional abnormalities
372
What is the general treatment for lower UTI?
nitrofurantoin or trimethoprim, increase fluid intake
373
What added investigations would you want to do in a complication UTI?
renal US, cystoscopy, KUB-XR
374
Treatment of an upper UTI?
ABCDE, rehydration, IV antibiotics, drain hydronephrosis, catheter, percutaneous nephrostomy
coamoxiclav, ciprofloxacin, OR gentamycin and cefuroxime IV
375
DD of acute pyelonephritis?
acute appendicitis, diverticulitis, cholecystitis, ruptured ovarian cyst, ectopic pregnancy
376
What protein inhibits bacterial adhesion in the urinary tract?
Tamm-Horsfall protein
377
Host factors against UTI?
urinary IgA, vaccine therapy, antegrade flushing of urine, gag layer resists adhesion, low urine pH, high osmolality
378
Bacterial factors that increase UTI risk?
capusule, toxins, enzymes, urease to make the urine more alkaline, a fimbril attachments, fimbriae/pili
