Pathology Flashcards
(358 cards)
1
Q
What is a typical presentation of UTI?
A
Dysuria, frequency increased, smelly urine
2
Q
Presentation of UTI in very young?
A
Unwell, failure to thrive
3
Q
Presentation of UTI in very old?
A
Incontinence, off their feet
4
Q
What is the content of normal urine?
A
Low pH, high osmolality and high ammonia
5
Q
Is the urinary tract sterile?
A
Yes except for the term a urethra
6
Q
Why is a initial urine sample not useful?
A
Because initial urine is heavily contaminated by urethral floral bacteria
7
Q
What type of urine sample do we use?
A
MSSU (mid-stream specimen of urine0
8
Q
How is MSSU cultured?
A
Sent to a museum hahah jk I’m losing my mind
Dip slide method (agar and moist sponge) 24hr incubation at 37degrees
9
Q
At what level of a MSSU culture is there an infection?
A
10(5) Per ml
10
Q
Is there an infection in MSSU culture is 10(3)-10(4)
A
If symptoms probably an infection, if no symptoms 50% chance
11
Q
Problems with MSSU?
A
Difficult to collect in young children and elderly and
Some bacteria species are no not normally present in terminal urethra/ rectal flora and may be pathogenic at low colony numbers
12
Q
What bacteria commonly causes a UTI?
A
E.coli
13
Q
What is urethritis
A
Urethra inflammation
14
Q
What is cystitis
A
Bladder inflammation
15
Q
What is ureteritis
A
Is inflammation of ureter
16
Q
What is acute pyelonephritis?
A
Inflammation of kidney
17
Q
What are the predisposing factors to a UTI?
A
Stasis of urine, pushing bacteria up urethra from below, generalised predisposition to infection
18
Q
What causes stasis of urine?
A
Obstruction or loss of “feeling” of full bladder
19
Q
What are causes of pushing bacteria up urethra from below?
A
Sexual activity in females and catheterisation
20
Q
Why is stasis of urine a predisposing factor to UTI?
A
Because bacteria that get higher up don’t get flushed out
21
Q
What happens int he urinary system if there is a urethra obstruction?
A
There is upper urethral and bladder dilatation, causing bilateral hydroureter causing bilateral hydronephrosis and eventually chronic renal failure
22
Q
What are consequences of obstruction within the urinary system?
A
Proximal dilatation, there is slowed urine flow causing bacteria not being able to be flushed out and causing an infection, sediments also form due to slowed urine flow creating calculous which cause additional obstruction
23
Q
Major renal tract abnormality causing a UTI in a child?
A
Vesicoureteric reflux
24
Q
What is vesicoureteric reflux?
A
Decreased angulation of ureter entering the bladder
25
Common cause of obstruction of renal tract in adult male?
Benign prostatic hyperplasia
26
Common cause of obstruction of renal tract in adult female?
Uterine prolapse
27
Common cause of obstruction of renal tract in both sexes?
Tumours and calculus
28
Why does a spinal cord/ brain injury cause stasis of urine?
There is decreased sensation, so there is no sense of when to micturate and no sense of when bladder is completely empty soo urine in bladder (residual volume) causing stasis of urine
29
Why is the female sex predisposed to getting UTIs from bacteria being pushed up the urethra from below?
Short urethra,
Lack of prostatic bacteriostatic secretion,
Closeness of urethral orifice to rectum,
Sexual activity,
Pregnancy (puts pressure on ureters and bladder0
30
Acute complication of a UTI?
Severe sepsis and septic shock
31
Chronic complication of UTI
Chronic pyelonephritis which can cause hypertension and chronic renal failure
Or calculi can cause obstruction, causing hydronephrosis, which will cause hypertension and chronic renal failure
32
What are mesangial cells?
“Tree-like” group of cells that support capillaries
33
What does the efferent arteriole contain ?
Plasm, unfiltered proteins such as albumin and antibodies
34
What is glomerulonephritis?
Disease of the glomerulus
35
What are the 4 common presentations of glomerulonephritis?
Haematuria, heavy proteinuria, slowly increasing proteinuria, acute renal failure
36
Main causes of haematuria?
UTI, urinary tract stone, urinary tract tumour, glomerulonephritis
37
Investigations for haematuria?
Urine culture, ultrasound, check results then check his clotting and proceed to renal biopsy
38
What is IgA glomerulonephritis?
IgA is stuck within the mesangium, clogging up with mesangium with IgA, the IgA irrritates the mesangial cells causing them to proliferate and produce more matrix
39
In IgA glomerulonephritis what would you expect to see in light microscopy?
Acccumulation of pink mesangial matrix and too many mesangial cells
40
In IgA glomerulonephritis what would you expect to see in immunoflourescence?
IgA immunoglobulin and complement component C3 in mesangial area of all glomeruli
41
In IgA glomerulonephritis what would you expect to see in electron microscopy?
Deposits of IgA with prominent mesangial cells, the IgA cause increased proliferation of mesangial cells
42
What is IgA nephropathy prognosis?
Return to normal as usually self-limiting, a small % go onto develop chronic renal failure via continued deposition of matrix
43
What is membranous glomerulonephritis
Thickened glomerular basement membrane due to IgG deposits between basal lamina and podocyte, causing protein in the urine
44
What does membranous glomerulonephritis look like on light microscopy?
Thickened glomerular basement membrane
45
What does membranous glomerulonephritis look like on silver stain microscopy?
Spikes of new basement membrane matrix material underneath podcytes
46
What does membranous glomerulonephritis look like on electron microscopy?
Deposits of IgG, basal lamina spike and thickened membrane
47
What affect does IgG have between the basal lamina and podocyte?
IgG activates complement (C3) which punches holes in the filter, creating a leaky filter that allows albumin to be filtered into urine causing nephrotic syndrome
48
Cause of diabetic glomerulonephritis?
There is glycated molecules causing matrix deposition in basal lamina underlying the endothelium and in mesangial matrix, this causes thickened but leaky basement membranes and the mesangial matrix compresses the capillaries
49
What would diabetic nephropathy look like on light microscopy
Small compressed capillary lumens, adhesions to Bowmans capsules, thickened capillary wall which is leaking albumin, increased mesangial matrix (which compresses capillaries), thickened narrowed arterioles (reduced blood flow to glomerulus)
50
What is nodules of mesangial matrix a sign of?
Kimmelsteil-Wilson lesion
51
What does rapidly rising creatinine represent/
Acute renal failure
52
What does crescentic glomerulonephritis look like in histology
Early endothelial damage with fibrin deposition, cellular proliferation and influx of acrophages (forming a crescent) around glomerular tuft, within the Bowman’s space
53
What are the causes of crescentic glomerulonephritis?
Granulomatosis with polyangiitis, microscopic polyarteritis, antiglomerular basement membrane disease, other forms of glomerulonephritis
54
What is granulomatosis with polyangiitis?
A form of vasculitis which affects vessels in the kidneys, nose and lung
55
What antibodies can you test for in granulomatosis with polyangiiits?
Presence of anti-neutrophil cytoplasmic antibodies (ANCA)
56
What do anti-neutrophil cytoplasmic antibodies do within the body/
They are directed against proteinase 3 and myeloperoxidase, antibodies produce tissue damage via interaction with primed neutrophils and endothelial cells
57
Granulomatosis with polyangiitis prognosis?
Fatal if left untreated, 75% complete remission with cyclophosphamide
58
What staging criteria is used for ACute Kidney Injury?
RIFLE
59
Definition of risk of acute kidney injury?
Increase in serum creatinine level (1.5x) or decrease in GFR by 25% or UO <0.5ml/kg/h for 6 hours
60
Definition of Injury of kidneys, a stage in acute kidney injury/
Increase in serum creatinine level (2x) or
decrease in GFR by 50% or
UO<0.5mL/kg/h for 12 hours
61
Definition of failure of kidneys, in acute kidney injury?
Increase in serum creatinine level (3x) or
Decrease in GFR by 75% or
Serum creatinine level >355umol/l with acute increase of >44umol/L or
<0.3ml/kg/h for 24 hours or
Anuria for 12 weeks
62
define the loss stage of acute kidney injury?
Persistent ARF or complete loss of kidney function >4 weeks
63
Define the end-stage kidney disease stage of acute kidney injury?
Complete loss of kidney function >3 months
64
Presentation of chronic renal failure
Asymptomatic, tiredness, anaemia, oedema, high blood pressure, bone pain due to renal bone disease, pruritus, n/v, dyspnoea, pericarditis, neuropathy, coma
65
Infection of ureter
Ureteritis
66
Iatrogenic/ trauma disease that can occur to ureter?
Inadvertently cut or tied during hysterectomy or colon resection
67
Neoplasia disease of the ureter?
TCC of ureter, TCC of bladder obstructing the VUJ, prostate cancer obstructing VUJ, pelvic malignancy, pelvic or para-aortic lymphadenopathy
68
Hereditary diseases of the ureter?
PUJ obstruction, VUJ reflux
69
Obstruction disease of the ureter?
Intra-luminal (stone, blood clot), intra-mural (scar tissue, TCC), extra-luminal (pelvic mass, lymph nodes)
70
Presentation of ureter diseases?
Pain, pyrexia, palpable mass, haematuria, renal failure
71
Infection disease of bladder?
Cystitis
72
Inflammation disease of the bladder?
Interstitial cystitis, Colombo diverticulitis resulting in colo-vesical fistula
73
Iatrogenic/ trauma diseases of the bladder
Bladder rupture, bladder injury from hysterectomy (resulting in vesisco-vaginal fistula)
74
Neoplasia disease of the bladder/
TCC of bladder, SCC of bladder
75
Idiopathic conditions of the bladder?
Overactive bladder syndrome
76
Degenerative diseases of the bladder?
Chronic urinary retention
77
Neurological diseases of the bladder
Neurogenic bladder dysfunction
78
Presentation of bladder disease
Pain, pyrexia, haematuria, lower urinary tract symptoms, recurrent UTIs, chronic urinary retention, urinary lark from vagina (vesico-vaginal fistula), pneumaturia (colo-vesical fistula)
79
What are storage LUTS
Frequency, nocturia, urgency, urge incontinence
80
What are voiding LUTS
Poor flow, intermittency, terminal dribbling
81
What are the common causes of LUTS
Bladder pathology, bladder outflow obstruction, pelvic floor dysfunction, neurological causes
82
What are some neurological causes of LUTS?
Supra-pontine lesions (stroke, Alzheimer’s, Parkinson’s),
infra-pontine supra-sacral lesions (spinal cord injury, disc prolapse, spina bifida),
Infra-sacral (multiple sclerosis, diabetes, causes equine compression, surgery to retroperitoneum)
83
Systemic disorders that can cause LUTS?
Chronic renal failure, cardiac failure, diabetes mellitus, diabetes insipidus
84
What controls bladder sesnsation and conscious inhibition of micturation?
The cortical centre
85
What is known as the micturation centre?
Pons
86
What are the sacral segments uncontrolled of micturation?
S2-S4
87
Relaxation of internal urethral sphincter is via what nerves?
S2-S4 autonomic- sympathetic
88
Relaxation of external urethral sphincter is via what nerves?
Somatic n.
89
Contraction of detrusor muscle is via what nerves?
Autonomic- parasympathetic
90
What are the 2 stages within the micturation cycle?
Storage/ filling phase ans voiding phase
91
Types of infection/ inflammation diseases of bladder outflow tract?
Prostatitis, balanitis
92
Iatrogenic/ trauma disease of the bladder outflow tract?
Pelvic floor damage after traumatic vaginal delivery or hysterectomy, urethral injury from catheterisation or pelvic fracture
93
Neoplasia of bladder outflow tracts?
Prostate cancer, penile cancer
94
Idiopathic diseases of the bladder outflow tracts?
Chronic pelvic pain syndrome
95
Obstruction disease of bladder outflow tract?
Primary bladder neck obstruction, benign prostatic enlargement causing obstruction, urethral stricture, mental stenosis, phimosis
96
Presentation of bladder outflow tract diseases?
Pain, pyrexia, haematuria, voiding LUTS (hesitancy, intermittency, poor flow, terminal dribbling, incomplete bladder emptying), overflow incontince, stress urinary incontinence, recurrent UTIs, acute urinary retention, chronic urinary retention
97
Why is voiding LUTS causes in bladder outflow tract disease?
Because of bladder outflow obstruction
98
Why is overflow incontinence a symptom of bladder oputflow tract diseases
Due to high pressure chronic urinary retention
99
Define acute urinary retention
Painful inability to void with a palpable and percussible bladder
100
What are the residuals of acute urinary retention
Vary from 500ml to 1 litre
101
What are some risk factors of acute urinary retention?
Benign Prostatic Obstruction, UTI, urethral stricture, alcohol excess, post-operative causes, acute surgical or medical problems
102
Patients with acute urinary retention due to BPO are usually triggered because of what/
Constipation, alcohol excess, post operative causes, urological procedure
103
What is treatment of acute urinary retention
Catheterisation
104
Define chronic urinary retention
Painless, palpable and percussible bladder after voiding
105
What are the chronic urinary retention residuals?
400ml to >2 litres
106
What is the main aetiological factor of chronic urinary retention?
Detrusor underactivity
107
How does chronic urinary retention present?
Can be asymptomatic,
LUTS,
Or as complications (UTI, bladder stones, overflow incontinence, post-renal or obstructive renal failure)
108
In chronic urinary retention when the bladder reaches full capacity and bladder pressure is in excess of 25cm water what symptoms can be expected/
Overflow incontinence, renal allure
109
What is the immediate treatment of chronic urinary retention?
Catheterisation
110
What are some subsequent treatment methods of chronic urinary retention?
CISC- clean intermittent self catheterisation
| TURP- transurethral resection of prostate (if due to benign prostatic obstruction)
111
What is required to diagnosis UTI?
Microbiological evidence and symptoms/ signs
112
What microbiological evidence is neeeded to diagnose a UTI?
Bacterial count of 10(4)cfu/ml from MSSU specimen with no more than 2 species of micro-organisms
113
What symptoms/ signs are required to diagnose UTI?
At least one of the following:
| Fever >38, loin/flank pain or tenderness, suprapubic pain or tenderness, urinary frequency, urinary urgency, dysuria
114
What are the 2 types of UTI?
Uncomplicated (young sexually active females) or Complicated (everyone else)
115
What types of organisms can cause UTIs?
E.coli, staph. Saprophyticus, klebsiella, proteus, pseudomonas, staph aureus
116
What complications can occur from UTIs?
Infection: sepsis (especially in pyelonephritis), perinephric abscess, renal failure, bladder malignancy (SCC), acute urinary retention, frank haematuria, bladder of renal stones
117
What investigations are used to diagnose a UTI?
MSSU/ CSU
Lower tract- flow studies, residual bladder scan, cystoscopy
Upper tract- USS kidneys, IVU/CT- KUB, MAG-3 renogram, DMSA scan
118
Name some emergencies related to urinary tract diseases?
Acute renal failure, sepsis due to UTI, renal colic, severe haematuria, metastatic disease causing metabolic derangements, acute urinary retention, chronic high-pressure urinary retention, iatrogenic injury/ trauma, testicular torsion, paraphimosis, priapism
119
What are the methods for measuring excretory renal function
Inulin clearance, isotope GFR, 24hr urine collection plus blood test, GFR estimating equations
120
What is creatinine generated from?
Breakdown of muscle
121
What factors need to be taken into account when measuring the GFR with serum creatinine?
Age, ethnicity, gender, weight, other isssues eg liver disease
122
What is the formula for COckgroft Gault
{[140-age]x weight x 1.23)/ SCr x (0.85 if female)
123
What is the formula for MDRD 4 variable equation?
175 x [SCr/88.4](power -1.154) x [age](power -0.203) x (0.742 if female) x (1.212 if black)
124
If someone has a GFR of >90ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 1:
| Kidney damage/ normal or high GFR
125
If someone has a GFR of 60-89ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 2
| Kidney damage/ mild retention in GFR
126
If someone has a GFR of 45-59ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 3a
| Moderately impaired
127
If someone has a GFR of 30-44ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 3b
| Moderately impaired
128
If someone has a GFR of 15-29ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 4
| Severely impaired
129
If someone has a GFR of <15ml/min/1.73m2 what stage are they at on the international CKD classification system?
Stage 5
| Advanced or on dialysis
130
What can freely cross the GBM?
Water, electrolytes, urea, creatinine
131
What crosses the GBM but is reabsorbed in the proximal tubule?
Glucose, low molecular weight proteins (alpha2 microglobulin)
132
What does not cross the GBM?
Cells (RBC, WBC), high molecular weight proteins (albumin, globulins)
133
How can you assess kidney filtering function
Urinalysis (dipstick), protein quantification (PCR, ACR)
134
Define Chronic kidney disease?
Presence of kidney damage (abnormal blood, urine or x-ray findings) or
GFR<60ml/min/1.73m2
That is present for >/= to 3 months
135
Name some common aetiology of CKD?
Diabetes, glomerulonephritis, hypertension, renovascular disease, polycystic kidney disease
136
What is the clinical approach taken to chronic kidney disease?
Detection of the underlying aetiology:
-treat the specific disease
Slowing the rate of renal declin:
-genetic therapies
Assessment of complications related to reduced GFR:
-prevention and treatment
Preparation for renal replacement therapy
137
Symptoms of chronic kidney disease?
Anaemia-pallor, hypertension, SOB, itch and cramps, cognitive changes- language and attention, anorexia, vomiting, taste disturbance, uraemia odour, polyuria or oliguria, nocturia, haematuria, proteinuria, peripeheral oedema
138
With someone with chronic kidney disease, what could the kidney look like on ultrasound?
Bilaterally small with thinned cortices suggesting intrinsic disease (eg glomerulonephritis),
Unilateral small Kidney which may indicate renal arterial disease,
Clubbed calyces and cortical scars suggesting reflux with chronic infection or ischameia,
Enlarged cystic kidneys suggesting cystic kidney disease
139
How would you manage slowing the rate of renal decline, in someone with chronic kidney disease?
```
BP control,
Control proteinuria (ACE inhibitors/ ARBs), treat underlying cause
```
140
What are some complications that are related to reduced GFR?
Acidosis, anaemia, bone disease, CV risk, death and dialysis, electrolytes, fluid overload, gout, hypertension, iatrogenic issues
141
How to manage the complications related to reduced GFR?
Acidosis- bicarbonate
Anaemia- Erythropoietin and iron
Bone disease- diet and phosphate binders
CV risk- BP, aspirin, cholesterol, exercise, weight
Death and dialysis- counsel and prepare
Electrolytes- diet and consider drugs
Fluid overload- salt and fluid restriction, diuretics
Gout- optimise +/- meds
Hypertension- weight, diet, fluid balance, drugs
142
Preparation needed for end stage renal disease and renal replacement therapy
Education and information, selection of modality (HD, PD, transplant), planning access, deciding when to start RRT and MDT
143
what is glomerulonephritis?
An inflammatory disorder of the kidney which is classified based on morphology
144
Glomerulonephritis common features?
Haematuria, proteinuria, hypertension, renal insufficiency
145
What can be the source of haematuria?
Kidney, ureter, bladder, prostate, urethra
146
In which condition could you expect to see haematuria more? Nephrotic or nephritic?
Nephrotic
147
Is renal insufficiency and hypertension more common in nephritic syndrome or nephrotic?
Nephritic
148
Describe the presentation of nephritic state?
Active urine sediment- haematuria, dysmorphic RBCs, cellular casts,
Hypertension,
Renal impairment
149
Describe the presentation of nephrotic syndrome?
Oedema, proteinuria >3.5g/day, hypoalbuminemia, hyperlipidemia, can be caused by primary or secondary glomerular diseases
150
Name some differential diagnosis of nephrotic suyndrome?
Congestive heart failure- however will have normal albumin
| Hepatic disease- however no proteinuria
151
What are the 2 categories that glomerulonephritis can be split into?
Proliferative or non-proliferative
152
What does diffuse, focal, global and segmental nomenclatures mean in relation to the glomerulus?
Diffuse >50% of glomeruli affected
Focal <50% of glomeruli affected
Global- all glomerulus affected
Segmental- part of the glomerulus affected
153
What are the different classes of proliferative glomerulonephritides?
Diffuse proliferative (eg post-infective nephritis), focal proliferative (eg mesangial IgA disease), focal necrotising (crescentic nephritis), membrano-proliferative nephritis
154
What can you expect from post infective glomerulonephritis in microscopy?
Congested cells, immune deposits and lumps
155
When is it common to get a post-streptococcal glomerulonephritis?
10-21 days after infection typically of throat or skin
156
What is the most common group that causes post-streptococcal glomerulonephritis
Lance field group A streptococci
157
What genes can cause a genetic predisposition to post-streptococcal glomerulonephritis?
HLA-DR, -Dp
158
How would you treat post-infective glomerulonephritis?
Antibiotics (debatable), loop diuretics (eg frusemide) for oedema, vasodilator drugs (eg amlodipine) for hypertension
159
What kind of proliferative glomerulonephritis is post-infection nephritis?
Diffuse proliferative glomerulonephritis
160
What kind of proliferative glomerulonephritis is IgA nephropathy
Focal proliferative
161
How is IgA nephropathy characterised?
IgA deposition in the mesangium + mesangial proliferation
162
How does IgA nephropathy present?
Microscopic haematuria + proteinuria, nephrotic syndrome and IgA crescentic glomerulonephritis
163
What is the prognosis for IgA nephropathy?
Up to 40% can progress to end stage kidney disease
164
Causes of crescentic glomerulonephritis/
Anti-neutrophil cytoplasmic antibody (ANCA)(microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis) or
Anti-glomerular basement membrane (GBM) eg anti_GBM nephritis or Goodpasture’s syndrome or
Others- IgA vasculitis, post-infective glomerulonephritis, SLE
165
How to treat Crescentic glomerulonephritis?
High dose steroids, cyclophosphamide, plasma exchange
166
How does anti-GBM disease present?
Nephritis (anti-GBMM glomerulonephritis) and nephritis + lung haemorrhage (Goodpasture’s sydnrome)
167
How is anti-GBM disease diagnosed?
Anti-GBM antibodies in serum and kidney
168
How is Anti-GBM disease treated?
Aggressive immunosuppressive: steroid, plasma exchange, cyclophosphamide
169
How is crescentic glomerulonephritis treated?
Immunosuppresion- corticosteroids, plasma exchange, cytotoxic eg cyclophosphamide, B-cell therapy eg rituximab, complement inhibitors
170
Name the types of non-proliferative glomerulonephritis?
Minimal change disease, focal and segmental glomerulonephritis, membranous nephropathy
171
How to you generally treat nephr0tic syndrome with regards to the common symptoms/
Loop diuretics + salt and fluid restriction (for oedema), Renin-angiotensin-aldosterone-blockade (for hypertension), Heparin or warfarin (reduced risk of thrombosis), pneumococcal vaccine (for reduced risk of infection), statins (to treat dyslipidemia)
172
How is minimal change nephrotic syndrome characterised?
Common in children, sudden onset of oedema in days, proteinuria
173
Is there a high relapse rate in minimal change nephrotic syndrome?
Yes, 2/3rd of patients relapse
174
How is minimal change disease treated/
Prednisolone (1mg/kg for up to 16 weeks), once remission is achieved there is a slow taper over 6 months.
The initial relapse is treated with further steroid course, however if relapse again, it is treated with:
Cyclophosphamide, cyclosporine, tacrolimus, mycophenolate mofetil, rituximab
175
What is minimal change disease’s prognosis?
Relapse common but risk of end stage kidney disease is low,
| Steroid toxicity can occur due to multiple exposure to steroids
176
What is normal serum albumin levels?
>35g/l
177
How does focal and segmental glomerulonephritis present?
Nephrotic syndrome
178
What does pathology reveal for focal and segmental glomerulonephritis
Reveals focal and segmental sclerosis with distinctive patterns:
Tip lesion, collapsing, cellular perihilar
179
What is the prognosis of focal and segmental glomerulonephritis?
High chance of progression to end stage kidney disease
180
What is the treatment of focal and segmental glomerulosclerosis?
General mesasure, trail of steroids (gerneally steroid resistant), cyclosporin, cyclophosphamide, and rituximab
181
What is membranous nephropathy
Commonest cause of nephrotic syndrome in adults, can be idiopathic or associated with other infections/ diseases. Renal biopsy shoes diffuse global subepithelial deposits within the glomerulus
182
What are the serological markers of membranous nephropathy?
Anti-phospholipase A2 receptor (PLA2R) antibody positive,
| THrombospondin type 1 domain containing 7A (THSD7A)
183
What are some possible secondary causes of membranous nephropathy?
Malignancies, SLE, rheumatoid arthritis, drugs (NSAIDs, gold, penicillamine)
184
How to treat membranous nephropathy?
General measure for at least 6 months, use immune suppression if symptomatic nephrotic syndrome or rising proteinuria or deteriorating renal function,
Cyclophosphamide and steroids (alternate months) for 6 months, cyclosporin,
Rituximab
185
What is the prognosis of membranous nephropathy?
Resolved spontaneously in a third of patients,
Good in treated patients whose proteinuria resolves
About 25% are on dialysis at 10 years and
Can recur in renal transplants
186
Define acute renal failure?
Rapid loss of glomerular filtration and tubular function over hours to days, resulting in the retention of urea/ creatine and sometimes oliguria
187
Define AKI stage 1 using KDIGO criteria?
Increase in serum creatinine:
1.5-1.9 times baseline in the past 7 days OR
>/=26.5umol/l increase
AND
<0.5ml/kg/h urine output for 6-12hours
188
Define AKI stage 2 using KDIGO criteria?
Increase in serum creatinine:
2.0-2.9 times baseline in the past 7 days
AND
<0.5ml/kg/h urine output for >/=12hours
189
Define AKI stage 3 using KDIGO criteria?
Increase in serum creatinine:
3.0 times baseline in the past 7 days OR
>/=354umol/l increase OR
Initiation of renal replacement therapy
AND
<0.3ml/kg/h urine output for >/=24hours OR
Anuria for >/12 hours
190
What are the dangerous consequences of AKI?
```
Acidosis
Electrolyte imbalance
Intoxication
Overload
Uraemic complications
```
(AEIOU)
191
What are the 3 groups of causes of AKI?
Pre-renal (blood flow to kidney)
Renal (damage to parenchyma)
Post-renal (obstruction to urine exit)
192
Name some intrinsic causes of AKI?
```
Acute tubular injury:
Prolonged pre-renal AKI, rhabdomyolysis, haemoglobinuria, nephrotoxins
Tubulointerstitial injury,
Glomerulonephritis,
Myeloma,
Vasculitis:
Lupus, ANCA associated,
Acute tubular necrosis
```
193
Pre-renal causes of AKI?
Sepsis, hypovolaemia (haemorrhage, burns, vomiting/ diarrhoea, diuretics, dehydration), hepatorenal syndrome, cardiac failure, hypotension (medications), shock, liver failure, arterial occlusion, vasomotor (NSAIDs/ACE inhibitors)
194
Post-renal causes of AKI?
Obstruction:
Intraluminal- calculus, clot, sloughed papilla
Intramural- malignancy, ureteric stricture, radiation fibrosis, prostate disease
Extramural- RPF, malignancy
195
What are the risk factors for Radiocontrast nephropathy
DM, renovascular disease, impaired renal function, paraprotein, high volume of radiocontrast
196
What presentation can you expect from renal dailure in myeloma?
Cast nephropathy, light chain nephropathy, amyloidosis, hypercalcaemia, hyperuricaemia
197
Blood tests to be completed for AKI?
U&Es, bicarbonate, LFTs, bone, FBC, clotting
198
What are the risk factors for AKI?
```
Age >75,
Previous AKI,l
Heart failure,
Liver failure,
Chronic kidney disease,
DM,
Vascular disease,
Cognitive impairement
```
199
What are some risk events of AKI?
Sepsis (eg pneumonia, cellulitis, UTI),
Toxins (eg X-ray contrast, NSAIDs, gentamicin, herbal remedies)
Hypotension (eg relative to baseline blood pressure),
Hypovolaemia,
Major surgery
200
What is the STOP AKI prevention care bundle?
S- sepsis
T- toxins: avoid (eg Gentamicin, NSAIDs, IV iodinated contrast)
O- optimise BP and volume status
P- prevent harm (daily U&Es, fluid balance and medication review
201
If sepsis is suspected, what steps are suggested?
```
Sepsis 6,
Blood cultures,
urine output monitoring and U&Es,
Fluids,
Antibiotics,
Lactate level,
Oxygen saturation monitoring
```
202
If a patient is hypovolaemic, what fluids would you suggest?
IV fluids- resuscitation fluids 250-500mls IV crystalloid bolus over 15 mins and review response
203
If the AKI is a post-renal problem what is a good starting management?
A catheter
204
What are the 5Rs for IV prescribing?
Rescuscitation- urgent to restore circulation
Routine maintenance- If cannot take orally
Replacement- additional to maintain
Redistribution- abnormal internal fluid resdistribution
REASSESSMENT
205
What is normal fluid intake and output?
2500ml intake
| 2100-2600 output
206
What is an early sign of hyperkalaemia on an ECG?
Peaked T waves
207
What are signs of hyperkalaemia on an ECG?
```
Peaked T waves,
P wave widens and flattens,
PR segment lengthens,
P waves eventually disappear,
Prolonged QRS internal,
High grade AV block,
Conduction block,
Sinus bradycardia
```
208
Hyperkalaemia treatment?
```
Calcium gluconate (stabilise myocardium)
Salbutamol and insulin-dextrose (to shift K+ intracellularly)
Diuretics, dialysis, anion exchange resins (to remove)
```
209
How to treat intoxication from AKI?
Morphine, digoxin
210
Advantages of HD?
Rapid solute removal,
Rapid volume removal,
Rapid correction of electrolyte disturbances,
Efficient treatment for hypercatabolic patient
211
Disadvantages of HD?
Haemodynamic instability,
Concern if dialysis associated with hypotension,
Fluid removal only during short treatment time
212
Advantages of CRRT?
Slow volume removal associated with greater haemodynamic stability,
Absence of fluctuation in volume and solute control over time,
Greater control over volume status
213
Disadvantages of CRRT
Need for continuous anticoagulation, may delay weaning/ mobilisation, may not have adequate clearance in hypercatabolic patient
214
Define End-stage renal disease
Irreversible damage to a persons kidneys so severely affecting their ability to remove or adjust blood wastes that, to maintain life, they must have either dialysis or a kidney transplant
215
What is the syndrome of advanced CKD called?
Uraemia
216
How big is anormal prostate?
15cc, increases with age
217
Wha are the McNeal’s Prostatic zones?
Transition, central, peripheral and anterior fibromusclar stroma zones
218
What is Benign prostatic hyperplasia?
Fibromuscular and glandular hyperplasia of the prostate, predominantly affecting the transition zone, it is part of aging process in men
219
Symptoms of benign prostatic hyperplasia?
Moderate to severe LUTS in 50% of men
220
What do they look at in the international prostate symptom score sheet?
Incomplete emptying, frequency, intermittency, urgency, weak stream, straining, nocturia
221
What is classed as mild, moderate and severe in the international prostate symptom score sheet?
Mild: 0-7,
Moderate: 8-19
severe: >/=20
222
How can you assess LUTS?
Symptom scoring systems, frequency volume charts
223
Symptoms of voiding LUTS
Hesitancy, poor stream, terminal dribbling, incomplete emptying
224
Symptoms of storage LUTS?
Frequency, nocturia, urgency +/- urge incontinece
225
If you believe someone has a prostate problem what examinations would you complete?
```
Abdomen:
? Palpable bladder
Penis:
? External urethral mental stricture,
? Phimosis
DRE:
Assess prostate size and consistency,
? Suspicious nodules or firmness
Urinalysis:
? Blood,
? Signs of UTI
```
226
Investigations if you beleive someone has a prostate problem?
```
MSSU,
FLow rate study,
Post-void bladder residual USS,
Bloods- PSA, urea and creatinine,
Reanal tract USS,
Flexible cytoscopy,
Urodynamic studies,
TRUS-guided prostate biopsy
```
227
At was level of Qmax do you have a big chance of BOO?
Qmax <10ml/s
| 90% chance of BOO
228
Treatment of uncomplicated BPO?
```
Waiting,
Alpha blockers,
5 alpha reductase inhibitors,
TURP,
Open retro public or transvesical prostatectomy,
Endoscopic ablative procedures
```
229
How do alpha blockers work in BPO?
The sympathetic alpha-adrenergic nerves innervate the smooth muscle of bladder neck and prostate, so the alpha blockers cause smooth muscle realisation and antagonise the “dynamic” element to prostatic obstruction
230
What are the types of alpha blockers?
Non-selective: phenoxybenzamine
Selective short acting: prazosin, indoramin
Selective long acting: alfuzosin, doxazosin, terazosin
Highly selective: tamsulosin
231
How do 5a-reductase inhibitors work?
5a-reductase converts testosterone to dihydrotestosterone
So 5a reductase inhibitors block this and reduce prostate size and reduce risks of progression of BPE, reduce LUTS and reduce prostatic bleeding
232
Side effects of 5a-reductase inhibitors?
Impaired sexual function, breast growth
233
Name the 2 5a-reductase inhibitors currently available?
Finasteride (5AR type II inhibitor)
| Dutasteride (5AR type I and II inhibitor)
234
What is TURP?
Transurethral resection of prostate
235
complications of TURP?
Bleeding, infection, retrograde ejactulation, stress urinary incontinence, prostatic regrowth causing recurrrent haematuria or BOO
236
Alternative surgical procedures used for BPO?
Transurethral laser vaporisation, urolift
237
Complications of BOO?
Progression of LUTS, acute urinary retention, chronic urinary retention, urinary incontinence (overflow), UTI, bladder stone, renal failure from obstructed ureteric outflow due to high bladder pressure
238
Treatment of Complicated BOO?
Cystolitholapaxy and TURP (BPO and bladder stones),
| Long term urethral or suprapubic catheterisation, clean intermittent self-catheterisation
239
Treatment of acute urinary retention?
Catherterisation, if no renal failure alpha blocker and remove catheter in e days
240
Complications from acute urinary retention?
UTI, post-decompression haematuria, pathological duresis, renal failure and electrolyte abnormalities
241
What is the main aetiological factor causing chronic urinary retention?
Detrusor underactivity
242
Complications of chronic urinary retention/
UTI, post0decompression haematuria, pathological diuresis, electrolyte abnormalities, persistent renal dysfunction
243
What are the features of pathological diuresis?
Urine output >200ml/hr + postural hypotension+ weight loss + electrolyte disturbance
244
Intrinsic causes of obstructuion at PUJ?
Stone, ureteric tumour, blood clot,fungal ball
245
Extrinsic causes of obstruction at PUJ?
Crossing vessels au PUJ, lymph nodes (tumour), abdominal mass (tumour)
246
Intrinsic causes of a obstruction at the ureter
Stone, ureteric tumour, scar tissue, blood clot, fungal ball
247
Extrinsic causes of a obstruction at the ureter
Lymph nodes (tumour, retroperitoneal fibrosis), iatrogenic, abdominal/ pelvic mass (tumour, pregnant uterus)
248
Intrinsic causes of a obstruction at the VUJ?
Stone, bladder tumour, ureteric tumour
249
Extrinsic causes of a obstruction at the VUJ
Cervical tumour, prostate cancer
250
Symptoms of upper urinary tract obstruction?
Pain, frank haematuria, symptoms of complications
251
Signs of upper urinary tract obstruction?
Palpable mass, microscopic haematuria, signs of complications
252
Complications of upper urinary tract obstruction?
Infection and sepsis, renal failure
253
Treatment of Upper urinary tract obstruction?
Emergency treatment of obstruction; percutaneous nephrostomy insertion or retrograde stent insertion
treat underlying cause:
Stone- ureteroscopy and laser lithotripsy +/- basketing or ESWL
Ureteric tumour- radial nephro-ureterectomy
PUJ obstruction- laparoscopic pyeloplasty
254
What is a nephrostomy?
Percutaneous puncture + tube
255
Describe a ureteric stent?
Silicone, polyurethane, nickel titanium stent inserted into ureter, causing dilation
256
Lower urianry tract obstruction presentation?
LUTS, acute urinary retention, chronic retention, recurrent UTI and sepsis, frank haematuria, formation of bladder stones, renal failure
257
Emergency treatment of lower urinary tract obstruction
Urethral/ suprapubic catheterisation
258
Definitive treatment of lower urinary tract obstruction?
```
Treat underlying cause:
BPE-TURP,
Urethral stricture- optical urethrotomy,
Meatal stenosis- meatal dilatation,
Phimosis- circumcision
```
259
High pressure chronic urinary retention presentation?
Painless, incontinent, raised creatinine, bilateral hydro-nephrosis
260
Low pressure chronic urinary retention?
Painless, dry, normal creatinine, normal kidneys
261
Complications of urinary retention?
Decompression haematuria, post obstructive diuresis
262
Describe decompression of haematuria?
Shearing of small vessels due to differing compliance of tissue layers, self limiting
263
Describe post obstructive diuresis?
Greater than 200ml/hr, can lead to life threatening Na and H2O depletion
264
Most common site of urothelial tumours?
Bladder- 90%
265
Risk factors for transitional cell carcinoma of the bladder
Smoking, aromatic amines, non-hereditary genetic abnormalities
266
Risk factors for squamous cell carcinoma
Schistosomiasis (S.haematobium only), chronic cystitis, cyclopjosphamide therapy, pelvic radiotherapy,
Adenocarcinoma- urachal
267
Bladder cancer presentation?
Painless visible haematuria,
Symptoms due to invasive or metastatic disease
Haematuria may be frank or microscopic,
Recurrent UTI,
Storage bladder symptoms- dysuria, frequency, nocturia +/- urge incontinence, bladder pain- suspect CIS
268
Investigations of haematuria?
Urine culture, CT urogram (IVU), ultrasound scans, cystourethroscopy, urine cytology, BP and U&E’s
269
If someone has frank haematuria within wheat time should they have a flexible cystourethroscopy?
Within 2 weeks
270
If someone has microscopic haematuria within what time should they have a flexible cystourethroscopy?
Within 4-6 weeks
271
Describe the grades of TCC
G1- well diff- commonly non-invasive,
G2- mod diff- often non-invasive,
G3- poorly diff- often invasive,
Carcinoma in situ
272
A what T stages of bladder TCC is it muscular invasive?
T2a and above
273
Low grade non-muscular invasive bladder cancer treatment?
Endoscopic resection + single insillation of intravesical chemotherapy within 24hours,
Need endoscopic follow up,
Can consider prolonged course of intravesical chemotherapy
274
High grade non-muscle invasion bladder cancer or CIS treatment
Endoscopic resection not sufficient,
Consider intravesical BCG therapy,
If refractory to BCG- need radical surgery
275
Muscle invasive bladder cancer treatment?
Neoadjuvant chemotherapy, followed by...
Radical radiotherapy and/or,
Radical cystoprostatectomy (men) or anterior pelvic exenteration with urethrectomy (women), with extended lympahdenectomy and/ or
Radical surgery combined with i continent urinary diversion (ileal) conduit, continent diversion (bowel pouch with catheterisable stoma) or orthotopic bladder substitution
276
Upper tract TCC presenting features?
```
Frank haematuria,
unilateral ureteric obstruction,
Flank or loin pain,
Symptoms of nodal or metastatic disease:
Bone pain, hypercalcaemia, lung, brain
```
277
Upper tract TCC diagnostic investigations?
CT-IVU (CT urogram), urine cytology, ureteroscopy and biopsy
278
How does a CT-IVU Diagnosis a upper tract urothelial cancer?
It shows a filling defect in the renal pelvis
279
Treatment for Upper Tract Urothelial cancer
Nephro-ureterectomy
280
Indications fo nephron-sparing endoscopic treatment in upper tract urothelial cancer?
If unfit for nephro-ureterectomy or has bilateral disease,
So get ureteroscopy can lasers ablation
Will needed regular surveillance ureteroscopy
281
Why do all cases of upper tract urothelial cancer need surveillance cystoscopy?
Because there is a high risk of synchronous and metachronous bladder TCC
282
Types of benign renal tumours?
Oncocytoma, angiomylipoma
283
Histological subtypes of renal adenocarcinoma?
Clear cells, papillary, chromophobe, Bellini type dictaphone carcinoma
284
Risk factors of renal adenocarcinoma?
Family history (vHL, familial clear cell RCC, hereditary papillae RCC), smoking, anti-hypertensive medication, obesity, end-stage renal failure, acquired renal cystic disease
285
Presentation of renal adenocarcinoma?
Asymptomatic- 50% present
Flank pain, mass and haematuria- 10% present
Paraneoplastic syndrome: anorexia, cachexia, pyrexia, hypertension, hypercalcaemia and abnormal LFTs, anaemia, polycythaemia and raised ESR - 30%
MEtastatic disease: bone, brain, lungs, liver -30%
286
TNM staging of renal cancer
T1- tumour <7cm confined within the renal capsule
T2- tumour >7cm and confined within capsule
T3- Local extension outside capsule
T3a-into adrenal or peri-renal fat
T3b- intro renal vein or IVC below diaphragm
T3c- Tumour thrombus in IVC extends above diaphragm
T4- tumour invades beyond Gerota’s fascia
287
Renal adenocarcinoma spread methods?
Direct spread (invasion) through the renal capsule, venous invasion to renal vein and vena cava, haematogenous spread to lungs and bones and lymphacic spread to paracaval nodes
288
Renal adenocarcinoma investigations?
CT scan of abdomen and chest, provides radiological diagnosis and complete TNM staging, assess contra lateral kidney
Bloods: U+Es, FBC, LFTs,
Ultrasound, DMSA or MAG-3 renogram
289
Treatment of renal adenocarcinoma?
Laparoscopic radial nephrectomy,
| Palliative cytreductive nephrectomy
290
Renal adenocarcinoma with metastases treatment?
RCC is radioresistant and chemoresistant so treat with multitargeted receptor tyrosine kinase inhibitors (suntinib, sorafenib, panzopanib, temsirolimus),
Immunotherapy (interferon alpha, interleukin-1)
291
What muscle do the ureters pass by?
Psoas major
292
What is the trig one in the bladder?
A triangular area between the ureteric and urethral orifices
293
Indications for renal imaging?
Renal colic and renal stone disease, haematuria, suspected renal mass, UTIs, hypertension
294
Contrast imaging studies used to view KUB?
IV urogram, Pyelography, micturating cystourethrography
295
What is a pyelography?
Injection of contrast into the ureters
296
What would you use a Doppler ultrasound for?
Renal artery stenosis
297
Isotope scans used for renal diseases, and why they are used?
DMSA- to look for renal scarring
MAG3- assess renal function and drainage
Bone scan- metastatic disease
298
What is the best imaging modality to diagnose renal tract stones and stage renal tumours?
CT
299
Types of urinary stones?
Calcium oxalate, calcium oxalate + phosphate, “triple phosphate”, calcium phosphate, Utica acid, cystine
300
What is the most common type of urinary stone?
Calcium oxalate
301
Symptoms and signs of urinary stones?
```
Renal pain,
ureteric colic (radiating to groin),
Dysuria/ haematuria/ testicular or vulval pain,
Urinary infection,
Loin tenderness,
Pyrexia
```
302
Investigations for urinary stones?
```
Blood tests- FBC, U&E, creatinine,
Calcium, albumin, urate,
Parathormone,
Urine analysis and culture,
24hr urine collections,
Radiology- ultrasound KUB, IVU, CT KUB,
```
303
Indications for surgical treatment for urinary stones?
```
Obstruction,
Recurrent gross haematuria,
Recurrent pain and infection,
Progressive loss of kidney function,
Patient occupation
```
304
Types of surgical treatment for urinary stones?
Open surgery, endoscopic surgery, Extracorporeal Shock Wave Lithotripsy (ESWL), Percutaneous nephrolithotomy (PCNL)
305
Indications for open surgery for urinary stones?
Non functioning infected kidney with large stones,
| For technical reasons cannot be managed another way
306
Types of o[pen surgery for urinary stone removal?
Simple pyelolithotomy, simple radial partial or total nephrotomy
307
When would toy complete a simple partial or total nephrectomy for urinary stones?
If
A non functioning kidney with large staghorn stones or
Elderly frail patients with complex stones and normal contralateral kidney
308
Indications for a percutaneous nephrolithotomy?
Large stone burden, associated PUJ stenosis, infundibular stricture, calyceal diverticulum, morbid obesity or skeletal deformity, ESWL resistant stones eg cystine
309
Contraindications for PCNL
Uncorrected coagulopathy, active UTI, obesity or unusual body habitus unsuitable for X-ray tables, relative contraindications include small kidneys and severe perirenal fibrosis
310
Local complications of PCNL?
Pseudoaneurysm or AV fistula,
| UT injury: pelvic tear, ureteral tear, stricture of PUJ
311
Injury’s that can occur to adjacent organs due to PCNL?
Bowel injury,
| Pneumothorax,
312
Systemic complications of PCNL?
Fever, sepsis, MI
313
What is ESWL?
Extracorporeal Shock Wave Lithotripsy
314
When is ESWL not effective?
Stones >2cms,
Less effective for lower pole stones,
Not effective after 2 treatments,
Ineffective for treating cystine stones
315
Indications for ureteroscopy?
```
Sever obstruction,
uncontrolled pain,
Persistent haematuria,
Lack of progression,
Failed ESWL,
Patient occupation
```
316
Minor complications of ureteroscopy?
Haematuria, fever, small ureteric perforation, minor vesico-ureteric reflux
317
Major complications of ureteroscopy?
Major ureteric perforation,
Ureteric avulsion,
Ureteral necrosis and stricture formation
318
Bladder stones presentation?
```
Suprapubic/groin/ penile pain,
Dysuria, frequency, haematuria,
Urinary infection persistent,
Sudden interruption of urinary stream,
Usually secondary to outflow obstruction
```
319
Name the types of aorta/large vessel arteritis
Takayasu arteritis, giant cell arteritis
320
Name the types of medium artery vasculitis?
Polyarteritis nodosa,
| Kawasaki disease
321
Name the types of small vessel vasculitis?
Granulomatosis polyarteritis,
Microscopic polyarteritis,
Churg-Strauss syndrome
322
Describe granulomatosis polyangiitis?
A granulomatous inflammtion in the respiratory tract, type of focal necrotising inflammation with crescents, more common in males and the age group 40-60y
323
Describe the systems affect3ed by granulomatosis polyangiitis and the subsequent symptoms?
Upper Resiratpry tract- epistaxis, basal deformity, sinusitis, deafness
Lower respiratory tract- cough, dyspnoea, haemoptysis, pulmonary haemorrhage
Kidney- glomerulonephritis
Joints- arthralgia, myalgia,
Eyes- scleritis
Heart- pericarditis
Systemic- fever, weight loss, vasculitic skin rash
324
Diagnostic tests for vasculitis
Urine (blood/proteins),
Renal function (raised urea/creatinine)
Biochemistry (raised alkaline phosphate, CRP, low albumin)
Haematology (anaemia, thrombocytosis, leukocytosis)
Immunology (hyperglobulinaemia, positive ANCA)
renal biopsy
325
The ANCA that’s diagnosis for granulomatosis polyangiitis?
C-ANCA
326
The ANCA that’s diagnosis for microscopic polyarteritis
P-ANCA
327
Infections that cause infective endocarditis?
Staphylococcus aureus, Vivian’s streptococci, enterococci
328
How does infective endocarditis lead to affecting the kidney
It leads to glomerulonephritis +/- vessel vasculitis due to immune complex function
329
If a patient has infective endocarditis, how can you tell that the renal system is affected?
Abnormal urea/creatinine
Haematuria, red cell casts,
Reduced complement levels
330
What is multiple myeloma?
A monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
331
What are the clinical features of multiple myeloma?
```
Markedly elevated ESR,
Anaemia,
Weight loss,
Fractures,
Infections,
Back pain/ cord compression
```
332
How is multiple myeloma diagnosed?
Bone marrow aspirate >10% clonal plasam cells,
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones protein,
Skeletal survey- lytic lesion
333
Presentation of renal failure in myeloma
```
Cast nephropathy- “myeloma kidney”
Light chain nephropathy,
Amyloidosis,
Hypercalcaemia,
Hyperuriacaemia
```
334
What history points could make you suspect systemic disease with renal involvement?
Fever, malaise, weight loss, arthralgia, myalgia, skin rash, gritty eyes, breathlessness, haemoptysis, epistaxis, haematuria, oedema
335
What signs would you expect if you suspected systemic disease with renal involvement?
Hands- splinter haemorrhages, purpura, Raynaud’s
Face- scleritis, uveitis, nasal cartilage deformity, retinal vasculitis, hypertensive retinopathy
Skin- vasculitic rash, scleroderma
CVS- hypertension, murmur
Chest- crepitations, haemoptysis,
Locomotor- joint swelling, tenderness
CNS- stroke, enccephalopathy
336
Peak age group for prostate cancer?
50-70
337
What is the diagnostic triad of prostate cancer?
PSA, DRE, TRUS-guided prostate biopsies
338
What is the normal serum range of PSA?
```
0-4.0ug/ml
<50 yrs- 2.5 is upper limit,
50-60 - 3.5,
60-70- 4.5
>70- 6.5
```
339
What can cause elevation in PSA?
```
UTI,
Chronic prostatitis,
Instrumentatio eg cateterisation)
Physiological (eg ejaculation)
Recent urological procedure
BPH
Prostate cancer
```
340
What is the half life of PSA?
2.2 days
341
What is the Gleason Grading of prostate cancer?
Score biggest and second biggest area of tumour a score of 3-5 (well to poorly differentiated) and add together the scores
342
What are the 4 stages of prostate cancer?
Localised stage, locally advanced stage, metastasic stage, hormone refractory stage
343
How would you stage a localised prostate cancer?
DRE, PSA, transrectal US guided biopsies, CT, MRI
344
Treatment of localised prostate cancer?
```
Watchful waiting,
Radiotherapy (external-beam, brachytherapy)
Radical prostatectomy (open, laparoscopic, robotic)
```
345
Treatment of locally advanced prostate cancer?
Watchful waiting,
Hormone therapy followed by surgery,
Hormone therapy followed by radiation,
Hormone therapy alone
346
Types of hormonal therapy for prostate cancer?
```
Surgical castration:
Bilateral orchidectomy
Medical castration:
LHRH analogues- goserelin, leuprorelin
LHRH antagonists
Anti-androgens
Oestrogens- diethylstilboestrol
```
347
How does oestrogens help on prostate cancer?
Inhibitots LHRH and testosterone secretion,
Inactivates androgens
Direct cytotoxic effect on prostatic epithelial cells
348
What is the PSA level at localised, locally advanced and metastatic prostate cancer?
localised <20
Locally advanced 20-100
Metastatic- >100
349
How does testicular cancer nornmally present?
Painless lump
350
What are some other presentations of testicular cancer other than painless lump?
Tender inflamed swelling, history of trauma
351
Risk factors of testicular cancer?
3rd decade, Caucasians
Testicular maldescent, infertility, strophic testis, previous cancer in contrallateral testis,
Testicular germ cell neoplasia in situ is a precursor lesion
352
What are the types of testicular cancer tumour markers?
AFP (alpha-fetoprotein) (teratoma)
BHCG (Human Chorionic Gonadotrophin)(seminoma)
LDH (lactate dehydrogenase)
353
Testicular cancer investigations?
MSSU, testicular ultrasound scan and CXR, tumour markers
354
Treatment of testicular cancer?
Radical orchidectomy
355
Lymphatic drainage of testis?
Para-aortic lymph nodes
356
Types of testicular germ cell tumours?
```
Seminomatous GCT (classical, spermatocytic or anaplasic)- normally affects 30- 40yrs
Non seminomatous GCT (teratoma, yolk sac, choriocarcinoma, mixed GCT)-normally affects 20-30yrs
```
357
Types of testicular cancer non-GCT?
sex cord/ stromal
| Leydig, sertoli, lymphoma
358
What are the 4 stages of testicular cancer?
Stage 1- disease is confined to the testis
Stage 2- infradiaphragmatic nodes involved
Stage 3- supradiaphragmatic nodes involved
Stage 4- extralymphatic disease
