RENAL Flashcards
What are the eGFR values for the different stages of CKD
Stage 1: >90 mL/min - normal/ slightly high- only CKD if other evidence of kidney damage
Stage 2: 60-89 - normal - only CKD if other evidence of kidney damage
Stage 3a: 45-59 - low
Stage 3b: 30-44 - moderately low
Stage 4: 15-29 - severely low
Stage 5: <15 - renal failure
At what stage of CKD do you start to see complications
Stage 4 - 15-20 mL/min
What is the ‘steady state’ that is required to measure creatinine, what limitations does this have, and what conditions might you see this in
The steady state is an assumed state where the amount of creatinine produced (from muscle breakdown) is equalised to that excreted from kidneys - so that if you measure serum creatinine and it is high or low this can be interpreted as kidney injury/ failure.
The limitation of this is that, is there is a problem in the kidney it may take some time for serum creatine to rise - t/f falsely reassuring.
Or, certain conditions or people will generate more creatine than normal, eg those with cachexia - muscle wasting - may not reflect kidneys failing. Or liver disease.
Or those with high muscle mass. This will mean their eGRF is underestimated.
What antibiotic can cause an increase in eGFR and why
Trimethoprim. Inhibits creatinine secreation in renal tubule, so get retention in serum. Is not a sign of renal failure.
But also, trimethoprim is nephrotoxic, so also could be!
What level of albuminuria is indicative of glomerular damage
1g upwards
Below this is probably bc of hypertension or CVS
What effects do NSAIDs have on GFR and what is the mechanism
Inhibit prostaglandins
Prostaglandins usually dilate the afferent arteriole
If inhibit these, get vasoconstriction of afferent arteriole
= less blood into glomerus
= decrease in GRF
What effects do ACE inhibitors have on GFR and how
Angiotensinogen II regulates vasoconstriction of efferent arteriole
If block AII by ACE inhibitor = dilation of efferent arteriole
= blood flows through glomerulus quicker
= decrease GFR
What is the most metabolically active areas of the nephron - what injury is this most susceptible to
Proximal - bc most solute re-absorption happens here
tf v susceptible to ischemic injury
What are the main complications of kidney disease
Cardiovascular disease - fluid overload - heart failure
Why are ACE inhibitors or ARBs indicated in proteinuric CKD
They dilate the efferent arteriole which will lower the GFR and decreased protein leak. This also isnt good for kidney but bc proteins injury the nephron it is more beneficial to lower GFR and prevent proteins getting into tubule, basically tolerate drop in GRF to preserve tubule and longer term kidney function.
When should ACEX or ARBs be stopped in pts with CKD
If they get infection/ malaise, bc BP can start to drop, so this + BP drop from ACE inhibitors can facilitate sepsis
What determines K+ excretion in the kidney
Na+ delivery to distal tubule
Aldosterone
*NB- K+ is freely filtered in glomerulus, then reabsorbed in proximal tubule & LoH.
It is exchanged for Na+ in distal and collecting duct. If get increase in Na+ delivery to distal tubule (via loop diuretic, furosemide), will exchange all this for K+ = hypokalemia
What are the main functions of the kidney
Homeostasis -Filtration & reabsorption -Blood pressure - RAAS -Potassium -Acid/ bicarb balance Vitamin D & Bone Erythropoetin
List two side effects of spironolactone
Hyperkalemia Metabolic acidosis (renal tubular acidosis type I)
This is bc, principal cells that have ENac channels (Na+ in exchange for K+) are blocked by spironolactone, so you don’t get movement of K+ from blood into urine in exchange for Na+
K+ is exchanged for H+, If block ENac = decreased K+ in lumen (urine) to exchange with H+ in cells, so retain H+ = acidosis.
List the side effects of loop (furosemide) and thiazide diuretics (distal tubule)
Hypokalemia
Bc, of ENaC channels.
Exchange Na+ for K+. If increase Na+ deliver = increase K+ movement into urine.
Renal tubule acidosis type 1 occurs where in nephron and what drugs can cause it
In collecting ducts - spironolactone can cause it in susceptible ppl - depends on their acid load (think about high protein diet where pt will probably have excess H+)
Renal tubular acidosis type 2 occurs where in nephron - what conditions/ pathology could cause this
In proximal tubule - where 90% of bicarb is reabsorbed
Anything that causes ischemia to these cells - hypotension, sepsis etc - bicarb resorption fails = metabolic acidosis
What are the criteria to identify a AKI
When thinking about AKI, try to remember the rule with:
“2,4,6,8 rule
Doubling
Halving”
1.increase in creatinine of 26 micromols/L within 48 hours
2.Creatinine doubling
Has creatinine gone half way to doubling? 1.5x BL within 7 days
3.Urine halved
Has the patients urine output per hour halved, based on the BW? eg. <0.5 mL/kg/hr in 6 consecutive hrs
BL* can be the best creatinine figure over the last 6 months
How many of the KDIGO criteria do you need for diagnosing AKI
1 out of 3
What blood test should be done if you suspect rhabdomyolisis may have happened in a patient
Bloods for creatinine phosphokinase
Lactate dehydrogenase
(Enzyme that catalyses phosphate groups onto creatinine - these are used as an energy reservoir for highly metabolic tissues, eg skeletal muscle; if muscle breaks down - creatinine kinase is released into blood)
How does rhabdomyolisis cause AKI
Release of muscle contents - myoglobin - protein that when broken down is toxic to kidney
Which gonal vein drains into a renal vein
Left gonadal into left Renal vein
Right gonadal direct into IVC
What is the main medical emergency associated with AKI
Hyperkalemia
Describe what happens in AKI induced hyperkalemia
Potassium is not being excreted by kidneys - increase in serum K+
K+ controls the resting membrane potential of cardiac myocytes and nerves
If serum K+ increases this alters the membrane potential of cardiac cells and inhibits Na+/K+ pump
Myocytes fail to repolarise properly and they accumulate Na+ and Ca2+ in the cell bc of pump breakdown.
=water into myocytes (odema) + contraction without action potential (causes ischemia) + cell undergoes programmes cell death
=this is “depolarisation arrest” - can’t repolarise properly, lose impulse-contraction coupling - ischemia - and cell starts to die.
HR starts to decrease, BP starts to drop
Muscle twitching bc of increased charge in cells
What are the signs of hyperkalemia on ECG
Tall, tented T waves (repolarisation inhibited) in V1-6
Increased R wave (myocytes hyper-ionised) in V1-6
Increased PR interval (depolarisation of atria slower bc lost fast Na+ channels?)
Small or absent p wave
What are the common complications of AKI
Hyperkalemia, acidosis, fluid overload - pulmonary oedema, uremia
What investigations should you do on a patient with suspected AKI
Bloods - U&E (ureamia?), creatinine
Imaging - ultrasound, CT, contrast Xray/ MRI
Urine dipstick - protein to creatinine ratio, blood, pH, microscopy for infections
Outline the management for a patient with AKI
Try to identify cause and treat it, manage complications
History and exam
Bloods and imaging
Urine dipstick
IV fluids
Drugs review - anything causing hypotension - ACE inhibitors?
Put patient on fluid balance to monitor input/ output
What are the risk factors for AKI
Age
Comorbidities
Reasons for admission
Drugs
What are the common causes of AKI
Pre-renal - anything that causes BP to drop - think about causes of shock + drugs that lower BP
Renal – Tubular , Glomeruli , Interstitial , Vascular (HUS)
Post-renal – Luminal , Mural , Extrinsic compression
Stones, malignancy, stricture
What is the best way to prevent AKI
Drug review in patient - review anything that can cause hypo or is nephrotoxic
What are the indications for dialysis in AKI
Refractory pulmonary oedema Persistent hyperkalaemia Severe metabolic acidosis Uraemic encephalopathy or pericarditis Drug overdose – BLAST ( Barbiturate, Lithium, Alcohol-ethylene glycol, Salicylate, Theophylline)
Difference between AKI and renal failure
AKI = abrupt decline in renal function
Renal failure = end stage chronic kidney disease - kidneys cannot function and need dialysis
What information can you get from urinary dipstick to help inform a cause of AKI
Protein - the higher it is, the more likely it is to be glomarulus problem
Blood - if high protein likely to be intrinsic problem - think about TTP and HUS
Glucose - diabetes, pregnancy, proximal tubule pathology
What can an USS tell you about kidney disease
If <9cm indicated CKD
Asymmetry = vascular problem
Causes of renal failure (end stage CKD, stages 4 & 5)
Diabetes
Hypertension
Atherosclerosis
Nephrotic syndrome
Lupus (autoimmune)
Genetic - polycystic kidney disease
How can CKD be classified
GFR, Albuminuria
Common causes for CKD
- Diabetes
- Glomerulonephritis
- Hypertension/ renovascular disease
Common causes for CKD
- Diabetes (damaged filter)
- Glomerulonephritis
- Hypertension/ renovascular disease (damage to vasculature)
What is the criteria to diagnose CKD
> 3 months of kidney damage, defined by permanent decrease in GFR, and/or proteinuria, haematuria, anatomical abnormality
What is the criteria to diagnose CKD
> 3 months of kidney damage, defined by permanent decrease in GFR, and/or proteinuria, haematuria, anatomical abnormality
GFR <60
What are the clinical features of CKD
Anaemia
Bone disease - osteomalacia, osteoperosis, secondary hyperparathyroidism
Neurological complications - occur in nearly all pt with severe CKD - improved on dialysis.
CVS - MI, cardiac failure, sudden cardiac death
How would you differentiate between AKI and CKD
CKD has more anaemia (normocytic) and bone features bc of changes to epo and calcitriol release.
AKI doesnt have these.
What is the management of CKD
Treat the cause, eg, vasculitis - immunosuppressive meds; tight metabolic control in diabetes; hypertension - control
Reduce CVS risk - diet & lifestyle (get good BP), weight loss, cholesterol (statins), stop smoking, normal protein diet
Treat complications - anemia
Dose adjustments for prescribed medicines
Correct complications - hyperkalaemia, calcium & phosphate, anaemia (Fe2+), acidosis, infections - vaccinations
What immunosuppressant used after renal transplantation can cause cancer
Ciclosporin
Bc of inhibition of NK cells and less neoplasm surveillance
Define what CKD is
Abnormal kidney structure of function, present for >3 months, with implications for health
If not decrease in GRF, could be proteinuria, small kidneys (<9 cm)
What is oligouric and anuric
Oligouric is urine output less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL or 500 mL per 24h in adults - this equals 17 or 21 mL/hour.
Anuric is no urine output
At what stage of CKD does urine output reduce/ stop (oligouria, anuria)
Stage 5
Stage 1- 4, pts have normal urine output
Signs of hypovolaemia
Tachy Pulse Low BP Reduced tissue turgor JVP - low Tongue - dry Urine output - reduced Weight - reduced
Symptoms of hypovolemia
Thirst
Dizziness
Lab results for hypovolaemia
increased creatinine (kidneys not filtering)
Causes of hypovolaemia
Anything that causes fluid loss Diuretics Dehydration (heat; not enough intake) Burns Diarrhoea
Signs of hypervolaemia
Normal pulse Increased BP JVP - high Pitting odema (bc of transudate, low protein, nothing to pull water back after pressure) Tongue - normal Tissue turgor - normal Urine - normal Wight increased
Symptoms of fluid overload (hypervolaemia)
Breathlessness
Leg odema
Blood results for hypervolaemia
Low creatinine (bc increased filtration) Or may be varied?
What is nephrotic syndrome
It is a syndrome characterised by:
- Very high prontinuria (>3g)
- Low serum albumin (<30)
- Odema
What are the causes of nephrotic syndrome
Usually idiopathic Other causes are: Drugs - NSAIDS - anything that can cause damage to filter Autoimmune - SLE Malignancy Infection
Describe the pathology of nephrotic syndrome
Proteins deposited on the outer aspect of the basement membrane - IgG and compliment often deposited
Basement membrane expands to reabsorb proteins - this makes filter more leaky.
Starting point is usually a problem with the podocytes
What is the differential diagnosis for oedema
Congestive heart failure
Nephrotic syndrome
Cirrhosis
Jugular venous pressure can differentiate nephrotic syndrome - it is not raised in this
What investigations would you do on a patient you suspect has nephrotic syndrome
Urinalysis - protein, GFR, haematuria, microscopy
Bloods - U&E, serum creatinine, albumin, serology - autoimmune
Imaging - ultrasound, XR, CT
Outline the principles of management for nephrotic syndrome
Diuretics - to manage fluid overload
ACE inhibitors - to manage proteinuria
+treat underlying disease if there is one, eg Lupus - rituximab etc
What is the cause of glomerulonephritis - list the most common
Usually infection or a disease that has stimulated the immune system to cause inflammation on histology
Most common is beta hemolytic group A strep - bacterial antigen gets stuck in filter and get inflammatory response
How do you diagnose glomerulonephritis
Renal biopsy
Common causes of glomerulonephritis
Infection & autoimmune
Post-strep GN
Small vessel vasculitis
IgA nephropathy (IgA lodges in kidney and sets of inflammation)
Goodpastures - anti-glomerular basement membrane (auto-antibodies again collagen type IV)
Rapidly progressive GN
How do you manage glomeruonephritis
As per CKD, BP control and inhibit RAAS.
Specific treatment depends on histology, severity and co-morbidities.
What is seen on renal biopsy in rapidly progressing glomerulonephritis
Glomerular cresent formation - this is WBC collecting in bowmans space
Define glomerulonephritis
Encompassing terms for conditions that cause inflammatory infiltrate around the glomerular filtration barrier. Causes - infection, autoimmune.
This causes proteinuria + haematuria
What is rapidly progressive glomerulonephritis
This is any aggressive GN, where the condition progresses to renal failure in days to weeks.
Small vessel/ ANCA vasculitis
Lupus nephritis
IgA nephropathy
What is diagnostic of rapidly progressive glomerulonephritis
Cresents of inflammatory cells in bowmans capsule
What investigations should be done on a patient that you suspect has GN
Bloods - FBC (look for white cells etc), CRP, U&E, LFT, Serology - autoantibodies (ANA, ANCA, Anti-GBM, IgA), serum albumin, culture
Urinalysis - GFR, p:cr, microscopy - red cell casts; microbiology
Biopsy - essential for diagnosis
CXR - look for GPA in lungs
Ultrasound - size of kidneys - look for renal vein thrombosis
How do you manage rapidly progressive GM
As per AKI - manage emergencies (hyperkalemia etc)
Identify the cause & treat it - eg Infection - antibiotics
Plasma transfusion is needed for IgA nephropthy
What is the treatment for small vessel vasculitis
High dose steroids/cyclophosphamide/biologics
Difference between post-streptococcal GN and IgA nephropathy
IgA you get upper respiratory tract symptoms a couple of days before, post-strep a couple of weeks before
How would you identify IgA vasculitis, how is it different from IgA nephropathy
IgA vasculitis has a purpuric rash
IgA nephropathy - no extra renal disease
What is the most prevalent pattern of glomerular disease
IgA nephropathy (in lecture)
What are the clinical features of IgA nephropathy
Episodic macroscopic haematuria ( synpharyngitic haematuria) in 40-50% of cases in second or third of life.
A symptomatic urine testing identifies 30-40% of cases in most reported series.
Nephrotic syndrome occurs in only 5% of all cases.
AKI at presentation could be due to ATN or crescentic GN.
Diagnosis: biopsy: Diffuse mesangial IgA deposits, subendothelial and sub epithelial deposits on EM is not uncommon.
What is the treatment of IgA nephropathy
Supportive care: BP control with RAAS inhibitors, Diet, Lower Cholesterol
Immunosuppression: Induction: Steroids, Cyclophosphamide
Remission: Steroids, Azathioprine
What patient group is lupus and lupus nephritis more common in
Lupus and Lupus Nephritis are 3-4 times more common in African Americans, Afro-Carribeans, Hispanics and Asians
Outline the different stages of lupus nephritis
Class I Normal Glomeruli on LM, but mesangial Immune deposits on IF
Class II Mesangial Hypercellularity with mesangial immune deposits
Class III Focal segmental Proliferative Lupus nephritis
Class IV Diffuse Proliferative Lupus nephritis
Class V Membranous Lupus
Class VI Advanced Sclerosing Lupus nephritis
What is the treatment for lupus nephritis
Class I, II – No specific renal therapy.
Induction and Maintenance:
Supportive care: BP control, Diet, Lower Cholesterol
Proliferative Lupus: Good RCT evidence for Steroids, Cyclophosphamide (Euro Lupus trial: 3 months Cyclophosphamide followed by Azathioprine)
Membranous Lupus: Supportive care, Steroids, small RCT evidence for Cyclophophamide,CNIs,Azathioprine..
Causes of nephrotic syndrome
Secondary MN: Associated with Autoimmune conditions, viruses, drugs and tumours.
Primary MN: Glomerular podocyte membrane PLA2R antigen is the target antigen in 70%-80% cases of primary MN. Recent metanalysis showed 99% specificity and 78% sensitivity for PLA2R ab in diagnosing primary MN.
What are renal calcui (stones) most commonly made of
Calcium oxalate
What is polycystic kidney disease
Autosomal dominant inherited disease. Mutation on PKD2 gene - causes cysts to grow in kidney.
1 in 400-1000
Presentation increased with age
Symptoms relate to size of cysts and hemorrhage bc of cysts
What is the presentation of polycycstic kidney disease
May be asymptomaic if mild and kidneys working ok Loin pain Visible haematuria (if cyst has bled) Infection Kidney stones
Can have extra-renal features
How would you investigate/ rule out polycystic kidney disease
Ultrasound scan Kidneys will be enlarged and have cysts Diagnosis criteria based on age. 15 - 40 - 3 or more cysts 40-60- 2 cysts in each kidney
What is the average liters of urine passed per day
1-1.5L
How is urine passed down the ureters
By peristalsis
Where are the internal and external urethral sphincters
Internal - neck of bladder
External - urogenital diaphragm
What is the name of the bladder muscle
Detrusor
What nerve regulate the bladder, micturation and voiding
Sympathetic nerve (hypogastric plexus - T11-L2) NA. Action = relax detrusor during filling, contracts internal urethral sphincter Parasympathetic nerve (pelvic nerve, S2,3,4) Ach. Action = stimulate detrusor muscle during voiding, relax internal urtheral sphincter Somatic nerve = pudendal nerve (S2,3,4) Ach. Action = stimulate/ contract external urethral sphincter so stays closed Afferent pelvic nerve = sensory input to brain and spinal cord from detrusor muscle
What property of the detrusor muscle prevent pressure back up from the bladder to the ureters and kidney
Receptive relaxation - keeps pressure low.
Lots of elastin in walls.
What are the 4 centers involved in micturition and voiding
- Cerebral cortex - guarding
- Pontine micturition centre/ periaquiductal grey: coodinating of voiding
- Sacral micturition centre
- Onuf’s nucleus - guarding reflex - cell bodies of pudendal nerve
Describe the neural regulation of bladder filling
Bladder fills with urine
Detrusor muscle - receptive relaxation
Sensory nerve from detrusor muscle sends slow pulse to sacral and micturition centres - slow impulse triggers sympathetic outflow to detrusor = relaxation + internal urethral sphincter contraction
+ activation of pudendal nerve = external urethral sphincter contraction
= no urine output
Describe the neural regulation of voiding (sacral reflex)
Sensory nerve from detrusor (sensory pelvic nerve) send fast pulse to sacral micturition centre.
This causes a reflex through parasympathetic activation to detrusor and contraction.
+ Inhibition of pudendal nerve
= Urine output
*NB, start getting increase pulses from sensory nerve from about 200 mls urine. Bladder can go up to about 500 mls.
Describe the neural regulation of guarding
Bladder filling >200ml. Pelvic sensory nerve sends fast pulses to scaral and pontine micturition centre.
Cortex sends signal to pontine micturition centre to inhibit voiding.
Signal from pontine to onufs nucleus = stimulation of pudendal nerve and sympathtic nerves to detrusor.
=More bladder relaxation and no urine output.
What stage is the bladder in 98% of the time
filling
Where does voluntary control of micturition come from
Cortex and PMC
Where is onuf’s nucleus and what is it important for
It is in ventral horn of sacral spinal cord.
Contains cell bodies for pudendal nerve (S2,3,4)
Important in guarding
List some differentials for a male patient with LUTS
Prostate enlargement (more cells, hyperplasia)
Detrusor muscle weakness (muscle in bladder)
UTI
Prostate cancer
Neurological disease
What type of cancer is prostate cancer
Adenocarcinoma
Where are prostate cancers most commonly located in the prostate
Peripheral zone - this means you should be able to feel for a mass with DRE
What is the international prostate symptom score, and what is it used for
It’s a questionnaire used to assess the severity of LUTS . It is used to assess (screen for) and monitor LUTS associated with benign prostatic hyperplasia. It helps diagnose BPH and monitor the patients symptoms.
It is not a screening tool for prostate cancer.
What are volume-flow charts, when are they used and what for
They are urine input/ output diaries that the patient completes daily.
They input the volume of liquid they intake and urine output.
Volume out can give you a flow rate, can tell you about OBSTRUCTION.
Anything below 10ml/s = 88% obstructed
10 - 15 ml/s = 54% obstructed
>15 ml/s = 24% obstructed
Normal, for a man over 60 years is 30 ml/s. Need to pass 125 mls to achieve this.
Can also calculate POST VOID RESIDUAL (PVR) VOLUME which can tell you about retention and hydronephritis risk
Anything >250 = risk of hydronephritis
Consider detrustor underactivity as cause of high PVR
What are volume-flow charts, when are they used and what for
They are urine input/ output diaries that the patient completes daily.
They input the volume of liquid they intake and urine output.
Volume out can give you a flow rate, can tell you about OBSTRUCTION.
Anything below 10ml/s = 88% obstructed
10 - 15 ml/s = 54% obstructed
>15 ml/s = 24% obstructed
Normal, for a man over 60 years is 30 ml/s. Need to pass 125 mls to achieve this.
Can also calculate POST VOID RESIDUAL (PVR) VOLUME which can tell you about retention and hydronephritis risk
What are volume-flow charts used for
Help work out if LUTS are obstructive, and if so, how much (work out by flow rate). Or if LUTS are being caused by increased frequency but no flow problems (irritative bladder - detrustor overactivity).
Or if LUTS are being caused by underactive bladder - risk of hydronephritis.
What are the complications of BPH
Disease progression Acute retention - painful (1L) Chronic retention - UTI risks Interactive obstructive uropathy - hydronephrosis Stones Haematuria
What is the treatment for mild BPH
watch and wait
What medical treatment is used for BPH
- Alpha1 blockers - should improve voiding problems
- Alpha 5 reductase inhibitors - shrink hyperplasia
- Antimuscurinics - for overactive bladder
What is the surgical treatment for BPH
When is this indicated
TURP - transurethral resection of prostate RUSHES Retention UTIS Stones Haematuria Elevated creatinine Symptom deterioration
What investigations would you do on a pt that you suspect has BPH
Urinalysis - UTI, proteinuria (msu) DRE - mass Bloods - U&Es, FBC, PSA Imaging - transrectal US Biopsy
What is the best medical treatment for BPH and why
combination alpha blockers and alpha-5 reductase inhibitors
The alpha-5 reductase inhibitors reduce retention risk and need for surgery (deal with obstruction)
Alpha blockers - give quick symptomatic relief of voiding problems - improve flow and post dribbling etc (deal with immediate problems)
What are the complications of TURP surgery
Can take out internal sphicter with resection = incontinence
Sepsis
Summary of BPH lecture
- LUTS can be divided into storage or voiding symptoms
- Evaluation of LUTS includes hx, exam, symptom score, FR and RU (rectal ultrasound), renal function
- Treatment of symptomatic BPE can be medical with alpha-adrenergic antagonists or 5-alpha-reductase inhibitors or combination of both
- Surgical treatment of BPE - often TURP
- Acute retention is painful and pain is relived by a catheter
- Interactive obstructive uropathy is rare
- Usually large residual, renal dysfunction which improves with a catheter. Long term treatment managment is TURP or long term catheter
What investigation do you need to diagnose prostate cancer
Biopsy
Describe the pathology of prostate cancer and how this links to treatment
Adenocarcinoma
Prostate gland secretes protein that liquidises (alkinates) semen
Cancer is in peripheral zone (contrast to BPE - transitional)
Oncogene ERG attaches to androgen sensitive gene, this means that when androgen stimulates the innocuous gene, this upregulates the oncogene = cell proliferation
What are the symptoms of prostate cancer
LUTS - obstruction
Nocturia, hesitancy, poor stream, terminal dribbling
+ Weight loss
+ Bone pain if metastasised
What investigations would you do on a 70 year old patient that has LUTS to rule out/ confirm prostate cancer
DRE - palpable mass - hard/ craggy
If mass - Bloods for prostate specific antigen
If PSA >3 ng/ mL discuss what this means with patient and referral
What investigations are required to diagnose prostate cancer, which one is diagnostic
DRE Bloods - PSA + others (PSMembrane A) Urinalysis - prostate cancer products Transrectal ultrasound Biopsy + Grade * Diagnostic Staging
Outline the treatment options for prostate cancer
Localised - Curative - Surgery, RTX, Hormone therapy
Locally advancer - Local control - Surgery, TRX, Hormone therapy
Advanced - palliative - hormone therapy
Why is prostate screening not rolled out in UK
- PSA is not specific for prostate cancer, this means that an elevated PSA result does not mean a patient has prostate cancer. 1/4 with high PSA will have PC.
- Inconclusive whether screening improves survival
- The natural disease course of localised prostate cancer is unknown, this means that their is currently no evidence about whether starting treatment for localised prostate cancer is beneficial or more risky to the patient than the natural disease course.
If a patient has a high PSA level (>3) what is their chance of having PC
25 - 33%
If a patient has a normal PSA level (>3) what is their chance of having PC
15%
A 50 year old male wishes to discuss having a PSA test for prostate cancer - he is asymptomatic. What information should you include in the discussion?
- PSA is not prostate cancer specific - so if you have a high level it wont confirm whether you have cancer
- A normal level won’t completely exclude cancer - some men with prostate cancer don’t have elevated PSA (6%)
- If high level - undergo more tests (Bloods, ultrasound, biopsy etc) to confirm diagnosis
- If do get diagnoses, there is no evidence that treatment will improve disease progression or survival - the benefits vs risks of treatment for asymptomatic PC is unknown - it may be more harmful to get treatment
- PSA levels increase as men get older bc the prostate enlarges- This means that an elevated PSA level does not mean you have cancer
What is the family risk of prostate cancer
5-10%
What conditions raise PSA levels
UTI
Prostatitis
BHE
What are the pros and cons of prostate screening
Pros:
Early detection of curable localised prostate cancer
Early detected of advanced treatable prostate cancer and better palliation
Cons:
Natural course of disease unknown
Inconclusive whether screening improves survival
Inconclusive whether diagnosis causes benefit or more risks than natural course of disease
What is the most common renal cancer, who is the demographic
Renal cell carcinoma
M>F
Middle aged
What is the main differential with renal cancer
Polycystic kidney disease - share similar symptoms
Haematuria
Loin pain
Enlarged kidneys
Difference - weight loss, palpable mass
What are the symptoms of RCC
Haematuria Loin Pain Abdominal mass Weight loss Hypertension (bc of EPO) Polycythemia (headache)
What investigations should be done for a pt you suspect with RCC
Ultrasound - rule out/ confirm PKD
May then want CT or MRI
Bloods - Include ALP for bone mets
Urinalysis - cytology
Where does renal cell carcinoma metastasise to
Bone
Liver
Lungs
Brain
Describe the staging of Renal cell carcinoma and treatment
Stage 1 = <7cm
Stage 2 = >7cm
Stage 3 = in renal vein
Stage 4 = broken through fascia
Treatment - nephrectomy
What is the most common bladder cancer - what are the risk factors of bladder cancer to include in your history
Transitional cell carcinoma Smoking Rubber dyes (aromatic amines) - occupational Chronic cystitis Paraplegic - cathether
What is the presentation of bladder cancer
Painless visible haematuria
Irritative voiding symptoms - frequency, urgency, nocturia
recurrent UTIs
What investigations should be done for a pt with suspected bladder cancer
Cystoscopy + biopsy *this is what is diagnostic
CT not helpful in small tumours
Urinalysis - cytology
Can do CT urogram on larger tumours
How is bladder cancer staged
T1- in mucosa - most present at this stage (80). Can observe or burn cancer off using transurethral resection of bladder tumour (TURBT), or immunotherapy to get immune system to kill it, or chemo (BCG)
T2 - in wall - cystectomy +- radio and chemo therapy
What is the rule for 2 week referral on bladder cancer
> 50 years, unexplained V haematuria (no UTI)
50 years, unexplained V haematuria with recurrent UTI
60 years, unexplained non visible haematuria with dysuria or raised white cell count on blood test
Non urgent referral when…
>60 with recurrent unexplained UTI
Causes of haematuria (V or NV)
Infection: UTI, pyelonephritis, TB Malignancy: anywhere in tract Stones: bladder, kidney, ureteric Trauma: penetrating Vs Blunt Nephrological: diabetes, nephropathy (proteinuria)
What is the common pathology of testicular cancer
Seminoma (most common - germ cell cancer)
2 - teratoma (also germ cell but younger one)
Presentation of testicular cancer
Male 20-40s
Painless testicular lump
Chest involvement - if metastasised
What is the differential for testicular cancer - how would you conduct the examination
- Can you get above the lump - no, hernia, hydrocele
- Is it separate from testis - if so, cyst, epididymitis, varicocele
- Cystic or solid - hydrocele, cyst etc
What are the signs of testicular torsion
Acutely inflamed Swollen Red Hot Painful
What cancer markers are there in the blood for testicular cancer
Beta human chorionic gonadatropin hormone
Risk factors for testicular cancer
Undescended testis
Infertility
Infant hernia
Treatment for testicular cancer
Orchidectomy
+ Radiotherapy - seminoma
Where does testicular cancer spread to
Lymph nodes
Liver
Lungs
What pathogen is associated with renal stones
Proteus
Causes of UTI
Sex Catheterisation Enlarged prostate Renal tract tumours Renal stones
What are the common UTI pathogens
Escherichia coli Proteus mirabilis Klebsilla spp - hospital acquired Staph saprophyticus Staph epidermidis Enterococci
What are the common investigations for UTI
Mid stream urine - to avoid contamination with vagina/ perineum
Direct microscopy - neutrophils, pus etc = pyuria
Culture
CLED, MacConkey
Sensitivity testing - antibiotics
What culture medium is used for gram negative pathogens and why
MacConkey agar - contains bile salts to inhibit gram positives
What culture medium is used for urine pathogens
CLED
What is the criteria for treating a UTI with antibiotics
1 severe, or >3 UTI symptoms
In what type of UTI should nitrofurantoin not be used
Pylonephritis
Pregnancy - 3rd trimester
Common antibiotics prescribed for UTIs
Amoxicillin Trimethoprim Cephalexin Nitrofurantoin Co-Amoxiclav Genatmicin
What are the features of renal colic pain
Extremely painful 12/10 Writing - cant get comfortable Acute onset Spasmodic "colic" Radiates to groin
How would you differentiate renal pain caused by pyelonephritis vs renal colic
Differentiating features
Pylonephritis - Fever, inflammatory markers, Sepsis risk - watch BP, not colic pain, less likely to radiate to groin, Pyuria
Renal colic - colic pain, “crescendo”, loin to groin, very intense pain
What investigation should not be used for kidney stones
USS
When should USS be used for renal pain (loin) and to rule out what
When you suspect upper urinary tract obstruction and hydronephritis - can be useful in pregnancy
Causes of renal stones (calculi)
Diet - high Na, Ca, protein (lowers ph), oxalate (spinach nuts) - ANYTHING that causes supersatuarated urine Hydration - dehydrated Parathyroid - PHT Idiopathic UTI
Presentation of renal tract obstruction
Pain 12/10 - loin -> groin
Writhing - helps diff to pertinonitis
Colic pain
UTI symptoms
Investigations for renal stones
Non contrast CT USS or MRI - pregnancy Bloods, everything - look for infection + Ca level Urinalysis - look for UTI Midstream culture - MCS
What are the complications of renal obstruction
Sepsis and shock
Pyonephritis (infection + obstruction - think about the staghorn stone) - watch for signs of fever, loin pain, vomiting and nausea
How are chlamydia, gonorrhoea and syphillis transmitted
vaginal, anal, oral sex, vertical transmission (mother to baby)
Who is most commonly affected by chlamydia
Young females, early 20s
In stable relationship
Who is most commonly affected by gonorrhoea
Males - late 20’s
New partner
What type of pathogens are chlamydia trachomatis and N gonorrhea
Gram negative cocci
What are the symptoms of chlamydia and gonorrhoea
Dysuria
Uretheral discharge
Which is more symptomatic of chlamydia and gonorrhoea
Gonorrhoea in males
How many asymptomatic early 20’s females have chlamydia
approx 10%
What investigations should you do for chalmydia in a female and male
Female - vaginal or cervical swab
Male - 1st pass urine
Then NAAT - nucelic acid amplification test
What investigations would you do to confirm gonorrhoea in a male and female
Uretheral swab
Vaginal swab
Can do microscopy (diplococci - gram -ve)
+ culture and NAAT
What is the management of chlamydia and gonorrhoea
Chlaymdia = not problem w resistance
Treat with doxycycline + erythromycin (gram -ve cover)
Pregnant = azithromycin
Gonorrhoea = problems with resistance - check local guidelines
Currently - ceftriaxone - IM
+ Azithroymycin
Which of chlamydia and gonorrhoea is treated IM
Gonorrhoea
What should be done on ALL STI diagnoses
Partner notification & follow up
Why is partner notification done
To prevent disease progression in asymptomatic person
To prevent reinfection of index patient who is being treated
What is shyphillis, who is affected by it and how is it transmitted
Gram -ve spirochaetes. T Pallidum
Males mainly - in 30s
Vaginal, oral, anal sex, verticle transmission
What is the presentation of shyphillis
Primary infection - ~month - chancres - genitals, mouth
Secondary ~ 6-8 months - palmar rash, papular trunk rash, fever, lymphadenopathy etc
Latent - >2 years - disease but no symptoms
Tertiary - CNS, CVS, gummas
How would you investigate a pt that you suspect has shyphillis
If have ulcer - swab and microscopy
+ Bloods - serology to exclude
+Bloods - EIA to confirm
What is the treatment for shyphillis
IM penicillin
What investigation would you do in a patient that you are suspicious of bladder cancer
Flexible cystoscopy
Who is most at risk of bladder cancer
Males - over 40
The risk of bladder cancer goes up with age
Females - risk starts to go up after 60
What percentage of bladder cancers reach the bladder wall when invading
20%
(i.e. 80% are not in the wall on presentation - T1)
Aka, 80% have superficial disease - a lot more treatment options avaiable for this
What is NMIBC
Non muscle invasive bladder cancer
What percentage of NMIBC progress to MI (muscular invasion)
15%
What percentage of NMIBC will recur
70%
What are the risk factors for developing bladder cancer
Paraplegia
Smoking
Occupational risk - aromatic amine exposure through paints
Bladder stones or schistosomiasis infection
How would you treat T1 bladder cancer
“Conservative treatment”
Diathermy (burn it off)
via transuretheral resection of the bladder
BCG - stimulates nonspecific immune response for multiple small tumours
+ chemo
95% survival at 5 yrs
How would you treat T2 bladder cancer
“Radical treatment”
Cystectomy or RTX
(RTX - worse prognosis)
Requires aggressive treatment
What is the prognosis of bladder cancer
50% survival 10 years - depends on grade really
What is the best investigation for kidney stones
Non contrast CT
When is an XRAY KUB useful in the management of renal stones
Monitoring/ good follow up tool.
NB, stones smaller than approx 5mm should pass on their own, with hydration advice and analgesic for pt. So would take Xray to compare with 2 weeks later to check stone has gone. Use X ray to confirm stone has gone.
This is “conservative” management of a kidney stone
Offering chlamydia tests in pharmacies is a type of what prevention
Secondary - pt already has disease, aim it to diagnose and treat to prevent disease progression
What is the triad of symptoms for pyelonephritis
Loin pain
Fever
Pyuria
Is polycystic kidney disease dominant or recessive
Autosomal dominant - means you have to inherit one copy of the gene - dont need both parents to be carriers but one must have it
What is the first mediciation you would give to a pt with hyperkalemia to give cardio protection
Calcium gluconate - this protects against the hyperexcitability stage of hyperkalemia where the cells is vulnerable to AF/ VF
Then treat with Insulin & dextrose to take K+ into cells and clear from blood to stabalise
What is actrapid
Insulin
What would you do if you have a patient with urosepsis who has a history of CVS
Stop ACEx or ARBs - will exacerbate sepsis
What would be the signs if stones on a non contrast CT
Hydronephrosis - dilated renal pelvis and parenchyma
Perinephritic stranding - fat stranding around it
Perinephric tissues
Cortical thickness
Hydronephrosis +/- hydroureter
Stones
Outline the management of stones >2cm
Drainage - think about sepsis etc
Decompression by uteric stent of percutaneous nephrostomy insertion
Shock Wave Lithotripsy
Then plan for surgery
