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Week 14 Flashcards

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1
Q

What are the functions of the kidneys?

A 
control of solutes and fluid status
blood pressure control
acid /base
drug metabolism / excretion
endocrine functions
metabolic waste excretion
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2
Q

What is the primary role of the kidneys?

A

to maintain fluid and electrolyte homeostasis in response to blood pressure and hormones

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3
Q

What is the function of the glomeruli?

A

filter plasma

not supposed to let through protein / cells / large molecules

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4
Q

What is the function of the tubules?

A

adjust filtrate content, with collecting ducts absorbing water

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5
Q

Describe measuring urinary protein excretion

A

24hr urine collection (grams/24hrs)

protein: creatinine ratio (PCR) on morning spot sample (mg/mol)
albumin: creainine ratio (mg/mol)

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6
Q

Describe haematuria

A

can be blood detectable on dipstick (non-visible haematuria)
visible haematuria-can come from anywhere in the urinary tract (kidneys, stones, infection, malignant, cysts, inflammation)

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7
Q

What is measured in U&Es?

A 
sodium
potassium
chloride
urea
creatinine
eGFR
\+/- bicarbonate
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8
Q

Describe creatinine

A

breakdown product of muscle so plasm concentration affected by muscle mass
concentration affected by plasma volume
affected only slightly by diet
up to 15% secreted by renal tubule, so total urinary excretion = glomerular filtration + tubular secretion
Trimethprim blocks this - artificially raised

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9
Q

Describe urea

A 
used less than plasma creatinine concentration because urea concentration is more affected by non kidney factors:
diet
dehydration
tissue breakdown - e.g corticosteroid
liver failure (lower levels
up to 40% may be reabsorbed
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10
Q

What is clearance?

A

volume of plasma which would be cleared of the substance per unit of time

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11
Q

What is renal clearance?

A

urine concentration X urine volume
/ plasma concentration of substance
usually expressed as ml/min
usually described as glomerular filtration rate

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12
Q

What is used to calculate the eGFR?

A

plasma creatinine concentration
age (adults only)
gender
race

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13
Q

Describe in what way eGFR assumes stable renal function

A

if today’s plasma creatinine concentration = 100micromols/L, but the patent has no kidneys or is making no urine, GFR=0
important for drug dosing
not suitable for AKI

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14
Q

Describe the staging of chronic kidney disease

A

> 90 - with another abnormality otherwise regard as normal = 1
60-89 - with another abnormality otherwise regard as normal = 2
30-59 - moderate impairment - 3
15-29 severe impairment = 4
<15 advanced renal failure = 5

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15
Q

Describe the basics of glomerulonephritis

A 
inflammatory diseases involving the glomerulus and tubules
rare
variable natural history 
may be primary or secondary
few specific treatments
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16
Q

What are the targets for injury in glomerulonephritis?

A 
mesangial cells
basement membrane (collagen IV)
epithelial cells (podocytes)
capillary endothelial cells
vasculature
tubular structures
integrity of glomerulus and tubules
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17
Q

What are the extrinsic mechanisms of glomerulonephritis?

A 
antibodies
immune complexes
complement
cytokines
lymphocytes
other infiltrating cells
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18
Q

What are the intrinsic mechanisms of glomerulonephritis?

A 
cytokines
growth factors 
TGF-beta, PDGF, IFN gamma
vasoactive factors
proteinuria
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19
Q

Describe kidney biopsy

A

required for clinical diagnosis of glomerulonephritis
biopsy of kidney cortex examined under:
light microscopy (glomerular and tubular structure)
immunoflourescence (looking for Ig and complement)
electron microscopy (glomerular basement membrane and deposits)
many diseases are a clinical and pathological spectrum

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20
Q

Describe RPGN

A

rapidly progressive glomerulonephritis - rapid rise in serum creatinine
crescentic damage
vasculitis / lugs. IgA: often have other clinical features

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21
Q

Describe nephritic syndrome

A

blood and protein in urine, high blood pressure, rising sCr
proliferative / acute inflammation
IgA / lupus / post-infectious

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22
Q

Give overview of nephrotic syndrome

A

> 3.5g/day proteinuria, low salt, oedema
non-proliferative, podocyte damage
minimal change/ FSGS/ membranous

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23
Q

Describe nephrotic syndrome

A

3.5g proteinuria per 24 hr
serum albumin <30
oedema

hyperlipidaemia
risk of venous thrombosis and infection also increased

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24
Q

Describe IgA nephropathy

A

infection? production of IgA
mesangial deposition of IgA
lysis of mesangium proliferation of MC, matrix production, healing or scarring
glomerulosclerosis, tubular loss, hypertensive damage
may be secondary to HSP, cirrhosis, coeliac disease
abnormal production of IgA, C3 deposition

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25
What are the clinical features of IgA nephropathy?
``` haematuria proteinuria hypertension renal impairment resolve, persist, progress to ESFR ```
26
How is IgA nephropathy treated?
antihypertensives ACE I ARBs
27
Describe the pathophysiology of membranous GN
primary - production of Ab Secondary - tumour? drugs? CTD? deposition of, or formation of, IC in the GBM and mesangium altered GBM charge, altered permeability, thickened GBM glomerulosclerosis tubular loss hypertensive damage
28
Describe the clinical features of membranous GN
proteinuria nephrotic syndrome hypertension renal impairment
29
Describe membranous GN
disease of adults presents with the nephrotic syndrome can be secondary to malignancy, CTD, drugs anti-phospholipase A2 receptor antibody in 70% IC in basement membrane / sup-epithelial space
30
How is membranous nephropathy treated?
treat underlying disease if secondary supportive non -immunological - ACEi, statins, diuretics, salt and fluid restriction specific immunotherapy - steroids, alkylating agents (cyclophosphamide), cyclosporin, alternatives (rituximab) outcomes - complete remission, partial remission, ESRD, relapse, death
31
Describe minimal change disease
commonest form of GN in children causes nephrotic syndrome EM - foot process fusion idiopathic but may be secondary to malignancy acute presentation - may follow URTI GFR - normal or reduced due to intravascular depletion relapsing course
32
What is the treatment of minimal change disease?
high dose steroids (prednisalone 1mg/kg for up to 8 weeks | cyclophosphamide / calcineurin inhibitor
33
Describe the pathophysiology of post infectious GN
``` infection - streptococci, production of Ab/IC deposition of AB/IC in mesangium etc complement activation infiltration of leukocytes destruction of glomerular cells proliferation of epithelial cells crescent formation glomerulosclerosis tubular loss hypertensive damage ```
34
Describe the clinical features of post infectious GN
``` nephritic/ RPGN haematuria proteinuria hypertension renal impairment ```
35
Describe post-infectious glomerulonephritis
production of cross reactive Ab after group A strep infection sub-epithelial I/C deposition complement consumption and hypocomplementaemia 10-21 day latent period oliguric ARF resolves over weeks in most cases may require dialysis
36
Describe crescentic GN / RPGN
a group of conditions linked by natural history./ histology crescents on biopsy progression to ESRF over a few weeks, untreated high mortality
37
What are common causes of crescentic GN / RPGN
goodpastures syndrome - anti-GBM antibody pauci immune - microscopic polyangiits - MPO antibody (postive pANCA) granulomatosis with polyangiitis (GPA) - PR3 antibody (positive cANCA post infectious / bacterial endocarditis lupus idiopathic rarely others - IgA nephropathy
38
What tests for diabetic nephropathy?
HbA1c / random glucose
39
What tests for vasculitis?
ANCA / anti GBM
40
What tests for membranous GN?
ANA/ PLA2R / virology
41
What tests for lupus?
complement / ANA / dsDNA
42
What tests for MPGN, FSGS?
complement / virology (hepB, C, HIV) Igs, RF
43
What tests for amyloid / light chain deposition?
SEP / BJP / SFLC
44
Name 4 systemic diseases associated with renal dysfunction
diabetes mellitus atheromatous vascular disease systemic lupus erythematosis amyloidosis
45
In what 5 ways can systemic diseases manifest in the kidneys?
``` acute kidney injury chronic kidney disease nephritic syndrome proteinuria nephrotic syndrome ```
46
Describe the pathophysiology of diabetic nephropathy
``` hyperglycaemia volume expansion intra-glomerular hypertension hyperfiltration proteinuria hypertension and renal failure ```
47
Describe the structural changes the glomerulus in diabetes mellitus
thickening of the glomerular basement membrane, fusion of foot processes, loss of podocytes with denudling of the glomerular basement membrane, and mesangial matrix expansion
48
What does the evidence recommend for the reduction of risk of diabetic nephropathy?
Tight glycaemic control Good BP control - ACEi /ARB, SGLT2 inhibitors aim for BP <130/80
49
Describe the action of SGLT2 inhibitors
prevent reabsorption of glucose and sodium lowers blood pressure and blood glucose main side effect- UTIs can't be used in late stage kidney disease
50
Describe the pathogenesis of renovascular disease
progressive narrowing of renal arteries with atheroma perfusion falls by 20% GFR falls but tissue oxygenation of cortex and medulla maintained RA stenosis progresses to 70% cortical hypoxia causes microvascular damage and activation of inflammatory and oxidative pathways parenchymal inflammation and fibrosis progress and become irreversible restoration of blood flow provides no benefit
51
Describe the management of renal artery stenosis
BP control (not ACEi / ARB) statin if diabetic - good glycaemic control lifestyle - smoking cessation, exercise, (low sodium diet) angioplasty - rapidly deteriorating renal failure, uncontrolled high BP on multiple agents flash pulmonary oedema
52
Describe amyloidosis
deposition of highly stable insoluble proteins material in extracellular space kideny, heart, liver, gut specific ultrastructural features (8-10nm fibrils) high affinity for the constituents of the capillary wall
53
What is the appearance of amyloid on light microscopy?
congo red stain | apple green befreingence
54
What is the appearance of amyloid on electromicroscopy?
amyloid fibrils | cause mesangial expansion
55
What are the 2 classes of amyloid?
AA - systemic amyloidosis - (inflammatory or infection | AL - immunoglobulin fragments from haematological condition - myeloma
56
HOw is amyloid treated?
AA - treat the underlying source of inflammation / infection AL - treat the underlying haematological condition
57
Describe systemic lupus erythematosis
auto-immune disease immune complex mediated glomerular disease multiple auto-ABS - directed against DNA, histones, snRNPs, transcriptional / translational machinery
58
Describe the pathophysiology of lupus nephritis
``` auto-antiboeis produced against dsDNA or nucleosomes (anti-dsDNA, anti-histone) form intravascular immune complexes or attach to GBM activate complement (low C4) renal ddadmage ```
59
Describe the diagnosis of lupus nephritis
renal biopsy to confirm diagnosis and stage disease | treatment - immunosuppresion - steroids / MMF/ cyclophosphamide / rituximab
60
What is a cyst?
sac like structure containing fluid in the kidneys - these arise from the tubules cause problems by compressing other structures, replacing useful tissue, becoming infected, bleeding, pain
61
Describe adult polycystic kidney disease
commonest inherited kidney disorder autosomal dominant PDK1 gene mutation (C16), most common and aggressive PDK 2 gene mutations
62
Describe the impact of PKD1 and 2 gene mutations
code for polycystic 1 and 2 polycystins are located in the renal tubular epithelia (and in liver and pancreas ducts) overexpressed in cyst cells membrane proteins involved in intracellular calcium regulation mechanism for cyst formation is poorly understood genetic testing not routine
63
Describe the natural history of APKD
cysts gradually enlarge kidney volume increases some compensation eGFR falls, usually 10 years before kidney fails
64
Describe the diagnosis of APKD
differentiate between simple renal cysts which are common as people get older should get ultrasound at 21 if family history - 2 cysts, screened again at 30 if no cysts no family history - 10 or more cysts on each side CT or MRI more sensitive
65
What are the renal complications of APKD?
50% risk ESRD by age 50 | cyst accidents 60%
66
What are the other complications of APKD?
``` hypertension intracranial aneurysms mitral valve prolapse aortic incompetence colonic diverticular disease liver / pancreas cysts hernias - volume of kidneys ```
67
What is the management of APKD?
``` supportive early detection and management of blood pressure treat complications manage extra renal associations renal replacement therapy ```
68
Describe Von HIppel Lindau
autosomal dominant condition causing multiple bengin and malignant neoplasms renal cysts and multifocal renal cell carcinomas other unusual tumours - phaechromoctytoma, haeangioblastoma, clear cell carcinoma of CNS
69
Describe tuberous sclerosis
autosomal dominant benign hamartomas of multiple systems: brain, eyes, heart, lung, liver, kidney and skin variable phenotype up to 80% renal involvement - multiple renal cysts, renal angiomyolipomas, renal cell carcinoma most have epilepsy, 50% have learning difficulties
70
Describe medullary cystic kidney disease
autosomal dominant cysts at the corticosteroids-medullary junction small to normal sized kidneys hyperuricaemia and gout
71
Describe Alport's syndrome
usually X-linked - collagen 4 abnormalities - alpha 3 gene mutation, alpha 4 gene mutation or alpha 5 gene mutation deafness and renal failure (can affect other organs including eyes) microscopic haematuria, proteinuria, and ESRF mainly on dialysis bu age 40 sensineural hearing loss late childhood female aport's carrier - 12 % ESFR by age 40
72
Describe Fabry's disease
X-linked storage disorder alpha galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3) Gb3 accumulates in glomeruli, particularly podocytes causing proteinuria and ESFR - average age of onset 34 also causes neuropathy, cardiac and skin features diagnosis - measure alpha Gal A activity in leukocytes renal biopsy management - enzyme replacement therapy
73
Describe cystitis
``` infection of the bladder dysuria frequency urgency suprapubic pain haematuria ```
74
Describe pyelonephritis
``` infection of the kidney cystitis symptoms plus fever >38 chills / riots flank pain costo-vertebral angle tenderness nausea / vomiting ```
75
What are the risk factors for UTI
``` infancy abnormal urinary tract female bladder dysfunction / incomplete emptying foreign body diabetes mellitus renal transplant immunosuppressants ```
76
How are UTIs diagnosed?
multisite microscopy / flow cytometry urine culture
77
Describe urine culture for UTI
obtain before starting antibiotics | clean catch supra pubic aspiration, catheter specimen
78
Describe antibiotics treatment of UTI
IV - ceftriaxone, gentamicin | oral - trimethoprim , cephalosporin, co-ampxiclav, nitrofurantoin
79
What are the pros and cons of ultrasound in UTI?
radiation free readily available good for dilated drainage tracts and cysts operator dependent less sensitive for scarring, parenchymal damage
80
Describe MCUG pros and cons
gold standard for VUR and PUV radiation invasive - UTI risk
81
Describe DMSA (static)
``` gold standard for scars ectopic - duplex differential fucntion timing - acute or chronic differentiating scars vs dysplasia radiation ```
82
Describe MAG3 indirect cystogram
used for VUR study with no catheter needed differential function need continence and cooperation on bladder emptying no PUV info available misses low grade VUR
83
Describe MAG3 diureses renogram
gold standard for obstruction furosemide also needed operator interpretation
84
What are the risk factors for renal scarring?
``` age high grade VUR anatomical obstruction dysfunctional voiding frequent episodes of APN therapeutic delay bacterial virulence factors host response low birth weight prenatal dysplasia ```
85
Name congenital abnormalities of jidey and urinary tract (CAKUT)
vesico-ureteric reflux (VUR) | obstruction of urinary drainage tracts
86
Describe VUR
retrograde passage of urine from the bladder to the upper urinary tract higher risk of UTI and pyelonephritis some will resolve spontaneously
87
Describe the management of VUR and UTI
medical - antibiotic prophylaxis for high grade VUR until toilet trained surgical - recurrent , febrile UTI, new scarring, sting procedure
88
Describe causes of bladder outlet obstruction
posterior urethral valve prostatic hypertrophy function obstruction - neurogenic bladder prune belly syndrome
89
Describe posterior urethral valve
commonest cause of obstruction in male infants valve leaflets or circumferential diaphragm presentation - antenatal hydronephritis, UTI, poor urinary stream, renal dysfunction chronic renal failure management- valve resection, antibiotic prophylaxis, CKD care
90
Describe PUJO
commonest cause of hydronephritis in children frequently noted on antenatal ultrasond abdominal mass, pain, haematuria, UTI
91
Describe vesicle-ureteric junction obstruction
anatomical narrowing v functional obstruction | antenatal dilatation: UTI, abdominal mass, haematuria
92
What is AKI?
decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatinine
93
What are the classifications of AKI and give examples of each type
pre renal - circulatory failure "shock" Renal - the cells of the kidney post renal - obstruction
94
Give examples of pre-renal causes of AKI
``` hypotension hypo-volaemia hypo-perfusion hypoxia sepsis drugs toxins ```
95
What can cause renal obstruction?
calculi tumours (ureter, bladder, prostate, cervix, ovarian) lymph nodes (compression) prostate
96
What are the renal causes of AKI?
glomerulonephritis drugs -gentamicin tubulo-intersitial nephritis, rhabdomyolysis
97
Describe ATN
acute tubular necrosis any pre renal cause of AKI if severe or prolonged usually reversible
98
What are the causes of ATN?
hypotension sepsis toxins
99
What toxins can cause ATN?
exogenous - drugs, contrast, poisons endogenous - myoglobin, haemoglobin, immunoglobulins, calcium, urate
100
How is AKI diagnosis established?
bloods - both creatinine and urea up potassium urine output usually less than 400ml day clinical assessment of fluid status (BP, JVP, oedema, heart sounds) underlying diagnosis (history, exam and meds)
101
Describe the treatment of AKI
immediate airway and breathing circulation - shock - restore renal perfusion, hyperkalaemia, pulmonary oedema remove causes - drugs, sepsis exclude obstruction and consider renal causes ask for help - renal or ICU
102
How is the cause of AKI established?
``` history and exam drugs urinalysis renal ultrasound GN screen - ANCA. ANA, immunoglobulins, EP, complement, aGBM, urine bench jones protein others - blood film, LDH, CK etc ```
103
What level of potassium is a medical emergency?
>6.5
104
What is the treatment of hyperkalaemia?
calcium glucondate 10ml 10% as cardiac membrane stabiliser insulin 10-15 units actrapid + 50ml 50% dextrose moves potassium into cells reduce absorption from gut - calcium resonium 15g 4 X day orally
105
How should acidosis be treated in AKI?
if raised potassium and HCO3 <16 also worth bicarb supplementation IV NaBicarb 1.26% IV
106
What are absolute indications for dialysis?
refractory potassium >6.5 mol/l | refractory pulmonary oedema
107
What are relative indications for dialysis?
acidosis (pH <7.1) uraemia - pericarditis, encephalopathy toxins (lithium, ethylene glycol etc)
108
Describe recovery from ATN
often a polyuric phase for 48-72 hours may be up to 6 L urine / day often subsequent low K, Ca, Mg as low quality urine tubules fail to concentrate urine
109
What is CKD?
kidney damage of GFR <60ml/min for 3 month or more
110
What are problems with serum creatinine as indicator of renal function?
slow recognition of loss of the first 70& of renal function surprise at the sudden rise in creatinine with late renal referral overestimation of function in women overestimation of function in elderly overestimation in inhere low muscle mass groups - amputees, quadriplegics, RA
111
What can cause CKD?
``` diabetic nephropathy renovascular disease chronic glomerulonephritis reflux nephropathy ADPKD obstructive uropathy ```
112
What are the symptoms of advanced CKD?
``` pruritus nausea, anorexia, weight loss fatigue leg swelling breathlessness nocturia joint / bone pain confusion? ```
113
What are the signs of advanced CKD?
``` peripheral and pulmonary oedema pericardial rub rash/excoriation hypertension tachypnoea cachexia pallor / lemon yellow tinge ```
114
What are the general principles of CKD management?
targeted screening interventions to slow rate of progression of CKD and reduce cardiovascular risk medicines to replace impaired individual functions of the kidney advanced planning for future renal replacement therapy renal replacement therapy
115
How can the progression of CKD be slowed?
``` aggressive BP control good diabetic control diet smoking cessation lowering cholesterol treat acidosis ```
116
Describe ACEi use in CKD
drug of choice if tolerated reduction in eGFR of up to 25% in first few weeks is a good thing will get more of a reduction if critical reduced renal perfusion sick day rules
117
Describe anaemia in CKD
common, particularly late iron absorption and utilisation suboptimal replace iron, B12 and folate first if low ESA eg darbepoietin alfa 30m every 2 weeks trigger usually Hb<100, target Hb - 100-120 higher associated with adverse CV events
118
Describe bone mineral control in CKD
Don't remove phosphate as well don't metabolise vitamin D calcium low, phosphate huh more PTH produced - further phosphate elevation and bone depletion sometimes parathyroid gland can become metaplastic or form nodules and be unresponsive to serum calcium levels
119
Describe CKD- MBD treatment
activated vitamin D - alfacalcidol occasional Mg supplementations phosphate binders calcium based - calcium carbonate / acetate non calcium - sevelamer, lanthanum, aluminium calcimetic - cinacalcet paratyhroidectomy
120
What are the options in RRT?
conservative care home based therapies hospital based therapies - haemodialysis transplant
121
When should dialysis be started in CKD?
``` individual based on symptoms most GFR - 6-8 no benefit to early start weight loss and persistent nausea persistent hyperkalaemia, acidosis, severe hyperphosphataemia or pruritis problematic fluid overload best to have permanent access ```
122
What is pharmacokinetics?
the science of the rate of movement of drugs within biological systems, as affected by the absorption, distribution, metabolism and elimination of medications
123
What is pharmacodynamics?
tidy of the biochemical and physiological processes underlying drug action
124
What is bioavailability ?
fraction of the administered drug dose that reaches the systemic circulation
125
What is the clearance?
volume of plasma cleared of drug per unit of time
126
What is half life?
time required for serum plasma concentration to decrease by half determined by clearance and volume of distribution
127
Describe the influence of age on pharmacokinetics
decrease in total body water and increases in total body fat | variable changes in first pass metabolism due to variable decline in hepatic blood flow
128
Give examples of water soluble drugs and the impact of ageing on their serum levels
lithium, aminoglycosides, alcohol, digoxin | serum levels may go up due to decreased volume of distribtion
129
Give examples of fat soluble drugs and the impact of ageing on their serum levels
diazepam, thiopental, trazadone | half life increased with increased body fat
130
Describe the influence of age on the liver
acetylation and conjugation fo not change with age oxidative metabolism through cytochrome P40 system does decrease with ageing, resulting in a decreased clearance of drugs hepatic blood flow variable
131
Describe the influence of age on pharmacodynamics
some effects increased - alcohol, opiates, sedatives, theophyilline some decreased - diminished HR response to isoproterenol and beta blockers
132
give examples of drug disease interactions
patient with PD have increased risk of drug induced confusion NSAID can exacerbate CHF urinary retention in BPH patients on decongestants oe anticholinergics constipation worsened by calcium, anticholinergics, calcium channel blockers neuroleptics and quinolone lower seizure thresholds
133
Give examples of common drug -drug interactions in the elderly
statines and erythromycin and other antibiotics verapamil and beta blockers warfarin and multiple drugs ACEi increase hypoglycaemic effect of sulfonylureas
134
Describe the effects of renal disease on pharmacokinetics and pharmacodynamics
decreased elimination decreased protein binding decreased hepatic metabolism altered sensitivity to drug effect adverse effects
135
Which drugs are affected by decreased elimination in renal disease?
``` aminoglycosides lithium digoxin methotrexate penicillins ```
136
Describe reduced protein binding in renal disesae
``` renal failure leads to acid retention acidic drugs less bound to albumin increased free drug in plasma usually not important but for phenytoin the target concentration should be lower in renal failure ```
137
Give examples of nephrotoxins
amphoteracin, gentamicin
138
Give examples of important prescribing in renal disease
``` antibiotics - reduce dose LMWH - reduce dose metformin - avoid NSAIDs- avoid digoxin - reduce dose phenytoin - reduce dose ACE inhibitors -caution ```
139
In what ways the hepatic impairment impact pharmacokinetics and pharmacodynamics?
first pass metabolism activation of prodrugs decreased protein binding decreased elimination altered sensitivity to drugs
140
Which drugs have profound changes in bioavailability when first past metabolism is reduced?
cholmethioazole verapamil paracetamol
141
Which drugs is the first pass activation reduced when there is hepatic impairment?
enalaprilm perindopril
142
Describe high extraction drugs of the liver
metabolised at a high rate by the liver rate varies with delivery affected by changes in blood flow morphine, verapamil, lignocaine
143
Describe low extraction drugs of the liver
metabolised at a low rate by the liver independent of blood flow sensitive to changes in liver enzyme acitivty chloramphenicol, theophylline
144
describe the effects on pharmacodynamics of drugs in liver impairment
``` sensitive to sedatives sensitivity to oral anticoagulants precipitation of encephalopathy fluid retention hepatorenal syndrome ```
145
Which drugs need care when prescribing to a patient with hepatic impairment?
``` some antibiotics valproate warfarin sedatives verapamil ```
146
What impacts can congestive cardiac failure have on drugs?
absorption hepatic elimination renal elimination (due to fluid retention)
147
What gastrointestinal conditions can have an effect on drugs?
achlorydia Crohn's disease post-operative issues
148
What are the risk factors for prostate cancer?
``` age familial genetic factor - 1q, 8p, Xp, BRCA2, PTEN, TP53 hormones racial factors geographic variations ```
149
What are the symptoms of prostate cancer?
``` often asymptomatic painful or slow micturation urinary tract infection haematuria urinary retention lymphodema ``` metastatic- bone pain, renal failure - ureteric obstruction raised PSA level
150
How is prostate cancer diagnosed and screened for?
DRE - digital rectal examination PSA - prostate-specific antigen TRUS - guided needle biopsy
151
Describe the pathology of prostate cancer
majority is primary adenocarcinoma usually arises in peripheral zone of prostate gleason grading
152
Describe prostate specific antigen
serine protease secreted into seminal fluid responsible for liquefaction of seminal coagulation small proportion leaks into circulation tissue not tumour specific tends to rise with age depends on prostate size
153
What are the treatment options for localised prostate cancer?
``` watchful waiting active surveillance radiotherapy radical prostatectomy cryotherapy TURP if symptomatic ```
154
What are two serious metastatic complications of prostate cancer?
spinal cord compression | ureteric obstruction
155
What are the treatment options of advanced prostate cancer?
androgen ablation therapy - medical castration (LNRH analogue) or surgical castration (orchidectomy) chemothrerapy TURP for relief of symptoms radiotherapy
156
What are the risk factors for bladder cancer?
``` age race environmental carcinogens chronic inflammation - stones, infection, long term catheters drugs - phenacetin, cyclophosphamide pelvic radiotherapy occupation ```
157
Describe presentation and diagnosis of bladder cancer
classically painless frank haematuria all should have cystoscopy, renal USS/ KUB cystoscopy is mandatory some present with microscopic haematuria
158
Describe the pathology of bladder cancer
transitional cell carcinoma (superficial / invasive) squamous carcinoma adenocarcinoma other secondaries
159
Describe the initial treatment of bladder cancer
diagnosed at flexible cystoscopy urgent TURBT CT IVU bimanual examination carried out at TURBT intravesicle mitomycin reduces risk of recurrence
160
Describe the treatment of low grade superficial transitional cell carcinoma
low risk of progression flexible check cystoscopy 3 months 30% chance recurrence course of 6 weekly mitomycin treatments given for specific tumours
161
Describe the treatment of bladder cancer in situ
high recurrence risk high risk of progression to muscle invasive disease do early check cytlscopy and re biopsy treat with intravesical BCG immunotherapy course of 6 weekly installations then further cystoscopy / biopsy cystectomy if treatment fails
162
Describe the treatment of invasive bladder cancer
require radical therapy radical cystectomy or radiotherapy radiotherapy poor if multifocal disease r widespread CIS neo-adjuvant chemotherapy
163
Describe radical cystectomy
bladder and prostate / uterus removed urine diverted into an ilial conduit or an orthotropic neobladder complex surgery high mortality sometimes required after radiotherapy failure
164
Describe the treatment of metastatic bladder cancer
often pulmonary treat with chemotherapy classic M-VAC- methotrexate, vinblastine, doxorubicin, cisplatin highly toxic
165
What are the main types of renal cancer
renal cell carcinoma transitional cell carcinoma sarcoma metastases
166
What are the risk factors for renal cancer?
``` smoking obesity hypertension acquired renal cystic disease haemodialysis genetics - VHL, tuberous sclerosis ```
167
What is the presentation of renal cancer
``` 80% incidental systemic symptoms - night sweats, fever, fatigue, weight loss, haemoptysis classic triad - mass, pain, haematuria varicocele lower limb oedema paraneoplastic syndrome ```
168
What are the paraneoplastic syndromes associated with renal cancer?
polycythaemia hypercalcaemia (PTH like substance or osteolytic hypercalcaemia) hypertension deranged LFTs ACTH, enteroglucagon, prolactin, insulin, gonadotropins
169
Describe the diagnosis of renal cancer
``` USS FBC, UE, LFT, CRP, bone profile, LDH CT kidneys / MRU renal biopsy CT chest ```
170
What is the is the treatment of a small renal mass?
biopsy treatment nephron sparing surgery, partial nephrectomy, cryotherapy, radical nephrectomy, surveillance
171
What are the indications for NSS?
single kidney CKD CV risk factors pT1a tumours
172
Describe radical nephrectomy
removal of kidney and Gerota's fascia | sparing adrenal gland
173
What are the risk factors for testicular cancer?
age - 20-45 cryporchidism HIV caucasian
174
What are the clinical features of testicular cancer?
majority - painless lump | investigations - tumour markers, alpha-fetoprotein, beta hCG, LDH
175
What are the different classes of testicular cancers?
``` seminoma teratoma mixed yolk sac leydig sertoli lymphoma metastases ```
176
What is the treatment of testicular cancer?
radical orchidectomy chemotherapy para-aortic nodal radiotherapy retroperitoneal lymph node dissection
177
Describe penile cancer
rare associated with HPV virus and smoking premalignant lesions even rarer in males circumcised at birth
178
What is the treatment of penile cancer?
``` circumcision topical treatment penectomy lymphadenectomy chemo-radiotherapy ```
179
Why do kidney stones form?
abnormal urine urinary obstruction urinary infection
180
How do stones for from abnormal urine?
``` under-saturated too much salt not enough water lack of inhibitors abnormal proteins ```
181
Describe how stones can form as a result of too much salt
abnormal blood- too much calcium - hyperparathyroidism, sarcoid etc too much acid - metabolic syndrome abnormal urine = renal tubular acidosis Hypercalciuria - excrete excess calcium with normal serum caclium hyperoxaluria - primary - kidney dysfucntion enteropathic - short bowel
182
What are the normal inhibitors of stone formation?
citrate magnesium pyrophosphate glyoproteins
183
What are substances that promote stone formation?
THP | matrix substance A
184
What factors affect stone formation?
low volume low pH low citrate low magnesium high uric acid high calcium high oxalate
185
Describe urinary obstruction of renal stones
``` congenital medullary sponge kidney PUJ obstruction mega ureter ureterocele ``` acquired ureteric stricture anastomotic stricture
186
Describe how urinary infections can lead to stones
urease producing organisms proteus mirablis splits urea- forms ammonium raises urine pH struvite (magnesium, ammonium phosphate and some calcium phosphate)
187
What type of stones are there?
calcium - mixed calcium oxalate monohydrate or dehydrate, calcium phosphate infection - struvite uric acid stone- not seen on xray (rising with obesity) others
188
How do stones present?
incidental pain haematuria UTI or sepsis
189
What are the initial investigations for stones?
history and exam bloods - U&E, CRP, FBC urine - non visible haematuria imaging - CT KUB
190
Describe the biochemical workup of first stone
``` U&E calcium urate urine dip sodium nitroprusside stone analysis ```
191
Describe the workup for recurrent stones
``` U&E calcium urate venous bicarbonate 2 X24 hour urine analysis ```
192
How are stones managed?
observation medical therapy - dissolution therapy (urate) non invasive therapy invasive therapy
193
What is the medical management of stones causing acute pain?
analgesia NSAIDs or opiates? medical expulsive therapy
194
What are the surgical options for treatment of kidney stones?
``` extracorporeal shockwave lithotripsy Rigid uteroscopy and fragmentation / basket extraction flexible ureteroscopy percutaneous nephrolithotomy emergency stent or nephrostomy ```
195
Describe ESWL
best for proximal ureteric stones generate shockwaves external to break down stones needs analgesia stone density
196
Describe ureteroscopy
best for ureteric stones or renal <2cm rigid or flexible basket and laseer needs anaesthetic
197
Describe PCLN
best for stones >2cm in kidney direct access to kidney via skin to fragment or extract stones needs general anaesthetic
198
Describe laparoscopic and open surgery for kidney stones
huge ureteric stones non functioning kidney reconstruction needed
199
Describe infected obstructed systems
urological emergency full history and exam sepsis 6 renal function, inflammation markers, coagulation screen urgent imaging - USS/ CT urgent decompression of an obstructed infected collecting system by nephrostomy or ureteric stenting
200
What are the absolute indications for RRT?
hyperkalaemia acidosis uraemia fluid overload
201
What are the symptoms in CKD which prompt start of dialysis?
``` anorexia vomiting itch restless legs weight loss metallic taste ```
202
What are the aims of dialysis?
``` homeostasis removal of nitrogenous waste products maintenance of normal electrolyse maintenance of normal extracellular volume correction of metabolic acidosis ```
203
What are the two aims of haemodialysis?
removal of solutes - potassium, urea (by diffusion) | removal of fluid ) convection
204
Describe diffusion in dialysis
movement of solutes by diffusion down a concentration gradient so blood solute concentration falls
205
Describe convection in dialysis
movement of fluid by convection down a pressure gradient so blood volume falls
206
Describe the practicalities of HD
hospital or home based standard 4h / 3 days per week home based treatment gives greater flexibility and empowerment but need carer, space and capital investment
207
How is vascular access achieved in HD?
anteriovenous fistula - radiocephalfc / brachiocephalic | tunneled line
208
What are the complications of HS?
``` crash hypertension dialysis disequilibrium cramps fatigue hypokalaemia air embolism blood loss access problems ```
209
What are the principles of peritoneal dialysis?
peritoneal membrane - diffusion | glucose as osmotic agent- osmosis
210
Describe the practicalities of PD
``` home based therapy better with some residual renal function different glucose concentrations of dialyse to provide more or less filtration gradual treatment- not good for AKI simple procedure once taught maintain independence ```
211
What are the complications of PD?
``` infections - peritonitis glucose load - diabetes, weight gain hernia, diaphragmatic leak, dislodged catheter peritoneal membrane failure hypoalbuminaemia encapsulating peritoneal sclerosis ```
212
Which patients are not suitable for PD?
grossly obese intra-abdominal adhesions frail home not suitable
213
What choice considerations are used to decide on RRT?
``` lifestyle frailty time carer physical -concurrent medical problems, disseminated malignancy, sever dementia, severe psychiatric disease ```
214
What problems are not addressed by dialysis?
anaemia renal bone disease neuropathy endocrine disturbances
215
What are the pros of kidney transplant?
``` no dialysis better level of renal function can live more independently better life expectancy better fertility ```
216
What are the cons of kidney transplant?
``` immunosuppressive medication increased cardiovascular risk increased infection post tranplant diabetes skin and other malignancies ```

Phase 3 (15 decks)

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