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Phase 2 > RENAL > Flashcards

RENAL Flashcards

1
Q

What are the eGFR values for the different stages of CKD

A

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

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2
Q

At what stage of CKD do you start to see complications

A

Stage 4 - 15-20 mL/min

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3
Q

What is the ‘steady state’ that is required to measure creatinine, what limitations does this have, and what conditions might you see this in

A

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.

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4
Q

What antibiotic can cause an increase in eGFR and why

A

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!

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5
Q

What level of albuminuria is indicative of glomerular damage

A

1g upwards

Below this is probably bc of hypertension or CVS

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6
Q

What effects do NSAIDs have on GFR and what is the mechanism

A

Inhibit prostaglandins
Prostaglandins usually dilate the afferent arteriole
If inhibit these, get vasoconstriction of afferent arteriole
= less blood into glomerus
= decrease in GRF

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7
Q

What effects do ACE inhibitors have on GFR and how

A

Angiotensinogen II regulates vasoconstriction of efferent arteriole
If block AII by ACE inhibitor = dilation of efferent arteriole
= blood flows through glomerulus quicker
= decrease GFR

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8
Q

What is the most metabolically active areas of the nephron - what injury is this most susceptible to

A

Proximal - bc most solute re-absorption happens here

tf v susceptible to ischemic injury

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9
Q

What are the main complications of kidney disease

A

Cardiovascular disease - fluid overload - heart failure

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10
Q

Why are ACE inhibitors or ARBs indicated in proteinuric CKD

A

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.

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11
Q

When should ACEX or ARBs be stopped in pts with CKD

A

If they get infection/ malaise, bc BP can start to drop, so this + BP drop from ACE inhibitors can facilitate sepsis

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12
Q

What determines K+ excretion in the kidney

A

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

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13
Q

What are the main functions of the kidney

A 
Homeostasis
-Filtration &amp; reabsorption
-Blood pressure - RAAS
-Potassium
-Acid/ bicarb balance
Vitamin D &amp; Bone 
Erythropoetin
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14
Q

List two side effects of spironolactone

A 
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.

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15
Q

List the side effects of loop (furosemide) and thiazide diuretics (distal tubule)

A

Hypokalemia
Bc, of ENaC channels.
Exchange Na+ for K+. If increase Na+ deliver = increase K+ movement into urine.

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16
Q

Renal tubule acidosis type 1 occurs where in nephron and what drugs can cause it

A

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+)

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17
Q

Renal tubular acidosis type 2 occurs where in nephron - what conditions/ pathology could cause this

A

In proximal tubule - where 90% of bicarb is reabsorbed

Anything that causes ischemia to these cells - hypotension, sepsis etc - bicarb resorption fails = metabolic acidosis

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18
Q

What are the criteria to identify a AKI

A

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

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19
Q

How many of the KDIGO criteria do you need for diagnosing AKI

A

1 out of 3

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20
Q

What blood test should be done if you suspect rhabdomyolisis may have happened in a patient

A

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)

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21
Q

How does rhabdomyolisis cause AKI

A

Release of muscle contents - myoglobin - protein that when broken down is toxic to kidney

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22
Q

Which gonal vein drains into a renal vein

A

Left gonadal into left Renal vein

Right gonadal direct into IVC

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23
Q

What is the main medical emergency associated with AKI

A

Hyperkalemia

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24
Q

Describe what happens in AKI induced hyperkalemia

A

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

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25
Q

What are the signs of hyperkalemia on ECG

A

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

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26
Q

What are the common complications of AKI

A

Hyperkalemia, acidosis, fluid overload - pulmonary oedema, uremia

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27
Q

What investigations should you do on a patient with suspected AKI

A

Bloods - U&E (ureamia?), creatinine
Imaging - ultrasound, CT, contrast Xray/ MRI
Urine dipstick - protein to creatinine ratio, blood, pH, microscopy for infections

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28
Q

Outline the management for a patient with AKI

A

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

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29
Q

What are the risk factors for AKI

A

Age
Comorbidities
Reasons for admission
Drugs

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30
Q

What are the common causes of AKI

A

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

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31
Q

What is the best way to prevent AKI

A

Drug review in patient - review anything that can cause hypo or is nephrotoxic

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32
Q

What are the indications for dialysis in AKI

A 
Refractory pulmonary oedema
Persistent hyperkalaemia
Severe metabolic acidosis
Uraemic encephalopathy or pericarditis
Drug overdose – BLAST ( Barbiturate, Lithium, Alcohol-ethylene glycol, Salicylate, Theophylline)
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33
Q

Difference between AKI and renal failure

A

AKI = abrupt decline in renal function

Renal failure = end stage chronic kidney disease - kidneys cannot function and need dialysis

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34
Q

What information can you get from urinary dipstick to help inform a cause of AKI

A

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

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35
Q

What can an USS tell you about kidney disease

A

If <9cm indicated CKD

Asymmetry = vascular problem

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36
Q

Causes of renal failure (end stage CKD, stages 4 & 5)

A

Diabetes
Hypertension
Atherosclerosis

Nephrotic syndrome
Lupus (autoimmune)
Genetic - polycystic kidney disease

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37
Q

How can CKD be classified

A

GFR, Albuminuria

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38
Q

Common causes for CKD

A
  1. Diabetes
  2. Glomerulonephritis
  3. Hypertension/ renovascular disease
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39
Q

Common causes for CKD

A
  1. Diabetes (damaged filter)
  2. Glomerulonephritis
  3. Hypertension/ renovascular disease (damage to vasculature)
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40
Q

What is the criteria to diagnose CKD

A

> 3 months of kidney damage, defined by permanent decrease in GFR, and/or proteinuria, haematuria, anatomical abnormality

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41
Q

What is the criteria to diagnose CKD

A

> 3 months of kidney damage, defined by permanent decrease in GFR, and/or proteinuria, haematuria, anatomical abnormality

GFR <60

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42
Q

What are the clinical features of CKD

A

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

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43
Q

How would you differentiate between AKI and CKD

A

CKD has more anaemia (normocytic) and bone features bc of changes to epo and calcitriol release.
AKI doesnt have these.

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44
Q

What is the management of CKD

A

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

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45
Q

What immunosuppressant used after renal transplantation can cause cancer

A

Ciclosporin

Bc of inhibition of NK cells and less neoplasm surveillance

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46
Q

Define what CKD is

A

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)

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47
Q

What is oligouric and anuric

A

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

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48
Q

At what stage of CKD does urine output reduce/ stop (oligouria, anuria)

A

Stage 5

Stage 1- 4, pts have normal urine output

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49
Q

Signs of hypovolaemia

A 
Tachy
Pulse
Low BP
Reduced tissue turgor 
JVP - low
Tongue - dry 
Urine output - reduced
Weight - reduced
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50
Q

Symptoms of hypovolemia

A

Thirst

Dizziness

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51
Q

Lab results for hypovolaemia

A

increased creatinine (kidneys not filtering)

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52
Q

Causes of hypovolaemia

A 
Anything that causes fluid loss
Diuretics
Dehydration (heat; not enough intake)
Burns
Diarrhoea
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53
Q

Signs of hypervolaemia

A 
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
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54
Q

Symptoms of fluid overload (hypervolaemia)

A

Breathlessness

Leg odema

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55
Q

Blood results for hypervolaemia

A 
Low creatinine (bc increased filtration) 
Or may be varied?
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56
Q

What is nephrotic syndrome

A

It is a syndrome characterised by:

  • Very high prontinuria (>3g)
  • Low serum albumin (<30)
  • Odema
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57
Q

What are the causes of nephrotic syndrome

A 
Usually idiopathic 
Other causes are:
Drugs - NSAIDS - anything that can cause damage to filter
Autoimmune - SLE
Malignancy 
Infection
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58
Q

Describe the pathology of nephrotic syndrome

A

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

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59
Q

What is the differential diagnosis for oedema

A

Congestive heart failure
Nephrotic syndrome
Cirrhosis

Jugular venous pressure can differentiate nephrotic syndrome - it is not raised in this

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60
Q

What investigations would you do on a patient you suspect has nephrotic syndrome

A

Urinalysis - protein, GFR, haematuria, microscopy
Bloods - U&E, serum creatinine, albumin, serology - autoimmune
Imaging - ultrasound, XR, CT

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61
Q

Outline the principles of management for nephrotic syndrome

A

Diuretics - to manage fluid overload
ACE inhibitors - to manage proteinuria

+treat underlying disease if there is one, eg Lupus - rituximab etc

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62
Q

What is the cause of glomerulonephritis - list the most common

A

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

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63
Q

How do you diagnose glomerulonephritis

A

Renal biopsy

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64
Q

Common causes of glomerulonephritis

A

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

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65
Q

How do you manage glomeruonephritis

A

As per CKD, BP control and inhibit RAAS.

Specific treatment depends on histology, severity and co-morbidities.

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66
Q

What is seen on renal biopsy in rapidly progressing glomerulonephritis

A

Glomerular cresent formation - this is WBC collecting in bowmans space

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67
Q

Define glomerulonephritis

A

Encompassing terms for conditions that cause inflammatory infiltrate around the glomerular filtration barrier. Causes - infection, autoimmune.
This causes proteinuria + haematuria

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68
Q

What is rapidly progressive glomerulonephritis

A

This is any aggressive GN, where the condition progresses to renal failure in days to weeks.
Small vessel/ ANCA vasculitis
Lupus nephritis
IgA nephropathy

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69
Q

What is diagnostic of rapidly progressive glomerulonephritis

A

Cresents of inflammatory cells in bowmans capsule

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70
Q

What investigations should be done on a patient that you suspect has GN

A

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

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71
Q

How do you manage rapidly progressive GM

A

As per AKI - manage emergencies (hyperkalemia etc)
Identify the cause & treat it - eg Infection - antibiotics
Plasma transfusion is needed for IgA nephropthy

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72
Q

What is the treatment for small vessel vasculitis

A

High dose steroids/cyclophosphamide/biologics

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73
Q

Difference between post-streptococcal GN and IgA nephropathy

A

IgA you get upper respiratory tract symptoms a couple of days before, post-strep a couple of weeks before

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74
Q

How would you identify IgA vasculitis, how is it different from IgA nephropathy

A

IgA vasculitis has a purpuric rash

IgA nephropathy - no extra renal disease

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75
Q

What is the most prevalent pattern of glomerular disease

A

IgA nephropathy (in lecture)

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76
Q

What are the clinical features of IgA nephropathy

A

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.

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77
Q

What is the treatment of IgA nephropathy

A

Supportive care: BP control with RAAS inhibitors, Diet, Lower Cholesterol

Immunosuppression: Induction: Steroids, Cyclophosphamide
Remission: Steroids, Azathioprine

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78
Q

What patient group is lupus and lupus nephritis more common in

A

Lupus and Lupus Nephritis are 3-4 times more common in African Americans, Afro-Carribeans, Hispanics and Asians

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79
Q

Outline the different stages of lupus nephritis

A

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

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80
Q

What is the treatment for lupus nephritis

A

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..

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81
Q

Causes of nephrotic syndrome

A

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.

82
Q

What are renal calcui (stones) most commonly made of

A

Calcium oxalate

83
Q

What is polycystic kidney disease

A

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

84
Q

What is the presentation of polycycstic kidney disease

A 
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

85
Q

How would you investigate/ rule out polycystic kidney disease

A 
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
86
Q

What is the average liters of urine passed per day

A

1-1.5L

87
Q

How is urine passed down the ureters

A

By peristalsis

88
Q

Where are the internal and external urethral sphincters

A

Internal - neck of bladder

External - urogenital diaphragm

89
Q

What is the name of the bladder muscle

A

Detrusor

90
Q

What nerve regulate the bladder, micturation and voiding

A 
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
91
Q

What property of the detrusor muscle prevent pressure back up from the bladder to the ureters and kidney

A

Receptive relaxation - keeps pressure low.

Lots of elastin in walls.

92
Q

What are the 4 centers involved in micturition and voiding

A
  1. Cerebral cortex - guarding
  2. Pontine micturition centre/ periaquiductal grey: coodinating of voiding
  3. Sacral micturition centre
  4. Onuf’s nucleus - guarding reflex - cell bodies of pudendal nerve
93
Q

Describe the neural regulation of bladder filling

A

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

94
Q

Describe the neural regulation of voiding (sacral reflex)

A

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.

95
Q

Describe the neural regulation of guarding

A

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.

96
Q

What stage is the bladder in 98% of the time

A

filling

97
Q

Where does voluntary control of micturition come from

A

Cortex and PMC

98
Q

Where is onuf’s nucleus and what is it important for

A

It is in ventral horn of sacral spinal cord.
Contains cell bodies for pudendal nerve (S2,3,4)
Important in guarding

99
Q

List some differentials for a male patient with LUTS

A

Prostate enlargement (more cells, hyperplasia)
Detrusor muscle weakness (muscle in bladder)
UTI
Prostate cancer
Neurological disease

100
Q

What type of cancer is prostate cancer

A

Adenocarcinoma

101
Q

Where are prostate cancers most commonly located in the prostate

A

Peripheral zone - this means you should be able to feel for a mass with DRE

102
Q

What is the international prostate symptom score, and what is it used for

A

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.

103
Q

What are volume-flow charts, when are they used and what for

A

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

104
Q

What are volume-flow charts, when are they used and what for

A

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

105
Q

What are volume-flow charts used for

A

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.

106
Q

What are the complications of BPH

A 
Disease progression
Acute retention - painful (1L)
Chronic retention - UTI risks
Interactive obstructive uropathy - hydronephrosis 
Stones
Haematuria
107
Q

What is the treatment for mild BPH

A

watch and wait

108
Q

What medical treatment is used for BPH

A
  1. Alpha1 blockers - should improve voiding problems
  2. Alpha 5 reductase inhibitors - shrink hyperplasia
  3. Antimuscurinics - for overactive bladder
109
Q

What is the surgical treatment for BPH

When is this indicated

A 
TURP - transurethral resection of prostate
RUSHES
Retention
UTIS
Stones
Haematuria
Elevated creatinine
Symptom deterioration
110
Q

What investigations would you do on a pt that you suspect has BPH

A 
Urinalysis - UTI, proteinuria (msu)
DRE - mass
Bloods - U&amp;Es, FBC, PSA
Imaging - transrectal US
Biopsy
111
Q

What is the best medical treatment for BPH and why

A

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)

112
Q

What are the complications of TURP surgery

A

Can take out internal sphicter with resection = incontinence

Sepsis

113
Q

Summary of BPH lecture

A
  • 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
114
Q

What investigation do you need to diagnose prostate cancer

A

Biopsy

115
Q

Describe the pathology of prostate cancer and how this links to treatment

A

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

116
Q

What are the symptoms of prostate cancer

A

LUTS - obstruction
Nocturia, hesitancy, poor stream, terminal dribbling

+ Weight loss
+ Bone pain if metastasised

117
Q

What investigations would you do on a 70 year old patient that has LUTS to rule out/ confirm prostate cancer

A

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

118
Q

What investigations are required to diagnose prostate cancer, which one is diagnostic

A 
DRE
Bloods - PSA + others (PSMembrane A)
Urinalysis - prostate cancer products
Transrectal ultrasound 
Biopsy + Grade * Diagnostic 
Staging
119
Q

Outline the treatment options for prostate cancer

A

Localised - Curative - Surgery, RTX, Hormone therapy
Locally advancer - Local control - Surgery, TRX, Hormone therapy
Advanced - palliative - hormone therapy

120
Q

Why is prostate screening not rolled out in UK

A
  • 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.
121
Q

If a patient has a high PSA level (>3) what is their chance of having PC

A

25 - 33%

122
Q

If a patient has a normal PSA level (>3) what is their chance of having PC

A

15%

123
Q

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?

A
  • 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
124
Q

What is the family risk of prostate cancer

A

5-10%

125
Q

What conditions raise PSA levels

A

UTI
Prostatitis
BHE

126
Q

What are the pros and cons of prostate screening

A

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

127
Q

What is the most common renal cancer, who is the demographic

A

Renal cell carcinoma
M>F
Middle aged

128
Q

What is the main differential with renal cancer

A

Polycystic kidney disease - share similar symptoms
Haematuria
Loin pain
Enlarged kidneys

Difference - weight loss, palpable mass

129
Q

What are the symptoms of RCC

A 
Haematuria
Loin Pain
Abdominal mass
Weight loss
Hypertension (bc of EPO)
Polycythemia (headache)
130
Q

What investigations should be done for a pt you suspect with RCC

A

Ultrasound - rule out/ confirm PKD
May then want CT or MRI
Bloods - Include ALP for bone mets
Urinalysis - cytology

131
Q

Where does renal cell carcinoma metastasise to

A

Bone
Liver
Lungs
Brain

132
Q

Describe the staging of Renal cell carcinoma and treatment

A

Stage 1 = <7cm
Stage 2 = >7cm
Stage 3 = in renal vein
Stage 4 = broken through fascia

Treatment - nephrectomy

133
Q

What is the most common bladder cancer - what are the risk factors of bladder cancer to include in your history

A 
Transitional cell carcinoma
Smoking
Rubber dyes (aromatic amines) - occupational
Chronic cystitis
Paraplegic - cathether
134
Q

What is the presentation of bladder cancer

A

Painless visible haematuria
Irritative voiding symptoms - frequency, urgency, nocturia
recurrent UTIs

135
Q

What investigations should be done for a pt with suspected bladder cancer

A

Cystoscopy + biopsy *this is what is diagnostic
CT not helpful in small tumours
Urinalysis - cytology
Can do CT urogram on larger tumours

136
Q

How is bladder cancer staged

A

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

137
Q

What is the rule for 2 week referral on bladder cancer

A

> 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

138
Q

Causes of haematuria (V or NV)

A 
Infection: UTI, pyelonephritis, TB
Malignancy: anywhere in tract
Stones: bladder, kidney, ureteric
Trauma: penetrating Vs Blunt
Nephrological: diabetes, nephropathy (proteinuria)
139
Q

What is the common pathology of testicular cancer

A

Seminoma (most common - germ cell cancer)

2 - teratoma (also germ cell but younger one)

140
Q

Presentation of testicular cancer

A

Male 20-40s
Painless testicular lump
Chest involvement - if metastasised

141
Q

What is the differential for testicular cancer - how would you conduct the examination

A
  1. Can you get above the lump - no, hernia, hydrocele
  2. Is it separate from testis - if so, cyst, epididymitis, varicocele
  3. Cystic or solid - hydrocele, cyst etc
142
Q

What are the signs of testicular torsion

A 
Acutely inflamed
Swollen
Red
Hot 
Painful
143
Q

What cancer markers are there in the blood for testicular cancer

A

Beta human chorionic gonadatropin hormone

144
Q

Risk factors for testicular cancer

A

Undescended testis
Infertility
Infant hernia

145
Q

Treatment for testicular cancer

A

Orchidectomy

+ Radiotherapy - seminoma

146
Q

Where does testicular cancer spread to

A

Lymph nodes
Liver
Lungs

147
Q

What pathogen is associated with renal stones

A

Proteus

148
Q

Causes of UTI

A 
Sex
Catheterisation
Enlarged prostate
Renal tract tumours
Renal stones
149
Q

What are the common UTI pathogens

A 
Escherichia coli
Proteus mirabilis
Klebsilla spp - hospital acquired
Staph saprophyticus
Staph epidermidis 
Enterococci
150
Q

What are the common investigations for UTI

A

Mid stream urine - to avoid contamination with vagina/ perineum
Direct microscopy - neutrophils, pus etc = pyuria
Culture
CLED, MacConkey
Sensitivity testing - antibiotics

151
Q

What culture medium is used for gram negative pathogens and why

A

MacConkey agar - contains bile salts to inhibit gram positives

152
Q

What culture medium is used for urine pathogens

A

CLED

153
Q

What is the criteria for treating a UTI with antibiotics

A

1 severe, or >3 UTI symptoms

154
Q

In what type of UTI should nitrofurantoin not be used

A

Pylonephritis

Pregnancy - 3rd trimester

155
Q

Common antibiotics prescribed for UTIs

A 
Amoxicillin
Trimethoprim
Cephalexin
Nitrofurantoin
Co-Amoxiclav
Genatmicin
156
Q

What are the features of renal colic pain

A 
Extremely painful 12/10
Writing - cant get comfortable
Acute onset 
Spasmodic "colic"
Radiates to groin
157
Q

How would you differentiate renal pain caused by pyelonephritis vs renal colic

A

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

158
Q

What investigation should not be used for kidney stones

A

USS

159
Q

When should USS be used for renal pain (loin) and to rule out what

A

When you suspect upper urinary tract obstruction and hydronephritis - can be useful in pregnancy

160
Q

Causes of renal stones (calculi)

A 
Diet - high Na, Ca, protein (lowers ph), oxalate (spinach nuts) - ANYTHING that causes supersatuarated urine
Hydration - dehydrated
Parathyroid - PHT
Idiopathic 
UTI
161
Q

Presentation of renal tract obstruction

A

Pain 12/10 - loin -> groin
Writhing - helps diff to pertinonitis
Colic pain
UTI symptoms

162
Q

Investigations for renal stones

A 
Non contrast CT 
USS or MRI - pregnancy
Bloods, everything - look for infection + Ca level
Urinalysis - look for UTI
Midstream culture - MCS
163
Q

What are the complications of renal obstruction

A

Sepsis and shock
Pyonephritis (infection + obstruction - think about the staghorn stone) - watch for signs of fever, loin pain, vomiting and nausea

164
Q

How are chlamydia, gonorrhoea and syphillis transmitted

A

vaginal, anal, oral sex, vertical transmission (mother to baby)

165
Q

Who is most commonly affected by chlamydia

A

Young females, early 20s

In stable relationship

166
Q

Who is most commonly affected by gonorrhoea

A

Males - late 20’s

New partner

167
Q

What type of pathogens are chlamydia trachomatis and N gonorrhea

A

Gram negative cocci

168
Q

What are the symptoms of chlamydia and gonorrhoea

A

Dysuria

Uretheral discharge

169
Q

Which is more symptomatic of chlamydia and gonorrhoea

A

Gonorrhoea in males

170
Q

How many asymptomatic early 20’s females have chlamydia

A

approx 10%

171
Q

What investigations should you do for chalmydia in a female and male

A

Female - vaginal or cervical swab
Male - 1st pass urine

Then NAAT - nucelic acid amplification test

172
Q

What investigations would you do to confirm gonorrhoea in a male and female

A

Uretheral swab
Vaginal swab

Can do microscopy (diplococci - gram -ve)
+ culture and NAAT

173
Q

What is the management of chlamydia and gonorrhoea

A

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

174
Q

Which of chlamydia and gonorrhoea is treated IM

A

Gonorrhoea

175
Q

What should be done on ALL STI diagnoses

A

Partner notification & follow up

176
Q

Why is partner notification done

A

To prevent disease progression in asymptomatic person

To prevent reinfection of index patient who is being treated

177
Q

What is shyphillis, who is affected by it and how is it transmitted

A

Gram -ve spirochaetes. T Pallidum
Males mainly - in 30s
Vaginal, oral, anal sex, verticle transmission

178
Q

What is the presentation of shyphillis

A

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

179
Q

How would you investigate a pt that you suspect has shyphillis

A

If have ulcer - swab and microscopy
+ Bloods - serology to exclude
+Bloods - EIA to confirm

180
Q

What is the treatment for shyphillis

A

IM penicillin

181
Q

What investigation would you do in a patient that you are suspicious of bladder cancer

A

Flexible cystoscopy

182
Q

Who is most at risk of bladder cancer

A

Males - over 40
The risk of bladder cancer goes up with age
Females - risk starts to go up after 60

183
Q

What percentage of bladder cancers reach the bladder wall when invading

A

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

184
Q

What is NMIBC

A

Non muscle invasive bladder cancer

185
Q

What percentage of NMIBC progress to MI (muscular invasion)

A

15%

186
Q

What percentage of NMIBC will recur

A

70%

187
Q

What are the risk factors for developing bladder cancer

A

Paraplegia
Smoking
Occupational risk - aromatic amine exposure through paints
Bladder stones or schistosomiasis infection

188
Q

How would you treat T1 bladder cancer

A

“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

189
Q

How would you treat T2 bladder cancer

A

“Radical treatment”
Cystectomy or RTX
(RTX - worse prognosis)
Requires aggressive treatment

190
Q

What is the prognosis of bladder cancer

A

50% survival 10 years - depends on grade really

191
Q

What is the best investigation for kidney stones

A

Non contrast CT

192
Q

When is an XRAY KUB useful in the management of renal stones

A

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

193
Q

Offering chlamydia tests in pharmacies is a type of what prevention

A

Secondary - pt already has disease, aim it to diagnose and treat to prevent disease progression

194
Q

What is the triad of symptoms for pyelonephritis

A

Loin pain
Fever
Pyuria

195
Q

Is polycystic kidney disease dominant or recessive

A

Autosomal dominant - means you have to inherit one copy of the gene - dont need both parents to be carriers but one must have it

196
Q

What is the first mediciation you would give to a pt with hyperkalemia to give cardio protection

A

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

197
Q

What is actrapid

A

Insulin

198
Q

What would you do if you have a patient with urosepsis who has a history of CVS

A

Stop ACEx or ARBs - will exacerbate sepsis

199
Q

What would be the signs if stones on a non contrast CT

A

Hydronephrosis - dilated renal pelvis and parenchyma
Perinephritic stranding - fat stranding around it
Perinephric tissues
Cortical thickness
Hydronephrosis +/- hydroureter
Stones

200
Q

Outline the management of stones >2cm

A

Drainage - think about sepsis etc
Decompression by uteric stent of percutaneous nephrostomy insertion
Shock Wave Lithotripsy
Then plan for surgery

Phase 2 (12 decks)

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