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2a Bateman - Phase 2a MASTER DECK > Renal and Urogenital System > Flashcards

Renal and Urogenital System Flashcards

1
Q

What is the function of the urinary tract?

A

To collect urine produced continuously by the kidneys

To store collected urine safely

To expel urine when socially acceptable.

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2
Q

What kind of organs are the kidneys?

A

Retroperitoneal.

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3
Q

Where are the kidneys located?

A

T11-L3.

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4
Q

Where is the blood supply to the kidneys from?

A

Blood supply from renal artery direct from aorta at L1 level

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5
Q

How many nephrons does each kidney contain and how much urine is produced each day?

A

Each kidney contains around 1 million nephrons and produces 1-1.5L of urine per day.

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6
Q

Where do the ureters run?

A

Run over psoas muscle, cross the iliac vessels at the pelvic brim and insert into trigone of bladder.

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7
Q

How is reflux of urine prevented?

A

valvular mechanism at the vesicoureteric junction.

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8
Q

What does the Bladder, Sphincter and Urethra look like?

A
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9
Q

What is the nervous control of the bladder and spincters?

A

Parasympathetic Nerve (pelvic nerve) S2-S4
Acetylcholine neurotransmitter
Involuntary control
Sympathetic Nerves (hypogastric plexus) T11 – L2
Noradrenaline neurotransmitter
Involuntary control
Somatic Nerve (pudendal nerve) S2-S4
“Onuf’s nucleus”
Acetylcholine neurotransmitter
Afferent pelvic nerve
Sensory nerve
Signals from detrusor muscle

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10
Q

What is each of these doing in neural control?

Cortex

Pontine Micturition Centre

Sacral Mictruition Centre

Onuf’s Nucleus

A

Cortex: voluntary control

Pontine Micturition Centre/Periaqueductal Grey: Co-ordination of voiding

Sacral Micturition Centre: Micturition reflex

Onuf’s Nucleus: Guarding reflex

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11
Q

What are the different phases of micturition?

A

Storage.

Guarding Reflex.

Micturition Reflex.

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12
Q

What happens in the storage phase of mictruition?

A

Bladder fills continuously as urine is produced by kidney and is passed through the ureters into the bladder

Normal adult bladder capacity 400-500ml with first sensation at 100-200ml

As the volume in the bladder increases the pressure remains low due to “receptive relaxation” and detrusor muscle compliance

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13
Q

What happens during the filling phase of mictruition?

A

At lower volumes the afferent pelvic nerve sends slow firing signals to the pons via the spinal cord.

Sympathetic nerve (hypogastric plexus) stimulation maintains detrusor muscle relaxation.

Somatic (Pudendal) nerve stimulation maintains urethral contraction.

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14
Q

What happens during the voiding phase?

A

Micturition reflex is an autonomic spinal reflex

Higher volumes stimulate the afferent pelvic nerve to send fast signals to the sacral micturition centre in the sacral spinal cord

Pelvic parasympathetic nerve is stimulated and the detrusor muscle contracts

Pudendal nerve is inhibited and the external sphincter relaxes

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15
Q

What happens during bladder emptying and what is needed?

A

Coordinated detrusor contraction with external sphincter relaxation to expel urine from bladder

A positive feedback loop is generated until all urine is expelled

Detrusor relaxation and external sphincter contraction after complete emptying of bladder

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16
Q

What happens during the guarding reflex?

A

Afferent signals from the pelvic nerve are received by the PMC/PAG and transmitted to higher cortical centres

If voiding is inappropriate the guarding reflex occurs

Sympathetic (hypogastric) nerve stimulation results in detrusor relaxation

Pudendal nerve stimulation results in contraction of the external urethral sphincter

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17
Q

What does the urinary tract have to do?

A

Convert a continuous process of excretion (urine production) to an intermittent process of elimination.

Store urine insensibly.

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18
Q

What do the detrusor muslce and distal spincter have to do in mictruition?

A

Detrusor muscle
Relaxes during storage (compliant)
Contracts during voiding

Distal sphincter mechanism
Contracts during storage
Relaxes during voiding

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19
Q

What are some lower urinary tract symptoms?

A

Storage symptoms
Frequency
Nocturia
Urgency
Urgency incontinence.

Voiding symptoms
Hesitancy
Straining
Poor/intermittent stream
Incomplete emptying
Post mictruition dribbling

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20
Q

What are these definitions?

BPH?

BPE?

BOO?

LUTS?

A

Benign prostatic hyperplasia.

Benign prostatic enlargement

Bladder outflow obstruction

Lower urinary tract symptoms

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21
Q

WHAT IS BPH?

A

Increase in epithelial (glandular)

and stromal (musculofibrous)

cell numbers in the periurethral area of the prostate

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22
Q

What is the incidence of BPH?

A

Older men affected

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23
Q

What are the symptoms of BPH?

A

Lower urinary tract symptoms (LUTS)

AND

Haematuria
Bladder stones
UTIs

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24
Q

What tests would you do for BPH?

A

DRE
Enlarged prostate

‘Rule out’ cancer
PSA raised
Transrectal USS ± biopsy.

Ultrasound (large residual volume, hydronephrosis)
Visulise kidneys

MSU (midstream specimin of urine)
Bacteria

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25
Q

What are the management options for BPH?

A

Lifestyle

Drugs

Surgery

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26
Q

What are the lifestyle management options for BPH?

A

Lifestyle
Avoid caffeine, alcohol (to decrease urgency/nocturia).
Relax when voiding.
Void twice in a row to aid emptying.
Control urgency by practising distraction methods (eg breathing exercises).

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27
Q

What are the drug management options for BPH?

A

Drugs

1st line Alpha-blockers
Tamsulosin
They Decrease smooth muscle tone (prostate and bladder).

2nd line 5alpha-reductase inhibitors
Finasteride
Decreases testosterone’s conversion to dihydrotestosterone

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28
Q

What are the surgery management options for BPH?

A

Surgery
Transurethral resection of prostate
Transurethral incision of the prostate
Transurethral laser-induced prostatectomy (TULIP)
Retropubic prostatectomy is an open operation

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29
Q

What are the side effects of alpha blockers?

A

Dry mouth

Weight gain

Dizziness

Hypotension

Sexual dysfunction

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30
Q

What is a requirement of BPH but not BPE?

A

Androgens.

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31
Q

WHERE CAN YOU GET STONES?

A

Anywehere from collecting duct to external urethral meatus (EUM).

Upper urinary tract
Renal Stones
Ureteric Stones

Lower urinary tract
Bladder stones
Prostatic stones
Urethral stones

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32
Q

What is the epidemology of stones?

A

Common: lifetime incidence up to 15%

Peak age: 20–40yr

Male more than females

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33
Q

Why do patients get stones?

A

Anatomical factors

Urinary factors

Infection

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34
Q

Why do patients get stones anatomical factors?

A

Anatomical factors
Congenital (horseshoe, duplex)
Acquired (obstruction, surgery)

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35
Q

Why do patients get stones urinary factors?

A

Urinary factors
Metastable urine, promotors and inhibitors
Calcium, oxalate, urate, cystine
Dehydration

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36
Q

How are stones formed?

A

Nucleation theory suggest that stones form from crystals in supersaturated urine.

Solubility point and formation point play factors

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37
Q

What are stones made of?

A

80% calcium - oxalate, phosphate.

10% uric acid.

5-10% struvite - infection stones.

1% cystine - congenital.

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38
Q

How can stones be prevented?

A

Overhydration.

Low salt

Normal dietary intake

Healthy protein intake

Reduce BMI

Active lifestyle

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39
Q

How can you prevent uric acid stones?

A

Only form in acid urine

Deacidification of urine to ph7-7.5 preventative

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40
Q

How do you prevent cystine stones?

A

Excessive overhydration

Urine alkalinisation

Cysteine binders

+/- genetic counselling

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41
Q

What symptoms can urinary tract stones cause?

A

Asymptomatic

Loin pain

Renal colic

UTI symtpoms
Dysuria, stangury, urgency, frequency

Recurrent UTIs

Haematuria
Visible and non-visible (85%)

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42
Q

WHAT IS RENAL COLIC?

A

Pain resulting from upper urinary tract obstruction.

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43
Q

Where are the three main places where stones get stuck?

A

Pelvi-ureteric junction

Pelvic brim

Vesico-ureteric junction

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44
Q

What are the symptoms of renal colic?

A

Severe unilateral loin pain

Rapid onset

Unable to get comfortable - writhing

Radiates to groin and ipsilateral testis/labia

Associated nausea / vomiting

Spasmodic / colicky, worse with fluid loading

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45
Q

How do you investigate a renal colic?

A

Blood and urine tests

Imaging

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46
Q

How do you investigate a renal colic blood and urine?

A

Bloods
Calcium, Phosphate, Uric acid

Urine
Urinalysis, MSU if positive

24hr urine for stone substances

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47
Q

How do you investigate a renal colic imaging?

A

Imaging

Kidney, ureters and bladder (KUB) XR
70%

Spiral non contrast CT
Look for stones 99%

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48
Q

What are the differential diagnosis of renal colic?

A

Ruptured AAA

Diverticulitis, appendicitis

Pyelonephritis

Testicular torsion

Musculoskeletal

Ectopic pregnancy, ovarian (cyst) torsion

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49
Q

How do you manage renal colic?

A

Pain relief
Diclofenac or opioids; abxif infection suspected

Stones <5mm diameter
90%+ pass spontaneously

Stones >5mm diameter:
Medical therapy (nifedipine or tamsulosin)
Extracorporeal shockwave lithotripsy
Percutaneous nephrolithotomy

If obstruction + infection
Ureteric stent may be needed

Prevention
Drink plenty

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50
Q

Why does infection matter?

A

Pyonephrosis

Can lose renal function in 24hrs

Systemic sepsis leading to septic shock

IV antibiotics.

Drainage

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51
Q

How can kidney stones be dangerous?

A

Smaller ones can migrate into ureter

Larger stones occlude calyces and/or PUJ

Can acutely obstruct – renal or ureteric colic

Chronic renal damage (esp. if infection stone)

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52
Q

WHAT ARE THE GENERAL SYMPTOMS OF CANCER?

A

Systemic or Constitutional
Non-specific
Specific
Paraneoplastic syndromes

  • *Local**
    e. g. Haematuria in Bladder Cancer
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53
Q

What are the constitutional non-specific symptoms of cancer?

A

Non-specific
Weight Loss
Anorexia
Fever
Anaemia (normocytic)

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54
Q

What are the specific constitutional symptoms of cancer?

A

Hypercalcaemia
Anorexia
Thirst
Confusion
Collapse

Marrow replacement
Purpura
Anaemia
Immune suppression

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55
Q

WHAT IS PROSTATE CANCER?

A

Cancer of the prostate

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56
Q

What is the epidemology of prostate cancer?

A

Most commonly diagnosed cancer in men

A disease of the industrialised West.

Old age

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57
Q

What type of cancer is prostate cancer?

A

Adenocarcinoma

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58
Q

What are the risk factors of prostate cancer?

A

+ve family history

Increased testosterone

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59
Q

Where does prostate cancer occur in the prostate?

A

Occurs in peripheral zone of prostate

85% of tumours are multifocal

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60
Q

How does prostate cancer spread and where does it spread to?

A

Spreads locally through prostate capsule

Metastasises to
Lymph nodes
Bone (sclerotic)
Lung, liver and brain

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61
Q

What are the biomarkers for prostate cancer?

A

Tissue

Serum
Prostate-specific Antigen (PSA)
Prostate-specific membrane antigen (PSMA)

Urine
PCA3
Gene fusion products (TMPRSS2-ERG)

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62
Q

What is PSA?

A

Prostate specific antigen

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63
Q

What does PSA do, what happens in BPH?

A

Serine protease responsible for liquefaction of semen

Small amount of retrograde leakage

Detected in small quantities in the blood

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64
Q

What does PSA show in prostate cancer?

A

PROSTATE SPECIFIC not CANCER SPECIFIC

Elevated in benign prostate enlargement, urinary tract infection, prostatitis

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65
Q

What are the symptoms of prostate cancer?

A

Asymptomatic or nocturia

Hesitancy

Poor stream

Terminal dribbling, or obstruction

Weight loss ± bone pain suggests mets

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66
Q

How can you diagnose prostate cancer?

A

DRE
Hard and irregular

Prostate specific antigen (PSA)
Increased

Prostate biopsy

Transrectal ultrasound scan (TRUSS)

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67
Q

What is the gleeson score? What is the T score?

A

Most common grade + highest grade
Grades 1 - 5

T staging

T1 Non palpable

T2 Palpable + confined to prostate

T3 Palpable + through capsule

T4 Palpable + invade other structures

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68
Q

What is the treatment for localised prostate cancer?

A

Surgery - radical prostatectomy

Radiotherapy - external beam

Observation - watchful waiting

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69
Q

What is the treatment for locally advanced prostate cancer?

A

Surgery

Radiotherapy and neoadjuvant hormone therapy.

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70
Q

What is the treatment for metastatic prostate cancer?

A

Hormone therapy

LHRH analogues
Goserelin

LH antagonists
Degarelix

Peripheral androgen receptor antagonists

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71
Q

What is the differential diagnosis of renal, bladder and testis cancer?

A

Infection: UTI, pyelonephritis, TB.

Malignancy: anywhere in tract

Stones: bladder, kidneym ureteric

Trauma: penetrating Vs Blunt

Nephrological: diabetes, nephropathy

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72
Q

What are the side effects of hormone replacement?

A

Osteoporosis

Gynaecomastia

Sexual dysfunction

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73
Q

WHAT IS BLADDER CANCER?

A

Cancer of the bladder

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74
Q

What are the different types of bladder cancer?

A

Transitional cell carcinoma

Some are
Squamous cell carcinoma
Adenocarcinoma

Rare: sarcoma, lymphoma, melanoma and secondaries

CIS: poorly differentiated, but confined epithelium, 50% become MI.

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75
Q

What are some risk factors of developing bladder cancer?

A

Paraplegia

Smoking

Occupational (rubber, cable, textile, printing)

Drugs (phenacetin, aspirin, cyclophosphamide)

Bladder stones

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76
Q

How can bladder cancer present?

A

85% painless VH (visible haematurtia)

Irritative voiding / recurrent UTI’s (CIS)

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77
Q

How can you diagnose a bladder tumour?

A

CT
Urogram is both diagnostic and provides staging

Cytoscopy
Diagnostic

Biopsy

Urine
Microscopy/cytology (cancers may cause sterile pyuria).

MRI or lymphangiography may show involved pelvic nodes.

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78
Q

What are the different stages of bladder cacner?

A

Ta surface

T1 lamina propria, not hit the muscle

T2 hit the muscle

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79
Q

How can you treat bladder tumours?

A

T1
Surveillance
Transurethral resection of bladder tumour (TURBT) Transurethral cystoscopy + diathermy
+/- maintenance chemo

T2-3
Radical cystectomy
Chemo (either post-op or neoadjuvant)
Preserve bladder function – orthotopic bladder reconstruction or urostomy

T4
Palliative chemo/radio

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80
Q

WHAT IS RENAL CANCER?

A

Cancer of the kidney

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81
Q

What are the types of renal cancer?

A

95% renal cell carcinoma (RCC)
An adenocarcinoma

TCC (transitional cell carcinoma) <5%

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82
Q

What is the cause of renal cancer?

A

Short arm chromosome 3

VHL tumour suppressor gene mutation

IGF-1 has free rein

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83
Q

What is the pathology of renal cancer?

A

Form from epithelial cell in proximal convulted tubule

Polygonal epithelial cells
Clear cytoplasm with carbohydrates and lipids

IGF-1 causes
Dysregulated cell growth
Hypoxia causing more angiogensis

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84
Q

What is the epidemology of renal cancer?

A

Sporadically
One tumour
Older men
Smokers

Inherited
E.g. Von Hippel-Lindau disease
Younger men and women
Both kidneys

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85
Q

What are the symptoms of renal cancer?

A

Most found incidentally!

Haematuria

Flank pain

Mass

Weight loss

Paraneoplastic syndromes

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86
Q

What are the paraneoplastic syndromes renal cancer?

A

Erythropoetin - more red blood cells, polycythemia

Renin - Increase blood pressure

PTHrP

ACTH - cortisol

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87
Q

What does a tumour of the left kidney cause that the right doesn’t?

A

Varicocles due to vein going into renal vein before IVC

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88
Q

How is renal cancer staged?

A

Using the TNM system.

T - Size, growth into nearby vein

N - Spread to lymph nodes

M - Degree of metastasis

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89
Q

How is renal cancer diagnosed?

A

BP
Increased from renin secretion.

Blood
FBC (polycythaemia from erythropoietin secretion);
ESR; U&E, ALP (bony mets?).

Urine
RBCS
Haematuria

Imaging
US; CT/MRI; IVU (filling defect ± calcification); CXR (‘cannon ball’ metastases).

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90
Q

What is the treatment of renal cancer?

A

Resection if localised

Biological therapies if metastasized

Immunomodulation
Chemokines
Antibodies

Molecular targeted therapies
VEGF receptor
Sunitinib, bevacizumab and sorafenib

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91
Q

WHAT ARE EPIDIDYMAL CYSTS?

A

Masses that lie above and behind the testis

Lie on the epididymus

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92
Q

When do epididymal cysts develop?

A

Usually develop in adulthood

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93
Q

What is the causes of epididymal cysts?

A

Unknown

Theroies
Blockage
Trauma
Inflammation

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94
Q

What do epididymal cysts contain?

A

Clear or milky (spermatocele) fluid.

Dead sperm cells

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95
Q

What are the symptoms of epidiymal cysts?

A

Usually none

Can cause
Pain
Discomfort
Heaviness

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96
Q

What are the tests for epidiymal cysts?

A

Usually discoered incidentally - physical exam

Trans-illumination - if light passes through shows fluid

Ultrasound

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97
Q

What is the treatment of epidiymal cysts?

A

Usaully none

Medications
NSAIDs

Surgery
Spermatocoelectomy

Aspiration and sclerotherapy
Draw fluid out and something put back in

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98
Q

WHAT IS A HYDROCELE?

A

Result of excessive fluid in tunica vaginalis (serous space surrounding testes)

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99
Q

What are the different types of hydrocoeles?

A

Primary or secondary

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100
Q

What is the primary type of hydrocele?

A

Associated with a patent processus vaginalis

Typically resolves during the 1st year of life

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101
Q

What is the secondary type of hydrocoele?

A

Testis tumour/trauma/infection.

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102
Q

Which hydrocoele is more common?

A

Primary hydroceles are more common, larger, and usually in younger men.

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103
Q

What is the difference between communicating and non-communicating hydroceles?

A

Communicating is peritoneal fluid collection

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104
Q

What are the symptoms for hydrocele?

A

Painless mass

Sometimes
Pain
Heaviness

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105
Q

What are the tests for hydrocele?

A

Physical exam

Painless smooth mass

Ultrasound

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106
Q

What are the managements for hydrocele?

A

Asymptomatic - Nothing

Symptomatic - Aspiration, resection

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107
Q

WHAT ARE VARICOELES?

A

Dilated veins of pampiniform plexus.

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108
Q

Which side of the testis of more affected by varicoceles?

A

Left side more commonly a effected.

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109
Q

Which is the cause of varicoceles?

A

Left side unknown

Right side venous obsturction from tumour

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110
Q

What are the symptoms of varcoceles?

A

Dull ache.

Bag of worms

Heavy

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111
Q

What are the tests for varicoceles?

A

Physical exam
Valsalva monuver.

Semen analysis

Ultrasound

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112
Q

What are the treatments for varicoceles?

A

Surgical treatment

Vascular ablation or embolization

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113
Q

WHAT IS EPIDIDYMITIS?

A

Inflammation of the epidiymis.

Acute epididymitis mostly occurs in young males.

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114
Q

What is the epidemology of epididmytis?

A

Acute epididymitis mostly occurs in young males.

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115
Q

What are the causes of epididymitis?

A

E. coli

Chlamydia

Gonorrhea

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116
Q

What is the pathology of epididymitis?

A

Organisms may get to Epididymis by retrograde spread from prostatic urethra & seminal vesicles or less commonly, through blood stream.

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117
Q

What are the symptoms of epididymitis?

A

Severe scrotal pain

Fever

Swollen scrotal area

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118
Q

What are the tests for epididymitis?

A

Prehn’s sign - lift testicules to see if pain improves

Ultrasound - check for torsion

Urethral swabs

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119
Q

What is the treatment of epididymitis?

A

Doxycycline

If gonorrhoea suspected add
Ceftriaxone

Scrotal elevation

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120
Q

Why do you remove the testicle out through the groin?

A

Damage testicle, release tumour cells into skin.

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121
Q

WHAT IS TESTICULAR CANCER?

A

Cancer of the testis

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122
Q

What are the different types of testicular cancer?

A

Seminomas (germ cell) – slow growing, classic appearance

Non-seminoma

Sex cord (stromal)

Mixed

Lymphoma

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123
Q

What is the epidemology of testicular cancer?

A

The commonest malignancy in males aged 15–44

124
Q

What is the staging of testicular cancer?

A

Stage 1 - Confined to testicle

Stage 2 - Spread but below diaphragm

Stage 3 - Above diaphragm or in solid organs.

Stage 4 - In lungs

125
Q

What are some risk factors for testicular tumours?

A

Cryptochidism - undecended testicle.

Fhx - family history.

Previous testicular tumour.

Poorly understood.

126
Q

What is the differential diagnosis for testicular cancer?

A

Inguinal hernias.

Epididymitis

Infection.

Torsion.

Catheters, UTI.

Hydrocele.

127
Q

What are the symptoms of testicular cancer?

A

80% painless lump in testis (hard/craggy, lies within testis, can be felt above).

Abdominal mass

HYDROCOELE

PAIN

METASTASES

128
Q

What are some investigations for testicular tumour?

A

Scrotal US

Biopsy

Tumour markers
AFP alpha feta protein (1/2 life 5 days) - also liver cancer, secreted by placenta
B-hcg (24-48)
LDH - lactacte dehydrogenase - shows turnover of cells.

CXR if respiratory symptoms

Staging CT

129
Q

What operations do you do for testicular tumour?

A

Early inguinal orchidectomy if malignant.

Types of tumour -

SEMINOMAS are very radiosensitive.

NON-SEMINOMAS (TERATOMAS) - cytotoxic chemotherapy.

bleomycin + etoposide + cisplatin.

130
Q

WHAT ARE THE FUNCTIONS OF THE KIDNEY?

A

Homeostasis

Filtration and reabsorption

Blood pressure

Potassium.

Vitamin D and bone disease

Erythropoeitin.

131
Q

What happens with homeostasis?

A

Filtration - Blood minus cells and large negatively charged molecules.

Reasborption and secretion.

132
Q

What is there a net excretion of?

A

Sodium.

Phosphate.

Potassium.

Acid.

Uraemic toxins.

133
Q

What is the glomerular filtration rate? What percentage of cardiac output does it take?

A

120ml/min = 170L/day.

20% of cardiac output.

134
Q

What happens when you progressively worse CKD?

A

Anaemia.

Bone disease.

135
Q

At what eGFR is dialysis end stage disease needed?

A

7-10.

136
Q

How do you calculate eGFR?

A

Predict creatinine generation from age, gender, race.

Require steady state.

Extremes of muscle mass may be misleading.

137
Q

What can make serum creatinine look worse?

A

Creatinine is secreted as well as filtered:

Creatinine clearnace > GFR

More porminant at low GFR

Inhibitors of this secretion will make serum Cr rise and function look worse

Inhibitors of secretion: trimethoprim.

138
Q

How can you measure how leaky the glomerulus is?

A

Look at the levels of Albumin.

>30mg Normal.

30-300mg Microalbuminuria

>300mg macro albuminuria

>1g Heavy’ glomerular pathology likely

>3g Nephrotic range

139
Q

How can you work out how much Albumin a person produces in one day?

A

Get the proportion of creatinine and use this in Albumin.

140
Q

What happens at the proximal tubule?

A

70% filtered sodium.

Phosphate.

Glucose

Amino acids.

141
Q

What happens with acute tunular necrosis?

A

Proximal tubules don’t get an adequte blood supply and subsequently die.

142
Q

What is Fanconi syndome?

A

Proximal tubular insult.

Glycosuria

Acidosis with failure of urine acid secretion

Phosphate wasting; rickets/osteomalacia

Aminoaciduria.

Various causes: Cystinosis, tenofovir, paraprotein disease.,

143
Q

How do the kidneys control blood pressure?

A

Volume

Vascocontriction.

144
Q

How is volume control done?

A

All about sodium.

70% in proximal tubule

25% loop of Henle

5% distal tubule

2% collecting duct.

145
Q

What happens at the loop of Henle? What is the disease assocaited with this?

A

Concentration gradient,

Dilute at top of loop

Concentrated at bottom of loop

Used at collecting ducts, passive transport of water.

Diabetes insipidus.

146
Q

When do you get extra water retention? How can you treat this?

A

Kidney failure

Heart failure

Liver failure

Loop diuretics.

Thiazides (distal tubule)

Aldosterone antagnosit (collecitng duct) - Spiraloactone - pottasium sparing diuretic.

Aquaporins - vasopressin antagnoist.

147
Q

What happens at the juxtaglomerular apparatus?

A

Macula densor cells next to the afferent arterioles.

Sense amount of sodium in the distal convoluted tuble.

More blood = more filtered, more delivered to distal tubule.

Drop in delivery secretes renin and then opens up afferent arteriole.

148
Q

What is the renin-angiotensin pathway?

A

Angiotensinogen + Renin->

Angiotensin + ACE ->

Anginotensin 2->

Vasoconstriciton (increase blood pressure) and Aldosterone (affects reabsorption of sodium).

149
Q

What happens in renal artery stenosis?

A

Kidneys are getting less blood,

Renin gets reduced.

Retain more sodium.

More vasoconstriction.

Blood pressure goes higher until adequete flow.

150
Q

What do NSAIDs do to the kidneys?

A

Lower the amount of prostaglandin, prostaglandin preferentially dilates the afferent arteriole and therefore gets constricted.

Angiotensin 2 preferentially constricts the efferent arteriole, block this and it will dilate.

Therefore little blood flow in + more coming out = no filtration.

151
Q

What can Albumin do to the kidneys if it is filtered?

A

Damages the kidneys on the way through.

152
Q

What can treat proteinuric CKD?

A

ACE inhibitors and ARB.

A small drop in eGFR is okay.

153
Q

Where is potassium control done?

A

K freely filtered and mostly absorbed in proximal tubule/loop of Henle.

Distal secretion determines renal excretion.

154
Q

What is potassium control governed by?

A

Distal delivery of Na.

Aldosterone. (help pumps working)

Distal tubule - sodium reabsorption and potassium secretion. 1 for 1.

155
Q

How is buffereing of acute changes controlled?

A

Insulin and catecholamines drive cellular potassium uptake.

156
Q

Why do ACE inhibtors, aldosterone inhibitors give hyperkalemia?

A

Block aldosterone, end up with low sodium and high potassium and high hydrogen.

157
Q

How is vitamin D activated?

A

7-dehydrocholesterol to cholecalciferol (vitamin D3) using UV light.

Cholecalciferol to 25-hydroxyvitamin D.

25 to 1-25 in kidney

calcitriol = active vitamin D.

158
Q

What does calcitriol do?

A

Increases calcium and phosphate absorption from the gut.

Suppresses parathyroid hormone.

Deficiency causes secondary hyperparathyroidism.

PTH has effects on bone health.

159
Q

What does renal anaemia do?

A

Erythropoetin deficiency in advanced kdiney disease leads to reduced haemopoesis and anaemia.

Exacerbated by functiuonal iron deficiency in renal disease.

Seldom seen until eGFR below 30.

160
Q

WHAT IS ACUTE KIDNEY INJURY?

A

Rapid reduction in kidney function over hours to days

161
Q

How do you diagnose acute kidney injury?

A

Rise in creatine > 26 micromol/L in 48 hrs (above baseline).

Rise in creatinine > 50% (best figure in last 6 months).

Urine output < 0.5 ml/kg/hr for > 6 consecutive hours.

162
Q

How many of the diagnosis do you need to diagnose a AKI?

A

1 out of the 3.

163
Q

What are the risk factors for acute kidney injury?

A

Age >75
Chronic kidney disease
Cardiac failure
Peripheral vascular disease
Chronic liver disease
Diabetes
Drugs (esp newly started)
Sepsis
Poor fluid intake/increased losses
History of urinary symptoms

164
Q

What are the most common causes of AKI?

A

Commonest are ischaemia, sepsis and nephrotoxins, although prostatic disease causes up to 25% in some studies and has the best prognosis.

165
Q

What are the pre-renal causes of AKI?

A

Renal hypoperfusion,

Hypotension
Renal artery stenosis ± ACE-i.

166
Q

What are the Intrinsic renal causes of AKI?

A

Acute tubular necrosis

Autoimmune

Glomerulonephritis

Vasculitis

167
Q

What are the post renal causes of AKI?

A

Caused by urinary tract obstruction

Stones
Malignancy
Extrinsic compression

168
Q

What are some nephrotoxic drugs?

A

ACE inhibitors/ ARBs

Results in dilated efferent arterioles decreasing GFR

NSAIDs

Inhibits cyclooxygenase which causes excess vasoconstriction of the afferent arteriole

Aminoglycosides (10-15% incidence of Acute Tubular Necrosis)

169
Q

What is the presentation of AKI?

A

Depends on underlying cause and severity

Oliguria or anuria

Nausea, vomiting

Dehydration

Confusion

Hypertension

Urinary retention (large painless bladder)

Postural hypotension

170
Q

How can you assess AKI?

A

Full examination

Renal
Creatinine
U+E
Glucose
Urine dipstick
Renal USS

Liver enzymes
Clotting
Autoantibodies (anti-GBM, ANCA)

171
Q

How can you treat AKI?

A

Euvolaemia

Stop nephrotoxic drugs

Treat underlying cause

Manage complications

172
Q

What is a complication of AKI?

A

Hyperkalaemia

173
Q

What would you see on a hyperkalemic ECG?

A

Peaked T waves.

Small or indiscernible P waves.

174
Q

How can you manage hyperkalaemia?

A

Insulin and Dextrose ( insulin drive potasssium into cell)

Dextrose compensate for sugar

Calcium gluconate. (to protect heart)

IV fluid.

Salbutamol.

Calcium resonium.

175
Q

What do you do before referral?

A
  • Proper history and examination
  • Blood tests & Imaging
  • IV fluid
  • Urine dip sticks
  • Review of drugs
  • Fluid balance ( intake /output )
  • Current volume status
176
Q

When do you refer to a Nephrologist?

A
  • Treat the urgent causes first !
  • Hyperkalaemia or fluid overload unresponsive to medical treatment
  • Urea > 40mmol/L +/- signs of uraemia
  • No obvious cause
  • Creatinine > 300 or rising > 50micromol/L per day
177
Q

When will you start dialysis?

A
  • Refractory pulmonary oedema
  • Persistent hyperkalaemia
  • Severe metabolic acidosis
  • Uraemic encephalopathy or pericarditis
  • Drug overdose – BLAST ( Barbiturate, Lithium, Alcohol-ethylene glycol, Salicylate, Theophylline)
178
Q

WHAT IS GLOMERULONEPHRITIS?

A

Inflammation in the glomerulus.

179
Q

What is the basic difference between nephritic and nephrotic syndrome?

A

Nephrotic syndrome involves the loss of a lot of protein

Nephritic syndrome involves the loss of a lot of blood

180
Q

What are the consequences of glomerulonephritis?

A

Damage to the glomerulus restricts blood flow, leading to compensatory increased BP

Damage to the filtration mechanism allows protein and blood to enter the urine

Loss of the usual filtration capacity leads to acute kidney injury

181
Q

What is the spectrum of glomerulonephritis disease?

A

1 Blood pressure: normal to malignant hypertension

2 Urine dipstick: proteinuria mildnephrotic; haematuria mildmacroscopic

3 Renal function: normal to severe impairment

182
Q

What are the causes of glomerulonephritis?

A

Syndrome Common primary causes Common secondary causes

Nephrotic
Membranous
Minimal change
FSGS
Mesangiocapillary GN

Diabetes
SLE (class V nephritis) Amyloid
Hepatitis B/C

Nephritic

IgA nephropathy​
Mesangiocapillary GN

Post streptococcal
Vasculitis
SLE (other classes of nephritis)
Anti-GBM disease
Cryoglobulinaemia

183
Q

WHAT IS NEPHRITIC SYNDROME?

A

Haematuria
+++ blood on urine dipstick (macro/microscopic)
Red cell casts (distinguishing feature)

Proteinuria
++ protein on urine dipstick

Hypertension

Low urine volume (<300ml/day)

184
Q

What happens to the podocytes in nephritic syndrome?

A

Podocytes develop large pores so blood and protein can escape through into urine

185
Q

What are some causes of nephritic syndrome?

A

Post-streptococcal glomerulonephritis

IgA nephropathy

Rapidly progressive glomerulonephritis (Goodpasture’s syndrome/vasculitis disorders)

186
Q

When does nephritic syndrome normally appear?

A

Often appears days-weeks after URTI

IgA nephropathy – days after URTI

Post-streptococcal glomerulonephritis – weeks after URTI

187
Q

What is the treatment for nephritic syndrome?

A

Treat underlying cause

188
Q

WHAT IS IgA NEPHROPATHY?

A

IgA accumulates in nephron and causes inflammation

189
Q

What are the clinical features of IgA nephropathy?

A

Haematuria

190
Q

How can you diagnose IgA nephropathy?

A

Biopsy.

191
Q

What is the management of IgA nephropathy?

A

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

Immunosuppression

192
Q

WHAT IS NEPHROTIC SYNDROME?

A

Proteinuria

Hypoalbuminaemia

Oedema

193
Q

What are the causes of nephrotic syndrome?

A

Primary
Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis

Secondary
Hepatitis
Diabetic nephropathy
Drug-related

194
Q

What is the pathophysiology of nephrotic disease?

A

Injury to the podocyte

195
Q

What are the test for nephrotic syndrome?

A

Urine dip (protein +++)

Bloods (show low albumin)

Biopsy (adults)

196
Q

What are the complications of nephrotic syndrome?

A

Susceptibility to infection
Loss of immunoglobulin in urine and also immunosuppressive treatments

Thromboembolism
Increase clotting factors and platelet abnormalities.

Hyperlipidaemia
Hepatic lipoprotein synthesis, response to low oncotic pressure

197
Q

What is the treatment of nephrotic syndrome?

A

Steroids in children

Diuretics for oedema

ACE-i for proteinuria

Treat underlying cause

198
Q

WHAT IS MEMBRANOUS GN?

A

Thickening of glomerular capillary wall.

IgG, complement deposit in sub epithelial surface causing leaky glomerulus.

199
Q

What are the different types of membranous GN?

A

Primary MN:
PLA2R antigen is the target antigen in 70-80% cases of primary MN.

Secondary MN:
Associated with autoimmune conditions, virsues, drugs and tumours.

200
Q

What are the clinical features of MN?

A

Nephrotic syndrome, benign urinary sediment.

201
Q

What is the diagnosis for MN?

A

Serum PLA2R Ab

Renal biopsy.

202
Q

What is the treatment for MN?

A

Supportive treatment- control of oedema, hypertension, hyperlipidemia and proteinuria.

RAS blockade, anti coagulation( only retrospective reviews)

Immunosuppression( steroids/ cyclophosphamide/ CNI)

203
Q

WHAT IS MINIMAL CHANGE DISEASE?

A

Commonest cause of nephrotic syndrome in children

In adults it can be idiopathic or in association with drugs (NSAIDS) or paraneoplastic (usually Hodgkin’s lymphoma).

204
Q

What is the pathology of minimal change disease?

A

T cells secrete inflammatory cytokines and damage foot processes on podocytes

Charge is lost

Albumin let through

Ig not let through

205
Q

What is the presentation of minimal change disease?

A

Nephrotic syndrome, benign urine sediment.

206
Q

What are the diagnosis options for minimal change disease?

A

Biopsy: Normal under light microscopy (hence the name).

Electron microscopy shows enhacement of the podocyte foot processes.

207
Q

What is the treatment of minimal change disease?

A

Steroids

Relapsing- remitting course treated with:

Cyclophosphamide or ciclosporin/tacrolimus

208
Q

WHAT IS CHRONIC KIDNEY DISEASE?

A

Impaired renal function for >3 months based on abnormal structure or function, or GFR <60mL/min/1.73m2 for >3 months with or without evidence of kidney damage

209
Q

What are the different stages of chronic kidney disease?

A

Stage GFR (mL/min) Notes

1 >90 Normal or GFR with other evidence of renal damage*

2 60–89 Slight GFR with other evidence of renal damage*

3A 45–59

3B 30–44 Moderate GFR with or without evidence of other renal damage*

4 15–29 Severe GFR with or without evidence of renal damage*

5 <15 Established renal failure

210
Q

After what stages are symptoms seen?

A

Symptoms usually only occur once stage 4 is reached (GFR <30).

End-stage renal failure (ESRF) is defined as GFR <15 mL/min/1.73m2 or need for renal replacement therapy (RRT—dialysis or transplant).

211
Q

What are some causes of chronic kidney disease?

A

Congential/inherited
Polycystic kidney disease,

Renal artery stenosis

Hypertension
Accelerated hypertension

Glomerular diseases
IgA nephropathy, Wegener’s granulomatosis, amyloidosis,

Interstitial diseases
Reflux nephropathy, tuberculosis, schistosomiasis, multiple myeloma

Systemic inflammatory disease
SLE, vasculitis

Diabetes mellitus.

Unknown

212
Q

What is the most useful sign of chronic kidney disease?

A

One of the most useful signs is bilaterally small kidneys on USS.

213
Q

What are the symptoms of chronic kidney disease?

A

Malaise, loss of appetite, insomnia, nocturiaand polyuria due to inability to concentrate urine, itching due to high levels of urea, N/V/D, symptoms of anaemia, peripheral and pulmonary oedema, bruising, bone pain due to metabolic bone disease.

In more advanced disease
CNS symptoms such as mental slowing, seizures, or myoclonus.

Eventually there may also be oliguria, which tends to occur in ARF and in the very late stages of CRF.

214
Q

HOW IS ERECTILE FUNCTION CONTROLLED?

A

Erection is a neurovascular phenomenon under hormonal control
Arterial dilatation, smooth muscle relaxation, activation of the corporeal veno occlusive mechanism

215
Q

What is erectile dysfunction?

A

The persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance

216
Q

What is the aeitology of erectile dysfunction?

A

Organic
Vasculogenic
Neurogenic
Hormonal
Anatomical
Drug induced

Psychogenic

217
Q

What are some common risk factors for erectile dysfunction?

A

In common with CVS disease
Lack of exercise
Obesity
Smoking
Hypercholesterolaemia
Metabolic syndrome

Diabetes x 3 risk of ED

218
Q

What diseases are associated with erectile dysfunction?

A

Diabetes mellitus

Cardiovascular disease
MI, hypertension

Liver disease and alcohol

Renal failure

Trauma
Pelvic fracture

Iatrogenic
Prostatectomy

219
Q

How can you diagnose ED?

A

Indicators of psychological aetiology

IIEF (International index for Erectile Function)
Erectile function, orgasmic function, sexual desire, ejaculation, intercourse and overall satisfaction

Physcial examination

220
Q

What are some indicators of psychological aetiology?

A

Sudden onset of ED

Good nocturnal and early morning erections

Situational ED

Younger patient

221
Q

What are you looking for on a physical examination for erectile dysfunction?

A

BP and heart rate

Hepatosplenomegaly

Genitalia
Peyronie’s disease

Prostatic enlargement or cancer

Hypogonadism
Small testes, secondary sexual characteristics

222
Q

What is Peyronies disease?

A
223
Q

What labratory tests can you do?

A

Fasting glucose

Lipid profile

Morning testosterone
If low testosterone perform prolactin, FSH, LH

Rarely done:
Nocturnal penile tumescence and rigidity
Intracavernosal injection test
Duplex USS of penile arteries
Arteriography

224
Q

What are the treatment options for ED?

A

Goal is to treat underlying condition
ie treat reversible factors

Identify and treat reversible causes of ED

Lifestyle and risk factor modification

Patient and partner involvement in education and counselling

225
Q

What are some curable causes of ED?

A

Hormonal causes
Testosterone deficiency
Primary testicular failure
Pituitary/hypothalamic failure

Testosterone replacement
Contraindicated if history of prostate cancer
Check DRE and PSA beforehand
Monitor for hepatic or prostatic disease

Psychosexual counselling
Variable results

226
Q

What is each line of treatment for ED?

A

First Line
Phosphodiesterase (PDE5) inhibitors

Second Line
Apomorphine SL
Intracavernous injections
Intraurethral alprostadil
Vacuum devices

Third Line
Consider penile prosthesis implantation

227
Q

What do PDE5 inhibitors do?

A

PDE5 inhibitors result in increased arterial blood flow, vasodilatation, and erection

Action on Nitric oxide

3 PDE5 inhibitors have been approved. Not initiators of erections – require sexual stimulation

228
Q

What are some examples of ED drugs?

A

Sildenafil (Viagra)
Effective 30-60 mins after administration
Reduced efficiency after fatty meal

Tadalafil (Cialis)

Vardenafil

229
Q

What are some common side effects from ED drugs?

A

Headache

Flushing

Dyspepsia

Nasal congestion

Dizziness

Visual disturbance

230
Q

What is Sublingual Apomorphine?

A

Centrally acting dopamine agonist

Sublingual 2 or 3mg

Not contraindicated with nitrates

Lower efficiency than PDE5 inhibitors

Limited in mild to moderate ED

231
Q

HOW ARE CHLAMYDIA TRACHOMATIS AND NEISSERIA GONORRHOEAE TRANSMITTED?

A

Adult
Urethra
Endocervical canal
Rectum
Pharynx
Conjunctiva

Neonate
Conjunctiva

Atypical pneumonia also in neonatal CT

232
Q

What are the symptoms for GC and CT for a male?

A

Dysuria and urethral discharge

233
Q

How long is incubation, how many are asymptomatic in males and what is the transmission from feamle to male?

A

Incubation
GC 2-5 days CT 7-21 days

Asymptomatic
GC 10% CT at least 50%

Transmission female to male
GC 20 – 60-80% CT 70%

234
Q

What are the complications of CT for a male?

A

Epididymo-orchitis; reactive arthritis

235
Q

What are the symptoms for GC and CT for a female?

A

Non-specific symptoms – discharge, menstrual irregularity, dysuria

236
Q

How long is incubation, how many are asymptomatic in females and what is the transmission from male to female?

A

•Asymptomatic

–GC 50% CT over 70%

•Incubation

–GC up to 10 days CT ill-defined

•Transmission male to female

GC 50-90% CT 70%

237
Q

What are some GC and CT female complications?

A

Pelvic inflammatory disease
Tubal factor infertility
Ectopic pregnancy
Chronic pelvic pain

Neonatal transmission
Ophthalmia neonatorum
Atypical pneumonia with CT

Fitz Hugh Curtis syndrome – peri-hepatitis

238
Q

What is used for chlamydia diagnosis?

A

Nucleic Acid Amplification Tests (NAAT)
High specificity and sensitivity
Sensitivity not 100%
negative test ≠ not infected

Female
Self collected vaginal swab
endocervical swab
first void urine – lower sensitivity. Sometimes used in community based asymptomatic screening

Male
first void urine

239
Q

What is involved with community screening for chlamydia?

A

Community based studies show prevalence of about 10% in asymptomatic <25 year olds

Asymptomatic carriage of Chlamydia for a number of years is well described

Diagnosis of Chlamydia in an asymptomatic person does not necessarily imply recent partner change

Community screening aims to reduce complications by reducing the prevalence of asymptomatic infection

240
Q

What is the chlamydia treatment?

A

Partner management

Azithromycin or Doxycycline

Erythromycin or Azithromycin in pregnancy

Antibiotic resistance not a clinically important problem

241
Q

What is the Gonorrhoea diagnosis?

A

Near patient test
Microscopy of gram stained smears of genital secretions looking for gram negative diplococci within cytoplasm of polymorphs
Male urethra
Female endocervix
Rectum

Culture on selective medium to confirm diagnosis

Sensitivity testing

NAAT

242
Q

What is the Gonorrhoea treatment?

A

Partner notification!

Continuous surveillance of antibiotic sensitivity

Single dose treatment preferred

Aim to cure at least 95% of people at first visit

Ceftriaxone IMI with Azithromycin orally

243
Q

What is the importance of partner notification?

A

Prevent re-infection of index patient

Prevent complications in asymptomatic contacts

244
Q

What are the different infectious syphilis?

A

Treponema pallidum subspecies pallidum

Early infectious syphilis (within 2 years of infection)
Primary, Secondary and Early Latent

Late syphilis (over 2 years since infection)
Late latent, CNS, CVS, gummatous
245
Q

How can syphilis be transmitted?

A

Safer sex – Men who have sex with men avoiding unprotected anal intercourse

BUT

Syphilis highly transmissible through oral sex

246
Q

What are the symptoms of syphilis?

A

Primary chancre - 95% genital skin, also nipples, mouth

Incubation ‘9-90 days’ - usually 21-35 days

Dusky macule - papule- indurated clean based non-tender ulcer. 50% solitary

Regional nodes 1-2/52 after chancre

Untreated - heals without scarring 4-8/52

247
Q

How do you diagnose syphilis?

A

Early moist lesions – may be able to identify motile spirochetes on wet mount using dark ground microscopy

Mainstay of diagnosis is serology
Genital ulcer
Serology usually positive if ulcer present for 2 or more weeks. If serology negative, repeat at 6 and 12 weeks to exclude diagnosis
Rash or other features of suspected secondary syphilis, serology can confidently confirm or refute the diagnosis

248
Q

What are the serology tests for syphilis?

A

Screening EIA

Confirmatory tests for samples which screen positive
Treponema pallidum particle agglutination test (TPPA)

Non- treponemal test to assess disease activity
VDRL or RPR
Titratable – negative, positive in neat serum, 1:2 dilution, 1:4. 1:8. 1:16., 1:32, 1:64 etc

249
Q

What is the treatment for syphilis?

A

Penicillin by injection is mainstay

Efficient follow up and partner notification essential

250
Q

WHAT IS THE DEFINITION OF A UTI?

A

The presence of a pure growth of >105 organisms per mL of fresh MSU

251
Q

What are some UTI syndromes?

A

Lower tract
Cystitis
Prostatitis
Epididymitis/orchitis
Urethritis

Upper tract
Pyelonephritis

252
Q

What is the classification of UTIs?

A

Asymptomatic bacteriuria

Uncomplicated
Normal renal tract + function

Complicated
Abnormal renal/GU tract, voiding difficulty/obstruction, decreased renal function, impaired host defences, virulent organism

Recurrent
Further infection with a new organism

Relapse
Further infection with the same organism

253
Q

What is pyuria?

A

Presence of leucocytes in the urine

Associated with infection

Sterile pyuria

254
Q

Where does uncomplicated and complicated UTIs take place?

A

Uncomplicated
Non pregnant women

Complicated
Pregnant
Men
Catheterised
Children
Recurrent/persistent infection
Immuncompromised
Noscomial infection
Structural abnormality
Urosepsis
Associated urinary tract disease

255
Q

What is the most common pathogen for UTIs?

A

E.coli.

256
Q

Why might a UTI occur?

A

UTIs may occur either because of the pathogenicity of the organism, the susceptibility of the host or a combination of both factors.

257
Q

How can you diagnose UTIs?

A

MC&S of MSU [GOLD]

Dipstick

Bloods

258
Q

What can be investigated with Microscopy?

A

White blood cells

Red blood cells

Casts
Give clues to renal pathology
Can be indicative of infection
Damage to kidney epithelium (glomerulonephritis)

Bacteria

Epithelial cells

259
Q

What are the signs and symptoms of UTIs?

A

Loin/abdopain

Offensive-smelling urine

Haematuria

Fever

260
Q

What is the Investigation of recurrent/complicted UTI?

A

MSU

Examination including DRE/PV

Post void bladder scan

USS scan of renal tract/pelvis

+/- Xray/KUB/NCCT KUB to rule out stones +/- CT

+/- Flexible cystoscopy

261
Q

What are the first line antibiotics for UTIs?

A

Avoid broad spectrum antibiotics

Nitrofurantoin
Pregnancy
Renal function

Trimethoprim
Pregnancy

262
Q

What are the risk factors for UTIs?

A

Female

Intercourse

Pregnancy

Menopause

UT obstruction

Malformations

Immunosuppression

Catheterization

263
Q

WHAT IS CYSTITIS?

A

Cystitis is inflammation of the bladder, usually caused by a bladder infection

264
Q

What are the symptoms of cystitis?

A

Frequency

Dysuria

Urgency

Haematuria

Suprapubic pain.

265
Q

What are the investigations for cystitis?

A

Urine analysis

Cystoscopy

Biopsy

266
Q

What is the treatment for cystitis?

A

Nitrofurantoin or Trimethoprim

Cefalexin if preggers

267
Q

WHAT IS PROSTATITIS?

A

Inflammation/swelling of the prostate gland

268
Q

What is the epidemology of prostatitis?

A

Affects 35-50% men

Common In men of all ages

269
Q

What is the pathogenesis of prostatitis?

A

Ascending infection from the urinary tract

Haematogenous spread

Gram negative organisms
E.coli, proteus, Klebsiella

270
Q

What are the symptoms of prostatitis?

A

Pain

Low back pain

Few urinary symptoms

Swollen or tender prostate

271
Q

What is the diagnosis of prostatitis?

A

Urinalysis and MSU

Bloods including cultures

STI screen

Urodynamic tests

Imaging

TRUSS +/- CT abdo and pelvis

272
Q

What is the treatment of prostatitis?

A

Trimethoprim OR

Nitrofurantoin

273
Q

WHAT IS URETHRITIS?

A

Inflammation of the urethra

274
Q

What are the symptoms of urethritis?

A

Painful/difficult urination

275
Q

How is urethritis transmitted?

A

Predominantly sexually transmitted

Gonococcal vs non gonococcal

Chlamydia trachomatis

Ureaplamsa urealyticum

T.vaginalis

M.genitalium

HSV

276
Q

What is the treatment of urethritis?

A

Requires sexual health referral

Treatment (Abx depends on cause)
Ceftriaxone
Azithromycin
Oflaxacin
Doxycycline

277
Q

WHAT IS EPIDIDYMO-ORCHITIS?

A

Inflammatory process of the epididymis +/- testes

278
Q

How does epididymo-orchitis present?

A

Presents with acute onset of pain and swelling

279
Q

What is epididymo-orchitis caused by?

A

Sexually transmitted pathogens ascending from the urethra or non-sexually transmitted uropathogens spreading from the urinary tract.

280
Q

What does pathogenesis of epididymo-orchitis depend on?

A

Pathogenesis depends on age and lifestyle

–Age <35 – STI>UTI

–Age >35 – UTI>STI

Take a sexual history
Elderly predominantly catheter related

281
Q

What are the epididymo-orchitis aetiology?

A
282
Q

What is epididymo-orchitis signs and symptoms?

A

Symptoms
Acute onset –usually unilateral scrotal pain +/- swelling
Urethritis symptoms
UTI Symptoms

Signs
Unilateral swelling and tenderness of epididymis +/- testes, urethral discharge, hydrocoele, erythema +/- oedema of scrotum, pyrexia

283
Q

What are the investigations for epidiymo-orchitis?

A

Samples
Urethral smear
Dipstick/MSU

Laboratory investigation
Urethral swab: Gonorrhoeae
First pass urine (FPU)/ urethral swab for nucleic acid amplification test (NAAT) for N. gonorrhoeae and C. trachomatis
MSU: MC&S
CRP &ESR

284
Q

What is the treatment for epididmo-orchitis?

A

Analgesia

Antibiotics

Sexual abstinence

Supportive underwear

Contact tracing

285
Q

What are the antibitotics for epididymo-orchitis?

A

Sexually transmitted
Ceftriaxone and Doxycycline OR
Ofloxacin
14 days
Refer to GUM

Non sexually transmitted
Ofloxacin or Ciprofloxacin
14 days

286
Q

What is a disease you must rule out for epididymo-orchitis?

A

MUST RULE OUT TORSION
Any doubt = surgical scrotal exploration
Surgical emergency

Features suggestive of torsion
Short duration of pain
Associated nausea/abdo pain
Previous short duration orchalgia

287
Q

WHAT IS TESTICULAR TORSION?

A

Testicular torsion happens when a spermatic cord becomes twisted, cutting off the flow of blood to the attached testicle.

288
Q

What are the symptoms of testicular torsion?

A

Sudden onset of pain in one testis, which makes walking uncomfortable. Pain in the abdomen, nausea, and vomiting are common.

289
Q

What are the signs of testicualr torsion?

A

Inflammation of one testis—it is very tender, hot, and swollen. The testis may lie high and transversely.

290
Q

What are the differential diagnosis of testicular torsion?

A

Epididymo-orchitis

Tumour

Hydrocele

291
Q

What are the tests for testicular torsion?

A

Doppler USS may demonstrate lack of blood flow to testis, as may isotope scanning.

292
Q

What are the treatments for testicular torsion?

A

Orchidectomy

Could return to scrotum

293
Q

WHAT IS PYELONEPHRITIS?

A

Infection of the renal parenchyma and soft tissues of renal pelvis /upper ureter

294
Q

What is the epidemology of pyelonephritis?

A

Predominantly affects

women <35

295
Q

What are the symptoms of pyelonephritis?

A

Classical triad

Loin pain

Fever

Pyuria

296
Q

What are the pyelonephritis routes of infection?

A

Ascending
Urethra colonised with bacteria. Massage of the urethra during intercourse can force bacteria into the female bladder

Haematogenous
S.aureus/Candida

Lymphatic spread
Rare

297
Q

What are the investigations for pyelonephritis?

A

Abdominal examination
Tender loin
Renal angle tenderness
PV: rule out tubal/ovarian/appendix pathology

Bloods including cultures

U/S scan
Rule out obstruction in upper tract

MSU

298
Q

What is the treatment for pyelonephritis?

A

Ciprofloxacin or co-amoxiclav

Surgery if needed

299
Q

What are the pyelonephritis complications?

A

Sepsis

Renal abscess

Progression to chronic pyelonephritis

300
Q

WHAT IS POLYCYSTIC KIDNEY DISEASE?

A

Polycystic kidney disease (PKD) is an inherited kidney disorder. It causes fluid-filled cysts to form in the kidneys.

301
Q

What are the different types of polycystic kidney disease?

A

Dominant and recessive

302
Q

What is are the dominant gene mutations?

A

85% have mutation in PKD1 – reach ESRF by 50s

15% have mutation in PKD2 – reach ESRF by 70s

Family screening important - MRI

303
Q

What are the recessive gene mutations?

A

Rarer

Variable signs, may present in infancy with multiple renal cysts and congenital hepatic fibrosis

No specific treatment

304
Q

What do the PKDs do?

A

Polycystinsregulate tubular and vascular development in the kidneys but also in other organs.

305
Q

What are the signs of polycystic kidney disease?

A

Excessive water and salt loss

Nocturia

Loin pain (due to renal haemorrhage, stones and UTIs)

Hypertension

Bilateral kidney enlargement

Gross haematuria following trauma

Renal colic due to clots

UTI and pyelonephritis may be presenting features

Renal stones are twice as common than in the general population

306
Q

What are the tests for PKDs?

A

Ultrasound diagnostic criteria

At least two unilateral or bilateral renal cysts at age <30 years

At least two cysts in each kidney between the ages of 30-59 years

At least four cysts in each kidney at age >60 years

The diagnosis is supported by hepatic or pancreatic cysts

307
Q

What are the treatment options for polycystic kidney disease?

A

No cure

Counselling and support for patients & family members

Monitor for disease progression

Treat hypertension, UTIs, stones, give analgesia

Dialysis for end-stage renal failure

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