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Phase 2a > RENAL > Flashcards

RENAL Flashcards

1
Q

Vertebral levels of the kidney?

A

T12 to L3

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2
Q

Order of renal blood flow from renal atery to renal vein?

A

Renal artery

Segmental artery

Interlobar

Arcuate

Cortical

Afferent

Glomerular capillaries

Efferent

Peritubular capillaries

Cortical

Arcuate

Interlobar

Renal vein

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3
Q

Where do Loop, thiazide and spironolactone?

A

Loop - ascending loop

Thiazide - distal convoluted tubule

spironolactone - distal convoluted tubule and cortical collecting

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4
Q

Layers of renal surfaces?

A

Renal fascia - attach

Adipose Capsule - shock

Renal Capsule-shape

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5
Q

Glomerular filtration barrier?

A

Endothelium

Basement Membrane

Podocyte

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6
Q

GFR calculation?

A

GFR = net ultrafilteration pressure X filtration rate

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7
Q

Juxtaglomerular complex?

A

Juxtaglomerular cells - Renin - on the walls of afferent

Macula densa cells - Adenosine - DCT

Extraglomerular mesangial cells - supportive - macrophages and signalling

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8
Q

Endocrine functions?

A

Renin

EPO

Vitamin D

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9
Q

Autocrine function?

A

Prostaglandin

EPO

Renal natriuretic peptide

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10
Q

Renal blood

A

P.RA - PRV / RESISTANCE IN ARTERIOLES

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11
Q

Factors that increase arteriolar resistance and decrease blood flow?

A

Adrenaline

  • Alpha 1 receptors on blood vessels
  • Blood flow away from kidneys to vital organs

Angiotensin 2

- Binds to receptors of efferent and afferent arterioles constrictions

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12
Q

Factors that decrease arteriolar resistance and increase blood flow?

A

ANP + BNP - Decrease cardiac workload

Prostaglandins E2, I2

Dopamine - binds to dopamine receptors - constricts capillaries of skin and muscle and dilates small vessels of the heart and kidney

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13
Q

Autoregulation of the kidney?

A
  1. Myogenic mechanism - smooth muscle contracts when there is very high systemic pressure
  2. Tubularglomerula mechanism - Macula densa of DCT detect the high sodium and chloride so release adenosine to afferent arteriole to constrict (increase resistance and increase GFR)
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14
Q

Measuring blood flow?

A

Fick principle - the amount of blood that flows into an organ is the same that flows out of an organ - if the organ doesn’t produce or breakdown products

Para-aminohippuric acid - used to measure renal blood flow

EFFECTIVE RENAL PLASMA FLOW = UPAH X URF / PLASMA CONC OF PAH FROM PERIPHERAL VEIN

RENAL BLOOD FLOW = RENAL PLASMA FLOW / 1 - HAEMATOCRIT

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15
Q

Symptoms of renal disease?

A

Oliguria - low urine output over several hours (AKI and stones) - hypotension and hypovolaemia

Anuria - Exclude obstruction - no urine but strongly want to urinate - palpate mass and insert catheter/ Asses hypovolaemia - BP, JVP, Pulses and electrolytes / Management of AKI

Haematuria

Dysuria - Pain on micturition (Inflammation of urethra or bladder , LUTS, Inflammation of vagina or glans penis

Polyuria - DI or CKD

Nocturia - BPH

Pain - infection, stone cyctic renal disease

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16
Q

Proteinuria?

A

Albumin >200mg/l due to increase permeability, decreased reabsorption, excess plasma proteins and physiological

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17
Q

Microalbuminaemia?

A

Increase in urinary albumin undetectable by conventional methods

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18
Q

Haematuria?

A

Blood in urine

Start - urethra

End- bladder or prostate

Throughout - above the bladder

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19
Q

UM: white cells?

A

UTI

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20
Q

UM: Sterile pyuria?

A

Pus cells without bacteria

UTI

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21
Q

UM: red cells

A

Haematuria

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22
Q

UM: Hyaline casts?

A

Precipitation of materials in renal tubules and they can also become incorporated in cells

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23
Q

Muddy brown casts?

A

Acute tubular necrosis

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24
Q

UM: Red cell casts?

A

Glomerulonephritis

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25
Q

UM: White cell casts?

A

Acute pyelonephritis

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26
Q

UM : Granular casts?

A

The disintegration of cellular debris

Chronic kidney disease

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27
Q

Ultrasonography?

A

Mass or cyst

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28
Q

Antegrade pyelography?

A

Identify the level of obstruction - pelvis, calyx + ureter

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29
Q

Retrograde pyelography?

A

Ureter to bladder - more invasive and risk of infection

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30
Q

2 types of renal scintigraphy?

A

measure perfusion and excretion - anatomical + functional abnormalities or kidneys and ureters

Dynamic - renal blood flow

Static - assess size and position of kidneys and parenchymal affects

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31
Q

What can cause bleeding of the urinary tract?

A

Bleeding disorder

Trauma

Cysts

Tuberculosis

Glomerulonephritis

Carcinoma

Infarct

Papillary necrosis

Stone

Uteric neoplasm or stone

Parasites

Infection

Stone

Carcinoma or papilloma

Prostatic enlargement

Urethral - trauma, infection or tumour

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32
Q

Glomerulonephritis?

A

Inflammation

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33
Q

Glomerulonephropathy?

A

The disease of the kidney without inflammation

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34
Q

Focal?

A

some of the glomeruli not all

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35
Q

Segmental?

A

A section of individual glomeruli

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36
Q

Diffuse?

A

>75% / most of the glomeruli

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37
Q

Global?

A

All of the glomeruli involved

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38
Q

Proliferative?

A

Increase in cell numbers due to hyperplasia of 1 or more resident glomerular cells +/- inflammation

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39
Q

Membrane alteration?

A

Thickening of the capillary wall due to deposition of immune deposits in the BM

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40
Q

Crescent formation?

A

Epithelial cell proliferation with mononuclear cell infiltration in Bowmans space - rapidly progressive glomerulonephritis

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41
Q

Nephrotic syndrome?

A

Haematuria

Proteinuria

Hypoalbuminemia

Hyperlipidaemia - increase hepatic lipogenesis and decreased clearance

Lipidura

Oedema - decreased oncotic and osmotic pressure

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42
Q

Acute glomerulonephritis?

A

Abrupt onset of haematuria of haematuria with cysts, dystrophic red cells, non-nephrotic range proteinuria, oedema, hypertension and transient renal impairment

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43
Q

Rapidly progressive glomerulonephritis?

A

Features of acute nephritis

Focal necrosis

Crescent formation

Rapidly progressive renal failure over weeks

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44
Q

Asymptomatic haematuria or proteinuria?

A

Incidental finding on urine dipstick or early indicator of renal disease

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45
Q

Types of nephrotic syndrome?

A

Structural and functional abnormalities of podocytes which increases the filtration of macromolecules

  • Membranous nephropathy
  • Focal segmental glomerulosclerosis
  • Minimal change disease
  • IgA nephropathy
  • Mesangial proliferative glomerulonephritis
  • Good pasture
  • Post-strep glomerulonephritis
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46
Q

Membranous glomeronephropathy?

A

Subepithelial deposits which also activate the alternate complement pathways - damage of podocyts and mesangium

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47
Q

Antibodies found in membranous glomerulonephropathy?

A

AUTOANTIBODIES TO GBM -

M type phospholipase A2 receptor

Neutral endopeptidase

COMPLEXES OUTSIDE OF KIDNEY THAT GET DEPOSITED -

Cationic bovine serum albumin

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48
Q

EM and immunofluorescence of membranous glomerulonephropathies?

A

EM - spike and dome + effacement of podocytes

IM - granular casts

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49
Q

Management of membranous glomerulonephropathy?

A

Idiopathic - steroids

Secondary - treat underlying disease or infection or drugs

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50
Q

Focal segmental glomeruloscelrosis (FSG)?

A

Segmental sclerosis and hyalinosis

Primary - podocytes are damaged and allow proteins and lipids to be filtered out - trapped in glomeruli = hyalinosis which leads to sclerosis

believed to be a continuation of minimal change disease

Secondary - sickle cell, HIV, heparin or renal hyperperfusion

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51
Q

Histo, EM and IM of FSG?

A

Histo - segmental sclerosis and hyalinsis

EM - podocyte effacement

IM - non-specific focal deposits of IgM and complement

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52
Q

Minimal change disease?

A

mostly affects children - a common cause of nephrotic syndrome in boys

Damage to the podocytes which leads to selective proteinuria without haematuria - T cells release cytokines that damage the for processes of podocytes

EM - podocytes effacement

IM - No immunoglobulins

Treated with corticosteroids

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53
Q

Type 1 mesangial proliferative glomerulonephritis?

A

1a - Circulating immune complexes due to chronic infection deposit in glomeruli and activate complement

1b - inappropriate activation of the alternate complement pathway by a nephritic factor (IgG that stabilized C3 convertase)

  • Deposit in subendothelial space - inflammation of the wall and it thickens - mesangial interposition through the BM = tram track appearance on LM and granular appearance on IM
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54
Q

Type 2 mesangial proliferative glomerulonephritis?

A

Dense deposit disease

Only complement deposits in the basement membrane (nephritic factor) - causing inflammation and decreased C3

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55
Q

Type 3 mesangial proliferative glomerulonephritis?

A

Immune complexes and complement in subendothelial and subepithelial space

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56
Q

IgA nephropathy (berger’s syndrome)?

A

Galactose deficient IgA and anti-glycan IgA antibodies form complexes - get trapped in the mesangium and causes activation of complement pathway and inflammation

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57
Q

IgA nephropathy clinical features?

A

present in childhood or during infection of the mucosal lining

Increase galactose deficient IgA and anti-glycan IgG

Hypertension

58
Q

IgA nephropathy management?

A

Control BP

Prevent immune complexes - corticosteroids

59
Q

Good pasture syndrome?

A

Haematuria and Haemoptosis

Autoantibodies to alpha 3 chain of type 4 collagen - once they nine to type 3 they activate complement (type 2 ) - which attracts neutrophils which release enzymes that increase free O2 radicals that damage BM, endothelium and the organ

60
Q

Risk factors of good pastures syndrome?

A

HLA-DR5

The environmental damage that exposes alpha 3 chain - infection, smoking, hydrocarbon-based solvents, oxidative stress

61
Q

Investigations and management of good pastures syndrome?

A

Kidney biposy - inflammation of BM

Immunofluorescence - anti-BM autoantibodies

Management - corticosteroids, immunosuppressants or plasmapheresis (filter plasma)

62
Q

Post-strep glomerulonephritis?

A

Caused by Lancefield A beta-haemolytic streptococci - specific antigens, streptolysin (RBC) and nephritogenic - M protein virulence factor

Immune deposits in the subendothelial space and GBM - activate complement and inflammation

63
Q

Clinical features of post-strep glomerulonephritis?

A

Haematuria + proteinuria - dark cola urine

Oliguria

Fluid retention - peripheral and periorbital oedema

Inflammation

64
Q

Investigations and management of post-strep glomerulonephritis?

A

LM - enlarged and hypercellular glomeruli

EM - subepithelial deposition

IM - stary sky and granular appearance

Blood - decreased C3 and anti-DNaseB (antigen against step)

Management - supportive but some children - renal failure and 1/4 of adults rapidly progressive glomerulonephritis

65
Q

Acute glomerular nephritis?

A

Bacterial antigens become trapped in the glomeruli resulting in inflammation

Haematuria, proteinuria, Hypertension oedema, oliguria and uraemia

Investigations - Baseline (GFR, Urinary proteins, Serum albumin, U+E), Culture, Urine microscopy, Serum antibodies, Cryoglobulins

Management - Supportive management, monitor fluid balance, fluid restriction if oliguric and immunosuppressants if SLE or vasculitis

66
Q

What can cause rapidly progressive glomerulonephritis?

A

Acute nephrotic syndrome

Good pasture

Anti-neutrophilic cytoplasmic antibodies - vasculitis

67
Q

Pathogenesis of UTI?

A

Bacteria from patients own bowel flora travels up the urethra - E.coli is the biggest baddie

68
Q

Risk factors of UTI?

A

Post menopausal women

Sexual activity

Catheter or instruments of urinary tract

UT stones or stasis

DM or immunosuppressants

69
Q

Clinical features of LUTS?

A

Frequency, urgency, dysuria - smelly urine, tenderness and even haematuria

70
Q

Clinical features of acute pyelonephritis?

A

Loin pain, tenderness, vomiting and fever

71
Q

Investigations to confirm UTI?

A
  • History of infection or UT instrument use
  • Dysuria, frequency or urgency
  • culture of midstream urine + sterile pyuria
  • Dipstick - leukocyte elastase and nitrites

Renal imagining or CT needed for recurrent infection or if symptoms persist after medication

72
Q

Management of UTI?

A

Trimethoprim- Sulfamethoxazole - Nitrofurantoin

Amoxicilin - Trimethoprim - Cephalosporin

singe shot

Lots of fluid

IV antibiotics

First time acutely ill - renal ultrasound

73
Q

single shot management of UTI?

A

Amoxicillin or co-trimethoprim

Bladder symptoms lasting more than 36 hours

74
Q

Difference between relapse and Reinfection UTI?

A

Relapse - same organisms bacturia within 7 days of treatment - associated with renal tract abnormality

Reinfection - same or different organisms 2 weeks after stopping treatment

75
Q

Acute pyelonephritis?

A

Neutrophil infiltration in the parenchyma - small cortical abscess and streaks of pus in the medulla - acute deterioration of the kidneys

76
Q

Difference between acute and chronic tubulointerstitial nephritis?

A

Both are injury to renal tubules and interstitium that results in decreased renal function

ACUTE - cellular infiltrate and variable tubular necrosis

allergic drug reaction of penicillin family or NSAIDS - fever, eosinophilia and mild proteinuria

CHRONIC - prolonged use of analgesics - tubular damage to the medullary area so difficulty concentrating urine - polyuria, proteinuria and uraemia

77
Q

Accelerated hypertension?

A

Fibrinoid necrosis in afferent arterioles and fibrin deposits in arteriole walls causing hypertension

Increase arteriolar lesions - renal damage - increased renin released - increase BP - progressive uraemia

78
Q

What can cause renal artery stenosis?

A

Atheroma

PVD or CAD

Fibromuscular hyperplasia

All-cause decreased renal perfusion causing ischaemia

79
Q

Most common causes of urinary tract obstruction?

A

Prostatic enlargement

Caliculi

Gynae tumour

80
Q

Hydronephrosis?

A

Dilation of renal pelvis - compression and thinning of renal parenchyma and decreased size of the kidney

81
Q

Clinical features of UT obstruction?

A

Dull ache pain in flank or loin made worse by increase urine volume

Anuria or polyuria (full or partial obstruction that may have caused tubular damage)

Obstruction of bladder outlet - hesitancy, poor stream, dribble, incomplete emptying – urinary retention

82
Q

Investigations of UT obstructions?

A

Pelvic exam or rectal exam

Ultrasound and excretion urography

Radionuclide studies - long standing obstruction

Retrograde and anterograde pyelography

83
Q

Management of UT obstruction?

A

Surgery

Insert catheter

Stent

Management of prostatic enarlgement, cancer or caliculi

84
Q

Pathophysiology of kidney stones?

A

supersaturation of solutes - precipitate out and forms nidus which crystallises and causes obstruction of the urinary tract

85
Q

What inhibits crystallisation of kidney stones?

A

Magnesium

Citrate

86
Q

Calcium oxalate?

A

Black/ dark brown

Radiopaque

Acidic urine

87
Q

Calcium phosphate?

A

Dirty white

Radiopaque

Alkaline urine - renal tubular acidosis causes failure to reabsorb bicarbonate

88
Q

Uric acid stones?

A

Red/ Brown

Radiolucent

Monosodium urate crystals associated with gout

89
Q

Struvite stones?

A

Dirty white

Radiopaque

Magnesium, ammonium and phosphate

Bacteria causes urea to break apart into CO2 and ammonia causing urine to be more alkaline

Staghorn crystals - branch out of different calyx

90
Q

Bacteria associated with struvite stones?

A

Klebsiella

Proteus Mirabilis

Pseudomonas

91
Q

Cystine stones?

A

Yellow/ pink stones

Excessive excretion of cystine

Radiopaque

92
Q

Xanthine stone?

A

Red/ Brown

Excessive purine breakdown

Radiolucent

93
Q

Clinical features of kidney stones?

A

Dull, localised flank pain

Renal colic - sharp and consistent pain that lasts hours

Haematuria

UTI

Urinary infrequency

Outflow obstruction

Painful bladder distention

94
Q

Management of renal stones?

A

<5mm - pass through urine

High fluid intake

Pain relief

Reduce stone formation - potassium citrate

Help stone pass - Alpha-adrenergic receptor or a calcium channel blocker

Shockwave lithotripsy - high-intensity acoustic pulses to break apart the stone

Surgery for massive stones

95
Q

Management of uric acid or Xanthine stones?

A

Allopurinol - makes more soluble hypoxanthine and inhibits xanthine oxidase

96
Q

Management of cystine stones?

A

V high water intake

D penicillamine - chelates cysteine forming a more soluble complex

97
Q

Causes of hyperoxaluria?

A

Genetic defect causing increased oxalate excretion

Increase oxalate containing food - rhubarb, spinach, nuts

Decreased calcium

98
Q

AKI?

A

Abrupt disruption in renal function over hours or days which is seen by decreased urine output and increased serum urea and creatinine

99
Q

Criteria used to indicate the degree of renal damage and have a predictive value of mortality?

A

RIF (U+C) LE

Risk

Injury

Failure

Loss > 4 weeks

End-stage renal failure > 3 months

100
Q

Causes of pre-renal, renal and post-renal AKI?

A

Pre-renal - Hypovolaemia, hypotension, low CO, NSAIDs or ACEi

Renal - Acute tubular necrosis, acute tubulointerstitial nephritis or pyelonephritis

Post-renal - obstruction

101
Q

Clinical features of AKI?

A

Oliguria

Biochem - Increase K, Decrease Na, Ca and phosphate - metabolic acidosis

symptoms - weakness, fever, fatigue, nausea, confusion, pruritus and bruising

Breathless - anaemia and pulmonary oedema

Impaired platelet function

Inffection

102
Q

Investigations of uraemic emergency?

A
  1. Acute or chronic
  2. Degree of renal damage - Urea and creatine and urine output
  3. Pre-renal, renal or post-renal
103
Q

Investigations of AKI?

A

Blood - Anaemia and increased ESR

Urine and blood cultures

Urine dipstick and microscopy - red cell casts, haematuria and proteinuria

Urinary and serum electrolytes

Renal ultrasound - mass or obstruction?

CT - renal scarring

Histology

Serum antibodies

104
Q

Management of AKI?

A

Optomise fluid balance and volume expansion

Monitor weight, fluid and bP

Remove nephrotoxins

EMERGENCY - prevent high potassium and pulmonary oedema, prevent further renal damage, consult nephrologist and adjust dose of drugs

105
Q

Management of hyperkalaemia?

A

Calcium gluconate

Salbutamol

Insulin

106
Q

CKD?

A

GFR <90ml/min/1.7m2 for greater than 3 months

107
Q

Causes of CKD?

A

Hypertension - ischaemia injury due to walls of arterioles becoming thicker = TGFB1 causes mesangial cells to go back to mesangioblasts - secrete more extracellular matrix = GLOMERULOSCELROSIS

Diabetes - non-enzymatic glycations of the efferent arteriole - backflow and hyperfiltration - mesangial cells secrete more extracellular matrix - expanding the size of the glomerulus = HYALINATERIOSCLEROSIS

Tubulointerstitial disease

Congenital kidney disease

UT obstruction

Systemic disease

Prolonged medication

Infection

108
Q

Clinical features of CKD?

A

Azotemia - Decreased appetite, nausea, encephalopathy (asterixis), pericarditis, bleeding because platelets don’t stick as well, uremic frost (uric acid crystals in the skin)

Electrolytes - increased potassium and decreased sodium, calcium and phosphate

Anaemia - decreased EPO

Hypertension - increased renin

109
Q

Investigations of CKD?

A

Changes in GFR over time <90 and if really bad <60

Renal biopsy - glomerulosclerosis

110
Q

Management of CKD?

A

Renoprotective - good BP control and monitoring, ACEi or ARB, Diuretics and calcium channel blockers

Reduce cardiovascular risk - statins, no smoke, control diabetes, control bP

Decrease potassium - Dietary restriction, stop drugs that retain potassium, ion exchange resins so less potassium absorbed in the GI

Anaemia - recombinant EPO

Acidosis - sodium bicarbonate

111
Q

ADPKD?

A

AD condition where multiple cysts develop on both kidneys causing an increase in size as the cysts fill up with fluid

Develop in both cortex and medulla and obstruct blood flow of neighbouring nephron which causing decreased blood flow and activates renin - hypertension

Also compresses collecting duct - urinary stasis

Also prone to getting cysts on other places of the body

112
Q

Aetiology of ADPKD?

A

mutation of PKD1 or PKD2 - polycystin protein of tubules and vasculature - abnormal sp they don’t allow calcium to enter so water flows in and you get uncontrolled cell proliferation

113
Q

Clinical features of ADPKD?

A

Hypertension

Acute loin pain

Abdo discomfort

Progressive renal impairment

Liver cyst

Subarachnoid haemorrhage

Mitral valve prolapse

114
Q

Investigations of ADPKD?

A

Hypertension

Enlarged kidneys

Family history

Maybe hepatomegaly

115
Q

Management of ADPKD?

A

Nothing can slow down progression

Monitor BP and serum creatinine

Dialysis or transplant

Children given early ultrasonography

116
Q

ARPKD?

A

mostly in infancy

mutation of PKHD1 - fibrocystin which is associated with polysytin - renal failure before birth

OLIGOHYDROAMNIOS - decreased urine in the amniotic fluid which leads to potters sequence - uterine walls crush the baby and cause deformities - respiratory insufficiency

Also prone to congenital hepatic fibrosis - portal hypertension and it affects the intrahepatic ducts and common bile duct

117
Q

Medullary sponge kidney?

A

Dilated collecting ducts and cysts on the collecting ducts

Congenital abnormality of the induction of the urteric bud and metanephric blastoma

Increased excretion of calcium, phosphate and oxalate = nephrolithiasis

increased risk of UTI and infection

Metabolic acidosis

118
Q

Symptoms of medullary sponge?

A

Stones - pain and haematuria

UTI - fever and pain

119
Q

Investigations of Medullary sponge?

A

Intravenous pyelogram - dilated collecting ducts and cysts

Excretion urography

120
Q

Management of medullary sponge?

A

Prevent stones - stay hydrated, citrate or bicarbonate supplements to stop calcium leaving the bone

Small stones - pass or shockwave lithotripsy

infection - antibiotics

121
Q

Horseshoe kidney?

A

Fusion of the inferior poles of the kidney - they end up low in the abdomen due to getting caught by the IMA

either by mechanical fusion or teratogenic cause - posterior nephrogenic cells migrate to the inferior poles can cause a parenchymal isthmus

More predisposed - hydronephrosis, stones, infection, chromosomal disorders, kidney cancer

122
Q

PSA?

A

Prostate-specific antigen is a glycoprotein expressed by normal or neoplastic prostatic tissue and is detected in blood

123
Q

Factors that can increase Exercise PSA?

A

BPH

Carcinoma

Mechanical manipulation of prostate

124
Q

Which zone of the prostate increases the most in BPH?

A

Transitional zone

125
Q

Clinical features of BPH?

A

Frequency

Nocturia

Hesitancy

Dribble

Urinary retention

Smooth lump on rectal exam

126
Q

Investigations of BPH?

A

Serum PSA

Prostate biopsy

Rectal exam

Ultrasonography to rule out renal disease

127
Q

Management of BPH?

A

Tamsulosin - relaxes bladder neck and prostate (selective alpha adrenoreceptor antagonist) - increase urine flow and decrease obstructive symptoms

Finasteride - 5 alpha-reductase inhibitor - inhibits the conversion of testosterone to dihydrotestosterone

Urethral catheterization

Prostatectomy or permanent catheter

128
Q

Clinical features of prostatic cancer?

A

Hard irregular prostate - peripheral zone

PSA

Bladder outflow obstruction

Bone meets

129
Q

Investigations of prostate cancer?

A

Transrectal ultrasound

Transrectal prostate biopsy

Serum PSA > 16

Endorectal coil - stage

130
Q

Management of prostatic carcinoma?

A

Watch and wait

Radical prostatectomy

Remove androgenic drive - orchidectomy, synthetic LH or antiandrogens

131
Q

Testicular tumours?

A

Most common in younger men

Seminoma or Teratoma

CF: Painless lump on testes, lung mets (cough and dyspnoea) and para-aortic lymph nodules (back pain)

Investigations - ultrasound, serum tumour markers, CXR, CT

132
Q

Serum tumour markers of testicular cancer?

A

Alpha-fetoprotein (AFP)

Beta subunit of human chorionic gonadotropin (B-HCG)

Teratoma - both high

Seminoma - Only B-HCG is high

133
Q

Management of testicular tumour?

A

Orchidectomy

Radiotherapy - seminoma that mets below the diaphragm

Chemo - widespread teratoma

offer sperm banking to these people before treatment is started

134
Q

Where do most kidney cancers arise?

A

Proximal tubular epithelium

135
Q

Clinical features of kidney cancer?

A

Haematuria

Loin pain

Mass on flank

Fever, malaise and weight loss

Left scrotal varicocies

Mets - bone, liver and lung

136
Q

Investigations of kidney cancer?

A

Ultrasonography

CT

MRI

137
Q

Management of renal cancer?

A

Local - radical or partial nephrectomy or ablasive technique

meets - IL2 or interferon, Termsirlimus - inhibit vascular endothelial growth factor and mTOR

138
Q

Urothelial tumours?

A

Bladder is the most common of urothelial tumours

RF: smoking, indi=ustrial chemicals, drugs and chronic inflammation

CF: painless haematuria and symptoms of UTI with not bacteria

Anyone over 40 years old with haematuria has a urethral tumour until proven otherwise

Management: Nephrouterectomy

Bladder - local diathermy, cystoscope resection, bladder resection, radio or chemo

139
Q

2 factors that ensure continence?

A

Low intravesical pressure - a stretch of bladder wall and stability of detrusor

Sphincter mechanism

140
Q

Types of incontinence?

A

Stress - post-prostatectomy or childbirth or urethral atrophy (cough, laugh or stand up)

Urge - strong desire to void but the patient can’t hold in urine (Detrusor spasms, bladder retaining urine and bladder hypersensitivity)

Overflow - caused by an obstruction (leaks and distended bladder)

Neurogenic - Brainstem damage (incoordination of sphincter or detrusor), Reduced outflow pressure (alpha-adrenergic blockers) or autonomic neuropathy (distended atonic bladder, diabetes or decreased excitability of detrusor)

Elderly - immobile, dementia (antisocial incontinence), Diuretics

Phase 2a (7 decks)

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