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Flashcards in Week 3 Deck (173):
1

What is agenesis?

Absence of one or more kidneys.

2

Hypoplasia of the kidneys

Small kidneys but normal function

3

What is a horseshoe kidney?

Kidneys joined at either pole. Usually inferior.

4

What is a duplex system?

Two kidneys on one side.

5

Describe polycystic kidney disease (infantile type)

Inherited defect leading to bilateral enlargement of the kidneys with cysts in the renal cortex and medulla.

6

How is infantile polycystic kidney disease inherited?

Autosomal recessive (ARPKD)

7

How does infantile polycystic disease present?

Infants with worsening renal failure and hypertension.
Bilateral renal enlargement with elongated cysts
Dilation of medullary collecting ducts
New borns may present with Potter sequence.

8

What is potter sequence?

Refers to the typical appearance and associated pulmonary hypoplasia associated with oligohydramnios (lack of amniotic fluid). Due to the newborn missing one or both of its kidneys.

9

What is infantile polycystic kidney disease associated with?

congenital hepatic fibrosis (leads to portal hypertension) and hepatic cysts.

10

How would you investigate polycystic kidney disease?

Ultrasound
CT or MRI

11

Why do people get adult polycystic disease (genetic)?

Due to a mutation on chromosome 16 in APKD1 (90% of cases)
Or on chromosome 4 in APKD2 (better prognosis)

12

What are the 4 B's for adult polycystic kidney disease?

B- big- abdominal mass is how it can present
B- berry aneurysm- in the circle of willis
B- bilateral
B-bleeding- presents with haematuria (occurs due to cysts bursting)

13

What other symptoms may someone with adult polycystic kidney disease present with?

Abdominal pain
Cyst infection
Renal calculi
Hypertension
Progressive renal failure
Reduced urine concentrating ability resulting in enuresis (involuntary urination)

14

Why is genetic counselling important in adults with polycystic kidney disease?

Offspring of affected people are at a 50% higher risk of having the disease

15

Name the 5 benign renal tumours

Fibroma
Adenoma
Angiomyolipoma
Juxtaglomerular cortical tumour
Oncocytoma

16

Describe a fibroma of the kidney

Most common tumour in the kidney- found with no clinical signs
Medullary in origin
White nodules

17

Describe an adenoma of the kidney

Yellowish nodules <2cm
Cortical in origin

18

Describe an angiomyolipoma of the kidney

Mixture of fat, muscle and blood vessels. Can be multiple or bilateral. Associated with tuberous sclerosis
Can cause haemorrhage.

19

Describe a juxtaglomerular cortical tumour?

Produce renin and can cause secondary hypertension.

20

Describe an oncocytoma tumour of the kidney?

3-7% of renal masses.
Stellate/central scar on CT- no definitive diagnosis until nephrectomy.

21

Name the malignant tumours you can get in the kidney

Nephroblastoma
Renal cell carcinoma
Transitional cell carcinoma
Adenocarcinoma
Squamous cell carcinoma
Embryonal rhabdomyosarcoma

22

What is the other name for a nephroblastoma?

Wilms tumour.

23

Where do nephroblastomas arise from?

Residual primitive renal tissue (blastema- immature kidney mesenchyme)

24

Who are nephroblastomas common in?

Most common malignant renal tumour in children - average age is less than 3.

25

How do nephroblastomas present?

Large
Unilateral flank mass.
Haematuria
Hypertension.

26

What is a renal cell carcinoma (cell type)?

Adenocarcinoma of the PCT

27

Who are renal cell carcinomas common in?

Its the commonest primary renal cell tumour in adults.

28

The classic triad of renal cell carcinoma

Flank pain
Palpable mass
Haematuria

29

Other presenting symptoms of renal cell carcinoma

Fever
Weight loss
Paraneoplastic syndrome (a set of signs that are a consequence of cancer)- hypercalcaemia, polycythaemia (erythropoietic stimulating substance)

30

Appearance of a renal cell carcinoma

Large, well circumcised mass.
Yellow colour with solid cystic, necrotic and haemorrhage areas.

31

Extension into what structure is common in renal cell carcinoma?

Renal vein. Can extend into the vena cava and right atrium.

32

Where does renal cell carcinoma commonly spread too?

Lung and bone (via the blood).
Lymphatic spread occurs later.

33

What cell type is commonest in renal cell carcinoma? What are they rich in?

Clear cell type. Tumour cells are rich in glycogen and lipid.

34

How would you diagnose a renal cell carcinoma?

Ultrasound
CT- triple phase contrast
Biopsy- however high false negative rate.

35

Risk factor for renal cell carcinoma

Smoking

36

Treatment of renal cell carcinoma?

Surgery- radical nephrectomy
Partial nephrectomy (nephron sparring)
Radiofrequency ablation.

37

Where do transitional cell carcinomas arise from?

The urothelial lining of the renal pelvis, ureter, bladder and urethra.

38

Where do transitional cell carcinomas usually occur?

The bladder. Most common LUT tumour.

39

Risk factors for transitional cell carcinomas

Smoking
Napthylamine dyes
Rubber industry
Long term cyclophosphamide or phenacetin use
analgesics
schistosomiasis.

40

How does a transitional cell carcinoma present?

Most commonly presents as haematuria (painless)

41

What are the two types of transitional cell carcinomas?

Papillary (80%)
non-papillary (20%)

42

Where in the bladder do transitional cell carcinomas usually occur?

In the trigone (75%)

43

Describe the two distinct pathways that transitional cell carcinomas arise through?

Flat/solid- develop as high grade flat tumour and then invades. Associated with early p53 mutation.
Papillary- develop as a low grade papillary tumour and then invade. They have a thicker lining and normal urothelium.

44

Quick description of an adenocarcinoma of the kidney?

Malignant proliferation of glands. Causes glandular metaplasia (extroversion)

45

Where does an adenocarcinoma arise from?

urachal remnant (tumour develops at the dome of the bladder), cystitis cystica (glandularis) or exotropgy (congenital failure to form the caudal portion of the anterior abdomen and bladder wall.

46

Quick description of squamous cell carcinomas.

Malignant proliferation of squamous cells- usually involving calcification of the bladder.
Arises from metaplasia- normal bladder lining is not squamous.

47

Quick description of embryonal rhabdomyosarcoma?

Commonest malignant bladder tumour in children. Muscle origin.

48

Difference between glomerular nephritis and pyelonephritis

Glomerular nephritis- non infective inflammation of the kidney
Pyelonephritis- infective cause of inflammation of the kidney.

49

Where do infections in pyelonephritis normally affect in the kidney?

Renal calyx.

50

How does pyelonephritis present?

Can present acutely but chronic is more common.

51

What organisms are likely to cause pyelonephritis

E coli is the commonest organism.
Then pseudomonas
Klebsiella species
Enterococcus (strep) faecalis.

52

How does pyelonephritis occur?

Rarely by blood borne infection.
More commonly but ascending infection. Cystitis is often also present.

53

What are the risk factors for developing pyelonephritis?

Females
Pregnancy- hormonal and anatomical effects.
Instrumentation (surgery)
Vesico-uteric reflex
Diabetes

54

How does chronic pyelonephritis often present?

Often there is no history of UTI- symptoms seem vague.
Hypertension and/or uraemia (nitrogenous waste products in the blood)
Large volume of urine

55

What will renal imaging show of chronic pyelonephritis?

Scarring and distortion of calyxes.

56

What is tuberculous pyelonephritis?

Haematogenous spread- usually from the lung. Vague symptoms of weight loss, fever, loin pain, dysuria (pain on urination)
Pyuria (pus in urine)

57

What is cystitis?

Inflammation of the bladder (not always due to infection)

58

What common organisms cause cystitis?

E coli
Klebsiella
Proteus
Psuedomonas

59

How does cystitis present?

Dysuria
Urinary frequency
Urgency
Suprapubic pain
Systemic signs absent

60

What is uretitis and cystitis cystica?

Following any infection in the bladder you get changes to the lining- it is important to biopsy these to make sure they aren't tumours.
Multiple small fluid filled cysts projecting into the lumen.
It is a reactive process but can resemble tumours.

61

What is schistosomiasis?

Parasitic infection of the bladder by S haematobium. Common in tropical countries.

62

What does schistosomiasis predispose too?

Malignancy- especially squamous cell carcinoma.

63

You can have a bladder infection causes by tuberculosis. True or false.

True- urinary spread of mycobacterium following renal disease with tb.

64

Who usually gets urethral urinary tract obstruction?

Usually males due to it being longer.

65

What can cause urethral obstruction in males?

Stricture
Posterior valves
Prostatic disease.

66

What causes prolonged bladder outflow obstruction?

Hypertrophy of the detrusor muscle. Increased risk of diverticulum formation.

67

What is hydronephrosis?

Dilatation of the renal pelvis with associated atrophy of the renal parenchyma (functional units of the kidney)

68

What causes hydronephrosis?

Urinary tract obstruction.

69

If the hydronephrosis is bilateral, where would this suggest the obstruction is and what can cause it?

Obstruction in the urethra.
Vesiculoureteric reflux (back flow of urine from the bladder to the ureter.
Neurogenic disturbance
Bilateral ureteric obstruction.

70

If the hydronephrosis is unilateral, what would this suggest?

Renal calculi, neoplasms, pelvic-ureteric obstruction, strictures.

71

If the hydronephrosis is sudden and complete there will be..... pelvicacyeal dilatation and ..... urine production.

Little
Urine production ceases.

72

If the hydronephrosis is gradual and partial there will be..... pelvicacyeal dilatation.

A lot of dilatation.

73

If hydronephrosis is severe, what changes will occur in the kidney?

Marked cortical thinning, atrophy and fibrosis.

74

What often follows hydronephrosis?

Pyelonephritis.

75

Describe squamous cell carcinoma of the penis?

Proliferation of squamous cells on the penile skin. Not common.

76

Risk factors for developing squamous cell carcinoma of the penis?

High risk- HPV (16)
Lack of circumcision (foreskin acts as a site for inflammation/irritation if not properly maintained/cleaned.
Poor hygiene

77

Where on the penis do squamous cell carcinomas generally develop?

On the glans/prepuce

78

Describe the gross appearance of squamous cell carcinoma

Ulcerating indurated tumour or exophytic mass
Red- raised area with a pungating foul smell.

79

Name and describe the precursor lesions for squamous cell carcinoma of the penis?

Bowens disease- in situ carcinoma of the penile shaft or scrotum that presents as leukoplakia- dry crusty appearance.

Erythroplasia of queyrat- in situ carcinoma on the glans that presents as erythroplakia- on prepuce or shaft of penis.

Bowenoid papulosis- in situ carcinoma that presents as multiple reddish papules. Seen in young patients (40's) relative to Bowen disease and erythroplasia of queyrat. Does not progress to invasive carcinoma.

80

Histologically what occurs to the tissues in squamous cell carcinoma of the penis?

Full thickness dysplagia (alteration in cells) of the epidermis

81

What occupational exposure makes you susceptible to squamous cell carcinoma of the penis?

Chimney sweeps

82

Significance of benign nodular hyperplasia of the prostate

Common disorder in most older men (at least 75% of men over 70 affected).
Not all show symptoms.

83

What tissue undergoes proliferation in BNHP?

Both glandular and stromal prostatic tissue.

84

What issues can benign nodular hyperplasia of the prostate cause and how would these present?

Physical obstruction to the urethra. Presents with hesitancy, poor stream, overflow incontinence. Collectively these symptoms are termed prostatism.
Physiological interference- peri-urethral glands at internal urethral meatus.

85

Name some complications of benign nodular hyperplasia of the prostate?

Bladder hypertrophy.
Diverticulum formation.
If untreated can lead to hydronephrosis.

86

Management of benign prostatic hyperplasia?

Surgery- transurethral resection
Drugs (alpha blockers e.g. tamsulosin, 5 alpha reductase)

87

Benign prostatic hyperplasia of the prostate Is pre-malignant. T or F.

False.

88

You have an increased risk of developing prostate carcinoma if a 1st degree relative has had it. True or false.

True.

89

Prostate carcinoma is associated with benign prostatic hyperplasia. True or false.

False- however both conditions can occur in the same gland.

90

Where does carcinoma of the prostate affect?

Peripheral ducts and gland particularly on the posterior lobe.

91

When is the peri-urethral zone involved in prostate carcinoma?

Late stages.

92

Describe latent carcinoma of the prostate.

Small cancerous foci found incidentally on biopsy or during surgery. Some may progress to clinically significant disease.

93

Where does prostate carcinoma spread locally?

Urethral obstruction, capsular penetration, seminal vesicles, bladder, rectum.

94

Lymphatic spread of prostatic carcinoma is likely to affect where?

Sacral, iliac and para-aortic nodes.

95

Haematogenous spread of prostatic carcinoma is likely to spread to where?

Bone (lumbrosacral area), osterosclerotic metastases, lungs and liver.

96

How would you diagnose prostatic carcinoma? (investigations)

Rectal examination
Imaging- ultrasound, skeletal X-rays, bone scans.
Biochemistry- prostatic specific antigen (PSA). Increased levels in most (but not all) prostate cancers.
Biopsy- transurethral resection- multiple (8-12) needle core biopsies under ultrasound control.

97

Treatment of carcinoma of the prostate?

Hormonal therapy- usually for elderly patients with advanced disease- anti-androgen treatment, oestrogen, cyproterone.
Radiotherapy- bone metastases
Surgery- radical prostatectomy.

98

Risk factors for developing testicular cancers?

Maldescent.

99

What is the presentation of testicular tumours usually like?

Painless swelling of the testicles. Can occur with hydrocele (sac filled with fluid), gynaecomastia and general effects of malignant disease.

100

What type of testicular tumours make up 90%?

Germ cell tumours- teratoma, seminoma.

101

What other tumours could you possibly get in the testicles?

Lymphoma/leukaemia. Stromal tumours.

102

Give examples of paratesticular tumours?

Adenomatoid tumour.
Sarcomas.

103

What is the commenest germ cell tumour?

Seminoma

104

Who usually gets seminomas?

30-50 year olds. (very rare before puberty)

105

Gross appearance of seminomas?

Solid, homogenous, pale, macroscopic appearance
Potato like.

106

Describe the cells making up the seminomas?

Large, clear tumour cells with variable external lymphocytic infiltrate.

107

What are the two variants of seminomas?

Spermatocytic and anaplastic.

108

Where do seminomas spread too?

Spread via lymphatics too para-aortic lymph nodes.
Blood spread to lungs and liver.

109

Seminomas are sensitive too?

Extremely sensitive too radiotherapy.

110

Who usually gets teratomas?

Peak in 20-30 year olds however can occur in childhood.

111

How are teratomas classified?

Differentiated teratoma (TD)
Malignant teratoma intermediate (MTI)
Malignant teratoma undifferentiated (MTU)
Malignant teratoma trophoblastic (MTT)

112

Gross appearance of teratomas?

Completely random- areas of haemorrhage, areas of necrosis ect.

113

What tumour markers are likely to be raised in seminoma?

Placental alkaline phosphatase.

114

The most malignant type of teratoma- and its tumour marker?

Trophoblastic
bHCG.

115

In yolk sac teratomas, what is likely to be raised?

Alpha feto protein. (also produced by hepatocellular carcinoma).

116

Where do loop diuretics act? and what channel on?

They act on the thick ascending limb of the loop of Henle. They block the sodium/pottasium/2chloride channel (bind to the chloride site) inhibiting the reabsorption of sodium.

117

Give an example of a loop diuretic?

Furosemide

118

What actions (in terms of ion concentrations) do loop diuretics cause? Also what adverse effects do they cause?

Loss of potassium.
Loss of magnesium and calcium.
Metabolic alkalosis
Hypovolaemia
Hyperglycaemia
Hyperuricaemia
Hearing loss (same channel in the bony part of the ear)

119

Clinical indications to use loop diuretics

Acute pulmonary oedema
Chronic heart failure
Chronic kidney failure
Nephrotic syndrome
Hepatic cirrhosis with ascites
Increase urine volume in acute kidney failure
Hypecalcaemia and renal stones

120

Where do thiazide diuretics act? which channel?

Early distal convoluted tubule. Act on Na/Cl co-transporter inhibiting sodium reabsorption.

121

Give an example of a thiazide diuretic?

Bendoflumethazide.

122

What effects do thiazide diuretics have on ion concentrations? and in general?

Decrease sodium reabsorption so higher conc of Na+ reaches the collecting duct. Increase potassium excretion. Increase calcium reabsorption.
Have a vasodilator effect.

123

Adverse effects of thiazide diuretics?

Hyponatraemia
Hypokalaemia
Hypomagnesia
Hypercalcaemia
Hyperuricaemia
Hyperglycaemia
Hyperlipideamia
Metabolic alkalosis.

124

Clinical indications for using thiazide diuretics?

Hypertension
Mild heart failure
Occasionally used in severe resistant oedema, nephrolithiasis and nephrogenic diabetes insipidus.

125

Where do potassium sparing diuretics act? What subtypes are their and where do they act?

Act in the collecting duct.
Aldosterone antagonists compete with aldosterone binding to intracellular receptors. This causes reduced gene expression and reduced synthesis of a protein mediator that activates sodium channels in the apical membrane.
Amiloride and triamterene block the apical sodium channel decreasing sodium reabsorption.

126

How effective are potassium sparing diuretics? Why are they acceptable in patients with low potassium?

They are weak diuretics alone- however used in conjunction with loop or thiazide they increase the effect.
They don't excrete potassium unlike loop and thiazide diuretics.

127

Clinical uses of pottasium sparing diuretics?

Moderate to severe heart failure
Secondary and primary hyperaldosteronism
Resistant essential hypertension

128

Adverse effects of pottasium sparing diuretics?

Hyperkalaemia- not to be used in conjunction with potassium supplements.

129

Triamterone is 10 x more potent than amiloride. T or F.

False- other way round.

130

Which drug is absorbed better from the GI tract, amiloride or triamterone?

Triamterone.

131

Carbonic anhydrase inhibitors are not used as diuretics anymore. True or false?

True

132

What are carbonic anhydrase inhibitors used for?

Used in glaucoma to reduce production of acqeous humour.
Used in alkolinase urine
Some forms of infantile epilepsy and acute mountain sickness.

133

How do carbonic anhydrase inhibitors work?

They inhibit the carbonic anhydrase enzyme present on the PCT causing excretion of bicarbonate along with Na+, K+ and water.

134

Effects of carbonic anhydrase inhibitors on ion concentrations? Also adverse effects?

Hyponatraemia
Hypokalaemia
Metabolic acidosis.

135

Why do loop diuretics and thiazide diuretics cause hypokalaemia?

Increased load of Na+ is sent to the distal convoluted tubule and collecting duct. This means enhanced reabsorption of sodium occurs here and potassium is secreted as a consequence.

136

How do low potassium levels present?

Weakness, fatigue, arrhythmias and myalgia.

137

How are osmotic diuretics given?

Only by IV.

138

Give an example of an osmotic diuretic and why they are favourable to use?

Manitol- pharmacologically inert
Not metabolised in the body
Does not enter cells
Freely filtered at the glomerulus
Undergoes limited reabsorption.

139

What clinical situations are osmotic diuretics used?

Raised intracranial pressure and intraocular preussre- acute glaucoma.
Prevention of inpending acute renal failure

140

How do osmotic diuretics work?

Extract water from the brain parenchyma, CSF and aqueous humor.

141

Side effects of osmotic diuretics?

Hyponatraemia headache is common.

142

Why are ADH analogues effective in low sodium?

They allow you to have water loss without losing sodium.

143

What receptors do ADH analogues act on?

V (vasopressin)- 2- causes vasodilation and water reabsorption in the CD.

144

Name an ADH analogue and compare its effectiveness to ADH?

Dermopressin- more potent than vasopressin (ADH)

145

Clinical uses of ADH analogues?

Diabetes insipidus-
neurogenic- lack of vasopressin release from the post pituitary
Nephrogenic- inability of the nephron to respond to

Also used in bedwetting/nocturnal enuresis in children
Control variceal bleeding in portal hypertension.

146

How do aquaretics/vaptans work?

They are competitive antagonists of vasopressin receptors (V1A, V1B and V2)
V2 mediate water reabsorption in the CD by directing aquaporin 2 containing vesicles to the apical membrane.

147

Clinical indications for using aquatics/vaptans?

Excess ADH conditions
Syndrome of innapropriate antidiuretic hormone
CHF
Cirrhosis

148

Define urinary incontinence?

The involuntary leakage of urine.

149

Name the types of urethral urinary incontinences?

Urge incontinence
Overflow incontinence
Stress incontinence
Mixed.

150

What do most men present with in terms of urinary incontinence?

Overflow incontinence

151

What is the most common type of urinary incontinence?

Stress

152

Describe the two phases of the micturition cycle?

Storage phase- bladder starts to fill. Pressure increase is stopped by accommodation from the detrusor muscle in the bladder wall keeping it constant.
Voiding phase- There is now an increased vesicular pressure causing the urethral sphincters to relax and allow emptying.

153

What nerve supply controls the storage phase?

Sympathetics (via T10-L2 hypgastric nerves)

154

What nerve supply controls the voiding phase?

Parasympathetics (pelvic splanchnic nerves S2-S4)

155

Describe overflow incontinence?

Usually occurs due to an obstruction to the urethra causing retention in the bladder. Over time (months to years) if it is chronic retention- the bladder will start to fill up more and more with urine stretching the detrusor muscle. Eventually it will stop working.

156

Presentation of overflow incontinence?

Incontinence at night and in places that are not sensible (they do not realise their bladder is full)
Due to an increase in intravesicular pressure (due to the detrusor muscle losing compliance) there is an increase in pressure in the renal pelvis causing acute kidney disease.

157

Presentation of urge incontinence

Daytime frequency (every 15-20 mins)
Small voided volumes
Sense of urgency
Eneuresis (leakage of urine at night)

158

What causes urge incontinence?

Could be due to detrusor overactivity- detrusor contractions occurring during inhibition of voiding.
Diagnosed by urodynamics.

Also could be due to afferent nerves being over-stimulated. Occurs when something is irritating the bladder e,.g. bladder stones or tumours.

Could be due to excess central facilitation- overactivity of pudendal nerve allowing relaxation of the external sphincter.

Or paraplegia- loss of central inhibition

Destruction of the S2 S3 centre- bladder becomes inert bag.

Pelvic surgery or fracture damaging parasympathetic nerves.

159

Describe stress incontinence?

Incontinence due to increased intra-abdominal pressure without detrusor contraction.

160

What causes stress incontinence?

Due to damage to the pelvic floor or urethral function during childbirth.

161

When are people likely to experience stress incontinence?

When they are sneezing, coughing, laughing ect.

162

How can the bladder be described and examined in overflow incontinence?

Painless, palpable mass arising from the pelvis.
Cannot get below it
Dull on percussion

163

How would you treat overflow incontinence?

Assess renal function using ultrasound.
Treat the obstruction.
Catheterise patient
Rehabilitate the bladder
Teach intermittent self catheterisation.

164

How would you treat urge incontinence?

Dietary discretion- e.g. avoid caffeine.
Pharmacotherapy- antimuscurins- e.g. oxybutylin, tolterodine. Also beta 3 adrenergic- mirabegron
Botox toxin (not licensed in the UK)
Neuromodulation (pacemaker for bladder muscle)
Surgery (enterocystoplasty)
Biofeedback- allows you to see how well your pelvic floor exercises are working.

165

How would you treat stress incontinence?

Lose weight.
Stop smoking
Pelvic floor exercises- physiotherapy
Pharmacotherapy- small role- duloxetin (serotonin 5-HT and noradrenaline reuptake inhibitor)
Surgical correction- minimally invasive tape procedures.

166

How would you go about treating mixed incontinence?

Combination of urge and stress incontinence. You have to figure out which is more dominant.

167

Why do the elderly get urinary incontinence?

Multifactorial- immobility, dementia, drugs, obstruction, neuropathy, pelvic floor weakness.

168

What are alternative forms of urinary incontinence (not urethral)?

Extraurethral route- ectopic ureter- rare and congenital
-fistula- vesico-vaginal fistula- important in developing countries due to obstructed labour.

169

How would you diagnose a renal cell carcinoma clinically?

Do an ultrasound or CT. These pick up tiny abnormalities so then you need to biopsy to find out which are dangerous.

170

What is balantis xerotica obliterans?

Lichenus sclerosis et atriphicus.
White scarred tissue on the glans and prepuce of the penis. Completely benign however scar tissue affects function.
May need circumcision.

171

How would you treat squamous cell carcinoma in situ e.g. Bowens disease, erythroplasia of Qeuyrat?

Topical 5 flourouracil.

172

How does carcinoma of the penis generally present?

Foul smelling, red raised area
Phimosis (foreskin won't go back)

173

What surgery can be performed on carcinoma of the penis?

Total/partial penectomy
Reconstruction.