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ESA 3 steven > Urinary > Flashcards

Urinary Flashcards

0
Q

What is the overall structure of the urinary system?

A

Each kidney connects to the bladder via a ureter. The bladder then empties via the urethra

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1
Q

What are the main functions of the kidney?

A

Regulation, excretion, endocrine and metabolism

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2
Q

Where are the kidneys located?

A

Between T12 and L3

Right kidney is slightly more caudal

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3
Q

What part of the trilaminar disc is the kidney derived from?

A

Intermediate mesoderm

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4
Q

What part of the kidney forms first, when and what does it do?

A

Pronephros - week 4 - it has no function as a kidney but extends the pronephric duct which drives the later stages

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5
Q

What is the second part of the kidney that forms, when and what does it do?

A

Mesonephros - end of week 4 - acts as an embryonic kidney and sprouts the ureteric bud for the definitive kidney. No part of the mesonephros becomes the definitive kidney

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6
Q

What is the third part of the kidney that forms, when and what does it do?

A

Metanephros - week 5 - becomes the final kidney. The collecting system is derived from the ureteric bud and the excretory system is formed from the mesoderm under the influence of the ureteric bud

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7
Q

Describe the ascent of the kidneys

A

Undergoes an apparent caudal to cranial shift as the embryo moves but the kidney does not. Laterally displaced and rotated 90 degrees

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8
Q

What is renal agenesis and how might it occur?

A

Failure of the renal system to develop. Due to the ureteric bud failing to interact with intermediate mesoderm

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9
Q

What are some potential problems with the migration of the kidneys?

A

May not cross the arterial fork and stay lower down

The kidneys ascend close together and may fuse to make a horseshoe kidney

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10
Q

What is the pathology behind an ectopic ureter?

A

Ureteric bud splits. Opening could be elsewhere

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11
Q

What are the types of cystic kidney disease?

A

Multicystic - ureter atresia

Polycystic - poor prognosis

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12
Q

How might abnormal renal vessels form and why are they problematic?

A

As the kidney ascends it creates new blood supply and destroys the old ones. Sometimes they aren’t lost however. Problematic because they are an end artery and the area they supply isn’t reached my the main renal artery

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13
Q

What does the urogenital sinus become?

A

Upper - bladder

Lower - pelvic and phallic

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14
Q

What is the difference between the male and female urogenital sinus?

A

Male gets independent openings from the ureteric bud and the mesonephric ducts. Female just gets the opening from the ureteric bud as the mesonephric duct regresses

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15
Q

What are the parts of the male urethra?

A

Preprostatic
Prostatic
Membranous
Spongy

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16
Q

Explain exstrophy of the bladder

A

Bladder is outside the abdominal wall

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17
Q

What is hypospadias

A

The urethra opens on the ventral wall of the penis not at the end of the glans

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18
Q

What is the excretory portion and the collecting portion of the kidney?

A

Excretory - nephron

Collecting - collecting duct, pelvis, ureter, bladder and urethra

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19
Q

What is the epithelium in the PCT, thin and thick limb of the loop of Henle, DCT, ureter and bladder

A 
Simple cuboidal with brush border
Simple squamous
Simple cuboidal - no brush border
Simple cuboidal - no brush border
Transitional
Transitional
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20
Q

How does the concentration of various substances in the ultrafiltrate compare to the plasma?

A

They’re the same except the ultrafiltrate has no large proteins and cells

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21
Q

What forces contribute to filtration?

A

Hydrostatic pressure in capillary
Hydrostatic pressure in Bowmans capsule
Osmotic pressure difference between capillary and tubular lumen

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22
Q

How is filtration auto regulated?

A

Myogenic response - BP increase causes afferent arteriole constriction and vice versa
Tubular glomerular feedback - if GFR increases Na+/Cl- increases in the DCT, detected by macula densa cells which release adenosine causing constriction. If it falls the prostaglandins are released causing dilation

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23
Q

What is the physiological range for GFR in men and women?

A

Men: 115-125
Women: 90-100

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24
Q

Define clearance

A

Volume of plasma from which any substance is completely removed by the kidney in a given time

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25
Q

What is GFR

A

The glomerular filtration rate is the amount of plasma the kidney filters. It is estimated using creatinine clearance rate as creatinine is neither reabsorbed or secreted

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26
Q

What happens if a clearance rate is over 125ml/min? Or under?

A

Over means its being secreted

Under means its being reabsorbed

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27
Q

What is transport maximum?

A

The maximum transport capacity. Anything over this is not reabsorbed and excreted in the urine

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28
Q

From deep to superficial what are the layers of tissue that surround the kidney?

A

Renal capsule
Peri renal fat
Renal fascia
Pararenal fat

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29
Q

Outline the passage urine takes within the kidney

A

Renal pyramid/minor calyx/major calyx/pelvis/ureter

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30
Q

Describe the locations of the kidneys vasculature

A

Right renal artery is longer and posterior to IVC. Distal to superior mesenteric
Left renal vein is longer and anterior to AA

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31
Q

Where do the ureters turn anteromedially?

A

Ischial spine

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32
Q

Where are ureteric narrowings?

A

Uretopelvic junction
Pelvic brim
Ureters entrance to bladder

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33
Q

Why are ureters vulnerable during an ovarectomy and hysterectomy?

A

Pass close to ovaries and posterior to uterine artery

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34
Q

What defines the trigone?

A

Two ureters and urethra

Smooth wall

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35
Q

How is Na+ taken in and removed?

A

Food

Sweat, faeces, urine

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36
Q

What are the percentages of Na+ reabsorbed in the various parts of the nephron?

A

PCT - 67
LoH - 25
DCT - 5
CD - 3

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37
Q

What is Na+ reabsorbed along with in the PCT?

A

Glucose, amino acids, H+, phosphates, water and chloride

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38
Q

What drives water reabsorption?

A

Osmosis, hydrostatic forces and oncotic forces

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39
Q

How are salts and water reabsorbed in the loop of henle?

A

Descending limb - just water

Ascending - salts via NaKCC2 channels

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40
Q

What channels facilitate Na+ reabsorption in the DCT and the CD?

A

NCC

ENaC

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41
Q

What four neurohormonal ways does the body control blood volume over long time periods?

A

Renin angiotensin aldosterone system
Sympathetic nervous system
Anti diuretic hormone
Atrial natriuretic peptide - opposes the other 3

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42
Q

Outline the RAAS pathway

A

Renin converts angiotensinogen into angiotensin I which is converted to angiotensin II by ACE

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43
Q

What are the effects of angiotensin II? And the other effect of ACE?

A

Vasoconstrict, increase aldosterone production, increase Na+ reabsorption in the kidney! increase thirst

Breakdown bradykinin thereby causing further vasoconstriction

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44
Q

How does the sympathetic nervous system affect blood volume?

A

Decreases blood flow and therefore Na+ excretion
Increase NHE and Na pumps
Increase renin production

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45
Q

How does ADH affect blood volume?

A

Increase Na+ and water retention

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46
Q

How does ANP affect blood volume?

A

Dilate afferent arteriole this increasing GFR

Inhibit Na+ reabsorption

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47
Q

What do prostaglandins do and what are they affected by?

A

Clinical use as vasodilators

NSAIDS stop there formation

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48
Q

What are the two types of hypertension?

A

Essential - unknown cause - 95%

Secondary - as a result of a primary condition - 5%

49
Q

Explain how renal artery stenosis can cause secondary hypertension

A

Narrowing of the artery reduces perfusion and therefore increases the RAAS system

50
Q

What are some adrenal causes of hypertension?

A

Conn’s syndrome
Cushings
Pheochromocytoma

51
Q

How do you treat hypertension?

A 
ACE inhibitors
Diuretics
Vasodilators
Beta blockers
Exercise, diet, reduce Na+ and alcohol intake
52
Q

What happens to plasma osmolarity if water intake < excretion

A

Increases

53
Q

What senses plasma osmolarity?

A

Hypothalamic osmoreceptors

54
Q

Where is ADH released from, what stimulates it and what is its effect?

A

Posterior pituitary
An increase in osmolarity
Increase water reabsorption and slightly increases salt reabsorption

55
Q

What is the ADH mechanism of action?

A

ADH–>G protein–>ATP->cAMP–>PKA–>insert aquaporin into apical membrane

56
Q

What is SIADH

A

Syndrome of inappropriate ADH secretion

ADH isn’t inhibited by low osmolarity so excess water is retained causing hyponatremia

57
Q

Outline the basis of the corticocapillary osmotic gradient

A

Filtrate enters the descending limb
Water moves out and into the vasa recta which remove it. This concentrates the filtrate
Ascending limb pumps out salts creating a gradient for water

58
Q

What are some causes of hypercalcaemia and symptoms? How is it treated?

A

Primary hyperparathyroidism, (non)haematological malignancies, PTHrP
Stones, depression, constipation
Increase hydration and diuretics to increase excretion
Bisphosphatase stop inhibit bone breakdown

59
Q

What is the effect on the body of alkalaemia?

A

Parasthesia and tetany

60
Q

What is the effect on the body of acidaemia?

A

Affect muscle contractility, glycolysis and hepatic function

61
Q

How does the kidney respond to acidaemia?

A

Recover all HCO3- and make more using the CO2 produced by the kidney. The H+ is excreted in urine

62
Q

How is acid secretion in the urine kept safe?

A

Buffered by phosphate

Attached to ammonia

63
Q

Explain the anion gap

A

If HCO3- is replaced but not by Cl-

It increases if metabolic acid is produced

64
Q

What is the kidneys response to alkalosis and why might this not always be possible

A

Excrete HCO3-

Because if there is volume depletion HCO3- is recovered along with Na+

65
Q

What is the function of ICF potassium?

A

Maintain volume, regulate pH, control enzymes, DNA/protein synthesis, cell growth

66
Q

What is the effect on the cell membrane if ECF K+ increases?

A

Depolarise the membrane as it’s less negative inside

67
Q

Where in the nephron is the controllable portion of K+ secretion?

A

Principal cells

68
Q

What factors increase K+ excretion and how?

A

Aldosterone - increase Na pumps and ENaCh
Hyperkalaemia - increase aldosterone
Alkalaemia

69
Q

What increases K+ movement from ECF to ICF?

A

High concentration, insulin, Catecholamines, aldosterone, alkalosis

70
Q

What is the effect of hyper and hypokalaemia on the heart?

A

Hypo - hyperpolarise cell making more excitable

Hyper - depolarise cell making less excitable as fewer Na+ channels open

71
Q

What factors increase chance of a UTI?

A

Shorter urethra - females
Obstruction - prostate, pregnant, stone, tumours
Neurological - incomplete emptying
Ureteric reflux - ascending infection

72
Q

What factors enable bacteria to infect? What is the usual bacteria?

A

Fimbriae to attach
Urease break down urea for favourable environment
Capsule
Coliforms like E. coli gram -ve

73
Q

What are symptoms of UTIs?

A

Lower - fever, dysuria, frequency, urgency

Upper - fever, loin pain

74
Q

What investigations do you do for a UTI?

A

Uncomplicated - don’t culture
Complicated (male, child, recurrent, pregnant) - mid stream urine sample/collection bag/catheter - urine dipstick and cultures

75
Q

When is it not useful to use dipstick tests?

A

Acute uncomplicated women
Men with severe
Catheters
Older

76
Q

How are UTIs treated?

A

Fluids
Treat underlying disorder
3-5 day course of trimethoprim
Pyelonephritis - 14 days co amoxiclav

77
Q

How and when should UTIs be prevented?

A

3+/year and no treatable cause

Trimethoprim prophylactic

78
Q

Why might you have sterile pyuria?

A

Can’t culture UTI due to antibiotics, chlamydia, TB, appendicitis

79
Q

Define dieresis and when are diuretics used?

A

Increased formation of urine by kidney

When water and Na+ retention causes ECF expansion

80
Q

What are the main types of diuretic, where do they work and on what channel?

A

Loop diuretics - loop of Henle - NaKCC
Thiazides - early DCT - NaCl
Spironolactone - CD/late DCT - inhibit aldosterone
Amiloride - CD/late DCT - ENaC

81
Q

When might loop diuretics be used?

A

Heart failure, nephrotic syndrome, renal failure, hypercalcaemia
Very potent

82
Q

When might thiazides be used?

A

Hypertension

Less potent

83
Q

When are K+ sparing diuretics used?

A

Hyperaldosteronism, cirrhosis

84
Q

Explain how congestive heart failure causes oedema

A

Increase venous pressure –> oedema

Decrease CO –> RAAS –> fluid retention –> oedema

85
Q

Explain how nephrotic syndrome and cirrhosis lead to oedema

A

Decrease protein –> decrease oncotic pressure –> oedema

86
Q

Explain the mechanism behind loop diuretics causing hypokalaemia

A

Increase Na+ and H2O excretion means a faster flow and more K+ washed away. Blocking NaKCC means less K+ reabsorbed

87
Q

What else has diuretic effects and why?

A

Alcohol - decrease ADH
Coffee - increase GFR and decrease Na+ reabsorption
Diabetes

88
Q

What are the three layers of the Detrusor muscle and the function of this arrangement?

A

Inner longitudinal
Middle circular
Outer longitudinal

Strength in all directions

89
Q

What are the internal and external urethral sphincter made of?

A

Smooth muscle - physiological sphincter and main continence muscle

Pelvic floor muscles - anatomical sphincter under somatic control

90
Q

What is the innervation to the Detrusor muscle and the urethral sphincters?

A

Detrusor - parasympathetic - pelvic nerve - contract
Sympathetic - hypogastric nerve - relax
Internal urethral sphincter - sympathetic - hypogastric - contract
External urethral sphincter - somatic - pudendal - contract

91
Q

Outline the voiding reflex pathway

A

Brain micturition centres –> spinal micturition centres –> parasympathetic neurones –> Detrusor contracts –> cerebral cortex stimulates external urethral sphincter to relax

92
Q

Outline how the bladder stores urine

A

Distend so pressure doesn’t increase
Sympathetic via hypo gastric cause the Detrusor to relax and internal urethral sphincter to contract
Pudendal nerve contracts external urethral

93
Q

Explain the main types of incontinence

A

Stress urinary incontinence - leakage on exertion (sneezing)
Urge urinary incontinence - urge to urinate
Mixed urinary incontinence
Overflow urinary incontinence - bladder struggles to empty so overflow causes a leak

94
Q

What are risk factors for incontinence?

A

Weak pelvic floor muscles - childbirth

95
Q

How is urinary incontinence managed?

A

Modify fluids, stop smoking, lose weight, reduce caffeine
Pelvic floor muscle training
Bladder training
Anticholine and botulinum to reduce Detrusor contraction
Women - vaginal tape
Men - artificial sphincter

96
Q

What is acute kidney injury?

A

An abrupt decline in GFR

<0.5ml urine 6 hours

97
Q

What are the causes of acute kidney injury?

A

Pre renal
Intrinsic renal
Post renal

98
Q

Explain pre renal causes of AKI

A

Reduced perfusion - hypovolaemia, systemic vasodilation, cardiac failure
Compensation overwhelmed - NSAIDS constrict afferent arteriole, ACE inhibitors dilate

99
Q

Explain acute tubular necrosis

A

Ischaemia, nephrotixins, sepsis cause

Cells can’t reabsorb salts and water so fluid resuscitation can overload

100
Q

Contrast pre-renal and ATN when diagnosing

A

In pre-renal Na+ is actively reabsorbed so low urinary Na+

ATN it is higher >20mmol

101
Q

Name some nephrotoxins

A

Myoglobin, bilirubin

ACEi, amino glycosides, NSAIDS, gentamicin

102
Q

What is rhabdomyolysis?

A

Muscle necrosis releasing myoglobin. A crush injury

Elderly people, unconscious drug users, wars

103
Q

Explain post renal failure

A

An obstruction such as stones, tumour, prostate, stricture

104
Q

What are some risk factors for AKI?

A 
Old
Female
Heart/liver disease
Diabetes
Sepsis
Ill
Trauma
105
Q

How is AKI treated?

A 
Treat underlying cause
Reduce Na+ and water
Ca2+ gluconate and reduce K+
Sodium bicarbonate
Dialysis
106
Q

What is nephrotic syndrome?

A

A non specific disorder that damages the kidneys and leak protein

Proteinuria, hypoalbuminaemia, oedema

107
Q

What is nephritic syndrome?

A

Collection of signs associated with disorders affecting the kidneys - small pores in podocytes allowing protein and RBCs to enter

108
Q

Differentiate between nephrotic and nephritic syndrome

A

Nephritic - abrupt onset, raised blood pressure, red cell cast
Nephrotic - more oedema and proteinuria than nephritic. Low BP

109
Q

What are some risk factors for prostate cancer?

A

Age, family history, ethnicity (black>white>Asians)

110
Q

What are some problems due to screening?

A

Overdiagnosis and treatment
Reduced quality of life due to treatment
Costs
Other causes for positive test - infection, inflammation and large prostate all cause raised PSA

111
Q

How might a patient with prostate cancer present?

A

Asymptomatic
Urinary symptoms
Bone pain
Haematuria

112
Q

What investigations are done if prostate cancer is suspected?

A

Digital rectal exam, serum PSA

113
Q

How is prostate cancer treated?

A

Prostatectomy, surveillance, radiotherapy, hormones

114
Q

Suggest some causes for haematuria

A

Cancer - renal/transitional/bladder/prostate

Stones, infection, inflammation, prostate hyperplasia

115
Q

Define chronic kidney disease

A

Irreversible, sometimes progressive loss of renal function over a period of months/years

116
Q

What are some causes of chronic kidney disease?

A

Glomerulonephritis, pyelonephritis, polycystic kidney disease, hypertension, diabetes

117
Q

What are the pros and cons of haemodialysis?

A

Effective, 4/7 days free, less responsibility

Fluid/diet restriction, limit holiday, access problems, CVS instability

118
Q

What are the pros and cons of peritoneal dialysis?

A

Done at home, done by self, mobility, less food/fluid restriction

Frequent 4x a day, peritonitis, responsibility

119
Q

What are the pros and cons of a renal transplant?

A

Restore renal function and improved survival

Limited supply, operation risk, immunosuppresion

ESA 3 steven (5 decks)

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