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PPE Revision > Urinary > Flashcards

Urinary Flashcards

1
Q

What are the actions of angiotensin II?

A
  1. Vasoconstriction of efferent arteriole of glomerulus - increases resistance to blood flow
  2. Stimulates aldosterone release from adrenal cortex
  3. Arteriolar vasoconstriction - increases blood pressure
  4. Stimulates release of ADH - increases aquaporin channels in collecting duct
  5. Breaksdown bradykinin (vasodilator) - causes vasoconstriction
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2
Q

In response to what is renin released and from where?

A

Macula densa cells detect low Na in juxtaglomerular apparatus which stimulates renin release from juxtaglomerular cells

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3
Q

What apical channels can be found in the PCT?

A
  1. Na+/Glu, AA or peptide cotransporter
    • Na+/Glu cotransporter = SGLUT2
  2. Na+/H+ exchanger coupled with H+/organic cation exchanger
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4
Q

What channels are present in the ascending loop of Henle?

A
  • NaK2Cl cotransporter
  • ROMK
  • Chloride channel (basolateral membrane)
  • Na/K-ATPase (basolateral membrane)
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5
Q

What channels are present in the early DCT?

A
  • Na/Cl cotransporter
  • Calcium channel - under control of PTH
  • NCX (basolateral membrane)
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6
Q

What channels are present in late DCT/collecting duct?

A

Principle cells

  • ENaC
  • ROMK
  • Aquaporin II - ADH controlled

Intercalated cells

  • K+/H+ exchanger
  • Cl- channel
  • Cl/HCO3- exchanger (basolateral)
  • Cl and K channels (basolateral membrane)
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7
Q

At what channel do the following act? Give an example where indicated

  1. Loop diuretics
  2. Thiazides
  3. Aldosterone antagonists
  4. ADH
  5. Aldosterone
A
  1. Loop diuretics - NaK2Cl cotransporter (LoH) - Furosemide
  2. Thiazides - Na/Cl cotransporter (early DCT) - Bendroflumethiazide
  3. Aldosterone antagonists - Block action of aldosterone (late DCT/CD) - spironolactone
  4. ADH - Increase aquaporin channels (late DCT/CD)
  5. Aldosterone - Increases expression of ENaC, ROMK and Na/K-ATPase
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8
Q

What spinal level do the kidney start and at what spinal level does the hilum sit?

A

T11/T12

L1/L2 = hilum

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9
Q

What are the functions of the kidney?

A
  1. Regulation
  2. Excretion
  3. Endocrine
  4. Metabolism
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10
Q

Describe the progression of blood vessels from renal artery to renal vein

A
  • Renal artery
  • Segmental artery
  • Interlobar artery
  • Arcuate artery
  • Interlobular artery
  • Afferent arteriole
  • Glomerulus
  • Efferent arteriole
  • Peritubular capillaries
  • Interlobular vein
  • Arcuate vein
  • Interlobar vein
  • Renal vein
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11
Q

Which muscle do the ureteres run anterior to?

A

Psoas major

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12
Q

What are the common places for kidney stones to become lodged?

A
  1. Ureteropelvic junction
  2. Pelvic brim
  3. As ureters enter kidney
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13
Q

What is the medial imbilical ligament a remanent of?

A

Urachus

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14
Q

What is the difference between males and females with regards to urethral sphincters

A

Only males have the internal urethral sphincter

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15
Q

Briefly describe main stages of embryonic development of the kidneys

A
  1. Pronephros
    • Produces pronephric duct
  2. Mesonephros
    • Mesonephric duct which sprouts ureteric bud (induces development of definitive kidney)
  3. Metanephros forms from ureteric bud as metanephric blastema
    • Collecting system derived from ureteric bud
    • Excretory component derived from intermediate mesoderm
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16
Q

From which embryonic tissue do the kidney develop?

A

Intermediate mesoderm

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17
Q

Describe a defect that can occur during migration of kidney during development

A

Kidney get caught going past the arterial fork (inferior mesenteric artery) then they can fuse to form a horseshoe kidney

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18
Q

Briefly describe development of bladder

A
  • Hindgut derivative
  • Cloaca is split into two by urorectal septum
    • Into urogenital sinus and anorectal canal
  • Urogenital sinus is divided into 3 parts (bladder, pelvic part and phallic part)
  • Allantois is a diverticulum of the hingut that extends into umbilical cord - becomes urachus that drains urinary bladder in utero
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19
Q

Briefly describe development of openings into bladder

A

Males

  1. Mesonephric ducts reach urogenital sinus
  2. Ureteric buds sprout from mesonephric ducts
  3. Smooth muscle begins to develop from mesonephric ducts on bladder
  4. Ureteric buds and mesonephric ducts make independent openings into bladder

Females

  • Same happens except that mesonephric ducts regress due to lack of androgens
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20
Q

What is hypospadias?

A

Failure of urethral folds to fuse

Urethra opens onto ventral surface rather than end of glans

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21
Q

What is the epithelial lining of:

  1. PCT
  2. Descending LoH
  3. Ascending LoH
  4. DCT
  5. Collecting duct
A
  • PCT - simple cuboidal epithelium with brush border, active transport
  • Descending LoH - Simple squamous, no active transport
  • Ascending LoH - Simple cuboidal, active transport
  • DCT - Simple cuboidal with few microvilli
  • Collecting duct - suboidal epithelium
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22
Q

What do the collecting ducts of kidney terminate to form?

A

Papillary ducts of Bellini which then connect to form minor calyx

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23
Q

Describe muscularture of ureter

A

2 layers of smooth muscles

A third layer appears in lower third of ureter

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24
Q

What is the epithelial layer of:

  • Calyx of kidneys
  • Ureters
  • Bladder
  • Inital part of urethra
A

All transitional epithelium

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25
Q

What is the epithelial layer of male and female urethra?

A

Male - Stratified columnar below ejaculatory ducts then becomes stratified squamous

Females - Stratified squamous

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26
Q

Decribe detrusor muscle

A

3 layers of muscle

Longitudinal-circular-longitudinal

Covers all areas except trigone

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27
Q

What feature of basement membrane and podocytes prevents proteins being filtered?

A

Negatively charged glycoproteins

28
Q

What affects glomerular filtration rate?

A
  1. Hydrostatic pressure in capillary
  2. Hydrostatic pressure in Bowman’s capsule
  3. Osmotic pressure gradient between capillary and tubular lumen
29
Q

Where does the majority of secretion occur in the nephron? And what is secreted?

A

Collecting duct

H+, K+, ammonium (NH4+), creatinine, urea, some hormones and drugs

30
Q

Describe secretion of organic cations

A
  1. OC enters through basolateral membrane via faciliated diffusion
    • Down concentration and electrical gradients (Na/K-ATPase)
  2. Secreted into lumen by H+/OC exchanger, driven by H+ gradient set by Na/H antiporter
31
Q

What is the renal threshold for glucose?

A

200mg/100ml

32
Q

Define clearance with regards to filtration

A

Volume of plasma from which a substance can be completely cleared to the urine per unit time

i.e. volume of plasma cleared of substance per minute

33
Q

What is normal GFR for males and females?

A

Males = 115-125ml/min

Females = 90-100ml/min

34
Q

What is the renal plasma flow?

A
  • Kidney recieves ~1.1L/min of blood
  • 45% is RBC, 55% is plasma = 605ml/min
  • 20% of all plasma is filtered = 121ml/min
35
Q

Describe the myogenic response

A

Mechanosensory channels are activated in response to stretch (e.g. increase in BP) causing influx of Ca2+ resulting in vasoconstriction

36
Q

Describe tubular glomerular feedback

A

Macula densa cells detect amount of NaCl present in filtrate

If NaCl increases then adenosine is released causing vasoconstriction of afferent arteriole

If NaCl decreases then prostaglandins are released causing vasodilation of afferent arteriole

37
Q

What is the difference between general overflow and specific overflow aminoaciduria?

A

General is all amino acids present in urine, normally due to inadequate deamination in liver or increased GFR

Specific is one amino acid present in urine, genetic inability to break down one amino acid - e.g. phenylalanine in PKU

38
Q

What proportion and amount of fluid is found in the ICF?

A

25L

63% of total fluid

39
Q

What proportion and amount of fluid is found in ECF?

A

15L

38% of all fluid

40
Q

Describe glomerulotubular balance

A

Balance between GFR and rate of reabsorption must be kept constant

Therefore regardless of amount 67% of Na will always be reabsorbed in PCT

41
Q

What are the four mechanisms that control BP?

A
  1. RAAS System
  2. Sympathetic Nervous System
  3. Antidiuretic Hormone
  4. Atrial Natriuretic Peptide
42
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma of adrenal glands

Causes hypertension and hypokalaemia

43
Q

What is pheochromocytoma?

A

Tumour of adrenal medulla causing secretion of NA and adrenaline

Increases sympathetic stimulation

44
Q

How is osmolarity detected and what are the effects?

A

Detected by hypothalamic osmoreceptors in OVLT (organum vasculoum of the laminae terminalis)

Causes release of ADH from posterior pituitary and stimulates thirst (thirst is insensitive, requires >10% change)

45
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion

ADH not inhibited by lowering of blood osmolarity, and causing excessive water retension resulting in increased BP, dilutional hyponatreamia, lowered blood osmolarity

46
Q

Explain how the corticopapillary osmotic gradient is set up and maintained

A
  1. Counter-current multiplication
    • Loop of Henle acts as counter current multiplier due to descending limb being permeable to water and ascending limb permabile to ions
    • Sets up gradient
  2. Counter-current exchange
    • Vasa recta run alongside loop of Henle and flow in opposite direction
    • They remove water and ion quickly to maintain gradient set by counter-current multiplication
47
Q

How does PTH control serum calcium?

A
  • Low serum calcium detected by parathyroid gland
  • Releases PTH
  • PTH increases osteoclast activity
  • Also increases conversion of calcidiol to calcitriol and increases Ca2+ reabsorption but increases phosphate excretion in kidney
48
Q

What are the causes of hypercalcinaemia?

A
  1. Primary hyperparathyroidism
  2. Haematological malignancies
  3. Non-haematological malignancies - squamous cell carcinoma of lung producing PTHrP
49
Q

What is normal blood pH?

A

7.38 - 7.42

50
Q

What pH is severe and life threatening acidaemia?

A

Severe = <7.1

Life threatening = <7.0

51
Q

What is the consequence of acidosis and alkalosis?

A

Acidosis = lethal denaturing of enzymes

Alkalosis = reduced solubility of calcium, so moves out of ECF (hypocalcaemia) making nerves more excitable

52
Q

How do the kidneys produce new HCO3-?

A
  • Metabolism of CO2 in intercalated cells of late DCT/CD - required carbonic anhydrase
  • H+ pumped into lumen to react with hydrogen phosphate (HPO42- - titratable acid)
  • HCO3- enters blood
53
Q

How is H+ buffered in urine?

A
  1. Titratable acid (HPO42-) - reacts with H+ to form HPO4- which limits rise in free H+ in tubule
  2. Attach H+ to ammonia (NH3) which is synthesised by PCT metabolism of glutamine - also produces new HCO3- to go into blood
54
Q

What are the pathophysiological factors that alter potassium concentrations?

A
  1. Acid base balance - acidosis causes reciprocal shifts in K
  2. Cell lysis - release of K into ECF
  3. Exercise - net release of K during recovery phase of action potential of skeletal muscles, also skeletal muscle is damaged during exercise. Uptake of K by non-contracting tissues prevents dangerously high K. [K] proportional to exercise intensity
  4. Plasma osmolarity - increased plasma osmolarity causes water to move into ECF, this increases ICF [K] due to less water so K moves from ICF into ECF
  5. Drug related changes - diuretics, ACE inhibitors
55
Q

What are the common causes of UTIs?

A
  • Coliforms - E. coli
  • Staphylococcus saprophyticus
56
Q

Describe innervation of bladder

A

Parasympathetic = pelvic nerve (S2-S4) = M3 receptors = contraction

Sympathetic = hypogastric never (T10-L2) = B3 receptors = relaxation

Somatic (external urethral sphincter) = pudendal nerve (S2-S4) = relaxation to urinate

57
Q

Define acute kidney injury

A

Decline in GFR that occurs during a period of less than 2 weeks with an increased urea and creatinine

58
Q

What is difference between oliguria and anuria?

A

Oliguria - little urine (<500ml per day)

Anuria - no urine (<100ml per day)

Normal = 1.5L per day

59
Q

Describe a pre-renal AKI

A
  • Renal hypoperfusion
  • Caused either by reduced effective circulating volume
    • Hypovolaemia
    • Systemic vasodilation e.g. sepsis, cirrhosis, anaphylaxis
    • Cardiac failure
  • Or impaired renal autoregulation
    • Preglomerular vasoconstriction e.g. sepsis, hypercalcaemia, NSAIDs
    • Postglomerular vasodilation e.g. ACE inhibitors, angiotensin II receptor antagonists
60
Q

Describe intrinsic AKI

A
  • Direct injury to kidney
  • Causes:
    • Nephrotoxic (damage epithelial cells causing cell death and shedding into lumen) - myoglobin, urate, bilirubin, NSAIDs, ACEi, aminoglycosides (gentamicin)
    • Inflammatory - glomeruonephritis, acute tubule-interstitial nephritis
    • Ischaemic - pre-renal cause or acute tubular necrosis (from ischaemic or nephrotoxic cause)
61
Q

Describe a post-renal AKI

A
  • Caused by obstruction in urinary tract (ureters, bladder, urethra)
  • Ostruction can be:
    • Within lumen - calculi, blood clot, tumour
    • Within wall - congenital, ureteric stricture
    • Pressure from outside - prostatic hypertrophy, mlaignancy, aortic aneurysm
62
Q

Name some primary causes of nephrotic syndrome

A

Usually due to damage of podocyte/subepithelial layer

  • Minimal change glomerulonephritis - fusion of podocyte foot processes
  • Focal segmental glomerulosclerosis - circulating permability factor
  • Membranous glomerulonephritis - immune complex deposition in sub-spithelial space (commonest cause in adults)
63
Q

What are the 4 sites of glomerular injury?

A
  1. Subepithelial - affects podocytes
  2. Glomerular basement membrane
  3. Subendothelial
  4. Mesangial/paramesangial
64
Q

Name common secondary causes of nephrotic syndrome

A
  • Diabetic mellitus
  • Amyloidosis
65
Q
A

PPE Revision (16 decks)

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