Renal Physiology Flashcards

Question

What is a antiporte?

Answer 1

transporters that move two (or more) molecules in opposite directions e.g. Na+/H+ antiporte

Answer 2

Movement of multiple solutes through the same channel

Answer 3

Create an electrochemical gradient for sodium on the base lateral surface using primary active transport to favour movement of Na into the cell form the tubule lumen

Answer 4

Made up of the: 1. Pars convolute - 2 segments: S1 and proximal S2 - in the renal cortex 2. Pars recte - straight segment: distal S2 and S3 - in the outer medulla

Answer 5

Paracellular - transports solutes through the cell Transcellular - transports solutes between the cells through intercellular space

Answer 6

Sodium glucose linked transporter Secondary AT Apical membrane - check? Glucose, lactate and amino acids 100% reabsorbed into blood

Answer 7

As Na moves in cells, obligatory water reabsorption occurs - waters feels obliged to follow from kidney tubules into bloodstream via osmosis 65% each - Na and Water reabsorbed

Answer 8

Juxtaglomerular cells + macula densa

Answer 9

Modified muscular layer of the afferent arteriole •Increased number of smooth muscle cells •Less actin/myosin but many granules (renin) Low BP → less distended walls → renin release

Answer 10

Cardiac output ~ 5 L/min Renal blood flow ~ 1 L/min Urine flow ~ 1 ml/min

Answer 11

AA ↓ Renal artery ↓ Interlobar artery ↓ Arcuate artery ↓ Interlobular artery ↓ Afferent arteriole ↓ Glomerular Capillary -> IVC -> Renal vein -> Interlobar veins -> Arcuate veins -> Interlobular veins -> Vasa recta -> Peritubular capillaries -> Efferent arteriole

Answer 12

Distal part of the nephron (tubule) responsible for secretion and reabsorption

Answer 13

Factors determining filtration: A.Pressure B.Size of the molecule C.Charge D.Rate of blood flow E.Protein binding

Answer 14

Glomerular capillary blood pressure (PG)

Answer 15

Fluid pressure in Bowman’s space (PBS) Osmotic forces due to protein (πG)

Answer 16

Small molecules and ions up to 10kDa can pass freely e.g. glucose, uric acid, potassium, creatinine Larger molecules increasingly restricted e.g. plasma proteins

Answer 17

Fixed negative charge in GBM (glycoproteins and proteoglycans) repels negatively charged anions e.g. albumin, phosphate, sulfate, organic anions

Answer 18

E. Protein binding Albumin has a molecular weight of around 66kDa but is negatively charged ∴ cannot easily pass into the tubule Filtered fluid is essentially protein-free Tamm Horsfall protein in urine produced by tubule Affects substances that bind to proteins e.g. drugs, calcium, thyroxine etc

Answer 19

filtration volume per unit time (minutes) GFR = KF (PG - PBS) - (πG) KF is the filtration coefficient Net filtration is normally always positive

Answer 20

GFR determined by 1.Net filtration pressure 2.Permeability of the filtration barrier 3.Surface area available for filtration (approx. 1.2-1.5m2 total)

Answer 21

Calculated by measuring excretion of marker (M) CM = UMV/PM V = urine flow rate (ml/min) UM = urine concentration of marker PM = plasma concentration of marker

Answer 22

Properties of a good marker: -freely filtered -not secreted or absorbed -not metabolised ∴ All the M that is filtered will end up in the urine, no more (as it is not secreted) and no less (as it is not reabsorbed)

Answer 23

Normal GFR = 125ml/min

Answer 24

Creatinine usually used -muscle metabolite -constant production Properties of a good marker: -freely filtered ✓ -not secreted or absorbed ✗ (tubular secretion) -not metabolised ✓

Answer 25

- medications - creatinine supplements - dietary protein intake - age, gender, ethnicity, height and weight - renal tubular handling

Answer 26

Endogenous: Cystatin C Non-glycosylated protein produced by all cells Properties of a good marker: -freely filtered -not secreted or absorbed -not metabolised Influenced by thyroid disease, corticosteroids, age, sex and adipose tissue Others - Exogenous: Inulin (gold standard) Properties of a good marker: -freely filtered -not secreted or absorbed -not metabolised 51Cr EDTA, 99mTc-DTPA , Radioisotopes, Iohexol Inulin (gold standard) Properties of a good marker: -freely filtered ✓ -not secreted or absorbed ✓ -not metabolised ✓

Answer 27

Aim to maintain renal blood flow and GFR over defined range 80-180 mmHg Protects against extremes of pressure Independent of renal perfusion

Answer 28

1. Renal auto regulation 2. Neural regulation 3. Hormonal regulation 4. Intrarenal regulation 5. Extracellular fluid volume 6. Blood colloid osmotic pressure 7. Inflammatory mediators

Answer 29

Myogenic mechanism: •Intrinsic ability of renal arterioles •Able to constrict or dilate Tubuloglomerular feedback: •Juxtaglomerular apparatus •Stimulus NaCl concentration •Influences AFFERENT arteriolar resistance

Answer 30

BP → stretches blood vessel wall → opens stretch-activated cation channels → membrane depolarisation → opens voltage-dependent calcium channels → ↑ intracellular calcium → smooth muscle contraction → ↑ vascular resistance → minimises changes in GFR ↓BP causes the opposite ONLY PRE-GLOMERULAR RESISTANCE VESSELS

Answer 31

Sympathetic nervous system: •Vasoconstriction of AFFERENT arterioles •Important in response to stress, bleeding or low BP

Answer 32

Renin-Angiotensin-Aldosterone System (RAAS): •Renin released from JGA •Initiates cascade •Aldosterone influences Na reabsorption at distal tubule which influences blood volume and pressure Atrial Natriuretic Peptide (ANP): •Released by atria •Stimulus of blood volume •Vasodilation of AFFERENT arterioles

Answer 33

•Respond to changes in pressure in glomerulus •Influence diameter of AFFERENT arterioles

Answer 34

•Changes in blood volume •Resultant hydrostatic pressure

Answer 35

•Oncotic pressure exerted by proteins •Local release of prostaglandins, nitric oxide, bradykinin, leukotrienes, histamine, cytokines, thromboxanes

Answer 36

N - decrease Epinephrine - Decrease Endothelin - decrease Angiotensin 2 - same - prevents decrease Endothelial derived nitric oxide - increase Prostaglandins - increase

Answer 37

(Decreased resistance) - prostaglandins - nitric oxide - high blood pressure Results in: - increased RBF - increased Pg - Increased GFR

Answer 38

(Increased resistance) - sympathetic NS - angiotensin 2 Results in: - decreased RBF - decreased Pg - decreased GFR

Answer 39

(Decreased resistance) - prostgalndins - increased RBF? - High blood pressure Results in: - increased RBF - increased Pg - increased GFR

Answer 40

(Increased resistance) - sympathetic NS - angiotensin 2 Results in: - decreased RBF - decreased Pg - Decreased GFR

Answer 41

Umbrella term •Causes: infection (bacterial/viral), autoimmune disorders, systemic diseases •Presentation: haematuria, proteinuria, hypertension, impaired kidney function

Answer 42

Umbrella term •Increased permeability of glomerular filtration barrier •Presentation: triad of oedema + proteinuria + low albumin

Answer 43

Deposition of IgA antibody in the glomerulus •Resultant inflammation and damage •Cause: immune-mediated •Presentation: haematuria, potentially following resp/GI infection

Answer 44

Thickening of GBM •Most common cause of nephrotic syndrome in adults •Cause: primary or secondary •Presentation: proteinuria (often leading to nephrotic syndrome)

Answer 45

Prolonged exposure to high blood glucose •Presentation: initially asymptomatic then progresses to proteinuria, hypertension and reduced kidney function

Answer 46

Type of nephrotic syndrome, only in children •Only visible under electron microscope

Answer 47

Genetic disorder affecting GBM (X linked or autosomal recessive) •Progressive kidney damage •Potentially includes hearing loss and eye abnormalities

Answer 48

20-25% - 1200ml/min blood flow

Answer 49

Only plasma can cross glomeruli structures 600-700ml/min plasma flow (RPF) – organic and anorganic solutes freely filtered GFR – 120 ml/min or 180 L/d UO 1.5 L/d

Answer 50

Confined to renal cortex Active reabsorption of multiple things –amino acids, glucose, bicarbonate, phosphate, salt and water, potassium, chloride, urate Metabolically active cells

Answer 51

PCT is the only site of glucose reabsorption Glu is co-transported with Na via sodium glucose transporter 2 (SGLT2) Defect → failure of glucose reabsorption glucose in urine SGLT2 inhibitors (gliflozins) are now establishes as treatement for type 2 diabetes

Answer 52

AR inherited disorder - tubular defect in uptake of amino acids Defect: mutations in the SLC3A1 and SLC7A9 genes which encode basic amino acid transporter (rBAT) Genetic test available, but not routinely used in clinical practice Failure of cystine reabsorption, increased urinary cystine concentration – stone formation Renal colic, recurrent stone formation usually in childhood or adolescence

Answer 53

High fluid intake: High urine flow, lower concentration Dietary restriction (reduced animal protein intake) Alkalinise urine: Increases solubility of cystine Chelation: Penicillamine, captopril Management of individual stones (percutaneous treatment, surgery etc)

Answer 54

Unable to reabsorb phosphate Commonest form is X-linked hypophosphataemic rickets (XLH) Defect in PHEX gene – zinc dependent metalloprotease PHEX mutation results in increased FGF-23 levels, (overactivity of the protein), reduces phosphate reabsorption by the kidneys, leading to hypophosphatemia and the related features of hereditary hypophosphatemic rickets

Answer 55

Bow legged deformity, muscle weakness, slow growth and are shorter than their peers. They develop bone abnormalities that can interfere with movement and cause bone pain. Phosphate replacement

Answer 56

Bow legged deformity, muscle weakness, slow growth and are shorter than their peers. They develop bone abnormalities that can interfere with movement and cause bone pain. Phosphate replacement

Answer 57

Defect: Na/H antiporter Mechanism: Failure of bicarbonate reabsorption Bicarbonate wasting, acidosis, impaired growth Associated with myeloma, Fanconi syndrome, drugs or inherited Alkali replacement

Answer 58

Mechanism: Generalised proximal tubular dysfunction, possibly due to failure to generate sodium gradient by Na/K ATPase Causes: Genetic (eg cystinosis, Wilson’s disease), myeloma, lead poisoning, cisplatin Commonly seen with T2 RTA Glycosuria, aminoaciduria, phosphaturic rickets, renal tubular acidosis

Answer 59

Generates medullary concentration gradient via countercurrent system Active Na reabsorption in thick ascending limb Development of a hypertonic interstitum in the medullary regions of the kidney Production of a dilute (hypo-osmotic) filtrate entering the distal tubule.

Answer 60

Defect: NKCC2, ROMK, ClCKa/b, Barrtin AR inherited disorder Mechanism: Failure of sodium, potassium and chloride cotransport Salt wasting, hypokalaemic alkalosis, volume depletion, failure of voltage dependent calcium & magnesium absorption

Answer 61

Similar to effects of loop diuretics (eg furosemide, bumetanide) Clinical features Antenatal: Polyhydramnios, prematurity, delayed growth, nephrocalcinosis Classical: Delayed growth, polyuria, polydipsia, cramps, lower BP Treatment: - Replace potassium, amiloride, ACEI

Answer 62

Distal tubule and cortical collecting ducts allow “fine tuning” of sodium reabsorption, potassium and acid-base balance Impermeable to passive movement of water and sodium Uses NCCT co transporter to reabsorb 5% of sodium Specific epithelial channel absorbs calcium, paracellular route Ca and Mg Hypokalemia due to increased delivery of sodium to collecting duct

Answer 63

Defect: NCCT (thiazide sensitive chloride channel) Mechanism: Failure of sodium/chloride cotransport in distal tubule, hypokalaemic alkalosis due to volume contraction, impaired magnesium absorption, increased calcium reabsorption (unknown mechanism) Similar to thiazide diuretics Polyuria, polydipsia, tetany

Answer 64

Defect: AD = SCL4A1 (Na channel), AR = H-ATPase Mechanism: Failure of acid secretion Hypercalciuria, nephrocalcinosis, stones Associated with autoimmune diseases, drugs, medullary sponge kidney Treat underlying cause, alkaline treatment

Answer 65

Defect: Activating mutation of ENaC, AD Mechanism: Sodium channel always open so constant aldosterone like effect Increased Na absorption, loss of K, hypertensive Amiloride (blocks ENaC)

Answer 66

Defect: Vasopressin V2 receptor in principal cells or aquaporin 2 water channel Mechanism: Failure of water reabsorption in the collecting duct, resulting in inability to concentrate urine Clinical features Polyuria, polydipsia, hypernatraemia

Answer 67

Clinical correlations Tolvaptan: V2 receptor antagonist Induces polyuria and free water loss (“aquaresis”) Licensed for hyponatraemia related to SIADH Also reduces cyst formation/progression in adult polycystic kidney disease

Answer 68

180L/days of filtrate volume - 400ml-20L/24h pH - 4.5-8 Na - 100-300mmol/24h K - 50-450mmol/24h glucose <1mmol/24h amino acids v. little HCO3 - 1mmol/24h

Answer 69

Proximal = bulk absorption = leaky Distal = fine tuning = impermeable

Answer 70

Proximal Tubule bulk reabsorption: Na, Cl, glucose, amino acids, HCO3; secretion of organic ions Loop of Henle more Na reabsorption, urinary dilution and generation of medullary hypertonicity Distal Tubule fine regulation of Na, K, Ca, Pi, separation of Na from H2O Collecting Duct similar to distal tubule, + acid secretion, regulated H2O reabsorption concentrating urine

Answer 71

Bulk reabsorption •Driven by the basolateral NaKATPase •Secondary active transport for reuptake of glucose, amino acids, lactate •Highly efficient; mostly achieved in first half •Cl follows Na in the second half •Big workload, determined by filtered load •High H2O permeability

Answer 72

Similar to glucose •Various cotransporters responsible for groups of amino acids (cationic, anionic, neutral,...) •Aminoaciduria, glycosuria and bicarbonate wasting are features of proximal tubule pathology

Answer 73

Transcellular and paracellular

Answer 74

Endogenous compounds •Creatinine •Urate •Bile salts •… Drugs •Furosemide •Penicillin •Salicylate •Acetazolamide •Trimethoprim* •Cimetidine* *Inhibit creatinine secretion

Answer 75

•More filtered load is matched by more proximal tubular reabsorption: 1.Greater filtration fraction increases the osmotic pressure in the downstream peritubular capillaries; sucks more back 2.Efferent arteriolar constriction reduces peritubular capillary hydrostatic pressure

Answer 76

The descending limb is water permeable and the ascending limb is H2O impermeable Solute reabsorption occurs in the thick ascending limb

Answer 77

Aim: to generate a hypertonic medullary interstitium so that H2O can be sucked out of the tubule in impermeable distal segments, thus concentrating the urine.

Answer 78

1. Solute reabsorption in the impermeable ascending limb lowers the lumenal osmolality and increases the medullary interstitial osmolarity 2. Increased interstitial osmolarity draws H2O out of the permeable thin descending limb, increasing the lumenal osmolality. 3. The continuous flow of fluid pushes the hyperosmotic fluid from end of the thin limb in to the ascending limb. Process repeats Generating a medullary interstitial osmotic gradient

Answer 79

backleak of urea out of the medullary collecting duct also contributes to medullary hypertonicity

Answer 80

Due to: - Vasa recta •Long capillaries extend into the medulla •Permeable to solute/water

Answer 81

Continues the active dilution of urine by reabsorption of Na+ in water-impermeable setting. We want distal delivery of dilute urine which can be concentrated at will

Answer 82

highly water impermeable, surrounded by hypertonic medullary interstitium •regulated Na reabsorption and K secretion •acid secretion •regulated water reabsorption •2 cell types: principal cell and intercalated cell

Answer 83

Increases transcription (steroid receptor) of ENaC (and NaKATPase) •This increases apical Na influx •This charge movement facilitates K efflux •Thus aldosterone drives both Na reabsorption and K secretion

Answer 84

Hypotonic urine enters the collecting duct •Main osmolyte is urea (most Na reabsorbed) •The limits of urine osmolarity are determined by how dilute it can enter the distal segment and how hypertonic the medullary interstitium is (driving H2O reabsorption)

Answer 85

principal cells •adenylyl-cyclase coupled vasopressin receptor (V2R) •kinase actions culminate in insertion of vesicles containing aquaporin 2 into the apical membrane •increases water permeability

Answer 86

Genetic defects in carbonic anhydrase produce a mixed proximal/distal renal tubular acidosis ●Inhibited by acetazolamide – mild diuretic effect and induces a metabolic acidosis ●Used to treat altitude sickness – allows more rapid compensation of respiratory alkalosis

Answer 87

Steroid hormone – predominantly acts on transcription ●Increase expression of ENaC, Na/K ATP-ase ●Mineralocorticoid receptor also activated by cortisol ●Cortisol entry to renal tubular cells prevented by 11-beta hydroxysteroid dehydrogenase

Answer 88

Defect: Chimeric gene – 11beta hydroxylase and aldosterone synthetase ●Mechanism: Aldosterone is produced in the adrenal in response to ACTH, so levels inappropriately high ●Treatment: Suppress ACTH using glucocorticoids

Answer 89

●Defect: 11-beta hydroxysteroid dehydrogenase ●Mechanism: Cortisol not broken down in the renal tubules, therefore activates mineralocorticoid receptor. ●Treatment: Spironolactone (mineralocorticoid receptor antagonist)

Answer 90

●Defect: Low aldosterone levels ●Mechanism: Reduced generation of electrochemical gradient, resulting in failure of H+ and K+ excretion ●Common in elderly patients with diabetes ●Treatment: Diuretics or fludrocortisone

Answer 91

Negative log [H+]

Answer 92

Disorder tending to make blood more acid than normal

Answer 93

Disorder tending to make blood more alkaline than normal

Answer 94

Acidemia = Low blood pH •Alkalemia = High blood pH

Answer 95

Measures of metabolic component of any acid-base disturbance •Absolute bicarbonate is affected by both respiratory and metabolic components •Standard bicarbonate is the bicarbonate concentration standardised to pCO2 5.3kPa and temp 37 •Bicarbonate and std bicarbonate are calculated not actually measured

Answer 96

Quantity of acid required to return pH to normal under standard conditions •Standard base excess corrected to Hb 50g/L •Can be used to calculate bicarbonate dose to correct acidosis 0.3xWtxBE (but not generally used in practice) •Base excess is negative in acidosis, can be referred to as base deficit

Answer 97

pH •pO2 •pCO2 •Std HCO3- •Std Base excess •May include other measures (eg lactate, Na+, K+)

Answer 98

•Henderson •Stewart’s theory (strong ion difference)

Answer 99

pH = pKa + log([A-]/[HA]) •pH = pKaH2CO3 + log([HCO3-]/[H2CO3]) •pH = 6.1 + log([HCO3-]/0.03 x pCO2)

Answer 100

Principle: pH and HCO3- are dependent variables governed by: •pCO2 •Concentration of weak acids (ATOT) ◦ATOT = Pi + Pr + Alb •Strong ion difference (SID) ◦SID = Na+ + K+ + Mg2+ + Ca2+ – Cl- – other strong anions (eg lactate, ketoacids)

Answer 101

Identifies the factors controlling pH

Answer 102

Disorders can be divided into acidoses – disorders that tend to make the blood acid and alkaloses •Disorders can be respiratory (ie driven by changes in CO2 excretion) or metabolic (ie driven by changes in acid load, acid excretion or bicarbonate recycling) •Different disorders can co-exist (mixed patterns)

Answer 103

Dilutional •Failure of H+ excretion: Renal failure, hypoaldosteronism, type 1 renal tubular acidosis •Excess H+ load: Lactic acidosis, Ketoacidosis, ingestion of acids (eg salicylate, ethylene glycol •HCO3- loss: Diarrhoea, type 2 renal tubular acidosis

Answer 104

Dilutional •Failure of H+ excretion: Renal failure, hypoaldosteronism, type 1 renal tubular acidosis •Excess H+ load: Lactic acidosis, Ketoacidosis, ingestion of acids (eg salicylate, ethylene glycol •HCO3- loss: Diarrhoea, type 2 renal tubular acidosis

Answer 105

Clinical features: Sighing respirations (Kussmaul’s resps), tachypnoea •Compensatory mechanism: Hyperventilation to increase CO2 excretion

Answer 106

Clinical features: Sighing respirations (Kussmaul’s resps), tachypnoea •Compensatory mechanism: Hyperventilation to increase CO2 excretion

Answer 107

Difference between measured anions and cations •Anion gap = [Na+] + [K+] – [Cl-] – [HCO3-] •Normal 10-16 •Wide anion gap: Lactic acidosis, ketoacidosis, ingestion of acid, renal failure •Narrow anion gap (ie high chloride): GI HCO3- loss, renal tubular acidosis

Answer 108

Difference between measured anions and cations •Anion gap = [Na+] + [K+] – [Cl-] – [HCO3-] •Normal 10-16 •Wide anion gap: Lactic acidosis, ketoacidosis, ingestion of acid, renal failure •Narrow anion gap (ie high chloride): GI HCO3- loss, renal tubular acidosis

Answer 109

Causes: ◦Alkali ingestion ◦Gastrointestinal acid loss: Vomiting ◦Renal acid loss: Hyperaldosteronism, hypokalaemia •Compensatory mechanism: Hypoventilation (but limited by hypoxic drive), renal bicarbonate excretion

Answer 110

CO2 retention, leading to increased carbonic acid dissociation •Causes: Any cause of respiratory failure •Compensatory mechanism: Increased renal H+ excretion and bicarbonate retention (but only if chronic)

Answer 111

CO2 depletion due to hyperventilation •Causes: Type 1 respiratory failure, anxiety/panic •Compensation: Increased renal bicarbonate loss (if chronic)

Answer 112

- Normal diet generates non-volatile acid such as sulphuric and phosphoric acid from Protein metabolism, lactate from anaerobic metabolism of Glucose and volatile acid co2 primarily from carbohydrate metabolism. •Kidneys excrete the acid load and also reclaim filtered bicarbonate. •Lungs mediate excretion of co2.

Answer 113

- reclaim the filtered HCO3- - regenerate HCO3 - - excretion of H+ ions buffered by phosphate or ammonia

Answer 114

It is defined as low arterial pH with in conjunction with a reduced serum HCO3- concentration

Answer 115

Causes: •Alkali ingestion •Gastrointestinal acid loss: Vomiting •Renal acid loss: Hyperaldosteronism, hypokalaemia •Compensatory mechanism: Hypoventilation (but limited by hypoxic drive), renal bicarbonate excretion

Answer 116

CO2 retention, leading to increased carbonic acid dissociation •Causes: Any cause of respiratory failure •Compensatory mechanism: Increased renal H+ excretion and bicarbonate retention (but only if chronic)

Answer 117

- depressed central drive - abnormal neuromuscular transmission - muscle dysfunction - enhanced ventilatory demand - increased dead space ventilation - augmented airway flow resistance - lung stiffness - pleural/chest wall stiffness

Answer 118

•CO2 depletion due to hyperventilation •Causes: Type 1 respiratory failure, anxiety/panic •Compensation: Increased renal bicarbonate loss (if chronic)

Answer 119

Forms a ridge of issue on the posterior abdominal wall •Both the renal and genital systems develop from it

Answer 120

From intermediate mesoderm: 1. Pronephros - develops in week - 4/40 (disappears by 5/40), Non-functional, rudimentary 2. Mesonephros - develops In week - 4/40, Part of it persists in males. 3. Metanephros - 5/40; starts to function at 12/40, Definitive kidney

Answer 121

•Excretory tubules develop with a group of capillaries •Capillaries > glomerulus •Tubules > Bowman’s capsule •Collecting duct called the mesonephric duct forms •Gonad starts to develop

Answer 122

•Excretory tubules develop with a group of capillaries •Capillaries > glomerulus •Tubules > Bowman’s capsule •Collecting duct called the mesonephric duct forms •Gonad starts to develop

Answer 123

Females: Tubules and mesonephric duct degenerate Males: A few tubules and the mesonephric ducts remain: •mesonephric duct = vas deferens •tubules = ducts of testis

Answer 124

Definitive kidney •Develops in the pelvic region •Collecting system and excretory system develop differently •Starts to function in week 12 of gestation

Answer 125

Definitive kidney •Develops in the pelvic region •Collecting system and excretory system develop differently •Starts to function in week 12 of gestation

Answer 126

Develops from the ureteric bud •The ureteric bud grows out from the mesonephric duct •Covered over by a ‘cap’ of metanephric tissue •Bud grows into the cap = renal pelvis

Answer 127

Bud splits into two parts = major calyces •Continued subdivision and formation of tubules = ureter, renal pelvis, major and minor calyces, collecting tubules

Answer 128

Develops from metanephric cap •Development promoted by the developing collecting tubules •Development of each is dependent on the other •Metanephric tissue forms renal vesicles •Vesicles become tubular and capillaries develop = glomerulus •Form nephrons

Answer 129

Ureter •Renal pelvis •Major and minor calyces •Collecting tubules

Answer 130

•Kidney ascends in utero •During ascent, new vessels are derived from more proximal parts of the aorta and lower vessels regress •Kidney starts to function in week 12 (12/40) •Urine is formed and excreted into the amniotic fluid

Answer 131

Renal agenesis •Nephrons and collecting ducts don’t develop •Can result if signaling between ureteric bud and metanephric tissue fails •Unilateral or bilateral – bilateral is rare but incompatible with life •Seen in many genetic conditions

Answer 132

1/600 •Lower poles of the kidneys fuse •Ascent obstructed by the IMA •Usually asymptomatic and found incidentally

Answer 133

Fusion of the upper and lower poles of the kidney.

Answer 134

As the kidneys ascend, lower vessels do not regress

Answer 135

Cloaca = common cavity for urogenital system and the gut Urorectal septum divides cloaca: •urogenital sinus •anal canal

Answer 136

Gives rise to 3 parts: •Upper part = bladder •Middle / pelvic part = part of the male urethra •Phallic part = develops differently in males and females

Answer 137

Rare •Failure of anterior abdominal wall to close •Bladder is exposed

Answer 138

Develops from the ureteric bud •Ureter directly enters the bladder after the distal part of the mesonephric duct merges into the bladder wall.

Answer 139

Mesonephric duct: develops into the vas deferens in males, regresses in females)

Answer 140

Mesonephric duct: develops into the vas deferens in males, regresses in females)

Answer 141

Double ureter (duplication) •Ureteric bud splits early in development

Answer 142

Ectopic ureter •Development of two ureteric buds •One enters bladder •Other enters bladder, urethra, vagina or epididymal region

Answer 143

The fetal kidney is functional. The fetal kidney ascends from the pelvis to the abdomen