Huge Review Flashcards
Osmolality of ICF
280-310mmol/L
Anatomy of kidney
Retroperitoneal
T11/12 - L2/3
3 narrowings of ureter
Vesicouterine junction
pelvic brim
Pelvi-uterine junction
Blood flow through kidney
Renal artery, segmental artery, interlobar artery, arcuate artery, cortical blood vessels
What happens at glomerulus, PCT, LOH, DCT, CD
glomerulus = ultrafiltration
PCT = reabsorption
LOH = concentration
DCT = more reabsorption
CD = water reabsorption
Types of nephron
Cortical = most common, shorter LOH, more renin
Juxtamedullary = bigger glomerulus
Embryology of kidney
Intermediate mesoderm —> Pronephros —> mesonephric system (no water storage)
Mesonephric duct —> ureteric bud (induces development of Metanephric system)
Ureteric bud —-> ureter
Urogenital sinus and GI tract develop from
Cloaca of hindgut
When is urogenital sinus created
Urorectal septum divides cloaca into bladder and and GI tract
Urogenital sinus connects to
Umbilical cord via urachus
Ascent of kidney
Elongation of embryo
Old vessels become accessory vessels
What is renal agenesis
When ureteric bud fails to interact with intermediate mesoderm
Outcomes of poor migration
Pelvic kidney, horseshoe kidney,
What is duplication defect
partial or complete splitting of ureteric bud giving ectopic urethral opening
What is hypospadias
Failure of spongy urethra to form as genital folds don’t fuse properly
Urethra opening is not at end of penis
When are urorectal fistulas formed
When the urorectal septum does not divide the urogenital sinus and GI tract by bursting cloacal membrane
urachus part of urogenital tract closes at birth to give
Median umbilical ligament
Normal GFR
90-120 ml-min
Measuring GFR
Inulin was used but requires IV and catheter
51 Cr-EDTA is radioactive and used in children and kidney transplant patients
Creatinine is used but GFR is 10-20% higher than usual
As kidney function worsens you secrete
More creatine into tubules
EGFR is less accurate with mild kidney disease because
There’s a reduction of GFR, nephron hypertrophy, reduced filtration of creatinine giving an increase in serum levels and secretion
Features of glomerulus
Only found in cortex
Only 20% of blood will be filtered
Filtration barrier
Endothelium of capillaries
Basement membrane (-)
Primary podocytes
3 different pressures acting on glomerulus
Hydrostatic pressure in glomerulus
Hydrostatic pressure in Bowman’s capsule
Oncotic pressure in glomerulus
Features of autoregulation
Myogenic mechanisms (afferent contracts or relaxes)
Tubuloglomerular feedback (macula densa in DCT detect increase in Na+ and Cl-)
Sympathetic NS (vasoconstriction during haemorrhage)
How does tubuloglomerular feedback work
Macula densa in DCT detect Cl- and Na+
GFR increase = more chloride uptake via NaKCC
Juxtaglomerular apparatus release adenosine
Constriction of afferent arteriole through A1, dilates efferent through A2 receptors
Low chloride/GFR = prostaglandins dilate the afferent arteriole
Short term bp regulation
Baroreceptor reflex in aortic arch and carotid sinus signal to the medulla
Causes myogenic reflex and tubuloglomerular feedback
Long term regulation of BP (5)
RAAS
Sympathetic NS
Prostaglandins
ADH
ANP
RAAS
Reduced NaCl delivery to DCT, reduced kidney perfusion
Renin released from granular cells of juxtaglomerular apparatus
AG1 —> AG2 by ACE
AG2 —> vasoconstriction on afferent and efferent, drop GFR, ADH release, thirst, increased Na+ reabsorption and aldosterone)
How does aldosterone work
Acts on principal cells of CD
Stimulate Na and water reabsorption by activating ENaC and ATPases
ANP
Causes vasodilation
Inhibits Na reabsorption
Works opposite to RAAS ADH and SNS
Pathology of RAAS
Pressure natriuresis (higher pressure means more sodium excreted)
Renovascular disease, coarctation of the aorta, primary hyperaldosteronism, Cushing’s
Renovascular disease causing hypertension
Narrowing of renal artery giving less perfusion
By atheroma?
RAAS activated
Primary hyperaldosteronism causing hypertension
XS aldosterone causes hypertension but does not impact renin or angiotensin
Liquorice can
Prevent conversion of cortisol, binds to aldosterone receptors causing increase in BP
Changes in osmolality are detected by
Osmoreceptors in the OVLT of hypothalamus
Thirst response is stimulated by
10% increase in plasma osmolality
(ADH response is short term)
Aquaporin 3 and 4 are always found
On basolateral membrane of DCT and CD
ADH causes
Increased aquaporin 2 on apical membrane
Low plasma ADH will cause
Diuresis
What is central diabetes insipidus
Too little ADH released
What is nephrogenic diabetes insipidus
Kidneys cannot respond to ADH
Diabetes mellitus urinary outcomes
Polyuria and polydipsia
What happens in SIADH
Too much ADH is released - high urine osmolality (less water in urine causes more concentration)
Features of urea recycling
Acts as osmole in nephron
Moves from ascending LOH, through DCT and CD to interstitium and back again
Acts as osmole in interstitium to increase conc grad in deep medulla
Responsive to ADH as requires aquaporin to move
How is counter current multiplier effect preserved
Vasa recta
Absorbs majority of remaining water and salts after PCT
How is counter current multiplier effect set up
Ascending LOH by juxtamedullary nephrons, sodium into interstitium
Interstitium osmolarity increases
Descending limb loses water to match higher osmolarity of interstitium
New fluid will enter descending limb,
sodium from ascending limb pumped out
Descending limb will equilibrate again
Process repeated again and again
Conc grad isotonic at cortex
Conc grad increases down LOH
Kidney control of H+
Phosphate and ammonium buffer H+ in urine
Bicarbonate production in kidney
Calcium in kidney
Needs magnesium (inhibitor) or would crystallise to give stones
Mostly binds to albumin or is freely excreted
Hypercalcaemia causes
Decreased PTH and increased calcitonin
More calcium excretion and less absorption due to less calcitriol
Symptoms and causes of hypocalcaemia
Fatigue, muscle weakness, tetany, laryngospasm, memory loss, confusion, long QT
Vit D deficiency, lack of PTH, reduced intake, malabsorption, diarrhoea, loop diuretic
Calcium reabsorption
Only free calcium filtered
Paracellularly in PCT
NCKK in TAL
Ca2+ channel in DCT
Calcium not reabsorbed in CD= kidney stones can develop
When is potassium intake affected
Na/K/ATPase
Activity increased with increased K+ conc, insulin, and NA effect on B2 receptors
Features of K+ reabsorption
PCT = paracellular transport
Thick ascending limb = NCKK
DCT and CD = ROMK and K+ATPase
What is the aldosterone paradox
Aldosterone allows NaCl retention with minimal K+ secretion but can also allow K+ secretion without Na retention
Symptoms of hypokalaemia
Weakness, polyuria (ADH resistance), constipation and arrhythmias, U wave on ECG
Symptoms of hypomagnasaemia
Fatigue, muscle spasms, depression, headache, tetany, seizures
Where is recovery of bicarbonate
Mostly in PCT but also in descending loop of henle
What is oliguria
Production of 500ml or less of urine a day
Types of kidney stone
Calcium oxalate, calcium phosphate, uric acid
Difference between acute and chronic urinary retention
Acute is painful
Acute causes of urinary retention
Male = BPH, prostate cancer, urethral stricture, prostatic infection
Female = prolapse, pelvic masses, treatment from stress urinary incontinence
AKI presentation and investigation
Increased K+, urea and creatine
decrease in bicarbonate, metabolic acidosis,
3 different types of AKI
Pre renal = reduction in perfusion
Intrinsic kidney disease = starved of oxygen (acute tubular necrosis)
Post renal disease = obstruction to urine flow
Where can you get transitional cell carcinoma
Renal pelvis, calices, ureter, bladder, urethra
Presentation of transitional cell carcinoma
Haematuria, CT, lymphoedema, hydronephrosis
Where can you get renal cell carcinoma
Parenchyma/PCT
Presentation of renal cell carcinoma
Haematuria, findings on CT, palpable mass, Varicocoele, PE, weight loss
Diagnosis of renal cell carcinoma
Clear cell full of glycogen are seen amongst pleomorphic cells
Spread of renal cell carcinoma
Regional spread
Lymph nodes and organs (liver)
IVC to right atrium and cause PE or right Varicocoele
Prostate cancer
Peripheral zone
PSA
Urinary symptoms, bone pain, change in bowel habits
Gleason grading system, PSA screening, DRE, biopsy, MRI
Treatment of prostate cancer
Removal
Radioactive iodine
LHRH agonists
Features of bladder cancer
90% are transitional cell carcinomas
Other 10% are squamous cell carcinomas (irritation of bladder)
Polycystic kidney disease
Autosomal dominant PKD1 or PDK 2
Cysts grow in kidney: pain, infection, need ultrasound
Measuring CKD
Bp and urine dipstick tests, creatinine levels,
Features of renal replacement therapy
When eGFR below 10
Haemodialysis, peritoneal dialysis, transplant
Causes of chronic kidney disease
Diabetes, hypertension, infection, genetic (PKD and Alport), obstruction
Staging and management of CKD
GFR decreases, stage increases 1-5
Stop smoking and obesity, exercise, statins and ACEi
Complications of CKD
Acidosis: can’t produce bicarbonate, give tablets
Hyperkalaemia: stop ACEi, avoid K+ high foods
Uraemia
Anaemia: less EPO, replace iron
Mineral bone disease: build up of phosphate prevents action of vitamin D, PTH produced, osteodystrophy, non bone calcification
Fluids
Dextrose: 1L 5%, all compartments
Colloid: 1L, go into plasma (burns victims and hypovolaemic)
Saline: 1L 0.9%, ECF (water depletion)
Staging CKD
Nephrotic vs nephritic
