Huge Review Flashcards

(82 cards)

1
Q

Osmolality of ICF

A

280-310mmol/L

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2
Q

Anatomy of kidney

A

Retroperitoneal
T11/12 - L2/3

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3
Q

3 narrowings of ureter

A

Vesicouterine junction
pelvic brim
Pelvi-uterine junction

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4
Q

Blood flow through kidney

A

Renal artery, segmental artery, interlobar artery, arcuate artery, cortical blood vessels

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5
Q

What happens at glomerulus, PCT, LOH, DCT, CD

A

glomerulus = ultrafiltration
PCT = reabsorption
LOH = concentration
DCT = more reabsorption
CD = water reabsorption

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6
Q

Types of nephron

A

Cortical = most common, shorter LOH, more renin
Juxtamedullary = bigger glomerulus

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7
Q

Embryology of kidney

A

Intermediate mesoderm —> Pronephros —> mesonephric system (no water storage)

Mesonephric duct —> ureteric bud (induces development of Metanephric system)

Ureteric bud —-> ureter

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8
Q

Urogenital sinus and GI tract develop from

A

Cloaca of hindgut

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9
Q

When is urogenital sinus created

A

Urorectal septum divides cloaca into bladder and and GI tract

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10
Q

Urogenital sinus connects to

A

Umbilical cord via urachus

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11
Q

Ascent of kidney

A

Elongation of embryo
Old vessels become accessory vessels

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12
Q

What is renal agenesis

A

When ureteric bud fails to interact with intermediate mesoderm

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13
Q

Outcomes of poor migration

A

Pelvic kidney, horseshoe kidney,

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14
Q

What is duplication defect

A

partial or complete splitting of ureteric bud giving ectopic urethral opening

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15
Q

What is hypospadias

A

Failure of spongy urethra to form as genital folds don’t fuse properly

Urethra opening is not at end of penis

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16
Q

When are urorectal fistulas formed

A

When the urorectal septum does not divide the urogenital sinus and GI tract by bursting cloacal membrane

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17
Q

urachus part of urogenital tract closes at birth to give

A

Median umbilical ligament

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18
Q

Normal GFR

A

90-120 ml-min

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19
Q

Measuring GFR

A

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

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20
Q

As kidney function worsens you secrete

A

More creatine into tubules

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21
Q

EGFR is less accurate with mild kidney disease because

A

There’s a reduction of GFR, nephron hypertrophy, reduced filtration of creatinine giving an increase in serum levels and secretion

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22
Q

Features of glomerulus

A

Only found in cortex
Only 20% of blood will be filtered

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23
Q

Filtration barrier

A

Endothelium of capillaries
Basement membrane (-)
Primary podocytes

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24
Q

3 different pressures acting on glomerulus

A

Hydrostatic pressure in glomerulus
Hydrostatic pressure in Bowman’s capsule
Oncotic pressure in glomerulus

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25
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)
26
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
27
Short term bp regulation
Baroreceptor reflex in aortic arch and carotid sinus signal to the medulla Causes myogenic reflex and tubuloglomerular feedback
28
Long term regulation of BP (5)
RAAS Sympathetic NS Prostaglandins ADH ANP
29
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)
30
How does aldosterone work
Acts on principal cells of CD Stimulate Na and water reabsorption by activating ENaC and ATPases
31
ANP
Causes vasodilation Inhibits Na reabsorption Works opposite to RAAS ADH and SNS
32
Pathology of RAAS
Pressure natriuresis (higher pressure means more sodium excreted) Renovascular disease, coarctation of the aorta, primary hyperaldosteronism, Cushing’s
33
Renovascular disease causing hypertension
Narrowing of renal artery giving less perfusion By atheroma? RAAS activated
34
Primary hyperaldosteronism causing hypertension
XS aldosterone causes hypertension but does not impact renin or angiotensin
35
Liquorice can
Prevent conversion of cortisol, binds to aldosterone receptors causing increase in BP
36
Changes in osmolality are detected by
Osmoreceptors in the OVLT of hypothalamus
37
Thirst response is stimulated by
10% increase in plasma osmolality (ADH response is short term)
38
Aquaporin 3 and 4 are always found
On basolateral membrane of DCT and CD
39
ADH causes
Increased aquaporin 2 on apical membrane
40
Low plasma ADH will cause
Diuresis
41
What is central diabetes insipidus
Too little ADH released
42
What is nephrogenic diabetes insipidus
Kidneys cannot respond to ADH
43
Diabetes mellitus urinary outcomes
Polyuria and polydipsia
44
What happens in SIADH
Too much ADH is released - high urine osmolality (less water in urine causes more concentration)
45
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
46
How is counter current multiplier effect preserved
Vasa recta Absorbs majority of remaining water and salts after PCT
47
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
48
Kidney control of H+
Phosphate and ammonium buffer H+ in urine Bicarbonate production in kidney
49
Calcium in kidney
Needs magnesium (inhibitor) or would crystallise to give stones Mostly binds to albumin or is freely excreted
50
Hypercalcaemia causes
Decreased PTH and increased calcitonin More calcium excretion and less absorption due to less calcitriol
51
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
52
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
53
When is potassium intake affected
Na/K/ATPase Activity increased with increased K+ conc, insulin, and NA effect on B2 receptors
54
Features of K+ reabsorption
PCT = paracellular transport Thick ascending limb = NCKK DCT and CD = ROMK and K+ATPase
55
What is the aldosterone paradox
Aldosterone allows NaCl retention with minimal K+ secretion but can also allow K+ secretion without Na retention
56
Symptoms of hypokalaemia
Weakness, polyuria (ADH resistance), constipation and arrhythmias, U wave on ECG
57
Symptoms of hypomagnasaemia
Fatigue, muscle spasms, depression, headache, tetany, seizures
58
Where is recovery of bicarbonate
Mostly in PCT but also in descending loop of henle
59
What is oliguria
Production of 500ml or less of urine a day
60
Types of kidney stone
Calcium oxalate, calcium phosphate, uric acid
61
Difference between acute and chronic urinary retention
Acute is painful
62
Acute causes of urinary retention
Male = BPH, prostate cancer, urethral stricture, prostatic infection Female = prolapse, pelvic masses, treatment from stress urinary incontinence
63
AKI presentation and investigation
Increased K+, urea and creatine decrease in bicarbonate, metabolic acidosis,
64
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
65
Where can you get transitional cell carcinoma
Renal pelvis, calices, ureter, bladder, urethra
66
Presentation of transitional cell carcinoma
Haematuria, CT, lymphoedema, hydronephrosis
67
Where can you get renal cell carcinoma
Parenchyma/PCT
68
Presentation of renal cell carcinoma
Haematuria, findings on CT, palpable mass, Varicocoele, PE, weight loss
69
Diagnosis of renal cell carcinoma
Clear cell full of glycogen are seen amongst pleomorphic cells
70
Spread of renal cell carcinoma
Regional spread Lymph nodes and organs (liver) IVC to right atrium and cause PE or right Varicocoele
71
Prostate cancer
Peripheral zone PSA Urinary symptoms, bone pain, change in bowel habits Gleason grading system, PSA screening, DRE, biopsy, MRI
72
Treatment of prostate cancer
Removal Radioactive iodine LHRH agonists
73
Features of bladder cancer
90% are transitional cell carcinomas Other 10% are squamous cell carcinomas (irritation of bladder)
74
Polycystic kidney disease
Autosomal dominant PKD1 or PDK 2 Cysts grow in kidney: pain, infection, need ultrasound
75
Measuring CKD
Bp and urine dipstick tests, creatinine levels,
76
Features of renal replacement therapy
When eGFR below 10 Haemodialysis, peritoneal dialysis, transplant
77
Causes of chronic kidney disease
Diabetes, hypertension, infection, genetic (PKD and Alport), obstruction
78
Staging and management of CKD
GFR decreases, stage increases 1-5 Stop smoking and obesity, exercise, statins and ACEi
79
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
80
Fluids
Dextrose: 1L 5%, all compartments Colloid: 1L, go into plasma (burns victims and hypovolaemic) Saline: 1L 0.9%, ECF (water depletion)
81
Staging CKD
82
Nephrotic vs nephritic