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Urinary > Huge Review > Flashcards

Huge Review Flashcards

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
Q

Features of autoregulation

A

Myogenic mechanisms (afferent contracts or relaxes)
Tubuloglomerular feedback (macula densa in DCT detect increase in Na+ and Cl-)
Sympathetic NS (vasoconstriction during haemorrhage)

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26
Q

How does tubuloglomerular feedback work

A

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

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27
Q

Short term bp regulation

A

Baroreceptor reflex in aortic arch and carotid sinus signal to the medulla

Causes myogenic reflex and tubuloglomerular feedback

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28
Q

Long term regulation of BP (5)

A

RAAS
Sympathetic NS
Prostaglandins
ADH
ANP

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29
Q

RAAS

A

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)

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30
Q

How does aldosterone work

A

Acts on principal cells of CD
Stimulate Na and water reabsorption by activating ENaC and ATPases

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31
Q

ANP

A

Causes vasodilation
Inhibits Na reabsorption

Works opposite to RAAS ADH and SNS

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32
Q

Pathology of RAAS

A

Pressure natriuresis (higher pressure means more sodium excreted)

Renovascular disease, coarctation of the aorta, primary hyperaldosteronism, Cushing’s

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33
Q

Renovascular disease causing hypertension

A

Narrowing of renal artery giving less perfusion
By atheroma?
RAAS activated

34
Q

Primary hyperaldosteronism causing hypertension

A

XS aldosterone causes hypertension but does not impact renin or angiotensin

35
Q

Liquorice can

A

Prevent conversion of cortisol, binds to aldosterone receptors causing increase in BP

36
Q

Changes in osmolality are detected by

A

Osmoreceptors in the OVLT of hypothalamus

37
Q

Thirst response is stimulated by

A

10% increase in plasma osmolality

(ADH response is short term)

38
Q

Aquaporin 3 and 4 are always found

A

On basolateral membrane of DCT and CD

39
Q

ADH causes

A

Increased aquaporin 2 on apical membrane

40
Q

Low plasma ADH will cause

A

Diuresis

41
Q

What is central diabetes insipidus

A

Too little ADH released

42
Q

What is nephrogenic diabetes insipidus

A

Kidneys cannot respond to ADH

43
Q

Diabetes mellitus urinary outcomes

A

Polyuria and polydipsia

44
Q

What happens in SIADH

A

Too much ADH is released - high urine osmolality (less water in urine causes more concentration)

45
Q

Features of urea recycling

A

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
Q

How is counter current multiplier effect preserved

A

Vasa recta

Absorbs majority of remaining water and salts after PCT

47
Q

How is counter current multiplier effect set up

A

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
Q

Kidney control of H+

A

Phosphate and ammonium buffer H+ in urine

Bicarbonate production in kidney

49
Q

Calcium in kidney

A

Needs magnesium (inhibitor) or would crystallise to give stones

Mostly binds to albumin or is freely excreted

50
Q

Hypercalcaemia causes

A

Decreased PTH and increased calcitonin

More calcium excretion and less absorption due to less calcitriol

51
Q

Symptoms and causes of hypocalcaemia

A

Fatigue, muscle weakness, tetany, laryngospasm, memory loss, confusion, long QT

Vit D deficiency, lack of PTH, reduced intake, malabsorption, diarrhoea, loop diuretic

52
Q

Calcium reabsorption

A

Only free calcium filtered

Paracellularly in PCT
NCKK in TAL
Ca2+ channel in DCT
Calcium not reabsorbed in CD= kidney stones can develop

53
Q

When is potassium intake affected

A

Na/K/ATPase

Activity increased with increased K+ conc, insulin, and NA effect on B2 receptors

54
Q

Features of K+ reabsorption

A

PCT = paracellular transport
Thick ascending limb = NCKK
DCT and CD = ROMK and K+ATPase

55
Q

What is the aldosterone paradox

A

Aldosterone allows NaCl retention with minimal K+ secretion but can also allow K+ secretion without Na retention

56
Q

Symptoms of hypokalaemia

A

Weakness, polyuria (ADH resistance), constipation and arrhythmias, U wave on ECG

57
Q

Symptoms of hypomagnasaemia

A

Fatigue, muscle spasms, depression, headache, tetany, seizures

58
Q

Where is recovery of bicarbonate

A

Mostly in PCT but also in descending loop of henle

59
Q

What is oliguria

A

Production of 500ml or less of urine a day

60
Q

Types of kidney stone

A

Calcium oxalate, calcium phosphate, uric acid

61
Q

Difference between acute and chronic urinary retention

A

Acute is painful

62
Q

Acute causes of urinary retention

A

Male = BPH, prostate cancer, urethral stricture, prostatic infection

Female = prolapse, pelvic masses, treatment from stress urinary incontinence

63
Q

AKI presentation and investigation

A

Increased K+, urea and creatine

decrease in bicarbonate, metabolic acidosis,

64
Q

3 different types of AKI

A

Pre renal = reduction in perfusion
Intrinsic kidney disease = starved of oxygen (acute tubular necrosis)
Post renal disease = obstruction to urine flow

65
Q

Where can you get transitional cell carcinoma

A

Renal pelvis, calices, ureter, bladder, urethra

66
Q

Presentation of transitional cell carcinoma

A

Haematuria, CT, lymphoedema, hydronephrosis

67
Q

Where can you get renal cell carcinoma

A

Parenchyma/PCT

68
Q

Presentation of renal cell carcinoma

A

Haematuria, findings on CT, palpable mass, Varicocoele, PE, weight loss

69
Q

Diagnosis of renal cell carcinoma

A

Clear cell full of glycogen are seen amongst pleomorphic cells

70
Q

Spread of renal cell carcinoma

A

Regional spread
Lymph nodes and organs (liver)
IVC to right atrium and cause PE or right Varicocoele

71
Q

Prostate cancer

A

Peripheral zone
PSA

Urinary symptoms, bone pain, change in bowel habits

Gleason grading system, PSA screening, DRE, biopsy, MRI

72
Q

Treatment of prostate cancer

A

Removal
Radioactive iodine
LHRH agonists

73
Q

Features of bladder cancer

A

90% are transitional cell carcinomas
Other 10% are squamous cell carcinomas (irritation of bladder)

74
Q

Polycystic kidney disease

A

Autosomal dominant PKD1 or PDK 2

Cysts grow in kidney: pain, infection, need ultrasound

75
Q

Measuring CKD

A

Bp and urine dipstick tests, creatinine levels,

76
Q

Features of renal replacement therapy

A

When eGFR below 10

Haemodialysis, peritoneal dialysis, transplant

77
Q

Causes of chronic kidney disease

A

Diabetes, hypertension, infection, genetic (PKD and Alport), obstruction

78
Q

Staging and management of CKD

A

GFR decreases, stage increases 1-5

Stop smoking and obesity, exercise, statins and ACEi

79
Q

Complications of CKD

A

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
Q

Fluids

A

Dextrose: 1L 5%, all compartments
Colloid: 1L, go into plasma (burns victims and hypovolaemic)
Saline: 1L 0.9%, ECF (water depletion)

81
Q

Staging CKD

A
82
Q

Nephrotic vs nephritic

A

Urinary (20 decks)

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