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Year 2 Conditions > Urinary > Flashcards

Urinary Flashcards

1
Q

What is AKI?

A

Abrupt drop in renal function causing a reversible build up of nitrogen waste products
Occurs over days to weeks

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2
Q

What are some pre-renal causes of AKI?

A

Decreased blood flow

Hypovolaemia - dehydration, haemorrhage, D&V, burns
Decreased CO - heart failure, MI
Decreased peripheral resistance - anaphylaxis, septic shock

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3
Q

What are some intra-renal causes of AKI?

A

Nephrotoxic injury - drugs (NSAIDs), rhabdomyolysis
Interstitial nephritis
Acute glomerulonephritis

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4
Q

What are some post-renal causes of AKI?

A

Obstruction to renal outflow

BPH
Bladder ca
Renal calculi

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5
Q

What is rhabdomyolysis?

A

Release of myoglobin due to muscle necrosis
Treated w/ IV fluids
Occurs in IVDU, elderly ppl or post earthquakes

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6
Q

What is acute tubular injury?

A

Cell damage due to ischaemia, nephrotoxins & sepsis
Generally not necrosis, but cells are damaged so it cannot be reversed
More likely if there is reduced perfusion AND a nephrotoxin

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7
Q

What is the management of AKI?

A

Volume overload - restrict Na & water intake
Hyperkalaemia - calcium gluconate, dextrose & insulin, restrict dietary intake
Sepsis - abx

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8
Q

What is CKD?

A

Gradual, irreversible drop in renal function

Takes months - years

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9
Q

What are the signs & Sx of CKD?

A

Uraemia
Proteinuria
Haematuria

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10
Q

What is the aetiology of CKD?

A 
Diabetes - most commonly 
Hypertension 
Immunological - glomerulonephritis 
Genetic - APCKD, Alport’s 
Obstruction 
Acute tubular necrosis
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11
Q

What is the management of CKD?

A

Modifiable risk factors - smoking, exercise, diet
Control diabetes
Control HTN - anti-hypertensives, diuretics, fluid restriction
Control proteinuria
Control lipids - statins

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12
Q

What are some complications of CKD?

A

Acidosis
Anaemia
Mineral bone disease
Altered drug metabolism

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13
Q

Why do pts get anaemia after CKD?

A 
Decreased EPO
Absolute iron deficiency 
Blood loss 
Short RBC life span 
Bone marrow suppression from uraemia 
B12 & folate deficiency
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14
Q

Why do pts get mineral bone disease after CKD?

A

Reduced activation of vitamin D => decreased Ca2+ absorption from gut => decreased serum Ca2+ => stimulation of PTH => increased osteoclast activity => break down of bone

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15
Q

What is end stage renal failure?

A

When death is likely without renal replacement therapy

eGFR <15ml/min

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16
Q

What are some Sx of end stage renal failure?

A 
Overwhelming fatigue 
Difficulty sleeping
Sx of volume overload; SoB, oedema 
Nausea &amp; vomiting 
Pruritis
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17
Q

What are some examples of renal replacement therapy?

A

Haemodialysis
Peritoneal dialysis
Transplant

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18
Q

What are the advantages & disadvantages of haemodialysis?

A

Advantages:
Less responsibility for pt
Can I have “days off”

Disadvantages
Travel & waiting time => massive restrictions
Big restriction on food & fluid intake

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19
Q

What are some advantages & disadvantages of peritoneal dialysis?

A

Advantages:
Allows independence
Generally less food & fluid restriction
Can travel more easily

Disadvantages:
Frequent daily changes
Responsibility is on pt

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20
Q

What is diabetes insipidus?

A

Inadequate reabsorption of water => diuresis

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21
Q

What are the two types of diabetes insipidus?

A

Central and nephrogenic

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22
Q

What is central diabetes insipidus?

A

Low plasma ADH

Due to damage to hypothalamus & posterior pituitary eg brain injury, tumour

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23
Q

What is nephrogenic diabetes insipidus?

A

Acquired insensitivity to ADH

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24
Q

What is the treatment for diabetes insipidus?

A

ADH injection or nasal spray

Low sodium diet

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25
Q

What is adult polycystic kidney disease?

A

An autosomal dominant condition resulting in growth of cysts on kidneys

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26
Q

What is the clinical presentation of APCKD?

A 
Pain
Bleeding into cyst
Infection 
Renal stones 
Hypertension 
Intra-cranial aneurysms 
Heart valve abnormalities
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27
Q

How is APCKD managed?

A

Treat HTN by blocking RAAS
Diet changes - low salt, don’t eat excessive protein
Tolvaptan - blocks ADH, affects how cysts grow

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28
Q

What is hyponatraemia?

A

When serum conc of Na is 135mmol

Most commonly caused by too much fluid - relative hyponatraemia

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29
Q

What causes hyponatraemia?

A

True Na loss: D&V, diuretics, renal failure, peritonitis

Changes to ADH secretion: heart failure, kidney disease, liver disease, tumours (small cell carcinoma)

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30
Q

What is the treatment for hyponatraemia?

A

Fluid restriction

Symptomatic pts can be treated w/ hypertonic saline & furosemide

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31
Q

What causes hyperkalaemia?

A

Decreased renal excretion; AKI, CKD, drugs blocking K+ secretion, low aldosterone state
DKA
Metabolic acidosis
Exercise

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32
Q

What is the emergency treatment for hyperkalaemia?

A

Reduce effect on heart; IV calcium gluconate
Shift K+ to ICF; glucose & IV insulin
Removal of excess K+ ; dialysis

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33
Q

What is the long term treatment of hyperkalaemia?

A

Treat cause eg managing diabetes to prevent DKA
Reduce intake
Removal of excess; dialysis

34
Q

What are the clinical features of hyperkalaemia?

A

Altered excitability of the heart => arrhythmias & heart block
Neuromuscular dysfunction in the GI tract => paralytic ileus
Acidosis

35
Q

What causes hypokalaemia?

A

Excessive loss of K+ ; D&V, renal loss (diuretics)

Metabolic alkalosis

36
Q

What is the treatment of hypokalaemia?

A

Treat underlying causes
K+ replacement - IV or oral
If due to increased aldosterone => potassium sparing diuretics or block action of aldosterone

37
Q

What are the clinical features of hypokalaemia?

A

Heart; arrhythmias
GI; neuromuscular dysfunction, paralytic ileus
Skeletal muscle; muscle weakness
Renal; nephrogenic DI

38
Q

What is urinary incontinence?

A

A condition in which a pt loses the ability to control micturition
Occurs when the bladder pressure is greater than the urethral sphincter pressure

39
Q

What is stress incontinence?

A

Involuntary leakage on increased intra-abdominal pressure eg coughing, sneezing

40
Q

What is urge incontinence?

A

Involuntary leakage preceded by urgency

41
Q

What is mixed incontinence?

A

A mix of stress and urge incontinence

42
Q

What investigations are done for incontinence?

A 
Urine dipstick
Non-invasive urodynamics; frequency volume chart, bladder diary 
Invasive urodynamics 
Pad tests 
Cystoscopies
43
Q

What is nephrotic syndrome?

A

Injury to podocytes or basement membrane resulting in proteinuria, hypoalbuminaemia & oedema

44
Q

What causes nephrotic syndrome?

A

Primary renal disease:
Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis

Secondary renal disease:
DM, SLE, amyloidosis

45
Q

How is nephrotic syndrome managed?

A

Oedema;
Diuretics, salt & fluid restriction

Increased cholesterol;
Statins

Proteinuria;
ACE-I

46
Q

What is nephritic syndrome?

A

Damage to endothelium or vessel resulting in haematuria (can get some proteinuria) and hypertension

47
Q

What causes nephritic syndrome?

A

Inflammation of glomerular basement membrane
Anti-GBM, vasculitis
Post infection

48
Q

How is nephritic syndrome managed?

A

HTN/proteinuria/oedema;
ACE-i, salt & fluid restriction, diuretics

Treat underlying cause; generally immunosuppression

49
Q

What is glomerulonephritis?

A

Inflammation of glomeruli

Can cause damage to capillary endothelium, basement membrane, mesangial cells or podocytes

50
Q

What is the clinical presentation of glomerulonephritis?

A

Asymptomatic proteinuria or haematuria

Nephrotic syndrome

51
Q

What is systemic lupus erythmatosus?

A

A type of vasculitis
Autoimmune condition which can affect multiple systems
Can cause either nephrotic or nephritic syndrome

52
Q

What is diabetic nephropathy?

A

A glomerulonephropathy

Most common cause of end stage renal disease

53
Q

What changes occur in diabetic nephropathy?

A 
Hyperfiltration 
Glomerular basement thickening 
Mesangial expansion 
Podocyte injury 
Glomerular sclerosis
54
Q

What occurs in hyperfiltration in diabetic nephropathy?

A

More NaCl & glucose is filtered out => increased reabsorption in PCT
Less salt is delivered to the macula densa
Makes macula densa thinks there is low perfusion => release of renin

55
Q

What are signs and symptoms of diabetic nephropathy?

A

Hyperfiltration & hypertrophy => increased GFR
Microalbuminuria (earliest stage, not picked up on dipstick)
Overt proteinuria develops over many years => progressive drop in GFR => ESRD

56
Q

What is the primary prevention of diabetic nephropathy?

A

Tight blood glucose control

Tight blood pressure control

57
Q

How are microalbuminuria and proteinuria in diabetic nephropathy managed?

A 
Inhibition of RAAS;
Reduces glomerular hyperfiltration, slows progression 
Blood pressure kept below 130/80 
Statins 
Moderate protein intake 
Tight blood glucose control
58
Q

What host factors increase risk of a UTI?

A

Shorter urethra in women
Obstruction from large prostate, pregnancy, stones or tumour
Neurological problems eg incomplete bladder emptying and residual volume
Ureteric reflex

59
Q

What features of bacteria contribute to a UTI?

A

Fimbriae allow attachment
Haemolysis damages host membrane
Urease breaks down urea => favourable environment
K antigens provide protection against host defences w/ polysaccharide capsule

60
Q

What are some clinical syndromes associated with a UTI, and what are their features?

A

Cystitis;
Lower UTI
Presents with frequency, urgency and dysuria

Acute pyelonephritis;
Upper UTI
Systemic therefore pt has a fever
Presents w/ renal angle tenderness

Chronic pyelonephritis

Asymptomatic bacteriuria;
Usually doesn’t need treatment
However needs to be treated in pregnant women

61
Q

What is an uncomplicated UTI?

A

An infection by a usual organism in a pt with a normal urinary tract (no catheter) and normal urinary function
Can occur in males and females of any age

62
Q

What is a complicated UTI?

A

When the pt has one or more predisposing factors to persistent infection, recurrent infection or failure of treatment

Abnormal urinary tract; vesicoureteric reflux, indwelling catheter
Virulent organism; S. aureus
Impaired host defences; poorly controlled diabetes, immunosuppression
Impaired renal function

Typically affects men, children and pregnant women

63
Q

What investigations are done for a UTI?

A

Dipstick tests;

64
Q

What is the treatment for UTIs?

A

Uncomplicated;
3 day course of trimethoprim

Complicated;
5-7 day course of trimethoprim, nitrofurantoin or cephalexin

Pyelonephritis;
14 day course of abx
IV initially unless pt is well enough for PO

65
Q

What are the different types of ureteric obstruction?

A

Intraluminal;
Stones, sloughed papilla, clots

Intramural;
Pelvic-ureteric junction obstruction, congenital
Upper TCC
Benign strictures, TB, surgical injury

Extraluminal;
Retroperitoneal malignancy, metastases to lymph nodes
Retroperitoneal fibrosis
Tumour => direct obstruction (bladder or prostate ca)

66
Q

What is acute renal colic?

A

Flank pain radiating to groin which comes and goes
Usually unilateral
Generally caused by a stone, but can be caused by clots or sloughed papilla
Can present w/ infection - pyonephrosis

67
Q

What is pyonephrosis?

A

Infection of the collecting system in kidneys
Pus collects in renal pelvis and causes distension of the kidney
Can cause kidney failure

68
Q

How does chronic ureteric obstruction typically present?

A

Generally painless, typically an incidental finding

Can present with:
Renal failure, pyonephrosis

69
Q

What is obstructive uropathy?

A

Renal impairment due to uni- or bilateral ureteric obstruction
Results in high pressure chronic retention

Can result in hyperkalaemia

70
Q

How are upper urinary tract obstructions diagnosed?

A

USS confirms hydronephrosis
CT can show cause of obstruction

Functional tests;
Diuretic renography,

71
Q

How can the upper urinary tract be drained in when there is obstruction?

A

JJ stent;
Facilitates drainage to bladder
Good for pts w/ clotting disorder
Internal

Nephrostomy;
Direct tube from kidney to bag
Good for pts who can’t have GA

72
Q

What happens in a pelviureteric junction obstruction?

A

Dilation of the renal pelvis and calyces
Congenital condition, can present w/ hydronephrosis on antenatal USS
However can present whenever

73
Q

What are symptoms in pelviureteric junction obstruction?

A

Can be asymptomatic

Loin pain caused by intermittent blockage eg alcohol consumption => swelling of renal pelvis

74
Q

What is treatment for pelviureteric junction obstruction?

A

Pyeloplasty

75
Q

What are causes of retroperitoneal fibrosis, and how does it affect the urinary tract?

A

Causes:
Idiopathic, malignancy, AAA, autoimmune conditions, drugs

Scar tissue interferes with peristalsis of ureters

76
Q

What is the treatment for retroperitoneal fibrosis?

A

Stents to decompress
Need to exclude malignancy
Steroids/immunosuppression

77
Q

What are some causes of intravesical obstruction?

A 
BPH (most common) 
UTI
Neurological dysfunction 
Surgery 
Drugs 
Urethral strictures 
Pelvic masses (fibroids, tumours)
78
Q

How does acute urinary retention present, and what is the treatment?

A

Painful inability to void

Treatment:
Catheterise and record residual volume 
Treat obvious cause 
α-blocker in men relaxes prostate
TURP
79
Q

How does chronic urinary retention present?

A

High pressure:
Abnormal U&E
Hydronephrosis

Low pressure;
Normal urinary function
No hydronephrosis

80
Q

How is chronic urinary retention treated?

A

Catheterise and record residual volume

Monitor for post-obstructive diuresis;
Salt and water overload
Causes diuresis
Can lead to salt and water imbalance => fluid replacement

Year 2 Conditions (3 decks)

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