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Kofi: Pure Clinical Sem 3 > Urinary: Obstruction > Flashcards

Urinary: Obstruction Flashcards

1
Q

What is the management of a patient with Haematuria?

A
  • Stabilise the patients
  • Blood
  • 3 way catheter and irrigation
  • CT angiogram if significant bleed
  • If it doesn’t settle then intervention such as cystoscopy/interventional radiology
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2
Q

Which substances presents with false negatives?

A

-Vitamin C

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3
Q

What is the mechanism for acute urinary retention?

A
  • Bladder outlet obstruction
  • Low bladder contractile power
  • Interrupted sensory or motor innervation of bladder and/or sphincter
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4
Q

What are investigations done for acute urinary retention?

A
  • History and examination
  • Bloods
  • Bladder scan
  • Neurological documentation important
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5
Q

What are the causes of acute urinary retention in men?

A
  • BPH
  • Prostate cancer
  • Urethral stricture
  • Prostatic infection
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6
Q

What are the causes of acute urinary retention in women?

A
  • Prolapses
  • Masses
  • Post botox
  • Fowler’s syndrome
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7
Q

What are the causes of acute urinary retention in both males and females?

A
  • Clots
  • Drugs
  • Pain
  • Major abdominopelvic surgery
  • Spinal cord compression
  • Spinal cord injury
  • Spina bifida
  • Urinary tract infections
  • Constipation
  • Urethral damage/rupture
  • Diabetic nephropathy
  • Neurological degeneration
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8
Q

What are management options for acute urinary retention?

A
  • Urethral Catheterisation
  • Suprapubic (if difficult)
  • Preferable as long-term condition
  • Risk of bowel perforation with insertion
  • Should have ultrasound if laparotomy
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9
Q

What differentiates acute urinary retention from chronic?

A

It is very painful

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10
Q

Where can stones from in the urinary tract?

A
  • Renal
  • Ureteric (constrictions)
  • Bladder (due to incomplete emptying)
  • Prostatic calculi (no clinical significance )
  • Urethral calculi in men (rare)
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11
Q

What are the effects of a ureteric obstruction?

A
  • Therefore, a unilateral obstructive stone globally impairs renal function.
  • Can also get bilateral calculi of kidney or ureters
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12
Q

What are features of renal and ureteric colic?

A
  • Causes a lot of pain
  • Present with renal colic
  • Loin to groin pain
  • Testicular pain sometimes
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13
Q

What are the investigations dow for renal and ureteric colics?

A
  • History
  • Examination
  • Urinalysis
  • CT KUB non-contrast
  • Abdominal X-ray
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14
Q

What are the management options for renal and ureteric colics?

A
  • Conservative management
  • Non- Invasive management (Shockwave lithotripsy)
  • Invasive management (Cystoscopy + lasertripsy, Percutaneous nephrolithotomy, Uteroscopy)
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15
Q

What are signs and symptoms of ureteric stones?

A
  • Very painful
  • Impairment in renal function
  • May get stuck
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16
Q

What are the management options for ureteric stones?

A

Symptoms and stone size guide treatment

  • Most stone will pass if small enough (less than 4mm)
  • Pain mandates a stent and sometimes primary URS + lasertipsy
17
Q

What is the pathophysiology of urosepsis?

A
  • Blocked upper renal tract to ureteric orifice
  • Standing column of septic urine in the upper urinary tract including the kidney is called pyelonephroisis
  • Infection can spread to blood
18
Q

What is the management for urosepsis?

A
  • Stenting
  • Nephrostomy

To drain urine

19
Q

What are causes of AKI?

A
  • Pre-renal
  • Renal vein
  • Renal artery
  • Small vessel disease – intrinsic
  • Glomerular disease - intrinsic
  • Acute tubular necrosis – intrinsic
  • Acute interstitial nephritis - intrinsic
  • Intratubular obstruction
  • Post renal obstruction
20
Q

What is imaging undertaken in AKI?

A
  • Ultrasound – perform if obstruction suspected. Not need for pre-renal/ATN
  • Chest X-ray – to look for fluid overload
21
Q

Why is biopsy taken if AKI suspected?

A
  • Pre-renal and post-renal AKI ruled out
  • A confident diagnosis of ATN cannot be made
  • Systemic inflammatory symptoms/sign are present
22
Q

What is the pathophysiology of pre-renal failure in AKI?

A
  • Actual GFR is reduced due to decreased renal blood flow.
  • No cell damage so kidney works hard to restore blood flow
  • Avidly reabsorbs salt and water (ADH + Aldosterone)
  • Responds to fluid resuscitation
23
Q

What are causes of pre-renal failure in AKI?

A
  • Hypovolaemia – blood loss, fluid loss
  • Systemic vasodilation – sepsis, cirrhosis, anaphylaxis
  • Pre-glomerular vasoconstriction – sepsis, NSAIDs
  • Post glomerular vasodilation – Ang2 antagonist, ACE inhibitors
24
Q

How does the kidney attempt to correct pre-renal failure and what happens if it fails?

A
  • In mild hypo-perfusion, autoregulation ensures renal blood flow preserved
  • Dilation of afferent arteriole - prostaglandin
  • Constriction of efferent arteriole - RAAS
  • If compensatory responses overwhelmed, AKI occurs
  • Occurs below 80mmHg or higher if hypertensive
25
Q

How do ACE inhibitor and NSAIDs affect renal perfusion to cause pre-renal failure?

A
  • NSAIDs acts against vasodilators (prostaglandins)
  • ACE inhibitors act against formation of Ang 2
  • The intrinsic auto-regulatory mechanism are overridden
26
Q

What is the pathophysiology in acute tubular necrosis?

A
  • Cells are damaged which cannot be reversed immediately but can be eventually if treated
  • Damaged cells cannot reabsorb salt and water efficiently or expel excess water
  • Proximal tubule is particularly at risk of ischaemia if pre-renal AKI persists
27
Q

What are the causes of acute tubular necrosis?

A
  • Ischaemia
  • Nephrotoxins
  • Sepsis
  • Thombotic-microangiopathy
  • Acute tubule-interstitial nephritis
28
Q

What examples of endogenous nephrotoxins?

A
  • Myoglobin
  • Urate
  • Bilirubin
29
Q

What are examples of exogenous nephrotoxins?

A
  • Endotoxin
  • X-ray
  • Drugs
  • Poisons
30
Q

How can myoglobin cause damage to the kidney?

A

-Due to muscle necrosis leading to rhabdomyolysis. Myoglobin filtered at glomerulus and is toxic to tubule cells. Can also cause obstruction

31
Q

What can increase myoglobin?

A
  • Crush injury
  • AKI in wars and natural disasters
  • Drug users (unconscious so don’t move)
  • Elderly - fall
32
Q

What is the pathophysiology of thrombotic microangiopathy?

A
  • Caused by endothelial damage
  • Platelet thrombi
  • Partial obstruction of small arteries
  • Destruction of Red Blood cells
  • Leads to micro-angiopathic anaemia
33
Q

What can cause acute tubule-insterstitial nephritis?

A
  • Toxin induced (Many drugs)

- Infections (Caused by an inflammatory response)

34
Q

What is the pathophysiology of post renal failure?

A
  • Obstruction with continuous production
  • Rise in intraluminal pressure
  • Dilatation of renal pelvis (hydronephrosis)
  • Decrease in renal function
35
Q

What are the causes of post renal failure?

A
  • Within the lumen (stones, blod clot, tumours)
  • Within the wall (congenital megareter, stricture post TB)
  • Pressure from outside (enlarge prostate, tumour, aortic aneurysm, ligation of ureter)
36
Q

How is AKI managed?

A
  • Treat volume overload (restriction of sodium and water, diuretic)
  • Treat hyperkalemia (restrict dietary K, Calcium gluconate)
  • Treat acidosis
  • Dialysis
37
Q

When is dialysis used in the AKI?

A
  • High K+ refractory to treatment
  • Metabolic acidosis where the sodium bicarbonate is not appropriate
  • Fluid overlaod refractory to diuretic
  • Signs of uraemia
  • Presence of dialysable nephrotoxin

Kofi: Pure Clinical Sem 3 (44 decks)

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