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Flashcards in Deck 4 - GU Deck (19)
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1. Q. Describe the fluid distribution in the body

A. Total body volume = 42 L, 60% body weight
B. Intracellular fluid = 28L (2/3 of total body weight)
C. Extracellular fluid = 14L (1/3 of total body weight), interstitial fluid (11L, 80%) + plasma volume (3L, 20%of ECF)


1. Q. Describe the ion distribution in the body

A. Plasma: mainly Na+, Cl-, (some K+, Mg2+, protein and HCO3-)
B. Interstitiual: mainly Na+, Cl- (some K+, Ca, Mg2+, protein and HCO3-)
C. Intracellular: K+, Ca2+ (Some Mg+, Na+, protein, Cl+, SO42-, PO43-, HCO3-)
D. Extracellular = intersitital + plasma


1. Q. What is daily fluid intake for relatively sedentary lifestyle?

A. 1.5-2L for a relatively sedentary lifestyle


1. Q. Name two causes of fluid loss

A. Heat, burns, vomiting, diarrhoea etc


1. Q. Name two ways fluid balance may be assessed initially, name two associated symptoms (CKD)

A. Pulse, BP, JVP, tissue turgor, tongue, urine output, weight
B. Fluid assessment: vital signs, fluid balance charts, stool charts, weight charts
C. Thirst, dizziness/breathlessness, leg oedema


1. Q. Name two patients at risk of hypovolaemia and two patients at risk of hypervolemia. Describe the symptoms and management of each.

A. Hypovolaemia: elderly, ileostomy/colostomy, short bowel syndrome, bowel obstruction, diuretics
Tx: Oral/IV fluids
B. Hypervolemia: acute kidney injury, chronic kidney disease, HF, liver failure
Symptoms: SOB, pulmonary oedema, leg oedema
Tx: Diuretics oral/IV e.g. furosemide, bumetanide, spironolactone, metolazone, fluid restriction, treat reversible cause


1. Q. What is acute kidney injury? What may cause it?

A. Sudden onset, sustained decline in renal function: associated with nitrogenous water, electrolyte and fluid balance disorders
B. Based on: serum creatinine, urine output, need for dialysis

C. Causes:
a. Pre-renal: decreased renal perfusion
F - Failure-cardiac/liver/skin (burns)
I - Infection/Sepsis + Intrarenal haemodynamics (NSAIDs, ACEi)
R - Red cell haemorrhage: Volume losses
S - Sick –GI losses: Stenosis (RAS) - Poor perfusion
T – Thrombosis
a. Intrinsic renal: renal parenchyma damaged
a. Vascular: large (renal artery/vein thrombosis, cholesterol emboli), small (vasculitis, HUS/TTP, malignancy HT)
b. Glomeruli: glomerulonephritis, nephrotic syndrome
c. Tubulointerstitum: acute interstitial nephritis (drugs), cast nephropathy (myeloma), ischemia, acute tubular necrosis
d. Vasculitis: may be renal limited or systemic
e. Haemolytic uraemia syndrome: thrombotic microangiopathy, haemolytic anaemia
f. Nephrotic syndome
b. Post-renal: outflow obstruction (tumour, stones, retroperitoneal fibrosis – ureter, bladder prostate)
D. Associated with: diarrhoea, haematuria, haemoptysis, hypotension, urine retention
E. Consequence: fluid excess – SOB and oedema
F. Present in 20-60% critically ill ots


1. Q. How can kidney function be investigated?

A. Blood tests: creatinine
B. eGFR, urine output


1. Q. What occurs in acute tubular necrosis (acute tissue injury)

A. Very common, esp. in hospital patients
B. Oliguric/non-oliguric
A. Decreases in renal perfusion


1. Q. Name 3 common PCs of acute kidney injury (AKI)

A. Uraemic: lethargy, nausea, anorexia, itch, confusion
B. Systemic: rash, joint pains, red eyes, nasal stuffiness/bleeding, haemoptysis
C. Ask: if reduced urine output/adequate fluid intake
D. PMH: comorbidities/risk factors e.g DM, CKD, prostate cancer, elderly
E. DH: current (dosing – may need to reduce/stop!), Recent change in meds, INCLUDE over-the-counter


1. Q. Name 5 features of examination of a pt with AKI

A. Volume/haemodynamic status: Pulse, JVP, Blood pressure (postural), Oedema (sacral/peripheral), skin turgor, Urine volumes (if available)
B. Urinalysis
C. Important: serum creatinine, urine output
D. Airways: O2 sats, RR, chest (haemoptysis)
E. Pericardial rub (if very uraemic)
F. Abdomen: suprapubic percussion dull
G. Skin rash


1. Q. What changes may be seen on ECG of an AKI patient? Why?

A. Hyperkalemic ECG changes:
a. Mild to moderate: prolongation of PR interval and development of peaked T waves
b. Severe: widening of QRS complex, ECG complex may evolve to a sinusoidal shape
B. Elevated potassium: increases activity of K+ channels and speeds up membrane repolarization. Also causes an overall membrane depolarization that inactivates many sodium channels – causing sluggish conduction of the electrical wave around the heart = small P waves and widening of QRS.


1. Q. What are urinary stones formed from?

A. 80%: ca2+ based, oxalate, phosphate
B. 10% uric acid (more common in obese/female patients)
C. 5-10% struvite – infection stones
D. 1% cysteine – congenital
E. Rare – drug stones, including indinavir, ephedrine


1. Q. How can stones be prevented? Name 3 ways

A. Over-hydration, low sodium diet, normal dairy intake, healthy protein intake, reduce BMI (metabolic syndrome), active lifestyle (PTH?)
B. Uric acid stones: only form in acidic urine, de-acidification of urine ton aim for 7-7.5 pH
C. Cystine stones: excessive over-hydration, urine alkalinisation, cysteine binders e.g. captopril, penicillamine


1. Q. Name 5 features of stone presentation

A. Asymptomatic
B. Loin pain
C. “renal colic” – rapid onset unilateral loin pain, unable to look comfortable, writhing, radiates from loin to groin, associated nausea and vomiting, spasmodic/colicky, worse with fluid loading, classically severe 12/10, “worse than labour”
D. UTI symptoms: dysuria, strangury, urgency, frequency
E. Recurrent UTIs
F. Haematuria: visible and non-visible


1. Q. What imaging technique is most appropriate for ureteric colic?

A. Non-contrast CT: 99% sensitivity, 90% specific
B. Kidney, ureter, bladder XR (KUBXR): historical first line, only 50-50 sensitivity (if stone is visible then greatly aids follow up – avoid repeated CTs)
C. (MRI has limited value as stones not seen – role in pregnancy)


1. Describe the treatment of ureteric colic

A. Analgesia – NSAIDS rectally, opiates
B. Antiemetics
C. +- admit, +-IV fluids, (may make pain worse as diuresis ensures)
D. Observe for sepsis!


1. Name two complications of ureteric colic

A. Migration into ureter
B. Larger stones occlude calyces and/or PUJ
C. Chronic renal damage: abscecss, fistulae, xanthogranulomatous pyelonephritis (chronic inflammatory disorder of the kidney, destructive mass that invades the renal parenchyma)


1. Q. Describe the treatment of ureteric/bladder stones

A. Ureteric stone: conservative, drainage if sepsis, Extracorporeal shock wave lithotripsy – acoustic pulse (ESWL), ureteroscopy, laparoscopy (open surgery)
B. Bladder stone: conservative, endoscopy, laparoscopic (open surgery)

13. CKD: Oncotic pressure – what affects it? Why may Cr rise? Why may CKD patients by oligouric/anuric??