Deck 4 - GU Flashcards
- 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)
- 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
- Q. What is daily fluid intake for relatively sedentary lifestyle?
A. 1.5-2L for a relatively sedentary lifestyle
- Q. Name two causes of fluid loss
A. Heat, burns, vomiting, diarrhoea etc
- 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
- 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
- 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
- Q. How can kidney function be investigated?
A. Blood tests: creatinine
B. eGFR, urine output
- 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
- 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
- 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
- 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.
- 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
- 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
- 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
