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Finals > Renal > Flashcards

Renal Flashcards

1
Q

Defintion & Stages of CKD

A

Def: markers of kidney damage and/or reduced kidney function over 3mths or more

Stages:
G1: eGFR >90
G2: eGFR 60-89
G3: eGFR 45-59 (A) 30-44 (B)
G4: eGFR 15-29
G5: eGFR <15

A1: ACR <3 mg/mmol
A2: ACR 3-30
A3: ACR >30

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2
Q

Causes/Risk Factors for CKD

A 
Hypertension
Diabetes
Older Age (RF)
Obstructive nephropathy
Ischaemic nephropathy (due to vascular disease)
Glomerulopathies
Inherited kidney disease e.g. PKD
Tubulointerstitial disease
Medications e.g. Lithium
Smoking (RF)
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3
Q

Clinical presentation of CKD

A

Generally asymptomatic
Non-specific sx tend to start when eGFR <45

Symptoms: Anoxeria, nausea, weakness, fatigue, muscle cramps, pruritus, dyspnoea

Signs: fluid overload, pallor (anaemia), hypertension

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4
Q

Investigations for CKD

A

U&Es - eGFR, hyperK
Urinalysis - dipstick for haematuria (consider 2WW), ACR
Renal USS +/- biopsy - if considering PKD or obstructive picture

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5
Q

Management of CKD

A
  1. Renoprotection - BP control (ACEI & aim <140/90), statin therapy, antiplatelet therapy & lifestyle (stop smoking)
  2. Treat complications - anaemia (EPO stimulating agents or Fe infusions), hyperK (monitor U&Es, CKD & ACEI both can cause), bone & mineral disorders (VitD supplements, low phosphate diet, bisphosphonates for osteoporosis)
  3. RRT - dialysis, peritoneal dialysis or renal transplant
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6
Q

Definition & Criteria for AKI

A

Acute decline in renal function occurring over hours/days
Rise in Cr >25 umol/L in 48hrs or >50% in 7days
Urine output <0.5ml/kg/hr for >6hrs

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7
Q

Causes of AKI

A

Pre-renal; hypovolaemia, reduced cardiac output, systemic vasodilation

Renal; vascular (thromboembolic, dissection, stenosis), glomerular, tubulointerstitial (ATN)

Post-renal; obstruction (stones, malignancy, BPH)

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8
Q

Investigations for AKI

A

History (meds) & examination (fluid status)

Bloods - guided by cause (FBC, U&Es, ABG)

Urinalysis for protein, blood, leucocytes, nitrites and glucose.

Leucocytes and nitrites suggest infection
Protein and blood suggest acute nephritis (but can be positive in infection)
Glucose suggests diabetes

Ultrasound of the urinary tract is used to look for obstruction. It is not necessary if an alternative cause is found for the AKI.

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9
Q

Management of AKI

A

Prevention - hydration& med reviews

Treat/reverse cause: hydrate (pre renal), stop nephrotoxic meds (renal), reverse obstruction (post renal)

Consider specialist input if AKI stage 3 or post renal AKI

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10
Q

RENAL DRS 25 Mnemonic

A 
Record baseline Cr & regular U&Es
Exclude obstruction
Nephrotoxic drugs stopped
Assess fluids status
Losses +/- cauterisation 
Dipstick - blood/protein
Review medications
Screen - acute renal screen
25 - rise in Cr = AKI
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11
Q

Urinary Calculi - composition, clinical features

A

Types: calcium phosphate/oxalate (80%), magnesium ammonium phosphate (10-20%)

• Can be asymptomatic 
• Loin to groin flank pain a/w nausea & vomiting 
	○ May also radiate to testicles, abdominal area
• Sharp, sudden, severe pain - may be intermittent 
• Haematuria
	○ can be microscopic or frank
• Dysuria Urinary frequency/urgency/retention
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12
Q

Urinary Calculi - investigations & management

A

Bedside
• Observations - HR, BP, temp (check if septic)
• Examination
• Urinalysis - dipstick, microscopy, C&S (r/o UTI & check for haematuria)

Bloods
• FBC inc WCC
• U&Es (check renal function, hydration status, AKI)
• Calcium, urea & phosphate levels

Imaging
• X-ray KUB - 90% of stones are radio-opaque so should show on X-ray
• USS - can be used to show any dilatation or if radiation is CI

• Conservative/medical - observation, analgesia, fluids (IV or oral), alpha blockers to help with ureteric relaxation 
	○ Suitable if stones are <5mm, should pass 
• Removal of calculi - ureteroscopy 
	○ Indicated if obstructed stone or continued pain or pyrexia 
• Lithotripsy - non invasive, break up stone into smaller fragments to allow it to pass if stone <2cm & no obstruction
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13
Q

Definition of Nephrotic Syndrome

A

Syndrome with a triad of heavy proteinuria >3.5g/day, hypoalbuminemia and oedema

Structural damage to basement membranes leads to loss of protein & albumin

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14
Q

Clinical Features of Nephrotic Syndrome

A 
Signs of fluid overload 
Fatigue
SOB
Peripheral oedema
Pulmonary oedema
Swelling of face, abdomen & genitals
Foamy urine - due to protein 	
Poor appetite
Haematuria
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15
Q

Investigations - Nephrotic Syndrome

A

Diagnosis based on presence of classical triad of symptoms
• Urinalysis
• Bloods - FBC, U&Es, LFTs (albumin), glucose, lipids, ESR/CRP
• Renal biopsy - usually needed to determine diagnosis

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16
Q

Management - Nephrotic Syndrome

A 
Treat oedema
	• Fluid & Na restriction
	• Diuretics - furosemide
Treat cause
	• For example - minimal change --> high dose steroids +/-immunosuppression

Monitor
• Blood pressure
• U&Es
• Fluid chart & weight

Manage complications

17
Q

Complications - Nephrotic Syndrome

A 
• Thromboembolic disease 
		○ Anticoagulation
	• Hyperlipidaemia 
		○ Statin therapy 
	• Recurrent infections
	• AKI/renal damage
18
Q

Definition & Aetiology - Nephritic Syndrome

A

the presence of haematuria, variable proteinuria, renal impairment, and hypertension.

Post Streptococcal Glomerulonephritis (esp. Group A beta-Haemolytic Streptococcus)
IgA Nephropathy - Berger’s Disease - the commonest Glomerulonephritis
Vasculitis/SLE

19
Q

aetiology of polycystic kidney disease & clinical presentation

A

Inherited AD condition - mutations in PKD1 (80%) & PKD2 (20%)
May be asymptomatic, often presents in 30/40s can be incidental

Flank/abdo/back pain - large cysts or ruptures
Haematuria - ruptures
Polyuria/polydipsia/nocturia

Large palpable kidneys
Hepatomegaly
Hypertension

20
Q

Investigations & Management of Polycystic kidney disease

A

Bloods (U&Es, Cr, eGFR) & urinalysis (dipstick, C&S, microscopy & ACR)
Diagnosis on imaging - CT/USS will show multiple cysts & enlarged kidneys, >2 cysts on patients <30

BP control (ACEi) - slows decline of renal function 
RRT/dialysis - by 60s half of p
21
Q

Risk factors for Pyelonephritis

A

Obstructed urinary tract, including BPH
Spinal cord injury, resulting in a neuropathic bladder

Female gender (due to a short urethra)
Indwelling catheter or ureteric stents / nephrostomy tubes in-situ
Structural renal abnormalities, such as vesico-ureteric reflux (VUR)

Diabetes mellitus, corticosteroid use, HIV infection (untreated)

Renal calculi
Sexual intercourse
Oestrogen depletion (menopause)
22
Q

Clinical Features - Pyelonephritis

A

fever, unilateral loin pain (or rarely bilateral), and nausea & vomiting, typically developing over the course of 24-48 hours.

(frequency, urgency, dysuria), as well as visible (or non-visible) haematuria.

23
Q

Differential Dx - Pyelonephritis

A

potential ruptured AAA.

Other differentials include renal calculi, acute cholecystitis, ectopic pregnancy or pelvic inflammatory disease, lower lobe pneumonia, or diverticulitis

24
Q

Investigations - Pyelonephritis

A

Bedside
• Observations - temp (suspicion of sepsis)
• Urinalysis - dipstick, C&S, microscopy
• Pregnancy test - if any lady of child bearing age
Bloods
• FBC - WCC, Hb
• CRP/ESR - inflammation
• U&Es - dehydration, renal function, electrolytes
• LFTs
• Amylase - r/o pancreatitis
Imaging
• All cases of pyelonephritis should have a renal US scan performed for evidence of obstruction (as an infected obstructed system is a urological emergency)
• If obstruction is suspected, non-contrast CT imaging of the renal tract should be performed (CT KUB).

25
Q

Management - Pyelonephritis

A

Start empirical antibiotics based on local protocols and IV fluids as appropriate
Tailor once sensitivities are available

Analgesia and anti-emetics

Whilst many uncomplicated cases can often be treated in the community, consider admission in those cases who are clinically unstable, significant dehydration, or with co-morbidities such as diabetes mellitus, renal transplant graft, immunocompromised

26
Q

IgA nephropathy - pathophysiology, S&S, investigations & management

A

Most common primary glomerulonephritis - occurs when IgA immune complexes deposit in kidney in the renal mesangium, causing damage

Macroscopic haematuria (a/w infections e.g. URTI, gastroenteritis), asymptomatic micro haematuria & proteinuria, hypertension, loin pain, low grade fever

observations(BP), urine dipstick & microscopy, bloods (baselines n U&Es), USS KUB
diagnosed via kidney biopsy - H&E stain, immunofluorescence, electro micro

lifestyle measures (w/l, stop smoking, diet), ACEI/ARB to control BP, steroids no longer used routinely as shown to be no benefit - reserved for special cases & in those where renal function is deteriorating significantly

Finals (16 decks)

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