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Year 3 - Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Acute Kidney Injury (AKI) - state the following:
- Pathophysiology (outline causes later)
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Defined as an acute reduction in renal function
- Pre-renal, renal and post-renal causes
- Classification based on serum creatinine vs baseline OR urine output

Presentation:
- Reduced renal function
- Measured by increased serum creatinine OR reduced renal output
- Suspect in unwell patients with declining renal function or urine output

Investigations:
- Routine bloods including FBC, U&Es, LFTs, CRP, creatinine kinase
- Blood pressure
- Bladder scan
- Urine dipstick and MC&S
- ECG
- USS KUB
- CT / Chest x-ray

Management:
Treat the underlying cause!!
- IV fluids if hypovolaemic
- Refer to specialist if renal/intrinsic cause, if there is no clear cause or if complications develop
- Stop any nephrotoxic medications e.g. NSAIDs or antihypertensives
- Relieve obstructions if possible e.g. catheter

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2
Q

List some potential causes of raised urea

A

Usually a sign of poor kidney function
- AKI (including dehydration)
- CKD
- GI haemorrhage
- Medications

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3
Q

Outline the causes of acute kidney injury

A

Pre-renal (reduced perfusion):
- Hypotension: hypovolaemia / dehydration / anaphylaxis / sepsis
- Congestive heart failure
- Anti-hypertensives e.g. ACEi
- NSAIDs
- Renal artery stenosis

Renal (intrinsic):
- Acute tubular necrosis
- Glomerulonephritis
- Interstitial nephritis
- Vasculitis

Post-renal (obstructive):
- Ureteric strictures
- Masses leading to obstruction
- BPH
- Renal calculi (bilateral)
- Retro-peritoneal fibrosis

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4
Q

Outline the classification for AKI

A

Classification:
- Assessed by measuring serum creatinine compared to baseline or by urine output
- Chose the worst one

Serum creatinine:
Stage 1: serum creatinine 1.5 - 2 X baseline
Stage 2: serum creatinine 2 - 3 X baseline
Stage 3: serum creatinine > 3 X baseline

OR

Urine output:
Stage 1: urine output < 0.5mls/kg/hr (35ml/hr) for 6-12 hrs
Stage 2: urine output < 0.5mls/kg/hr (35ml/hr) for > 12 hrs
Stage 3: urine output < 0.3mls/kg/hr (20ml/hr) for > 24 hrs OR anuria for > 12 hrs

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5
Q

Outline the risk factors for AKI

A
  • Increased age
  • Cognitive impairment
  • Chronic kidney disease
  • Heart failure
  • Diabetes
  • Liver disease

Use of nephrotoxic medications:
- Anti-hypertensives
- NSAIDs
- Contrast medium (for CT scans)

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6
Q

Outline the 4 biochemical complications of an AKI

A
  • Hyperkalaemia (can’t secrete K via ROMK)
  • Metabolic acidosis (can’t produce sufficient HCO3)
  • Fluid overload (can’t fluid balance)
  • Uraemia (can’t be cleared from blood)
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7
Q

Chronic Kidney Disease (CKD) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management principles

A

Pathophysiology:
- Chronic deterioration in renal function
- Deterioration is permanent and progressive
- Classification based on eGFR (G SCORE) OR urine albumin:creatinine ratio (A SCORE)

Presentation:
May be asymptomatic and diagnosed on routine testing
- Pruritus
- Pallor
- Oedema
- Hypertension
- Nausea / loss of appetite
- Muscle cramps
- Peripheral neuropathy

Investigations:
- Measure eGFR and calculate urine albumin:creatinine ratio
- Urine dipstick to check for haematuria
- Ultrasound to check for causes including haematuria, CKD, obstruction

Management principles:
- Slow progression
- Reduce complications and treat complications
- Reduce risk of cardiovascular disease

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8
Q

Outline some ways to reduce the progression of chronic kidney disease and to reduce the risk of complications

A

Reduce CKD progression:
- Good diabetes control
- Good hypertension control
- Manage glomerulonephritis

Reduce risk of complications:
- Be healthy (no smoking, reduce alcohol, exercise)
- Diet modifications: sodium, potassium, fluid intake and phosphate
- Statins for primary prevention of cardiovascular disease (Atorvastatin 20mg)

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9
Q

Outline some long term complications of CKD and how they are treated

A

Anaemia of chronic disease:
Treatment: exogenous erythropoietin and iron supplements

Renal bone disease:
Treatment: active forms of vitamin D and low phosphate diet

Cardiovascular disease:
Treatment: primary prevention (Atorvastatin 20mg) and control risk factors e.g. hypertension, diabetes

End-stage renal failure (ESRF)
Treatment: dialysis or renal transplantation

Metabolic acidosis:
Treatment: oral sodium bicarbonate

Peripheral neuropathy (uraemic neuropathy):
Treatment: neuropathic pain relief

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10
Q

Outline the pathophysiology of renal bone disease

A

Key issue = reduced functioning of kidneys
(1) High phosphate levels due to reduced clearance
(2) Reduced vitamin D activation at the kidneys
(3) Low Ca (due to reduced vitamin D)

Results in:
- Low Ca and high phosphate detected by the parathyroid glands
- Increased PTH production
- Bone resorption = renal bone disease

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11
Q

Describe the 2 main types of dialysis, including subtypes

A

Peritoneal dialysis:
- Uses peritoneal membrane as a filtration membrane
- Requires a Tenckhoff catheter to insert and remove the dialysis solution
- Can be done at home
1) Continuous ambulatory - fluid in all the time, replaced at regular intervals (manual exchange)
2) Automated - fluid in overnight replaced continuously by a machine (automated exchange)

Haemolysis dialysis:
- Filtered by a haemodialysis machine at the hospital
- Generally 3 days a week, for approx. 4 hrs each time
- Can use either an arterio-venous fistula or a tunneled cuffed catheter

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12
Q

Outline the indications for acute dialysis

A

Basically if the patient is symptomatic (matters less about the eGFR)

Suffering from complications of severe AKI (AEIOU):
- (Acidosis) Metabolic acidosis
- (Electrolytes) Hyperkalemia
- (Intoxication) Overdose of certain medications
- (Oedema) Fluid overload
- (U) Uraemia

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13
Q

Outline the indications for long term dialysis

A
  • End stage renal failure / stage 5 CKD
  • Complications of severe AKI continuing long term
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14
Q

List some complications of peritoneal dialysis

A
  • Infection (bacterial peritonitis) due to glucose solution
  • Sclerosis / fibrosis
  • Ultrafiltration failure (due to absorbing Dextrose solution and reducing gradient)
  • Weight gain (due to absorbing Dextrose solution)
  • Psychological effects
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15
Q

Outline 2 veins commonly used for tunneled cuffed catheter (in haemodialysis)

A

Subclavian vein
Jugular vein
Despite which entry, catheter ends up in the SVC or right atrium

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16
Q

Outline some complications of haemodialysis, in relation to catheters and AV fistulas

A

Tunneled cuffed catheter:
- Infection
- Thrombosis
- Pneumothorax

AV fistula:
- Infection
- Bleeding risk
- Thrombosis
- Aneurysm
- STEAL syndrome
- High output heart failure

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17
Q

Outline which arteries and veins are typically connected in an AV fistula for haemodialysis (2)

A

Brachio-cephalic (brachial artery and cephalic vein)
Radio-cephalic (radial artery and cephalic vein)

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18
Q

List some complications associated with renal transplantation and associated immunosuppression

A

Related to organ:
- Infection
- Transplant failure
- Transplant rejection
- Electrolyte imbalances

Related to immunosuppression:
- Malignancy (non-Hodgkin’s lymphoma and squamous cell carcinoma imparticular)
- More frequent or severe infections
- Atypical infections e.g. PCP, CMV, TB
- Steroid-induced T2DM
- Ischaemic heart disease

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19
Q

Diabetic nephropathy - state the following:
- Pathophysiology
- Presentation and screening
- Management

A

Pathophysiology:
- Scarring of the glomerulus, due to high flow of glucose (uncontrolled diabetes)
- Leads to damage of the glomerulus, allowing proteins to leak through the glomerulus, into the urine
- Most common cause of glomerular pathology and CKD in UK

Presentation and screening:
- Frothy urine (proteinuria)
- Signs of uncontrolled diabetes e.g. high HbA1C, peripheral neuropathy, vision changes
- Regular screening for diabetic nephropathy using albumin:creatinine ratio and U&Es

Management:
- Control of diabetes (good blood sugar control)
- BP control with ACEi

20
Q

Outline Nephrotic Syndrome and it’s pathophysiology

A

Nephrotic syndrome:
- A clinical syndrome characterised by: proteinuria, hypoalbuminaemia and oedema + hyperlipidaemia
- Caused by damage to the basement membrane in the glomerulus leading to increased permeability and leakage of protein

Pathophysiology:
- Cytokines damage podocytes causing them to fuse together and destroy charge of the glomerular basement membrane.
- Increased permeability and massive protein loss
- Also leeds to low serum albumin (beyond the ability of the liver to replace them)
- Due to the loss of albumin, disruption to oncotic pressure with fluid leaking into interstitial = oedema
- As an attempt to maintain oncotic pressure, the liver tries to compensate by increased synthesis of lipids
- Also in a hypercoagulable state due to urinary loss of antithrombin 3
- Also in an immunosuppressed state due to urinary loss of immunoglobulins

21
Q

Outline the most common causes of Nephrotic Syndrome (in children and adults) as well as a couple of other common causes

A

Most common cause in children: Minimal change disease

Most common cause in adults: Membranous glomerulonephritis

Other common causes:
- Systemic diseases: SLE and amyloidosis
- Diabetes mellitus
- Focal segmental glomerulosclerosis (FSGS)

22
Q

Outline the presentation, investigations and management for Nephrotic Syndrome

A

Presentation:
- Oedema (peripheral and periorbital)
- (Proteinuria, hypoalbuminaemia and hyperlipidaemia)

Investigations:
- Urine dipstick / urinalysis
- Serum albumin
- Blood pressure
- Creatinine
- Renal biopsy only if unresponsive to treatment or diagnosis is unclear

Management:
- High dose steroids for 12 weeks (treat underlying cause, which is damage by cytokines)
- Diuretics, may need large doses
- Fluid and salt restriction
- ACEi (vasodilate EA, helps to reduce pressure which reduces loss of protein)
- Statins (hyperlipidaemia)
- Anticoagulants (hypercoagulable state)
- May need to manage underlying cause if clear e.g. SLE

23
Q

List the complications of Nephrotic Syndrome

A
  • Thromboembolism (hypercoagulable state due to urinary loss of antithrombin 3)
  • Infection (immunosuppressed state due to urinary loss of immunoglobulins)
  • Hyperlipidaemia (overcompensation of liver to replace albumin)
  • Hypocalcaemia (loss of vit D in urine)
  • Acute renal failure (acute tubular necrosis)
24
Q

Outline the 2 main types of interstitial kidney disease and key causes, including brief outline of management

A
  1. Acute interstitial nephritis
    - Acute inflammation of the interstitium and tubules
    - Mainly a hypersensitivity reaction to a trigger
    Key causes:
    - Hypersensitivity reaction to drugs e.g. NSAIDs and Antibiotics
    - Hypersensitivity reaction to infection
    Management:
    - TREAT UNDERLYING CAUSE
    - Steroids may have some role
  2. Chronic tubulo-interstitial nephritis
    - Chronic inflammation of the interstitium and tubules
    - Presents with CKD
    Key causes:
    - Many causes including: infection, autoimmune, iatrogenic, granulomatous disease
    Management:
    - TREAT UNDERLYING CAUSE
    - Steroids may have some role
25
Q

Outline the presenting triad of symptoms for acute interstitial nephritis

A

Interstitial hypersensitivity reaction causes:
- Erythematous rash
- Fever
- Eosinophilia

26
Q

Outline some drugs that can cause acute interstitial nephritis

A
  • NSAIDs
  • Diuretics
  • PPI
  • Antibiotics (e.g. penicillins, sulfa drugs, cephalosporins and quinolones)
  • Allopurinol
  • Rifampicin
27
Q

Acute tubular necrosis - state the following:
- Pathophysiology
- Common causes
- Investigations
- Management

A

Pathophysiology:
- Damage and death of the epithelial cells of the renal tubules
- Most common cause of AKI
- However is reversible (recovery in 1-3 weeks)
Common causes
1. Ischaemia secondary to hypoperfusion e.g. sepsis, hypovolaemia, shock
2. Toxins e.g. contrast dye, NSAIDs, Gentamicin, Heroin, Lithium

Investigations:
Urinalysis - shows ‘muddy brown casts’ (pathognomonic for ATN)

Management:
Similar management to AKI
- Treat underlying cause
- Supportive management
- IV fluids
- Stop any nephrotoxic medications

28
Q

Briefly outline the 4 types of renal tubular acidosis (type 1 and 4 are likely to be examined)

A

Type 1:
- Distal tubule unable to excrete H+
- Leads to build up of H+ in the blood = metabolic acidosis

Type 2:
- Proximal tubule unable to reabsorb HCO3-
- Leads to excessive HCO3- in urine, reduced HCO3- in the blood = metabolic acidosis

Type 3:
- Mix of type 1 and type 2
- Pathology in both the distal tubule and proximal tubule

Type 4:
- Reduced aldosterone (normally Na reabsorption and K+ / H+ excretion)
- So low aldosterone = Na loss and K+ / H+ retaining
- Hyperkalaemia suppresses ammonia production; low ammonia levels leads to more acidic urine

29
Q

Type 1 renal tubular acidosis - state the following:
- Pathophysiology
- Common causes
- Clinical findings (blood, urine)
- Management

A

Pathophysiology:
- Distal tubule unable to excrete H+
- Leads to buildup of H+ in the blood = metabolic acidosis

Common causes:
- Genetic
- SLE / Sjogren’s / PBC
- Hyperthyroidism
- Marfan’s syndrome
- Sickle cell anaemia

Clinical findings (blood, urine):
- Metabolic acidosis
- Alkaline urine
- Hypokalaemia

Management:
- Oral bicarbonate (correct hypokalamia as well)

30
Q

Type 4 renal tubular acidosis - state the following:
- Pathophysiology
- Common causes
- Clinical findings (blood, urine)
- Management

A

Pathophysiology:
- Reduced aldosterone (normally Na reabsorption and K+ / H+ excretion)
- So low aldosterone = Na loss and K+ / H+ retaining
- Hyperkalaemia suppresses ammonia production; low ammonia levels leads to more acidic urine

Common causes:
- Adrenal insufficiency
- Medications e.g. ACEi or Spironolactone
- SLE
- Diabetes
- HIV

Clinical findings (blood, urine):
- Metabolic acidosis
- Acidic urine
- Hyperkalaemia
- High Cl-

Management:
- Fludrocortisone (Aldosterone replacement)
- Sodium bicarbonate
- May require treatment of hyperkalaemia

31
Q

Haemolytic uraemic syndrome - state the following:
- Pathophysiology
- Presentation (classic triad)
- Management

A

Pathophysiology:
- Occurs when there is thrombosis in small blood vessels throughout the body
- Triggered by the shiga toxin

Presentation (classic triad):
- Haemolytic anaemia
- AKI
- Thrombocytopenia (low platelets)

Management:
- Supportive management
- Antihypertensives
- Blood transfusions
- Dialysis

32
Q

List things that are released during muscle cell breakdown (in rhabdomolysis)

A
  • K+
  • Creatine kinase
  • Myoglobin
  • Phosphate
33
Q

List some causes of rhabdomyolysis

A
  • Extremely vigorous exercise (beyond the capabilities of the individual)
  • Falls in long lie / prolonged immobility
  • Compartment syndrome
  • Crush injuries
  • Seizures
34
Q

List some symptoms and signs of rhabdomyolysis

A
  • Red-brown urine
  • Muscle aches/pain
  • Oedema
  • Confusion
  • Fatigue
35
Q

Outline the key management of rhabdomyolysis

A

IV fluids = encourage filtration and hydrates

IV Sodium Bicarbonate = more alkaline urine, less toxic to kidneys

IV Mannitol = increase GFR to encourage filtration and reduce oedema

Treat any complications e.g. hyperkalaemia

36
Q

List some causes of hyperkalaemia

A

Conditions:
- Rhabdomyolysis
- AKI
- CKD
- Adrenal insufficiency
- Tumour lysis syndrome

Medications:
- Aldosterone antagonists (diuretics e.g. Spironolactone)
- ACEi / ARB
- NSAIDs
- K+ supplements

37
Q

Outline the management for hyperkalaemia
< 6 mmol/L and stable renal function
> 6 mmol/L and ECG changes
> 6.5 mmol/L

A

< 6 mmol/L and stable renal function = mild changes e.g. stopping hyperkalaemic drugs or modifying diet

> 6 mmol/L and ECG changes = urgent treatment

> 6.5 mmol/L = urgent treatment, regardless of other signs

Management:
- Insulin + Dextrose fluid = drives glucose into cells, takes K+ with it
- IV Calcium Gluconate = stabilise cardiac muscle cells
- IV Calcium Resonium = draws K+ into stool
- IV fluids = increase urine output and K+ excretion in urine

38
Q

List some common causes of CKD

A

2 most common:
- Diabetes
- Hypertension
+
- Glomerulonephritis
- Polycystic kidney disease
- Chronic use of nephrotoxic medications e.g. NSAIDs, Lithium, PPIs
- Age-related decline

39
Q

What is the best blood test to detect rhabdomyolysis

A

Serum creatine kinase (CK)

40
Q

List some drugs that should be stopped in AKI (nephrotoxic and renally excreted drugs)

A

Nephrotoxic drugs:
- NSAIDs
- Aminoglycosides e.g. gentamicin
- ACE inhibitors/ARBs
- Diuretics

Renally excreted drugs:
- Metformin
- Lithium
- Digoxin

41
Q

List 3 absolute contraindication for renal transplant

A
  • Metastatic cancer
  • Active infections
  • Severe comorbidity
42
Q

Alport’s syndrome - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Rare X-linked inherited nephropathy due to abnormal glomerular basement membrane (defective type 4 collagen)
- Problems with the eyes, ears and kidneys

Presentation:
- Gross haematuria
- Sensorineural hearing loss
- Vision changes

Investigations:
Quite general!
- Routine bloods e.g. FBC, U&Es
- Audiometry and ophthalmoscopy
- Renal biopsy
- Genetic testing

Management:
- Ongoing annual monitoring e.g. U&Es
- Manage comorbidities or manifestations e.g. HTN
- ACEi if proteinuria
- May eventually need dialysis

43
Q

What drugs should be stopped in AKI? (DAMN)

A

DAMN

D- Diuretics
A - ACEi and aminoglycosides
M - Metformin
N - NSAIDS

44
Q

Outline some clinical signs of a patient with CKD

A
  • Coarse crackles or reduced breath sounds (pulmonary oedema)
  • Peripheral pitting oedema
  • Excoriation marks from pruritus
  • Evidence of CKD replacement therapy e.g. AV fistula or permacath
45
Q

Outline 2 pros and 2 cons for both live kidney donation and decreased kidney donation

A

Live kidney donation:
+ planned surgery (elective)
+ generally a better match / better quality kidney, reduced risk of failure
- hard to find a donor
- emotional turmoil if it fails

Decreased kidney donation:
+ don’t have to find the donor
+ no connection to donor
- not always the best match, increased risk of failure
- surgery can be at short notice and longer waiting times

Year 3 - Medicine (8 decks)

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