Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AKT > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

Pre-renal causes of AKI

A

Due to inadequate blood supply to kidneys reducing the filtration of blood. Inadequate blood supply may be due to:

Dehydration
Hypotension (shock)
Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Renal causes of AKI

A

This is where intrinsic disease in the kidney is leading to reduced filtration of blood. It may be due to:

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Post-renal causes of AKI

A

Caused by obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:

Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Nephrotoxic drugs include

A

NSAIDS and ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What gives GFR better than creatinine

A

Cystatin C - produced in the body at a constant rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Creatine clearance calculation

A

U (urine concentration) x V (urine flow rate) / P (plasma concentration) x 24 x 60 = creatinine clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

G Score of ranking kidney failure

A

G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is needed for diagnosis of CKD

A

eGFR of < 60 or proteinuria for a diagnosis of CKD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Albumin creatine ratio?

A

Measures proteinuria
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Drug for patients with CKD

A

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Xray changes in CKD

A

Spine xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Indications for acute dialysis in patients with a severe AKI

A

A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Peritoneal Dialysis

A

Peritoneal dialysis uses the peritoneal membrane as the filtration membrane. A special dialysis solution containing dextrose is added to peritoneal cavity. Ultrafiltration occurs from the blood, across the peritoneal membrane, in to the dialysis solution. The dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a Tenckhoff catheter?

A

This is a plastic tube that is inserted into the peritoneal cavity with one end on the outside. It allows access to peritoneal cavity. This is used for inserting and removing the dialysis solution.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Continuous Ambulatory Peritoneal Dialysis?

A

This is where the dialysis solution is in the peritoneum at all times. There are various regimes for changing the solution. One example is where 2 litres of fluid is inserted into the peritoneum and changed four times a day.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is automated dialysis ?

A

This involves peritoneal dialysis occurring overnight. A machine continuously replaces dialysis fluid in the abdomen overnight to optimise ultrafiltration. It takes 8-10 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Complications of peritoneal dialysis

A

Bacterial peritonitis. Infusions of glucose solution make the peritoneum a great place for bacterial growth. Bacterial infection is a common and potentially serious complication of peritoneal dialysis.

Peritoneal sclerosis involves thickening and scarring of the peritoneal membrane.

Ultrafiltration failure can develop. This occurs when the patient starts to absorb the dextrose in the filtration solution. This reduces the filtration gradient making ultrafiltration less effective. This becomes more prominent over time.

Weight gain can occur as they absorb the carbohydrates in the dextrose solution.

Psychosocial effects. There are huge social and psychological effects of having to change dialysis solution and sleep with a machine every night.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Options for blood supply for haemodialysis

A

Tunnelled cuffed catheter
Arterio-venous fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Positioning of a tunnelled cuffed catheter

A

Tube inserted into the subclavian or jugular vein with a tip that sits in the superior vena cava or right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Examine an AV fistula

A

Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
Stereotypical “machinery murmur” on auscultation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is STEAL syndrome

A

STEAL syndrome is where there is inadequate blood flow to the limb distal to the AV fistula. The AV fistula “steals” blood from the distal limb. The blood is diverted away from where is was supposed to supply and flows straight into the venous system.

This causes distal ischaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is high output heart failure?

A

Where there is an A-V fistula blood is flowing very quickly from the arterial to the venous system through the fistula. This means there is rapid return of blood to the heart. This increases the pre-load in the heart (how full the heart is before it pumps). This leads to hypertrophy of the heart muscle and heart failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Procedure of kidney transplant

A

The patient’s own kidneys are left in place.

The donor kidney’s blood vessels are connected (anastomosed) with the patient’s pelvic vessels, usually the external iliac vessels.

The donor kidney’s ureter is anastomosed directly with the patient’s bladder.

The donor kidney is placed anterior in the abdomen and can usually be palpated in the iliac fossa area. They typically use a “hockey stick incision” and there will be a “hockey stick scar”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Immunosuppressants for kidney transplant

A

Most common
Tacrolimus
Mycophenolate
Prednisolone

Other possible immunosuppressants:
Cyclosporine
Sirolimus
Azathioprine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

The most common cause of nephrotic syndrome in adults

A

Focal segmental glomerulosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common cause of primary glomerulonephritis (not caused by another disease)?

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most common type of glomerulonephritis overall

A

Membranous glomulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Membranous glomulonephritis histology

A

IgG and complement deposits on the basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Classic presentation of Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)

A

Patients are typically under 30 years. It presents as:

1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
They develop a nephritic syndrome
There is usually a full recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Goodpasture syndrome presentation

A

Patient that presents with acute kidney failure and haemoptysis (coughing up blood).

Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What two conditions may cause both haemoptysis and acute renal failure?

A

Goodpasture syndrome and granulomatosis with polyangiitis (AKA Wegener’s granulomatosis).

32
Q

Granulomatosis with polyangiitis

A

Type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA).

33
Q

Acute interstitial nephritis presents with

A

Acute kidney injury and hypertension. There is acute inflammation of the tubules and interstitium.

34
Q

Cause of acute interstitial nephritis

A

Usually caused by a hypersensitivity reaction to:

Drugs (e.g. NSAIDS or antibiotics)
Infection

35
Q

What can cause direct damage to kidney tubules

A

Radiology contrast dye
Gentamycin
NSAIDs

36
Q

Urinalysis unique to kidney tubular necrosis

A

Muddy brown casts and renal tubular epithelial cells

37
Q

Renal tubular acidosis

A

Metabolic acidosis due to pathology in the tubules of the kidney. The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and urine and maintaining a normal pH.

38
Q

What is Type 1 Renal Tubular Acidosis?

A

Type 1 renal tubular acidosis is due to pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions.

39
Q

Causes of type 1 renal tubular acidosis

A

Genetic. There are both autosomal dominant and recessive forms.
Systemic lupus erythematosus
Sjogren’s syndrome
Primary biliary cirrhosis
Hyperthyroidism
Sickle cell anaemia
Marfan’s syndrome

40
Q

Signs type 1 renal tubular acidosis

A

Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)

41
Q

Lab results for type 1/2 tubular acidosis

A

Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)

42
Q

Treatment for type 1/2 renal acidosis

A

Treatment is with oral bicarbonate. This corrects the other electrolyte imbalances.

43
Q

What is Type 2 Renal Tubular Acidosis?

A

Type 2 renal tubular acidosis is due to pathology in the proximal tubule. The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood. Excessive bicarbonate is excreted in the urine.

44
Q

Main cause of type 2 renal tubular acidosis

A

Fanconi’s syndrome

45
Q

What is Type 4 Renal Tubular Acidosis?

A

Type 4 renal tubular acidosis is caused by reduced aldosterone.

Reduced urine buffering capacity

46
Q

Cause of type 4 renal tubular acidosis

A

This can be due to adrenal insufficiency, medications such as ACE inhibitors and spironolactone or systemic conditions that affect the kidneys such as systemic lupus erythematosus, diabetes or HIV.

47
Q

Lab results for type 4 renal tubular acidosis

A

Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH

48
Q

Management of type 4 renal tubular acidosis

A

Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.

49
Q

Triad of haemolytic uraemia syndrome

A

Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)

50
Q

Cause of HUS

A

Most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin and can cause HUS.

51
Q

Classic presentation of HUS, timeline and symptoms

A

E. coli 0157 causes a brief gastroenteritis often with bloody diarrhoea.

Around 5 days after the diarrhoea the person will start displaying symptoms of HUS:

Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising

52
Q

What component of muscle cells in rhabdomyolysis causes AKI

A

Myoglobin in particular is toxic to the kidney in high concentrations.

53
Q

Causes of rhabdomyolysis

A

Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found

Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition)

Crush injuries

Seizures

54
Q

Rhabdomyolysis investigations

A

Creatine Kinase (CK) blood test is a key investigation in establishing the diagnosis. It will be in the thousands to hundreds of thousands of Units/L. CK typically rises until 12 hours, then remains elevated for 1-3 days, then falls gradually. A higher CK increases the risk of kidney injury.

Myoglobinurea is myoglobin in the urine. It gives urine a red-brown colour. This will cause a urine dipstick to be positive for blood.

Urea and electrolytes (U&E) blood tests for acute kidney injury and hyperkalaemia.

ECG is important in assessing the heart’s response to hyperkalaemia.

55
Q

Management of rhabdomyolysis

A

IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products.

Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence on this is not clear and there is some debate about whether to use it.

Consider IV mannitol. This aims to increase the glomerular filtration rate to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.

56
Q

ECG hyperkalemia

A

Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes

57
Q

Hyperkalemia management

A

Insulin (e.g. actrapid 10 units) and dextrose (e.g. 50mls of 50%) drives carbohydrates into cells and takes potassium with it, reducing the blood potassium.

Calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias.

58
Q

Extra-renal manifestations of PKD

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation

59
Q

Autosomal recessive polycystic kidney disease (ARPKD) presents in pregnancy with

A

Oligohydramnios as the fetus does not produce enough urine. Leads to underdevelopment of the lungs resulting in respiratory failure shortly after birth.

They can have dysmorphic features such as underdeveloped ear cartilage, low set ears and a flat nasal bridge. They usually have end-stage renal failure before reaching adulthood.

60
Q

Treatment for PKD

A

Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease.

61
Q

What is Alport syndrome ?

A

Alport syndrome is a genetic disorder leading to mutations on collagen type 4. This type of collagen is found in the basement membrane of the kidney, the eye, and the cochlear leading the renal, hearing and eye problems.

62
Q

Genetics of Alport syndrome

A

It is commonly X-linked but may be seen in a less severe, lyonization pattern in affected females. It can also present in a dominant or recessive fashion. Diagnosis is made on tissue biopsy and genetic testing.

63
Q

Drug to reduce phosphate

A

Calcium carbonate

Sevelamer (non calcium phosphate binder)

64
Q

What does the 4-parameter Modification of Diet in Renal Disease (MDRD) formula include?

A

Creatinine, ethnicity, gender and age only

CAGE

65
Q

What does base excess tell us ?

A

Indicates metabolic component
Positive base excess - metabolic alkalosis
Negative base excess - metabolic acidosis

Then use anion gap to work out cause

66
Q

Paracetamol overdose

A

Paracetamol overdose tends to be indolent at the beginning of the syndrome with general nausea and vomiting. Right upper quadrant pains can be seen when liver damage occurs.

67
Q

Acute interstitial nephritis causes findings of

A

An ‘allergic’ type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function

68
Q

Hyaline casts may be seen in the urine of patients taking

A

Loop diuretics

69
Q

Dialysis disequilibrium syndrome

A

Array of neurological manifestations that are seen during or following dialysis, primarily after the new initiation of dialysis.

Due to cerebral oedema

70
Q

Why is sarcoidosis a RF for diabetes insipidus

A

Sarcoidosis can result in the formation of granulomas in the pituitary gland which leads to neurogenic diabetes insipidus.

71
Q

What is the key indication that kidney disease is chronic and not acute

A

Hypocalcaemia

72
Q

KDIGO staging of

A

Stage 1 Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage 2 Increase in creatinine to 2.0 to 2.9 times baseline, or
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3 Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

73
Q

What is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys

A

Alfacalcidol

74
Q

Diagnosis of Post-streptococcal glomerulonephritis

A

Raised anti-streptolysin O titres are used to confirm the diagnosis of a recent streptococcal infection

75
Q

Distinguishing between prerenal uraemia and acute tubular necrosis

A

Look the urine sodium and osmolality and the serum urea : creatinine ratio.

In prerenal uraemia, the body is trying to retain fluids. Hence, it is going to retain sodium to increase them, resulting in high blood sodium and low urine sodium.

In ATN normal serum urea:creatinine ratio would be expected. On urine tests, sodium levels higher than 40 mmol/, low osmolality, and muddy brown casts would be expected.

76
Q

What does urea:creatine ratio tell us about AKI?

A

Urea to creatinine ratio above 100 is a landmark characteristic of a pre-renal acute kidney injury.

AKT (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions