Brainscape's Knowledge GenomeTM

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


See full index

METABOLIC > RENAL - KIDNEY DISEASE > Flashcards

RENAL - KIDNEY DISEASE Flashcards

1
Q

What are the functions of the kidneys?

A

Elimination of metabolic waste
Water homeostasis
Electrolyte homeostasis
Acid base homeostasis
Blood pressure control
Synthesising vitamin D, EPO and renin
Excretion of drugs and drug metabolites

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

Explain why there is a non-linear relationship between serum creatinine and kidney function?

A

Kidney function needs to drop by 50% before creatinine levels become abnormal I.e. its no sensitive to small changes in function

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

What is eGFR calculated from?

A

Creatinine, age, gender ethnicity

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

Why do we use eGFR for chronic kidney disease not acute?

A

Because its the best measure for use when stable renal function

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

How do we classify CKD?

A

EGFR <60 or kidney damage
Must be present for over 3 months

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

What is the staging for CKD?

A

EGFR stages
g1 - >90
G2 - 60-89
G3a - 45-59
G3b - 30-44
G4 - 15-29
G5 - <15

Or ACR categories. <3 is A1, 3-30 is A2 and >30 is A3

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

What’s the eGFR threshold for symptoms?

A

<30

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

Do you always see urine volume decrease in kidney disease?

A

No. In slowly progressive kidney disease can see urine volume actually increase, as failing tubular function leads to a salt and water wasting state. This is because the concentrating ability in the tubules fails

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

What are the risk factors for CKD?

A

Age, hypertension, diabetes, smoking, poor socioeconomic status, use of nephrotoxic medications

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

What are some causes of CKD?

A

Diabetes or hypertension
Atherosclerosis
Immune mediated diseases e.g. membranous nephropathy, IgA nephropathy and SLE
Drugs
Infectious diseases e.g. HIV, HBV, TB, HCV
Polycystic kidneys
Obstructions e.g. tumours or stone

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

Normally CKD is asymptomatic but what signs and symptoms may suggest it?

A

Pruritus
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension

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

How do we investigate CKD?

A

EGFR from U&E blood test - 2 tests required 3 months apart
Urine dipstick for proteinuria and haematuria
Renal ultrasound

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

What must eGFR be for a diagnosis of CKD?

A

<60 (or proteinuria)

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

Why can anaemia occur in CKD?

A

EPO deficiency
But it can also be from a number of other causes… increased blood loss, bone marrow toxins, haematuria deficiency, increased red cell destruction, ACEi use

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

How much does CKD increase the risk of cardiovascular disease?

A

16 fold

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

Why can CKD cause pruritus?

A

Accumulation of nitrogenous waste products of protein catabolism
Iron deficiency
Hyperparathyroidism
Hypercalcaemia and hyperphosphataemia

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

What are some complications of CKD?

A

Cardiovascular disease
Hypertension
Oedema
Electrolyte abnormalities
Metabolic acidosis
Mineral-bone disease
Anaemia
Uraemia
Altered drug metabolism

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

What are some general measures for managing CKD?

A

Treat any modifiable underlying cause
Address CVD risk factors e,g, smoking cessation, exercise, weight loss
Avoid nephrotoxic drugs
Immunise against influenza and pneumococcus

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

How do we correct hyperkalaemia in CKD?

A

FAR

Force K+ into cells - 20 ml 10% dextrose and 10-20 units of insulin. Or sodium bicarbonate. Or beta 2 agonist like salbutamol
Antagonise K+ - 10ml 10% calcium gluconate
Remove K+ - sodium-calcium resonium or dialysis as a last resort

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

Which drugs must be stopped in CKD?

A

Contrast media
ACEi/ ARBs
NSAIDs
Diuretics
Anti-microbials - Aminoglycosides, sulfamethoxazole, penicillins, rifampicin, amphoterecin, aciclovir
Anti convulsants - lamotrigine, valproate, phenytoin
Lithium
Anaesthetic agents - methoxyflurane and enflurane
Ethylene glycol

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

What causes renal bone disease?

A

We get low active vitamin D which is essential in calcium absorption from the intestines and kidneys
Secondary hyperparathyroidism occurs due to parathyroid glands reacting to low serum calcium and high serum phosphate - this increases osteoclast activity = absorption of calcium from bone

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

How quick does AKI come on?

A

Hours - days

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

How to we measure AKI?

A

Using creatinine and urine output

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

What are the creatinine and urine output values for stage 1 AKI?
Stage 2?
Stage 3?

A

Stage 1 - 50-100% creatinine increase. Or <0.5ml/kg/hour for 6 hours urine
Stage 2 - 100-200% creatinine increase. Or <0.5ml/kg/hour for 12 hours urine
Stage 3 - >200% creatinine increase or <0.3ml/kg/hour for 24 hours or anuria for 12 hours or needs dialysis

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

What are the risk factors for AKI?

A

Older age
Diabetes
Hypertension
Heart disease
Liver disease
CKD
Meds - diuretics, ACEi/ARB, NSAID, gentamicin, vancomycin, chemotherapy

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

What are pre-renal causes of AKI?

A

Perfusion failure e.g hypovolemia, hypotension, low cardiac output or blockage of renal artery
Medications

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

What are common intra-renal causes of AKI?

A

Diseases that affect the kidney tissue e.g. vascular is, SLE, multiple myeloma, interstitial nephritis

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

What are post-renal causes of AKI?

A

Obstruction to urinary system e.g, stones, tumours, blocked catheters

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

What are the main complications of AKI?

A

Death
Infections
Anaemia
Metabolic acidosis
Hypertension
CKD
Altered drug metabolism
Oedema
Electrolyte abnormalities

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

What are the clinical signs of nephrotic syndrome?

A

Heavy proteinuria (>3.5g/day) which also leads to hypoalbuminaemia
Peripheral oedema due to salt and water retention
Hyperlipidaemia and lipiduria
Loss of antithrombin III (and protein S and C)
Loss of thyroglobulin and vitamin D

Marked peripheral pitting oedema, pleural effusion, pericardial effusion and ascites
Hypercoagulability
Hypertension (not s marked as nephritic)
Frothy urine

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

What are the causes of nephrotic syndrome?

A

When the glomerular filtration barrier is damaged leading to increased protein leak
focal segmental glomerulosclerosis
membranous glomerulonephritis
minimal change disease
diabetic nephropathy
Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the complications of nephrotic syndrome?

A

Thromboembolism
Infections
Hyperlipidaemia
Malnutrition
CKD and occasionally AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why can nephrotic syndrome cause thromboembolism?

A

increased excretion of antithrombotic factors by the affected kidneys and increased production of pro-thrombotic factors by the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do we treat nephrotic syndrome?

A

Loop diuretics
Salt restriction
ACEi or ARBs to reduce proteinuria
Thrombo-prophylaxis
Treat underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Why can nephrotic syndrome cause Hyperlipidaemia?

A

Due to increased synthesis of lipoproteins as a direct consequence of low plasma albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are some primary causes of nephrotic syndrome?

A

Minimal change nephropathy
Congenital nephrotic syndrome
Focal segmental glomerular sclerosis
Membranous nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some secondary causes of nephrotic syndrome?

A

Amyloidosis
Diabetic nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the clinical features of minimal change disease?

A

Most common in children, particularly boys
Proteinuria is highly selective where albumin, but not higher molecular weight proteins are lost in urine
Oedema is usual and in children presents mostly around the face
Accounts for 25% of adult nephrotic syndromes
Doesn’t lead to CKD
Minimal changes on light microscopy but electron microscopy shows fusion of the foot processes of podocytes
Treated with high dose prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What’s the pathophysiology of minimal change disease?

A

Effacement of foot processes in glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What’s the pathophysiology of congenital nephrotic syndrome?

A

An autosomal recessive lay inherited disorder due to mutations in the gene coding for nephron. This loss of function results in massive proteinuria shortly after birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is focal segmental glomerulosclerosis?

A

Progressive glomerular scarring that can occur in all ages
Present as massive, non-selective proteinuria, haematuria, hypertension and renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is amyloidosis?

A

a group of rare, serious conditions caused by a build-up of an abnormal, insoluble protein called amyloid in organs and tissues throughout the body
Can affect the kidneys, manifesting as nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Outline the pathology of diabetic nephropathy?

A

glucose will non-enzymatically combine with proteins and lipids to form pro-inflammatory molecules (non-enzymatic glycation). These molecules cause inflammation of efferent arteriole leading to arteriosclerosis. Overall effect is thickening of arteriole which increases the pressure proximal to the arteriole which causes an increase in GFR. Mesangial cells respond by secreting transforming growth factor beta = extracellular matrix release = fibrosis (glomerulosclerosis) = drops GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the clinical features of nephritic syndrome?

A

Proteinuria <3G a day. May have frothy urine
Haematuria (macroscopic or microscopic) - Cola coloured urine
Sterile pyuria (raised WCC in urine but no growth on cultures)
Hypertension
Temporary oliguria or uraemia
Azotemia
Oedema - liver can compensate for quite a bit of this so less marked than in nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are some of the causes of nephritic syndrome?

A

Anything that damages the glomerular endothelium and causes inflammation or is immune mediated
Rapidly progressive GN
IgA nephropathy
Henoch-schonein purpura
Alport syndrome
Haemolytic uraemic syndrome (HUS)
SLE
Anti-GBM GN
ANCA vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is post-streptococcal glomerulonephritis?

A

Occurs in childhood
Acute nephritis 1-3 weeks after a group A streptococcal infection (streptococcal throat infection, otitis media or cellulitis)
Caused by immune complex deposition in glomeruli (type 3 hypersensitivity)
Presents with flu-like sympotms, haematuria, proteinuria, hypertension and oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is IgA nephropathy?

A

The most common form of glomerulonephritis worldwide
Presents with asymptomatic haematuria and (classically) 12-72 hours after an upper RTI
Associated with HSP, coeliac disease and alcohol cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What age group does IgA nephropathy tend to present in?

A

Teens-late thirties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Alports syndrome?

A

A rare hereditary nephritis characterised by chronic kidney disease, hearing loss and eye abnormalities
X-linked dominant inherited disease due to a defect in type IV collagen = abnormal GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the mortality from patients with AKI?

A

About 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Is pre-renal, renal or post-renal the most common cause of kidney failure?

A

Pre-renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the surgical triad for common cause of hospital acquired AKI?

A

Post-operative volume depletion
Infection
Nephrotoxic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which drugs are nephrotoxic?

A

ACEi and ARB - cause efferent vasodilation
NSAIDs - cause afferent vasodilation
PPIs - cause interstitial nephritis
Aminoglycosides
Contrast mediums

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is acute uraemia?

A

A rise in blood urea and other products of metabolism which is often but not invariably accompanied by oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is oliguria?

A

A volume of urine below which at maximum urinary concentration the body cannot excrete the products of metabolism
A decrease in urine output relative to fluid input of <0.5mg/kg/h for 12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What would you see on ECG in hyperkalaemia?

A

Tenting of T waves
Widening of QRS
Disappearance of p waves
Sine wave pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What clinical methods are used to assess intravascular fluid volume?

A

Body weight
Skin turgor
Postural bp
Mucous membranes
JVP
Lung bases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does absolute anuria mean until proven otherwise?

A

Urinary tract obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is RIFLE classification?

A

Risk - GFR decreases >25%
Injury - GFR decreases >50%
Failure - GFR decreases >75%
Loss - dialysis dependant >4 weeks
End stage kidney disease - dialysis dependant >3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is oliguria?

A

<400mls/day or <0.5ml/kg/hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is anuria?

A

No urine output I.e. <50mls/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What do we think when we see macroscopic haematuria compared to microscopic?

A

Macroscopic usually indicates bleeding within the urinary tract
Microscopic more commonly indicates glomerular haematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the common sites of obstruction in post renal renal failure?

A

Bilateral pelvicoureteric junction
Bilateral ureteric junction
bladder outflow
Urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Which hormones does the kidney produce?

A

1,25 dihydroxy D3
EPO
Renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are some symptoms and signs of uraemia?

A

Anorexia
Change in taste
Nausea
Vomiting
Pruritis
Neuropathy
Pericarditis
Confusion
Encephalopathy
Coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are some common symptoms of hypovolemia seen in an AKI?

A

Thirst, orthostatic symptoms and postural hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is secondary glomerulonephritis?

A

When the kidney damage is as a result of another disease process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Why do patients with nephrotic syndrome have an increased risk of infection?

A

Due to losses of immunoglobulins and immune mediators in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What’s the difference between the oedema seen in nephrotic syndrome and the oedema in nephritic syndrome?

A

In nephrotic syndrome low oncotic pressure due to hypoalbuminaemia and high hydrostatic pressure from fluid retention
in nephritic syndrome oliguria causes na+ and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the main 2 causes of nephrotic syndrome in children?

A

Minimal change disease
Focal segmental glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the main causes of nephrotic syndrome in adults?

A

Membranous glomerulonephritis
Focal segmental glomerulosclerosis
Diabetic nephropathy
SLE, amyloidosis, Hep B C and HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is steroid responsive nephrotic syndrome?

A

Because most children with nephrotic syndrome will have MC disease and most will respond to steroids, you can treat without a biopsy - this is what we call steroid responsive nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is relapsing nephrotic syndrome?

A

When children relapse on steroid withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is steroid dependant nephrotic syndrome?

A

Children who need continuous steroid therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is steroid resistant nephrotic syndrome and what is the likely cause?

A

Children who’s nephrotic syndrome does not respond to steroids
They need a biopsy
Usually caused by inherited abnormalities of podocyte proteins or quite often focal segmental glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the most common cause of nephritic syndrome in children?

A

Post-streptococcal glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What’s the most common cause of nephritic syndrome in adults?

A

IgA nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Briefly outline the pathophysiology of post-streptococcal glomerulonephritis?

A

Streptococcal antigens deposit in the glomerulus forming immune complexes and causing inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is Henoch-Schonlein purpura?

A

an inflammation of the small blood vessels of the skin, joints, bowels and kidneys.
It can cause nephritic syndrome
Presents with a rash on extensor surfaces, polyarthtisi, abdominal pain, GI haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Why is the histology crescentic in rapidly progressive glomerulonephritis?

A

Because sudden breaks in the glomerular basement membrane allow an influx of inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

How does anti-GBM antibody disease present?

A

Rapid renal function decline and pulmonary haemorrhage (SOB and haemoptysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What’s the classical presentation of IgA nephropathy?

A

Visible haematuria 1-2 days following an upper resp tract infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What lesions are commonly seen histologically in diabetic nephropathy?

A

kimmelsteil wilson lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the 3 types of amyloidosis?

A

AL (primary)
AA (secondary)
Familial ATTR amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are some secondary causes of nephrotic syndrome?

A

Diabetes
Lupus
Amyloidosis
Malaria
Hep B and C
HIV
SLE
Drugs - gold, NSAIDs, heroin, lithium
Malignancies - lymphoma and leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What can cause pre-renal azotemia?

A

Absolute fluid loss e.g. haemorrhage, vomiting, diarrhoea, severe burns
Relative fluid loss - congestive heart failure causing low CO, hypotension, NSAID use, ACEi ARB use, cyclosporine use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What causes azotemia?

A

High serum levels of nitrogen and creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What can cause intra-renal azotemia?

A

Acute tubular necrosis
vascular causes e.g. vasculitis
Acute tubulointerstitial nephritis
Glomerulonephritis (aka nephritic syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are the 3 types of ATN?

A

Ischemic-Induced Acute Tubular Necrosis e.g. MI or haemorrhage
Nephrotoxic-Induced Acute Tubular Necrosis (aminoglycosides, myoglobin secondary to rhabdomyolysis, radiocontrast agents, lead)
Sepsis-Induced Acute Tubular Necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are some nephrotoxins that can cause acute tubular necrosis?

A

Aminoglycosides
Heavy metals
Myoglobin
Uric acid in tumour lysis syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is acute tubulointerstitial nephritis?
What can cause it

A

inflammation that affects the tubules of the kidneys and the interstitium
Hypersensitivity reaction to drugs such as penicillins, NSAIDs or PPIs.
It can also be caused by infections e.g. pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What can cause a post-renal AKI?

A

BPH
Tumours
Stones

93
Q

Is pre-renal AKI reversible?

A

Yes but prolonged can lead to ischaemic intra-renal AKI

94
Q

How can you investigate pre-renal causes of AKI?

A

Check fluid status of patient
Calculate fractional excretion of Na+ and urea

95
Q

How can you investigate intra-renal causes of AKI/

A

Urinanalysis
Urine microscopic sensitivity
Urine casts
Renal ultrasound
Urine creatinine ratio and albumin creatinine ratio

(Think about intra causing inflammation = WBC casts. Alternatively glomerulonephritis causing haematuria)

96
Q

How can we investigate post renal causes of AKI/

A

Bladder scan for urinary retention
Check catheter to see if its blocked/kinked
Imaging to check for obstruction

97
Q

What are the indications for acute dialysis?

A

Acidosis (refractory)
Electrolyte imbalance (refractory severe hyperkalaemia)
Intoxication (Salicyclic acid, Lithium, Isopropanol, Magnesium laxatives, Ethylene glycol)
Overload with fluid
Uraemic complications e.g. pericarditis, platelet dysfunction

98
Q

What should you be thinking when you see a raised MCV and raised GGT?

A

Alcohol!

99
Q

Why can hypertension cause kidney failure?

A

We get thickening of vessel walls and luminal narrowing of the small arteries and arterioles which leads to chronic ischaemia and gradual loss of nephrons

100
Q

Outline how atherosclerotic renal disease can cause secondary hypertension?

A

Hypoperfusion of the kidney causes renin release -> angiotensin 2 release -> aldosterone release -> increased blood volume due to sodium and water retention -> hypertension

101
Q

What is interstitial nephritis?

A

A type 1 hypersensitivity reaction usually in response to antibiotics, NSAIDs or diuretics

102
Q

Outline the investigations for renal failure?

A

Urinanalysis and cultures
ABG - for acidosis
VBG - hyperkalaemia, raised urea and creatinine
CXR, AXR and ultrasound
Renal biopsy
ECG to look for hyperkalaemia

103
Q

What is hydronephrosis?

A

The swelling of the kidneys due to a build up of urine - indicates a backward pressure

104
Q

Why should you treat complications of AKI before the cause?

A

Because the complications will kill you faster

105
Q

Outline management for AKI?

A

Protect myocardium from hyperkalaemia - calcium gluconate
Remove K+ - insulin and dextrose
Diuretics for pulmonary oedema
Bicarbonate for any acidosis (or dialysis if refractory)
Then treat underlying cause

106
Q

What are the indications for dialysis?

A

Complications of uraemia e.g. encephalopathy
Refractory hyperkalaemia
Refractory fluid overload
Anuria

107
Q

Why is the BUN: creatinine ratio so important to look at?

A

As acutely urea will go up faster than creatinine (larger ratio)
But chronically creatinine will be higher than urea (smaller ratio)

108
Q

What GFR is end-stage renal failure?

A

<15ml/min

109
Q

What are the 3 most common causes of CKD?

A

DM
Hypertension
Glomerulonephritis

110
Q

What are come manifestations of CKD?

A

Peripheral neuropathy, restless leg syndrome, fatigue - urea affects nervous system
Taste perception
Accelerated atherogenesis!!!
Renal osteodystrophy and bone cysts
Electrolyte imbalances
Anaemia of chronic disease (EPO)
Bruise easily (impaired platelet function due to uraemia)

111
Q

What do most CKD patients die of and why?

A

Heart disease due to accelerated atherosclerosis

112
Q

Why does CKD cause renal osteodystrophy?

A

reduces absorption of calcium due to failure of hydroxylation of 25-dehydroxycholecalciferol. This low calcium level leads to hyperparathyroidism.

113
Q

How can we reduce the risk of heart disease in CKD patients?

A

We prescribe all CKD patients statins
BP control, blood sugar control etc

114
Q

What is a renal diet?

A

low in sodium, phosphorous, and protein. Some patients may also need to monitor potassium and calcium too

115
Q

What’s a normal potassium range?

A

3.5-5.0mmol/l

116
Q

What is mild hyperkalaemia? And what is severe?

A

5-6mmol/l is mild
>6mmol/l is severe (or a lower level but with ECG changes)

117
Q

What are the main causes of hyperkalaemia?

A

Renal failure
Drugs - combination of ACEi, K+ sparing diuretics and NSAIDs
Increased K+ release - acidosis, haemolysis, cytotoxic drugs, rhabdomyolysis

118
Q

What do we worry about when hyperkalaemia is accompanied by acidosis?

A

Ventricular tachyarrythmias

119
Q

Although its usually asymptomatic, what symptoms can be seen with hyperkalaemia?

A

Muscle weakness and flaccid paralysis

120
Q

How do you treat severe hyperkalaemia?

A

Protect the myocardium from K+ - 10ml 10% calcium glauconate IV
Remove K+ from the blood using 10 units actrapid insulin (check blood glucose!) and 50ml 50% dextrose IV.
You may give calcium resonium
you may also give 2.5mg salbutamol as this will also help drive K+ into cells

121
Q

Outline who we screen for CKD and how?

A

Those taking medicines that can adversely affect kidney function such as lithium or NSAIDs should have their GFR monitored at least annually

122
Q

How does screening for CKD happen after an AKI?

A

You should monitor patients for at least 3 years even if eGFR has returned to baseline

123
Q

What are some symptoms that suggest CKD rather than AKI?

A

Fatigue
Weight loss
Anorexia
Nocturia
Pruritus

124
Q

How does hypertension cause CKD?

A

Hypertension causes renal artery walls to thicken. Narrow lumen = ischaemic injury to nephrons glomerulus = immune cells secrete growth factors = mesangial cells regress to mesangioblasts which secrete extracellular matrix = glomerulosclerosis (scarring) which diminishes the ability to filter the blood

125
Q

How does diabetes cause CKD?

A

Non-enzymatic glycation = stiff and narrow efferent arterioles (hyaline arteriosclerosis) = increased pressure in glomerulus = hyperfiltration = mesangial cell expansion (glomerulosclerosis) = diminishes ability to filter blood

126
Q

What electrolyte imbalances are present in CKD?

A

Hyperkalaemia
Hypocalcaemia

127
Q

Which types of drugs are typically excreted directly via the kidneys?

A

Hydrophilic (hydrophobic must first undergo biotransformation before)

128
Q

How does urinary pH impact excretion?

A

Drug ionisation changes depending on the alkaline or acidic environment. Increased excretion of weakly acidic drugs occurs with basic urine and vice versa.

129
Q

What can impact kidney drug excretion?

A

Renal disorders
Age - kidney function naturally declines with ages
Pathologies that impact renal blood flow or urine flow e.g. congestive HF

130
Q

Why are ACEi contraindicated in patients with bilateral renal artery stenosis?

A

due to risk of azotemia resulting from preferential efferent arteriolar vasodilation in the renal glomerulus.

131
Q

What are the main causes of oedema?

A

Medication
Pregnancy
Underlying disease e.g. kidney disease, liver cirrhosis, congestive heart failure

132
Q

What are the main causes of proteinuria?

A

Glomeruli disease
Urine infections
First warning of eclampsia in pregnancy
Intense exercise
Stress
Fever
Prolonged exposure to cold temperatures

133
Q

What’s the structure of immunoglobulins?

A

they are heterodimic proteins composed of 2 heavy and 2 light chains. They are separated functionally into variable domains that bind antigens and constant domains that specify effector functions e.g. activating complement of binding to Fc receptors.

134
Q

What are the 5 main classes of heavy chain C domains of immunoglobulins?

A

IgM, IgG, IgA, IgD, IgE

135
Q

What’s the function of IgM?

A

They are membrane bound and found on the surface of immature and mature B cells.
They are the first antibody produced in primary response to an antigen
They are efficient in binding antigens with many repeating epitopes and activate the complement
Responsible for early stages of immunity

136
Q

What’s the function of IgG?

A

The most abundant class with 4 isotopes.
They have the highest opsonisation and neutralisation activities

137
Q

What’s the function of IgA?

A

expressed in mucosal tissues and secretions
Forms dimmers after secretion
First lune of defence against infection by microorganism

138
Q

What’s the function of IgD?

A

Membrane bound immunoglobulin on the surface of matur B cels with no biological effector function known

139
Q

What’s the function of IgE?

A

Found mainly in tissues
Associated with hypersensitivity reactions and defend against parasite infections

140
Q

What’s the function of Th1 cells? What cytokines do they release?

A

They drive activation of monocytes, macrophages and cytotoxic T lymphocytes.
they have a key role in protection against intracellular pathogens
Release INF gamma and TNF alpha

141
Q

What’s the function of Th2 cells? What cytokines do they release?

A

Drive antibody responses and promote eosinophil granulocyte functions
Protect against extracellular parasites and immune responses that underlie allergic disease
Secrete IL-4, IL-5 and IL-13

142
Q

What’s the function of Th17 cells? What cytokines do they release?

A

Drive inflammatory responses, especially via recruitment of neutrophil granulocytes
Protect against fungal infections and have a role in chronic inflammatory diseases
Secrete IL-17

143
Q

What’s the function of T follicular helper cells? What cytokines do they release?

A

helping B cells produce antibody against foreign pathogens.
Secrete IL-21

144
Q

What’s the function of T regulatory cells? What cytokines do they release?

A

maintaining peripheral tolerance, preventing autoimmune diseases and limiting chronic inflammatory diseases
Secrete IL-10 and TGF-beta

145
Q

What is the function of cytotoxic CD8 T cells?

A

They kill virus infected cells following recognition of viral peptide HLA class 1 complexes.

146
Q

What are the 3 mechanisms that CD8 T lymphocytes can kill?

A

Cytotoxic granule proteins e.g. perforin
Toxic cytokines
Death inducing surface molecules

147
Q

What’s the most common cause of AKI?

A

Infections and nephrotoxic drugs

148
Q

What’s the definition of nephrotoxic drugs?

A

Any drugs who act directly on the kidneys

149
Q

What are the diagnostic criteria for AKI?

A

A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days.
A fall in urine output to less than 0.5mL/kg/hour for more than 6 hours.

150
Q

What’s the diagnostic criteria for a CKD?

A

CKD is a reduction in kidney function or structural damage present for more than 3 months
It includes all individuals with markers of kidney damage or those with an eGFR of less than 60ml/min/1.73m2 on at least 2 occasions 3 months apart

151
Q

Why do we use eGFR for CKD and not AKI?

A

eGFR calculations assume that the level of creatinine in the blood is stable over days or longer

152
Q

What are the 2 reasons that CKD can cause hypocalcaemia?

A

increased serum phosphorus and decreased renal production of 1,25 (OH)2 vitamin D.

153
Q

Outline BUN:Cr, FENA and urine osmolality in pre-renal AKI?

A

BUN:Cr ratio >20:1 - this is because the functioning units of the kidney have not been affected so they can still excrete creatinine and retain urea as normal
Fractional excretion of sodium (FENA) <1% and urine osmolality >500 (very conc) - because urine urea is low and sodium and water follow the urea into the blood

154
Q

Outline BUN:Cr, FENA and urine osmolality in intra-renal AKI?

A

BUN:Cr ratio will be <15:1 as urea can’t be reabsorbed and creatinine can’t be excreted (tubular cells damaged).
FENA is >2% and osmolality <350. The low GFR stimulates RAAS but kidney tubules can’t respond to aldosterone. Na+ and water follow urea into urine.
Doesn’t respond to fluid challenge

155
Q

Outline BUN:Cr, FENA and urine osmolality in post-renal AKI?

A

Early stages - will resemble pre-renal AKI as kidney tubules are functioning BUN:Cr >20:1
In later stages it will resemble intra-renal AKI as kidney tubules are no longer functioning BUN:Cr <15:1

156
Q

How do you rule out post-renal causes?

A

Renal ultrasound (alternatively CT, bladder scan etc)

157
Q

What are the 3 ways in which glomerulonephritis can present?

A

asymptomatic urinary abnormalities
acute nephritis (nephritic syndrome)
rapidly progressive glomerulonephritis.

158
Q

Which chromosome is most likely affected in autosomal dominant Polycystic kidney disease?

A

Chromosome 16

159
Q

How can we measure renal plasma flow?

A

By measuring para aminohippuric acid

160
Q

What proportion of renal flow is the GFR usually?

A

20%

161
Q

What is a nephrostomy?

A

a thin, plastic tube (catheter) that is inserted through the skin on your back, and into a kidney - drains the kidney

162
Q

Why are the kidneys and lungs commonly affected at the same time?

A

They both have plenty of basement membranes

163
Q

When are ACEi Reno-protective?

A

In patients with renal disease and diabetes

164
Q

What are the contraindications for ACEi?

A

hyperkalemia, renal artery stenosis, pregnancy, or prior adverse reaction to an ACEI including angioedema.

165
Q

What can increase serum urea?

A

High protein diet
Increased catabolism e.g. surgery, infection, trauma
Steroid therapy
Renal disease

166
Q

What can decrease serum urea?

A

Hepatic dysfunction
Physiological increased filtration e.g. pregnancy
Low protein diet
Reduced catabolism e.g. old age

167
Q

What form of investigation is diagnostic for kidney injury?

A

Renal biopsy

168
Q

What associated sympotms are present with a obstruction in post-renal failure?

A

Vomiting

169
Q

How do you treat hyperphosphataemia

A

Phosphate binders e.g. calcium carbonate or calcium acetate

170
Q

How do you treat uraemic encephalopathy?

A

Renal replacement therapy

171
Q

Whats the classic picture of pulmonary oedema on x-ray?

A

Bat wing distribution of a heterogeneous opacity
Fluid filled fissure
Kerley B lines

172
Q

At what mean arterial pressure does perfusion to the kidney stop?

A

65mmHg

173
Q

How does acute interstitial nephritis present?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

174
Q

When should you refer to a nephrologist concerning an eGFR?

A

referring to a nephrologist from primary care if eGFR falls below 30 or progressively by > 15 in a year

175
Q

Whats the difference between Contrast media nephrotoxicity and contrast-induced nephropathy?

A

Contrast media nephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media. Contrast-induced nephropathy occurs 2 -5 days after administration.

176
Q

How can you prevent contrast induced nephropathy?

A

intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure
And stop metformin for a minimum of 48 hours and until the renal function has been shown to be normal - prevents lactic acidosis

177
Q

Whats the most commonly isolated organism in peritonitis associated with peritoneal dialysis?

A

Staphylococcus epidermidis

178
Q

On biopsy, what does a sample for post-streptococcal glomerulonephritis show?

A

IgG, IgM and C3 immune complex deposition
Endothelial proliferation with neutrophils

179
Q

Whats the most common type of glomerulonephritis in adults?

A

Membranous glomerulonephritis

180
Q

How does membranous glomerulonephritis present?

A

Nephrotic syndrome or proteinuria

181
Q

What can cause membranous glomerulonephritis?

A

Causes
idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

182
Q

How do you manage membranous glomerulonephritis?

A

ACEi or ARB to reduce proteinuria
Anticoagulation for high risk patients
Severe and progressive disease - corticosteroids and cyclophosphamide

183
Q

Whats the prognosis for membranous glomerulonephritis?

A

one-third: spontaneous remission
one-third: remain proteinuric
one-third: develop ESRF

184
Q

What are the complications of nephrotic syndrome?

A

Increased risk of thromboembolism
Increased risk of acute coronary syndrome, stroke etc
CKD
Infections
Hypocalcaemia

185
Q

Why can nephrotic syndrome increase the risk of thromboembolism?

A

increased excretion of antithrombotic factors by the affected kidneys and increased production of pro-thrombotic factors by the liver.

186
Q

Why is there an increased risk of acute coronary syndrome and or stroke in nephrotic syndrome?

A

Due to the hyperlipidaemia

187
Q

Why does nephrotic syndrome cause hyperlipidaemia?

A

increased hepatic lipogenesis, a non-specific reaction to falling oncotic pressure secondary to hypoalbuminemia.

188
Q

Why does nephrotic syndrome increase risk of infections?

A

As immunoglobulin are lost in the urine

189
Q

Why does nephrotic syndrome put you at risk for hypocalcaemia?

A

As vitamin D and binding protein are lost in the urine

190
Q

What are the 3 main things that can cause nephritic syndrome?

A

Small vessel vasculitis
Immune complex deposition
Anti-GBM autoantibodies

191
Q

What are examples of how immune complex deposition can cause nephritic syndrome?

A

SLE
Post-streptococcal glomerulonephritis
IgA nephropathy
Cryoglobulinaemia

192
Q

What is ANCA-associated vasculitis?

A

An umbrella term for
- Microscopic polyangiitis (MPA)
- Granulomatosis with polyangiitis (GPA): previously known as Wegener’s granulomatosis
- Eosinophilic granulomatosis with polyangiitis (EGPA): previously known as Churg-Strauss syndrome

193
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibody (autoantibodies that target self antigens leading to a vasculitis

194
Q

What is anti-GBM disease?

A

a rare small-vessel vasculitis that results from the formation of GBM antibodies that target type IV collagen within the basement membrane. This results in linear deposition of IgG in the glomerular capillaries.

195
Q

Whats the aetiology of nephrotic syndrome?

A

Structural damage = loss of negative charge at the GBM means the loss of the selectivity of permeability
=massive non-selective loss of protein

196
Q

Whats the aetiology of nephritic syndrome?

A

Inflammation of glomerulus = cytokine release = leaky capillaries = leakage of proteins and RBC

197
Q

What does ‘diffuse’ mean?

A

Affecting >50% of glomeruli

198
Q

What does ‘focal’ mean?

A

Affecting <50% of glomeruli

199
Q

What does ‘global’ mean?

A

Entire glomerulus is affected

200
Q

What does ‘segmental’ mean?

A

Only part of the glomerulus is affected

201
Q

What does ‘proliferative’ mean?

A

An increased number of cells in glomerulus

202
Q

What does ‘membranous’ mean?

A

Thickening of GBM

203
Q

What does ‘sclerosis’ mean?

A

Scarring of glomerulus

204
Q

What are examples of mixed nephrotic and nephritic syndrome causes?

A

Membranoproliferative GN
Poststreptococcal GN

205
Q

What is rapidly progressive glomerulonephritis?

A

A nephritic syndrome which rapidly progresses to renal failure in days/weeks
It can be caused by ANCA–associated small-vessel vasculitis, lupus nephritis and anti-GBM disease
It may be associated with pulmonary haemorrhage

206
Q

What is seen on renal biopsy in rapidly progressive GN?

A

Crescents - breaks in the GBM allow an influx of inflammatory cells

207
Q

Whats the treatment for rapidly progressive glomerulonephritis?

A

Corticosteroids
Cyclophosphamide
Plasma exchange

208
Q

What is seen on renal biopsy in IgA nephropathy?

A

Mesangial hypercellularity
Positive immunofluoresence for IgA and C3

209
Q

How is IgA nephropathy treated?

A

ACEi/ARBs to reduce proteinuria
If after 3-6 months of this there is persistent haematuria… Corticosteroids

210
Q

What is Henoch-schonlein purpura?

A

(A systemic variant of IgA nephropathy)
IgA deposition in skin, joints, gut and kidneys
Presents with a purpuric rash on extensor surfaces, poly arthritis, abdominal pain (GI bleeding) and nephritic syndrome

211
Q

What is found on renal biopsy in Henoch-schonlein purpura?

A

Mesangial hypercellularity
Positive immunofluoroscence for IgA and C3

212
Q

What does Alport syndrome look like on renal biopsy?

A

Longitudinal splitting of laminate dense of GBM = basket weave appearance (on electron microscopy)

213
Q

How is Alport syndrome managed?

A

ACEi/ARBs may slow progression of disease but most patients require dialysis or transplant

214
Q

What is membranoproliferative glomerulonephritis?

A

A mixed nephritic/nephrotic syndrome
Due to either immune complex deposition secondary to autoimmune conditions, infections of Cryoglobulinaemia. OR due to C3 glomerulopathy
Effacement of foot processes of pdodocytes with electron dense deposits on electron misciospy

215
Q

What is a C3 glomerulopathy?

A

A genetic or acquired defect in the C3 complement pathway

216
Q

How can a recent streptococcal infection be confirmed?

A

Positive anti-streptolysin O titres

217
Q

What is seen on renal biopsy for PSGN?

A

Acute, diffuse, proliferative glomerulonephritis
Immunofluorescence shows a granular starry sky appearance

218
Q

What is minimal change disease?

A

A nephrotic syndrome that’s usually idiopathic but may be due to drugs, paraneoplastic or infectious mononucleosis
Typically affects children
Causes a highly selective proteinuria - mainly albumin and transferrin leak

219
Q

Whats seen on renal biopsy in minimal change disease?

A

No changes on light microscopy but effacement of foot processes of podocytes on electron microscopy

220
Q

How is minimal change disease managed?

A

Steroids

221
Q

What is focal segmental glomerulosclerosis?

A

A cause of nephrotic syndrome
Scarring of GBM that can be idiopathic or secondary to HIV/heroine/lymphoma/other forms of GN
High recurrence rate even after renal transplant

222
Q

What is seen on renal biopsy in focal segmental glomerulosclerosis?

A

Focal and segmental sclerosis
Effacement of foot processes of podocytes on electron miscioscpy

223
Q

What is membranous glomerulonephritis?

A

The most common cause of nephrotic syndrome
May be primary to anti-phospholipase A2 antibodies or secondary to infections/malignancy/drugs/autoimmune conditions

224
Q

Whats seen on renal biopsy in membranous glomerulonephritis?

A

Spike and dome pattern on electron microscopy - deposition of antibodies between podocytes and basal membrane

225
Q

How is membranous glomerulonephritis managed?

A

Ponticelli regime - IV methylprednisolone, prednisolone tablets, cyclophosphamide tablets

226
Q

Whats the most common cause of end-stage renal failure?

A

Diabetic nephropathy

227
Q

What is seen on renal biopsy in amyloidosos?

A

Nodular glomerulosclerosis with apple green birefringence due to amyloid deposition with Congo red stain

228
Q

What are the main causes of focal segmental glomerulosclerosis?

A

FSG is caused (mostly) by the 4H’s

  • Huh? - idiopathic
  • Hurt kidney - secondary to other nephropathies
  • HIV
  • Heroin
229
Q

What casts are seen on acute tubular necrosis?

A

Brown granular casts

METABOLIC (43 decks)

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