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Week 5 Flashcards

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1
Q

What drugs vasoconstrict the afferent arteriole? What does this cause?

A

NSAIDs e.g. naproxen.

Causes decreased glomerular filtration rate.

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2
Q

What drugs vasodilator the afferent arteriole? What does this cause?

A

ANP
Prostaglandins
Increases glomerular filtration rate.

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3
Q

What drugs vasoconstrict the efferent arteriole? What does this cause?

A

Angiotensin II
ANP
Noradrenaline
Causes an increase in glomerular filtration.

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4
Q

What drugs vasodilator the efferent arteriole? What does this cause?

A

ACEI
ARB
Causes a decrease in glomerular filtration rate.

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5
Q

What is renal osteodystrophy?

A

When the kidneys become damaged in chronic kidney disease- it means they hydrolysing vitamin D to its active form. This means that calcium isn’t absorbed from the gut to replace that lost from the bone. This causes weak bones.

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6
Q

Acute kidney injury can be…

A

Pre, intra or post renal.

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7
Q

Causes of pre-renal AKI?

A

Due to hypoperfusion of the kidney e.g. from renal artery stenosis, hypovolaemia due to diarrhoea, sepsis causing hypovolaemia, hypotension due to cardiac causes e.g. MI.

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8
Q

What would happen if AKI wasn’t treated?

A

It would mean the kidney would undergo acute tubular necrosis due to lack of oxygen.

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9
Q

How would you diagnose AKI?

A

Ultrasound is needed to check for obstruction and to check the size of the kidneys (to check for acute exacerbation of chronic kidney disease which will mean the kidneys are often smaller)

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10
Q

What would you do if the ultrasound reveals no apparent cause of hypoperfusion of the kidneys and they appear to be normal size?

A

Urgent renal biopsy

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11
Q

What is the treatment for hyperkalaemia?

A

Calcium gluconate 10% 10mls IV- cardioprotective against arrhythmias.
10 units of act rapid insulin and 50mls of glucose 50%IV- insulin causes potassium to move into cells and glucose prevents the subsequent hypoglycaemia it would cause.
2.5mg of salbutamol. Beta agonists cause pottasium uptake in cells.

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12
Q

Will the acute treatment of hyperkalaemia suffice?

A

Patient is most likely to need heamo-dialysis as the acute treatment is only temporary.

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13
Q

What are the stages of chronic kidney disease?

A

Stage 1- GFR normal- >90. Has to have evidence of kidney damage.
Stage 2- GFR 60-90. Need evidence of kidney damage.
Stage 3- GFR 30-59.
Stage 4- GFR of 15-30
Stage 5- GFR of less than 15 OR on renal replacement therapy.

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14
Q

Pathogenesis of diabetic nephropathy

A

High blood glucose causes release of vasoactive mediators that dilate the afferent arteriole increasing GFR. Also causes a release of growth factors causing renal hypertrophy and mesangial expansion.
This causes nodule formation and diffuse glomerulosclerosis.
This causes inflammation, proteinuria (due to GBM thickening and podocyte dysfunction) and tubulointerstitial fibrosis.

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15
Q

How would you diagnose diabetic nephropathy?

A

History of DM
Albuminuria/proteinuria
Presence of other diabetic problems (if they have retinopathy they are likely to have issues with their kidney)
Renal impairment (late finding)

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16
Q

Describe the 3 stages of diabetic nephropathy

A 
Stage 1: Pre 
- renal hypertrophy
-GFR increases 
Stage 2: Incipient 
- microalbuminuria
-hypertension
Stage 3: Overt
-proteinuria
-nephrotic syndrome
-mesangial nodules (Kimmel-steil wilson lesions)
-tubulointerstitial fibrosis
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17
Q

How would you prevent and manage diabetic nephropathy?

A

Prevention- good glycaemic control
Antihypertensive therapy- tight BP control (< 130/80) using ACE inhibitors and ARBs
Lipid control.

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18
Q

How do you slow the progression of diabetic nephropathy?

A

Reduce proteinuria.

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19
Q

What is ischaemic neuropathy?

A

Refers to the reduced GFR associated with reduced renal blood flow beyond the level of auto regulatory compensation.
Over time- can lead to renal atrophy and progressive CKD.

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20
Q

What can cause ischaemic neuropathy?

A

Essential hypertension
Secondary hypertension- due to atherosclerosis in the renal arteries causing stenosis
Or fibromuscular dysplagia

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21
Q

What occurs if the renal is under-perfused?

A

It activates a series of hormonal and neuronal responses resulting in an increase in systemic bp.

This is due to the increased blood pressure trying to overcome the blockage and perfuse the kidneys. It compensates a bit. When you then treat the high blood pressure- the kidneys become even more under-refused hence the AKI.

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22
Q

Who gets atherosclerotic renal vascular (renal artery stenosis) disease?

A

Older patients (greater than 50)
Males affected more than females
Usually unilateral

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23
Q

Clinical presentation of renal vascular disease?

A 
Renovascular hypertension
AKI after treatment for hypertension
CDK with diffuse vascular disease
Flash pulmonary oedema
Abdominal bruits.
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24
Q

What investigation would you use to look into renal artery stenosis?

A 
Renal artery US
Renal artery duplex studies
CT angiography
MR angiography
Conventional angiography
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25
How would you treat renal artery stenosis?
Medical therapy- Statin Antiplatelet ACE inhibitor Interventional therapy- angiography +/- stenting.
26
When are ACE inhibitors as treatment for renal artery stenosis contraindicated?
When it is bilateral disease. In unilateral they protect the other kidney by lowering the bp and preventing further damage. However they also decrease GFR and if both kidneys are already affected by stenosis- the GFR will already be very low. Therefore ACE inhibitors will not be helpful.
27
What is fibromuscular dysplagia?
Non atherosclerotic, non-inflammatory disease of the blood vessels that results in abnormal growth in the vessel walls.
28
What can fibromuscular dysplagia be associated with?
Ehler danlos syndrome.
29
What other artery can fibromuscular dysplagia cause?
Other than the renal artery can involve the cerebral artery.
30
What is myeloma?
Cancer of plasma cells (B lymphocytes) | They normally produce antibodies.
31
What occurs in myeloma?
Multiple plasma cells accumulate in the bone marrow impairing production of normal blood cells. They produce a paraprotein (abnormal antibody) that causes renal dysfunction.
32
Symptoms of myeloma?
Bone pain Weakness Fatigue Weight loss
33
Signs of myeloma?
``` Anaemia Hypercalcaemia Renal failure Amyloidosis Recurrent infections. ```
34
Classical presentation of myeloma?
Back pain and renal failure.
35
Glomerular manifestations of myeloma?
AL Amyloidosis | Monoclonal immunoglobulin depositation.
36
Tubular manifestations of myeloma?
Light chain cast nephropathy
37
Miscellaneous renal manifestations of myeloma?
Dehydration, hypercalcaemia, contrast, bisphosphonates, NSAIDs.
38
How would you diagnose myeloma?
Need a high index of suspicion Bloods- serum free light chains. Serum free electrophoresis. Urine- presence of bence jones protein Bone marrow and renal biopsy
39
Management of myeloma?
Chemotherapy | Stem cell transplant
40
What type of vasculitis normally affects the kidney?
Small vessel.
41
How would patients present with small vessel vasculitis?
Fever, arthralgia, weight loss, malaise
42
What is ANCA associated small vessel vasculitis?
Necrotising polyangitis that affects capillaries, venules and arterioles.
43
Who gets ANCA associated small vessel vasculitis?
People tend to present in their 5,6 or 7th generation.
44
How would you diagnose small vessel vasculitis?
Urinalysis Bloods- look for raised inflammatory markers, AKI and anaemia. Immunology- ANCA, Anti-MPO and Anti PR3 Renal biopsy
45
Presentation fo granulomatosis with polyangitis?
Predominantly anti PR3 antibodies | Inflammation most commonly affects the respiratory tract.
46
Presentation of microscopic polyangitis?
Predominantly anti MPO antibodies. | Small vessel vasculitis with no granulomas.
47
Presentation of eosinophilic granulomatosis?
Asthma and eosinophilia. Also sometimes skin involvement.
48
Management of small vessel vasculitis?
Immunosupression- steroids and cyclophosphamide. Plasma exchange Supportive dialysis.
49
What renal involvement do lupus patients get?
Most frequently observes abnormality if proteinuria. | A number of types of renal disease can occur and are differentiated by renal biopsy.
50
Describe the classification of lupus nephritis?
``` Class I- minimal mesangial Class II- Mesangial proliferative Class III- Focal proliferative Class IV- Diffuse proliferative Class V-Membranous Class VI-advanced sclerosing. ```
51
What is renal replacement therapy?
Either transplantation or dialysis
52
Two types of dialysis?
Haemodialysis and peritoneal dialysis
53
How does haemodialysis work?
The blood is filtered into a tube that runs alongside a semi-permeable membrane. On the other side of the tube is dialysis fluid containing water, small amounts of sodium, urea and potassium and large amounts of bicarbonate. Due to the concentration difference- the large amounts of sodium, potassium and urea in the blood move across to the dialysis fluid creating an equilibrium. The bicarbonate moves the opposite way into the blood (to stop acidosis in the patient). Water moves across by a negative pressure from the blood into the dialysis fluid.
54
How can you gain access to a patients blood?
Need to either put in a fistula or a tunnelled venous catheter.
55
What is a fistula?
A vein is attached directly into an artery. This makes a high pressure system and the vein starts to get bigger. This is a good place for blood to be taken as it is strong.
56
Pros and cons of fistulas?
Pro's- good blood flow | Cons- takes 6 weeks to prepare after surgery.
57
What is a tunnelled venous catheter?
A line straight into the jugular vein. Good for emergency situations e.g. AKI. However higher risk of infection.
58
What is peritoneal dialysis?
Instead of using an artificial membrane- the peritoneum is used as a membrane. It can be done either over night automated peritoneal dialysis, or 4 times daily for half an hour (continuous peritoneal dialysis).
59
What is in the dialysis fluid in peritoneal dialysis?
High levels of glucose to attract water by osmosis. | Low levels of potassium, urea, and sodium to attract these to diffuse across.
60
What can go wrong with peritoneal dialysis?
Peritonitis- usually infection by staph aureus. If you cough- strep. Thickening of the peritoneal membrane meaning water cannot diffuse across. Hernias (increased intraabdominal pressure and interfere with dialysis)
61
Describe the restrictions a dialysis patient will have to endure?
``` Water restriction- no more than 1 litre per day Salt restriction Pottasium restriction Phosphate restriction (have to take phosphate binding pills) ```
62
What metabolic complications can you get from end stage renal failure?
``` Phosphate retention Leading to hypocalcaemia and release of parathyroid hormone Low 1,25 vitamin D Anaemia- low epo and iron deficient Salt and water retention ```
63
When would you start a patient on dialysis?
``` On bloods GFR<5 or Resistant hyperkalaemia or Urea >45 Unresponsive acidosis ``` Or based on symptoms- fatigue, lethargy, nausea/vomiting, itch
64
Define acute kidney injury?
An abrupt reduction in kidney function defined as a serum creatinine of >26.4 Or an increase in creatinine by >50% Or a reduction in urinary output.
65
KDIGO staging of AKI
Based on serum creatinine or urine output (in practice- creatinine) Stage 1- >26 or 1.5-1.9 x reference creatinine Stage 2- 2-2.9 x reference creatinine Stage 3- > or = 3 x reference creatinine or >354 or need for RRT. Urine ratios Stage 1- <0.5ml/kg/hour for >6 hours Stage 2<0.5ml/kg/hour for >12 hours Stage 3<0.3mk/kg/hour for >24 hours.
66
Risk factors for AKI
``` Diabetes Older age Chronic kidney disease Peripheral vascular disease Heart failure Liver disease ```
67
How is AKI classified?
Pre-renal Intrinsic Post renal
68
Pre-renal causes of AKI
All result in hypo perfusion of the kidney - Hypovolaemia due to fluid/blood loss. Could be haemorrhage or D and V - Hypoperfusion- ACEi/ARBs. NSAIDs - Hypotension- cardiogenic shock, disruptive shock.
69
What does untreated pre-renal AKI lead too?
Acute tubular necrosis.
70
What can cause acute tubular necrosis?
Rhabdomyalysis- breakdown/injury of muscle Sepsis and severe dehydration Drug toxicity
71
Treatment of pre-renal AKI?
Assess for hydration- Cap Refill, BP, HR, UO, oedema 0.9% NaCl solution- give bolus of fluid and then reassess as necessary If greater than 1000mls and no improvement- get help.
72
Causes of intrinsic renal AKI?
Disease causing inflammation or damage to the cells causing AKI - blood vessels- vasculitis - glomerular disease-glomerular nephritis - tuberlar injury- acute tubular necrosis, drugs (gentamicin), rhabdomyolysis, contrast - interstitial injury- drugs, infection, systemic
73
Signs and symptoms of Aki
Anorexia, fatigue, weight loss, lethargy Nausea and vomiting Itch Fluid overload (oedema, SOB) Signs- pleural and pulmonary effusions due to fluid overload Uraemia, itch Oligouria
74
What would give you a clue that it is a renal cause?
Sore throat, rash, joint pains, D&V, haemoptysis Recent contrast Vascular bruits
75
What initial investigations would you do into AKI?
``` U&E's- Potassium high?, creatinine? FBC and coagulation screen- abnormal clotting, anaemia Urinalysis- proteinuria, haematuria USS- size of kidney? Obstruction? Immunology- ANCA, Anti-GBM, ANA ```
76
When would you biopsy in AKI?
Urgent- suspected rapidly progressing GN -Positive immunology and AKI Semi urgent- unexplained AKI to gain a diagnosis Rule out obstruction, volume depletion and AVN
77
Further treatment of AKI?
Establish good perfusion- fluid resus. If still not adequate perfusion then use inatropes/vasopressors. Treat underlying cause- antibiotics it sepsis Stop nephrotoxics Dialysis if remains anuric and uraemia.
78
Life threatening complications of AKI?
``` Pulmonary oedema Acidosis Hyperkalaemia Uric >40 Ureamic pericardial effusion ```
79
What is post renal AKI?
Blockage or obstruction leading to back pressure on the kidney (hydronephrosis) and stopping of function.
80
Causes of post renal AKI?
Stones, cancers, strictures, extrinsic pressure.
81
Treatment of post renal AKI?
Relieve obstruction Catheter Nephrostomy
82
ECG changes in hyperkalaemia
Depressed ST segment Peaked T waves Flattened P waves

Renal (5 decks)

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