MET3 Revision: Renal II Flashcards

1
Q
A
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2
Q

What are the two ways of classifying CKD? [2]

A

Via GFR; and albumin excretion

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3
Q

What are the classifications of CKD by GFR? [5]

A

· Stage 1: any kidney problem, but eGFR >90
· Stage 2: any kidney problem, eGFR 60-90
· Stage 3a: eGFR 45-59
Stage 3b eGFR 30-44
· Stage 4: eGFR 15-30
· Stage 5: eGFR < 15

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4
Q

What are the classifications of CKD by albuminuria? [6]

A

A1:
* Albumin excretion (mg/24hr): < 30
* ACR: < 3

A2:
* Albumin excretion (mg/24hr): 30-300
* ACR: 3-3-

A3:
* Albumin excretion (mg/24hr): >300
* ACR: >30

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5
Q

What are primary renal disease causes of CKD:

Glomerular [1]
Tubolinterstitial [1]
Blood flow [1]
Cystic / congenital [1]
Transplant [1]

A

What are primary renal disease causes of CKD:

Glomerular: MCD; membranous nephropathy
Tubolinterstitial; UTI; pyelonephritis; stones
Blood flow: renal limited vasculitis
Cystic / congenital: renal dysplasia
Transplant: recurrence of renal disease

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6
Q

What are systemic causes of CKD:

Glomerular [1]
Tubolinterstitial [1]
Blood flow [1]
Cystic / congenital [1]
Transplant [1]

A

What are systemic causes of CKD:

Glomerular: diabetes; amyloid
Tubolinterstitial: drugs, toxins, sarcoid
Blood flow: heart failure
Cystic / congenital: alport syndrome
Transplant: rejection, calcineruin toxicity

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7
Q

Who manages stages 3-5 of CKD? [3]

A

Stage 3 CKD with eGFR 30-60: the most important effect of this is the increase on your vascular risk: mostly managed by GP to reduce vascular risk and prevent progression of CKD to the point where it needs serious intervention + likely dialysis.

Stage 4 CKD: is also quite poor kidney function and will likely need nephrology attention.

Stage 5 CKD: patients need immediate nephrology attention and are very close to needing dialysis.

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8
Q

State 5 pathological systemic consequences of CKD [5]

A

Anaemia
Renal bone disease
HTN
Acid / base imbalance
Uraemia

(Basic roles of the kidneys

  1. Get rid of fluid (and sodium)
  2. Control serum pH
  3. Control serum potassium
  4. Regulate BP
  5. Regulate Hb via EPO production
  6. Control bone and mineral metabolism both through Ca/PO excretion and through Vit D

So, in cases of CKD, all of these things go wrong as they cannot go ahead as normal like they do in a healthy kidney)

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9
Q

Describe how anaemia can occur due to CKD [5]
Which stage of CKD does this occur in? [1]

A
  • Reduced secretion if EPO; relative deficiency
  • Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • Reduced absorption of iron
  • Anorexia due to uraemia
  • Reduced RBC survival}}

G3B+

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10
Q

How can acidosis occur due to CKD? [2]

A

Increased tendency to retain hydrogen ions (due to abnormalities in acid-base homeostasis)
Leads to low levels of bicarbonate

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11
Q

Describe what the mineral disturbances in CDK MBD (CKD mineral bone disorder) are [3]

A

Disturbances in Ca & P metabolism, causing:
High serum phosphate (reduced excretion)

Low vitamin D activity - causing low serum calcium (healthy kidneys metabolise vitamin D into it’s active form, which is essential for Ca reabsorption& regulating bone turnover

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12
Q

What are the pathological consequences of low Ca2+ in CKD MBD? [3]

A

Low serum calcium and high serum phosphate causes the parathyroid glands to excrete more PTH: secondary hyperparathyroidism.

PTH stimulates osteoclast activity, increasing calcium absorption from bone. This results in osteomalacia

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13
Q

What is the name for this radiographical finding of CKD MBD? [1]

Describe why this occurs [2]

A

Rugger jersey spine

Sclerosis of both ends of each vertebral body (denser white)
Osteomalacia in the centre of the vertebral body (less white)

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14
Q

How do you manage CKD MBD? [3]

A

· Vitamin D analogues & dietary supplements
· Dietary restriction of phosphate and prescribe phosphate binders around the time of meals
· Calcimimetics: bind to PTH receptors and mimic the normal action of calcium to prevent PTH release

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15
Q

What level of serum P do you treat CKD bone-mineral disease at? [1]

A

P > 1.5mmol/L

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16
Q

What is the BP aim for patients with CKD? [1]

What is the BP aim for patients with CKD & DM or ACR > 70? [1]

A

What is the BP aim for patients with CKD? [1]
* < 140/90
What is the BP aim for patients with CKD & DM or ACR > 70? [1]

:< 130/80

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17
Q

When should you refer a patient to a renal specialist? [5]

A
  • eGFR less than 30 mL/min/1.73 m2
  • Urine ACR more than 70 mg/mmol
  • proteinuria > 30 mg/mmol & haematuria
  • Accelerated progression (a decrease in eGFR of 25% or 15 mL/min/1.73 m2 within 12 months)
  • 5-year risk of requiring dialysis over 5%
  • Uncontrolled hypertension despite four or more antihypertensive
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18
Q

Describe the managment for CKD patients:

To slow disease progression [2]

To reduce risk of complications [1]

A

Slow disease progression:
- ACE inhibitors (or angiotensin II receptor blockers)
- SGLT-2 inhibitors (specifically dapagliflozin)

To reduce risk of complications:
- Atorvastatin 20mg (prevents CV disease)

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19
Q

Which CKD patients should be offered ACE inhibitors? [3]

When is a SGLT-2 inhibitor be given to CKD patients? [1]

A

ACE inhibitors are offered to all patients with:
* Diabetes plus a urine ACR above 3 mg/mmol
* Hypertension plus a urine ACR above 30 mg/mmol
* All patients with a urine ACR above 70 mg/mmol

SGLT-2 Inhibitors
Dapagliflozin is the SGLT-2 inhibitor licensed for CKD. It is offered to patients with:
* Diabetes plus a urine ACR above 30 mg/mmol

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20
Q

What is normal protein daily excretion? [1]

A

< 150mg/day

21
Q

First line treament for reducing proteinuria is? [2]

A

ACE inhibitors
ARBs

22
Q

How do you treat anameia of CKD? [2]

A

Iron deficiency is treated before using erythropoietin.

Anaemia may be treated with erythropoiesis-stimulating agents, such as recombinant human erythropoietin.

23
Q

Why do blood transufusions need to be carefully considered when treating anaemia of CKD? [1]

A

Blood transfusions can sensitise the immune system (allosensitization), increasing the risk of future transplant rejection.

24
Q

How does HIV-associated nephropathy appear on US? [1]

A

Chronic HIV-associated nephropathy will have large/normal sized kidneys on ultrasound

25
Q

Name the two most common loop diurertics [2]

A

Furosemide & Bumetanide

26
Q

At high doses, explain what AE loop diuretics can cause

A

Tinnitus & hearing loss:
- A similar NaCl2K transporter is found in the inner ear which regulates endolymph

27
Q

Describe which pathology chronic loop diuretic use can lead to [2]

A

Gout: due to inhibition of uric acid secretion

28
Q

Loop diuretics have the potential to effect drugs excreted by the kidneys.

Name and describe three examples [3]

A

Lithium: have reduced excretion, so have increased levels occur

Digoxin toxicity increased: due to diuretic associated hypokalaemia

Aminglycosides can become more nephrotoxic

29
Q

What is important to note regarding furosemide prescription in patients with pulmonary oedma? [1]

A

bioavailbility (the proportion of furosemide absorbed from the gut) is reduced to gut wall oedema.

Manage by giving IV furosemide or bumetanide

30
Q

Describe the MoA of thiazide-like diuretics [1]

A
  • Block Na/Cl channel from urine into DCT
  • Blockage of the Na/Cl channel increases the flow of ions through the Na/Ca channel, resulting in increased calcium reabsorption into the interstitium in exchange for Na return to the DCT.
31
Q

Describe common AEs of thiazide like diuretics [5]

A

Hypokalemia. Most widely recognized, the first adverse effect of thiazide diuretics is hypokalemia.

Hyponatremia. The MOA of thiazide diuretics is to decrease sodium reabsorption and therefore decreased fluid reabsorption; this directly causes decreased levels of circulating sodium.

Metabolic alkalosis. Patients on thiazide diuretics may experience a hypokalemic metabolic alkalosis due to the increase in aldosterone-mediated K and H ions excretion in the intercalated cells of the CT.

Hypercalcemia. By increasing calcium reabsorption from the luminal membrane into the interstitium in exchange for sodium, thiazides reduce urine calcium levels and increase blood calcium. However, if indicated, this effect of thiazide diuretics makes thiazides useful for nephrolithiasis and osteoporosis treatment. Decreased urinary calcium decreases stone development in the kidney, and increased blood calcium is beneficial for patients with osteoporosis and promotes bone health.

Hyperglycemia. Thiazide diuretics cause hypokalemia; at the level of the pancreatic B cells, this hypokalemia causes hyperpolarization of the B cell and decreases insulin secretion. Decreased K in the interstitium keeps the K channels open for an extended time, which causes the hyperpolarization of the cell. This hyperpolarization does not allow the voltage-gated calcium channels to open. When intracellular calcium does not increase through calcium influx via the voltage-gated calcium channels, exocytosis of insulin granules does not occur in the pancreatic B cells.

Hyperuricemia: increases risk of gout

32
Q

Thiazides effectiveness are reduced by which drug class? [1]

A

NSAIDs

33
Q

Describe the main advantage of using a tunnelled catheter c.f. an AV fistula / graft? [1]

A

Can be used almost automatically, unlike AV fistula in which we need to wait for healing and maturing to occur.

34
Q

Describe exactly how a tunnelled catheter is put into place [3]

A

Inserted into the subclavian or jugular vein with a tip in the superior vena cava or right atrium.

It has two lumens, one for blood exiting the body (usually red) and one for blood entering the body (usually blue).

They can stay long-term and be used for regular haemodialysis.

35
Q

Name 4 AV fistula features to examine in an OSCE

A

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

36
Q

How can an AV-fistula cause high output heart failure? [3]

A

Blood flowing quickly from the arterial to the venous system through an A-V fistula.

There is a rapid return of blood to the heart: increasing the pre-load (how full the heart is before it pumps).

This leads to hypertrophy of the heart muscle and heart failure.
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37
Q

What are the indications for short term dialysis? [5]

A

A – Acidosis (severe and not responding to treatment)

E – Electrolyte abnormalities (particularly treatment-resistant hyperkalaemia)

I – Intoxication (overdose of certain medications)

O – Oedema (severe and unresponsive pulmonary oedema)

U – Uraemia symptoms such as seizures or reduced consciousness

38
Q

Haemodialysis requires good access to an abundant blood supply.

Two tubes are needed, one to remove the blood and one to put the blood back in.

The options for longer-term access are what? [3]

A

Tunnelled cuffed catheter:
* catheter that sits in a central vessels tunnelled under the skin and is usually present on the chest wall
Tunneled Central Line for Childhood Cancer Patients - Together by St. Jude™

Arteriovenous fistula:
* the most common and optimum. Surgical procedure takes place between an artery and a vein. The common sites are radio-cephalic, brachio-cephalic or brachio-basilic.
Haemodialysis access with an arteriovenous fistula

AV graft:
* PTFE graft placed between artery and vein which can be used for dialysis

39
Q

Describe how an AV fistula works for dialysis [3]

A

An AV fistula is an artificial connection between an artery and a vein. It bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein.

This provides a permanent, large, easy-access blood vessel with high-pressure arterial blood flow.

Creating an A-V fistula requires a surgical operation and a maturation period of 4-16 weeks before it can be used.

40
Q

Which three locations can an AV fistula be placed in? [3]

A

Radiocephalic fistula at the wrist (radial artery to cephalic vein)

Brachiocephalic fistula at the antecubital fossa (brachial artery to cephalic vein)

Brachiobasilic fistula at the upper arm (less common and a more complex operation)

41
Q

What is STEAL syndrome of an AV fistula? [2]

A

Inadequate blood flow to the limb distal to the fistula.

The AV fistula “steals” blood from the rest of the limb.

Blood is diverted away from the part of the limb it was supposed to supply, leading to ischaemia. Instead, it flows through the fistula and into the venous system.

42
Q

State 5 access complications of dialysis [5]

A

Thrombosis of any 3 types

· Infection (common in tunnelled dialysis)

· Failure of access due to stenosis of central vessels or thrombosis, or no option for AV

· Fistula can become aneurysmal

· If there is high flow from a distal you can get distal ischemia known as steal syndrome

43
Q

State 3 complications of the diaylsis process [3]

A

· Hypotension during dialysis
· Reactions such as cramps and headaches
· Inadequate dialysis dose
· Staphylococcus epidermis infection

44
Q

Describe the process of peritoneal dialysis [3]

A

Peritoneal dialysis uses the peritoneal membrane to filter the blood.

A special dialysis solution containing dextrose is added to the peritoneal cavity.

Ultrafiltration occurs from the blood, across the peritoneal membrane, into the dialysis solution. The dialysis solution is replaced, taking away the waste products that have filtered out of the blood.

45
Q

What is the name of the catheter used in peritoneal dialysis? [1]

A

Tenckhoff catheter

This plastic tube is inserted into the peritoneal cavity, with one end on the outside, allowing access to the peritoneal cavity to insert and remove the dialysis solution.

46
Q

Describe the two types of peritoneal dialysis [2]

A

Continuous ambulatory peritoneal dialysis:
- dialysis solution is always in the peritoneal cavity
- The peritoneal cavity that is drained through a closed system via gravity

Automated peritoneal dialysis:
- Machine continously replaces the dialysis fluid every 8-10hrs

47
Q

Describe the complications of peritoneal dialysis [5]

A

Bacterial peritonitis(infections in the high-sugar environment are common and serious)

Peritoneal sclerosis (thickening and scarring of the peritoneal membrane; life threatening)

Ultrafiltration failure (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective)

Weight gain (due to absorption of the dextrose)

Psychosocial implications

48
Q

[] is the most common cause of peritonitis secondary to peritoneal dialysis

A

Coagulase-negative Staphylococcus is the most common cause of peritonitis secondary to peritoneal dialysis. e.g. Staphylococcus epidermidis