personal Learning Carry Home Flashcards

(21 cards)

1
Q

Allupurinol and azathioprin interactions
Allupurinol and Febuxostat

Zurich (Febuxostat) non purine based xanthine oxidase inhibitor that is metabo-lised by the LIVER. The dose range is 40–80 mg daily.

No dose adjustment is necessary in patients with mild to moderate renal impairment (GFR 30–60 ml/min)

A

Zyloric
Its most important side effect is a skin rash that may vary in severity from mild and remitting with reduction in dose, to severe and life threatening including toxic EPIDERMAL NECROLYSIS and STEVENS-JOHNSON syndrome. It also has an important drug interaction with aza-thioprine that can lead to life threatening NEUTROPENIA . Under these circumstances the
options are to reduce dose of azathioprine by 75 % or switch to mycophenolate which does not interact with allopurinol

Coprescription of febuxostat and azathio-prine carries the SAME RISK of neutropenia as allo-purinol and azathioprine.
Other drugs that can be used to lower uric acid levels include the uricosu-ric agents probenecid, sulfi npyrazone and losartan though they are seldom effective when GFR <60 ml/min

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2
Q

Asymptotic Bacteriurea Treat or not

Short answer is NO but few cxeptions

A

Exceptions to the ‘don’t treat’ rule are PREGNANT women with asymptomatic bacteriuria who are otherwise at risk of ascending infection and acute pyelonephritis;
RECENTLY TRANSPLANTED kidney patients on high doses of immunosup-pression; and possibly CHILDREN with vesicoure-teric REFLUX whose kidneys have not yet stopped growing

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3
Q

Prophylactic dosages of antibiotics

for women who experience three or more symp-tomatic infections during a 12 month period or whenever the woman thinks that her life is being adversely affected by frequent recurrences

A

Prophylactic Doses of Antibiotic

for Recurrent Urinary Tract Infection

Antibiotic Dose Frequency

Trimethoprim 100 mg daily

Nitrofurantoin 50 or 100 mg daily

Cefaclor 250 mg daily

Cephalexin 125 or 250 mg daily

Ciprofl oxacin 125 mg daily

31.1 Objectives: Urinary Tract Infec

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4
Q

Targeted Medical Therapies for

Stone Disease

A

Drink plenty to maintain high urine output

Maintain good calcium intake but do not take calcium supplements

Consider THIAZIDE for hypercalciuria

ALLUPURINOL to dissolve urate stones

PENICILLAMINE to dissolve cystine stones

ALKALINISE urine for URATE & CYSTINE stones

Further Reading

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5
Q

Describe the drug therapy of neuropathic pain in dialysis patients.

A

The drugs available for neuropathic pain include the tricyclic antidepressant, amitriptyline and the anti-convulsant drugs carbamazepine, valproate and gabapentin (only med requiring dose reduction in Ckd)

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6
Q

Pregnancy in transplant patients

1avoid 1 year in live donors
2 avoid 2 years deceased donors

A

modify the immunosuppression so as to avoid sirolimus (rapamycin) and mycophenolate mofetil (MMF) both of which may cause foetal malformation. The combination of tacrolimus and predniso-lone with or without azathioprine is usually recommended.

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7
Q

Pregnancy outcome

A

Pre-preg creatinine (μmol/L)

Loss of >25 % renal function during pregnancy (%)

Progression to ESRF after 1 year (%)

<125 2%. 0

125–180 40%. 2

> 180 70% 35

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8
Q

Pregnancy outcome

A

Pre-preg creatinine (μmol/L)

Loss of >25 % renal function during pregnancy (%)

Progression to ESRF after 1 year (%)

<125 2%. 0

125–180 40%. 2

> 180 70% 35

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9
Q

Minimal change variants: (mesangio proliferative GN)

Mesangial proliferation
IgM nephropathy
C1q nephropathy

A

these present with minimal changes on bx and are believed to be part of MCD-FSGS spectrum.Base on finding of mesengial proliferation and additional EM findings sub groups are made in Mesengioproliferative GN
IgA also present similary but with IgA deposits

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10
Q

CLINICAL PRESENTATIONS OF MESENGIOPROLIFERATIVE GN

HEMATUREA.(good prognosis usually)
Nephrotic syndrome (not so good)
A

usually treated with steroid and +- cyclophosphaide

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11
Q

IGM NEPROPATHY

c1 q Nephropathy

A

mesangial proliferative glomerulonephritis have prominent diffuse mesangial deposits of IgM and complement but contrary to MCD less responsive to steroids

C1q nephropathy refers to a disorder in which mesangial proliferation is associated with mesangial deposits on EM strong C1q deposits on immunofluorescence microscopy

C1q nephropathy may be a COMBINATION of several disease groups rather than a single disease entity].
C1q nephropathy may be associated with either MCD, FSG, or proliferative glomerulonephritis.

CRITERIA for the illness include predominant C1q deposits on immunofluorescence microscopy and no clinical evidence of systemic lupus erythematosus.

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12
Q

LESISIONS TO BE CONFUSED WITH MCD

A

n addition to minimal change disease (MCD), three disorders present with the nephrotic syndrome and initially show only minor changes on light microscopy. These include idiopathic
1 mesangial proliferative glomerulonephritis,
2 IgM nephropathy, and
3 C1q nephropathy. All disorders are diagnosed by biopsy.

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13
Q

Dialysiates BIcarb

Typical dialysate bicarbonate: 35 mmoL/L. • Suggested target serum bicarbonate before hemodialysis: 22–24 mmoL/L (18–23 mmoL/L).

• If pre-dialysis serum bicarbonate is low (<20 mEq/L):

A
If pre-dialysis serum bicarbonate is high (>27 mEq/L)
@High protein intake 
@ketoacodidosis
@Diarrhoea
@RespirTory alkalosis compensation
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14
Q

If pre-dialysis serum bicarbonate is high (>27 mEq/L):–
-compensatory state of respiratory acidosis
– Malnutrition

A

Suggested target serum bicarbonate after hemodialysis: <28 mmoL/L (20–28 mmoL/L)

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15
Q

A dialysate bicar-bonate concentration of 35 mEq/L is usually pre-scribed for maintenance hemodialysis patients. Many hemodialysis centers use a dialysate bicar-bonate concentration of 32–39 mEq/L.

A

If pre-dialysis bicarbonate is low (<20 mEq/L), patients need alkali administration via a high dialy-sate bicarbonate concentration (>35 mEq/L) with oral sodium bicarbonate in interdialytic period.

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16
Q

DDS of dec bicarb
Clinicians should evaluate the other factors associated with metabolic acidosis (high-protein intake, gastrointestinal

bicarbonate loss,

  • ketoacidosis,
  • lactic acidosis, etc.) or compen-sated state of respiratory alkalosis (central —nervous system stimulation, hypoxemia,
  • drugs, -cardiac failure,
  • mechanical ventilation, etc.).
A

Clinicians also evaluate the other causes of meta-bolic alkalosis (upper gastrointestinal acid loss due to persistent vomiting or nasogastric suction, excess exogenous bicarbonate loads, loop diuret-ics, etc.) or compensated state of respiratory aci-dosis (airway obstructive or parenchymal lung disease, drugs that act on the central nervous sys-tem, etc.)

17
Q

High vs low efficiency dialysed

HEMO and the European Membrane Permeability Outcome (MPO) study, overall mortality did not differ significantly between high-flux and low-flux groups. However, the subgroup of patients undergoing long-term hemodialysis (>3.7 years) in HEMO and the subgroup of patients with a low serum albumin

But long term dialysis

HEMO and the subgroup of patients with a low serum albumin level (<40 g/L) in MPO experienced a mortality ben

-efit from high-flux dialyzers. Because some studies showed decreased mortality after using high-flux dialyzers, many dialysis centers now recommend tha

A

A blood flow rate of 300 mL/min is acceptable, but the rate can range from 200 to 800 mL/min.

Summary of dialysate flow rate prescription
• Dialysate flow rate is typically 500 mL/ min.
• Dialysate flow rates higher than 600 mL/ min may offer limited or no benefit.

4 

18
Q

Dose of heparin in dialysis

A

European best practice guidelines for HD recommend administering

50 IU/kg UFH into the arterial access needle for an initial loading dose. The maintenance dose of heparin is

800–1500 IU/h, given via constant infusion into the arterial line using an infusion pump

maintenance infusion is stopped 30–60 min

19
Q

Heparin free dialysis

A

The heparin-free hemodialysis protocol requires pretreating both the dialyzer and blood lines with 2000–5000 units of heparin contained in a liter of normal saline. The heparinized saline is flushed from the extracorporeal lines prior to the start of the dialysis treatment so that heparin is not administered to the patient. Extracorporeal blood flows are rapidly increased to 250–500 mL/ min and maintained throughout the treatment, and 25–30 mL saline flushes are administered every 15–30 min into the arterial tubing line ( h t t p : / / w w w. u p t o d a t e . c o m / c o n t e n t s / hemodialysis-anticoagulation).

The minimum-dose heparin hemodialysis pro-tocol usually involves boluses of 500 units of heparin every 30 min to keep the activated clot-ting time >150 but <200 s. Al

20
Q

Benefits of lmwh

A

Benefits of LMWH include higher bioavail-ability (less nonspecific binding to platelets and plasma proteins
), improved lipid profile,
reduced risk of hyperkalemia and osteoporosis, and lower incidence of HIT type II.

21
Q

Intra Dialytic Hypotension CAUSES

@ water can be removed up to 20% of plasma at the appropriate ultrafiltra-tion (UF) rate since the physiological compensa-tion occurs to reward hypovolemia. If water removal is too excessive or too quick, e.g., UF rate > 0.35 mL/min/kg, hypotension can occur

A
PATIENT factors
-DYSAUTONOMIA IN DM
-STRCUCTURAL HEART DISEASE 
ANAEMIA
BLEEDING
SEPSIS
INC ANTIHYPERTENSIVE

DIALYSIS FACTORES
incompatible dialyser
Factors-related dialysis processes include use of low sodium or low calcium dialysates, use of acetate dialysis or bioincompatible dialyzers (K/DOQI 2005).