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SIU6 Special patient group > AKI and CKD > Flashcards

AKI and CKD Flashcards

1
Q

what are the common causes of kidney failure?

A

-PHDNHN
1 Pyelonephritis : inflam of pyelonephrons due to infection, antigens
2 Hypertension : chronic overloading of kidney with fluid and electrolytes
3 Diabetes mellitus : disturbed sugar metabolism, acid- base balance
4 Nephrotoxic drugs, metals : aminolycosides, gentamycin, lithium
5 Hypovolemia : reduced blood flow to kidney cause renal ischeamia
6 Neophroallergens : compounds may trigger IMR and nephritic syndrome

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2
Q

define Uremia

A

reduced glomerular filtration caused by acute kidney disease

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3
Q

two General approaches for

dose adjustment in renal disease

A

Methods based on drug clearance

OR elimination half-life

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4
Q

what are the three common markers used in estimating glomerular filtration rate?

A
  1. insulin (but long time to reach Css)
  2. creatinine (but also actively secreted, gives an over-estimation)
  3. BUN, blood urea nitrogen: urea (end pro of protein metab)
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5
Q

assumptions we made regarding to the use of creatinine cl to reflect renal function

A
  1. constant production from liver
  2. constant conversion in striatal muscle
  3. freely filtered by kidney not secreted or reabsorbed
  4. measurement of serum/ urine cr is accurate
  5. renal collection is complete (24h)
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6
Q

Production and release of creatinine from muscle is directly proportional to…. but it’s hard to measure so we use….

A

LBW- muscle
we use IBW BUT,
low muscle, more fat in elderly, females, children, muscle wasting pt. so lower CR than that calculated with IBW
greater muscle in athelets, so higher CR than calculated value
food (meat) intake

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7
Q

ways to determine Clcr - number 1

A

rate of excretion of Cr = C x Cl
Cl= rate of excretion of Cr from urine/ serum conc of Cr = C x Vol of urine/ Conc
unit ml/min

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8
Q

ways to determine Clcr - number 2

A

cockcroft- gault empirical equation for male and female

unit: ml/min

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9
Q

ways to determine Clcr - number 3

what is the relationship between age and Clcr?

A

nomogram of Clcr based on age, wt, sex, Ccl, Rate, gives Clcr
linear decline of creatinine clearance with increased age

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10
Q

what is normal renal function based on estimated Clcr

A

> 80ml/min

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11
Q

what is mild/ moderate renal impairment baed on Clcr

A

mild 50-80ml/min

moderate 30-50ml/min

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12
Q

what is severe renal impairment baed on Clcr

A

<30ml/min

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13
Q

what is ESRD

and what may the patient require?

A

end stage renal disease

require dialysis

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14
Q

what are the two types of dialysis

A 
peritoneal dialysis (fliter: peritoneal mem from abdomen)
haemodialysis (filter: artifical membrane in machine)
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15
Q

describe dialysis- is it an artificial process

  • purpose
  • process
A

yes

  • to remove accumulated drug and metabolites form body fluid
  • diffusion of drug from body fluid to dialysis fluid through either peritoneal/artificial membrane by equilibrium
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16
Q

the requirements for dialysable drugs

A
  • hydrophilic
  • not protein bound bc based on diffusion
  • low WM<500
  • low Vd preferred or time consuming as rate limitor is vol of blood influx to the machine
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17
Q

describe haemoperfusion

when is it used in clinic

A

pass blood though an adsorbent material to remove drugs and back to patient
used in overdose/poisoning

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18
Q

describe haemofiltration

A

pass blood through hollow artificial fibres or mem to remove eletrolytes and small mw subs by low pressure flow

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19
Q

what are the PK implication for kidney impairment?

A
  • change in BA
  • increase in Vd (more total body water)
  • reduced drug protein binding (more urea)
  • reduced clearance/ filtration/ elimination rate constant k
  • increased half life
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20
Q

properties of glomerular filtration measuring markers

A
  • freely filtered at the glomerulus
  • not be reabsorbed nor actively secreted by renal tubules
  • not be metabolized
    not bind significantly to plasma proteins
  • not have an effect on filtration rate nor alter renal function
  • be nontoxic
  • may be infused in sufficient dose (simple, accurate quantitation)
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21
Q

What are the signs of AKI?

A

1 Anaemia (reduced erythropoietin)
2 Abnormal BP (increase renin to increase BP)
3 Increased serum Cr, protein in urine, reduced eGFR (reduced waste excretion)
4 Reduced calcium, increased phosphate (reduced excretion) and parathyroid hormone level (kidney cannot change vitD into active form to increase Ca)
5 UE imbalance (sodium and potassium maybe affeted as kidney cannot repond to antidiuretics and aldosterone to reabsorb water)

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22
Q

is acute kidney injure a long term process?

A

no, sudden reduction in kidney function

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23
Q

how to access the stages of AKI in terms of serum Cr

A

stage 1: 1.5-2x of the baseline Cr
stage 2: 2-3x of the baseline cr
stage 3: over 3x of the baseline

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24
Q

why trimethoprim is not recommended to use in patient with AKI/CKD?

A
  1. trimethoprim increases serum Cr level by changing the metabolic rate of muscle producing creatinine (can false AKI)
  2. hyperkalaemia in CKD pateint- think alternatives
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25
What are the three main time periods where AKI can occur?
Pre-renal, intrinsic, post renal
26
What are the examples of causations of AKI in those three time period
Pre-renal : volume depletin (hypovolemia) dehydration (NV) Sepsis Cardiogenic Intrinsic : prolonged pre-renal insult cuasing tubular necrosis Inflammation in nephron Drugs Post renal : outflow obstruction by clot in bladder (use catherter) Prostate enlargement Ureter
27
nice guideline: Consider .....in adults, children and young people with diarrhoea, vomiting or sepsis until their clinical condition has improved and stabilised
temporarily stopping ACE inhibitors and ARBs
28
nephrontoxic drugs: CANDA
C - Contrast media A - Angiotensin converting enzyme inhibitor N - Non steroidal anti-inflammatory drugs D - Diuretics A - Angiotensin II receptor blockers (ARB)
29
Things to do before giving contrast media to AKI 2/3 patient
Oral hydration or NaCl 0.9% IV fluid Hold/ review nephrotoxins Check UO, serum Cr
30
UR’INE TROUBLE! How to manage AKI | URINE
U- Underlying cause: treat PHDNHN, sepsis, dehydration, cardiac failure R- Rehydration: with IV fluid, water I- Investigate: renal tract imaging, avoid iodine contrast, daily UE N- Nephrotoxic drugs: stop CANDA, metformin, posttium sparing diuretics spironolactone E- Escalate, observe: hourly UO
31
what are the 5 key functions of kidney?
1 Excrete toxins, drugs-- high Cr in blood, low eGFR 2 Control BP-- increase renin production, HT, monitor BP 3 RBC production --low erythropoietin, anaemia, monitor FBC, give ESA: Darbepoetin IV or iron IV 4 Electrolyte balance-- low response to antidiuretic, aldosterone, low re-ab of water, monitor UE daily, give iv fluid 5 Make strong bones-- low activation of vitD from diet to alpha-calcidol, low Ca but high Pi/PTH, monitor Ca, Pi and PTH
32
Chronic kidney disease (CKD) is a ....condition defined as an estimated glomerular filtration rate (eGFR) of... and/or kidney damage (haematuria or proteinuria) present for ...
progressive and irreversible <60 mL/min/1.73 m2 at least 3 months
33
what is the first method of calculating GFR? (from cappillaries to bowmans cap)
GFR= urine conc x flow (of urine?) / serum conc
34
GFR is .... of a solute, the solute has to be
the clearance rate of a solute | freely filtered and not actively re-ab or secreted
35
what is the kinetic relationship (graph) between serum cr level and GFR?
non- linear
36
one way to estimate GFR?
Use CrCl
37
How long a complete urine collection got to last? What is the disadvantage?
24 h, unwidely used. urine collection can be inaccurate/ incomplete
38
How to calculate crcl?
Rate in =rate out Rate out= urine conc x urine vol Rate out= C x crcl Crcl= urine conc x urine vol / C (cr in serum)
39
What is the unit for crcl?
Volume, but can change into flow rate by dividing by hours or mins. 2L/day = 1.4 ml/min
40
How to estimate crcl? (instead of collecting 24h urine sample)
COCKROFT-GAULT ecrcl= (140-age) x wt (kg) x constant / serum cr (micro mol/ L) Constant: 1.23 male, 1.04 femal
41
What are the other eq used to estimate GFR?
MDRD study | CKD EPI
42
disad of MDRD eq | unit?
Give standardised result for BSA 1.73m2 Doesn’t adjust for body mass Inaccurate for GFR>60ml/min ml/min/1.73m2
43
Which is the recomd method for estimating eGFR by NICE?
CKD EPI (chronic kidney disease epidemiology collaboration)
44
Why is CKD EPI better than MDRD? It is more accurate when… and less accurate when…
Includes age, sex, ethinicity, more accurate espcially at higher GFR >60ml/min Less accurate in person eg obesed, black female
45
disad of cockcroft-gault in estimating crcl?
Not accurate when CrCl <20ml/min and when person has extreme body mass (athelet with lots of muscles, ecrcl tend to be overestimated)
46
crcl is more accurate for dose adjustment what type of pt
elderly with low body weight, low muscle
47
What are the signs and symptoms of CKD?
``` Pale appearance Hypertension (due to toxin build up in body) SOB (fluid overload lung, low O2 in HB) Kidney size and shape (small kidney) Urine output (polyuria, nocturia Haematuria / proteinuria (dipstick test Itching, cramp (due to toxin in muscle Congnitive function (language/ confusion GI symptoms (NV Peripheral oedema (due to na retention) ```
48
why is a low Hb target needed in patient with CKD? | Aim to maintain Hb between 10-12g/dL
because high Hb level can cause ADR: hypertension CVD/ motality loss of dialysis access
49
What causes osteoporosis in CKD patients
Reduced hydroxylation of vitD by kidney, reduced ca absorption Impaired phosphate excretion, increased serum phosphate These increase PTH (parathyroid hormone) production, lead to osteoblast then osteoclast actvity of bone resorption More ca is release bone is weaken
50
renal bone disease- treatment options inc diet
``` Alfacalcidol (start low, 250ng 3 x per week Phosphate binders (1st ca acetate-phosex or ca carbonate-calcichew w food, 2nd sevelamer, non-ca phophate binder) Dietary phosphate restriction ```
51
what trt is used to trt muscle cramps in CKD
quinine at night
52
CKD impaired homeostasis of acid-base balance can cause.... | can be trt with...
metabolic acidosis | sodium bicarbonate : to bind with excess H+
53
CKD impaired homeostasis of fluid (retention) can cause.... | can be trt with... which med?
hypertension | antihypertensives, diuretics, furosemide 20-40OM
54
drugs which extensively excreted by kidney are (2 example)
Aciclovir | Gabapentin 100% renal excreted
55
how does CKD affect the normal drug PK in terms of absorption
reduced absorption due to gastric oedema | EX fluid in GIT, cant absorb
56
CKD effect on drug distribution
for plasma protein bound drug: phenytoin, warfarin, diazepam, propanolol. the distribution increase due to ureamia (high urea level- displaces drug from protein binding sites so more free fraction) frequent TDM is required if narrow therapeutic window lower albumin level gives reduced protein binding
57
CKD effect on drug metabolism
reduced metabolism for vitD hydroxylation and insulin | so less insulin is needed in CKD pt
58
CKD effect on drug excretion
reduced excretion for extensively renally excreted drugs eg aciclovir, gabapentin (100% renal excreted), methotraxate (Once a week not as bad) and digoxin. prolonged half life opiates - active metabolites of which half life is prolonged
59
what type of kidney disease pt needs a kidney transplant?
``` Diabetes Hypertension Blockage – stone, prostate, cancers Glomerulonephritis Congenital abnormalities including polycystic kidney disease ```
60
what is SKP in kidney transplant for diabetic pt
simultaneous kidney pancrease | transplant both organs - get pt off insulin
61
hospital stay for kindey donor after kidney is removed. what are the three remaining steps?
1. PCA for 24h 2. 3-day inpatinet stay 3. annul review
62
descirbe the kidney recipient hospital stay
Immunosuppression started 48 hours before admission if elective target 5 days inpatient (short!) experience less discomfort than donors Intensive (3x /w) follow up for first 3 months Life long follow up at transplant centre/ referring renal unit.
63
what meds to stop/ continue before transplant?
``` stop: Antihypertensives Cholesterol lowering agents Phosphate binders Alfacalcidol Erythropoietin continue: B- blockers diabetic meds gastroprotective med omeprazole ```
64
give 2 IM suppression meds used on induction | explain how they work
basiliximab- il2 inhibitor- on surface of T lymphocytes | alemtuzumab
65
3 Im suppressant meds on maintenance
- steroid - Calcinurine inhibitor: CNI Tacrolimus/ciclosporin - Antiproliferative agent Mycophenolate/azathioprine (reserved)
66
how does CNI work?
Inhibit calcineurin activity preventing T cell proliferation
67
how does antiproliferative agents: mycophenolate, azathioprine work?
Impairs T and B cell proliferation
68
Typical prescription heart beating or living kidney recipient (DBD/LKD) -brain stem death
basiliximab prednisolone - w food tacrolimus - not w food
69
Typical prescription non-heart beating kidney transplant recipient (DCD) -circulatory death
basiliximab prednisolone tacrolumus mycophenolate (added if high risk)
70
what do tacrolimus/ciclosporin interact with? how does the interaction affect their conc?
``` conc increased by (enzyme inhibitor) marcolides eg erthyromycin, antifugal eg fluconazone grapefruit juice conc reduced by (enzyme inducer) st.johns wort rifampicin ```
71
trt for organ rejection
Methylprednisolone pulses ATG (Rabbit anti-human thymocyte immunoglobulin) Polyclonal antibody -T lymphocyte depletion
72
are Transplant recipients exempt from prescription charges
no
73
advice for pt after transplant?
1. vaccinations but not live ones 2. avoid nasid or other nephrotoxic drug 3. healthy diet, lifestyle 4. watch out for interaction w herbals

SIU6 Special patient group (6 decks)

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