Brainscape's Knowledge GenomeTM

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


See full index

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

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

define Uremia

A

reduced glomerular filtration caused by acute kidney disease

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

two General approaches for

dose adjustment in renal disease

A

Methods based on drug clearance

OR elimination half-life

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

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

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

ways to determine Clcr - number 2

A

cockcroft- gault empirical equation for male and female

unit: ml/min

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

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

what is normal renal function based on estimated Clcr

A

> 80ml/min

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

what is mild/ moderate renal impairment baed on Clcr

A

mild 50-80ml/min

moderate 30-50ml/min

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

what is severe renal impairment baed on Clcr

A

<30ml/min

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

what is ESRD

and what may the patient require?

A

end stage renal disease

require dialysis

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

what are the two types of dialysis

A 
peritoneal dialysis (fliter: peritoneal mem from abdomen)
haemodialysis (filter: artifical membrane in machine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

describe haemofiltration

A

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

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

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

is acute kidney injure a long term process?

A

no, sudden reduction in kidney function

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

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

What are the three main time periods where AKI can occur?

A

Pre-renal, intrinsic, post renal

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

What are the examples of causations of AKI in those three time period

A

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

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

nice guideline:
Consider …..in adults, children and young people with diarrhoea, vomiting or sepsis until their clinical condition has improved and stabilised

A

temporarily stopping ACE inhibitors and ARBs

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

nephrontoxic drugs: CANDA

A

C - Contrast media
A - Angiotensin converting enzyme inhibitor
N - Non steroidal anti-inflammatory drugs
D - Diuretics
A - Angiotensin II receptor blockers (ARB)

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

Things to do before giving contrast media to AKI 2/3 patient

A

Oral hydration or NaCl 0.9% IV fluid
Hold/ review nephrotoxins
Check UO, serum Cr

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

UR’INE TROUBLE! How to manage AKI

URINE

A

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
Q

what are the 5 key functions of kidney?

A

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
Q

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 …

A

progressive and irreversible
<60 mL/min/1.73 m2
at least 3 months

33
Q

what is the first method of calculating GFR? (from cappillaries to bowmans cap)

A

GFR= urine conc x flow (of urine?) / serum conc

34
Q

GFR is …. of a solute, the solute has to be

A

the clearance rate of a solute

freely filtered and not actively re-ab or secreted

35
Q

what is the kinetic relationship (graph) between serum cr level and GFR?

A

non- linear

36
Q

one way to estimate GFR?

A

Use CrCl

37
Q

How long a complete urine collection got to last? What is the disadvantage?

A

24 h, unwidely used. urine collection can be inaccurate/ incomplete

38
Q

How to calculate crcl?

A

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
Q

What is the unit for crcl?

A

Volume, but can change into flow rate by dividing by hours or mins.
2L/day = 1.4 ml/min

40
Q

How to estimate crcl? (instead of collecting 24h urine sample)

A

COCKROFT-GAULT ecrcl= (140-age) x wt (kg) x constant / serum cr (micro mol/ L)
Constant: 1.23 male, 1.04 femal

41
Q

What are the other eq used to estimate GFR?

A

MDRD study

CKD EPI

42
Q

disad of MDRD eq

unit?

A

Give standardised result for BSA 1.73m2
Doesn’t adjust for body mass
Inaccurate for GFR>60ml/min
ml/min/1.73m2

43
Q

Which is the recomd method for estimating eGFR by NICE?

A

CKD EPI (chronic kidney disease epidemiology collaboration)

44
Q

Why is CKD EPI better than MDRD? It is more accurate when… and less accurate when…

A

Includes age, sex, ethinicity, more accurate espcially at higher GFR >60ml/min
Less accurate in person eg obesed, black female

45
Q

disad of cockcroft-gault in estimating crcl?

A

Not accurate when CrCl <20ml/min and when person has extreme body mass (athelet with lots of muscles, ecrcl tend to be overestimated)

46
Q

crcl is more accurate for dose adjustment what type of pt

A

elderly with low body weight, low muscle

47
Q

What are the signs and symptoms of CKD?

A 
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
Q

why is a low Hb target needed in patient with CKD?

Aim to maintain Hb between 10-12g/dL

A

because high Hb level can cause ADR:
hypertension
CVD/ motality
loss of dialysis access

49
Q

What causes osteoporosis in CKD patients

A

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
Q

renal bone disease- treatment options inc diet

A 
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
Q

what trt is used to trt muscle cramps in CKD

A

quinine at night

52
Q

CKD impaired homeostasis of acid-base balance can cause….

can be trt with…

A

metabolic acidosis

sodium bicarbonate : to bind with excess H+

53
Q

CKD impaired homeostasis of fluid (retention) can cause….

can be trt with… which med?

A

hypertension

antihypertensives, diuretics, furosemide 20-40OM

54
Q

drugs which extensively excreted by kidney are (2 example)

A

Aciclovir

Gabapentin 100% renal excreted

55
Q

how does CKD affect the normal drug PK in terms of absorption

A

reduced absorption due to gastric oedema

EX fluid in GIT, cant absorb

56
Q

CKD effect on drug distribution

A

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
Q

CKD effect on drug metabolism

A

reduced metabolism for vitD hydroxylation and insulin

so less insulin is needed in CKD pt

58
Q

CKD effect on drug excretion

A

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
Q

what type of kidney disease pt needs a kidney transplant?

A 
Diabetes 
Hypertension
Blockage – stone, prostate, cancers
Glomerulonephritis
Congenital abnormalities including polycystic kidney disease
60
Q

what is SKP in kidney transplant for diabetic pt

A

simultaneous kidney pancrease

transplant both organs - get pt off insulin

61
Q

hospital stay for kindey donor after kidney is removed. what are the three remaining steps?

A
  1. PCA for 24h
  2. 3-day inpatinet stay
  3. annul review
62
Q

descirbe the kidney recipient hospital stay

A

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
Q

what meds to stop/ continue before transplant?

A 
stop: Antihypertensives 
Cholesterol lowering agents
Phosphate binders
Alfacalcidol 
Erythropoietin 
continue: B- blockers
diabetic meds 
gastroprotective med omeprazole
64
Q

give 2 IM suppression meds used on induction

explain how they work

A

basiliximab- il2 inhibitor- on surface of T lymphocytes

alemtuzumab

65
Q

3 Im suppressant meds on maintenance

A
  • steroid
  • Calcinurine inhibitor: CNI Tacrolimus/ciclosporin
  • Antiproliferative agent
    Mycophenolate/azathioprine (reserved)
66
Q

how does CNI work?

A

Inhibit calcineurin activity preventing T cell proliferation

67
Q

how does antiproliferative agents: mycophenolate, azathioprine work?

A

Impairs T and B cell proliferation

68
Q

Typical prescription heart beating or living kidney recipient (DBD/LKD) -brain stem death

A

basiliximab
prednisolone - w food
tacrolimus - not w food

69
Q

Typical prescription non-heart beating kidney transplant recipient (DCD) -circulatory death

A

basiliximab
prednisolone
tacrolumus
mycophenolate (added if high risk)

70
Q

what do tacrolimus/ciclosporin interact with? how does the interaction affect their conc?

A 
conc increased by (enzyme inhibitor)
marcolides eg erthyromycin, 
antifugal eg fluconazone
grapefruit juice 
conc reduced by (enzyme inducer)
st.johns wort 
rifampicin
71
Q

trt for organ rejection

A

Methylprednisolone pulses
ATG (Rabbit anti-human thymocyte immunoglobulin)
Polyclonal antibody -T lymphocyte depletion

72
Q

are Transplant recipients exempt from prescription charges

A

no

73
Q

advice for pt after transplant?

A
  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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions