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Medicine > Renal > Flashcards

Renal Flashcards

1
Q

causes of CKD

A

diabetes
ht
age related decline
glomerulonephritits
AKI- had got
ADPKD
meds- nsaids, acei, armb, ppi, lithium
SLE
alport disease

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2
Q

whats ckd and things show its chronic not acute

A

chronic reduction in kideny function
have anemia
low vit D
osetomalacia
osteosclerosis
osteoporosis
= rugger jersey spine on xray
high PTH
high phosphate serum
hypertension
metabolic acidosis
hyperkalaemia
cv disease
peripheral neuropathy

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3
Q

what risk factors of ckd

A

diabetic
ht
obesity
cv disease
older age
smoking
using meds that are nephrotoxic

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4
Q

s and s of ckd

A

often find on incidental finding

can have
itching
loss appetite
nasuea
oedema
muscle cramps
peripheral neuropathy
pallor
ht
any of complications
hyperkaleamia
metabolic acidosis

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5
Q

inveestigfatins for ckd and diagnsosi

A

diagnosed by 2 eGFR 3 months apart = need eGFR less than 60 / protienuria to diagnose ckd
use ACR (early morning urine saple) or eGFR scores to do stages of ckd

can do serum creatinine
ACR urine to check for proteinuria- 3 or more mg/mmol is signficant

urine dipstick = haematuria- more than 1 is sig check also for malginany

renal us if accelerated cks, fam hist of adpkd

bmi, bp, serum hba1c, lipid profile to asses cv risk factors

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6
Q

whats g score and whats a score

A

ways to stage ckd
a1 with g1/g2 not ckd

g score is eGFR
A score is ACR

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7
Q

complications of ckd

A

anemia
renal bone disease- ckd-mbd
cv disease
dialysis issues

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8
Q

how to manage ckd

A

manage complications = oral sodium bicarbonate= treat metabolic acidosis
iron and erhtropoeitin- treat anemia
vit d= treat renal bone disease
dialsys and transplant in end stage renal disease = eGFR less than 15

slow progression by optomising rf= diabetes, gt, treat glomerulonephritits
redice cv risk
recude complications by exercsie, weight loss, stop smoking, reduce phosphate intake, reduce k intake and water and sodium keep an eye on in diet

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9
Q

how do you trea tht in pt with ckd

A

ACEi irst line with ckd

offer treatment if diabetetic and ACR more than 3

if got ht and acr over 30

all pt with acr over 70

aim for bp to be below 140/90 or if acr ver 70 aim for under 130/80

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10
Q

what do you need to monitor in paitnets on ht treatment with ckd

A

serum potassium

ckd and also acei cause hyperkalameia

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11
Q

how to treat anemia of ckd

A

exogenous erythropoeitin

if low iron give iv iron/ oral before erythropoetin

try not to do blood transfusion cus if need transplant later may rejet it

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12
Q

whats renal bone disease

A

osteomalacia
osteoporosis
osteosclerosis

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13
Q

what do you see on xray f the spine with pt with ckd

A

rugger jersey spine
edges of vertebra more dense white(osteoscleorsis)
middle of vertebrae less white (osteomalacia)

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14
Q

how does renal bone disease occur

A

high serum phosphate becasue not being excreted by kidenys well
also got ow vit d becasue not being activated and so this leads to low ca
both of these leads to secondary hyperparathryoidism which causes increase osteoclast activity and so reabsrob ca from bones

get osteomalacia due to increased bone turnover without enough ca

get osteosclerosis because have increased osteoblast actvity to match increase osteoclast but the tissue is mineralised properly

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15
Q

trat renal bone disease

A

vit d= calcitrol/ alfacalcidol
bisphosphonates if osteoporisis - due to age, rf and steroid use

decrease phospahte in diet

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16
Q

will you see high or low serum phosphate in ckd

A

high

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17
Q

will you see how or low k in ckd

A

high

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18
Q

will you see metabolic acidosis or alkalosis in ckd

A

acidosis

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19
Q

whats does glomeruloneprhtis mean

A

inlam of or aroud the glomerulus

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20
Q

how do you treat most glomerulonephrtis

A

steroids
bp control- ACEi/ARB

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21
Q

whats the type of glomerulonphritis

A

IgA nephropathy = bergers disease
anti GBM = good pastures
post infectious streptoccocal glomerulonephritis
memnranous glomerulonepthritis
minimal change disease
focal segmental glomerulosclerosis
rapidly progressive glomerulonepthritis

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22
Q

whats the criteria have to have to be nephrotic sydrome

A

set of sytpoms not a diagnosis
have to have
proteinuria of more than 3g per 24hrs
hypoalbuminaemia= less than 25g per l
peripheral oedema

also may have hypercholesteramiae and dyslipidaemia and hypercoaguability

this is because liver tries to make more proteins cus low alumin

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23
Q

s and s of nephrotic syndrome

A

peripheral oedema
frothy urine- proteinuria
intravacual depletion= dizzy, abdo cramps
hypercoagulability= DVT, MI, PE
chest pain = PE
SOB= oedema
xanthlosmata

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24
Q

investigations for nephtrotic syndrome

A

urine disptick= proteinuria and look for microscopic haematuria
midstream urine for culture amd microscopy
ACR in ealy moring sample
FBC and coag screen
lipid profile and fasting glucse
u and e and lft

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25
Q

whats the most common cause of nepthrotic syndrome in children

A

minimal change disease

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26
Q

whats the most common casue of nephrotic syndrome in adults

A

focal segemental glomerulosclerosis

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27
Q

other causes of nephrotic syndrome

A

sle, diabetes, infection, sickle cell, alport, drugs, amyloid

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28
Q

treat nephrotic syndrome

A

corticosteroids
oedema- low salt intake, fluid restriction, diuretics
bp control- ACEi/ ARB

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29
Q

whats nephritic syndrome

A

doesnt have to fit exact criteria like nephrotic

haemaitria- micor or macro
oliguria
proteinuria but not more than 3 cus then nephrotic
fluid retention- some oedmea= periorbital, peripheral, pulmonary
ht

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30
Q

causes of nephritic syndrome

A

post streptococall glomerulonephritis
other casues of glomerulonepthritis
bacteria infections, viral infection eg. hep b, mumps
malaria
sle, anti gbm
guillain barre syndrome
diptheria, pertusiss and tetanus vaccine
amyloid
igA

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31
Q

whats the most common cause of primary glomerulonephritis

A

IgA nephropathy

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32
Q

whats the most comon type pf glomerulonephritis overall

A

membranous glomerulonephritis

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33
Q

whats IgA nephropahty and histology finings

A

most common casue of primary glomerulonephritits
esp in 20s
histology= IgA depsosits and mesagnial expansion/proliferation
can affect bv too

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34
Q

histology findings are IgG and complement depostis on basement membrane of glomerulus
what is this

A

membranous glomerulonepthritis

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35
Q

whats membranous glomerulonephtiris

A

most common type of glomerulonephritis overall
20 and 60s
histology= IgG and complement depositis on BM
most are idiopathic = antibodies to phospholipase A2R on podocytes
can be secondary to maligancy, rhematoid disroders, drugs- nsaids

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36
Q

pt had tonsilits
2 weeks later theyre not weeing much and have soe bloodin their urine
what is this

A

post streptococcal glomerulonephritis

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37
Q

whats post strephtococcal glomerulonepthrits

A

also called diffuse proliferative glomerulonephritis
under 30s mainy
1-3 weeks after strep infection - tonsilits/ impetigo
nephritic syndrome

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38
Q

post streptococcal glomerulonephritis/ diffuse proliferative glomerulonepthritis shows nephrotic or nephritic syndrome

A

nephrititc

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39
Q

patient has reduce urine output
n and v
cofusion
coughing up blood

what is this

A

goodpastures syndrome/ anti GBM

aki and haemoptysis = anti gbm

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40
Q

whats anti GBM/ good pastures syndrome

A

anti GBM antibodiees attack GBM and pulmonary basement membrane
get glomerulonephritis and pulmonary haemorrhage
its type 2 hypersenticity rxn
rf is smoking
antibodies to alpha 3chain type 4 collagen

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41
Q

whats rapidly progressive glomerulonephritis

A

histology= cresentic glomerulonephritis
v acute illners
often secondary to anti gbm

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42
Q

patient has diabetes
have protein in urine

what is this

A

diabetic nephropathy

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43
Q

whats tha pathophysiology of diabetic nephropathy

A

poor glycemic control= high blood glucose

activtes RAAS

increase angiotensin 2 in renal

afferent arteriole dilate
efferent arteriole constrict

inital increase gfr

dec creatine in blood and hyperfiltration

increase pressure state

causes sheer stress on glomerulus

this casues
mesangial expansion
podocyte loss
increase permeability to protien
glomeruloscleorisis
glomerular ht
tubulointerstial fibrosis
tubular atrophy

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44
Q

whats the three main thigs that happen in diabetic nephropathy

A

mesagnial expansion
nephron ischemia
increase pressure state

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45
Q

why mesangial expansion occur in DKD

A

increase pressure state
wider and thicker = fibrosis and inflatation casuing glomerular dysfunction and atrophy
dec filtration sa
gaps
protien gets through into tubules and so into urine

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46
Q

why does nephron ischemia occur in dkd

A

efferent arteriole constrict due to raas activcation due to high glucose
efferent arteriole supplies blood to the tubules
constricted so less blood
increased turbulence

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47
Q

s and s of dkd

A

proteinuria

maybe haematuriea
increase gfr initially
low gfr and renal failure

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48
Q

how to prevent dkd

A

regular screening of ACR
optomise bp, statins , glycemic control
educate
weight loss
dec salt

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49
Q

how to manage dkd

A

OPTOMISE BLOod sugar
optomise blood pressure
even if normal bp pts with diabetic nephropathy be on acei or arb

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50
Q

what bp meds is for pt with diabetic nephropahty

A

ACEi or ARB

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51
Q

whats acute tubular necrosis

A

damage and death to tubular epithelial cells
most common casue of AKI
epithelila cells can regernate- 7-21 days recovery

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52
Q

whats the most common cause of AKI

A

acute tubular necrosis

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53
Q

whats causes of acute tubular necrosis

A

ischemia = secondary hypoperfusion
shock
sepsis
dehydration

toxins = direct damage
radiology contrast dye
gentamicin
NSAIDs
lithium
heroin

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54
Q

what antibiotic causes acute tubular necrosis

A

gentamicin

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55
Q

s and s of acute tubular necrosis

A

s and s of aki

decreased urine output
vomit nausea
diarrhoea
confusion
hyperkalemia
metabolic acidosis

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56
Q

urinalysis shows muddy brown casts
what is this

A

acute tubular necrosis

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57
Q

what ivestigfations for acute tubular necrosis

A

urialysis = muddy brown casts = pathognomic finding specific to acute tubular necrosis

may also see renal tubular epithelial cells in urine

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58
Q

hpw to manage acute tubular necrosis

A

same as other aki
supportive
iv fluids
stoph nephrotxic meds
treat complications

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59
Q

whats renal tubular acidosis

A

metabolic acidosis with normal anion gap due to pathology in the kidney tubules

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60
Q

hyperkalaemia
high chloride
metabolic acidosis
low urine ph

what is this

A

type 4 renal tubular acidosis

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61
Q

whats type 1 renal tubular acidosis

A

to do with hydrogen ions not being able to be excreted in the DCT

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62
Q

causes of type 1 renal tubular acidosis

A

genetic
sle
sjorgens syndrome
primary biliary cirrhosis
hyperthryoidism
sickle cell anameia
marfdans sydrome

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63
Q

singns symptoms of type 1 renal tubular acidosis

A

failure to thrive in children
hyperventilation trying to compensate
ckd
osteomalacia
high ca in urine

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64
Q

results if type 1 renal tubular acidosis

A

hypokameia
metabolic acidosis
alkalotic pH - high urine ph over 6

65
Q

treatment of type 1 renal tubular aicdosis

A

oral bicaarbonate- also sorts out electrolyte balance

66
Q

hypokalaemia
high urine ph
metabolic acidosis

what could this be

A

type 1 or 2 rneal tubular acidosis

67
Q

most common type of renal tubular acidosis

A

type 4 - to do with low aldosterone

68
Q

whats type 2 renal tubular acodisi

A

due to PCT
not able to reabsrob bicarbonate

69
Q

cause of type 2 renal tubular acidosis

A

fanconi syndrome

70
Q

whats fanconi syndrome

A

genetic
seen in jews
bone marrow suprresion
acute myeloid leukameia
cafe au lait spots
facial features
abscence of radius bone bilaterally
type 2 renal tubular acidosis

71
Q

reuslts if type 2 renal tubular acidosis

A

hypokalaemia
metabolic acidosis
high urine ph - alklalotic

72
Q

treat type 2 renal tubular acodisis

A

oral bicarb

73
Q

which types of renal tubular acidosis are similar in results and treatment

A

type 1 and 2
both have hypokalemia
metabolic acidosis
high urinary ph
treat oral bicarbonate

1 to do with h ions not excreted from dct
2 is bicarb not reabsorbed in pct

74
Q

whats type 3 renal tubular acidosis

A

1 and 2 combined
pct and dct pathology

75
Q

whats type 4 renal tubular acidosis

A

low alodsterone or not able to respond to aldosterone

76
Q

whats most common type of renal tubular acidosis

A

type 4
aldosterone low

77
Q

what cause and how work type 4 renal tubular acidisos

A

low aldosterone
alodsterone casues rebasorbtion of na
excretion of h and k in dct

k and h not excreted so metabolic acidosis and hyperkalaemia
hyperkalaemia supresses the normal excretion of ammonia into urine to stop being acidoc urine but this is supressed by high k so have acidic urine

78
Q

results of type 4 renal tubular acidosis

A

hyperkalaemia
metabolic acidosis
high chloride
low urine ph

79
Q

s and s of type 4 renal tubular acidosis

A

cardiac arhtymia
paralysis
due to high k

80
Q

causes of type 4 renal tubular acidosis

A

low aldosterone =>
ACEi/ arb
spironolactone
sle
diabetes
hiv
addisons disease ]nsaids
ckd
heparin use

81
Q

treatment type 4 renal tubular acidosis

A

fludrocortisone
sodium bicarbonate
treat hyperkaelamie = volume expansion, potassium wasting diuretics - furusomide

82
Q

s and s of type 1 and 2 renal tubular acidosis

A

hypokalemia =
muscle weakness
hyporelfexia
osteomalacia

83
Q

whats HUS

A

thrombosis in small bv throughout body casued by shiga toxin

84
Q

what toxin casues HUS

A

shiga toxin

85
Q

what pathogens can produce shiga toxin

A

Ecoli 0157 ( most common)
shigella

86
Q

patient had blood diarrhoea for a few days and they took loperamide
they now have abdo pain and not weeing much

whst is this

A

HUS

87
Q

what increases risk of getting HUS

A

treating the gastroenteritis with anitbiotics or anti motility agents- loperamide

88
Q

whats the casue of HUS

A

get e coli 0157 or shigella pathogen
this casues gastroennteritis
the bacteria produce shiga toxin
this toxin casues thrombosis in small bv thorughout the body and block bv

89
Q

classic triad of hus

A

haemolytic anaemia
AKI
low platelt count- thrombocytopenia

90
Q

s and s of hus

A

start with gastroenteritis- blood diarrhoa
brief

then 5 days after they start developing signs of hus

dec urine output - aki
lethargy and ittiability - anemia
bruising - low patlets
haematuriea/ dark brown urine
abdo pain
confusion
hypertension

91
Q

treat hus

A

med emergency
10% die
supportive
antihypertentisves
blood transfusion
dialysis

92
Q

athlete did ultramarathon
painful aches in musces
red-brown urine
oedema
what is this

A

rhamdomyolysis

93
Q

when to suspect rhabdomyloysis

A

anyone with a long lie, prlonged immobility, crush injury,
extreey rigourous exercise
seizure

94
Q

whats rhabdomyloysis

A

myocytes undergo apoptosis
release potassium
phosphate
myoglobin
creakine kinase

filtrered by kidnyes and casues injury to kidneys

95
Q

why is rhabdomyolsis initally so bad

A

potassium- hyperkalemia -cardiac arryhtmia esp vf

96
Q

what injures kidneys in rhabdomylosis

A

myoglobin toxic to kideys
casues AKI

97
Q

s and s of rhabdomylosysis

A

muscle aches and oains
oedema
fatigue
confusion- esp old
red-brown urine

98
Q

investigations rhabdomylosis

A

creatine kinase bloods- diagnositic - in thousandds
initally rises in first 12 hrs then stays elevated for 1-3 days the gradually falls ]

urine dipstick= postive for blood- myoglobinurea

u and e= aki and hyperkalaemia
ecg= high pot

99
Q

causes of rhabdomyloysis

A

prlonged immbolility
extremly rigourous exericse beyond person ability- crossfit competion, ultramarathon, triathlon
crush injuries
seizures

100
Q

treat rhabdomylosyis

A

iv fluids
maybe sodium bicarb as make urine less acididc and reduc toxic myoglobin = debated
maybe iv mannitol- debated and ensure hypovolameia corrected first

treat complications esp hyperkalameia
aki= iv fluids, nicarb, dialysis
compartment syndrome = m ischemaia= trat by fascitomy
treat hyperphosphatameia - diuretics/ dialysis
hypocalcamiea = leave as will go back to normal probs but check

101
Q

casues of hyperkalaemia

A

conditions=
AKI
CKD
rhabdomylosis
aldrenal insufficiency = addisons
tumour lysis syndroe

meds=
nsaids
ACEi
ARB
k supllements
aldosterone antagonsits- spirnolactone, eplerenone

102
Q

how to diagnose hyperkalamiea

A

u and e blood test
haemmolysis pof sample can give falsely high levels
ECG - do on all patients if k above 6mmol/l

103
Q

ecg changes in hyperkalameia

A

tall peaked t waves
broad QRS complex
flatening or asbcence of p waves

104
Q

manage hyperkalemia

A

iv insulin and dextrose= drives carbs into cells and takes k with
calcium gluconate = stabiolse cardiac muscle

have defo those two

other options=
nebulised salbutamol= tempriary drives k into cells
iv fluids= increase urine out put = encoirage k excretion= be careful if pt renal failire overlaoding them

oral caclium resonium= draws k out of gut into stool = for milder cases
sodium bicarboante= if acidotic and renal fialure acidosis fixed and the k goes into cells d
dialysis if v bad

105
Q

when to treat hyperkalaemia

A

ifeuqal or less than 6mmol/l and stable rneal function then change meds and diet

if 6 or more mmol/l and got ecg changes then urgent treatment

if 6.5mmol/l or more regardless of ecg changes urgent treatment

106
Q

broad qrs complex
tall peaked t waves
flat p waves

what is this

A

hyperkalameia

107
Q

whtas the genes and chromososomes for autosoal dominant polycystic kidney disease

A

PKD 1 - CHROMOSOME 16= MOST COMMON

PKD2- chromosome 4

108
Q

whats the extra renal manifestations of adpkd

A

cerbeal anyerysm
hepatic, ovarian , prostatic, splenic cysts
cardiac valve disease- mitral regurg
colonic diverticula
aortic root dilatation

109
Q

complications of adpkd

A

chronic lion pain
ht
cv disease
gross hameatruai when cysts burts- resolves
renal stones more common
end stage renal failure at 50

110
Q

how to diagnose adpkd

A

kidney US
genetic testing

111
Q

s and of adpkd

A

hypertension- headaches
blood in urine
fluttering/ pounding of heart ( cardaic vavle issues)
frequent bladder/ kidney infections
nocturia
loin pain
enlarge kidney on examination

112
Q

whats autosomal recessvie polycistic kidney disease

A

cyts develop in kindeys and renal failure but thus is more severe then the dominatn type
on chromosome 6

113
Q

how does autosomal recessive pkd present

A

in oregancy with oligohydroamnios

this casues underdevelopment of the lungs so when born have resp failure and require dialsysis in forst few days of life

also have underdeveloped ear cartilage
low set ears
flat nasal bridge
end stage renal failure before adulthood

114
Q

management of adpkf

A

tolvaptan = slows pregoression of renal failure and cyst developement
support comolications
antihypertensives for ht
analgesia for renal colic
antibiotics for infection / drain cysts
dialysis
transplant
genetic counselling
regular us monitor of cysts
regular bp cehck
regular blood check renal fucntion
avoid anti inflammatroy and anti coagulation meds
avoid contact sport to reduce risk of cyst rupture
mr angiogram for diagnosing intracranial anyeursym

115
Q

how do you match for renal tranplsant

A

hla type a,b,c on chromosome 6
dont need full match

116
Q

renal trnaplant procedure briefly and oe after findings

A

own kidneys left in
donor kidneys bv anastamose with pelvic bv
donor ureter connected to bladder of pt
kiney placed anterioly in abdomen
can palpate kindey in iliac fossa area
see hockey stick scar

117
Q

complcations to transplant

A

rejection- hyperacute, acute, chronic
failure
electrolyte imbalnace

issues with immunosupressants =
ischemic heart disease
t2 diabetes due to steroids
infections inc and more severe
unusual infections- PCP, CMB, PJP, TB
non-hodgkin lymphoma
skin cancer esp squamous cell carcinoma

118
Q

what meds needed for pos transplant

A

kideny starts fucnctioning immediatelty
life long immunosupression:
tacrolimus
mycophenolate
prednisolone

others
cyclosporine
sirolimus
azathioprine

119
Q

whats interstial kidney disease

A

interstial nephritis = inflam of sapce between the cells and tubules = interstitum
acute and chronic

120
Q

causes ofacute interstial nephritis

A

usulat hypersensitivity rx to :
drugs- nsaids / abx
infection

121
Q

s and s of acute interstial nephritis

A

aki
hypertension

other features with hypersentvity rxn
rash

fever
eosinophilia

122
Q

manage acute interstial nephritis

A

treat underlying cause
steroids to reduce inflammation

123
Q

causes of chronic interstial nephritits

A

autoimmune
infectious
iatrogenic
granulomatous disease

124
Q

s and s of chronic interstial nephritis

A

ckd symtoms

125
Q

manage chronic interstial nephritis

A

treat underlying cause

126
Q

whats AKI

A

acute drop in kidney function diagnosed by serum creatinine

127
Q

how to diagnose aki

A

serum creatinine levels
rise in creatine of 25 micromol/l or more in 48 hrs

rise in creatine of 50% or more in 7 days

urie output of les tha 0.5ml/kg/hr for 6 hrs or more

128
Q

s and s of aki

A

decreased urine output / changes to urine colour
confusion, fatigue, drowsiness
n and v
diarhoea
evidence of dehydration
oedema
high bp

129
Q

causes of aki - pre renal

A

pre renal:
most common= inadequate blood supply to kidneys so decreased filtration of blood occurs

dehydration
hypotension- shock
heart failure/mi = dec cardiac output
nsaids= durgs that lower bp, dec circulating volume, decrease renal blood flow
fluid loss- hypovolamiea = bleeding, severe diarrhoea
burns
majory surgery

130
Q

causes of aki - renal

A

intrinsic disease leading to decreased filtration of blood

toxins and drugs= chemo, contrast, antibiotics= aminoglycosides
vascualar= vasculitis, thrombosis, embolism, dissection
glomerulnephritits
sepsis
interstial nephritis
acute tubular necrosis

131
Q

what anitbiotic can cause aki

A

aminoglycosides

132
Q

causes of post renal aki

A

obstruction to outflow=
kidney stones
masses- abodmen and pelvis eg. cancer
ureter/urethral strictures
enlarged prostate/prostate cancer

133
Q

what are risk factors ofr AKI

A

recent surgery
CKD
diabetes
over 65
heart failure
dehydration
aminoglycosides = esp if ill and not drinking much casues renal vasoconstriction
nephrotoxic drugs= NSAIDs, ACEi, ARB, diuretics
liver disease
ct contrast
infection- sepsis
cognitive impairement- not drinking

134
Q

what investigations to do for suspected aki

A

serum creatine!!
urialysis = leucocyes and nitrites=infection
protein and blood= acute nephritits
glucose= diabetes
ultrasound if susepct post renal pbstruction
GFR

135
Q

urinalysis shows nitirites in blood
what this mean

A

infection

136
Q

urinalysis showed leucocytes and nitrites in blood
what this mean

A

infection

137
Q

protein and blood in urinalysis mean what

A

acute nephritits or infection

138
Q

management of AKI

A

prevention= avoid nephrotoxic drugs
and have adequate fluid input

fluid rehydration with iv fluids if pre renal

stop nephrotoxic meds

releive obstruction if post= catheter

dialysis if bad

139
Q

what complications of AKI

A

hyperkalaemia
metabolic acidosis
fluid overload, heart failure, pulmonary oedema
uraemia => encephalopathy/ pericarditits

140
Q

what indications suggest a need for acute dialysis

A

AEION
acidosis= severe and not responding to rx
Electrolyte imbalance - severe and not responding to rx
intoxication= overdose of certain meds
oedema= sevre and unrepsoponsie pulmonary oedema
uraemia symptoms= seizures, decreased consiousness.

141
Q

indications for long term dialysis

A

end stage renal failure - CKD stage 5
acute indications lasting long term

142
Q

what options are there for maintence dialysis

A

contionuous abulatory peritoneal dialysis
automated peritoneal dialysis
haemodialysis

143
Q

whats peritoneal dialysis

A

uses peritoneal membrane as filtration membrane
dialysis solution contains dextrose
ultrafiltration
involves tenckhoff catheter

144
Q

whats the difference between continuous ambulatory peritoneal dialysis and automated peritoeal dialysis

A

continuous ambulaotry= dialsysis solution in peritoneum at all times. cahnged / amount put in varies
automated=
occurs overnight
machine replaces dialysis fluid
8-10 hrs

145
Q

complications of peritoneal dialysis

A

bacterioal peritonitis! = glucose in ad bateria likes glucose so increase bacterial growth
peritoenal sclerosis
ultrafilatration failure
weight gain- absorb some of the carb
pschycosocial effects

146
Q

how haemodialsysis occur

A

blood filtered
4 hrs a day 3 days a week
need abundant blood supply
tunneled cuffed catheter into subclavian or jugular vein and sit in svc or right atrium, infection and clots an issue
or av fistual = allows high pressure blood from artery to vein bypassing capillaries= radioacephalic, brachiocephalic or brachiobascilic

147
Q

how to examine an av fistula

A

skin integrity
aneurysm
palpable thrill
machinery murmur on auscultation

148
Q

av fistula complications

A

anyeursm
stenosis
thrombosis
high output heart fialure = rapid return to heart = have increased pre load and so get hypertrophy of heart and heart failure
STEAL syndrome= inadquate blood flow to limb distal to av fistuala= distal ischemia

149
Q

someone is on dialysis
they have a tube connecting to their blood vessel
do you take blood from this?

A

no
never take blood from a fistula

150
Q

a pateint has a raised serum creatine
you check their medications to see if they are on what drug that raises theur creatine levels

A

trimethoprim
can raise serum creatine levels

151
Q

when may you have falsley raised serum creatine levels

A

on / been on rcently trimethoprim
recent pregnacy
during pregnacy serum creatine levels can decrease so if ahve levels checked after recent preg then could appear to be raised compared to recent ones but actually its they were preg and so levels were lower and now they back to their normal

152
Q

what extra renal features are there of ADPKD

A

heart murmur
hepatic cysts that manifest as hepatomegaly
diverticulosis
intracranial anyeursm
ovarian cysts

153
Q

ats the most common extra renal minfestation of ADPKD

A

Liver cysts are the commonest extra-renal manifestation of ADPKD

154
Q

cuassative agent of peritonitits assocaited with peritoneal dialyssis

A

most common is Staphylococcus epidermidis

155
Q

urine dip for aki casues pre renal, renal and post renal

A

pre renal- normal
renal- lots of protein (leaking through) and some blood
post renal- lots blood and not much if any protein

156
Q

urea higher than creatine proportionally for AKI casue

A

dehydration or upper gi bleed

157
Q

pt has pyeloneprititis and then is treated with abx. then they develop an AKI but no infection symtpoms present. casue for the aki

A

gentamicin

158
Q

immediate rejection of renal trasnplant - within 48hrs- casued by what

A

Signs of rejection within the immediate (24-48h) post-transplant period should always raise suspicions of hyperacute rejection, the rapidity of which is caused by pre-existing of antibodies against a donor’s ABO/HLA antigens

Cell-mediated (cytotoxic T-cell) mediated rejection is a cause of acute rejection but usually manifests within the first 6 months as oppose to the first 24h

Medicine (11 decks)

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