Renal Flashcards
(158 cards)
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
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
3
Q
what risk factors of ckd
A
diabetic
ht
obesity
cv disease
older age
smoking
using meds that are nephrotoxic
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
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
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
7
Q
complications of ckd
A
anemia
renal bone disease- ckd-mbd
cv disease
dialysis issues
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
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
10
Q
what do you need to monitor in paitnets on ht treatment with ckd
A
serum potassium
ckd and also acei cause hyperkalameia
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
12
Q
whats renal bone disease
A
osteomalacia
osteoporosis
osteosclerosis
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)
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
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
16
Q
will you see high or low serum phosphate in ckd
A
high
17
Q
will you see how or low k in ckd
A
high
18
Q
will you see metabolic acidosis or alkalosis in ckd
A
acidosis
19
Q
whats does glomeruloneprhtis mean
A
inlam of or aroud the glomerulus
20
Q
how do you treat most glomerulonephrtis
A
steroids
bp control- ACEi/ARB
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
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
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
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
25
whats the most common cause of nepthrotic syndrome in children
minimal change disease
26
whats the most common casue of nephrotic syndrome in adults
focal segemental glomerulosclerosis
27
other causes of nephrotic syndrome
sle, diabetes, infection, sickle cell, alport, drugs, amyloid
28
treat nephrotic syndrome
corticosteroids
oedema- low salt intake, fluid restriction, diuretics
bp control- ACEi/ ARB
29
whats nephritic syndrome
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
30
causes of nephritic syndrome
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
31
whats the most common cause of primary glomerulonephritis
IgA nephropathy
32
whats the most comon type pf glomerulonephritis overall
membranous glomerulonephritis
33
whats IgA nephropahty and histology finings
most common casue of primary glomerulonephritits
esp in 20s
histology= IgA depsosits and mesagnial expansion/proliferation
can affect bv too
34
histology findings are IgG and complement depostis on basement membrane of glomerulus
what is this
membranous glomerulonepthritis
35
whats membranous glomerulonephtiris
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
36
pt had tonsilits
2 weeks later theyre not weeing much and have soe bloodin their urine
what is this
post streptococcal glomerulonephritis
37
whats post strephtococcal glomerulonepthrits
also called diffuse proliferative glomerulonephritis
under 30s mainy
1-3 weeks after strep infection - tonsilits/ impetigo
nephritic syndrome
38
post streptococcal glomerulonephritis/ diffuse proliferative glomerulonepthritis shows nephrotic or nephritic syndrome
nephrititc
39
patient has reduce urine output
n and v
cofusion
coughing up blood
what is this
goodpastures syndrome/ anti GBM
aki and haemoptysis = anti gbm
40
whats anti GBM/ good pastures syndrome
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
41
whats rapidly progressive glomerulonephritis
histology= cresentic glomerulonephritis
v acute illners
often secondary to anti gbm
42
patient has diabetes
have protein in urine
what is this
diabetic nephropathy
43
whats tha pathophysiology of diabetic nephropathy
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
44
whats the three main thigs that happen in diabetic nephropathy
mesagnial expansion
nephron ischemia
increase pressure state
45
why mesangial expansion occur in DKD
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
46
why does nephron ischemia occur in dkd
efferent arteriole constrict due to raas activcation due to high glucose
efferent arteriole supplies blood to the tubules
constricted so less blood
increased turbulence
47
s and s of dkd
proteinuria
maybe haematuriea
increase gfr initially
low gfr and renal failure
48
how to prevent dkd
regular screening of ACR
optomise bp, statins , glycemic control
educate
weight loss
dec salt
49
how to manage dkd
OPTOMISE BLOod sugar
optomise blood pressure
even if normal bp pts with diabetic nephropathy be on acei or arb
50
what bp meds is for pt with diabetic nephropahty
ACEi or ARB
51
whats acute tubular necrosis
damage and death to tubular epithelial cells
most common casue of AKI
epithelila cells can regernate- 7-21 days recovery
52
whats the most common cause of AKI
acute tubular necrosis
53
whats causes of acute tubular necrosis
ischemia = secondary hypoperfusion
shock
sepsis
dehydration
toxins = direct damage
radiology contrast dye
gentamicin
NSAIDs
lithium
heroin
54
what antibiotic causes acute tubular necrosis
gentamicin
55
s and s of acute tubular necrosis
s and s of aki
=
decreased urine output
vomit nausea
diarrhoea
confusion
hyperkalemia
metabolic acidosis
56
urinalysis shows muddy brown casts
what is this
acute tubular necrosis
57
what ivestigfations for acute tubular necrosis
urialysis = muddy brown casts = pathognomic finding specific to acute tubular necrosis
may also see renal tubular epithelial cells in urine
58
hpw to manage acute tubular necrosis
same as other aki
supportive
iv fluids
stoph nephrotxic meds
treat complications
59
whats renal tubular acidosis
metabolic acidosis with normal anion gap due to pathology in the kidney tubules
60
hyperkalaemia
high chloride
metabolic acidosis
low urine ph
what is this
type 4 renal tubular acidosis
61
whats type 1 renal tubular acidosis
to do with hydrogen ions not being able to be excreted in the DCT
62
causes of type 1 renal tubular acidosis
genetic
sle
sjorgens syndrome
primary biliary cirrhosis
hyperthryoidism
sickle cell anameia
marfdans sydrome
63
singns symptoms of type 1 renal tubular acidosis
failure to thrive in children
hyperventilation trying to compensate
ckd
osteomalacia
high ca in urine
64
results if type 1 renal tubular acidosis
hypokameia
metabolic acidosis
alkalotic pH - high urine ph over 6
65
treatment of type 1 renal tubular aicdosis
oral bicaarbonate- also sorts out electrolyte balance
66
hypokalaemia
high urine ph
metabolic acidosis
what could this be
type 1 or 2 rneal tubular acidosis
67
most common type of renal tubular acidosis
type 4 - to do with low aldosterone
68
whats type 2 renal tubular acodisi
due to PCT
not able to reabsrob bicarbonate
69
cause of type 2 renal tubular acidosis
fanconi syndrome
70
whats fanconi syndrome
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
reuslts if type 2 renal tubular acidosis
hypokalaemia
metabolic acidosis
high urine ph - alklalotic
72
treat type 2 renal tubular acodisis
oral bicarb
73
which types of renal tubular acidosis are similar in results and treatment
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
whats type 3 renal tubular acidosis
1 and 2 combined
pct and dct pathology
75
whats type 4 renal tubular acidosis
low alodsterone or not able to respond to aldosterone
76
whats most common type of renal tubular acidosis
type 4
aldosterone low
77
what cause and how work type 4 renal tubular acidisos
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
results of type 4 renal tubular acidosis
hyperkalaemia
metabolic acidosis
high chloride
low urine ph
79
s and s of type 4 renal tubular acidosis
cardiac arhtymia
paralysis
due to high k
80
causes of type 4 renal tubular acidosis
low aldosterone =>
ACEi/ arb
spironolactone
sle
diabetes
hiv
addisons disease ]nsaids
ckd
heparin use
81
treatment type 4 renal tubular acidosis
fludrocortisone
sodium bicarbonate
treat hyperkaelamie = volume expansion, potassium wasting diuretics - furusomide
82
s and s of type 1 and 2 renal tubular acidosis
hypokalemia =
muscle weakness
hyporelfexia
osteomalacia
83
whats HUS
thrombosis in small bv throughout body casued by shiga toxin
84
what toxin casues HUS
shiga toxin
85
what pathogens can produce shiga toxin
Ecoli 0157 ( most common)
shigella
86
patient had blood diarrhoea for a few days and they took loperamide
they now have abdo pain and not weeing much
whst is this
HUS
87
what increases risk of getting HUS
treating the gastroenteritis with anitbiotics or anti motility agents- loperamide
88
whats the casue of HUS
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
classic triad of hus
haemolytic anaemia
AKI
low platelt count- thrombocytopenia
90
s and s of hus
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
treat hus
med emergency
10% die
supportive
antihypertentisves
blood transfusion
dialysis
92
athlete did ultramarathon
painful aches in musces
red-brown urine
oedema
what is this
rhamdomyolysis
93
when to suspect rhabdomyloysis
anyone with a long lie, prlonged immobility, crush injury,
extreey rigourous exercise
seizure
94
whats rhabdomyloysis
myocytes undergo apoptosis
release potassium
phosphate
myoglobin
creakine kinase
filtrered by kidnyes and casues injury to kidneys
95
why is rhabdomyolsis initally so bad
potassium- hyperkalemia -cardiac arryhtmia esp vf
96
what injures kidneys in rhabdomylosis
myoglobin toxic to kideys
casues AKI
97
s and s of rhabdomylosysis
muscle aches and oains
oedema
fatigue
confusion- esp old
red-brown urine
98
investigations rhabdomylosis
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
causes of rhabdomyloysis
prlonged immbolility
extremly rigourous exericse beyond person ability- crossfit competion, ultramarathon, triathlon
crush injuries
seizures
100
treat rhabdomylosyis
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
casues of hyperkalaemia
conditions=
AKI
CKD
rhabdomylosis
aldrenal insufficiency = addisons
tumour lysis syndroe
meds=
nsaids
ACEi
ARB
k supllements
aldosterone antagonsits- spirnolactone, eplerenone
102
how to diagnose hyperkalamiea
u and e blood test
haemmolysis pof sample can give falsely high levels
ECG - do on all patients if k above 6mmol/l
103
ecg changes in hyperkalameia
tall peaked t waves
broad QRS complex
flatening or asbcence of p waves
104
manage hyperkalemia
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
when to treat hyperkalaemia
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
broad qrs complex
tall peaked t waves
flat p waves
what is this
hyperkalameia
107
whtas the genes and chromososomes for autosoal dominant polycystic kidney disease
PKD 1 - CHROMOSOME 16= MOST COMMON
PKD2- chromosome 4
108
whats the extra renal manifestations of adpkd
cerbeal anyerysm
hepatic, ovarian , prostatic, splenic cysts
cardiac valve disease- mitral regurg
colonic diverticula
aortic root dilatation
109
complications of adpkd
chronic lion pain
ht
cv disease
gross hameatruai when cysts burts- resolves
renal stones more common
end stage renal failure at 50
110
how to diagnose adpkd
kidney US
genetic testing
111
s and of adpkd
hypertension- headaches
blood in urine
fluttering/ pounding of heart ( cardaic vavle issues)
frequent bladder/ kidney infections
nocturia
loin pain
enlarge kidney on examination
112
whats autosomal recessvie polycistic kidney disease
cyts develop in kindeys and renal failure but thus is more severe then the dominatn type
on chromosome 6
113
how does autosomal recessive pkd present
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
management of adpkf
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
how do you match for renal tranplsant
hla type a,b,c on chromosome 6
dont need full match
116
renal trnaplant procedure briefly and oe after findings
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
complcations to transplant
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
what meds needed for pos transplant
kideny starts fucnctioning immediatelty
life long immunosupression:
tacrolimus
mycophenolate
prednisolone
others
cyclosporine
sirolimus
azathioprine
119
whats interstial kidney disease
interstial nephritis = inflam of sapce between the cells and tubules = interstitum
acute and chronic
120
causes ofacute interstial nephritis
usulat hypersensitivity rx to :
drugs- nsaids / abx
infection
121
s and s of acute interstial nephritis
aki
hypertension
other features with hypersentvity rxn
rash
fever
eosinophilia
122
manage acute interstial nephritis
treat underlying cause
steroids to reduce inflammation
123
causes of chronic interstial nephritits
autoimmune
infectious
iatrogenic
granulomatous disease
124
s and s of chronic interstial nephritis
ckd symtoms
125
manage chronic interstial nephritis
treat underlying cause
126
whats AKI
acute drop in kidney function diagnosed by serum creatinine
127
how to diagnose aki
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
s and s of aki
decreased urine output / changes to urine colour
confusion, fatigue, drowsiness
n and v
diarhoea
evidence of dehydration
oedema
high bp
129
causes of aki - pre renal
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
causes of aki - renal
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
what anitbiotic can cause aki
aminoglycosides
132
causes of post renal aki
obstruction to outflow=
kidney stones
masses- abodmen and pelvis eg. cancer
ureter/urethral strictures
enlarged prostate/prostate cancer
133
what are risk factors ofr AKI
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
what investigations to do for suspected aki
serum creatine!!
urialysis = leucocyes and nitrites=infection
protein and blood= acute nephritits
glucose= diabetes
ultrasound if susepct post renal pbstruction
GFR
135
urinalysis shows nitirites in blood
what this mean
infection
136
urinalysis showed leucocytes and nitrites in blood
what this mean
infection
137
protein and blood in urinalysis mean what
acute nephritits or infection
138
management of AKI
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
what complications of AKI
hyperkalaemia
metabolic acidosis
fluid overload, heart failure, pulmonary oedema
uraemia => encephalopathy/ pericarditits
140
what indications suggest a need for acute dialysis
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
indications for long term dialysis
end stage renal failure - CKD stage 5
acute indications lasting long term
142
what options are there for maintence dialysis
contionuous abulatory peritoneal dialysis
automated peritoneal dialysis
haemodialysis
143
whats peritoneal dialysis
uses peritoneal membrane as filtration membrane
dialysis solution contains dextrose
ultrafiltration
involves tenckhoff catheter
144
whats the difference between continuous ambulatory peritoneal dialysis and automated peritoeal dialysis
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
complications of peritoneal dialysis
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
how haemodialsysis occur
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
how to examine an av fistula
skin integrity
aneurysm
palpable thrill
machinery murmur on auscultation
148
av fistula complications
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
someone is on dialysis
they have a tube connecting to their blood vessel
do you take blood from this?
no
never take blood from a fistula
150
a pateint has a raised serum creatine
you check their medications to see if they are on what drug that raises theur creatine levels
trimethoprim
can raise serum creatine levels
151
when may you have falsley raised serum creatine levels
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
what extra renal features are there of ADPKD
heart murmur
hepatic cysts that manifest as hepatomegaly
diverticulosis
intracranial anyeursm
ovarian cysts
153
ats the most common extra renal minfestation of ADPKD
Liver cysts are the commonest extra-renal manifestation of ADPKD
154
cuassative agent of peritonitits assocaited with peritoneal dialyssis
most common is Staphylococcus epidermidis
155
urine dip for aki casues pre renal, renal and post renal
pre renal- normal
renal- lots of protein (leaking through) and some blood
post renal- lots blood and not much if any protein
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urea higher than creatine proportionally for AKI casue
dehydration or upper gi bleed
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pt has pyeloneprititis and then is treated with abx. then they develop an AKI but no infection symtpoms present. casue for the aki
gentamicin
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immediate rejection of renal trasnplant - within 48hrs- casued by what
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
