renal Flashcards

1
Q

what are the different types of renal stones

A

Calcium oxalate, 65%
Calcium phoshphate 20%
Uric acid 10%

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2
Q

epidemiology and prevalence of renal stones

A

lifetime risk 10-15% age 20-40 is peak

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3
Q

Risk factors of stone formation

A
Dehydration - largest risk factor 
pre existing kidney disease 
PCKD 
UTI- Proteus 
Urinary factors - Hypercalcemia 
thiazide= increase uric acid
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4
Q

Prevention of stone formation

A
Overhydration 
reduce salt and sodium 
normal dairy
moderate protein 
reduce BMI
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5
Q

where can stones form

A

upper, renal pelvis or ureter

lower bladder urethra prostate

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6
Q

Presentation of renal stones

A
Majority asymptomatic 
renal colic (associated with nausea and vomiting)
Pallor
sweating 
haematuria 
Auria 
UTI symptoms, voiding symptoms 
no signs on examination ( look out for gout tophi as a sign of excess uric acid
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7
Q

what is renal colic

A

severe abd pain, loin to groin
sudden onset
radiates to ipsilateral testicle or labia
writhing pain, unable to find comfortable position
colicky pain
pain usually subsited after a few hours
made worse by exercise or diuretics or alcohol

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8
Q

Investigations and diagnoses of renal stones

A

Before starting investigations start on Analgesia and antiemetics to stabilize patent

Non contrast CT of kidney ureter and bladder NCCT-KUB - diagnostic of stone

identify cause of stone: Bloods, Serum Ca, Serum uric acid. U and E. MC and S of MSU

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9
Q

differential diagnoses for patient present with renal colic

A

AAA
Gynae causes, Torsion of ovaries or ruptured ectopic
MSK
Torsion

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10
Q

Management of renal stones

Include preventative measures

A

Analgesia, NSAIDs, antiemetics
potentially give IV fluid if you want them to pass the stone
watch for sepsis
if stone <1 cm then conservative (hydrain, pain and antiemetic)
stone =2-3cm then lithotripsy (Extracorporeal shock wave lithotripsy)
stone >2cm Ureteroscopic laser

ureteric stent

Prevention of further if hypercalciuria ( thiazide
if hyperuricemia (allopurinol)

trimethoprim or gentamycin

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11
Q

Complication of Renal stones

A

can cause sepsis
obstruction of UT can cause dilation and dilation of the kidney is hydronephrosis. if there was an infection present it could cause pyonephrosis

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12
Q

what is pyonephrosis and presentation

A
pyelonephritis +hydronephrosis (infection of the kidney)
Loin pain 
fever 
Nausea and vomiting 
haematuria 
proteinuria 
sterile pyuria 
leads to sepsis
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13
Q

treatment of pyonephrosis

A
Iv antibiotics (gentamicin) + oxygen + drain 
watch for sepsis and potentially transfer to ITU
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14
Q

what does Acute kidney injury mean

A

Spectrum of kidney disease ranging from mild improvement to full kidney failure requiring RRT

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15
Q

What is creatinine and why is it used in

A

its a muscle breakdown product that is filtered freely in the kidney and not reabsorbed so gives indication of kidney filtration levels. elevated serum creatinine suggest reduced filtration

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16
Q

criteria to diagnose AKI

A

> 26 mmol/L rise in serum creatinine
50% increase in serum creatinine
oliguria less than 0.5ml/kg/Hr

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17
Q

what is the time frame for acute kidney injury and chronic kidney injury

A

3 month

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18
Q

risk factors for kidney injury

A
Diabetes 
liver disease 
sepsis
reduced fluid intake 
age >75 
CKD
Cardiovascular problems 
PMH of urinary symptoms 
urinary symptoms 
Drugs - NSAIDs and ACEi
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19
Q

why can NSAIDs and ACEi have an effect on Kidney

A

Prostaglandins cause afferent dilation which improves GFR
Angiotensin 2 causes efferent constriction whic also improves GFR
having ACEi and NSAIDS blocks this and causes Reduced GFR

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20
Q

causes of AKI

A

commonest are ischemia, sepsis, nephrotoxins
Pre renal - commonest cause (70%)
renal-
Post renal causes- least common

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21
Q

causes of AKI

pre renal

A

hypoperfusion, any reason. HV shock, D and V , sepsis

ACEi or NSAIDs.

renal artery stenosis

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22
Q

causes of AKI

renal

A

acute tubular necrosis (commonest renal cause of AKI)
glomerular cause, autoimmune, SLE, or Glomerulonephritis
interstitial, drugs like aminoglycans
vascular: SLE, ischemic, increased BP

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23
Q

causes of AKI

post renal

A

any obstruction to outflow tract-
lumina, stones, clots
intramural, BPH, Malignancy of bladder, ureter, prostate
extraluminal: compressive malignancy

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24
Q

What can cause Acute tubular nephrosis

A

nephrotoxins,

myoglobinuria by rhabdomyolysis

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25
Q

name some nephrotoxins

A

aminoglycans, Vancomycin
Lithium
Methotrexate

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26
Q

assessment and investigations of a patient with AKI

A

assess history: which drugs they are on, Risk factors PMH Urgent Hyperkalemia examination

Examination: look for palpable kidney (PCKD) bladder or masses in abdomen , check volume status- BP, JVP, edema, skin turgor.

bed tests: Dip stick, looking for nitrates or leukocytes, Microscopy and cultures to look for crystals, cultures

blood tests, U and E, FBC, clotting LFT, ESR, CRP, potentially serology

Imaging- renal USS, CTKUB,

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27
Q

Urgent examination to carry out in AKI

A

Urgent K+ and ECG checking for Hyperkalemia

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28
Q

Investigations and Imagining of AKI

A

Ultrasound looking for hydronephrosis or obstruction,
if hydronephrosis and over 65 suspect BPH and catheterise
if not relieved do NCCTKUB to look for stones etc

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29
Q

presentation of AKI

A

Usually asymptomatic and only detected on Blood tests but can present with nausea vomiting, confusion and a wide variety of symptoms (on another flashcard

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30
Q

Signs and symptoms of AKI

A

early: nausea, vomiting, reduced urine output, dizziness, lethargy

due to fluid retention, pul odema, nocturnal dyspnea, orthopnea, peripheral oedema

due to B, hyper or hypotension , Orthostatic hypotension, tachycardia

Confusion
haematuria

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31
Q

general managment of AKI

A
monitor for hyperkalemia 
assess fluid volume levels and aim to acheive euvolemia, give fluids or restrict fluids.
stop any nephrotoxic drugs, 
stop NSAIDS, ACEi, Metfroim
manage underlying dieseas
32
Q

Managment of AKI
pre renal
renal
post renal

A

Pre renal, if spsis, antibiotics. fluid challange if not CCF

Post renal, catheterise, if that doesnt work then NCCT KUB to see if there was stone and clear

Renal- may need dialysis or refered to nephrologist

33
Q

WHat are indications for dialysis in AKI

A

Fluid overload signs and symptoms, JVP, Oedema , Orthopnea, nocturnal Dysnpnoea
or Anuria
Hyperkalemia
metabolic acidosis
Uraemic complications like encephalopathy or pericarditis
drug overdose

34
Q

Indications to refer AKI to nephrologist

A

Hyperkalemia

35
Q

what are the complications of uremia

A

confusion coma
pericarditis pericardial rub
uremia induced platelet dysfunction, GI bleeds
neuropathy, nausea and vomiting, cramps

36
Q

complications of AKI

A

Hyperkalemia
edema
uremia
acidosis

37
Q

Prevention of AKI

A

monitoring drugs they are taking, temporarily stopping them if they have D and v
ensure patients in hospital are well hydrated use fluid volume charts
Med review if D and V

38
Q

ECG changes of hyperkalemia

A

High T wave
absent P wave
increased PR interval
wide QRS

39
Q

Treatment of Hyperkalemia

A

IV insulin and Glucose

since insulin stimulates uptake of Glucose

40
Q

what is chronic kidney disease, time to become chronic

A

Renal impairment for more than 3 Months

41
Q

how is chronic kidney disease staged and what symptoms are found at each stage

A

EGFR
stage 1 > 90 just has risk factors
stage 2 = 60-90 proteinuria
stage 3 = 30-59 still asymptomatic, N and V
stage 4 = 15-30 this is when symptoms usually start to show
end stage renal failure <15 - needs RRT at this stage

42
Q

causes of CKD

A
Diabetes M type 2 more than 1 
glomerulonephritis (commonest cause)- SLE, Vasculitis, nephropathy 
Congenital - PCKD 
Hypertension or renovascular disease 
Pyelonephritis 
following from AKI
43
Q

Symptoms of CKD

A

symptoms usually start when there is uremia

Anaemia, Pallor lethargy SOB
Platelet abnormality - Bruising, epistaxis
Skin - pigmentation and pruritus and purpura
GI- anorexia, D and V nausea
Endo - amenorrhea, erectile dysfunction
CNS- confusion, encephalitis
CVD, Pericarditis, pericardial rub, hypertension cardiomegally
Renal- nocturia, polyuria
oedema and pul oedema, dyspnea orthopnea
MSK, weakness

44
Q

commonest symptoms of CKD

A

Uraemic tinge, pigmentation
Increased BP
Fluid overload signs

45
Q

Investigations and examination of CKD

A

look for signs of fluid overload and oedema- signs and symptoms, cardiomegaly

Bloods: HB, normal or normocytic anemia, ESR and CRP, Ca low , PTH high, PO4- low or High

Urinalysis: dipstick, Haematuria, (glomerulonephritis) proteinuria, suggests Glomerular disease. MSand C shows albumin creatinine conc

Biochem: creatinine clearance test, estimates GFR and is a screening tool

Renal ultrasound for all renal patients, look for hydronephrosis, do biopsy if still unknown

46
Q

Management of CKD conservative

A

stop nephrotoxic drugs,
Limit progress, lower BP
Bone disease: use Vit D analouges to lower PTH
CVD: statins, Lifestyle and BP
Diet, avoid high phosphate food, Potassium restrictions

47
Q

Management of CKD stage 1 to 4

A

Main cause of death is CVD

so ACEi or ARB plus statins plus diuretics plus CCB if needs be

48
Q

Management of CKD symptoms

A

anemia, Iron B12 Folate
Acidosis, sodium carbonate
oedema, diuretics, loop diuretic furosemide
prepare for RRT
Treat underlying conditions, BPH, Diabetes

49
Q

what is RRT and how to prep for it

A

Hemodialysis- insert AV fistula
Peritoneal dialysis
Renal transplant

50
Q

what glomerular nephritis

A

disease of the glomerulus
term for inflammation of glomerulus and nephron
can have nephrotic or nephritic presentation

51
Q

Nephrotic syndrome presentation

A
Proteinuria
Mild hypertension 
Mild impairment of GFT
Hypoalbuminemia 
Oedema
52
Q

pathophysiology of nephrotic syndrome

A

Damage to podocytes so protein can leak though causing hypoalbuminemia and oedema .
due to reduced albumin in blood liver works more produced more albumin and causes Hyperlipidemia

53
Q

causes of nephrotic syndrome

A

Primary, Membonous, minimal change, FSGS, focal segmental Glomerulosclerosis

Secondary- Diabetes, SLE Amyloid, Hep B or C

54
Q

complication of Nephrotic syndrome

A

Due to loss of Immunoglobulins- increased risk of infection

due to hyperlipidemia, Increased Risk of Thromboemboli to Mi or Stroke

55
Q

Treatment of Nephrotic syndrome

A

Oedema, Loop diuretic furosemide
Proteinuria: ACEi or ARB
Prevent atheromas by statins and anticoagulation
Treat underlying cause, usually steroids, glucocorticoids

56
Q

Nephritic syndrome Presentation

A

Haematuria, Proteinuria, Oliguria

Mod to severe increase in BP and Decrease in GFR

57
Q

nephritic syndrome Pathophysiology

A

Excess damage to nephron and glomerulus so Blood and protein leak though. reduction in GFR causes oliguria.
there is compensatory increase in BP

58
Q

nephritic syndrome causes

A

Commonest cause is IgA nephropathy (primary cause)
other primary cause is mesangiocapillary GN

Secondary causes. SLE, ANti GBM disease, Goodpasture’s. Post streptococcus infection, Hep b or C
vasculitis
Drugs, penicillamine

59
Q

Investigations for Glomerulonephritis

A

Bloods, FBC, U and E, LFT ESR CRP, Serology anti ANA, Anti DsDNA
Urinalysis - dip stick and MC and S- look for streptococcus, RBCs, WBCs, albumin

Renal Biopsy is gold standard-

60
Q

management of Glomerulonephritis

A
Refer to nephrologist
maintain Bp  
Diuretics for oedema (more in nephrotic)
ACEi for proteinuria 
statins and anticoagulation 
diet for hyperlipidemia (more in nephrotic)
Treat underlying cause potentially steroids or glucocorticoids
Potential antibiotic therapy
61
Q

nephrotic or nephritic syndromes that need Immunosuppressive therapy (prednisolone)

A

IgA nephropathy
SLE
Anti Glomerular basement membrane disease
Vasculitis

62
Q

whos is screened for Chronic kidney disease

A
screen at risk patients 
Diabetes 
Hypertension 
CVD
BPH 
Recurrent UTI 
Family history of ESRD
Congenital kidney disease like PCKD
63
Q

how is screening for Chronic kidney disease done

A

Albumin creatinine ratio
urinalysis
serum creatinine

64
Q

What is polycystic kidney disease

A

inherited disorder either autosomal recessive or dominant.

65
Q

Prevalence of PCKD and what gene does it affect

A

PKD1 and 2 on chromosome 16

1 in 1000

66
Q

Progression of PCKD

A

85% progress to ESRD

can cause increased risk of forming renal stones and calculi

67
Q

Signs for PCKD

A
Palpable kidney, Think PCKD
Abdominal pain 
haematuria (from Cyst hemorrhage)
Hypertension 
progressive renal failure 
 SAH 
UTIs
68
Q

pathophysiology of PCKD

A

cysts in kidney, causing enlargement. they can hemorrhage leads to haematuria
cyst infection can cause renal stones
Increased risk of renal cell carcinoma

69
Q

extrarenal signs and pathology/complications of PCKD

A
liver cysts
intracranial aneurysm- SAH 
ovarian cyst
Diverticular disease 
Mitral valve prolapse
70
Q

complications of PCKD

A

hypertension, increased cardiovascular morbidity and mortality, chronic renal failure, ruptured intracranial aneurysm, and end-stage renal disease

71
Q

Investigations to confirm this is PCKD

A

Renal ultrasound

CT or MRI if not found on Ultrasound

72
Q

Investigations to carry out in PCKD to assess damage and other complications

A

Urinalysis to look for UTI, increased albumin, haematuria. these indicate more likely to progress to severe disease
ECG - suspected LV dysfunction
Brain CT if suspected SAH
Can screen for SAH with MRI angiography

73
Q

Management of PCKD

A

Monitor kidney function U and E
Control BP to 130/90
Treat Infections
if painful, Laparoscopic removal of cyst
Diet, increase water reduce sodium and avoid caffeine
ESRD, Dialysis or transplant
Screen relatives and genetic counseling

74
Q

Screening for PCKD

A
Screen in relatives
USS
less than 40 YO, up to 3 cyst is normal 
40-60 year old, Up to 2 cysts per kidney 
60 or more up to 4 cysts per kidney
75
Q

Who to screen for SAH

A

1st degree relative with PCKD plus SAH

Screen using MRI angiography