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year 5 > Renal > Flashcards

Renal Flashcards

1
Q

A 5-year-old boy presents with a short history of facial oedema that has now progressed to total body swelling involving the face, abdomen, scrotum, and feet. Other symptoms include nausea, vomiting, and abdominal pain. The parents report that the child had a viral illness with fever a few days before the development of the swelling. On examination, he has facial oedema, ascites, scrotal oedema, and pitting oedema of both legs up to the knees.

A

minimal change nephropathy

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2
Q

A 42-year-old white man with no previous medical history presents to his primary care physician with progressively increasing oedema of both lower extremities. There is no family history of renal failure. The patient has pitting pedal oedema. Urinalysis reveals marked proteinuria (3+).

A

FSGS

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3
Q

A 48-year-old man presents to his family doctor with a recent lower-extremity swelling that is gradually worsening. Over the last few weeks, he has also noticed puffiness under his eyes. A urinalysis demonstrates significant proteinuria, and a 24-hour urine collection confirms proteinuria of 12 g. He has no history of diabetes, macroscopic haematuria, or hypertension.

A

membranous nephropathy

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4
Q

A 50-year-old man with a 15-year history of type 2 diabetes presents with oedema, fatigue, and impaired sensation in the lower extremities. He is found to have proteinuria, a reduced eGFR, anaemia, background diabetic retinopathy, and peripheral neuropathy

A

diabetic nephropathy

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5
Q

A 23-year-old white man with an unremarkable past medical history presents to the clinic for a routine physical examination including a urine analysis required for his job. This shows invisible haematuria and mild proteinuria. The physical examination reveals no significant abnormal findings

A

IgA nephropathy, berger’s

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6
Q

A 41-year-old woman is discharged from hospital following a diagnosis of community-acquired pneumonia, to be managed at home on amoxicillin. A day later she returns to the emergency department with a low-grade fever, widespread erythematous rash and pain throughout her joints and lower back, with her initial bloods showing a significantly elevated creatinine.

A

AIN

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7
Q

A 20-year-old woman presents with a 5-day history of painless light brown coloured urine. She has experienced 3 episodes of this over the 5 days. There is no dyspareunia, urgency or pain elsewhere. As of now, she is afebrile though she alludes to being ill with a respiratory infection around three weeks ago.

A

post strep GN

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8
Q

A concerned mother attends your GP surgery with her 7-year-old son. She is very concerned as she reports that ‘there is blood in his urine.’ Urine dipstick is ++++ for blood with no leukocytes, nitrates or protein. The boy reports that he first noticed the haematuria this morning. Physical examination is unremarkable, with normal heart and lung sounds and a soft non-tender abdomen. He is afebrile and does not have any symptoms of a urinary tract infection. His past medical history is unremarkable but his mother reports that he recently had a cold 2 days prior and has had several colds over the past year.

A

IgA nephropathy

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9
Q

5 causes of nephrotic syndrome

A

primary glomerular disease

  1. minimal change
  2. FSGS
  3. membranous nephropathy

systemic

  1. diabetes
  2. amyloidosis
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10
Q

nephritic syndrome causes

A
  1. post-strep glomerulonephritis
    small vessel vasculitis
    anti GBM disease

iga nephropathy

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11
Q

causes of crescenteric nephritis or RPGN

A
  • SVV small vessel vasculitis
  • SLE
  • anti GBM good pasture’s
  • aggressive phase of other inflammatory nephritis
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12
Q

acute intersitial nephritis causes AIN

A

Allergic

  • drug
  • autoimmune

Infective
-Toxic- noxious

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13
Q

chronic interstitial nephritis causes

A
  • AIN where the cause continues
  • in assoc. with glomerulonephritis
  • allergic/ immune- sarcoidosis, autoimmune-sjorgen
  • infective
  • toxic Ig light chains, heavy metals, Li
  • development/ congenital - reflex nephropathy and renal dysplasias
  • inhertied- metabolic, nephrocalcinosis
  • ischaemia/ papillary necrosis- sickle cell, analgesic nephropathy
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14
Q

haematuria causes

A 
UTI
stones
tumours
prostate gland disease
-glomerulonephritis
schistosomiasis
  • not haematuria
  • menstruation
  • dyes in food
  • transient haematuria from strenuous exercise
  • if on warfarin more likely to get more significant
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15
Q

signs of glomerulonephritis

A 
haematuria
proteinuria 
one of 
blood pressure
oedema
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16
Q

visible haematuria management

A

-exclude menstruation/ UTI
check BP, renal function

refer to urology for USS/ CT renal tracts/ cystoscopy

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17
Q

persistent non visible haematuria diagnosis

A

need 2 out of 3 positive dipsticks

exclude menstruation and UTI

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18
Q

persistent non visible haematuria and normal renal function and BP but over 40

A

refer to urology

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19
Q

persistent non visible haematuria and normal renal function and BP but under 40 and symptomatic

A

refer to urology

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20
Q

persistent non visisble haematuria and normal renal function and BP but under 40 and not symptomatic

A

keep under observation

-annual urinalysis and renal function and BP check

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21
Q

persistent non visible haematuria and abnormal renal function and BP

A

refer to renal

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22
Q

persistent non visible haematuria and fhx of renal disease or evidence of systemic disease

A

refer to renal

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23
Q

inx options for haematuria

A

-hx
-urinalysis
-urine culture
-urine microscopy
BP
-renal function
-urine ACR

all patients >40 and persistent non visible haematuria get cystoscopy and imaging along with visible haematuria patients

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24
Q

who to send to renal for haematuria

A
  • hx of fhx of renal disease
  • evidence of systemic disease
  • abnormal BP or renal function
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25
Q

what is loin pain haematuria syndrome

A

-name given to the syndrome in which people suffer loin or flank pain and have blood in their urine, in whom no other cause is found

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26
Q

types of oedema

A

-localised

generalised- ascites, pleural effusion, facial - can with increased severity be in the genitalia and abdomen

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27
Q

inx for oedema

A

hx and exam
urinalysis
bloods- labumin

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28
Q

4 mechanisms of oedema

A

increased ECF
increased hydrostatic pressure
increased capillary permeability
lowered oncotic pressure

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29
Q

what can cause increased ECF

A
  • sodium retention by kidneys renal failure
  • heart failure
  • nephrotic syndrome- low albumin
  • liver failure
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30
Q

signs of general increased in hydrostatic pressure

A

-venous pressure is high in heart or renal failure
raised JVP
nephrotic syndrome - except get a normal JVP as intravascualr deplete

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31
Q

signs of local increased in hydrostatic pressure and cause

A

-venous pressure will be raised by DVT or venous insufficiency or by extrinsic obstruction such as pregnancy or tumour
-non pitting localised oedema- lymphoedema
also some infections, malignancy and radiation

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32
Q

causes of increased capillary permeability

A

infection
sepsis
protein leaks into the interstuitium which reduces the oncotic pressure gradient so draws fluid out

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33
Q

lowered oncotic pressure of blood

A
  • low serum albumin due to reduced synthesis or increased loss
  • assoc. with avid sodium retention by the kidneys
  • liver failure is reduced synthesis
  • nephrotic syndrome- increased loss of proteins
  • malnutrition reduced synthesis

hold onto fluid

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34
Q

management of oedema

A

diuretics
salt and fluid restriction depending
compression

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35
Q

unilateral leg oedema suggests

A

a mechanical problem

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36
Q

oedema with hyponatraemia suggest

A

whole body sodium is increased but water is increased more - hypervolaemic hyponatraemia so needs restriction of water and salt but caution diuretics

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37
Q

proteinuria what does it signify

A

renal disease

-protein in the urine always comes from the kidney

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38
Q

three main causes of proteinuria

A

-glomerular disease
increased protein production
low reabsorption at proximal tubule

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39
Q

main causes of proteinuria

A
  • nephrotic syndrome
  • glomerular disease -glomerulonephritis, diabetes
  • CKD
  • autoimmune- lupus, goodpasture
  • urine infection
  • systemic- congestive heart failure, eclampsia
  • dehydration
  • htn
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40
Q

less important causes of proteinuria

A

-fever
strenuous exercise
absent in the morning but occurs in the later in the day-orthostatic proteinuria
occurs only during a urine infection

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41
Q

inx proteinuria

A

-dipstick urine

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42
Q

indication for further inx of proteinuria

A

-proteinuria >100
haematuria- think glomerulonephritis
-raised serum creatnine/ low eGFR
-HTN
-symptoms of systemic disease eg vasculitis such as rash, arthralgia
-previous hx or fhx suggesting significant renal disease

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43
Q

further inx for proteinuria

A

quantify proteinuria creatinine
urine albumin creatinine ratio
uss of kidneys
consider referral renal biopsy

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44
Q

what is assoc, to proteinuria

A

cardiovascular disease

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45
Q

quantification of proteinuria inx

A

-PCR or ACR urine

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46
Q

what is normal protein loss in urine

A

about 0.3g/day

but virtually no albumin

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47
Q

management of low level proteinuria

A

-absence of heavy proteinuria <1g day, haematuria, HTN, renal function, symptoms: monitor urine test and renal function at 6 month intervals

> 1g consider renal biopsy

see flow chart

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48
Q

voiding symptoms

A 
persistent dribbling
intermittent stream
straining
hesitancy 
poor flow 
bladder outflow obstruction
double voiding
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49
Q

storage symptoms

A

frequency
urgency
nocturia
incontinence

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50
Q

end stage renal failure symptoms

A 
-thirst 
twitching
pallor
fatigue
nausea
vomiting 
bone pain
breathlessness
pigmentation
coma
confusion
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51
Q

causes of haematuria

A

-cysts
-tumours
-vascular malofrmations
-glomerular disease
0interstitial disease
-infection
-cancer
-stones
-trauma
-clotting disorders

-excerise
malnutrition

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52
Q

def of oliguria

A

<400

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53
Q

anuria def

A

<100

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54
Q

causes of oliguria/ anuria

A

urinary obstruction eg prostate, tumour, stone
lack of renal perfusion- aortic dissection
RPGN

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55
Q

AKI stage 1 is

A

creatinine >1.5-1.9

urine <0.5 for >6 hours

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56
Q

AKI stage 2

A

creatinine 2-2.9

urine <0.5 for 12 hours

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57
Q

AKI stage 3

A

> 3 creatinine

urine <0.3 for 24 hrs or anuric 12 hours

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58
Q

how do NSAIDs act at as predisposing drugs to AKI

A

NSAIDS inhibit prostaglandin production which inhibits the dilatation of the afferent arteriole

which is aimed at increasing glomerular pressure

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59
Q

how do ACEi act as predisposing drugs to AKI

A

ACEi inhibit angiotensin II production which prevents constriction of the efferent arteriole

which is aimed at increasing glomerular pressure

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60
Q

causes of AKI

A

usually multifactorial
-dehydration- SEVERE hypovolaemia
pre-existing renal damage
predisposing drugs

overall get decreased glomerular pressure that is required for proper filtration

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61
Q

predisposing drugs to AKI

A 
-ACEi
NSAID
aminoglycosides
diuretics 
IV contrast
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62
Q

classification of AKI

A

-pre-renal
renal
post-renal

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63
Q

pre renal causes for AKI

A
  • circulation- systemic and local (RAS)
  • bp
  • cardiac ouput
  • sepsis
  • fluid balance reduced
  • reduced arterial circualtion
  • intrarenal microcirculation
  • blood loss
  • dehydration
  • vascular occlusion
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64
Q

inx for AKI

A
  1. renal u and e
    2, urinalysis
  2. renal USS
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65
Q

INX findings for pre-renal AKI

A

urine osmolality increases
sodium urine decreases- hold onto sodium
serum urea: creatinine increases

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66
Q

intrinisc renal AKI causes

A
  • ATN acute tubular necrosis-prolonged pre-renal
  • inflammation: glomerulonephritis, interstitial nephritis, pyelonephritis
  • vascular- renal vein thrombosis, cholesterol emboli, renal infarction, malignant hypertension, recent angiography
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67
Q

Acute tubular necrosis pathology

A

-get an injury to the tubule which leads later to necrosis of the tubule and fibrosis

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68
Q

intrinisic renal AKI inx findings

A

urine osmolality decreased

urine sodium increased- loose sodium

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69
Q

post-renal AKI causes

A
  • neurological
  • stones, crystals blocking
  • kidneys, bladder
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70
Q

approach to the patient with oliguria

A
  1. is it real- check bladder recordings?
  2. check circulation
  3. fluid balance
  4. drug chart
  5. previous result and hx
  6. uss and dipstick
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71
Q

elevated creatinine diff dx

A
  1. aki
  2. ckd
  3. aki on background of ckd
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72
Q

KDIGO criteria for AKI 3

A
  1. increase in serum creatinine by >26.5 micromol within 48 hours
  2. increase in serum creatinine by >1.5 x baseline within the prior seven days
  3. urine volume <0.5ml/kg for >6 hours
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73
Q

what suggest a dx of AKI rather than CKD

A
  1. normal kidney size on USS
  2. normal haemoglobin (RBC half life 120 days so wont be acute presentation)
  3. normal PTH (also takes time to develop)

if in doubt assume AKI and inx promptly

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74
Q

pre renal AKI clinical features

A

-hypotensive, tachycardic, poor peripheral perfusion, delayed CRT, postural hypotension

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75
Q

management of pre-renal AKI

A

-fluid resus will work providing tubules intact

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76
Q

acute tubular necrosis causes

A
  • when hypotension is very severe or prolonged, ATN may develop due to ischaemic injury
  • prolonged pre-renal goes onto develop ATN

which is when urinary sodium begins to increase and osmolality decrease as can no longer absorb sodium and water back through tubules

also toxic causes

  • drugs- aminoglycosides, cisplatin, tenofovir, methotrexate, iodinated contrast
  • rhabdomyolysis
  • myeloma light chains
  • crystals
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77
Q

management of ATN

A
  • fluid resuscitiation aggressive and early

- once ATN has developed fluid resus alone will not be enough as kidney tubules take time to regenerate

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78
Q

mortality ATN

A

50% due to assoc. organ failure

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79
Q

Anti GBM immunofluorescence presentation

A

ribbon pattern

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80
Q

immune complex deposition disease presentation

immunofluorescence

A

granular or starry sky pattern

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81
Q

vasculitis immunofluorescence presentation

A

negative

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82
Q

causes of RPGN

A

-vasculitis
anti GBM
post-infectious glomerulonephritis

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83
Q

post renal AKI causes

A

-obstruction
to flow in renal tract- NEEDS TO BE BILATERAL
-Most likely benign prostatic hypertrophy
-also tumours, external compression

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84
Q

presentaton of post-renal AKI

A

-anuria
or
-polyuria

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85
Q

systematic approach to patient with AKI

A
  1. is the AKI renal- check renal function
  2. could it be pre-renal failure
    - access circualtory state eg BP,JVP, mucous membranes, check fluid balance, check medications eg any new medications
  3. could it be post-renal
    -bladder palpable?
    -person at high risk eg male >60, hx of bladder cancer, loin pain, visible haematuria
    order USS scan
  4. could it be an intrinsic renal cause
    Toxic ATN
    AIN-eosinophilic count and leucocytes
    glomerulonephritis- blood and protein
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86
Q

management of established AKI

A

-drug chart stop nephrotoxic drugs
-fluids
control intake of fluid, resus, match sodium loss, no potassium initially
-hyperkalaemia management
-acidosis give sodium bicarb if pH<7
-diet: low protein and phosphate
-prevent infection
-consider PPI reduce risk Upper GI bleeds
-treat obstruction if needed

others
-dialysis

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87
Q

what drugs need stopping in AKI

A

-NSAID
-AceI
-AMINOGLYCOSIDES
-ARB
diuretics
metformin
lithium
digoxin

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88
Q

indications in AKI for dialysis8

A
  1. dangerous hyperkalaemia
  2. pulmonary oedema
  3. severe symptoms or complications
  4. poor biochemical results and unlikely to recover function quickly
  5. pericarditis
  6. neurological signs eg uraemic encephalopathy
  7. need for high fluid intake eg for nutrition during oliguria
  8. to enable nutrition
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89
Q

dialysis of choice for AKI

A

haemodialysis

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90
Q

why is there a polyuric phase after AKI

A

-excess electrolytes and fluid retained during AKI but also because the tubules are recovering from injury so are less responsive to ADH/ ang so dont appropriately retain salt and water

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91
Q

management of after AKI Fluid

A

-rough guide is to ensure total fluid is equal to urinary volume from the day before
unless signs of overload

may also need to supplement bicarb, potassium

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92
Q

prognosis of AKI after

A
  1. full recover
  2. acute on chronic disease
  3. AKI to ESRD
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93
Q

what do people with AKI die of 4

A
  1. hyperkalaemia
  2. pulmonary oedema
  3. uraemia
  4. infection
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94
Q

long term risks of aki

A
  • recover often incomplete
  • long term increased risk of ESRF
  • poor outcomes are more likely with increasing severity and duration of the insult
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95
Q

biopsy sign of ATN

A

vacuolation

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96
Q

rf for aki

A

chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over

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97
Q

CKD stages

A 
1 >90
2 60-90
3 30-60
4 15-30
5 <15
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98
Q

eGFR variables

A 
cage
Creatinine
age
gender
ethnicity
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99
Q

dx of CKD

A

eGFR of <60 on at least 2 occasions 90 days apart

abnormalities of kidney function or structure present for more than 3 months

irereversible deterioration of renal function

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100
Q

main causes of CKD

A 
diabetes mellitus
interstitial disease
glomerular disease
hypertension
systemic inflammatory disease
renovascular disease
cogenital and inherited
unknown
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101
Q

clinical features CKD

A 
<15 gfr
-tired
breathless
renal anaemia
pruuritus 
anorexia 
weight loss
n and v
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102
Q

risk factors for developing ESRD

A 
-severity 
proteinuria
haematuria
high BP
young age
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103
Q

inx

A 
blood tests
urinalysis and proteinuria
ACR 
HEPATitis testing
renal USS
CT/ MRI angiography
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104
Q

referral CKD to nephrologist

A
  • eGFR <30
  • rapid deterioration >25% from past yr
  • significant proteinuria unless known to be due to diabetes ACR >70
  • ACR >30 with non visible haemturia
  • HTN that remains poorly controlled despite 4 medications
  • suspicion of renal involvement in multisystem disease
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105
Q

AKI def

A

1.5 x baseline 7days
cr 26.5 in 48hrs
0.5 urine for 6hrs ?

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106
Q

when to refer to renal unit -immediate

A 
suspect acute renal failure
oliguria
obstruction
ARF on CRF
severe new renal failure
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107
Q

cause ckd 4-5

A 
often multifactorial
diabetes and renal artery stenosis
inflammation eg glomerulonephritis
circulatory
obstruction
inherited eg pkd
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108
Q

management CKD 3

A

-assess- features, urinalysis, medication, PMH
-monitoring: aim to keep BP <140/90
management of CVD- stain
refer for specialist
-proteinuria
haematuria
rapid deteriorating renal function
young age
fhx of renal failure
poorly controlled HTN

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109
Q

CKD managemenet

A 
-BP control
<130/80 if albuminuria
ACEi if proteinuria
bicarbonate for acidosis
dietary avoid potassium
salt restriction 
avoid high protein diet
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110
Q

complications of CKD

A 
-HTN
potassium
acidosis
anaemia
renal osteodystrophy
CVD risk
malnutrition
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111
Q

acidosis rx in ckd

A

sodium bicarb

avoid too much protein

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112
Q

anaemia of ckd is

A

normochromic normocytic anaemia

make sure from renal and not another cause

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113
Q

anaemia pathology CKD

A

recombinant EPO
IV iron
-definiciency of EPO
decreased response to EPO, toxic effect of uraemia, reduced RBC survival

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114
Q

renal osteodystrophy pathology

A

low vitamin D
high PTH- high phosphate levels stimualte PTH
decreased calcium absortion
osteoclastic bone resporption

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115
Q

rx of renal bone disease

A

phosphate binders eg calcium carbonate

calcitriol alfacalcidol

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116
Q

drugs to stop taking on sick days

A 
ACEi
ARB
NSAID
diuretics
metformin
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117
Q

indications for dialysis

A 
fluid overload- acute pulmonary oedema
hyperkalaemia
uraemia-encephalopathy
metabolic acidosis
bleeding diathesis
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118
Q

ESRD options

A

conservative treatments

dialysis

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119
Q

types of dialysis

A 
hospital haemodialysis
home haemodialysis 
peritoneal dialysis
-continuous ambulatory peritoneal
automated peritoneal dialysis
120
Q

haemodialysis preparation

A

-anticoagulation
-vascular access
monitoring

121
Q

SE haemodialysis

A 
hypotension
muscle cramps
bacteraemia
hypotension
cardiac arrhythymias
haemorrhage
air embolism
dialyser
pulmonary oedema
sepsis
122
Q

types of haemodialysis

A

haemofiltration-mostly AKI

haemodiafiltration- haemodialysis and ultrafiltration

123
Q

continuous ambulatory peritoneal dialysis

A

-4 x 2L fluid exchanges dialy
4-6 hrs with a gap overnight
each bag takes 30-60 minutes

124
Q

automated peritoneal dialysis

A

overnight 8-9hrs as sleep

125
Q

disadvantages of peritoneal dialysis

A 
peritoneal infection
peritonitis
catheter site exit infection
ultrafiltration failure 
sclerosing pertinoitis
126
Q

contraindication to PD

A 
major abdo surgery
peritoneal adhesions
inguinal hernias
severe respiratory compromise
inability to perform the technique safely and hygenically
127
Q

sclerosing peritonitis is

A

major complication of PD usually by staph epidermidis or bowel organism
-abdo pain, fever, cloudy PD
antibiotics needed

128
Q

ESRD definition

A

implies a level of renal function at which death is likely within weeks or months
symptoms

129
Q

immunosuppression for transplant

A

triple therapy

  1. MMF mycophenalate mofetil or azathioprine
  2. tacrolimus or cyclosporine
  3. relatively low dose prednisolone
130
Q

risks of immunosuppression therapy for transplant

A
  1. increased SCC risk
  2. cardio toxicity
  3. renal failure nephrotoxicity
131
Q

rejection from transplant

A

5 days to 2 weeks

  • give high dose steroids
  • tubulointerstitial inflammatory infiltrates
132
Q

what is hyper-acute rejection

A

minutes to hours
due to pre-existing antibodies
HLA type 1 antigens
type II reaction

133
Q

complication of transplant

A
  1. ischaemia reperfusion injury- interruption of blood supply, build up toxicities, organ damage
  2. delayed graft function- more common cadaveric so may need dialysis initially - oliguric after transplant
  3. technical problems
  4. acute rejection
    <6 months post-transplant
    signs and symptoms of infection
    mismatched HLA
    rise in creatinine
  5. chronic rejection >6 months both antibody and cell mediaated mechanism cause fibrosis or due to recurrence of original disease
  6. infections- CMV especially
  7. CMV
  8. anastomosis damage or infection
  9. arterial thrombosis
  10. cardiac event at transplantation
    immunosuppression risks
134
Q

BK virus transplant

A 
also called polyomavirus 
only causes problems in transplant 
most people who carry it have no symptoms
biopsy 
Blood PCR testing
urine cells 
attacks transplant

balance risk of developing this on immunosuppression
-reduce immunosuppressive drugs

135
Q

AIN causes

A

allergic
NSAID, PPI, antibiotics-penicillin, allopurinol, furosemide

immune-autoimmune
-TINU syndrome-tubulointerstitial nephritis and uveitis
-AIN only
sjorgen syndrome 
sarcoidosis 
transplant rejection

infective
toxic- drugs most common

136
Q

inx for AIN

A 
-eosinophilia
leucocytes
drug induced generalised signs of drug hypersensitivity
white cell cast
sterile urine 
biopsy shows inflammation
137
Q

management AIN

A

withdrawal of drug
high dose steroids
treat cause

138
Q

chronic interstitial nephritis is

A

renal dysfunction with firbosis and infiltration of the renal parenchyma by lymphocytes, plasma cells and macrophages

139
Q

cause chronic interstitial nephritis

A

-persistent AIN
glomerulonephritis
immune
-sarcoidosis, sjorgen ,chronic transplant rejection, SLE

myeloma-bence jones protein -cast nephropathy

posions eg lead poisoning

drugs eg gentamicin, chemo, tenofovir, all drugs from AIN, lithium, ciclosporin, tacrolimus

infection

inherited
-VUR, renal dysplasias, wilson disease, sickle cell

metabolic- hypokalaemia, calcium phosphate crystals

unknown sometimes especially Asian race in UK

140
Q

cast nephropathy causes

A

-form casts seen in

loop diuretics, myeloma

141
Q

fanconi syndrome is

A

renal glycosuria in normal blood sugars
damage to proximal tubules
crystals form in proximal tubules
excess glucose, uric acid,phosphates being excreted

142
Q

signs of CIN

A 
HTN
small kidneys
CKD
impaired concentration abilities 
sodium and water deplete
143
Q

CIN management

A

supportive
correct acidosis and hyperkalaemia
renal replacement therapy if irreversible renal damage has occurred

144
Q

ATN causes

A
  1. prolonged pre-renal aki
  2. severe infection- v.low BP
  3. toxicity
  4. myeloma
  5. crystals
  6. rhabdomyolysis
145
Q

nephrotic to nephritis

A

minimal change
FSGS
Membranous nephropathy
diabetic nephropathy

MCGN
Post strep
vasculitis
GBM

146
Q

nephrotic syndrome triad

A

heavy proteinuria >3.5g/24hrs
hypoalbuminuria <30g/l
peripheral oedema formation - due to avid sodium and fluid retention by the kidneys

147
Q

cause nephrotic

A

damage to podocyte or non inflammatory architectyal alterations of the glomerulus

148
Q

minimal change disease

A 
normal glomeruli on micoroscopy
can get podocyte foot process effacement
most common cause children
in adults assoc. to NSAID nand hodgkin
high dose steroids
149
Q

FSGS focal segmental golmeruli sclerosis

A 
focal scarring
idiopathic, HIV, reflux nephropathy, obesity
primary= idiopathic- treat with steroids
secondary- gradual onset, causal, ACEi
variable response to steroids
may progress to renal failure 
tends to be younger people
150
Q

membranous nephropathy

A

usually idiopathic, some drugs, rarely malignancy
more common elderly
1/3 progress to renal failure
thickened glomerular capillary walls and basement membrane
basememnt membrane spikes on silver staining
immune complex deposition
often primary in adults and secondary in children

151
Q

amyloidosis

A

early manifestation often
amyloid protein depositis
more common elderly

152
Q

SLE

A

usually young women

153
Q

management nephrotic syndrome

A

diet control salt intake
diuretics often loop
-careful and stop if signs of increasing creatinine or hypovolaemia

ACEI 
anticoagulation
statin
infection
steroids and PPI
154
Q

nephrotic oedema 2 main factors

A

sodium retention directly by renal

secondary sodium retention in which the low plasma oncotic pressure due to hypoalbuminaemia promotes the movement of fluid from the vascular space into the interstitium

155
Q

complications of nephrotic syndrome

A 
susceptibility to infection
increased risk DVT
high cholesterol
hypercoaguability
protein malnutrition
hypovolaemia 
AKI
156
Q

nephritic syndrome presentation

A

haematuria- often non visible
hypertension
reduction in renal function

157
Q

pathology nephritic syndrome

A

inflammation in the glomeruli which damages and disrupts the glomerular basement membrane GBM, allowing red blood cells to enter the urinary space

allows RBC to enter into the urinary space
increased permeability

158
Q

RPGN presentations

A
  1. post strep- ASOT, c3, c4
  2. anti GBM
  3. small vessel vasculitis - ANCA
  4. lupus- ds DNA ANA c3 c4
159
Q

mild glomerulonephritis presentations

A
  1. IgA nephropathy IgA and HSP
  2. mesangiocapillary glomerulonephritis MCGN- c3, c4 hiv, hep b, ANA dsDNA
  3. Alport syndrome -genetic screening, hearing test
160
Q

RPGN crescenteric nephritis

A

severe and rapid nephritic syndrome
exhibits many cellular “crescents”

presentation

  • non visible haematuria
  • severe nephritic syndrome
  • acute onset of haematuria, HTN, oedema
  • pulmonary haemorrhages good pastures
  • systemic features vasculitis
161
Q

main causes of RPGN

A

post strep
vasculitis
anti GBM
Lupus

162
Q

treatment of RPGN

A

pulse methylprednisolone then daily oral prednisolone
IV cyclphosphamide or rituximab
plasmapharesis

163
Q

IgA nephropathy

A 
common disease
most common worlwide
often slowly evolving over decades
can occur as HSP 
IgA deposited in the mesangium of glomeruli
164
Q

post- strep GN

A 
-10-14 days after strep throat
fluid retention
hypertension
oedema
haematuria 
reduced GFR 
diffuse proliferation of cells on renal biopsy
165
Q

small vessel vasculitis

A

usually assoc. with antibodies to neutrophil granule enzyme ANCA
other systemic features

-microscopic polyangiitis
wegner disease
if severe can cause crescenteric nephritis

166
Q

MCGN mesangiocapillary glomerulonpehritis

A

either

can be caused by persistent infection or other diseases or occur alone

167
Q

IgA presentation

A 
-most common asymptomatic
visible haematuria 
dark brown urine
discomfort in kidneys 
rarely sa nephrotic syndrome
hypertension 
young male 
occurs with or a few days after resp infection
168
Q

diagnosis of IgA nephropathy

A

hx of passing blood at same time as infection
urinalysis blood
bloods= raised IgA
renal biopsy- immune deposits

169
Q

management of IgA nephropathy

A
  1. ACEi
  2. Steroids if haematuria and either renal dysfunction, proteinuria
  3. fish oil
  4. immunosuppression- cyclophosphamide, cyclosporin -most not needed
  5. 1/3 develop CKD and need dialysis and some need transplant
170
Q

prognosis Iga NEPHROPATHY

A

1/3 devlop chronic kd

171
Q

vasculitis pathology

A

ANCA antibodies to neutrophil cytoplasmic antigens, granule enzymes such as myeloperoxidase

172
Q

presentation of 2 main small vessel vasculitis

A
  • wegner granulomatosis with polyanggitis-sinusitis
  • MPA microscopic polyangiitis -kidney, gut and skin
  • HSP; children, abdo pain, rash, haematuria, weakness
173
Q

dx of SVV

A

ANCA positive
antibodies to myeloperoxidase
biopsy

174
Q

presentation of SVV

A

systemically unwell
renal
RPGN
pulmonary haemorrhage, rash

175
Q

management of SVV

A

-cyclophosphamide, steroids and plasma exchange

176
Q

post strep GN

A 
asymptoamtic
microscopic haematuria
full blown acute nephritic- headahce, malaise
light brown urine
children
oedema gross haematuria and HTN
usually 1-3 weeks after strep throat
177
Q

inx for post-strep GN

A 
in children 
-urinalysis
serology antibodies
renal function 
no biopsy
178
Q

biopsy signs of post strep GN

A

diffuse GN
starry night
neutrophils
deposition of IgG and c2

179
Q

diff dx for post-strep GN

A

need to consider if lasts beyond 2 weeks

membranoproliferative GN -lasts longer
IgA nephropathy -shorter time interval

180
Q

management post -strep GN

A

supportive

181
Q

minimal change disease

A 
often hx of recent viral illness
oedematous puffy child 
facial oedema, abdominal and scrotum
HTN is rare
can have nausea and vomiting
182
Q

diagnosis of MCD

A

dont biopsy in children-trial steroids first

biopsy appears normal on light microscopy
on electron microscopy can see podocyte foot processes

183
Q

causes of MCD

A 
-infectious
90% cause unknown
allergic reaction
asoc. to other disease
drugs eg ibuprofen
hodgkin's
184
Q

prognosis MCD

A

1/3 frequent relapse
1/3infrequent relapse
1/3 only one episode

185
Q

management MCD

A

give high dose of prednisolone
if dont respond
-wrong disease or
-need a combination of treatment

186
Q

relapsing MCD treatment

A

cylophosphamide 8-12 week course of drug can prevent relapses for many months or years
in patients with frequent relapses

cyclosporin
tacrolimus

187
Q

FSGS pathology

2 types

A

diseases that damage the glomeruli in small areas and leave scarring = secondary FSGS

primary FSGS= occurs without any known reason- idiopathic

188
Q

biopsy of FSGS shows

A

only some / focal areas of glomeruli show scarring

189
Q

assoc. to primary FSGS

A

WEST AFRICA

apoliprotein 1

190
Q

secondary FSGS causes

A

-presents with more modest proteinuria than primary

  1. HUS
  2. cholesterol emboli
  3. toxins
  4. genetic
  5. HIV, severe obesity
191
Q

presentation of FSGS

A

nephrotic
all ages
sometimes responds to steroid treatmnet- not always
kidney function can be abnormal
can cause complete kidney destruction and need dialysis
can come back after transplantation

192
Q

diff dx FSGS

A

can be mistaken for MCD if biopsy taken of a normal part of glomeruli

193
Q

primary FSGS treatment

A

steroids

194
Q

secondary FSGS treatment

A

depends on cause

ACEI to prevent progression

195
Q

membranous nephropathy pathology

A

in membranous nephropathy the filtering layer becomes thickened and there is a protein leak into the urine

  • attack on the cells within the glomerulus that make the GBM known as podocytes
  • most common cause of nephrotic syndrome in caucasian adults
  • antibodies attack podocytes
196
Q

causes of membranous nephropathy

A

-2/3 idiopathic (anti PLA2)
-arthritis lupus
drugs pencillamine, gold, captopril
cancer
infections hepatitis
toxins eg mercury, formaldehyde

197
Q

histology of membranous nephropathy

A

thickened GBM
subepithelial spikes
PLA2

198
Q

presentation of membranous nephropathy

A

asymptomatic
proteinuria
peripheral oedema
hypercoaguable state

199
Q

prognosis membranous nephropathy

A

5-15% remission
30-40% partial remission
25% disease will progress and cause slow loss of function , lead to ESRF

200
Q

factors that increase the chance of loss of kidney function

A 
male >50
high proteinuria
kidney biopsy scarring
BP not well controlled
kidney function abnormal at dx
hepatitis - known cause cant be cured
201
Q

management membranous nephropathy

A 
-monitoring
steroids
-immunosuppressive cyclophosphamide, cyclosporin 
bp treatment 
diuretics
202
Q

mesangiocapillary glomerulonephritis pathology

A

pattern of injury seen on renal biopsy characterised by an increase in mesangial cellularity with thickening of glomerular capillary walls

203
Q

presentation MCGN

A

nephrotic or nephritis

204
Q

types of MCGN

A 
1st= deposition of IG into glomeruli, assoc. to chronic infections
2nd= deposition of complement into glomeruli , assoc. inherited or acquired abnormalities in complement pathway, dense deposit disease
205
Q

treatment of MCGN

A

immunoglobulin type eg MMF, cyclophosphamide

complement type eg eculizumab

206
Q

lupus markers

A

ANA

anti DS DNA

207
Q

management of Lupus

A 
MMF
cyclophosphamide
azathioprine 
cytotoxic agents
anti B cell antibodies rituximab
208
Q

thiazides side effects

A

hyponatraemia
hypocalciuria
hypokalaemia

209
Q

action thiazides

A

inhibit reabsorption of NaCl in tubules

210
Q

loop diuretics action

A

inhibit reabsorption of NaCL in loop henle

211
Q

spironalactone

A

aldosterone antagonist

inhibits sodium potassium exhange

212
Q

SE of loop diuretics

A 
hypercalciuria 
hyponatraemia
hypokalaemia
hypomagnesia
ototoxic
213
Q

Ace inhibitors side effects

A 
hypotension
dry cough
rash
hyperkalaemia
renal dysfunction
214
Q

calcium channel side effects

A

constipation in verapamil

bradycardia

215
Q

drugs to avoid in renal failure

A 
ACEi
ARB
gentamicin
nitrofurantoin
NSAID
opiates
heparin LMWH use UFH
vancomycin
216
Q

alport syndrome pathology

A

defect in type 4 collagen
GBM deteriorates with time leading to progressive loss of glomeruli often with deafness
rare
loss of alport protein- autoimmune

217
Q

histology alport

A

basket weaving

thick and thin GBM

218
Q

presentation of alport

A 
male
renal problems
sensorineural hearing loss 
women only get partial symptoms if carriers
x-linked worse in me
219
Q

thin GBM disease

A

often runs in families
benign familial haematuria
thin GBM
some also carry one copy of alport protein gene mutation

220
Q

benign familial haematuria

A

-inherited cause for blood appearing in urine

often related to Thin GBM

221
Q

nail patella syndrome

A

-poorly formed nails
2. patella missing
3. elbows often dont straighten properly
4. iliac horns
5. scolitosis
6. abnormality GBM
7. glaucoma
autosomal dominant
get nephrotic syndrome
LMX1B-collagen

222
Q

good pasture’s disease is

A

an autoimmune condition in which there can be severe inflammation affecting kidneys and lungs
antibodies develop against the a3 chain of type 4 collagen
young patients

223
Q

anti GBM presentation

A 
-haematuria
nephritic
renal failure 
RPGN can get more severe features
signs of kidney failure
lung haemorrhages 
dry cough and minor breathlessness
haemoptysis
224
Q

diagnosis anti GBM

A

early symptoms often vague
biopsy
anti GBM antibodies
check for ANCA

225
Q

management AntiGBM

A

steroids
cyclphosphamide
plasma exchange

226
Q

DIABETIC NEPHROPATHY

A

late microvascular complication of diabetes mellitus
typically appears more than 20yrs type 1 dm
most already have diabetic retinopathy and neuropathy

227
Q

phases of diabetic nephropathy

A

phase1= hyperfiltration
-elevated GFR
hypertension
microalbuminuria

phase 2= over diabetic neuropathy
-overt proteinuria
dipstick test positive
BP can start to lose dip at night 
GFR starts to go back to normal

phase 3= incipient nephropathy
htn
proteinuria
npehortic syndrome

phase 4
progressive renal failure
CKD

228
Q

histo features of diabetic nephropathy

A

mesangial expansion in glomerulus
slit diaphragm break down and protein leak
kimmelstiel- nodules of matrix
arterio hyalinolysis

229
Q

risk factors diabetic nephropathy

A

poor diabetic control
duration of diabetes
presence of retinopathy and other microvascular complications
fhx susceptibility to HTN

230
Q

diagnosis of diabetic nephropathy

A

ACR urine albumin creatinine ratio more sensitive
GFR renal function
if atypical then renal biopsy might be considered aka rapid onset not indicating diabetic nephropathy

231
Q

prevention of diabetic nephropathy

A

blood sugars control
bp control
ACEI for proteinuria
diet protein restrict

232
Q

management diabetic nephropathy no proteinuria

A 
monitoring 
aim BP <130/80
hba1c <7
diet advice
stop smoking
233
Q

management diabetic nephropathy proteinuria

A 
close monitoring 
monitor urine protein
aim BP <125/75 
further BP drugs 
cholesterol
ACEI
234
Q

who needs a renal biopsy for diabetic with kidney problems

A
  1. Type 1dm <10 yrs failing kidneys
  2. rapid progression proteinuria
  3. rapid deterioration renal function
  4. absence retinopathy
  5. presence severe haematuria
  6. additional systemic symptoms such as weight loss
235
Q

polycycstic kidney disease presentation

A 
abdominal pain
early satiety 
palpable mass 
urinary tract infection
haematuria
hypertension 
asymptomatic initially 
renal failure
236
Q

PKD pathology

A

autosomal dominant inherited
50% with PKD1 progresss to ESRD
PKD2 tends to be milder

237
Q

dx PKD

A

-USS
cyts not detectable till in 20s
so cant use for screening in teens
can also be hepatic cysts

MRI
berry aneurysm if fhx of them sudden death or high risk job

renal function
can be fairly normal till late stage

238
Q

management pkd

A

tolvaptan
ADH vasopressin V2 receptor antagonist
slows rate of growth of cyst and GFR loss
risk of dehydration due to polyuria

50% dialysis and renal transplant

239
Q

complications of PKD

A
  1. hepatic cysts= hepatomegaly
  2. diverticulosis
  3. berry aneurysms- subarachnoid haemorrhages
  4. ovarian cysts
  5. mitral valve prolapse
  6. kidney stones
240
Q

infantile PKD pathology

A 
autosomal recessive
rare
different gene
PKHD1 gene fibrocystin
also cysts in liver
pulmonary fibrosis
severe illness
241
Q

alport syndrome pathology

A 
x-linked young men 
recessive
women as carriers get a lesser disease
due to lyonisation get inactivation in some cells 
collagen 4 absent or normal
242
Q

histology alport

A

basket weave

243
Q

presentation alport

A

deafness sensorineural
eye involvement -lenticonus of lens
progressive haematuria, proteinuria then renal failure in teens

244
Q

management alport

A

acei limit progression

245
Q

renal anaemia is

A

normochromic normocytic anaemia

due to deficiency in EPO

246
Q

management of renal anaemia

A

look for contributing causes- dont assume renal
need to ensure IRON replete before giving EPO
erythropoiesis stimulating agents 2-3 injections a week
IV iron

247
Q

se of EPO treatment

A 
HTN
encephalopathy
bone aches
urticaria
pure red cell aplasia- antibodies develop
248
Q

haemoglobin target for renal anaemia

A

100-110

avoid predisposing to thrombosis

249
Q

renal artery stenosis pathology

A

arteriosclerosis of renal arteries
reduction in renal perfusion pressure activates the RAS system
increase in angII
vasoconstriction and increased aldosterone so retain sodium
global renal ischaemia leads to shrinkage of kidney

> 70% stenosis haemodynamically significant effects
most common cause secondary HTN

250
Q

main cause of RAS in young patients

A

fibromuscular dysplasia
-uncommon
-hypertrophy of the media which narrows artery
more often women <50
distal main renal artery or the intra-renal branches

251
Q

presentation of RAS

A

usually HTN
classic but rare presentation is with recurrent episodes of sudden flashing lights
flash pulmonary oedema-usually at night

252
Q

RAS is more likely if

A 
severe HTN
asymmetrical kidneys
flash pulmonary oedema
peripheral vascular disease of lower limbs
renal impairment
renal function has deteriorated on ACEi
253
Q

inx RAS

A 
dipstick
blood- hypokalaemia secondary aldosteronism increased renin
MRI/ CT angiography
USS
RENAL ARTERIOGRAPHY GOLD STANDARD
254
Q

Management RAS

A

-fibromuscular dysplasia patients often resond to balloon dilatation
1st line
-medical therapy

2nd line
interventions
angioplasty - balloon

255
Q

indications for management angioplasty RAS

A 
young <40
BP intractable
flash pulmonary oedema
malignant HTN
deteriorating renal function
256
Q

what is ischaemic nephropathy

A

CKD that results from RAS

257
Q

acute renal infarction

A

sudden occlusion of the renal arteries
loin pain, non visible haematuria
severe HTN

can be caused by thrombosis of a renal artery or thromboemboli from a distant source

258
Q

thrombotic microangiopathy pathology

A

diseases are assoc. with platelet thromboses in small blood vessels
damage to endothelium
plateelt thromboses in small vessels

259
Q

causes of thrombotic microangiopathy

A 
HUS
TTP
DIC
malignancy
systemic sclerosis
PET
260
Q

diagnosis

A

BLood film

  • microangiopathic haemolytic anaemia MAHA
  • schistocytes= fragments of RBC

blood
raised LDH
elevated unconjugated bilirubin
thrombocytopaenia

261
Q

thrombotic thrombocytopaenia purpura pathology

A

haematological, CNS and renal pathology
-autoimmune disorder against antibodies to ADAMTS-13
this is involved in regulating platelet aggregation
low serum ADAMTS 13
USUALLY helps to break down vWF larger versions
so get abnormal build up of large vWF

262
Q

presentation of TTP

A 
-MAHA
thrombocytopaenia purpura
neurological manifestations
fever
renal disease
AKI
schistocytes on blood film
petechiae
lower abdominal pain 
fatigue 
typiclaly female
263
Q

causes of TTP

A 
post infection
pregnancy 
drugs- ciclopsorin, OCP, penicillin, clopidogrel
tumours
SLE
HIV
264
Q

inx findings for TTP

A 
thrombocytopaenia
renal failure
anaemia
schistocytes 
direct coomb's test will be negative 
low ADAMTS13
265
Q

management TTP

A

plasma exchange therapy and steroids

capacuzimab

266
Q

HUS haemolytic uraemic syndrome pathology

A

typical
-blood diarrhoea in children from E.coli toxin
shiga toxin causes endothelial damage which causes platelet activation and clumping
-activates GB3 receptors
-these then destroy red blood cells as they get damaged passing through- MAHA

atypical
-to do with complement dysregulation
chronic disease both children and adult

267
Q

HUS presentation

A 
anaemia
 thrombocytopaenia
AKI
schistocytes 
typical often children with bloody diarrhoea
268
Q

other causes of HUS

A

pneumococcal infection
HIV
SLE

atypical
CTD
Drugs eg quinine, cytotoxic
malignancy

269
Q

management HUS

A

typical
supportive only
dialysis if severe renal failure

in those with fhx atypical HUS may benefit from complement inhibitors
plasma exchange
ECULIZUMAB for atypical types

270
Q

DIC management

A

haemostasis

replace clotting factors

271
Q

cholesterol emboli presentation

A 
renal impairment 
haematuria
proteinuria
sometimes eosinophilia
vasculitis
can be ischaemic toes
272
Q

patient undergoes cardiac arteriiography then gets renal failure

A

suspect cholesterol emboli

273
Q

myeloma and renal pathology

A

hypercalcaemia

free light chains can be toxic to tubular cells and cause cast nephropathy and acute tubular necrosis

274
Q

myeloma and renal presentations

A
  1. cast nephropathy
  2. fanconi syndrome- uric and phosphate … all excreted
  3. amyloidosis nephrotic
  4. monoclonal immunoglobulin deposition disease
  5. hypercalcaemia
275
Q

3 main causes of amyloidosis

A
  1. AL amyloid due to light chains eg from myeloma
  2. ALL amyloid due to proteins in chronic infection or inflammation eg rheymatoid
  3. diabetes amyloid
276
Q

HIV nephropathy presentation

A

collapsing FSGS
Proteinuria, nephrotic, progressive renal imapirment
responds to HAART if treated early enough

277
Q

sodium risks

A

up too fast= cerebral pontine myelinolysis

low too fast= cerebral oedema

278
Q

hypernatraemia causes

A

-reduced water intake eg coma, depression
-increased losses -hypovolaemic
increased loss via gut, skin, tract
-iatrogenic salt administration
-diabetes insipidus

279
Q

features hypernatraemia

A 
thirst
oliguria
concentrated urine
weakness
nausea
loss of appetitie
reduced cerebral function
280
Q

inx findings hypernatraemia

A

increased plasma urea

281
Q

management hypernatraemia

A

oral replacement
-water normal
-5% dextrose and .9% saline if severe
5% dextrose if mild

282
Q

hypontaraemia causes

A 
euvolaemic
SIADH 
primary polydipsia
hypothyroidism
beer potomania
poor diet intake of sodium

hypervolaemic
excess water exceeds excess sodium
cardiac liver or renal failure
RAAS

hypovolaemic 
large electrolyte losses
Addison
diuretic
vomiting
diarrhoea
GI 
cerebral salt waste syndrome
283
Q

clinical features of hyponatraemia

A 
often asympatomatic
acute <48hrs
chronic >48hrs
oedema
confusion
drowsy
n and v
seizure
chovstek and trosseau
284
Q

chronic hyponatraemia >48hrs

A

hypovolaemic give 0.9% saline

euvolaemic: fluid restrict, tolvaptan, vasopressin siadh
hypervolaemic: fluid and salt restrict,

285
Q

acute hyponatraemia <48hrs rx

A

if also signs of cerebral oedema

need to restore rapidly using hypertonic sodium chloride 1.8%

286
Q

drugs causing hyponatraemia

A 
thiazide
nsaid, antibiotics, PPI
SIADH drugs: antidp, antipsychotics, carbarmazepine, anti cancer, opioids, MDMA
Venlafaxine
MDMA
287
Q

hyperkalaemia causes

A 
increased intake
tissue breakdown- rhabdomyoloysis
hyperglycaemia and acidosis cause relase
addison
spironalactone
impaired excretion AKI and CKD
drugs
288
Q

signs of hyperkalaemia

A

rare
asymptomatic
progressive muscle weakness

289
Q

ECG changes hyperkalaemia

A
  1. tented t waves
  2. loss of p waves
  3. wide QRS
  4. sine waves
290
Q

treatment hyperkalaemia

A
  1. give IV calcium gluconate to stabilise the membrane
    2.IV glucose and insulin
    50ml 50% and 5units actrapid
  2. salbutamol
  3. sodium bicarbonate
  4. IV fluids
  5. dialysis
  6. potassium biding resins -calcium resonium
  7. loop diuretics
291
Q

hypokalaemia causes

A 
<3.5
loss of potassium from the GI tract eg vomiting
shift into cells eg insulin
endocrine eg hyperaldosteronism
drugs
decreased intake
increased excretion eg cushing
excessive liquorice
RTA
292
Q

clinical features low K

A

asymptomatic
lethargy
muscle weakness
in chronic can get noctyria, polyuria, polydipsia

293
Q

inx

A

ECG flatten and inversion t waves

can often seem normal potassium as not measuring intracellular

294
Q

management hypokalaemia

A

give KCL IV
rich diet
potassium bicarb if acidosis

295
Q

hypercalacaemia ssymptoms

A 
stones
bones
throans
psychiatric overtones
moans
296
Q

management high calcium

A 
IV 0.9% saline
IV bisphosphonates
steroids
calcitonin
calcimimetics
parathyroidectomy

year 5 (9 decks)

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