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Year 3 > Block 34 Week 1 > Flashcards

Block 34 Week 1 Flashcards

1
Q

functions of the kidney - homeostasis?

A
  • Elimination of metabolic waste
  • Water homeostasis
  • Electrolyte homeostasis
  • Acid base homeostasis
  • Blood pressure control
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2
Q

kidney functions - synthesis of?

A
  • activatesVitamin D
  • Erythropoietin
  • Renin
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3
Q

kidney functions - excretion of?

A

drugs and drug metabolites

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4
Q

what is serum creatinine affected by?

A
  • influenced by gender ethnicity, age, body mass, diet, exercise
  • not sensitive to small changes in function
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5
Q

eGFR?

A
  • Calculated from creatinine, age, gender, ethnicity
  • Better reflection of kidney function
  • Best measure for use in stable renal function
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6
Q

classification of CKD

A
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7
Q

CKD =

A
  • eGFR of under 60
  • or kidney damage (e.g. abn blood, urine, imaging)
  • must be present for more than 3 months
  • irreversible and tends to progress
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8
Q

systemic disease causing KD?

A
  • diabetes
  • HTN
  • atherosclerosis
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9
Q

Immune mediated causes of KD?

A
  • membranous nephropathy
  • IgA nephropathy
  • SLE
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10
Q

Drugs that can lead to KD?

A

nsaids

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11
Q

infections that can lead to KD?

A
  • HIV
  • HBV
  • HCV
  • TB
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12
Q

Genetic diseases -> CKD?

A
  • polycystic kidneys
  • cystinosis
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13
Q

RF for progression of CKD?

A
  • Untreated underlying disease e.g. SLE, polycystic kidney disease
  • modificable
  • worse proteinuria
  • older age
  • smoking
  • uncontrolled P
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14
Q

complications of CKD - main cause of death?

A
  • Cardiovascular disease (main cause of death)
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15
Q

other complications of CKD - electrolyte abn?

A
  • Salt/water retention (oedema)
  • Electrolyte abnormalities (↕ Na/K)
  • Metabolic acidosis
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16
Q

other complications of CKD?

A
  • Hypertension
  • Mineral-bone disease (vitamin D, PTH, PO4)
  • Anaemia (erythropoietin)
  • Uraemia
  • Altered drug metabolism
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17
Q

general management of CKD?

A
  • Control blood pressure
  • Reduce proteinuria (if present) – ACEi/ARB
  • Stop smoking
  • Avoid nephrotoxic drugs (eg NSAIDs)
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18
Q

treating complications of CKD - bone related?

A
  • 1α vitamin D
  • Phosphate restriction/binding
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19
Q

treatment for complications of CKD - dietary changes?

A
  • Salt restriction
  • Bicarbonate supplementation
  • EPO replacement
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20
Q

Preparation for CKD 5 (if progressing)?

A
  • Dialysis
  • Transplant
  • End of life care
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21
Q

AKI stage 1?

A

Creatinine

  • > 26mmol rise
  • 50-100% from baseline
  • urine output <0.5ml/kg/hr for 6 hrs
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22
Q

stage 2 AKI?

A
  • 100-200% inc in creatinine
  • <0.5ml/kg/ hr for 12 hrs
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23
Q

stage 3 AKI?

A
  • > 200% inc in creatinine
  • or >354
  • or needs dialysis
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24
Q

urine output in stage 3 AKI?

A
  • <0.3ml/kg/hr for 24 hrs
  • or anuria for 12 hrs
  • or needs dialysis
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25
Q

AKI staging

A
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26
Q

who is at risk of AKI?

A
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27
Q

causes of AKI - pre-renal?

A
  • Perfusion failure (“Shock” or blockage of renal artery)
  • Made worse by medication eg
  • Antihypertensives
  • ACEi/ARB, NSAID – interfere with renal autoregulation
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28
Q

ACE, ARB, NSAID can lead to ? AKI

A

pre-renal

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29
Q

Renal causes of AKI?

A

Disease affecting the kidney tissue (vasculitis, SLE, multiple myeloma, interstitial nephritis)

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30
Q

Post-renal causes of AKI?

A

Obstruction of the urinary system (eg stones, tumours, blocked catheters)

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31
Q

Complications of AKI?

A
  • death - mainly sepsis
  • HTN
  • metabolic acidosis
  • salt/water retention - oedema
  • anemia - from EPO
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32
Q

general management of AKI?

A
  • Careful fluid balance
  • Dietary restriction if needed (eg low potassium)
  • Safe prescribing (eg reduce dose of antibiotics)
  • Appropriate clinical setting (eg HDU/ITU if needed)
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33
Q

gen management of AKI - dialysis?

A

Dialysis if needed to control complications (eg pulmonary oedema, hyperkalaemia, acidosis, uraemia)

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34
Q

what is needed for there to be nephrotic syndrome?

A
  • Heavy proteinuria
  • Clinical evidence of peripheral oedema
  • Hyperlipidaemia
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35
Q

heavy proteinuria in nephrotic syndrome?

A
  • 24 hour urine collection >3-3.5g protein/24 hour or
  • Spot urine PCR >300-350 mg/mmol
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36
Q

when does nephrotic syndrome occur?

A
  • when glomerular filtration barrier is damaged leading to inc protein leak
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37
Q

primary diseases causing nephrotic syndrome?

A
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Minimal change disease
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38
Q

secondary causes of nephrotic syndrome?

A
  • Diabetes Mellitus
  • Cancers
  • Drugs
  • Infections (eg HIV, HBV, HCV)
  • sLE
  • Amyloid
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39
Q

Complications of nephrotic syndrome - haematological?

A
  • Thromboembolism
  • DVT +- PE
  • Renal vein thrombosis
  • Arterial (rare)
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40
Q

other complications of Nephrotic S?

A
  • Infection
  • Hyperlipidaemia
  • Malnutrition
  • Acute kidney injury
  • Chronic kidney disease
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41
Q

tx of nephrotic syndrome - pharm?

A
  • Diuretics (loop eg furosemide) if massive fluid overload
  • Proteinuria reduction – ACEi/ARB
  • Thrombo-prophylaxis
  • Salt restriction
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42
Q

what is nephritic syndrome?

A
  • proteinuria - <3g protein/ 24 hrs or spot urine PCR <300-350mg/mmol
  • haematuria
  • oedema
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43
Q

Nephritic syndrome is a ?

A

medical emergency

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44
Q

what is nephritic syndrome caused by?

A
  • caused by damage to the glomerular endothelium, often inflammation/ immune mediated
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45
Q

what are the autoimmune causes of nephritic syndrome?

A
  • autoimmune diseases - SLE, ANCA vasculitis, Anti-glomerular basement membrane antibody disease
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46
Q

infection related nephritic syndrome?

A

postinfectious glomerulonephritis, bac endocarditis, HCV

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47
Q

How do patients w CKD present?

A
  • Commonly through routine monitoring of eg hypertension, SLE, drug monitoring
    *I ncidental finding (eg routine medical, routine urinalysis, found during investigation for something else)
  • Family with genetic disease (eg polycystic kidneys)
  • Sometimes symptoms (eg pain in polycystic kidney)
  • Symptoms caused by lost renal fu nction – only at a late stage (CKD4/5)
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48
Q

how do patients present w AKI?

A
  • Usually in high risk patients in hospital (eg trauma, GI bleed, post surgery)
  • Symptoms due to underlying disease (eg SLE, vasculitis)
  • Monitoring of known chronic disease (eg prostate disease, chemotherapy)
  • Sometimes due to nephritic syndrome (oedema, generally unwell)
  • Haematuria (rare)
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49
Q

CKD summary?

A
  • slow - months to years
  • eGFR used to measure function
  • caused by chronic diseases, genetic diseases, glomerular diseases - diseases that can nephotic syndrome
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50
Q

AKI summary?

A
  • fast - hours to days
  • measure serum creatinine or urine output
  • caused by acute illness, immune mediated dieasses e.g. nephritic syndrome
  • aim is to restore baseline function
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51
Q

urine in nephrotic syndrome?

A

oedema, frothy urine

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52
Q

what is important in nephritic syndrome?

A
  • immunology tests e.g. ANA, ANCA is important in nephritic syndrome
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53
Q

Most common Ix for renal issues?

A

US

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54
Q

Proteinuria + haematuria could be

A

glomerulonephritis

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55
Q

mortality from AKI is?

A

50%

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56
Q

principle causes of acute renal insuffiency?

A
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57
Q

common causes of hosp acquired AKI?

A

the surgical triad -post-op volume depletion, infection and nephrotoxic drugs

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57
Q

at rism groups for AKI?

A
  • elderly
  • diabetics
  • vasculopaths
  • known chronic renal impairment
  • sig cardiac dysfunction
  • CLD
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58
Q

drugs related to AKI - ACEI?

A
  • ACE-inhibitors and angiotensin II receptorblockers– efferent vasodilatation
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59
Q

drugs related to AKI - NSAIDs?

A
  • NSAIDS– afferent vasodilatation
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60
Q

drugs related to AKI - PPI?

A
  • Proton pump inhibitors– Interstitial nephritis
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61
Q

Other drugs leading to AKI?

A
  • Aminoglycosides
  • Contrast medium – 20% risk of AKI
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62
Q

Ix for AKI?

A
  • urine dipstick
  • haematology - FBC, coagulation profile, eosinophils, palsma viscosity
  • CRP, glucose
  • microbiology
  • radiology - US, CXR
  • immunology - ANA, ANCA, ANTI-GMB
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63
Q

life threatening complications of AKI?

A
  • Hyperkalaemia
  • Pulmonary oedema
  • Intravascular volume depletion
  • Uraemic encephalopathy
  • Pericardial fluid

requires dialysis

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64
Q

What is glomerulonephritis?

A
  • inflammation of glomerulus
  • 3 cell types of glomerulus: endothelial, epithelial, mesangial cells - produces mesangial matrix
  • can be primary or secondary
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65
Q

histology of glomerulonephritis?

A
  • diffuse: all glomeruli affected
  • focal: some glomeruli affected
  • global: whole glomerulus affected
  • segmental: only part of the glomerulus is affected
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66
Q

features of nephrotic S?

A
  • peripheral oedema - pitting oedema
  • proteinuria - more than 3.5g/day
  • hypoalbuminaemia
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67
Q

what occurs in nephrotic syndrome that increases the thromboembolic risk?

A
  • hypercholesterolaemia
  • (inc risk of infection and inc risk of thromboembolic risk)
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68
Q

Nephrotic S - low serum albumin ->

A

imbalance in starling forces -> fluid in IS space -. secondary hyperaldosteronism -> peripheral oedema

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69
Q

What are the causes of nephrotic syndrome in children?

A
  • minimal change glomerulonephritis - most common cause
  • focal segmental glomerulosclerosis - 2nd most common cause
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70
Q

minimal change?

A
  • person has Nephrotic S but light microscopy is normal
  • fusion of foot processes on EM
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71
Q

types of minimal change disease?

A
  • Treat w steroids without a biopsy - steroid responsive nephrotic syndrome
  • some relapse on steroid withdrawal - relapsing nephrotic syndrome
  • steroid dependent NS - requires cont steroid therapy
  • steroid resistant nephrotic syndrome
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72
Q

most common cause of nephrotic syndrome in adults?

A

membranous glomeruloneophritis -

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73
Q

other causes of nephrotic syndrome in adults?

A
  • IgA nephropathy
  • diabetic nephropathy
  • SLE, amyloidosis
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74
Q

Membranous GN?

A
  • most common finding is thickening of capillary loops - spikes on them are characteristics
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75
Q

How does membranous GN present?

A
  • adults
  • presents w proteinuria +/- renal impairment
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76
Q

prognosis of memb GN?

A
  • 1/3 spont recovery, 1/3 persistent proteinuria, 1/3 ESRF
  • majority autoimmune
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77
Q

mem GN is associated with?

A
  • adenocarcinoma (lung and GI)
  • hep B
  • SLE
  • drugs - gold. penicillamine - used be used to treat RA
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78
Q

how does IgA nephropathy present?

A
  • commonly presents w visible haematuria 1-2 days following URTI in 75% of younger patients
  • can present w nephrotic S, renal failure
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79
Q

IgA nephropathy can be benign but can ?

A

but 1/3 progress to ESRF/ death over 20 yrs

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80
Q

when is prognosis worse for IgA nephropathy?

A
  • proteinuria
  • HTN
  • scarring on biopsy
  • male
  • abn renal function
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81
Q

Alport’s syndrome?

A
  • genetic defect in the gene for alpha-5- chain of type 4 collagen found in the basement membrane
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82
Q

forms of alport’s syndrome?

A
  • X linked
  • autosomal recessive
  • autosomal dominant
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83
Q

X linked form of alport’s syndrome?

A
  • young males
  • haematuria
  • proteinuria
  • progressive renal failure
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84
Q

what else can be seen with alport’s syndorome?

A
  • haematuria
  • proteinuria
  • progressive renal failure
  • sensorineural deafness
  • anterior lenticonus - displacement of the lens of the eye
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85
Q

Female carriers of alports syndrome tend to have?

A
  • non-visible haematuria
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86
Q

How does nephritic syndrome present?

A
  • visible haematuria - smoky urine
  • HTN
  • AKI
  • often oliguria
  • some proteinuria
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87
Q

oedema in nephritic syndrome?

A
  • oedema may be present - secondary to oliguria causing salt and water retention, not proteinuria
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88
Q

urine

what is charactistic of nephritic syndrome?

A

red cell cast in urine

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89
Q

most classical cause of nephritic syndrome in children?

A

post-streptococcal GN

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90
Q

other causes of nephritic syndrome in children?

A
  • haemulytic uraemic syndrome
  • henoch-schonlein purpura
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91
Q

classic causes of nephritic syndrome in adults?

A
  • goodpasture’s
  • ANCA-assocuated vasculitis
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92
Q

Other causes of nephritic syndrome in adults?

A
  • SLE
  • primary/ secondary mesangiocapillary GN
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93
Q

Post-streptococcal GN?

A
  • presents w diffuse proliferative GN
  • Typically 10-14 days after a streptococcal throat infection
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94
Q

post-strep GN requires?

A
  • supportive care
  • spontaneous recovery
95
Q

henoch-schonlein purpura (HSP) typically presents w ?

A
  • Typically presents w a rash, back of the legs and buttocks
  • extensor surfaces, arms
  • joint pain, abd pain,
  • GI haemorrhage
96
Q

Rapidly progressive GN?

A
  • adults
  • AKI developing over days to weeks
97
Q

Histology in rapidly progressive GN?

A
  • crescentic glomerulonephritis - BS filled w cells and debris -> crescent
  • vascular necrosis - BV wall destroyed
98
Q

GN - cANCA?

A

associated w granulonatosis w polyangilitis - wegener’s

99
Q

GN - pANCA?

A

microscopic polyangitis

100
Q

tx of rapidly progressive GN?

A
  • steroids/ cyclophosphamide
  • rituximab
101
Q

antiglomerular BM ab disease/ goodpasture disease?

A
  • adults usually
  • presents w AKI
  • pulm haemorrhage
102
Q

Serology of goodpasture disease?

A
  • igG against type 4 collagen in the BM of the glomerulus
103
Q

histology of goodpasture disease?

A
  • cresenteric glomerulonephritis
  • linear igG dep
  • anti-GBM antibody positive
104
Q

Treatment of goodpastures?

A
  • steroids
  • cyclophosphamide
  • plasma exchange
105
Q

mesangiocapillary GN?

A
  • A.k.a membranopoliferative
  • any age
106
Q

secondary glomerulonephritis - most common cause?

A

diabetic nephropathy

107
Q

other causes of secondary glomerulonephritis?

A
  • amyloidoisis
  • subacute bacteria endocarditis and systemic lupud erythematosus - associated w hypocomplementaemia
108
Q

MGGN causes

A
109
Q

Lesions seen in diabetic nephropathy?

A
  • kimmelsteil-wilson lesions
110
Q

amyloid?

A
  • usually presents w nephrotic syndrome
  • stains w congo red
  • apple green on microscopy
111
Q

when does amyloid A inc?

A
  • secondary GN
  • serum amyloid component A - acute phase protein. Inc by any condition that causes chronic inflammation
  • e.g. RA, Crohns, ankylosing spondylitis, psoriatic arthiris
112
Q

hereditary amyloid A?

A
  • hereditary - familial mediterranean fever
  • chronic pyogenic infection - bronchiectasis, osteomyelitis
113
Q

AA amyloid presentation?

A
  • renal - 90%
  • hepatospenomegaly
  • bleeding, dysmotility, malabs
  • cardiac - 9%
  • adrenal
114
Q

AL amyloid causes?

A
  • primary GN
  • involves serum amyloid A component + light chain fragment complexing
  • paraprotein in blood or urine in more than 90%
115
Q

AA vs AL amyloid?

A
  • AA: secondary GN
  • AL: primary GN
116
Q

causes of AL amyloid?

A
  • myeloma - most common
  • lymphoma
  • MGUS
117
Q

what is the most common cause of AL amyloid?

A

myeloma

118
Q

organs affected in AL amyloid?

A
  • predom: kidney and heart
  • can also: SI, carpal tunnel, nerves, skin, tongue
119
Q

where is renin released from?

A

granular cells of the renal juxtaglomerular apparatus(JGA)

120
Q

What are the 3 triggers for renin release?

A
  • Reduced sodium delivery to the distal convoluted tubule detected bymacula densacells.
  • Reduced perfusion pressure in the kidney detected bybaroreceptorsin the afferent arteriole.
  • Sympathetic stimulation of the JGA via β1adrenoreceptors.
121
Q

what inhibits renin release?

A
  • release of renin is inhibited by ANP which is released by stretched atria in response to increases in BP
122
Q

renin converts ?

A
  • Renin convers angiotensin to angiotensin 1
  • angio 1 -> angio 2 by ACE - in the lungs
123
Q

effects of Angiotensin 2?

A
  • Systemic vasoconstriction
  • acts on hypothalamus increasing thirst
124
Q

angiotensin 2 acts on ? to release more ADH?

A
  • acts on posterior pituitary to release more ADH which causes more water reabs
125
Q

Angiotensin causes increased release of?

A
  • Causes SNS to release NA -> inc cardiac output, vasoconstriction of arterioles, release of renin
126
Q

where is aldosterone released from?

A
  • released from zona glomerulasa of the adrenal cortex
127
Q

where does aldosterone act?

A
  • Aldosterone acts onthe principal cellsof thecollecting ductsin the nephron.
  • It increases the expression of apical epithelial Na+ channels (ENaC) to reabsorb urinary sodium and water
  • causes potassium to exit (activation of sodium potassium pump) causing hypokalaemia
128
Q

summary of the effects of aldosterone?

A
  • increased sodium and water in blood -> inc blood pressure
  • causes potassium to leav e-> hypokalaemia
129
Q

Imp of HTN in kidney disease?

A
  • HTN can damage BVs leading to decreased kidney function over time
  • accelerates progression of other kidney diseases such as diabetic nephropathy and glomerulonephritis
  • renal function decline aggrevates hypertension
130
Q

ACEi and renal impairment?

A
  • most ACEi are renally excreted
  • in renal impairment, ACEI can accumulate
  • GFR in an ACE inhibitor treated kidney is blood pressure dependent, so a small drop in blood pressure reduces GFR, causing further accumulation of ACE inhibitor and so on.
131
Q

ACEi in the case of bilateral renal artery stenosis?

A
  • the glomerular filtration pressure is dependent on the vasoconstriction of the efferent arteriole because the resistance of the afferent blood vessels has been pathologically increased
  • vasoconstriction of the efferent arteriole is mediated by angiotensin II
  • administration of an ACE inhibitor abolishes the vasoconstriction of the efferent arteriole resulting in an abrupt fall in the glomerular filtration rate
132
Q

primary nephrotic syndrome?

A

Due to a primary renal glomeruli injury
* Minimal change disease
* Focal segmental glomerulosclerosis
* Membranous nephropathy

133
Q

secondary nephrotic syndrome?

A

Glomerular injury due to a wider systemic illness

  • Diabetes mellitus
  • Amyloidosis
  • Human immunodeficiency virus
134
Q

symptoms of nephrotic syndrome?

A
  • fatigue
  • poor appetite
  • peripheral oedema
  • SOB - typically from pleural effusions and/or pulmonary oedema
  • Foamy urine: due to excess protein loss
135
Q

nephrotic syndrome - signs of fluid overload?

A
  • Oedema: peripheral, periorbital
  • Ascites: fluid in the peritoneal cavity
  • Effusions: dull percussion note and reduced air entry
136
Q

Diagnosis of Nephrotic S is based on the triad of?

A
  • Nephrotic-range’ proteinuria(> 3.5 g/day)
  • Hypoalbuminaemia(< 35 g/L)
  • Oedema(e.g. peripheral, periorbital)
137
Q

complications of nephrotic syndrome?

A
  • DVTs and PE - loss of natural ACs
  • hyperlipademia
  • recurrent infections
  • AKI
138
Q

minimal change disease is resp for 90% of ? cases in children

A

nephrotic syndrome

139
Q

minimal change causes?

A
  • majority idiopathic
  • secondary - drugs like NSAIDs,
  • Malignancy(e.g. lymphoproliferative disorders),
  • Infections(e.g. syphilis - rarely)
140
Q

what can be seen in minimal change?

A
  • fusion of podocyte foot process under em
  • related to immune dysfunction
  • treated w systemic glucocorticoids e.g. prednisolone
141
Q

What happens in primary focal segmental glomerulosclerosis?

A
  • Primary FSGS is thought to occur due to a circulating factor that damages podocytes in the glomeruli leading tofoot process effacement.
  • This refers to a loss of podocyte foot process structure, causing them to spread out and this reduces the effectiveness of the filtration barrier.
    *
142
Q

what happens in secondary FSGS?

A
  • secondary: adaptive response to renal injury
  • This response is a combination of glomerular hypertrophy (increase in cell proliferation) and hyperfiltration (abnormally high glomerular filtration rate)
  • obesity, reflux nephropathy, reduction in kdiney mass are classic causes
143
Q

Membranous nephropathy?

A
  • one of the most common causes in adults
  • characterised by glomerular basement membrane thickening in the absence of significant cellular proliferation on histology
144
Q

what enables a serological diagnosis of membranous nephropathy?

A
  • presence of typical abn antibodies e.g. anti-PLA2R) that are seen in primary MN enables a serological diagnosis
145
Q

what occurs in renal amyloidosis?

A
  • excess deposition of amyloid fibrils in the glomerulus leading to nephrotic syndrome.
146
Q

AL vs AA amyloidosis?

A
  • AL amyloidosis(excess light chains due to plasma cell disorders) and
  • AA amyloidosis(excess precursor protein due to chronic inflammation).
147
Q

diagnosis of amyloid?

A

congo red stain

148
Q

What are the nephrotoxic drugs?

A
  • NSAIDs
  • ACEi and ARBs
  • diuretics
  • ab - ciprofloxacin, vancomycin, flucloxacillin, aminoglycosides
  • metformin
  • lithium
  • digoxin
149
Q

AKI vs CKD summary table

A
150
Q

preventing AKI?

A
  • increase fluid intake during an infection
  • increase fluid intake on hot days
  • stop taking nephrotoxic drugs and follow sick day rules until you are well and have been eating and drinking for 24-48hours
151
Q

AKI is most commonly ? in nature?

A

pre-renal, typically occuring secondary to renal hypoperfusion.

152
Q

what can cause renal hypoperfusion?

A
  • renal hypoperfusion can be due to hypovolaemia,
  • reduced cariac output,
  • systemic vasodilation (e.g. sepsis),
  • arteriolar changes (e.g. secondary to ACE-inhibitor or NSAID use).
153
Q

impacts of renal hypoperfusion

A
  • Renal hypoperfusion causes ischaemia of the renal parenchyma.
  • Prolonged ischaemia can lead to intrinsic damage and the development of acute tubular necrosis (ATN).
  • ATN is the most common cause of intrinsic renal AKI.
154
Q

what is the most common cause of renal/ instinsic AKI?

A

acute tubular necrosis (from prolonged ischaemia)

155
Q

causes of intrinsic AKI?

A
  • Renal artery stenosis
  • renal artery thrombosis
  • dissections e.g. aortic
  • glomerular pathology
  • ATN - secondary to prolonged renal hypoperfusion
156
Q

post renal aki is?

A

obstructive

157
Q

common causes of post-renal AKI?

A
  • Common causes of obstructive uropathy include urinary stones (urolithiasis),
  • malignancy (inc. intraluminal, intramural and extramural tumours),
  • stricturesand
  • bladder neck obstruction (e.g. benign prostatic hyperplasia).
158
Q

What are the RF for AKI?

A
  • Age(> 65 years old)
  • History of AKI
  • CKD
  • Urological history(e.g. stones)
  • Cardiac failure
  • Diabetes mellitus
  • Sepsis
  • Hypovolaemia
  • Nephrotoxic drug use
  • Contrast agents
159
Q

CFs of AKI?

A
  • usually non specific and related to underlying cause
  • raised JVP
  • bibasal crackles
  • gallop rhythm
  • peripheral oedema
  • dry membranes and thirst
  • postural drop
  • tachycardia
160
Q

what do patients usually present w in the case of pre-renal AKI?

A
  • Patients usually present with clinical features of hypovolaemia & dehydration.
  • Reduced capillary refill time
  • Dry mucous membranes
  • Reduced skin turgor
  • Thirst
  • Dizziness
  • Reduced urine output
  • Orthostatic hypotension
161
Q

Features associated w fluid loss?

A
  • features associated w fluid loss: excesive sweating, vomiting, diarrhoea, polyuria
  • elderly: confusion
162
Q

How may patients w intrinsic renal AKI present?

A
  • Those with intrinsic glomerular pathology may present with features of nephritic syndrome (e.g. haematuria, proteinuria, oliguria and hypertension)
  • or nephrotic syndrome (e.g. heavy proteinuria, hypoalbuminaemia and oedema).
163
Q

intrinsic renal AKI - ppts w tubulointerstitial disease?

A
  • Patients with a tubulointerstitial disease (e.g. acute interstitial nephritis) may complain of arthralgia, rashes and fever.
  • Eosinophilia is frequently seen.
164
Q

how may patients w renal stones present?

A
  • Patients with urinary stones may present with classical loin-to-groin pain, haematuria, nausea and vomiting.
165
Q

how may ppts w prostatic problems present?

A
  • Those with prostatic problems may have lower urinary tract symptoms (e.g. dysuria, frequency, terminal dribbling, hesitancy).
166
Q

obstruction at the bladder neck can be associated w?

A

palpable bladder and a tender suprapubic area.

167
Q

Ix for AKI - beside?

A
  • Urine dipstick
  • Urine microscopy
  • Urine osmolality and electrolytes
  • ECG
168
Q

bloods to do for AKI?

A
  • FBC
  • U&Es
  • bone profile
  • blood gas
  • Creatine kinase
  • Vasculitis screen(e.g. ANCA, ANA)
  • Clotting
  • Blood film
  • Complement
  • Immunoglobulins
  • Serum electrophoresis
  • Virology(hepatitis B/C)
168
Q

which imaging modality is key for AKI?

A
  • US is key - can look for evidence of obstructive uropathy (e.g. hydronephrosis). If there is ahigh degree of suspicion of urinary stones, a non-contrast CT may be completed.
169
Q
A
169
Q
A
170
Q

What can be done to assess renal vascular function?

A
  • Renal doppler - renal vascular assessment
  • MR angiography for vascular assessment
171
Q

what can be done to look for signs of overload?

A

CXR

172
Q

management of AKI?

A
  • stop nephrotoxic drugs
  • volume dysregulation -> fluids
  • hypervolaemic -> diuretics and fluid restriction
173
Q

AKI vs CKD on imaging?

A
  • renal US
  • most ppts w CKD have bilateral small kidneys
  • exceptions to this rule:
  • autosomal dominant polycystic kidney disease
  • diabetic nephropathy (early stages)
  • amyloidosis
  • HIV-associated nephropathy
174
Q

Other features suggesting CKD rather than AKI?

A
  • hypocalcaemia(due to lack of vitamin D)
  • AKI: sudden decline in GFR
  • usually reversible
175
Q
A
176
Q
A
177
Q
A
178
Q

ckd involves presence of dec GFR for?

A
  • CKD: presence of decreased GFR for more than 3 months
  • caused by long term diseases such as diabetes or hypertension.
179
Q

AIN presentation?

A
  • Patients present with acute or subacute deterioration in renal function (suggested in this patient who is passing less urine), joint pain, and hypersensitivity features (fever and rash).
  • Urinalysis will show a raised urine white cell count.
180
Q

drugs causing AIN?

A
  • often caused by NSAIDs
  • penicillins
  • PPIs
  • rifampicin
  • diuretics
  • allopurinol
181
Q

Use of 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes = risk of

A

hyperchloraemic metabolic acidosis

182
Q

all diabetic patients require screening for?

A

ACR) in early morning specimens

183
Q

Exudate vs transudate pleural effusions ?

A

EXudate = EX-life i.e. cell death
Transudate = Failures

184
Q

which type of LC causes more cavitating lesions?

A

sq cell > other types

185
Q

types of anticancer treatments?

A
  • cytotoxic: * Largely work by damaging DNA and inducing programmed cell death (apoptosis)
  • hormone: tamoxifen
  • immunotherapy: herceptin
  • targeted: tyrosine receptor kinase inhibitors
186
Q

Adjuvant chemo =

A

Treatment used to mop up micrometastatic disease post surgery in order to prolong surgery e.g. breast, lung and colorectal cancers.

187
Q

Neoadjuvant chemo =

A

Used to downstage tumours prior surgery e.g. oesophageal and rectal cancers.

188
Q

Curative chemo =

A

Chemotherapy is used as the sole, or main, modality to cure malignancy e.g. testicular cancers, lymphomas, leukaemias and many paediatric malignancies.

189
Q

Palliative chemo =

A

Chemotherapy is used to relieve symptoms, improve quality of life, and prolong life, but is not curative.

190
Q

acute side effects of chemo - generally reversible?

A
  • Myelosuppression
  • Nausea and Vomiting
  • Diarrhoea
  • Alopecia
  • Skin and nail changes
  • Local reactions
191
Q

late - usually irreversible side effects of chemo

A
  • Neuropathies
  • Sterility
  • Cardiovascular
  • Pulmonary fibrosis
  • Renal insufficiency
192
Q

Myelosuppression?

A
  • red cells - lethargy, dyspnoea
  • white cells - infections
  • platelets - purpura, bleeding
193
Q

The main mechanism for processing antigen from the donated kidney and presenting it to the host’s immune system.

A

dendritic cell

194
Q
A
194
Q
A
195
Q
A
195
Q

The principal effector for interleukin-2 production, which promotes the immune response

A

T cell

196
Q

Principle source of antigen in rejecton?

A

HLa system

197
Q

A 37 year old man with a 19 year history of type 1 diabetes is noted to have a lesion on the anterior aspect of her right shin. The lesion is not painful.

A

Necrobiosis lipoidica diabeticorum

198
Q

A 73 year old woman with a 3 year history of type 2 diabetes attends the surgery for dressing to a lesion on her shin. The nurse asks you to review this. The lesion is not painful and has been present for several weeks. The patient reports that her mobility has been poor for some time due to arthritis in her hips.

A

venous ulcer

199
Q

A 58 year old man with a 32 year history of type 1 diabetes is seen in the podiatry clinic. An image of his foot is shown. He was not initially aware of this problem and he does not have any pain

A

neuropathic ulcer

200
Q

how do sulfonylureas woek?

A

increase insulin sensitivity in skeletal muscle tissue

201
Q

Tx of neuropathic ulcers?

A

provision of protective footwear

202
Q

A 45 year old man with type 2 diabetes attends his GP surgery for a screening test to look for diabetic nephropathy. What would be the most appropriate and cost effective screening test to perform?

A
  • Albuminuria is the first sign of diabetic nephropathy. Initially the quantity of albumin is too low to be detected by a urine dipstick (previously called microalbuminuria).
  • early morning ACR needed
203
Q

What can ppint towards type 2 diabetes as opposed to type 1?

A

ketonuria

204
Q

when should SGLT2 inhibitors be avoided?

A

avoid initiation if eGFR <60ml

205
Q

biochemical abn seen in addisons?

A
  • hyponatreamia and hyperkalaemia
206
Q

Low aldosterone in addisons?

A
  • hyperkalaemic metabolic acidosis
207
Q

initial test for cushings?

A

24 hr urine free cortisol

208
Q

raised ASO titre suggests?

A

Raised ASO titre suggests recent Streptococcal infection. Acute post- infective nephritis causes a diffuse proliferative glomerulonephritis

209
Q

Blotchy skin rash + fever + eosinohilia + elevated urea and creatinine ->

A

acute interstitial nephritis

210
Q

barrier to live donor transplant?

A

Daughter’s cancer history excludes her from transplant for a minimum of 3 years post curative therapy.

211
Q

hyperkalaemia does NOT occur w?

A

cushings syndrome - hypokalaemic metabolic acdisosis

212
Q

normal casts in urine?

A

hyaline casts

213
Q

IgA nephropathy?

A
  • young adults
  • haematuria a day or 2 after an URTI
214
Q

post-streptococcal glomerulonephritis?

A

10-14 days after infection but IgA nephropathy occurs soon after

215
Q

what can cause ESKD in children?

A

autosomall recessive polycystic kidney disease

216
Q

hyperparathyroidism on bone scan?

A

diffuse inc in activity

217
Q

Pagets disease bone scan?

A

localised activity

218
Q

MM bone scan?

A

multiple myeloma is lytic and does not cause changes on an isotope scan.

219
Q

A 48 year old woman presents with a painless swelling in the left lobe of the thyroid gland. An isotope scan shows increased uptake of isotope in a solitary nodule. What is the most likely diagnosis?

A

Increased activity on an isotope scan is most characteristic of a functioning adenoma.

220
Q

marrow failure is associated with…

A

Marrow failure is associated with fat deposition and affects all blood-forming elements except lymphocytes which are formed in lymph nodes

221
Q

A 36 year old woman is to be counselled about the long term effects of chemotherapy for her cancer. What will it be important to include in the discussion?

A

new tumour formation

222
Q

What is the most common acute manifestation of radiation toxicity?

A

mucositis

223
Q

MTOR side effect?

A
  • hypothyroidism - in a quarter of ppts
224
Q

TKI inhibit which pathway?

A

VEGFR pathway which is more prev in cancer

225
Q

pain relief in renal colic?

A

1) NSAIDs - diclofenac
2) codeine

226
Q

insulin used in continuous subcut insulin infusion pumps?

A

insulin lispro - short acting insulin

227
Q

drug to prevent diabetic nephropathy?

A

ACEi

228
Q

what is not impacted by dialysis?

A

All of the electrolytes can cross a semipermeable membrane and may improve with dialysis alone. Haemoglobin will only improve with the administration of erythropoietin +/-iron

229
Q

osteomyelitis affects?

A
  • infection of bone
  • diabetes or those w PAD
230
Q

Symptoms of osteomyleitis?

A
  • pain, warmth, erythema
  • systemic features - fever and malaise
231
Q

Charcots athropathy?

A
  • swelling of the foot
  • redness and warmth
  • improves on elevation of the foot - infectious causes do not improve
232
Q
A

Year 3 (45 decks)

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