Renal Flashcards

1
Q

Causes of AKI

A

Pre- renal (decreased vascular flow)

Renal (damage to glomerulus, intersitium or vessels)

Post-renal- blockage of urinary tract

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2
Q

Pre-renal causes of AKI

A
  • hypovolaemia (dehyd, haemorrhage, D+V, burns, shock)
  • reduced CO- HF, MI, sepsis
  • Meds- ACEI, ARB, NSAIDs, loop diuretics, aminoglycosides
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3
Q

Renal Causes of AKI

A
  • acute tubular necrosis
  • *- vasculitis
  • Glomerulonephritis
  • *- infiltration- amyloidosis, myeloma, renal cancer
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4
Q

Post-renal causes of AKI

A
  • Intrinsic- stones, clot, UT tumour

- Extrinsic- prostate, neurogenic bladder, blocked catheter

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5
Q

Presentation of AKI

A
  • reduced UO
  • colour change of urine (dark, brown)

Fluid overload

  • Peripheral oedema
  • pulm oedema- SOB, orthopnoea, PND, cough, crackles)

Uraemia

  • confusion
  • fatigue
  • drowsiness, GCS
  • N+V
  • seizures
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6
Q

Diagnostic criteria fro AKI

A

1 of:

  • raised Cr >=26 in 48hrs
  • > =50% rise in Cr above baseline
  • UO <0.5ml/kg/hr for at least 6 hours
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7
Q

definition of oliguria

A

<1ml/kg/hr infants

<0.5ml/kg/hr children

Adults:
<400-500ml daily in adults
17-21ml/hour
0.3-0.5ml/kg/hr

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8
Q

ix for ?AKI

A
  • UO
  • FBC, UE, CRP, Coag, LFT, CK
  • *- urinalanysis
  • *- immunology (autoantibs)
  • renals USS
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9
Q

what urinanalysis results would suggest different causes of AKI

A
  • negative- pre-renal
  • blood and protein- glomerular
  • white cell- infection/intersitital nephritis
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10
Q

what clasificaiton is used for AKI (stages)

A
  • KIDGO
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11
Q

complications of AKI

A
  • anaemia (EPO lacking)
  • hyperkalaemia
  • metabolic acidosis
  • pulm oedema
  • uraemia pericarditis
  • total renal failure
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12
Q

Management of AKI

A

Pre-renal cause

  • IV fluids
  • Sepsis 6
  • major haemorrhage protocol

Renal

  • stop meds
  • steroids

Post-renal

  • catherterise
  • surgery

General

  • fluid balance (BP, skin turgor, JVP, fluid chart)
  • monitor Na, K, Ca, Cr, glucose
  • tx hyperkalaemia
  • refer if no ID cause/moderate AKI

severe- haemodialysis

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13
Q

what is acute tubular necrosis

A
  • ischaemic or nephrotoxic injury to tubular epithelial cells causing AKI
  • results in detachment from BM
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14
Q

sx of acute tubular necrosis

A
  • *- hypotension, fluid depletion
  • exposure to nephrotoxic substances- contrast, aminoglycoside, abx, CT
  • oligo/anuria
  • *- poor oral intake, anorexia
  • dizziness, malaise
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15
Q

ix ?acute tubular necrosis

A
  • urinanalysis- muddy brown casts (epithelial cells)

* *****- urine Na conc, urine osmolality (ie conc)– high

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16
Q

management of acute tubular necrosis

A
  • fluid balance

- remove toxic agents

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17
Q

definition of anuria

A

<100ml/day

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18
Q

what is the most common cause of CKD

A

diabetes

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19
Q

causes of CKD

A

diabetes
hypercholesterolaemia
HTN
glomerular disease

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20
Q

presentation of CKD

A
  • asx in stages 1-4
  • N+V, diarrhoea, anorexia, wt loss
  • **- polyuria, nocturia, haematuria
  • oedema, pleural effusions (SOB, cough, chest pain, orthopnoea)
  • HTN
  • *- bone pain, # (Ca, phosphate reab issues)
  • *- prox muscle weakness (Ca, reabs issues)
  • neuro- polyneuropathy, confusion
  • uraemic pericarditis- chest pain worse on insp and lying), coughing
  • skin pigmentation/darkening- pigments that are usually excreted are retained
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21
Q

ix ?CKD

A
  • UE
  • FBC- anaemia
  • HbA1c, lipids
  • PTH, Ca, Phosphate, vit D
  • urinanalysis- proteinuria, haematuria
  • urine albumin-Cr ratio– >3mg/mmol clinically relevant pronteinuria
  • renal USS- obstruction, FH PCKD
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22
Q

Classification of CKD

A
1- eGFR >90 plus kidney damage (strctural/haematuria/proteinuria >3m)
2- eGFR 60-89 plus kidney damage
3a- eGFR 45-59 
3b- eGFR 30-44
4- eGFR 15-29
5- eGFR <15
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23
Q

management of CKD

A
  • monitor eGFR and alb-Cr ratio
  • smoking, alcohol, wt/diet
  • avoid NSAIDs and other nephrotoxics
  • pneumococcal and flu jabs
  • bisphos, vit D and Ca supplements
  • PO iron, IV iron, recombinant EPO/erythropoietic stimulatign agent
  • manage HTN
  • statins
  • antiplatelets
  • renal replacement
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24
Q

indications for renal replacement therapy

A

Severe AKI

  • unresponsive acidosis
  • unreposnsive electrolyte abnormalities, esp hyperkalaemia
  • oedema
  • uraemia, seizure, GCS, encephalopathy
  • pericarditis

LT
- CKD stage 5

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25
Q

types of renal replacement therapy

A

Intermittent haemodialysis-

  • AV fistula
  • *- 3-4 times p/w, 3-4 hours
  • infection, thrombosis, aneurysm in fistula, stenosis, STEAL syndrome (distal limb ischaemia), **high output HF (increased venous retrun to heart)

Peritoneal dialysis

  • pt can do in own time, independence
  • bacterial peritonitis, peritoneal sclerosis, wt gain, **LT ascites

Continuous-

  • on ward, more unwell pts
  • no toxin build up
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26
Q

what would suggest O/E of a renal transplant

A
  • mass palpable in iliac fossa (usually R)
  • Rutherford Morrison (reverse hockey stick ie long curved scar, usually in RIF).
  • may have palpable AV fistula
  • may have mutiple abdo scars due to dialysis insertion/exit sites (peritnoeal)
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27
Q

pathopysiology of renal arteyr stenosis

A
  • atherosclerosis
  • impaired renal BS
  • juxtaglom apparatus detects
  • renin released
  • RAAS activated
  • HTN
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28
Q

RAAS system

A
  • low BP detected by juxtoglomerulus apparatus
  • renin released
  • angiotensinogen–> angiotensin I
  • ACEI causes angio I–> II
  • angio II causes aldosterone from adrenals plus vasoconstriction
  • alosterone– reabs Na and water
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29
Q

where is angiotensinogen released from

A

liver

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30
Q

sx of renal artery stenosis

A
  • **Flash pulm odema (recurrent)
  • dyspnoea
  • orthopnoea
  • cough- frothy, blood
  • wheezing
  • weak, thirst, confusion, irritable (hypernatraemia)
  • twitches, cramps, paralysis, arrhythmias (hypokalaemia)
  • *- confusion, tremor (metabolic alkalosis)
  • double vision, headaches
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31
Q

signs of renal artery stenosis

A
  • sudden onset HTN
  • tx resistant HTN
  • worsening eGFR (ischaemia)- esp after starting ACEI
    deranged U&Es
  • metabolic alkalosis
  • HTN retinopathy on fundocscopy
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32
Q

ix ?renal artery stenosis

A
  • UE, aldosterone to renin ratio
  • renal USS
  • duplex/doppler US
  • CT/MRI angiography
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33
Q

tx renal artery stenosis

A
  • diuretics
  • angioplasty, stenting
  • lifestyle
  • manage diabetes
  • antiplatelets, statins
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34
Q

presentation of glomerulonephritides

A
  • asx
  • nephritic or nephrotic syndromes
  • chronic/end-stage- anaemia, bone disease
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35
Q

ix ?glomerulonephrtides

A
  • bloods- inflam markers, protein levels, antibodies

- renal biopsy

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36
Q

What is Nephrotic Syndrome

A
  • large proteinuria (>=3.5g/day)
    AND
  • hypoalbuminaemia (<=30g/L)
  • cause by non-proliferative glomerulonephritis
  • also has hyperlipidaemia- liver compensates fro reduces albumin by also increasing lipid production
  • loss of Ig proteins
  • loss of antithrombotic proteins
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37
Q

sx nephrotic syndrome

A
  • oedema- ascites, effusion
  • immunosupression, recurrent infections
  • clotting (urinary loss of antithrombotic proteins, increased prod of prothombotic factors)- renal vein thromb, PE, DVT
  • frothy urine (proteinuria)
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38
Q

What is nephritis syndrome

A
  • small proteinuria
  • haematuria (micro or macro)
  • reduced renal function– reduced UO– HTN
    +- oedema
  • caused by proliferative glomerulonephritis
  • red cell casts in urine (indicate glomerular damage)
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39
Q

Name some non-proliferative glomerulonephritis

A
  • focal segmental glomerulosclerosis
  • minimal change
  • membranous glomerulonephritis
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40
Q

what type of renal syndrome do non-proliferative glomerulonephritides cause

A
  • nephrotic
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41
Q

who does focal segmental glomerulosclerosis affect

A

adults

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42
Q

pathophysio of focal segmental glomerulosclerosis

A
  • non proliferative
  • segmental scarring of glomeruli and fusion of foot processes
  • idiopathic
  • HIV, lupus, reflux nephro
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43
Q

who does minimal changes disease tend to affect

A

2-6yo

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44
Q

causes of minimal change disease

A
  • idiopathic
  • paraneoplastic- Hodgkins
  • drugs
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45
Q

sx of minimal change disease

A
  • oedema / wt gain

- in a child

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46
Q

pathophysio of membranous glomerulonephritiis

A
  • non-proliferative
  • IgG deposition, thickening of glomerular cap wall
  • glomerular PLA2R antigen targetting
  • mostly caused by autoimmune disease
  • can also be caused by infection, drugs, tumour
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47
Q

presentation of focal segmental glomerulosclerosis and membranous glomerulonephritis

A
  • facial swelling
  • oedema
  • HTN
  • renal failure (reduced UO)
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48
Q

who does membranous glomerulonephritis tend to affect

A

adults, slow

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49
Q

ix of non-proliferative glomerulonephritides/nephrotic syndromes (focal segmental glomerulosclerosis, minimal change, membranous)

A
  • urinanalysis- large proteinuria
  • PLAR2 ab in urine (membranous)
  • renal biopsy
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50
Q

management of non-proliferative glomerulonephritides/nephrotic syndromes (focal segmental glomerulosclerosis, minimal change, membranous)

A
  • prednisolone
    cyclophosphamide/ciclosporin
  • salt/fluid restriction
  • correct cause (infection, drug, autoimmune disease)
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51
Q

what would yuo see on renal biopsy of the different non-proloferative glomerulonephritides

A

focal segmental glomerulosclerosis

  • segmental scarring of glomeruli
  • fusion of foot processes

minimal changes

  • no changes on light micro
  • effacement of podocyte foot process on electrone
  • no deposits or ig complements

Membranous

  • Ig deposits on immunofluoresent staining
  • thickened BM
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52
Q

Name proliferative glomerulonephritis

A
  • IgA (berger’s)
  • post- strep
  • anti-glomerular BM
  • rapidly progressive
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53
Q

what renal syndrome do proliferative glomerulonephritides tend to cause

A

nephritic

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54
Q

what is igA nephropathy

A
  • igA deposits
  • proliferative glomerulonephritis
  • occurs post- URTI
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55
Q

sx of igA nephropathy

A
  • frank haematuria
  • after URTI
  • can cause henoch-schonlein purpura in children- deposits in skin, GI tract
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56
Q

management f igA nephropathy

A
  • ARB, ACEI (BP control)
  • low cholesterol diet
  • immunosupresison- steroids, cyclophosphamide, azathioprine for remission
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57
Q

most common proliferative glomerulonephritis

A

igA nephropathy/Berger’s

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58
Q

most common non-proliferative glomerulionephritis

A

adult- focal segmental glomerulosclerosis

children- minimal change

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59
Q

ix for any cause of ?nephritic syndrome/proliferative glomerulonephritis (frank haematuria)

A
  • dipstick
  • renal biopsy- to find cause
  • serology for autoab
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60
Q

what is post-strep glomerulonephritis

A
  • proliferative glomerulonephritis
  • immune glomerular injury triggered by strep infection (2w following)
  • generally self limiting
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61
Q

what is the specific antibody found in post- strep glomerulonephritis

A

anti-streptococcal antibody titres

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62
Q

management of post-strep glomerulonephritis

A

fluid balance
supportive
self limiting

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63
Q

what is anti-glomerular basement membrane disease

A
  • autoimmune attack of basemement membrane antigens located in glomeruli and alveoli
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64
Q

sx anti-glomerular BM disease

A
  • nephritic syndrome- haematuria, HTN, oedema

- haemoptysis, cough, SOB- Goodpasture’s syndrome!

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65
Q

what is a sepcific antibody found in anti-GBM disease

A
  • anti-GBM antibodies
66
Q

renal biopsy findings of the different nephritic, proliferative diseases

A

IgA- mesangial cells and matrix, crescents, igA deposits

Post-strep- exudative and proliferative, subepithelial humps

anti-GBM- igG deposits along basement membrane

67
Q

What vasculitic diseases can affect the kidneys?

A
  • necrotising small vessel vasculitis

- granulomatosis with polyangitis (wegner’s)

68
Q

sx of necrotising small vessel vasculitis

A

rash
sinusitis
malaise, fever, wt loss

69
Q

tx of necrotising small vessel vasculitis/ granulomatosis with polyangiitis

A
  • steroids
  • cyclophosphamide
  • metho, azathioprine
70
Q

sx of granulomatosis with polyangitis (wegner’s)

A

sinusitis
glomerulonephritis- proteinuria, haematuria
cough, haemoptysis
purpura, arthritis, scleritis/episcleitis
fever, malaise, weakness, wt loss

71
Q

What is haemolytic uraemic syndrome

A

shiga toxin /verotoxin producing e.coli

  • thrombin and fibrin deposition in renal, GI and CNS microvasculature
  • haemolysis
  • plts sequestered
72
Q

sx of haemolytic uraemic syndrome

A
  • after e.coli infection- gastroeneritis
  • bloody diarrhoes, pain, vomiting
  • haematuria
  • oliguria
  • jaundice
  • anaemia sx
73
Q

ix for haemolytic uraemic syndrome

A
  • low plt, low Hb, elevated LDH, raised WCC
  • red cell fragments on blood film
  • rise in Ur and Cr
  • LFTs to ddx HELLP
  • CRP
  • clotting- reduced values
  • stool PCR, urine culture
  • urinanalysis- haematuria, proteinuria
74
Q

tx haemolytic uraemic syndrome

A
  • fluid and electrloytes
  • anti-HTNs
  • dialysis
  • plasma exchange
  • liver, kidney transplants
75
Q

what is lupus nephritis, sx

A
  • lupus (fever, malaise, joint pain, malar rash)

- haematuria, proteinuria (forthy), HTN, oedema

76
Q

tx lupus nephritis

A
  • BP ctornol
  • electrolyte and fluid
  • steroids, cyclophosphamide
77
Q

what is fanconi syndrome

A
  • inadequate reabs in the Prox renal tubules

- caused by hypoxia, drugs, genetics, infiltration (myelome, wilsons)

78
Q

sx of fanconi

A
  • polyuria, polydipsia, dehydration
  • rickets and osteomalacia (loss of phosphate)
  • electrolyte disturbances– hypokalaemia
79
Q

tx fanconi syndrome

A
  • replace electrolytes and fluids

- kidney transplant

80
Q

what inheritance pattern is PCKD

A

dominant OR recessive!

81
Q

presentation of autosomal dominant PCKD

A

asx unless cysts large/haemorrhagic

  • loin pain
  • haematuria
  • stones
  • HTN
  • cyst infection- fever, pain, sepsis
  • UTI, pyelonephritis
82
Q

management of dominant PCKD

A
  • annual monitoring USS< BP, UE
  • drink water
  • HTN control
  • tx infections
  • CT guided cyst aspiration
  • tolvaptan- slows growth
  • renal replacement therapy
83
Q

sx of recessive PCKD

A
  • affects fetus
  • oligohydramnios
  • underdeveloped lungs

infance

  • abdominal mass
  • resp failure
  • portal HTN (cirrhosis)
  • underdeveloped ear cartiliage, low set ears, flat nasal bridge
84
Q

tx recessive PCKD

A
  • tx renal failure, portal HTN

- renal replacement- most will dies in childhood if dont have this

85
Q

what is alport syndrome

A

x linked

  • defect in type IV collagen
  • affects glomerular BM, cochlea, eyes
86
Q

sx alport

A
  • haematuria, proteinuria
  • sensorineural deafness
  • cataracts, corneal erosion later in life
87
Q

management of alport syndrmoe

A

ACEI
renal replacement therpay
renal transplant

88
Q

ix for inhertied renal disease (PCKD, alport)

A

UE, urinanalysis
USS
genetic testing
renal biopsy

89
Q

cell type of renal cancer

A

95% RCC

90
Q

sx renal cancer

A

2/3 are asx

  • haematuria
  • flank pain
  • abdo mass
  • HTN
  • anorexia, wt loss
91
Q

ix ?renal cancer

A
  • HTN- aggressive (renin)
  • FBC- polycythemia due to EPO
  • ESR, UE
  • ALP (bony mets)
  • renal USS
  • CT/MRI
92
Q

what is the 2ww criteria for ?RCC

A

> =45 yo and
unexplained frank haematuria without UTI
OR
frank haematuria that perissts/recurs after successful tx of UTI

93
Q

tx RCC

A
  • surgical- nephrectomy

- CT/RT resistant

94
Q

what is a wilms tumour

A

nephroblastoma

  • children
  • embryonal tumour of the kidney
95
Q

sx wilm’s tumour

A
  • abdo mass
  • otherwise well child
  • haematuria
  • HTN
96
Q

ix ?wilms tumour

A
  • US/CT/MRI abdo

- assess function of contralateral kidney

97
Q

tx wilms tumour

A

CT
excision, nephrectomy
RT

98
Q

what is rhabdomyolysis

A
  • breakdown of damage skeletal muscle
  • causes myoglobin release
  • kidney damage
99
Q

causes of rhabdomyolysis

A
  • trauma (crush, burns, ischaemia)
  • heat (lightning, heat stroke)
  • exertion (long lie, shivering, seizures)
  • genetic disorders in metabolism
  • hypothyroidism
  • DKA
  • electrolyte imbalances
  • DUchenne
  • infection
  • inflammation
  • drugs
100
Q

what drugs may cause rhabdomyolysis

A
  • statin (safety net muscle pain)
  • cyclosporin
  • erythro
  • colchicine
  • cocaine, ampehtamines, ecstasy, LSD
101
Q

sx rhadomyolysis

A
  • weakness
  • soreness
  • bruising
  • dark urine
  • fatigue, malaise, fever, N+V,
  • confusion, agitation
102
Q

ix ?rhabdomyolysis

A
  • CK
  • myoglobin- serum and urine
  • K- may leak from injured tissue
  • Cr
103
Q

tx rhadomyoloysis

A
  • IV fluids stat
  • sodium bicarbonate meds- binds to myoglobin and alkalanises the urine
  • diuretics
  • tx and monitor for hyperkalaemia, hypocalacaemia
  • dialysis
104
Q

sx acute retention

A
  • urgency, but cannot urinate
  • lower abdo pain.discomfort
  • normal renal function
105
Q

sx chronic retention

A
  • polyuria (8x p/d)
  • hesitancy
  • weakn/intermittent stream
  • feeling need to urinate post-mic
  • nocturia
  • leakage
  • urge incontinence
  • cant tell when bladder is full
  • mild discomfort lower abdo/pelvis
106
Q

ix to differentiate acute and chronic retention

A

Residual volume
>1L in chronic
<1L in acute

Kidney function
deranged in chronic
normal in acute

107
Q

what is high pressure urinary retention

A
  • chronic retention with high intra-vesical pressure

- back up to kidneys- BL hydronephrosis

108
Q

causes of retention

A

Obstruction

  • stones
  • strictures
  • constipation
  • mass in pelvis/GI
  • blood clot
  • foreigh bodies
  • urethritis, cystitis, balanitis, prastatitis

Meds

  • amphetamines
  • Anticholinergics
  • sypathomimetics
  • muscle relaxants
  • MSADs
  • antipsychotics
  • tricyclics
  • opioids

Neuro- CNS damage, diabetes, MS, parkisons

Iatrogenic- spinal, joint surgery

BPH, prostate cancer, penile cotnriction bands, meatal stenosis, paraphimosis/phimosis

Gynae cancers, prolapse

109
Q

name some antimuscarinic/anticholinergic drugs

A
  • Antihistamines- promethazine, hydoxyzine, chlorpheniramine
  • oxybutynin, solifenacin
  • procyclidine (parkinsons)
  • tiotropium/irpatropium
  • atropine
110
Q

anticholinergic drug mechanism

A

block the parasympathetic nervous system:

  • block cholinergic or acetylecholin receptors
  • antimuscarinics block muscarinic receptors
  • antinicotinics block nicotinic receptors
111
Q

effects of anticholinergic drugs on the body

A
  • decreased smooth muscle motility in UT and increase tone of sphincters contorlling urination
  • increase the heart rate,
  • minimize vestibular issues
  • help with motor sx in parkinsonss
  • decrease gastric acid secretion
  • relax muscles in airways
112
Q

SE anticholinergics

A

Can’t pee, can’t see, can’t spit, can’t shit

  • dry mouth, sore throat
  • urinary retention
  • mood changes, hallucinations, confusion
  • above are sx of an overdose too
113
Q

ix for retention

A
  • genital and rectum
  • urinanalysis
  • post void residual volume, urodynamic testing
  • cystoscopy
  • USS, CT
114
Q

tx retention

A
  • 2 way catheter
  • surgical dilatation
  • analgesia
  • acute- alpha-adrenoreceptor blocker (doxazosin, tamsulosin)
  • chronic- intermittent catheterisation, indwelling

Men

  • alpha adrenoceptor blocker (alfuzosin, doxazosin, tamulosin– selective alppa1)
  • bethanechol chloride
  • 5alpha reductase inhib- finasteride
  • surgery
115
Q

post obstructive diuresis

A
  • UO >200ml/hr over 2 hours

- can cause electrloyte disurbance and hypotension

116
Q

management of post obstructive diuresis

A
  • monitor (bloods, wt, ABG, obs)
  • USS renal
  • CT KUB
  • IV fluid relplacement, hartmans 50% of UO
  • catheter- indwelling
  • never TWOC
117
Q

Hydronephrosis- what is it?

A

UT obstruction cause increased pressure in the kidneys

  • kidney distension
  • damage and loss of function
118
Q

sx hydronephrosis

A
  • flank/back pain- can be dull if chronic
  • N+V
  • fever
  • infants- listelessness, FTT
119
Q

ix ?hydronephrosis

A
  • USS- distended
  • urogram
  • CT/MRI if ?cancer
  • creatinine
  • urinanalysis- ??infection
120
Q

tx hydronephrosis

A
  • watch and wait if mild
  • preventative abx
  • anatomical correction
  • surgery to unobstruct
121
Q

sx of renal vein thrombosis

A
  • loin/flank pain
  • oliguria
  • haematuria
  • N+V
  • may also have PE
  • asymmetrical lower leg oedema- back flow of venous blood
  • frothy urine if due to nephrotic syndrmoe
122
Q

signs of renal vein thromb

A
    • lef variocele if L renal vein thrombosed
  • dilated abdo veins
  • peripheral oedema
  • proteinuria
123
Q

ix ?renal vein thrombosis

A
Cr, urinary protein
doppler USS
IV urogram
CT/MRI ?cancer
biopsy if ?nephrotic syndrome
124
Q

management of renal vein thrombosis

A
  • warfarin
  • streptokinase to lyse if acute
  • statin
  • ACEI/ARBC or proteinuria
  • tx underlying cause
  • thrombectomy
  • surgery- IVC filters, nephrectomy
125
Q

Where to loop diuretics act in the kidneys, how do they work

A
  • loop of henle- thick ascending
  • inhibit NKCC2 transporter
  • stop Na, K and Cl reabs
  • reduced water reabs
126
Q

SE loop diuretic

A
  • hypokalaemia- stops K reabs
127
Q

Where do thiazide- like diuretics act in the kidney, mechanism of action

A

DCT
NaCa cotransporter inhibition- less Cl ions and Na reabs from tubule into blood
Less water reabs

128
Q

SE thiazide like diuretics

A
  • gout flare

- hyperglycaemia

129
Q

egs of thiazide like diuretics

A

indapamide

bendroflumethiazide

130
Q

EGs of aldosertone antagonsists

A

spironolactone

eplerenone

131
Q

location of action of aldosterone anatgonsists

A

DCT- inhibit aldosterone from binding

prevents water and Na reabs

132
Q

SE of alosetrone anatgonsists

A

Hyperkalaemia

agranulocytosis

133
Q

SE of ACEI

A

dry cough

hyperkalaemia

134
Q

SE ARB

A

hyperkalaemia

135
Q

eg of ACEI

A

ramipril

- pril

136
Q

eg of ARB

A

losartan
candesartan
- sartan

137
Q

CCBs mechanism of action

A

block Ca channels on BV and heart

relaxes smooth muscle

138
Q

eg of CCBs

A

amlodipine

verapamil

139
Q

SE CCBs

A
  • peripheral oedema
  • flushing
  • constipation
140
Q

Sx of pyelonephritis

A
  • fever, N+V, aching, fatigue, confusion
  • abdo/flank pain
  • dysuria
  • cloudy urine, haematuria, pyuria
  • urgency/frequency
  • fishy odour
141
Q

organisms that commonly cause pyelonephritis

A

Gram -ve

  • e.coli
  • proteus
  • klebsiella
  • enterbacter
142
Q

ix ?pyelonpehritis

A
  • urinanalysis
  • if catheter- check
  • bloods, culture
  • -> can make dx if loin/flank pain and confirmed UTI

diagnostic uncertainty:

  • CTKUB ?stone
  • kidney USS if recurrent, voiding custourethrography
  • DMSA- radionucleotide
143
Q

tx pyelonephritis in non pregnant women, men, indwelling catheters

A

1st line

  • cefalexin 500mg BD 7 days
  • coamox 500/125mg TDS 7 days
  • trimethoprim 200mg BD 14 days
  • cipro 500mg BD 7 days
144
Q

tx pyelonephritis in pregnant women

A

cefalexin 500mg BD 7 days

145
Q

what are kidney stones often made up of

A
  • Ca oxalate
  • Ca phosphate
  • uric acid- dont show on XR
  • struvite (mg, ammon, phos)
  • cysteine
  • Xanthine- dont show on XR
146
Q

sx kidney stone

A
  • flank pain
  • becomes severe
  • renal colic- spasmodic
  • loin to groin
  • haematuria
147
Q

ix kidney stone

A

CT KUB

urinanalysis- blood

148
Q

tx stone

A
  • <5mm- can pass (CCBs, alpha adrenergic eg tamsulosin)
  • hydration
  • analgesia
  • potassium citrate reduce formation
  • lithotripsy
  • surgery and stent
149
Q

sx stress incontinence

A
  • physical stress
  • coughing, sneezing, laughing, bending. lifting, jumping, running, having sex
  • muscles that support urethra are weak
150
Q

sx of urgency incontinence/OAB

A
  • sudden urge to urinate due to bladder contracting
151
Q

sx overflow incontinence

A
  • dribbling after micturition

- due to obstruction

152
Q

medications that can cause incontinence

A
  • diuretics
  • antihypertensives
  • sleeping tablets
  • sedatives
  • muscle relaxants
153
Q

food,drink that can cause incontinence

A
  • caffeine
  • fizzy drinks
  • chocolate,
  • chillis, spice
  • citrus, vit c
  • alcohol
154
Q

conditions/diseases that can cause incontinence

A
  • neuro
  • stones, UTI
  • obstruction (tumour, constipation, prostate
  • cauda equina
  • retention (nocturnal)
  • prolapse
155
Q

ix incontinence

A
  • bladder diary
  • physical exam- pelvic floor, PR
  • diptick
  • USS bladder (overflow, retention)
  • cystoscopy
  • urodynamics
156
Q

tx stress incontinence

A
  • pelvic floor exercises
  • topical oestrogen
  • pessary/urethral insert
  • bulking agents injected
  • surgery- sling
  • catheter
  • absorbent pads
157
Q

tx overactive bladder

A
  • bladder training
  • anticholinergics- oxybutynin, solifenacin
  • mirabegron- beta-3-adrenergic agonist
  • topical oestrogen
  • imipramine- tricyclic
  • botox
    catheter
  • absorbent pads
158
Q

tx cystitis

A
  • trimethoprim 200mg BD 3 days OR
  • nitro 100mg BD for 3 days
    If recurrent
  • trimethoprim 200mg within 2 hours of sex
  • 6m course of trimethoprim or nitro 100mg at night
159
Q

what is interstitial cystitis, sx

A

chronic, mech unknwn

  • urgency, frequency, nocturia
  • suprapubic/pelvic pain
  • may rdiate to groin, sacrum, vagina
  • pain worse when bladder full
  • dysuria
  • pain better post void
  • sx worse during menstruation
  • dyspareunia
  • often coincides with functional issues, SLE, asthma, TMJ
160
Q

ix ?intersitial cystitis

A

rule out other causes:

  • urinanalysis
  • cervical swab (STI)
  • urodynamics
  • men- urethral swabs, prostatic secretion cultures– chronic prostatits
  • cystoscopy with biopsy for diagnosis
161
Q

tx intersitial cystitis

A
  • reduce caffeine, alcohol, acidic foods and drink
  • stress
  • analgesia
  • amytriptyline,. cimetidine
  • pentosan - polysulfate sodium
  • oxybutynin
  • gabapentin
  • ciclosporin
  • intravescical lidocaine, botulinum toxin
  • surgical ablaiton, augmentation cystoplasty