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PACES Hawthorne > Medical Abdomen > Flashcards

Medical Abdomen Flashcards

1
Q

Chronic liver disease

On examination

Inspect: general, hands, face, trunk, ankles

Abdo: inspect/palpate

sig negatives!

A

Peripheral Inspection

  • General
    • Jaundice
    • Ascites
    • Cachexia
    • Tattoos and track marks
    • Pigmentation
  • Hands
    • Clubbing (esp. in PBC)
    • Leukonychia
    • Terry’s nails (white proximally, red distally)
    • Palmer erythema
    • Dupuytren’s contracture
  • Face
    • Pallor: ACD
    • Xanthelasma: PBC
    • Keiser-Fleischer rings
    • Parotid enlargement (esp. c¯ EtOH)
  • Trunk
    • Spider naevi
    • Gynaecomastia
    • Loss of 2O sexual hair
  • Ankles
    • Peripheral oedema

Abdomen

  • Inspection
    • Distension ± Para- / umbilical hernia
    • Dilated veins
    • Drain scars
  • Palpation
    • ± hepatomegaly
    • ± splenomegaly
    • Shifting dullness

Significant Negatives

  • Evidence of decompensation
    • Jaundice
    • Encephalopathy: asterixis, confusion
    • Foetor hepaticus: ammonia and ketones
    • Hypoalbuminaemia: oedema and ascites
    • Coagulopathy: bruising
  • Evidence of SBP: esp. if ascites
  • Cause: xanthelasma, pigmentation, KF rings, tattoos
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2
Q

Definition of Chronic liver disease

A

Progressive destruction of the liver parenchyma over a period greater than 6 months leading to fibrosis and cirrhosis

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3
Q

CLD

Differentials

(common/rare)

A
  • Common
    • EtOH
    • Viral
    • NASH
  • Rarer
    • Genetic: HH
    • AI: AH
    • Drugs: methotrexate
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4
Q

History Qs in CLD case

(cases)

A
  • EtOH
  • Sexual Hx, IVDU, transfusions
  • FH
  • Other AI disease: e.g. DM, thyroid
  • DH
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5
Q

Investigations in CLD case

Initial work up

(and 2 ‘other’)

A

Initial Workup

  • Urine: dip ± MC+S (? UTI)
  • Bloods: FBC, U+E, LFTs, INR, glucose
    • LIVER SCREEN!
  • Ascitic tap: chemistry, cytology, MC+S, SAAG
    • PMN >250mm3 indicates SBP
  • US + PV duplex
    • Liver size and texture
    • Focal lesions
    • Ascites
    • Portal vein flow
  • Other:
    • liver biopsy
    • MRCP: PSC
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6
Q

CLD

Liver screen

(7-think ‘cause’)

A
  1. EtOH: MCV, GGT, AST:ALT >2
  2. Viral: Hep B and C serology
  3. NASH: lipids
  4. AutoAbs: SMA, AMA, pANCA, ANA
  5. Ig: ↑IgG – AIH, ↑IgM – PBC
  6. Genetic: caeruloplasmin, Ferritin, α1-AT
  7. Ca: AFP, Ca 19-9
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7
Q

Treatment of CLD

General/specific (to cause)

A

General

  • MDT: GP, hepatologist, dietician, palliative care, family
  • EtOH abstinence
  • Good nutrition
  • Cholestyramine for pruritus
  • Screening: liver screen
  • HCC: US + AFP
  • Varices: OGD (propranolol+banding, acute UGI bleed: terlipressin)

Specific

  • HCV: protease (-) + ribavarin
  • PBC: ursodeoxycholic acid
  • Wilson’s: penicillamine
  • HH: venesection, desferrioxamine
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8
Q

Complications of CLD

(7)

A
  1. Varices: β-B, banding
  2. Ascites: fluid and salt restrict, spiro, fruse, tap, daily wt
  3. Coagulopathy: Vit K, FFP, platelets
  4. Encephalopathy: avoid sedatives, lactulose, rifaximin
  5. Sepsis / SBP: tazocin or cefotaxime
    • Avoid gent: nephrotoxicity
  6. Hypoglycaemia: dextrose
  7. Hepatorenal syndrome: IV albumin + terlipressin
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9
Q

Causes of CLD

(common-3/other-5)

A

Common

  1. Chronic EtOH
  2. Chronic HCV (and HBV)
  3. NAFLD / NASH

Other

  1. Congenital: HH, Wilson’s, α1ATD, CF
  2. AI: AH, PBC, PSC
  3. Drugs: Methotrexate, amiodarone, isoniazid
  4. Neoplasm: HCC, mets
  5. Vasc: Budd-Chiari, RHF, constrict. pericarditis
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10
Q

4 important complications of CLD

A
  1. Liver failure / decompensation
  2. SBP
  3. Portal HTN: SAVE (splenomegaly/ascites/varices/encephalopathy)
  4. HCC
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11
Q

Child-Pugh Grading of cirrhosis

A

Evaluates prognosis in Cirrhosis
Graded A-C using severity of 5 factors

  1. Albumin
  2. Bilirubin
  3. Clotting
  4. Distension: ascites
  5. Encephalopathy

A.5-6 = [0] 1 yr Mortality

B.7-9 = [20] 1 yr Mortality

C.10-15 = [50] 1 yr Mortality

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12
Q

CLD Decompensation precipitants

(HEPATICS)

A
  • Haemorrhage: e.g. varices
  • Electrolytes: ↓K, ↓Na
  • Poisons: diuretics, sedatives, anaesthetics
  • Alcohol
  • Tumour: HCC
  • Infection: SBP, pneumonia, UTI, HDV
  • Constipation (commonest cause)
  • Sugar (glucose) ↓: e.g. low calorie diet
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13
Q

General Management of CLD decompensation

(5)

A
  • HDU or ITU
  • Rx any precipitant
  • Good nutrition: e.g. via NGT c¯ high carbs
  • Thiamine supplements
  • Prophylactic PPIs vs. stress ulcers
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14
Q

Important monitoring in CLD decompensation

(3)

A
  • Fluids: urinary and central venous catheters
  • Bloods: daily FBC, U+E, LFT, INR
  • Glucose: 1-4hrly + 10% dextrose IV 1L/12h
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15
Q

Management of (6) Complications of decompensated CLD

A
  • Ascites: daily wt, fluid and Na restrict, diuretics, tap
  • Coagulopathy: Vit K, FFP, platelets
  • Encephalopathy: avoid sedatives, lactulose, rifaximin
  • Sepsis / SBP: tazocin or cefotaxime
  • Hypoglycaemia: dextrose
  • Hepatorenal syndrome: IV albumin + terlipressin
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16
Q

PAthophysiology of encephalopathy (CLD)

A

↓ hepatic metabolic function -> Diversion of toxins from liver directly into systemic system. -> Ammonia accumulates and pass to brain where
astrocytes clear it causing glutamate → glutamine -> ↑ glutamine → osmotic imbalance → cerebral oedema

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17
Q

Presentation of encephalopathy

(5)

A
  • Asterixis, Ataxia
  • Confusion
  • Dysarthria
  • Constructional apraxia
  • Seizures
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18
Q

Single key invesigation in encephalopathy (CLD)

A

Plasma NH4 (raised!)

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19
Q

Teatement of encephalopathy

A
  • Nurse in well lit, calm environment
  • Correct any precipitants
  • Avoid sedatives
  • Lactulose
    • ↓ nitrogen-forming bowel bacteria
    • 2-4 soft stools/d
  • Rifaximin PO: kill intestinal microflora
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20
Q

Hepatorenal syndrome

pathophysiology

(and classification)

A

Renal failure in pts. c¯ advanced CLF

Pathophysiology: “Underfill theory”
Cirrhosis → splanchnic arterial vasodilatation → effective
circulatory volume → RAS activation → renal arterial
vasoconstriction. Persistent underfilling of renal circulation → failure

  • *Type 1:** rapidly progressive deterioration (survival <2wks)
  • *Type 2**: steady deterioration (survival ~6mo)
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21
Q

Treatment of hepatorenal syndrome

A
  1. IV albumin + terlipressin
  2. Haemodialysis as supportive Rx
  3. Liver Tx is Rx of choice
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22
Q

SBP

Presenation

A

Pt. c¯ ascites and peritonitic abdomen
Complicated by hepatorenal syn. in 30%

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23
Q

SBP: Common organisms

A

Common organisms: E. coli, Klebsiella, Streps

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24
Q

SBP: 1 key investigation

A

ascites PMN >250mm3 + MC+S

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25
Q

SBP management

A

taxocin

or

cefuroxime

until sensitivities known

prophylaxis: high recurrence therefore long term cipro given

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26
Q

Poor prognosis in CLD (4 factors)

A

Worsening encephalopathy
↑ age
↓ albumin
↑ INR

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27
Q

Ascites

examination

inspection: cause

abdo

completion

sig negatives

A
  • Peripheral inspection: Cause
    • Signs of CLD
    • CCF: ↑ JVP, bibasal creps, peripheral oedema
    • Nephrotic: periorbital oedema
    • Budd Chiari: abdo pain, hepatomegaly, jaundice
  • Abdomen
    • Shifting dullness
    • Portal HTN: splenomegaly
  • Completion
    • CVS and Resp for CCF
    • Urine dip: proteinuria in nephrotic syndrome
  • Significant Negatives
    • CLD
    • Acute liver failure / decompensation
    • Cause: ↑ JVP, periorbital oedema
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28
Q

Causes of ascites

3: common

‘SAAG’

A

Commonest

  1. Cirrhosis
  2. CCF
  3. Carcinomatosis

Serum Ascites Albumin Gradient (SAAG) = Se albumin – Ascites Albumin

SAAG ≥1.1g/dL = Portal HTN (97% accuracy) (transudate)

  • Cirrhosis in 80%

SAAG <1.1g/dL (exudate)

  • Neoplasia: e.g. peritoneal mets or ovarian Ca
  • Inflammation: pancreatitis
  • Nephrotic syndrome
  • Infection: TB peritonitis
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29
Q

Portal HTN Causes

pre/hep/post

A

Portal pressure >10mmHg (norm 5-10): 80% cirrhosis in UK

Pre-hepatic

  • Portal vein thrombosis
    • PV, ET (polycythemia vera (PV), essential thrombocythemia (ET))
    • PNH
    • Nephrotic syndrome

Hepatic

  • Cirrhosis

Post-hepatic

  • Cardiac: RHF, TR, constrictive pericarditis
  • Budd-Chiari (hepatic vein thrombosis)
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30
Q

History Qs in ascites

A
  • SBP: fever, abdo pain
  • Cause
    • Liver disease
    • Cardiac failure, MI
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31
Q

Key investigations in ascites

Bedside/bloods/special/imaging

A

Bedside

  • Urine: dip ± MC+S
    • Exclude nephrotic syn.
    • ? UTI

Bloods

  • FBC
  • U+E
  • LFTs: esp. albumin
  • INR
  • Glucose
  • Liver screen

Ascitic tap

  • Chemistry
  • Cytology: malignancy, PMN (>250/mm3 = SBP)
  • Bacteriology: MC+S, Ziehl-Neelson Stain
  • SAAG

US + PV duplex

  • Liver size and texture
  • Focal lesions
  • Ascites
  • Portal vein flow
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32
Q

Treatment of ascites

(general/diurectic/therapeutic paracentesis)

A

General

  • EtOH abstinence
  • Daily wts: aim for ≤0.5kg/d reduction
  • Fluid restrict: <1.5L/d
  • Low Na diet: 40-100mmol/d

Diuretics

  • Spironolactone
  • Add frusemide if response poor

Therapeutic Paracentesis

  • Temporary insertion of pig-tail drain or Bonnano catheter
  • Indications
  • Respiratory compromise
  • Pain / discomfort
  • Renal impairment
  • Risks
  • Severe hypovolaemia: replenish albumin
  • SBP
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33
Q

Treatment of refractory ascites

A

TIPSS

Transplant

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34
Q

Treatment/prophylaxis of SBP

A
  • *Rx**: Tazocin or cefotaxime until sensitivities known
  • *Prophylaxis**: high recurrence -> cipro long-term
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35
Q

Medical jaundice

  • examination (cause)*
  • Abdo*
  • completetion*
  • sig negatives*
A

Cause

  • CLD
  • Pancreatic Ca: cachexia, Virchow’s node
  • Haemolysis: pallor

Abdomen

  • Excoriations and pruritus
  • Splenomegaly
  • Hepatomegaly
  • Palpable gallbladder: Ca head of pancreas

Completion

  • Urine dip: look for BR, urobilinogen and Hb

Significant Negatives

  • Acute liver failure / decompensation
  • CLD
  • Organomegaly
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36
Q

Differential for medical jaundic

(CLD/splenomeg/hepatomeg/none)

A
  • CLD: EtOH, viral, NAFLD
  • Splenomegaly
    • Haemolysis
    • CLD ( → portal HTN)
    • Viral hepatitis: e.g. EBV
  • Hepatomegaly
    • Hepatitis
    • CLD
  • No CLD or organomegaly
    • Biliary obstruction
    • Haemolysis
    • Drugs: fluclox, OCP
    • Gilberts
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37
Q

Liver transplant

Examination: peripheal general/immunosupp

abdo

sig negatives

A

Peripheral Inspection

  • General
    • Evidence of CLD
    • Pigmentation: HH
    • Tattoos and needle marks: Hep B/C
  • Immunosuppressant Stigmata
    • Cushingoid
    • Skin tumours: AKs, SCC (100x ↑ risk), BCC and MM
    • Gingival hypertrophy: ciclosporin

Abdomen

  • Mercedes-Benz scar

Significant Negatives

  • Evidence of CLD or cause for Tx
  • Evidence of immunosuppression
  • Absence of features of liver failure = working Tx

Differential for Mercedes Benz Scar

  • Hepatobiliary surgery
    • Liver transplant
    • Segmental resection
    • Whipples’: pancreaticoduodenectomy
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38
Q

History for liver transplant patient

causes/Tx/current/DHx

A
  • Cause
    • EtOH
    • Sexual Hx, IVDU, transfusions
    • FH
    • Other AI disease: e.g. DM, thyroid
    • DH
  • Transplant
    • adaveric or live segmental
    • Any complications
  • Current health
    • Acute rejection: fever, graft pain
    • Immunosuppression
      • Infection: e.g. CMV pneumonitis
      • Skin Ca
  • DH
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39
Q

Investigations for liver tranplant

bloods/other

A

Bloods

  • FBC: infection
  • U+E: ciclosporin can → renal impairment
  • LFTs: assess graft function
  • Clotting
  • Fasting glucose: tacrolimus and steroids → DM
  • Drug levels: ciclosporin, tacrolimus

Other

  • Liver biopsy: if rejection suspected
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40
Q

Top causes for liver tranplatnt (3)

A
  • Cirrhosis
  • Acute liver failure
    • Hep A, B
    • Paracetamol overdose
  • Malignancy
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41
Q

Success of liver transplant

A

80% 1 year survival

70% 5 year survival

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42
Q

Liver transplant immunosuppression regime

A

Tacrolimus/ciclosporin

azathioprine

prednisolone (+/- withrawal @3mo)

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43
Q

Hepatomegaly

  • Examination:*
  • peripheral: causes*
  • abdo*
  • completion*
  • sig negatives*
A
  • *Peripheral Inspection**
  • Cause*
  • CLD
  • EtOH: palmar erythema, Dupuytren’s
  • HH: skin discolouration
  • Ca: cachexia
  • CCF: ↑ JVP, bibasal creps, ascites, peripheral oedema
  • Haematological: pallor, bruising, purpura, LNs

Abdomen

  • Hepatomegaly
    • Define fingerbreadths below costal margin at which liver edge palpable.
      • Moves inferiorly on inspiration
      • Can’t get above it
      • Dull PN
    • Features to note
      • Edge: smooth, craggy, nodular
      • Tenderness
      • Pulsatile
    • Percuss above and below to confirm enlargement
    • Auscultate for liver bruit
    • HCC
  • Other
    • Splenomegaly
    • Inguinal nodes
    • Ascites

Completion

  • CVS and Resp: CCF

Significant Negatives

  • Splenomegaly
  • Acute liver failure / decompensation
  • Cause: CLD, ↑JVP, pallor, bruising, LNs
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44
Q

Hepatomegalu

common causes (3)

Other causes (MACHO)

A

Common Causes

  • Hepatitis: EtOH, viral, NAFLD
  • CLD
  • Congestion 2O to cardiac failure

Other Causes: MACHO

  • Malignancy: 2O
  • Anatomical: Riedel’s lobe, hyperexpanded chest
  • Congestion: TR, Budd Chiari
  • Haem: leukaemia, lymphoma, myeloproliferative, SCD
  • Other: sarcoidosis, amyloidosis, Gaucher’s, ADPKD
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45
Q

Key history Qs

Hepatomegaly (3)

A
  • Hepatitis / CLD: EtOH, viral exposure, FH
  • Cardiac: dyspnoea, PND, previous MI, rheumatic fever
  • Haem: tiredness, bruising, infections, bone pain
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46
Q

Hepatomegaly investigations

bedide/bloods/imaging/histology

A

Urine dip

  • BR, urobilinogen
  • Proteinuria: amyloid

Bloods

  • FBC
  • ↓Hb: malignancy, chronic disease
  • Lymphocytosis: hepatitis viruses, EBV (atypical)
  • U+E: CCF → renal impairment
  • LFT
  • Clotting
  • Liver screen

Imaging

  • Abdo US + PV and hepatic duplex
    • Liver size and texture
    • Focal lesions
    • Ascites
    • Portal vein flow
    • Hepatic veins: thrombosis
  • CT: e.g. for tumour
  • MRI: good quality images of liver parenchyma

Liver Biopsy

  • Check clotting first
  • Nodular Pattern
    • Micronodular: EtOH, HH, Wilson’s
    • Macronodular: viral
  • Iron: Pearl’s stain
  • Copper: Rhodamine stain
  • α1ATD: PAS stain (α1AT globules accumulate in liver)
  • Amyloid: apple-green birefringence c¯ Congo Red
  • Granulomata: PBC
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47
Q

Causes of hepatomegaly

(6)

A
  • EtOH: abstinence + support
  • Viral: supportive or anti-viral therapy
  • HH: venesection ± desferrioxamine
  • Wilson’s: penicillamine
  • CCF: ACEi, β-B and diuretics
  • Haematological: monitoring or chemo
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48
Q

Splenomegaly

Examination

Peripheral: cause

abdo:inspect/palpate

completion

sig negatives

A

Peripheral Inspection: Cause

  • Haematological: pallor, bruising, purpura, LNs, cachexia
    • Cervical, axilla, inguinal
  • Portal HTN: CLD signs
  • IE: splinter’s, clubbing
  • Felty’s Syndrome: rheumatoid hands
  • *Abdomen**
  • Inspection*:Asymmetry
  • Palpation*
  • Splenomegaly
    • Can’t get above it
    • Moves inferiorly toward RIF on respiration
    • Notch
    • Dull PN
    • Not ballotable
  • Size: big or small?
  • Hepatomegaly?
  • Inguinal nodes?

Completion

  • Cardio and Resp exam: IE and sarcoid
  • Urine dip: haematuria (IE), proteinuria (amyloid)

Significant Negatives

  • Hepatomegaly
  • Haem: pallor, bruising, LNs
  • CLD
  • IE: splinters, clubbing
  • RA hands: Felty’s Syndrome
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49
Q

(isolated) Big spleen: limitted differential (4 categorieS)

A
  • Myeloproliferative: CML, MF
  • Lymphoproliferative: CLL, lymphoma
  • Infiltrative: amyloidosis, Gaucher’s
  • Developing world: malaria, visceral leishmaniasis
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50
Q

Small spleen (common/other)

A

Common

  • Haem: myelo- / lympho-prolif disorders, haemolysis
  • Portal HTN: mostly 2O to cirrhosis
  • Infection: EBV

Other

  • Infection: herpes viruses, hepatitis virus, IE, malaria
  • Inflammation: RA, SLE, Sjogren’s
  • Rare: sarcoidosis, amyloidosis, Gaucher’s, CVID
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51
Q

Hepatosplenomegaly:

A

same differentials as isolated splenomegaly (except inflammatory)

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52
Q

causes of MASSIVE splenomegaly

A

Causes of Massive Splenomegaly: >20cm

  • CML
  • Myelofibrosis
  • Malaria
  • LeishManiasis
  • Gaucher’s (AR, glucocerebrosidase deficiency)
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53
Q

History Qs in splenomegaly (4)

A
  • Haem: tiredness, bruising, infections, bone pain
  • CLD: EtOH, viral exposure, FH
  • Infections: fever, sore throat, jaundice, foreign travel
  • Inflammation: arthritis
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54
Q

Haematological Ix in splenomegaly

splenomegaly= haematological + infective + liver Ix

A
  • FBC
    • CML: ↑↑↑WBC – PMN, basophils, myelocytes
    • MF: pancytopenia
    • CLL: lymphocytosis
    • Haemolysis: ↓ Hb, ↑MCV, ↑RDW
  • Film
    • MF: leukoerythroblastic c¯ teardrop poikiolcytes
    • CLL: smear cells
    • Haemolysis: spherocytes, reticulocytosis
  • Other Bloods
    • DAT
    • U+E and urate: ↑ malignancy → uropathy
  • Imaging
    • Abdo US
    • CT chest and abdomen
    • PET scan
  • Histology / Cytology
    • LN biopsy
    • BM aspirate or trephine biopsy (MF)
  • Genetic Analysis
    • CML: Ph Chr, t(9:22)
    • MF: Jak2+ in 50%
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55
Q

Infective Ix in splenomegaly

splenomegaly= haematological + infective + liver Ix

A
  • Urine Dip
    • Haematuria: IE
  • Bloods
    • FBC: lymphocytosis (may be atypical in EBV)
    • U+E: renal impairment in IE
    • Thick and thin films
  • Imaging
    • Abdo US
    • Echo: IE
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56
Q

Liver Ix in splenomegaly

splenomegaly= haematological + infective + liver Ix

A
  • Bloods
    • FBC
    • LFT
    • Clotting
    • Liver screen
  • Imaging
    • Abdo US + PV duplex
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57
Q

Myloproliferative Disorders

CML

  • symptoms*
  • genetics*
A

CML
Clonal proliferation of myeloid cells
15% of leukaemia

Symptoms

  • Hypermetabolism: wt. loss, fever, night sweats, lethargy
  • Massive HSM → abdo discomfort
  • Bruising / bleeding (platelet dysfunction)
  • Gout
  • Hyperviscosity

Philadelphia Chromosome

  • Reciprocal translocation: t(9;22)
  • Formation of BCR-ABL fusion gene
    • Constitutive tyrosine kinase activity
  • Present in >80% of CML
  • Discovered by Nowell and Hungerford in 1960
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58
Q

CML

Investigations

A
  • ↑↑WBC
    • PMN and basophils
    • Myelocytes
  • ± ↓Hb and ↓plat (accelerated or blast phase)
  • ↑urate
  • BM cytogenetic analysis: Ph+ve
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59
Q

CML

management

A
  • Imatinib: tyrosine kinase inhibitor
    • → >90% haematological response
    • 80% 5ys
  • Allogeneic SCT
    • Indicated if blast crisis or TK-refractory
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60
Q

Primary myelofibrosis

symptoms (/presentation)

A

Clonal proliferation of megakaryocytes → ↑ PDGF →Myelofibrosis
Extramedullary haematopoiesis: liver and spleen

Symptoms

  • Elderly
  • Massive HSM
  • Hypermetabolism: wt. loss, fever, night sweats
  • BM failure: anaemia, infections, bleeding
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61
Q

Investigations of myelofibrosis

A
  • Film: leukoerythroblastic c¯ teardrop poikilocytes
  • Cytopenias
  • BM: dry tap (need trephine biopsy)
  • 50% JAK2+ve
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62
Q

Treatment of primary myelofibrosis

A
  • Supportive: blood products
  • Splenectomy
  • Allogeneic BMT may be curative in younger pts.
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63
Q

Prognosis of myelofibrosis

A

5 yr median survival

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64
Q

Anatomy of the spleen

A

Intraperitoneal structure lying in the LUQ
Measures 1x3x5 inches
Weighs ~7oz
Lies anterior to ribs 9-11

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65
Q

Function of spleen

A

Function: part of the mononuclear phagocytic system

  • Phagocytosis of old RBCs, WBCs
  • Phagocytosis of opsonised bugs: esp. encapsulates
  • Antibody production
  • Sequestration of formed blood elements
    • Platelets, lymphocytes and monocytes
  • Haematopoiesis
66
Q

What is hypersplenism

A
  • Pancytopenia due to pooling and destruction w/i an enlarged spleen.
  • Anaemia, bruising, infections
  • Sequestration crisis in SCD → hypovolaemic shock
67
Q

causes of hyposplenism (4)

A
  1. splenectomy
  2. coeliac disease
  3. IBD
  4. SCD
68
Q

Four findings on a bloodfilm indicative of hyposplenism

A
  1. ↑ platelets transiently after splenectomy
  2. Howell-Jolly bodies
  3. Pappenheimer bodies
  4. Target cells
69
Q

Management of hyposplenism (3)

A
  1. Immunisations:
    • Pneumovax
    • HiB
    • Men C
    • Yrly flu
  2. Daily Abx: Pen V or erythromycin
  3. Warning: Alert Card and/or Bracelet
70
Q

Indications for splenectomy (6)

A
  • Trauma
  • Rupture: e.g. 2ndary to EBV
  • AIHA
  • ITP
  • HS
  • Hypersplenism
71
Q

Complications of splenectomy

A
  • Redistributive thrombocytosis → early VTE
    • Temporary post-op aspirin prophylaxis
  • Gastric dilatation: transient ileus
    • May disturb gastro-omental vessel ligatures
    • Prophylactic NGT post-op
  • Left lower lobe atelectasis
  • Pancreatitis: tail shares blood supply c¯ spleen
  • ↑ susceptibility to infections
    • Encapsulates: haemophilus, pneumo, meningo
72
Q

Enlarged kidneys

Examination findings

  • peripheral: renal impariment/replacement/immsupp*
  • Abdo: inspect, palpate, ausc*
  • completion*
  • sig negatives*
A

Peripheral Inspection

  • Renal Impairment
    • HTN
    • Pallor
  • Renal Replacement Therapy
    • AV fistula (or scar)
    • Tunnelled dialysis lines (or scar)
    • Tenchkhoff catheter (or scar)
  • Immunosuppressant Stigmata
    • Cushingoid
    • Skin tumours: AKs, SCC, BCC and MM
    • Gingival hypertrophy: ciclosporin

Abdomen

  • Inspection
    • Nephrectomy scar
    • Rutherford Morrison scar
    • Tenchkhoff catheter (or scar)
  • Palpation
    • Palpable Kidney
      • Flank mass
      • Can get above it
      • Ballotable
      • Moves inferiorly c¯ respiration
      • Resonant PN
    • Hepatomegaly
    • Renal Transplant
  • Auscultation
    • Renal bruit

Completion

  • External genitalia: hydrocele 2O to RCC
  • Urine dip: proteinuria, haematuria
  • CVS: mitral valve prolapse

Significant Negatives

  • Unilateral enlargement
  • Hepatomegaly
  • Evidence of RRT or immunosuppression
73
Q

Enlarged kidneys differential

(bilateral, 4 + unilateral, 4)

A

Bilateral

  • ADPKD
  • Bilateral RCC (5%)
  • Bilateral cysts: e.g. in VHL
  • Amyloidosis

Unilateral

  • Simple renal cyst
  • RCC
  • Compensatory hypertrophy
    • contralateral nephrectomy: ADPKD
74
Q

History Qs in enlarged kidneys (3 key)

A
  • ADPKD: FH, loin pain, haematuria, headaches
  • RCC: haematuria, loin pain
  • Compensatory hypertrophy: previous infections, stones
75
Q

Key investigations in enlarged kidneys

bedside/bloods/imaging/other

A

Urine

  • Dip: haematuria, proteinuria
  • Cytology

Bloods

  • FBC: ↓Hb 2ndary to ESRF
  • U+E: ↓eGFR, electrolyte disturbance
  • Bone profile: ↓Ca, ↑ PO4, ↑PTH

Imaging

  • Abdo US
    • Confirm renal enlargement
      • Cysts
      • Hydronephrosis
      • Masses
    • Liver enlargement
  • CT/MRI
    • MRA: Berry aneurysms
    • CT abdo: esp. if RCC suspected

Other

  • Genetic studies to look for mutation in
    • PKD1 gene on Chr 16: 85%
    • PKD2 gene on Chr 4: 15%
  • Family screen
76
Q

Management of ADPKD

  • general*
  • medical*
  • surgical*
A

General

  • ↑ water intake, ↓ Na, ↓ caffeine (may ↓ cyst formation)
  • Monitor U+E and BP
  • Genetic counselling
    • 50% chance of transmission
    • 10% are de novo mutations
  • MRA screen for Berry aneurysms

Medical

  • Rx HTN aggressively: <130/80 (ACEi best)
  • Rx infections

Surgical: Nephrectomy

  • Recurrent bleeds or infections
  • Abdominal discomfort
77
Q

ADPKD progression…

A

ESRF in 70% by 70yrs
Mx complications: CRF HEALS
Dialysis or transplant

78
Q

ADPKD

Epidemiology

A
  • Prev: 1:1000
  • 5% of ESRF in UK
  • Genetics
    • PKD1 gene on Chr 16: 85%
    • PKD2 gene on Chr 4: 15%
    • Involve cell-cell interactions
79
Q

Presentation of ADPKD

A
  • Age: 30-50s
  • HTN
  • Recurrent UTIs
  • Loin pain: cyst haemorrhage or infection
  • Haematuria
80
Q

Extra-renal involvement of ADPKD (3)

A
  • Hepatic cysts → hepatomegaly
  • Intracranial Berry aneurysms → SAH
  • MV Prolapse: mid-systolic click + late systolic murmur
81
Q

ARPKD epidemiology

prev/genetics

A
  • *Prev**: 1:40000
  • *Genetics**: PKHD1 (fibrocystin) gene on Chr6
82
Q

Presentation of ARPKD (4)

(and extra-renal involvement 1)

A
  • Perinatal
  • Oligohydramnios: may → Potter sequence
    • Clubbed feet, pulm. hypoplasia, cranial abnormalities
  • Bilateral abdominal masses
  • HTN and CRF

Extra-renal involvement: comgenital hepatic fibrosis-> portal HTN

83
Q

Prognosis of ARPKS

A

ESRF by 20yrs!

NEED transplant

84
Q

Simple renal cyst

A
  • Common: 1/3 of pts over 60yrs
  • May present as renal mass and haematuria
  • Contain fluid only: no solid elements
  • Main differential is RCC
85
Q

Dialysis associated with renal cysts

A
  • Seen after prolonged dialysis
  • 2O to obstruction of renal tubules by oxalate crystals
  • ↑ risk of RCC in cyst: 15% of pts on haemodialysis
86
Q

Tuberous Sclerosis (Bourneville’s disease) (3)

A

AD condition c¯ hamartomas in skin, brain, eye, kidney

  • *Skin**: nasolabial adenoma sebaceum, ash-leaf macules, peri-ungual fibromas
  • *Neuro**: ↓IQ, epilepsy, astrocytoma
  • *Renal**: cysts, angiomyolipomas
87
Q

RCC epidemiology (%/age/sex)

A
  • *90**% of renal cancers
  • *Age**: 55yrs
  • *Sex**: M>F=2:1
88
Q

RF for RCC (5)

A
  • Smoking
  • Obesity
  • HTN
  • Dialysis: 15% of pts. develop RCC
  • 4% heritable: e.g. VHL syndrome
89
Q

Pathophysiology of RCC

A 
*Adenocarcinoma from proximal renal tubular epithelium
Clear Cell (glycogen) subtype: 70-80%*
90
Q

Presentation of RCC

A

50% incidental finding
Triad: Haematuria, loin pain, loin mass
Invasion of L renal vein → varicocele (1%)
Cannonball mets → SOB

91
Q

Paraneoplastic features of RCC (5)

A

EPO → polycythaemia

PTHrP → ↑ Ca

Renin → HTN

ACTH → Cushing’s syn.

Amyloidosis

92
Q

Spread of RCC

A
  • Direct: renal vein
  • Lymph
  • Haematogenous: bone, liver and lung
93
Q

Investigations of RCC

(blood/urine/imaging)

A
  • Blood: polycythaemia, ESR, U+E, ALP, Ca
  • Urine: dip, cytology
  • Imaging
    • CXR: cannonball mets
    • US: mass
    • IVU: filling defect
    • CT/MRI
94
Q

Management of RCC

Med/surg +prognosis

A

Medical

  • Reserved for pts. c¯ poor prognosis
  • Temsirolimus (mTOR inhibitor)

Surgical

  • Radical nephrectomy
  • Consider partial if small tumour or 1 kidney

Prognosis: 45% 5ys

95
Q

Von Hippel-Lindau

A
  • Autosomal Dominant
  • Renal and pancreatic cysts
  • Bilateral renal cell carcinoma
  • Haemangioblastomas (Often in cerebellum → cerebellar signs)
  • Phaeochromocytoma
  • Islet cell tumours
96
Q

Renal tranplant

Examination

  • Peripheral inspection: renal imp/replacement/immsupp/cause*
  • abdo:insp/palp/ausc*
  • completion*
  • sig negative*
A

Peripheral Inspection

  • Renal Impairment
    • HTN
    • Pallor
  • Renal Replacement Therapy
    • AV fistula (or scar)
    • Tunnelled dialysis scars
    • Tenchkhoff catheter scars
  • Immunosuppressant Stigmata
    • Cushingoid
    • Skin tumours: AKs, SCC (100x ↑ risk), BCC and MM
    • Gingival hypertrophy: ciclosporin
  • Cause
    • DM
      • Finger pricks from BM monitoring
      • Insulin marks on abdomen, lipodystrophy
    • Cystic Kidney Disease
      • Nephrectomy scars or ballotable kidneys
    • Connective Tissue Disease
      • SLE, SS, RA

Abdomen

  • Inspect
    • Rutherford Morrison Scar in RIF
    • Nephrectomy scars
    • Tenchkoff catheter scars
  • Palpate
    • Smooth oval mass under scar
    • Dull PN
    • Can get below it
    • Doesn’t move with respiration
  • Auscultate
    • Renal bruit over transplant

Completion

  • Dipstick: haematuria and proteinuria
  • Drug chart: any potentially nephrotoxic drug (e.g. ACEi)
  • BP: HTN common post-Tx

Significant Negatives

  • Evidence of immunosuppression

Signs of a cause: DM and PKD
Working Tx
Renal replacement therapy not in use
No pain over Tx site

97
Q

Gum hypertrophy differential

(5)

A
  • Drugs: ciclosporin, phenytoin, nifedipine
  • Familial
  • AML
  • Scurvy
  • Pregnancy
98
Q

History Qs in Renal Transplant

A
  • Cause
    • DM
    • GN
  • Transplant
    • Cadaveric or live
    • any complications: e.g. urinary leaks, infection
  • Current health
    • Acute rejection: fever, graft pain
    • Graft function: Cr levels, BP, urine output
    • Immunosuppression
      • Infection: e.g. CMV pneumonitis
      • Skin Ca
    • CV risk
  • DHx
99
Q

Renal transplant

Investigations

Urine/blood/other

A

Urine

  • Dip: haematuria, proteinuria
  • MC+S

Bloods

  • FBC: infection
  • U+E: eGFR – look @ trend
  • LFTs: ciclosporin can → hepatic dysfunction
  • Fasting glucose: tacrolimus is diabetogenic
  • Drug levels: ciclosporin, tacrolimus

Other

  • Renal biopsy: if rejection suspected
100
Q

Commonest indications for renal transplant

(4)

A
  • Diabetic nephropathy
  • GN
  • Polycystic Kidney Disease
  • Hypertensive nephropathy
101
Q

Assessment of Renal Transplant

(pre-transplant)

A
  • Virology: CMV, HIV, VZV, hepatitis
  • Co-morbidities: esp. CVD
  • ABO
  • anti-HLA Abs: may be acquired from blood transfusion
  • Haplotype
    • Importance: HLA-DR > HLA-B > HLA-A
    • 2 alleles @ each locus → 6 possible mismatches
    • ↓ mismatches → ↑ graft survival
  • Pre-implantation cross-match
    • Recipient serum vs. donor lymphocytes
102
Q

Contraindications to renal transplant

A
  • Active infection
  • Cancer
  • Severe co-morbidity
  • Failed pre-implantation x-match
103
Q

Types of renal transplant grafts (4)

A
  1. Cadaveric: brainstem death c¯ CV support
  2. Non-heart beating donor: no active circulation
  3. Live-related
    • Optimal surgical timing
    • HLA-matched
    • Improved graft survival
  4. Live unrelated
104
Q

Immunosuppression in renal transplant

(pre/post-op)

A
  • *Pre-op**: campath / alemtuzumab (anti-_CD52_)
  • *Post-op:**
  • Short-term: prednisolone
  • Long-term: tacrolimus or ciclosporin
105
Q

Prognosis for renal trasplant grafts

Cadaveris vs HLA identical live

A

15yrs vs >20yrs

106
Q

Complications

(post-op, 4/rejections, hyperacute/acute/chronic)

A

Post-op

  • Bleeding
  • Graft thrombosis
  • Infection
  • Urinary leaks
  • *Rejection**
  • *Hyperacute** rejection: minutes
  • Path: ABO incompatibility
  • Presentation: thrombosis and SIRS

Acute Rejection: <6mo

  • Path: Cell-mediated response
  • Presentation
    • Fever and graft pain
    • ↓ urine output
    • ↑ Cr
  • Rx: Responsive to immunosuppression

Chronic Rejection: >6mo

  • Presentation: Gradual ↑ in Cr and proteinuria
  • Path: Interstitial fibrosis + tubular atrophy
  • Rx: supportive, not responsive to immunosuppression
107
Q

Drug toxicity in renal transplant

Ciclosporin/tacrolimus/steroids

A

Ciclosporin: calcineurin inhibitor (blocks IL2 production)

  • Nephrotoxic: may contribute to chronic rejection
  • Gingival hypertrophy
  • Hypertrichosis
  • Hepatic dysfunction

Tacrolimus: calcineurin inhibitor (blocks IL2 production)

  • < nephrotoxicity cf. ciclosporin
  • Diabetogenic
  • Cardiomyopathy
  • Neurotoxicity: e.g. peripheral neuropathy

Steroids → Cushing’s Syndrome

and of course immunosuppression…

108
Q

SE of immunosuppression in renal transplant patients

A

↑ risk of infection: CMV, PCP, fungi, warts
↑ risk of malignancy

  • Skin: SCC, BCC, MM, Kaposi’s
  • Post-Tx lymphoproliferative disease (2O EBV)
109
Q

CVD in Renal patients

A

Hypertension
Atheromatous vascular disease
A leading cause of death

110
Q

Indications for renal replacement therapy (3)

A
  • Suggested to start when GFR<15ml/min + symptoms
  • Psychological preparation necessary
  • PD vs. HD depends on med, social and psych factors
111
Q

General dialysis complications

A
  • 20% annual mortality
  • Cardiovascular disease
  • Malnutrition
  • Infection
    • uraemia → granulocyte dysfunction → ↑ sepsisrelated mortality
  • Amyloidosis
    • β2-microglobulin accumulation
    • Carpal tunnel, arthralgia
  • Renal cysts → RCC
112
Q

Haemodyalysis

counter-current flow/ultrafiltration

A

Counter-current flow

  • Blood flows on one side of semipermeable membrane
  • Dialysate flows in the opposite direction on the other side.
  • Solute transfer by diffusion

Ultrafiltration: Fluid removal by creation of –ve transmembrane pressure by decreasing the hydrostatic pressure of the dialysate.

113
Q

Complications of Haemodialysis

A
  • Disequilibration syndrome (usually only 1st dialysis)
    • Rapid changes in plasma osmolarity → cerebral oedema
    • n/v, headache and ↓GCS
  • Fluid balance: BP↓, pulmonary oedema
  • Electrolyte imbalance
  • Aluminium toxicity (in dialysate) → dementia
  • Psychological factors
114
Q

Haemofiltration

(where is it used?)

A

Usually only used in ITU
Takes longer cf. HD but there is less haemodynamic
instability.

115
Q

Mechanism of haemofiltration

A
  • Use a Vas Cath
  • Blood filtered across a highly permeable membrane by hydrostatic pressure and water and solutes are removed by convection.
  • Ultrafiltrate is replaced by isotonic replacement.
116
Q

Mechanism of peritoneal dialysis

A
  • Dialysate introduced into peritoneal cavity by Tenchkhoff catheter.
  • Uraemic solutes diffuse into fluid across peritoneum
  • Ultrafiltration: addition of osmotic agent (e.g. glucose)
  • ~3L 4x /day c¯ ~4h dwell times
117
Q

Types of peritoneal dialysis (2)

A

Continuous Ambulatory Peritoneal Dialysis CAPD: fluid exchange during day c¯ long dwell @ night
Assisted Peritoneal Dialysis​ APD: fluid exchanged during night by machine c¯ long dwell throughout day.

118
Q
A
119
Q

Adbantages (3) and disadvantages (3) of peritoneal dialysis

A

Advantages

  • Simple to perform
  • Requires less equipment-> Easier @ home or on holiday
  • Less haemodynamic instability -> useful if cardio disease

Disadvantages

  • Inconvenience
  • Body image
  • Anorexia
120
Q

Complications of peritoneal dialysis

A
  • Peritonitis
  • Exit site infection
  • Catheter malfunction
  • Obesity (glucose in dialysate)
  • Mechanical: hernias and back pain
121
Q

AV fistula examination

(inspection/palpation/austultation/sig negatives)

A

Inspection

  • Swelling c¯ surgical scar over distal forearm or @ elbow
  • Evidence of use: needle marks
  • Evidence of infection

Palpation

  • Check if painful
  • Temperature
  • Palpable thrill

Auscultate

  • Audible bruit

Significant Negatives

  • Evidence of infection, stenosis, aneurysm
122
Q

Definition of AV fistula

(location,3/connection)

A

Surgically created connection between artery and vein

  • Radio-cephalic @ wrist = Cimino-Brescia
  • Brachio-cephalic @ the elbow

Venous limb (from machine) is proximal

Side-to-side anastomosis c¯ ligation of the distal vein

123
Q

Advantages (3) and Disadvantages (3) or AV fistula

A

Advantages

  • High flow rates, low recirculation (<10%)
  • Low infection rates
  • Less chance of stenosis cf. grafts

Disadvantages

  • Take ~6 weeks to arterialise
  • Affect pts. body image
  • Must take care: avoid shaving, don’t take BP/blood here
124
Q

Complications of AV fistula (4)

A
  • Thrombosis and stenosis
  • Infection
  • Bleeding
  • Aneurysm
125
Q

Steal syndrome

(AV fistulas)

A
  • Distal tissue ischaemia
    • Pallor, pain, ↓ pulses
    • May → necrosis
  • ↓ wrist:brachial pressure index
  • Rx: banding (plication)
126
Q
A
127
Q

What is a tunnelled cuff catherer (and AKA?)

A

Two lines tunnelled under skin and entering IJV

aka: Tessio Lines

128
Q

disadvantages of Tunnelled cuffed catheter for renal access

A

Disadvantages

  • May have ↑ recirculation cf. AVF
  • Lower flow rates
  • ↑ risk of infection and thrombosis

(advantages ==>DON’t have to…

  1. wait ~6 weeks for AVF to arterialise
  2. Suffer same affect on pts. body image
  3. don’t have to take care: e.g. avoid shaving, taking BP/blood from AVF arm)
129
Q

Complication of Tunnelled cuffed Catheters (4)

A
  • Adverse events @ insertion: e.g. pneumothorax
  • Line or tunnel infection
  • Blockage
  • Retraction
130
Q

Features and classification of CRF

A
  • Kidney damage ≥3mo indicated by ↓ function
  • Symptoms usually only occur by stage 4 (GFR<30)
  • ESRF is stage 5 or need for RRT
131
Q

Causes of CRF

Common, 2 Other, 7

A

Common:

  • DM
  • HTN

Other

  • RAS
  • GN
  • CTD: SLE, SS, RA
  • Polycystic disease
  • Drugs: e.g. analgesic nephropathy
  • Pyelonephritis: usually 2O to VUR
  • Myeloma and amyloidosis
132
Q

Investigations for CRF patient

urine/bloods: function+renal screen/imaging/histology

A

Urine

  • Dip: haematuria, proteinuria, glycosuria
  • PCR
    • Normal = <20mg/mM
    • Nephrotic = >300mg/mM
  • BJP: myeloma

Function

  • FBC: ↓Hb
  • U+E: ↓ eGFR
  • Bone: ↓Ca, ↑PO4, ↑PTH, ↑ALP

Renal Screen

  • DM: fasting glucose, HbA1c
  • ESR
  • Immune
    • SLE: ANA, C3, C4
    • Goodpasture’s: anti-GBM
    • Vasculitis: ANCA
    • Hepatitis: viral serology
  • Se protein electrophoresis

Imaging

  • CXR: pulmonary oedema
  • Renal US
    • Usually small (<9cm)
    • May be large: polycystic, amyloid
  • Bone X-rays: renal osteodystrophy (pseudofractures)
  • CT KUB: e.g. cortical scarring from pyelonephritis

Renal biopsy: if cause unclear and size normal

  • Histology subtype
  • Amyloid: apple-green birefringence c¯ Congo Red
133
Q

Complications of CRF

(CRF HEALS)

A
  • *C**ardiovascular disease
  • *R**enal osteodystrophy
  • *F**luid (oedema)
  • *H**TN
  • *E**lectrolyte disturbances: K, H
  • *A**naemia
  • *L**eg restlessness
  • *S**ensory neuropathy
134
Q

Features of Renal osteodystrophy (5)

A
  1. Osteoporosis: ↓ bone density
  2. Osteomalacia: ↓ mineralisation of osteoid (matrix)
  3. 2O/3O HPT → osteitis fibrosa cystica
    • Subperiosteal bone resorption
    • Acral osteolysis: short stubby fingers
    • Pepperpot skull
  4. Osteosclerosis of the spine → Rugger Jersey spine
    • Sclerotic vertebral end plate c¯ lucent centre
  5. Extraskeletal calcification: e.g. band keratopathy
135
Q

Pathophysiology of renal osteodystrophy

A
  • ↓ 1α-hydroxylase → ↓ vit D activation → ↓Ca → ↑PTH
  • Phosphate retention → ↓Ca and ↑PTH (directly)
  • ↑PTH → activation of osteoclasts ± osteoblasts
  • Also acidosis → bone resorption
136
Q
A
137
Q

Management of CRF

General (and CV risk), Specific (HTN,Oedema,Bone,Anaemia,Restless)

A

General Mx

  • Rx reversible causes
  • Stop nephrotoxic drugs
  • Na, K, fluid and PO4 restriction

Optimise CV Risk

  • Smoking cessation, exercise
  • Statin + antiplatelet
  • Rx DM
  • *Specific Mx**
  • *Hypertension**
  • Target <140/90 (<130/80 if DM)
  • In DM kidney disease give ACEi/ARB (inc. if normal BP)
  • *Oedema**: frusemide
  • *Bone Disease**
  • Phosphate binders: calcichew, sevelamer
  • Vit D analogues: alfacalcidol (1 OH-Vit D3)
  • Ca supplements
  • Cinacalcet: Ca mimetic

Anaemia

  • Exclude IDA and ACD
  • EPO to raise Hb to 11g/dL (higher = thrombosis risk)

Restless Legs: clonazepam

138
Q

Diabetic nephropathy

pathophysiology

A

Commonest cause of ESRF: >20%
Advanced / ESRF occurs in 40% of T1 and T2 DM
Pathology

Diabetic nephropathy describes conglomerate of lesions occurring concurrently.

  • Hyperglycaemia → hypertrophy and ROS production
  • Hallmark is glomerulosclerosis and nephron loss
  • Nephron loss → RAS activation → HTN
139
Q

Clinical signs of diabetic nephropathy

and screening test

A
  • Microalbuminuria
    • 30-300mg/d or albumin:creatinine >3mg/mM
    • Strong independent RF for CV disease
  • Progresses to proteinuria: albuminuria >300mg/d
  • Usually coexists c¯ other micro- and macro-vasc disease
  • Screening: T2DMs should be screened for microalbuminuria 6moly
140
Q

Management of Diabetic nephropathy

A
  • Good glycaemic control delays onset and progression
    • UKPDS: UK Prospective Diabetes Study
    • DCCT: Diabetes Control and Complications Trial
  • Control HTN: BP target 130/80
  • ACEi/ARB: even if normotensive
  • Stop smoking
  • Combined kidney pancreas Tx possible in selected pts
141
Q

Rheumatoid arthritis association with CRF

3 processes

A
  1. NSAIDs → ATN
  2. Penicillamine and gold → membranous GN
  3. AA amyloidosis occurs in 15%
142
Q

Pathogenesis of SLE association with CRF…and treatment

A

Pathogenesis

  • Involves glomerulus in 40-60% → ARF/CRF
  • Immune complex deposition → T3 hypersensitivity
  • Typically membranous GN
  • Proteinuria and ↑BP

Rx

  • Proteinuria: ACEi
  • Aggressive GN: immunosuppression
143
Q

Diffuse systemic sclerosis and CRF

association and treatment

A
  • Renal crisis: malignant HTN + ARF
    • Commonest cause of death
  • Rx: ACEi if ↑BP or renal crisis
144
Q

Pathophysiology of myeloma and CRF

A
  • Excess production of monoclonal Ab ± light chains (excreted and detected in 60% as urinary BJP).
  • Light chains block tubules and have direct toxic effects → ATN.
  • Myeloma also assoc. c¯ ↑↑Ca2+
145
Q

Presentation and treatment of CRF in myeloma

A

Presentation

  • ARF / CRF
  • Amyloidosis

Rx

  • Ensure fluid intake of 3L/d to prevent further impairment
  • Dialysis may be required in ARF
146
Q

Cause of Renovascular disease

A

Cause

  • Atherosclerosis in 80%
  • Fibromuscular dysplasia
  • Thromboembolism
  • External mass compression
147
Q

Presentation investigation and management of Renovascular disease

A

Presentation

  • Refractory hypertension
  • Renal bruits
  • Worsening renal function after ACEi/ARB
  • Flash pulmonary oedema (no LV impairment on echo)
  • Other signs of PVD

Ix

  • CT/MR angio
  • Renal angiography

Rx

  • Rx medical CV risk factors
  • Angioplasty and stenting
  • AVOID ACEi/ARB
148
Q

IBD Examination

  • Peripheral: general/hands/eyes/mouth/legs*
  • abdo: inspection/palpation*
  • completion*
A

Peripheral Inspection

  • General
    • Often young female pt.
    • Laparotomy scars
    • Malnutrition or wt. loss
    • Cushingoid
    • Pallor
  • Hands
    • Clubbing
    • Leukonychia
    • Beau’s lines
  • Eyes
    • Pale conjunctivae
    • Iritis, episcleritis
  • Mouth
    • ​Aphthous ulcers
    • Gingival hypertrophy (ciclosporin)
  • Legs
    • Erythema nodosum
    • Pyoderma gangrenosum

Abdominal

  • Inspection
    • Scars
      • May be multiple and atypical in Crohn’s
      • Healed stoma sites
      • Healed drain sites
    • Stomas or healed stoma sites
    • Enterocutaneous fistulae
  • Palpation
    • Tendernes
    • RIF mass
    • ± hepatomegaly

Completion

  • Inspect perineum for perianal disease
  • Examine for extra-intestinal features
    • Large joint monoarthritis
    • Sacroileitis
    • Bronchiectasis
149
Q

Differential diagnosis for IBD (4)

A
  • Crohn’s
  • UC
  • Malabsorption: coeliac
  • Mid-line lap: FAP
150
Q

Important History Qs in IBD

A
  • Symptoms
    • Wt. loss, fever, malaise
    • Abdominal pain
    • Diarrhoea, blood and/or mucus PR
  • Peri-anal disease: abscesses, fistulae
  • Extra-intestinal: EN, arthritis, iritis, gallstones, PSC
  • Therapy
    • Admissions
    • Medical therapy
    • Operations
151
Q

Investigations of IBS

(bloods, stool, imaging, endoscopy)

A

Bloods

  • FBC: ↓Hb, ↑WCC
  • U+E: dehydration, ↓K
  • LFTs: ↓ albumin, deranged LFTs
  • Clotting: ↑INR
  • ↑ ESR, ↑ CRP: used to monitor activity
  • Haematinics: Fe, B12, folate
  • Markers of Activity in CD: ↓Hb, ↑ESR, ↑CRP, ↑WCC, ↓albumin

Stool

  • Culture + CDT: exclude infective causes
    • Campy, Yersinia, Shigella, C. diff, TB

Imaging

  • AXR
    • Toxic megacolon in UC
    • Bowel obstruction 2O to strictures in Crohn’s
  • Contrast studies
    • Ba or Gastrograffin enema in UC
    • Small bowel follow-through in Crohn’s
  • MRI: perianal disease in Crohn’s

Endoscopy

  • Ileocolonoscopy + regional biopsy
    • Ix of choice
    • Safe in acute disease
    • Distinguish UC from Crohn’s
    • Assess disease severity
  • Wireless capsule endoscopy
152
Q

Differentiate Pathology

UC vs Crohns

A
153
Q

Differential complications

UC Vs Crohn’s

A
154
Q

Scoring system for severe exacerbation in IBD (3 key factors, 6)

A

Dx: True-Love and Witts Criteria

  1. Symptoms
    • BMs >6 x /d
    • Large PR bleed
  2. Systemic Signs
    • ↑ HR >90
    • Pyrexia >37.8
  3. Laboratory Values
    • ↓ Hb <10.5g/dL
    • ESR >30mm/Hr
155
Q

Management of IBD

Crohn’s

general/inducing remision/maintaining/surg

(passmed)

A

General points

  • patients should be strongly advised to stop smoking
  • some studies suggest an increased risk of relapse secondary to NSAIDs and the combined oral contraceptive pill but the evidence is patchy

Inducing remission

  • glucocorticoids (oral, topical or intravenous) are generally used to induce remission.
    • enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)
    • 5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
    • azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy. Methotrexate is an alternative to azathioprine
    • infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
    • metronidazole is often used for isolated peri-anal disease

Maintaining remission

  • as above, stopping smoking is a priority (remember: smoking makes Crohn’s worse, but may help ulcerative colitis)
  • azathioprine or mercaptopurine is used first-line to maintain remission
    • methotrexate is used second-line
    • 5-ASA drugs (e.g. mesalazine) should be considered if a patient has had previous surgery

Surgery: around 80% of patients with Crohn’s disease will eventually have surgery

156
Q

UC

Management

Inducing/maintaining remision

(passmed)

A

Inducing remission

  • treatment depends on the extent and severity of disease
  • rectal (topical) aminosalicylates or steroids: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids and oral aminosalicylates
  • oral aminosalicylates
    • oral prednisolone is usually used second-line for patients who fail to respond to aminosalicylates. NICE recommend waiting around 4 weeks before deciding if first-line treatment has failed
  • severe colitis should be treated in hospital. Intravenous steroids are usually given first-line

Maintaining remission

  • oral aminosalicylates e.g. mesalazine
  • azathioprine and mercaptopurine
    • methotrexate is not recommended for the management of UC (in contrast to Crohn’s disease)
    • there is some evidence that probiotics may prevent relapse in patients with mild to moderate disease
157
Q

IBD management

surgery UC vs Crohns’

A

Ulcerative colitis

  • Elective indications for surgery include disease that is requiring maximal therapy, or prolonged courses of steroids.
  • Longstanding UC is associated with a risk of malignant transformation. Dysplastic transformation of the colonic epithelium with associated mass lesions is an absolute indication for a proctocolectomy.
  • Emergency presentations of poorly controlled colitis that fails to respond to medical therapy should usually be managed with a sub total colectomy. Excision of the rectum is a procedure with a higher morbidity and is not generally performed in the emergency setting. An end ileostomy is usually created and the rectum either stapled off and left in situ, or, if the bowel is very oedematous, may be brought to the surface as a mucous fistula.
  • Patients with IBD have a high incidence of DVT and appropriate thromboprophylaxis is mandatory.
  • Restorative options in UC include an ileoanal pouch. This procedure can only be performed whilst the rectum is in situ and cannot usually be undertaken as a delayed procedure following proctectomy.
  • Ileoanal pouch complications include, anastomotic dehiscence, pouchitis and poor physiological function with seepage and soiling.

Crohns disease

  • Surgical resection of Crohns disease does not equate with cure, but may produce substantial symptomatic improvement.
  • Indications for surgery include complications such as fistulae, abscess formation and strictures.
  • Extensive small bowel resections may result in short bowel syndrome and localised stricturoplasty may allow preservation of intestinal length.
  • Staging of Crohns will usually involve colonoscopy and a small bowel study (e.g. MRI enteroclysis).
  • Complex perianal fistulae are best managed with long term draining seton sutures, complex attempts at fistula closure e.g. advancement flaps, may be complicated by non healing and fistula recurrence.
  • Severe perianal and / or rectal Crohns may require proctectomy. Ileoanal pouch reconstruction in Crohns carries a high risk of fistula formation and pouch failure and is not recommended.
  • Terminal ileal Crohns remains the commonest disease site and these patients may be treated with limited ileocaecal resections.
  • Terminal ileal Crohns may affect enterohepatic bile salt recycling and increase the risk of gallstones.
158
Q

Indications for surgery in IBD (5)

A
  • Obstruction
  • Megacolon
  • Perforation
  • Severe GI bleeding
  • Failure to respond to medical therapy
159
Q

Key extra-intestinal features in IBD

A
  • Skin
    • Clubbing
    • Erythema nodosum
    • PG (esp. UC)
  • Mouth Aphthous ulcers
  • Eyes
    • Anterior uveitis
    • Episcleritis
  • Joints
    • Large joint arthritis
    • Sacroileitis
  • Hepatic
    • Fatty liver
    • Chronic hepatitis → cirrhosis
    • Gallstones (esp. CD)
    • PSC + cholangiocarcinoma (esp. UC)
  • Other
    • AA amyloidosis
    • Oxalate renal stones
160
Q

Gen management UC vs Crohns

gen/induction/maintenance

A

PACES Hawthorne (18 decks)

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