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Medicine and Surgery Mushkies > Abdo Mushkies > Flashcards

Abdo Mushkies Flashcards

1
Q

Liver screen?

A
  1. Alcohol = FBC, LFT, GGT
  2. Viral = Hep B and C Serology
  3. NASH = Lipids
  4. Abs = SMA, AMA, pANCA, ANA
  5. Ig = IgG (AIH), IgM (PBC)
  6. Malignancy = AFP, Ca19-9
  7. Genetic = caeruloplasmin, ferritin, a1-AT
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2
Q

Management of chronic liver disease classification?

A
  1. General
  2. Cause
  3. Complications
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3
Q

General Mx of chronic liver disease?

A
  1. MDT = GP, hepatologist, dietician, palliative care
  2. Alcohol abstinence
  3. Good nutrition
  4. Cholestyramine for pruritis
  5. Screening = HCC (US + AFP), OGD for varices
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4
Q

Complications of chronic liver disease?

A

VACESHH

  1. Varices
  2. Ascites
  3. Coagulopathy
  4. Encephalopathy
  5. Sepsis/SBP
  6. Hypoglycaemia
  7. Hepatorenal syndrome
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5
Q

Mx of complications of chronic liver disease?

A
  1. Varices = BB, banding
  2. Ascites = fluid and salt restrict, spiro, furos, tap, daily wt, TIPSS
  3. Coag = Vit K, FFP, plts
  4. Encephalopathy = avoid sedatives, lactulose, rifaximin
  5. Sepsis/SBP = tazocin or cefotaxime
  6. Hypoglycaemia = dextrose
  7. Hepatorenal syndrome = IV albumin + terlipressin
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6
Q

Causes of chronic liver disease?

A
  1. Alcohol
  2. Autoimmune = AIH, PBC, PSC
  3. Drugs = methotrexate, isoniazid, amiodarone
  4. Viral = HCV, HBV
  5. Metabolic = HH, Wilsons, a1ATD, CF
  6. Malignancy = HCC or mets
  7. Vascular = Budd-Chiari, RHF, Constrictive pericarditis
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7
Q

Child-Pugh Grading of Cirrhosis?

A

ABCDE

  1. Albumin
  2. Bilirubin
  3. Clotting
  4. Distension (Ascites)
  5. Encephalopathy
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8
Q

Child-Pugh Gradindg A,B,C scores?

A
  1. A = 5-6
  2. B = 7-9
  3. C = 10-15
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9
Q

Precipitants of hepatic decompensation?

A

HEPATICS

  1. Haemorrhage = varices
  2. Electrolytes, hypokalaemia/natraemia
  3. Poisons = diuretics, sedatives, anaesthetics
  4. Alcohol
  5. Tumour = HCC
  6. Infection = SBP, pneumonia, UTI, HDV
  7. Constipation (most common cause)
  8. Sugar = low calorie diet
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10
Q

Monitoring of hepatic decompensation?

A
  1. Fluids = urinary and central venous catheters
  2. Bloods = daily FBC, U&E, LFT, INR
  3. Glucose = 1-4hrly + 10% dextrose IV 1L/24hrs
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11
Q

Pathophysiology of hepatic encephalopathy?

A

Reduced hepatic metabolic function –> diversion of ammonia from liver directly into systemic circulation –> brain where astrocytes cause conversion of glutamate into glutamine –> causes osmotic imbalance –> cerebral oedema

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12
Q

Presentation of hepatic encephalopathy?

A

ACDCS

  1. Asterixis, Ataxia
  2. Confusion
  3. Dysarthria
  4. Constructional apraxia
  5. Seizures
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13
Q

MOA of lactulose for hepatic encephalopathy?

A

Reduces nitrogen forming bowel bacteria

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14
Q

What is hepatorenal syndrome?

A

Renal failure in patients with advanced CLD

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15
Q

What is the pathophysiology of hepatorenal syndrome?

A

‘Underfill theory’

  1. Cirrhosis –> splanchnic arterial vasodilatation –> reduced effective circulatory volume –> RAS activation –> renal arteriole vasoconstriction
  2. Persistent underfilling of renal circulation –> failure
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16
Q

3 most common SBP organisms?

A
  1. E. coli
  2. Klebsiella
  3. Strep
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17
Q

Mx of SBP?

A

Tazocin or cefotaxime until sensitivities known

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18
Q

SBP cell level?

A

> 250/mm3

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19
Q

3 commonest causes of ascites?

A

3 Cs

  1. Cirrhosis
  2. Cancer
  3. CCF
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20
Q

SAAG?

A

Serum ascites albumin gradient

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21
Q

SAAG <1.1g/dL?

A

Portal HTN (97% accuracy), due to cirrhosis in 80%

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22
Q

SAAG >1.1g/dL?

A
  1. Infection = TB peritonitis
  2. Inflammation = pancreatitis
  3. Malignancy = peritoneal mets/ovarian Ca
  4. Nephrotic syndrome
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23
Q

HVPG?

A

Hepatic Venous Pressure Gradient

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24
Q

Portal HTN HVPG?

A

HVPG greater than or equal to 5 mm Hg and is considered to be clinically significant when HVPG exceeds 10 to 12 mm Hg

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25
Q

Causes of portal HTN?

A
  1. Pre-hepatic
  2. Hepatic
  3. Post-hepatic
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26
Q

Pre-hepatic causes of Portal HTN?

A
  1. Portal vein thrombosis
  2. Splenic vein thrombosis
  3. AV fistula
  4. Splenomegaly (increased portal blood flow)
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27
Q

Hepatic causes of portal HTN?

A

All hepatic disease tings

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28
Q

Post-hepatic causes of portal HTN?

A
  1. Cardiac = RHF, TR, constrictive pericarditis
  2. Budd-Chiari
  3. IVC obstruction
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29
Q

Ascites bloods?

A

FBC, U&E, LFTs, INR, Glucose, Liver screen

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30
Q

Mx of ascites?

A
  1. General = fluid restrict (<1.5L). low Na diet (40-100mmol/d), daily wts (<0.5kg/d reduction)
  2. Medical = spironolactone and furosemide if response poor
  3. Therapeutic paracentesis
  4. Refractory ascites = TIPSS/transplant
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31
Q

3 indications for therapeutic paracentesis?

A
  1. Resp compromise
  2. Pain/discomfort
  3. Renal impairment
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32
Q

2 risks of therapeutic paracentesis?

A
  1. Severe hypovolaemia (replenish albumin)

2. SBP

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33
Q

Urobilinogen in causes of jaundice?

A
  1. Prehepatic = yes
  2. Hepatic = yes
  3. Posthepatic = no
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34
Q

3 immunosuppressant stigmata?

A
  1. Cushingoid
  2. Skin tumours
  3. Gingival hypertrophy (ciclosporin)
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35
Q

Liver transplant scar?

A

Mercedes Benz

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36
Q

DDx for Mercedez Benz scar?

A

HPB surgery

  1. Liver transplant
  2. Segmental resection
  3. Whipples
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37
Q

2 types of liver transplant?

A
  1. Cadaveric

2. Live segmental

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38
Q

3 most common indications for liver transplant?

A
  1. Cirrhosis
  2. Malignancy
  3. Acute liver failure = Hep A/B, paracetamol OD
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39
Q

Liver transplant prognosis?

A
  1. 80% 1 yr survival

2. 70% 5 yr survival

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40
Q

Immunosuppression regimen for liver transplant?

A

TAP

  1. Tacrolimus/ciclosporin
  2. Azathioprine
  3. Prednisolone +/- withdrawal at 3mo
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41
Q

Causes of hepatomegaly?

A

3Cs, 2Is, 2Bs

  1. Cancer = primary or secondary
  2. Cirrhosis = early, usually alcoholic
  3. Cardiac = CCF, congestive pericarditis
  4. Infiltration = fatty, haemochromatosis, amyloidosis, sarcoidosis
  5. Infection = Viral, Malaria, Abscess
  6. Blood = leukaemia, lymphoma, myeloproliferative, haemolytic
  7. Biliary = PBC, PSC
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42
Q

3 features of hepatomegaly?

A
  1. Moves inferiorly on inspiration
  2. Cant get above it
  3. Dull percussion note
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43
Q

Features to note about hepatomegaly?

A
  1. Edge = smooth/craggy/nodular
  2. Tenderness
  3. Pulsatile
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44
Q

What is Riedel’s lobe?

A

A common anatomical variant of the liver, which is a tongue-like, inferior projection of the right lobe of the liver beyond the level of the most inferior costal cartilage, wrongly assumed to be hepatomegaly

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45
Q

Hepatomegaly bloods?

A
  1. FBC
  2. U&E
  3. LFT
  4. Clotting
  5. Liver screen
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46
Q

Hepatomegaly Ix?

A
  1. Bedside = urine dip (protein, urobilinogen)
  2. Bloods
  3. Imaging = US, CT, MRI
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47
Q

What are we looking for on liver US?

A
  1. Liver size and texture
  2. Focal lesions
  3. Ascites
  4. Portal vein flow
  5. Hepatic veins: thrombosis
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48
Q

What must one check before performing a liver biopsy>

A

Clotting

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49
Q

Causes of macronodular and micronodular cirrhosis (cut-off 3mm)?

A
  1. Micro = alcohol, HH, Wilsons

2. Macro = viral

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50
Q

Stains for liver biopsy?

A
  1. Perl’s Prussion Blue = Iron
  2. Rhodamine = Copper
  3. a1ATD = PAS (a1AT globules accumulate in liver)
  4. Amyloid = apple green birefringence with Congo Red
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51
Q

Features of splenomegaly on palpation/

A
  1. Cant get above it
  2. Moves towards RIF on respiration
  3. Notch
  4. Dull PN
  5. Not ballotable
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52
Q

What other examinations must you do with splenomegaly?

A
  1. Cardio = IE

2. Resp = Sarcoid

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53
Q

Causes of splenomegaly?

A
  1. Myeloproilferative = CML, MF
  2. Lymphoproliferative = CLL, lymphoma
  3. Infective = Visceral leishmaniasis, Malaria
  4. Infiltrative = Gaucher’s, amyloidosis
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54
Q

Gaucher’s disease?

A

A genetic disorder in which glucocerebroside accumulates in cells (esp. WBCs and macrophages) and certain organs, caused by a hereditary deficiency of the enzyme glucocerebrosidase

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55
Q

CML defn?

A

A leukaemia characterised by clonal proliferation of myeloid cells

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56
Q

CML Fx?

A
  1. Constitutional
  2. Anaemia, Bleeding, Infections
  3. Massive HSM –> abdo discomfort
  4. Gout
  5. Hyperviscosity
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57
Q

Most common cause of CML?

A

t(9;22) translocation leading to formation of BCR-ABL fusion gene

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58
Q

CML FBC?

A
  1. Raised WBC

2. Low Hb and Plts

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59
Q

Mx of CML?

A
  1. Imatinib = tyrosine kinase inhibitor with 90% ham response, leading to 80% survival at 5 years
  2. Allogeneic SCT = indicated if blast crisis or TK-refractory
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60
Q

Myelofibrosis film?

A

Leukoerythroblastic with teardrop poikilocytes

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61
Q

Myelofibrosis Mx?

A
  1. Supportive = blood products
  2. Splenectomy
  3. Allogeneic BMT may be curative in younger pts
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62
Q

Prognosis of primary myelofibrosis?

A

5 year median survival

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63
Q

Anatomy of the spleen?

A
  1. Intraperitoneal structure lying in the LUQ
  2. Measuring 1x3x5 inches
  3. Weighing 7 oz
  4. Lying anterior to ribs 9-11
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64
Q

Function of the spleen?

A

Part of the mononuclear phagocytic system

  1. Phagocytosis of old RBCs and WBCs
  2. Phagocytosis of opsonised pathogens
  3. Ab production
  4. Sequestration of formed blood elements
  5. Haemopoiesis
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65
Q

Hypersplenism?

A
  1. An overactive spleen, that can either be primary or secondary to being an enlarged spleen
  2. Leads to a pancytopenia –> anaemia, bruising, infections
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66
Q

Massive splenomegaly defn?

A

> 1kg

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67
Q

What transiently rises after splenectomy?

A

Platelets

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68
Q

Hyposplenism film?

A
  1. Howell-Jolly bodies
  2. Pappenheimer bodies
  3. Target cells
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69
Q

Mx of hyposplenism?

A
  1. Conservative = Alert card/bracelet

2. Medical = Immunisations (Pneumovax, HiB, Men C, influenza) and Abx (Pen V/erythromycin)

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70
Q

Indications for splenectomy?

A
  1. Trauma
  2. Rupture = e.g. secondary to EBV
  3. AIHA
  4. ITP
  5. Hereditary spherocytosis
  6. Hypersplenism
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71
Q

5 complications of splenectomy?

A
  1. Infections = haemophilus, pneumo, meningo
  2. Pancreatitis = tail shares blood supply with spleen
  3. LLL atelectasis
  4. Gastric dilatation due to transient ileus
  5. Redistributive thrombocytosis –> early VTE
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72
Q

Why to give early post-op aspirin after splenectomy?

A

To prevent early VTE due to redistributive thrombocytosis

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73
Q

Why can gastric dilatation occur post splenectomy?

A

May disturb gastro-omental vessel ligatures

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74
Q

Features of a palpable kidney?

A
  1. Flank mass
  2. Cant get above it
  3. Ballottable
  4. Moves inferiorly on respiration
  5. Resonant PN
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75
Q

3 things to complete examination of an enlarged kidney?

A
  1. CVS = mitral valve prolapse
  2. Urine dip = proteinuria, haematuria
  3. External genitalia = hydroecele 2ary to RCC
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76
Q

5 causes of bilaterally enlarged kidneys?

A
  1. ADPKD
  2. Bilateral RCC
  3. Bilateral cysts
  4. Amyloidosis
  5. Hydropnephrosis
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77
Q

4 causes of unilaterally enlarged kidney?

A
  1. RCC
  2. Simple renal cyst
  3. Compensatory hypertrophy
  4. ADPKD (with contralateral nephrectomy)
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78
Q

ADPKD genetics?

A
  1. PKD1 on Chr16 = 85%

2. PKD2 on Chr4 = 15%

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79
Q

ADPKD Mx?

A
  1. Conservative = high water intake, low salt intake, less caffeine, genetic counselling
  2. Medical = HTN aggressively (<130/80), Rx infections
  3. Surgical = Nephrectomy if recurrent bleeds/infections or abdo discomfort –> Dialysis/Transplant
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80
Q

ADPKD Ix?

A
  1. Bedside = Urine dip, MC&S
  2. Bloods = FBC, U&E, Bone profile
  3. Imaging = US, CT, MRI head
  4. Genetic studies to look for mutation
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81
Q

ADPKD Prognosis?

A

ESRF in 70% by 70 y/o

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82
Q

ADPKD prevalence?

A

1/1000

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83
Q

ADPKD presentation?

A
  1. 30-50 y/o
  2. HTN
  3. Recurrent UTIs
  4. Haematuria
  5. Loin pain: cyst haemorrhage/infection
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84
Q

3 extra-renal features of ADPKD?

A
  1. Hepatic cysts –> hepatomegaly
  2. Berry aneurysms –> SAH
  3. MV prolapse –> mid-systolic click and late murmur
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85
Q

ARPKD prevalence?

A

1:40,000

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86
Q

ARPKD genetics?

A

PKHD1 (fibrocystin) gene on Chr6

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87
Q

Presentation of ARPKD?

A
  1. Perinatal
  2. Oligohydramnios, may –> potter sequence
  3. Bilateral abdominal masses
  4. HTN and CKD
88
Q

ARPKD extra-renal involvement?

A

Congenital hepatic fibrosis –> portal HTN

89
Q

ARPKD prognosis?

A

ESRF by 20yrs

90
Q

Simple renal cysts Fx?

A
  1. Common = 1/3rd pts >60y/o
  2. May present as renal mass and haematuria
  3. Contain fluid only, no solid elements
  4. Main DDx is RCC
91
Q

Dialysis associated renal cysts Fx?

A
  1. Seen after prolonged dialysis
  2. 2ary to obstruction of renal tubules by oxalate crystals
  3. Increased risk of RCC in cysts
92
Q

Tuberous sclerosis aka?

A

Bourneville’s disease

93
Q

Tuberous sclerosis defn?

A

AD condition characterised by hamartomas in skin, brain, eye and kidneys

94
Q

Skin, neuro and renal fx of TS?

A
  1. Skin = adenoma sebaceum, Shagreen patch, axillary freckling, ash leak macules, peri-ungual fibromas
  2. Neuro = reduced IQ, epilepsy, astrocytoma
  3. Renal = cysts, angiolipomas
95
Q

RCC epidemiology?

A
  1. 90% of renal cancer
  2. 55y/o typically
  3. 2M:1F
96
Q

RCC Rfs?

A
  1. Smoking
  2. Obesity
  3. HTN
  4. Dialysis (15% develop RCC)
  5. Congenital = e.g. vHL
97
Q

RCC presentation triad?

A
  1. Haematuria
  2. Loin pain
  3. Loin mass
98
Q

5 paraneoplastic Fx of RCC?

A
  1. EPO –> polycythaemia
  2. PTHrP –> raised Ca
  3. Renin –> HTN
  4. ACTH –> Cushings
  5. Amyloidosis
99
Q

RCC spread?

A
  1. Direct = renal vein
  2. Lymph
  3. Haematogenous = bone, liver, lung
100
Q

RCC Ix?

A
  1. Bedside = urine dip and cytology
  2. Bloods = FBC, U&E, LFTs, bone, ESR
  3. Imaging = CXR (cannonball), US, IVU (filling defect), CT/MRI
101
Q

RCC Mx?

A
  1. Medical = for pts with poor prognosis, mTOR inhibitors (e.g. Temsirolimus)
  2. Surgical = radical nephrectomy
102
Q

RCC prognosis?

A

45% at 5 yrs

103
Q

5 fx of vHL?

A
  1. Renal and pancreatic cysts
  2. Bilateral RCC
  3. Haemangioblastomas in cerebellum
  4. Islet cell tumours
  5. Phaeochromocytomas
104
Q

vHL inheritance?

105
Q

Renal transplant palpation Fx?

A
  1. Smooth oval mass under Rutherford Morrison scar
  2. Dull PN
  3. Can get below it
  4. Doesnt move with respiration
106
Q

Auscultation of renal transplant?

A

Maybe hear a bruit

107
Q

5 causes of gum hypertrophy?

A
  1. Drugs
  2. Pregnancy
  3. Familial
  4. AML
  5. Scurvy
108
Q

3 drugs that cause gum hypertrophy?

A
  1. Ciclosporin
  2. Nifedipine
  3. Phenytoin
109
Q

Renal transplant pt bloods?

A
  1. FBC = infection
  2. U&E = eGFR trend
  3. LFTs = ciclosporin
  4. Glucose = ciclosporin is diabetogenic
  5. Drug levels = ciclosporin, tacrolimus
110
Q

4 commonest indications for renal transplant?

A
  1. DM
  2. GN
  3. ADPKD
  4. HTN
111
Q

4 C/I to renal transplant?

A
  1. Active infection
  2. Cancer
  3. Severe co-morbidity
  4. Failed pre-implantation x-match
112
Q

Types of renal transplant?

A
  1. Cadaveric
  2. DBD/DCD
  3. Live related
  4. Live unrelated
113
Q

3 benefits of live related donor?

A
  1. Optimal surgical timing
  2. HLA Matched
  3. Improved graft survival
114
Q

Renal transplant immunosuppression?

A
  1. Pre-op = Alemtuzumab (anti-CD52)
  2. Post-op short term = prednisolone
  3. Post-op long term = tacrolimus/ciclosporin
115
Q

Alemtuzumab aka?

116
Q

Half life of cadaveric grafts?

117
Q

Half life of HLA-identical live grafts?

A

> 20 years

118
Q

Classification of renal transplant complications?

A
  1. Post-op
  2. Rejection
  3. Drug toxicity
  4. CVD
119
Q

Renal transplant post-op complications?

A
  1. Bleeding
  2. Graft thromboses
  3. Infection
  4. Urinary leaks
120
Q

Renal transplant rejection types?

A
  1. Hyperacute
  2. Acute
  3. Chronic
121
Q

Hyperacute renal transplant rejection fx?

A
  1. Mins
  2. Path = ABO incompatability
  3. Presentation = thrombosis and SIRS
122
Q

Acute renal transplant rejection fx?

A
  1. <6m
  2. Path = cell-mediated response
  3. Presentation = fever and graft pain, reduced urine output, raised Cr
  4. Rx = Immunosuppression
123
Q

Chronic renal transplant rejection fx?

A
  1. > 6m
  2. Path = Interstitial fibrosis and tubular atrophy
  3. Presentation = gradual increase in Cr and proteinuria
  4. Rx = supportive, not responsive to immunosuppression
124
Q

Ciclosporin/Tacrolimus MOA?

A

Calcineurin inhibitor, blocks IL2 production

125
Q

Ciclosporin 4 s/e?

A
  1. Nephrotoxic
  2. Hepatotoxic
  3. Gingival hypertrophy
  4. Hypertrichosis
126
Q

Tacrolimus 4 s/es?

A
  1. Nephrotoxicity (less than ciclo tho)
  2. Diabetogenic
  3. Cardiomyopathy
  4. Neurotoxicity e.g. peripheral neuropathy
127
Q

S/e of reduced immune function for renal transplant?

A
  1. Infection = CMV, PCP, fungi, warts

2. Malignancy = PTLD (EBV), Skin (SCC, BCC, MM, Kaposi’s)

128
Q

CVD complications of renal transplant?

A
  1. HTN

2. Atheromatous vsacular disease

129
Q

3 types of Renal replacement therapy?

A
  1. Haemodialysis
  2. Peritoneal Dialysis
  3. Haemofiltration
130
Q

Indication for renal replacement therapy?

A
  1. Suggested when eGFR <15ml/min + symptoms
  2. Psychological preparation necessary
  3. PD vs. HD depends on med, social and psych factors
131
Q

Annual mortality of dialysis?

132
Q

Complications of dialysis?

A

20% annual mortality

  1. Infection
  2. Inflammation = amyloidosis
  3. Malignancy = from renal cysts
  4. Malnutrition
  5. CVD
133
Q

MOA of dialysis infections?

A

Uraemia –> granulocyte dysfunction –> increased sepsis related mortality

134
Q

MOA of dialysis amyloidosis?

A

B2 microglobulin accumulation

135
Q

Mechanism of haemodialysis?

A
  1. Countercurrent flow = blood flows on one side of semipermeable membrane, dialysate flows in opposite direction on other side, solute transfer by diffusion
  2. Ultrafiltration = Fluid removal by creation of negative transmembrane pressure by decreasing the hydrostatic pressure of the dialysate
136
Q

5 complications of haemodialysis?

A
  1. Disequilibration syndrome
  2. Fluid balance = low BP and pulmonary oedema
  3. E- imbalance
  4. Aluminium toxicity in dialysate –> dementia
  5. Psychological factors
137
Q

What is disequilibration syndrome?

A

Rapid changed in plasma osmolarity that leads to cerebral oedema, that usually only occurs on the 1st dialysis

138
Q

Peritoneal dialysis mechanism?

A
  1. Dialysate introduced into peritoneal cavity by Tenchkoff catheter, uraemic solutes diffuse into fluid across peritoneum
  2. Ultrafiltration = addition of osmotic agent e.g. glucose
  3. 3L 4x/day with approx 4hr dwell times
139
Q

Types of peritoneal dialysis?

A
  1. CAPD = fluid exchange during day with long dwell at night

2. APD = fluid exchanged during night by machine with long dwell throughout day

140
Q

CAPD?

A

Continuous ambulatory peritoneal dialysis

141
Q

APD?

A

Automated Peritoneal dialysis

142
Q

3 advantages of peritoneal dialysis?

A
  1. Simple to perform
  2. Requires less equipment –> easier at home or holiday
  3. Less haemodynamic instability (useful if CVD)
143
Q

3 disadvantages of peritoneal dialysis?

A
  1. Inconvenience
  2. Body image
  3. Anorexia
144
Q

5 complications of peritoneal dialysis?

A
  1. Peritonitis
  2. Exit site infection
  3. Catheter malfunction
  4. Obesity (glucose in dialysate)
  5. Mechanical = hernias and back pain
145
Q

Where is haemofiltration typically only used?

146
Q

Haemofiltration MOA?

A
  1. Uses a Vas Cath
  2. Blood filtered across a highly permeable membrane by hydrostatic pressure and water and solutes are removed by convection
  3. Ultrafiltrate is replaced by isotonic replacement
147
Q

2 types of renal access?

A
  1. AV fistula

2. Tesio line

148
Q

AV fistula examination?

A
  1. Inspection = swelling with surgical scar over distal forearm or elbow, evidence of use of needle marks, evidence of infection
  2. Palpation = painful, temperature, thrill
  3. Auscultation = bruit
  4. Significant negatives = infection, stenosis, aneurysm
149
Q

What is an AV fistula?

A

A surgically created connection between an artery and vein, venous limb is proximal

150
Q

2 types of AV fistula?

A
  1. Radiocephalic at wrist = Cimino-Brescia

2. Brachiocephalic at elbow

151
Q

3 advantages of AV fistulas?

A
  1. High flow rates, low recirculation (<10%)
  2. Low infection rates
  3. Less chance of stenosis cf. grafts
152
Q

3 disadvantages of AV fistulas?

A
  1. Takes 6 weeks to arterialise
  2. Affects pt body image
  3. Must take care: avoid shaving, dont take BP/blood here
153
Q

4 complications of AV fistulas?

A
  1. Thrombosis and stenosis
  2. Infection
  3. Bleeding
  4. Aneurysm
  5. Steal syndrome
154
Q

(Vascular Access) Steal syndrome?

A

A syndrome caused by ischemia resulting from an AV fistula, presenting with distal tissue pallor, pain, and reduced pulses, with potential to eventually develop into necrosis

155
Q

Mx of steal syndrome?

A

Revasculariation or Banding techniques

156
Q

Tesio line?

A

Two lines tunnelled under skin and entering the IJV

157
Q

3 disadvantages of Tesio line?

A
  1. Lower flow rates
  2. Increased risk of infection and thrombosis
  3. May have increased recirculation cf. AVF
158
Q

4 complications of Tesio line?

A
  1. Insertion e.g. pneumothorax
  2. Line/tunnel infection
  3. Blockage
  4. Retraction
159
Q

CKD stages?

A 
G1. >90 
G2. 60-89
G3. 30-59
G4. 15-29
G5. <15
160
Q

When is CKD diagnosed?

A

When they have abnormalities of kidney structure or function present for at least 3 months

  1. All individuals with markers of kidney damage (see below) or those with an eGFR of less than 60 ml/min/1.73m2 on at least 2 occasions 90 days apart (with or without markers of kidney damage).
  2. Markers of kidney disease may include: albuminuria (ACR > 3 mg/mmol), haematuria (or presumed or confirmed renal origin), electrolyte abnormalities due to tubular disorders, renal histological abnormalities, structural abnormalities detected by imaging (e.g. polycystic kidneys, reflux nephropathy) or a history of kidney transplantation
161
Q

How is CKD classified?

A

According to eGFR and ACR categories (see diagram)

162
Q

ACR (Albumin:Creatinine ratio) categories?

A

A1. Normal/mildly increased <3 mg/mmol
A2. Moderately increased 3-30 mg/mmol
A3. Severely increased >30 mg/mmol

163
Q

CKD Ix?

A
  1. Urine = Dip, PCR, BJP
  2. Bloods = FBC, U&E, Bone
  3. Renal screen
  4. Imaging
  5. Renal biopsy
164
Q

CKD Renal screen components?

A
  1. DM
  2. ESR
  3. Serum protein electrophoresis
  4. Immune
165
Q

CKD Renal immune screen components?

A
  1. SLE = ANA, C3, C4
  2. Goodpasture’s anti-GBM
  3. Vasculitis = ANCA
  4. Hepatitis = viral serology
166
Q

CKD Imaging?

A
  1. CXR = pulmonary oedema
  2. Renal US = usually small (<9cm), may be large (polycystic, amyloid)
  3. Bone X rays = renal osteodystrophy
  4. CT KUB
167
Q

Normal vs. nephrotic PCR values?

A
  1. Normal = <20mg/mM

2. Nephrotic = >300mg/mM

168
Q

CKD complications?

A

A WET BED + 3

  1. Acid-base
  2. Water
  3. Electrolytes
  4. Toxins
  5. BP –> CVD
  6. Erythropoiesis
  7. Vitamin D
  8. Restless legs
  9. Sensory neuropathy
  10. Renal osteodystrophy
169
Q

What is renal osteodystrophy?

A

Alteration in bone morphology in pts with CKD

170
Q

5 features of renal osteodystrophy?

A
  1. Osteoporosis = reduced BMD
  2. Ostemalaxia = reduced mineralisation of osteoid
  3. 2/3ary HPT –> osteitis fibrosa cystica
  4. Osteosclerosis of the spine (Rugger Jersey spine)
  5. Extraskeletal calcification
171
Q

Mechanism of renal osteodystrophy?

A
  1. Reduced 1a hydroxylase activity –> raised PTH
  2. Phosphate retention –> raised PTH
  3. Acidosis –> bone resorption
172
Q

CKD Mx?

A
  1. Conservative
  2. Medical
  3. Surgical
173
Q

Conservative CKD Mx?

A
  1. Optimise CVD risk with smoking cessation, exercise + medical
  2. Stop nephrotoxic drugs
  3. Na, K, fluid and PO4 restriction
174
Q

Medical CKD Mx?

A
  1. Underlying Cause
  2. Complications
    a. HTN
    b. Oedema = furosemide
    c. Anaemia = EPO
    d. Restless legs = clonazepam
    e. Bone disease
175
Q

Mx of renal osteodystrophy?

A
  1. Phosphate binders = Calcichew, sevelamer
  2. Vit D analogues = alfacalcidol
  3. Ca supplements
  4. Cinacalcet = Ca mimetic
176
Q

Commonest cause of ESRF?

177
Q

Pathology of diabetic nepropathy?

A
  1. Hyperglycaemia –> hypertrophy and ROS production
  2. Hallmark is glomerulosclerosis and nephron loss
  3. Nephron loss –> RAS activation –> HTN
178
Q

Hallmark of DN on histology?

A

Glomerulosclerosis and nephron loss

179
Q

Detection of diabetic nephropathy clinically?

A
  1. Microalbuminaemia = 30-300mg/d or ACR >3mg/mM, is a strong independent RF for CVD
180
Q

When should T2DM be screened for microalbuminuria?

181
Q

Mx of diabetic nephropathy?

A
  1. Good glycaemic control delays onset and progression
  2. Control HTN <130/80, ACEi/ARB even if normotensive
  3. Combined Pancreas Kidney Transplant in select pts
182
Q

Commonest cause of death in diffuse systemic sclerosis?

A

Renal crisis with malignant HTN and AKI

183
Q

4 causes of RAS?

A
  1. Atherosclerosis in 80%
  2. Fibromuscular dysplasia
  3. Thromboembolism
  4. External mass compression
184
Q

Fibromuscular dysplasia defn?

A

A non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery. FMD has been found in nearly every arterial bed in the body although the most common arteries affected are the renal and carotid arteries

185
Q

RAS presentation?

A
  1. Refractory HTN
  2. Renal Bruits
  3. Renal function worsening after ACEi/ARB
  4. Flash pulmonary oedema
186
Q

RAS Ix?

A
  1. CT/MR angio

2. Renal angiography

187
Q

RAS Mx?

A
  1. Rx medical CV risk factors
  2. Angioplasty and stenting
  3. AVOID ACEi/ARB
188
Q

IBD Ix?

A
  1. Bedside = stool culture + CDT
  2. Bloods = FBC, U&E, LFTs, Clotting, ESR, CRP, haematinics
  3. AXR = toxic megacolon/obstruction
  4. Contrast (Ba/Gastrograffin enema)
  5. MRI = perianal diseas
  6. Colonoscopy
  7. Wireless capsule endoscopy
189
Q

Differences between UC and CD classification?

A

Macroscopic and microscopic

190
Q

Macroscopic difference b/w UC and CD?

A
  1. Location
  2. Distribution
  3. Strictures
191
Q

Microscopic difference b/w UC and CD?

A
  1. Fibrosis
  2. Ulceration
  3. Granulomas
  4. Pseudopolyps
  5. Inflammation
  6. Fistulae
192
Q

UC macroscopic features?

A
  1. Location = rectum + colon + backwash ileitis
  2. Distribution = contiguous
  3. Strictures = No
193
Q

CD macroscopic features?

A
  1. Location = mouth to anus, esp. terminal ileum
  2. Distribution = skip lesions
  3. Strictures = Yes
194
Q

UC microscopic features?

A
  1. Fibrosis = None
  2. Ulceration = Shallow, broad
  3. Granulomas = None
  4. Pseudopolyps = Marked
  5. Inflammation = Mucosal
  6. Fistulae = No
195
Q

CD microscopic features?

A
  1. Fibrosis = Marked
  2. Ulceration = Deep, thin and serpiginous (Cobblestone mucosa)
  3. Granulomas = Present
  4. Pseudopolyps = Minimal
  5. Inflammation = Transmural
  6. Fistulae = Yes
196
Q

Truelove and Witts UC criteria?

A
  1. Symptoms = BM>6/d, Large PR bleed
  2. Signs = HR > 90, Pyrexia > 37.8
  3. Lab values = Hb < 10.5, ESR >30
197
Q

General Mx of acute IBD flare?

A
  1. Resus = admit, NBM, hydration
  2. Hydrocortisone = 100mg IV QDS + PR if rectal disease
  3. Thromboprophylaxis = LMWH
  4. Dietician review
198
Q

Acute IBD flare monitoring?

A
  1. Bedside = daily examination, vitals, stool chart

2. Bloods = FBC, U&E, ESR, CRP

199
Q

Crohns flare acute Mx?

A
  1. Abx = metronidazole PO/IV
  2. Consider parenteral nutrition
  3. Improvement –> oral pred 40m/d
  4. Refractory = methotrexate +/- infliximab
200
Q

UC flare acute Mx?

A
  1. Improvement –> oral pred + 5-ASA

2. Refractory - ciclosporin or infliximab

201
Q

Indications for surgery during acute IBD flare?

A
  1. Obstruction
  2. Perforation
  3. Haemorrhage
  4. Failure to respond to medical Mx
  5. Megacolon
202
Q

CD complications?

A
  1. Fistulae
  2. Perianal abscess
  3. Strictures
  4. Malabsorption
  5. Toxic dilatation
203
Q

UC complications?

A
  1. Obstruction
  2. Perforation (toxic megacolon)
  3. Haermorrhage
  4. Malignancy (Colorectal/cholangio)
  5. VTE
204
Q

Extra-intestinal features of IBD?

A
  1. Skin
  2. Eyes
  3. Mouth
  4. Joints
  5. Hepatic
  6. Other
205
Q

IBD skin features?

A
  1. Clubbing
  2. Erythema nodosum
  3. Pyoderma gangrenosum
206
Q

IBD mouth features?

A

Aphthous ulcers

207
Q

IBD eye features?

A
  1. Anterior uveitis

2. Episcleritis

208
Q

IBD joint features?

A
  1. Large joint arthritis

2. Sacroiliitis

209
Q

IBD hepatic features?

A
  1. Fatty liver
  2. Cirrhosis due to chronic hepatitis
  3. Gallstones (esp. CD)
  4. PSC + Cholangiocarcinoma (esp. UC)
210
Q

IBD ‘other’ features?

A

AA amyloidosis

Oxalate renal stones

211
Q

General Mx of mild-moderate IBD?

A
  1. MDT = GP, gastroenterologist, dietician, nurses, surgeon
  2. Nutrition = ADEK vitamins, high fibre diet (esp. CD)
  3. Induction
  4. Maintenance
212
Q

UC induction meds?

A
  1. 5-ASAs
  2. Prednisolone
  3. Ciclosporin/infliximab
  4. Topical = enemas/foams: 5-ASA/pred
213
Q

CD induction meds?

A
  1. Ileocaecal = budesonide
  2. Colitis = sulfasalazine
  3. Prednisolone
  4. Methotrexate
  5. Infliximab/adalimumab
214
Q

UC maintenance meds?

A
  1. 5-ASA
  2. Azathioprine
  3. Infliximab/Adalimumab
215
Q

CD maintenance meds?

A
  1. Azathioprine
  2. Methotrexate
  3. Infliximab/adalimumab
216
Q

Which drug classes are largely used for each of CD and UC?

A
  1. UC = aminosalicylates

2. CD = methotrexate

Medicine and Surgery Mushkies (52 decks)

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