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PATH FINAL > Body PATH > Flashcards

Body PATH Flashcards

1
Q

Polyarteritis Nodosa (PAN)
- Epi
- Affected parts ?
- Association ?
- Prognosis ?

A

Epi
- PAN is more common in MAN

Affects
- Renal (90% - microaneurysms), GI, Cardiac, CNS (aneurysms)
- spares Lung

Associations
- Hep B and C**

Prognosis
- Fatal if untreated (progressive renal failure or gastrointestinal complications)

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2
Q

PAN patho

A

PAN: Immune complex mediated

Wegners, Churg Strauss, Microscopic Polyangiitis: ANCA

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3
Q

HSP
- features

A

Most common vasculitis in Children
Systemic disease (GI most common)

Feature
- Painful bloody diarrhea
- Common lead point for Intuss
1) Intussusception
2) Scrotum with massive skin oedema
3) Colitis (thumb printing on x-ray)

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4
Q

Behcets
- Clinical presentation ?
- Feature

A

Clinical
- Mouth and genital ulcers
- Turkish descent
- Aortic thickening

Feature
- Pulmonary artery aneurysm (likely shown)*
- pericarditis
- CNS: T2 hyperintensities (thalamus, midbrain, and internal capsule): most common

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5
Q

Esophageal web
- location
- association

A

Location
- Upper esophagus

Association
- Plummer-Vinson syndrome: iron deficiency anemia, glossitis, and cheilosis
- graft-versus-host disease
- gastro-oesophageal reflux disease
- Radiation

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6
Q

Esophageal web
- Circumferential or Semi-circumferential

A
  • Semi-circumferential (typically arise from the anterior wall and never from the posterior wall)*
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7
Q

Zenkers Diverticulum vs Killian-Jamieson location

A

Zenkers
- “Killian triangle” Hypopharynx (not cervical esophagus)
- Midline posterior wall of distal pharynx
- Pulsion type
- FALSE diverticulum (Traction diverticulum is TRUE diverticulum)
- increased risk for aspiration. Surgically treated with an endoscopic, surgical diverticulectomy, or diverticulopexy.

Killian-Jamieson
- Cervical esophagus (below cricopharyngeus)
- “Killian-Jamieson space”
- Anterolateral
- Pulsion type
- FALSE diverticulum (Traction diverticulum is TRUE diverticulum)

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8
Q

Epiphrenic Diverticula vs Para-esophageal hernia location

A

Epiphrenic Diverticula
- just above the Diaphragm (usually right)
- pulsion type

Para-esophageal hernia
- on the left
- pulsion type

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9
Q

Barrett esophagus
- Metaplasia of what to what ?
- Increased risk for ?

A

Cause
- Intestinal (Columnar) metaplasia of esophageal squamous epithelium

Increased risk
- 40x increased risk for adenocarcinoma* (10% progresses to adenocarcinoma*)

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10
Q

Barrett esophagus
- Microscopic finding

A
  • Goblet cells (diagnostic), secrets mucin
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11
Q

Barrett Esophagus stricture at high, mid or low esophagus ?

A

Mid esophagus

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12
Q

Carcinoid
- risk factors

A
  • Autoimmune chronic gastritis
  • MEN-1
  • NF-1 (gist also NF-1 RF)
  • TS
  • VHL
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13
Q

How common is Carcinoid syndrome

A
  • Uncommon (<10%)
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14
Q

Other syndrome Carcinoid can cause ?

A

Zollinger Ellison

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15
Q

What can one measure for Carcinoid tumor

A
  • 24 hour urine 5-HIAA (metabolite of serotonin)
  • Chromogranin-A
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16
Q

What are the antibodies found in Celiac disease

A
  • transglutaminate IgA antibodies (most sensitive), antigliadin IgA or IgG, and anti-endomysial antibodies.
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17
Q

Right vs Left clinical symptoms of Colon cancer

A

Caecal and right-sided colon cancers: Fatigue and weakness due to iron-deficiency anaemia.

Left-sided: Occult bleeding, changes in bowel habits.

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18
Q

Explain the classic adenoma-carcinoma sequence

A

Accounts for up to 80% of sporadic colon tumours ie. Majority arise from polyps (1st path way, the other pathway is Microsatellite instability pathway)

  • “First hit” is either sporadic or inherited mutation of the APC allele followed by loss of the intact second
    copy of APC which is the second hit.
  • Further mutations of KRAS or inactivation of p53 accumulate then lead to the development of carcinoma.
  • Lose capacity to degrade B-catenin -> B-catenin accumulates -> Triggers cell proliferation

** KRAS gene is part of the signalling pathway that regulates cell growth

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19
Q

Ascending vs Descending colon cancer macroscopy

A

Ascending colon:
- Polypoid, exophytic masses, may be ulcerated
- Rarely obstruct

Descending colon:
- Annular lesions and cause luminal narrowing.
- Most are well to moderately differentiated adenocarcinomas with varying degrees of glandular differentiation and mucus production.

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20
Q

Menetrier disease involvement which part of stomach

A
  • Involves Fundus, spares Antrum
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21
Q

How does Pancreatic cancer cause Gastric Varices ?

A
  • Splenic vein thrombosis –> Gastric varices
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22
Q

All findings in Crohn’s

A
  • Cobble stone
  • Creeping fat
  • Crypt abscesses (UC also gets this)
  • Non-caseating granulomas
  • Pseudopolyps
  • Transmural with Lymphoid aggregates (UC has NO mural thickening - serosal surface normal)
  • Enlarged nodes (UC no enlarged nodes)
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23
Q

What are the 2 types of gastric cancer

A

Intestinal
- Preceded by Intestinal metaplasia*
- Bulky mass
- Form Glands*
- Broad cohesive fronts
- “neoplastic cells often contain apical mucin vacuoles”
- APC loss of function and gain of b-catenin function (c.f. Diffuse type)

Diffuse
- NO preceding intestinal metaplasia*
- Infiltrative
- Signet ring cell
- Don’t form glands
- Loss of e-cadherin (c.f. Intestinal type APC and b-catenin)
- Desmoplastic reaction*

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24
Q

Most common location of Gastric cancer in stomach

A
  • Lesser curve, Antrum*
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25
Q

Risk factors for GIT lymphoma

A

H-pylori (chronic inflammation) -> MALtoma - indoldent marginal B-cell lymphoma (ANTRUM)

Celiac disease -> T-cell lymphoma in proximal small bowel

Immunodeficiency, AIDS

Mediterranean lymphoma: Background of mucosal plasmacytosis

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26
Q

Causes of Chronic Gastritis

A

H-Pylori

Autoimmune Gastritis (Pernicious anemia)

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27
Q

Juvenile polyps
- associations
- Morphology

A
  • Sporadic (no malignant potential)
  • Syndromic (Malignant potential of colonic adenocarcinoma)
  • Have association with pulmonary AVMs.

Morphology
- characteristic cystic spaces representing dilated glands filled with mucin and inflammatory debris.

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28
Q

Peutz-Jeghers Syndrome
- increased risk for what ?

A
  • Cervical cancer (adenoma malignum)
  • Breast (50%)
  • Pancreas (36%)
  • Uterine, Ovary, Testis cancer
  • Lung
  • Intussusception*
  • GI tract adenocarcinomas*
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29
Q

FAP mostly inherited or sporadic ?

A

Inherited (75%)

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30
Q

Gardner syndrome consists of ?

A
  • Osteomas
  • Desmoids tumours
  • Epidermoid cysts
  • Dental abnormalities
  • Hypertrophy of the retinal pigment epithelium
  • Follicular thyroid carcinoma
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31
Q

Most common syndromic form of colon cancer ?

A

HNPCC

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32
Q

HNPCC more common which side ?

A

Right side

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33
Q

HNPCC inheritance ?

A

AD
- MSH2 and MSH1

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34
Q

HNPCC increased risk for what cancers ?

A
  • Endometrium
  • Stomach
  • Ovary
  • Uterus
  • Brain
  • Small bowel
  • Biliary tract
  • Pancreas
  • Skin
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35
Q

Which phase of Ischemic bowel does the most damage

A

two phases:
1. Initial hypoxic injury
2. Reperfusion injury: Greatest damage occurs

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36
Q

SCC esophagus Risk factors

A

HPV, smoking, alcohol, poverty, caustic oesophageal injury, achalasia, tylosis, Plummer-Vinson syndrome, radiation, diets deficient in fruit/veg and frequent consumption of very hot beverages

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37
Q

Causes Pneumatosis Coli

A
  • Cystic Fibrosis, Asthma
  • COPD
  • IBD*
  • Steroids and Chemo
  • Scleroderma (and other connective tissue disease)
  • Gas producing bacteria e.g. clostridium
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38
Q

Is Pseudomembranous colitis specific to C-diff ?

A

Pseudomembranes are not specific and can be seen in ischaemic bowel and necrotising infections.

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39
Q

Appendiceal carcinoid clinical presentation ?

A
  • Usually asymptomatic and discovered incidentally at surgery*
  • Otherwise may present with appendicitis or mucocele (less common) due to obstruction
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40
Q

Appendiceal carcinoid benign or malignant ?

A
  • Almost always benign and distant spread is exceptionally rare*
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41
Q

Mucocele cause

A
  • Mucocoele = macroscopic appearance of the appendix when it is distended with mucus.

Cause
- benign or malignant chronic obstruction of the appendix such as mucosal hyperplasia, adjacent caecal tumor, mucinous cystadenoma/adenocarcinoma

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42
Q

Mucocele ruptures often, T or F ?

A

F, rarely ruptures

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43
Q

Celiac disease bowel changes

A
  • Dilated jejunum with complete loss of folds
  • Jejunum loses folds and look like normal ileum (reversal)
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44
Q

Whipples disease involvement site

A

Proximal jejunum

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45
Q

Whipple’s ddx ? (pseudo-whipples)

A

MAI (instead of T.Whipplei)
- distinction done with acid fast stain

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46
Q

Spigelian Hernia location

A
  • At the lateral border o f the rectus (Semilunar line)
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47
Q

Richter Hernia

A

Contains only one wall of bowel and therefore does not obstruct.

These are actually at higher risk for strangulation.

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48
Q

Femoral hernia location

A
  • Inferior to inferior epigastric
  • Medial to common femoral vein (often indents it)
  • Below the pubic tubercle* (both inguinal hernias above)
  • Obstruction more common than others*
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49
Q

Which side of paraduodenal hernia more common ?

A

Left

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50
Q

Features of left vs right paraduodenal hernia

A

Left (fossa of Lanzert)
- behind IMV
- DDx (Lesser sac hernia - behind stomach)

Right (fossa of Waldeyer)
- associated with Malrotation
- behind SMA and below duodenum

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51
Q

Sigmoid vs Caecal volvulus features

A

Sigmoid
- Haustra lost
- Points RUQ

Caecal volvulus
- Haustra maintained
- Dilated small bowel loops

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52
Q

Giant Hemangioma features and complication

A

Features:
- Incomplete fill in
- Peripheral calcifications
- Hemorrhage, Necrosis

Complications:
- Kasabach-Merritt syndrome: consumptive coagulopathy due to thrombocytopenia

  • Rupture with hemoperitoneum
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53
Q

FNH test to do ?

A

Sulfur colloid hot

HIDA scan

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54
Q

OCP affect on FNH ?

A
  • OCP use has a trophic effect, but does not cause FNH**
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55
Q

FNH association

A
  • Hemangiomas
  • Hepatic adenomas
  • Meningioma, Astrocytoma
  • AVMs
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56
Q

4 Cirrhosis microscopic changes ?

A
  1. Bridging fibrous septae
  2. Regenerative nodules
  3. Architectural disruption
  4. Vascular derangement
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57
Q

Hepatic adenoma 3 types

A

Inflammatory
- most common
- risk to bleed if >5cm
- associated with NAFLD, obesity, OCP
- small definite risk of cancer
- dystrophic vessels “telangiectatic”

HNF-1a
- ONLY in women
- associated with OCP
- Fat containing
- Multiple masses

B-catenin
- Cancer risk
- associated with Anabolic steroids, Glycogen storage disease, FAP
- MEN and WOMEN

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58
Q

Hepatic adenoma Microscopic finding

A
  • Absence of portal and central vein and bile ducts**
  • Contains fat mainly in HNF-1a
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59
Q

Management and prognosis of Hepatic adenoma (eg. b-catenin type)

A
  • B-catenin type resected even if asymptomatic
  • Tumors may regress on withdrawal of OCPs
  • Risk of rupture is increased in pregnancy**
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60
Q

Serum AFP sensitivity for HCC screening

A
  • Serum AFP is elevated in 50% of patients with advanced HCC
  • Insensitive as a screening test as can be normal in patients with premalignant or early HCC.
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61
Q

HCC major and other risk factors ?

A

Major
- HBV, HCV, alcohol, NASH

Others:
- Hereditary haemochromatosis, alpha-1 antitrypsin deficiency, Wilson disease, tyrosinaemia, glycogen storage disorders, Primary biliary cholangitis/cirrhosis, Hepatic adenoma

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62
Q

PBC pathology and imaging and complication

A

Path:
- Destruction of small intrahepatic bile ducts, portal inflammation, and progressive scarring
- High AMA

Imaging:
- Lace-like fibrosis and periportal halo sign are seen together the sensitivity for primary biliary cholangitis can approach 70%
- Regional lymphadenopathy: tends to dominate in the gastrohepatic ligament and porta hepatis

Complication
- Cirrhosis

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63
Q

HCC genetic changes

A

Early changes
- Activation of b-catenin
- Inactivation of p53

Precursors
- dysplastic nodule
- small cell change
- large cell change

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64
Q

Hepatic adenoma associations/RFs

A
  • Diabetes**
  • Metabolic syndrome*
  • Obesity
  • Glycogen storage disease
  • Anabolic steroids
  • OCPs
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65
Q

HBV transmission route in high vs low prevalence areas

A

High prevalence
- Transmission during childbirth accounts for 90% of HBV cases in high prevalence areas

Low prevalence
- Unprotected sex and IVDU are the chief modes of spread

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66
Q

Aetiologies of Hepatitis

A
  • Viral hepatitides
  • Parasites
  • Drug induced (Paracetamol, ETOH)
  • Autoimmune
  • Steatohepatitis
  • Metabolic disease
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67
Q

Hepatitis B
- how many % ends in chronic infection ?
- how many % makes full recovery and clearance ?
- How many % get acute fulminant hepatitis ?

A
  • 10% get chronic infection (c.f. HCV 90% chronic infection and 20% develops cirrhosis)
  • 90% make full recovery and clearance
  • 1% get acute fulminant hepatitis (HCV also very rare)
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68
Q

Hepatitis B dsDNA or RNA ?

A
  • Partially dsDNA (c.f. HCV ssRNA)
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69
Q

Hepatitis C association ?

A
  • Associated with Metabolic syndrome
  • Will give rise to insulin resistance and NAFLD
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70
Q

Majority or Minority of HCV will clear virus ?

A
  • only Minority will clear virus* (c.f. Hep B Majority)
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71
Q

Which hepatitis dependent on HBV ?

A

Hep D dependent on HBV either as co-infection or superinfection*

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72
Q

Hepatitis E high mortality rate in what demographic ?

A
  • High mortality rate in pregnant women*
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73
Q

Pancreatic serous cystadenoma
- Location
- Benign or malignant

A

Location
- Pancreatic head (most common)

Path
- Lots of small cysts , tend to be < 10mm separated by fibrous septa radiating from a central scar which may be calcified
- Benign

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74
Q

Mucinous cystadenomas
- how many % associated with invasive component ?

A

Can be precursors to invasive pancreatic carcinoma, around 20% associated with invasive component –> need to be resected

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75
Q

What pancreatic lesion is Peutz-Jegher associated with

A
  • IPMN
  • Pancreatic ductal adenocarcinoma
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76
Q

Classic feature of Pancreatic insulinoma

A
  • Amyloid deposition**
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77
Q

Features of Glucagonoma

A
  • Diabetes and skin rash
  • sometimes DVT and PE
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78
Q

Features of VIPoma

A
  • Diarrhea
  • Hypokalemia
  • Achlorydia
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79
Q

Features of Somatostatinoma

A
  • Diabetes
  • Biliary dyskinesia with stones
  • Steatorrhea
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80
Q

Clinical findings of PBC including labs

A

Usually identified on work up of raised ALP and GGT when it is asymptomatic.

When symptomatic, there are insidious findings of fatigue and pruritus.

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81
Q

What’s unique about PBC cirrhosis ?

A
  • Hepatomegaly cirrhosis (rather than shrunken)
  • Not all end stage PBC end up with cirrhosis
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82
Q

What microscopic lesion is diagnostic of PBC ?

A
  • Florid duct lesion: small bile ducts are actively destroyed by lymphoplasmacytic inflammation with or without the formation of granulomas.
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83
Q

Lab findings of PBC

A
  • characteristic laboratory finding is antimitochondrial antibodies. ALP and GGT are raised.
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84
Q

Echinoccoccus granulosus vs Echinococcus multilocularis

A

Echinoccoccus granulosus (more common)
- dogs definitive host
- sheeps intermediate host
- human accidental host
- better prognosis*

Echinococcus multilocularis
- fox definitive host
- rodent intermediate host
- worse prognosis* - more invasive

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85
Q

Which layer of Hydatid cyst gives rise to daughter cyst

A
  • Endocyst layer
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86
Q

Type I Hypersensitivity reaction
- type ?
- examples ?

A

Type I Hypersensitivity reaction
- Immediate
- IgE and Mast cell mediated

Examples
- Anaphylaxis
- Bronchial asthma
- Allergic rhinitis
- Food allergies

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87
Q

Type II Hypersensitivity reaction
- type ?
- examples ?

A

Type II Hypersensitivity reaction
- Antibody mediated*
- IgG or IgM tags cell for phagocytosis

Examples
- Autoimmune haemolytic anaemia
- Pemphigus
- ANCA vasculitis
- Goodpasture
- Acute rheumatic fever
- Graves, myasthenia
- Pernicious anaemia

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88
Q

Type III Hypersensitivity reaction
- type ?
- examples ?

A

Type III Hypersensitivity reaction
- Immune complex mediated
- Inflammation and tissue injury from immune complex deposition

Examples
- SLE
- Post strep GN
- PAN
- Serum sickness
- Reactive arhtirits

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89
Q

Type IV Hypersensitivity reaction

A

Type IV Hypersensitivity reaction
- T-cell mediated
- Caused by inflammation resulting from cytokines produced by CD4 T cells, and cell killing by CD8 T cells

Examples
- Rheumatoid arthritis
- MS
- T1 DM
- IBD
- Psoriasis
- Contact sensitivity
- Tuberculin reaction

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90
Q

Stages of Cysticercosis/neurocysticercosis

A
  1. Larval tissue invasion
  2. Vesicular
  3. Colloidal vesicular
  4. Granular nodular
  5. Calcified
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91
Q

Who gets a Nutmeg liver ?

A

Nutmeg liver: Inhomogeneous mottled appearance
- Budd Chiari
- Hepatic veno-occlusive disease
- Right heart failure
- Constrictive pericarditis

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92
Q

Who gets massive caudate lobe hypertrophy ?

A
  • Budd-Chiari (chronic phase, caudate hypertrophy and peripheral atrophy)
  • Primary Sclerosing Cholangitis
  • Primary Biliary Cirrhosis
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93
Q

Is portal HTN a contraindication to Liver transplant ?

A
  • NO, only makes it more challenging
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94
Q

Normal transplant liver US features

A
  • Rapid systolic upstroke
  • RI between 0.5 - 0.7
  • Hepatic artery peak velocity <200cm/s
  • Hepatic artery is KING in a transplanted liver, it is the primary source of blood flow for the bile ducts
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95
Q

PSC vs AIDS Cholangitis

A

AIDS Cholangitis
- Infection of the biliary epithelium {classically Cryptosporidium)
- Appearance mimics PSC with intrahepatic and/or extrahepatic multifocal strictures.
- The classic association/finding is papillarv stenosis (which occurs 60% of the time).

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96
Q

Oriental Cholangitis (Recurrent pyogenic cholangitis) Features and Association ?

A
  • Dilated ducts that are full of pigmented stones
  • “Straight rigid intrahepatic ducts”
  • The anatomically longer, flatter left biliary system tends to make the disease burden left dominant
    (the opposite of hematogenous processes
    which favor the right lobe).

Association
- Clonorchiasis, ascariasis, and nutritional deficiency.

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97
Q

Causes of Portal Vein Pulsatility:

A

Right-sided CHF, Tricuspid Regurg, Cirrhosis with Vascular AP shunting.

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98
Q

Causes o f Portal Vein Reversed Flow:

A

The big one is Portal HTN (any cause).

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99
Q

Amyloidosis stains

A

Congo red stain – under ordinary light imparts a pink/red colour to tissue deposits

Apple-green birefringence of the stained amyloid when observed by polarised light microscopy

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100
Q

Which type of amyloidosis worst prognosis and which one good

A
  • Prognosis very poor for AL type (<2 year survival).
  • Secondary amyloidosis AA type prognosis is better (Chronic inflammation, RA, TB, RCC etc)
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101
Q

Cholesterol gallstone RF ?

A

female sex

middle age

obesity

positive family history

recent rapid weight loss**

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102
Q

Sickle cell and Crohn disease cause what type of gallstone ?

A

Black Pigmented stone

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103
Q

Acute vs Chronic hepatitis morphology ?

A

Periportal inflammation only seen in Chronic*

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104
Q

Cholangiocarcinoma risk factors ?

A
  • BRCA2
  • Opisthorchis spp. and Clonorchis spp.
  • PSC, PSC, hepatolithiasis, Caroli disease, choledochal cysts
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105
Q

Wilson’s disease lab findings ?

A
  • FREE serum copper: Increased (*serum copper reduced)
  • Urinary copper: Increased

(everything else, including ceruloplasmin are reduced)

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106
Q

Wilson’s disease manifestations ?

A

Hepatic
- Acute hepatitis
- Chronic hepatitis
- Cirrhosis
- Fulminant hepatic necrosis

Brain
- Abnormal T2 hyperintensity in the putamina is the most common MRI abnormality, followed by midbrain, pons, and thalamus
- dysarthria, dystonia, tremor, parkinsonism, choreoathetosis, and ataxia and gait anomalies

MSK
- premature osteoarthritis
- osteopenia

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107
Q

List out Calcium, PTH, and phosphate levels for the 3 types of Hyperparathyroidism

A

Primary hyperparathyroid - high Ca, low phosphate, high PTH

Secondary hyperparathyroid - TRUE, low Ca, high PTH, and high phosphate

Tertiary hyperparathyroid - high Ca, and VERY high PTH, low phosphate

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108
Q

Features may indicate that a polyp is higher risk

A

> 2cm

> 3 adenomas

high grade dysplasia

Villous features

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109
Q

What are secondary causes of hemochromatosis ?

A
  • Iron transfusion
  • Thalassemia, Sickle cell
  • Bantu siderosis
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110
Q

Differentials for Hemochromatosis

A

Amiodarone Therapy
- Iodine-containing antiarrhythmic medication
- Diffuse, homogeneously dense liver on NECT

Glycogen Storage Disease
- ↑ or ↓ attenuation of liver on NECT
- Depends on specific type of disease
- Associated with multiple hepatic adenomas (60%)

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111
Q

Other signs of Hemochromatosis apart from liver

A
  • Dilated cardiomyopathy
  • Hepatomegaly: 90%
  • Arthralgia: 50%
  • Diabetes: 30%
  • Dilated cardiomyopathy
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112
Q

GIST associated syndromes

A
  • Carneys triad
  • Carneys Stratakis syndrome
  • NF-1
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113
Q

GIST
- arise from what cell ?
- stains what ?
- genetic mutation of what ?

A
  • Arise from interstitial cell of Cajal
  • CD117 (c-KIT) positive stain
  • SDH subunit gene alternation
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114
Q

What is Medullary spong kidney disease

A

sporadic condition where the medullary and papillary portions of the collecting ducts are dysplastic and dilated and in most cases develop medullary nephrocalcinosis.

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115
Q

What are the associated syndromes of GIST ?

A

Carneys triad
- Extra-adrenal Paraganglioma
- GIST
- Pulmonary Chondroma

Carneys stratikis

NF-1

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116
Q

What are the causes of Caecal volvulus ?

A
  1. Developmental failure of peritoneal fixation allows the proximal colon to be free and mobile: this occurs in 11-25% of the population
  2. Restriction of the bowel at a fixed point within the abdomen, acting as a fulcrum for rotation, e.g. adhesion, abdominal mass, scarring from calcified lymph nodes
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117
Q

Renal TB seen in what kinda patients ?

A

Immunocompromised
- results from haematogenous spread at the time of primary infection

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118
Q

Renal TB radiology findings

A

Early
- papillary necrosis

Progressive
- multifocal strictures and hydronephrosis
- mural thickening and enhancement (on cross-sectional imaging

End stage
- Shrunken kidney with amorphous dystrophic calcifications
- Autonephrectomy

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119
Q

Renal TB DDx

A
  • Medullary sponge kidney
  • Papillary necrosis
  • XGP
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120
Q

What are the indications for TIPS ?

A

Transjugular intrahepatic portosystemic shunt (TIPS)
- bypass the liver by forming communication between Portal vein and Hepatic vein ( The target portosystemic gradient after TIPS formation is <12 mmHg)

Indications
- Portal HTN with
- variceal bleed
- ascites refractory to treatment
- hepatorenal syndrome
- Budd-Chiari
- Malignant compression of hepatic or portal veins

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121
Q

how does one get Tuberous Sclerosis ?

A
  • Spontaneous (80%)
  • AR (20%)
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122
Q

Lipid poor AML DDx

A
  • RCC (calcification, irregular, large, invade sinus)
  • Retroperitoneal liposarcoma invading kidney
  • Oncocytoma (May contain fat)
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123
Q

AMLs are part of what group ? and are composed of what components ?

A

PEComas (perivascular epitheliod cells tumor group)
- Others include LAM

Composed of
- blood vessels (-angio) lacking elastic tissue, plump spindle cells (-myo), and adipose tissue (-lipo).

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124
Q

XPG (Xanthogranulomatous pylonephritis)
- causative organism ?

A
  • Escherichia coli and Proteus mirabilis
  • Struvite stones
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125
Q

Pheochromcytoma associations

A
  • MEN2a/2b: Almost never extra-adrenal, almost always bilateral
  • VHL
  • NF1
  • Carney triad (extra-adrenal pheo)
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126
Q

Pheochromocytoma arises from what cell ?

A
  • Chromaffin cells of the Adrenal medulla
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127
Q

Locations of Pheochromocytoma

A

10% extra-adrenal: more likely to be malignant and metastasise

Along the sympathetic chain as well as in the urinary bladder and organ of Zuckerkandl (origin of IMV).

Thoracic paragangliomas are rare and only account for 1-2% of all cases of phaeochromocytoma

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128
Q

Pheochromocytoma genetics mutation

A

(SDHB) gene mutations

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129
Q

Can you differentiate pheochromcytoma benign to malignant ?

A
  • No
  • Need to see invasion of adjacent structures
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130
Q

Clinical features and radiology of Pheochromocytoma

A

Secondary hypertension and positive urinary catecholamines

Usually large and heterogeneous adrenal masses, with cystic and necrotic components

Vivid enhancement in arterial/portal venous phase is suggestive: >110-120 HU

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131
Q

Management of Pheochromocytoma

A

Definitive treatment is surgical, and if complete resection is achieved, without metastases, then surgery is curative and hypertension usually resolves.

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132
Q

MEN-1
MEN-2

A

MEN-1
- Parathyroid hyperplasia (most common)
- Pituitary adenoma (Prolactinoma)
- Pancreatic Neuroendocrine tumor (Gastrinoma > Insulinoma)

MEN-2
- Pheochromocytoma
- Medullary thyroid cancer
- Parathyroid hyperplasia

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133
Q

3 types of Cholangiocarcinoma ?

A

Intraductal

Periductal

Mass forming

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134
Q

Classification for resectability of Cholangiocarcinoma

A

Bismuth-Corlette classification

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135
Q

Innervation of Anal Sphincters

A

Internal anal sphincter:
- parasympathetic and sympathetic fibres from the superior and inferior hypogastric plexus

External anal sphincter:
- Pudendal nerve (inferior rectal and deep perineal branches)

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136
Q

Anal tumor vs Rectal tumor staging ?

A

Anal tumor staging is mostly based on size and extension, rather than wall invasion.

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137
Q

Anal tumor most common type (adeno, scc etc.)

A

SCC

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138
Q

Anal tumor risk factors

A

HIV
HPV
Immunosuppression

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139
Q

Two sub types of rectal tumor ?

A

Adenocarcinoma (majority)
1. Mucinous adenocarcinoma
2. Signet ring cell adenocarcinoma

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140
Q

Prognostic factors of rectal tumor

A

EMVI (extra mural venous invasion)
Tumor deposits
Lymph node metastases
CRM (Circumferential resection margin) less than 1-2mm is poor prognosis

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141
Q

Layers of the rectum

A

From inside to out
- Muscularis Mucosa
- Submucosa (T1)
- Muscularis propria (T2)

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142
Q

Most useful sequence for rectal cancer MRI

A

High Resolution T2 with 1.0mm voxel

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143
Q

Rectal cancer T2 or T3 ? What is this MRI artifact called ?
Sagittal: Rectum bent and not straight, shows clearly intact muscularis propria
Axial: Appears to invade through muscularis propria

A

Partial volume artifact
- Look at sagittal for confirmation as axial will have partial voluming artifact

143
Q

T staging of rectal cancer ?

A

T1: tumour invades submucosa

T2: tumour invades muscularis propria

T3: tumour invades through the muscularis propria
- T3a: tumour extends <1 mm beyond muscularis propria
- T3b: tumour extends 1-5 mm beyond muscularis propria
- T3c: tumour extends 5-15 mm beyond muscularis propria
- T3d: tumour extends 15 mm beyond muscularis propria

T4a: tumour penetrates to the surface of the visceral peritoneum
T4b: tumour directly invades or is adherent to other organs or structures

144
Q

What are good MRI protocols for rectal cancer ?

A
  1. Sagittal HR T2
  2. Axial HR T2
  3. Small FOV T2
  4. Diffusion weighted imaging (optional)
145
Q

Complications of Percutaneous Cholecystostomy

A
  • Catheter Migration
  • Bile leakage and bile peritonitis
  • Bowel Injury
  • Sepsis
146
Q

Gastric adenocarcinoma risk factors ?

A
  • Pernicious anemia
  • Atrophic Gastritis
  • Bill Roth 2 procedure
  • Smoking
  • Type A blood group
147
Q

Name 4 eponymous names associated with Gastric nodal mets

A
  • Sister mary joseph’s node
  • Krunkenberg’s node
  • Irish node
  • Virchow’s node
148
Q

What is the most common subtype of gastric adenocarcinoma ? name other types

A
  • Mucinous gastric adenocarcinoma (Most common subtype)
  • The other WHO subtypes are tubular, papillary, and poorly-cohesive.
149
Q

Name some non-neoplastic gastric polyps

A
  • Hyperplastic polyps
  • Inflammatory polyps
  • Harmatomatous polyps
150
Q

Name hamartomatous polyposis syndromes

A
  • Peutz-Jeghers syndrome
  • Juvenile polyposis syndrome
  • Cowden syndrome
  • Cronkhite-Canada syndrome
151
Q

Why are esophageal cancers prone to focal spread ?

A
  • Lacks serosal layer*
152
Q

Esophageal carcinoma complications

A
  • Esophago-pulmonary or mediastinal fistula
  • Perforation
152
Q

Name a few types of Esophageal carcinoma

A
  • Squamous cell carcinoma (most common world wide)
  • Adenocarcinoma
  • Mucoepidermoid carcinoma
  • Adenoid cystic carcinoma
  • Lymphoma
153
Q

How is the malignant potential of a gastrointestinal stromal tumour (GIST) determined?

A

tumour size, mitotic count, site of origin — correct!

Explanation
Several factors determine the malignant potential of a gastrointestinal stromal tumour (GIST). These include the tumour’s size, mitotic count (rate of cell division), site of origin within the gastrointestinal tract (gastric lesions are less aggressive), and perforation. These criteria help classify GISTs into risk categories, guiding clinicians in assessing the tumour’s aggressiveness and determining the most appropriate course of treatment.

154
Q

Diagnostic criteria GENE mutation for GIST ?

A
  • KIT and/or DOG1 immunopositivity
  • SDHB gene mutation in SDH-deficient GISTs

SDH gene mutation seen in
- sympathetic paragangliomas, head and neck paragangliomas, phaeochromocytomas, renal cell carcinoma (RCC), and gastric gastrointestinal stromal tumours (GIST)

155
Q

prostatic utricle cyst associations

A

hypospadias

cryptorchidism

unilateral renal agenesis

anorectal malformations e.g. imperforate anus

156
Q

How to differentiate Prostatic utricle cyst from Müllerian duct cyst ?

A

Müllerian duct cyst
- older age (second or third decade of life)
- usually large and tear drop shape
- may extend above base of prostate

157
Q

Prostatitis grading

A

I: acute bacterial prostatitis
II: chronic bacterial prostatitis
III: chronic prostatitis and chronic pelvic pain syndrome (CPPS)
IV: asymptomatic inflammatory prostatitis

158
Q

What is granulomatous prostatitis

A
  • nodular form of chronic prostatitis. It is usually diagnosed on biopsy.
159
Q

Causes of granulomatous prostatitis

A
  • idiopathic
  • TB
  • iatrogenic: Bacillus Calmette–Guérin (BCG) vaccine
  • intravesical BCG therapy for bladder cancer
  • post-radiotherapy
  • sarcoidosis
  • autoimmune
160
Q

BPH treatments

A
  • Alpha-blocker (5 alpha reductase)
  • Transurethral resection of the prostate (TURP)
  • Prostatic arterial embolisation (PAE) = microsphere and micro
161
Q

Embolisation agents

A

Temporary
- starch microsphere
- gel foam
- blood clot

Permanent
- microparticles
- coils

162
Q

Prostate cancer risk factors

A
  • Obesity
  • Smoking
  • BRCA2
  • Elderly
163
Q

Causes of small bowel intussusception ?

A

Meckel diverticulum, lipoma, GIST or polyps

164
Q

What does Faecal calprotectin do ?

A

Faecal calprotectin (FCAL) is a protein marker of gut inflammation. It is used for:

  1. distinguish inflammatory bowel disease from irritable bowel syndrome
  2. assess disease activity in inflammatory bowel disease, including acute exacerbations and response to treatment
165
Q

Extra-intestinal manifestations of Crohns?

A
  • Erythema Nodosum
  • Sacroilitis
  • Uveitis
  • Gallstones
  • PSC (more common in UC)
  • Interstitial lung disease
166
Q

Ogilvie syndrome risk factors

A

It is a parasympathetic dysfunction
(risk factors same as acalculous cholecystitis)
- Burns
- Trauma
- Diabetes
- Recent surgery
- Parkinsons

167
Q

Name 2 bowel and mesenteric injury grading system for CT

A

RAPTOR
- multifocal haematoma
- extravasation
- bowel haematoma
- devascularization
- faecalisation
- pneumoperitoneum
- fat pad injury (abdominal wall seat belt sign)

BIPS

168
Q

Name another watershed areas for ischemic colitis besides Splenic flexure (Griffith’s point)

A

Rectosigmoid junction (Sudek point)
- IMA and Superior rectal artery

That said, the Sudeck point is less susceptible to ischaemia than the Griffiths point, thanks to the submucosal arterial plexus formed by branches of the superior, middle, and inferior rectal arteries

169
Q

Complications of Ischemic Colitis

A

Gangrenous colitis (20%)

Non-Gangrenous colitis (80%)
- stricture colitis (non reversible)
- chronic colitis (non reversible)

170
Q

When is surgery required for ischemic colitis ?

A

Peritonitis
Perforation
Haemorrhage
Sepsis
Symptomatic stricture

171
Q

Occlusive or non-occlusive mesenteric ischemia has higher mortality rate ?

A

Occlusive (90%) higher morality rate

172
Q

What can faecaloma lead to?

A
  • stercoral colitis
  • stercoral perforation

Faecaloma:
- mass of faeces most frequently noted in the rectum and sigmoid colon, and is considered a severe/extreme form of faecal impaction.

173
Q

Causes of toxic megacolon

A
  • UC (most common cause)
  • Ischemic colitis
  • C-diff colitis
  • Radiation colitis
  • Colonic Lymphoma
174
Q

When is surgical treatment required in Diverticulitis ?

A

1.Who progress to stage III or IV
- Peritonitis, Pneumoperitoneum, generalized ascites(III)
- Faecal Peritonitis with findings same as above (IV)

2.Who fail medical management

3.Whom carcinoma cannot be excluded

4.Who have multiple (≥2) attacks

5.Who develop fistulas

175
Q

Indications for CT colonography ?

A

screening test for colorectal carcinoma

colon evaluation after incomplete or unsuccessful optical (conventional) colonoscopy

assessment of strictures

to better evaluate the colon proximal to obstructing neoplasms detected by conventional colonoscopy

patients with contraindications to or refusing optical colonoscopy

176
Q

Absolute contraindications for Colonography ?

A
  • Acute inflammatory conditions such as acute diverticulitis, active stage of ulcerative colitis or Crohn disease
  • Recent abdominal or pelvic surgery
177
Q

Colonography technique

A
  1. Bowel preparation
    - can tag residual stool with gastrografin
  2. Bowel distention
  3. IV contrast (optional)
  4. Antispasmodic agent
    - Buscopan
    - IV glucagon
178
Q

Why T2 vs T3 rectal tumor important to differentiate ?

A

T3 and/or N1 disease can receive preoperative down-staging with radiotherapy alone (more common in Europe) or combined chemo-radiotherapy (more common in the US)

179
Q

Complications of Mirrizi syndrome

A
  • Cholecystobiliary fistula
  • Cholecystocutaneous fistula
  • Cholecystoenteric fistula -> Gallstone ileus
  • Biliary stricture
  • Biliary cirrhosis
180
Q

What study besides ultrasound can be used to confirm acalculous cholecystitis ?

A

Tc99m Cholescintigraphy (HIDA scan)
- considered a highly reliable test and may be performed even in acutely ill patients. Ideally, there is non-visualisation of the gallbladder

181
Q

Why is it important to identify acalculous cholecystitis ?

A

The importance of recognising acalculous cholecystitis lies in the fact that these patients have a high rate of recurrence when treated with medical management. As such, cholecystectomy is the definitive treatment.

182
Q

Management of xanthogranulomatous cholecystitis ?

A

Cholecystectomy
- because cant differentiate from gallbladder carcinoma

183
Q

Associations of Primary sclerosing cholangitis

A
  • UC
  • Reidels thyroiditis
  • Sjogrens syndrome
  • Retroperitoneal fibrosis
  • Mediastinal fibrosis
  • Autoimmune hepatitis
  • Orbital pseudotumour
184
Q

Markers for Primary sclerosing cholangitis ?

A
  • ANA
  • AntiSMA
  • P-ANCA
185
Q

Primary sclerosing cholangitis complications

A
  • Cholangiocarcinoma
  • HCC
  • Gallbladder carcinoma
  • Colorectal carcinoma
186
Q

Typical vs Atypical FNH

A

Typical
- has central scar
- has central artery

Atypical
- no central scar
- no central artery

187
Q

Nuclear medicine imaging for FNH ?

A

Sulfur colloid and HIDA
- Hot on FNH due to uptake by Kupffer cells (c.f. Hepatic adenoma no uptake due to low Kupffer cells)

  • Can be used to distinguish focal nodular hyperplasia from other liver lesions which do not contain normal liver cellularity, such as hepatic adenomas, hepatocellular carcinoma, and hepatic metastases.
188
Q

3 types of HCC ?

A
  • Focal
  • Multifocal
  • Infiltrative
189
Q

Treatment options for HCC ?

A
  • Partial hepatectomy (for small lesion)
  • Liver transplant (need to meet Milan criteria)
  • TACE (chemo embolization), TARE (radioembolization)
190
Q

3 types of Cholangiocarcinoma ?

A
  • Periductal (Klatskin)
  • Intraductal
  • Mass forming
191
Q

When is hilar peri-hilar cholangiocarcinoma unresectable ?

A
  • Bismuth type IV: bilateral secondary biliary radicle involvement
  • Main portal vein encasement/occlusion
  • Atrophy of a liver lobe with contralateral portal vein or hepatic artery encasement
  • Atrophy of a liver lobe with contralateral secondary biliary radicle involvement
  • Involvement of both hepatic arteries
192
Q

Mass forming cholangiocarcinoma imaging appearance ?

A

DWI: Targetoid

CT: minor peripheral enhancement with gradual centripetal enhancement, Capsular retraction, Calcification (20%)

193
Q

Fibrolamellar HCC imaging apparance ?

A
  • Large
  • Central scar (enhance on delay)
  • Calcification
  • Capsule
  • Arterial heterogeneous
  • No uptake with Primovist
  • No uptake on Sulfur colloid (no Kupffer cell)
194
Q

Complications of pancreatitis

A
  1. Acute peripancreatic fluid collection
  2. Pseudocyst
  3. Acute necrotic collections
  4. Walled off necrosis
  5. Emphysematous pancreatitis (infected)
  6. Haemorrhage: erosion of vessels
  7. Pseudoaneurysm
  8. Splenic vein thrombosis
  9. Portal vein thrombosis
195
Q

Complications of pancreatic trauma

A
  • Pancreatitis (most common)
  • Haemorrhage
  • Fistula
  • Pseudocyst
  • Abscess
196
Q

A pancreatic laceration involves the main pancreatic duct. What AAST grade is this injury?

A

Grade 3

197
Q

Risk factors for pancreatic ductal adenocarcinoma

A
  • Smoking
  • Chronic pancreatitis
  • Diabetes
  • Diet rich animal fat and protein
  • Obesity
  • BRCA2
  • HNPCC
  • Peutz-Jeghers syndrome
198
Q

Precursors of pancreatic ductal adenocarcinoma

A

Pancreatic intraepithelial neoplasia (PanIN): responsible for more than 90% of pancreatic cancers

IPMN

Mucinous cystic neoplasm

199
Q

When is pancreatic ductal adenocarcinoma not resectable

A
  • SMA and Celiac axis involved
  • Metastasized
200
Q

What can be done to differentiate pancreatic mucinous neoplasm types ?

A

EUS ± FNA cytopathology, CEA, and CA 19-9 in differentiating cyst type

201
Q

Pancreatic serous cystadenoma associated syndrome

A

VHL

202
Q

Give examples of pancreatic neuroendocrine tumours

A

Insulinoma: Hypoglycemia

Gastrinoma: Zollinger-Ellison syndrome

Glucagonoma: Diabetes, Depression, DVT, Dermatitis
- most likely malignant

203
Q

Marker for Neuroendocrine tumor

A

Chromogranin-A

Synaptophysin

203
Q

What tests to do to differentiate pancreatic tail neuroendocrine tumour (pNET) from splenunculus ?

A
  • DOTATATE
  • RBC study
203
Q

Differentials for pancreatic pNET

A
  • Hypervascular mets (RCC, Melanoma, Thyroid cancer)
  • Splenunculus (if in tail)
  • Solid serous cystadenoma
204
Q

Treatment for pNET if functional ?

A
  • Resection
205
Q

Treatment for pNET if non-functional ?

A
  • Resect if >2cm
206
Q

What are some complications of a Whipples procedure ?

A
  • Gastric outlet obstruction / delayed gastric emptying
  • Anastomotic leakage (usually occurs within two weeks)
  • Pancreatic fistula
  • Pancreatitis of the residual gland
  • Biliary stricture
  • Wound infection
  • Abdominal abscess
  • Intra-abdominal haemorrhage
207
Q

How is pancreas transplant usually done ?

A

SPK: simultaneous pancreas and kidney transplant (~78% of cases)

-> The donor pancreas is removed along with the duodenum
-> the pancreas + duodenum then attaches to the recipient’s intestine

208
Q

Complications of pancreas transplant ?

A

Same as renal transplant
- Graft rejection
- Anastomotic breakdown and hemorrhage
- Stenosis or thrombosis of arterial inflow or venous outlflot
- Small bowel obstruction usually from adhesions, but internal hernia may occur
- Peripancreatic fluid collection
- Pancreatitis

209
Q

Risk factors for TB peritonitis

A

concomitant HIV infection

peritoneal dialysis

cirrhosis

210
Q

3 types of TB peritonitis ?

A
  • Wet type (most common)
  • Dry type
  • Fibrotic-fixed type
211
Q

Left Gastric vein vs Oesophageal varices which one more likely to bleed ?

A

Gastric varices

  • Considered distinct from oesophageal varices in that they have a propensity to haemorrhage at comparatively lower portal pressures
  • Associated with higher mortality rate with haemorrhage (range 14-45%)
212
Q

2 types of esophageal varices

A

Uphill (most common)
- Portal HTN
- Shunts portal vein to SVC via “Azygos vein”

Downhill
- SVC obstruction

213
Q

Name a few types of internal hernia

A
  • Left paraduodenal hernia (30%)
  • Right paraduodenal hernia (13%)
  • Pericaecal hernia (13%)
  • Foramen of Winslow, intersigmoid and transmesenteric hernias each comprise less than 10%.
214
Q

Location of obtuator hernia ?

A

Obturator hernias are characterised by bowel herniating between the obturator and the pectineus muscles.

215
Q

Obtuator hernias are usually asymptomatic unless what ?

A
  • Compress the obturator nerve: Howship-Romberg sign (only present in approximately half of cases)
  • Contain bowel which obstructs/strangulates/incarcerates
216
Q

Pseudomyxoma peritonei may be divided into two pathological subtypes which have aetiological and prognostic significance, which two ?

A

Peritoneal adenomucinosis
- Peritoneal neoplasm composed of mucin with minimal cytological atypia and mitosis
- primary tumor from adenoma

Peritoneal mucinous carcinoma
- Marked cytological atypica
- Primary tumor is mucinous adenocarcinoma

217
Q

Treatment and prognosis of Pseudomyxomatous peritonei

A
  • Surgical debulking followed by intra-peritoneal chemotherapy infusion
  • Recurrent bowel obstruction common due to fibrosis and adhesions
218
Q

Why stanford A dissection (before right brachiocephalic trunk) needs surgical treatment ?

A

Leads to:
- Coronary occlusion
- Aortic valve insufficiency
- Rupture into pericardium leading to cardiac tamponade

219
Q

Findings predictive of impending rupture

A

Increased aneurysm size on serial imaging (rate of 10 mm or more per year)

> 7 cm

Reduced thrombus size

Thrombus fissuration

Discontinuity in calcification

High-attenuation crescent sign: well-defined peripheral crescent of increased attenuation within the thrombus of a large abdominal aortic aneurysm

220
Q

Treatment for rupture AAA ?

A

Endovascular aneurysm repair (EVAR) or open surgery

220
Q

Aortoiliac occlusive disease symptoms

A
  • Erectile dysfunction
  • Pulselessness
  • Thigh claudication
  • Pallor
221
Q

Classificaiotn of Aortoiliac occlusive disease (Leriche syndrome)

A

type I: confined to the distal abdominal aorta and common iliac arteries

type II: as above with extension into the external iliac arteries

type III: aortoiliac segment and femoropopliteal vessels

222
Q

Pathophysiology of Aortoiliac occlusive disease (Leriche syndrome)

A

Endothelial damage resulting in inflammation and lipid accumulation in the tunica media

223
Q

Causes of Aortoiliac occlusive disease (Leriche syndrome)

A
  • arteriosclerosis
  • thrombosis
  • vasculitis
224
Q

Aorto-Enteric fistula causes ?

A

Primary: associated with a complicated abdominal aortic aneurysm
- ectopic gas adjacent to or within the aorta

Secondary: associated with graft repair)
- pseudoaneurysm formation
- disruption of aneurysmal wrap

225
Q

primary retroperitoneal malignancy

A

Liposarcoma (most common)
Undifferentiated pleomorphic sarcoma (MFH)
Leiomyosarcoma
Rhabdomyosarcoma

226
Q

Most frequent location of retroperitoneal Leiomyosarcoma ?

A

IVC

227
Q

Complications of Boerhaave

A

acute mediastinitis

oesophagopleural fistula

pneumonia

empyema

sepsis

228
Q

Duplication cysts of the gut embryology ?

A

Result from an aberration of the posterior division of the embryonic foregut at 3-4 weeks gestation

229
Q

Duplication cysts of the gut association

A
  • Spina bifida
  • Oesophageal atresia
  • Other duplication cysts of the gut
230
Q

Duplication cysts of the gut complications ?

A
  • Carcinoma develop within the cyst
  • Peptic ulceration
  • Perforate, hemorrhage or erode adjacent structures (rare)
231
Q

Duplication cyst of the gut management ?

A
  • Surgical removal if symptomatic
  • Biopsy is normally avoided due to the risk of infection and mediastinitis.
232
Q

Oesophageal intramural pseudodiverticulosis associations ?

A
  • Esophageal strictures (90%)
  • Esophageal carcionma
  • Esophageal candidiasis
  • Esophageaal reflux
233
Q

Chagas disease pathogen

A

Trypanosoma cruzi

234
Q

What is Ivor lewis procedure

A

For esophageal cancer with Esophagectomy, the stomach is “pulled up” into the thoracic cavity, appearance mimics achalasia

235
Q

Ivor lewis complications

A

Stricture, leak, recurrent laryngeal nerve palsy, and aspiration

236
Q

Describe the 2 stomach volvulus

A

Organo-axial volvulus
- rotates along LONG axis

Mesenteric-axial volvulus
- rotates along SHORT axis
- displacement of antrum above gastro-oesophageal junction

237
Q

Associations of gastric volvulus

A

Wandering spleen

Congenital diaphragmatic hernia

Diaphragmatic eventration

Laparoscopic adjustable gastric banding

238
Q

Describe Gastroparesis

A

Abnormal gastric motility with delayed stomach emptying in the absence of mechanical obstruction and results in gastric distension.

239
Q

Causes of Gastroparesis

A
  • Idiopathic
  • Diabetes mellitus
  • Post-surgical: e.g. vagotomy, gastric fundoplication, gastric bypass surgery
  • Medications: e.g. opiates, calcium channel blockers, alcohol
  • Infection: e.g. Chagas disease, Clostridium botulinum
240
Q

Best study to check for Gastroparesis ?

A

Nuclear medicine: Solid meal gastric scintigraphy

  • 60-120 minutes. Measurement of the half-emptying time is the simplest way to assess gastric transit (normal 60 -105 minutes)
241
Q

Complications of Billroth procedures

A

dumping syndrome

gastrojejunocolic fistula

afferent loop syndrome

increased risk of gastric adenocarcinoma, 15-20 years post-surgery

242
Q

What is Roux-en-Y gastric bypass used for ?

A

used to treat morbid obesity.

243
Q

Explain Afferent loop syndrome

A

Intermittent partial or complete mechanical obstruction of the afferent limb (always the excluded limb where food doesn’t pass) of a gastrojejunostomy.

Seen in:

Partial gastrectomy
- Billroth II gastrojejunostomy

Gastric bypass
- Roux-en-Y gastric bypass

Pancreaticoduodenectomy

244
Q

Complications of Roux-en-Y gastric bypass

A

Early
- Anastomotic leak: usually at the gastrojejunal anastomosis
- Acute ischaemia

Late
- Anastomotic narrowing/stenosis/stricture
- Dumping syndrome
- Ulceration
- Adhesions, potentially leading to small-bowel obstruction
- Internal hernia

245
Q

Reasons to do Fundoplication

A

Treatment of gastrooesophageal reflux disease after failure of medical treatment and the first line of treatment of paraoesophageal hernia.

246
Q

Complications of Fundoplication

A

Tight fundoplication: manifests as dysphagia and achalasia-like symptoms and occurs when the fundoplication is tight and long (>2 cm)

Slippage: the fundoplication surrounds the stomach with retraction of the gastrooesophageal junction into the chest; it manifests as recurrent gastrooesophageal reflux

Disruption: the most common complication and occurs when the fundal sutures slip; it manifests as recurrence of reflux symptoms

Twisted fundoplication and gastric volvulus: rare and urgent complication

247
Q

Meckels diverticulum Rule of 2s

A

occur in 2% of the population
are 2 inches (5 cm) long
are 2 feet (60 cm) from the ileocaecal valve
2/3 have ectopic mucosa
2 types of ectopic tissue are commonly present (mostly gastric and pancreatic)
the commonest age at clinical presentation is 2 years

248
Q

Pathology findings of Celiac disease

A
  • Villous atrophy
  • Crypt hyperplasia
248
Q

Causes of small bowel strictures ?

A
  • NSAID**
  • Radiation
  • Crohn disease
  • Tuberculosis
  • Eosinophilic enteritis
249
Q

What are the grades of perianal fistula

A

grade 1: simple linear intersphincteric

grade 2: intersphincteric with abscess or secondary tract

grade 3: transsphincteric

grade 4: transsphincteric with abscess or secondary tract within the ischiorectal fossa

grade 5: supralevator and translevator extension

250
Q

Associations of Perianal fistula

A

Spontaneous
- diverticulitis: perhaps the most common cause in developed countries
- Crohn disease
- tuberculosis

Iatrogenic: post-surgical complication
- post-ultralow anterior resection
- hysterectomy
- post-pelvic radiotherapy

Childbirth

Pelvic malignancies

251
Q

What tests can be done to evaluate Perianal fistula other than MRI ?
What is its major drawbacks ?

A

Fistulography
- difficult to assess secondary extensions secondary to lack of proper filling with contrast material
- inability to visualise the anal sphincters and to determine their relationship to the fistula

Ultrasound
- endoanal ultrasound (EAUS)
- transvaginal ultrasound (TVUS)
- transperineal ultrasound (TPUS)

252
Q

What are the pros and cons of Ultrasound over MRI for peri-anal fistula evaluation ?

A

Pros of US
- ease of access and lower cost

Cons of US
- less sensitive than endoanal MR for deep supra levator disease

253
Q

What are the 3 methods to do US for perianafistula ?

A

endoanal ultrasound (EAUS)

transvaginal ultrasound (TVUS)

transperineal ultrasound (TPUS)

  • Infusion of hydrogen peroxide into the fistulous tract renders it hyperechoic, thus facilitating its delineation
  • Doppler interrogation can show hyperaemia in active Crohn disease.
254
Q

List out the Fibropolycystic liver diseases

A
  1. Congenital hepatic fibrosis
  2. Autosomal dominant polycystic liver disease
  3. Caroli disease
  4. Biliary hamartomas
  5. Choledochal cysts
255
Q

Congenital hepatic fibrosis inheritance ?

A

AR

256
Q

Congenital hepatic fibrosis associated with ?

A

Caroli disease (AR)

257
Q

What are the 2 types of Caroli disease ?

A

Type 1 (Simple caroli disease)
- cystic dilatation of larger intrahepatic bile ducts

Type 2 (Caroli syndrome - fibrotic type)
- small bile duct dilatation and congenital hepatic fibrosis or cirrhosis +/- portal HTN

258
Q

Caroli disease associations

A
  • Medullary sponge kidney
  • ARPKD
  • ADPKD (very rarely)
259
Q

Caroli disease Complications

A

Simple type
- intrahepatic stone formation
- recurrent cholangitis that may lead to bacteraemia and sepsis
- hepatic abscesses
- Cholangiocarcinoma

Periportal fibrosis type
- cirrhosis and portal hypertension
- hepatomegaly
- ascites
- varices
- Cholangiocarcinoma

260
Q

Caroli disease prognosis ?

A

Poor
- segmentectomy or lobectomy for localised disease
- transplant or conservative management for diffuse disease

261
Q

Test used for hydatid cyst ?

A

Casoni skin test

262
Q

How can the aetiology of the hepatic abcess be inferred ?

A

Identification of E. histolytica specific antigen or DNA in stool samples

Antiamoebic antibodies in blood serum

263
Q

Liver Amoebic abscess extrahepatic pathologies

A
  • Pleural effusion
  • Perihepatic fluid
  • Gastric or colonic involvement
  • Retroperitoneal extension
264
Q

Treatment differences between Amoebic vs Pyogenic liver abscess ?

A

Traditionally, amoebic abscesses are treated with medical therapy as the first line, as opposed to percutaneous or surgical drainage, which is the first line of treatment in pyogenic liver abscesses.

265
Q

Budd Chiari Aetiology

A
  • Idiopathic (most common)
  • Congenital: Hepatic vein or IVC web
  • Venous thrombosis: Sepsis, Polycythemia, Antiphospholipid
266
Q

Budd Chiari complications

A

Patients with chronic Budd-Chiari syndrome are at risk for hepatocellular carcinoma (HCC) and therefore should be monitored with serum alpha-fetoprotein (AFP)

267
Q

Intraductal papillary neoplasm of the bile duct (IPNBD)

A
268
Q

The criteria for biliary cystadenomas include

A
  • Cyst lined by cuboidal or columnar epithelium that resembles normal biliary epithelium
  • No communication with bile ducts
  • Variable amount of mucin producing epithelium
  • Associated with ovarian type subepithelial stroma
269
Q

Prognosis of biliary cystadenoma

A
  • Often recurs after resection
  • Potential to turn into biliary cystadenocarcinoma
  • radiological differentiation from the more sinister biliary cystadenocarcinoma is unreliable, surgical excision is usually done.
270
Q

3 types of liver transplant

A

Deceased donor
- most common

Live donor
- right lobe for adult
- left lobe for child

Split transplant
- deceased donor liver split to 2 or more portions and given to 2 or more people

271
Q

Indications for liver transplant

A
  • Cirrhosis with refractory complications
  • Fulminant Acute liver failure
  • HCC with local disease only
  • alpha-1-antitrpsin deficiency, Wilson disease
272
Q

Liver Pre-transplant evaluations include

A

Donor
- Volume of liver
- Parenchymal disease (diffuse or local)
- Vascular anatomy
- Biliary anatomy

Recipient
- Vascular anatomy
- Milan criteria

273
Q

Liver Post-transplant evaluations NORMAL findings

A

Normal findings:
- Perihepatic haematoma
- Right-sided pleural effusion
- Minimal ascites
- Periportal oedema

274
Q

Liver Post-transplant evaluations COMPLICATIONS

A
  • Rejection (diagnosed via biopsy)
  • Hepatic arterial thrombosis: (most common vascular complication)
  • Portal vein thrombosis
  • Hepatic vein thrombosis
  • IVC thrombosis
  • Hepatic abscess
  • Biliary stricture / ischemia
  • Bile leak**
275
Q

Explain TIPS

A

Transjugular intrahepatic portosystemic shunt (TIPS or TIPSS)
- treatment for portal hypertension in which direct communication is formed between a hepatic vein and a branch of the portal vein, thus allowing some proportion of portal flow to bypass the liver.

  • The target portosystemic gradient after TIPS formation is <12 mmHg.
276
Q

Indications for TIPS

A
  • Portal HTN
  • Variceal bleed (recurrent or when medical therapy fails)
  • Hepatorenal syndrome
  • Budd-chiari syndrome
  • Malignant compression of portal or hepatic veins
  • Ascites refractory to medical treatment
277
Q

Absolute and Relative contraindications of TIPS

A

Absolute contraindications:
- arguable none
- possible severe right heart failure as the flow diversion from TIPS will increase pre-load
- uncontrolled sepsis as there is a substantially increased risk of stent infection

Relative contraindications
- Right heart failure
- Cavernous transformation
- Cystic hepatic disease
- Occluded MAIN portal vein thrombus
- Polycystic kidney disease
- Hepatic malignancy or hemangioma

278
Q

Describe pancreatic divisum

A
  • Characterised, in the majority of cases, by the dorsal pancreatic duct (i.e. main pancreatic and Santorini ducts) directly entering the minor papilla with no communication with the ventral duct (a.k.a duct of Wirsung) and thus, the major papilla.
279
Q

3 subtypes of Pancreatic divisum

A
  1. Classic type
    - No connection at all
  2. Absent ventral duct: Minor papilla drains all pancreas while major papilla drains bile duct
  3. Functional
    - Filamentous or inadequate connection between dorsal and ventral ducts
279
Q

Pancreatic divisum can result in what

A
  • Santorinicele, which is a cystic dilatation of the distal dorsal duct (duct of Santorini), immediately proximal to the minor papilla.
280
Q

Embryology of Annular pancreas

A

Annular pancreas develops due to failure of the ventral bud to rotate with the duodenum, causing encasement of the duodenum.

(pancreas develops from a single dorsal and two ventral buds from foregut)

281
Q

2 types of annular pancreas

A

Complete surround

Incomplete surround

282
Q

Annular pancreas complications

A
  • Pancreatitis (common in adults)
  • Duodenal obstruction
283
Q

Annular pancreas associations

A

Down syndrome

pancreas divisum

pancreatitis

pancreatic cancer

intraductal papillary mucinous neoplasm (IPMN)

284
Q

Worriesome features of IPMN

A
  • main pancreatic duct over 5 mm
  • cyst diameter ≥3 cm
  • presence of a contrast-enhancing mural nodule ≥5 mm
  • presence of solid mass
  • thickened and enhancing cyst wall
  • growth rate ≥5 mm/year
285
Q

What are some features of IPMN that may guide surgery

A
  • Increased CA19-9
  • EUS FNA: increased CEA
  • new onset jaundice
286
Q

Solid pseudopapillary tumour of the pancreas prognosis

A

While most lesions are benign, ~15% can be malignant. Complete resection is associated with long-term survival even in the presence of metastatic disease.

287
Q

Test to do to differentiate between sclerosing mesenteritis and malignant mesenteric involvement.

A

FDG PET-CT

288
Q

What are the 3 types of peritoneal mesothelioma

A

epithelioid (most frequent, 60 to 80%)

sarcomatoid (10 to 12%)

biphasic (mixed epithelioid - sarcomatoid,10 to 15%)

289
Q

Aetiology of retroperitoneal fibrosis

A
  • Idiopathic (most common)
  • Autoimmune (IgG4-related)
  • NSAIDS
  • Malignant: Lymphoma, Desmoplastic reaction
  • Asbestos
290
Q

SMA criteria

A

aortomesenteric angle: 6° to 22°

aortomesenteric distance: 2-8mm

291
Q

Causes of Cholangitis ?

A

Infective cholangitis
- recurrent pyogenic
- ascending cholangitis (Escherichia coli)

Chemotherapy induced cholangitis **

PSC

eosinophilic cholangitis

292
Q

VHL findings

A
  • RCC
  • Renal cysts
  • AML
  • Pancreatic cysts
  • Pancreatic NETs
  • Pancreatic serous cystadenomas
  • Pheochromocytoma
  • Hemangioblastoma
293
Q

VHL genetics and prognosis ?

A

AD (mostly - 80%)

Poor prognosis
- survival 50 years
- most common death RCC and Hemangioblastoma
- need active surveillance

294
Q

HNPCC due to what ?

A

DNA Mismatch repair gene mutation (MMR)
- MLH1 and MSH2 gene

295
Q

Management of HNPCC

A
  • Screening of the colon every 1 to 2 years starting from 25-40 years of age
  • may require colectomy
  • Due to the risk of endometrial and ovarian cancer, transvaginal ultrasound screening and serum CA-125 can be considered in women’s early 30s
  • In those post childbearing or over 40 years, prophylactic hysterectomy and bilateral salpingo-oophorectomy should be offered
296
Q

What are some AIDS-defining illnesses

A

candidiasis

CMV

TB, histoplasmosis

Pneumocystis pneumonia

Kaposi sarcoma

PML

cervical cancer: invasive

297
Q

Diffuse/distal esophageal spasm (DOS) gold standard for diagnosis ?

A

Manometry

298
Q

Clinical presentation of diffuse oesophageal spasm (corkscrew oesophagus).

A

Chest pain
Dysphagia

299
Q

Management of Hepatic adenoma ?

A

≥5 cm: resection (due to risk of hemorrhage)
<5 cm: biopsy

300
Q

Pancreatic AAST grading

A

The proximal pancreas is defined as the gland to the right of SMV.

grade I: haematoma with minor contusion or superficial laceration without duct injury

grade II: major contusion or laceration without duct injury

grade III: distal transection or deep parenchymal injury with duct injury**

grade IV: proximal transection or deep parenchymal injury involving the ampulla (and/or intrapancreatic common bile duct)

grade V: massive disruption of the pancreatic head (“shattered pancreas”)

301
Q

Management of Pancreatic injury

A

Injuries with pancreatic duct disruption are more likely to undergo endoscopic stenting

Whereas surgical intervention such as wide drainage, and distal pancreatectomy is preferred for grade III to V injuries

302
Q

When can one get hemorrhagic pancreatitis ?

A

Complication of severe necrotizing pancreatitis or Rupture of pseudoaneurysm (GDA or Splenic artery)

303
Q

What is the gleason score ?

A
  • measures aggressiveness of the prostate cancer
  • based on the histological patterns of prostate cancer cells, specifically how much the cancer tissue resembles normal prostate tissue.

A pathologist examines biopsy samples and identifies the two most prevalent cell patterns. These patterns are graded on a scale from 1 to 5:

Grade 1: Cells look almost like normal prostate cells (well-differentiated).
Grade 5: Cells look very abnormal and undifferentiated.
The two most common patterns are then added together to give a total score:

For example, if the most common pattern is grade 3 and the second most common is grade 4, the Gleason score will be 3+4 = 7.

304
Q

Management for Prostate cancer ?

A

Gleason score of <7 and a PSA of <10 ng/L are considered to have a potentially curable disease.
- These patients undergo prostatectomy, “brachytherapy”, or “external beam radiation”.

Patients that do not meet these criteria will usually undergo a combination of androgen deprivation therapy, immunotherapy, radiotherapy, or chemotherapy.

304
Q

What are poor prognostic indications for Prostate cancer ?

A

Extracapsular extension
- neurovascular bundle involvement
- obliteration of the rectoprostatic angle
- involvement of the urethra
- seminal vesicle invasion (normal seminal vesicles have a high signal on T2)

Lymphadenopathy

304
Q

Waterhouse Friderichsen syndrome is due to what ?

A

Due to Septicemia:

Neisseria meningitidis (meningococcus): classic
Haemophilus influenzae
Pseudomonas aeruginosa
Escherichia coli
Streptococcus pneumoniae

305
Q

Explain the vascular supply to the gallbladder and how this affects the pattern of local invasion in gallbladder carcinoma.

A

Answer:

Arterial supply: The gallbladder is primarily supplied by the cystic artery, a branch of the right hepatic artery.

Venous drainage: Venous blood from the gallbladder drains into the portal vein.

Relevance: Gallbladder carcinoma tends to invade the adjacent liver early (segments IV and V) due to its close proximity and shared blood supply.

306
Q

What are the key indications for performing a Whipple procedure?

A

Pancreatic ductal adenocarcinoma of the head of the pancreas that is resectable.

Periampullary carcinoma (including ampullary adenocarcinoma and distal cholangiocarcinoma).

Duodenal adenocarcinoma.

Chronic pancreatitis (when causing severe symptoms such as intractable pain or biliary/pancreatic duct obstruction).

Occasionally performed for benign tumors or cystic neoplasms if there is a high risk of malignancy or significant symptoms

307
Q

Describe the anatomical structures resected during a Whipple procedure.

A

Head of the pancreas (and sometimes part of the body).

Distal bile duct and common bile duct.

Gallbladder.

Duodenum (usually the first and second parts).

Distal stomach (in a classic Whipple procedure, although pylorus-preserving variants spare the distal stomach).

Regional lymph nodes. After resection, anastomoses are created to reconstruct the gastrointestinal tract, including pancreaticojejunostomy, hepaticojejunostomy, and gastrojejunostomy.

308
Q

What are the common post-operative complications associated with the Whipple procedure?

A

gastric outlet obstruction / delayed gastric emptying

anastomotic leakage (usually occurs within two weeks)

pancreatic fistula

pancreatitis of the residual gland

biliary stricture

wound infection

abdominal abscess

intra-abdominal hemorrhage

other: hepatic infarction, portomesenteric venous thrombosis

309
Q

How does treatment for Esophageal vs. Gastric varices differ ?

A

Esophageal varices are treated more easily with band ligation (EVL) due to their superficial location and smaller size.
Gastric varices, being deeper, larger, and having more complex blood flow, are better treated with cyanoacrylate glue injection or more invasive interventions like TIPS or BRTO in refractory cases.

Gastric Varices:
1. Endoscopic cyanoacrylate glue injection (for bleed)
2. Balloon-occluded Retrograde Transvenous Obliteration (BRTO) - (for bleed)
3. TIPS (for bleed)

Esophageal varices:
1. Non-selective beta-blockers (prophylaxis)
2. Endoscopic variceal ligation (for bleed)
3. TIPS (for bleed)

310
Q

Esophageal varices vs Gastric varices venous drainage and collateral flow ?

A

VENOUS DRAINAGE AND PORTAL HTN:
Esophageal varices
- increased pressure in the left gastric vein and the esophageal veins.

Gastric varices
- increased pressure in the left gastric vein, posterior gastric vein and the left gastroepiploic vein, which drain into the splenic vein.

COLLATERALS:
Esophageal varices
- Collateral between portal vein and SVC, via the azygos vein

Gastric varices
- gastro-renal shunts
- gastro-caval shunts
- spleno-renal shunts

311
Q

Findings of Angiodysplasia

A

focal areas (<5 mm) of contrast enhancement in the bowel wall (most prominent in the enteric phase)

enlargement of the feeding mesenteric artery (e.g. ileocecal artery in cecal angiodysplasia)

early filling and/or dilatation of the draining mesenteric vein (e.g. ileocecal vein in cecal angiodysplasia)

312
Q

What are some uses of Sulfur collloid study ?

A
  1. Gastric emptying study
  2. FNH (all other lesions are cold) and ectopic spleen
  3. Lymphoscintigraphy: lymphatic mapping in sentinel lymph node biopsy procedures
  4. Gastrointestinal tract bleeding: particularly for slow or intermittent bleeds that might not be detected by angiography.
313
Q

Indications for TACE

A

unresectable hepatocellular carcinoma (HCC): usually Barcelona Clinic Liver Cancer (BCLC) stage B

either as palliative treatment or as a bridge to a liver transplant

may be an adjunct to radiofrequency ablation or anti-angiogenic agents

hepatic metastases: most commonly from colorectal carcinoma

intrahepatic cholangiocarcinoma

314
Q

Spigelian hernia associated with ?

A

ipsilateral cryptorchidism (75%)

315
Q

What pre-disposes bilateral adrenal hemorrhage ?
(unilateral usually from trauma)

A
  • Waterhouse-Friderichsen syndrome (sepsis from N.meningitidis)
  • DIC
  • adrenal tumor
  • heparin
  • primary anti-phospholipid syndrome
316
Q

Imaging findings of Hepatic Schitosomiasis ?

A

CT
- Widened hepatic fissures deeply dividing the segments of the liver along the portal vein branches
- Capsular calcifications
(Tortoise shell liver)

317
Q

Budd-Chiari with Cirrhotic liver with multiple enhancing lesions no washout showing surrounding halo

A
  • Regenerative nodules
318
Q

What influences prognosis of Biliary cystadenocarcinoma ? What other complications

A

Complications:
- Rupture into peritoneum or retroperitoneum
- Recurrence common

Prognosis:
- Tumors with ovarian stroma found in women have indolent course and good prognosis
- Tumors without ovarian stroma found in both sexes have aggressive clinical course and poor prognosis
Risk of malignant transformation to adenocarcinoma up to 30%

319
Q

US features of post transplant hepatic artery stenosis

A
  • Slow systolic upstroke
  • RI < 0.5 (low resistance)
  • PSV > 200
320
Q

Locations of TIPS

A

Most common route: Right HV → right PV → main PV

320
Q

Other post liver transplant complications

A

Biliary leak
- from entry of T-tube: easily treated
- from biliary anastomosis: requires revision
- from intrahepatic ducts: leads to biliary necrosis -> catastrophic

Biliary anastomosis narrowing
- see proximal dilatation

Hepatic artery pseudoaneurysm

Allograft rejection

HA thrombosis

321
Q

What PSV is considered TIPS shunt malfunction ?

A

Shunt velocity < 90 or > 250 cm/s at any point

322
Q

Pregnant lady with abdomen pain, shown liver with hemorrhage or infarct.. think ?

A

HELLP syndrome
- haemolysis
- elevated liver enzymes and
- low platelets

IMAGE
- hepatomegaly: especially the right lobe
- haemorrhage, subcapsular haematoma, rupture
- hepatic infarction

323
Q

Liver imaging findings of HHT

A
  • Large, tortuous extrahepatic ± intrahepatic arteries with early filling and enlargement of hepatic ± portal veins
  • Heterogeneous enhancement of hepatic parenchyma
  • Telangiectasias: Small vascular spots
324
Q

Hepatic Peliosis

A

Rare, benign disorder characterized by sinusoidal dilation and presence of multiple blood-filled lacunar spaces within liver

Portal phase: Centrifugal or centripetal enhancement without mass effect on hepatic vessels

Delayed phase: Late, diffuse, homogeneous enhancement

Hyperintense on T2WI

Multiple foci of ↑ signal due to presence of subacute blood (hemorrhagic necrosis)

Tx
- Do not drain as can BLEED!

325
Q

What are the 3 morphology of Pancreas Serous Cystadenoma ?

A
  • Polycystic (70%)
  • Macrocystic
  • Honeycomb

lined by glycogen-rich epithelium*

Tx
- Almost all benign -> observation

326
Q

Major complications of Post pancreas transplant

A

Imaging of major complications

Allograft pancreatitis: Edema, enlargement, and heterogeneous pancreas with peripancreatic fluid

Acute rejection: Enlargement and edema of graft with increased T2 signal on MR

Chronic rejection: Small and atrophic graft with decreased T1 and T2 signal on MR

Vascular complications: Venous thrombosis is more common than arterial

Intraabdominal fluid collections: May represent abscess, seroma, lymphocele, urinoma, or pseudocyst

327
Q

Pancreatic transplants typically performed in which 2 groups

A
  1. Patients with end-stage renal disease who have or will have kidney transplant: Pancreas transplant improves odds of kidney survival by preventing hyperglycemia
  2. Patients with severe diabetic complications who fail insulin therapy may undergo pancreas transplant even in absence of chronic kidney disease
328
Q

post pancreatic transplant complications

A

Pancreatic fistula: Leakage of amylase-rich fluid from pancreatic duct => Focal fluid collection, ectopic gas, or hematoma directly adjacent to pancreaticojejunostomy

Abscess: Can be intrahepatic, in pancreatic bed, or in subphrenic, subhepatic, or retroperitoneal spaces

Gastrojejunostomy and hepaticojejunostomy leaks: Suspect when focal fluid collection or ectopic gas in close contiguity to anastomosis

Postoperative pancreatitis

Liver infarct

Anastomotic strictures: Suspect when progressive biliary or pancreatic ductal dilatation without obstructing tumor at anastomotic site

Delayed gastric emptying: Gastric remnant markedly dilated with large retained ingested material and fluid

329
Q

Benefit of US guided abdominal biopsy benefit vs CT

A

One of the most important benefit for deep targets is that pressure with the ultrasound probe can decrease the needle distance up to nearly 50% for targets deeper.

CT, a posterior paraspinal approach would be fairly straightforward, ensuring that the planning images were obtained during end expiration to avoid the lower lung edge.

330
Q

Indications for CT enterography

A
  • Crohn’s disease (most common indication)
  • Suspected small bowel bleed (performed after negative endoscopy)
  • Small bowel polyposis syndrome, Carcinoid
  • Celiac disease
  • Obstruction (adhesions)
331
Q

CT enterography technique explained

A

Bowel prep
1. fast for 4-6 hrs
2. drink 1.5L of oral contrast over 1hr
- adequate luminal distension is necessary as collapsed bowel loops may mimic pathology
- CT enterography utilises negative or neutral oral contrast (attenuation similar to that of water - e.g. water, PEG, mannitol, methylcellulose, locust bean gum, and low-density barium sulphate preparations (Volumen, 0.1% W/V)

Procedure
1. CT with IV contrast
2. ​data interpretation with the use of axial and coronal reformatted images for proper evaluation

332
Q

What are the major features of LIRADS 5

A

Major features - which makes this a LR-5 lesion:

  1. lesion > 20mm
  2. Arterial phase hyperenhnacement
  3. non-peripheral washout
  4. Threshold growth is increase in size of 50% or more within 6 months
  5. Have capsule
333
Q

When can only LIRADS be used ?

A

LIRADS can only be used in patients with:

  1. Cirrhosis (Not congenital hepatic fibrosis or by other causes like Budd-Chiari, Cardiac congestion)
  2. Hep-B patient
  3. Current or prior HCC
334
Q

What are some strategies to reduce Partial volume artifact ?

A

Increase Slice Resolution: Use thinner slices to reduce the overlap of tissues in each slice. This can be achieved by lowering slice thickness on CT and MRI, which can help differentiate small or closely spaced structures.

Optimize Acquisition Settings: Adjust settings such as higher resolution and field of view (FOV) specific to the region of interest. Using a smaller FOV can minimize partial volume effects by focusing on the area needing high detail.

Utilize Multi-Planar and Volume Reconstructions: Advanced imaging techniques, like multi-planar reconstructions (MPR) or 3D volume reconstructions, can help visualize structures from different angles, reducing artefacts caused by averaging of different densities.

Select Appropriate Reconstruction Algorithms: For CT scans, iterative reconstruction algorithms often provide a clearer distinction between structures, especially in high-contrast regions, thus minimizing the partial volume artefact.

335
Q

How to reduce chemical shift artifact in MRI ?

A

Increase Bandwidth: A higher receiver bandwidth decreases the time available for chemical shift to occur, reducing the artifact. However, increasing bandwidth may reduce the signal-to-noise ratio, so a balance is needed.

Optimize Field Strength: Chemical shift artifacts are more pronounced at higher magnetic field strengths. Using lower field strengths can help reduce the artifact, though this may not always be feasible depending on diagnostic needs.

Use Frequency Selective Fat Suppression: Techniques like fat saturation (fat-sat) or STIR (Short Tau Inversion Recovery) can suppress fat signal selectively, minimizing the chemical shift between fat and water.

Modify the Imaging Sequence: Certain sequences, like spin-echo, are less susceptible to chemical shift artifacts than gradient echo sequences. Choosing an appropriate sequence can help manage the artifact.

Use Opposed-Phase Imaging: Acquiring images in opposed-phase conditions can help in canceling out the chemical shift artifact, especially useful in assessing fatty infiltrations or differentiating fat-containing lesions.

336
Q

What is Aliasing artifact MRI ?

A

Aliasing on MRI, also known as wrap-around, is a frequently encountered MRI artifact that occurs when the field of view (FOV) is smaller than the body part being imaged. The part of the body that lies beyond the edge of the FOV is projected onto the other side of the image

337
Q

What causes fatty pancreatic atrophy ?

A
  • Aging
  • Corticosteroids
  • Cystif fibrosis
  • Metabolic syndrome/Obesity
337
Q

Describe prognostic groups for seminomatous tumors

A

Good prognosis:
- Tumor has not spread to other organs other than the lung
- AFP normal, bHCG and LDH can be at any level

Intermediate prognosis:
- Tumor has spread to other organs other than the lung
- AFP normal, bHCG and LDH at any level

Poor prognosis
- No poor prognostic group for seminomatous tumors

338
Q

What are some differentiating features between PSC and autoimmune cholangiopathy ?

A

PSC is
- Associated with IBD (UC / CD)
- Younger patient
- Less acute
- Does not respond to steroids
- Shorter segments of stricturing

339
Q

What pathological process is responsible for symptoms of pseudomembranous colitis

A

Toxin B

340
Q

What study can you do to differentiate necrotizing pancreatitis to interstitial ?

A

Dual-energy CT
- with virtual non-contrast reformats
- can depict hematoma and differentiate it from parenchymal enhancement on contrast-enhanced images. It also improves the detection of non-calcified gallstones and isoattenuating cholesterol stones which may be the causative factor in the patient’s pancreatitis

Dual-energy CT dual-phase protocols with virtual non-contrast reformats can also offer lower radiation doses than conventional triple-phase CT imaging of the pancreas

341
Q

Epiphrenic diverticula real or false diverticula

A

False
- pulsion type

342
Q

Epiphrenic diverticula associations?

A

achalasia

hiatus hernia

esophageal stricture

esophageal web

343
Q

Angiodysplasia treatment?

A

Approximately 50% of gastrointestinal hemorrhage from angiodysplasia ceases without intervention.

Endovascular treatment is generally not effective and first-line treatment is interventional endoscopy.

344
Q
A

PATH FINAL (12 decks)

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