Gastro Flashcards

1
Q

hepatic causes of jaundice (high indirect bilirubin)

A

Gilbert’s (decr UDPG activity)
Crigler Najjar (no UDPG)
Hepatitis
Newborn jaundice (not enough UDPG or lignin to deal with incr haem catabolism from conversion of HbF to HbA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hepatic causes of jaundice (high direct bilirubin)

A
Hepatitis 
Drugs that impair excretion
Rubin Johnson syndrome (no cMOAT for excretion)
Tumours 
Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Post-Hepatic causes of jaundice

A

Due to high conjugated bilirubin:

Gallstones
Biliary strictures/obstruction
Cholangitis
Pancreatic or biliary tree cancer

All lead to cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens to bilirubin when it is unconjugated in the blood and liver?

A

Blood - bound to albumin

Liver - bound to ligandin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What sort of bilirubin is toxic and what does it cause in the brain?

A

Indirect is insoluble so cannot be excreted and builds up

Kernicterus due to brain toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which enzyme conjugates bilirubin and what happens if it is not present or has decr activity?

A

UDPG

Decr activity: Gilbert’s
Not present: Crippler Najjar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what happens to bilirubin in the gut?

A

Converted to urobilinogen via gut bacteria
then 90% is converted to stercobilin and excreted in faeces

10% absorbed into portal circulation and goes back to liver. 9% of this is recycled back to gut and 1% goes to kidneys and is excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What colour is the pee and poo with:
obstructive jaundice?
pre-hepatic jaundice?

A

Obstructive: Dark wee, pale poo

Pre-hepatic: dark wee and poo (overwhelm liver conjugating enzymes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a potential consequence of pre-hepatic jaundice?

A

Excess haem from haemolysis results in excess synthesis of bile salts which can result in precipitation of GALLSTONES

-> cholestasis -> obstructive jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

4 categories of mechanisms of diarrhoea

A

Osmotic
(excess unabsorbed substrates in gut lumen retain fluids)

Secretory
(stimulation of excretory mechanisms from enterocytes)

Inflammatory
(altered membrane permeability leads to exudation of protein, blood, mucus)

Altered intestinal motility
(slow or fast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Common underlying cause of osmotic diarrhoea

A

FODMAPS (IBS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Common underlying causes of secretory diarrhoea

A

Bacterial toxins

  • ETEC
  • Cholera

Laxative abuse

Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Common underlying causes of inflammatory diarrhoea

A

IBD

Invasive bacteria

  • Shigella
  • Salmonella
  • Clostridium difficile
  • Campylobacter

Entamoeba histolytica
CMV colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Common underlying causes of altered motility diarrhoea

A
SLOW:
Anatomical defects causing intestinal stasis 
-strictures
-blind loops (diverticulitis)
-surgery

FAST:

  • IBS
  • Thyrotoxicosis
  • Diabetic neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
Appearance of poo with 
- inflammatory
- secretory
- osmotic 
Diarrhoea
A

Inflamm - blood and mucus, small volume

Secretory: watery, >1Lvol

Osmotic: fatty,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute abdomen - which causes need laparotomy and which don’t

A

Need laparotomy:

  • Generalised peritonitis (perf ulcer, diverticulum, appendix, bowel, gallbladder)
  • Ruptured organ (liver, spleen, AAA, ectopic pregnancy)

Doesn’t need:

  • local peritonitis (cholecystitis, diverticulitis, salpingitis)
  • suspected abscess
  • localised ileus
  • colicky pain (patient restless)

Maybe:
-SBO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Management of Acute abdomen

A
Treat shock w 2 large bore cannulas w crystalloid (Hartmann's) fluids
ECG
Vitals
Group and hold
Blood cultures
Antibiotics (cef and met)
Analgesia (IV morphine PRN)
IV fluids 
Plain AXR and erect CXR 
Nil by mouth 
Antiemetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management of abdominal trauma (blunt)

A

§ ABCs, fluid resus and stabilisation

§ Surgery ?
□ Hollow organ injuries -> laparotomy
□ Solid organ injuries -> laparotomy if hemodynamically unstable or high transfusion requirements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management of abdo trauma (penetrating)

A
§ ABCs
§ Fluid resuscitation and stabilization
§ Gunshot wounds require laparotomy 
§ Laparotomy if penetrating trauma and
	□ Shock
	□ Peritonitis
	□ Evisceration
	□ Free air in abdomen
	□ Blood in NG tube, catheter or on DRE

§ Local wound exploration in some instances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment for peritonitis

A

IV rehydration and electrolyte balance correction

IV antibiotics (cephalosporin, tazosin or carbepenem)

Laparotomy - exploratory peritoneal lavage and correction of anatomical defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Treatment of ascites

A
1st line
	○ Salt restriction (>2g daily)
	○ Diuretics: spironolactone, frusemide
	○ Weight loss 
If refractory (treatment with diuretics is inadequate)
	○ Therapeutic/palliative ascitic taps
	○ IV albumin 
         ? Liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Complications of ascites and the treatment

A

Spontaneous bacteiral peritonitis if they develop fever, chills, abdo pain, hypotension, ARF etc

Treatment: IV antibiotics (cephalosporin) and IV albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Investigations for a suspected hernia

A

Ultrasound +/- CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List different types of hernias

A

Inguinal hernias (direct vs indirect)

Femoral hernia

Umbilical

Paraumbilical (below or above umbilicus)

Epigastric (through lines alba above umbilicus)

Incisional hernia

Obturator hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
  1. What does reducible mean?

2. What does irreducible mean?
hernia

A
  1. contents can be pushed back into their rightful position
  2. hernia cannot be pushed back into their right place = stuck = incarcerated.
    May or may not be strangulated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does incarcerated mean? (hernia)

A

Herniated tissue is trapped in a hernial sack and cannot be pushed back into position (=irreducible)

Doesn’t imply anything about blood supply.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

obstructed vs strangulated in conte

A

Obstructed - bowel caught in hernia obstructing the passage of bowel contents through

Strangulated - Blood supply is compromised and bowel becomes ischaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 questions to ask about a lump found on examination

A
  1. Can you get above it? (no-> hernia)
  2. Yes -> Is it separate to the testes? (No-> testicular tumour)
  3. Does it transilluminate? (Yes -> fluid as in cyst or hydrocoel; no-> solid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Direct vs indirect hernia

A

Direct: directly through defect in abdominal wall. older patients.
- Medial to inferior epigastric artery)

Indirect: through deep inguinal ring into inguinal canal. Associated w congenital defect in males (patent processes vaginalis). younger patients.
- Lateral to inferior epigastric artery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the site that direct hernias usually occur in called and why are the anatomical landmarks?

A

Hasselbach’s triangle

  • lateral edge of rectus sheath
  • inferior epigastric vessel
  • inguinal ligament
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where do femoral hernias occur?

A

Femoral canal: medial to femoral vein, below inguinal ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which type of hernia is more common in women and what is a common complication?

A

Femoral hernia . More likely to be irreducible and to strangulate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Complications of hernias

A

Incarceration
Strangulation
Richter’s hernia
Obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Richter’s hernia - what is it? how might a patient present?

A

Once side of small bowel wall becomes incarcerated in a hernia which may strangulate that section of bowel wall. presents w sepsis and tachycardia + lump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When might you perform surgery for a hernia?

A

Emergency if hernia is strangulated.

Elective if:

  • obstruction (change in bowels)
  • Pain
  • Nuisance, aesthetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Contents of the spermatic cord

A
Vas deferens
testicular artery & vein
genital branch of genitofemoral nerve
lymphatics
cremaster muscle
\+/- hernial sac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the management of hernia?

A

Do nothing if small and asymptomatic.

Surgery to prevent strangulation or evisceration, for pain or aesthetic. Laparoscopic or open mesh repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What genetic alleles is coeliac associated wiht?

A

HLA-DQ2 and HLADQ8 are found in close to 100% patients but also in 20% of the general population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What sort of hypersensitivity is coeliac disease?

A

Type 4 hypersensitivity against gliadin, found in gluten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Histopathology of coeliac disease: 3 features

A
  1. Villous atrophy and crypt hyperplasia
  2. Increased #s plasma cells and lymphocytes in LP
  3. Increased IELs (CD4 T cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What part of bowel does coeliac mainly affect? What affect does this have on absorption?

A

Duodenum and jejunum

Affects absorption of Vitamin B, C and folate (proximal), mostly

Protein, fat and fat soluble vitamins (A, E, D, K) distally. absorbed so only affected in severe disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What sort of anaemia is associated w Coeliac disease?

A

Iron deficiency (microcytic)

or pernicious anaemia (B12, macrocytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Symptoms of coeliac disease

A

D • Diarrhoea, steatorrhea
• Weight loss, fatigue
• Bloating, gas
• Anaemia - iron deficiency &raquo_space; B12, folate deficiency
• Symptoms of vitamin, mineral deficiency (apthous ulcers, angular stomatitis)
• Osteoporosis in older people
• Failure to thrive in infants
• Symptoms improve with gluten free diet and relapse when gluten reintroduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Diagnosis of coeliac

A

Small bowel biopsy before starting GF diet

Bloods: FBE, Iron studies, UEC, B12, folate

Serology (anti gliadin and anti tTG antibodies + IgA)

HLA-DQ typing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does coeliac put you at risk for?

A

Other autoimmune conditionts (autoimmune thyroiditis, T1D)

Cancers - EATL small bowel lymphoma, adenocarcinoma of small bowel and oesophageal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the main symptoms for Crohn’s vs UC

A

Crohns: abdominal cramps, diarrhoea, weight loss (malnutrition), fever

UC: rectal bleeding, urgency, tenesmus, abdominal cramps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Physical distribution of Crohns vs UC

A

Crohn’s

  • anywhere from mouth to anus
  • Skip lesions
  • Commonly terminal ileum

UC

  • rectum -> colon (not proximal to ileocaecal jan)
  • continuous
  • always starts in rectum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Potential complications of UC vs Crohns

A

Crohns:

  • Strictures
  • Fissures -> risk of perforation
  • Abscess
  • Fistulae
  • Perianal disease

US

  • toxic megacolon -> risk of perforation
  • incr risk colon cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Extra colonic manifestations of Crohn’s vs UC

A

Crohns

  • perianal fistulae and skin tags
  • renal stones
  • cholelithiasis
  • oral ulcers

Both

  • rashes, erythema nodosum
  • arthritis, analysing spondylitis
  • uveitis, episcleritis
  • PSC
  • fatty liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Cobblestoning and mucosal islands are a feature of what IBD condition?

A

Crohn’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Effect of surgery in crohn’s vs UC

A

Crohn’s - recurrence is common

UC - surgery can cure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Treatment of IBD

A

Crohns: stop smoking + only fluids during exacerbation

  • Steroids (C-oral pred; UC-IV methylpred)
  • 5ASA therapy +/- antibiotics
  • Immunosuppressants (azathioprine, methotrexate, infliximab)
  • Surgery for:
    • Crohn’s: presence of complications
    • UC: failed medical therapy, toxic megacolon, bleeding, pre-cancerous change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Investigating IBD

A

Bloods (FBE, CRP, UEC, LFT, blood cultures)

Stool MCS (shigella, campylobacter, e coli, C. diff, salmonella -> all inflamm pattern diarrhoea)

Abdo x-ray
Erect CXR (perf?)

Colonoscopy and biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

management of IBS

A

Low FODMAPS diet
Incr fibre intake
Antismasmotic (hyoscine) before meals

Reassurance, relaxation or stress reduction therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Red flags that rule out IBS as a DDX

A
Weight loss
Fever
Nocturnal defecation
anaemia
blood or pus in stool
abnormal gross finding on endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the criteria for IBS?

A

Abdo pain relieved w defecation
Abdo pain assoc w change in fréquency OR consistency of stool

+/- bloating, passing mucus, straining, urgency, incr or decr stool frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Managing an acute abdomen

A
  1. ABCDE
    - Airway, breathing, circulation
    - Disability: BSL, GCS
    - E: expose patient (Evidence for trauma/aneurysm/GI bleed?)
  2. insert 2 large bore (18 or 16gu) cannulas
  3. Bloods: blood cultures, group and hold, FBE, UEC, LFT, CRP, ABG, Trop, beta HCG
  4. ECG
  5. Check obs: pulse, BP, JVP, saO2
  6. ECG if > 50
  7. Ceftriaxone and metronidazole
  8. IV morphine PRN, metaclopramide
  9. IV fluids: hartmann’s
  10. FAST scan +/- Portable plain erect CXR and AXR
  11. Call surgical reg
  12. Prep for theatre
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Preparation for theatre

A
  1. Nil by mouth
  2. DVT prophylaxis: LMWH, 3. TEDs
  3. Catheterise (IDC)
  4. NGT (decompression and prevents aspiration)
  5. PPIs
    +/- analgesia, antiemetic, anxiolytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Management of abdominal trauma

A
  1. ABCDE primary surgery (+/- O2 or intubation)
  2. secondary surgery + NGT, IDC
  3. Bloods (incl group and hold), urinalysis
  4. FAST scan (free fluid), Abdominopelvic X-ray (bone breaks, pneumoperitoneal, air fluid levels, hernias) , CT (not if haemodynamically unstable)
  5. Fluid resuscitation (2 large bore cannulas w hartmann’s )
  6. Surgery - laparotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Management of appendicitis

A

IV fluids + electrolyte correctance
Prompt appendectomy
Metronidazole +ceftriaxone pre-op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Complications of appendicitis

A

Perforation

Abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Examination tests for appendicitis

A

Tenderness at McBurney’s point (1/3 from ASIS to umbilicus)

Rovsing’s sign: when LIF is pressed, pain felt more strongly in RIF than left

Psoas sign = retrocaecal appendix (pain on flexion of hip against resistance OR passive hyperextension of hip)

Obturator sign =pelvic appendix (flexion then external or internal rotation about R hip causes pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Where does diverticular disease usually affect? where is the pain generally felt?

A

Sigmoid colon

LLQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Management of diverticular disease

A

Diverticulosis: high fibre diet, avoid seeds and nuts.

Diverticulitis (acute episode):

  • Conservative: NPO, IV fluids and IV cef and met
  • surgical treatment is Hartmann procedure if refractory to medical MX, or complications present.
65
Q

What is hartmann’s procedure

A

Surgical resection of sigmoid and rectum w closure of rectal stump and formation of end colostomy.
Colostomy can be later reversed and the 2 ends of bowel sewed together.

66
Q

What side of body are ileostomies vs colostomies?

A

Colostomies: LIF

Ileostomies: RIF

67
Q

Complications of diverticulitis

A
Recurrence
Abscess
Fistulae
Perforation
Bleeding
Obstruction
68
Q

Investigations for suspected diverticulitis

A

FBC
CT
Erect AXR (pneumoperitoneum)
Colonoscopy or flexible sigmoidoscopy

69
Q

Investigating suspected ectopic pregnancy + mX

A

beta HCG
Transvaginal US

Laparoscopic surgery (or methotrexate if beta HCG low and ectopic is small)

70
Q

Courvoisier’s law

A

in a patient w painless jaundice and a palpable RUQ mass, the cause is unlikely to be gallstones -> more likely to be obstructing pancreatic or biliary neoplasm

71
Q

Charcot’s triangle - what is it for and what is that?

A

for ascending cholangitis (infection of CBD caused by bacteria)

  1. fever
  2. jaundice
  3. RUQ pain
72
Q

Reynold’s pentad

A

for ascending cholangitis

  1. fever
  2. jaundice
  3. RUQ pain
  4. Mental state changes
  5. Hypotension
73
Q

Does bleeding happen more commonly in diverticulitis or diverticulosis?

A

Diverticulosis

Bleeding v rare with diverticulitis.

74
Q

Key features of bowel obstruction

A
  1. Vomiting, nausea, LOA
  2. Constipation (distal obstruction - no faeces or flatus passed; prox obstruction - some faeces or flatus may be passed)
  3. Distension

+/- Colicky pain (from peristalsis)

75
Q

Causes of Small bowel obstruction

A

Functional (ileus)

Mechanical obstruction

  • Adhesions
  • Bulge (Hernias)
  • Cancer (adenocarcinoma)

Rare causes

  • foreign body
  • intusseption (prox segment of bowel collapses into distal bowel lumen, commonly ileum through ileo-caecal valve)
  • CD (IBD) stricture
  • Gallstone ileus (stone lodges in ileocaecal valve - v rare!!)
76
Q

Causes of large bowel obstruction

A

Functional (ileus)

Mechanical obstruction

  1. Cancer
  2. Diverticulitis
  3. Volvulus

Rarer causes

  • Adhesions
  • Constipation
  • Volvulus (sigmoid or caecal)
77
Q

How to distinguish between small and large bowel on AXR?

A

Small bowel - plicae circulares (valvulae conniventes), more centrally located. no larger than 3cm

Large bowel - No larger than 6cm. Has haustra which don’t completely cross lumen.

78
Q

What sorts of SBO do you manage conservatively vs perform emergency surgery?

A

Conservative:

  • Partial SBO
  • Ileus
  • Adhesions
  • Crohn’s stricture

Emergency surgery

  • LBO
  • Strangulation
  • Complete or recurrent SBO
79
Q

What are potential complications of bowel obstruction

A

Strangulation -> ischaemic bowel

Perforation -> peritonism, fever, incr WCC

80
Q

What is achalasia? what appearance do you get on barium swallow?

A

Oesophageal motility disorder characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter relaxation in response to swallowing.

Barium swallow -> dilated oesophagus tapering to beak-like narrowing

81
Q

Investigations for motility disturbance w dysphagia?

A

Upper GI endoscopy - rule out malignancy

Barium swallow (older patients, rule out pharyngeal pouch)

Esophgeal manometer (assesses competence of oesophageal sphincters and oesophageal motility)

+/- CT if significant weight loss to rule out malignant infiltration

82
Q

Treatment achalasia

A

Pneumatic dilatation - first line, + PPI

OR: 
Botulinum toxin (Decr tone of LES transiently)
83
Q

Gastritis - common causes of acute flares

A

Alcohol
ASpirin/NSAIDs
Stress
H. Pylori

84
Q

Diagnosis of H pylori

A

Urea breath test
Serology and stool Ag test
Biopsy -> histology, rapid urease test

85
Q

Treatment of H pylori

A

Triple therapy for 7-14 days

  • PPI
  • Amoxicillin
  • Clarithromycin
86
Q

Potential complications of H pylori gastritis

A
peptic ulcer - 15%
gastric malignancy (carcinoma and MALT lymphoma) - 0.5%
87
Q

Predisposing factors for colon cancer

A
Neoplastic polyps
FAP or HNPCC genes
IBD
Smoking and alcohol
HX cancer
88
Q

most common form of colon cancer.

A

adenocarcinoma

89
Q

What is the sreening program for bowel cancer?

A

people 60-75 years old are screened using Faecal occult blood home testing kits. NOT diagnostic -> need colonscopy if postive

90
Q

What common cause of iron deficiency anaemia in people over 50

A

Colon cancer until proven otherwise.

91
Q

Where does colon cancer go to commonly ?

A

liver, lung, bone

92
Q

What is the name of the staging criteria for bowel cancer? What are the stages?

A

Duke’s
○ A: Limited to muscularis mucosae
○ B: extension through muscularis mucosae
○ C: involvement of regional lymph nodes
○ D: Distant metastases

93
Q

When would you use radiotherapy and chemotherapy with bowel cancer?

A

Radiotherapy

  • palliative mostly
  • post-op for tumours with high chance of recurrence

Chemo

  • dukes B and C
  • palliation
94
Q

RIsk factors for acute pancreatitis

A
Alcohol 
Middle aged women; young-middle aged men
Gallstones
Hyperlipidaemia
Causative meds
ERCP 
HIV/AIDS
SLE
95
Q

Causes of acute pancreatitis

A
"I GET SMASHED"
Idiopathic
Gallstones
Ethanol
Trauma
Scorpion/spider bite
Malignancy/mumps (and other infections)
Autoimmune
Steroids 
Hyperlidaemia/hypercalcaemia/hyperparathyroidism
ERCP
Drugs
96
Q

Causes of chronic pancreatitis

A

ALCOHOL IS #1!!!

Then CF, protein malnutrition, genetics etc rarer causes

97
Q

3 clinical features of chronic pancreatitis

A

Severe upper abdo pain radiating to back

Steatorrhea

Diabetes

98
Q

Complications of pancreatitis

A
○ Pseudocyst complications
	• Persistence of pseudocyst
	• Haemorrhage
	• Infection
	• Rupture  
○ CBD obstruction
○ Duodenal obstruction
99
Q

MX of chronic pancreatitis

A

Alcohol abstinence!!!
Analgesia
+/- pancreatic enzyme replacement

Surgery

100
Q

MX of acute pancreatitis

A
IV fluids
Nutritional support (enteral feeds of TPN)
\+/-:
Analgesia
Antiemetics
O2 
NG tube
Ca, Mg replacements
Antibiotics if infected
Insulin 
Benzo and vitamin, mineral replacement if alch-induced 

Surgery if gall-stone induced

  • cholecystectomy
  • ERCP w sphincterotomy
101
Q

In what cases would you genetic test for hereditary polyposis in colon cancer?

A

DNA test if FHX of FAP of HNPCC or cancer DX before age 50

102
Q

What are the 2 main hereditary forms of colon polyps?

A

FAP - onset at puberty, surgery by 17-20

HNPCC - onset from 20

103
Q

Treatment for FAP and HNPCC

A

Surgery: Total colectomy with ileorectal anastomosis
With yearly endoscopy surveillance

FAP: also chemotherapy

104
Q

Which form of hereditary polyposos is associated w 100s of 1000s of polyps by age 20?

A

FAP

105
Q

What are SX of volvulus due to?

A

Obstruction

Bowel ischeamia

106
Q

What is cirrhosis?
Describe.

Is it reversible?

A

Anatomical term. describes conversion of liver into state of abnormal ANATOMY, occurring with chronic renal disease (ESLD).

Description: Nodules of regenerating hepatocytes surrounded by bands of fibrous scar tissue.

Irreversible.

107
Q

Causes of cirrhosis. The big 3

A

THE BIG 3:

  1. Alcohol
  2. HBV
  3. HCV
108
Q

Causes of cirrhosis. The autoimmune 3

A

AUTOIMMUNE 3

  1. Autoimmune hepatitis
  2. Primary biliary cirrhosis
  3. Primary sclerosing cholangitis
109
Q

Causes of cirrhosis. The metabolic 3

A

METABOLIC 3

  1. Haemochromatosis (too much Fe)
  2. Wilson’s disease (too much Cu)
  3. Alpha-1 antitrypsin deficiency
110
Q

Causes of cirrhosis. The other 3

A

OTHER 3:

  1. Nash
  2. Budd Chiari
  3. Chornic biliary obstruction (tumour, CF)
111
Q

4 stages of progression of chronic liver injury to cirrhosis

A

○ Stage 1: enlarged portal tracts w no septa

○ Stage 2: septa extending towards central vein but not much linking between portal tracts

○ Stage 3: portal-to-portal bridging

○ Stage 4:Cirrhosis (network of nodules separated by fibrous scar tissue)

112
Q

Pathophys of cirrhosis.

A

Chronic liver injury -> inflammation, necrosis, fibrosis

113
Q

What is the coagulopathy in CLD due to?

How would you measure this - what blood test?

A

Lack of coagulation factors (factor VIII) due to impoaired synthetic function of liver

Low platelet count due to splenomegaly from portal HTN

-INR

114
Q

What are the signs you get in the decompensation phase with CLD?

A

Encephalopathy -> drowsiness, metabolic flap

Jaundice

Ascitites + peripheral oedema

Leukonychia

Bruising/coagulopathy

Variceal bleeding

115
Q

When ALT and AST are elevated more so over ALP and GGT, which pattern suggests acute hepatitis vs cirrhosis?

A

AST > ALT -> cirrhosis

ALT > AST -> acute liver disease

116
Q

What scoring system is used for prognosis in CLD?

A

Child-Pugh score

□ Based on ascites, encephalopathy, bilirubin, albumin, prothrombin time (INR)

117
Q

What is the MELD score used for?

What does it predict and what is it based on?

A

Used to stratify patients w CLD on transplant list.

Predict 3 month survival.
Based on creatinine (hepatorenal syndrome), INR (coagulopathy) and total bilirubin (ductal obstruction w cirrhosis).

118
Q

What are the most common causes of death in cirrhosis?

A

Renal failure (hepatorenal syndrome)
Sepsis
GI bleed (Varicies)
Hepatocellular carcinoma

119
Q

What is the diagnosis of pancreatitis based on?

A

2/3 things to diagnose pancreatitis - clinical decision.

  • Lipase > 2x upper limit of normal
  • Characteristic pain
  • CT w characteristic changes (inflammation around pancreatitis)
120
Q

Classic triad of features of ruptured AAA

A
  • Pain
  • Hypotension
  • Pulsative abdo mass
121
Q

What is hepatorenal syndrome?

A

Renal failure due to CLD and portal HTN.

Bc there is more blood in the portal system, less blood to kidneys -> apparent drop in renal perfusion -> chronic renal arteriolar vasoconstriction -> ischaemia and infarction of kidney

122
Q

What are complications of cirrhosis?

A

Hepatorenal syndrome
HCC
Sodium and water retention
Osteoporosis
Hepatic hydrothorax (ascites leaks into pleural space, causing SOB on exertion)
Metabolic failure
Spontaneous bacterial peritonitis from ascites

123
Q

Investigations for CLD

A
  • Abdominal ultrasound of liver
  • Bloods: FBE, UEC, LFT, INR, Albumin, serology for Hep B and C, Fe studies, Caeruloplasmin etc
  • Liver biopsy
  • Fibroscan
124
Q

When do you refer for liver transplant

A

Anyone with decompensated CLD (ascites, variceal bleeding, encephalopathy, coagulopathy, hepatorenal syndrome, HCC)

125
Q

When not to refer for liver tarnsplant?

A

Too early
Substantial co-morbid illness
Psychosocial rasons
HCC not meeting criteria for transplant

126
Q

Treatment for HBV

A
Oral nucleos(t)ide analogues
PEGlyated IFN
127
Q

Treatment for HCV

A

Peg IFN + ribaviron +/- new agents

128
Q

Do transplants work with Hep C?

A

No reinfection occurs 100% of the time

129
Q

Why might you have a low pH in liver failure?

A

impaired hepatic metabolism results in lactic acidosis

130
Q

Causes of acute liver failure

A

Paracetamol overdose - toxic dose is 10g

Ischaemic hepatitis (caused by decr blood flow due to shock, acute severe heart failure)

Acute viral hepatitis
- Hep A, D, E , EBV

131
Q

Treatment of paracetamol overdose

A

N acetyl cysteine (NAC) for paracetamol poisoning, within 8 hours of ingestion of paracetamol

+Coagulation factors
May need liver transplant

132
Q

What conditions is paracetamol overdose associated with?

Why?

A

Alcoholism and starvation

  • Both reduce glutathione levels which mops up excess of the toxic paracetamol metabolite NAPQI
133
Q

What is budd Chiari syndrome?

A

Autoimmune liver condition

-Obstruction in the post-hepatic venous sinusoids (draining system of liver), resulting in back pressure and damage to liver cells

134
Q

What is the definition of fulminant hepatic fialure/acute liver failure?

A
  • Rapid deterioration of liver function in previously normal liver
  • Jaundice to encephalopathy within <8weeks
  • INR >1.5
135
Q

Pathology of fulminant hepatic failure

A

Fulminant hepatocellular necrosis: Widespread hepatocellular necrosis beginning in thecentrizonal distribution(zone 3, around central vein) and progressing towardsportal tracts (relative preservation of portal tracts)

136
Q

Investigations for ALF (FHF)

A

Paracetamol levels and toxicology screen
Hep A, B, C serology; EBV PCR
Liver ultrasound

137
Q

Features of ALD on histology

A

○ Hepatocyte necrosis with surrounding zone III inflammation

○ Mallory denk bodies
○ Chicken wire fibrosis

138
Q

Inherited liver diseases

A
  1. Wilson’s disease - excess Cu (keiser fleicher rings)
  2. Haemochromatosis -excess Iron storage (brone/grey skin)
  3. Alpha 1 antitrypsin deficiency
139
Q

Investigations and basic treatment of Wilson’s disease

A

Ix: serum ceruloplasmin, Urinary copper, incr Cu on liver biopsy, genetic analysis

Mx: chelation therapy

140
Q

HAemochromatosis

- diagnosis and basic MX

A

FBE: transferrin saturation and ferritin elevated
Gene analysis

MX: lifelong phlebotomy if primary, or chelation therapy if secondary cause.

141
Q

Clinical features of acute viral hepatitis

A

Most subclinical.

Flu-like syndrome (nausea, vomiting, anorexia, headaches, fatigue, myalgia, fever, arthralgia)

Some progress to icteric phase - lasts days-weeks

  • pale stool, dark urine, jaundice
  • hepatomegaly, RUQ pain
  • splenomegaly, cervical lymphadenopathy
142
Q

Treatment for ascending cholangitis

A

Drainage via ERCP ideally

Antibiotics: tazocin or ceftriazone and metronidazole or carbapenem

143
Q

How might you get a liver abscess?

A

Direct spread from:
- biliary tract infection

Portal spread from GI infx

Systemic infx (endocarditis)

144
Q

What is sclerosing cholangitis?

list 3 causes

A

Inflammation of biliary tree leads to scarring and lumen obliteration

1. Primary: assoc w IBD (UC)
Secondary:
2. chronic choledocholilithiasis
3. cholangiocarcinoma
4. post-surgery/trauma/ERCP
145
Q

What is primary biliary cirrhosis and what are 2 common causes

A

Autoimmune
chornic inflammation and fibrous obliteration of intrahepatic bile ductules

  1. Sjogrens
  2. scleroderma
146
Q

treatment biliary colic vs acute cholecystitis

A

Bilairy colic: analgesia and rehydration with elective cholecystecomy

Acute cholecystitis:

  • admit, hydrate, NPO, NG tube, analgesics
  • cefazolin
  • cholecystectomy early
147
Q

where does most pancreatic cancer occur (what part of hte pancreas?) and how does it manifest clinically?

A

Head of the pancreas in 70%
- Systemic SX, obstructive jaundice, vague constant mid-epigastric pain, painless jaundice, courvoisier’s sign
+/- palpable tumour mass

148
Q

what type of cancer is pancreatic cancer most of the time?

A

Ductal adenocarcinoma

149
Q

What is a Whipple’s procedure?

A
Pancreaticoduodenectomy - removes 
- CBD
-GALLbladder
-Duodenum
-Pancreatic head
\+/- distal stomach
150
Q

Clinical features of acute viral hepatitis

A

Mostly subclinical

Flu-like prodrome preceding jaundice by 1-2 weeks
Nausea, vomiting, anorexia, headache, fatigue, myalgia, low-grade fever
Arthralgia and urticaria (HBV)

Jaundice: Some progress to icteric phase, lasting days to weeks
Pale stool and dark urine
Hepatomegaly and RUQ pain
Splenomegaly and cervical lymphadenopathy (10-20% cases)

151
Q

DDX for hepatitis

A
Viral (Hep A-E, EBV, CMV, YF)
Alcohol
Drugs
Immune-mediated (autoimmune)
Toxins (paracetamol)
152
Q

Investigations

A

AST, ALT (hugely elevated)
ALP and bilirubin (minimally elevated)
Viral serology (anti - :hep, EBV, CMV, YF), IgM

153
Q

Complications of Hep A

A

Fulminant hepatic failure and subsequent death (<5% time)

Relapse

154
Q

Complications of Hep B

vs Hep C

A

HBV:
• Cirrhosis (8-20% of those without treatment)
• HCC
• Co or super-infection with HDV

HCV:
• 80% become chronic
• 20% of chronic cases become Cirrhosis
• HCC
• Can cause cryoglobulinemia, assoc w membranoproliferative GN, lymphoma

155
Q

Blood tests for HBV what do the following mean:

HBsAg
Anti-HBs
HBeAg
Anti-HBC IgM and IgG 
HBV DNA
A
  • HBsAg is a marker of infected state!
  • HBeAg is a marker of high HBV viral load!
  • Anti-Hbs is a marker of resolved infection/immunity
  • Anti-HBc IgM markers acute infection
  • Anti-HBc IgG marks chronic or resolved infection
  • HBV-DNA: viral load
156
Q

Treatment for HBV

A

• Counselling
• Screening for HCC with ultrasound every 6 months
• Treatment goal: reduce HCV DNA to undedetectable level
• Medications: IFN, tenofovir, entacavir, adefovir
• Vaccinate against HAV
Blood and sexual precautions

157
Q

Serum markers for HCV?

Treatment HCV

A

Serum anti-HCV and HCV-RNA (monitor response tot treatment)

  • Blood precautions
  • Vaccinate against HBV and HCA
  • Avoid alcohol
  • Direct acting anti-virals (ribavirin, sofosbuvir)
  • Pegylated IGN-alpha + ribaviron
  • Measure HCV-RNA @ 1 and 3 months after starting treatment
158
Q

histology of chrons

A

Chronic inflammation and granuloma formation (epithelioid macrophages and giant cells )