GI Flashcards

1
Q

IBS diagnosis and symptoms

A

for at least 6 months:
abdominal pain, and/or
bloating, and/or
change in bowel habit
altered stool passage (straining, urgency, incomplete evacuation)
abdominal bloating (more common in women than men), distension, tension or hardness
symptoms made worse by eating
passage of mucus
Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis
No blood/ weight loss

full blood count
ESR/CRP coeliac disease screen (tissue transglutaminase antibodies)
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2
Q

Management of IBS

A
Pain- antispasmodic agents
	Constipation - laxative (not lactulose - osmotic due to bloating?)
	Diarrhoea - loperamide
	2nd line Amitriptyline
	Olso
Talking therapy
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3
Q

Caeliac microscopy

A

villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia

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4
Q

UC clasification

A

• mild: < 4 stools/day, only a small amount of blood
• moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

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5
Q

Pathology of UC

A

• red, raw mucosa, bleeds easily
• no inflammation beyond submucosa (unless fulminant disease)
• widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
• inflammatory cell infiltrate in lamina propria
• neutrophils migrate through the walls of glands to form crypt abscesses
• depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

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6
Q

UC how to induce remission

A

Rectal aminosalicylates (mesalasine) or rectal steriods
Oral mesalasine
Oral pred
If severe IV steroids

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7
Q

UC maintain remission

A

Oral mesalaasine (5ASA)
Aza or mercaptopurine (6MP similar to aza, must assess TMPT first)
Not MTX
Priobiotics may help

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8
Q

CD inducing remission

A

Oral, topical or IV steroids
Elemental diet (esp children)
Mesalazine second line
Aza or mercaptopurine (after assessing TMPT)
Infliximab if refractory/ fistulating
Metronidazole (also anti inflam) if isolated perianal disease

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9
Q

CD maintaining remission

A

Stop smoking
Aza or mercapto
MTX second line
5-ASA possible

Surgery

Often ileocaecal resection
Segmental small bowl resection
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10
Q

Symptoms of coeliac

A
Chronic or intermittent diarrhoea
	Failure to thrive or faltering growth (in children)
	Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
	Prolonged fatigue ('tired all the time')
	Recurrent abdominal pain, cramping or distension
	Sudden or unexpected weight loss
	Unexplained iron-deficiency anaemia, or other unspecified anaemia
	Other automimmune stuff e.g. Thyroid, T1DM
Complications

anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes rare: oesophageal cancer, other malignancies
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11
Q

Investigations into coeliac

A

eintroduce gluten for at least 6 weeks prior to testing.

Immunology
tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
endomyseal antibody (IgA)
anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
anti-casein antibodies are also found in some patients
	Jejunal biopsy
	villous atrophy
	crypt hyperplasia
	increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
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12
Q

Describe bowel cancer screening

A

60-74 (50-74 in Scotland) years get invited
Every 2 years
Send in poo poo
FOB (Faecal occult blood) and colonoscopy

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13
Q

Describe prognostic risk of liver cirrhosis

A
Child-Pugh - gives 1/2 year prognosis
Bilirubin
Albumin
PTT
Ascites
Encephalopathy

Also

MELD - model for end stage liver disease

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14
Q

Complications of liver cirrhosis

A
Portal
		Varices
		Caput madusae
		Splenomegaly
	HCC risk
	Ascites
	Coagulopathy/ SBP
	Encephalopathy
Hypoglycaemia
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15
Q

Management of liver cirrhosis full!! General, ascites, SBP, Enceph, Renal failure, (varices separate)

A

Good nutrition
Alcohol abstinence
Avoid NSAIDs, sedatives and opiates
Colestyramine for pruritis
US and aFP every 6 months
Specific treatment e.g. ursodeoxycholic in PBC, penacillamine
Ascites
Fluid restriction
Low salt
Spirono
Add frusemide
Therapeutic paracentesis with albumin infusion
SBP
Abx propyclaxis
Pipercillin and tazobactam
Encephalopathy
Lactulose and rifaximin (non absorbing abx which kills N forming bacteria),
Renal failure
(decreased hepatic clearence leads to trapping in kidneys e.g. IgA also HRH syndrome in fulminant LD)
Give terlipressin for pressure (ADH analogue, also used for bleeding esophageal varices
Haemodyalysis
Transjugular intrahepatic porto-systemic shunt (TIPSS)

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16
Q

Oesopahgeal varices treatment and prevention

A
VBL
			Baloon tamponage
			Transfusion
			FFP if needed
			Terlipressin (constrictor)
			Abx
			Sengstaken- Blakemore tube if needed
Failure then consider TIPSS
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17
Q

Hepatic encephalopathy symptoms

A

Sleep disturbance
Altered mood/behaviour
Dyspraxia - 5 pointed atar

		Liver flap
		Personality change
		Confusion/ lethargy
		Restless/ stupor
Coma
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18
Q

Hereditary haemochromotosis path

A

Increased intestingal iron absorption
Iro deposition in joints, liver, heart, panc, pit, adrenals, skin
Middle aged men (women protected for 10more years by menstrual blood loss)
Auto rec?
Freq 1 in 200-400
Multiple different mutations

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19
Q

Hered haemo symptoms

A
Early
		Nil or tiredness
		Arthralgia (2 and 3 MCP and knee pseudogout)
		Low libido
	Later
		Slatye grey skin pigmentations
		Signs of CLD
		Hepatomegaly
		Cirrhosis 
		Dilated cardiomyopathy
		DM (bronze diabetes from iron in panc)
Hypogonadism from pit dysfunction
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20
Q

Hered haemo investigation

A
LFTs
	Ferritin (inflam can increase too)
	Transferrin saturation increased]
	HFE genotyping (ciommonest gene)
	Xray
		Chondrocalcinosis in stressed more than relaxed (compare dominant hands)
	Liver biopsy
Perl's stain quantifies iron loading
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21
Q

Gered haemo management

A

Venection- 0.5-2 units every 1-2 weeks until ferritin <50mcg
Maintainence needed for life
If not desferrioxamine
Monitor LFT and glucose (HbA1c not reliablke)
Limit iron e.g. from over the counter drugs but don’t limit diet intake
No alcohol
No uncooked seafood (bacteraemia)

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22
Q

Wilsons disease patho and onset

A

autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13.

The onset of symptoms is usually between 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease

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23
Q

Wilsons symptoms

A

Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis
neurological: basal ganglia degeneration, speech and behavioural problems are often the first manifestations. Also: asterixis, chorea, dementia
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

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24
Q

Wilson’s diagnosis

A

reduced serum caeruloplasmin
reduced serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
increased 24hr urinary copper excretion

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25
Q

Management of Wilson’s disease

A

penicillamine (chelates copper - binds and makes easier to excrete) has been the traditional first-line treatment
trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
tetrathiomolybdate is a newer agent that is currently under investigation

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26
Q

Primary biliary cirrhosis (cholangitis) RFs and patho

A

MIddle aged females
Autoimmune although unsure
Chronic inflam in interlobular bile ducts (within liver) causing cholestasis and cirrhosis

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27
Q

Presentation of Primary biliary cirrhosis

A

Itching in middle aged women
Associated with Sjorgens, RA, Systemic sclerosis and thyroid
Liver symptoms

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28
Q

Diagnosis of PBC

A

anti-mitochondrial and sentive and specific

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29
Q

Management of PBC

A

Pruritis: cholestyramine
Fat soluble vitamin supps
Ursodeoxycholic acid
Liver transplant (rare to have recurrence)

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30
Q

Features of primary sclerosing cholangitis

A

Jaundice and pruritis
RUQ pain
Fatigue

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31
Q

Investigation of primary sclerosing cholangitis

A

ERPC - beaded apprearence

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32
Q

Complications of primary scelerosing cholangitis

A

Cholangio carcinoma

Colorectal cancer

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33
Q

Investigation into autoimmune hep

A

Young females

ANA/ SMA but other types too

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34
Q

Features of autoimmune hep

A

CLD
Acute hepatits - fever, jaundice
Amenorrhoea (cholesterol?)
Liver biopsy

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35
Q

Management autoimmune hep

A

Steroids
Aza
Liver transplant

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36
Q

Which hepatitis virus give acute disease which are self limiting?

A

A
E
B (if in adults and can be chronic too)
Small % of C

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37
Q

Which serology marker of Hep B current infection

A

HBsAg

38
Q

Which serology marker of Hep B immunity

A

anti- HBS

39
Q

Whicih serology marker of Hep B current or past infection?

A

anti-hBC

40
Q

Which serology marker of Hep B infectivity

A

anti-HBSAe

41
Q

previous immunisation:

:

A

anti-HBs positive, all others negative

42
Q

previous hepatitis B (> 6 months ago), not a carrier

A

anti-HBc positive, HBsAg negative

43
Q

previous hepatitis B, now a carrier:

A

anti-HBc positive, HBsAg positive

44
Q

When can you vaccinate against hep B

A

Passive can be given after high risk exposure

45
Q

Treatmetn of hep B

A

Liver inflam get antivirals -48weeks pegylated (PEG) interferon alpha or nucleoside anologues e.g. tenofovir entecavir - aim to lower HBsAg (HB surface antigen)

46
Q

Type of virus hep B

A

DNA

47
Q

Type of virus hep C

A

RNA flavivirus

48
Q

Hep C progression and comps

A
Rarely acute
		85% silent chronic infection (opposite to Hep B)
		Cirrhosis and HCC risk
		F for progression
			Male Older
			Higher viral load
			Alcohol
			HIV HBV
		Glomerulonephritis
		Thyroiditis
		Autoimmune hep
PAN - polyarteritis nodosa - systemic necrotizing vasculitis - tissue (muscle) ischaemia
49
Q

Treatment of B cell MALT lymphoma

A

Management - eradication may be achieved with a 7 day course of
a proton pump inhibitor + amoxicillin + clarithromycin, or
a proton pump inhibitor + metronidazole + clarithromycin

50
Q

Treatment of GORD

A

Lifestyle, weight, food, smoking, caffeine, alcohol, citrus
Antacids/ PPO, H2
Nissen fundoplication laproscopic

51
Q

Risks of upper GI bleed score

A

Rockall score - pre and post endoscopy score to predict mortality

52
Q

Treatment of acute peptic ulcer bleed

A

Endoscopic haemostasis - clips, cautery adn adrenaline.
IV or oral PPI
Consider H pylori

53
Q

Cannular for rapid IV fluids

A

14 or 15g

54
Q

Symptoms or gord

A

Heartburn lying, after meals, straining
Acidregurg
Salivation
ODynopghagia from oesophagitis

Extraoesoph:

Nocturnal asthma
Chronic cough
Laryngitis

55
Q

GORD comps

A

Iron deficiency anaemia
Ulcers
Benign strictures
Barretts ACC

56
Q

Investigation GORD

A

Endoscope if dysphagia or alarm symptoms. 24hr pH monitoring or manometry if endoscope normal

57
Q

Types of hiatus hernia and sequelae

A

Sliding - junction above diaphragm - more likely to have GORD

Rolling - junction below diaphragm but outpouching - risk of strangulation

PPI or operation.

Very common, esp fat women

58
Q

Barrets treatment

A

PPI and endoscopic mucosal resection or radiofrequency ablation

59
Q

5 Good questions for dysphagia

A

Solids or liquids from the start?
Stricture benign or malig = solid
Motility = both

Problem initiating swallow?
-neuro related, bulbar (CN) palsy

Odonyphagia?
Ulcer (malig, oesophagitis, candida) or spasm

All the time and getting worse?
If not think spasm
Worse - malig

Neck bulge or gurgle on drinking?
Pharyngeal pouch

60
Q

Chronic panc cause

A

Around 80% of cases are due to alcohol excess with up to 20% of cases being unexplained. Smoking, , Ax, CF, Haemochromotosis, stones/ tumour causing obstruction

61
Q

Chronic panc symptoms

A
Asmptomatoc
Dull pain after a meal - 15 to 30mins. Relieved sitting forward, Bores into back.
NV
Weight loss
Steatorrhoea after 5 years of pain
DM after 20 years
62
Q

Chronic panc investigations

A

CT - better for calcification, focal or diffuse enlargement or duct dialtions
Fecal elastase - measure exocrine function
ECRP to visualise with contrast to classfy and give prognosis
- dialtion and clubbing of branches = mild
- Severe = dilated branches

63
Q

Chronic panc treatment

A

Stop alcohol and smoking
Pancreatic enzyme supps with PPI (better with less acidity)
Analgesia not NSAIDs
Antioxidants in early disease
Enteral feeding better (e.g. PEG) - low fat may help symptoms
Octreotide may relieve pain and maybe decrease inflam

Fluid drainage percutaneously or endoscopically

64
Q

Amylase and lipase in chronic panc

A

Usually normal

65
Q

Bilioary colic path vs acute cystitis

A

CCK from fatty food
Causes gallbladder contraction
Gallstone in cystic duct
(same as acute cystitis but passes through cystic sooner not getting stuck)

Acute cystitis - growth of gallbladder due to inflammation and mucins and E coli growth
Move to RUQ and rebound tendernitis. hence fever. Can lead to ischaemia and gangrene. Sepsis/ rupture possible

66
Q

Biliary colic pain graph

A

Increase for 15
Stops after 6 (if acute cholecystitis it remains lodged and pain stays)-
Starts several hrs after food

67
Q

Pathophys cause of ascending cholangitis

A

Bacteria infection of CBD due to
Choledocholithiasis (stone in CBD)
Stricture e.g. cancer

68
Q

Reynold’s pentad?

A

fever, RUQ and jaundice

AND

Hypotension
Conusion (sepsis)

69
Q

Treatment of ascending cholangitis

A

Rehydration and abx

Remove obstruction - ERCP and shockwave lithotripsy

Stent in ducts

Cholecystectomy if gall stone related

70
Q

Panc cancer RFs

A
Male old
Smoking alcohol
DM
Chronic pain
Central adiposity
71
Q

Commonest type of panc cancer

A

Ductal carcinoma

60%in head, 25% body

72
Q

Presentation of most panc cancers

A

Very similar to chronic
In head most commonly painless obstructive jaundic
May cause acute pajnc

Thrombophlebitis migrans - swollen and red,
Hypercalcaemia
Portal hypertension
Neprosis (renal vein met)

Palpable gallbladder
Hepatomeg
Splenomeg
Lymphadenopathy
Ascites
73
Q

What is Courvoisier’s law

A

Courvoisier’s law (or Courvoisier syndrome, or Courvoisier’s sign or Courvoisier-Terrier’s sign) states that in the presence of a palpably enlarged gallbladder which is nontender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones. Usually, the term is used to describe the physical examination finding of the right-upper quadrant of the abdomen. This sign implicates possible malignancy of the gallbladder or pancreas and the swelling is unlikely due to gallstones.

74
Q

Treatment of carcinomas of the pancreas

A

Pancreatoduodenectomy/ Whipple’s only if no mets

If tial - lap excision
Post op chemo

75
Q

How to prescribe insulin

A

Always prescribe by brand name and include the concentration of insulin

76
Q

Most strong insulin and how is it given?

A
Very potent
U500 - 5x stronger than normal insulin
For insulin resistant patients
Normally TDS before meals
Prescribed in marks not U
Marks based on 0.3 or 0.5ml insulin syringe. 1 mark = 0.01ml = 5 units
77
Q

Who needs an insulin infusion

A
DKA
HHS - Hypersmolar hyperglycaemic state
Surgical patients - NBM and missing more tna one meal
Vomiting
Major vasc event - ACS and Post CVA
TPN/ entral fed patients
Steroid use
Metabolically unwell not eating and drinking
-most cortisol related
78
Q

Practical aspects of IV insulin. What would you do?

A

To make 50 units of Human Actrapid
50 units of actrapid and 49.5ml of NaCl aline ina 50ml luer lock syringe so conc of 1unit/1ml
Non returnable valve
No more than 24 hrs as crystalises
Volumetric pump used
Rate used that gives 6-10mmols/L of glucose
Discard after 24hrs
In most cases needs substrate (glucose)
Different degrees of insulin sensitivity accounted for
Patients have different sensitivities to insulin to adjust accordingly related to weight, concurrent illness and medication (steroids)
Tables for rate guides
CBGs done hourly for first 24h

79
Q

Which patients should be kept over 6mmols/L during IV insulin (normally 4)

A

In patients with ACS or stroke do not let CBGs drop below 6

80
Q

Explain discontinuation proceedure for IV insulin

A

Stop 30 mins after usual diabetes treatment begins and patient can eat and drink
Check CBGs after 1 hr and 4x in next 24 hrs - rebound hyperglycaemia

81
Q

Who needs haemodyalysis in AKI?

A
- AEIOU - who needs HD?
		○ Acidosis
		○ Electrolytes
			§ Particularly K and HCO3
		○ Intoxicants eg ethylene glycol (antifreeze) (needs dialysing out - digoxin also)
		○ Oedema (usually oligo/ anuria)
		○ Uraemia
			§ Uraemic pericarditis, encephalopy 
Symptoms not neccessarily urate(?) Levels
82
Q

high Na what fluid to give?

A

5% dex

Give Saline if Na normal or low

83
Q

Hypernatraemia symptoms

A
Thirst
Weakness
Nause
Loss of appetite
Confusion 
Muscle twitching
Seizures
Coma
84
Q

Treatment of renal bone disease

A

Vit D
Cinacalcet consider
Dietary restriction of PO4 consider
If secondary hyperpara consider parathyroidectomy

85
Q

Causes of bone disease in CKD

A

Low calcium and high PO4 cause secondary hyperparathyroidism
Low Vit D.

Even if PTH kept low by meds, still get adynamic bone disease due to loss of remodeling (loss of blasts and clasts) - associated with low PTH/ resitance to PTH

86
Q

Alternate to fistula in haemodialysis

A
Graft
			Similar to fistula
			Not able to join e.g. DM or IV drug user
			Graft into plastic
			Can be used much earlier than fistulas
			Risks 
				Larger operation that fistula 
				Increased risk of infection
		Permcath
			Right IJV
			Tunnel under skin
			Suboptial dialysis as less blood flow
Can start immediate dialysis
87
Q

How does heamodyalisis anticoag?

A

Anticoag
Tinsiparin used in cirucit (extracorporeal)
Only do patient if history of clotting fistula etc.

88
Q

Types of PD?

A
CAPD - continous anmbulatory PD
				Bag throughout day
				Multiple bag exchanges throughout the day
			Automated PD
				Exchanges carried out at night
				More frail?
Cant fit in exchange during day
89
Q

Functions of the liver

A
Nutrition/metabolic\
		Glycogen
	Detox
		Bilirubin
	Clotting factors
	Immune function
		Kupfer cells
		Bacteria from portal vein
	Detoxification
		Drug excretuin
		Alcohol
		Ammonia
	Manufactures proteins
		Albumin
Binding proteins
90
Q

Investigation into acute/ chronic diverticular disease

A

Patients presenting in clinic will typically undergo either a colonoscopy, CT cologram or barium enema as part of their diagnostic work up. All tests can identify diverticular disease. It can be far more difficult to confidently exclude cancer, particularly in diverticular strictures.

Acutely unwell surgical patients should be investigated in a systematic way. Plain abdominal films and an erect chest x-ray will identify perforation. An abdominal CT scan (not a CT cologram) with oral and intravenous contrast will help to identify whether acute inflammation is present but also the presence of local complications such as abscess formation.

91
Q

Pathology of diverticular disease

A

Diverticular disease is a common surgical problem. It consists of herniation of colonic mucosa through the muscular wall of the colon. The usual site is between the taenia coli where vessels pierce the muscle to supply the mucosa. For this reason, the rectum, which lacks taenia, is often spared.

92
Q

Treatment diverticular disease

A

Increase dietary fibre intake.
Mild attacks of diverticulitis may be managed conservatively with antibiotics.
Peri colonic abscesses should be drained either surgically or radiologically.
Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication for a segmental resection.
Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually a stoma. This group have a very high risk of post operative complications and usually require HDU admission. Less severe perforations may be managed by laparoscopic washout and drain insertion