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Phase II > GI > Flashcards

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
Management of Wilson's disease
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
26
Primary biliary cirrhosis (cholangitis) RFs and patho
MIddle aged females Autoimmune although unsure Chronic inflam in interlobular bile ducts (within liver) causing cholestasis and cirrhosis
27
Presentation of Primary biliary cirrhosis
Itching in middle aged women Associated with Sjorgens, RA, Systemic sclerosis and thyroid Liver symptoms
28
Diagnosis of PBC
anti-mitochondrial and sentive and specific
29
Management of PBC
Pruritis: cholestyramine Fat soluble vitamin supps Ursodeoxycholic acid Liver transplant (rare to have recurrence)
30
Features of primary sclerosing cholangitis
Jaundice and pruritis RUQ pain Fatigue
31
Investigation of primary sclerosing cholangitis
ERPC - beaded apprearence
32
Complications of primary scelerosing cholangitis
Cholangio carcinoma | Colorectal cancer
33
Investigation into autoimmune hep
Young females | ANA/ SMA but other types too
34
Features of autoimmune hep
CLD Acute hepatits - fever, jaundice Amenorrhoea (cholesterol?) Liver biopsy
35
Management autoimmune hep
Steroids Aza Liver transplant
36
Which hepatitis virus give acute disease which are self limiting?
A E B (if in adults and can be chronic too) Small % of C
37
Which serology marker of Hep B current infection
HBsAg
38
Which serology marker of Hep B immunity
anti- HBS
39
Whicih serology marker of Hep B current or past infection?
anti-hBC
40
Which serology marker of Hep B infectivity
anti-HBSAe
41
previous immunisation: | :
anti-HBs positive, all others negative
42
previous hepatitis B (> 6 months ago), not a carrier
anti-HBc positive, HBsAg negative
43
previous hepatitis B, now a carrier:
anti-HBc positive, HBsAg positive
44
When can you vaccinate against hep B
Passive can be given after high risk exposure
45
Treatmetn of hep B
Liver inflam get antivirals -48weeks pegylated (PEG) interferon alpha or nucleoside anologues e.g. tenofovir entecavir - aim to lower HBsAg (HB surface antigen)
46
Type of virus hep B
DNA
47
Type of virus hep C
RNA flavivirus
48
Hep C progression and comps
``` 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
Treatment of B cell MALT lymphoma
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
Treatment of GORD
Lifestyle, weight, food, smoking, caffeine, alcohol, citrus Antacids/ PPO, H2 Nissen fundoplication laproscopic
51
Risks of upper GI bleed score
Rockall score - pre and post endoscopy score to predict mortality
52
Treatment of acute peptic ulcer bleed
Endoscopic haemostasis - clips, cautery adn adrenaline. IV or oral PPI Consider H pylori
53
Cannular for rapid IV fluids
14 or 15g
54
Symptoms or gord
Heartburn lying, after meals, straining Acidregurg Salivation ODynopghagia from oesophagitis Extraoesoph: Nocturnal asthma Chronic cough Laryngitis
55
GORD comps
Iron deficiency anaemia Ulcers Benign strictures Barretts ACC
56
Investigation GORD
Endoscope if dysphagia or alarm symptoms. 24hr pH monitoring or manometry if endoscope normal
57
Types of hiatus hernia and sequelae
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
Barrets treatment
PPI and endoscopic mucosal resection or radiofrequency ablation
59
5 Good questions for dysphagia
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
Chronic panc cause
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
Chronic panc symptoms
``` 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
Chronic panc investigations
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
Chronic panc treatment
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
Amylase and lipase in chronic panc
Usually normal
65
Bilioary colic path vs acute cystitis
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
Biliary colic pain graph
Increase for 15 Stops after 6 (if acute cholecystitis it remains lodged and pain stays)- Starts several hrs after food
67
Pathophys cause of ascending cholangitis
Bacteria infection of CBD due to Choledocholithiasis (stone in CBD) Stricture e.g. cancer
68
Reynold's pentad?
fever, RUQ and jaundice AND Hypotension Conusion (sepsis)
69
Treatment of ascending cholangitis
Rehydration and abx Remove obstruction - ERCP and shockwave lithotripsy Stent in ducts Cholecystectomy if gall stone related
70
Panc cancer RFs
``` Male old Smoking alcohol DM Chronic pain Central adiposity ```
71
Commonest type of panc cancer
Ductal carcinoma | 60%in head, 25% body
72
Presentation of most panc cancers
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
What is Courvoisier's law
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
Treatment of carcinomas of the pancreas
Pancreatoduodenectomy/ Whipple's only if no mets If tial - lap excision Post op chemo
75
How to prescribe insulin
Always prescribe by brand name and include the concentration of insulin
76
Most strong insulin and how is it given?
``` 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
Who needs an insulin infusion
``` 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
Practical aspects of IV insulin. What would you do?
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
Which patients should be kept over 6mmols/L during IV insulin (normally 4)
In patients with ACS or stroke do not let CBGs drop below 6
80
Explain discontinuation proceedure for IV insulin
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
Who needs haemodyalysis in AKI?
``` - 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
high Na what fluid to give?
5% dex | Give Saline if Na normal or low
83
Hypernatraemia symptoms
``` Thirst Weakness Nause Loss of appetite Confusion Muscle twitching Seizures Coma ```
84
Treatment of renal bone disease
Vit D Cinacalcet consider Dietary restriction of PO4 consider If secondary hyperpara consider parathyroidectomy
85
Causes of bone disease in CKD
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
Alternate to fistula in haemodialysis
``` 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
How does heamodyalisis anticoag?
Anticoag Tinsiparin used in cirucit (extracorporeal) Only do patient if history of clotting fistula etc.
88
Types of PD?
``` 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
Functions of the liver
``` 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
Investigation into acute/ chronic diverticular disease
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
Pathology of diverticular disease
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
Treatment diverticular disease
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

Phase II (18 decks)

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