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Case 11 Flashcards

1
Q

What are the consequences of diarrhoea ?

A

Electrolyte imbalances and dehydration

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2
Q

A px has a stool culture which comes back negative, what does this mean ?

A

Problem does not have a bacterial cause

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3
Q

What are the 3 main causes of low Hb?

A

Blood loss , Fe deficiency in diet , Fe absorption failure

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4
Q

What deficiencies are shown in micro and macrocytic anaemia ?

A 
Micro = Fe def (MCV falls) 
Macro = b12/folate def
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5
Q

What are the layers of the GI tract from superficial to deep ? ( 10)

A 
CT layer (serosa) 
Longitudinal muscle 
Myenteric plexus 
Circular muscle 
Submucosal plexus 
Submucosa 
Muscularis mucosa 
Lamina propria 
Epithelium 
Lumen
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6
Q

Where are Brunner’s glands found and what is their function ?

A

Located in the submucosa of the duodenum

The secrete HCO3

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7
Q

Where are intestinal glands and goblet cells located relative to the duodenal villi ?

A

Goblet cells are on the outer surface just inside of the enterocytes
Intestinal glands are in the gaps between the villi

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8
Q

How is the jejunum structured differently to the duodenum ?

A

Highly folded or max absorption (SA^)
Plica circulares is the name for one group of villi
No Brunner’s glands (so no HCO3)

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9
Q

How would you differentiate between the ileum and the rest of the SI under a microscope ?

A

The ileum contains Peyer’s patches, found between muscalris and sub mucosa. They’re important for immune function through monitoring of bacteria, prevent pathogenic growth

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10
Q

How would a blood capillary appear on a histological section ?

A

Small oval/circle filled with lots of red dots

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11
Q

Where are B12, folate and Iron absorbed in the body ?

A

Dude I just feel ill bro
Duodenum = Iron
Jejunum = Folate
Ileum = B12

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12
Q

Along with Fe, what other structures are absorbed in the duodenum ?

A

Ca and monosaccharides

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13
Q

How are microcytic anaemias broken down ?

A

Absorption or malnutrition problems. Think of px’s age e.g. doubt 40 yo man is anorexic

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14
Q

What is a tTG test used for and what other test would you have to issue with it and why?

A

IgA tissue transglutaminase (tTG) is used to indicate coeliac. A high result = +ve
You also have to run a total immunoglobulin A test to check for a deficiency, because this would give false -ve for coeliac (if IgA was low)

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15
Q

What is scalloping ?

A

Appearance under an endoscopy is inflammed, swollen with worse definition. The bumping looks similar to cobble stones.

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16
Q

What is the significance of inflammation in the villi/mucosa ? Give an example enzyme in the brush border …

A

Inflammatory cells block off villi/mucosa so nutrients don’t come into contact with brush border -> enzyme digestion decreases
Lactase breaks down lactose in BB

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17
Q

What is the trigger of bile ?

A

Fat in the duodenum causes CCK release from I cells.

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18
Q

What is the consequence on digestion of inflammation ?

A

No CCK release because I cells inflamed
Brunner’s glands can’t release HCO3 to neutralise the acidic chyme
Long chain fatty acids can’t be endocytose by enterocytes

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19
Q

How is diarrhoea defined ?

A

Passage of 3 or more loose or liquid stools per day (or more frequent than is normal for the px). Roughly 200g

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20
Q

What are the 4 main types of diarrhoea ?

A

Osmotic , Inflammatory , Secretory and Mobility

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21
Q

What is osmotic diarrhoea ?

A

non absorbable substance means H2O moves into lumen. Retention of H2O in bowel. Often due to lactate deficiency or use of sugar substitutes (slow absorption but cause rapid motility)

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22
Q

What type of diarrhoea; water not absorbed through walls so remains in stool. Mainly colon causes abdominal pain, fever and bloody diarrhoea ?

A

Inflammatory pathogens e.g.; shigella, salmonella, campylobacter, e.coli and c.diff
IBD shows inflammatory

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23
Q

What are the secretions in secretary diarrhoea ?

A

Mucosal lining secretes Cl and HCO3 into fluid. Electrolyte absorption affected, H2O released into SI. Common during infection or certain drug use

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24
Q

What is the difference between acute (watery and blood) and persistent diarrhoea ?

A

Acute, lasts several days and includes cholera
Bloody = dysentery
Persistent, 14+ days

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25
Q

What type of diarrhoea ; watery diarrhoea expelled violently with gas ? Common cause ?

A

Explosive , commonly due to bacterial infections

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26
Q

What is steatorrhea ?

A

Less fat absorbed in the intestines so more present in stools. Causes; diet, kidney disease, CD, coeliac, gallstones

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27
Q

What is the key ingredient in chillies that causes the burning sensation and sometimes burning diarrhoea ?

A

Capsiacin

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28
Q

What is lassitude ?

A

Lack of energy without exertion

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29
Q

Where is B12 absorbed ?

A

Terminal ileum

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30
Q

What condition is referred to as transmural ?

A

Crohn’s disease, affects whole wall

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31
Q

What is cobblestoning ?

A

Ulcers form in the terminal ileum that reduce the SA of villi and appear hard and bumpy like cobblestones

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32
Q

What is pyloric gland metaplasia ?

A

Pits in the ileum heal poorly and lead to fall in SA and efficiency

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33
Q

How would you tell if there is infection on a histological section of the ileum ?

A

Shows Casciation, can be seen as ‘cheese blocks’ under section.

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34
Q

What does a high fat content show in a stool sample ?

A

May be an indicator or steatorrhea of lactose intolerance

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35
Q

What is the first course of tx when a px is in shock ?

A

ABC and calm them down.

Rehydrate in order to active ADH to ^ retention. Can give hydrocortisone (steroid) or prednisone to help

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36
Q

What are the key indicators of dehydration ?

A

Creatinine and urea ^

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37
Q

What is Chaggers disease and how would you identify it ? Would can it cause ?

A

Large bowel enlargement due to SM dysfunction not maintaining tone. Shows ‘thumb printing’ on Xray. Can lead to toxic megacolon, CVD.

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38
Q

What are pseudopolyps and what can they cause ?

A

Projecting masses of scar tissue that project form granulation tissue during healing phase of repetitive cycles of ulceration. Rest of mucosa becomes inflamed/ulcerated -> destroyed

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39
Q

What does a decrease in albumin show ?

A

Fluid imbalance , possibly from not eating or drinking properly

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40
Q

What is the significance of diarrhoea and a job involving food handling ?

A

Have to wait for 2 days for sx/illness to pass before returning to work.

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41
Q

When would you report infectious diarrhoea ?

A

Every time no matter the occupation.

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42
Q

What do FBC and CRP levels indicate ?

A

full blood count shows inflammatory markers

C reactive protein shows infection+inflammation produced by liver

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43
Q

How would you obtain a stool culture ?

A

Obtain sample. Culture specimen on selective blood agar plate with abx that inhibit most faecal flora.
Incubated in warm temps with no O2
Look under microscope and identify organism

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44
Q

What are the microbiological characteristics of Campylobacter ?

A

Red rod like worms. Gram -ve , helical. Possible cause of IBD

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45
Q

What are the two most common bacterial causes of gastroenteritis ?

A

Salmonella and Campylobacter

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46
Q

What are the bacterial causes of gastroenteritis that arise from poor hygiene and food poisoning ?

A

E. coli and Staphylococcus

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47
Q

What is diverticulosis ?

A

Bits of inner mucosa push through deeper layers of gut forming pouches. More common with age from ^ wear and tear.

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48
Q

What are the 5 complications of diverticulitis ?

A 
Inflammation/infection 
Diverticular abscess 
Strictures, cause LB obstruction
Fistula -> pneumaturia and faecal leakage obstruction 
Perforation or bleeding
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49
Q

What are the risk fx for C.diff? (6)

A 
multiple/lengthy abx (most common) 
long stay in hospital 
frailty and immunosuppression 
Exposure to PPIs 
Age >65 
Comorbitides eg. renal failure
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50
Q

What are pseudomembranes ?

A

Appear to be raised bits of mucosa under endoscope, countless bits of yellow mold bumps.

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51
Q

What is pseudomembranous colitis ?

A

Secondary to C.diff infection. Mucopurulent exudate erupts out of crypts. Under biopsy each one looks like a mushroom cloud.

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52
Q

What is the issue with superficial crypts during pseudomembranous colitis ?

A

They cause patchy necrosis that leads to dilation of the membrane. Leads to end stage of disease, entire crypts necrotic, resembles ischemic colitis.

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53
Q

How would you tx pseudomembranous colitis ? (3)

A

Re establish fluid balance (oral or IV)
Stop causative abx
Give vancomycin and metronidazole (if serious)

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54
Q

What tx would you use to treat recurrent C diff ?

A

FMT, faecal microbiota therapy (stool transplant).

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55
Q

What are the two layers that enclose the abdominal cavity ?

A

Greater and lesser omentum

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56
Q

What is the name for the double layers of peritoneum and what is their function ?

A

Mesentery

Carry blood vessels and lymphatics supplying the organs

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57
Q

List the retroperitoneal organs …

A

Suprarenal glands, Aorta/IVC, Duodenum (2-4 parts), Pancreas , Ureters , Colon ( ^ + descending) , Kidneys , Eosophagus , Rectum

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58
Q

Peritoneal fluid usually absorbed by pores in peritoneal membrane. What is the term for when fluid ^ ?

A

Ascites, often blockage occurs due to metastatic tumours.

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59
Q

Which two organs are connected by the lesser omentum?

A

Liver and stomach

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60
Q

What is the name of the hole that connects the two sacs ?

A

Epiploic foramen

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61
Q

What is the name of the procedure used to drain the greater sac and what is the process ?

A

Paracentesis , needle into the anterolateral abdominal wall.

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62
Q

Where would an accumulation of fluid in the infra colic compartment track to in an erect individual and why?

A

Pouch of Douglas , lowest point so gravity flow

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63
Q

What is Morrison’s patch ?

A

Space between right kidney and liver, allows fluid to move from infra to supra colic compartment via the paracolic glottis.

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64
Q

What is air under the diaphragm referred to as ?

A

Pneumoperitoneum , black on X-ray due to less dense that air.

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65
Q

Where does the primordial foregut meet the midgut ?

A

2nd region of the duodenum and the ampulla of Vater

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66
Q

What is the ligament that attaches the end of the duodenum to the post abdominal wall ?

A

Ligament of Trietz , attaches the duodenal flexure. Landmark for surgery because it remains constant.

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67
Q

What are the normal diameters of the SI, LI and caecum?

A

SI = 3cm , LI = 6 , Caecum = 9cm

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68
Q

What is the name of the junction between the ileum and LI and where is it located ?

A

Ileocecal valve

In the RLQ

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69
Q

What is intussusception ?

A

Intestines slide into adjacent regions causing blockage and potential vascular obstruction.

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70
Q

When the appendix becomes inflamed its lumen can be obstructed leading to distention and swelling. Where is the pain felt ?

A

Umbilical region.

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71
Q

How is pain felt if the structures are innervated by the autonomic NS ?

A

generalised dull aching pain

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72
Q

After appendix inflammation the parietal peritoneum becomes involved. How does the pain change?

A

Innervated by somatic, segmental nerves so pain is severe highly localised and sharp. Pain is felt in the Right Iliac fossa.

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73
Q

Name same conditions where appendicitis may be in a different location ?

A

Pregnancy, growing uterus pushes appendix ^
Citus inverts, R/L axis swap so pain in LIF
Some have appendix behind colon

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74
Q

What is the name given to the surface position for the appendicular orifice used in surgical excision of the appendix ?

A

McBurney’s point

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75
Q

Removal of the appendix would require ligation of which artery running in the mesoappendix ? Where does it arise?

A

The appendicular artery. Arises from the ileocolic branch of the SMA

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76
Q

Which parts of the colon are intraperitoneal ?

A

distal 1/3 transverse and sigmoid

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77
Q

What 3 features of the LI can be used to distinguish it from the SI in surgery ?

A

Haustra (small pouch sac formation) , Teni Coli (longitudinal ribbons along length) , size/diameter

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78
Q

What is a haemorrhoid ? How are the felt during a PR exam?

A

Enlargment of the veins due to straining (piles). On the surface of anus/rectum as little bumps.

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79
Q

What is the difference between internal and external haemorrhoids ?

A

Internal, originate from sup rectal veins, are painless due to have no nerve supply (endoderm)
External, from the inf rectal veins, are acutely painful.

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80
Q

Which blood vessel acts as a landmark to distinguish between two types of inguinal hernia ?

A

Inferior epigastric vessels; indirect - lateral and direct - medial

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81
Q

What are the two types of inguinal hernia ?

A

Direct, bowel enters abdominal cavity ‘directly’ through weakness in the post wall. ^ with age, due to ^ intra abdominal pressure and wall laxity.
Indirect, bowels enters inguinal canal through deep inguinal ring due to failure of closure of the process vaginalis - deemed congenital in origin.

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82
Q

For direct inguinal hernias, what is the weakness in the post wall referred to as ?

A

Hesselbach’s triangle

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83
Q

Where does the sympathetic and parasympathetic innervation arise from in the gastrointestinal system ?

A

Sympa - sympathetic trunk in the thorax

Para - from the vagus and pelvic splanchnic nerves

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84
Q

What are the spinal levels of the fore, mid, and hindgut and so what are there areas of referred pain ?

A 
Fore = T5-T9 -> anywhere above umbilicus 
Mid = T10/11 -> umbilicus 
Hind = L1/2 -> hips and ASIS
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85
Q

Which CN provides para innervation of the gut up until the splenic flexure of transverse colon ?

A

Vagus , ‘wandering’ in latin. It’s the longest

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86
Q

What is Hirschprung’s disease and what are the signs?

A

Congentical megacolon. Ganglia absent from myenteric plexus causes constipation and reduced gut motility

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87
Q

What are the 3 branches of the aorta that supply the gut and their spinal levels ?

A

Coeliac trunk (T12) , SMA (L1/2), IMA (L3)

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88
Q

What are the main beneficial properties of intestinal bacteria ? (3)

A

Enterohepatic circualtion; breakdown of food, drugs aid absorption
Nutrition; metabolise vits eg. B7 9 12, K
Infection, normal flora prevent growth of endogenous and limit infection from exogenous.

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89
Q

How might a poor gut lead to clotting disorders ?

A

Poor gut nutrition means Vit K isn’t metabolised so specific fx aren’t made.

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90
Q

What are the properties of C diff bacteria and how is it spread?

A

Gram +ve rod, mostly LB disease, destroys normal gut flora. Spread faecal orally due to poor hygiene.

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91
Q

Why are C diff recurrent infections common ?

A

Spores are resistant to chemicals and heat so won’t dry out. They are then able to replicate in the gut and cause infection.

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92
Q

How would you manage a C diff infection on an individual and multiple scale ?

A

Fluid balance, anti C diff abx , surgery.

Isolate cohort / environmental cleaning.

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93
Q

What abx would you use for a C diff infection ?

A

Coamoxiclav (combo of amoxicillin and Clavulanic acid) used as broad spectrum abx.
Then narrow to target gut; Metronidazole for moderate and Vancomycin for severe (often now used 1st line)

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94
Q

What is the advantage of a FMT during C diff infection?

A

Faecal microbiota transplant

px restores normal biota and limits C diff migration sites.

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95
Q

What bacteria are curved motile gram -ve rods , that are the commonest cause of IID ?

A

Campylobacter , Infectious intestinal disease

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96
Q

How long do sx of campylobacter last and how are they resolved ?

A

normally 2-7 days , usually self limiting but persistent / recurrent if px is immunocompromised

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97
Q

How do you ^ prevention of campylobacter infections ?

A

better kitchen hygiene and isolation of sx patients.

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98
Q

Salmonella is a grame -ve motile rod. What 2 major problems does it cause via which subtypes ?

A

Food poisoning , S enteritidis

Thypoid (enteric fever) , S typhi and S parathyphi

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99
Q

How long does a salmonella infection last ?

A

Ilness normally 48-96 hrs. Can take up to 9 weeks, asymptomatic shedding is a major problem

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100
Q

What tx can be used in Salmonella becomes serious ? (Wouldn’t use meds if mild)

A

Quinolones, macrolides, cephalosporins

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101
Q

What is enteric fever ?

A

Salmonella cause febrile illness with cough and constipation common.

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102
Q

What condition would you treat a px with fluoroquinolone?

A

Enteric fever.

Can also use Ceftriaxone, azithromycin

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103
Q

What are the 4 types of E coli ?

A

Enterotoxigenic , Verocytotoxin , enteroinvasive, Enteropathogenic

104
Q

Where does VTEC act and what can it cause ?

A

Verocytotoxin (E coli)
direct attachment to terminal ileum and colon, shows widespread outbreaks eg. in food.
Can cause HUS (haemolytic uremic syndrome - RBC breakdown)

105
Q

How do you treat cholera ?

A

Aggressively rehydrate initially

Vaccines available for travellers to ^ risk areas.

106
Q

How is shigella spread ?

A

non motile Gram -ve rods. small infectious dose spread through faecal oral spread in poor hygiene.

107
Q

What is the norovirus ?

A

non enveloped ssRNA virus that affects SB. Can last in air for hours.

108
Q

How long is the incubation period for norovirus and what sx are seen during this time?

A

24-48 hrs , fever vomit diarrhoea.

109
Q

What is the commenest cause of infant diarrhoea that affects the small bowel with types A+B effecting humans ?

A

Rotavirus

110
Q

How would you detect and manage the rotavirus ?

A

Detection using ELISA test

Management; isolation using careful transport and then clean the environment

111
Q

What is the two stage life cycle of intestinal protozoa giardia lamblia ?

A

flagellate trophozoite in host duodenum attaches to epithelium and reproduces by binary fission. Cyst then passed to stool where it’s highly infectious

112
Q

How would you diagnose Giardia ?

A

Stool microscopy, iodine stain to reveal cysts. Ag detection assays used to test px post outbreak/tx

113
Q

What is the 1st line tx for Giardia ?

A

Metronidazole , Tinidazol can also be used.

114
Q

Cryptosporidium; what is it, where does it multiply, what does it cause ?

A

Intestinal sporozoa that multiplies in SI. 1-5 oocytes cause infection. Major diarrhoea cause in immunocompromised

115
Q

What is Cryptosporidium resistant to and how is it transferred between hosts ?

A

Resistant to Chlorine and Disinfectant

Transferred via H2O, mainly mammal hosts

116
Q

What are the sx of Cryptosporidium and what are the major complications that can develop ?

A

Diarrhoea with abdominal cramps and weight loss, may develop cholangitis and cholecystitis

117
Q

What is the special method through which Cryptosporidium is diagnosed ?

A 
Oocytes may be seen in stool microscopy. 
Modified ZN (Ziehl-Neelson) stain which is acid fast staining that causes bacilli to be pink 
Has to be used on structures which are resistant to Gram staining
118
Q

What key investigations would show an ^ as a result of malabsorption ?

A

FBC , WCC (inflam) and anaemia

119
Q

What are the +/- of biopsy ?

A

May be useful in C diff for diagnosis and to exclude IBD

Risk of perforation ^ so avoid where possible

120
Q

How would these specimens look on an agar plate; campylobacter , E coli , Salmonella , Vibrio cholerae ?

A

Campylobacter; black with white hashtag
E coli ; Pink with white spots
Salmonella ; red with white spots
Vibrio cholerae ; grey with fluorescent green lines

121
Q

What are the main causes of malnutrition ? (5)

A

Anorexia (disease,anxiety,depression) , difficulty in food to mouth/chewing , oral intake contra, enforced fasting (religious) , sedations comatose

122
Q

What occurs in the period after starvation (24 weeks starved then 12 not) ?

A

Rapid ^, fat ^ to higher than previous value. Depression ^ during fasting period.

123
Q

What is marasmus ?

A

Malnourishment of a child causing them to be significantly under projected weight percentiles. Normally metabolically stable to chronic fall in food intake

124
Q

What effect does malnourishment/anorexia have on these systems; wound response, gut, CV, Resp, CV, Res, Renal, Liver, Pancreatic, Intestines ?

A

Wound response; collagen made of protein so healing takes longer and is worse
Gut; integrity falls as tight junctions break -> leaky
CV; ventricular mass and CO falls -> Brady/hypertension
Resp; ventilatory drive/cell mediated immunity falls. Cough P down so ^ chest infections. need ventilatory support for longer
Renal; gradual loss of function. less able to concentrate urine in renal medulla so lower conc grad -> polyuria
Liver; nothing until near death. glycogen and fat stores used up.
Pancreatic; atrophies -> endo/exocrine function falls

125
Q

What is the effect on the intestines during malnourishment ?

A

presence of nutrients in the gut needed for mucosal growth/function through activation of trophic GI hormones. ^blood flow (activation of ANS). malnutrition -> less absorption, less motility, immune impairment

126
Q

How can a loss of weight affect absorption?

A

Villi height falls, atrophy and thinning of mucosa so SA down. Less brush border enzyme activity -> steatorrhea/diarrhoea ^.

127
Q

What is sarcopenia ?

A

loss of body muscle but retention of fat, appear obese but lean mass is normal

128
Q

What is Kwashiorkor malnutrition ?

A

Fluid retention due to lack of protein in the diet. Shows poor response to infection, loss of electrolytes. ^urinary nitrates.

129
Q

What are the fat soluble vitamins ?

A

A, caretonoids for vision, antioxidants
D, made using sunlight. def -> rickets, depression, schizophrenia, asthma. Muscle weakness (OA)
E, antioxidants. Role in stroke prevention/cancer/HD
K, attributes to blood clotting fx. def -> internal bleeding

130
Q

What is Beri Beri syndrome ?

A

B1 def. neck veins enlarged, fluid in lungs, ^ HR, swelling in legs. Coordination problems, reflexes slow.

131
Q

Name some water soluble vitamins ?

A

B1 (thiamine) carb metabolism
B2 (riboflavine) energy metabolism. def > angular colitis/stomatitis/glossitis.
B6 (pyridoxine) , B7 (biotin) def > alopecia, B12 (cobalamin)

132
Q

What is the WAASP assessment for nutritional tx?

A

Weight, appetite, ability to eat, stress, pressure (sores/wounds)

133
Q

What are the example screening questions during a nutritional assessment ?

A

Have you lost weight recently?
Has your appetite lessened ?
Are your clothes or dentures loser than normal ?

134
Q

What is the estimated requirements of a 46 yo women post op in terms of calories and protein ?

A

Calories - 1668

Protein - 74 g

135
Q

What is the cascade process that causes ^ P53 and what is P53 ?

A

APC > K-ras > SMAD4 > P53

Gene that codes for a protein that regulates the cell cycle so acts as a tumour suppressor

136
Q

What are the common presentations of bowel cancer ? (3)

A

Anaemia bleeds on R side > tiredness/SOB
Change in bowel habits, >3/day and/or up at night to poo
Obstruction, vomit pain abdo distention and constipation

137
Q

What is the difference between proto-oncogenes and oncogenes ?

A

Protooncogenes are the normal form which help regulate cell growth and proliferation
Oncogenes, activated so cell activity ^

138
Q

What is the consequence of a single or double gene mutation in TS genes ?

A

Tumour suppressor
1 is ok because the other still regulates/’acts as breaks’
2 means there’s no regulation > rapid proliferation.

139
Q

What are the risk fx for colorectal cancer ? (

A

Famalial, diet (lack of fibre, ^ red meat, ^ processed food)

140
Q

What is SNP ?

A

Single nucleotide polymorphism , single base changes that can cause variety of effects when totalled

141
Q

What are the properties of cancer cells that allow them to rapidly proliferate ? (3)

A

Create own vascular supply (central tumour cells would self deprive themselves of O2)
Metastasis , can help to avoid the immune response
Insensitive to growth inhibitory signals. Evasion of apoptosis

142
Q

How is FAP normally regulated ?

A

Familial adenomatous polyposis
APC gene on Ch5 regulated by b catenin
APC binds to GSK3b > destruction complex > breakdown of b catenin to keep levels low.

143
Q

How does FAP develop when b catenin isn’t broken down?

A

B catenin moves into cell > activates oncogene > proliferation > apoptosis > uncontrolled growth

144
Q

What are the extra intestinal manifestations of FAP ?

A

CHRPE (congenital hypertrophy of retinal pigment epithelium) - black spots on back of the eye
Desmoid tumour, growth of fibroblasts (produce collagen) . Benign but rapid growth so remove surgically.

145
Q

Post op (for FAP) what is the tx plan for the px ?

A

^GI surveillance because risk of polyps and cysts in stomach and GI tract ^

146
Q

How would you diagnose colorectal polyps ?

A

DNA extraction from WBC or lymphocyte. Tested in genetics diagnostic service. Abnormal stop codon in gene > mutation so not enough APC (for example) made

147
Q

What is the difference between Ulcerative colitis and Crohn’s disease ?

A

UC - diffuse mucosal inflammation limited to colon, normally rectum. May extend symmetrically to LI. Diagnose using an endoscope
Crohn’s - Patchy transmural inflammation anywhere on GI tract. Typically non bleeding. SB involvement with rectum sparing.

148
Q

What is the normal appearance of the colon and how does this differ to severe UC ?

A

Norm, shiny purple/pink and retains delicate reticulated vascular pattern
Severe, macro ulceration with mucopurelent exudate and spontaneous haemorrhage

149
Q

What are the common sx of UC ?

A

bleeding (rectal can lead to anaemia), diarrhoea (not present in proctitis), urgency to poo, abdominal pain

150
Q

What is proctitis ?

A

Rectal inflammation subset of UC. No diarrhoea, poo forms further round colon therefore just mucous and blood comes from the rectum.

151
Q

What is an early radiological sign of toxic colitis ?

A

Gas accumulation over the colon. Luminal diameter is slightly smaller with scalloped margins from edema/spasm

152
Q

What is the danger with toxic megacolon ? where is the dilation largest ?

A

Perforation or peritonitis.

Dilation at max in the transverse colon because fluid collects in flaccid bowel when supine

153
Q

In toxic megacolon how would you redistribute the gas and what effect would this cause ?

A

Rotate the px in supine , redistributes the gas and decompresses the colon.

154
Q

What are perforations ?

A

complication of UC, subserosal dissection of luminal gas into the bowel wall.

155
Q

What is the advantage of colonoscopy in decreasing colorectal cancer risk ? What is the first cancer sign?

A

Highlights bowel structure targets abnormal areas to avoid biopsy.
First sign = visual dysplasia

156
Q

Name some extra intestinal manifestations related to IBD (4)

A

Aphthous stomatitis (mouth ulcers) , Orofacial granulmoatosis (OFC) lip swelling w/ fissures, inflam etc. , Episcleritis and uvetis (eyes) painful red eye light causes iris to contract pain due to inflam , Arthritis etc.

157
Q

What is the most common extracolonic manifestation of colitis ?

A

Peripheral arthritis. Joint inflam similar to RA but affects large joints , no synovial destruction and is asymmetrical.

158
Q

How would you differentiate between peripheral arthritis and RA ?

A

Peripheral arthritis is seronegative (-ve in blood test for rheumatoid fx)

159
Q

What is the difference between Erythema nodosum and Pyoderma gangrenosum?

A

Erythema nodosum - bowel activity down > pale coloured skin with red spots. Seen in Crohn’s self healing
Pyoderma gangrenosum - trauma lesions red area w purple edge on shins, hands etc. Seen in UC need tx

160
Q

What conditions are associated with HLA-B27 on Ch6?

A

Central athropathy, ankylosing spondylitis (fibrosis/fusing of vertebrae) , spondylitis, sacroilitis

161
Q

What is sclerosing cholangitis ?

A

Bile ducts becomes distorted, truncated and have segmental areas (narrowing/bleeding)

162
Q

What major types can Crohn’s disease develop into ?

A

Obstructive , fiscalisation and Ileitis

163
Q

What is obstructive Crohn’s disease ?

A

1st stricturing > inflam+fibromusclar proliferation, collagen deposition in intestinal walls > narrows lumen.

164
Q

Px presents with post prandial cramps and vomiting. They have also noted weight loss recently. What is your diagnosis ?

A

Obstructive Crohn’s. Food distention causes cramping most evident after meals. Vomiting is from high grade obstruction. Weight loss could be due to avoiding food.

165
Q

What is the Fistulation that is seen in Crohn’s disease ?

A

wall thickens, lumen narrows penetrative ulcers form. Culminates in sinus tracts + fistulae formation to adjacent structures.

166
Q

What different sx would be experienced depending on the location of the fistulae ?

A

Enteroenteric ; may be asymptomatic
Enterovesical; recurrent UTIs , pneumaturia (gas in urine)
Retroperitoneal; psoas abscess (back, hip, thigh pain)
Enterocutaneous; (stomach contents leak into skin) drainage via scar
Perianal; pain swelling pus.
Rectovaginal

167
Q

How would you tx a perianal or rectovaginal fistula ?

A

Perianal - anal suture ‘seton’ used to tie knot prevents fistula blockage
Rectovaginal - drainage

168
Q

What is the cause of a perianal fistula ?

A

Crypts of morgagni in anus spread through internal sphincter muscle > intersphincteric, isorectal supralevator abscess etc.

169
Q

Which condition shows; modularity, ulceration, narrowing and irregularity of the lumen. Overall transmural inflammation and lymphoid proliferation ?

A

Ileitis as a result of Crohn’s , irregular intestinal loops form as lumen narrows and wall thickens with mesenteric hypertrophy.

170
Q

What is the ‘string sign’ ?

A

Combination of transmural thickening with erratic spasms in the terminal ileum indication ileitis.

171
Q

If a px presents with major perianal lesions with a history of IBD, what is the likely diagnosis and what can you rule out ?

A

Likely is Crohn’s

Never seen in UC

172
Q

Px presents with fistulation into surrounding tissue and organs around the bowel in an asymmetrical pattern. What is your diagnosis ?

A

Crohn’s

173
Q

What are the differentials between IBD and IBS ? (5)

A

IBD +ve for; anaemia (platelets ^ albumin drop) , weight loss/fever , perianal disease, bloody stools , faecal WBC count.

174
Q

What is the faecal calprotectin test ?

A

Test to rule out IBD. If a little +ve then useless because could still be both. If very +ve = IBD. If -ve then not IBD (IBS)

175
Q

When are the peaks of onset for Crohn’s and UC ?

A

Late adolescence/early adult has a peak for both. Crohn’s has a 2nd peak in 60’s/70’s.

176
Q

IBD has ^ too rapidly to just be a cause of genetics. What are the other possible causes and during which time period ?

A

Urbanised living ^ , industrialisation/pollution

Influence occurs during childhood

177
Q

How does an appendectomy affect UC and Crohn’s ?

A

In young px (<20) prior to UC shows protective effect
After onset procedure shows no difference.
Crohn’s shows no difference whatsoever

178
Q

Name some drug tx that can be used for UC and Crohn’s (4)

A

Mesalazine (anti inflam) works in UC
Corticosteroids used in both
Azathioprine (immunosuppressants) oral works in both
Anti TNF used in both, injected

179
Q

What are anti TNF antibodies ? Give examples when they would be used…

A

Used instead of steroids normally. Monoclonal antibodies that target TNF bound to membrane, fast acting.
Infection’ infliximab and Vedolizumab > lymph traffic inhibitor binds to interns on surface lymphocytes

180
Q

What is Sulfasalzine ?

A

Cause of clinical toxicity, especially in px who are slow acetylators. Composed of aminosalicyclic acid (5-ASA) - an aspirin analogue - bound to a diazo bond.

181
Q

How is sulfasalzine activated ?

A

Intestinal bacteria cleave the di-azo bond, releasing 5-ASA which causes drug toxicity.

182
Q

How is Sulfasalzine absorbed and metabolised ?

A

30% upper GI/kidneys. Most absorbed by liver excreted in urine.

183
Q

What is the drug tx ladder for UC ?

A

mild = Mesalazine . Severe = Anti TNF then corticosteroid. Maintenance of remission = Mesalazine and azathioprine / 6-mercaptopurine

184
Q

What is the drug tx ladder for Crohn’s ?

A 
Mild = Budesonide (locally active corticosteroid) with dietary therapy and abx 
Severe = Anti TNF > Corticosteroids 
Maintenance = azithioprine and anti TNF
185
Q

What is the link between Azathioprine and 6-mercaptopurine ?

A

Azathioprine is a pro drug quickly converted to 6-mercapotpurine via non enzymatic nucleophilic attack by sulfahydryl compounds (glutathione) present in RBC and other tissues

186
Q

What abx can be used in tx of Crohn’s ?

A

Metronidazole and Ciproflaxacin

187
Q

What conditions might Methotrecate and Ciclosporin be used for and why ?

A

Methotrecate (Crohn’s) and Ciclosporin (UC) are immunosuppressive drugs

188
Q

What is the function of Vedolizumab ?

A

Used in infection, gut specific lymphocyte traffic inhibitor. Response to MAdCAM-1 allowing lymph straight past inflammatory site therefore preventing response.

189
Q

What is Mebeverine ?

A

Antispasmodic used in IBS. MOA unclear, but decreases Ca entry into gastric SM cells so fewer spasm episodes.

190
Q

What drug could have ADR on a px of; indigestion, constipation, rash and dry skin ?

A

Mebeverine

191
Q

What drug tx is used as an antidiarrhoeal eg. for acute non infective diarrhoea ?

A

Loperamide , mu opioid receptor agonist. Decreases myenteric plexus electrical activity that then relaxes GI SM tone ^ peristalsis.

192
Q

What brand name is Loperamide often sold under ?

A

Imodium

193
Q

What is prednisolone?

A

Anti inflammatory, can be used in UC. binds to steroid receptor, acts as gene transcription regulator ^ anti inflammatory protein synthesis but decreases inflammatory immune factor synthesis.

194
Q

What are the contraindications of prednisolone ?

A

If immunosuppressed or have active infection

195
Q

Why might Cinchocaine and hydrocortisone by used together ?

A

Haemorrhoid tx. Combinations often include peripheral vasoconstrictors eg. phenylephrine + LA + Anti inflam.

196
Q

What is the function of a LA ?

A

Local anaesthetic. Blocks Na voltage gated channels in nociceptive nerve fibres. Forces nerve to ^ refractory period and prevent pain AP along axon to CNS.

197
Q

When would you not give Cinchocaine for haemorrhoid tx ?

A

Heart block or WPWS arrhythmias. If already on class 1 anti arrhythmic drugs

198
Q

At what vertebrae levels are the 4 parts of the duodenum?

A

Bulb at L1
Sup duodenal flexure to inf flexure L2
Inf duo flexure to midline L3
Midline to ligament of Treitz L2

199
Q

Which parts of the duodenum are retroperitoneal ?

A

Parts 2, 3 and 4

200
Q

How would you test for Perforation ?

A

Use an erect chest X ray, view collection around the ‘hole’

201
Q

How would you distinguish the small and large bowel in an abdominal x ray ?

A

Small; central location, gas/fluid filled, calculate conniventes, calibre <3 cm diameter
Large; Peripheral location, faeces, hausfrau, calibre <5 cm diameter.

202
Q

How would the large bowel change during toxic megacolon or perforation ?

A

Calibre ^ to above normal range. Abnormal >8cm.

Haustra disconnected, don’t cross entire width of wall.

203
Q

What is pneumatosis ?

A

Gas within the wall of the bowel. Just before the bowel perforates. Bowel wall ischemic as under too much pressure

204
Q

What is the name given to abnormal gas filled loops in the colon ?

A

Pseudo obstruction. Common in the elderly, tend to be on Parkinson’s medication

205
Q

How would perforation be indicated on a chest X ray ?

A

px has to be erect long enough for gas to rise. Air released into peritoneal space. Free air under diaphragm shows upper edge of liver and lower edge of diaphragm (usually isn’t seen due to soft tissue and fluid).

206
Q

What are Rigler’s signs ?

A

Air is seen on both sides of intestine (lumen and peritoneal side of wall). Triangles of gas (low density=dark) show leakage into peritoneal space.

207
Q

What is the term given to a large pneuma-peritoneum where gas rises above abdominal wall?

A

Falciform or Football sign. Liver rises from falciform ligament, shows gases either side.

208
Q

How is a Ba follow through carried out and how would Crohn’s be indicated ?

A

Just SB, px drink liquid containing Barium to coat the lumen.
Crohn’s shows superficial inflammation (cobblestoning). deep ulceration through bowel. Contrast goes through bowel wall transmurally.

209
Q

What test would be used to assess the colon mucosa in detail to help identify cancers and polyps ?

A

Barium enema, just LB. Px given laxative and rectal tube inserted (Ba + CO2) in a double contrast study.

210
Q

What is diverticular disease and what does it have a similar presentation to ?

A

Out pouches of mucosa through bowel wall. Can lead to inflammation and fever with an acute presentation similar to appendicitis.

211
Q

What are the limitations of a Ba enema ?

A

Mobility (requires regular turning) , anal tone, inadequate bowel prep common, overlap of bowel oops common

212
Q

What is the advantage of using an IV contrast during CT scans ?

A

Gives an enhanced view of the soft tissue and tumours. Useful for identifying blocked areas. Contains Iodine

213
Q

How does the appearance of an oral contrast vary ?

A

Contains -ve (H2O) which is dark. Enhances wall/mucosal pattern. Shows outside of bowel.
And the +ve (iodine based drink) which is bright. Helps identify fistulas.

214
Q

What is Comb sign ?

A

The hyperactive mesentery seen with Crohn’s disease. Lines of inflammation look like a hair comb.

215
Q

How is the pain felt in; haemorrhoids, fissures and fistulas and how would you tx them initially ?

A

Haemorrhoids, intense pain with palpable lump when bowel opens
Fissures, tearing of anus able to pinpoint pain when straining
Fistulas, passage of outside of anus through sphincter that causes intense pain or asymptomatic.
Relax the anal can with GTN spray or Dilitiazem cream

216
Q

What is an end colonoscopy ?

A

End of colon exposed, Hartmann’s op removes rectum+sigmoid , contents similar to stool. Used in early management

217
Q

What are the complications with ileostomy ?

A

More problems in op and may be watery so need antidiarrhoeals to prevent dehydration.

218
Q

What are the two types of ileostomy?

A

End; UC px removes LB, green and thick contents relative to amount of SB still present
Loop; Some SB attached to skin, diverts the stool downstream of the stoma.

219
Q

What is a Colostomy and what are the advantages over CTC ?

A

Direct visualisation of inside of bowel that allows for biopsy (CTC doesn’t with same prep).
Look right into terminal ileum so useful for Crohn’s/UC diagnosis.
CT colonography

220
Q

What is ERAS , give some examples ?

A

Enhanced recovery after surgery
stop smoking, anaesthetic choice, pre-op nutrition etc.
Helps delay fear, hypothermia, organ dysfunction, electrolyte imbalance etc.

221
Q

What is the advantage of laparoscopic over open surgery?

A

Smaller incision so less pain and able to breath better post op. Coughing/breathing deeply post op can be painful. More likely to mobilise faster and to ^ level.

222
Q

What are the two curves of the colon ?

A

Right - Hepatic flexure

Left - Splenic flexure

223
Q

The SM cells within the GI are syncytium , what does this mean ?

A

group of cells that share cytoplasm so act as one. AP spreads rapidly from cell to cell and allows electrolytes to move freely between cells.

224
Q

What are cajal cells ?

A

Sit between layers of SM, act as pacemaker cells of the gut SM. Initiate slow wave pattern that oscillates between resting and -40mv.

225
Q

What is the myenteric plexus ? what sensory info do they deliver ?

A

Interconnection of neurones above musculature of the gut. Has afferent sensory nerves that deliver info to interneurones in plexus; stretch and chemo.

226
Q

What is the response when a strong impulse is initiated in stretch and chemo receptors ?

A

Stretch/chemo > info to interneurons > efferent nerves to SM cells > stimulation with AP (spike waves) > muscle contraction.

227
Q

Apart from stretch/chemo receptors, how else is contraction stimulated ? How does this relate to tx?

A

ACh from parasympathetic nerves.

Anticholinergic meds help constipation eg. antihistamines (Benadryl).

228
Q

What are the effects of ; parasympathetic , sympathetic and stress on peristalsis ?

A

Para; stimulates
Sypma; inhibits in extremes , high A/NA all or nothing
Severe stress; complete stop

229
Q

What is the effect of a bolus of food intake ?

A

Stimulates stretch receptors > circular muscles contract then longitudinal muscles contract to shorten tube. Then circular again just after bolus rely to push food down in waves.

230
Q

Where does the roughly 9L of fluid/day go and how is it absorbed ?

A

100ml/day in urine excretion. SI absorbs 8.5L. LI absorbs 100-400ml but can be up to 9L.
Absorbed through passive osmotic forces, paracellularly through tight junctions in lining of SI/LI.

231
Q

What is the effect of some drugs eg. Epsom salts, on absorption ?

A

Can alleviate constipation (Mg sulphates).

Poorly absorbed creates osmotic force that pulls H2O out of body to liquify the stools. Lactulose does the same

232
Q

What is the difference between trans and paracellular movement ? How is the lumen charged ?

A

Transcellualr resistance > para due to voltage difference between SI lumen and intestinal fluid surrounding cells. Lumen is -ve because Na are the main ion to be absorbed.

233
Q

What can cause abnormalities of the tight junctions ?

A

TJ targeted by E coli, they break them down allowing bacterial products/dietary antigens through into lamina propria. This then allows larger structures eg. dendritic cells, macrophages to pass through.

234
Q

What are the key proteins that regulate tight junction function ?

A

Claudins, occludins and includins

235
Q

Where is Na absorbed, through what method, which carrier, how can this be used in tx?

A

Absorbed in the jejunum through co-transport with glucose (SGLT1) and H+.
Can be used for rapid oral rehydration through Na dependant glucose uptake SGLT1 drugs ^ H2O uptake.

236
Q

Where is K absorbed and secreted. What is secretion stimulated by in different membranes ?

A

Absorbed in jejunum. Secreted throughout SI, in colon secretion stimulated by ^ aldosterone channels in apical membrane and ^NaK ATPase in basolateral membrane.

237
Q

How is Ca absorption stimulated and how is this substance made ?

A

active absorption stimulated by Calcitriol. Released from kidneys (produced using Vit D). Vit D taken up/broken down by liver, goes to kidneys and converted to Calcitriol.

238
Q

How is Ca absorbed passively, where does this take place, through what channels. What do the channels respond to ?

A

Paracellular uptake in Duo/ileum through TRPV (transient receptor potential channels).
Channels respond to ^temp (pain, curry - Capsasin)

239
Q

How is ferric state iron (found in meat) absorbed ?

A

converted in SI to Ferras (Fe2+) ^ h2o solubility through reductase enzymes and conc of H/bile acids in duodenum. Uptake in duo through enterocytes. Either stored as ferritin or taken out of basolateral membrane and complexed into transferrin.

240
Q

What is transferrin ?

A

Large macromolecular that prevents iron loss in portal circulation. Used to transport iron.

241
Q

Where are Cl and HCO3 absorbed ?

A

Cl, duodenum passive (lumen -ve pd) cotransport with Na/HCO3 exchange
HCO3, ileum. HCO3 in LI neutralises bacterial flora.

242
Q

What are the action of NANC ?

A

enteric hormones, non adrenergic non cholinergic. Release VIP > acts through PKA + cAMP to ^ Cl by ^ pKa/cAMP to ^ H2O loss.

243
Q

What is Verner-Morrison syndrome ?

A

Pancreatic tumour that ^ VIP to give watery diarrhoea.

244
Q

What is the function of EC cells and how is this related to SSRIs ?

A

Enterochromaffin. secrete serotonin > stimulates pKc > ^Ca turnover in enterocytes > ^ Cl out.
Antidepressants (eg. Fluoxetine) targets CNS but gives ADR of diarrhoea because can also target the gut

245
Q

What is the function of D cells ? what problems can arise if they malfunction ?

A

Produce somatostatin which regulates Na/Cl absorption.

Patho - DM, diarrhoea, weight loss etc.

246
Q

Enteric neurones can release enkephalins, what is their function ? How can this relate to clinical drugs ?

A

They are opioid transmitters important for NaCl absorption. Diarrhoea relief tablets contain emprimide (opioid substance) that helps dry out the stools.

247
Q

What substances give excitatory and inhibitory effects during SI/LI motility ?

A

Excite - substance P + ACh

Inhibit - VIP, NO (short half life)

248
Q

What is the meaning of ‘segmentation’ during post prandial SI contractions ?

A

Circular muscle creates pinching affect around bolus in non propulsive movement in preparation for peristaltic waves.

249
Q

What is the migrating motility complex and when does it occur ?

A

Occurs during fasting every 1.5 Horus. Long range contraction ‘flushes’ contents along the whole length of the intestine.

250
Q

What response does a moving bolus initiate ?

A

triggers stretch receptors, widen path ahead narrows lumen behind.
Longitudinal muscle in front of bolus contract and behind it relaxes
Circular in front relaxes and behind contracts.

251
Q

What is the SIP synctium composed of ?

A

SM cells , Interstitial cells of cajal (ICCs) , Platelet derived growth factor receptor a+ cells (PDGFRa+)

252
Q

What are the function of N cells in the ileum ?

A

Release neurotensin in terminal SI in response to fat. decreases motility (fat normally all absorbed in ileum so if any might get through neurotensin ^ to allow ^ time for absorption).

253
Q

What is the function of L cells and what do they respond to?

A

In the distal ileum they release GLP-1 to reduce motility and ^ absorption.
Released in response to ^ glucose and fat

254
Q

What cells release motilin in response to ^ fat and acid. What is the effect of Motilin ?

A

M cells in the duodenum.

^ Sensitivity reflex in SI so normal intrinsic activity ^. Used in fasting to wash away any small debris. §

255
Q

What is Hirschprung’s disease ?

A

SM prefers contraction it needs inhibitory neurones to relax. Myenteric plexus becomes ganglionic so no relaxation occurs. Proximal build up of mass/matter

256
Q

What type of muscle is the external anal sphincter and what nerve is it innervated by ?

A

Skeletal muscle (voluntary) . innervated by the pudendal nerve (poodendal).

test (14 decks)

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