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GI Flashcards

1
Q

What are the 2 patterns of movement in the GI tract

A

Peristalsis - reflex response -result of wall stretch
segmentation - mixes lumen content

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2
Q

Electrical activity of GI tract

A

spontaneous rhythmic fluctuation with MP -64 and -45
specialised cells aka interstitial cells of cajal
spike potential→ increase tension→ cause contraction
Depo→ ca2+ influx
Repo→ K+ efflux
stimulated by stretch, ACh, Parasympathetic

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3
Q

3 ways GI motility is regulated

A
  1. Reflexes from outside the digestive system
  2. Reflex from inside digestive system (enteric ns)
  3. GI peptides
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4
Q

The extrinsic nervous system (Sympathetic)

A

originate between T5 &L2 of the spinal cord
innervated all of GI tract
Nerve ending secrete mainly NE and epinephrine
Stimulation = inhabits GI activity

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5
Q

The extrinsic nervous system (parasympathetic)

A

divided into cranial and sacral
cranial PN fibres are almost in the vagus nerves except to mouth and pharyngeal
sacral originates from 2-2 sacral segment of spinal cord
it passes through pelvic nerve to distal half of large intestine
stimulation causes increased activity

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6
Q

ENS (layers of cells)

A

-Lumen
-Mucosa (epithelium, lamina propria, muscularis mucosa)
-Submucosa (submucosal plexus)
- Muscularis propria (circular muscle, myenteric plexus, longitudinal plexus)
- Serosa

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7
Q

6 main polypeptides of GI

A

Cholecystokinin
Secretin
GIP
GLP-1
Gastrin
Motilin

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8
Q

CCK

A
  • produced by I cells in duodenum and jejunum
  • also secreted by neurons in the brain
  • stimulates contraction of gall bladder for bile release
  • Stimulation of pancreatic enzyme release
  • relaxes Sphincter of Oddi
  • inhibits gastric emptying by slowing contraction,
  • promotes intestinal motility
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9
Q

Secretin

A
  • produced by S cells of upper small intestine mucosa.
  • mildly affects gastric emptying,
  • promotes pancreatic secretion of HCO3
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10
Q

GIP

A
  • secreted by “K cells” mainly in duodenum
  • slows the rate of stomach emptying when SI is overloaded.
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11
Q

GLP-1

A
  • produced by “L cells” in distal small intestine mucosa.
  • delays gastric emptying
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12
Q

Gastrin

A
  • released from the gastric antrum G cells by stomach distension.
  • increases motility in the stomach
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13
Q

Motilin

A
  • secreted by “M-cells” in the upper small intestine.
  • secreted during fasting, and the only known function of this hormone is to increase gastrointestinal motility - migrating motor complex
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14
Q

3 segments of the Oesophagus

A

cervical

thoracic

Abdominal

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15
Q

Innervation and muscle types of the oesophagus

A

Proximal 1/3 → striated:
- innervated by somatic motor neurons of vagus nerve
distal 2/3 → smooth muscle
- innervated by visceral motor neurons of vagus nerve
- synapse with postganglionic neurons

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16
Q

Lower oesophageal sphincter (LOS)

A
  • Mainly closed
  • ACH causes intrinsic sphincter to contract (closes)
  • NO &VIP → inhibitory (opens)
  • Function: prevent reflux
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17
Q

3 phases of swallowing

A
  • Oral → voluntary
  • Pharyngeal
  • Oesophageal
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18
Q

5 features that make up the anti- reflux barrier

A
  • LOS
  • normal oesophageal peristalsis
  • Crural fibres of the diaphragm
  • Length of the abdo oesophagus
  • Gravity (small effect)
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19
Q

4 aspects of gastric motility

A
  • Filling
    accommodates 20-fold change in its volume by receptive relaxation:
  • vago-vagal reflex from stomach to brainstem and back; reduces tone of muscular wall.
  • the proximal stomach relaxes to store food at low
    pressure whilst it is acted upon by acid and enzymes.
    • Storage
  • Mixing
    Peristaltic contraction (PC) usually begin in body of stomach down
    PC becomes more vigorous as it reaches the antrum.
    This propels the chyme forward
  • Emptying
    A small portion of the chyme is pushed through the “partially” open sphincter into the duodenum

When PC reaches the pyloric sphincter, the sphincter closes tightly→ No further emptying

Chyme not delivered into duodenum is forced backward into the stomach – “retropulsion.”

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20
Q

3 parts of the stomach

A
  • Body normally stores food; has weak contraction & numerous oxyntic glands
  • Antrum has thick muscularis externa, vigorous contractions & numerous pyloric glands - (secrete gastrin)
  • Pylorus regulates passage of chyme into duodenum
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21
Q

Entry of food into duodenum depends on:

A
  • Hypertonic chyme, low pH
  • Presence of a.a and peptides
  • Fatty acids and monoglycerides → slows gastric emptying
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22
Q

Emesis

A
  • A regulation of the gut motility function following excessive irritation or distension of any part of upper GI
  • signals initiating vomiting mainly originate from upper GI - pharynx, oesophagus, stomach and duodenum.
  • nerve impulses are transmitted by vagal and sympathetic afferent nerve to v. centre.
  • sufficient stimulation of v. centre leads to vomiting act;
  • involves forceful expulsion of gastric (and duodenal) contents through the mouth;
  • often preceded by salivation, nausea, rapid irregular heart beat, dizziness, retching.
  • Vomiting can also be elicited by drugs or by rapid change in direction
  • some emetics stimulate duodenal receptors, others act on receptors on floor of 4th ventricles called CTZ
  • motion stimulates receptors in vestibular labyrinth centre, then to CTZ.
  • It represents a defence reaction to protect the body against intake of dangerous agents.
    • Toxins in the GI tract can be recognised either
      • before absorption via visceral parasympathetic and sympathetic afferent fibres.
      OR
      • after absorption into the blood via the chemoreceptor trigger zone (CTZ) located in the area postrema.
  • Thus CTZ integrates both the afferent signals from the gastrointestinal tract and the chemical signals from the blood.
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23
Q

Motility of the Small intestine (SI)

A
  • SI is 5m in length, has 3 sections
  • It takes 2-4 hrs for chyme to traverse it
  • Basic electrical rhythm is entirely intrinsic.
  • Movements of SI can be
    • peristaltic (propulsive contractions)
    • mixing (segmentation) contractions
    • migrating contractions
  • Segmentation is characterised by closely spaced contractions of circular muscles
  • Slow waves of smooth muscle causes segmental contractions backed by myenteric nerve plexus.
  • Peristaltic contraction progressive, moves content in orthograde direction, about 2 cm/sec
  • net movement along SI averages 1cm/min
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24
Q

Regulation of SI

A
  • Peristaltic contraction
    • Neural by local reflex mediated via ENS, but can be extrinsic innervation
    • Hormonal factors:
      • gastrin, CCK, insulin, motilin, and serotonin enhance intestinal motility
      • Secretin, VIP and glucagon inhibit
      • Drugs such as codeine & other opiates decrease motility
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25
Q

Innervation of large intestine

A

Parasympathetic

  • Vagus: - caecum, ascending & transverse
  • Pelvic: - descending, sigmoid rectum anal canal

Sympathetic

  • proximal part mainly via sup. mesenteric plexus
  • distal – via inf. mesenteric / sup. Hypogastric
  • rectum & anal canal – inf. hypogastric plexus
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26
Q

Motility of Large intestine

A
  • Segmental or Haustral contractions
    • combined contraction of circular and longitudinal muscle to form bag like sacs - called haustration
    • mix and shuttle contents slowly to enhance water and electrolytes absorption.
    • progress of colonic content slow, 5-10cm/hr.
    • modulated by vagus & pelvic nerves
  • Peristalsisslow in comparison to small intestine; 8 -15hrs transit time.Mainly in caecum and ascending colon
  • Mass movement
    powerful contraction of mid-transverse colon, sweeps colon contents into rectum

occurs usually after first meal of day

associate with gastro-colic reflex

stimulates the urge to defecate

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27
Q

Incontinence

A
  • Faecal incontinence – involuntary or inappropriate passage of stool.
  • Continual dribble of faecal matter is prevented by tonic contraction of;
    • internal anal sphincter (smooth muscle), which contributes up to 90% of resting anal canal pressure.
    • external anal sphincter (striated muscle), voluntary innervation by pudendal nerve, contributes 20% resting anal tone
    • puborectal muscle wraps around posterior aspect of anorectal junction.Physiology of incontinence
  • Damage to anal sphincters may be associated with dysfunction of;
    • smooth muscle: – leads to faecal leakage without awareness.
    • Striated muscle: – presents with faecal urgency
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28
Q

The 3 salivary glands

A

parotid gland - only serous

submandibular gland - both serous and mucinous

Sublingual gland - a mix

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29
Q

2 major components of saliva and what they contain

A

-Serous component carries out digestive function and has: water, electrolytes,
enzymes, IgA
-Mucinous lubricates; principally contains lubricating glycoproteins mucin.

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30
Q

regulation of salivary secretion

A

Parasympathetic fibres activation leads to a copious flow of saliva
mediated by Ach activation of acinar cell muscarinic receptors (M1 & M3).
stimulation of mAChRs on salivary acinar cells to lead G proteins activation to increase
intracellular calcium levels.
Sympathetic postganglionic transmitters – noradrenaline acts α1- & β1-
adrenoreceptors

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31
Q

nerves which stimulate mucinous and serous saliva

A

ACh released at submandibular ganglion of the facial nerve (VII) stimulates muscarinic receptors on
acinar cells & triggers serous and mucinous saliva secretion.
 ACh released at otic ganglion of the glossopharyngeal nerve (IX) stimulates muscarinic receptors &
triggers serous saliva secretion

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32
Q

gastric secretion

A

2 distinctive cell types are involved in gastric secretions:
Parietal cells – HCL, Intrinsic factor
Chief cells – Pepsinogens and gastric lipase

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33
Q

Pancreatic exocrine secretion

A

Major components are:
 HCO3 ions:- making the juice alkaline (pH 7.1-8.2).
 Digestive enzymes:
 amylases (starch to oligosaccharides)
 proteases (trypsin, chymotrypsin, elastase, etc.)
 lipases (major triglyceride enzymes)
 Activities of these enzymes highest in upper jejunum, declines further
down the intestine.

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34
Q

Phases of secretion

A

Cephalic phase: nerve signals
from brain causes Ach release in
pancreas.
 Gastric phase: nervous
stimulation of enzyme secretion
continues.
 Intestinal phase: chyme with low
pH enters intestine; secretin
released in response; pancreatic
secretion is more copious.

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35
Q

Bile secretion

A

1st secretion by hepatocytes into bile
canaliculi; this contains bile acids,
cholesterol, bilirubin & phospholipids.
2nd stage secretion is made of water,
bicarbonate, NaCl when by ductal
epithelial cells are stimulated by Ach
& Secretin

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36
Q

What is achalasia

A
  • Primary motor disorder of oesophagus; due to inflammatory destruction of inhibitory nitrinergic neurons in oesophagus
  • Elevated resting LOS tone (spasm); may be due to
    • selective destruction of the n.a.n.c inhibitory neurones
    • damage to oesophageal innervation
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37
Q

Risk factors for achalasia

A
  • infection
  • autoimmunity
  • genetics
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38
Q

Signs and symptom of achalasia

A

chest pain

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39
Q

Investigations foe achalasia

A
  • Upper GI endoscopy and biopsy of LOS
  • Timed barium oesophagram to assess oesophageal emptying; dilated oesophagus appears tapers to beak-like at G-O junction.
  • Oesophageal manometry:
    • To assess the motor function of the UOS, LOS and oesophageal body
    • Assess cause of regurgitation (e.g. reflux of stomach acids into oesophagus)
    • Dysphagia (determine cause of swallowing difficulty)
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40
Q

Management for achalasia

A
  • Dilatation, Surgery, Drugs & Botulinum toxin:
  1. Pneumatic dilatation – to stretch out sphincter.
  2. Laparoscopic cardiomyotomy – to divide the muscle fibres across the lower oesophageal sphincter; relieves dysphagia in 90% of patients
  3. Botulinum toxin injection – selectively blocks Ach release.
  4. Calcium-channel blockers and nitrates to reduce pressure in the LOS.
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41
Q

GORD?

A

Gastro-intestinal reflux disease (GORD) is a condition characterised by retrosternal, and sometimes epigastric pain, as a result of reflux of the acidic contents of the stomach into the oesophagus

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42
Q

Risk factors for GORD

A

-Hiatus hernia
-Eating certain foods – fat, chocolate, caffeine
-Smoking
-Obesity
-Dysfunction of the lower oesophageal sphincter (LOS)
-Alcohol
-Helicobacter Pylori
-“Stress”

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43
Q

Pathophysiology of gord

A

unintentional relaxation of the LOS
Fundic distension due to overeating
delayed gastric emptying secondary to the high-fat western diet and impaired oesophageal defences (e.g. saliva).

distension causes the sphincter to be taken up by the expanding fundus,

o exposing the distal 3cm of squamous epithelium of the oesophagus to gastric juice leads to inflammation.

o Patient compensates by increased swallowing, allowing saliva to bathe the injured mucosa and alleviate the discomfort.

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44
Q

Signs and symptoms of GORD

A
  • heartburn/chest pain
  • Acid brash - the feeling of a bitter, acid-like taste in the mouth
  • Nausea and vomiting
  • Cough
  • Dysphagia
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45
Q

Investigation for GORD

A

Orifice Test

  • OGD - endoscopy to visualise the oesophagus is useful to investigate and determine the severity of Oesophagitis.
    • If other causes such as malignancy are suspected, biopsies can also be taken.
    • Capsule endoscopy can be done as a less invasive alternative

X-ray/Imaging

Barium swallow - if excluding an alternative cause for symptoms, such as malignancy, a barium swallow may be a useful imaging modality

Special Tests

  • Manometry - can be useful to investigate motility disorders such as achalasia
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46
Q

Management for GORD

A

Treatment aims to decrease amount of reflux:

  • Lifestyle changes:
    • avoiding foods and beverages that can weaken the LOS; e.g. chocolate, peppermint, fatty foods, coffee, and alcoholic beverages.
    • eating meals at least 2 to 3 hours before bedtime may lessen reflux.
    • stopping smoking
  • Drugs: antacids, alginates, H2 receptor blockers, PPI
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47
Q

Complications for GORD

A

Barret’s oesophagus
Anaemia
Benign oesophageal stricture
gastric volvulus
Webs

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48
Q

4 types of lactose intolerance

A

primary (the most common) →lactase production falls sharply in adulthood

secondary→ n coeliac dx.

congenital→ in babies born prematurely

developmental. → lack of lactase at birth, inherited.

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49
Q

Risk factors for lactose intolerance

A
  • black, Native American, Asian, Hispanic, or Jewish ethnicity
  • adolescence and early adulthood
  • family history of lactase deficiency
  • enteritis/gastroenteritis
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50
Q

Pathophysiology of lactose intolerance

A

Lactose intoleranceoccurs when your small intestine doesn’t produce enough of an enzyme (lactase) to digest milk sugar (lactose)

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51
Q

Signs and symptoms of lactose intolerance

A

Abdominal pain/discomfort
borborygmi
flatulence
skin rashes

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52
Q

Investigation for lactose intolerance

A
  • trial of dietary lactose elimination
  • FBC
  • lactose hydrogen breath test
  • stool culture
  • faecal pH
  • faecal reducing substance/sugar
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53
Q

Mangement for lactose intolerance

A

change in diet

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54
Q

Complication for lactose intolerance

A

Diseases associated with secondary lactose intolerance includeintestinal infection, celiac disease, bacterial overgrowth and Crohn’s disease

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55
Q

What is peptic ulcer disease

A

Ulcer found in the lower oesophagus, stomach, and duodenum

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56
Q

What causes peptic ulcer disease

A

caused by infection with helicobacter Pylori

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57
Q

Risk factor for peptic ulcer disease

A

common in men

poor hygiene

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58
Q

Signs and symptoms for peptic ulcer disease

A

upper abdominal pian
vomiting
For DU’s, the pain is when you are hungry, and GU’s the pain is when you eat
nausea
weight loss

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59
Q

Investigation for peptic ulcer disease

A

Urea breath test- test for H. pylori

Serological test for IgG

Stool test

Endoscopy

FBC

U+E

FOB

patient over 55 → straight to endoscopy
Barium meal test

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60
Q

Management for peptic ulcer disease

A

smoking cessation

First line therapy –Triple therapy –
patients will be treated with a proton pump inhibitor, and two antibiotics

Second line therapy –
Sometimes Tripotassium dicitratobismuthate may be taken (bismuth chelate).

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61
Q

Complication for peptic ulcer disease

A

Perforation

Haemorrhage

Malignancy

Anaemia

Penetration of adjacent organs

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62
Q

What is Jaundice and what is the normal levels in micromol

A

Jaundice describes the yellow pigmentation of the skin, sclera, and mucous membrane resulting from raised plasma bilirubin.

Normal levels are below 21micromol

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63
Q

Normal bilirubin metabolism

A

Haem→ biliverdin (by haem oxygenase) →Unconj. Bilirubin (by Biliverdin reductase) → Conjugated bilirubin (by glucoronyl- transferase 1)

Urobilin→ urine colour

Stercobilin→ faces colour

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64
Q

Physiology and causes of Pre-hepatic causes of jaundice

A

Physiology: haem degraded in macrophages, occurs in spleen and liver mainly but can occur in skin and kidneys too. once broken down it is released bound to plasma albumin and transported to the liver to be conjugated and excreted. Unconjugated is water insoluble

Causes:

  • Overproduction- Haemolytic anaemia
  • Reduced uptake- Gilberts syndrome
  • Conjugation defects:
    • acquired - neonatal, maternal milk, Wilsons disease
    • Inherited- Crigler-Najjar syndrome
  • Drugs
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65
Q

Physiology and causes of intra-hepatic causes of jaundice

A

Physiology: in the liver unconjugated bilirubin is removed from the blood by hepatocytes. it is then conjugated in the hepatocytes with glucuronic acid, and it became soluble to be excreted in bile.

Causes:

  • Biliary obstruction
  • Intrahepatic cholestasis:
    • primary biliary cholangitis
    • viral hepatitis
  • Hepatocellular injury - Acute or Chronic
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66
Q

Physiology and causes of post-hepatic causes of jaundice

A

Physiology: conjugated bilirubin is transported through the liver and cystic ducts in bile and stored in the gallbladder or passes into the duodenum. In the intestine, some is excreted in the stool and the rest is metabolised by gut flora into urobilinogen and reabsorbed and excreted by the kidney.

Causes:

  • Gallstones
  • Surgical strictures
  • Extra-hepatic malignancy
  • Pancreatitis
  • Parasitic infection
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67
Q

RF for jaundice

A

Alcohol misuse

Factors that increased risk of hepatitis

Travel to high-risk areas

High BMI

Metabolic syndrome

IBD

Pregnancy

FHx

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68
Q

SS for Jaundice

A

Fever

Abdominal pain

change in skin colour

Dark coloured urine or clay coloured stool

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69
Q

Ix for jaundice

A

FBC

U+E

LFTs

Clotting screen

Hep a,b,c

Urine dipstick

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70
Q

Complication for jaundice

A

Most are admitted or referred as it can be indicative of an underlying cause

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71
Q

Whts is acute pancreatitis

A

Acute pancreatitis refers to inflammation of the pancreas.
The inflammation is believed to occur due to atypical premature activation of pancreatic enzymes inside the pancreas.
Pancreatitis can range from mild to life-threatening

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72
Q

Pathophysiology of acute pancreatitis

A
  • There are a wide variety of causes, with gallstones and alcohol being the two most common.

Theinflammationin acute pancreatitis is typically caused by hypersecretion or backflow (due to obstruction) of exocrine digestive enzymes, which results inautodigestionof the pancreas.

Pancreatic damage can be classified into two major categories:

  • Interstitial oedematous pancreatitis: most common, better prognosis
  • Necrotising pancreatitis: less common, around 5-10%, more severe

The damage that occurs during acute pancreatitis ispotentially reversible(to varying degrees), whereaschronic pancreatitisinvolves ongoing inflammation of the pancreas that results inirreversible damage.

Chronic pancreatitis is associated withendocrine and exocrine dysfunction, as well as chronic abdominal pain.

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73
Q

Causes of acute pancreatitis

A

IGETSMASHED
Idiopathic

Gallstones

Ethanol(alcohol)

Trauma

Steroids

Malignancy/mumps

Autoimmune

Scorpion venom

Hypercalcemia or hyperlipidaemia

ERCP examination

Drugs

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74
Q

RF for acute pancreatitis

A
  • Male gender
  • Increasing age
  • Obesity
  • Smoking
  • Alcohol
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75
Q

SS of acute pancreatitis

A
  • Abdominal pain which radiates to the back and may be relieved by sitting forward.
  • Systemically unwell in a hypovolemic state, and may be pyrexial
  • Specific signs to look out for on examination are;
    • Cullen’s sign (periumbilical bruising)
    • Grey Turner’s sign (Bruising on flanks)
  • Nausea and vomiting
  • decreased appetite
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76
Q

Ix for acute pancreatitis and one clinical tool

A

abdo CT scan
MRCP
clinical tool- Glasgow score

77
Q

Diagnosis of acute pancreatitis

A

requires 2 of the following:
- Typical history
- Raised serum amylase or lipase more than 3 ULN
- Imaging

78
Q

Classification of acute pancreatitis

A
  • Mild:most common, no organ dysfunction/complications, resolves normally within a week
  • Moderate:initially some evidence of organ failure which improves within 48 hours
  • Severe:persistent organ dysfunction for greater than 48 hours, together with local or systemic complications
79
Q

Immediate management for acute pancreatitis

A
  • IV fluid resus and correction of electrolyte disturbances
  • Analgesia
  • Anti-emetics
  • Nil by mouth
  • Control of blood glucose
80
Q

management for gallstone induced acute pancreatitis

A
  • Endoscopic retrograde cholangiopancreatography (ERCP)
  • Cholecystectomy
81
Q

Management for alcohol induced pancreatitis

A
  • Benzodiazepines to treat withdrawal agitation and seizures
  • Thiamine, folate, and vitamin B12 replacement
82
Q

Early complication for acute pancreatitis

A
  • Necrotising pancreatitis
  • Infected pancreatic necrosis occurs when necrosing pancreatic tissue becomes infected, patients require antibiotics and necrosectomy
  • Pancreatic abscess: occurs when peripancreatic collections of fluid become infected, urgent drainage is required
  • Acute respiratory distress syndrome (ARDS): associated with the SIRS response of acute pancreatitis. Typical CXR appearance of widespread bilateral pulmonary infiltrates
83
Q

Late complication for acute pancreatitis

A
  • Pancreatic pseudocysts: collections of fluid that are not surrounded by epithelium. They are typically amylase-rich and can become infected, rupture or bleed. Pseudocysts typically accumulate within four weeks after acute pancreatitis. Only 40% resolve spontaneously, therefore intervention is usually advised (drainage/excision).
  • Portal vein/splenic thrombosis: secondary to ongoing inflammation, anticoagulation required
  • Chronic pancreatitis:repeated attacks of acute pancreatitis can lead to ongoing inflammation and fibrosis of the pancreas
  • Pancreatic insufficiency: the exocrine function of the pancreas is more commonly affected (whilst the endocrine function is typically maintained).
84
Q

Pathophysiology of chronic pancreatitis

A
  • Chronic pancreatitis has numerous causes namely alcoholism, trauma, congenital (cystic fibrosis), drugs (Steroids, azathioprine), idiopathic, genetics and chronic obstruction secondary to numerous causes.
  • All these numerous causes result in pancreatic fibrosis
85
Q

RF for chronic pancreatitis

A
  • Alcohol intake is the main cause of chronic pancreatitis
  • Smoking
  • Hypercalcaemia
  • Hypertriglyceridaemia
  • Autoimmune disease
  • Medications (Thiazide diuretics, tetracyclines, oestrogens)
86
Q

SS for chronic pancreatitis

A
  • Abdominal pain (usually dull, epigastric pain, which may radiate to the back, or localise to RUQ).
  • The pain may be relieved by sitting upright and leaning forward
  • Pain is made worse by eating, may be chronic or intermittent
  • Other symptoms may include: nausea, vomiting, decreased appetite, weight loss, offensive stools/diarrhoea
  • Abdominal tenderness (around epigastrium) & guarding
  • Abdominal distension
  • Signs of malnutrition (assess the BMI)
  • Jaundice
  • Signs of chronic liver disease
87
Q

Ix for chronic pancreatitis

A

Bloods

  • FBC/LFT/RFT/Lipase/Amylase/HBA1c/Triglycerides/Calcium

Orifice Test

  • PR exam might show slimy faecal matter

X-ray/Imaging

  • CT/magnetic resonance cholangiopancreatography

Special Tests

  • faecal elastase if malabsorption. Biopsy.
88
Q

Management for acute pancreatitis

A

Conservative management

  • Reduce alcohol consumption
  • Offer smoking cessation

Medical management

  • Treat any hypercalcaemia
  • Pain management. Opioids typically used
  • Malabsorption can be managed with pancreatic enzymes like Creon.

Surgical management

  • Utilised if medical management is not effective.
  • This may involve ERCP, pancreatic resection
89
Q

Complication for Chronic pancreatitis

A
  • Diabetes
  • Pseudocyst
90
Q

Pathophysiology of pancreatic cancer

A

poorly understood

95% mutation in K-RAS2 proto-oncogene, the activation ofwhich leads to increased cell proliferation,loss of the normal response to apoptotic signals, dysplasia and ultimately cancer

91
Q

RF for pancreatic cancer

A
  • Smoking
  • Family history
  • Chronic pancreatitis
  • Diet (High BMI, red meat)
  • Age (above 60s, very rare below 40)
  • Diabetes
92
Q

SS for pancreatic cancer

A
  • Non specific symptoms like epigastric/back pain. Painless progressive jaundice
  • Itching
  • Dark urine/pale or fatty stools
  • Weight loss/reduced appetite
  • Abdominal swelling
  • Nausea and vomiting if stomach compressed
  • Haematemesis
  • Ascites
  • Lymphadenopathy (virchow’s node)
  • Epigastric mass
  • Jaundice
93
Q

Ix Pancreatic cancer

A

Bloods

  • FBC (might show normocytic anaemia or thrombocytopenia), LFTS (raised liver markers), Tumour markers like CA19-9 (good for baseline and follow up but of little diagnostic value), Glucose (hyperglycaemia in the absence of previous diabetes history)

X-ray/Imaging

  • Ultrasound abdomen (May show dilated bile duct, lymph nodes but limited by bowel gas). Abdominal CT is the investigation of choice
94
Q

Management for pancreatic cancer

A
  • Tissue biopsy is important for prognosis and suitability for radiotherapy/chemotherapy. It is also used to determine the histology of pancreatic neoplasm
  • Staging is ranked from stage 0 to 4. The TNM staging (Tumour, Node, Metastasis) also used.
  • Management includes surgery and chemotherapy/radiotherapy
  • Only 10-20% of tumours are resectable. Distal pancreatectomy is used for cancers of the body and tail of the pancreas. Whipple’s procedure is used for proximal pancreatic cancers, this procedure preserves the stomach, pylorus and 4cm of the duodenum.
  • About 80% of pancreatic cancers are non resectable. Management plans for the non resectable cancers include stenting of the bile duct to relieve obstruction and palliative radiotherapy/chemotherapy.
  • Where pain control is difficult patients should be referred to the palliative team
  • Malabsorption can be managed with pancreatic supplements e.g Creon
95
Q

Complication for pancreatic cancer

A
  • Obstructive jaundice
  • Refractory pain
96
Q

What is cholelithiasis

A

AKA gallstones

3 types of gallstones:

  • Cholesterol
  • Mixed
  • Pigment stones
97
Q

Pathophysiology of cholelithiasis

A

The stones form from concentrated bile in the bile duct, and most are made of cholesterol.

Begins with the secretion of bile, supersaturated with cholesterol from the liver.

Imbalance of cholesterol, phospholipid and bile salt→ precipitation of cholesterol microcrystals → aggregation of microcrystal →formation of cholesterol gallstones

98
Q

the 4 F’s for RF for cholelithiasis

A

Fat

Fair

Female

Forty

99
Q

examples of medication that can cause cholelithiasis

A

Medication (octreotide, GLP1 analogues, ceftriaxone)

100
Q

SS of cholelithiasis

A

majority is asymptomatic

Biliary colic→ intermittent right upper quadrant pain caused by gallstones irritating bile ducts

Pain triggered by meal and last between 30 min -8 hours, may radiate to right shoulder tip.

Vomiting/ Nausea

symptoms can manifest as other complication

LFTS are normal

101
Q

Ix for cholelithiasis

A

Stones in gallbladder or cystic duct → unlikely to show abnormal results

stones in common bile duct→ accounts for symptoms and abnormal lab results.

LFTS→ increased bilirubin, ALP and ALT

Ultrasound→ Gold standard

102
Q

Management of cholelithiasis
1st line, GP, ED and inpatient management

A
  • 1st line → Analgesia:
    • intermittent mild- moderate pain → paracetamol or NSAID e.g., diclofenac
    • Severe pain - Diclofenac or an opioid
  • In GP→ request abdo ultrasound
  • In ED→ if pain controlled by analgesia and normal bloods and obs then send home
  • Inpatient→ refer to Gen surg
103
Q

Complications for cholelithiasis

A

acute cholecystitis

acute cholangitis

pancreatitis

104
Q

What is acute cholecystitis

A

Acute inflammation of the gallbladder

Major complication of gallstones

105
Q

Pathophysiology of acute cholecystitis

A

impacted gallstones causes complete obstruction of the cystic duct

leads to inflammation within gallbladder wall

106
Q

RF acute cholecystitis

A

Gallstones

107
Q

ss acute cholecystitis

A

Nausea

Vomiting

Contant RUQ pain lasting more than 8 hrs

Palpable gallbladder

Fever

Raised inflammatory marker WCC+CRP)

Murphys signs

108
Q

Ix acute cholecystitis

A

Abdominal ultrasound- gold standard

CT

109
Q

Management acute cholecystitis

A

Analgesia

Nil by mouth

IV fluid

Antibiotics

In GP → send patient to ED if suspicions of acute cholecystitis

In secondary care → Referral to General Surgeons for consideration of “Hot Lap Chole”

If not for hot lap chole →routine elective surgery after 6 weeks

110
Q

Complication for acute cholecystitis

A
  • Sepsis
  • Gallbladder empyema
  • Gangrenous gallbladder
  • Perforation
111
Q

Chronic cholecystitis

A
  • May occur after one or more episodes of acute cholecystitis.
  • Results from chronic irritation or repeated episodes of acute inflammation leading to fibrosis of the gallbladder wall.
  • Can initially be asymptomatic and occur from the presence of gallstones in the gallbladder
  • Patients may present abdominal pain similar to biliary colic or constant abdominal pain similar to that of acute cholecystitis but less severe and self-limiting
  • Gallbladder wall thickening and the presence of gallstones will be seen on imaging.
  • Unlike acute cholecystitis – no pericholecystic fluid, no gallbladder distention on imaging.
112
Q

What is choledocholithiasis

A

The presence of gallstones migrated from the gallbladder within the bile ducts

113
Q

SS for choledocholithiasis

A

Nausea

vomiting

Constant RUQ pain

Pale stools

Dark urine

Afebrile

Bloods→ Inflammatory markers normal in simple choledocholithiasis

  • Raised bilirubin/LFTs = OBSTRUCTIVE JAUNDICE
114
Q

Gold standard Ix for choledocholithiasis

A

MRCP

115
Q

Management for choledocholithiasis

A

Analgesia

Prophylactic Abx

ERCP

116
Q

What is cholangitis

A

Acute bacterial infection of the biliary tree in the setting of bile stasis

Predominantly Gram-negative enteric bacteria, most commonly E.coli

HIGH MORTALITY

117
Q

RF for cholangitis

A
  • age >50 years
  • cholelithiasis
  • benign stricture
  • malignant stricture
118
Q

SS for cholangitis

A

Nausea, vomiting

Charcot’s Triad:

  • Jaundice, Fever, RUQ pain

pale stool

confusion

dark urine

119
Q

Ix for cholangitis

A

Bloods → raised inflammatory marker and deranged LFT

Gold standard→ MRCP

120
Q

Mangement for cholangitis

A

ERCP as URGENT to remove the obstruction

Supportive treatment

IV antibiotics, IVF, analgesia, low threshold to refer to ITU for organ support

121
Q

Complications for cholangitis

A

Hepatic abscess, portal venous thrombosis

122
Q

What is meant by acute liver failure

A
  • sudden onset of liver dysfunction
  • Absence of prior liver disease
  • Resulting in encephalopathy (brain dysfunction) within 8 weeks of onset
123
Q

Cause and pathophysiology of acute liver disease

A

causes:

  • common→ Paracetamol
  • Non paracetamol: e.g. preg, viral, malignancy

Liver injury → liver cell death → loss of critical hepatocyte mass → Failure of liver to perform functions → Multiorgan dysfunction

124
Q

RF for acute liver disease

A
  • Hepatotoxic drugs
  • Contaminated food/water (enteric viruses – Hep A and E)
  • Blood borne virus risks (Hep B)
    • Unprotected sex
    • Tattoos/piercing with unclean equipment
    • Recreational drug use – shared paraphernalia
  • Recreational drugs – mushrooms, ecstasy
  • Threshold for liver injury reduced if underlying liver disease
125
Q

SS for acute liver failure

A
  • Right upper quadrant pain
  • Nausea/Vomiting
  • A general sense of feeling unwell (malaise)
  • Sweet smelling/musty breath (fetor)
  • Disorientation, confusion, agitation, sleepiness, flapping tremor (features of encephalopathy)
126
Q

Ix for acute liver failure

A
  • liver function tests
  • prothrombin time/INR
  • basic metabolic panel
  • FBC
127
Q

Management for acute liver failure

A

REsus
NAC
Empirical antibiotic

128
Q

Complication for acute liver failure

A

coagulopathy

Infection

renal failure

129
Q

Paracetamol metabolism

A

see notes

130
Q

RF for paracetamol overdose

A
  • High doses
  • chronic alcohol consumption
  • Drugs→ anti-seizure, opioids
  • Advanced age
  • Malnutrition
  • Chronic liver disease
131
Q

What is Acute hepatitis

A
  • Acute inflammation of the liver, of any cause, causing sudden increase in liver tests
  • Usually manifests as an increase in aminotransferases (ALT and AST)
    • Intracellular enzymes
    • Released in the setting of liver inflammation causing disruption/death of hepatocytes
  • Could be interchangeably referred to as acute liver injury
  • In some cases, if ongoing hepatocyte necrosis and loss of critical liver cell mass, can lead to acute liver failure
132
Q

Some examples of drugs that cause acute hepatitis

A

-Paracetamol
- NSAIDS
- Amiodarone
- Anabolic steroids
- Chlorpromazine
- statins

133
Q

other causes of acute hepatitis

A
  • Viral
  • (Drugs)
  • Autoimmune
  • Genetic/inherited
  • (Alcohol)
  • Ischaemic
  • (Pregnancy)
  • Malignancy
134
Q

Ix for acute hepatitis

A
  • FBC, U&E, LFT, GGT, blood clotting, glucose
  • ABG
  • Blood cultures
  • Arterial blood gases
  • Blood cultures
  • ultrasound
  • ct
  • biopsy
135
Q

Difference between acute and chronic hepatitis

A

see notes

136
Q

What is Cirrhosis

A

Chronic liver disease is continual destruction of the liver parenchyma and its gradual substitution with fibrous tissue. It is a long-term process (>6 months)

This process ultimately leads to liver cirrhosis

Cirrhosis → Irreversible distortion of liver architecture by scar tissue and nodule formation

This affects the liver’s synthetic, metabolic and excretory actions

137
Q

Causes of cirrhosis

A
  • Commonest cause worldwide = chronic viral hepatitis B and C
  • Commonest causes in Western world
    • Alcohol, chronic viral hepatitis B and C, MAFLD
138
Q

Compensated vs decompensated

A
  • Compensated— when the liver can still function effectivelyand there are no, or few, noticeable clinical symptoms
  • Decompensated— when the liver is damaged to the point that it cannot function adequately, andovert clinicalcomplications(such as jaundice, ascites, variceal haemorrhage, and hepatic encephalopathy) are present. Events causing decompensation include infection, portal vein thrombosis, and surgery.**
139
Q

RF for cirrhosis

A

alcohol misuse

HEP b and c infection

Obesity

type 2 diabetes

autoimmune liver disease

140
Q

SS for cirrhosis

A
  • suspect in high-risk groups if they have malaise, fatigue, anorexia, nausea, weight loss, muscle wasting or Abdo pain
  • hepatomegaly
  • chronic liver disease→ spider naevi, palmar erythema, white nails, muscle wasting.
  • signs of decomp liver disease →jaundice, abnormal bruising, peripheral oedema, ascites, sepsis, variceal bleeding, encephalopathy
141
Q

Ix for Cirrhosis

A

FBC → Low platelet count

LFT → high AST to ALT ratio, high bilirubin, low albumin, increase prothrombin time and INR

transient elastography

142
Q

Management for Cirrhosis

A

REFER

Lifestyle changes

Alcohol cessation

143
Q

Complications for Cirrhosis

A

Portal HTN

Ascites

Hepatic encephalopathy

Haemorrhage from oesophageal varices

infection

144
Q

Some withdrawal symptoms of alcohol

A
  • Tremors
  • Sweating
  • Fever
  • Nausea, vomiting
  • Anxiety
  • Agitation
  • Anorexia
  • Insomnia
145
Q

Management for alcohol related liver disease and withdrawal

A

Benzodiazepines

146
Q

Whts is oesophagitis

A

Inflammation of the oesophagus

147
Q

Causes of oesophagitis

A
  • GORD
  • Medications- NSAIDS, bisphosphonates, tetracycline antibiotics)
  • immune mediated- eosinophilic oesophagitis
148
Q

RF for oesophagitis

A

Eating just before bed

Excessive alcohol, caffeine, chocolate

Greasy or spicy food

Cigarette smoking

Obesity

Hiatus hernia

Certain medications

149
Q

SS of oesophagitis

A

Epigastric or chest pain

Burning (“hearburn”)

Acidic/sour taste

Dysphagia

Odynophagia

Hoarseness

Persistent cough

Epigastric abdominal tenderness to

palpation

150
Q

Ix for oesophagitis

A

Oesophagogastric duodenoscopy (OGD) with oesophageal biopsies

151
Q

Management for reflux oesophagitis

A
  • Avoid greasy/spicy foods, citrus, chocolate, peppermint, caffeine, alcohol
  • Smoking cessation
  • Weight loss
  • PPI
152
Q

Management for eosinophilic oesophagitis

A
  • Refer to allergist
  • Avoidance of food allergies
  • Daily PPI
  • Topical steroids
    • Fluticasone MDI without spacer
      • Sprayed into patient’s mouth, then swallowed
153
Q

Management for drug induced eosophagitis

A
  • Discontinue offending medication, if possible
  • Offer alternative
  • Remain upright 30 minutes after consuming
  • Liquid version
154
Q

Complications of oesophagitis

A

Strictures

Barrett’s oesophagus

  • Abnormal cellular changes of oesophagus
  • ~1% progress to oesophageal cancer

Oesophageal cancer

155
Q

What is anal fissure and what are the 2 classifications

A

Tear or ulcer in lining of anal canal

Classification:

  • acute - less than 6 weeks
  • Chronic- more than 6 weeks
156
Q

RF for primary anal fissure

A

Trauma secondary to hard or loose stools

157
Q

RF for secondary anal fissure

A
  • IBD
  • STIs (HIV, syphilis, HSV)
  • Colorectal cancer
  • Psoriasis
  • Bacterial, fungal, viral skin infections
  • Anal trauma (previous anal surgery or anal sex)
  • Pregnancy, childbirth
158
Q

SS for anal fissure

A

Anal pain on defecation

Tearing sensation on passing stool

Bright red blood on stool or toilet paper

Fissure visible on anal exam

Sentinel pile

159
Q

Examination finding on acute anal fissure

A

Superficial with well-demarcated edges

160
Q

Examination finding on chronic anal fissure

A
  • Wider and deeper with muscle fibres visible in the base
  • Edges often swollen
  • +/- skin tag
161
Q

Examination finding on primary anal fissure

A
  • Singular
  • Posterior midline of anus
162
Q

Examination finding on secondary anal fissure

A
  • Multiple
  • Irregular outline
  • Location may be lateral
163
Q

Management for Anal fissure

A

Ensure stool is soft
Treat constipation (if indicated)
Increased fluid intake and dietary fibre
Keep anal area dry and clean
Manage pain (Paracetamol or ibuprofen)
Sitz bath
lidocaine -apply prior to defecation
if symptoms persist for more than week then rectal GTN ointments and consider secondary causes

164
Q

Complications of anal fissure

A

Anorectal fistula
Infection / abscess

165
Q

What is anorectal abscess

A

Infection of soft tissue around the anus or rectum

May cause sepsis

166
Q

RF for anorectal abscess

A

Immunodeficiency

Diabetes

Receptive anal intercourse

Crohn’s disease

167
Q

SS for anorectal abscess

A

perianal pain
erythema
discharge
fever
bleeding
Malaise
Swelling
Perianal fluctuance
Purulent discharge

168
Q

Ix for anorectal abscess

A

Clinical diagnosis by digital rectal exam and other signs
Ultrasound, MRI
Culture and sensitivity of discharge

169
Q

Management for anorectal abscess

A

Prompt drainage of abscess
perianal - outpatient incision & drainage
Perirectal - surgical drainage
Sitz bath
Antibiotic (cover anaerobes and gram neg)
Ampicillin/sulbactam or cefoxitin + metronidazole or ciprofloxacin or clindamycin

170
Q

What are colorectal polyps

A

Projections arising from colonic mucosal surface
(Most commonly adenomatous polyps)

171
Q

What genetic condition predispose someone to colorectal polyps

A

Familial adenomatous polyposis (FAP) syndrome

Autosomal dominant

  • Hundreds to thousands of colorectal adenomas
  • Near100% risk for colorectal cancer by age 4
172
Q

4 types of colorectal polyps

A

Tubular
Serrated
Tubulovillous
Villous

173
Q

SS for colorectal polyps

A

Usually asymptomatic

Rectal bleeding

Frank red blood, melaena

Mucus discharge

Tenesmus

Post-defecation sensation that rectum was incompletely evacuated

Change in bowel habits

174
Q

Diagnosis for colorectal polyps

A

May be found incidentally on colonoscopy

Colonoscopy with biopsy/excision of polyp

Ordered if concern for colorectal cancer

  • Iron deficiency anaemia in persons age ≥60, positive faecal occult blood test, change in bowel habit etc
175
Q

What is the management for adenomatous polyps

A

Removed endoscopically
Surveillance - colonoscopy frequency dependent upon number/size of polyps, family history, patient age

176
Q

What is the management for hyperplastic/ metaplastic polyps

A

No action required

177
Q

management for familial adenomatous polyposis syndrome

A

colectomy

178
Q

RF for colorectal cancer

A

Increasing age

Genetics

FHx

Inflammatory bowel disease

Obesity

alcohol

179
Q

SS for colorectal cancer

A

Increase freq and looser stools (change in bowel habits)
bleeding
distension
pain
weight loss
appetite loss
unexplained fever
conjunctival pallor palpable lymp nodes

180
Q

When to give urgent 2 ww referral (4 pts , colerectal cancer)

A
  • Positive faecal occult blood test
  • Age ≥40 with unexplained weight loss and abdominal pain
  • Age ≥50 with unexplained rectal bleeding
  • Age ≥60 with:
    • Iron-deficiency anaemia or
    • Change in bowel habit
181
Q

Ix for colorectal cancer

A

colonoscopy with biopsies

182
Q

Management for colorectal cancer

A

Surgical resection

Chemoradiotherapy

Chemotherapy

183
Q

What is coeliac disease

A

Chronic, autoimmune systemic disorder triggered by gluten exposure

184
Q

Pathophysiology of coeliac disease

A

Genetic predisposition (human leukocyte antigen (HLA) alleles found)
Gluten presence triggers immune activation within small bowel epithelium → Deveolpment of coeliac-specific autoantibodies + intraepithelial lymphocytosis →villous atrophy →small bowel enteropathy with systemic symptoms

185
Q

SS for coeliac disease

A

Diarrhoea
steatorrhea
Constipation
Weight loss
Heartburn
pain
Bloating
Flatulence
Fatigue
Rash
Tenderness
dermatitis herpetiformis

186
Q

Diagnosis for coeliac disease

A

Serum IgA tissue transglutaminase antibody (tTGA) and serum total IgA
Endoscopy intestinal biopsy (confirms diagnosis and only done if indicated by positive serology)

187
Q

Coeliac disease management

A

Gluten-free diet
supplement for any nutritional deficiency
annual FBC monitoring

188
Q

Complication for coeliac disease

A

reduced qualy
depression and anxiety
delayed puberty
Nutrional deficiency
Hypersplenism

PA- FCM (10 decks)

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