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Phase 2A extra > Extra GI and liver > Flashcards

Extra GI and liver Flashcards

1
Q

MALABSORPTION

A

/////

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2
Q

What is malabsorption?

A

The failure to fully absorb nutrients either because of the destruction to the epithelium or due to a problem in the lumen meaning food cannot be digested.

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3
Q

Name 4 disorders of the small intestine resulting in malabsorption

A
  1. Coeliac disease
  2. Tropical Sprue
  3. Crohn’s
  4. Parasite infection
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4
Q

Describe the pathophysiology behind Coeliac disease

A
  1. In wheat, in gluten the prolamin a-gliadin is resistant to digestion from protease enzymes (pepsin and chymotrypsin) in the proximal small bowel.
  2. The gliadin peptides then passes through the epithelium and are deaminated by tissue TRANSGLUTAMINASE
  3. They interact with antigen-presenting cells via HLA-DQ2 or HLA-DQ8
  4. These activate gluten-sensitive CD4+ T cells
  5. T-cells produce pro-inflammatory cytokines and initiate an inflammatory cascade.
  6. Cascade ➞ metaloproteinkinases and other mediators ➞ villous atrophy, crypt hyperplasia and intraepithelial lymphocytes ➞ malabsorption
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5
Q

Why do you get anaemia in coeliac disease?

A

The mucosal damage can mean that B12, folate and iron cannot be absorbed resulting in anaemia.

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6
Q

Why does mucosal damage severity decrease towards the ileum?

A

Gluten is digested into small “non-toxic” fragments.

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7
Q

What is dermatitis herpetiformis? What causes it?

A

Raised red patches of skin, can be blisters that burst with scratching. Found on elbows, knees, buttock, torso and scalp.
Caused due to IgA deposition in the skin.

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8
Q

What is angular stomatitis?

A

Angular cheilitis, also known as angular stomatitis and perlèche, causes swollen, red patches in the corners on the outside of your lips.

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9
Q

INFLAMMATORY BOWEL DISEASES

A

//////

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10
Q

What are IBDs?

A

Chronic, autoimmune diseases when the mucosal immune system exerts an inappropriate response to luminal antigens, such as bacteria, which may enter the mucosa via a leaky epithelium. You can have ulcerative colitis or Crohn’s disease.

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11
Q

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

A

Ulcerative colitis: ONLY affects the colon

Crohn’s: affects ANY PART of the GI tract

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12
Q

Macroscopic features of Ulcerative colitis

A
  1. ONLY colon affected
  2. Starts at the rectum, can progress as far as the ileocaecal valve.
  3. Circumferential and continuous inflammation- no skip lesions
  4. Ulcers and pseudo-polyps in severe disease
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13
Q

Microscopic features of Ulcerative colitis

A
  1. Mucosa ONLY inflamed (not transmural)
  2. Crypt abscesses
  3. Depleted goblet cells
  4. No granulomata
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14
Q

Name the layers of the GI tract inner to outer

A
  1. Lumen
  2. Mucosa
  3. Submucosa
  4. Muscularis propria
  5. Serosal surface
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15
Q

Macroscopic features of Crohn’s

A
  1. Affects ANY part of GI tract (mouth to anus)
  2. Non-continuous inflammation and skip lesions
  3. Cobblestone mucosa appearance - ulcers and fissures in the mucosa
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16
Q

Microscopic features of Crohn’s

A
  1. Transmural inflammation
  2. Granulomas (non-caseating)
  3. Increased chronic inflammatory cells and lymphoid hyperplasia.
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17
Q

What is Erythema Nodosum?

A

Tender red bumps that are seen symmetrically on shins

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18
Q

What is pyoderma gangrenosum?

A

Painful ulcers on the skin

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19
Q

AMINOSALICYLATE

  • what is it?
  • active component?
  • examples
A

Aminosalicylate 5-ASA acts topically in the colonic lumen to induce remission.
The active component: 5-aminosalicylic acid (5-ASA) which is absorbed in the small intestine so they have to bind to something else to reach the colon.
examples: sulfasalazine, mesalazine, olsalazine.

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20
Q

What are the indications for surgery in Crohn’s disease?

A
  1. failure to medical therapy
  2. obstruction from strictures
  3. fistulae, abscesses, perianal disease
  4. toxic dilatation and perforation.
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21
Q

IRRITABLE BOWEL SYNDROME

A

////

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22
Q

Name 4 theories on the pathophysiology of IBS

A

Dysfunction in the brain-gut axis resulting in:
- disorders of intestinal motility
- enhanced visceral hypersensitivity
OR microbial dysbiosis (imbalance)

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23
Q

Red flag symptoms for colon cancer

A
  1. Unexplained weight loss
  2. Bleeding on defecation/wiping
  3. Abdo/rectal mass
  4. Raised inflammatory markers
  5. Anaemia
  6. FHx of bowel or ovarian cancer
  7. Age over 50
  8. Nocturnal symptoms
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24
Q

FODMAP’s

A

Fermentable, oligosaccharides, disaccharides, monosaccharides and polyols. e.g. apples, cherries, peaches, lactose, legumes, green vegetables (broccoli, sprouts, cabbage, peas), artificial sweeteners.

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25
Q

Soluble fibre

A

GOOD FOR IBS-C

  • Dissolve in water
  • broken down by bacteria
  • softens stool
  • barley, oats, beans, prunes, figs
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26
Q

Insoluble fibres

A

BAD FOR IBS D

  • makes diarrhoea worse
  • doesn’t dissolve in water
  • passes through gut unchanged
  • bulks up faeces
  • increases gut motility
  • cereals, whole- wheat bread, lentils, apples, avocados
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27
Q

APPENDICITIS

A

////

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28
Q

Pathophysiology behind appendicitis

A
  1. Occurs when lumen of appendix becomes obstructed by lymphoid hyperplasia, filarial worms, faecoliths (stones of poo).
  2. This causes gut organisms to enter into the appendix wall
  3. Causes oedema, ischaemia, necrosis, proliferation and inflammation
  4. Eventually the appendix ruptures, leaking out all of the contents e.g. faeces, organisms ext»>escapes into peritoneum»>peritonitis»life threatening.
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29
Q

Where is the appendix located?

A

McBurney’s point:

2/3 of the way from the umbilicus to the anterior superior iliac spine.

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30
Q

Why does the pain start in the periumbilical region and then migrate to the right iliac fossa, specifically McBurney’s point?

A
  1. Internal organs and the visceral peritoneum have no SOMATIC INNERVATION so the brain attributes the visceral signs to a physical location where the dermatome corresponds to the same entry-level in the spinal cord.
  2. NO LATERALITY (can’t tell right from left) to the visceral unmyelinated c-fibre pain signals which enter bilaterally and at multiple levels
  3. Early inflammation irritates structures and walls of the appendix and you get REFERRED pain to the mid-abdomen
  4. As inflammation gets worse it irritates the parietal peritoneum and then you get somatic localised pain at McBurney’s point.
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31
Q

Presentations of acute liver injury

A
  1. Malaise
  2. Nausea
  3. Anorexia
  4. +/- Jaundice
    Rare: COnfusion, bleeding, Liver pain, hypoglycaemia
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32
Q

Presentations of chronic liver injury

A
  1. Ascites
  2. Oedema
  3. Haematemesis
  4. Malaise, nausea, anorexia, wasting
  5. Easy bruising
  6. Pritusis
  7. Hepatomegaly
  8. Abnormal LFT’s
    Rare: Jaundice and confusion
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33
Q

What does a serum liver function test look at?

A
  1. Serum albumin
  2. Bilirubin
  3. Prothrombin time
  4. Liver biochemistry ( Aminotransferases, Alkaline phosphate)
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34
Q

What does the levels of albumin show?

A

The severity of CHRONIC liver disease.

The falling serum albumin is a bad prognostic sign

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35
Q

Unconjugated bilirubin

A

Unconjugated bilirubin is a waste product of haemoglobin breakdown that is taken up by the liver, where it is converted by the enzyme uridine diphosphoglucuronate glucuronosyltransferase (UGT) into conjugated bilirubin.

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36
Q

Conjugated bilirubin

A

Conjugated bilirubin is water-soluble and is excreted into the bile to be cleared from the body

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37
Q

What is the pro-thrombin time? What is it a sensitive indicator of?

A

Prothrombin time (PT) is a blood test that measures how long it takes blood to clot. Indicator of acute and chronic liver disease.

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38
Q

Other than the chronic and acute liver disease when else would you see a prolonged pro-thrombin time?

A
  1. Vit K deficiency

2. Biliary obstruction (low concentration of bile salts»>poor absorption of Vit k )

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39
Q

Aminotransferases

A

These enzymes are contained in hepatocytes and leak into the blood with liver cell damage. Examples are aspartate aminotransferase and alanine aminotransferase, GGT

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40
Q

Gamma-glutamyltransferase

A

GGT is an enzyme found throughout the body, but it is mostly found in the liver. When the liver is damaged, GGT may leak into the bloodstream. High levels of GGT in the blood may be a sign of liver disease or damage to the bile ducts. Bile ducts are tubes that carry bile in and out of the liver.

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41
Q

Where are damaged erythrocytes broken down?

A

They are broken down by macrophages in the spleen, bone marrow and in the kupffer cells of the liver.

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42
Q

Asterixis

A

Asterixis is a tremor of the hand when the wrist is extended, sometimes said to resemble a bird flapping its wings.

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43
Q

Fector hepaticus

A

Sweet and musty breath/urine

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44
Q

Liver disease progression

A

Stage 1: Inflammation. In the early stages, your liver will be inflamed and could be tender. Or it may not bother you at all.
Stage 2: Fibrosis/scarring. If you don’t treat the inflammation, it will cause scarring. As scar tissue builds up in your liver, it stops blood flow, which keeps the healthy parts from doing their job and makes them work harder.
Stage 3: Cirrhosis. The scar tissue takes over, and with less and less healthy tissue to do its job, your liver won’t work well, or it won’t work at all.
Stage 4: End-stage liver failure/disease. This is an umbrella term for several conditions, including swollen liver, internal bleeding, loss of kidney function, fluid in your belly, and lung problems. Only a liver transplant can cure it.

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45
Q

HEPATITIS

A

inflammation of the liver

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46
Q

Give 6 non-infective causes of acute and chronic hepatitis.

A
  1. Alcohol
  2. Drugs
  3. Toxins/poisoning
  4. Pregnancy
  5. Autoimmune
  6. Hereditary metabolic
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47
Q

Give 2 infective causes of acute hepatitis.

A
  1. Hep A and E

2. Herpes viruses e.g. EBV, CMV, VZV, COVID-19

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48
Q

Give 2 infective causes of chronic hepatitis

A
  1. Hepatitis B (+/- D)

2. Hepatitis C

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49
Q

Hepatitis A is what type of virus?

A

Picornavirus
- Replicates in the liver, is excreted in bile and then excreted in the faeces for about 2 weeks before the onset of clinical illness and for up to 7 days after. The disease is MAXIMALLY infectious JUST BEFORE the onset of jaundice.

50
Q

Pathology of Hepatitis B

A
  • DNA virus that comprises an inner core or nucleocapsid, surrounded by an outer envelope of surface protein (HBsAg).
  • HBsAg produced in excess by the infected hepatoytes and can exist separately in the serum and bodily fluids.
  • After penetration into hepatocytes the virus loses its coat and the virus core is transported to the nucleus without processing.
51
Q

Why is it hard to develop a vaccine for HCV?

A

There are 7 genotypes and rapid mutations so envelope proteins change rapidly so its hard to develop a vaccine.

52
Q

CIRRHOSIS

A

////

53
Q

Main causes for cirrhosis

A
  1. Chronic alcohol abuse
  2. Non-alcoholic fatty liver disease
  3. Hepatitis B +/- D
  4. Hepatitis C
54
Q

Describe the pathophysiology behind cirrhosis

A
  1. Liver injury causes necrosis and apoptosis, releasing cell contents and reactive oxygen species
  2. This activates the stellate and kupffer cells of the liver
  3. Stellate cells release cytokines that attract neutrophils and macrophages to the liver»> more inflammation and necrosis»fibrosis.
  4. Kupffer cells phagocytose these necrotic cells and secrete pro-inflammatory mediators:
    TGF-beta = stellate cells to myofibroblasts
    PDGF= myofibroblasts proliferation
  5. Increased myofibroblasts = progressive collagen deposition&raquo_space;>fibrosis and scar accumulation of liver.
  6. This leads to severe liver functioning as fibrosis is non-functioning.
55
Q

Micronodular cirrhosis

A

Regenerating nodules are usually <3mm in size with uniform involvement of the liver. It is often caused by alcohol or biliary tract disease.

56
Q

Macronodular cirrhosis

A

These nodules are varying in size and normal acini may be seen within the larger nodules. Often due to chronic viral hepatitis.

57
Q

What is Leuconychia due to?

A

White discolourations on nails due to hypoalbuminaemia.

58
Q

Xanthelasma

A

Yellow fat deposits under the skin usually around eyelids. Xanthos= yellow elasma= metal plates

59
Q

PORTAL HYPERTENSION

A

////

60
Q

What is the portal vein formed from?

A

Union of the superior mesenteric and splenic vein. Bring the blood with all the nutrients absorbed in the GI tract.

61
Q

Normal pressure of the portal vein

A

5-8mmHg

62
Q

Post hepatic cause of portal hypertension

A
  1. Right heart failure
  2. Congestive pericarditis
  3. IVC obstruction
63
Q

Pathophysiology of portal hypertension

A

From many different causes the blood flow from the portal system to IVC meets resistance.
The contraction of activated myofibroblasts (mediated by NO, endothelin, prostaglandins) contributes to increased reistance to blood flow.

64
Q

Varices

A

Enlarged/swollen veins

65
Q

Intial management for varices

A
  1. Resuscitate until haemodynamically stable
  2. Blood transfusion if anaemic
  3. Vit K and platelet infusion
  4. Vasopressin (IV TERLIPRESSIN/IV SOMATOSTATIN) to cause vasoconstriction.
  5. Prophylactic antibiotics
  6. Variceal banding/ Balloon tamponade/ transjugular intrahepatic portocaval shunt
66
Q

Initial management for varices

A
  1. Resuscitate until haemodynamically stable
  2. Blood transfusion if anaemic
  3. Vit K and platelet infusion
  4. Vasopressin (IV TERLIPRESSIN/IV SOMATOSTATIN) to cause vasoconstriction.
  5. Prophylactic antibiotics
  6. Variceal banding/ Balloon tamponade/ transjugular intrahepatic portocaval shunt
67
Q

How can you prevent a variceal haemorrhage?

A
  1. Beta-blocker (propranolol) to reduce resting pulse and decrease portal pressure
  2. Variceal banding repeatedly
  3. Liver transplant
68
Q

Diagnosis of portal hypertension

A
  1. Physical exam
  2. Ultrasound:
    - diameter of portal vein >13-15mm
    - doppler to find velocity of blood <16cm/s
    - reopening of umbilical vein
  3. Hepatic venous pressure gradient : pressure difference between the portal vein and IVC
69
Q

How are oesophageal varices formed?

A

Oesophagal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren’t designed to carry large volumes of blood.

70
Q

Drugs that cause hepatotoxicity

A
  1. Anti-biotics
  2. CNS drugs
  3. Immunosuppressants
  4. Analgesics&raquo_space;diclofenac
  5. GI drugs
71
Q

Drugs that DO NOT cause hepatotoxicity

A
  1. Low dose aspirin
  2. NSAID’s except diclofenac
  3. Beta-blockers
  4. Ace inhibitors
  5. Thiazides
  6. CCB’s
72
Q

Asprin is metabolised by what?

A

Asprin➞Salicylic acid by esterases

Salicylic acid ➞ Salicyluric acid + Salicyl phenolic glucuronide

73
Q

What happens in aspirin overdose?

A
  1. The two pathways become saturated
  2. Kidney excrete more salicylic acid
  3. Salicylates stimulate the respiratory centre and increase the depth and rate of respiration = inducing respiratory alkalosis
  4. Compensatory mechanisms: renal excretion of bicarbonate and potassium = metabolic acidosis
  5. Disruption of oxidative phosphorylation= increased lactate, pyruvate and ketone bodies.
74
Q

BILIARY TRACT DISEASE

A

///////

75
Q

Biliary colic

A

Pain associated with temporary obstruction of the cystic or common bile duct by a stone migrating from the gall bladder. It is a sudden onset, severe but constant pain and has a crescendo characteristic.

76
Q

Cholecystitis

A

Gallbladder inflammation

77
Q

Cholangitis

A

Inflammation of the bile duct

78
Q

ALCOHOLIC LIVER DISEASE

A

/////

79
Q

How does alcohol damage the liver?

A
  1. Ethanol is metabolised in the liver by two pathways leading to an increase in the NADH/NAD ratio
  2. This alters the redox potential and results in the more fatty acid synthesis and less fatty acid oxidation>fatty- acids accumulate in the liver and are esterified to glycerides.
  3. This is minimal with small amounts of alcohol but with large amounts, the cells become swollen with fat (steatosis)
  4. The changes in redox potential also impair carbohydrate and protein metabolism and cause centrilobular necrosis of hepatic acinus.
  5. TNF-alpha cells released by the kupffer cells cause an increase in reactive oxygen species leading to tissue injury and fibrosis
  6. Acetaldehyde is formed from the oxidation of ethanol and its effect on hepatic proteins could be a factor in producing liver cell damage.
80
Q

What can alcohol enhance in the liver?

A

The effects of toxic metabolites of drugs e.g. paracetamol on the liver.

81
Q

What type of cirrhosis is alcoholic cirrhosis?

A

Classically of the micronodular type but the mixed pattern can also be seen accompanying fatty change.

82
Q

What does alcoholic hepatitis involve?

A
  1. fatty acid deposition in hepatic cells= fatty liver
  2. Infiltration of polymorphonuclear leucocytes and hepatocyte necrosis
  3. Dense cytoplasmic inclusions: Mallory bodies and giant mitochondria are sometimes seen
83
Q

PANCREATITIS

A

////

84
Q

How do gall stones cause pancreatitis?

A

The gallstone blocks the pancreatic duct so enzymes can get out»>they start to digest the pancreas as intracellular Ca2+ increases and activates trysinogen>trypsin»»EXTENSIVE ACINAR DAMAGE.

85
Q

HAEMOCHROMATOSIS

A

/////

86
Q

Pathophysiology of haemochromatosis

A
  1. The HFE gene protein interacts with transferrin receptor 1, which is a mediator in intestinal iron absorption.
  2. Excessive iron is taken up by the mucosal cells of the small intestine, exceeding the binding capacity of transferrin.
  3. HFE decreases the hepatic expression of the hepcidin protein so you get iron overload.
  4. Excess iron is taken up by the liver and pancreas mainly but also in the heart, skin and endocrine glands.
  5. Fibrosis and cirrhosis is a late feature.
87
Q

WILSON’S DISEASE

A

/////

88
Q

Pathophysiology

A
  1. Dietary copper usually absorbed in the stomach and upper small intestine, then transported to the liver bound loosely to albumin.
  2. In the liver it is incorporated into ceruloplasmin and secreted into the blood, excessive is lost in bile and in faeces.
  3. In Wilsons, there is an error in the copper metabolism (specific not known) that causes the copper to be deposited in the liver, basal ganglia (globus pallidus and putamen), cornea.
89
Q

Fulminant hepatic failure

A

The clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function.

90
Q

Classifications of fulminant hepatic failure

A 
Hyperacute= encephalopathy within 7 days of jaundice onset
Acute= encephalopathy within 8-28 days of jaundice onset 
Subacute= encephalopathy within 5-26 weeks days of jaundice onset
91
Q

GASTRIC CANCER

A

/////

92
Q

How can Helicobacter pylori infection cause gastric cancer?

A

Normal gastric mucosa➞ H. pylori infection ➞ ACUTE GASTRITIS ➞ Chronic active gastritis ➞ Atrophic gastritis ➞ Intestinal metaplasia ➞ DYSPLASIA ➞ advanced gastric cancer

93
Q

Describe intestinal adenocarcinoma (type 1)

A
  • Well-formed and differentiated glandular structures
  • Tumours: polyploid, ulcerated lesions with heaped up rolled edges.
  • In the surrounding mucosa intestinal metaplasia
  • Most common: distal stomach
94
Q

Describe diffuse adenocarcinoma (type 2)

A
  • Poorly cohesive undifferentiated cells
  • Tumours: infiltrate the gastric wall
  • Can involve any part of the stomach, especially the cardiac
  • worse prognosis than intestinal
95
Q

Inguinal hernia

A

The protrusion of abdominal contents through the inguinal canal

96
Q

Spermatic cord contents

A

3 ARTERIES: testicular artery, cremasteric artery, artery of the Vas
3 VEINS: Pampiniform plexus of testicular veins, cremasteric vein, a vein of the Vas
3 NERVES: Ilio-inguinal nerve, genitofemoral nerve, sympathetic nerves
3 OTHERS: Vas deferens, lymph vessels, tunica vaginalis

97
Q

What does your ilioinguinal nerve supply?

A

Skin sensation to anterior 1/3 of external genitalia

98
Q

What does your genitofemoral nerve supply?

A

To cremasteric muscle

99
Q

What do your sympathetic nerves supply in the penis?

A

to the vas and testicular pain

100
Q

DIARRHOEA

A

/////

101
Q

Acute diarrhoea

A

Is defined as that lasting less than 2 weeks

102
Q

Chronic diarrhoea

A

Is defined as that lasting more than 2 weeks

103
Q

Organic causes of diarrhoea?

A

associated with changes in the structure of an organ or tissue resulting in symptoms- increased stool weights

104
Q

Functional causes of diarrhoea?

A

Conditions where there is no physical cause for symptoms e.g. irritable bowel syndrome

105
Q

Decreased consistency of stool caused by what?

A
  1. Water
  2. Fat
  3. Inflammatory discharge
106
Q

GORD

A

////

107
Q

Pathophysiology

A
  1. Between swallows the muscles of the oesophagus are relaxed except the upper and lower oesophageal sphincters.
  2. The LOS in the distal oesophagus remains closed unless swallowing is initiated, allowing food to enter the stomach and some reflux is normal
  3. In GORD there is excessive transient lower oesophageal sphincter relaxations as the LOS has reduced tone»» allowing gastric acid to flow back into the oesophagus
  4. Allowing for prolonged contact of gastric contents with the mucosa.
  5. Increased mucosal sensitivity to acid and reduced oesophageal clearance of acid contributes
  6. A hiatus hernia can impair anti-reflux mechanisms and contribute.
108
Q

PEPTIC ULCERS

A

///

109
Q

How do NSAIDs e.g. aspirin and naproxen produce gastric ulcers?

A

Usually, gastric mucosa is protected by a layer of mucin that is produced by gastric mucus-secreting cells. Mucous secretion is stimulated by prostaglandins.
Cyclo-oxygenase 1 is needed for prostaglandin synthesis. NSAID’s inhibit COX-1&raquo_space;>reduced mucosal defence.

110
Q

How do Helicobacter pylori infections produce gastric ulcers?

A
  1. They inhabit the mucus layer or just beneath it and cause major destruction to the mucin layer.
  2. Cause decrease in duodenal HCO3-»>increasing acidity of the stomach
  3. Secrete urease= urea +ammonia
    Ammonia + H+ = ammonium that is toxic to the gastric mucosa and less mucus made. Secreted proteases, phospholipase and vacuolating cytotoxin A can then begin attacking the gastric epithelium.
  4. Increase gastrin = more acid release from parietal cells.
  5. Decrease somatostatin = more acid released.
111
Q

How can ischaemia of the gastric cells cause peptic ulcers?

A

Causes gastric cells to produce less mucin» less protection from gastric acid.

112
Q

How can too much acid production cause ulcers?

A

Too much acid overwhelms the mucin and results in ulceration. Stress can cause increased acid productions.

113
Q

INTESTINAL OBSTRUCTION

A

/////

114
Q

Bowel obstruction

A

Arrest/blockage of the onward propulsion of intestinal contents.

115
Q

Three types of bowel obstruction

A
  1. Small bowel obstruction
  2. Large bowel obstruction
  3. Pseudo-obstruction
116
Q

What might be causing the intestinal obstruction (pathology)?

A
  1. Obstruction of the lumen
  2. Disease in the wall of the bowel
  3. Disease outside the bowel
117
Q

Obstruction of the lumen

A
  1. Tumors (carcinomas, lymphomas)
  2. Diaphragm disease
  3. Meconium ileus (neonates the bowel is sticky)
  4. Gallstone ileus
118
Q

Disease in the wall of the bowel

A
  1. Inflammatory ( Crohn’s, diverticulitis)
  2. Neural: Hirschpungs’s disease
    In neonates, they are born without full innervation to the colon/rectum so peristalsis won’t happen efficiently leading to faeces build up and gut dilatation.
119
Q

Disease outside the wall of the bowel

A
  1. Adhesions (MOST COMMON CAUSE OF OBSTRUCTION)
    commonly occurs after surgery, adhesions means loops of small and large intestine can’t move around freely, they get stuck together and on the abdominal walls, at the sites of adhesions the intestine can twist on itself, resulting in obstruction of blood supply or the normal movement of the contents of the intestines.
  2. Volvulus
  3. Peritoneal tumour
120
Q

How do hernias cause SBO?

A

Due to intestinal contents being unable to pass through a strangulated loop

Phase 2A extra (7 decks)

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