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year 2 sem 1 > wk 5 GI > Flashcards

wk 5 GI Flashcards

1
Q

anemia def.

A
  • When serum haemoglobin is 2 standard deviations below the normal
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2
Q

iron deficiency def.

A

¢ Iron deficiency anaemia affects 2-5% of adult males and non-menstruating females.
¢ Of these around 10% will have an underlying GI malignancy
¢ If iron deficient but not anaemic, around 1% will have an underlying malignancy
¢ Means that patients should be referred on urgent caution of cancer

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3
Q

iron deficiency anaemia (IDA) causes

A
  • Poor intake of dietary iron
  • Reduced absorption (malabsorption) e.g coeliac, post surgical
  • Increased iron (blood) loss e.g. menstruation, cancer
  • Increased demand e.g. pregnancy, adolescence
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4
Q

IDA symptoms and signs

A

¢ Often none (asymptomatic)
¢ Common symptoms: tiredness, dyspnoea, headache
¢ Common signs: pallor, atrophic glossitis
¢ Rarer signs: koilonychia, leuconychia, tachycardia, angular cheilosis

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5
Q

what are the 2 different forms of dietary iron

A
  • haem iron (ferrous)

- non-haem iron (ferric)

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6
Q

ferrous iron

A
  • Fe2+
  • Found in red meat and seafood
  • Readily absorbed by the body
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7
Q

Ferris iron

A
  • Fe3+
  • Less absorbable
  • As needs to be changed to Fe2+ in iron rich environments in order to be absorbed
  • Some ferric iron can be absorbed but at a much lower rate than ferrous iron
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8
Q

haemochromatosis

A
  • Too much iron is absorbed in the body
  • Once iron absorbed = no mechanism for excretion
  • 2-4 x as much as should be is absorbed
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9
Q

ferritin

A
  • body stores iron in cells as ferritin
  • So, ferritin is a marker of total body iron stores
  • Not serum iron – this is just showing iron being moved around the body
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10
Q

how are ferritin levels interpreted

A
  • If ferritin is low, then you have low total body iron stores
  • If ferritin is normal you can still be deficient
  • Bc ferritin can be an acute phase reactant
  • Elevated if there’s inflammation
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11
Q

anaemia of chronic disease signs in full blood count

A
  • MCV – size of the cell
  • Small in IDA and ACD
  • MCH – blood in each
  • Similar
  • Don’t do bone marrow tests on everyone
    So on blood tests look vv similar
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12
Q

how to tell the diff. between IPA and ACD

A
  • If ferritin low = iron deficiency anaemia
  • Serum iron is unhelpful
  • Look at TRANSFERRIN
  • If body low in iron = more transferrin
  • If body has full stores of iron in ACD = low/ normal transferrin
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13
Q

mechanisms of AoCD

A
  • Occurs when there’s ongoing inflammatory stimulus
  • Eg cancer, infection, chronic inflammatory conditions
  • Effects blood and iron in 4 ways
  • Increases HEPCIDIN
  • Which inhibits release of iron form endothelial system
  • So body has enough iron but it’s being held in the wrong place/ not released
  • Inhibits ERYTHROPOIETIN release
  • Dec. erythropoetic stimulation
  • So don’t make as much RBC as bone marrow not stimulated
  • Esp. since there’s less iron available to them to make blood
  • Giving more iron won’t help therefore
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14
Q

whats the gold standard for investigating IDA

A
  • Bidirectional endoscopy
  • Endoscopy and colonoscopy

but not always done

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15
Q

standard endoscopy

A
  • Put camera down back of throat
  • Round the back of the pharynx
  • Pharynx normally numbed to stop gag reflex
  • Look at oesophagus, stomach and duodenum
  • Either performed under…
  • Topical anaesthetic spray (lidocaine) at back of throat - awake
  • Topical lidocaine and sedation (conscious sedation – awake and aware but anterograde amnesia so don’t remember much)
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16
Q

capsule endoscopy

A
  • On vv few patients
  • See small and middle bowel
  • Takes photos
  • Take pret
  • One use only pill – photos downloaded wirelessly

Looking for angiodysplasia
- Thin blood vessels that bleed and ooze

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17
Q

investigation strategy for IDA

A
  • Once colon and upper GI tract have been assessed then no further GI investigations required for the majority
  • No formal diagnosis is common
  • Ensure not losing blood from renal tract
  • Investigate small bowel if recurrent IDA
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18
Q

hyperplasia

A
  • Tissue growth due to inc. in cell number

- Can be physiological or pathological

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19
Q

metaplasia

A
  • Change from one fully differentiated cell tyoe to another fully differentiated cell type
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20
Q

dysplasia

A
  • Descriptive term -> pattern of disordered growth, architecture and maturation within a tissue in nature
  • Unlike metaplasia and neoplasia, it does not describe a pathological process rather an appearance seen down the microscope
  • Important to recognise as gives clue to the fact a tissue has underlying genetic abnormality in regulation of cell growth and differentiation
  • Cells showing dysplasia may already be neoplastic or show pre-neoplastic changes
  • But dysplasia can revert back to normal
  • Dysplasia divided into high- and low-grade dysplasia depending on how growth pattern differs from that of surrounding tissue
  • In epithelial tissues severe dysplasia often referred to as carcinoma in situ
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21
Q

features of dysplasia

A
  • Hyperchromatism
  • Dark staining of nuclei reflecting an increase in DNA content eg polyploidy
  • Nuclear pleomorphism
  • Variation in nuclear shape (and size)
  • Loss of orientation
  • Many normal epithelial cells show “polarity”
  • Cell crowding and stratification
  • Reflects loss of normal contact inhibition
  • Increased and/ or abnormal mitotic figures
  • Reflects increased cell proliferation
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22
Q

neoplasia

A
  • Uncontrolled cell growth, abnormal mass of tissue, uncoordinated to normal tissue, persists after evoking stimulus
  • Aetiology
  • Benign/ malignant
  • Routes of metastasis
  • Nomenclature
  • Staging and grading
23
Q

examples of epithelial cancer

A

CARCINOMAS
adenocarcinoma
squamous cell carcinoma

24
Q

examples of soft tissue cancers

A

SARCOMAS
osteosarcomas
chondrasarcoma

25
Q

effects of benign tumours

A
  • bleeding
  • space occupying lesions within the skull
  • compression of adjacent structures
  • obstructions of lumina/ hollow organs
  • hormonal effects
  • inc. or dec. prod.
26
Q

borderline tumours

A

Such tumours tend to fall into 2 categories

  • tumours show extensive local invasion but almost never metastasise, these are prone to local recurrence
  • tumours that appear entirely benign at the time of diagnosis, but can develop distant metastases, often presenting many years after the initial diagnosis
27
Q

symptoms of neoplasia of the GI tract

A
  • various and non-specific
  • tiredness (anaemia)
  • bleeding
  • anorexia and vomiting
  • weight loss
  • pain caused by obstruction
  • dysphagia
  • alteration in bowel habit (for colon)
28
Q

what are the common types of oesophageal carcinomas worldwide vs UK

A 
squamous cell carcinoma 
-	90% of oesophageal cancers worldwide
-	80% in developing countries
Risk factors
-	Tobacco and alcohol
-	Diet
-	Infection
-	Fungal oesophagitis?
-	Human papillomavirus?
-	Genetic factors

Adenocarcinoma

  • Most common in the UK
  • Most associated with acid reflux and Barrett’s oesophagus
  • Tobacco and alcohol less important
29
Q

prognosis for oesophageal/ gastric carcinomas

A
  • Poor
  • Tumour stage is most important prognostic factor for squamous cell and adenocarcinomas
  • Good prognosis for tumours confined to the mucosa
  • Many tumours picked up late
  • 10-20% survival for adenocarcinomas involving deep muscularis propria
30
Q

whats the most common carcinoma of the stomach

A

adenocarcinomas

  • Highest rates in japan, east asia, eastern Europe and S America
  • Low rates in N America, N Europe, Africa
  • Failing incidence and mortality
31
Q

what are the 2 main histological patterns of adenocarcinomas in the stomach

A

Intestinal

  • Majority of cases in high incidence areas
  • Increased risk in patients with FAP

Diffuse

  • Relatively more common in low incidence areas
  • Often younger patients
  • Female > male
  • Mutations or inactivation of CDH1 gene a common feature
32
Q

types of neoplasias of the small intestine

A
  • Uncommon
  • Maybe bc content of small bowel are liquid and so pass quicker
  • Less content with dietary carcinogens
  • May be other factors
  • Adenocarcinoma
  • Neuroendocrine tumours
  • GISTs
  • Lymphoma
  • Enteropathy type T-cell lymphoma (EATL) in coeliac disease
  • Others
33
Q

neuroendocrine tumours

A
  • Epithelial tumour associated with the synthesis of hormones or neurotransmitter-like substances
  • Eg serotonin
  • Range from well-differentiated benign -> poorly differentiated malignancy
  • Small cell carcinoma is vv aggressive
  • Can be difficult to predict their behaviour
  • Risk depends on size, site and grade (based on mitotic activity

YELLOW

34
Q

gastrointestinal stromal tumour (GISTs)

A
  • Soft tissue tumour that can arise anywhere in the GI tract
  • Commonest in stomach
  • Related to “pacemaker” cells in muscularis propria
  • Malignant tumours are type of sarcoma
  • 75-80% of GISTs have activating mutations in the KIT receptor tyrosine kinase gene
  • Can be difficult to predict behaviour
  • Risk dependant on site, size and proliferative activity
35
Q

colorectal polyps

A
  • Inflammatory – IBD, lymphoid
  • Hamartomatous eg
  • Juvenile polyps and polyposis
  • Peutz-jegher syndrome
  • Hyperplastic
  • Seen in sigmoid and rectum commonly
  • Lesions in the submucosa eg lipoma presenting as a “polyp”
36
Q

neoplastic polyps / cancer in the colon/ rectum

A 
Adenomas
-	Tubular
-	Tubulovillous
-	Villous
(The more villous the more likely there’s high-grade dysplasia)

adenocarcinomas

]Adenomas are precursors for adenocarcinomas (cancer)

37
Q

colorectal adenocarcinoma

A
  • peak incidence 60-79
  • no gender diff.
  • but rectal cancer M>F
  • 55% in rectum/sigmoid
  • 22% of tumours in caecum/ ascending colon
  • Most sporadic
  • About 5% are associated with IBS or FAP or IBD
38
Q

dietary risk factors of colorectal adenocarcinoma

A
  • Excess calories
  • Low fibre
  • Too much refined carbohydrates
  • High intake of red meet
  • Low intake of protective vitamins
  • Exact mechanisms unclear
  • Bacteria involved\
39
Q

genetic pathways involved with colorectal carcinoma

A

APC/B- catenin pathway

Micro-satellite instability pathways

serrated neoplasia pathway

40
Q

familial colorectal carcinoma

A
  • About 1% associated with FAP
  • Up to 5% ass. With HNPCC/ Lynch syndrome
  • > 80% ass. With an inherited defect
  • Having 1st degree relarive with CRC inc. risk by up to 8 fold
41
Q

defintion of the acute abdomen

A

• An abdominal condition of abrupt onset associated with severe abdominal pain (resulting from inflammation, obstruction, infarction, perforation, or rupture of intra-abdominal organs).

42
Q

visceral pain

A
  • Transmitted by C fibres that are found in muscle, periosteum, mesentery, peritoneum, and viscera
  • Most painful stimuli from abdominal viscera are conveyed by this type of fibre and tend to be dull, cramping, burning, poorly localised, and more gradual in onset and longer in duration than somatic pain
  • Because abdominal organs transmit sensory afferents to both sides of the spinal cord, visceral pain is usually perceived to be midline in the epigastrium, periumbilical region, or hypogastrium
43
Q

somatic pain

A
  • Mediated by A-gamma fibres which are distributed principally to skin and muscle
  • Signals from the neural pathway are perceived as sharp, sudden, well-localised pain, such as follows an acute injury
  • Somatic-parietal pain arising from noxious stimulation of the parietal peritoneum is more intense and more precisely localised than visceral pain
  • Lateralization of the discomfort of parietal pain is possible because only one side of the NS innervates a given part of the parietal peritoneum
44
Q

referred pain

A
  • Felt in areas remote from diseased organ
  • May be linked to embryological development
  • Eg pain in right shoulder in gall stone disease
45
Q

what to ask about in acute abdomen

A

GI symptoms
- Nausea, vomiting, anorexia, hematemesis, diarrhea, constipation, bloody stools, melena stools
GU symptoms
- Dysuria, frequency, urgency, hematuria, incontinence
Gyn symp.
- Vaginal discharge, vaginal bleeding, pain during sex
General
- Fever, lightheadedness

46
Q

what are the main categories of acute abdomen

A 
abdominal pain and shock
generalised peritonitis
localised peritonitis
intestinal obstruction
"medical" illness
47
Q

what could cause abdominal pain and shock

A

Ruptured AA (aortic aneurysm)

  • Acute abdominal pain
  • Back pain
  • Hypotension
  • Background of vascular problems
  • HIGH. MORTALITY

Ruptured ectopic pregnancy

  • Acute abdominal pain
  • Hypotension
  • Bleeding in the abdomen
  • Pos. pregnancy test

Acute mesenteric ischaemia

  • Blood supply to bowel compromised
  • Signif. Abdominal pain
  • When it leads to shock its normally to late!!!!
  • Mortality quite high
  • Severe acute pancreatitis

Severe intense abdominal pain

  • Radiates to the back
  • Predisposing factor (gallstones/ alcohol consumption)
  • all these cases cause rise in amylase

closed loop intestinal obstruction

  • blockage in bowel causing bowel to twist
  • inc. pressure in lumen and reduce blood supply into the bowel
48
Q

what can cause generalised peritonitis

A

perforated ulcer
- stomach or duodenum

colonic perforation

perforated appendicitis

  • spillage of enteric contents into abdomen causing chemical reaction
  • leading to rigid abdomen
  • REMEMBER AMYLASE
  • As can mimic pancreatitis
  • As you don’t operate on pancreatitis
49
Q

what can cause localised peritonitis

A

AN INFLAMMED ORGAN IN A CERTAIN QUADRANT

  • Acute appendicitis
  • Acute diverticulitis
  • Acute cholecystitis
  • Ruptured ovarian cyst- ovarian torsion
50
Q

symptoms of abdominal obstruction

A

Central colicky pain
Distention
Constipation
Vomiting

51
Q

what are the differences in LBO and SBO

A
  • SBO is managed conservatively unless there’s suspicion of compromise of blood supply to the bowel
  • LBO is usually managed ASAP

This is because…

  • In small bowel there’s a decompression valve
  • So contents don’t go through
  • Instead patient vomits
  • So pressure inside colon is alleviated
  • Also alleviated medically by putting tube through the nose to decompress the stomach

But…

  • In LBO is there’s a blockage in eg descending colon
  • There’s a valve in the cecum that doesn’t allow backflow from large bowel to small bowel
  • So things can’t pass down or up so pressure increase
  • Progressive distention leads to perforation
52
Q

volvulus

A
  • Bowel twisting around it’s axis
  • Leading to inc. pressure like in LBO
  • Leads to perforation quickly
  • If there’s a volvulus in the small bowel or large bowel you must do surgery on this
53
Q

imaging in acute abdomen

A
  • RUQ pain, lower abdominal pain in female patients -> ultrasound
  • Almost all other types -> CT scan
  • Because you need to establish diagnosis before operating
54
Q

what groups are important to consider in acute abdomen

A
  • the elderly
  • children
  • immunocompromised
  • critically ill patients
  • morbidly obese
  • pregnant (appendicitis)

year 2 sem 1 (13 decks)

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