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Year 2 - Semester 1 > Gastro - week 4 > Flashcards

Gastro - week 4 Flashcards

1
Q

what is anaemia

A

when the serum haemoglobin is 2 standard deviations below normal

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2
Q

what is iron deficiency

A

when the total body iron is low due to absorption not matching demand

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3
Q

what is the epidemiology of iron deficiency anaemia

A

Iron deficiency anaemia affects 2-5% of males and non-menstruating females
Of these 10% have an underlying GI malignancy
If iron deficient but not anaemic, 1% will have underlying malignancy

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4
Q

what are some causes for IDA

A
  • Poor intake of dietary iron
  • Poor absorption e.g. coeliac or post-surgery
  • Increased iron (blood) loss e.g. menstruation or cancer
  • Increased demand e.g. pregnancy, adolescence
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5
Q

what are the symptoms of IDA

A 
•	Often none
•	Tiredness, dyspnoea, headache
•	Common signs
       o	Pallor, atrophic glossitis
•	Rarer signs
       o	Koilonychia, leuconycia, tachycardia, angular 
                cheilosis
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6
Q

what are the two types of iron

A

Ferrous iron – Fe2+ is found in red meat and seafood and is readily absorbed by the body – how the body wants it
Ferric iron – Fe3+ - less absorbable – needs to be changed to ferrous iron

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7
Q

what are iron absorption enhancers

A
  • Vitamin C
  • Fructose
  • Sorbitol
  • Alcohol
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8
Q

what are iron absorption inhibitors

A
  • Tannins (tea)
  • Calcium, manganese, copper
  • Egg and pulse proteins
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9
Q

describe ferritin

A

Iron stored in the body as ferritin - can be raised if the body is inflamed
If ferritin is normal there is no good way of testing iron deficiency

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10
Q

describe chronic disease anaemia

A

On a haematological test, iron deficiency anaemia and anaemia of chronic disease look the same.
Chronic disease could be anything like cancer
Inhibits release of iron from the reticular endothelial system
Also reduces erythropoietin release

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11
Q

how can you tell if someone has IDA and not CDA

A

Ferritin levels and bone marrow iron stores can be used to check for iron deficiency anaemia (would both be low) - transferrin will also be high to move what little iron there is around

Iron deficiency anaemia defined as low haemoglobin in the presence of
• Low ferritin
• Low serum iron in the presence of transferrin >3.0

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12
Q

what is the treatment for IDA

A
  • Optimise diet
  • Supplement with iron tablets for 3 months after iron deficiency is corrected
  • Main side effects are constipation, GI upset and dark stools
  • If unable to tolerate then some evidence to suggest once daily dosing/alternate day dosing is effective
  • If unable to tolerate that then IV iron can be considered – can be dangerous as body absorbs all of this and only as much oral iron as it needs
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13
Q

describe dysplasia

A

Dysplasia – disordered growth, architecture and maturation in a tissue, seen down a microscope - an appearance rather than a process
Dysplastic tissue may be neoplastic, show pre-neoplastic changes or revert back to normal
In epithelial tissue, severe dysplasia can be referred to as carcinoma in situ (intraepithelial neoplasm) – not yet able to invade into surrounding tissue

Features

• Hyperchromatism
o Dark staining of nuclei reflecting an increase in DNA content

• Nuclear pleomorphism
o Variation in nuclear shape (and size)

• Loss of orientation
o Many normal epithelial cells show polarity

• Cell crowding and stratification
o Reflects a loss of normal contact inhibition

• Increased and/or abnormal mitotic figures
o Reflects increased cell proliferation

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14
Q

what are soft tissue or connective tissue malignancies called?

A

called sarcomas

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15
Q

what is intussesception

A

where a polyp on the bowel is dragged by waves of peristalsis causing the bowel to “telescope”. This causes obstruction of the lumen and compresses the venous drainage, leading to ischaemia

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16
Q

what are the two types of borderline tumours

A
  • Tumours that show extensive local invasion but almost never metastasise. Prone to local recurrence if incompletely excised
  • Tumours that appear benign but which can develop distant metastases
17
Q

what are symptoms of GI neoplasia

A
  • Weight loss
  • Tiredness (anaemia)
  • Anorexia and vomiting
  • Pain caused by obstruction
  • Dysphagia
  • Alteration in bowel habit
18
Q

what types of oesophageal cancer are most common where?

A

Squamous cell carcinoma of the oesophagus most common in the world but the most common oesophageal cancer in the UK in adenocarcinoma – most associated with barrett’s oesophagus

19
Q

describe gastric carcinoma

A

• More males than females
• Often presents late
• Familial link around 10%
• Aetiology multifactorial – but mostly things that cause chronic gastritis
• 2 types histologically
o Intestinal
 Increased risk in patients with FAP
o Diffuse
 Relatively more common in low incidence
areas
 Often younger patients
 Female>male
 Inactivation of CDH1 gene which codes
for E-cadherin, a cell adhesion molecule

20
Q

describe small intestine cancer

A
  • Uncommon
  • Adenocarcinoma

• Neuroendocrine tumours
o Epithelial tumours associated with the synthesis of
hormone or neurotransmitter-like substances
o Range from well differentiated benign to
aggressive poorly differentiated tumours

• Gastrointestinal stromal tumours
o Soft tissue tumour (sarcoma) that can arise anywhere in the GI tract – most commonly stomach
o Related to pacemaker cells in muscularis propria
o Many have activating mutations in the receptor
tyrosine kinase

• Lymphoma (in coeliac disease)

21
Q

where do colon cancers tend to metastasise?

A

to the liver

22
Q

describe colorectal polyps

A

• Inflammatory – IBD, lymphoid

• Hamartomatous
o Juvenile polyps and polyposis
o Peutz jegher syndrome – pigmentation of lips

  • Hyperplastic
  • Lesions in the submucosa

• Neoplastic
o Adenomas
 Tubular
 Tubulovillous
 Villous (the more villous the more likely it
is high grade or invasive)

23
Q

describe colorectal adenoma inc. risk factors and genetics

A
  • Older age cancer
  • No gender diff other than rectal which is more common in men
  • Most sporadic (not genetic)
•	Dietary risk factors
       o	Excess calories
       o	Low fibre
       o	High intake of refined carbs
       o	High intake of red meat
       o	Low intake of vitamins
•	Other risk factors
       o	Family history
       o	Inherited syndromes
       o	Alcohol
       o	Smoking
       o	IBD
       o  	Occupational factors
       o	Radiation
       o	Schistosomiasis

• Genetics
o APC/ beta catenin pathway
 Inactivation of APC gene (tumour
suppressor) – seen in about 80%
 Genetic basis of the inherited FAP
o Microsatellite instability pathway
 10-15% of sporadic colorectal carcinomas
(more right sided than left)
 Inactivation of DNA mismatch genes
 One of these involved in lynch syndrome
 Loss of one of these genes increases
mutation rate by up to 1000 fold
 Not associated with typical adenoma-
adenocarcinoma sequence
o Serrated neoplasia pathway
 More recently identified
 Associated with distinctive precursor
lesions showing similarities to
hyperplastic polyps
 More common in right bowel
 More rapid progression to malignancy

24
Q

where is alcohol metabolised?

A

about 10% in stomach and rest in liver

25
Q

what can portal hypertension lead to

A

varices

encephalopathy - flapping tremor, confusion and foetor hepaticus

ascites

26
Q

what are signs of liver failure

A

low albumin

prolonged prothrombin time

27
Q

what is 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).

28
Q

descibe visceral pain

A
  • It is transmitted by C fibers that are found in muscle, periosteum, mesentery, peritoneum, and viscera.
  • Most painful stimuli from abdominal viscera are conveyed by this type of fiber and tend to be dull, cramping, burning, poorly localized, 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 in the midline, in the epigastrium, periumbilical region, or hypogastrium
29
Q

describe what abdominal visceral nociceptors respond to

A

respond to mechanical and chemical stimuli.
• The principal mechanical signal to which visceral nociceptors are sensitive is stretch; cutting, tearing, or crushing of viscera does not result in pain
• Abdominal visceral nociceptors also respond to various chemical stimuli and are activated directly by substances released in response to local mechanical injury, inflammation, tissue ischemia and necrosis, and noxious thermal or radiation injury.

30
Q

describe somatic-parietal pain

A

Somatic-parietal pain is mediated by A-δ fibers that are distributed principally to skin and muscle.
Signals from this neural pathway are perceived as sharp, sudden, well-localized pain, such as that which follows an acute injury.
Somatic-parietal pain arising from noxious stimulation of the parietal peritoneum is more intense and more precisely localized than visceral pain.
Lateralization of the discomfort of parietal pain is possible because only one side of the nervous system innervates a given part of the parietal peritoneum.

31
Q

describe referred pain

A
  • Referred pain is felt in areas remote from the diseased organ
  • This convergence may result from the innervation, early in embryologic development, of adjacent structures that subsequently migrate away from each other.
32
Q

what should you ask in a patient history for acute abdomen

A

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

• GI
Past abdominal surgeries, h/o GB disease, ulcers; Fam Hx IBD
• GU
Past surgeries, h/o kidney stones, pyelonephritis, UTI
• Gyn
Last menses, sexual activity, contraception, h/o PID or STDs, h/o ovarian cysts, past gynecological surgeries, pregnancies
• Vascular
h/o MI, heart disease, AF, anticoagulation, CHF, PVD, Fam Hx of AAA
• Other medical history
DM, organ transplant, HIV/AIDS, cancer
• Social
Tobacco, drugs – Especially cocaine, alcohol
• Medications
NSAIDs, H2 blockers, PPIs, immunosuppression, warfarin

33
Q

what are some examples of abdominal pain and shock

A
  1. RUPTURED AAA
  2. RUPTURED ECTOPIC PREGNANCY
  3. Acute mesenteric ischemia
  4. Severe acute pancreatitis
  5. Closed loop intestinal obstruction
34
Q

what are some examples of Generalised peritonitis

A
  1. PERFORATED ULCER
  2. COLONIC PERFORATION
  3. PERFORATED APPENDICITIS
35
Q

what are some examples of Localised peritonitis

A
  1. ACUTE APPENDICITIS
  2. ACUTE DIVERTICULITIS
  3. ACUTE CHOLECYSTITIS
  4. RUPTURED OVARIAN CYST/OVARIAN TORSION

Year 2 - Semester 1 (13 decks)

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