GI Flashcards
what is dysphagia
cause
- an OBSTRUCTION that causes difficulty in swallowing
CAUSE: - carcinoma (presents late, usually inoperable)
- benign structure (associated with REFLIX OESOPHAGITIS)
- stroke
- neurological issues (eg motor neuron disease)
IMPLICATIONS:
there are serious implications (lack of food eg)
what is oesophagitis
- INFLAMMATION of oesophagael mucosa
- the LOWER OESOPHAGEAL sphincter is tonically closed (unless swallowing) protects against reflux of HCl
- GORD/GERD (gastro-oesopgeal reflex disease)
CAUSES:
- decrease in sphincter tone
- CNS depressant drugs
- alcohol
- pregnancy
ANATOMICAL CHANGES:
1) inflammatory cells in the squamous epithelial layer
2) Neutrohphils are markers of severe injury
TREATMENT:
- removal of acid
- sleep upright
- smaller meals
- surgery
what is Barrett oesophagus
- 10% of GORD patients develop Barrett oesophagus
- important risk factor for oesophageal carcinoma, bleeding and structure
- Squamous mucosa is replaced by metastatic columnar epitheli
- alteration of STEM CELL DIFFERENTIATION, there is a change in cell type to resemble THE STOMACH
what is gastritis
- inflammation of gastric mucosa ACUTE: - neutrophil invasion CHRONIC: - lymphocytes, intestinal metaplasia and atrophy. - ULCER --> damage can cause breach and bleeding - loss of superficial mucosa (erosion) - acute GI bleeding
ASSOCIATED WITH:
- NSAID’s, aspirin, Alcohol and tobacco, Bacterial and viral infection, Severe stress, Chemotherapy treatment
MECHANISM:
- anything that increased HCl, decreased HCO3 or reduces blood flow will cause disruption to the mucus layer and direct damage to the epithelium
TREATMENT:
- most commonly it is SELF-LIMITING and doesn’t require more than simple OTC treatment
CHRONIC:
1) H.Pylori
- common
- can penetrate through the mucus bicarbonate layer
- survives in stomach by metabolising UREA
- diagnosed by biopsy, bacteria or urease enzyme activity or urea breath test or stool sample
- treatment: 3x antibiotic
2) Chronic alcohol and tobacco
- cessation is req
3) Immunologic loss (autoimmune) of parietal function (10%) leading to ACHYLORDIA
- immune system targets the PARIETAL CELLS (atrophy of them)
- diagnosed: by testing for PARIETAL CELL ANTIBODIES
- the parietal cells also make INTRINSIC FACTOR O due to having fewer parietal cells there will be less intrinsic factor. More likely to have pernicious anaemia
- Anaemia [low Hb/Fe stores, especially in a man or postmenopausal woman]
COMPLICATIONS:
- bleeding (slow bleeding over long period –> anaemia)
- perforation of stomach/duodenum (SERIOUS and life threatening). Diagnosed by CT scan or endoscopy
- causes: severe pain, rigid abdomen and will require surgery
- post surgery there can be OBSTRUCTION FROM SCARRING/SWELLING
TREATMENT:
- Al/Mg hydroxide (Gaviscon)
- Histamine H2 receptor antagonists
- Poroton-pump inhibitors
- antibiotics
what is the importance of differential diagnosis
- difficult to differentiate the severity of the condition between an ulcer and perforation
- the older a person is the less severe they perceive pain in their abdomen
- we can measure HOW THICK the erosion to the mucosa is
- it is a PEPTIC ULCER if the erosion is below the muscularis mucosae
- if there is erosion THROUGH THE SEROSA then there is a PERFORATION
- can differentiate using GASTROSCOPY
what are the malabsorption syndroms (in the small intesitine) that cause DEFECTIVE INTRALUMINAL DIGESTION
- Pancreatic insufficiency (no bicarbonate, no enzymes (amylase, hydrolase, proteases). Can be caused by pancreatitis, cystic fibrosis (Cl- transporter problem O not able to produce bicarbonate O secretions are at wrong pH and not fluid)
- Biliary insufficiency (no bile secreted O dietary fat is not emusified and digested, can be caused by gall stones/gall bladder removal O no storage of bile at specific times )
- Bacterial overgrowth in small intestine (SIBO)
what are the malabsorption syndroms (in the small intesitine) that affect the MUCOSA
- Disaccharridase deficiency (lactose intolerance)
- Abetolipoproteinaemia (no Apo B 48 (if there is no MTP, Apo B 48 cannot be added to new chilomicron O chylomicron cannot leave cell O unable to form chylomicrons) O causes fat malabsoroption leads to abetalipoproteinemia
- Primary bile acid malabsorption (ileal bile acid transporter O bile is not reabsorbed and leads to fat malabsoroption )
what are the malabsorption syndroms (in the small intesitine) that cause REDUCED SMALL INTESTINE SURFACE AREA
- these are less common
- Coeliac disease (flattening of villi O reduced surface area)
- Crohn disease (may req surgery which removes a section O this leads to reduced length and surface area)
what other factors can cause malabdroption syndromes
- lymphatic obstruction (can be important as when fat is absorbed, it goes into the lymphatic system and joins at the throacic duct. If there is obstruction of lymphatic system this can be impaired. can be due to LYMPHEDEMA or LYMPH NODE REMOVAL)
- GI infections can have an ACUTE effect on absorption. is transient
describe Disaccharide Deficiency
- Most common is lactase
- Activity high at birth, declines during childhood, low in adults
- 15% Caucasians; 70-90 % Other Ethnic Group
- high lactose in GI tract will change OSMOLALITY of gut lumen causing body to adjust osmolarity by water moving from extracellular fluid to lumen
- this makes peristalsis more efficient (substances move through gut more quickly)
- if enzyme deficiency: then diarhoea, flatulence, abdominal bloating (once lactose enters colon, bacteria start to ferment the sugar and produce gas), pain
TREATMENT - stop consuming lactose
what are the General Clinical Features of maldigestion and malabsorption
- Chronic Diarrhea
- Steatorrhea (fatty stools, often pale in olour)
- Weight loss/failure to thrive
- Anorexia (loss of appetite)
- Abdominal distension (due to gas)
- Borborygami (audible bowel sounds)
- Muscle wasting (most visible on arms and legs)
- Almost impossible to differentiate based on symptoms alone
describe fat malabsoption
- Greasy stools which do not flush away (Steatorrhea)
- Bile insufficiency (no fat emulsification, stools will be white/yellow)
- Pancreatic lipase deficiency (no enzymatic digestion)
- Mucosal defects (no chylomicron assembly
CONFIRMATION:
faecal fat tests
wdescribe Coeliac’s disease
- gluten sensitive enteropathy
- Primarily in Caucasions
- can be diagnosed in infancy through middle-age
- HLA phenotype DQ2 or 8
- Linked with dermatitis herpetiformis (skin blistering lesion, 100 %)
- autoimmune conditions and linked with others inc thyroid disease, Type 1 diabetes (strong link)
- Sensitivity to gluten (gliadin) from wheat and closely related grains (oat (not actually in oats but it is often contaminated), barley, rye)
- T-cell mediated inflammatory reaction
- in a blood test Anti-gliadin antibodies IgA and tTG (Tissue Transglutaminase Antibody) by blood test (95 % sensitivitity)
- only way to have 100% accuracy in diagnosis is by SI BIOPSY
what is dermatitis herpetiformis
- Skin manifestation of coeliac disease in 15-25 % of patients
- Fluid filled blisters (appearance similar to herpes)
in a biopsy to diagnose Coeliac’s what can be seen
characteristic features
- Atrohy and loss of villi (and microvilli)
- Intra-epithelial lymphocytes
- Crypts elongated
- Overall mucosal thickness is unchanged
- Mucosal histology reverts to near-normal following period of gluten exclusion
- Re-biopsy ± rechallenge
