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BDS2 BAMS > gastro meds > Flashcards

gastro meds Flashcards

1
Q

Medications used in GI disease

A

1 antacids (ELIMINATING acids)

REDUCING acid secretion
2. H2 receptor blockers
3. Proton pump inhibitors

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2
Q

examples of Antacids

A
  • gaviscon
  • rennie
  • alkalis that neutralises acid
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3
Q

function of H2 receptor blockers

A
  • preventing histamine activation of acid production
  • limited effectiveness because gastrin and Ach pathways still operative
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4
Q

function of Proton pump inhibitors

A
  • blocks acid secretion irrespective of whether the simulation continues at the bottom
  • much more effective clinically than H2
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5
Q

what is ome/lanso/pantoprazole

A

PPI

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6
Q

what is cimetidine

A
  • cimetidine
  • ranitidine
    both are H2 receptor blockers
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7
Q

Upper GI disease

A
  • Oral diseases
  • Oesophageal
    o Dysphagia
    o GORD
  • Gastric
    o Hiatus hernia
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8
Q

Dysphagia

A
  • difficulty swallowing
  • dysmotility = fibrous replacement of elastic and muscle tissue
  • external compression
  • feel of food sticking
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9
Q

causes of dysphagia

A
  • external compression
  • GORD
  • scleroderma
  • neuromuscular dysfunction
    o Parkinsons
    o Diabetes
    o Achalasia

refer to the notes for more info

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10
Q

GORD Causes

A
  • defective lower oesophageal sphincter
  • impaired lower clearing
  • impaired gastric emptying
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11
Q

effects of GORD

A
  • ulceration
  • inflammation – erythema due to burning by acid
  • Barrett’s oesophagus metaplasia – change in oesophagus epithelium from stratified squamous to columnar epithelium
  • Precancerous adenocarcinoma – chronic inflammation can lead to potentially malignant lesion
  • Dysphagia
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12
Q

Signs and symptoms of gord

A
  • epigastric burning
  • abdominal pressure
    increasing
  • dysphagia
  • stricture
  • oesophagitis
  • dysmotility
  • GI bleeding FOB test
  • severe pain
  • heartburn after excessive food or drink mimicking MI
  • oesophageal muscle spasm
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13
Q

Management of Gord

A
  • stop smoking improves sphincter
  • lose weight as abdominal fat can pressure ad force food back up
  • stop excess coffee
  • antacids
  • H2 blockers
  • PPI
  • drugs to increase gut motility and gastric emptying to reduce backfilling into the oesophagus
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14
Q

2 types of hernia

A
  • part of stomach in thorax

o 1 => sliding hernia where the hernia moves with the oesophagus
o 2=> rolling hernia where the oesophagus and hernia behave independently

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15
Q

symptoms of hernia

A
  • similar symptoms to GORD
  • the diaphragmatic muscles cannot help to compress the lower sphincter making it easier for gastric contents to pass up from stomach back into oesophagus and cause GORD
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16
Q

Peptic ulcer disease affects which part of the git

A
  • oesophagus
  • stomach
  • duodenum often affected by PUD
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17
Q

causes of peptic ulcer disease

A
  • High acid secretion in ddn and oesophagus
  • Normal acid secretion but lost ability to neutralise acids (Helicobacter pylori) (stomach)
  • Drugs like nsaids and steroids
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18
Q

Types of peptic ulcer disease

A
  1. bleeding ulcer – gone through lining and submucosa, eroded to an artery causing significant bleeding
  2. perforated ulcer – burn can extend through artery or viscous wall into peritoneum
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19
Q

where does Helicobacter pylori usually affect

A
  • infects lower part of stomach (antrum)
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20
Q

what does h pylori do to the stomach

A
  • bacteria gets through the mucus layer, removes it, allows attack on stomach lining, leading to inflammation
  • loss of mucus layer protection
  • chronic gastric wall inflammation
  • activates lymphoid tissues in gastric wall
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21
Q

can lymphoma caused by H.pylori disappear?

A

yes, with triple therapy. (2 antibiotics and 2 PPI)

  • when stimulus is removed ie H. pylori, the lymphoma will disappear
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22
Q

what is MALT

A

lymphoma on the stomach (peptic ulcer disease) is a MALT (mucosa associated lymphoid tumour)

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23
Q

Signs and symptoms of PUD

A
  • asymptomatic
  • epigastric burning pain
  • significant bleeding and perforation ulcers may cause there to be change in amount of blood in circulation, could be a drop in blood pressure
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24
Q

Investigations for peptic ulcer diseases

A
  • endoscopy, biopsy
  • radiology
  • anaemia
    o FBC and FOB
    o chronic bleeding in the stomach may cause a decrease in Hb content (fbc)
    o bleeding in git shown by positive test of Hb in stools for FOB
  • H. pylori
    o antibodies in blood
    o mucosa biopsy
    o metabolic products of bacteria in breath sample
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25
Q

Complications of peptic ulcer disease

A

Local more serious
o perforation
o haemorrhage
o stricture
o malignancy

Systemic
o anaemia

refer to notes for more info

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26
Q

tx of peptic ulcer disease

A

o stop smoking

o small regular meals

o eradication therapy, removing H.pylori using triple therapy

o ulcer healing drugs like PPIs

o reduce acid secretion using H2 receptor blockers and PPI

o improve mucosal barrier by eliminating H.pylori with triple therapy and stopping NSAIDs and steroids

Surgical
o gastrectomy used when there is stricture, ACUTE bleeding, perforation, malignancy

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27
Q

what is gastrectomy

A

surgical excision of the ulcer, part of the stomach

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28
Q

Bilroth 1 vs 2

A

Bilroth 1 – duodenum connected to upper part of stomach

Bilroth 2 – duodenum sewn up, stomach connected to small bowel

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29
Q

what is vagotomy

A

vagotomy – divide the main vagus trunk into small branches to the stomach to reduce acid secretion

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30
Q

what is coeliac disease

A

sensitivity to alpha-gliaden component of gluten!

Gluten found in wheat, barley, rye etc

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31
Q

Where does coeliac disease affect?

A
  • Small bowel
  • mainly JEJUNUM
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32
Q

what disease has to do with malabsorption

A

disease of the small intestines like

a. Pernicious anaemia
b. Coeliac disease
c. Crohn’s
d. Small bowel disease

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33
Q

where are haematinics absorped in git?

A

b12 terminal iluem
iron and folate in jejunum

** iron and folate deficiency may be due to coeliac disease

b12 deficiency due to diseases affecting terminal ileum like crohns

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34
Q

coeliac disease may cause what deficiency

A

iron and folate

35
Q

crohns may cause what deficiency

A

b12

36
Q

Causes of coeliac disease

A
  • genetic susceptibility
  • environmental triggers
  • gluten ALPHA GLIADEN COMPONENT
37
Q

what does alpha glaiden do to the small intestine?

A

o alpha gliaden in gluten passes through the bowel wall causing an immune reaction that produces antibodies

o T cells and antibodies destroy the villous tissue resulting in villous atrophy

  • loss of projections
  • decrease in SA
  • reduction in absorption
38
Q

signs and symptoms of coeliac

A
  • failure to grow due to malabsorption
  • abdominal pain
  • oral aphthae (ulcers)
  • tongue papilla loss
  • steatorrhea (oily stools)
  • dysphagia
  • iron, folate deficiency
  • fat deficiency
39
Q

Investigations for coeliac

A
  • autoantibody test
    o serum transglutaminase (TTG)
    o anti gliaden antibodies
  • jejunal biopsy
  • loss of projections seen on endoscopy
  • faecal fat increased if malabsorption
  • haematinics
40
Q

can Gluten free diet reverse coeliac disease?

A

yes , FULLY reverses jejunal villous atrophy

  • complete and full absorption restored
41
Q

what is dermatitis herpetiformis

A

Coeliac disease associated diseases

o little blisters on skin filled with fluid
o autoantibodies against the skin
o granular IgA deposited in skin and mucosa
o itch and blisters
o antibodies binding to the JE between the connective tissue and the epithelial surface, loss of adhesion causing the epithelium to lift up

42
Q

which disease has granular IgA deposited in skin and mucosa

A
  • dermatitis herpetiformis which is a coeliac disease associated disease
43
Q

if you see oral aphthous ulcer and blisters, what could you link it to?

A

Coeliac disease associated diseases

deficiency of haematinics

44
Q

what is Pernicious anemia

A

disease caused by vitamin b12 deficiency either because

a. B12 intake not enough
b. B12 not absorbed in terminal ileum

45
Q

what might cause lack of b12 absorption in terminal itleum?

A

a. parietal cells disease, usually autoimmune, Intrinsic factor not produced

b. inflammatory bowel disease of the terminal ileum like Crohn’s

c. bowel cancer at ileocaecal junction

46
Q

Treatment of Pernicious anaemia

A
  • increase b12 intake
  • supplements
  • IM injections of b12
47
Q

Importance of B12

A
  • nerve function without it may have permanent neuromuscular damage
  • bone marrow production of RBC
48
Q

where is bowel cancer occuring

A
  • usually means colonic cancer
  • large bowel
49
Q

who gets bowel cancer more commonly

A

UK screening from age 50
man > woman

50
Q

Symptoms of bowel cancer

A
  • usually none
  • low level anaemia
  • rectal blood loss (high risk symptom)
  • abdominal pain/tenderness
51
Q

how to screen for bowel cancer?

A

o Faecal immunochemical test (FiT)
o endoscopy if positive ie see blood in stool

52
Q

causes of bowel cancer?

A
  • carcinomas arise from POLYPS
  • patient controlled factors
  • medical and familial factors
53
Q

how to stage bowel cancer?

A

Staged by degree of invasion into bowel wall

  1. A => SM
  2. B => Muscularis
  3. C => Lymph nodes
  4. D => Liver
54
Q

best Treatment of bowel cancer

A

best tx is to detect early and remove polyps

  • surgery
  • hepatic metastases drugs to control spread in liver
  • radiotherapy
  • chemotherapy
55
Q

what are intestinal polyps

A

genetically inherits a tendency to form lots of polyps in the bowel, each polyp has a risk of developing a cancer therefore increase polyp number = increase risk of cancer

56
Q

is small intestine polyps high risk or low risk

A

low risk

large intestine -> high risk

57
Q

how long for polyps to progress to malignancy?

A

about 5 years
frequent screening is good, remove early polyps can prevent bowel cancer

58
Q

what gene may increase risk of bowel cancer

A

o genetics p53 gene in 75% of bowel cancer patients

59
Q

what gastro diseases may increase risk of bowel cancer?

A

o Ulcerative colitis

60
Q

what diet might cause increased risk of bowel cancer?

A

o diet low in fibre, high in fat, low vegetables
o alcohol

61
Q

where does crohns and ulcerative colitis appear?

A

crohns - anywhere in git but popular site is ileocaecal junction

UC - colon and rectum, always in rectum

62
Q

cause of crohns

A
  • Crohn’s could be caused by transmission of mycobacteria through milk from cattle with Johne’s disease
  • Food intolerance
  • persisting viral infection
  • smoking
  • genetics
63
Q

is drinking pasteruised milk safer to prevent crohns?

A

no
- Ultra heat transmission kills mycobacteria, pasteurisation does not kill mycobacteria

64
Q

Microscopic features of crohns

A

oedema
granuloma
transmural
narrowing of lumen

65
Q

why is there odema in crohns?

A

o giant cells occupying the drainage channels and preventing fluid from draining
o fluid build up causing oedema

66
Q

what disease has a cobblestone appearance?

A

crohns
o areas of oedema between fibrous bands causing a cobblestone appearance

67
Q

can crohns appear in the mouth?

A

yes
- extend onto skin or perianal tissues

68
Q

symptoms of crohns

A

if crohns in small bowel,
o pain
o malabsorption
o obstruction

if crohns in the mouth
OFG

69
Q

orofacial granulomatosis vs oral crohns disease

A

OFG if only mouth affected

oral crohns if extension of crohns disease from other parts of git

70
Q

presentation of ofg

A

o lip and oral swelling
o no identifiable trigger
o oedema of mouth and face
o cobblestone/ fissures
o full thickness inflammation to surface of skin from mouth

71
Q

why do we need Growth monitoring for kids with OFG

A

, May go on to develop Crohn’s later in life, if there is failure to grow according to normal rate, failing to absorb nutrients, necessary for other investigations maybe calprotectin levels or endoscopy

72
Q

which disease has continuous level of inflammation throughout the bowel?

A

UC

  • start as the distal part and moves forward through the large intestine
  • continuous level of inflammation throughout the bowel
73
Q

Microscopic features of UC

A

VASCULAR

mucosal only, doesnt extend through the wall, superficial layers only

74
Q

clinical appearance of UC

A
  • erythema
  • inflammatory change
75
Q

Symptoms of UC

A
  • diarrhoea
  • abdominal pain
  • rectal bleeding
76
Q

Investigations for Inflammatory bowel disease

A
  • blood tests
    o anaemia
    o c reactive protein
    o erythrocyte sedimentation rate
  • faecal calprotectin
  • endoscopy
  • leukocyte scan
  • barium studies
  • bullet endoscopy
77
Q

what calprotectin?

A

inflammatory protein secreted by epithelial cells in large or small bowel into lumen

78
Q

link between UC and bowel cancer or carcinomas in general

A
  • ulcerative colitis can develop into carcinoma
  • inflammatory change present for many years
79
Q

TX of Inflammatory bowel disease

A
  • Medical (immunosuppressive drugs) both steroidal and non steroidal
  • Surgical colectomy; drain abscess/ close fistulae; remove obstructed bowel segments
80
Q

what steroidal drugs are used for crohns and what are used for UC

A

crohns -
systemic steroidal + antiinflammatory 5ASA drugs

UC -
systemic and local (topical rectal) steroidal + antiinflammatory 5ASA drugs

81
Q

Non steroidal drugs for inflammatory bowel disease

A

 NS immunosuppressant
* keeps inflammatory response under control

 anti TNFa therapy
* suppress part of inflammatory process
* biological drugs
* monoclonal antibodies
* moderate to severe disease
* change quality of life

82
Q

be aware of the oral lesions seen in Crohns

A

OFG

The detection of specific oral manifestations often preceded by painless gingival enlargement (diffuse lip and buccal mucosal swelling, oral cobblestoning, buccal sulcus ulceration and mucosal tags)

and/or unspecific or ancillary ones (cheilitis, scaly perioral erythematous rashes and frank intraoral abscess formation, labial and tongue fissuring, glossitis and aphthous stomatitis) is mandatory for the early diagnosis of intestinal Crohn’s disease.

83
Q

crohns vs UC need to know

comparing location, site, serosa, clinical appearance, continuity, rectum involvement, anal fissures, vascularity, carcinoma potential etc

A

** transmural vs mucosa only

** discontinuous vs continuous

** rectum always involved in UC

** crohns non vascular

** UC has carcinoma potential

84
Q

can a colectomy fully cure uc?

A

yes

BDS2 BAMS (27 decks)

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