Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haroon flashcards > GI > Flashcards

GI Flashcards

1
Q

What is Achalasia?

A

Osephageal dysmotility (impaired peristalsis)
-failure of the lower oesophageal sphincter to relax in response to swallowing.
- rate and idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Symptoms of achalasia?

A

-Non progressive dysphagia (struggle swallowing anything)
-Chesty Substernal pain
-Food regurgitation
-Aspiration pneumonia-food or liquid is breathed into the airways or lungs, instead of being swallowed.
-Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Investigations to diagnose Achalasia?

A

Barium swallow with “bird beak” appearance of the distal oesophagus
- manometry (measure pressure across LOS) = diagnostic

endoscopy to exclude malignancy anytime there is dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Complication of Achalasia?

A

May increase risk of oesphageal squamous cell lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment for Achalasia?

A

There is no cure for achalasia, but treatment can help relieve the symptoms and make swallowing easier.

The pharmalogical agents used are either calcium-channel blockers (i.e., nifedipine, verapamil) or nitrates, taken prior to meals.- while awaiting definitive intervention.

endoscope botox to let los relax and lasts months to years

pneumatic dilatation- Air-inflated balloons are used to apply mechanical stretch to the lower oesophageal sphincter to tear its muscle fibres. Best option if surgery good option.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is appendicitis?

A

Acute inflamed appendix, usually due to luminal obstruction
SURGICAL EMERGENCY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Epidemiology and risk factors of appendicitis?

A

10-20yrs old
Male
Frequent antibiotic use
Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of appendicitis?

A

Blockages:
- Faecolith (hard mass of stool)
- foreign body
- lymphoid hyperplasia of Peyer’s patches (teens)
- fibrous strictures

Blockage is typically infected with e.coli and as pressure inside appendix increases, so does rupture risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mechanisms of pain in appendicitis?

A

Peri umbilical pain: inflammation of appendix and visceral peritoneum irritates autonomic nerves of the embrylogical midgut —> referred pain to the umbilical region

Right iliac fossa: due to localised inflammation of the parietal peritoneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Classic triad presentation of appendicitis?

A

1) central abdominal pain that migrates to right iliac fossa
2) low-grade pyrexia
3) anorexia

50% of patients present with this characteristic history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Symptoms of appendicitis?

A

1) periumbilical pain that migrated to the right iliac fossa (McBurney’s point) (rebound or percussion tenderness)
2) low grade fever >38°C
3) reduced appetite and anorexia
4) nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Signs of appendicitis?

A

1) Rosving’s sign (pressing on left Illiac fossa causes right illiac fossa pain to get worse)

2) Psoas sign (pain worsened by lying on left side and extending the right leg)

3) Obturator sign (pain worsened by flexing and internally rotating the hip)

4) elevation of the neutrophil count.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Complications of appendicitis?

A

Perforation (15-20%) - appendiceal rupture
Appendiceal mass
Periappendical abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Investigations to diagnose appendicitis?

A

CT abdominal + pelvis = gold standard
Ab ultrasound
Pregnancy test to rule out ectopic pregnancy ( presents with right iliac fossa pain)

FBC (high neutrophil)
CRP (elevated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment for appendicitis?

A

-Antibiotics and then appendectomy (laproscopic)
-Must drain abcesses - resistant to antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why must abscess be drained in appendicitis?

A

Abscess = walled off bacterial collection
-Resistant to systemic antibiotics so not useful
-Needs to be directly dealt with
- drainage + intra abscess antibiotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is ischemic colitis?

A

Ischemia of colonic arterial supply
- colon gets inflamed due to hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of ischemic colitis?

A

Affecting inferior mesenteric artery;
- thrombosis (+/- atherosclerosis) = most common
- emboli
- decreased CO + arrhythmias (eg history of AF) or due to shock
- combined oral contraceptive pill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Most common sites affected with ischemic colitis?

A

Watershed areas
- splenic flexure (most common)
- sigmoid colon + cecum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Symptoms of ischeamic colitis?

A

LLQ pain + bright bloody stool
+/- signs of hypovolemic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Investigations to diagnose ischemic colitis?

A

Colonoscopy + biopsy = gold standard
(Only after patient is fully recovered, prevents stricture formation + normal healing)
(first rule out other causes- eg. Stool sample for h pylori)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Complications of ischemic colitis?

A
  • perforation
  • tissue death
  • strictures (therefore obstruction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Treatment for ischeamic colitis?

A

If just symptomatic- IV fluids + antibiotics (prophylactic)
If gangrenous (infected colon)- only SURGERY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is mesenteric ischemia?

A

Ischemia of small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Two types of mesenteric ischemia?

A

AMI- acute attack “abdominal MI”
CMI- chronic and over a longer period of months “abdominal angina”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Causes of mesenteric ischemia?

A

Affecting superior mesenteric artery
- Thrombosis (most common)
- Emboli (due to AF often)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Symptoms of mesenteric ischemia?

A

Triad:
1) central/ RIF acute severe abdo pain
2) no abdo signs on exam (eg. Guarding, rebound tenderness)
3) rapid hypovolemic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Investigations to diagnose mesenteric ischemia?

A

CT angiogram
FBC+ABG = persistant metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Complication of mesenteric ischemia?

A

SBP (spontaneous bacterial peritonitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment of mesenteric ischemia?

A

Fluid resuscitation
Antibiotics
IV heparin ( decrease thromboemboli)

—> infarcted bowel is treated by surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are colorectal polyps vs adenomas?

A

Polyps = small growths on the inner lining of the colon => very common
Adenomas = type of polyp that may become cancerous => precursor

  • mostly spontaneous and benign
  • common with age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Risk factors for colorectal polyps and cancer?

A

-Familial inherited genetic predisposition
-Adenomas/ polyps
-Alcohol, smoking, ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

2 inherited conditions that massively increase the risk of polyps

A

1) familial adenomatous polyposis (FAP)
- Auto dom APC gene mutation
- causes 1000s of duodenal polyps
- inevitably will get colorectal cancer (93% risk by 50)

2) hereditary non polyposis colon cancer (HNP C-Lynch syndrome)
- auto dom MSH-1 mutation (or MSH-2) - a DNA mismatch repair gene
-Rapidly increases progression adenomas-> carcinoma
-MSH2 gene mutation is incorrect. This mutation is one of the mutations associated with Lynch syndrome (hereditary non-polyposis colorectal cancer), which predisposes individuals to colorectal cancer and other malignancies. Lynch syndrome typically does not present with the extensive polyposis seen in FAP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Common metastases of colon polyps/adenomas?

A

Liver and Lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Symptoms of colorectal polyps/adenomas?

A

Mostly in distal colon (from sigmoid onwards)
=> LLQ pain, bloody mucosy stools (fresh blood because in the distal colon closer to the anus)
Tenesmus (if rectal involvement) - a frequent urge to go to the bathroom without being able to go. It usually affects your bowels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Investigations to diagnose colorectal polyps/adenomas?

A

FIT test (fecal occult)
- screening for microscopic blood in poop
- done in all 60+ with Fe deficient anaemia and change in bowel habits

Gold standard= colonoscopy and biopsy

Patients with a +ve FIT and suspected colorectal cancer get referred for colonoscopy/biopsy within 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How are colorectal polyps/adenomas classified?

A

TNM system - Tumour, Node, Metastasis. T describes the size of the tumour. N describes whether there are any cancer cells in the lymph nodes. M describes whether the cancer has spread to a different part of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Treatment for colorectal adenomas/polyps cancer?

A

Surgery and chemo is the only curative option if there are no metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are gastric carcinomas?

A

Mostly adenocarcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Grading of gastric carcinomas?

A

T1 = well differentiated = better prognosis (mc)
T2 = undifferentiated “signet ring carcinomas” typically at proximal stomach = worse prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causes of gastric carcinomas

A

H.pylori
Smoking
CDH-1 mutation cashed in gene= 80% risk
Family history
Pernicious anemia (autoimmune chronic gastritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Symptoms of gastric carcinomas?

A

Severe epigastric pain (Same as gastritis, but worse)

Anemia (Fe deffieciency, occult loss)
- weight loss
- Tired all the time
- progressive dysphagia

Metastatic signs:
-jaundice due to liver metastases
-krukenberg tumour due to ovarian metastases from gastric cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Investigations to diagnose gastric carcinomas?

A

Gastroscopy+ biopsy
CT\mri for staging, PET to iD metastases
Staging= TNM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Treatment for gastric carcinomas?

A

Surgery + “ECF” chemo regimen, if resectable

E – epirubicin (eh-pee-roo-bih-sin)

C – cisplatin (sis-pla-tin)

F – fluorouracil (floor-oh-yoor-uh-sil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Two types of esophageal cancer?

A

Adenocarcinoma
Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Adenocarcinoma location and association?

A

Lower 2/3 of oesophagus
Associated with Barrett’s oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Squamous cell carcinoma location and association?

A

Upper 2/3 esophagus
Smoking and alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Symptoms of oesophageal cancers?⏰

A

Presents when advanced
ALARMS
Anemia
Loss of weight
Anorexic
Recent sudden symptom worsening
Melaena/Haematemesis
Swallowing progressive difficulty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Key symptom of esophageal cancer and differential diagnosis?

A

Progressive swallowing difficulty
- first hard to swallow potatoes, now it’s hard to swallow soup
If it’s non progressive it could be achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Investigations to diagnose esophageal cancer

A

OGD (oesophago-gastro-duodenoscopy)
+ biopsy with barium swallow
CT/PET for staging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Treatment for esophageal cancer?

A

Medically fit = chemo/radio + surgery
Unfit = palliative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Chance of small intestine carcinomas?

A

Small intestine is pretty tumour resistant so decreased chance of tumour here
1% of all GI tumours
Most are adenocarcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Risk factors of small intestine carcinomas

A

Chronic SI disease:
-Chron’s
-Coeliac’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Diagnosis and treatment of small intestine carcinoma?

A

Same as gastric carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is Coeliac’s?

A

Systemic autoimmune T4 hypersensitivity to gluten that effects the small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Pathophysiology of Coeliac’s

A

-Pathogenic component of gluten = gliadin
-Once absorbed, it is deamidated by tissue transglutaminase (tTG)
-In coeliacs, deamidated peptides are presented by antigen-presenting cells via HLA DQ2 or DQ8 to T helper cells to trigger immune response.
-Immune activation —> villous atrophy, lymphocyte accumulation and intestinal crypt hyperplasia —> malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Risk factors for Coeliacs

A

Family history
HLA-DQ2.5 / 2 and HLA-DQ8
Autoimmunity (thyroid disorders + addisons)
IgA deficiency
Down’s syndrome
Turner’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Signs and symptoms of coeliacs

A

Indigestion
Diarrhoea or steatorrhoea
Bloating and/or constipation
Weight loss and fatigue
Unexplained iron, vit b12 or folate deficiency
IBS in adults

Dermatitis herpetiformis- vesicular itchy rash that occurs due to IgA deposition along the dermal papillae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Investigations to diagnose coeliacs

A

If possible patients should be on a gluten containing diet for 6 weeks prior to investigations

Screening:
1st line: serological test for IgA antibodies against tTG (anti-tTG)
- total IgA must also be measured as may get false -ve in IgA deficient patients

2nd line: endomysial antibodies (IgA) if anti-tTG is weakly positive

Diagnostic: gold standard
Duodenal biopsy for all patients with positive serology
Findings: crypt hyperplasia, villous atrophy, intraepithelial lymphocyte infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Treatment for coeliacs

A

Gluten-free diet
Avoid : wheat, rye, barley sometimes oats
-Rice, potatoes and corn are gluten free

-Replace vitamins and mineral’s deficiency if needed
-Offer pneumococcal vaccination with boosters every 5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Complications of coeliacs

A

Dermatitis herpetiformis
Malignancy
Increased risk of osteoporosis
Calcium and vit D deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Differential diagnosis with coeliacsand treatment for it?

A

Sprue or tropical sprue (associated with tropical travel) = malabsorption syndrome
-Similar biopsy to coeliacs- crypt hyperplasia and villous atrophy
-Treatment = often antibiotics eg tetracycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Types of diarrhoea?

A
  • watery
  • secretory
  • osmotic
  • functional (IBS)
  • steatorrhoea
  • inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is diarrhoea?

A

A presenting symptom with many differential diagnoses
Classed as 3+ watery stools daily which are level 5-7 on Bristol stool chart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is bloody diarrhoea?

A

Dysentery
Eg. Amoebic dysentery
E.coli + salmonella + shigella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Levels of diarrhoea?

A

Acute < 14 days
Subacute 14-28 days
Chronic > 28 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Causes of diarrhoea?

A

IBD (Crohn’s, UC)
Coeliac disease
Hyperthyroidism
Inflammation or malignancy
Infective causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Infective causes of diarrhoea?

A

Viral = most common
- rotavirus (kids <3y)
- norovirus (adult)

Bacterial:
- campylobacter (most common bacterial cause)
- c. Diff
- salmonella
- shigella
- cholera
- E.coli

Worms

Parasites- Giardiasis (most common parasite cause)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Antibiotics as a cause of diarrhoea?

A

They increase the risk of C. Diff infection

4C’s - clindamycin, co-amoxiclav, ciprofloxacin, cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Treatment of diarrhoea?

A

Depends on underlying cause
Viral (mc) = self limiting

Fluids and dioralyte to rehydrate patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Complications of diarrhoea?

A

Dehydration
Electrolyte loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is diverticular disease?

A

-Outpouching of colonic mucosa
-Most frequently affects the sigmoid due to its small diameter
-due to increased intra-colonic pressure at naturally weaker parts of the colon, where penetrating arteries enter wall of the colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Define diverticulum

A

An outpouching at perforating artery sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Define diverticulosis

A

An asymptomatic outpouching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Define diverticular disease?

A

A symptomatic outpouching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Define diverticulitis

A

Inflammation of outpouching - infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What percentage of diverticula are asymptomatic?

A

95% and only 5% are symptomatic (diverticular disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is Meckel’s diverticulum?

A

Paediatric disorder
-Failure if obliteration of vitelline duct
-Rule of 2s:
2 years old
2 inches long
2ft from ileocaecal valve (umbilical)

Diagnostic= technetium scam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Risk factors for diverticular disease?

A

Connective tissue disorders (ED + M)
Ageing
Increased colon pressure
COPD + chronic cough
Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Complications of diverticulitis?

A

SBP- Spontaneous Bacterial Peritonitis
Obstruction
Fistulae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Symptoms of diverticulitis?

A

1) Left lower quadrant pain
2) constipation
3) fresh rectal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Investigations to diagnose diverticulitis?

A

CT abdominal/ pelvis with contrast = gold standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Treatment for diverticulosis?

A

Nothing, watch and wait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Treatment for diverticular disease

A

Bulk forming laxatives “isphagula husk”
Surgery is gold standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Treatment for diverticulitis

A

Antibiotics (Co amoxiclav)
Paracetamol
IV Fluid + liquid food
Rarely surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is dyspepsia?

A

Not a disease
A presenting symptom of “indigestion”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Signs of dyspepsia?

A

-early satiation
-epigastric pain + reflux (GORD like pain)
-extreme fullness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Cause of dyspepsia?

A

Often unknown
(“Functional disorder”)
Maybe related to ulcers (especially gastric)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Diagnosis of dyspepsia?

A

Need endoscopy to find underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is gastritis?

A

Mucosal inflammation and injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Causes of gastritis

A

Autoimmune (related to pernicious anaemia + anti intrinsic factor antibodies)
H. Pylori
NSAIDs (causes gastropathy- injury without inflammation)
Mucosal ischaemia
Campylobacter (GBS)

+ viral (CMV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Symptoms of gastritis?

A

Epigastric pain with diarrhoea
Nausea and vomiting
Indigestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is PUD (Peptic ulcer disease) a complication of?

A

Gastritis
Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Investigations to diagnose gastritis?

A

If H.pylori suspected:
- stool antigen test/ urea breath test
Gold standard= endoscopy + biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Treatment for gastritis/h. pylori?

A

H. Pylori = triple therapy CAP
Clarithromycin
Amoxicillin
PPI

96
Q

Pathophysiology of H.Pylori?

A

Commences in stomach- not usually diarrhoea causing
- Decreased virulence and is typically opportunistic
1) decreases stomatostatin
2) decreases luminal HCO3
3) secretes urease
4) inscreases gastrin release

Urea —urease—> CO2 + NH3
NH3 + N+ —reversible—> NH4+ (toxic)

97
Q

What is autoimmune gastritis?

A

Affects fundal portion of the stomach
Especially causes atrophy of parietal cells

98
Q

What kindof bacteria is C.difficile?

A

Gram +ve spore forming bacteria

99
Q

What is C.difficile mainly induced by?

A

Ciprofloxacin
Co-amoxiclav
Cephalosporins
Clindamycin
4 Cs

100
Q

What does C. difficile cause and how?

A

Pseudomembranous colitis
- normal GIT flora killed by antibiotics and C.diff replaces these
- results in dangerous severe diarrhoea ( very watery so increased dehydration) and is highly infectious

101
Q

Treatment for C.difficile?

A

Stop using these 4 antibiotics ( ciprofloxacin, Co-amoxiclav, cephalosporins, clindamycin)

=> give Vancomycin (now first line according to nice)

102
Q

What is E.Coli?

A

Major player in UTIs also
Gram -ve bacterialbacilli
Often commensal flora of GIT
Some strains/ “serotypes” are very virulent

103
Q

Strains of E.coli that lead to watery diarrhoea?

A

ETEC
EAEC
EPEC

104
Q

Strains of E.coli that lead to bloody diarrhoea?

A

EHEC

105
Q

Cause of haemolytic uremic syndrome?

A

Serotype 0157:H7 of E.coli
Leads to haemorrhagic diarrhoea
Nephrotic syndrome

106
Q

Treatment of E.coli?

A

Often amoxicillin, trimethoprim, nitrofurantoin

107
Q

What is H.pylori?

A

Gram -ve bacteriabacillus
Has a decreased virulence in the GIT

108
Q

Pathology of H.pylori?

A

1) causes decreased stomatostatin
2) increased luminal gastric acid (as more gastrin)
3) urease results in ammonia generation
4) therefore decreased HCO3- secretion

109
Q

Complications of h.pylori?

A

-PUD- Peptic ulcer disease
-gastritis
-gastric carcinomas

110
Q

Investigations to diagnose H.Pylori?

A

Biopsy
(Stool antigen + C-urea breath test often 1st line)

111
Q

Treatment for H.pylori?

A

Triple therapy:
Clarythromycin + amoxicillin + PPI

112
Q

What is GORD

A

Gastric-oesophageal reflux disease = reflux of gastric contents into oesophagus due to decreased pressure across lower oesophageal sphincter

113
Q

Causes of GORD

A
  • raised intragastric pressure= obesity + pregnancy
  • hiatal hernia (mostly with LOS sliding up through diaphragm)
  • Drugs anti-muscarinics, CCBs
  • Scleroderma (LOS = scarred)
114
Q

Symptoms of GORD

A

“Heartburn”
-Retrosternal burning chest pain that is exacerbated by lying flat
-Sour/bitter taste of acid in the back of the mouth
-dysphagia
-nausea
-chronic cough

115
Q

Investigations to diagnose GORD

A

If no red flags go straight to treatment (PPI)

Red flags (dysphagia, haematemesis, weight loss)
- endoscopy —> esophagitis or Barrett’s
- esophageal manometry —> measure functionality of LOS and gastric acid pH

116
Q

Treatment for GORD

A

-Conservative lifestyle changes (smaller meals, 3+hrs before bed, avoidance of trigger foods)

-medication review: consider reducing or stoppping medications that are causing symptoms eg CCB

-PPI offer full dose for 1-2 months
If symptoms persists use PPI at lowest dose possible as maintenance

If symptoms still persist or CI then use H2RA

117
Q

Last resort for GORD treatment?

A

Surgical treatment- laparoscopic fundoplication = mobilisation of fundus of stomach which is then wrapped around the lower oesophageal sphincter to tighten it

118
Q

Complications of GORD

A

-Barrett’s oesophagus
-oesophageal stricture - fibrous scarring and therefore narrowing of oesophageal lumen
-dental problems

119
Q

Barrett’s oesophagus

A

-10-15% develop Barrett’s
-Always involves hiatal hernia
-Metaplasia (SSNKE —>simple columnar)
-Increased risk of adenocarcinoma
-Diagnose with a Biopsy

Pathway for oesphagus changes:
Normal—> metaplasia (Barrett’s) —> dysplasia (adenocarcinoma)

120
Q

What is IBS?

A

Chronic, relapsing and often lifelong disorder that affects lower GI tract
- no discernible structure or biochemical cause => considered ‘functional’

121
Q

Cause of IBS

A

Multi factorial
Genetics + environmental + psychological (stress, anxiety) + dietary
Exact mechanism unknown

122
Q

Categorisation of IBS

A

IBS-C —> mostly constipation
IBS-D —> mostly diarrhoea
IBS-M —> mostly mixed; alternating C/D

123
Q

Risk factors of IBS

A

Young adults
Females
Family history
Dietary factors
Psychosocial cavities
Drugs

124
Q

Symptoms of IBS

A

-Abdominal pain and bloating relieved from defecation
-Altered stool form/frequency

125
Q

Diagnosis to exclude before diagnosing IBS

A

Coeliacs (serology)
IBD (check fecal calprotectin)
Infections (ESR/CRP/Blood cultures)

126
Q

Investigations to diagnose IBS

A

IBS is a diagnosis of exclusion so no specific investigation to confirm diagnosis

May use following to exclude other conditions:
- FBC
- ESR/CRP
- coeliac serology

127
Q

Treatment for IBS

A

1st line: conservative patient education, dietary advice and patient reassurance, address any cormorbid stress or anxiety
For IBS-C consider more fibre and for IBS-D consider probiotics

2nd line:
IBS-C —> laxatives (senna/Fybogel)
IBS-D —> antimotility drug (loperamide)

3rd line:
For severe abdominal pain consider low-dose trycyclic antidepressant (TCA eg amitriptyline)
- consider CBT for psychological support
- refer to gastroenterologist

128
Q

Complications of IBS

A

Mood disorders: more severe and frequent depression and anxiety
Poor quality of life: miss three times as many days off work

129
Q

What does inflammatory bowel disease comprise of? (IBD)

A

Ulcerative colitis
Crohn’s disease

130
Q

Pathophysiology of IBD?

A

Inflamed intestines
Associated with HLAB27 (Seronegative spondyloarthropathy)
Has a Bimodal age distribution (15-20, 55+)

131
Q

Extraintestinal manifestations of both Crohn’s and Ulcerative Colitis

A

Eyes:
Episcleritis = chrons>
Uveitis = UC>

Cutaneous:
Erythema nodosum
Pyoderma gangrenosum

Musculoskeletal:
Arthritis (most common manifestation in both)
Spondylarthritis “spine ache”
Osteoporosis
Clubbing

Also 90% of UC patients have PSC but also sometimes present in patients with Chron’s

Primary sclerosing cholangitis (PSC) is a chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and are eventually narrowed or blocked. When the bile ducts are narrowed or blocked, bile builds up in the liver and causes further liver damage.

132
Q

How to differentiate UC from Crohn’s particularly in the pediatric population?

A

Serum antibody markers:
- pANCA more associated with UC
- ASCA more associated with Crohn’s

133
Q

How to differentiate IBD from IBS?

A

Faecal calprotectin
Raised in IBD and not IBS

134
Q

Cause of Crohn’s disease?

A

Environmental and genetic
- CARD15/NOD2 mutation => strong genetic component
- bacteria trigger an immune mediated response (t-cells)

135
Q

What part of the gut does Crohn’s disease affect?

A

Whole gut
Especially terminal ileum and proximal colon (usually rectum is spared)
Throat to anus

136
Q

Risk factors for Crohn’s

A

Family history
Jewish
HLA-B27 gene
Smoking (2x as likely)
Caucasian

137
Q

Pathophysiology of Crohn’s

A

-Characterised by skip lesions (lesions with gaps in between) arising anywhere between the mouth and the anus
-End result is transmural inflammation (in all layers) with granuloma formation
=> resulting in fistulas, strictures and adhesions

138
Q

Signs and symptoms of Crohn’s disease?

A

-Diarrhoea- most significant symptom in adults
-Abdominal pain- most significant symptom in kids
-Gallstones and kidney stones
-Weight loss and lethargy
-B12/folate/ Fe deficiency due to malabsorption in small intestine
-Apthous mouth ulcers

139
Q

Investigations to diagnose Crohn’s

A

-Feacal calprotectein = raised (inflammation in GI tract + differentiates IBD from IBS)
-FBC
-CRP/ESR
-U&Es
-Colonoscopy = skip lesions, cobblestone mucosa, deep ulcers
-Biopsy = transmural inflammation, granulomas and goblet cells

140
Q

General management tips for Crohn’s

A

-Smoking cessation advice = crucial
-Some evidence that NSAIDs and/or combined oral contraceptive pill can increase risk of relapse

141
Q

Treatment given to induce remission in mild and moderate Crohn’s

A

Elemental diet (alone or with meds, particularly in young people)

Mild Crohn’s:
FIRST LINE : glucocorticoids (PO predinsolone or IV hydrocortisone)
SECOND LINE: aminosalicylate (eg mesalazine)

Moderate Crohn’s:
Add in:
FIRST LINE: azathioprine or mercaptopurine
SECOND LINE: Methotrexate

142
Q

Treatment for severe Crohn’s to induce remission that is unresponsive to conventional therapy

A

Infliximab or adalimumab as monotherapy or combined with other immunosuppressant

143
Q

Treatment for Crohn’s if it is refractory to medical therapy or disease limited to the distal ileum to induce remission

A

Surgery

144
Q

How to classify severity of Crohn’s

A

Mild:
- first prevention or
- 1 exacerbation in 12 months

Moderate:
- >= exacerbations in 12 months or
- glucocorticoid cannot be tapered for management of mild disease

Severe:
- unresponsive to conventional therapy AND
- >= symptoms eg weight loss, fever, severe abdominal pains
- usually >3 loose stools per day

145
Q

How to maintain remission in Crohn’s

A

1st line: azathioprine or metcaptopurine
2nd line: Methotrexate
Post surgery: consider azathioprine with or without methotrexate

146
Q

Frequency of surgery in Crohns patients?

A

Approx 80% of patients with Crohn’s will require surgery but this is not curative as entire bowel can be affected. By removing ‘x’, ‘y’ can flare up.

147
Q

Complications of Crohn’s

A

Peri-anal abscess
Anal fissure
Anal fistula
Strictures and obstruction

148
Q

Location of ulcerative colitis

A

COLON ONLY
start at rectum—> sigmoid colon—> proximal colon
Never proximally beyond illeocaecal valve
Doesn’t affect the anus

149
Q

Aetiology of ulcerative colitis

A

Not well understood
Autoimmune colitis associated with HLA B27 gene
Involves polygenic predisposition and env factors

150
Q

Risk factors for ulcerative colitis

A

Family history
HLA b27
Caucasian
Non-smokers
Bimodal age distribution 15-25 and 55-70yrs

151
Q

Symptoms of ulcerative colitis

A

-Abdominal pain in left lower quadrant
-Urgency and tenesmus (pain on defecation)
-Bloody mucosy watery diarrhoea

152
Q

Investigations to diagnose ulcerative colitis

A

-Increase in feacal calprotectin
-pANCA +ve
-FBCs
-CSR\ESR

  • colonoscopy = continuous, “leadpipe sign”
  • biopsy = raw/red mucosal with widespread shallow ulceration with crypt abscesses and goblet cell depletion
153
Q

How is disease activity measured in ulcerative colitis patients?

A

Truelove and Witt’s severity index

-how many bowel movements, blood?, HR, pyrexial?, anaemic?, esr?

154
Q

Treatment for ulcerative colitis to induce remission

A

Generally:
First line: topical ASAs -acetylsalicylic acid
Second line: Add high-dose oral ASA
Third line: Add topical or oral corticosteroid

For acute severe colitis admit into hospital and start iV corticosteroids
Add ciclosprin if no improvement in 72hr
Still no improvement consider surgery

155
Q

Treatment for maintenance of remission of ulcerative colitis

A

Low maintenance dose of ASA-aspirin

156
Q

Surgery with ulcerative colitis?

A

Total/partial colectomy is often curative

157
Q

Complications of ulcerative colitis

A

Toxic megacolon is the most common complication cause ulcerative colitis deaths

158
Q

Investigations to diagnose both types of intestinal obstruction?

A

1st line- X-Ray = shouldn’t be used however might be your exam answer according to lecturer but he is trying to get exam boards to change it💀💀

Gold standard = CT abdomen and pelvis with contrast, and is now often used as initial imaging modality where possible
- can idenitify dilated bowel loops, evidence of ischaemia and perforation as well as underlying cause

159
Q

What is a pseudo obstruction?

A

No mechanical obstruction, often a result of post operative state
-still have symptoms of intestinal obstruction

160
Q

Treatment for intestinal obstruction?

A

pain: analgesia
assess food balance: nasogastric tube, urinary catheter
resuscitate: iv fluids
alleviate nausea: nasogastric tube, select antiemetics
nutrition: if > 5 days without intake, may need parenteral feed

Most patients are two days without food before admission

161
Q

Two types of intestinal obstruction?

A

Small Bowel
Large Bowel

162
Q

Causes of intraluminal obstruction?

A

-tumour
- carcinoma
- lymphoma
- diaphragm disease (becoming more common due to NSAIDs)
- meconium Ileus - a baby’s first stool (feces), called meconium, is blocking the last part of the baby’s small intestine
- gallstone disease

163
Q

Causes of intramural obstruction?

A
  • inflammatory
    • Chron’s disease
    • diverticulitis
  • tumours
  • neural
    • Hirschsprung’s disease
164
Q

Causes of extraluminal obstruction?

A
  • adhesions
  • volvulus
  • tumour
    • peritoneal deposits
165
Q

Percentage of intestinal obstruction cases that involve large bowel?

A

25-40% of all cases

166
Q

Causes of large bowel obstruction?

A

Malignancy (90%)
Volvulus- mostly sigmoid colon, children
Intussusception (bowel telescopes in on itself -> most common in children)

167
Q

Symptoms of large bowel obstruction?

A

First constipation
Then vomiting
Gross distension + pain
Hyperactive, then normal, then absent bowel sounds

168
Q

Percentage of intestinal obstruction that is small bowel?

A

60-75% of all cases

169
Q

Causes of small bowel obstruction?

A

Adhesions (most common) 50%
Hernias 15%
Cancer 10%
Crohn’s

170
Q

Symptoms of intestinal obstruction?

A

Vomiting then constipations
Mild abdominal distension + pain
Tinkeling bowel sounds (*hyperresonant bowels on percussion in both types of intestinal obstruction)

171
Q

What is small bowel obstruction?

A

A form of intestinal failure causing malabsorption requiring iV supplementation or replacement

172
Q

Presenting history of small bowel obstruction?

A

-Pain in umbilical region that comes in waves = colic
-Bilious vomiting (dark green)
- bloating/ distension
- when did they last eat and drink?

173
Q

What to assess in a patient with potential small bowel obstruction?

A
  • hydration status
  • weight loss
  • pulse/bp
  • O2 stats
  • scars
  • abdominal distension
  • abdominal tenderness
  • Hernia orifices
  • PR exam
174
Q

Investigations to diagnose small bowel obstruction?

A

Full blood count
Urea and electrolytes
Lactate
C-reactive protein

CT SCAN = 🔑 NOT X RAY

175
Q

Why use a CT scan for suspected small bowel obstruction?

A

3D representation of problem
Localises site of obstruction
Indicates cause
Tells you if bowel is ischaemic:
- poor enhancement
- free fluid
- twisted mesentery

176
Q

How to treat patients with Small bowel obstruction due to adhesions?

A

Gastrograffin Challenge = administer soluble contrast and do x-ray to assess if operation needed

ischaemia/shock= resuscitate and operate

non operative management for up to 3 days

gastrografin challenge

176
Q

How to treat small bowel obstruction due to hernia?

A

Groin or umbilical - operate (almost always groin- ie. femoral)
High risk patient- Taxis (local anaesthesia and push back in)
High BMI- conservative measures
Incisional hernia- treat as adhesive SBO

177
Q

Types of operation given for small bowel obstruction?

A

-Key hole or open
-divide scar tissue
-risk of future scar formation
-minimally invasive surgery can help

178
Q

Most common complication of small bowel obstruction?

A

Renal failure

179
Q

When would you advise surgery in adhesive SBO?

A

Signs of ischemia on a CT scan

180
Q

Differential diagnosis for MWT?

A

Boerhaave’s syndrome
-spontaneous perforation of the oesophagus
-usually due to vomiting
-ruptures all the layers of the oesophageal wall (transmural)
-unlike MWT it’s a surgical emergency

181
Q

Risk factors of a Mallory Weiss Tear?

A

-Any condition that predisposes to retching or vomiting: gastroenteritis, bulimia, hyperemesis
- Alcoholism
- chronic cough
- hiatus hernia
- GORD
- Male
- age 40-60

182
Q

What if a patient has haematemesis and pulmonary hypertension?

A

oesophageal varices rupture

183
Q

Symptoms of MWT

A

Background of alcohol excess presenting with episodes of violent retching or vomiting
- Haematemesis
(Usually small to moderate volume of bright red blood which is self limiting)
- hypotensive in severe cases but unlikely

184
Q

Investigations to diagnose MWT

A

Upper GI endoscopy (gold standard) required for all patients depending on the Glasgow Blatchford score
- usuallay shows a single longitudinal tear (can be multiple) in the mucosa at the gastro-oesophageal junction

185
Q

Scoring system for upper GI bleeds

A

Glasgow Blatchford Score
Score >0 means patient require admission for inpatient endoscopy
Score 0 means patient can be discharged

Most accurate in identifying risk patients in need of transfusion

186
Q

What is the Rockall score?

A

Calculated after endoscopy to identify patients at risk of adverse outcomes after treatment for an upper GI bleed

187
Q

Treatment for MWT

A

Most spontaneously heal within 24h!

188
Q

What is Mallory Weiss Tear?

A

Linear lower oesophageal mucosal tear due to sudden increase in intra-abdominal pressure at the border of the gastro-oesophageal junction

Limited to mucosa and submucosa

189
Q

Typical presentation of Mallory-Weiss Tear?

A

Presents typically as a young male with acute history of retching and vomiting after a night out eventually causing haematemesis

Causes a laceration resulting in an upper GI bleed that is usually self-limiting.

190
Q

Location of Duodenal ulcers?

A

-Mostly at D1 and sometimes D2
-The gastroduodenal artery is located at the posteromedial aspect of D2 so deeply penetrating ulcers in this region can result in a torrential upper GI bleed

191
Q

Causes of duodenal ulcers

A

H. Pylori (causes 95% of duodenal ulcers)
NSAIDS
ZE Syndrome

192
Q

Symptoms of duodenal ulcers

A

Epigastric pain
- worse between meals
- better with food
* typically weight gain

193
Q

Investigations to diagnose duodenal ulcers

A

If no red flags:
- non-invasive testing
1. Urea breath test
2. Stool antigen test
If red flags:
Urgent endoscopy + biopsy
(Will see Brunner’s gland hypertrophy- more mucous production)

194
Q

What do you have to make sure of before testing for H.pylori?

A

If testing for h.pylori, patient must be off PPI for 2 weeks+ (all ulcers)
- otherwise you can get a false -ve

195
Q

Treatment for both gastric and peptic ulcers?

A

Stop NSAIDs
1) H.pylori +ve -> triple therapy
CAP
Clarythromycin
Amoxicillin
PPI (omeprazole)
(If they have a penicillin allergy replace amoxicillin with metronidazole)

2) H.Pylori -ve give PPI at initial high dose for a month until ulcer healed

Ensure all patients who have a proven ulcer have a repeat endoscopy 6-8 weeks later to confirm healing as well as h.pylori retesting

196
Q

What type of peptic ulcer is more common?

A

Gastric>Duodenal
Gastric is 2/3x more common

197
Q

What are peptic ulcer diseases?

A

Punched out round holes in either stomach or stomach or duodenum

198
Q

Where do gastric ulcers occur

A

Mostly at a lesser curve

199
Q

Causes of gastric ulcers

A

-H.pylori (causes of 75% of gastric ulcers)
-NSAIDs
-Zolinger Ellison syndrome:
- pancreatic tumour
- gastric acid hypersecretion
- widespread peptic ulcers

200
Q

Symptoms of gastric ulcers

A

Epigastric pain
- worse on eating
- better between meals + with antacids
* typically weight loss

201
Q

Investigations to diagnose gastric ulcers

A

If no red flags (55+, haematemesis/melaena, anaemia, dysphasia)
- non invasive tests:
c-urea breath test
Stool antigen test

If red flags
- urgent endoscopy + biopsy

202
Q

Complications of peptic ulcer disease

A

-Bleeding

-Perforation: life threatening as ulcer penetrates the duodenum or stomach into the peritoneal cavity; requires surgical intervention

-Gastric outlet obstruction: caused by obstruction at pylorus due to an ulcer and subsequently scarring. Presents with vomiting and nausea after food

203
Q

What is an anal fissure?

A

Tear in anal skin lining below dentate line
=> very painful due to strong sensory supply

204
Q

Most common causes of anal fissure?

A

Hard feaces

205
Q

Other less common causes of anal fissures?

A

Trauma (eg childbirth)
Crohn’s
UC

206
Q

Symptoms of anal fissures?

A

-Extreme defecation pain
-very itchy bum (pruritus ani)
-anal bleeding

207
Q

Treatment for anal fissures?

A

Stool softening (increase fibre intake + more fluids)
Topical creams (lidocaine ointment)
Definitive treatment=surgery (not usually done)

208
Q

What is an anal fistula?

A

Abnormal “tracks” form between inside of anus —> elsewhere
Eg subcutaneous skin (mostly)

209
Q

What does an anal fistula typically progress from?

A

= Perianal abscesses
- abscess discharges (toxic substances) which aid fistula formation as abscess grows

(Also Crohn’s and rectal cancer)

210
Q

Symptoms of anal fistulas?

A

Bloody/ mucosy discharge
Often very viable and painful

211
Q

Treatment for anal fistula?

A

Surgical removal + drainage (with antibiotics if infected)

212
Q

What are haemorrhoids?

A

Swollen veins around anus disrupt anal cushions
- parts of the anal cushions prolapse through tight anal passage
(Google pics at ur own discretion 🤮)

213
Q

Most common cause of haemorrhoids?

A
  • Constipation with increase straining
  • also anal sex
214
Q

2 types of haemorrhoids?

A

1) internal
- originate above internal rectal plexus (dentate line)
- less painful as has decreased sensory supply
- may feel “incomplete emptying”

2) external haemrrhoids
- originate below dentate line
- so painful patients can’t sit down!

215
Q

Symptom of haemorrhoids?

A

-Bright red flesh PR bleeding and mucosy bloody stool
-bulging pain
+/- pruritas ani (itchy bum)

216
Q

Investigations to diagnose haemorrhoids?

A

External haemorrhoids = PR exam (digital) - may be visible though
Internal haemorrhoids = proctoscopy

217
Q

Treatment for haemorrhoids?

A

Stool softener
Definitive= rubber band ligation

218
Q

What is a perianal abscess?

A

Walled off collections of stool + bacteria around anus

219
Q

Most common cause of perianal abscess?

A

Anal sex causing anal gland infection

220
Q

Symptoms of perianal abscess?

A

Pus in stool + constant pain (tender)

221
Q

Treatment for perianal abscess?

A

Surgical removal + drainage if walled off and resistant to oral antibiotic therapy

222
Q

In which people are pilonidal sinus and abscess commonly seen in?

A

In very hairy people (eg Asians)

223
Q

Symptoms of pilondial sinus and abscesses?

A

Swollen pus filled smelly abscess on bum crack
(Visible on exam)

224
Q

Treatment for pilondial sinus / abscess?

A

Surgery + hygiene advice

225
Q

What’s Meleana?

A

Blood in the stool that appears black

226
Q

Likely causes of GI bleeding?

A

Peptic ulcer= most common (50%)
Osephageal varices
Mallory-Weiss syndrome
Gastric carcinoma (uncommon)

227
Q

How to manage patients with GI bleeds?

A

A
B
C - iv fluids, blood transfusion?
D - AVPU, GCS, pupils, blood sugar
E - active, melaena, haematemesis

keep patient nil by mouth

228
Q

How to differentiate between variceal and non-variceal bleed?

A

Variceal bleed=
Suspect in patients with a history of liver - disease or alcohol excess.
Antibiotics and Terlipressin reduce mortality.
Endoscopy within 12 hours.

Non-variceal bleed
Suspect in patients with a history of peptic ulcers, using certain medications;
NSAIDs, anticoagulation or antiplatelets.
Consider proton pump inhibitors.
Endoscopy within 24 hours.

229
Q

What is most important when it comes to GI bleeding?

A

Initial assessment and management rather than endoscopy in most cases

230
Q

In the UK how often do you see upper GI bleeding?

A

Nearly one presentation every 6 minutes
= very common medical emergency

231
Q

What is Zenker’s diverticulum?

A

A pharyngeal pouch when some food goes down the pouch instead of totally down oesphagus

232
Q

Symptoms of Zenker’s diverticulum?

A

Smelly breath (food is accumulating in oesphagus)
Regurgitation and aspiration of food

233
Q

What are pilondial sinus/abscesses caused by?

A

Hair follicles that get stuck in natal cleft (bum crack)
Which :
1) forms small tracts (sinus)
2) get infected (abscesses)

234
Q

What is SIBO?

A

Small intestinal bacterial overgrowth syndrome (SIBO) can often present with similar symptoms to IBS (bloating, abdominal pain, diarrhoea or constipation). However, bloating is often strongly related to the time of day (occurring at night time due to chronic build-up of gas). Patients with SIBO often report having nausea and gastro-oesophageal reflux. As the vignette doesn’t provide any of these additional symptoms, it is more likely for the patient to be suffering from IBS than SIBO.

235
Q

Food allergies presentation

A

Food allergies can present in a range of ways - from abdominal bloating and change in bowel habits to anaphylaxis (with oedema, rash, and airway impairment). This patient reports a mild improvement in symptoms when avoiding nightshades, however, there are still symptoms present. This should reassure the student that this is unlikely to be the correct answer.

236
Q

Zollinger-Ellison syndrome

A

Zollinger-Ellison syndrome is a syndrome of excessive gastrin secretion from a gastrin secreting tumour of the pancreas or duodenum, and may be associated with MEN 1. A diagnosis is made with elevated serum gastrin at least 10 times the upper limit of normal, a reduced gastric pH, and a secretin stimulation test if those criteria are not met.

Haroon flashcards (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions