GI DJ Flashcards

1
Q

Where is Mucous cell found and it’s function?

A

Fundus. Produce protective mucous layer.

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2
Q

Where is ECL cell found and it’s function?

A

Fundus.

1) Produce histamine that stimulates parietal cells.

2) Histamine binds to H2 receptors on parietal cells, releases HCL.

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3
Q

Where is Parietal cells found and it’s function?

A

Fundus.

1) Produce HCL and intrinsic factor.

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4
Q

Where is Chief of cells found and it’s function?

A

Stomach

1) Secrete pepsinogen (zymogen) –
2) Stimulates lipolysis.

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5
Q

Where are D cells found, and it’s function?

A

Pylorus.

1) Produce somatostatin -> inhibits HCL/Histamine production.

2) Regulates the secretion of insulin and glucagon from the pancreas, helping to maintain stable blood sugar levels.

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6
Q

Where are G cells found, and it’s function? 1/2

A

Pylorus.

Secrete Gastrin

1) Binds to Parietal cells.

2) Enhances motility -> HCL production.

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7
Q

Where are I cells found, and it’s function?

A

Duodenum.

1) Secrete CCK - secretion of pancreatic enzymes: CCK lipase, proteases, and amylase

2) Contracts the gallbladder: releasing bile into the small intestine to help in the digestion and absorption of fats.

3) Inhibits gastric emptying: CCK slows down gastric emptying, which allows for a more gradual release of food into the small intestine and facilitates better digestion and absorption.

4) Reduces food intake: CCK acts as a satiety hormone

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8
Q

Where are M cells found, and it’s function?

A

Duodenum. Secrete motolin -> stimulates peristalsis and bile / pancreas secretion.

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9
Q

Where are S cells found, and it’s function?

A

duodenum

1) Releases secretin -> decrease HCL

and

2) promotes bicarbonate secretion from pancreas and bile.

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10
Q

Where are K cells found, and it’s function?

A

Duodenum.

1) Produce glucose-dependent insulinotropic peptide (GIP).

2) GIP –>releases insulin from Pancreas , which helps to lower blood glucose levels.

3) Decrease gastric emptying.

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11
Q

Where are Enteroendocrine cells found, and it’s function?

A

Duodenum.

1) Produce glucose-dependent insulinotropic peptide (GIP).

2) GIP –>releases insulin from Pancreas , which helps to lower blood glucose levels.

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12
Q

Where are Acinar cells found, and it’s function?

A

1)Pancreas (Exo).

2) Secrete digestive enzymes (salivary ducts/ pancreas)

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13
Q

Where are L cells found, and it’s function?

A

Iluem

1) GLP-1 plays a role in glucose homeostasis by stimulating insulin secretion from the pancreas, suppressing glucagon secretion, and delaying gastric emptying.

2) PYY acts as an appetite suppressant and regulates energy homeostasis by reducing food intake, and reducing fat storage. It also inhibits gastric motility and gastric acid secretion.

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14
Q

Where are GR cells found, and it’s function?

A

GR cells secrete Grehlin to make you hungry. Found in stomach.

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15
Q

Where are Delta cells found, and it’s function?

A

Islets of Langerhans.

Secrete the hormone somatostatin, inhibits insulin, glucagon, and gastrin.

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16
Q

Where are Duct cells found, and it’s function?

A
  1. Pancreas.
  2. Secrete bicarbonate-rich fluid.

Bicarb neutralizes chyme that enters duodenum so there is an optimal pH for the activation of digestive enzymes.

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17
Q

Flow of bile

A

Gall bladder-> Cystic duct -> common bile duct -> ampulla of vater -> duodenum

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18
Q

Where are Kupffer cells found and function?

A

Liver. Phagocytosis.

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19
Q

Where are Payer patches found and function?

A

Ileum. Immune system, protect against infections a (release IgA).

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20
Q

Flow of bile

A

Cystic duct -> common bile duct -> ampulla of vater ->S.o.O> duodenum

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21
Q

Liver function (5 points)

A

1.Bile production
2. Storage - glycogen
3. Detoxification
4. Nutrient synthesis - albumin and clotting factors
5. Phagocytosis - Kupffer cells

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22
Q

where is bile synthesized and by who

A

in the liver by hepatocytes and consists of bile salts, cholesterol, phospholipids, and bilirubin

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23
Q

stercobilin

A

gives poo dark colour

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24
Q

peyer’s patches (ileocaecal valve), which immunogoblin?

A

B cells which release IgA

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25
Gastrocolic reflex
presence of food, contractions of the colon and an urge to defecate, mediated by the parasympathetic nervous system. rest and digest baby
26
difficulty in swallowing both liquids and solids
motility condition
27
difficulty was initially with swallowing solids, and then started to occur also when having liquid;
mechanical obstruction.
28
Oesophageal Varices cause
Cause: Due to portal hypertension
29
Oesophageal Varices Management
Endoscopic variceal band ligation 1st line Terlipressin (vasocactive) Sengtaken- Blakemore TIPSS
30
Mallory-Weiss tear
Tear of the tissue of the lower oesophagus
31
Mallory-Weiss tear who gets it
big boozers
32
Mallory-Weiss Diagnosis:
Upper GI endoscopy
33
GORD, why it happens
incompetent LOS/ Barrett's oesophagus
34
Investigations GORD
Investigations: 1st line endoscopy, barium swallow, oesophageal manometry, 24 hr pH monitoring
35
GORD management
Proton pump inhibitor – 1st line H2-receptor antagonists – 2nd line
36
Barrett's oesophagus cell change
Squamous to Columnar
37
achalasia
relaxation issue of the lower oesophageal sphincter
38
Achalasia, degenerative loss of ganglia from
Auerbach's plexus
39
Investigations Achalia :
Oesophageal manometry (confirms) , on barium swallow (bird beak appearance)
40
Oesophageal cancer, upper and lower
Squamous cell carcinoma (upper/middle) ~ 90% Adenocarcinoma (lower)
41
Gastric Cancer 2 things
h. pylori, Signet ring cells
42
Gastric Cancer risk factors
'A' blood type, smoking
43
Gastroparesis
Delayed gastric emptying (NOT DUE TO OBSTRUCTION)
44
Cause Gastroparesis,
1. Idiopathic 2. diabetes mellitus, medications e.g. opiates anticholinergics
45
features Gastroparesis TOOTHLESS AGRESSION BENWA
Clinical features: Bloating Early satiety Nausea Weight Loss Abdominal Pain
46
Investigation:Gastroparesis
Investigation: Oesophageal Manometry
47
ALP
biliary damage
48
ALT
ALT hepatocyte damage
49
GGT
GGT general damage
50
Cholestatic tiny keyboard
ALP and GGT raised more than ALT
51
Hepatic, worlds greatest, keyboard
ALT > ALP and GGT.
52
Hep A, E
faecal-oral
53
Hep B, who gets in
BBV and sexually transmitted: GAYS, PWID, children of infected women.
54
who is likely: Hep C
BBV: PWID, transfusions, tattoo in developing world.
55
Anti-HBs (surface antibody) -
clearance of infection OR immunity in vaccinated.
56
Anti-HBc (core antibody) -
had caught, unclear if bug cleared.
57
Hepatitis A, which immunogoblin?
Clotted blood for HAV IgM confirms diagnosis
58
Hepatitis C, which immunogoblin? what test
IgG , PCR
59
Hepatitis E, which immunogoblin?
Blood for HEV IgM
60
HBsAg
evidence of active infection.
61
Hep C treatment
DAA's- 1.Protease inhibitors, 2. NS5 inhibitors 3. polymerase inhibitors. 8-12 weeks of combination DAA treatment -
62
NASH
If inflammation is also present - non-alcoholic steatohepatitis (NASH). Most common cause of liver failure
63
NAFLD risk factors
Risk factors - old age, obesity, diabetes
64
NAFLD Presentation
May complain of RUQ pain due to hepatomegaly.
65
acoholic liver disease, colin
AST > ALT
66
PSC (bile ducts), 4 main points
Males UC itching/pruritus higher ALP than bilirubin
67
PBC (bile ducts), 3 factors
1. Fat, Female, Fifties 2. Jaundice, skin pigmentation, xanthelasma, hepatosplenomegaly 3. AMA positive raised ALP, GGT, mildly raised ALT. AMA positive.
68
Autoimmune Hepatitis, Type 1
Adults
69
Autoimmune Hepatitis, Type 2
children and young adults.
70
Autoimmune Hep, whats raised
1. raised AST and ALT 2.elevated IgG. 3. Presence of ASMA
71
Treatment Autoimmune Hep ,
Immunosuppression - prednisolone and azathioprine.
72
Pancreatitis mnemonic
Causes = GET SMASHED’: Acute G - gallstones (common). E - ethanol. T - trauma. S - steroids. M - mumps. A - autoimmune. S - scorpion venom (NOT COMMON). H - hypertriglyceridemia or hypercalcemia. E - ERCP. D - drugs eg azathioprine.
73
Where is pain for Pancreatitis
Epigastric, to back
74
About Pancreatitis- 6 things
1. Mainly Adenocarcinoma, head of Panc. 2. T1/T2 Diabetics. 3. Painless jaundice 4.steatorrhea 5.dark urine 6. ascites
75
Gallstones, 5 f's
Risk factors - fat, fair, female, fertile, forty.
76
Gallstones pain
epigastric/RUQ pain due to transient cystic duct obstruction, no signs of infection
77
Chronic cholecystitis 3 points
chronic inflammation of the gallbladder, typically caused by gallstones that obstruct the cystic duct damage gallbladder wall.
78
Acute cholecystitis - 4 things whos sign
1. acute GB distension, 2. RUQ pain / shoulder 3. +/- fever. 4. Murphys sign - press hand below right costal margin, hold
79
Cholangiocarcinoma, where?
Cancer of the biliary tree
80
Cholangiocarcinoma causes - 3 things
PSC HCV diabetes,
81
Cholangiocarcinoma symptoms
fever, abdominal pain, malaise, raised bilirubin, raised ALP +/- ascites.
82
test IBD Inflammatory Bowel Disease test
Faecal calprotectin (> 90% sensitive and specific to IBD in adults)
83
Crohn’s Disease (NESTS)
N – No blood or mucous (less common than UC) E – Entire GI tract (mouth to anus) S – “Skip lesions” on endoscopy T – Terminal ileum most affected and Transmural inflammation S – Smoking is a risk factor (don’t set the nest on fire)
84
Chrohn's management
stop smoking: Corticosteroids Prednisolone. Budosenide. Immunosuppression Azathioprine Mercuptopurine Sulfasalazine. Methotrexate.
85
UC
*UC = Up Close (Close UP) C – Continuous inflammation L – Limited to colon and rectum O – Only superficial mucosa affected S – Smoking is protective E – Excrete blood and mucus U – Use aminosalicylates P – Primary Sclerosing Cholangitis
86
Poop classifcation for UC
- mild: < 4 stools/day, only a small amount of blood - moderate: 4-6 stools/day, varying amounts of blood, -severe: >6 bloody stools per day + tachycardia,
87
UC Management Mild / Moderate
First line: 5 ASA - Sulfasalazine - Mesalazine Second line: corticosteroids (e.g., prednisolone)
88
UC severe
-Severe disease Admit to hospital First line: IV corticosteroids (e.g. hydrocortisone)
89
UC maintaining remission
*Maintaining Remission Aminosalicylate (e.g. mesalazine oral or rectal) 5ASA
90
Giardiasis
floating fat poop, non bloody
91
E Coli 0157 -
shiga toxin and increased risk of HUS
92
Incubation period Gastroenteritis
1-6 hrs: Staphylococcus aureus, Bacillus cereus* 12-48 hrs: Salmonella, Escherichia coli 48-72 hrs: Shigella, Campylobacter > 7 days: Giardiasis, Amoebiasis
93
Cholera
severe watery diarrhea and dehydration. It is primarily spread through contaminated water can be treated with rehydration therapy and antibiotics.
94
Irritable Bowel Syndrome
woman, nervous
95
Irritable Bowel Syndrome signs
anxiety / depression female
96
IBS diagnostic, lucie city
Rome III diagnostic criteria Recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months associated with 2 or more of the following: Improvement with defaecation Onset associated with change in frequency of stool Onset associated with a change in the form of stool
97
IBS Management 1st line and 2nd line constipation (x) vs diarrhea ( y)
1st line: Dietary advice ‘If it upsets you, don’t eat it’ Increase fibre in IBS-C, decrease fibre in IBS-D 2nd line: constipation (Fybogel, ispaghula husk) diarrhea ( Loperamide , Imodium)
98
IBS Management 2nd line
Low FODMAP diet (second line) Group of short-chain carbohydrates poorly digested in small intestines leading to fermentation and osmotic changes in large bowel Eliminate all FODMAP for 2-6 weeks, then reintroduce gradually to identify triggers
99
IBS drugs IBS-D IBS-C
IBS-D - anti-diarrhoeals- Imodium (loperamide) IBS-C - Fybogel (bulk forming) that contains ispaghula husk (avoid stimulant laxatives) Patients may be given 4-week trial of probiotics
100
Coeliac
Presentation - diarrhoea and weight loss. Steatorrhoea. Abdominal pain. Bloating. Nausea and vomiting. Aphthous ulcers and angular stomatitis. Fatigue. Weakness. Failure to thrive. Iron deficiency anaemia. Dermatitis herpetiformis. Can be asymptomatic
101
Coeliac investigations
test measures levels of immunoglobulin A (IgA) antibodies against tissue transglutaminase (tTG)
102
PBC - PSC -
Probably Blowing C*** = Females Against Mum's Approval = AMA antibodies Probably Sucking Cl*t = Men Usually Cant finish = UC (association)
103
Bowel intussusception telescope
sigmoid volvulus old person
104
Globus hystericus
nervous
105
mechanism of cirrhosis are: 3 things
Hepatic stellate cells Myofibroblasts Collagen
106
Ursodeoxycholic acid (UDCA) is the
main treatment for PBC
107
Viral hep meds
peggy Peginterferon immune system
108
PSC fibrosis, where
Autoimmune destruction of intra- and extra-hepatic bile ducts resulting in fibrosis
109
direct inguinal hernia Indirect Inguinal Hernia
direct inguinal hernia- pops back out Indirect Inguinal Hernia- stays in
110
Charcot’s triad, which disease
ascending cholangitis Charcot’s triad of ascending cholangitis (RUQ pain, jaundice and fever).
111
colorectal cancer marker
CEA
112
CA-125: CA-19-9: AFP: PSA:
CA-125: ovarian cancer CA-19-9: Panc Cancer AFP: Liver cancer PSA: Prostate cancer
113
immunogoblin is present in nasal secretions
IgA
114
Main resistance vessels
Arterioles, play role in SVR and MAP
115
1. Primary pneumothorax = 2. Secondary pneumothorax= 3. Tension pneumothorax=
1. Primary pneumothorax = <2cm and asymptomatic= No action >2cm or symptomatic= needle aspiration 2nd IC space MCL , if unsuccessful then chest drain 2. Secondary pneumothorax= underlying lung issue. Admit. Chest drain 1st line mid aux line 5th ICS 3. Tension pneumothorax= Large Bore Cannula 2nd ICS M.C.L